Watchman News

Fitness enthusiasts all over social media are now jumping on the latest fitness trend — whole body vibration (WBV) therapy. You’ll see them standing on vibration plates, their bodies quivering and reverberating as they try to maintain their balance. Their goal? To trim their waistline and shed off a few pounds.

I’ve previously written about the benefits of using a vibration plate, and I’ve long emphasized that not all platforms are created equal. Among them, the Power Plate stands out as the most advanced option, offering superior technology and consistent results compared to generic vibration devices.

I believe that if you want to take your fitness to the next level, using this tool is one of the best ways to diversify your workout routine. But is WBV therapy truly helpful for weight loss? Let’s take a look at the evidence and what it says regarding this fitness trend.

The Science of Whole Body Vibration — How Does It Work?

In essence, whole body vibration is a specialized form of training that blends mechanical stimulation with active or passive exercise. The fact is, we’re constantly exposed to vibrations, also called oscillations, all around us — riding in a car, traveling on a plane or train, or even using a smartphone are some examples. The only difference is the frequency and intensity of these vibrations.

• The body detects vibrations through mechanoreceptors — These are found under the skin and near the bones.1,2 Vibrations are measured in Hertz (Hz), which is a complete cycle a vibrating object makes when it moves from one position to the other and back again.3

• Strong vibrations are harmful to your health, but milder ones are beneficial — The body is sensitive to vibrations that are between 1 and 100 Hz. When the vibrations go beyond this range, they can irritate and injure your musculoskeletal system. However, if the vibrations are mild enough, they can have therapeutic effects. This is how whole body vibration works. In WBV therapy, your body is subjected to rapid controlled vibrations on a specially designed platform.

• The concept of WBV isn’t new — WBV was first developed in the mid-20th century and was famously used by Russian scientists to help cosmonauts maintain muscle and bone mass during long periods in space. The method has since been adapted for fitness, rehabilitation, and performance enhancement.4

• In its modern form, WBV is applied using platforms — Each offer slightly different vibration patterns and intensities, and the frequency ranges from 12 to 90 Hz.5 Depending on the machine, the movement may be synchronous (both sides moving together) or side-alternating (mimicking a walking motion), and the amplitude — how far the platform moves — can be adjusted to control the strength of the stimulus.6
It’s important to note that these differences matter: not all machines deliver the same benefits. For years, I’ve highlighted Power Plate as the superior choice because of its unique tri-planar vibration technology, which provides more precise and effective stimulation than standard plates.

• When you step onto a WBV platform, your body instinctively works to stabilize itself — The constant, rapid vibrations cause your muscles to contract and relax automatically and repeatedly, far faster than they would during regular exercise. The result is a unique type of muscle activation that challenges your body in ways traditional workouts do not.7

Personal trainer Laura Wilson explains, “This stimulates a subconscious muscle activation each time the machine moves, meaning your muscles are activating far more than they would on a stable surface.”8

• The platform vibrates in a specific pattern — You can stand still with slightly bent knees for a gentler session, or you can increase intensity by performing squats, lunges, planks, push-ups, and other dynamic exercises directly on the platform. The vibration frequency typically ranges from 20 to 60 times per second.9

So, Does WBV Therapy Help with Weight Loss?

Whole body vibration has been linked to several well-documented health benefits (which I’ll outline later). But when it comes to shedding excess weight, the answer isn’t as straightforward as a simple yes or no.

• Vibration plates don’t magically shed off excess fat — The fact is that while using this equipment could help with your weight loss goals, it’s only beneficial if it’s part of a well-rounded fitness plan. To put it simply, standing on a vibration plate doesn’t mean you’ll easily burn off fat — you also need to pair it with a healthy diet and regular exercise. According to Michael Betts, a personal trainer and director at TrainFitness:

“Vibration plates are not a magic bullet or a replacement for traditional exercise. The benefits are modest and work best when combined with other forms of training.”10

• Its benefits are similar to that of walking — In terms of its effects on aerobic and calorie-burning, some experts compare using a vibration plate with moderate-intensity walking. The length and frequency of your sessions will influence the results you achieve.

• Still, there are studies showing promising results — A 2019 meta-analysis published in the Journal of Musculoskeletal and Neuronal Interactions reviewed seven controlled trials involving 280 participants and found that WBV training led to a statistically significant reduction in total fat mass.

• While the percentage change in body fat was small, the Power Plate produced greater fat reductions — Overall, the strongest and most consistent benefits appear to come from Power Plate and from WBV’s ability to increase lean muscle mass rather than markedly decrease body fat.

Published Research Highlights the Other Benefits of WBV Therapy

While the weight loss effects of WBV are yet to be confirmed, other published studies point to its other benefits to your health. There’s research supporting its potential for improving bone mass density,11 easing chronic pain,12 and moderating inflammation.13,14 This therapy offers hope for many health conditions, such as:

• Osteoporosis — A 2023 review article published in Cureus looked at nine clinical trials to determine the effects of vibration therapy on osteoarthritis and osteopenia patients. The researchers found that WBV helps increase bone mass and density in geriatric people and postmenopausal women.15

“Vibration therapy … shows promising results in regaining muscle mass and function after degeneration. It reinforces the blood supply to the bones and reduces osteoclast formation. It reactivates the inactive muscle fibers and the neuronal and proprioceptive sensory systems around them,” the researcher concluded.

“Vibration therapy can be regarded as an alternative to stimulating physically restricted patients with mechanical stimulation to rebuild musculoskeletal strength.”

• Fibromyalgia — A 2021 study published in the International Journal of Environmental Research and Public Health explored the effects of WBV therapy among fibromyalgia patients. The study involved 60 people between 35 and 65 years old (90% were women) who were asked to do WBV therapy for 12 weeks. According to the researchers, the therapy helped improve motor function and gait speed among those with this condition.16

• Knee osteoarthritis — A 2013 study published in the Annals of Rehabilitation Medicine examined the effects of WBV in people with chronic knee osteoarthritis. According to their findings, vibration plates “reduced pain intensity and increased strength of the right quadriceps and dynamic balance performance.”17

• Cognitive function — A 2018 study published in the Journal of Exercise Rehabilitation sought to identify how WBV benefits elderly women with mild dementia. In this study, the participants were asked to do WBV five times a week for eight weeks. The researchers recorded data before and after the training period. Results noted that they had elevated brainwave activity, and that using vibration plates is a viable method to help prevent functional decline in the brain.

A more recent study, published in 2022 in the Annals of Nuclear Medicine, also looked at the effects of WBV on mild cognitive impairment. Using SPECT (single-photon emission computed tomography) imaging, researchers noted that the 16 participants had increased regional cerebral blood flow, which may result in improved cognitive function.18

• Muscle strength — A 2007 study involving 16 healthy adults found that when they were asked to do various static and dynamic unloaded squats while using a vibration plate, the neuromuscular activation of their leg muscles increased.19 Another study highlighted that this therapy increased isometric muscle strength, explosive muscle strength, and overall muscle mass in their upper legs — possibly helping prevent sarcopenia.20

• Spinal injury — A study published in 2009 found notable improvements among people with chronic spinal injury after doing WBV. The research involved 17 participants who did the therapy three times a week for one month. According to their findings:

“The WBV intervention was also associated with statistically significant increases in cadence, and both the stronger and weaker legs exhibited increased step length and improved consistency of intralimb coordination. Changes in cadence and step length of the stronger leg were strongly correlated with improvements in walking speed.”21

Do You ‘Vibe’? Here’s What to Know About Different WBV Equipment

Although vibration plates are starting to become popular on social media — with users filming themselves “vibing” on their equipment and sharing how it has improved their fitness routine — these machines have actually been around for many years.

As I previously mentioned, different vibration platforms sold today have varying intensities and patterns. They also differ in terms of movement. Among all the different brands sold today, however, I believe the Power Plate offers the most advantages and gives you more bang for your buck.

• Why the Power Plate is my vibration plate of choice — Power Plate uses a unique “tri-planar” movement that improves upon commonly used vibrating plate technology. Called PrecisionWave™, it works by vibrating in three different directions: up and down, side to side, and front to back. PrecisionWave™ is considered to be the most precise vibration methodology so far, which is why Power Plate is now the most advanced vibration technology on the market.22

• There are other kinds of vibration plates today — One example is pivotal vibration, also known as oscillating vibration. It works like a seesaw, tilting up with a central pivot point. The tilting goes up and down rapidly, which is almost imperceptible. The disadvantage is that this type of tilting movement means you cannot perform dynamic exercises on the surface while using the vibration plate.

• Another type is linear vibration — This type of vibration plate moves back and forth along a straight line. The primary difference between this and pivotal vibration is the direction. Linear has a back-and-forth motion, while pivotal has a tilting motion. The advantage with this linear vibration machines is that they’re usually cheaper, making them ideal for first timers.

If you’re considering purchasing your own vibration equipment, I urge you to do your research first so you can evaluate the pros and cons of each machine. These can cost from $100 to $3,000, depending on their extra features, accessories, and speed options.23 Knowing your options will help you find a product that fits all your requirements so you don’t overspend. For a guide on how to choose a vibration plate, read “Utilize the Power of Vibrations to Promote Wellness.”

Safety Reminders When Using a Vibration Plate

Most healthy adults can use vibration plates safely without any issues, but as with other fitness equipment, there are some exceptions. If you fall under any of these groups, you may want to reconsider using this machine:

• People with certain medical conditions, such as heart disease, severe osteoporosis, head injury, or herniated disc
• Those who had a surgical procedure recently
• Pregnant women
• People with balance disorders, postural problems, or have a limited range or motion

Unless you have been cleared by your doctor or physician, it would be better to avoid using this machine.

• First time using a vibration machine? Take it slow — Dr. Leah Verebes, a physical therapist and assistant professor at Touro University’s School of Health Sciences, advises beginners to start slow and easy. Ideally, do five- to 10-minute sessions on the machine at a low intensity. “Moderation is key, as excessive use may lead to fatigue or injury,” she adds.

• Don’t overtrain — Meanwhile, Betts advises beginners to stick to two to three vibration sessions per week. Once your body is able to adjust to the training, you can gradually increase your sessions, but be careful not to overdo it. “As your body adapts, you can increase to 15- to 20-minute sessions up to 3 to 4 times a week. Never go over 30 minutes, as this can cause fatigue and joint stress,” he said.

Finally, remember that recovery is essential; make sure to leave at least 24 hours in between sessions. “Listen to your body and adjust accordingly,” Betts advises. “Quality of movement matters more than duration.”24

Frequently Asked Questions (FAQs) on Whole Body Vibration (WBV) Therapy

Q: What is whole body vibration therapy?
A: WBV therapy involves standing, sitting, or exercising on a platform that vibrates at controlled frequencies. These vibrations trigger rapid, automatic muscle contractions that enhance muscle activation, circulation, and coordination.

Q: Can WBV help with weight loss?
A: Yes, but results are modest. WBV works best when combined with a balanced diet and regular exercise. Standing on a vibration plate alone won’t burn significant fat.

Q: What other health benefits does WBV offer?
A: Research links WBV to improved bone density, increased muscle strength, better balance, enhanced cognitive function, reduced chronic pain, and potential rehabilitation support for certain injuries.

Q: Are all vibration plates the same?
A: No. Vibration plates differ in movement type (tri-planar, pivotal, or linear), frequency range, and amplitude. Devices like the Power Plate use advanced tri-planar technology for more precise stimulation.

Q: Is WBV therapy safe for everyone?
A: It’s safe for most healthy adults, but not recommended for those who are pregnant, have severe osteoporosis, cardiovascular issues, and certain spinal and balance disorders without medical clearance. People who recently had a surgical procedure are also advised to consult their physician before using a vibration plate.

Cerebrospinal fluid, the clear liquid that cushions your brain and spinal cord, carries away waste, including proteins linked to Alzheimer’s disease and Parkinson’s disease.1 Researchers have long known that it eventually drains into the lymph nodes in your neck, but the step they could never account for was how the fluid crosses the arachnoid membrane, which is the protective layer that separates your brain from the lymphatic vessels beyond it.2

That gap in the anatomy has stood open for roughly 250 years, ever since lymphatic vessels around the brain were first described.3

A research team based in South Korea now reports that it has found the missing exit route, along with evidence that the route deteriorates as animals age and can be functionally restored in aged mice. Their work, which also involved Finnish and American researchers, was published in the journal Cell.4

What the Cell Study Showed

The work was done almost entirely on mice, as well as two long-tailed macaque monkeys (whose brain structure sits closer to ours than a mouse’s does). The mice were specifically bred so their drainage vessels will glow green under a microscope, which let the researchers observe where fluid went. They also used a scanning electron microscope (SEM) to build a very high-magnification image5 on tissue from both mice and monkeys.6,7

The question that the researchers aimed to answer was how cerebrospinal fluid gets out. Either the drainage vessels connect straight to the fluid-filled space around the brain, or the fluid has to squeeze through gaps in the arachnoid membrane first. Researchers have argued over the two pathways for years. All along, a pathway nobody could find was carrying half the traffic.8

• The openings are real, tiny, and sit in one small patch — Under the SEM, the researchers found actual holes in the membrane, but only in one place — a strip of tissue lying over the perforated bone behind the bridge of your nose, which separates the brain from the nasal cavity.

