Watchman News

Do you enjoy alcoholic drinks every now and then? While it’s commonly believed that moderate drinking is fine,1 growing evidence suggests that alcohol, even in modest amounts, may harm your body. Previous research has shown that it increases your risk for premature death and cancer. Now, there’s a growing body of evidence showing that it also damages your brain, and may increase your risk of dementia.

Any Intake of Alcohol Raises Your Risk for Brain Damage

A study published in Neurology explored how alcohol consumption affects the brain over time, particularly in older adults.2,3 Researchers, based in Brazil, examined brain autopsies from 1,781 people who have an average age of 75 years old at death. Then, they compared those findings to how much alcohol each person drank throughout life as reported by family members. Here’s what they found:

• Defining the parameters of the study — The participants were split into four groups — those who never drank, moderate drinkers (up to seven drinks per week), heavy drinkers (eight or more drinks weekly), and former heavy drinkers who had quit.

A single drink was defined as containing 14 grams (g) of alcohol, which is roughly equivalent to 350 milliliters (mL) of beer, 150 mL of wine, or 45 mL of liquor.

• Those who drank regularly had more vascular brain lesions — Among heavy drinkers, 44% had vascular brain lesions. That compares to 40% for those who never drank, and 50% for former heavy drinkers.

Vascular brain lesions are also known as hyaline arteriolosclerosis, which is the thickening and stiffening of the small blood vessels in your brain. These lesions reduce blood flow (thus oxygen delivery) to brain cells, which may contribute to tissue damage, cognitive dysfunction, and long-term memory problems.

• The presence of lesions persisted even after quitting — Even former drinkers who quit years before death showed lasting damage. This suggests alcohol’s impact on your brain is not only acute, but also cumulative.

• Your lifestyle greatly influences the risk for brain lesions — After adjusting for other health factors like smoking, exercise, and age, heavy drinkers had a 133% higher chance of developing these brain lesions compared to those who never drank.

Former heavy drinkers weren’t far behind, with an 89% increased risk. Even moderate drinkers still had a 60% higher risk for brain damage than lifelong abstainers.

• Alcohol increases your risk for dementia — In addition to vascular damage, the researchers also examined another biomarker of brain degeneration called tau tangles. These are abnormal protein clumps that interfere with neuron function and are linked to Alzheimer’s disease.

Heavy drinkers had a 41% higher risk of developing tau tangles, while former heavy drinkers had a 31% increased risk compared to those who never consumed alcohol.

• Former heavy drinkers had a significantly lower brain mass ratio — This means this test group’s brains were smaller relative to their body size. Shrinking brain mass may set the stage for poor memory, slower thinking, and more difficulty managing daily tasks. Worse yet, this group also scored lower in cognitive function tests.

• Drinking is linked to a shorter lifespan in this study — Heavy drinkers died an average of 13 years earlier than those who never drank.

The findings raise serious concerns. Even if you feel fine now, and even if your drinking is within what’s often defined as “moderate,” your brain may be experiencing asymptomatic injury. These findings raise serious doubts about the assumption that a beer here or there is harmless.

Further Research Shows That No Alcohol Intake Is Safe for Your Brain

A study published in eClinicalMedicine set out to answer a long-standing hypothesis — does alcohol cause dementia, or are the two loosely associated?4

To answer that, researchers analyzed data from 313,958 United Kingdom (U.K.) participants who currently drank alcohol, all of whom were free of dementia when the study began (2006 to 2010). Over a follow-up period that lasted until 2021, researchers tracked those who developed dementia. They categorized alcohol consumption levels and matched these to genetic profiles designed to estimate lifelong alcohol exposure.

• Genes leaning toward higher alcohol intake were more at risk for dementia — Using individual-level analysis, researchers found that every increase in genetically predicted alcohol consumption pushed dementia risk higher. Interestingly, the strongest effects were seen in women. As noted by the researchers:

“Our analyses found a distinctly more significant association between alcohol consumption and dementia risk among women drinkers … who typically had lower rates of other risk factors, such as smoking, compared to men. For men, the presence of multiple risk factors could mask alcohol’s specific effects.”5

• The study also invalidated the idea that there’s a safe range for drinking — The researchers looked for a non-linear relationship — a curve where low-level drinking might be neutral or even protective, but didn’t find one. “Our findings suggested that there was no safe level of alcohol consumption for dementia,” the authors wrote.

• The data is clear regarding alcohol consumption — To check their results, the researchers created positive control criteria — a known consequence of alcohol use — such as alcoholic liver disease. Their model showed that people with alcohol-promoting genes had a much higher risk of liver damage.

Then, the researchers used age as a negative control (something alcohol doesn’t influence) and found no relationship. These comparisons confirmed that their models were functioning properly, and that the dementia link was genuine — not a statistical coincidence.

Cut Back on Alcohol and Repair the Damage Before It’s Too Late

I’ll admit that I bought into the many common myths about alcohol. I used to drink alcohol a few times a year, believing that it was relatively harmless — and even beneficial. But after diving into the research further, I’ve changed my stance.

Now, I don’t drink any alcohol at all, and I recommend you do the same. If you’re drinking regularly, even a few drinks a week, you may be putting your cognition at risk. As noted by the research earlier, there is no safe level of alcohol when it comes to protecting your memory, your ability to think clearly, or your overall brain health. It’s time for you to take control of your brain health again, starting with these strategies:

1. Cut your alcohol intake to zero — The most important step is to stop the damage at its source. If you’re drinking daily, or even several times weekly, this may be impairing blood flow to your brain and contributing to shrinkage in the areas responsible for memory and cognition.

If you’re not ready to quit completely, start by eliminating weekday drinking or limiting yourself to special occasions. But remember, “moderation” isn’t protective like some have suggested — the evidence increasingly challenges that idea. Your brain is better off without it.

2. Take N-acetylcysteine (NAC) before and after occasional alcohol use — It’s thought to support the liver’s handling of acetaldehyde, a byproduct of alcohol metabolism, though this is not a substitute for reducing alcohol intake.

If you choose to explore NAC or B-vitamin support around alcohol use, talk to a healthcare provider about whether it’s appropriate and what dose may make sense for you. But as mentioned earlier, there’s still no substitute for avoiding alcohol completely.

3. Replace alcohol with beverages that nourish you — If alcohol is your way to unwind, reward yourself, or deal with stress, it’s time to change your routine. Switch to other drinks, such as teas, freshly homemade juices with pulp, or pure sparkling water with natural flavors added.

4. Rebuild your mitochondria with healthy carbohydrate intake — Alcohol can impair mitochondrial function. To restore it, you need fuel, and that is glucose.

I recommend aiming for 200 to 250 grams of carbs per day, mostly from sources like white rice, fruit juices with pulp, and whole fruits. This gives your body what it needs to produce adenosine triphosphate (ATP), the energy currency of every cell, especially brain cells. And if you’ve struggled with brain fog or fatigue before, this shift alone has the power to drastically change your health for the better.

5. Start healing your gut to reduce endotoxin load — Alcohol may damage your gut, allowing endotoxins to be produced. Endotoxins are bacterial fragments that leak into your bloodstream and may contribute to inflammation, especially in your brain. To repair your gut, again, stop drinking alcohol. Moreover, add fermented foods into your diet to diversify your gut flora, allowing better crosstalk between your gut and brain.

Strategies for Eliminating Alcohol Consumption

Are you having trouble quitting alcohol? Dr. Brooke Scheller, founder of Functional Sobriety (a nutrition-based program for alcohol reduction) and author of “How to Eat to Change How You Drink,” offers several helpful tips:

1. Get curious and educate yourself — Read books, listen to podcasts, and learn about the health impacts of alcohol.

2. Find community support — Scheller runs an online community called the Functional Sobriety Network. There are many other support groups and resources available as well.

3. Examine your social media — Unfollow accounts that glamorize drinking and follow sober influencers instead.

4. Address the root causes — Look at why you drink — stress, social pressure, habit — and find healthier alternatives.

5. Support your body nutritionally — Supplements like L-theanine, L-glutamine, NAC, B-complex vitamins, and milk thistle are commonly used by some people to help with cravings and support detoxification.

6. Stabilize blood sugar — Increasing protein intake and eating regularly helps reduce alcohol cravings.

7. Be open about your choice — Scheller encourages people to simply say they’re not drinking for their health if asked.

One of the most powerful shifts Scheller advocates for is changing how you think about alcohol in your life in order to reframe your relationship with drinking:

“Previously, the only people who did quit drinking were people that identified themselves as having a problem or maybe had to quit. And so the first thing I’ll say if you’re listening and you’re interested is you don’t have to have a problem to decide that you want to explore this.

You don’t need to even be that regular of a drinker for you to say, ‘You know what? This is something I may want to explore.'”

In other words, choosing not to drink alcohol is a positive, empowering decision for your health and longevity — not a punishment or deprivation.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

Frequently Asked Questions (FAQs) About the Impact of Alcohol on Brain Health

Q: Is moderate drinking safe for my brain?

A: No. Even moderate drinking — defined as seven or fewer drinks per week — raises your risk for vascular brain lesions by 60% compared to people who never drank alcohol. These lesions reduce blood flow and oxygen in your brain, which may contribute to cognitive decline and memory issues over time.

Q: Does quitting alcohol reverse the brain damage?

A: According to the research, the answer is no. Former heavy drinkers in the study had even more brain lesions than current heavy drinkers and showed lower brain mass ratios and worse cognitive function. This suggests alcohol’s damage is long-lasting and accumulates over time, even after you stop.

Q: What exactly does alcohol do to the brain?

A: Alcohol has been linked to hyaline arteriolosclerosis, which is the hardening and narrowing of the brain’s small blood vessels. It also increases tau tangles, which are abnormal proteins linked to Alzheimer’s disease. These changes are associated with shrinking brain tissue, impaired memory, and reduced your ability to think clearly and manage daily tasks.

Q: Is there any safe level of alcohol that doesn’t affect dementia risk?

A: No. Genetic analysis from over 313,958 people showed a direct link between alcohol intake and dementia risk. Researchers found no evidence of a protective effect at any level of drinking — dementia risk increased steadily with every uptick in alcohol consumption.

Q: How can I protect my brain if I’ve been drinking regularly?

A: Start by eliminating alcohol completely to stop further damage. Support your detox pathways with N-acetylcysteine (NAC), repair your mitochondria with healthy carbs like fruit and white rice, and rebuild your gut by avoiding alcohol and adding fermented foods. These steps may help support brain function and reduce further damage.

Short-chain fatty acids (SCFAs) play an important role in human health, particularly within the gastrointestinal tract. They are produced in the colon through the bacterial fermentation of dietary fiber, the indigestible component of plant-based foods.

This fermentation process transforms complex carbohydrates into various SCFAs, including acetate, propionate and butyrate, each with distinct physiological effects. Among these, butyrate stands out for the properties that have drawn the most research attention in metabolic health.

A Primer on Butyrate — The Metabolic Powerhouse Fueling Your Gut

According to a review published in Pharmacological Research,1 butyrate has been reported to improve “body weight and composition, lipid profile, insulin sensitivity, and glycemia in animal models of MetS [metabolic syndrome].” The same review cautions that these animal results may not translate to people, because butyrate has poor systemic availability and is rapidly cleared, and notes that human trials to date have not demonstrated substantial benefit. But that’s not all researchers have examined. They also noted:

“In vitro studies have examined the influence of butyrate on intestinal cells, adipose tissue, skeletal muscle, hepatocytes, pancreatic islets and blood vessels, highlighting genes and pathways that may contribute to its beneficial effects. Butyrate’s influences in these cells have been attributed primarily to its epigenetic effects as a histone deacetylase inhibitor, as well as its role as an agonist of free fatty acid receptors.” 2

While fiber is essential for butyrate production, you need a healthy gut microbiome to reap the benefits of fiber. As discussed in my book “Your Guide to Cellular Health,” the vast majority of the population have damaged microbiomes due to exposure to metabolic poisons.

For these individuals, high fiber intake exacerbates existing issues by fueling pathogenic bacteria, leading to the production of endotoxins that compromise cellular energy and overall health. Later, I’ll explain why this occurs, as well as strategies to repair your gut health, enabling it to process fiber in a way that supports your health.Butyrate Is a Primary Fuel for Your Gut Lining

Unlike most cells in your body that rely on glucose for energy, your colonocytes draw heavily on butyrate. This metabolic adaptation highlights butyrate’s role in maintaining the health and function of your colonic epithelium, though previous reviews question whether butyrate is their exclusive preferred fuel.

Butyrate is transported into your colonocytes through several mechanisms, including passive diffusion, which is concentration-dependent, and active transport via other cell membrane transporters.3 Once inside your colonocytes, butyrate undergoes beta-oxidation within the mitochondria, your cells’ powerhouses.

This metabolic pathway breaks down butyrate into acetyl-CoA to generate ATP, the primary energy currency of your cells.4,5 This process is remarkably efficient, providing your colonocytes with up to 70% to 80% of their energy needs, a substantially higher proportion compared to other energy substrates like glucose or glutamine.6

This efficient energy use is central to maintaining colonocyte health.7,8 Furthermore, butyrate’s role as a primary fuel source for your colonocytes contributes to their ability to remove oxygen from your colon, which helps create the ideal environment for your beneficial gut bacteria to grow.9The Impact Butyrate Has on Your Gut Barrier Function

Your gut barrier, a dynamic and complex structure composed of a single layer of epithelial cells connected by tight junctions, along with a protective mucus layer, plays a vital role in selectively regulating the passage of substances between your gut and your bloodstream.

It prevents the entry of harmful bacteria, toxins and undigested food particles while allowing the absorption of essential nutrients. But how does it protect, to be exact? As explained in a narrative review published in Clinical Nutrition10 — drawing largely on rat, pig, and cell-culture studies:

“Butyrate strengthens the gut barrier by targeting three complementary elements: tight junctions, the mucus layer and the production of antimicrobial peptides. Many tight junction proteins are upregulated by butyrate (e.g., TJP1, claudin 7, cadherin 1 in the rat ileum; TJP1, claudin 3 and occludin in pig colons).

Tight junction protein 1 (TJP1; previously named ZO1) is particularly important, as it modulates tight junctions and is commonly used as a marker of intestinal permeability. In contrast, claudin 2, a tight junction protein that forms gap channels and contributes to a leaky gut barrier, is downregulated by butyrate …

In addition to altering the expression of tight junction proteins, butyrate promotes tight junction assembly by activating AMPK, reducing the permeability of colon cancer cell monolayers.”*

As noted earlier, the absorption of butyrate by the colonocytes also reinforces the colon, which may help limit inflammation and immune activation.11,12 Disruptions to gut barrier function have been linked to various gastrointestinal disorders, as well as metabolic diseases, according to a 2021 study published in Metabolites.13

*These findings are from laboratory or animal research and may not directly apply to human health.

Butyrate and Its Impact on Inflammation

Butyrate has been studied for its anti-inflammatory action, which it appears to exert through a variety of intricate mechanisms. A review published in Immune Network14 outlines mechanisms by which butyrate may down-regulate inflammation driven by pathogenic gut bacteria:

“Butyrate can down-regulate inflammation by inhibiting the growth of pathobionts, increasing mucosal barrier integrity, encouraging obligate anaerobic bacterial dominance and decreasing oxygen availability in the gut.

Butyrate can also decrease excessive inflammation through modulation of immune cells such as increasing functionalities of M2 macrophages and regulatory T cells and inhibiting infiltration by neutrophils.”15

What Animal Research Suggests About Butyrate and Body Weight

Research in mice published in the journal Gut16 found that butyrate influenced energy expenditure. In these animals, colon-absorbed butyrate was associated with increased energy expenditure in tissues including muscle, liver, and white and brown fat.

Additionally, the researchers observed that butyrate promoted fat oxidation and reduced fat accumulation in these mice. Oral butyrate also lowered food intake, an effect the authors attributed to appetite-regulating pathways in the gut and brain.

As reported by the authors,17 “Butyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating Bat [brown adipose tissue].”

Supporting these findings, a 2023 review published in Frontiers in Endocrinology18 — drawing predominantly on rodent research — reported associations between butyrate and measures of body weight, fat mass, and glucose regulation. In the animal studies reviewed, butyrate supplementation was associated with improvements in fasting glucose, insulin levels, markers of insulin resistance, and plasma triglyceride levels. According to this featured review:19

“Butyrate reduced lipid accumulation by regulating liver mitochondrial function, reducing liver mitochondrial energy efficiency and improving the capability of mitochondria to utilize fat as metabolic fuel …

Short-term oral administration of butyrate can alleviate diet-induced obesity in mice by stimulating mitochondrial function in skeletal muscle. Butyrate has also been reported to increase the number of mitochondria in skeletal muscle.”*

Similarly, a review published in Molecules20 described animal research in which butyrate reduced food intake by suppressing appetite. The same review reported effects on liver fat accumulation in mice fed a high-fat diet. “[Butyrate] is able to downregulate the expression of nine key genes involved in the intestinal cholesterol biosynthesis pathway and thereby it may inhibit hypercholesterolemia,” the researchers noted.21

*These findings are from laboratory or animal research and may not directly apply to human health.

Dietary Fiber Helps Produce Butyrate, but There Are Caveats

As shown in the featured studies, butyrate is far more than a simple metabolic byproduct. It serves as a major energy source for your colonocytes and supports your gut barrier, and research — much of it in animal and laboratory models — suggests it may also influence insulin sensitivity, inflammatory signaling, and appetite regulation.

In short, butyrate plays an important role in maintaining your gut health and overall well-being. However, while promoting butyrate production through dietary interventions like increasing fiber intake is generally recommended, this assumes that you have a properly functioning gut.

As I discuss in my book “Your Guide to Cellular Health,” for those with compromised gut health, simply going for a high-fiber intake to promote SCFA production is highly counterproductive. Why? Because when you eat fiber with an imbalanced gut microbiome, the bad bacteria (oxygen-tolerant bacteria) can ferment the fiber and produce endotoxins that undermine metabolism and cellular function.

To truly benefit from a high-fiber diet, you need to first heal and seal your gut so that beneficial bacteria can thrive. Getting enough carbs is an important part of that process.Building Your Gut from the Ground Up

Most adults need about 250 grams of targeted carbs a day from healthy, unprocessed sources — considerably more if you are very active. For most people with ordinary digestive complaints, well-cooked white rice and whole fruits are the place to start. Ripe, whole fruits provide essential nutrients, healthy carbohydrates and dietary fiber that your gut needs to produce butyrate and other SCFAs. As a bonus, your bowel movements may also become more regular.

If your gut is severely compromised, I recommend you kickstart your gut-healing with dextrose water. Simply mix pure dextrose with water and sip slowly over several hours to avoid spiking your insulin levels. After one to two weeks, start the transition to increasingly more complex carb sources — fruit juice with pulp, then pulp-free juice sipped slowly, then whole fruits, and finally complex carbs and starches like white rice.

Now, the question is, how do you know if you have a healthy gut? As detailed in “Your Guide to Cellular Health,” the five indicators of good gut health are:

• Regular bowel movements (one to three times daily)

• Minimal bloating or discomfort

• The ability to digest a wide variety of food

• Good energy levels

• Proper nutrient absorption Again, once your gut is functioning well, the key to increasing your butyrate production lies in dietary fiber. Think of it as the raw material for the butyrate “factory” in your gut. When you eat fiber-rich whole foods, your gut bacteria ferment that fiber, producing SCFAs as a byproduct. If your digestion still is not where you want it, build up to these gradually. Excellent sources of dietary fiber include fruits (like apples, berries and bananas) and vegetables (especially leafy greens, broccoli and carrots). Other gut-friendly carbs include:

• Well-cooked white rice

• Sourdough bread

• Root vegetables like potatoes and sweet potatoes

• Fresh, ripe fruits

• Masa harina, or traditionally made tortillas

Limit Linoleic Acid to Support Butyrate Production

Another dietary factor that impacts your gut health is excess intake of linoleic acid (LA), which I believe is one of the biggest contributors to metabolic dysfunction and poor gut health when consumed in large amounts. To be clear, your body still needs small amounts of LA to function optimally. However, the issue is that LA is so pervasive in the modern food supply, particularly in ultraprocessed foods.

A laboratory study of bacterial cultures published in Scientific Reports22 found that LA induced metabolic stress in Bifidobacterium breve DSM 20213, a beneficial gut bacterium, altering biosynthetic pathways for amino acids, carbohydrates and fats and slowing its growth.

Given LA’s pervasive presence in ultraprocessed foods, keeping its intake in check is an important part of protecting your health and supporting butyrate production. I recommend limiting your LA intake to less than 5 grams a day.

Keep in mind that LA is an essential fat — your body does require small amounts of it — so the goal is to return to the historical intake range, not to drive it toward zero.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.

Type 2 diabetes involves far more than high blood sugar. It’s characterized by high blood sugar because your body’s cells stop responding normally to insulin, making it harder to move glucose from your bloodstream into your tissues for energy. Early signs often include increased thirst, frequent urination, fatigue, blurry vision, slow-healing cuts and frequent infections. Left unchecked, it raises your risk of heart disease, kidney failure, nerve damage and vision loss.

Most conversations about diabetes risk begin and end with body weight, but that leaves out an important part of the picture. Your muscles are active metabolic tissue, and when they weaken or shrink while body fat increases, the metabolic consequences go well beyond what a bathroom scale can capture. Doctors call this combination of excess body fat and declining muscle mass and strength sarcopenic obesity, and it carries a metabolic risk far greater than either problem on its own.

Research confirms that this combination deserves far more attention than it currently receives, revealing that muscle health reshapes long-term diabetes risk in ways that weight alone can’t explain. The findings also highlight groups you might not expect to be most affected, reinforcing that muscle preservation is an investment worth making well before it feels urgent. So, what exactly does the evidence show, and why do your muscles hold so much influence over blood sugar control?

Muscle Strength Predicts Diabetes Risk Better Than Weight Alone

For a study published in Diabetes Care, researchers followed 479,607 adults from the UK Biobank who did not have Type 2 diabetes when the study began to determine whether having both excess body fat and poor muscle health created a greater diabetes risk than either condition alone.1

The researchers evaluated body composition, comparing body fat with measures of muscle strength and muscle mass to identify who developed Type 2 diabetes over time. The study also included a landmark analysis involving 53,107 participants to examine what happened when people’s body composition changed over time.

This allowed the researchers to determine whether improving or worsening muscle health altered future diabetes risk instead of simply capturing a single snapshot at the beginning of the study. Because of the study’s exceptionally large size and median follow-up of 14.2 years, the findings provide one of the strongest looks yet at how muscle health influences your long-term metabolic health rather than just your current condition.

• Losing muscle while gaining body fat created the greatest diabetes risk — During the follow-up period, 32,948 participants developed Type 2 diabetes. Researchers found that the combination of excess body fat and poor muscle health carried a substantially greater risk than either problem alone.

When researchers compared different body composition groups, they found that people with both excess body fat and low muscle mass and strength were more than 3.5 times more likely to develop Type 2 diabetes than those with healthy body composition. By comparison, obesity alone and low muscle mass alone each carried lower risks.

• Future risk changed when body composition changed — Researchers also looked at what happened when people’s body composition changed over time. They found that participants who developed sarcopenic obesity faced a sharply higher risk of developing Type 2 diabetes than those who maintained healthy body composition.

People who remained in this state over time faced an even greater risk, showing that the longer someone had both excess body fat and poor muscle health, the more their diabetes risk increased.

• Some groups faced even greater risk than others — Researchers found that women and adults younger than 60 experienced a larger increase in Type 2 diabetes risk from sarcopenic obesity than men and adults 60 and older.2 That finding challenges the common belief that muscle loss only becomes important late in life. The results suggest muscle preservation deserves attention decades before most people begin thinking about age-related muscle decline.

• Researchers showed muscle health adds information that body weight misses — The researchers concluded that evaluating both body fat and muscle health provides a more complete picture of who faces the greatest future risk for Type 2 diabetes. In practical terms, two people with similar body weights don’t necessarily have the same metabolic health. One person might carry more healthy muscle, while the other has less muscle and more body fat.

Although the scale shows similar numbers, their future diabetes risk could look very different. The researchers concluded that these findings support an “integrated assessment of muscle health and adiposity” when identifying people at higher risk for Type 2 diabetes. Put simply, muscle deserves a place beside body fat as a core measure of metabolic health, not an afterthought.

Protect Your Muscle to Protect Your Metabolism

Protecting your muscles is one of the most effective ways to lower your long-term risk of Type 2 diabetes. The goal isn’t simply to lose weight — it’s to build and preserve the muscle that helps your body regulate blood sugar every day. Focus on improving body composition because stronger muscles and less excess body fat work together to support a healthier metabolism.

1. Make muscle your first priority instead of focusing only on weight loss — If you’re trying to lose weight, don’t sacrifice muscle in the process. Losing muscle while losing fat works against your metabolism because muscle uses glucose for energy. Strength training several times each week, combined with regular daily movement such as walking, gives your muscles the stimulus they need to stay strong.

The research showed that people with both excess body fat and poor muscle health faced the greatest diabetes risk. That means preserving muscle isn’t simply about appearance; it’s one of the most effective ways to support healthy blood sugar and metabolic health over the long term.

2. Train smarter instead of simply training longer — More exercise isn’t always better. Research discussed by cardiologist Dr. James O’Keefe shows that strength training has a “sweet spot.”3 The greatest health benefits come from moderate amounts of resistance exercise, while excessive training causes those benefits to level off and eventually decline.

Keep most strength-training sessions to about 20 to 40 minutes, using a weight that becomes challenging after about 10 repetitions. Give your muscles a day or two to recover before the next workout. For most people, two or three strength-training sessions each week provide the greatest long-term benefit.

Once total strength-training time climbs beyond roughly two hours per week, the additional health gains become much smaller, and after about three to four hours weekly, they continue to decline.

3. Eat enough protein and healthy carbohydrates to support muscle growth — Your muscles need both building materials and fuel. I recommend aiming for about 0.8 grams of protein per pound of lean body mass (about 1.76 grams per kilogram), with one-third coming from collagen-rich sources like slow-cooked meats or bone broth.

Pair that with enough healthy carbohydrates to support cellular energy production. Most adults need about 250 grams of carbohydrates each day. Start with whole fruit and white rice if you have digestive issues, gradually adding in other well-tolerated carbohydrate sources as your gut health improves. Better fuel helps your muscles perform better during exercise and recover afterward.

4. Prioritize sleep to protect the muscle you’re building — Your muscles don’t grow during your workout — they grow while you recover, and sleep is when the bulk of that repair happens. During deep sleep, your body releases growth hormone, which drives muscle protein synthesis and tissue repair. Cut that short and the process stalls.

Poor sleep also raises cortisol, your body’s primary stress hormone, which breaks down muscle tissue and worsens insulin resistance, the exact combination this research links to the highest diabetes risk.

To support high-quality sleep each night, keep your bedroom cool and completely dark, stop eating at least three hours before bed and limit blue light exposure in the evening. If you’re doing everything right with training and nutrition but not seeing results, insufficient sleep is one of the first places to look.