The holes measured 2 to 12 micrometers across. To help you visualize, a micrometer is a thousandth of a millimeter, so about 15 of these openings would fit side by side across one human hair. That count comes from 73 holes across four mice. Nowhere else on the membrane had any, and two monkeys showed the same pattern in the same place. This is the piece that previous researchers had been missing: a physical doorway, in a specific spot, that can now be located and measured.

• Plugging the holes stopped the drainage — To test whether the holes actually carry fluid, the team corked them. They injected plastic beads into the fluid around the brain using two sizes: small ones fine enough to slip through, and large ones 50 times bigger, too wide to pass.

The next day, they injected a traceable dye. In the mice given small beads, and in the untreated controls, the dye reached the neck lymph nodes normally. In the mice whose holes were corked, almost none arrived. Blocking the openings stopped the drainage. That is the strongest evidence in the paper that these holes are the exit pathway.

• Damaging the nasal end slowed amyloid clearance, too — If this route matters, damaging it should slow drainage, and it did. The researchers used a chemical delivered into the nose to partially destroy the smell nerves and the drainage vessels beside them.

Dye clearance into the neck lymph nodes fell by 60% and 40% in the two sets of nodes. Repeating the test with a tagged version of amyloid-beta — the sticky protein that builds up in Alzheimer’s disease — clearance fell by 49% and 26%.

Scans showed no change in the brain’s fluid volume or in pressure inside the skull, so the slowdown came from the damaged route rather than from a pressure shift. This is the closest the study comes to the disease question. The route does not just carry dye — it carries amyloid-beta.

• Every part of the system was smaller in old mice — Comparing mice aged 85 to 100 weeks with young adults (8 to 12 weeks), the drainage network between the smell centers covered 58% less area, and the vessels that remained looked less healthy.

The holes themselves were 51% smaller and 59% fewer, with immune cells clinging to the membrane surface. The bone channels the vessels pass through were narrower and fewer. Drainage vessels in the lining of the nose were down by roughly half.

The decline is not observed in one component only, but across the whole route at once — and it happens over the same stretch of life when neurodegenerative disease becomes most common.9

• A growth factor restored the flow without repairing the holes — The researchers loaded the gene for a signaling protein called vascular endothelial growth factor C (VEGF-C), which prompts drainage vessels to grow, into a harmless virus and gave it to old mice as a nasal dose. Six weeks later, the vessels between the smell centers had doubled, with large gains in the lining of the nose.

The holes and the bone channels did not recover at all — they stayed exactly as they were. Fluid outflow returned anyway, back into the range seen in young mice. This is a notable finding because the plumbing downstream was able to make up for damage upstream, which is a more workable target. Note that it happened in mice, though, using an experimental gene therapy that does not exist for people as of this moment.

• What the researchers say is still unknown — Their methods cannot rule out other escape routes for very small molecules, and they could not watch the process happen live. They also do not know how long the growth-factor effect lasts, why the bone channels never recovered, or whether any of this improves how an aging brain works.

A Second Study Looked at Human Donor Brains’ Waste Clearance Capabilities

While the Cell study traces the route in animals, a separate research, published in Acta Neuropathologica Communications, asked whether failing waste clearance shows up in human brains. Working with donated tissue, they counted structures called wasteosomes — microscopic bundles the brain appears to use as sealed waste containers — and found more of them in people who had died with neurodegenerative disease.10,11

• The definition of wasteosome — It has a spherical shape measuring between 2 and 50 micrometers across, the largest about three-quarters the width of a human hair. Support cells in the brain build them, and what ends up inside depends on what was swallowed, such as the tau protein in Alzheimer’s disease that forms tangles inside nerve cells.

Once made, they can be released into cerebrospinal fluid, and they have been found in the deep lymph nodes of the neck — the same place the Cell study’s fluid ends up. This finding is relevant because if the brain wraps up its waste and ships it out through the drainage system, then counting the packages left behind is one way to ask, indirectly, whether the shipping worked.

• Limitations of the research — The team analyzed brain tissue from 185 donors: people who had died with Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), and two types of frontotemporal lobar degeneration (FTLD): FTLD with TDP-43 proteinopathy (FTLD-TDP) and FTLD with tau proteinopathy (FTLD-Tau). Donors with no brain disease served as the comparison group.

They set out to score 28 brain regions, but 21 of them had to be dropped from the analysis because the signal was too faint or the scores clustered too tightly to work with, leaving seven regions to carry every result reported. In addition, one donor fell out of the main calculation, leaving 184.

• Every disease group had more wasteosomes — All four disease groups carried more wasteosomes than the comparison group, and the rise was spread fairly evenly across regions rather than piling up in one spot. One statistical test placed every disease group above the comparison group; another test left the ALS group just short of their threshold.

• Age was an alternative explanation, since wasteosomes accumulate with age and the groups differed sharply in age at death — The Alzheimer’s donors averaged 85 years, and the ALS donors 61 years. So, the researchers retested everything holding age as a constant.

The gap between the disease and comparison groups mostly held, though the Alzheimer’s comparison narrowed to the point where they could no longer call it a clear difference. Age itself still mattered in the model. On that basis, they rule age out as the single shared explanation.

• The pattern followed the drainage routes, not the diseases — The extra wasteosomes did not pile up where each disease does its own damage. In the FTLD groups, the frontal lobe showed no increase. In ALS, the memory centers are untouched at the stages included here, yet they showed a rise anyway.

What the affected regions had in common was positioning — they sit around a deep vein at the center of the brain and along its inner surfaces — places that have been proposed as parts of the main drainage pathway. These observations matter because if wasteosomes built up because of each disease, they should track each disease. Instead, they tracked the plumbing, which hints that clearance could be the problem the diseases might share.

• The researchers say plainly that they cannot prove it — There is no way to know what any donor’s drainage system was doing while they were alive, so the link stays hypothetical rather than an explicit finding.

Wasteosomes may also be building up in drainage regions the study never looked at, including the nerves that carry smell signals and the smell centers themselves, where earlier work reported wasteosomes are especially concentrated. Ultimately, their own conclusion stays conditional — the findings are consistent with a long-underperforming drainage system in these diseases, and further study is required.

Everyday Habits That Support Cellular Energy While the Science Develops

The featured studies discussed here do not point to any brain-drainage intervention you can use today. What they do highlight is that clearance appears to be an active, energy-dependent process that falls off with age — and the everyday habits that support cellular energy remain the practical ground you can actually stand on. Neither study tested the steps below, but they reflect a broader strategy for supporting cellular energy.

1. Cut linoleic acid (LA) down to roughly 5 grams a day — LA, which is the dominant fat in seed oils, accumulates in your tissues over the years and can leak metabolites that may compromise mitochondrial function.

Replace canola, soybean, corn, sunflower, and similar oils with tallow, ghee, or grass fed butter for cooking, and scrutinize labels on packaged foods, sauces, dressings, and restaurant meals, where these oils hide. Nuts and seeds carry LA as well, and olive oil needs moderating because of its oleic acid content, which can contribute to metabolic dysfunction when consumed in excess, similar to LA.

2. Give your brain the fuel it runs on — Glucose is the preferred cellular fuel, and your brain alone requires a minimum of 125 grams of carbohydrate per day. For most adults, roughly 250 grams of targeted carbs daily supports cellular energy production, with more for anyone highly active. Whole fruits and white rice are reasonable starting points.

If gas, bloating, pain, or irregular stools show up when you add carbs, that usually points to gut function needing attention first, so build up gradually rather than jumping straight to high-fiber foods, which can raise endotoxin in a compromised gut.

3. Get outdoors daily, ideally around solar noon — Sensible sun exposure remains the preferred route to optimal vitamin D, which functions as an epigenetic regulator and supports AMP-activated protein kinase (AMPK) activation.

If you have been eating seed oils regularly, allow four to six months of reduced intake before pursuing high-intensity midday sun, since high-LA tissue increases susceptibility to sunburn. Pair sunlight with movement whenever you can — an hour of walking a day covers both, and standing more beats long, uninterrupted sitting.

4. Treat sleep as part of your brain’s maintenance schedule — Sleep has been consistently linked to enhanced glymphatic and lymphatic clearance of brain waste, and the pathway described in the Cell paper is part of that same broader clearance system.12

Create a consistent sleep window, get morning light to help reset your body’s master clock, and reduce nighttime electromagnetic field (EMF) exposure in the bedroom, since these invisible waves can disrupt cellular ion balance through voltage-gated calcium channels.

5. Know your numbers instead of guessing — A handful of inexpensive labs can tell you more about your metabolic status than any symptom checklist. These include fasting insulin and homeostatic model assessment for insulin resistance (HOMA-IR), 25(OH)D for vitamin D status with an optimal range of 60 to 80 nanograms per milliliter (ng/mL), ferritin with a target of 60 to 75 ng/mL, and HbA1c for longer-term glucose patterns.

Talk to your health care provider about whether these tests are appropriate for you. Then, retesting a few months after making dietary and lifestyle changes shows you whether the changes are landing.

Frequently Asked Questions (FAQs) About the Brain Waste Clearance System

Q: What exactly is a wasteosome?
A: A: This is a tiny sphere (2 to 50 micrometers across) that the brain appears to use as a sealed container for cellular debris. Support cells build them, and what ends up inside depends on what was swallowed. The Acta Neurologica Communications study counted more of them in all four disease groups than in donors without brain disease.

What that means is still open — nobody can know what a donor’s drainage system was doing in life, and 21 of the 28 brain regions had to be dropped from the analysis, leaving seven to carry the result.

Q: Does a fading sense of smell mean my brain isn’t draining properly?
A: Nothing in this research supports that. The confusion is understandable — the exit route sits directly above the smell centers, and when researchers deliberately damaged the smell nerves in mice, drainage dropped sharply. But that is damage causing reduced drainage in a mouse experiment, not smell loss signaling a drainage problem in a person, and neither study tested that direction.

A persistent, unexplained loss of smell is still worth raising with your health care provider for other reasons.

Q: What is the difference between the two drainage systems discussed in the featured studies?
A: One works inside brain tissue, moving fluid through it and picking up debris. The other takes over at the brain’s outer wrappings and carries that fluid the rest of the way to the lymph nodes in your neck. The Cell paper mapped the handoff between them. The second study looked only at the first, and never measured its flow directly.

Q: Could the growth factor that worked in the aged mice be given to people?
A: No. VEGF-C was not a supplement, a drug, or a nasal spray — the researchers packaged its gene inside a modified virus and delivered that into the noses of mice. It exists only in the laboratory, has never been tested in humans, and is available nowhere. No treatment based on this pathway is available for any condition, and the work remains preclinical.

The mouse result was narrower than it sounds, too. Drainage recovered, but no one checked whether amyloid or tau fell, or whether the animals’ brains worked any better.

Q: Can sleep help the brain clear waste?
A: Separate research has consistently linked sleep to better clearance of brain waste, and the route described in the Cell paper is part of that same broader system. Neither study here examined sleep, though — that link comes from other published studies. Still, the practical steps to support brain health remain, namely a consistent sleep window, and morning light to help reset your body’s master clock.

Q: Is there a test that shows how well my brain is draining?
A: Not currently. No clinical test of brain drainage exists as a routine assessment. Researchers have proposed that wasteosomes might one day serve as an indirect marker of long-term clearance problems, but they note that direct evidence linking these structures to drainage is still missing.

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.

Which of these is not a glucagon-like peptide-1 (GLP-1) weight loss drug?

Mounjaro
Ozempic
Metformin
Metformin is a different type of diabetes medication. Ozempic, Wegovy, and Mounjaro are commonly used in the GLP-1 drug category for diabetes or weight management. Learn more.
Wegovy

1 Which of these foods is a good source of vitamin K2?

Fermented foods
Fermented foods such as natto can provide vitamin K2, which helps direct calcium toward bones and teeth rather than soft tissues. Learn more.
Refined grains
Sugary cereals
Fruit juices

2 Which breathing technique may help calm the nervous system and support healthier blood pressure?

Alternate nostril breathing
Pursed-lip breathing
Box breathing
Box breathing uses a repeated four-second inhale, hold, exhale, and hold pattern that may help reduce stress signals that keep blood pressure elevated. Learn more.
Diaphragmatic breathing

3 What are dendritic cells?

Cells that store energy in muscles
Cells that carry oxygen in blood
Cells that build and repair bone
Immune cells that alert other immune defenders
Dendritic cells help the immune system recognize threats and direct other immune cells to respond to abnormal cells. Learn more.

4 Why do people often start a routine strongly and then lose consistency?

Their goals become less important
Motivation naturally fades over time
Motivation often provides an early push, but routines built only on enthusiasm may fade once everyday demands return. Learn more.
Their daily needs completely change
Their routine becomes too automatic

5 About how many daily steps were linked to the lowest risk of death?

6,000 to 7,500 steps
9,000 to 10,500 steps
Around 9,000 to 10,500 steps per day were associated with the lowest risk of death, even among people who spent long hours sitting. Learn more.
11,000 to 12,500 steps
13,000 to 14,500 steps

6 Where should you start when trying to reduce your exposure to air pollution?

At your workplace
Inside your vehicle
At outdoor parks
Inside your home
Most people spend about 90% of their time indoors, so reducing pollution inside the home can meaningfully lower daily exposure. Learn more.