5. Use blood flow restriction (BFR) training if heavy weights aren’t an option — If you’re older, have joint pain or are recovering from an injury, BFR, also called KAATSU training, offers another way to build muscle without lifting heavy weights. During BFR training, specialized bands partially restrict blood flow while you exercise with very light weights or, if you’re frail, even just your body weight.

This brief reduction in oxygen inside the working muscles stimulates muscle growth and increases the release of myokines, which are signaling proteins your muscles produce that support muscle repair and healthy metabolism. Because the resistance is so light, BFR places much less stress on your joints while still helping preserve or increase muscle mass. It also requires far less recovery time than traditional heavy lifting.

6. Measure your progress by your waist and strength, not just your weight — A bathroom scale doesn’t tell you how much muscle you’ve gained or lost. If your weight stays the same while your muscle increases and body fat declines, your metabolic health is moving in the right direction. To monitor your fat profile, track your waist-to-hip ratio.

To calculate it, divide your waist measurement by your hip measurement (using the same unit, such as inches or centimeters). Once you have the number, you can see how it lines up with risk categories:

Waist-to-hip ratio
Men
Women

Ideal
0.8
0.7

Low risk
0.85

You can also track grip strength at home with an inexpensive hand dynamometer; healthy grip strength generally falls above 72 pounds for men and 44 pounds for women, and improvements over time are one of the most reliable signs that your overall muscle health is heading in the right direction.

FAQs About Muscle Health and Type 2 Diabetes

Q: Why does muscle health matter if I’m more concerned about losing weight?
A: Muscle does much more than help you move. It’s one of the largest tissues in your body that actively absorbs glucose from your bloodstream, which directly helps keep blood sugar under control. The research found that people who had both excess body fat and poor muscle health faced a much higher risk of developing Type 2 diabetes than people with healthy muscle, showing that preserving muscle is just as important as reducing excess fat.

Q: Is muscle loss only a concern for older adults?
A: No. While muscle loss becomes more common with age, this study found that the link between poor muscle health and Type 2 diabetes was especially strong in adults younger than 60 and in women. That means protecting your muscle should begin long before you reach retirement age.

Q: How much strength training is enough to support healthy muscles?
A: More isn’t necessarily better. Research suggests that two or three resistance-training sessions per week, lasting about 20 to 40 minutes each, provides the greatest long-term health benefits for most people. Training far beyond that amount offers diminishing returns and can reduce some of the advantages associated with regular strength exercise.

Q: What if I can’t lift heavy weights because of joint pain or an injury?
A: BFR, also called KAATSU training, allows you to stimulate muscle growth using very light weights or even just your body weight. Because it places much less stress on your joints than traditional weightlifting, it offers an effective option for older adults and anyone who can’t safely perform heavy resistance exercise.

Q: What’s a better way to measure progress than watching the number on the scale?
A: Focus on changes that reflect better body composition instead of body weight alone. Improvements in strength, waist size and muscle mass provide a clearer picture of your metabolic health than the scale by itself. Two people can weigh the same yet have very different diabetes risk depending on how much muscle and body fat they carry.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

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In health communication, what does “identification” mean?

Remembering the facts in a message
Comparing several health recommendations
Understanding how a biological process works
Recognizing yourself in the person or situation
Identification occurs when people see their own experiences reflected in a story or situation, making the health message feel more personally relevant. Learn more.

Many chronic diseases, from heart disease and Alzheimer’s to cancer, share one thing in common — chronic inflammation. But while inflammation is thought to play a key role in disease progression, pinpointing where it occurs in the body has always been a challenge. Standard blood tests measure broad markers like C-reactive protein (CRP), but they fail to identify specific tissues or organs affected by inflammation.1

A study published in the journal Proceedings of the National Academy of Sciences2 (PNAS) has found a way to detect inflammation in specific areas using antibodies. This innovation could open the door to highly targeted diagnostic tests, allowing earlier detection of inflammatory diseases. These findings come from laboratory work in cell, animal, and human tissue samples, but the approach has not yet been validated as a clinical blood test.

How Does Inflammation Work?

Inflammation is how your body responds to threats, whether from injury or infection. It mobilizes immune cells, increases blood flow, and activates signaling molecules to contain damage and promote healing. But for this process to work properly, the immune system needs to maintain a balance between inflammation and resolution. When this stability is disrupted, inflammation becomes chronic, leading to long-term health problems.3
• Your body’s first line of defense — When you get injured or are exposed to harmful bacteria, your immune system jumps into action. Specialized immune cells called macrophages act like sentries, constantly patrolling your body. They detect distress signals from damaged cells or foreign invaders and respond quickly to keep you safe.4

• Cellular “alarms” trigger an immune response — When your immune system detects a threat, it sounds the alarm by releasing signaling molecules called cytokines and chemokines. These act like emergency alerts, calling in more immune cells to help. Cytokines also control how strong and long-lasting the inflammation is, making sure your body responds appropriately.5

• Increased blood flow fuels the battle — When your immune system detects a threat, your blood vessels widen to increase blood flow to the area. This delivers immune cells, including neutrophils, which attack invaders and clear out damaged tissue. Along with oxygen and nutrients, this surge helps fight infection and start the healing process, causing redness, swelling, and warmth, the classic signs of inflammation.6

• Immune cells attack and clear the threat — When your body detects a threat, neutrophils are the first to arrive. They quickly engulf harmful particles and release antimicrobial substances to kill invaders. If the threat persists, macrophages take over, clearing pathogens and cellular debris, while T-cells coordinate the immune response and destroy infected cells to prevent further damage.7

• Shutting down inflammation for recovery — Once the infection or injury is under control, your immune system releases anti-inflammatory molecules to slow down the response. This helps limit unnecessary damage to healthy tissue and helps your body transition from defense to repair.8,9

To learn more about the key differences between acute and chronic inflammation, early warning signs, and how to restore balance, check out “Warning Signs of Acute and Chronic Inflammation in the Body.”

Will This Approach Change How Inflammation Is Diagnosed?

The featured study, conducted by researchers at Case Western Reserve University,10 highlights a new antibody-based method to track traces of inflammation, pinpointing it at its source. This approach could offer a more precise way to detect inflammation-driven conditions.11

• A unique chemical reaction enables detection — Researchers found that when reactive oxygen species (ROS) — highly reactive molecules that damage DNA, proteins, and lipids — interact with certain compounds, they create a distinct chemical reaction. This reaction leaves a detectable marker, allowing antibodies to track inflammation at its source.12

• The role of reactive oxygen species — During inflammation, your immune cells release ROS to kill bacteria and fight infections. These molecules also come from environmental sources like UV light, pollution, radiation, and smoking. While ROS helps protect you, too much damages your cells and tissues and contributes to disease.13

• How ROS interact with fats in your cells — Researchers found that ROS reacts with linoleic acid (LA), a type of omega-6 fat in all cell membranes. This interaction creates compounds called epoxyketooctadecenoic acids (EKODEs), leaving behind markers that can be used to detect inflammation.14

• A breakthrough in biomarker detection — The study also found that EKODEs form a unique bond with cysteine, an amino acid. These compounds build up in tissues under oxidative stress, including the brain, heart, and liver. By raising antibodies against the EKODE-cysteine adduct in rabbits, the team detected these markers in human cells and brain tissue as well as in mouse tissue, paving the way for more precise inflammation detection.15

• Linking EKODEs to disease — The researchers aim to map EKODEs to specific diseases by identifying which organs and conditions these markers are most strongly associated with. One area of focus is the eye, where the team plans to examine EKODEs produced in response to age-related macular degeneration and diabetic retinopathy, both of which can lead to vision loss.16

The authors believe these findings could pave the way for a simple blood test that detects inflammation in specific organs. “This research opens up an amazing number of pathways for future studies,” said Greg Tochtrop, Ph.D., professor of chemistry at Case Western Reserve and senior author of the study. “It will lead directly to better understanding inflammation and detecting diseases, as well as to discovering new drugs.”17

How Lipid Peroxidation Products Fit into the Bigger Picture of Inflammation

While the groundbreaking inflammation detection method highlighted in this article offers new insight into chronic disease, understanding the molecular players driving inflammation will empower you to take control of your health at a deeper level. As biochemical reviews describe,18 EKODEs are just one of several lipid peroxidation products formed when polyunsaturated fats (PUFs), particularly LA, oxidize.

Two others that have been studied extensively are 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA), which also exert wide-ranging effects on your biological systems.19 These are signaling molecules that appear to protect or damage depending on how they interact in your cells. Their activity may help explain why inflammation can spiral out of control and why spotting them matters:

• EKODEs are double-edged signalers — EKODEs (epoxy-keto fats) feature both an epoxide ring and a keto group, giving them distinct bioactive properties. At low concentrations, EKODEs activate pathways that influence antioxidant defenses, inflammation, and metabolism. In animal studies, oxidized linoleic acid products have also been shown to influence pain signaling, though this work is early and has not been established for EKODEs specifically.20

However, when levels spike during oxidative stress, like in chronic disease, they appear to become damaging — modifying proteins, disrupting membranes, and amplifying cellular dysfunction. In this model they act as mediators in inflammation, tipping the balance between adaptation and damage.

• 4-HNE is a potent messenger of stress — 4-HNE is a highly reactive aldehyde that activates Nrf2 to boost detoxification enzymes. It can also increase cytokines, your body’s inflammatory alarm system. At low levels, 4-HNE acts as a signaling molecule that promotes cellular adaptation.

At high levels, 4-HNE shifts to a destructive role, binding to mitochondrial proteins, and promoting apoptosis in laboratory studies. Reviews of lipid peroxidation report elevated 4-HNE in conditions ranging from Alzheimer’s21 to atherosclerosis, though these are associations rather than demonstrated causes.22

Its electrophilic nature lets it “tag” proteins on cysteine or lysine residues, altering their function in ways that either support survival or accelerate cellular dysfunction. In inflammation, 4-HNE appears to shape both the magnitude and trajectory of the response.

• MDA is the silent cross-linker — Malondialdehyde, the dialdehyde cousin, plays a less overt — but equally damaging — role in oxidative stress. It excels at cross-linking proteins and DNA, leaving a trail of damage. It’s less a direct signaler and more a saboteur, quietly amplifying inflammation by compromising your cellular machinery.

Although MDA influences stress pathways indirectly, its real danger lies in chronic accumulation — elevated MDA has been observed in diabetes, aging, and cancer, where it is thought to erode structural integrity. MDA’s presence is treated as a marker of unresolved long-term oxidative stress.

• The interplay between these three compounds — These three lipid-derived compounds don’t act independently. During oxidative stress, they interact within the same biochemical environment, competing for nucleophilic targets — cysteines and lysines on proteins — and diluting each other’s effects. For example, if 4-HNE tags a key enzyme first, it blocks subsequent interactions by EKODEs.

In high-stress states (say, a heart attack or chronic infection), they are proposed to act together and overwhelm antioxidant defenses like glutathione — 4-HNE compromising mitochondria, MDA cross-linking DNA, and EKODEs destabilizing membranes.

At lower levels, EKODEs have been shown to activate antioxidant-response pathways, which may curb 4-HNE’s and MDA’s effects and offer a protective counterbalance. Note that this interplay is described from laboratory work and has not been mapped out in people.

• Why this matters to you — The behavior of these compounds serves not just as a scientific explanation but as a roadmap. These lipid peroxidation products are measurable (via assays like TBARS for MDA or mass spectrometry for 4-HNE), and their levels reflect your oxidative load.

The diagnostic approach discussed in this article could, in theory, spotlight their activity indirectly. Think of it as a window into their influence on your inflammatory response. That said, talk to your health care provider about whether this testing is appropriate for you should you be interested in it.

It’s also worth noting that what presents as oxidative stress often traces back to a deeper problem in how your cells produce energy — a reductive shift in the mitochondria that leaves reactive oxygen species with nowhere to go.

Seen this way, lowering lipid peroxidation isn’t just about neutralizing damage; it’s about restoring the cellular energy production that keeps these products in check in the first place.

The good news is that these lipid peroxidation products are factors you can influence. Understanding how they interact helps explain where inflammation begins. Research in this area points toward familiar levers: Dietary patterns that support the body’s own antioxidant response, and reducing omega-6 load by removing vegetable oils from the diet.

Is Our Understanding of Chronic Inflammation Flawed?

While researchers at Case Western Reserve University23 have identified biomarkers that reveal inflammation in specific organs, a new hypothesis-and-theory paper published in Frontiers in Immunology24 — a single-author framework proposal rather than new experimental data — challenges the long-held belief that chronic inflammation is simply unresolved acute inflammation. Instead, it suggests that chronic disease stems from a loss of anti-inflammatory mediators, not just excessive inflammatory signaling.

• Inflammation versus unalamation — Experts have long believed that chronic inflammation happens because the immune system stays too active. However, the author proposes that it results from a loss of anti-inflammatory mediators, disrupting a balance called unalamation. This challenges the conventional idea that suppressing inflammation is the ideal treatment.25

• The role of unalamation in health and disease — Your body uses inflammatory mediators like prostaglandins and cytokines to fight infections, heal wounds, and maintain tissues. Unalamation is the balance between these inflammatory and anti-inflammatory signals. When anti-inflammatory mediators drop too low, inflammation persists, even without an injury or infection, leading to long-term health problems.26

• Why standard anti-inflammatory drugs fall short — NSAIDs and other inflammation-blocking drugs help with short-term inflammation but do not, in this framework, correct chronic conditions like arthritis, heart disease, or neurodegenerative disorders. This is because they block inflammatory signals without restoring the missing anti-inflammatory ones, leaving the underlying imbalance unaddressed.27

• Cancer and the unalamation connection — The author also revisits the idea that chronic inflammation drives cancer. Tumors contain both inflammatory and anti-inflammatory signals, which suggests that they grow in a state of heightened unalamation, not just inflammation.

This may explain why blocking inflammation alone doesn’t stop cancer and, the author proposes, why unalamation may be worth investigating as a therapeutic direction. Again, keep in mind that this is a hypothesis, not a demonstrated treatment approach.28

This emerging research reshapes how we approach inflammation-related diseases. Instead of merely shutting down inflammatory pathways, future therapies may need to restore the body’s natural balance of pro- and anti-inflammatory mediators, offering a more sustainable path to healing.

What Are the ‘Four E’s’ That Drive Inflammation?

To break free from inflammation, it would be wise to address its root causes, not just treat symptoms. Today’s diets, daily habits, and environmental exposures create a constant inflammatory burden and overwhelm your body’s ability to maintain balance. I believe there are four primary drivers of inflammation — what I call the “Four E’s”:

1. Excess LA — An omega-6 polyunsaturated fat (PUFA), LA is found abundantly in vegetable oils and ultraprocessed foods. LA is essential in small amounts and required for mitochondrial function — the problem is quantity, not the fat itself.

In excess, LA is one of the most harmful components of the Western diet, and has been reported to negatively affect your metabolic health and gut microbiome,29 which are two of the most important factors for maintaining proper inflammatory responses and overall health. I recommend keeping LA intake between 2 and 5 grams per day.

2. Electromagnetic fields (EMFs) — EMFs are generated by everyday electronic devices such as cell phones, Wi-Fi routers, and microwaves, causing unseen harm to your health. In a mechanism laid out in Pall’s review of EMF effects,30 EMFs activate voltage-gated calcium channel (VGCC) receptors in your cells, leading to an influx of calcium ions. This surge in calcium is thought to catalyze the production of peroxynitrite, a potent oxidant that contributes to cellular stress and inflammation.

3. Endocrine-disrupting chemicals (EDCs) — Exposure to EDCs significantly impacts your health by over-activating estrogen receptors in your body. Microplastics are alarmingly prevalent in our environment, with research suggesting that the average person ingests the equivalent of a credit card’s weight in plastic each week.31

Plastic is often laden with harmful substances like phthalates and bisphenol A (BPA), both of which bind to estrogen receptors and disrupt normal hormonal functions. Elevated estrogen has been shown to raise intracellular calcium levels in cell studies,32 which is thought to drive the generation of peroxynitrite — a mechanism proposed to exacerbate inflammation and contribute to various chronic health conditions.

4. Endotoxins — Consuming ultraprocessed foods loaded with vegetable oils and high-fructose corn syrup (HFCS), as well as exposure to EDCs, disrupts your gut microbiome, increasing endotoxin production and systemic inflammation. Endotoxins are toxic substances released from the cell walls of certain bacteria, particularly gram-negative bacteria.

These bacteria are facultative anaerobes, meaning they thrive in both aerobic (with oxygen) and anaerobic (without oxygen) environments. This adaptability allows them to colonize various areas in the body, including the gut, where they contribute to inflammation.

When endotoxins from these bacteria enter the bloodstream — often due to a compromised gut barrier (leaky gut) — they trigger a strong inflammatory response known as endotoxemia. In review articles, this condition has been linked to various health issues, including metabolic syndrome and autoimmune diseases.33,34,35

Reducing these four inflammatory stressors lowers the burden on your system and supports the conditions your body needs to restore its natural balance of pro- and anti-inflammatory mediators. Learn how to address these root causes of inflammation in “Cellular Health Revolution — Unveiling Hidden Threats and Empowering Solutions.”

Frequently Asked Questions (FAQs) About Inflammation and Chronic Disease Q: Why is it hard to detect the exact location of inflammation?

A: Standard blood tests only measure broad inflammatory markers like CRP, which indicate inflammation but don’t reveal where it’s happening in the body. The new antibody-based test could change that by identifying inflammation in specific organs.

Q: What is unalamation, and why does it matter?

A: Unalamation refers to the functional balance between inflammatory and anti-inflammatory mediators. Chronic inflammation may not be caused by too much inflammation but rather by too little anti-inflammatory activity.

Q: Why do NSAIDs fail to treat chronic inflammation?

A: NSAIDs and other anti-inflammatory drugs block inflammatory mediators but do nothing to restore missing anti-inflammatory signals. Without correcting the underlying imbalance, inflammation persists.

Q: Is chronic inflammation really the cause of cancer?

A: One Frontiers in Immunology hypothesis paper proposes that tumors exist in a state of heightened unalamation, not just chronic inflammation. This means both inflammatory and anti-inflammatory mediators are present in excess, creating an environment the author argues may favor tumor growth. This is a proposed framework, not an established finding.

Q: What are the best ways to restore balance and fight chronic disease?

A: Researchers working in this area propose that, rather than blocking inflammation alone, future therapies may need to replenish anti-inflammatory mediators, reduce oxidative stress and support mitochondrial function. These are research directions rather than established treatments.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.

If you have ever abandoned a supplement routine, the problem may not have been discipline. It may have been its complexity. Most supplement routines ask you to add tasks to a day that already has too many, and before you know it, the routine of taking it falls by the wayside.

For a supplement to make a difference in your health, the formula needs to be designed for optimal effectiveness, yes, but it also needs to fit into the life you lead. This article series has addressed both sides of that proverbial coin: the science behind better nourishment and the everyday conditions that decide whether you can keep the practice in place long enough for it to matter.

The scientific rationale comes first. Nutrient form, amount, absorption, and delivery all matter. A poorly formulated supplement will have minimal impact even if you take it religiously. But the reverse also matters. A strong formula will do nothing for you if it sits untouched in a cabinet.

Most supplement makers will explain the chemistry of their product but leave it up to you to solve the adherence problem. They tell you what the nutrient does, but not how the routine fits into travel, fatigue, family life, or the week when everything gets off track. Health care often treats those details as secondary but in real life, they are central. The best routine is the one that respects both sides of the problem: the science of what goes into your body and the reality of how you live.

Why Identification Matters

People rarely change because they understand a biological mechanism. They change when the message feels relevant to them. That is why narrative health communication matters. Research in health messaging suggests stories can be more persuasive than plain informational messages because they allow people to identify with the situation, the problem, and the person in the story.

The notion that a narrative tends to be more persuasive for changing a health behavior than the same information delivered as bare facts and figures is well established in communication research.1

A 2022 study put that idea to a direct, head-to-head test. Researchers compared three ways of encouraging the very same health action — a personal story, a brief factual example, and a plain informational message — and the story produced a stronger intention to act than the dry, informational version did.2

More revealing was why. The story worked through two linked mechanisms the researchers measured: “transportation,” the feeling of being drawn into a narrative and carried along by it, and “identification,” the sense of recognizing yourself in the person or situation. Once people were absorbed in the story and saw themselves in it, the message took hold.

The relevance to a supplement routine is direct. Dosages and absorption pathways gives you nothing to step into or recognize yourself in. A routine described in the terms of your actual day — the rushed breakfast, the travel week, the morning after you’ve slipped and need to start again — does.

Supplement makers have typically relied on scientific language: milligrams, compounds, pathways, and clinical-sounding promises. That language has its place. It helps explain what is in the product and why a formula was built a certain way. But it does not answer the question most people face each morning: “How am I supposed to keep up this supplement regimen?” That is why so many bottles end up half-used. The routine never became part of the way you eat, plan, travel, or care for yourself.

A Better Test: Can You Picture Yourself Doing It?

A supplement routine with long-term potential must pass a simple test: Can you picture yourself doing it on an ordinary day? Not on the perfect day. Not on the day when the kitchen is clean, breakfast is planned, and you carefully follow every reminder. The ordinary day. The rushed day. The tired day. The day after you’ve already missed three days and need to restart.

That is where practical design comes in. For example, supplements that are designed to require fewer pills is one way to reduce resistance. Another is to design powder forms to be added directly to food, which is one of the strategies we’re pursuing for some of our supplements.

Powders designed to be added to food removes several friction points at once, including the difficulty of remembering, the dislike or difficulty of swallowing pills and capsules, and the generalized feeling that “it’s just too complicated.”

A scoop of powder stirred into a meal you already eat is as easy as adding a dash of salt or pepper. This food-centered format also keeps the supplement routine tied to nourishment instead of making it feel like a pharmacy ritual.

It can also encourage more positive responses to missed doses. Instead of berating yourself for being undisciplined, which tends to be a demotivating response, you can simply sprinkle the powder onto your next meal without self-reproach, because now you’re more apt to see it for what it actually is: a simple way to boost the nutrient content of the food you’re already eating, just like you add flavor by adding spice.

The supplement stops being a clinical chore you perform out of vague obligation and becomes part of your ongoing effort to simply eat well. That connection can help keep you on the adherence track, because the supplement is now properly associated with nutrition — food — rather than a separate health intervention on par with medication.

A routine you struggle to fit into your busy day will only survive as long as your willpower does. Meanwhile, a routine that doesn’t ask you to add additional tasks to your to-do list does not need much, if any, willpower to maintain.

The Bottom Line

A supplement routine has two jobs. First, it must make scientific sense. The forms, amounts, and delivery must be optimized. Second, it has to fit your life well enough that you can keep using it. The old pill-centered model focused almost entirely on the first job and left the second one to willpower. But willpower is a fragile foundation for a daily routine. Food-centered design works better.

That is the point of our food-first approach to supplements. Adherence to a supplement routine becomes easier when all you need to do is sprinkle it on top of your food.

That is what a supplement “built for you” means in practical terms. A powdered supplement you can add to food or beverages means your routine gets tied to something that happens every day, namely eating. And when a supplement routine is as easy as eating, you can return to it, one meal at a time.

Frequently Asked Questions

Q: Isn’t this just marketing — telling me a “story”?
A: A story can be used as marketing, but that is not the point here. The point is design. Health messaging research suggests stories can influence health intentions when people identify with the situation being described. That does not make “a story” a substitute for science. It means the science becomes more useful when the routine feels relevant to your life.

Q: Why does “seeing myself doing it” matter for whether I take a supplement?
A: Because a supplement routine depends on repeated behavior. When the routine feels separate from your day-to-day activities, it becomes one more task to remember. When it’s tied to something you already do, such as eating, it becomes easier to repeat and easier to restart after a missed day.

Q: Does the story matter more than the formula?
A: No. The formula still comes first. Nutrient form, dose, absorption, and delivery all matter. But even an excellent formula does nothing for you when you abandon it. The story matters because it helps connect a sound formula to a routine you can actually keep.

Q: What does “built for you” mean here?
A: It means something concrete: A powdered supplement you can add to food or beverages means your routine gets tied to something that happens every day, namely eating. It means the supplement was designed around real life rather than a perfectly organized day.

These statements have not been evaluated by the U.S. Food and Drug Administration.

This article is for general education. The products described are dietary supplements intended to support normal health and wellbeing as part of a food-first lifestyle. They are not a substitute for a varied diet, a healthy lifestyle, or the advice of your physician. If you are pregnant, nursing, taking medication, or managing a health condition, talk with your healthcare provider before beginning any supplement.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

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What is xanthan gum commonly used for in processed foods?

Adding sweetness for better palatability
Preserving color
Increasing protein and carb content
Thickening and stabilizing foods
Xanthan gum is commonly added to foods to improve thickness, stability, and texture without significantly changing flavor. Learn more.

Vitamin K is a fat-soluble vitamin that occurs in two forms, K1 (phylloquinone), found abundantly in green leafy vegetables, and K2. Vitamin K2 has several subforms, known as menaquinones, which are designated MK-4 through MK-13. These subforms differ primarily in the length of their side chains, which affects their distribution in the body, sources in the diet, and specific biological functions.

MK-7 through MK-13 are produced by various strains of bacteria in the gut, while MK-4 is primarily found in animal-based foods such as eggs, dairy products (like cheese and butter), and certain meats (especially liver).

Vitamin K1 and K2 play pivotal roles in various body functions, including bone health. In fact, being deficient in vitamin K is closely linked to an increased risk of fractures and osteoporosis, a condition characterized by weakened bones and a heightened susceptibility to breaks.

Studies highlight that individuals with optimal vitamin K levels exhibit greater bone mass and a lower incidence of fractures. For instance, research demonstrates that vitamin K is essential for the production of a protein that’s vital for bone mineralization.1

Additionally, vitamin K2 has been shown to work synergistically with vitamin D, enhancing bone mineral density and overall bone quality. These findings underscore the importance of maintaining adequate vitamin K levels through diet or supplementation to support bone health effectively.

Understanding Vitamin K’s Bone-Strengthening Benefits

Vitamin K is a key player in maintaining bone strength and may help prevent arterial calcification, helping ensure that calcium is directed to where it’s needed most — your bones and teeth, not your arteries.

• Vitamin K1 (phylloquinone) supports vascular health and bone retention — This form of vitamin K may help reduce calcification in blood vessels while helping bones retain calcium, which may help prevent unnecessary calcium buildup in the arteries.

• Vitamin K2 (menaquinone) activates vitamin D and directs calcium — K2 works by activating vitamin D-dependent proteins, allowing calcium to be efficiently transported out of the arterial system and into bones and teeth.2

• Vitamin K is vital for the carboxylation of osteocalcin — This is a process that enhances bone strength. It might sound complex, but it’s actually a straightforward process. To understand this, you need to first know what osteocalcin is — this is a small protein produced by osteoblasts during bone formation.3

• Carboxylation transforms osteocalcin into a functional hormone — Carboxylation is a process wherein osteocalcin is transformed from a simple protein into a sophisticated hormone involved in bone metabolism and broader metabolic regulation.

When your body lacks sufficient vitamin K, the carboxylation of osteocalcin is impaired. This means that osteocalcin cannot effectively bind calcium to the bone matrix. Over time, this contributes to osteoporosis, where bones become porous and more prone to fractures.

• Vitamin K deficiency may increase cardiovascular risk — When calcium is not directed to your bones where it’s needed most, it may not only decrease bone mineral density and increase fragility, but also raise the risk of cardiovascular conditions. This is because calcium accumulates in places like your blood vessels and arteries instead.

• Common causes of vitamin K deficiency — The underlying causes of vitamin K deficiency often stem from poor dietary intake, certain medical conditions, or the use of medications that interfere with vitamin K absorption. For instance, individuals with gastrointestinal disorders struggle to absorb this nutrient effectively. Additionally, long-term use of antibiotics disrupts gut bacteria, reducing your body’s natural production of vitamin K.

To learn more about the differences between vitamin K1 and K2, read “Vitamin K1 vs. K2 — Understanding Their Distinct Roles in Your Health.”

Vitamin K Plays an Essential Role in Enhancing Bone Health

A 2024 review investigated the multifaceted roles of both vitamin K1 and K2, as well as vitamin K-dependent proteins, in maintaining bone health, particularly emphasizing their interaction with vitamin D and their effects on calcium metabolism. The research examined how these vitamins may work together to support bone integrity, including in the context of osteoporosis.4

• Vitamin K activates key bone-building proteins — Vitamin K facilitates the carboxylation of osteocalcin and matrix Gla-protein (MGP), which are essential for binding calcium within the bone matrix. MGP is also a potent inhibitor of arterial calcification.

• Vitamin K enables calcium-binding through carboxylation — One of the researchers’ key findings was that vitamin K acts as a necessary cofactor for enzymes that convert glutamic acid residues in proteins into gamma-carboxyglutamic acid residues.* This chemical transformation is important for osteocalcin to effectively bind calcium. According to the researchers:

“The important effects of vitamin K on Ca and skeletal homeostasis are known to be mediated through its role as a cofactor for the γ-glutamyl carboxylase enzyme that promotes conversion of glutamate (Glu) residues to gamma-carboxyglutamic (Gla) residues in the post-translational carboxylation of osteocalcin (OC) and matrix Gla protein (MGP). This may have a significant impact on osteogenesis.”5

• Vitamin K2 plays a key role in bone remodeling — The review also revealed that vitamin K2 plays a significant role in bone remodeling. It assists in directing calcium to the bones and prevents its deposition in soft tissues, which leads to vascular calcification. This dual action supports both bone and cardiovascular health.*

• Vitamin K and vitamin D work together to regulate calcium balance — The research highlighted the synergistic relationship between vitamins K and D in regulating calcium homeostasis.

Vitamin D enhances calcium absorption in the gut, while vitamin K helps ensure that the absorbed calcium is appropriately utilized by the bones. This collaboration between the two vitamins may help support optimal bone density and reduce the risk of fractures.

“Vitamin D exerts effects directly on osteoblasts by promoting osteoblast maturation and OC synthesis. The multiple effects of vitamin D on bone are associated with a high expression of the vitamin D receptor in several types of bone cells.”6

• Researchers identified biomarkers for vitamin K status — The ratio of carboxylated osteocalcin (cOC) to undercarboxylated osteocalcin (ucOC) was used to assess functional vitamin K levels in the body. A lower cOC-to-ucOC ratio indicated an inadequate vitamin K status, which was associated with increased bone loss and a higher risk of hip fractures.

The biological mechanisms underlying these findings involve vitamin K’s role in activating proteins that regulate calcium placement in the body. By enabling osteocalcin and MGP to bind calcium effectively, vitamin K helps ensure that calcium is deposited in the bones rather than in the arteries or other soft tissues.

How Does Vitamin K’s Influence Energy Metabolism and Blood Sugar Levels?

Another review published in the journal Nutrients explored the role of vitamin K in both bone health and energy metabolism. The research examined how vitamin K interacts with proteins involved in bone formation and how its deficiency could impact overall metabolic processes.7

• Vitamin K is essential for both bone integrity and metabolic health — The review cites research on individuals with varying levels of vitamin K intake, analyzing their bone integrity and insulin sensitivity. Findings suggest that adequate vitamin K levels may help support strong bones and healthy blood sugar regulation, pointing to this nutrient’s potential relevance to osteoporosis and diabetes risk.*

• Osteocalcin links vitamin K to both bone and glucose metabolism — Activated osteocalcin contributes to bone strength and influences how the body regulates insulin and blood sugar levels. This dual function means that vitamin K deficiency could lead to both weakened bones and impaired glucose metabolism, heightening the risk of developing diabetes.

“[V]itamin K deficiency in the bone results in a lower production of OC and a low serum level of OC, predisposing to a state of glucose intolerance and diabetes mellitus that may then enhance bone matrix deterioration via the production of cross-linked advanced glycation end products (AGE), which have been further associated with bone fractures after adjustment of confounders.

We believe that as a whole, vitamin K deficiency plays an important role in glucose metabolism, ultimately leading to a disturbance of bone quality,” the researchers reported.8

• Vitamin K may help prevent arterial calcification and support cardiovascular health — In addition to its effects on bone and energy metabolism, vitamin K was found to play a role in preventing the calcification of soft tissues, such as blood vessels.* This may help reduce the hardening of arteries, which is a significant risk factor for cardiovascular diseases. The research suggested that vitamin K helps direct calcium to the bones rather than letting it accumulate in the arteries.

• Uncarboxylated osteocalcin (ucOC) is a marker of vitamin K deficiency — The review identified specific markers for vitamin K deficiency, such as elevated levels of uncarboxylated osteocalcin (ucOC) in the blood. Monitoring these markers will help in early detection of vitamin K insufficiency, allowing for timely interventions to maintain bone density and metabolic health.

• Low vitamin K intake is linked to a higher risk of fractures — Individuals with low vitamin K intake were found to have a higher incidence of hip and vertebral fractures across different populations. The research underscored the importance of maintaining adequate vitamin K levels through diet or supplementation to significantly reduce the risk of such fractures.*

Your Microbiome Also Influences Your Bone Health

In related news, a 2024 review published in the Gut Microbes journal explored how the gut microbiome, which is the community of microorganisms living in your intestines, works in collaboration with vitamin K2 to maintain strong and healthy bones, highlighting how these microorganisms contribute to bone density and the overall integrity of your skeletal system.9

• Gut bacteria naturally produce vitamin K2 — The research focused on understanding how variations in the gut microbiome affect the risk of developing bone-related conditions such as osteoporosis. It was found that certain beneficial gut bacteria species, like Bacteroides and Lactococcus lactis, produce vitamin K2 and help maintain adequate levels of this nutrient.*

• Dysbiosis lowers vitamin K2 levels, weakening bones — One of the key findings was that disruptions in the gut microbiome, a condition known as dysbiosis, decreases your vitamin K2 production,10 compromising bone strength and increasing your risk of fractures and osteoporosis.*

Vitamin K2 produced by gut bacteria activates proteins that are essential for bone formation and mineralization, and maintaining a balanced and healthy gut microbiome is essential for ensuring the proper synthesis of vitamin K2.

• Probiotics and prebiotics enhance bone health — The review also discussed the role of probiotics and prebiotics in enhancing bone health. Probiotics are live beneficial bacteria that are consumed through fermented foods or supplements, while prebiotics are non-digestible food ingredients that promote the growth of these healthy bacteria.11

Incorporating probiotics and prebiotics into your diet supports your gut microbiome, leading to increased production of vitamin K2 and improved bone density.

• The gut microbiome supports calcium and vitamin D absorption — The study also highlighted the interconnectedness between the gut microbiome and other aspects of bone metabolism, such as hormone regulation and immune system function.
Your gut bacteria influence the absorption of calcium and vitamin D as well, both of which are vital for bone health. Additionally, a healthy gut microbiome helps modulate the immune system, reducing inflammation that negatively impacts bone integrity.

• Antibiotics disrupt vitamin K2 production — The review also pointed out that antibiotic treatments, which disrupt the gut microbiome, lead to a significant reduction in vitamin K2 production.12 This not only affects bone health but also emphasizes the importance of being cautious when taking antibiotics, to preserve the beneficial bacteria responsible for maintaining bone integrity.

For a deeper dive into vitamin K’s role in bone and heart health, read “Vitamin K 101 — Essential Basics for Bone and Heart Health.”

Egg Yolks Are Your Best Source of Vitamin K2 as MK-4

Egg yolks are among the highest dietary sources of MK-4, a vital form of vitamin K2 that plays an important role in bone health, cardiovascular function, and calcium regulation. Including egg yolks in your diet significantly contributes to your MK-4 intake, supporting various aspects of your health.

• Egg quality is important — You need to be careful about your egg sources as most commercial egg sources — even free-range organic — have high PUFA levels as they are fed grains like soy and corn.

• Chickens should be fed low-PUFA grains for optimal egg quality — Ideally, chickens should be fed rice, barley, and split peas. I personally eat six egg yolks a day from chickens who are fed this and have 80% less linoleic acid than regular chickens.

Below is a comprehensive overview of egg yolks as a top source of MK-4, along with additional dietary sources and considerations.

6 Key Steps to Enhance Bone Health Through Vitamin K

To help support healthy vitamin K levels and optimal bone and overall health, consider the following:

1. Add more green leafy veggies into your diet — They are some of the best sources of vitamin K1. Collard and turnip greens, kale, spinach, broccoli, Brussels sprouts, cabbage, and lettuces are good choices.13

2. Boost your natural vitamin K2 production — Enhance your body’s natural vitamin K2 levels by incorporating fermented foods such as natto and fermented vegetables cultivated with specific bacterial cultures. Additionally, consume grass fed animal products like egg yolks, liver, and grass fed dairy to support K2 production.

3. Consider vitamin K2 supplementation — Research suggests that vitamin K2 — ideally 180 to 200 micrograms daily in the MK-7 form — may work synergistically with vitamin D3 and magnesium to support absorption and effectiveness, helping strengthen bones while supporting healthy calcium balance in the arteries.

Current guidance pairs 180 mcg of K2 with 5,000 IU of vitamin D3, so talk to a healthcare provider about what combination and dose make sense for you rather than following a fixed protocol.

Timing may also help. Some research suggests taking vitamin K2 with the day’s fattiest meal, since it’s fat-soluble, may improve absorption and support osteocalcin activation. Consistent timing may help maintain steadier vitamin K2 levels for bone and heart health.

4. Balance key nutrient cofactors — Getting sufficient calcium, magnesium, vitamin D3, and vitamin K2 — through diet and, where appropriate, supplementation — may help these nutrients work together to build and maintain bone density, promoting proper calcium utilization and bone matrix formation for optimal bone health.

5. Support your gut microbiome — Maintain a healthy intestinal environment to naturally boost vitamin K2 production. Focus on whole, unprocessed foods and consider targeted probiotic supplementation tailored to your microbiome.

6. Focus on bone-building exercises — Regular weight-bearing movement may help stimulate bone formation, while K2 may help support proper calcium deposition. Walking, resistance training and bodyweight exercises work together with K2 to help strengthen your skeleton. Some research suggests combining exercise with vitamin K2 may offer added benefit beyond supplementation alone, though direct comparative studies are limited.

*These findings are from research conducted in clinical settings and may not directly apply to human health.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

Frequently Asked Questions (FAQs) About Vitamin K and Bone Health

Q: What’s the main role of vitamin K in bone health?

A: Vitamin K helps direct calcium into bones, making them stronger and reducing the risk of fractures. It’s also thought to help prevent calcium from building up in arteries, which may support heart health.

Q: Do I need both vitamin K2 and vitamin D?

A: Yes, they work together. Vitamin D helps your body absorb calcium, and vitamin K2 helps direct it toward bone-building instead of arterial accumulation.

Q: Can vitamin K2 help prevent osteoporosis?

A: Some research suggests vitamin K2 may help support bone mineral density by activating osteocalcin, a key protein for bone formation, though clinical trial evidence on whether it reduces fracture risk remains mixed.

Q: How much vitamin K2 should I take daily?

A: Research suggests 180 to 200 mcg of vitamin K2 (MK-7) daily, taken with a meal containing healthy fats to help improve absorption, may support bone and heart health — talk to a healthcare provider about what’s appropriate for you.

For decades, xanthan gum has slipped into the food supply with almost no scrutiny. Manufacturers add it to gluten-free breads, salad dressings, sauces, ice cream, protein shakes, and countless packaged foods because it thickens, stabilizes, and improves texture without changing flavor. Many people don’t think twice when they see it on an ingredient label.

Yet that confidence rests on surprisingly little long-term safety data, and most of what does exist focuses on surface-level markers — weight, blood sugar, cholesterol — that can look perfectly normal while something deeper goes wrong.

Xanthan appears across so many product categories that anyone eating a modern processed diet likely consumes it multiple times a day without realizing it. People with swallowing disorders may take in even more, since xanthan gum-based thickeners are standard in clinical nutrition. The question scientists have largely failed to ask is what happens inside the digestive tract when that kind of exposure continues week after week.

An animal study finally looked in the right place, and what the researchers found beneath the surface contradicted everything the conventional safety profile would predict. Next, I’ll break down exactly what they discovered and why those changes deserve your attention.

Xanthan Gum Triggered Hidden Inflammation in the Colon

The study, published in PLOS One, investigated what happened when adult Wistar rats consumed xanthan gum every day for 10 weeks.1 The researchers examined the colon itself, measuring inflammatory chemicals, immune cell activity, gut barrier proteins, and changes in the gut microbiome.

They also tested three different xanthan gum doses designed to reflect different patterns of human consumption, from people who regularly eat processed foods to those who rely on xanthan gum-based thickeners because of swallowing disorders. The researchers wanted to determine whether continuous exposure altered the intestinal environment. That’s important because changes inside your digestive tract often develop long before routine blood work reveals a problem.

• The colon became inflamed even though the animals looked healthy on the outside — After 10 weeks, the rats showed no significant differences in body weight, food intake, body fat, blood glucose, triglycerides, cholesterol, or HDL cholesterol compared to animals that didn’t receive xanthan gum.

If a doctor looked only at those numbers, everything would appear normal. Yet microscopic examination of the colon told a very different story. The researchers found that xanthan gum promoted “an inflammatory state” across all doses and concluded that “dietary xanthan gum induced moderate-grade inflammation and modified the colon gut barrier.”

• Immune cells accumulated inside the intestinal wall as xanthan gum intake continued — When researchers examined colon tissue under the microscope, they found inflammatory cells had infiltrated the intestinal wall, especially in the groups receiving the medium and highest xanthan gum doses. Most of these cells were lymphocytes, a type of white blood cell involved in long-lasting immune responses rather than short-lived reactions.

The researchers also assigned inflammation scores based on the severity of tissue changes. Compared to the control animals, both the medium- and highest-dose groups had significantly higher scores, confirming that the inflammatory response was measurable rather than simply a microscopic observation.

• Proteins that help control what passes through your intestinal lining shifted in the wrong direction — Researchers found greater amounts of Claudin-2 in the xanthan gum groups. Claudin-2 is a protein that acts like adjustable caulking between intestinal cells; it controls how tightly those cells seal together. When Claudin-2 levels rise above normal, the seal loosens, allowing substances to slip through the intestinal lining that would normally stay inside the digestive tract.

The researchers also observed higher levels of inflammatory signaling molecules known to increase Claudin-2 and weaken the gut barrier, creating conditions that reinforce inflammation instead of allowing the tissue to recover.

• The gut microbiome changed in subtle but meaningful ways — Xanthan gum didn’t significantly alter the dominant bacterial groups known as Firmicutes and Bacteroidetes or the overall diversity of the microbiome.

Even so, the highest-dose group developed significantly higher levels of Elusimicrobiota, a relatively rare group of gut bacteria that scientists are still working to understand, while the medium-dose group showed a trend toward more Patescibacteria, another uncommon group of microbes often found in complex microbial communities.

These shifts matter not because scientists fully understand what these bacteria do, but because they didn’t occur in isolation — statistical analysis linked them directly to the inflammatory markers and barrier protein changes happening in the same tissue, suggesting the microbiome was responding to the inflammatory environment xanthan gum created rather than changing randomly.

• The findings offer a biological explanation for earlier concerns about xanthan gum — The researchers explained that their results support previous reports linking xanthan gum-containing thickeners with serious intestinal problems such as necrotizing enterocolitis — a life-threatening condition in which intestinal tissue becomes severely inflamed and begins to break down — in premature infants.

Although this study involved adult rats, it identified specific biological changes, including chronic inflammation, altered gut barrier proteins, and microbiome shifts, that help explain why long-term xanthan gum exposure deserves closer attention.

These findings come from an animal study. Additional research is needed to determine whether the same effects occur in humans.

How to Reduce Your Xanthan Gum Exposure at the Source

If your goal is a healthier gut, the smartest place to start is with the foods that introduce the problem in the first place. The research in this article showed changes in the colon after long-term xanthan gum exposure, not because of a nutrient deficiency but because of repeated intake of a common food additive. That means your greatest opportunity is to reduce the amount that enters your diet every day instead of searching for something that simply masks the effects afterward.

1. Find the hidden sources of xanthan gum before you eat them — Try a one-week label audit. Xanthan gum appears in a wide variety of foods, including gluten-free breads, tortillas, wraps, salad dressings, sauces, gravies, soups, protein powders, meal replacement shakes, nondairy products, ice cream, frozen meals, and many packaged snacks.

Make it a habit to read ingredient labels before you buy packaged foods. Every time you spot xanthan gum, choose a different product that doesn’t contain it whenever possible. You might be surprised by how often it appears. Once you recognize where it hides, avoiding it becomes much easier and eventually turns into second nature.

A simple rule of thumb: spend most of your shopping time around the perimeter of the grocery store where fresh foods are located, and less time in the center aisles where xanthan gum is most likely to appear.

2. Build your meals around fresh whole foods instead of products that rely on stabilizers — The easiest way to avoid xanthan gum is to eat foods that don’t need it in the first place. Fresh fruits, properly prepared vegetables, whole-food carbohydrate sources that fit your digestive tolerance, high-quality animal protein, and simple homemade meals eliminate many processed food additives.

I also recommend avoiding the highly processed foods that commonly contain xanthan gum along with other unwanted ingredients. That includes many packaged sauces, gluten-free convenience foods, protein bars, frozen meals, salad dressings, and similar products.

Cooking more of your own meals gives you complete control over every ingredient. If a recipe calls for xanthan gum as a thickener, try whole-food alternatives instead — pureed cooked potato or vegetables, or a simple reduction, can often achieve the texture you need without any additive at all.

3. Support your gut instead of overwhelming it with more processed foods — If your digestion already feels off, don’t assume adding more fiber or more processed “health foods” solves the problem. Focus first on removing foods that repeatedly irritate your digestive tract, including not only xanthan gum but also seed oils, which are high in linoleic acid (LA); they weaken your colon’s protective lining and make it harder for beneficial bacteria to thrive.

Begin with simple, easy-to-digest meals that minimize excessive fermentation and reduce the release of endotoxins — toxic compounds produced when certain gut bacteria break down. This gives your intestinal lining a better environment to recover. As your digestion becomes more consistent, gradually increase your carbohydrate intake using foods that your gut handles comfortably.

Start with whole fruit and well-cooked starches such as white rice, which provide glucose to fuel your cells without placing excessive demands on an already stressed digestive system. Next, introduce root vegetables, followed by non-starchy vegetables, then starchy vegetables such as squash and sweet potatoes. Save beans, legumes, and minimally processed whole grains for last, and only if your digestion remains stable. Most adults thrive on about 250 grams of carbohydrates per day.

4. Choose fats that support better metabolic health instead of processed seed oils — Xanthan gum often appears in the same packaged foods that contain seed oils. Those oils add another unnecessary burden to your metabolism. I recommend replacing soybean, corn, sunflower, safflower, cottonseed, grapeseed, and canola oils with more stable fats such as grass fed butter, ghee, or tallow. Avoid nuts and seeds as they’re also high in LA.

FAQs About Xanthan Gum and Colon Inflammation

Q: Does this study prove xanthan gum is harmful to people?
A: No. This research was conducted in rats, not humans, so it doesn’t prove the same effects occur in people. However, it showed that long-term xanthan gum consumption caused measurable inflammation, changes to proteins that regulate the gut barrier and shifts in the gut microbiome, giving scientists a biological reason to study its long-term effects in humans more closely.

Q: Why didn’t routine health measurements reveal a problem?
A: The rats maintained normal body weight, blood sugar, cholesterol, and other metabolic markers throughout the study. The concerning changes only became apparent when researchers examined the colon tissue under a microscope, showing that gut inflammation can develop long before standard health measurements change.

Q: What happened to the intestinal lining after long-term xanthan gum intake?
A: Researchers found increased amounts of proteins associated with a leakier intestinal barrier, along with higher levels of inflammatory signaling molecules. Together, these changes suggest the colon became less effective at keeping unwanted substances inside the digestive tract and more prone to ongoing inflammation.

Q: Where is xanthan gum commonly found in the food supply?
A: Xanthan gum is widely used as a thickener and stabilizer in processed foods. Common sources include gluten-free breads and tortillas, salad dressings, sauces, soups, protein powders, meal replacement shakes, frozen meals, nondairy products, ice cream, and many packaged snack foods. Reading ingredient labels is the easiest way to identify and avoid it.

Q: What’s the most effective way to reduce your exposure to xanthan gum?
A: Focus on replacing packaged foods with fresh, whole foods whenever possible. Preparing more meals at home, checking ingredient labels before you buy packaged products and choosing alternatives that don’t contain xanthan gum are practical ways to reduce your daily exposure while also cutting back on many other processed food additives.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

Test Your Knowledge with Today’s Quiz!
Take today’s quiz to see how much you’ve learned from yesterday’s Mercola.com article.

During rapid weight loss with GLP-1 medications, what type of tissue may also be lost along with fat?

Bone tissue
Muscle tissue
Glucagon-like peptide-1 (GLP-1) medications can lead to muscle loss along with fat loss, which may reduce strength and lower resting metabolism. Learn more.
Nerve tissue
Skin tissue

Antidepressants have a long, documented history of side effects while taking them. For example, they’ve been associated with blurry vision, increased anxiety, constipation, sleep disturbances, and loss of libido. Research suggests roughly 1 in 3 antidepressant users in primary care may no longer benefit from the drugs and could be ready to stop — and among those who do stop, about 56% report withdrawal symptoms.1

However, withdrawal symptoms are a real trade-off, and for some people they become severe enough that they resume the medication in an effort to feel functional again.

Long-Term Antidepressant Withdrawal Is Well-Documented

A study published in Epidemiology and Psychiatric Sciences set out to learn what happens after people stop taking antidepressants. Specifically, the researchers investigated a condition known as post-acute withdrawal syndrome (PAWS), where symptoms continue long after someone stops their medication.2

This paper was the first systematic review with a meta-narrative synthesis of its kind focusing solely on antidepressants like selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs).

Of the 1,286 records screened, seven studies met the selection criteria: three analyses of online self-reports from peer-support groups, one randomized controlled trial, one case series, one case report, and one prospective cohort study — an evidence base that the authors themselves describe as limited.

They also didn’t focus on patients in the early stages of stopping antidepressants — they focused on those experiencing symptoms months, or even years, after stopping.

• The effect of PAWS on your brain health — The researchers noted that PAWS involves a multitude of symptoms, including “dizziness, vertigo, tremor, nausea, insomnia, fatigue, mood dysregulation, anxiety, panic, irritability and agitation.” In severe cases, those in withdrawal report suicidal thoughts and behavior.3

• Symptoms can last for a long time — According to the studies reviewed, lingering symptoms lasted anywhere from 1.5 to 166 months (around 13.8 years). That upper figure is an outlier at the far end of a wide range, and it comes largely from online self-reports rather than controlled follow-up. Doctors usually tell patients that stopping antidepressants will be uncomfortable for a week or two, but this data tells a very different story.

• Paroxetine was linked to the most problems — The most consistent risk factor identified across these studies was long-term use of paroxetine, though the authors caution that most of the included studies could not speak to this question. According to the researchers:

“Two of the included studies indicate that in particular long-term paroxetine use may carry an increased risk of PAWS, but most studies were uninformative on this subject. One analysis of online self-reports further showed that the duration of tapering was positively correlated with the duration of withdrawal symptoms, suggesting that patients experiencing more persistent withdrawal symptoms try to taper more slowly.”

• PAWS is not a relapse — It’s not your original depression coming back. PAWS has its own distinct pattern, and the symptoms often feel different than the ones that led you to take antidepressants in the first place. That distinction is key because it helps explain why people may be misdiagnosed as having a “relapse,” when in fact they’re going through withdrawal:4

“[I]t appears that in both clinical research and practice, protracted and persistent withdrawal symptoms are frequently misdiagnosed as a relapse of the primary mental health condition (typically depression) or new emergent mental disorders, the latter being specifically embedded in the concept of persistent post-withdrawal disorders,” the study authors said.

• Stopping medication versus continuing usage — One noteworthy finding is that people who tapered off their antidepressant usage still had more recorded withdrawal symptoms than those who stayed on the medication.

The researchers cited a 2021 randomized controlled trial (RCT) published in The New England Journal of Medicine. Here, 478 patients were split into two groups — maintenance and discontinuation. By the end of 52 weeks, 135 people in the discontinuation group experienced withdrawal symptoms, and 92 in the maintenance group.5 Going deeper into the findings, the researchers noted:6

“In this study, 39 weeks after patients had started tapering citalopram, fluoxetine, sertraline or mirtazapine, the number of recorded withdrawal symptoms was still significantly increased compared to patients maintained on their antidepressant medication.

Of note, in the design of this RCT, the popular antidepressant drugs paroxetine and venlafaxine were deliberately excluded, because, as written by the authors, both are known to cause marked withdrawal symptoms when treatment is discontinued.”

• Effective treatment of PAWS is needed — After analysis, the researchers suggest that more RCTs are needed regarding PAWS. However, they recommend that the focus need to be on effective treatments, since there is little information regarding this topic:

“[R]igorous long-term RCTs are required to test the efficacy of treatment and management strategies. These studies would inform clinicians about effective interventions to mitigate the severity and duration of this impairing syndrome, as to date not a single clinical intervention has been formally evaluated.”

PAWS Is More Common Than You Think

A meta-analysis published in The Lancet Psychiatry investigated 79 studies — 44 RCTs and 35 observational studies — with a total of 21,002 participants. The review encompasses different treatment settings, and types of antidepressants, offering a bird’s eye view of PAWS.7

• Many are affected once medication is stopped — The team found that 31% of people who stop antidepressants experience some kind of withdrawal symptom. Severe ones were less common — 2.8% of everyone who discontinued an antidepressant, compared with 0.6% of those who discontinued placebo.