7 What does the body use to help support natural GLP-1 production in the intestine?

Cholesterol
Linoleic acid
Butyrate
Butyrate is a short-chain fatty acid (SCFA) made by beneficial gut bacteria that helps support intestinal cells involved in natural glucagon-like peptide-1 (GLP-1) production. Learn more.
Glucose

Test Your Knowledge with
The Master Level Quiz

1 Which types of cheese are rich in vitamin K2?

Ricotta and cottage cheese
Feta and cream cheese
Mozzarella and mascarpone
Gouda and Brie
Gouda and Brie are among the cheeses that provide vitamin K2, along with foods such as egg yolks, liver, and natto. Learn more.

2 Which test can help detect early kidney damage?

Complete blood count (CBC)
C-reactive protein (CRP)
Estimated glomerular filtration rate (eGFR)
Estimated glomerular filtration rate (eGFR) is a blood-based measure of kidney function that can help detect declining filtration before symptoms appear. Learn more.
Hemoglobin A1C (HbA1c)

3 How many grams (g) of protein per pound of ideal body weight are recommended?

0.2 to 0.4 g
0.6 to 0.8 g
Protein makes up a large part of bone structure. The recommendation is 0.6 to 0.8 grams per pound of ideal body weight, with about one-third from collagen-rich foods. Learn more.
1.0 to 1.2 g
1.4 to 1.6 g

4 Why might reducing salt alone not be enough to improve blood pressure?

Overall diet quality also matters
Aggressive salt restriction may raise stress hormones and insulin. Focusing on whole foods while limiting ultraprocessed foods may better support blood pressure control. Learn more.
Protein intake becomes too high
Calcium levels begin to fall
Digestion naturally slows down

5 Which is a possible symptom of small intestinal bacterial overgrowth (SIBO)?

Blurred vision
Joint swelling
Frequent headaches
Food intolerance
Small intestinal bacterial overgrowth (SIBO) can cause food intolerance along with bloating, gas, constipation, or diarrhea. Learn more.

6 Which type of cancer is especially common in Western countries?

Colorectal cancer
Colorectal cancer is among the most common cancers worldwide, with about 1.2 million cases diagnosed each year. Learn more.
Pancreatic cancer
Thyroid cancer
Kidney cancer

7 How many grams (g) of creatine per day are generally sufficient for most adults?

1 to 2 g
2 to 3 g
3 to 5 g
A daily intake of 3 to 5 grams is commonly used to maintain creatine stores, while higher amounts may increase bloating or digestive discomfort. Learn more.
8 to 10 g

8 Which group showed the strongest link between high artificial sweetener intake and faster cognitive decline?

Older adults over 70
Young adults under 30
Middle-aged adults under 60
Middle-aged adults under 60 showed the strongest association, while people with diabetes also experienced greater declines in memory and overall thinking skills. Learn more.
Adults between 60 and 70

9 What is the fiber paradox?

Some types of fiber are more useful for digestion than others
Too much fiber too soon can worsen gut symptoms
Fiber feeds beneficial gut bacteria, but people with gut imbalances may need to increase their intake gradually to avoid worsening digestive symptoms. Learn more.
Fiber only supports gut bacteria when eaten with fermented foods
Higher fiber intake always improves digestion once symptoms begin

10 Why can taking a supplement with a meal help build consistency?

Meals increase the supplement dose
Eating makes motivation stronger
Food removes the need for a routine
The meal becomes a regular cue
Linking a supplement to a meal creates a dependable cue, making the behavior easier to remember and repeat. Learn more.

11 How much of daily calorie intake can linoleic acid (LA) make up for some Americans?

25%
Linoleic acid (LA) intake has risen sharply in modern diets, largely because of vegetable oils and processed foods. Learn more.
15%
10%
5%

12 Which statement about the Motum movement program is not true?

It retrains basic movements such as rolling, crawling, and squatting
It may help reduce fear of movement and improve balance
It uses personalized corrections and different movement levels
It mainly relies on rest and avoiding physical activity
Motum encourages gradual, guided movement rather than inactivity. The program helps retrain motor control, build confidence, and make everyday movements feel more manageable. Learn more.

13 How long should you walk each hour to help break up long periods of sitting?

2 minutes
5 minutes
A five-minute walk every hour may offer a practical way to reduce long stretches of sitting while supporting energy, focus, and overall health. Learn more.
10 minutes
15 minutes

14 Which form of vitamin K is found in brain tissue and linked to brain health?

Menaquinone-7 (MK-7)
Phylloquinone (K1)
Menaquinone-4 (MK-4)
Menaquinone-4 (MK-4) is the primary form of vitamin K stored in brain tissue. Researchers found that a modified vitamin K compound could cross the blood-brain barrier and convert into MK-4. Learn more.
Menadione (K3)

15 What type of processed sugar is commonly found in sodas and processed snacks?

High-fructose corn syrup (HFCS)
High-fructose corn syrup (HFCS) delivers a concentrated fructose load to the liver, where excess amounts may be converted into fat and contribute to insulin resistance. Learn more.
Brown rice syrup (BRS)
Evaporated cane juice (ECJ)
Glucose syrup (GS)

16 What can help reduce air pollution inside your home?

A ceiling fan
A humidifier
An air freshener
A HEPA air purifier
A high-efficiency particulate air (HEPA) purifier can help remove airborne particles from indoor air, especially in rooms where you spend a lot of time. Learn more.

17 What process helps make slow-fermented bread easier to digest?

Refining
Fermentation
Fermentation gives microbes time to break down gluten and fermentable sugars, which can make bread easier to digest. Learn more.
Freezing
Fortifying

18 What is a major factor that can drive fatty liver disease?

Dehydration
Low calcium intake
Obesity
Obesity is a major driver of fatty liver disease, along with Type 2 diabetes and insulin resistance. Learn more.
Seasonal allergies

19 Besides body weight, what should you track when measuring weight loss progress?

Clothing size alone
Daily steps and strength
Tracking daily steps, strength, energy, and ease of movement gives a broader picture of physical function than relying on the scale alone. Learn more.
Calorie intake only
Weekly body weight

20 Which nuclear receptor is activated by oleoylethanolamide (OEA) and reduces glucose metabolism?

PPAR-gamma
PPAR-delta
PPAR-alpha
Peroxisome proliferator-activated receptor alpha (PPAR-alpha) is activated by oleoylethanolamide (OEA), signaling the body to burn more fat while reducing glucose metabolism. Learn more.
LXR-alpha

21 Which heavy metal was found to cause biochemical changes associated with Alzheimer’s disease?

Mercury
Mercury was found to trigger several biochemical abnormalities associated with Alzheimer’s disease, including changes involving tau and beta-amyloid. Learn more.
Aluminum
Cadmium
Lead

Weight loss grabs headlines, but what happens after the pounds come off matters just as much. Research presented at the Endocrine Society’s ENDO 2026 meeting tracked adults taking popular GLP-1 weight loss drugs such as Ozempic, Wegovy, Mounjaro, and Zepbound, and found something that runs counter to conventional wisdom: as participants lost weight, their day-to-day physical activity went down, not up.1

How easily you move through daily life tells a bigger story about your health than any number on the scale. GLP-1 receptor agonists reduce appetite and help people lose weight, but they also reduce lean muscle mass — the tissue responsible for strength, balance, and everyday physical function.

The new research adds another concern: People taking these medications also became less physically active, even though losing weight should make movement easier. That combination — less muscle and less movement — raises serious questions about whether the scale is telling the whole story, and whether there’s a better way to support your body’s own weight-regulation system.

People Became Less Active After Starting GLP-1 Drugs

The researchers behind this study started with a straightforward question: After people lose weight on GLP-1 medications, do they naturally start moving more? Rather than asking participants how much they exercised, the team analyzed objective activity data collected by Fitbit wearable devices alongside electronic health records from the National Institutes of Health’s All of Us Research Program.

That approach gave researchers a much clearer picture of what people actually did during everyday life instead of what they remembered or believed they did.

Instead of focusing only on pounds lost, the researchers examined how much participants walked each day and how much time they spent performing moderate-to-vigorous physical activity, which includes activities such as brisk walking, cycling, jogging, or anything that noticeably raises your heart rate. Those measurements paint a much broader picture of health because they reflect how active your body remains outside the doctor’s office.

• Hundreds of adults provided enough wearable data for detailed analysis — The researchers initially identified 1,950 adults with obesity who started a GLP-1 medication. Only 753 participants had enough Fitbit information before and after treatment to allow meaningful comparisons, making this one of the largest analyses of wearable activity data in people taking these medications. Most participants were women (78.6%), and the average age was 52.7 years.

This matters because wearable devices continuously collect movement data throughout the day. Instead of measuring activity during one clinic visit or relying on questionnaires completed months later, researchers observed how daily routines changed over time. That creates a more realistic picture of what happened after participants began treatment.

• The study challenged one of the biggest assumptions about weight loss — Many people expect that carrying less body weight automatically makes everyday movement easier. If climbing stairs requires less effort or walking becomes more comfortable, common sense suggests that people would naturally move more. The investigators found exactly the opposite.

Study leader Dr. Sajana Maharjan summarized the preliminary findings directly: “While many assume that weight loss leads naturally to increased physical activity, our study suggests otherwise.” She added that the results reinforce that “exercise cannot be optional for people taking these medications.”2 Those comments highlight the central message of the research: weight loss and physical activity are not interchangeable measures of health.

• Movement declined in more than one important way — The decline involved both everyday movement and structured exercise. Researchers reported that average daily step counts dropped from 5,047 steps before treatment to 4,487 afterward. Time spent in moderate-to-vigorous physical activity also fell from 28 minutes per day to 22 minutes per day.

Looking at both measurements together tells an important story. Participants didn’t simply skip gym workouts while staying active throughout the day. They walked less overall and also spent less time performing activities that strengthen the heart, lungs, and muscles. If you focus only on the number on the scale, you miss those important changes in daily habits.

• Some participants experienced even larger declines than others — Researchers found that the greatest reductions in physical activity occurred in men and in participants who reported joint or muscle pain. On the other hand, factors such as age, heart failure, and a previous stroke did not meaningfully change the overall findings.

If joint discomfort or muscle soreness already limits your activity, losing weight does not automatically solve that problem. Building a routine that protects muscle strength and encourages regular movement becomes even more important when pain makes exercise less appealing.

• GLP-1 medications reduce more than body fat; they also reduce lean muscle mass — This includes the muscles responsible for strength, balance, posture, and everyday movement. At the same time, participants became less physically active after starting treatment. Together, those two changes raise concerns about preserving physical function during weight loss.

Muscle does much more than help you lift heavy objects. It allows you to climb stairs, rise from a chair, carry groceries, maintain balance, and remain independent as you age. When you lose muscle and move less at the same time, you’re working against your long-term health on two fronts. That’s why the researchers stressed that exercise can’t become optional.

Preserving strength and maintaining regular movement provide a more complete picture of health than watching the scale alone.

But here’s what the study doesn’t address: your body already has a built-in system for regulating appetite and metabolism, and it doesn’t require a prescription. The fact that GLP-1 drugs can weaken muscle and discourage movement doesn’t mean you’re stuck choosing between a smaller waistline and a body that actually works well. It means the better path is restoring the biological machinery that handles both, and that starts in your gut.

Protect Your Muscle While You Support Your Body’s Natural GLP-1

The real solution isn’t to replace your body’s appetite-control system with a drug. It’s to support the biological system you already have. Your gut naturally produces GLP-1 through specialized cells in your colon, and those cells depend on butyrate, a short-chain fatty acid (SCFA) made by beneficial gut bacteria.

When your microbiome is healthy, it may help regulate appetite, blood sugar, and metabolism without injections. The goal is to rebuild that system from the ground up while preserving your strength and your ability to move.

1. Nurture the gut bacteria behind your body’s own GLP-1 signaling — Butyrate serves as the primary energy source for the cells lining your colon. SCFAs also interact with receptors on nearby L-cells, the gut cells involved in releasing GLP-1. Nurturing the microbial community behind these signals is one way to support your gut’s own GLP-1 activity from the ground up.

Akkermansia muciniphila is one of the species researchers study most closely here. Rather than producing butyrate directly, it lives in the gut’s mucus layer and releases SCFAs like acetate and propionate — the raw material that other resident bacteria use to make butyrate. In this way, a healthy Akkermansia population may help sustain the wider community of butyrate-producing microbes.

2. Remove the foods that interfere with butyrate production — I recommend eliminating seed oils, which are high in linoleic acid (LA), because they weaken your colon’s protective lining and make it harder for beneficial bacteria to thrive. These unstable fats also interfere with your colon cells’ ability to burn butyrate for energy, allowing oxygen levels inside the colon to rise.

That creates an environment where many beneficial bacteria struggle to survive. Keep LA intake below 5 grams per day, and ideally closer to 2 grams, so your microbiome has the opportunity to recover.

3. Calm your digestion before increasing fiber — If you deal with bloating, abdominal discomfort, or unpredictable bowel habits, avoid adding large amounts of fermentable fiber all at once. Start with simple, easy-to-digest meals that reduce excessive fermentation and the release of endotoxins — toxic fragments from bacterial cell walls — while your intestinal lining repairs itself.

As your digestion becomes more predictable, gradually increase carbohydrate intake using foods your gut tolerates well.

Whole fruit and well-cooked starches such as white rice provide glucose for cellular energy without overwhelming an already stressed microbiome. From there, add root vegetables first, followed by non-starchy vegetables, 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 daily once metabolic health improves.

4. Feed the bacteria that make 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 feeds beneficial bacteria.

As those microbes multiply, butyrate production increases, your gut barrier tightens, and inflammatory compounds remain inside your digestive tract instead of leaking into your bloodstream. That may help restore communication between your microbiome and the rest of your metabolism, helping your body regulate appetite and fat metabolism through its own biological signals.