According to the analysis, symptoms typically began within a few days of stopping the drug, but in many cases, they didn’t fully resolve for weeks. In addition, the presence of symptoms wasn’t necessarily linked to how long someone had taken the medication — a meta-regression found no significant association between withdrawal incidence and duration of antidepressant treatment, which ranged across the included studies from one to 156 weeks.

• What the 31% means once placebo is accounted for — The authors’ bottom-line estimate is lower than the raw figure. Subtracting the symptoms reported after placebo discontinuation, they put the incidence of genuine antidepressant withdrawal at “approximately 15%, affecting 1 in 6 to 7 patients who discontinue their medication” — a figure they say should inform patients “without causing undue alarm.”8

• Expectation alone can produce symptoms — People who stopped a placebo still reported symptoms at a rate of 17%, or roughly 1 in 6. The authors describe these as non-specific or “discontinuation-like” symptoms, consistent with a nocebo effect in which the expectation of discomfort produces real symptoms.

• Severity and type of symptoms weren’t uniform — Specifically, desvenlafaxine, venlafaxine, imipramine, and escitalopram were associated with the highest frequency of symptoms, while imipramine, paroxetine, and desvenlafaxine or venlafaxine were associated with greater symptom severity.

In contrast, drugs like fluoxetine (Prozac), which linger longer in the bloodstream, showed a much lower rate of withdrawal complaints. The researchers also suggested that the half-life of these drugs (how long they remain in the body) plausibly affects not just the severity of the symptoms, but their time of appearance as well.

• What the evidence says about tapering — Notably, this featured meta-analysis itself found no difference between studies that tapered the drug and studies that stopped it abruptly (31% versus 29%). The authors nonetheless point to separate research on how tapering is done:9
“Tapering of antidepressants is recommended in most guidelines, and there is research suggesting that prolonged and hyperbolic tapering of antidepressants will substantially reduce (although not completely exclude) withdrawal effects and increase the likelihood of successful discontinuation of antidepressants.”

The same authors add that hyperbolic tapering has also been criticized and, because its pragmatic feasibility is limited, may not be indicated for every patient.

Critics Say the Effects of Antidepressants Are Being Downplayed

Antidepressants are one of Big Pharma’s moneymakers. According to a market analysis report from Precedence Research, the global antidepressant market was valued at $19.53 billion in 2025, with North America contributing 47% of market revenue in 2024.10

That said, the labeling that acknowledges these side effects was imposed by regulators rather than volunteered by industry. Since mid-October 2004, the U.S. Food and Drug Administration (FDA) has required manufacturers to place a black box warning on all antidepressants distributed in the United States, stating that the medications “increase the risk of suicidal thinking and behavior (suicidality) in children and adolescents with major depressive disorder (MDD) or other psychiatric disorders.”

The expanded warnings section adds that anxiety, agitation, panic attacks, insomnia, irritability, hostility, impulsivity, akathisia, hypomania and mania “have been reported in adult and pediatric patients” treated with these drugs.11

Despite these warnings, industry-aligned research continues to characterize these effects as minor — a framing that critics say understates the harm patients report.

• Using science to give an air of legitimacy — In a report by investigative journalist Maryanne Demasi, Ph.D., she criticizes a 2025 JAMA Psychiatry meta-analysis of 50 studies and 17,828 participants12 which concluded that the mean number of discontinuation symptoms one week after stopping was “below the threshold for clinically significant discontinuation syndrome” — a finding widely reported as showing that withdrawal is only “mild.”13

One of the reasons Demasi did her analysis is because of the prestige behind the journal. When it releases an influential study, consumers and medical practitioners tend to accept that the findings are true and accurate.

• Media is brought in to help — Demasi argues that industry-aligned researchers mobilized mainstream media to push a narrative that antidepressants can be slowly stopped and, as mentioned above, only produce mild side effects in doing so:

“The authors mobilised a rapid media campaign to shape the public narrative, with the Science Media Centre issuing expert commentary to ‘reassure both patients and prescribers’ that most withdrawal symptoms were ‘not clinically significant.’”

• The methodology is flawed — Digging deeper into the issue, Demasi broke down the logic of the JAMA Psychiatry meta-analysis. According to her findings, the studies used in the review are either biased or poorly designed. For example, she pointed out that the study followed patients for just two weeks — this isn’t applicable to antidepressant users in America, as half of them have already been taking these medications for more than five years. Demasi continues:

“Worse, many trials enrolled patients already taking antidepressants — then abruptly withdrew them before randomisation. As a result, those assigned to placebo experienced withdrawal symptoms that blurred the difference between treatment and control groups, artificially minimising the harms.”

• Industry funded most of the included studies — Demasi noted that most of the studies included in the meta-analysis were funded by the pharmaceutical industry. Furthermore, the researchers excluded medications such as paroxetine and escitalopram, which are already strongly linked to severe PAWS.
For context, the Lancet Psychiatry meta-analysis cited earlier ran its own funding subgroup analysis and found little difference between industry-funded and independently funded studies (31% versus 28%), so funding alone does not account for the range of estimates in this literature.14

• A firsthand account of PAWS — In an interview with National Public Radio (NPR),15 a Canadian patient named Phillipa Munari described taking Effexor (venlafaxine) for 10 years. When she decided to stop taking it, problems started to appear even with the help of a doctor to taper it off.

According to Munari, she developed nerve pain, as well as chronic pain in her neck and shoulders. To make matters worse, she also had severe anxiety — all of which she didn’t have before. In an effort to manage her health issues, she went back to taking Effexor and then weaned off it again, much more slowly the second time.

• The effects of PAWS can be lasting — Munari shared that after her second round of Effexor (with a better tapering plan), her nerve pain and fatigue improved. However, the anxiety worsened. She describes about two years of severe symptoms and roughly four more years beyond that before she felt fully recovered.

Exercise Is a Powerful Support for Your Mental Health

If you’ve been feeling the blues lately, it’s worth knowing that a pill isn’t the only avenue — supporting the very systems that have been thrown off balance matters, too. And one of the most accessible ways to do that is getting regular exercise. In addition, decisions about starting or stopping a medication will need to be made with a qualified health care provider.

Exercise is not just a mood booster. Research suggests it may help support brain plasticity, nervous system regulation, and energy production at the cellular level. Barring any serious injury or physical ailment, I believe that it’s one of the best ways to support your mental health because it’s free and something that you can do right away.

• • Exercise compares favorably with standard care — In an umbrella review of 97 reviews covering 1,039 trials and 128,119 participants, published in the British Journal of Sports Medicine, researchers reported that physical activity was extremely beneficial for symptoms of depression, anxiety, and distress — about 1.5 times more effective than counseling or the leading medications. As noted by the lead author Ben Singh, Ph.D.:16

“Physical activity is known to help improve mental health. Yet despite the evidence, it has not been widely adopted as a first-choice treatment … Higher-intensity exercise had greater improvements for depression and anxiety, while longer durations had smaller effects when compared to short and mid-duration bursts.”

• Any exercise is better than nothing — Singh noted that moving your body, no matter how you do it, is beneficial. He explains:17

“We also found that all types of physical activity and exercise were beneficial, including aerobic exercise such as walking, resistance training, Pilates, and yoga. Importantly, the research shows that it doesn’t take much for exercise to make a positive change to your mental health.”

• Start with a walk — While it’s tempting to start off with an intense session at the gym, you can already gain plenty of benefits by going for a walk. In my interview with Dr. James O’Keefe, he noted that it’s a great way to boost your fitness — an average of 10,000 steps a day is associated with meaningful benefits. It’s also a moderate-intensity activity that is difficult to overdo for most people, which makes it sustainable as a daily habit. Aim for about an hour of walking a day.

• Strength training complements walking — Lifting weights is another beneficial strategy that goes hand in hand with your daily walks, however, it’s important that you don’t overdo it. According to O’Keefe, observational data suggest the additional mortality benefit appears to flatten,18 and may reverse, beyond roughly 130 to 140 minutes of total strength training per week:

“I’ve always been a fan of strength training … But again, the devil is in the details about the dosing. When you look at people who do strength training, it adds another 19% reduction in all-cause mortality on top of the 45% reduction that you get from one hour of moderate exercise per day.

When I strength train, I go to the gym and spend anywhere from 20 to 40 minutes, and … I try to use weights that I can do 10 reps with … After that, you’re feeling sort of like spent and … it takes a couple of days to recover. If you do that two, at the most three, times a week, that looks like the sweet spot for conferring longevity.”

• There are other useful strategies to support your mood — While exercise is effective, it’s not the only option available. I recommend supporting your gut with fermented foods (preferably homemade), given how closely gut health is intertwined with your brain function.

In addition, getting deep, restorative sleep is important for your mental health. Managing stress, as well as resetting your body’s internal clock by getting sun exposure within about 20 minutes of waking up, will also help support your mental and physical well-being. For an in-depth explanation of these tips, read “Depression Accelerates Physical Illness and Increases Disease Risk.”

Frequently Asked Questions (FAQs) About Post-Acute Withdrawal Syndrome

Q: What is Post-Acute Withdrawal Syndrome (PAWS) and how common is it after stopping antidepressants?
A: PAWS refers to long-lasting withdrawal symptoms that occur after discontinuing antidepressants such as selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs). These symptoms include dizziness, anxiety, tremors, insomnia, fatigue, and even suicidal thoughts.According to a 2024 meta-analysis from The Lancet Psychiatry, 31% of people who stop taking antidepressants report some form of withdrawal symptom — falling to approximately 15%, or about 1 in 6 to 7, once the symptoms reported after placebo discontinuation are subtracted. A separate 2025 systematic review of seven studies, drawn largely from online self-reports and case reports, found persistent symptoms lasting anywhere from one and a half months to about 13.8 years at the extreme.

Q: Are PAWS symptoms just a relapse of depression or something different?
A: No. PAWS symptoms are distinct from a relapse of depression. While often misdiagnosed as a return of the original mental health condition, PAWS has its own symptom profile and course. This misdiagnosis can lead to unnecessary reinstatement of medications and further confusion for patients.

Q: Which antidepressants are most associated with severe withdrawal symptoms?
A: In The Lancet Psychiatry meta-analysis, desvenlafaxine, venlafaxine, imipramine and escitalopram were associated with the highest incidence of withdrawal symptoms, and imipramine, paroxetine, and desvenlafaxine or venlafaxine with the greatest severity.

In contrast, longer-acting drugs like fluoxetine are associated with fewer issues. Tapering rather than stopping abruptly is recommended in most clinical guidelines, though that same meta-analysis found no difference in withdrawal incidence between studies that tapered and studies that stopped abruptly.

Q: Is the pharmaceutical industry downplaying the risks of antidepressant withdrawal?
A: Critics say yes. Investigative reporting by Maryanne Demasi, Ph.D., argues that pharmaceutical companies minimize the severity of withdrawal symptoms.

A 2025 meta-analysis published in JAMA Psychiatry found discontinuation symptoms fell below the threshold for clinical significance — widely reported as “mild” — but critics argue this rested on short follow-up, industry-funded research that excluded high-risk drugs, and poorly designed trials. Media campaigns, they say, further reinforced this framing.

Q: What supportive strategies are being discussed for antidepressant withdrawal?
A: No intervention has yet been formally tested for antidepressant withdrawal itself — the 2025 systematic review notes that “to date not a single clinical intervention has been formally evaluated” for PAWS, and calls for long-term trials. Separately, and for symptoms of depression and anxiety rather than withdrawal specifically, an umbrella review reported that physical activity was about 1.5 times more effective than counseling or the leading medications.

Activities like walking, strength training, yoga, and Pilates were all beneficial — even light exercise can make a meaningful difference. Any plan for tapering or stopping an antidepressant need to be made with a qualified health care provider.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.

Twelve-year-olds in the U.S. live in a world where smartphone access feels almost unavoidable, yet the decision to give a device at this age carries far more weight than some parents realize. Many families assume that a phone is simply a tool for convenience or safety, but the emerging data signals something deeper: Early access appears to shape how your child sleeps, handles stress, and interprets their social world.

Those early patterns influence confidence, learning, emotional steadiness, and even how your child relates to their own body. When a child enters the digital world before they have the emotional and neurological maturity to handle constant stimulation, their developing brain may adapt to an environment that never truly shuts off. That shift is thought to affect how they regulate attention, manage relationships, and interpret social pressure.

You see the results in subtle ways first — restlessness, heavier reliance on screens for comfort, later bedtimes — but the long-term patterns reveal why this conversation deserves your full attention. Your decisions about device access influence far more than screen habits; they shape foundational systems tied to sleep, mood balance, and healthy development.

Early Phone Ownership Shapes Health in Powerful Ways

A study published in Pediatrics investigated how early smartphone access influences depression, obesity, and sleep disruption in adolescents.1 The researchers set out to understand whether owning a smartphone at a younger age places a child on a different health trajectory than peers who don’t have these devices.

They analyzed data from 10,588 children in early adolescence, an age defined by rapid emotional growth and heightened sensitivity to social feedback. The findings showed higher odds of depression, obesity, and insufficient sleep among those who owned a smartphone at age 12 compared to those who did not.

• Health risks rise dramatically when phones enter a child’s life too soon — According to the study, adolescents who owned smartphones at age 12 had a 31% higher risk of depression, a 40% higher risk of obesity, and a 62% higher likelihood of insufficient sleep compared to peers without phones.

When you translate that into your child’s daily life, it means earlier ownership may shift mood, appetite, and energy patterns in ways that researchers say build with each earlier year of ownership — though the cited study followed outcomes only through age 13, not into adulthood.2

• The earlier a child gets a phone, the more those risks build year after year — Each year earlier that a child received a smartphone increased the odds of obesity by 9% and insufficient sleep by 8%. The researchers described this pattern as a “per-year effect,” meaning the timing itself matters, not just the presence of a phone.

This is consistent with the idea that delaying smartphone access may reduce cumulative risk, similar to how delaying exposure to other health-related stressors is thought to support long-term health.

• New smartphone access is linked to sharply diverging health paths — Among adolescents who did not own a smartphone at age 12, those who acquired one over the following year had a 57% higher likelihood of reporting clinical-level psychopathology and a 50% higher likelihood of insufficient sleep at age 13.

Even after adjusting for their baseline mental health, these differences held steady. This means the shift wasn’t simply explained by preexisting issues. The researchers describe this as an association, not proof that phone acquisition alone caused the change in behavioral and emotional patterns that followed.

• Sleep disruption from early phone exposure is a significant concern — While the study didn’t analyze specific app use or timing, insufficient sleep associated with phone ownership often reflects stimulation, nighttime alerts, late-night scrolling, and exposure to blue light, which disrupts melatonin, a hormone that regulates sleep-wake cycles.

Melatonin is primarily produced in your mitochondria in response to near-infrared light exposure, and healthy evening melatonin release depends partly on winding down light and screen exposure before bed. When melatonin drops in the evening, your child takes longer to fall asleep and experiences more fragmented rest. This pattern may reinforce fatigue-driven eating, lower movement, and mood instability.

• Smartphones expose children to increased social stressors — Smartphones expose adolescents to constant social feedback loops, including comparison, peer evaluation, and subtle forms of social exclusion. These experiences may influence cortisol — your body’s main stress hormone — which plays a role in energy balance, appetite, sleep quality, and emotional resilience.

When your child receives this type of stimulation before their brain has matured, stress patterns may form that are more difficult to unwind later.

Early Access to Smartphones May Alter Emotional Development in Lasting Ways

A related study published in the Journal of Human Development and Capabilities evaluated how childhood smartphone ownership influences emotional stability and psychological well-being in young adulthood.3

The researchers used data from the Global Mind Project, a worldwide mental health database, to determine whether the age a child receives a smartphone shifts measurable outcomes years later. The study population included 18- to 24-year-olds across multiple global regions, offering a broad view of how early smartphone exposure aligns with later emotional outcomes.

• Early phone ownership predicts deeper emotional struggles in young adulthood — Individuals who received a smartphone before age 13 experienced more suicidal thoughts, higher aggression, lower emotional resilience, and weaker self-worth as young adults. Girls reported the greatest emotional strain, while boys showed increased instability and reduced empathy compared to peers who received smartphones later.

Young adults who had smartphones earlier in childhood also experienced more symptoms described as “detachment from reality,” which means trouble staying grounded in real-world interactions and emotional experiences.

Early ownership was also associated with hallucinations, or perceiving things that aren’t present. The authors explained that these patterns were consistent across geographic regions, emphasizing that the phenomenon is not restricted to any single culture or social environment.

• The role of technology-driven stressors in worsening mental health — As the authors stated, emotional deterioration was linked to “social media access, cyberbullying, disrupted sleep, and poor family relationships,” all of which were more common among early smartphone recipients.

Cyberbullying refers to harassment or humiliation through digital platforms, and this form of stress often carries deeper psychological weight because it follows the child everywhere, without a break. Early access also increased exposure to algorithm-driven content, which reinforces comparison, insecurity, and compulsive scrolling patterns that affect emotional regulation.

• The earlier the phone, the worse the long-term results — The researchers noted a clear gradient: the younger the child at the time of ownership, the greater the severity of mental health symptoms in adulthood.4

The threshold at age 13 appeared especially important because neurological development at that age includes growth in impulse control and emotional regulation. When a child enters digital environments without these capacities in place, their coping systems may become shaped more by overstimulation than by healthy interpersonal feedback.

• Girls lose resilience and boys lose calm when phones arrive too early — Females who received smartphones before age 13 showed the largest drops in self-worth, confidence, and emotional resilience. These traits involve the ability to handle stress, recover from setbacks, and maintain a stable sense of identity.

For boys, the steepest changes involved emotional volatility, lower calmness, and reduced empathy. Early smartphone exposure disrupted the specific emotional strengths each group typically develops during adolescence.

• How family dynamics influence risk — According to the researchers, poor family relationships intensified the negative effects of early smartphone ownership, suggesting that children with less support experienced the steepest emotional declines. When a child receives a smartphone early without strong relational anchors, the device may become a significant emotional reference point, shaping beliefs, behaviors, and coping skills.

It’s worth noting that both studies discussed here are observational: They show associations between the timing of smartphone ownership and later health and mental health outcomes, not proof that smartphone ownership by itself causes these outcomes. The Journal of Human Development and Capabilities researchers note this as a limitation of their own work, even as they argue the scale of the potential impact justifies a precautionary approach.

Practical Steps to Protect Your Child’s Health in a Digital World

Your child’s brain and body respond to their environment more than you might realize, and early smartphone access may shape sleep, stress, and emotional development in ways that influence their long-term well-being.

That means your solutions have to target not only early smartphone exposure but also the root causes identified in the research: disrupted sleep, overstimulation, reduced movement, and constant exposure to digital social pressure. To take back control, structure your child’s environment with clear boundaries that support healthy rhythms. Straightforward steps create real progress without turning your home into a battleground.

1. Delay smartphone access until your child shows strong emotional regulation skills — You may help support healthy development when you match device access to your child’s maturity rather than their age alone.

If your child struggles with big emotions, impulsive choices, or social overwhelm, delaying a smartphone may help protect their confidence and long-term emotional health. When you present this as a skill your child is growing into rather than a hard restriction, they see that the goal is to make them stronger, not to punish them.

2. Keep smartphones out of the bedroom at all times — Protect your child’s sleep by removing nighttime triggers that may disrupt melatonin, disrupt sleep cycles, and interfere with emotional stability. This important boundary gives their nervous system a break from alerts, scrolling, and blue light. I recommend setting a family rule that all devices stay in a shared spot outside bedrooms, and taking regular phone breaks to manage smartphone dependence and give their mind a rest.

3. Limit wireless device use and reduce your child’s exposure to EMFs — Your child’s developing brain is thought to be more sensitive to wireless radiation than an adult’s, as their thinner skull bones are believed to offer less protection. If your child is constantly surrounded by wireless devices, they’re exposed to EMF levels that could disrupt mood regulation, impair focus, and raise risks of neurological problems over time.

I recommend treating wireless access as something used only when absolutely needed, not as a default.

To support your child’s long-term well-being, swap wireless connections for wired ones, turn off Wi-Fi when it’s not in use, and keep phones away from their body entirely. If your child reaches for a smartphone out of habit, build a simple routine together that replaces wireless use with safer alternatives. Treat it like a daily challenge they get to master, which strengthens their sense of control and lowers their total EMF load without creating conflict.

4. Create a predictable home routine that anchors sleep, movement, and downtime — You build stability by giving your child a rhythm that balances stimulation with recovery. If your child thrives on structure, set repeating anchor points throughout the day: morning sunlight, set meal times, walking breaks, and an early wind-down routine.

These anchors may help support healthy regulation of stress hormones and support mood resilience, especially for children who are regularly exposed to digital environments.

5. Use device rules that strengthen family connection instead of fueling conflict — Consistent rules give your child a clear framework, and that makes daily life smoother for both of you. Useful boundaries include things like no phones before school, no devices in bedrooms, and screen-free hours in the evening. If your child pushes back, involve them in choosing the exact times or places where phones stay off-limits.

You might agree on a “family tech-off night,” or designate a basket where phones go when everyone is home. Once they see why these rules matter — and once they help decide them — they’ll feel respected instead of controlled, and that shift may lower conflict while raising personal accountability.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

FAQs About Early Smartphone Use

Q: Why is age 12 such a sensitive time for smartphone ownership?
A: Age 12 sits in a window of rapid emotional and neurological development. The research suggests that receiving a smartphone at 12 or earlier is associated with disruptions in sleep, stress responses, and emotional balance. Earlier ownership also is associated with shifts in eating patterns, attention, and emotional coping skills in ways that appear to build year after year.

Q: What health risks rise when a child gets a smartphone too early?
A: Children who own a smartphone at age 12 face higher risks of depression, obesity, and insufficient sleep. These shifts influence confidence, learning, appetite regulation, and stress responses. For children who didn’t have a phone at 12, getting one between ages 12 and 13 was associated with sharply higher odds of clinical-level emotional symptoms by age 13.

Q: How does early smartphone access affect long-term mental health?
A: Young adults who received smartphones before age 13 reported more suicidal thoughts, lower emotional resilience, weaker self-worth, and symptoms of detachment from reality. Girls showed the greatest drops in confidence and resilience, while boys showed more emotional instability and reduced empathy.

Q: Why is sleep disruption such a key part of the problem?
A: Smartphones interfere with melatonin, the hormone that controls sleep-wake cycles. Nighttime scrolling, alerts, and bright screens delay sleep, fragment rest, and increase fatigue. Poor sleep then affects appetite, weight, stress tolerance, and emotional regulation.

Q: What practical steps help protect my child?
A: Delay smartphone access until your child demonstrates strong emotional regulation, keep phones out of bedrooms, limit wireless and EMF exposure, create a predictable daily rhythm, and use simple device rules that encourage cooperation rather than conflict. These steps target the root causes — overstimulation, sleep disruption, and emotional overload — and may support healthier long-term development.

GLP-1 medications have transformed how millions of people lose weight, but the number on the scale tells only part of the story. When appetite drops and pounds disappear quickly, it’s easy to assume everything is moving in the right direction. Yet experienced clinicians are raising a pointed question: what exactly are you losing?

If the answer includes a significant share of muscle along with fat, the consequences reach far beyond appearance. Muscle supports your strength, balance, mobility, and metabolism, and once it disappears, rebuilding it demands far more effort than preserving it in the first place.

At the same time, as prescriptions have surged, so have reports of medication-related problems reaching poison centers across the U.S. National data reveal a striking increase in reported exposures following approval of these drugs for weight management. A growing share of those cases proved serious enough to require professional medical evaluation.

The patterns behind those reports point less to a flaw in the medications themselves and more to gaps in education, dosing errors, and a population of newer users still learning how to handle the drugs safely.

Those trends highlight an important shift in the conversation. Success with these medications isn’t simply about losing pounds. It’s about preserving your health, protecting your metabolism, and avoiding preventable problems along the way. That starts with understanding why the quality of your weight loss matters every bit as much as the amount.

Muscle Loss Changes the Story Behind Weight Loss

In an MSN news report published in June 2026, interventional cardiologist Dr. Sanjay Bhojraj, who has more than 20 years of clinical experience, challenged the common belief that every pound lost on GLP-1 medications like Ozempic represents better health.1 Instead, he emphasized that the way you lose weight determines whether your health improves or declines. It’s worth noting that his comments come from a news interview and reflect his clinical perspective rather than findings from a formal study.

His message centered on a simple but often overlooked point: Successful treatment involves much more than taking a weekly injection. It requires a complete strategy that includes nutrition, exercise, and a realistic plan for maintaining results after the medication ends.

Instead of asking yourself only, “How much weight have I lost?” Bhojraj encourages you to ask a better question: “What exactly did I lose?” That shift in thinking changes the entire conversation because losing muscle carries very different consequences than losing excess body fat.

• Eating less doesn’t automatically make you healthier — One of Bhojraj’s strongest warnings addressed a mistake he frequently sees among patients who rely on appetite suppression alone. As he explained, “Not all weight loss on GLP-1 medications is healthy weight loss,” adding that “the biggest mistake I see? People confuse eating less with getting healthier.”

Your body still requires enough protein and regular physical activity while you lose weight. If your calorie intake drops sharply but your protein intake falls with it, your body begins breaking down muscle tissue to meet its energy needs.

• Protein and strength training help tell your body to protect muscle — Bhojraj explained that GLP-1 medications reduce appetite, but they don’t automatically protect lean body mass. Lean body mass refers to everything in your body that isn’t fat, including your muscles, bones, and organs. Muscle represents the largest part of that lean tissue and deserves special attention during weight loss.

His advice was straightforward. Prioritize adequate dietary protein while following a resistance-training program. Resistance training means exercises that force your muscles to work against a load, such as weight machines, free weights, resistance bands, or even your own body weight through movements like pushups, squats, and lunges. Those activities send your body a powerful signal that your muscles remain necessary and deserve to stay.

A practical way to monitor your progress is to track more than body weight. Notice whether everyday tasks become easier, whether you continue lifting similar weights in the gym, and whether your balance and stability remain strong. Those improvements provide evidence that you’re protecting the muscle that supports healthy aging instead of sacrificing it during rapid weight loss.

• Losing muscle slows the engine that burns calories every day — Bhojraj highlighted another consequence that many people overlook. Rapid weight loss frequently includes a significant amount of lean muscle loss, which he compares to sarcopenia — the loss of muscle tissue faster than the body replaces it.

Strictly, sarcopenia describes age-related muscle loss, while lean mass lost during rapid weight reduction is a related but distinct problem. Either way, the same two habits help protect muscle: adequate protein and resistance exercise.

Muscle requires energy even while you rest, which means people with more muscle naturally burn more calories throughout every day. When muscle disappears, your resting metabolic rate falls. Resting metabolic rate simply means the calories your body burns to keep your heart beating, lungs working, and organs functioning even while you sit or sleep.

This explains why some people struggle after stopping GLP-1 medication. A slower metabolism means your body requires fewer calories than before. If old eating habits return while calorie needs have dropped, regaining weight becomes much easier.

• Digestive health deserves attention throughout treatment — Another important point from Bhojraj’s discussion is that appetite suppression alone doesn’t equal complete metabolic health. He specifically included digestion among the factors people often ignore while focusing exclusively on the scale.

Digestion affects how efficiently your body breaks down food and absorbs the protein, vitamins, and minerals required to support muscles and normal body functions.

Simply eating less without paying attention to food quality leaves your body with fewer building blocks to repair and maintain healthy tissue. One useful habit is to review your routine every week instead of waiting until problems appear. Ask yourself whether you consistently eat enough protein, complete resistance exercise, tolerate meals comfortably, and maintain your energy throughout the day.

Those simple checkpoints help you judge your progress using real measures of health instead of relying only on body weight. The urgency to lose weight quickly doesn’t only affect what happens inside your body. It also shapes how quickly people take up the medications, and national data from poison centers track how sharply reported problems have grown alongside that uptake.

Poison Center Reports Revealed How Rapidly GLP-1 Problems Grew

A nationwide analysis, published in the Journal of Medical Toxicology, tracked how GLP-1 medication exposures changed after approval for weight loss.2 To understand how GLP-1 medication problems changed after semaglutide received U.S. Food and Drug Administration (FDA) approval for chronic weight management in 2021, researchers analyzed 10,033 exposures reported to the National Poison Data System between 2012 and 2023.

Semaglutide, sold under the brand names Ozempic and Wegovy, is the GLP-1 medication at the center of that growth.

The researchers focused on who experienced medication-related problems, what types of exposures occurred, and how often those events required medical care. Because the National Poison Data System collects reports from poison centers throughout the U.S., it provides a broad picture of real-world medication problems rather than the tightly controlled conditions found in clinical trials. That makes the findings especially valuable because they reflect what happens after medications reach everyday patients.

• Reported exposures more than doubled after weight-loss approval — The researchers identified 3,113 GLP-1 exposures before July 2021 and 6,920 afterward, meaning reports increased more than twofold following semaglutide’s approval for obesity treatment. Semaglutide-related poison center calls accelerated by an additional 9.9% every quarter after approval, confirming that the increase represented far more than routine year-to-year growth.

Semaglutide quickly became the medication involved in most reports. Before approval, it accounted for 24.6% of reported GLP-1 exposures. After approval, that figure jumped to 64.2%, making it the dominant product reported to poison centers. Other GLP-1 medications increased only slightly during the same period.

• The average age of reported exposures dropped from 57 years before approval to 51.6 years afterward — When the authors roughly estimated the age of just the newly exposed group, the average dropped to about 47.5 years — though they called this an approximation, and the data can’t tell whether someone was taking the drug for diabetes or for weight loss.

Women also represented a much larger share of reported exposures, increasing from 68.9% before approval to 78.2% afterward. Those changes reflect how the medications expanded beyond their original role in diabetes treatment. As more adults without diabetes began using GLP-1 drugs for obesity, poison center reports shifted toward a younger population that differed from the earlier patient group.

• Most reports involved dosing mistakes rather than intentional overdoses — Researchers found that therapeutic errors, meaning people accidentally took the medication incorrectly, accounted for the majority of reported exposures in both periods — 85.6% before approval and 81.0% afterward, a slight decline as a share even as the raw number rose. Examples include taking the wrong dose, injecting the medication too often, or misunderstanding how to use the injection pen.

The pattern also shifted toward first-time or short-term use. Acute exposures, meaning a single incorrect dose or one-time mistake, increased from 47.2% before approval to 58.7% afterward, while acute-on-chronic exposures, meaning problems that developed during ongoing regular use, declined. This supports the researchers’ conclusion that many reports involved newer users who were still learning how to use the medication correctly.

• More people needed medical evaluation even though many symptoms remained mild — The investigators found that the proportion of patients managed in or referred to a health care facility increased from 23% before approval to 33.5% afterward, representing a 46% higher likelihood of requiring professional evaluation.

Note that this category counts people who were already at a health care facility when the call was placed as well as those referred to one, so it is broader than “required professional evaluation.” At the same time, the study reported that most exposures still produced relatively mild gastrointestinal symptoms.

Even so, digestive symptoms sometimes became severe enough to require medical attention because repeated nausea and vomiting increase the risk of dehydration, meaning your body loses more water and minerals than it replaces. One death was reported across the 10,033 exposures — a patient who had undergone liposuction and developed colonic ischemia — and the authors state that causality cannot be determined from a single report.

They concluded that improved patient counseling and clearer poison center guidance may help reduce preventable therapeutic errors and unnecessary emergency evaluations.

• They are equally clear about what their data cannot do — Poison center reports “cannot establish causality,” and the study is descriptive pharmacovigilance rather than evidence that these medications caused the outcomes reported.

Two cautions the authors themselves raise are worth keeping in mind alongside these numbers. Because these drugs drew intense media and social media attention, the authors write that the rise in call volume “likely reflects a combination of rapid expansion in the user base and variable degrees of stimulated reporting.”

This means some of the increase reflects more people picking up the phone, not only more people having problems. At the same time, because reporting to poison centers is voluntary, the data may understate how often these problems actually occur.

Build the System That Regulates Your Appetite Naturally

Your body already contains the machinery to regulate appetite, burn fat, and protect muscle without a weekly injection. The problem isn’t that the system is broken beyond repair. The problem is that modern diets and lifestyle habits have suppressed the signals it depends on. GLP-1 medications reduce appetite, but they also introduce risks that range from muscle loss to medication errors and other complications.

Rather than replacing your body’s own appetite-regulating system with an injection, I recommend restoring the biological processes that already exist. Your colon naturally produces GLP-1 through specialized cells called L-cells,3 and those cells are thought to respond to butyrate,4 a short-chain fatty acid made by beneficial gut bacteria. When your microbiome functions the way it was designed, it helps regulate appetite, blood sugar, and metabolism while you preserve your strength instead of sacrificing it.

1. Remove the foods that prevent your gut from recovering — I recommend eliminating seed oils, such as soybean, corn, canola, sunflower, and safflower oil, because their high linoleic acid (LA) content degrades the gut environment that beneficial bacteria depend on to thrive. Excess LA is also thought to impair your colon cells’ ability to use butyrate for energy, weakening the protective lining of your digestive tract.

Use more stable traditional fats instead, such as tallow, ghee, or grass fed butter. Keep your LA intake below 5 grams per day, and ideally closer to 2 grams, to give your microbiome the opportunity to recover and begin producing the compounds that support healthy appetite regulation.

2. Heal your digestion before increasing fiber — If you struggle with bloating, abdominal discomfort, or irregular bowel habits, avoid loading your diet with large amounts of fermentable fiber all at once. Begin with simple, easy-to-digest meals that reduce excessive fermentation while your intestinal lining recovers. As digestion becomes more predictable, gradually increase carbohydrates using foods your body tolerates well.

Whole fruit and well-cooked white rice provide glucose for cellular energy without overwhelming an already stressed microbiome. Next, add root vegetables, followed by non-starchy vegetables and then starchy vegetables such as squash and sweet potatoes. Leave beans, legumes, and minimally processed whole grains until last, and only if your digestion remains comfortable. Most adults do best with roughly 250 grams of carbohydrates each day once metabolic health improves.

3. Feed the bacteria that produce butyrate — Once your gut becomes more stable, begin adding foods that nourish butyrate-producing microbes. Cooked-and-cooled white potatoes and green bananas contain resistant starch, a type of carbohydrate that reaches your colon intact and serves as food for beneficial bacteria.

As those microbes multiply, butyrate production increases, your gut barrier becomes stronger, and your body regains the natural metabolic signals that help regulate appetite and blood sugar.

A useful detail: You don’t have to eat potatoes cold to get the benefit. Cooking, cooling, and then gently reheating them retains most of the resistant starch, so a rewarmed baked potato or a pan of leftover roasted potatoes still feeds those beneficial bacteria effectively.

4. Protect your muscle while your metabolism recovers — Preserving muscle deserves as much attention as losing fat. Prioritize adequate protein and regular resistance exercise throughout your weight-loss journey. Aim for 0.6 to 0.8 grams per pound (1.32 to 1.76 grams per kilogram) of ideal body weight, with one-third coming from collagen-rich sources like slow-cooked meats or bone broth.

Weight training, resistance bands, and bodyweight exercises all help tell your body to hold onto muscle instead of breaking it down for energy. Strong muscles also keep your metabolism higher, making it easier to maintain your progress over the long term.

5. Judge success by how your body performs, not just by what you weigh — I encourage you to look beyond pounds lost. Your strength, daily movement, energy, and ability to handle everyday activities without strain tell you far more about your metabolic health than any number on a scale.

Those measurements tell you whether your metabolism is becoming healthier or simply becoming smaller. I explain how to restore your body’s own GLP-1 production through nutrition and metabolic support in my book, “Weight Loss Cure: Melt Fat Naturally with Your Own GLP-1,” where I outline practical strategies for rebuilding the biological systems that regulate appetite naturally.

FAQs About GLP-1 Medications and Weight Loss

Q: Why isn’t all weight loss on GLP-1 medications considered healthy?
A: The scale doesn’t distinguish between fat and muscle. If a significant portion of your weight loss comes from muscle, your metabolism slows, your strength declines, and maintaining your results becomes more difficult. Protecting muscle through adequate protein intake and resistance exercise is just as important as losing excess body fat.

Q: Why did poison center reports involving GLP-1 medications increase so quickly?
A: As these medications became widely prescribed for weight management, reports to poison centers rose sharply. Many cases involved accidental dosing mistakes rather than intentional overdoses, especially among newer users who were still learning how to administer the medications correctly.

The study’s authors add that intense media attention probably encouraged more people to call, so part of the rise reflects reporting behavior rather than a rise in problems alone — though because reporting to poison centers is voluntary, the data still likely understate how often these problems actually occur.

Q: What’s the biggest mistake people make while taking GLP-1 medications?
A: Focusing only on eating less instead of improving overall health. Appetite suppression alone doesn’t preserve muscle, support digestion, or build habits that last after the medication stops. A long-term plan includes nutritious meals, regular strength training, and attention to metabolic health.

Q: If I decide not to use a GLP-1 medication, how can I support healthy appetite control?
A: Restoring a healthy gut microbiome helps your body regulate appetite naturally. Removing foods that disrupt gut health, healing digestion, feeding beneficial bacteria, and preserving muscle all support the biological systems involved in healthy metabolism instead of relying on an injectable medication.

Q: How should I measure progress if the scale isn’t the whole story?
A: Look at more than your body weight. Improvements in strength, energy, balance, endurance, and your ability to perform everyday activities provide a much better picture of whether your metabolism and overall health are moving in the right direction. Your goal is lasting health, not simply a lower number on the scale.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

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Why is fluorine added to some medicines?

To increase vitamin content and bioavailability
To change the medicine’s color
To improve stability or how it moves through the body
Fluorine can help medicines resist breakdown, remain stable, or move through the body differently, but it usually does not provide the therapeutic effect. Learn more.
To provide the medicine’s main therapeutic effect

Fatty liver disease affects 38% of adults in the United States — a statistic that has increased by 50% in the past 30 years.1 This condition, characterized by the buildup of fat in liver cells, often progresses silently, with many people not realizing they have it until they start experiencing symptoms like fatigue, abdominal discomfort, or abnormal liver enzyme levels. When left unaddressed, fatty liver disease can advance to inflammation, fibrosis, and even cirrhosis.

Centuries ago, people naturally ate foods that are considered rich in prebiotic fiber nowadays. Garlic, onions, and leeks were common staples in traditional diets across Europe and Asia, prized not just for flavor but for how they “kept the body clean.” Modern research is currently examining whether these vegetables do more than aid digestion — and whether the fiber they contain shifts how gut microbes handle sugar, potentially easing the metabolic load on the liver. And this benefit comes from a natural fiber called inulin.

What the Research Found About the ‘Fiber Revolution’ in Your Gut

A study published in Nature Metabolism and conducted by researchers from the University of California, Irvine (UCI) School of Medicine revealed that inulin-rich vegetables — such as onions, garlic, leeks, and chicory — contain a fiber that, in mice, changed the way gut bacteria behave and reduced fructose-driven liver damage. In this animal model, increasing intake of the naturally occurring, plant-based fiber shifted microbial metabolism so that less fructose reached the liver.2

• What is inulin? To put it simply, inulin is a soluble, fermentable prebiotic fiber composed of fructose chains. It travels to the lower gut region where certain gut microbes digest and convert it into short-chain fatty acids (SCFAs) like butyrate and propionate.3 Inulin, as a dietary fiber, not only nourishes colon cells — it is also being studied for a second role, which is buffering the liver against the effects of high fructose intake.

• The researchers conducted the study on male mice — This group is more susceptible to fatty liver. The mice were divided into four main dietary arms:

◦ Standard chow with plain water (control)
◦ Standard chow with high-fructose corn syrup (HFCS) water, to induce liver fat and insulin resistance
◦ An inulin-supplemented diet with HFCS water
◦ A delayed-intervention arm that received HFCS water for 16 weeks before inulin was added for a further 14 weeks

A separate antibiotic-treated group was used to confirm the effect depended on the microbiome.

• The research was particularly focused on a model of lean metabolic liver disease who were not obese — This is a group that’s often overlooked when it comes to metabolic disease prevention. Many people assume only those who are overweight develop fatty liver, but human epidemiology indicates that even individuals with normal body weight can experience liver damage associated with high fructose consumption.4 Note that the experiments themselves were conducted entirely in mice — no human participants were enrolled.

• They tracked where the sugar went — The researchers used what’s called isotope tracing, meaning there are special forms of fructose and water that can be followed as they move through metabolic pathways. These tracers allowed them to track exactly where the fructose went — whether it was broken down in the gut, converted to fat in the liver, or transformed into amino acids and antioxidants. This gave them a real-time view of how inulin changed the animals’ internal chemistry.

• Here’s what they discovered — In mice given sugary HFCS water, adding inulin protected their metabolism. It prevented or reversed fatty liver, lowered harmful liver lipids, and improved insulin resistance. Mechanistically, it turned down fat-making, boosted fat-burning, and rerouted fructose to be broken down by gut microbes before it could overload the liver.

One important dose caveat — the researchers replaced 10% by weight of dietary starch with inulin, and noted that this level exceeds what humans typically tolerate (around 4%). It follows standard rodent-study practice, but it is not a human dose.

Why the Gut-Liver Axis Matters

Your liver and gut are in constant conversation. Every meal you eat, every sip of soda or bite of processed food, sends signals through this communication highway known as the gut-liver axis. This axis is anchored in a direct anatomical link: the hepatic portal vein, which is the vessel that carries nutrient-rich blood from your intestines directly to your liver for processing.5

• When your gut is healthy, this system functions like a well-tuned messaging network — But when your gut bacteria are unbalanced, what scientists call dysbiosis, more inflammatory compounds and microbial byproducts are thought to reach the liver. Researchers have linked sustained exposure of this kind to fat accumulation, oxidative stress, insulin resistance, and eventually, fatty liver disease.

• So what’s the role of inulin in this? According to Dr. Cholsoon Jang, inulin “changes the bacteria in the gut to promote the consumption of harmful dietary fructose.” In simpler terms, this means that the bacteria in the intestines become proactive and start eating up the sugar before it causes trouble. In the mice studied, the result was less sugar “spilling over” to the liver, less fat buildup, and a stronger antioxidant response within the liver.6

• Here’s one of the most fascinating findings from the featured study — Inulin’s protective process appears to begin earlier in digestion than scientists previously believed. The small intestine, not just the colon, hosts bacterial communities capable of fermenting inulin. This early fermentation means that sugar molecules like fructose can be intercepted before they reach the liver.

• The study showed that these bacteria literally consume fructose — They’re burning it as their own energy source before it spills into the bloodstream. This “sugar-buffering” effect is the mechanism the authors propose for the lower liver fat and improved insulin sensitivity they observed. Whether the same buffering occurs at the fiber intakes people can realistically tolerate has not yet been tested.*

• Inulin also helped prevent hepatic de novo lipogenesis — This is the biological term for the liver’s creation of new fat from excess sugar. When this process slows down, liver fat levels stabilize, blood sugar becomes easier to regulate, and inflammation declines. In this model, the change originated in the microbiome rather than in the liver itself.

• Once the gut was “trained” with inulin, the initial signs of fatty liver were reversed — These include reduced liver fat deposits and better antioxidant response. “Our findings provide insight into how fibre protects our health from harmful nutrients like fructose,” Jang commented.7

• The antioxidant activity was tied to an increase in the liver’s production of glutathione — Called “the master antioxidant,” glutathione is one of the most powerful detoxifying compounds in the body. Glutathione helps the liver neutralize reactive compounds and limit oxidative damage. In the inulin-fed mice, glutathione production rose and markers of fructose-induced lipid peroxidation fell. This is the authors’ proposed explanation for the improved antioxidant response.

These findings point toward a future of personalized nutrition strategies. By identifying which types of gut bacteria are most efficient at processing fructose, health care practitioners could one day design customized diet plans or match prebiotic or probiotic choices to different individuals. In Dr. Jang’s words:

“By checking how well someone’s gut bacteria clears fructose before the body absorbs it, we can choose the right prebiotic or probiotic supplement for that person to improve results and reduce side effects.”8

*These findings are from laboratory or animal research and may not directly apply to human health.

Food First — Onion and Garlic Are the Easiest Place to Start

Inulin is found in various vegetables, and chances are some of these are already in your kitchen pantry. These include onions, garlic, chicory root, artichokes, leeks, and asparagus. These may seem ordinary, but their prebiotic fiber is the raw material your gut microbes ferment. Among these, onion and garlic are not the richest sources — chicory root and Jerusalem artichoke are far higher — but they are the easiest to work into everyday meals:

• It’s okay to start small — Even modest, consistent intake of inulin-rich vegetables, especially onions and garlic, is a reasonable way to increase prebiotic fiber. A practical, food-first approach begins with a quarter to half a cup of cooked onion daily or half to one clove of garlic added to your regular meals. These portions are general tolerance-building suggestions for ordinary culinary use, not a therapeutic dose — no human intake level has been established for the liver effects observed in the mouse study.

Once your gut adjusts, small portions, like a teaspoon of finely chopped onion in a salad or a sliver of garlic in dressing two to three times per week can amplify the benefits.

• What matters most is consistency — Your gut bacteria need time to adapt and “learn” to process the inulin effectively. The research team found that microbial adaptation is what allowed the gut to intercept fructose in their animal model. Feeding your microbiome steadily is the pattern that mirrors how the effect was produced in that featured study.

• This gradual approach also taps into the principle of self-efficacy — This refers to the belief that small, repeatable actions can make a measurable difference. Seeing your digestion improve, your energy stabilize, and even your post-meal bloating diminish reinforces the motivation to stick with the habit. It’s not about restriction; it’s about building body confidence through achievable, everyday wins.

• To sustain the habit, personalize it — Connect your meals to outcomes that matter to you: clearer skin, lighter mornings, better digestion, or a sense of control over your health. Each time you chop garlic or caramelize onions, you’re not just cooking — you’re feeding the microbes that ferment prebiotic fiber — the same adaptation researchers are studying for its effects on sugar handling and liver fat.

This sense of personal mastery builds long-term adherence far better than fear-based restriction. As the featured study emphasizes, microbial adaptation depends on regular input rather than sporadic perfection. Each small meal you prepare is a step toward the steady pattern that adaptation requires.

Other Inulin-Rich Vegetables You Can Try

If you want to mix things up, there are other vegetables that work through the same gut-liver mechanism. Rotating your sources helps your gut bacteria thrive in diversity, improving overall metabolic balance. Here are some inulin-rich vegetables to add to your meals (per 100-gram serving):9

• Leeks (6.5 g) — The white and light green parts are excellent for soups and stir-fries. Their gentle sweetness and high inulin content make them a smooth next step once you’ve mastered onions.

• Chicory root (41.6 g) — Often found in herbal coffee substitutes, it’s one of the richest natural sources of inulin. Start small by adding just a teaspoon of chicory blend at a time to test your comfort level.

• Jerusalem artichoke or sunchoke (18 g) — This vegetable is particularly high in inulin, so begin with very small portions (a few thin slices roasted or blended into soup). Once tolerated, it becomes one of the densest food sources of the fiber your gut microbes ferment.

• Asparagus (2.5 g) — Although its inulin is not as high as other vegetables, this food has a well-rounded nutrition profile, offering minerals like copper, selenium, zinc, magnesium, and more.

These everyday inulin-rich vegetables are far more than garnishes — they’re accessible, everyday sources of prebiotic fiber you can prepare right in your kitchen. I recommend following this “food-first” approach, as it doesn’t require supplements or complex protocols — just consistency, mindfulness, and an understanding of how these humble kitchen staples fit into a diet that can support gut and metabolic health.

How About Inulin Supplements?

Inulin supplements often appear in health stores labeled as “gut health boosters” or “prebiotic powders.” While they might seem like an easy shortcut, it’s important to understand that supplements are not a substitute for real food. This distinction matters because these vegetables provide more than fiber — they deliver enzymes, minerals, and other cofactors that shape how your microbiome responds.

• When you eat a whole vegetable, you’re offering your gut bacteria a complete ecosystem — These include water, nutrients, and structural fibers that slow fermentation and make digestion smoother.

In contrast, a powdered supplement delivers inulin in a concentrated dose that your system might not be ready for. For someone with a balanced gut, this might not cause issues. But if your microbiome is fragile or underdeveloped, which is common after years of stress, low-fiber diets, or antibiotic use, jumping straight into concentrated inulin can backfire.

• That said, there are situations where inulin supplementation can be helpful — If you’re under medical supervision and tracking your Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) score, which is a valuable diagnostic tool that helps assess insulin resistance, adding a measured dose of inulin powder under clinical guidance could make sense.It’s a strategic choice for individuals who need more controlled intake or who can’t tolerate raw or cooked vegetables easily. Work with a knowledgeable clinician or nutritionist to help you identify a beneficial dose and gradually raise it while monitoring your response.
Talk to your healthcare provider about whether this testing is appropriate for you.
• Imagine it like strength training for your gut — You wouldn’t walk into a gym and lift 200 pounds on your first day. You start light, master your form, and increase gradually. The same goes for inulin. Whole foods are your training weights: gentle, consistent, and structured. Inulin powder, on the other hand, is advanced resistance: best reserved for when your body is ready for it.

Important Safety Considerations When Consuming Prebiotic Fibers Like Inulin

When you begin increasing prebiotic fiber — especially inulin — it’s common to experience temporary bloating or gas. These symptoms are usually a sign that your microbiome is adjusting rather than a cause for alarm — but persistent or worsening symptoms are worth discussing with your health care provider.

• Your gut bacteria are adjusting to a new energy source — As they ferment inulin, they produce gases like hydrogen and carbon dioxide, which can cause mild bloating in the first few days or weeks. This is part of the microbial retraining process.

• The key is pacing — Start with very small amounts and increase slowly over time. If you’re using food, that might mean starting with a tablespoon of cooked onion per meal or half a clove of garlic. If you’re under medical care and using a powder, begin with as little as one to two grams daily and work up gradually.These starting amounts are conservative, practical suggestions rather than doses drawn from the cited research. Jumping to a full serving too quickly overwhelms your microbiome and creates discomfort.

However, if you regularly feel bloated after meals, go days without a bowel movement or have frequent loose stools, even before you increase your inulin intake, your gut may be in poor shape and is not ready for high-fiber foods. These symptoms suggest an imbalanced gut microbiome or irritated gut lining. This is important, as you need to address the underlying gut problem before reintroducing fermentable fibers like inulin.

• Avoid fiber and fermentable carbs if your digestion is impaired — A damaged gut often cannot handle even “healthy” fiber-rich foods. Beans, leafy greens, cruciferous veggies, and whole grains all ferment quickly and feed the wrong microbes when your gut is compromised. That drives more bloating, inflammation and gas. In this phase, you want fuel that doesn’t backfire, like whole fruit and cooked starches like white rice, which digest more cleanly without fermenting too fast.

• Reintroduce fermentable fibers in small amounts once your gut calms — When your bloating stops and your digestion becomes regular, that’s your green light. Start with resistant starches like cooked-and-cooled white potatoes or green bananas.

These feed butyrate-producing bacteria — the strains associated with gut barrier integrity and inflammatory balance. This is also when you can slowly add in inulin-rich vegetables like onion, garlic, and leeks. Keep portions small and build up as your tolerance improves (the next section will help you with this).

• Those with gut conditions are advised to approach with extra care — These include Irritable Bowel Syndrome (IBS) or Small Intestinal Bacterial Overgrowth (SIBO). Both conditions involve bacterial imbalance, and adding prebiotics too fast can feed the wrong microbes before balance is restored.

• Listening to your body is the ultimate feedback loop — Discomfort often accompanies a shift in your microbial community; easing discomfort suggests it has adapted. This process embodies the principle of personalization — understanding your unique response and adjusting based on what your body tells you.

A 7-Day Micro-Plan to Build Tolerance

This seven-day micro-plan works like a gentle training schedule for your microbiome. Each day adds just enough new stimulus to encourage microbial diversity, reduce inflammation, and minimize discomfort.

• Days 1 and 2: 2 to 3 tablespoons of cooked onion in one meal — Add sautéed or roasted onion to your main meal, mixing it into rice or soup. Cooked onion introduces inulin gradually while also supplying antioxidants like quercetin, which have been studied for their antioxidant activity.

Observe how your body reacts. Bloating, gas, or changes in bowel movement are common while your microbes adjust. To manage these early effects, drink water slowly throughout the day and avoid eating too fast.

• Days 3 and 4: Add half a clove of cooked garlic — Garlic is slightly stronger than onion in both flavor and prebiotic potency. It contains allicin, a sulfur compound that has been investigated for antimicrobial and immune-related activity.

This step builds microbial endurance. The aim is to widen the range of fermentable fibers your gut can tolerate — the kind of adaptation the featured study links to changes in how the liver handles sugar and fat. If you feel gassy, it’s a byproduct of the fermentation that also produces SCFAs.

• Day 5: Include 2 tablespoons (cooked) leeks or chicory — These vegetables provide different strains of inulin and other prebiotic fibers, which encourage microbial variety. Chicory also contains polyphenols that act like fertilizers for your beneficial bacteria. Leeks, on the other hand, have a softer flavor and gentler fiber profile, making them perfect for soups and stews. This step marks the turning point where your gut begins to “graduate” from basic to intermediate tolerance.

• Day 6: Test 1 teaspoon raw onion in a dressing if tolerated — Raw onion introduces a stronger dose of inulin in an unheated form. If you’ve tolerated the previous steps without excessive discomfort, mix one teaspoon of finely minced raw onion into a salad dressing or salsa. This is simply a tolerance test for raw prebiotic fiber.