5. Measure success by how your body performs, not just by the scale — It’s important to track more than body weight. Pay attention to your daily steps, your strength, your energy, and how easily you move through everyday life.

If you’re preserving muscle while rebuilding your gut microbiome and restoring your body’s own GLP-1 production, you’re improving the systems that regulate appetite and metabolic health in the long term rather than relying on a medication like Ozempic that only temporarily replaces them.

My book, “Weight Loss Cure: Melt Fat Naturally with Your Own GLP-1,” available in ebook and hardcover, explains how to restore your body’s natural GLP-1 production through diet and metabolic support. When your gut microbiome produces enough SCFAs, especially butyrate, your body is better able to regulate appetite, metabolism, and fat loss through its own biological signals.

FAQs About Reduced Activity in People Taking GLP-1 Drugs

Q: Why did people taking GLP-1 weight loss drugs become less active?
A: Researchers found that people taking GLP-1 medications such as Ozempic, Wegovy, Mounjaro, and Zepbound took fewer daily steps and spent less time exercising after starting treatment, even though they lost weight. Average daily step counts fell from 5,047 to 4,487, while moderate-to-vigorous physical activity dropped from 28 minutes to 22 minutes per day. The findings show that weight loss alone doesn’t automatically lead to a more active lifestyle.

Q: Why is losing muscle during weight loss a concern?
A: GLP-1 medications reduce more than body fat; they also reduce lean muscle mass. Muscle supports strength, balance, posture, and everyday activities such as climbing stairs and carrying groceries. When muscle loss occurs alongside lower physical activity, physical function becomes harder to maintain, making regular movement and strength-building especially important.

Q: How does your body naturally produce GLP-1?
A: Your intestine already produces GLP-1 through L-cells. Those cells depend on butyrate, an SCFA made by beneficial gut bacteria when they ferment certain carbohydrates and fibers. Healthy butyrate production strengthens your gut barrier and supports the metabolic signals that help regulate appetite, blood sugar, and fat metabolism naturally.

Q: What foods help rebuild butyrate production?
A: Start by reducing seed oils, which are high in LA, and stabilizing your digestion before increasing fermentable fiber. As your gut health improves, gradually add whole fruit, well-cooked starches, root vegetables, and resistant starch foods such as cooked-and-cooled white potatoes and green bananas. These foods nourish butyrate-producing bacteria that support your body’s natural GLP-1 production.

Q: How should you measure success if you want lasting weight loss?
A: Don’t rely on the scale alone. Track your daily steps, strength, energy, and how easily you move through everyday life. Improving physical function while restoring your gut microbiome and your body’s own GLP-1 production provides a stronger foundation for long-term metabolic health than focusing only on body weight.

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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How can long-term air pollution affect your arteries?

It can encourage plaque buildup
Long-term air pollution can promote inflammation, oxidative stress, and artery damage, creating conditions that encourage plaque buildup. Learn more.
It can increase bone density
It can improve blood circulation
It can strengthen artery walls

First comes the air you breathe. Then comes what it quietly leaves behind. A large imaging study published in Radiology found that years of exposure to outdoor air pollutants, even at moderate levels, left measurable marks inside the coronary arteries, the vessels that deliver oxygen-rich blood to your heart.1 When those arteries gradually narrow or become blocked through plaque buildup, the condition is called coronary artery disease.

The condition often develops without warning signs — no chest pain, no shortness of breath, nothing to prompt a doctor’s visit — until a heart attack or another serious cardiovascular event forces the issue. Many people don’t connect that progression to the air they breathe every day, but that assumption leaves you vulnerable.

The exposures involved in this study weren’t the dramatic smog of heavily industrialized cities. They reflected the kind of air that surrounds millions of ordinary people going about their ordinary lives. And the damage showed up not just in one measurement but across multiple markers of how far artery disease had progressed.

Even Everyday Air Pollution Left a Measurable Mark
The Radiology study investigated whether years of exposure to common outdoor air pollutants were linked to more advanced coronary artery disease when examined with detailed heart CT scans rather than relying only on conventional risk factors.2

The researchers reviewed records from 11,128 adults who underwent cardiac CT between 2012 and 2023. Among them, 7,313 also received coronary CT angiography, a specialized scan that gives doctors a detailed view of plaque inside the heart’s arteries instead of simply showing calcium deposits.

Researchers estimated each person’s average exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) during the entire 10 years before the heart scan. PM2.5 includes particles no wider than 2.5 micrometers — roughly 30 times smaller than the diameter of a human hair — small enough to slip deep into your lungs and enter your bloodstream.

Daily exposure adds up slowly over time. Instead of asking whether a bad air-quality day affects your heart, the researchers examined whether years of breathing moderate pollution changed the arteries themselves.

• More pollution matched more disease inside the arteries — Higher long-term exposure to both PM2.5 and NO2 consistently matched greater coronary artery calcium and a greater overall plaque burden. Pollution tracked with multiple signs that coronary artery disease had progressed further.

Earlier studies often focused only on coronary calcium scores, but this study looked beyond hardened calcium deposits to evaluate the total amount of plaque present inside the arteries. That provides a more complete picture because plaque exists in different forms, and not all dangerous plaque has become heavily calcified.

• Even moderate pollution levels mattered — The median long-term PM2.5 exposure measured only 7.5 micrograms per cubic meter, with most participants living between 4.3 and 9.2 micrograms per cubic meter. Those numbers fall far below the extreme pollution many people imagine. Yet researchers still found significant relationships between those exposures and worsening artery disease. That means your attention shouldn’t focus only on heavily polluted cities or major industrial centers.

• Women experienced the strongest association with severe blockages. After researchers completed their most comprehensive statistical analyses, long-term exposure to both PM2.5 and NO2 was associated with obstructive coronary artery disease in women but not in men.3 Obstructive disease refers to arteries narrowed enough to significantly reduce blood flow through the heart.

Women exposed to higher levels of fine particle pollution were about 80% more likely to have severe blockages in the arteries that supply blood to the heart, while NO2 exposure also showed a statistically significant association. Researchers did not observe comparable statistically significant relationships in men after the same adjustments.

Instead of assuming everyone responds identically to environmental exposures, this study suggests your individual characteristics matter. If you are a woman with other cardiovascular risk factors, long-term air quality deserves a place on your personal checklist alongside blood pressure and blood sugar.

• Researchers identified why pollution damages arteries — Several biological processes work together to accelerate atherosclerosis, the gradual buildup of plaque inside artery walls. Instead of acting through one pathway, pollution creates stress throughout the cardiovascular system.

Inflammation and oxidative stress drive much of the damage. Oxidative stress occurs when harmful reactive molecules overwhelm your body’s natural defenses, damaging cells and tissues. According to the researchers, pollution increases systemic inflammation and oxidative stress, creating conditions that encourage plaque formation and progression. The artery lining also loses its normal protective function.

Healthy arteries have an inner lining called the endothelium that helps blood vessels relax, controls blood flow and discourages unwanted clot formation.

The researchers describe endothelial dysfunction, meaning that protective lining no longer works properly, as another important mechanism linking long-term pollution exposure with worsening coronary artery disease. They also note that pollution makes blood stickier and more prone to forming dangerous clots, which can trigger a heart attack even in arteries that aren’t yet severely narrowed.

• The design of the study strengthens confidence in the findings — This investigation included adults from multiple hospitals over an 11-year period, giving researchers access to one of the largest imaging-based analyses of long-term air pollution and coronary artery disease published to date.

Researchers repeated their analyses using several different approaches, including limiting participants to those living close to monitoring stations, excluding the COVID-19 period, separating lower and higher pollution exposure groups, and examining different exposure windows over one, five, and 10 years. The relationships remained broadly consistent across those analyses.

Although this study can’t prove direct cause and effect, the repeated patterns across multiple analyses strengthen the evidence that long-term exposure to moderate air pollution is closely associated with more advanced coronary artery disease.

Reduce Your Daily Exposure to Air Pollution and Strengthen Your Arteries
Air pollution isn’t something you can eliminate completely, but you can control many of the factors that determine how much reaches your body and how resilient your cardiovascular system remains. It’s important to both lower the environmental burden you face and build the habits that strengthen your arteries over the long term.

The Radiology study focused on long-term exposure to PM2.5 and NO2, two common air pollutants strongly linked to combustion from traffic, power plants, and other fuel-burning sources.

Within that broad category is an even smaller group called ultrafine particles (UFPs), which measure less than 100 nanometers across — about one-thousandth the width of a human hair. The study didn’t measure UFPs separately, but many of the same combustion sources that increase PM2.5 also produce enormous numbers of UFPs.

For years, I believed microplastics and nanoplastics represented the greatest environmental threat to your health. They remain a serious concern. But after I spent more time reviewing the research, another hazard emerged as even more significant: UFPs. They come from everyday combustion sources such as vehicle exhaust, industrial emissions, power plants, and gas stoves.

What surprised me most was the sheer number of these particles. In urban areas, you inhale roughly 10,000 to 30,000 UFPs in every cubic centimeter of air annually,4 and directly alongside major highways, that number can rise to about 160,000 particles per cubic centimeter.5 By comparison, estimates suggest people take in roughly 39,000 to 121,000 microplastic particles over an entire year through food, water, and air combined.6

By particle number, UFPs account for roughly 90% of the particles in polluted air.7 They’re the invisible majority. Their size makes them especially concerning. UFPs travel deep into your lungs, pass through the tiny air sacs where oxygen enters your bloodstream, and circulate throughout your body. Research links long-term exposure with inflammation, oxidative stress, and cardiovascular damage, and these particles have been detected in organs throughout the body, including the brain, liver, and placenta.

I no longer look at UFPs and microplastics as separate problems because they work together. Nanoplastics themselves fall within the ultrafine particle size range, and both trigger many of the same harmful biological responses, including oxidative stress, chronic inflammation, immune dysfunction, and cellular injury.

Both also transport other toxic substances into your tissues. Together they create a much greater burden than either exposure alone, making it even more important to reduce the amount of pollution you breathe and bring into your home whenever you have the opportunity.

1. Reduce the pollution you breathe every day — If you live near busy roads, industrial areas or places where wildfire smoke is common, make cleaner air part of your routine. Keep windows closed when air quality is poor, avoid strenuous outdoor exercise during periods of heavy pollution, and choose walking or cycling routes away from heavy traffic whenever possible. Every hour you spend breathing cleaner air reduces the burden on your cardiovascular system.

2. Upgrade the air inside your home — You spend about 90% of your time indoors,8 so the air inside your home contributes more to your total pollution exposure than the air outside. I recommend starting with your bedroom because you spend six to eight uninterrupted hours there every night. Run a high-efficiency particulate air (HEPA) purifier while you sleep to reduce the amount of fine particles you breathe during the hours your body performs much of its repair work.

Research also suggests cleaner air may support your brain’s glymphatic system, the built-in waste-removal network that becomes most active during deep sleep and clears away metabolic waste, including proteins associated with Alzheimer’s disease. Fine particles inhaled during sleep can trigger low-grade inflammation that interferes with this process, which makes cleaner nighttime air even more valuable.9

If you cook with a gas stove, use effective ventilation every time because gas appliances release nitrogen dioxide and fine particles directly into your home. Use a range hood that vents to the outside, not one that simply recirculates air through a filter. If you don’t have exterior ventilation, open a nearby window while cooking and run a box fan to push air out.

If you live near a busy road, highway or other major traffic corridor, keep your windows closed during morning and evening rush hours, when outdoor pollution is often highest. On days when outdoor air quality is good, however, open your windows to flush out pollutants that build up indoors from cooking, furniture, cleaning products, and building materials. Let current PM2.5 air-quality readings determine when to bring fresh air in and when to keep it out.

3. Protect the lining of your arteries with real food — Your artery walls respond to everything you eat. Build most meals around minimally processed foods such as ripe fruit, root vegetables, properly prepared vegetables, and high-quality protein while avoiding ultraprocessed foods, including seed oils, that drive chronic inflammation.

If you eat restaurant food several times each week, replace one restaurant meal each day with a homemade meal prepared from whole ingredients. Small victories become lasting habits.

4. Keep your cardiovascular risk factors under control — High blood pressure, elevated blood sugar, and smoking all increase stress on your arteries.

The study showed that pollution remained associated with more advanced coronary artery disease even after accounting for these factors, which means lowering those risks gives you another layer of protection rather than replacing the need to reduce pollution exposure. Make a checklist and track your progress instead of waiting until symptoms appear.

5. Move your body where the air is cleaner — Regular physical activity strengthens your heart and blood vessels, but location matters. If you’re an outdoor walker, choose parks, tree-lined neighborhoods, or other areas farther from heavy traffic whenever possible. Even shifting your route a few blocks away from congested roads lowers your direct exposure while allowing you to keep the benefits of exercise.

Think in decades instead of days. Every cleaner meal, every walk in fresher air and every step that lowers unnecessary inflammation becomes part of your long-term scorecard. Focus on steady progress instead of perfection, and those daily choices continue working for you year after year.

FAQs About Air Pollution and Coronary Artery Disease

Q: How does air pollution affect my heart?
A: Long-term exposure to air pollution contributes to inflammation, oxidative stress, and damage to the inner lining of your arteries. Over time, those changes encourage plaque to build up, increasing your risk of coronary artery disease and other cardiovascular problems.