If you feel mild bloating, reduce the portion or pair the meal with an acidic component such as vinegar or lemon. Many people find acidic pairings easier on digestion. This day is about testing boundaries safely.

• Day 7: Adjust upward or maintain based on comfort — This is where you customize your intake. If digestion feels light and your energy is stable, you can increase your portions slightly — maybe half a cup of cooked onion daily and one full clove of garlic spread across two meals. If you notice lingering discomfort, stay at your current level for a few more days before advancing. The goal is comfort and consistency, not speed.

This stage reinforces self-efficacy — you’re now in control of your microbiome’s pace of adaptation. You’ve built awareness around how your gut responds and learned to listen to your body’s cues. Over time, this approach strengthens both digestion and confidence in your ability to manage it.

A 7-Day Gut Training Plan — An Overview
Here’s a one-week plan to help your gut adjust to inulin-rich foods like onions and garlic — without bloating. This is a quick-reference summary of the micro-plan above, not a second protocol.

• Days 1–2: Eat 2 to 3 tbsp. of cooked onion. Eases digestion and introduces inulin gently.
• Days 3–4: Add 1/2 clove of cooked garlic for stronger prebiotic and immune support.
• Day 5: Include 2 tbsp. of cooked leeks or chicory for more fiber diversity.
• Day 6: Try 1 tsp. raw onion in a dressing if comfortable. Use vinegar or lemon to reduce gas.
• Day 7: Increase slightly or hold steady based on comfort.
Slow progression lets your gut bacteria adapt, build resilience, and support liver health naturally.

More Strategies to Support Liver Health

While inulin shows strong promise in helping protect your liver from sugar damage, it’s just one aspect of keeping this organ in optimal condition. Remember, your liver is your body’s central detox organ, and when it’s overloaded not only with sugar but with harmful fats, toxins, or nutrient gaps, it struggles to do its job efficiently. These tips address factors commonly implicated in liver stress.

1. Eliminate vegetable oils and alcohol — Vegetable oils are high in linoleic acid (LA), a polyunsaturated fat (PUF) that oxidizes and forms byproducts that may compromise your mitochondria, the powerhouses of your cells. Alcohol is also damaging, since it breaks down into a compound that injures liver cells. Cutting both is one of the highest-value changes you can make. For cooking, switch to grass fed butter, ghee, or tallow. Lastly, keep total LA intake between 2 and 5 grams per day.

2. Optimize your carbohydrate intake — Aim for 250 grams of targeted carbohydrates daily from whole, unprocessed foods, adjusting upwards if you are highly active, based on your microbiome. As your digestion strengthens, introduce complex carbohydrates and starches like white rice gradually to maintain balanced energy and support metabolic function.

3. Eat choline-rich foods to support liver health — Choline helps package up fats and ship them out so your liver doesn’t become clogged. Inadequate choline intake has been associated with fat accumulation in liver cells. The best food sources are pastured egg yolks and grass fed beef liver.

4. Consider taking a choline supplement if your diet falls short — Citicoline is one of the more widely studied forms. Research has examined daily doses in the range of 500 to 2,500 milligrams (mg) for effects on hepatic fat export and cognitive function. With this in mind, discuss dosing with a qualified health care provider before starting any supplement.

5. Repair with sunlight and smart vitamin D use — Your skin is designed to make vitamin D from sunlight, and daily exposure supports not only your bones and immune system but also your liver’s ability to metabolize fat. But here’s the catch: If you’re still using vegetable oils, the LA stored in your skin increases your risk of sun damage.Eliminate those oils for four to six months before building up to high-intensity sun exposure, with the aim of going out during solar noon. When sunlight isn’t an option, consider supplementing with vitamin D3.

It’s also important to test and track your vitamin D to stay on target. Instead of guessing, check your vitamin D levels with a simple blood test at least twice a year. Aim for 60 to 80 ng/mL (150 to 200 nmol/L). This range is the target I recommend to help support immune function and energy production.

Talk to your health care provider about whether this testing is appropriate for you.

Frequently Asked Questions (FAQs) About Inulin and Fatty Liver Disease

Q: Does inulin help fatty liver?
A: In mice, it did. A study published in Nature Metabolism found that inulin-adapted gut microbes intercepted fructose early in digestion, before it reached the liver, and that this reduced fat accumulation in liver cells and lowered markers of inflammation. The study was conducted entirely in animals at a fiber dose above typical human tolerance, so the same effect has not yet been demonstrated in people.
In simpler terms, inulin appears to help “train” the gut bacteria to eat up sugar first, so the liver doesn’t have to. Adding inulin-rich vegetables is a low-risk dietary change, and one field that researchers are actively studying for its metabolic effects.

Q: Is inulin good for liver health?
A: The evidence so far is promising but preclinical. In the mouse study, inulin increased the production of glutathione, your liver’s most powerful antioxidant molecule. Inulin also reduced the “spillover” of sugar from the gut into the bloodstream, which means the liver did not have to convert that excess sugar into fat. In that model, this was accompanied by lower oxidative stress.

Q: Which vegetables have the most inulin?
A: The richest sources of inulin are chicory root (41.6 g per 100 g) and Jerusalem artichoke (18 g), followed by garlic (12.5 g), leeks (6.5 g), onions (4.3 g) and asparagus (2.5 g). Cooked onions and garlic are the easiest and most tolerable ways to start, especially if you’re new to prebiotic fibers.
Leeks offer a gentle alternative that’s excellent for soups and stews, while chicory root and Jerusalem artichoke deliver higher doses for those further along in their gut restoration journey. Each of these vegetables nourishes your beneficial microbes, improves digestion, and supports your gut-liver communication loop.

Q: How much inulin is safe?
A: There’s no one-size-fits-all number, because everyone’s microbiome adapts differently. The key is not how much you eat, but how gradually you introduce it. Think of it as training your gut, not forcing it. Start with small servings — like a few tablespoons of cooked onion — and increase only when your digestion feels comfortable. This slow approach minimizes gas and ensures your bacteria adjust properly.

Q: Why does inulin cause gas or bloating?
A: When you first increase your intake of inulin, your gut bacteria begin fermenting it into short-chain fatty acids (SCFAs) — molecules that nourish your colon and reduce inflammation. This fermentation produces gas as a natural byproduct. If you experience bloating or mild discomfort, that’s usually a sign your microbes are adjusting to a new food source — though symptoms that persist or worsen are worth raising with your healthcare provider.
The best approach is to start low, go slow, and focus on cooked vegetables before introducing raw forms. As your microbial community becomes stronger and more balanced, these early symptoms typically fade.

Q: Is food-based inulin better than supplements?
A: For most people, yes. Whole foods provide inulin alongside natural cofactors like water, minerals, and enzymes that help your gut process fiber efficiently. Supplements, in contrast, deliver concentrated doses that can overwhelm an untrained gut.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.

Heart disease feels like a permanent feature of modern life, but it wasn’t always that way. In the late 1800s, coronary heart disease was uncommon, and most people died from infections rather than chronic vascular problems. Today, coronary heart disease sits at the center of cardiovascular mortality, bringing with it chest pain, breathlessness, fatigue, and sudden heart attacks that often appear after years of silent damage.

That contrast alone raises a basic question you deserve an honest answer to: What fundamentally changed? The usual explanations focus on longer lifespans, better diagnostics, or individual behavior. I don’t find those answers sufficient.

When I examined long-term mortality data, one pattern stood out: Something changed the internal environment of human arteries long before heart attacks became common. One change stands out because it happened quickly, affected nearly everyone, and reshaped what people ate every single day.

My paper, “Seed Oils as a Hypothesized Contributor to Heart Disease: A Narrative Synthesis,” published in the journal Cureus on January 21, 2026, explains why the widespread adoption of industrial seed oils deserves closer scrutiny.1

It synthesizes over 200 references showing that the rapid adoption of LA-rich industrial seed oils in the early 1900s preceded the surge in coronary heart disease deaths by 10 to 20 years — the exact timeframe needed for atherosclerotic plaques to develop — and that LA oxidation generates the same inflammatory aldehydes like 4-HNE now implicated in oxidative damage to the lining of blood vessels.

Coronary heart disease doesn’t begin with a heart attack. It begins quietly, with changes inside blood vessels that build year after year. To understand why heart disease became so widespread — and how you can change your own trajectory — you need to see how one dietary shift altered the internal environment of your arteries over time. I break down that evidence step by step in my paper, which you can read in full below.

> > > > > Click Here

When you hear “PFAS,” you probably think of nonstick cookware, waterproof jackets, or contaminated drinking water. You probably don’t think of the prescription sitting in your medicine cabinet. Yet fluorinated compounds classified as per- and polyfluoroalkyl substances (PFAS) are built into a surprisingly wide range of approved pharmaceuticals, often not because they’re essential to how those medicines treat disease, but because they make the drug easier to formulate.

If fluorine serves the manufacturer’s design goals more than the patient’s therapeutic needs, then every PFAS-containing medicine that passes through your body and into the water supply deserves a harder look, particularly now that researchers have mapped out whether effective alternatives already exist. An analysis published in Sustainable Chemistry and Pharmacy took on exactly that question, and the answer should change how we think about drug design going forward.1

PFAS-Free Drug Alternatives Already Exist Across Nearly Every Medical Category

For the study, researchers investigated whether PFAS-containing medicines are truly necessary or whether practical alternatives already exist.2 They reviewed approved active pharmaceutical ingredients (APIs), the part of a medicine that produces its therapeutic effect, and identified 111 PFAS-containing medicines used in humans and 28 used in veterinary medicine.3

The researchers found that 87% of the 111 human PFAS-containing medicines already have a non-PFAS alternative available, with alternatives in development for nearly all of the remainder — directly challenging the long-held belief that fluorinated medicines are medically indispensable.

According to the study’s lead researcher Dr. Michael Müller of the University of Freiburg, “The fact that PFAS-free alternatives already exist for almost all indications is a clear indication that, from a pharmacological point of view, per- or polyfluorination is not strictly necessary.”

• Fluorine usually improves drug performance rather than treating disease — The analysis found that fluorine is rarely responsible for a medicine’s therapeutic effect. Instead, drug developers often add fluorine because it helps medicines remain stable, resist breakdown, or move through the body differently. Those properties make medicines easier to design and formulate, but they’re separate from the drug’s intended medical action.

That distinction is important because it shows many medicines can achieve the same therapeutic result without relying on PFAS chemistry, creating opportunities to reduce persistent environmental contamination while maintaining effective treatment.

• Most PFAS-containing medicines eventually become another persistent environmental pollutant — Researchers found that 84% of the PFAS-containing medicines they examined have the ability to degrade into trifluoroacetic acid (TFA), a highly persistent PFAS compound that remains in the environment instead of breaking down naturally.

The study explains that once medicines are excreted, they enter wastewater systems and eventually reach rivers, lakes and groundwater. The researchers also note that removing TFA from drinking water is extremely difficult. For that reason, the authors argue that preventing TFA formation at the source is far more effective than trying to remove it later.

• PFAS-containing medicines are used across almost every area of health care — The researchers mapped PFAS-containing medicines using a classification system that groups medicines according to the conditions they treat. They found these medicines are spread across numerous therapeutic categories rather than concentrated in one specialty.

That means replacing PFAS-containing medicines isn’t a challenge limited to one disease or one group of patients. Instead, it requires evaluating each medicine individually and comparing it with available non-PFAS alternatives that provide the same therapeutic benefit rather than assuming every fluorinated medicine is required.

• The researchers argued that environmental persistence deserves greater attention during drug development — Their concern focuses on what happens after these medicines leave the body and enter the environment.

Researchers argue that environmental persistence deserves consideration alongside conventional measures such as safety, quality, and effectiveness during drug development and regulatory decision-making, particularly when equally effective non-PFAS alternatives already exist.

• The findings point toward a future where effective medicines no longer rely on PFAS — Because non-PFAS alternatives already exist for nearly every PFAS-containing medicine identified in the analysis, the researchers conclude that reducing the pharmaceutical industry’s reliance on these persistent chemicals is achievable.

Rather than forcing a choice between effective treatment and environmental protection, the findings suggest both goals can move forward together as future medicines are designed with persistence in mind from the beginning.

Reduce Your Overall PFAS Exposure One Choice at a Time

PFAS deserve attention because your exposure adds up over a lifetime. These “forever chemicals” break down extremely slowly, allowing them to accumulate in drinking water, soil, food and, ultimately, your body. Research has linked higher PFAS exposure to reduced immune response,4 liver damage, thyroid disorders, and reproductive and developmental problems,5 and separate research has associated PFAS-contaminated drinking water with an increased incidence of certain cancers.6

Since you encounter PFAS from many different sources every day, reducing unnecessary exposure wherever practical, including when equally effective PFAS-free medicines are available, is one way to lower your cumulative burden over time.

The research suggests that reducing PFAS exposure isn’t about making one dramatic change. It’s about lowering your total lifetime exposure wherever practical. Medicines are only one source. Drinking water, food packaging, stain-resistant fabrics, and many everyday consumer products also contribute. Every unnecessary source you eliminate chips away at your cumulative PFAS burden, and over a lifetime, those reductions compound.

1. Only take prescription medicines that you truly need — While some medicines are necessary, many people remain on drugs long after the original reason for taking them has disappeared. If you take one or more long-term medications, regularly evaluate whether each one is still needed or whether another approach addresses the underlying problem instead of simply managing symptoms.

Bring a complete list of every medication you currently take to your next appointment and ask your doctor to walk through each one. For every prescription, the question is straightforward: “Is this still necessary, or has my situation changed enough that we can reassess?”

That single conversation, repeated at each annual visit, keeps your medication list current and prevents unnecessary long-term exposure to any drug, PFAS-containing or otherwise. Reducing unnecessary prescriptions lowers your exposure to PFAS-containing medicines while also reducing the release of these persistent chemicals into the environment through wastewater.

2. Choose PFAS-free medicines when an equivalent option exists — The researchers found that 87% of PFAS-containing active pharmaceutical ingredients identified for human medicine already have a non-PFAS alternative available, with alternatives in development for nearly all of the rest. If two medicines offer comparable therapeutic benefits, ask whether a PFAS-free option is available. That simple conversation supports both your long-term exposure goals and cleaner pharmaceutical design.

A simple way to start that conversation: “I’m trying to reduce my exposure to persistent fluorinated chemicals. Does this medication contain fluorine, and if so, is there an equally effective alternative that doesn’t?” Many doctors won’t have encountered the request before, but framing it as a preference keeps the conversation productive and gives your provider room to weigh the clinical tradeoffs with you.

One quick way to check whether a medication you already take may contain PFAS: look at the generic name on the label. If it includes “fluor-” or “flu-,” as in fluoxetine, fluticasone, or ciprofloxacin, the drug contains fluorine. That doesn’t automatically mean you should switch, but it tells you which prescriptions are worth discussing with your doctor at your next visit.

3. Reduce PFAS from other everyday sources — Because PFAS exposure is cumulative, medicines are only part of the picture. Replace nonstick cookware with stainless steel, limit food packaged in grease-resistant wrappers or containers, avoid stain-resistant carpets and furniture treatments when possible, and choose personal care products that don’t contain fluorinated ingredients. Lowering exposure across multiple areas often has a much greater effect than focusing on one source alone.

4. Filter your drinking water — PFAS have been detected in drinking water supplies throughout many regions because they persist in the environment for decades. A high-quality filtration system certified to remove PFAS reduces one of the most consistent sources of everyday exposure. Cleaner drinking water lowers your ongoing exposure every single day.

5. Think about cumulative exposure instead of isolated products — Think of PFAS exposure the way you’d think about secondhand smoke. One exposure isn’t the entire story. The total amount you accumulate over years matters most. Every informed decision, whether it involves a prescription, your cookware, your drinking water, or the products you bring into your home, helps lower that cumulative burden and gives you greater control over your long-term health.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

FAQs About PFAS in Medications

Q: Why are PFAS used in some prescription medicines?
A: PFAS are often added during drug development because they help certain medicines remain stable, resist breakdown, or move through the body more efficiently. According to the research reviewed in this article, fluorine usually is not responsible for the medicine’s therapeutic effect. Instead, it mainly changes how the drug behaves, which means many medicines can achieve the same medical result without relying on PFAS.

Q: Should I stop taking a medicine if it contains PFAS?
A: No. The research doesn’t suggest that you should stop taking prescribed medications on your own. Instead, the findings encourage you to become an informed consumer by asking whether an equally effective PFAS-free alternative is available, particularly if you’re starting a new medication or reviewing long-term prescriptions.

Q: Why are PFAS called “forever chemicals”?
A: PFAS earned that nickname because they break down extremely slowly in the environment. After they’re released into water, soil or other parts of the environment, they remain there for many years. Some PFAS-containing medicines also degrade into TFA, another highly persistent compound that’s difficult to remove from water once it’s released.

Q: Besides medications, where else are PFAS commonly found?
A: Prescription drugs are only one source of exposure. PFAS are also found in nonstick cookware, grease-resistant food packaging, stain-resistant carpets and furniture, waterproof clothing, some cosmetics, and contaminated drinking water. Because exposure accumulates from multiple sources over time, reducing PFAS wherever practical lowers your overall lifetime burden.

Q: What are the most effective ways to reduce PFAS exposure?
A: Focus on the sources you can control. Review long-term medications to determine whether they’re still necessary, choose PFAS-free medicines when equivalent options exist, filter drinking water, replace nonstick cookware with safer alternatives such as stainless steel, and avoid consumer products marketed as stain-resistant or water-repellent whenever possible.

Small changes across several areas of your life often reduce total PFAS exposure more effectively than concentrating on just one source.

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What happens to the ovaries after reproductive function ends?

They stop all biological activity
They disappear gradually over time
They remain biologically active
In mouse studies, ovaries continued changing at the molecular level after reproduction ended, rather than becoming completely inactive. Learn more.
They continue releasing mature eggs

Nearly 18 million people lose their lives to cardiovascular disease every year, according to the World Health Organization (WHO),1 making it the most common cause of death worldwide. Coronary artery disease (CAD) is the most prevalent form, marked by plaque buildup that narrows or blocks blood flow to the heart.

Coronary artery disease often begins with subtle symptoms — fatigue, chest tightness, or shortness of breath — but if left unchecked, it could lead to heart attacks or even sudden death. The good news is that CAD doesn’t develop overnight, and that gives you time to change the outcome.

One key driver that could help you turn the tide is your gut health. A review found that reseeding your gut microbiota with beneficial bacteria strains could support your heart health.

Review Provides Strong Evidence Linking Probiotics to Help Lower CAD Risk

Published literature review in Cureus examined how probiotics influence cardiovascular risk, particularly coronary artery disease. The review analyzed a range of clinical trials, meta-analyses, and randomized controlled studies to determine how various probiotic strains affect major heart disease risk factors.2

• The review encompassed a wide range of participants — They ranged from individuals diagnosed with CAD to adults managing Type 2 diabetes, high cholesterol, obesity, or hypertension — groups most at risk for future cardiac events.

• The researchers focused on 10 key human studies — These consisted of seven randomized controlled trials (RCTs) and three meta-analyses. Each of these studies involved human participants with CAD or its major risk factors.

• One of the standout strengths of the methodology is the diversity of the data used — Trials came from countries including the U.S., Iran, China, Thailand, Greece, and Japan. That means the findings are not tied to one ethnicity or geographic population — they represent a much wider pool of data, which makes the conclusions more likely to apply across different lifestyles and genetic backgrounds.

• The research consistently showed that probiotics were associated with measurable changes in heart disease triggers — These include blood pressure, cholesterol, blood sugar, weight management, and inflammation.* According to the researchers:

“There are several risk factors for the development of CAD, which are hyperlipidemia, hyperglycemia, hypertension, inflammation, and oxidative stress, which increase patients’ risk of atherosclerosis and, in turn, lead to CAD.

In recent years, growing evidence has established the beneficial effect of the gut microbiota in influencing these cardiovascular risk factors. This microbial ecosystem plays a significant role in metabolic regulation, immune function, and systemic inflammation, all of which are significant to the development and progression of CAD.”3

• The study highlighted bacteria strains that provide significant benefits — For example, they noted that Lactobacillus acidophilus has a more significant effect on cholesterol levels compared to other strains, while Bifidobacteria has protective effects against atherosclerosis, especially if partnered with a lipid-lowering treatment. Bacteroides vulgatus and Bacteroides dorei helped prevent formation of atherosclerotic plaque.*

Probiotics Help Improve Heart Health by Fixing Gut Imbalance at the Source

So how exactly do probiotics work at the cellular level to help protect your heart? The researchers highlighted several key biological pathways, demonstrated by the studies they reviewed.

• Helping reduce inflammation by supporting the gut barrier — The paper emphasized that dysbiosis harms your gut lining, allowing endotoxins like lipopolysaccharides (LPS) to escape into the bloodstream. This may trigger inflammation that contributes to endothelial dysfunction and atherosclerosis.

The trials found that the probiotic strain Lactobacillus rhamnosus reduced LPS levels and inflammatory cytokines like IL-1β, which may help lower cardiovascular strain.

• Shifting short-chain fatty acid (SCFA) balance toward heart-protective molecules — SCFAs are byproducts of bacterial fermentation, and they have a significant impact on your metabolic health. The study found that probiotics promote the production of propionate — a SCFA that has been linked to reduced vascular inflammation and less fat accumulation in the liver. At the same time, it limits acetate, which may contribute to fat storage and cholesterol synthesis in excessive amounts.

Acetate is generally beneficial, as it supports mucus production. But if there’s too much of it, it could cause adverse effects, which is why balance is key. This shift supports healthy blood lipid levels and lowers the burden on your cardiovascular system.

• Reducing trimethylamine N-oxide (TMAO) production from gut microbes — TMAO is a compound created when certain gut bacteria break down foods like red meat and eggs, and having high levels is associated with arterial plaque buildup and heart attacks.

The study found that certain probiotics like Lactobacillus plantarum modulate bile acid metabolism and suppress TMAO-producing bacteria, which may help lower this risk. A separate analysis4 found that having high blood levels of TMAO increased the risk of dying from any cause fourfold in the next five years.

• Balancing blood pressure via nitric oxide and ACE pathways — Specific strains like Lactobacillus helveticus may help regulate blood pressure by influencing nitric oxide (NO), a molecule that relaxes blood vessels, and inhibiting angiotensin-converting enzyme (ACE) activity, which raises blood pressure.

A meta-analysis included in the review found that probiotic doses of 10¹⁰ colony-forming units (CFU) or more reduced both systolic (the top number in a reading) and diastolic (the bottom number) blood pressure, especially in older adults with hypertension.

• Improving cholesterol metabolism — Certain probiotics influence how your body processes cholesterol. For example, Ruminococcus helps convert cholesterol into bile acids that are excreted, while other strains incorporate cholesterol into their own membranes or convert it into non-absorbable forms like coprostanol. These actions may help reduce circulating low-density lipoprotein (LDL) levels and slow plaque formation.

• Supporting blood sugar and insulin sensitivity — Probiotics such as Bifidobacterium species may help increase GLP-1, a hormone that boosts insulin secretion and slows gastric emptying — both important for stable blood sugar. They may also help reduce oxidative stress and improve how cells respond to insulin, which may lower the risk of Type 2 diabetes.

Each of these pathways reflects how a healthier gut microbiome — powered by the right probiotics — creates a ripple effect through your entire metabolic system. These findings not only demonstrate how probiotics influence gut health, but how those changes may help lower some of the biological triggers of coronary artery disease.

“Probiotics have shown effective mechanisms to control risk factors and lower CAD. Their effect is produced through many mechanisms, such as their anti-inflammatory and antioxidative role,” the researchers concluded.

“Other mechanisms were addressed mainly through the reduction or prevention of CAD risk factors, which are achieved by the anti-glycemic and antihypertensive effects of the probiotics and by reducing metabolic disorders. These further prevent obesity and hypercholesterolemia, which in turn signify the effective role of probiotics in preventing CAD.”

Consuming Probiotics May Help Normalize Blood Pressure

Previous studies have also provided evidence on how probiotics help reduce cardiovascular incidents by modulating risk factors like hypertension. For example, an analysis of nine studies looked at the link between blood pressure levels and consuming probiotic-rich foods or probiotic supplements, and found favorable results.5

• Those who regularly took probiotics have lower blood pressure levels compared to those who did not — On average, their systolic blood pressure was 3.6 millimeters of mercury (mm Hg) lower, while their diastolic blood pressure was 2.4 mm Hg lower. The most significant benefit appeared to be among those whose blood pressure was higher than 130/85, and probiotics that contained a variety of bacteria lowered blood pressure to a greater degree than those containing just one type of bacteria.*

• Kefir demonstrated antihypertensive effects and more — In a 2018 study published in the FASEB journal6 researchers conducted an experiment on three groups of rats — one group had hypertension and was given kefir, the other had hypertension, but was not treated, and the third had normal blood pressure and was not treated. They found that rats fed kefir not only appeared to have lower blood pressure levels, but also had:*

◦ Improved balance of beneficial bacteria in the gut
◦ Improved intestinal structure with decreased intestinal permeability
◦ Lower levels of endotoxins
◦ Lower levels of inflammation in the central nervous system

“Our data suggest that kefir antihypertensive-associated mechanisms involve gut microbiota-brain axis communication during hypertension,” the researchers concluded.

• An earlier animal study found that probiotics help prevent hypertension from a high-salt diet — Published in the Nature journal, the researchers reported that the Lactobacillus Murinus bacteria was shown to help prevent salt-sensitive hypertension by modulating T helper 17 (TH17) cells in this animal model.* When the mice subjects were given this probiotic strain, it helped protect them from the adverse effects of excessive salt intake.

“Our results connect high salt intake to the gut-immune axis and highlight the gut microbiome as a potential therapeutic target to counteract salt-sensitive conditions,” the researchers concluded.7

Combining Probiotics with Plant Nutrients Could Make Them More Efficient

While probiotics alone are beneficial, there are ways to supercharge their effects. One way is to combine them with bioactive plant compounds. A review published in Food Chemistry Advances analyzed how probiotics and plant compounds impact your gut microbiota and may help reduce inflammation. The researchers reviewed evidence on the synergistic role of these compounds in managing metabolic diseases, particularly cardiovascular disease and Type 2 diabetes.8

• Those who have metabolic disorders and chronic inflammation may have seen some of the greatest benefits — In individuals with obesity, Type 2 diabetes, cardiovascular issues, or inflammatory bowel conditions, gut dysbiosis is a common denominator. Combining targeted probiotics and plant-derived bioactives helped reduce systemic inflammation, strengthen gut barrier function, and rebalance microbial diversity.

• Specific strains showed unique effects — For example, Lactobacillus rhamnosus and Lactobacillus plantarum boosted production of mucin, a slippery protein that forms protective mucus, helping make the gut lining stronger. Meanwhile, Bifidobacterium longum and Bifidobacterium breve work efficiently in breaking down fiber into SCFAs.

• Certain plant compounds improved probiotic performance — Polyphenols found in tea, berries, and cocoa supported the growth of beneficial bacteria while slowing the spread of harmful ones.