Q: Does air pollution only become dangerous in heavily polluted cities?
A: No. The Radiology study found that even moderate long-term exposure to PM2.5 and NO2 was associated with more advanced coronary artery disease.10 The pollution levels studied were similar to what millions of people experience every day rather than the severe smog often associated with major industrial centers.

Q: Why are UFPs a growing concern?
A: UFPs are extremely small pollution particles produced by vehicle exhaust, industrial emissions, power plants, and gas stoves. Because they’re much smaller than most airborne particles, they travel deep into your lungs, enter your bloodstream and spread throughout your body.

They also outnumber microplastics by an enormous margin — you may inhale more UFPs in a single breath near a highway than you absorb in microplastics over an entire year — making them one of the most underappreciated sources of daily particle exposure.

Q: What is the most effective way to reduce my exposure to air pollution?
A: Start inside your home because that is where most people spend about 90% of their time. Running a HEPA air purifier in your bedroom, using proper ventilation when cooking with gas, avoiding outdoor exercise near heavy traffic and opening your windows only when outdoor air quality is good all help reduce the amount of pollution you breathe.

Q: Besides cleaner air, what else helps protect your arteries?
A: Cleaner air is only one part of the solution. Eating minimally processed whole foods, avoiding ultraprocessed foods, and seed oils, maintaining healthy blood pressure and blood sugar, staying physically active in cleaner-air environments, and making those habits part of your daily routine all work together to reduce stress on your arteries and support long-term heart health.

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

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Take today’s quiz to see how much you’ve learned from yesterday’s Mercola.com article.

About how many hours per day do adults in high-income countries spend sitting?

7 to 8 hours
11 to 12 hours
Adults in high-income countries now spend about 11 to 12 hours sitting each day, which is more than three-quarters of their waking time. Learn more.
13 to 14 hours
15 to 16 hours

You might have noticed it yourself or heard it from friends that the bread in Europe seems to sit differently in your body than the bread you eat in the United States. People share stories of enjoying baguettes in Paris or pizza in Rome without the discomfort that often follows a sandwich or dinner roll at home. Social media echoes the same theme, with travelers and health-conscious eaters asking why bread varies so much between regions.1

The truth is that bread is not a single, uniform product. It reflects choices about farming, milling, fermenting, and baking that vary from place to place. When you sit down to eat, your body is responding to those choices, and they add up to create a very different experience. That divergence has roots both in the wheat itself and in how it is handled along the way, and it shapes not just the flavor and texture but how it interacts with your digestion and energy.

How Wheat Variety Shapes the Bread on Your Plate

When you think about what shapes bread, the type of wheat it’s made from is one of the most important details. In North America, much of the harvest comes from “hard” red wheat, which carries a high concentration of proteins. In Europe, fields are dominated by “soft” wheat, which contains fewer proteins. Because those proteins are the raw material for gluten, the variety of wheat grown in each region sets the stage for different outcomes in bread texture and structure.

• Gluten is a protein network, not a single substance — Gluten is formed mainly by two proteins called glutenin and gliadin. When flour is mixed with water, these proteins interact, stretch, and form bonds that create elasticity in dough. Hard wheat contains more of these proteins, so the gluten matrix becomes stronger and more resistant to breaking.2,3

This is why American flours are used for bagels, sandwich loaves, and other breads that hold a dense structure and a chewy bite. Soft wheat, which dominates European fields, produces weaker gluten networks, resulting in breads that are airier and more delicate in texture.

• Gluten load may influence digestive response — Bread made with high-gluten flour delivers more intact gluten proteins to the digestive tract. Gliadin, in particular, resists full enzymatic breakdown and reaches the small intestine in larger fragments, where it interacts with the gut lining and causes discomfort in sensitive individuals.4

• Climate and soil shape wheat cultivation — Hard wheat thrives in the hotter, drier regions of North America, while soft wheat is better adapted to Europe’s milder conditions. Over centuries, these growing environments shaped grain supplies and, in turn, local food traditions. French, Italian, and German breads often begin with soft wheat flour that naturally produces less gluten, aligning with regional preferences for lighter textures.5,6

• This difference does not mean that every loaf in Europe is low in gluten — Some European millers import hard wheat from North America and blend it into their flour to strengthen doughs for particular styles of bread.

While this practice exists, it’s difficult to determine how common it is, how much imported wheat is added, or how much it changes the overall gluten content in the final product. Still, the European grain system fundamentally rests on softer, lower-gluten varieties, while the American system tilts heavily toward harder, higher-gluten wheat.7,8

What you experience when you eat bread is shaped long before the dough is mixed. The variety of wheat grown in one region versus another determines how much gluten is present and how it behaves under fermentation and baking. That underlying difference helps explain why your body may feel a noticeable shift when you eat bread abroad compared with what you are used to at home.

Why Slow Fermentation Makes Bread Easier to Digest

One of the biggest differences between traditional and modern bread lies in how long the dough is fermented. Extended fermentation gives microbes time to transform the dough, breaking down gluten and sugars while enriching flavor and nutrition. That process explains much of why slow-fermented bread often feels easier on the body.9,10

• Microbes reshape dough during long fermentation — Many European bakeries maintain starters and ferment dough for 12 to 48 hours. These practices, handed down through generations, allow wild yeasts and lactic acid bacteria to break down proteins and carbohydrates using enzymes such as proteases and fructanases. Proteases dismantle gluten into smaller, more digestible fragments, while fructanases reduce fermentable sugars that otherwise tax the gut.11

• Fermentation improves flavor, texture, and nutrition — As lactic acid bacteria thrive, they produce organic acids that lower dough pH. This slows staling, adds flavor complexity, and reduces phytic acid, which increases the bioavailability of minerals like magnesium and zinc. In effect, time allows microbes to act as natural pre-digesters, converting flour into a food that delivers more nutrients with less digestive strain.12

• U.S. bread production often bypasses fermentation benefits — Commercial bakeries in the United States typically mix, proof, and bake within a few hours, using commercial yeast and chemical conditioners to achieve volume and structure. The process is efficient but skips the microbial transformations of slow fermentation. Gluten and sugars remain largely intact, leaving bread with a different nutritional and digestive profile.13,14

For a deeper look at how bread has changed over time and why your ancestors digested it differently than you might today, check out “The Truth About Bread — Why Your Ancestors Could Digest It (And Why You Might Not).”

Glyphosate Use — A Transatlantic Divide in Wheat Production

Glyphosate has become a cornerstone of American wheat farming, used both to suppress weeds and, in some regions, sprayed directly on the crop just before harvest to speed up drying, make harvest more predictable, and increase yield. However, it leaves more opportunity for residues to remain on the grain that becomes your bread. This single step in crop management is an important place to look to understand why bread in Europe feels different.

• In Europe, growers are bound by stricter rules — Farmers in Europe are not allowed to use glyphosate for pre-harvest desiccation, and its application throughout the season is more tightly regulated.15

Countries such as Austria and Germany have gone further, pushing toward bans or national phaseouts.16,17 This reflects Europe’s broader precautionary approach to agricultural chemicals. For consumers, this means loaves baked in Europe are less likely to contain glyphosate traces.

• Glyphosate disrupts gut microbes — Glyphosate works by blocking the shikimate pathway, an enzyme system in plants and bacteria. Human cells do not use this pathway, which is why regulators have often argued it is safe, but the bacteria in your gut do.18

Disrupting those microbial communities affects digestion, immune regulation, and even mood, since your microbiome interacts with nearly every part of your physiology. Animal and cell studies suggest glyphosate exposure alters gut flora balance and intestinal integrity, which amplifies symptoms in those with wheat sensitivity.19,20

• Global health authorities have raised broader concerns — In 2015, the International Agency for Research on Cancer (IARC) classified glyphosate as “probably carcinogenic to humans,” citing evidence from animal studies and human data.21 Other concerns raised in the scientific literature include potential endocrine disruption, oxidative stress, and links to metabolic disorders.22

The way glyphosate is regulated illustrates how policy choices shape the food you eat. For a deeper look at how this chemical affects your body, read “Roundup Weedkiller Linked to Multiple Cancers.”

Additives, Sweeteners, and the Engineering of Modern Bread

Bread is never just flour, water, salt, and yeast when it comes from most large-scale commercial bakeries in the United States. To achieve uniformity, speed, and shelf life, they add a number of additives, preservatives, and other chemicals that turn bread into as much of a manufactured product as a baked food.

• Dough conditioners, oxidizers, and emulsifiers — Ingredients such as mono- and diglycerides, L-cysteine, azodicarbonamide, and potassium bromate improve elasticity, gas retention, and resilience under high-speed mixing. These compounds make mass production possible by shortening fermentation times and stabilizing loaves for distribution.23

Potassium bromate, in particular, strengthens the structure and “spring” of dough, which is why it has been widely used by industrial bakeries. However, it’s not fully neutralized during baking, and studies show it increases the risk of cancer. For this reason, the European Union, Canada, the U.K., China, Brazil, and many other countries have banned it outright as a flour additive. Despite this, it remains legal in the U.S.24

• Bleaching and maturing agents — U.S. flour is often chemically bleached with agents like benzoyl peroxide and chlorine dioxide to create a whiter appearance and improve baking properties. Maturing agents accelerate protein cross-linking in the dough, again designed for speed and uniformity. The European Union bans or tightly restricts many of these compounds.25,26

• Mandatory enrichment and fortification — Since the 1940s, U.S. flour has been required to be enriched with iron and B vitamins to address nutrient deficiencies. More recently, folic acid was added to prevent neural tube defects.27,28

While these measures sought to improve public health outcomes, they also underscore how much nutrition is lost when bran and germ are stripped during milling. European countries vary in their enrichment policies but generally apply less across-the-board fortification.

• High-fructose sweeteners and other additives — Many U.S. breads include added sugars, often in the form of high-fructose corn syrup, to accelerate browning, enhance flavor, and appeal to sweet-leaning palates. European breads, especially traditional loaves, tend to avoid this practice. The difference means that even when bread looks similar, the metabolic response in your body is not the same.29

Taken together, these practices define two divergent approaches. One treats bread as a product engineered to endure long supply chains, and the other preserves bread as a food meant to be eaten fresh. For you, that difference shows up not only in flavor and texture but also in how comfortably your body receives it.

How to Choose Bread That’s Good for You

If you want bread that reflects the qualities you notice in European loaves, the key is knowing what to look for. A few simple checks will help you identify breads that are closer to traditional formulas and easier on your digestion.

• Check ingredient lists for simplicity — The closer a loaf is to flour, water, salt, and starter or yeast, the better. Extra conditioners, flavorings, or preservatives tell you that quality has been sacrificed for convenience.

• Choose authentic sourdough — A true sourdough loaf develops under the action of wild yeasts and lactic acid bacteria over many hours. This natural process breaks down gluten fragments, reduces fermentable carbohydrates, and produces organic acids that enhance flavor and extend freshness without chemical preservatives. When you choose sourdough, you’re choosing bread that is more digestible and closer to how bread has been made for centuries.

• Confirm the use of a real starter — Ask your baker about their starter and how long they ferment. Those who value tradition will be open about this, while shorter fermentation almost always indicates commercial shortcuts. On packaged bread, look for terms like “starter” or “levain.” If you see vinegar, lactic acid, or yeast boosters instead, you’re looking at imitation sourdough designed for speed, not authenticity.

• Prioritize flour quality — Look for unbleached, stone-ground, or high-extraction flours, as they retain more of the grain’s natural integrity and flavor. Many bakeries that follow European methods highlight their flour sources.

• Avoid loaves with added sweeteners — Commercial loaves in the U.S. often contain sugar, corn syrup, or syrups that soften flavor and texture. Authentic European-style bread rarely relies on them because fermentation creates its own depth.

• Seek out local bakeries for transparency — Independent bakers often bake daily and are more transparent about ingredients and methods. By asking questions and choosing bread with long fermentation, clean ingredient lists, and clearly sourced flour, you bring home loaves that reflect the standards you admire abroad.

• Reintroduce bread gradually into your diet if your gut is sensitive — If your gut health is compromised, the first step is not to load up on bread, even if it’s traditionally made. Complex carbohydrates feed microbial overgrowth and aggravate inflammation in a weakened digestive system.

Begin instead with gentler sources of carbs, such as ripe fruits or well-cooked then chilled white rice, which place less strain on digestion. As balance returns and symptoms improve, slowly add back more complex carbs, with slow-fermented sourdough being one of the best tolerated starting points.

When you take the time to select bread made with patience and simplicity, you not only taste the difference but also feel it in how your body responds. Choosing bread made this way supports your digestion and connects you to a tradition of baking that values nourishment as much as convenience.

Frequently Asked Questions (FAQs) About Bread

Q: Why does bread in Europe not bother me like bread in the U.S.?
A: You react differently because most European bread is made with soft wheat, longer fermentation, and fewer additives. That combination produces less intact gluten, fewer fermentable sugars, and more beneficial acids, which makes the bread easier on your digestion compared to the fast-produced, high-gluten, additive-heavy bread common in the U.S.

Q: Is sourdough bread really easier to digest?
A: Yes. Authentic sourdough goes through a long fermentation process where wild yeasts and lactic acid bacteria break down gluten and fermentable sugars, which reduces digestive strain. If you’re sensitive to bread, sourdough is one of the best places to start reintroducing it.

Q: Does glyphosate in U.S. bread affect my health?
A: Yes, it can. In the U.S., glyphosate is often sprayed on wheat crops before harvest, which increases residue in the flour that ends up in your bread. Glyphosate disrupts gut bacteria, weakens the intestinal barrier, and has been linked to other health concerns. European regulations are stricter, so bread there is less likely to contain glyphosate residues.

Q: If I have gut issues, can I still eat bread?
A: You’ll want to reintroduce it carefully. Start with gentler carbs like ripe fruit or well-cooked and chilled white rice until your digestion stabilizes. Then, slowly add back more complex carbs, with long-fermented sourdough as one of the best-tolerated options. This gradual approach helps your body adjust without aggravating symptoms.

Q: How do I know if sourdough bread is real?
A: Check the ingredient list. True sourdough only needs flour, water, salt, and starter. If you see vinegar, lactic acid, or yeast boosters, it’s likely imitation sourdough made to mimic flavor without the fermentation process — and it won’t give you the same digestive benefits.

Fatty liver disease not caused by alcohol is quickly emerging as a major public health concern in the United States.1 It often develops silently over many years, with contributors like obesity, Type 2 diabetes, and insulin resistance. Symptoms — such as a swollen belly, unexplained weight loss, extreme fatigue, and pain in the upper right abdomen — usually don’t show up until the condition has progressed.2

But even if it’s advanced, it’s not too late. Fatty liver is a reversible condition, and addressing it can lead to real improvements in your health.

Many doctors will recommend GLP-1 agonists like Ozempic for patients with liver disease, especially when there is co-existing obesity or Type 2 diabetes.3 However, there are many downsides to this approach, such as poor mental health, lower bone and muscle density, and a host of digestive issues. Worse, you can rebound from Ozempic, which means you’ll regain the weight you’ve lost once you stop taking the drug.4

The good news is there are far safer, healthier alternatives. The most important remedy for fatty liver disease is choline, as your body simply cannot get rid of liver fat without it, and choline deficiency is rampant (We’ll get back to that later). Researchers are also looking into niacin for fatty liver disease treatment, and while the results are promising, this is an incomplete picture — niacinamide is the better alternative, which I’ll also explain below.

Where Niacin Fits Into the Picture of Fatty Liver Disease

In a study published in Metabolism, researchers from Korea discovered the role of microRNA-93 (miR-93) in attenuating fatty liver disease.5 For context, miR-93 is a unique ribonucleic acid (RNA) that helps suppress the expression of certain genes. To perform the experiment, the team used transcriptome analysis, allowing them to identify how the process unfolded.

They also used a screening system to test drugs that can modulate miR-93 expression, particularly niacin. A preprint of the study sheds further light on these findings:6

• At the center of the findings sits miR-93 — Micro RNAs act like molecular messengers inside cells. They do not build proteins themselves. Instead, they tell cells which instructions to ignore. In this study, miR-93 blocked a protein called SIRT1, which plays a central role in cellular energy regulation. When miR-93 levels rose, SIRT1 activity dropped, and liver metabolism shifted toward fat storage rather than fat use.

The researchers showed that when miR-93 rose, liver cells lost control over a major energy pathway known as the LKB1-AMPK system. When energy runs low, AMPK pushes cells to burn fat and restore balance. Suppressing SIRT1 shuts that system down. As a result, fat piled up in liver cells, mitochondria slowed, and metabolic stress increased.

• Animal data strengthened the hypothesis — Mice engineered to lack miR-93 resisted fatty liver even when fed a high-fat diet. These mice also had lower liver fat, less inflammation, improved insulin sensitivity, and stronger mitochondrial activity. In contrast, normal mice with elevated miR-93 developed classic fatty liver features.

• How niacin enters the picture — The authors reported that niacin treatment suppressed miR-93 expression in liver tissue. When miR-93 levels fell, SIRT1 activity rebounded. That rebound restored AMPK signaling and improved fat handling inside liver cells. In both human liver samples and mouse models, niacin reversed the molecular fingerprint tied to fatty liver disease.

• AMPK sits downstream of SIRT1 and amplifies the effect — When AMPK remains active, liver cells burn fat, regulate glucose, and maintain insulin sensitivity. When AMPK shuts down, fat accumulates and metabolic chaos follows. The study showed that niacin restored this pathway, starting at miR-93 suppression and ending with improved mitochondrial output.

Another important finding involves the mitochondria themselves. The researchers linked high miR-93 levels to impaired mitochondrial respiration. When they falter, the liver shifts into fat storage mode. Niacin restored mitochondrial efficiency by reopening the SIRT1-AMPK pathway, allowing liver cells to generate energy instead of hoarding fat.

Does Niacin Improve Liver Fat or Enzymes?

The Metabolism study isn’t the only published research to make the connection between niacin and improved liver fat turnover. In a 2024 study published in JAMA Network Open, researchers investigated a similar angle — the role of dietary niacin intake on long-term survival of people diagnosed with fatty liver disease.7

A total of 4,315 people aged 20 and older with fatty liver disease were selected using data from the National Health and Nutrition Examination Survey (NHANES), which was conducted between 2003 and 2018. Over a median follow-up of 8.8 years, 566 participants died from any cause and 197 died from cardiovascular causes.

• Participants who ingested more niacin had better mortality odds — Those who had the highest dietary niacin intake showed a significantly lower risk of death from all causes compared with those with the lowest intake.
Specifically, participants consuming 26.7 milligrams (mg) of niacin per day or more had a 30% lower risk of all-cause mortality than those consuming 18.4 mg per day or less, even after adjusting for age, sex, body mass index, smoking, alcohol intake, physical activity, and overall diet quality.

• Consistency played an important role — The survival advantage emerged over nearly a decade of follow-up. This suggests niacin intake supports long-term metabolic stability rather than producing short-lived effects.

• The research showed niacin’s role in nicotinamide adenine dinucleotide (NAD+) metabolism — It acts as a central cofactor in cellular energy production, DNA repair, and mitochondrial function. When NAD+ availability declines, cells struggle to produce energy efficiently. In fatty liver disease, this energy deficit drives cellular stress and systemic dysfunction.

Higher niacin intake supports NAD+ synthesis. More NAD+ improves mitochondrial efficiency, enhances oxidative metabolism, and stabilizes cellular stress responses.

• Another study reinforces the benefits of niacin — In a study published in Therapeutic Advances in Chronic disease,8 researchers investigated how nicotinamide (a different form of niacin9) can help improve fatty liver disease and overall metabolic health.

Alanine aminotransferase, a liver enzyme that rises when liver cells sustain injury, dropped by an average of 26.6% in the nicotinamide group compared with 0.74% in the control group over the same period.

• Beyond liver enzymes, lipid markers improved — Participants receiving nicotinamide showed statistically significant reductions in total cholesterol and low-density lipoprotein (LDL) cholesterol compared with controls. These changes matter because dyslipidemia accelerates fatty liver progression and cardiovascular risk among diabetics. Improving lipid balance reduces the metabolic pressure that feeds liver dysfunction.

• Insulin resistance also improved — The nicotinamide group demonstrated a significant reduction in insulin resistance indices compared to the control group by week 12. Insulin resistance drives fat accumulation in the liver and worsens glycemic control. Improving this marker directly supports better glucose handling and metabolic stability.

The Ideal Niacin Dosage for Fatty Liver Disease

Now that you’re familiar with the importance of niacin, the next step is figuring out the optimal intake amount, as the featured studies showcased different doses. For example, the researchers from the Metabolism study administered 200 mg per kilogram (kg) of weight in test mice.10 In the JAMA Network Open study, 26.7 mg produced health benefits, but this was only an average intake — not a definite dosing recommendation.11

For better guidance, the recommended dietary allowance for niacin is listed below. These dosages are what the Office of Dietary Supplements recommends for healthy individuals; if you’re deficient, you likely need more:12

Age
Male
Female
Pregnancy
Lactation

Birth to 6 months
2 mg
2 mg
 
 

7 to 12 months
4 mg
4 mg
 
 

1 to 3 years
6 mg
6 mg
 
 

4 to 8 years
8 mg
8 mg
 
 

9 to 13 years
12 mg
12 mg
 
 

14 to 18 years
16 mg
14 mg
18 mg
17 mg

19 years and above
16 mg
14 mg
18 mg
17 mg

• Recommended niacin formulations — Due to the various niacin supplements out in the market, it can get confusing from the viewpoint of consumers. Look for “timed release” preparations, as well as similar terms such as controlled release, slow release, sustained release, prolonged release, and long-acting niacin.13 That said, there’s ample reason to opt for niacinamide instead of niacin, as I’ll explain in the next section.

• Top food sources of niacin — While supplementation has been shown to help, it’s not the only option available — you can also get it from your diet. Some of the foods with the highest amounts of niacin include grass fed beef liver, chicken breast (make sure to look for pastured organic chickens), wild-caught sockeye salmon, and potatoes.14

Why Niacinamide Is the Superior Choice Compared to Niacin

Where does niacinamide enter the picture, you may wonder? While it sounds like niacin (and the two are often erroneously interchanged), this is where the similarities end. To set the record straight, I generally recommend niacinamide over niacin because it’s the best NAD+ precursor, as the immediate breakdown product of NAD+ is niacinamide.

• NAD+ is a key molecule that fuels energy production in your mitochondria — When NAD+ levels become low, your cells won’t be able to convert the food you eat into energy, which forces your body to break down muscle tissue to survive — not an ideal situation.

Next, when NAD is used up, it gets broken down into niacinamide (also known as nicotinamide), which is recycled. It’s converted into nicotinamide mononucleotide (NMN), and then back into NAD+. The process is outlined in the image below.

• Dosing recommendation of niacinamide — For optimal results, I recommend taking 50 mg of niacinamide three times a day. In addition to being a more direct way to increase NAD+, niacinamide is also far more cost-effective — it will only cost you $25 a month if you get it as a powder.

• Niacinamide powder is the optimal form to take — Generally, a 1/64 teaspoon of niacinamide powder is around 50 mg. For your convenience, you can easily buy a measuring set on amazon that contains a 1/64 teaspoon.

Now, the reason why I recommend it in powder form is because you can easily control your intake. Most supplements brands set the lowest dose at 500 mg, which isn’t ideal — this high a dose actually decreases NAD+ due to negative feedback on NAMPT, the rate-limiting enzyme for NAD+, which controls the amount of NAD+ your body produces.

• Niacinamide doesn’t cause skin flushing — Both niacin and niacinamide are forms of vitamin B3, and in the context of typical low-supplement dosages, they are routinely considered interchangeable. However, niacin causes flushing, which is a temporary side effect wherein the blood vessels become dilated, causing the skin to become more redder or pinker than usual. Niacinamide does not cause this.

Key Risks to Discuss with Your Doctor

While the studies show that niacin offers important benefits, it’s essential to be aware of the possible risks, especially at higher doses or when combined with certain medications. Discuss the following concerns with your healthcare provider:

• Liver injury — High-dose (or extended release) niacin has caused clinically significant hepatotoxicity, including severe cases. Risk rises with sustained-release forms, dose escalation, and self-medication without monitoring. If any of these apply to you, stop immediately and seek care for possible jaundice, dark urine, severe fatigue, or itchy skin.15

• Glycemia and insulin resistance — High-dose niacin can worsen glucose tolerance in some patients. Intensify glucose monitoring if used.16

• Uric acid and gout — Niacin can raise uric acid and precipitate gout flareups among susceptible individuals.17

• Drug combinations — There are certain medications that can interfere with niacin supplementation. For example, isoniazid and pyrazinamide (tuberculosis medications) hamper niacin production from tryptophan. Moreover, isoniazid can inhibit NAD production.18

Choline — A Cornerstone of Fatty Liver Management

While your liver may benefit from niacinamide, increasing choline intake is a far better foundational strategy. That’s because choline is required to transport fat out of the liver.

Your liver produces very low-density lipoprotein (VLDL), which transports triglycerides and some cholesterol from your liver to other tissues. VLDL assembly requires phosphatidylcholine, which depends on adequate choline availability. When hepatic (liver) choline/phosphatidylcholine is too low, VLDL secretion is impaired, so triglycerides are less efficiently exported and accumulate in liver cells, resulting in fatty liver disease.

• Food is the best source of choline — Egg yolks (especially pastured ones) are the richest and safest way to meet your choline needs. Other sources include organic muscle meats and wild-caught fish, which provide moderate amounts.

Vegetables that contain small amounts of choline include cruciferous vegetables, such as broccoli, cauliflower, and Brussels sprouts. For those who follow a plant-based diet, you’ll likely need to take a supplement to support your liver health, as you simply cannot eat enough vegetables to meet the needs of your liver.

• Take a choline supplement if diet alone isn’t enough — There are several choline supplements available on the market, but the only one I recommend is citicoline, primarily due to its superior bioavailability.

• Recommended intake — Your choline intake will depend on your age. For example, adult men generally need 550 mg of choline per day, while adult women need 425 mg per day. Infants will need 125 to 150 mg per day while children (around 4 to 8 years old) will need 250 mg per day. Use this as a guide to know if you’re getting enough.

For a more in-depth understanding of how choline provides a vital line of defense for your liver, see “A Mortal Enemy of Your Liver, It’s Not Alcohol.”