Plant compounds and probiotics may also work together to help keep inflammation in check — in part by activating immune cells that release calming signals, which help tell your immune system to relax. At the same time, they help lower levels of chemicals that cause inflammation, which is often high in people with metabolic issues. For more information on this topic, read “The Science of Probiotics — How Beneficial Bacteria Support Health.”

How to Boost Your Gut Health to Help Avoid Heart Disease

Your gut is home to trillions of microbes that influence everything from how well you digest food to how effectively your immune system and metabolism function. But when these microbial populations get out of balance, your health starts to unravel at every level.

But getting your gut health back on track is not just about taking probiotics. There are a few important considerations to help your gut microbiome thrive. I recommend following these strategies:

1. Fix your gut microbiome before feeding it — Although fiber is essential for gut health, consuming too much if your gut health is imbalanced will only end up feeding the unhealthy microbes, triggering gas, bloating and toxic byproducts like endotoxins. This is called the fiber paradox — The very substance that promotes a healthy microbiome in the long term worsens symptoms in the short term if introduced too early.

If you’re dealing with inflammation or bacterial overgrowth, start by healing your gut. Remove ultraprocessed foods and focus on easy-to-digest carbohydrates like fruit and white rice until your symptoms stabilize. Afterward, you can add in small amounts of more fibrous carbs like root veggies.

Once your gut health is healed, expand your diet by adding non-starchy vegetables, starchy options (sweet potato or squash), beans, legumes, and eventually whole grains with minimal processing.

2. Prioritize bacteria that produce butyrate — Butyrate is an SCFA and is one of the most powerful healing compounds your body makes. It fuels the cells lining your gut, calms immune overactivation, and reduces whole-body inflammation.

Specific gut microbes are needed to produce butyrate, particularly Faecalibacterium prausnitzii, Roseburia, and Eubacterium. They thrive on fermentable fibers found in foods like cooked-and-cooled potatoes, green bananas, lentils, Jerusalem artichokes, and oats. Once your gut lining begins to heal, feeding these bacteria becomes a top priority.

3. Feed Akkermansia correctly — While not a butyrate producer itself, Akkermansia plays a supportive role by maintaining and thickening your gut’s mucus layer, creating an ideal environment for butyrate-producing microbes to thrive.

Having higher levels of Akkermansia is strongly associated with improved blood sugar control, lower inflammation, stronger gut barrier function, and even reduced body fat. Think of it as a gatekeeper that improves the terrain, while Faecalibacterium and others generate the fuel. Together, they create a microbiome that’s stable, anti-inflammatory and metabolically protective.

Polyphenol-rich foods like pomegranate, red grapes, cranberries, and green tea may help promote Akkermansia growth. So do inulin-containing plants like garlic, leeks, chicory root, and asparagus. Start with small amounts and build as tolerated.

Once your gut symptoms have stabilized — minimal bloating, consistent stool form for at least a week, and improving fiber tolerance — consider starting with a pasteurized Akkermansia postbiotic formula that uses enteric coating or microencapsulation, which helps more of it survive stomach acid and reach your colon. Live Akkermansia may be introduced later, once that tolerance is firmly established.

4. Support gut health at the cellular level — Beyond just adding fiber, you need to remove factors that actively damage your gut environment. One major culprit is excessive linoleic acid (LA) from vegetable oils, which disrupt your mitochondrial function, decreasing your cellular energy production and wrecking your gut environment. Switch to healthier fats like butter, ghee, or tallow instead.

Also, minimize exposure to endocrine-disrupting chemicals and electromagnetic fields (EMFs), as these further impair cellular energy and negatively impact the oxygen-free gut environment that beneficial bacteria like Akkermansia need to thrive.

5. Rebuild daily habits that reinforce microbial balance — Eating at regular times, getting early morning sunlight, sleeping deeply, getting enough daily exercise, and managing stress all shape your gut flora and contribute to your overall health.

*These findings are from laboratory or animal research and may not directly apply to human health.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

Frequently Asked Questions (FAQs) About Probiotics and Heart Health

Q: How do probiotics influence heart health?
A: Probiotics may help balance the gut microbiome, which has been associated with lower inflammation and improved metabolic function — including reduced cholesterol levels, better blood sugar control, and less vascular damage, all factors linked to coronary artery disease.

Q: Which probiotic strains are most effective for cardiovascular health?
A: Strains like Lactobacillus acidophilus, Bifidobacterium lactis, Lactobacillus plantarum, and Lactobacillus helveticus have been associated with reduced LDL (bad) cholesterol, improved insulin sensitivity, lower inflammatory markers, and better blood pressure regulation in the reviewed studies. Each strain works in different ways.

Q: What does gut health have to do with heart health?
A: Your gut and heart are deeply connected through what researchers call the “gut-heart axis.” When your gut microbiota is out of balance, it can produce inflammatory toxins that enter your bloodstream, damage blood vessels, and trigger atherosclerosis. A healthy gut lining and diverse microbiome may help protect against these effects and support lower cardiovascular risk.

Q: Which gut-derived compounds were linked to heart disease in the review?
A: The review highlighted acetate (in excessive amounts) and trimethylamine N-oxide (TMAO) as compounds that increase heart disease risk, while short-chain fatty acids (SCFAs) like propionate and butyrate were linked to reduced inflammation and improved cardiovascular outcomes.

Q: What types of people were included in the reviewed studies?
A: The research involved adults with coronary artery disease and those managing related conditions such as Type 2 diabetes, obesity, high cholesterol, and high blood pressure — groups at higher risk for cardiovascular complications.

1 Which pesticide has been linked to a higher risk of Parkinson’s disease?

Chlorpyrifos
Long-term chlorpyrifos exposure was associated with more than a 2.5-fold higher risk of Parkinson’s disease in agricultural communities. Learn more.
Atrazine
Permethrin
Malathion

2 What can happen when you take a larger supplement dose than your body can readily absorb?

Absorption always increases proportionally
The nutrient stays stored indefinitely
More of the dose may be excreted
Absorption does not always rise in proportion to the dose. For magnesium, the percentage absorbed can decrease as the amount taken increases. Learn more.
The nutrient becomes easier to absorb

3 How many extra calories per day did people eat on an ultraprocessed diet?

100 calories
250 calories
350 calories
500 calories
Twenty adults stayed at the NIH Clinical Center for four weeks and ate about 500 more calories per day on the ultraprocessed diet. Learn more.

4 What do you call someone who naturally prefers later bedtimes and wake times?

Morning chronotype
Evening chronotype
An evening chronotype describes people who naturally prefer later sleep and wake times. This group showed some of the strongest associations with brighter daytime light. Learn more.
Irregular sleeper
Short sleeper and an insomniac

5 Which muscles were linked to better future heart health?

Chest, back, and rib muscles
Healthier muscles in the chest, back, and between the ribs were associated with a lower likelihood of heart attack. Learn more.
Arm, shoulder, and hand muscles
Hip, thigh, and calf muscles
Neck, jaw, and facial muscles

6 Which antioxidant has been studied for supporting ovarian cell health in women with Polyendocrine Metabolic Ovarian Syndrome (PMOS)?

Lycopene
Lutein
Astaxanthin
Astaxanthin has been studied for its effects on oxidative stress, inflammation, insulin sensitivity, and the environment surrounding developing eggs. Learn more.
Beta-carotene

7 As the ovaries age, which type of activity becomes more prominent?

Digestive activity
Immune-related activity
Aging mouse ovaries showed greater activity in immune-related genes and accumulated more immune cells as reproductive functions declined. Learn more.
Bone-forming activity
Respiratory activity

Test Your Knowledge with
The Master Level Quiz

1 Which everyday task may become harder as Parkinson’s disease progresses?

Reading
Hearing
Tasting
Walking
Parkinson’s disease affects the brain circuits that control smooth movement, so walking, balance, and coordination may become more difficult over time. Learn more.

2 Which of these medications is not prescribed to induce sleep?

Zolpidem
Zopiclone
Loperamide
Zolpidem, zopiclone, and benzodiazepines are used as sleep aids, but they may disrupt brain rhythms involved in memory and waste clearance. Loperamide is not a sleep medication. Learn more.
Benzodiazepines

3 What is one way to reduce pesticide exposure from produce?

Buy more packaged foods
Grow your own produce at home
Growing your own fruits and vegetables gives you more control over pesticide use and can help reduce repeated exposure. Learn more.
Store produce at room temperature
Peel every fruit before eating

4 What can affect how much magnesium your body absorbs from a supplement?

The form and dose
A systematic review published in Nutrition found that magnesium absorption varies by form and dose, with organic forms generally better absorbed. Learn more.
The capsule size
The capsule color
The serving time

5 About how much magnesium do most adults need each day?

At least 400 mg
Magnesium needs vary by person, but the guidance given is at least 400 milligrams daily for most adults. Learn more.
About 200 mg
At least 600 mg
About 800 mg

6 What term is commonly used for the electric shock-like sensations some people report during SSRI withdrawal?

Muscle tremors
Sensory flashes
Nerve spasms
Brain zaps
Selective serotonin reuptake inhibitor (SSRI) withdrawal can include “brain zaps,” along with symptoms such as dizziness, sleep problems, anxiety, and mood changes. Learn more.

7 What is a practical first step for cutting back on ultraprocessed foods?

Count every calorie you eat
Avoid all packaged foods until you detox completely
Replace them with minimally processed foods
Replacing highly processed products with foods that have simpler ingredient lists can reduce ultraprocessed food intake without requiring a complete diet overhaul. Learn more.
Remove carbohydrates from meals

8 Which creative activity was linked to the largest difference in biological brain age?

Visual art
Tango dancing
In research published in Nature Communications, tango dancers showed the largest difference, with brains appearing more than seven years younger than their actual age. Learn more.
Strategy gaming
Playing music

9 Which essential amino acid helps signal muscle growth?

Glycine
Leucine
Leucine acts as both a building block for muscle and a metabolic signal that helps activate muscle protein synthesis and mitochondrial energy production. Learn more.
Taurine
Glutamine

10 What system helps regulate your sleep-wake cycle, hormone release, and daily alertness?

Circadian rest-activity rhythms
Circadian rest-activity rhythms help organize daily patterns of sleep, activity, hormones, and alertness across the 24-hour cycle. Learn more.
Autonomic reflex pathways
Metabolic feedback loops
Sensory processing rhythms

11 Which foods can help maintain beneficial bacteria in the gut?

High-fiber whole grains
Fermented vegetables without live cultures
Probiotic-rich foods
Probiotic-rich foods such as yogurt, kimchi, and kefir provide beneficial microbes that can help support a more balanced gut microbiome. Learn more.
Protein “fortified” cereals

12 Which pancreatic cells are responsible for producing insulin?

Beta cells
Beta cells in the pancreas produce insulin, which helps regulate blood sugar. In the adolescent mouse study, prolonged fasting was linked to fewer mature beta cells and lower insulin production. Learn more.
Alpha cells
Sigma cells
Delta cells

13 Besides exercise, what can help support healthier muscles?

Eating more protein each day
Avoiding carbohydrates after workouts
Training harder with minimal rest days
Protein, healthy carbohydrates, and recovery
Protein and carbohydrates provide nutrients and energy for muscle repair, while adequate recovery gives muscles time to adapt and strengthen. Learn more.

14 Which factor was much more important for obesity than daily energy expenditure?

Resting metabolic rate
Physical activity level
Immune system activity
Calorie intake
In a study published in the Proceedings of the National Academy of Sciences (PNAS), calorie intake was about 10 times more important for obesity than daily energy expenditure. Learn more.

15 What is the medical term for involuntary teeth grinding or clenching that often occurs during sleep?

Temporomandibular joint disorder
Sleep apnea
Bruxism
Bruxism affects about 8.6% of adults and can place substantial pressure on the teeth and jaw during sleep. Learn more.
Trigeminal neuralgia

16 Granulosa cells depend heavily on mitochondria for what purpose?

Storing reproductive hormones
Fueling egg cell development
Mitochondria provide the energy granulosa cells need to nourish and support developing eggs throughout the months-long maturation process. Learn more.
Producing follicular fluid
Controlling menstrual timing

17 Which of these habits may decrease butyrate production?

Eating too little dietary fiber
Gut bacteria make butyrate by fermenting fiber, so a low-fiber diet gives these bacteria less material to produce this short-chain fatty acid. Learn more.
Including resistant starches regularly
Staying sedentary most of the time
Eating fermented foods with probiotics

18 What kind of carbohydrate can provide dogs with a moderate source of glucose?

White rice
White rice provides carbohydrates that supply glucose, which dogs use for functions such as brain and red blood cell energy. Learn more.
Sweet potatoes
Rolled oats
Brown rice

19 When can changes associated with ovarian aging begin?

Only after age 70
Once all follicles are gone
Immediately after menopause
Years before menopause
Changes in cell communication, follicle development, and tissue remodeling began before reproductive cycles stopped. Learn more.

20 Which cells have stopped dividing but remain metabolically active in the body?

Stem cells
Immune cells
Senescent cells
Senescent cells no longer divide, but they remain active. Their buildup over time is associated with aging and age-related disease. Learn more.
Red blood cells

21 Which of these fish is a rich natural source of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)?

Wild-caught Alaskan salmon
Cold-water fatty fish such as wild-caught Alaskan salmon, mackerel, herring, and sardines are among the best natural sources of omega-3 fats. Learn more.
Farm-raised tilapia
Atlantic cod
Yellowfin tuna

Editor’s Note: This article is a reprint. It was originally published June 30, 2024.

I interviewed Dr. Ahvie Herskowitz, former clinical professor of medicine at the University of California, San Francisco, and founder of Anatara Medicine, a multidisciplinary integrative center in San Francisco.1 Herskowitz, an internist, has a deep foundational knowledge and science background that’s ideal for treating complicated health care cases.

We may be collaborating on a project in the future, but in the meantime at his center, they’re using advanced techniques to help people restore their health, including strategies for longevity and treatments for very ill patients, including those with autoimmunity, gut problems, cancer, and more.

Microbiome Issues, Leaky Gut Linked to Failure to Thrive

Herskowitz treats illness by looking at the foundational causes of disease. We discussed that a leading cause of death is, in my view, endotoxemia resulting in septic shock. This occurs when you secrete endotoxin from facultative anaerobes, otherwise called oxygen-tolerant bacteria, which shouldn’t be in your gut.

These pathogenic bacteria secrete a very virulent form of endotoxin, also known as lipopolysaccharides (LPS), which cause inflammation if they translocate across the compromised gut barrier into the systemic circulation. Leaky gut, or a disturbed microbiome, is considered by Herskowitz to be one of the foundational contributors to chronic disease.

Herskowitz explains, “I think that everyone that’s doing poorly and failing to thrive has a biome issue and a leaky gut issue, almost 100% … And in the standard allopathic intensive care units, it’s not considered a foundational issue.” When Herskowitz treats cancer patients, he says, they’re often in a state of failure to thrive.

“They’ve gotten so burdened by so many different layers of toxicity, that their system cannot keep up anymore enough,” he says. “And … that’s eventually due to mitochondrial failure throughout the body.”

Patients Overwhelmed by Toxicity and Nutritionally Depleted

Chronic diseases often result from a buildup of toxicities and a lack of nutrition and healing in the body to compensate for them. “All these toxicities affect every cell of the body simultaneously,” Herskowitz says.

“So, we all have relative strengths and weaknesses. And that comes up as to what organ is going to be the most involved. But we all have to almost decide whether we’re going to release these toxins on a day-to-day basis, otherwise our concept of longevity is going to be badly estimated.”

Herskowitz estimates that 80% to 90% of the U.S. population has metabolic syndrome, which increases the risk of heart disease, stroke, and Type 2 diabetes. Obesity is another epidemic. Both are due to several factors, including toxicity that started more than 50 years ago as the food supply became increasingly processed. Herskowitz explains:

“This is where you get to the concept of an infinite number of toxicities, feeding a system that only has a finite way of cellular responses … it’s the seed oils [containing] linoleic acid, it’s the ultraprocessed foods and snacks. So, when you go to a general store today …

The overwhelming majority of the food that’s sold there is not to be for human consumption … and then the concept of our farming system has evolved toward efficiency … listen, industry is not our friend. It’s not our partner … their job is to sell more stuff, and to do so in an efficient way.

… I watched it over 45 years, I mean, ‘70s, ‘80s, 90s, this stuff is getting worse. Now the most difficult group to get an appointment with in the hospital is not the cardiology department, because it’s usually the largest department, but it’s endocrine and rheumatology, neurology.”

In other words, exposure to ultraprocessed foods and other toxicities is wreaking havoc in the body, leading to widespread chronic disease. “It causes havoc within the communications network, so that hormones go awry, inflammation goes awry and the detoxification system is overwhelmed,” Herskowitz explains.

“This leads to all the different disorders … it’s a straightforward thing … you have this nutrient depletion, which obviously … you’re more susceptible to everything. And then each of us is reaching our limit, so to speak.”

Why You Should Pay Attention to ‘Nuisance Symptoms’

Herskowitz often sees patients when they’re very ill — but they don’t start out this way. He often looks back into their medical records over 25 years to see their past medical history. People who end up with serious diseases like Alzheimer’s disease often have far more “nuisance symptoms” over the years. This includes symptoms such as toenail fungus, indigestion, occasional diarrhea, hyperactivity or even high blood pressure.

In Herskowitz’s experience, his Alzheimer’s patients had 2.5 times more nuisance symptoms compared to a control group that didn’t have Alzheimer’s. This reflects Herskowitz’s own clinical observations from his practice, not a peer-reviewed published study. “It’s consistent with this toxicity type of concept,” he says. “When you’re toxic, you have all these little things going on, and you don’t pay attention to them, because they’re not severe.”

However, they’re clues that something is off balance in your body, which can likely be addressed in the early stages. Unfortunately, most physicians aren’t looking for these types of systemic problems.

Tests to Measure How Old You Really Are

One of the challenges facing longevity medicine is figuring out what to measure in order to get an idea of how old you really are — meaning your biological age, which is how well your body is functioning compared to your chronological age, the actual number of years you’ve been alive. Biological age can be younger or older than your chronological age depending on your lifestyle, environmental factors, and genetics.

Herskowitz believes oxidative stress is one useful measure to show where you are in a given moment in time over time. At his center, they use a urine test called 8-hydroxy-2-deoxyguanosine (8-OHdG) as a biomarker for oxidative damage and they use the lipid peroxides as a marker. He also uses tests to measure chronic immune function, mitochondrial function, and senescent cells.

Senescent cells are cells that have stopped dividing and entered a state of permanent growth arrest without undergoing cell death. These cells can no longer replicate, but they remain metabolically active.

Senescence is a natural part of the cellular lifecycle and serves as a mechanism to prevent the proliferation of damaged cells, which leads to cancer. However, the accumulation of senescent cells over time contributes to aging and various age-related diseases. According to Herskowitz:

“[We look for] concepts of the subtlety of how the immune system is being suppressed. And it’s not the current CBC [complete blood count]. It’s more on the chronic side. So how does it deal with biological toxins? And that’s more a journey into the complement immune cascade, which deals with chronic infection, chronic biological toxins and how to deal with it.

So, measures of complement cascades for autoimmunity as well. And then probably the biggest one, other than mitochondrial function and oxidative stress, to me is if we can measure the number of senescent cells we have in our body at any time. The higher it is, the worse you’re doing.”

Herskowitz also uses markers of metabolic pathways that measure glucose metabolism. “It’s not as simple as glucose,” he says. “It’s more inflammatory/metabolic/hormonal,” or the fact that patients are so nutrient deficient that their system isn’t generating sufficient energy. Further, on a day-to-day basis, Herskowitz uses serum ferritin level as an important marker of health.

I have also long stated that serum ferritin, which measures stored iron, is one of the most important tests that everyone should have done on a regular basis as part of a preventive, proactive health screen.

Innovative Test for Cancer Treatment

Meanwhile, Herskowitz described an innovative test for tumors that helps improve treatment decisions. Many people with cancer capitulate to taking chemotherapy, either because of fear, their own choice, or direction from loved ones or their oncologist.

Many alternative practitioners treating cancer patients say their biggest challenge is the fact that virtually no one comes to see them before they take chemotherapy, which they believe can compromise their body’s healing abilities.

Herskowitz, who uses antioxidants, nutrition, photobiomodulation, intravenous therapies, and other strategies for cancer, details a test he believes may change the way chemotherapy is given in the U.S.:

“There’s a new innovation you should be aware of. And that’s taking a slice of the tumor itself on the biopsy side, articulating the various genomic mutations, and looking for the same genomic mutations in the peripheral blood. Now, it’s not a new generation of circulating tumor cell counts, and this is all different generation. So, the goal here is, say, I’m on chemo.

I don’t want to be on it, unless it’s working. Whether it’s high-dose chemo, or even low-dose chemo, I want it to be working on my behalf. And unless these markers are going down, I’m going to switch. I can tell my oncologist to switch because the genomic data are universally accepted by any oncologist in any university setting.

And I think that’s going to change the way chemotherapy is given in the United States over time. These are approved tests for advanced cancers, and now they’re moving to get approvals for all cancers of any kind.”

Cellular Function Is Becoming Less Efficient

In his decades of clinical experience, Herskowitz says he’s seen our overall capacity for cellular function becoming less efficient. “Practicing now is just different,” he says. For instance, less than 2% of the population used to have autoimmunity, but now he believes it’s somewhere between 10% and 20% — and we could be reaching a tipping point.

“I don’t know where we’re going to be in 10 years … people are still functioning, which is remarkable … [but] I think that we’ve lost most of our reserves. Our reserve function is relatively gone. So, maybe more than 50% of our reserve function has now gone over the last four decades,” he says, referring to not only biological resiliency but also metabolic and mitochondrial function. Fortunately, there’s still hope to turn health around.

“Mitochondrial biogenesis is possible, at some point, so I think we still have a lot of hope that right now we can reverse by going clean. And the cleaner you go, the better you’ll feel anyway,” Herskowitz explains. The fact is, your body has unbelievable resiliency provided you identify what’s causing your problems and address it, including by eliminating ultraprocessed foods from your diet and reducing your exposure to other toxicities.

You can find out more about Herskowitz’s strategies for longevity and chronic disease at his website Anataramedicine.com. As mentioned, we’re going to be working together in the future so Herskowitz can further direct his knowledge and insights into correcting the faults in the system. He adds:

“I can tell you one thing. I’ll end it like this. There’s a lot of secrets going on, there’s a lot of mystery. There’s a lot of things we don’t know very much about. And the worst thing a doctor can do is have an arrogant attitude. They understand everything. And I think that as long as we remain open and honest now, and remain lifelong learners, we will all be in better shape.”

This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

In the video above, Dr. Jen Gunter walks through the basics of what menopause is, how the hormonal transition unfolds, and what you can do about common symptoms. It’s a useful primer, but it reflects the conventional understanding that the story essentially ends once the transition is complete. The research below picks up exactly where that thinking stops.

Menopause is officially defined as the point 12 consecutive months after your last period, but the dramatic symptoms most women associate with it — hot flashes, night sweats, sleep disruption, mood changes, vaginal dryness, and accelerated bone loss — actually belong to the transition leading up to that milestone, when the ovaries are actively winding down hormone production.

That’s where one of the biggest misconceptions takes hold: the assumption that by the time a woman reaches postmenopause, the ovaries have simply stopped working.

For a long time, the scientific consensus supported that view. Once the ovary’s supply of follicles ran out, researchers treated the organ as little more than inactive scar tissue, a structure that had finished its job and could be safely ignored. That assumption shaped decades of medical thinking and helped justify the routine removal of ovaries during unrelated surgeries.

Yet millions of women now spend decades in postmenopause, which raises a question science has only recently begun taking seriously: what are the ovaries actually doing during all those years? Now two studies are challenging the old view from complementary directions. One investigated how the ovary’s molecular and cellular identity transforms after reproduction ends and discovered an organ that, far from going quiet, appears to take on an entirely new biological role.1

The other built extraordinarily detailed spatial maps of the aging ovary and found that decline begins not with a sudden shutdown but with a gradual loss of the precise coordination among cell types that keeps the organ functioning.2 Together, they suggest the postmenopausal ovary deserves far more scientific attention than it has received, and that understanding what changes inside this organ is the first step toward understanding how it influences healthy aging throughout the rest of your body.

The Ovary Kept Changing Long After Reproduction Ended

A study published in Molecular Human Reproduction investigated what actually happens to the ovary after reproduction ends, a stage that scientists have historically viewed as biologically quiet. Instead of assuming the postmenopausal ovary simply remains in place without an important purpose, the researchers compared ovaries from reproductively young, reproductively old, and post-reproductive mice to determine how the organ continues to change after its reproductive years end.3

Because human postmenopausal ovarian tissue is difficult to study, the researchers used mice, whose ovarian aging follows many of the same biological patterns seen in women. The three groups were 2-month-old (reproductively young), 18-month-old (reproductively old), and 24-month-old (post-reproductive) mice, with three to four animals per group. The authors note that mice do not menstruate, but argue the model remains useful for identifying conserved mechanisms of ovarian aging.

Rather than focusing only on hormone production or egg loss, the team combined detailed tissue analysis with gene activity measurements to examine the ovary from multiple angles. This allowed them to identify structural changes, shifts in cellular behavior, and differences in which genes were switched on or off at each stage of aging. Their goal was to determine whether the post-reproductive ovary remains biologically active instead of becoming an inactive organ.

• Researchers found that ovarian aging continued after fertility ended — Most people assume menopause represents the final chapter of ovarian biology. According to the researchers, that assumption doesn’t match what they observed. Although the ovaries had already exhausted their supply of follicles, the organ continued changing at the molecular level long afterward.

Instead of reaching a stable endpoint, the ovaries developed an entirely different pattern of activity. The researchers wrote that “the ovary continues to undergo molecular changes after reproductive senescence,” meaning the transition didn’t stop once reproduction ended. That finding suggests your ovaries continue participating in important biological processes long after fertility disappears.

• The ovary gradually lost its reproductive identity and adopted a completely different one — Genes associated with normal ovarian function steadily became less active while an entirely different collection of genes became much more active. Genes work like instruction manuals that tell cells which jobs to perform. When different genes switch on, cells begin behaving differently.

Instead of producing instructions related to reproduction, the post-reproductive ovary increasingly expressed genes involved in immune activity and inflammation. The researchers described this as a shift “from reproductive functionality to an immune-dominant signature.” Rather than functioning primarily as a reproductive organ, the ovary appeared to take on responsibilities more commonly associated with the immune system.

• Immune cells steadily moved into the aging ovary — The genetic findings matched what researchers observed under the microscope. As the ovaries aged, increasing numbers of immune cells entered the tissue. These included T cells, which help coordinate immune responses, macrophages, which remove damaged cells and debris, and multinucleated giant cells, large immune cells that often appear during long-lasting tissue remodeling or inflammation.