Other Tips to Help Protect Your Liver from Further Damage

While the findings regarding niacin show promise, don’t rely on it alone to manage fatty liver disease. It would be wise to follow a holistic approach, as this can maximize your outcomes. Here are other strategies I recommend you follow:

1. Eliminate vegetable oils and alcohol right away — If your diet includes packaged or restaurant foods made with soybean, canola, corn, sunflower, or other vegetable oils, your liver is taking a nonstop hit. These oils are high in linoleic acid (LA), a fragile polyunsaturated fat (PUF) that drives fat accumulation in the liver and fuels oxidative damage.
Your body converts LA into oxidized linoleic acid metabolites (OXLAMs), which are unstable compounds that harm mitochondria and interfere with cellular energy production.

To protect your health, keep your LA intake to below 5 grams a day, but if you can keep it to below 2 grams, that’s even better. For better monitoring, sign up for the Pax health platform. It contains the Seed Oil Sleuth, a feature that can help monitor the LA in your food to a tenth of a gram. In addition, use healthy fats like grass fed butter, ghee, tallow, or coconut oil when cooking your food.

Alcohol also compounds the problem. When metabolized, it becomes acetaldehyde, a toxic byproduct that damages liver cells from the inside out. If you’re already showing signs of fatty liver or insulin resistance, removing both vegetable oils and alcohol is one of the fastest ways to give your liver a chance to heal.

2. Move daily and focus on reducing waist size — There’s no need for intense workouts or long gym sessions. A 10- to 20-minute brisk walk after meals, daily stretching, and a couple of weekly strength or bodyweight sessions are enough to make a difference.

Regular movement lowers insulin levels and improves blood flow and oxygen delivery to the liver. A waist circumference over 40 inches for men or 35 inches for women signals excess visceral fat, which is strongly associated with liver fibrosis.

3. Make high-quality sleep a priority to calm inflammation — Poor and/or insufficient sleep robs your liver of the recovery time it needs. Aim for deep, uninterrupted rest in a dark, cool environment.

Stop eating at least three hours before sleeping to avoid nighttime blood sugar disruptions. Even modest improvements in sleep quality can lower inflammation and gradually improve insulin sensitivity, easing the burden on your liver. For additional information, read “Subtle Signs You Are Not Getting Enough Sleep.”

Frequently Asked Questions (FAQs) About the Link Between Niacin and Fatty Liver Disease

Q: Does niacin help with fatty liver disease?

A: Yes. Research shows niacin can improve fatty liver by restoring key metabolic pathways that promote fat-burning instead of fat storage. Higher dietary niacin intake has also been linked to better long-term outcomes in people with fatty liver disease.

Q: Is niacin safe if I already have fatty liver?

A: It can be safe at low to moderate intakes, especially from food. High-dose niacin, particularly without supervision, can stress the liver. Anyone with fatty liver disease is advised to use niacin only with medical guidance and monitoring.

Q: What dose of niacin is used for fatty liver?

A: There is no established treatment dose. Benefits have been seen at dietary intakes around 26.7 mg per day. Higher supplemental doses raise safety concerns and should only be used under medical supervision.

Q: Does niacin worsen blood sugar or insulin resistance?

A: High doses can worsen blood sugar control in some people. Lower doses and certain forms, such as nicotinamide, have been shown to improve insulin resistance. Monitoring is important if you have diabetes.

Q: What is niacinamide and why is it better than niacin?

A: Niacinamide is a form of vitamin B3 that helps your body produce NAD+, a critical molecule needed for mitochondrial energy production and healthy metabolism. It’s considered better than niacin because it’s a more direct and efficient NAD+ precursor, is easier to dose in smaller amounts, and does not cause the uncomfortable skin flushing that niacin often triggers. It is also generally better tolerated, whereas high-dose niacin can carry greater risks like liver strain.

Q: Why is choline important for the management of fatty liver disease?

A: Your liver produces very low-density lipoprotein, or VLDL, which transports triglycerides and some cholesterol from your liver to other tissues. When choline intake falls too low, your liver cannot package and export fat efficiently, so triglycerides remain in liver cells and accumulate over time, resulting in fatty liver disease. To boost intake, food sources are the best, such as egg yolks, organic muscle meats, and wild-caught fish.

Americans are drinking more sugar than ever before, and it’s not just the amount that’s fueling today’s metabolic crisis. It’s the form. When refined sugar is consumed in liquid form, whether in sodas, flavored waters, or sports drinks — it bypasses your body’s natural defenses. There’s no chewing, no fiber, no fullness. Just a rapid flood into your bloodstream that forces your pancreas and liver to respond instantly.

This kind of metabolic ambush happens quietly at first, but over time, it rewires how your body handles insulin, stores fat, and manages energy. You might assume sugar only becomes a problem if you’re overweight. But research now shows that even lean people are at risk when that sugar comes from a bottle or can. The damage starts below the surface, long before you feel symptoms or see changes on a scale.

If you’re drinking soda daily, or if your children are, this isn’t just about empty calories. It’s about how those drinks hijack your metabolism, starting with the very first sip. And if you want to protect yourself from insulin resistance and its many downstream effects, understanding how different types of sugar behave in the body is the first step.

Why Processed Fructose Wrecks Your Liver, Energy, and Blood Sugar Balance

If you’ve been told that “sugar is sugar,” forget it. Not all sugars are processed the same way in your body. One type in particular, refined fructose, such as high-fructose corn syrup (HFCS), poses unique risks when it’s stripped from whole foods and dumped into drinks and processed snacks. Your liver is the one that ends up paying the price. Here’s why this matters for you:

• Whole fruits don’t cause this problem — When you eat an apple or a handful of berries, the fructose inside them is wrapped in fiber, water, and antioxidants. That natural packaging slows absorption, giving your body time to respond in a balanced way. It’s not just slower; it’s safer. Your liver doesn’t get slammed with a sugar overload.

• Processed fructose shows up as a flood, not a trickle — The HFCS in sugary sodas, fruit punches, and energy drinks isn’t attached to fiber or nutrients. It’s isolated, concentrated, and absorbed rapidly. Once it’s in your system, your liver has no choice but to process the entire load at once.

• Your liver is the only organ that handles fructose, so it gets overwhelmed fast — Unlike glucose, which your muscles and brain use immediately, fructose heads straight to your liver. When your liver receives more than it can handle, it turns the excess into fat. This leads to fatty liver disease and starts a domino effect: more fat in your liver, more insulin resistance, and more inflammation across your entire system.

• Fructose overload damages your cellular energy factories — Your mitochondria — the parts of your cells responsible for generating energy — are also impacted. They get hit with a surge of damaging byproducts when your liver processes too much fructose.

This causes what’s known as reductive stress, which leaves your cells inflamed, tired, and unable to function efficiently. If you’re dealing with fatigue, belly fat, or rising blood sugar, processed fructose is likely playing a central role. Pulling it out of your daily diet isn’t optional — it’s essential.

Sugary Drinks Spike Your Diabetes Risk, but Whole Food Sugars Do the Opposite

A meta-analysis published in Advances in Nutrition examined how different sources and forms of sugar affect your risk of developing Type 2 diabetes.1 The researchers analyzed 29 prospective cohort studies that tracked people’s diets and health outcomes over time, pooling data from a large population base. Their goal was to separate the effects of added sugar — especially in drinks — from the sugars naturally present in whole foods.

• People who drank sugary beverages daily had a sharply higher risk of Type 2 diabetes — The most consistent and alarming finding was that consuming sugar in liquid form significantly raised the risk. Each additional daily serving of sugar-sweetened beverages, like soda or sweetened iced tea, was associated with a 25% higher risk of developing Type 2 diabetes.

• Sugars in solid whole foods showed the opposite trend — In stark contrast, sugar from whole foods like fruits did not increase risk. In fact, the data showed that total sugar intake and sucrose intake were inversely associated with diabetes risk, meaning that when people got their sugars from natural, solid food sources, their odds of developing the disease went down.

• The difference lies in how your body processes liquid vs. solid sugar — When you drink sugar, your body absorbs it extremely fast, flooding your bloodstream with glucose and overwhelming your pancreas. Unlike solid food, sugary drinks bypass chewing and satiety signals — so you don’t feel full, and you’re more likely to overconsume. That rapid absorption spikes insulin levels, which over time contributes to insulin resistance, a key factor in Type 2 diabetes development.2

• Fructose’s effects varied depending on its source — While some studies within the meta-analysis reported that high fructose intake increased diabetes risk, others showed no effect or even protective effects, largely depending on whether the fructose was consumed in processed form, like HFCS, or in whole fruit. This variation underscores that fructose from fruit is not the same as fructose from soda, both in terms of how your body responds and how it impacts long-term health.

• Sugary drinks were the most consistent predictor of risk across studies — The strongest and most consistent relationship observed across all the studies was between sugar-sweetened beverage consumption and increased Type 2 diabetes risk. This relationship held true across age groups, geographies, and even when controlling for other dietary and lifestyle variables.

Sugary Drinks Drive Early Blood Sugar Problems in Boys

Research presented at the American Heart Association’s Lifestyle and Cardiometabolic Scientific Sessions summarized findings from a long-term adolescent health study.3 It showed that boys who regularly consumed sugary drinks had a significantly greater risk of developing insulin resistance and elevated blood sugar markers by their late teens. This research adds to growing evidence that the metabolic effects of sugary beverages begin far earlier than most people realize.

• The study focused on a large group of school-age children over several years — Boys with the highest intake of sugary drinks were already showing signs of prediabetes, including higher fasting glucose and lower insulin sensitivity. Each daily 8-ounce serving of sugary beverages was associated with a 34% increase in insulin resistance, a 5.6 mg/dL rise in fasting glucose, and a 0.12% increase in HbA1c levels, a marker of average blood glucose levels over the past two to three months.

• The metabolic changes were already underway by age 17 — Importantly, these weren’t hypothetical risks. The adolescents in this study had already developed measurable changes in their blood sugar regulation by the end of the study period. This suggests that the damage begins long before any symptoms of diabetes appear, and long before any formal diagnosis is made. That makes early prevention key, especially for families with a history of diabetes or metabolic disease.

• Prevention needs to start in childhood — The article emphasized that small dietary shifts in childhood, like cutting back on soda, could delay or even prevent serious problems later on. The earlier families make these changes, the more likely they are to protect their children’s long-term metabolic health.

Men Who Drink Soda Daily Face a Steadily Rising Risk of Diabetes, Even Without Weight Gain

A study published in the American Journal of Clinical Nutrition examined how daily consumption of sugar-sweetened beverages affected Type 2 diabetes risk in 40,389 U.S. men.4 Researchers followed participants over a 20-year period, collecting data on their diet, lifestyle habits, and health outcomes. The purpose was to determine whether sugary drinks were an independent risk factor for diabetes, even after accounting for weight, activity levels, and overall diet quality.

• The results showed a clear link between soda and diabetes, independent of body weight — Men who drank one or more servings of sugar-sweetened beverages per day had a 16% higher risk of developing Type 2 diabetes compared to those who rarely drank them. This increased risk remained even after adjusting for body mass index, smoking, exercise, and total calorie intake.

• Even small daily habits had a measurable effect on long-term health — Replacing just one sugary drink per day with a healthier alternative, like water or coffee, led to a 17% lower risk of developing diabetes over time. This finding is especially empowering if you’re looking to make small, sustainable changes. You don’t need to overhaul your entire diet overnight. Just cutting one daily soda makes a measurable difference in your future health.

• Cola was the worst offender among all sugary beverages studied — While all sweetened drinks raised risk, colas were the most damaging. The study found that drinks like fruit punches and lemonades had a weaker association, possibly because they were consumed less often or had different sweetener profiles. But colas, with their combination of high sugar and additives like caramel coloring, were consistently tied to the greatest increase in diabetes risk.

How to Protect Your Metabolism from Refined Sugars

If you’re trying to avoid diabetes, or reverse early signs of insulin resistance, the first and most important step is to stop flooding your system with liquid sugar. That’s what every piece of research we’ve looked at makes crystal clear. Refined sugar in soda, including HFCS, is absorbed fast and hits your pancreas hard.

If you drink soda and other sugary drinks daily, you’re giving your body zero time to recover between hits. What you do now matters. You don’t have to overhaul everything overnight, but you do need to stop the source of the damage before real improvement occurs. Start with these five steps:

1. Cut out sugary drinks, including soda — If you’re a soda drinker, this is the biggest favor you can do for your long-term health. Replace sugary beverages with water, unsweetened iced tea or sparkling water with lemon or lime. Remember, it’s not about total sugar — it’s about how it hits your bloodstream.

2. Replace one soda a day with black coffee or green tea — If you drink one or more sugary beverages per day, replacing just one of them with unsweetened coffee or tea significantly lowers your risk of Type 2 diabetes. That’s a small effort with big payoff. While the goal is to eliminate soda entirely, cutting back by one drink a day is a good start.

3. Eat your fruit — While HFCS in soda should be avoided, natural fructose in fruit is not problematic. Whole fruit is packed with fiber that slows sugar absorption, plus it fills you up and provides beneficial carbohydrates and fiber.

4. Stay hydrated to prevent automatic sugar grabs — Sometimes when you reach for a soda, you’re not craving sugar — you’re just thirsty. I recommend carrying a refillable glass or stainless-steel water bottle with you all day. Add lemon, lime, or cucumber slices for flavor. Once you’re consistently hydrated, you’ll notice fewer cravings and less temptation to default to sweet drinks.

5. Find replacements you enjoy so you don’t feel deprived — The key to long-term change is making it sustainable. Try different healthier options like herbal teas, unsweetened iced teas, or flavored sparkling waters until you land on something you actually like. Once you’ve found a go-to drink you enjoy, it’s much easier to skip the soda without feeling like you’re giving something up.