Think of macrophages as the body’s cleanup crew. They remove worn-out material and help organize tissue repair. T cells serve as coordinators that direct other immune cells where to respond. Finding substantially more of these cells inside the post-reproductive ovary tells scientists the organ remains biologically busy rather than dormant.

The authors read this shift as ovarian “inflammaging” and propose that “targeting the inflammatory milieu of the ovary may be the foundation for a non-hormonal, non-fertility therapeutic to maintain healthspan for women in the post-reproductive period.” In other words, the immune identity is presented as something to counteract, not as a second job the ovary has usefully taken on.

• Scar-like tissue remained elevated after follicles disappeared — The researchers examined collagen, the structural protein that helps support tissues throughout your body. Excess collagen creates fibrosis, meaning normal tissue becomes stiffer and more scar-like. Picrosirius Red staining, which detects collagen I and III, showed an increasing trend with age that remained elevated in the post-reproductive ovary. The authors report this as a trend rather than a statistically significant increase.

Total follicle numbers were significantly reduced at both 18 and 24 months compared with 2 months, with no further decline between 18 and 24 months, indicating follicle depletion was complete by 18 months.

The continued transformation after follicle depletion occurred mainly at the molecular level. Although the ovary’s physical fibrosis had reached a plateau, 230 genes were still differentially expressed between the reproductively old and post-reproductive stages. This distinction shows that the organ remained biologically dynamic even when its major structural changes had stabilized.

• The aging ovary appeared capable of communicating with the rest of the body — One of the study’s most intriguing discoveries involved proteins that aging ovaries appear capable of releasing into circulation. Researchers identified numerous genes whose protein products are predicted to be secreted outside the ovary. Secreted proteins act like biological messages because they travel to other tissues and influence how those tissues behave.

This finding raises an important possibility. Instead of remaining isolated after menopause, the ovary could continue influencing organs throughout the body by releasing inflammatory signaling molecules.

The authors concluded that the post-reproductive ovary “could be a source of pro-inflammatory signaling mediators with the potential to modulate extra-ovarian tissues.” This remains a computational prediction. The authors state that future studies are needed to validate whether the genes they identified actually produce secreted proteins, and whether those products can be detected in the blood.

None of that undercuts the study’s central finding, though. Instead of seeing the ovaries only as organs involved in fertility, this research suggests they remain active participants in whole-body aging. Scientists still need additional research, particularly in humans, but this work provides evidence that the post-reproductive ovary continues playing a meaningful biological role rather than quietly fading into inactivity.

Ovarian Cells Lost Their Perfect Timing Before Fertility Ended

That first study revealed what the ovary becomes after reproduction ends — an immune-active organ still participating in whole-body biology. But it left open the question of how the ovary gets there. A second study, published in Nature Aging, tackled that question by investigating how thousands of different ovarian cells coordinate their activities as the organ ages.4

The researchers built an exceptionally detailed spatial map of the aging mouse ovary using an advanced genetic mapping technique that captures which cells are active and exactly where they sit within the tissue. The study analyzed 22 mouse ovaries, generating 69 spatial maps that captured more than 610,000 individual measurement points across different stages of the reproductive cycle.

The investigators also developed new computer tools to identify and track 358 oocytes (immature eggs), 668 follicles, and 236 corpora lutea, the temporary structures that form after ovulation. By comparing young, middle-aged, and older mice that were still cycling, they discovered that important biological changes appeared long before reproduction stopped. The three age groups were 10 to 12 weeks, 36 to 40 weeks, and 52 to 54 weeks.

Instead of a sudden collapse at menopause, ovarian aging reflected a gradual breakdown in the precise timing and organization that normally keeps the ovary functioning efficiently.

• The ovary began losing its internal rhythm years before reproduction stopped — Ovarian aging started disrupting the timing of normal biological events while the animals were still reproductively active. Healthy ovaries carefully synchronize hormone signals, egg development, and tissue remodeling throughout every reproductive cycle. According to the researchers, that coordination steadily weakened with age instead of disappearing all at once.

Think of a symphony orchestra. Every musician still knows how to play, but if they gradually stop following the conductor’s cues, the music drifts out of sync long before anyone stops playing entirely. The researchers concluded that ovarian aging reflects “a progressive breakdown of tissue-level coordination,” meaning the individual cells still existed but no longer worked together with the same precision.

That finding matters because many women notice changes in menstrual cycles, hormone balance, and fertility years before menopause. This research suggests those changes begin when the ovary’s internal timing system starts drifting out of sync rather than when eggs suddenly run out.

• Egg development became less organized as neighboring cells stopped communicating efficiently — The study found that aging disrupted folliculogenesis, the carefully controlled process through which immature follicles grow and mature before ovulation. Instead of progressing through clearly defined stages, older ovaries lost much of the orderly communication that guides healthy follicle development.

Follicles don’t develop in isolation. Each one constantly exchanges chemical signals with surrounding support cells that deliver nutrients, hormones, and growth instructions. Researchers found that this coordinated conversation became increasingly disorganized with age, making follicle development less synchronized with the normal reproductive cycle.

The investigators also found that hormone-sensing patterns became uncoupled from cycle stage. In other words, ovarian cells no longer responded to hormonal signals with the same precision seen in younger ovaries, even before reproductive cycles had completely stopped.

• The ovary struggled to clean up after ovulation — Every ovulation creates a temporary structure called the corpus luteum, which produces progesterone before naturally breaking down to make way for the next cycle. The study found that this cleanup process became less efficient as ovaries aged.

Researchers observed an accumulation of late-stage, regressing corpora lutea that normally would have cleared. The authors identify these structures by their transcriptional signature rather than by age — they note the method cannot determine how old a corpus luteum is and describe the finding as failed timely clearance, suggesting that normal tissue turnover slowed with age.

Because proper removal of these structures helps prepare the ovary for the next reproductive cycle, delayed clearance disrupted the normal sequence of events.

This discovery gives scientists another explanation for why reproductive cycles often become irregular before menopause. It isn’t simply hormone production that changes. The ovary also becomes less efficient at resetting itself between cycles.

• The physical layout of the ovary became increasingly disorganized — Healthy follicles normally develop in carefully arranged neighborhoods inside the ovary. The researchers found that this spatial organization gradually disappeared with aging. Preantral and atretic follicles, which cluster tightly in young ovaries, became more scattered in aged ones, reducing the close communication that supports normal development.

Antral follicles behaved differently — they sit as relatively isolated “islands” in both young and old ovaries. Imagine trying to complete a team project after everyone has been moved into separate buildings. Communication slows, coordination suffers, and mistakes become more common. Researchers reached a similar conclusion about ovarian tissue. Loss of this spatial organization reduced the ability of neighboring follicles to influence one another through short-range signaling.

The study also found changes in the extracellular matrix (ECM), the supportive framework that surrounds cells — specifically reduced expression of matrix genes alongside increased matrix-degrading enzymes, which the authors describe as aberrant remodeling. They propose in their concluding model that loss of follicle clustering “may, in part, reflect increased ECM rigidity,” citing earlier work; this study did not measure tissue stiffness directly.

• Inflammation, tissue remodeling, and structural breakdown occurred as interconnected layers rather than separate processes — Rather than identifying one single cause of ovarian aging, the researchers found several biological processes working together. Increased inflammatory signaling, changes in the extracellular matrix, altered immune activity, and declining tissue organization reinforce one another.

The authors describe a propagating sequence rather than simultaneous onset: disrupted clearance of corpora lutea generates persistent inflammatory niches that “may initiate” broader immune remodeling, and local defects then “propagate across niches” to produce organ-level disorganization.

The authors described these changes as “interconnected layers of ovarian aging,” meaning each problem reinforced the others instead of occurring independently. As tissue organization weakened, immune remodeling increased. As inflammation increased, communication between cells deteriorated further. Together, these changes accelerated the decline in normal ovarian function.

Healthy organs depend on millions of cells working together in the right place at the right time. According to this research, ovarian aging isn’t defined by one damaged cell type or one failing hormone. It reflects the gradual loss of the remarkable coordination that normally keeps every part of the ovary working as a unified system.

That gradual unraveling is exactly what millions of women experience firsthand during perimenopause — the irregular cycles, the unpredictable symptoms, the sense that something has shifted before any test confirms it — and this research now offers a biological explanation for why the decline feels like a slow drift rather than a clean stop.

The authors draw the same parallel to human perimenopause, while stating that “validation in human tissue will be necessary for translating these findings into clinical applications.”

Note: The findings from both featured studies are from laboratory or animal research and may not directly apply to human health.

Support Healthy Ovarian Aging by Protecting the Tissue That Remains

The research shows that the ovary continues changing long after menopause instead of simply shutting down, which means the environment you create inside your body still matters. If the postmenopausal ovary is indeed releasing inflammatory signals that influence tissues throughout the body — and the early evidence points in that direction — then the internal environment surrounding that organ matters even more than previously understood.

Chronic inflammation, poor metabolic health, and reduced cellular energy place extra strain on tissues that are already adapting to a new biological role. Focus on creating an environment that supports healthy tissue function instead of accepting that everything after menopause is simply decline.

The studies also suggest that your goal after menopause is not simply replacing hormones. Instead, it’s supporting the metabolic and cellular environment that allows the tissues you still have to function as well as possible. Many of the same habits that protect your mitochondria, lower inflammation, and improve metabolic health also support healthier hormone balance throughout the rest of your body.

1. Reduce the inflammation that places extra stress on aging tissues — Chronic, low-grade inflammation became a defining feature of the aging ovaries in the research. To reduce this, build most meals around minimally processed whole foods while eliminating seed oils and ultraprocessed foods.

Seed oils, like soybean, canola, sunflower, or safflower oil, are rich in linoleic acid (LA), which contributes to inflammation and mitochondrial dysfunction. Keeping LA intake below 5 grams per day while replacing those oils with traditional fats such as grass fed butter, ghee, or tallow helps create a healthier environment for aging tissues.

2. Lower your exposure to estrogen-like chemicals in your environment — Even after menopause, your body continues responding to hormone signals from outside sources. Everyday plastics, personal care products, food packaging, and household products often contain endocrine-disrupting chemicals that behave like estrogen inside the body.

I recommend storing food in glass or stainless steel instead of plastic, avoiding heating food in plastic containers, choosing products without parabens or phthalates whenever possible, filtering your drinking water, and reducing unnecessary plastic use throughout your home.

3. Build a strong metabolic foundation instead of restricting your body — Healthy tissues require energy to repair themselves, and a postmenopausal ovary that remains biologically active needs that energy just as much as any other organ. I recommend eating enough healthy carbohydrates — about 250 grams daily for most adults, adjusted for activity level — along with adequate protein from bioavailable sources.

Aim for 0.6 to 0.8 grams per pound of ideal body weight (1.32 to 1.76 grams per kilogram), with one-third coming from collagen-rich sources like slow-cooked meats or bone broth.

Nutrients found in foods such as liver, pasture-raised eggs, and properly raised animal foods provide vitamin A, vitamin B6, and other compounds that are involved in normal hormone production and cellular energy metabolism. Daily sunlight, resistance exercise, regular walking, and restorative sleep further strengthen the metabolic foundation that every organ depends on.

4. Look beyond blood estrogen alone when evaluating hormone balance — Even after menopause, blood estrogen levels tell only part of the story because estrogen stored inside tissues doesn’t always match what appears in a blood test. One marker that I believe provides additional insight is prolactin, a hormone whose production rises in response to estrogen activity.

Elevated prolactin, particularly alongside reduced thyroid function, suggests increased estrogen signaling even when blood estrogen appears low. Looking at the broader hormonal picture provides a more complete understanding of what’s happening inside your body. Talk to your health care provider about whether this testing is appropriate for you.

5. Focus on restoring balance instead of replacing estrogen — If you’re considering hormone support, carefully weigh the total estrogen burden from medications and environmental exposures.

For many postmenopausal women, bioidentical progesterone, not synthetic progestins, offers a different strategy because progesterone opposes many estrogen effects. Where progesterone is used, I recommend transmucosal delivery of pharmaceutical-grade bioidentical progesterone mixed with natural vitamin E, rather than a transdermal cream.

The goal is creating an internal environment where the tissues that continue serving you after menopause remain as healthy and resilient as possible.

FAQs About the Ovaries After Menopause

Q: Do the ovaries become inactive after menopause?
A: No. The research reviewed in this article found that although the ovaries stop releasing eggs and lose their reproductive function, they remain biologically active. Both studies were conducted in mice, so this is not yet established in women. Instead of simply becoming inactive tissue, they continue changing at the molecular level and take on many characteristics associated with the immune system, suggesting they still influence your health long after menopause.

Q: What changes inside the ovaries as they age?
A: Scientists found that the aging mouse ovary gradually loses its reproductive identity while genes involved in immune activity become more active. The ovaries also accumulate immune cells, maintain elevated fibrosis after reproductive aging, and continue changing at the molecular level even after follicle depletion is complete.

Q: Does ovarian aging begin only after menopause?
A: No. The second study found that important changes begin years before menopause. Communication between ovarian cells becomes less coordinated, follicle development becomes less organized, tissue remodeling changes, and the ovary gradually loses the precise timing that keeps the reproductive cycle functioning normally.

Q: Why does this research matter if I’m already postmenopausal?
A: These findings suggest your ovaries continue participating in whole-body biology after reproduction ends. Rather than viewing menopause as the end of ovarian function, the research indicates that the postmenopausal ovary remains an active organ whose biological changes could influence healthy aging throughout the rest of your body. Both research teams state that validation in human tissue is still needed.

Q: What lifestyle habits support healthy ovarian aging after menopause?
A: Focus on the factors that influence cellular health rather than simply replacing hormones. That includes eating a minimally processed diet while avoiding seed oils, reducing exposure to estrogen-like chemicals from plastics and personal care products, maintaining healthy metabolism with adequate carbohydrates and protein, looking beyond blood estrogen alone when evaluating hormone balance, and considering whether bioidentical progesterone is appropriate instead of adding more estrogen.

This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.

Test Your Knowledge with Today’s Quiz!
Take today’s quiz to see how much you’ve learned from yesterday’s Mercola.com article.

What is the updated name for the condition formerly called polycystic ovary syndrome (PCOS)?

Polyendocrine metabolic ovarian syndrome (PMOS)
The name PCOS was changed to PMOS in 2026 to better reflect the condition’s multiple hormonal and metabolic features, not just ovarian changes. Learn more.
Polycystic metabolic ovarian disorder (PMOD)
Primary endocrine ovarian syndrome (PEOS)
Polymetabolic ovarian dysfunction (PMOD)

Owning a pet is one of the best things you can do to enrich your life. Be it a cat, a fish, or a bird, the friendship and love offered by a pet will be precious as you journey through life.

I, myself, have two beloved dogs, Joy and Grace. Their presence adds immense amounts of pleasure and satisfaction to my daily solar noon walks on the beach. They’ve also become parents themselves, giving birth to a litter of puppies back in March 2025.

My dogs also serve as my humble reminder of our connection to nature, as well as the importance of constantly moving forward, both literally and metaphorically speaking.

That said, I believe our pets deserve the same amount of attention when it comes to their diet. That’s why I’ve prepared this affordable, yet healthy meal plan for would-be pet parents in the hope of giving their dogs a great head start on life.

If you already have a dog, I still recommend following this nutrition plan — it contains everything your dog needs to live long and healthy.

The Staple Ingredients for Your Pup’s Homemade Meal

Raising a healthy, happy puppy doesn’t have to mean breaking the bank. With a bit of strategic shopping and a focus on nutritious basics, you can build a wholesome diet for your pup that’s both cost-effective and packed with essential nutrients. The table below outlines a set of affordable staple foods that serve as the foundation for a balanced homemade puppy diet.

These ingredients are rich in protein, fats, and important micronutrients. More importantly, they’re also readily available at budget-friendly prices if you know where to look. This list includes how much you need to buy, rough price estimates, and tips for sourcing them as cheaply as possible, including clever ways to ask your local butcher or shop bulk deals.

Item
How much?
Where and how to get it dirt-cheap

White rice
20-pound “Great Value” sack
Walmart sells it at $1 to $1.10 per pound. One bag is around $22.

Ground beef 70% lean/30% fat
Buy weekly family packs
Look at the club store or supermarket overstock.

Fattier blends are usually the loss-leader, which usually costs $2.50 to $3.00 per pound when on sale.

Beef neck bones
One per week
Helps keep their teeth clean and jaw strong.

Beef liver
Two to three pounds per month
Ask the butcher for frozen bulk liver.

You can also check Hispanic/Asian markets where it’s typically sold at $1.50 to $2.00 per pound.

Beef fat/suet (for tallow)
Five pounds raw renders around four pounds of tallow, which can last for months
Ask the butcher, “Do you have beef trimmings/suet you’d toss?” Many counters hand it over free or around $1 per pound.

Wholesale renderers list inedible-grade tallow at around $0.54 per pound.

Eggs
Five-dozen tray
Warehouse club or local farm (around $2.50/dozen)

• Dogs need protein — Dogs are scavenging carnivores by nature, which means most of their diet comes from the prey they consume, particularly protein. In one study, researchers noted that getting enough protein is important to help increase lean body mass in dogs, and they need more of it as they age.1

Aside from helping build muscle, protein is required by animals for important biological processes, such as synthesizing hormones and enzymes.2

• Fats are also important — Dietary fats play a crucial role in pet nutrition in different ways:

◦ It’s a concentrated energy source

◦ It makes up part of the membrane of cells and helps transport nutrients and other substances across the cell membrane

◦ It produces metabolites that help control inflammation

◦ It contributes to the formation of certain hormones, such as estrogen, testosterone, and progesterone, as well as the formation of bile acids that aid in digestion and absorption of nutrients

◦ It acts as a mechanical barrier, insulating the body against heat loss, protecting internal organs, and preventing excess water loss

• What about carbs? — Dogs typically don’t have a nutritional requirement for carbohydrates. Compounding the issue is that most kibble sold is carb-heavy (between 46% and 74%), leading to issues such as canine diabetes. However, dogs still need glucose. As noted in a study published in the Journal of the American Veterinary Medical Association:3

“Dogs do not have a dietary requirement for carbohydrate, except during pregnancy and lactation. However, dogs have a metabolic requirement for glucose. Similar to other species, certain tissues and cells (e.g., brain and RBCs) rely on glucose for energy needs.”

• Seed oil reset note — If your dog has been eating conventional kibble loaded with industrial seed oils, keep the menu locked on the white rice base for roughly six months; the simple starch gives tissues time to clear stored omega-6 fats. Brand new puppies raised on fresh, species-appropriate food from day one can transition sooner.

After the seed oil reset — or immediately for pups with no seed oil history — swap in up to half of the white rice portion with organic oat groats or bran. Oats bring ~10 g of mixed insoluble and soluble fiber per cooked cup, which will feed hindgut microbes and firm stools better than rice.

• This meal plan will minimize your vet bills — I believe that this recipe covers everything your puppy will need to grow into a healthy, strong dog. The other benefit here is that you’ll be minimizing your veterinary bills, which have been exponentially increasing.4

Don’t Throw Away Eggshells

Eggs are one of the most affordable superfoods for both you and your pet. They contain protein, healthy fats, and essential nutrients to support optimal health. Interestingly, eggshells, which most people never eat, also help meet important nutritional needs, namely calcium intake.

• Role of calcium in canine health — Like humans, dogs also need calcium for various reasons. In an article from Veterinary Clinics: Small Animal Practice, a calcium deficiency during growth increases the risk of limb deformities and fractures, making it essential to a growing pup.5

Calcium is important for other processes as well, such as muscle contraction, neurotransmitter communication, and blood clotting.6

• Eggshells membranes are nutritious — In the earliest days of dogs, they scavenged eggs from birds’ nests they were able to find, eating them all (even the shell). As it turns out, the membranes found in these shells are beneficial for joint health.7

• How to choose the best eggs — I recommend looking for organically raised, free-range, pastured eggs. This means that chickens roam and forage outside rather than being fed a grain diet high in linoleic acid (LA).

This ensures that the eggs you and your dog eat have lower polyunsaturated fat (PUF) levels compared to conventionally harvested eggs. To find pastured eggs, make the trip to your local farmers market or health food stores. For in-depth tips on finding the best eggs, read “How to Decode Egg Carton Codes.”

Now, how do you make eggshell powder? The process is quite simple — simply follow the recipe below:

Save shells, rinse, and dry.
Bake at 250 degrees Fahrenheit (121 degrees Celsius) for 10 minutes.
Grind shells to a powder. One teaspoon provides 2 grams of calcium.

Making Lightning-Easy Tallow in a Pressure Cooker

Tallow is fat derived from animals, mainly beef or lamb. If you haven’t cooked with it, I recommend giving it a try. It’s great for high-heat cooking because it has a high smoke point, as well as being rich in stable unsaturated fats. That said, here’s how to make your own tallow at home:

Load up to 5 pounds diced beef fat into the pressure cooker.
No water needed (the sealed steam prevents scorching).
Cook on high pressure for 60 minutes, then set to natural release for 15 minutes.
Pour the tallow through a strainer into jars, then allow it to harden. This helps the fat to last six months in the fridge, or one year in the freezer.

How to Cook the Puppy Power Meal

Once you have all the base ingredients, it’s time to create your very own Puppy Power Meal. Follow the recipe below.

Puppy Power Meal
Ingredients

4 pounds white rice
Up to 2 pounds organic oat groats/bran (optional; see Seed Oil Reset Note above)
3 pounds ground beef, 70% lean/30% fat
10 ounces homemade tallow
8 ounces beef liver
10 egg yolks
10 teaspoons eggshell powder
10 to 20 mg elemental zinc (chelated zinc or zinc gluconate; scale dose by body weight); supports skin, immune, and reproductive health
Pinch of iodized salt
1 fish-oil capsule per 20 pounds of puppy weight

Procedure

Cook the rice first, then allow it to cool. If using oat groats or bran, fold it into the cooked rice before cooling.
Add the ground beef raw.
Stir the tallow into the meat.
Dice/purée the liver and quick-sauté for two minutes.
Stir the raw egg yolks into the warm mixture.
Stir the eggshell powder, salt, fish oil, and zinc into the finished meal.

• Mix everything together — Once you’ve prepared all the ingredients, let everything cool, then create separate portions for your pup. Lastly, freeze the food to lock in the freshness.

• Additional nutrition boosters — Don’t forget to mix in the eggshells for calcium, the zinc, as well as salt and fish oil for additional trace minerals and omega-3 fats.

• Important feeding reminder — Serve 1 cup of Puppy Power Meal per 10 pounds of body weight. Add or reduce the portions as needed if ribs poke out or if your pup becomes pudgy. Done correctly, you should be able to cook an estimated 10-pound batch, which feeds a 10-pound pup for 10 to 12 days.

Those two micro-investments cost less than $1 a week yet address the two problems vets see most in adult dogs — dental disease and oxidative inflammation.

Checking the Cost of the Ingredients

Depending on where you get your ingredients, the total running cost of this Puppy Power Meal runs at around $1.60 to $1.90 per pound once cooked. This is more economical (not to mention healthier) compared to the mass-produced options below:

• Popular dry kibble — Around $1.84 to $2.10 per pound (Purina ONE Lamb and Rice Formula or Beneful 40-pound bags).

• Premium/vet formulas — The prices on these products climb up to $3 to $4 per pound. Meanwhile, boutique fresh-frozen subscriptions command higher premiums, which is around $4 to $10 per pound.

Quick Questions Answered for New Pup Owners

Being a new pet parent is a daunting task — you want to make sure you’re doing the best you can. To help you with your journey, here are some questions that you may have already asked while reading through this article:

• What are all the ingredients for? The ingredients cover a wide range of nutritional requirements. For example, liver plus yolks cover vitamins A, B, and K. Meanwhile rice supplies carbs/glucose, and the fish oil adds omega-3 fats.

• Do pups need veggies? Dogs don’t need veggies that much because their gut functions differently from humans. However, they still need some amounts to help promote digestive health and a balanced gut microbiome.

• What if the beef I got is leaner (80/20)? I recommend adding an extra spoon of rendered tallow per meal to bump up the fat portions again.

• Fresh versus frozen portions? Keep three days’ worth in the fridge for immediate feeding. Freeze the rest in silicone cubes or glass containers.

• Calcium for nursing moms? If you have a nursing dog, double the eggshell powder during lactation.

I recommend you share this article with other puppy parents. Gather the ingredients and invite them for one pressure cooker session. The food you make will help nourish their dogs for less than the price of “bargain” kibble.

Frequently Asked Questions (FAQs) About Raising a Puppy on a Budget

Q: What are the essential ingredients for a healthy and budget-friendly homemade dog diet?

A: The core ingredients include white rice, ground beef with a 70/30 fat-to-lean ratio, beef liver, beef fat, or suet rendered into tallow, whole eggs, and eggshell powder. Additionally, a pinch of iodized salt and a fish oil capsule (per 20 pounds of body weight) are recommended for essential trace minerals and omega-3 fatty acids.

These ingredients collectively provide protein, fats, vitamins, calcium, and the small amount of carbohydrates needed for energy. When sourced strategically, such as through bulk purchases, local butchers, or warehouse clubs, they remain highly affordable.

Q: Why is protein and fat important for my dog’s health?

A: Protein is vital because dogs are scavenging carnivores by nature, and it helps build lean muscle, supports various bodily functions, and plays a role in synthesizing hormones and enzymes. As dogs age, their need for protein actually increases.

Fats, on the other hand, serve as a dense energy source and contribute to several biological functions. They help with nutrient transport across cell membranes, play a role in reducing inflammation, and are involved in the production of important hormones and bile acids. Fat also acts as a physical barrier to prevent heat loss, protect internal organs, and minimize water loss.

Q: Do dogs really need carbohydrates like rice in their diet?

A: While dogs do not have a strict dietary requirement for carbohydrates, they do require glucose for certain metabolic functions, particularly for brain and red blood cell energy needs. White rice is included in the diet to fulfill this need in a moderate and controlled way.

Unlike most commercial kibbles, which can be excessively high in carbohydrates, this homemade approach includes enough rice to meet the dog’s glucose requirement without risking weight gain or metabolic diseases like canine diabetes.

Q: How do I store Dr. Mercola’s homemade Puppy Power Meal?

A: For storage, keep about three days’ worth of food in the refrigerator and freeze the rest in containers to preserve freshness. When feeding, provide 1 cup of this meal per 10 pounds of your dog’s body weight and adjust as needed based on your pet’s physique and appetite.

Q: How does the Puppy Power Meal compare to store-bought kibble in cost and nutrition?

A: The recipe costs around $1.60 to $1.90 per pound once cooked. This makes it more affordable than many dry kibble options, which typically range from $1.84 to $2.10 per pound, and significantly cheaper than premium or veterinary formulas, which can cost between $3 and $4 per pound.

Boutique fresh-frozen subscriptions are even more expensive, often reaching $10 per pound. Beyond the cost advantage, homemade food provides superior nutrition by relying on whole, fresh ingredients rather than heavily processed fillers and additives.