FAQs About Soda and Other Sugary Beverages

Q: What’s the biggest risk of drinking sugary beverages like soda every day?

A: Daily consumption of sugary drinks floods your bloodstream with fast-absorbing sugar, overwhelming your liver and pancreas. Over time, this leads to insulin resistance, a key driver of Type 2 diabetes, even if you’re not overweight.

Q: Is fructose from fruit the same as fructose from soda or processed foods?

A: No. Fructose in whole fruit is bundled with fiber, water, and antioxidants, which slow absorption and protect your metabolism. Processed fructose, such as high-fructose corn syrup, hits your system all at once and forces your liver to convert the excess into fat, triggering metabolic dysfunction.

Q: Do sugary drinks affect kids as much as adults?

A: Yes — likely even more. A long-term study found that each daily 8-ounce sugary drink raised insulin resistance in boys by 34% and increased fasting glucose and HbA1c levels. The damage often begins in childhood, before any symptoms appear.

Q: Can I lower diabetes risk just by changing my drink habits?

A: Absolutely. Replacing just one daily sugary drink with water, black coffee, or unsweetened tea lowered diabetes risk by 17% in a 20-year study. Small changes in what you drink create big changes in your long-term health.

Q: What’s the best way to protect myself and my family from the effects of liquid sugar?

A: Start by eliminating soda and sweetened drinks from your daily routine. Stay hydrated with water, enjoy whole fruits when you’re craving something sweet and experiment with healthier alternatives, like sparkling water with lime, you actually enjoy. The goal is to stop the metabolic stress before it turns into chronic disease.

Rates of neurological diseases continue to increase in America. For example, over 7 million people are currently diagnosed with Alzheimer’s disease, and this number is estimated to rise to almost 13 million by 2050.1

Treatment for neurological disease greatly varies, but medications are often the first line of strategy. However, these are riddled with side effects. In an effort to break new ground when it comes to preserving and boosting cognitive health, researchers are tapping into the power of nutrients found in food, namely vitamins K and A.

Vitamin K Analogue Shows Neuron-Boosting Power

In a study published in ACS Chemical Neuroscience, researchers explored how modifying vitamin K’s chemical structure can benefit brain health. The team designed 12 vitamin K analogues by attaching a retinoic acid-like side chain to them. For context, retinoic acid is the biologically active form of vitamin A, and is known for regulating cell growth and differentiation.2

The goal was to see if this newly synthesized form of vitamin K would be better at helping immature brain cells develop into fully functioning neurons. The experiments were carried out using neural precursor cells and mice models. These analogues were tested for their ability to pass through the blood-brain barrier, activate key receptors inside the brain, and trigger neuron development.

• One analogue stood out — Compound 7 not only reached the brain after oral administration but also transformed into menaquinone-4 (MK-4), the primary form of vitamin K stored in brain tissue.

Here, the blood-brain barrier acts like a high-security checkpoint, preventing most substances from entering. Many drugs fail here, which is why brain-related treatments are difficult to design. That said, compound 7 not only got through but was also converted into MK-4 once inside the brain, showing it was both bioavailable and metabolically useful.

• Compound 7 showed stronger effects in promoting neuronal differentiation compared to regular vitamin K — For context, differentiation means that the cells stopped behaving like generic, immature cells and instead took on the specialized shape and function of neurons. This process is like flipping the switch from “blank slate” cells into brain cells that can send signals, connect with other neurons, and contribute to learning and memory.

• Compound 7 activated several nuclear receptors — These are proteins inside cells that act like master switches for gene activity. Among them were retinoic acid receptors (RARs) and the steroid and xenobiotic receptor (SXR). By turning on these receptors, compound 7 influenced the expression of genes that drive neuron growth and survival.

• Another mechanism involved the metabotropic glutamate receptor 1 (mGluR1) — This receptor helps regulate synaptic signaling — the way neurons talk to each other. Computer modeling showed that compound 7 bonded more strongly to this receptor compared to regular vitamin K, suggesting it had a stronger effect on brain communication pathways. In other words, the analogue not only helped create more neurons, but also supported the chemical “language” used to exchange information.

• The benefits were not limited to test tubes — In mice, oral administration of compound 7 worked its way into the brain and eventually converted into MK-4. This shows the compound is not only theoretically effective but also practically deliverable through diet or supplementation in a living organism.

• Future implications — While this study focused on laboratory and animal models, it lays the groundwork for modifying existing nutrients that could open doors to new therapies. If regular vitamin K supports brain health, then new analogues like compound 7 could amplify those effects many times over.

Nutrient science is moving beyond simple supplementation and into precision-designed molecules tailored for specific effects. These findings demonstrate that vitamin K is not just useful for blood clotting or strengthening bones — it has the capacity, when optimized, to trigger the growth and development of neurons.

Brain Vitamin K Levels Predict Lower Dementia Risk

Digging deeper into the link between brain function and vitamin K, a study published in Alzheimer’s & Dementia: Translational Research & Clinical Interventions analyzed vitamin levels in the brains of older adults and linked the results to dementia outcomes.3

The population studied included 325 participants who agreed to annual cognitive testing during life and brain donation after death. The average age at death was 91, making this group especially relevant for understanding late-life cognitive decline.

• Higher brain concentrations of menaquinone-4 (MK-4) lowered risk of dementia — Specifically, the findings showed a 17% to 20% reduction of having dementia or mild cognitive impairment at the time of death. In simple terms, more MK-4 in the brain helped reduce memory loss, confusion, and disorientation in later years.

Digging into the specifics, those with higher MK-4 also showed less Alzheimer’s-type brain damage. Neuropathologists found fewer neurofibrillary tangles, which are twisted fibers of the tau protein that clog brain cells and disrupt communication. They also observed less overall Alzheimer’s pathology across multiple brain regions. These findings suggest vitamin K is not just a marker, but a meaningful agent that helps slow down disease progression.

• Comparing the odds of dementia across different vitamin K levels — Participants with more MK-4 in their brains had significantly reduced odds of advanced Braak stage, which is a way of rating how far Alzheimer’s pathology has spread. Specifically, the reduction ranged from 14% to 16% depending on the brain region studied.

• Duration of vitamin K intake matters — Because participants underwent annual cognitive testing for years before death, the researchers could compare brain vitamin levels with how thinking ability changed over time. Specifically, those with more MK-4 retained their cognitive function longer and declined more slowly.

• The strongest associations were observed in the midfrontal cortex — This part is involved in decision-making and executive function. People with higher MK-4 in this area were less likely to meet criteria for dementia at death. That means vitamin K presence was most protective in the part of the brain that helps you plan, organize, and think critically.

• Vitamin K is important for brain function — Comparing vitamin K to other variables, the effect was independent of age, gender, education level, and even total calorie intake. This suggests that the observed benefits were not simply the result of healthier overall lifestyles but had a specific link to vitamin K status. In other words, two people of the same age and educational background could still show different dementia outcomes depending on the vitamin K stored in their brain.

• The benefit lies in vitamin K’s multiple roles beyond blood clotting — The researchers theorize that MK-4 in the brain influences sphingolipid metabolism, a process important for the structure and stability of brain cell membranes. Thus, healthy membranes support efficient communication between neurons.

Vitamin K also regulates proteins that protect against oxidative stress and inflammation,4 both of which accelerate Alzheimer’s pathology. By acting on these cellular pathways, higher MK-4 levels translate into stronger resilience against neurodegeneration.

The takeaway here is straightforward — higher levels of MK-4 align with better cognitive outcomes and less Alzheimer’s-related damage. Unlike studies that stop at blood markers, this one directly ties brain tissue vitamin K to dementia, making its implications especially powerful for those concerned about aging and memory loss.

Retinoic Acid Impacts Learning and Memory

In a related study published in the Annual Review of Nutrition journal, researchers examined how vitamin A and its active form, retinoic acid, influence cognition and neurological disease. The focus was not only on aging brains, but also on how disruptions in retinoic acid signaling contribute to conditions like Alzheimer’s, depression, and schizophrenia.5

• Deficiency can affect anyone’s brain function — The review highlighted that vitamin A deficiencies or impairments in retinoic acid metabolism are not limited to malnourished populations. Even in developed countries, subtle deficiencies or signaling breakdowns appear in adults with cognitive impairment and neuropsychiatric disorders. That said, the authors emphasized that restoring proper retinoic acid pathways could help maintain memory, learning, and emotional regulation.

• How retinoic acid fine-tunes synaptic plasticity — This refers to the ability of neurons to strengthen or weaken their connections based on activity. Long-term potentiation, the cellular process that underpins memory formation, is strongly influenced by retinoic acid signaling. When that pathway falters, memory consolidation suffers.

• Retinoic acid signaling naturally decreases with age — This decline coincides with reductions in hippocampal neurogenesis, which is the brain’s ability to create new neurons.

In healthy youth, retinoic acid helps replenish and remodel memory circuits. In older age, diminished activity means fewer new neurons and less flexible synapses, making it harder to adapt or recover from cognitive challenges.

• Certain groups are vulnerable to disruption — Alzheimer’s patients often show reduced expression of retinoic acid receptors in brain regions like the hippocampus and cortex. This receptor loss correlates with the severity of their memory impairment.

In other words, that part of the Alzheimer’s disease pathology involves not only toxic proteins like amyloid and tau, but also a breakdown in nutrient signaling that normally sustains cognitive resilience.

• Impact of retinoic acid on other pathways — The authors also compared the effects of retinoic acid to other signaling molecules. They noted its strong interaction with neurotransmitters like acetylcholine, which is central to attention and memory.

When retinoic acid pathways are impaired, cholinergic signaling weakens, leading to the same deficits often targeted by current Alzheimer’s drugs. But instead of offering short-lived symptomatic relief, supporting retinoic acid signaling can address the upstream regulatory system that keeps acetylcholine functioning well.

• Why the benefits of retinoic acid are impactful — It mainly works through nuclear receptors, which are proteins inside brain cells that regulate which genes get turned on or off. By binding to these receptors, retinoic acid activates gene networks involved in synaptic proteins, neurotransmitter systems, and structural remodeling of neurons. This is not just about single pathways but about broad control of the brain’s adaptability.

Another mechanism involved mTOR, a key pathway that balances growth, energy use, and plasticity. Retinoic acid influences mTOR activity in ways that optimize both neuron survival and flexibility. That connection is significant because mTOR dysfunction has been implicated in everything from aging to autism. With proper retinoic acid signaling, mTOR operates in a balanced way, supporting healthy brain plasticity rather than tipping into disease states.

• How retinoic acid impacts mood and psychiatric health — Deficiencies or signaling breakdowns were linked not only to memory problems but also to depression-like symptoms. Animal studies cited by the researchers showed that restoring retinoic acid reversed these issues, suggesting that vitamin A’s role extends into strengthening emotional resilience as well.

Optimize Your Vitamin K and A Levels with These Strategies

Vitamin K continues to be an important nutrient for overall health. In a previous article, I noted how it serves as the body’s master regulator for calcium distribution that promotes better skeletal integrity and cardiovascular health. Now, the studies I discussed in this article show how important it is for optimal brain health.

While the featured study researchers used an analogue, I believe that getting vitamin K naturally is just as good for your health. That said, here are tips on how to optimize your intake for best results:

1. Eat natural sources of vitamin K2 — Make a point of adding natto (fermented soybeans) and other vegetables fermented with K2-producing bacteria to your daily meals. These foods are excellent sources of the MK-7 form of vitamin K2, known for staying active in the body longer.

Certain cheeses like Brie, Munster, and Gouda are also abundant in K2. In addition, grass fed organic animal products such as egg yolks, liver, butter, tallow, and dairy provide valuable amounts of this nutrient.

Now, why vitamin K2? In another article, I explained how it significantly impacts bone and heart health, giving it system-wide importance. Moreover, it also has higher bioavailability compared to vitamin K1.

2. Pair K2 with healthy fats — Because vitamin K2 is fat-soluble, consuming it alongside healthy fats helps your body absorb it more effectively. Choices include grass fed butter, ghee, or tallow.

3. Combine K2 with key cofactors — Vitamin K2 works alongside other vital nutrients, particularly calcium, vitamin D3, and magnesium. When supplementing with vitamin D3, be sure to include K2 as well, since this helps guide calcium into your bones rather than your arteries. This balanced approach strengthens your skeletal system while safeguarding heart and brain health.

4. Dosing recommendations — The recommended daily intake of vitamin K for an adult ranges between 150 and 200 micrograms. If you’re taking a supplement, keep this in mind. Again, for best absorption, take it alongside meals that contain healthy fats.

5. Dietary sources of vitamin A — This nutrient is found in vast sources of plant foods. Top examples include kale, spinach, broccoli, carrots, and sweet potatoes. It’s also found in tomatoes, red bell pepper, eggs, and beef liver.6

Just like vitamin K, vitamin A is also fat-soluble, which is why they work well together. However, take care not to go overboard with your consumption — toxicity is far more common than deficiency in America. Symptoms include blurry sight, dry skin, and bone pain.7

Frequently Asked Questions (FAQs) About Vitamins K and A for Brain Health

Q: Why are researchers focusing on vitamins K and A for brain health?
A: Rates of neurological diseases like Alzheimer’s are steadily rising, and current treatments often have limited effectiveness with unwanted side effects. Researchers are now exploring nutrients such as vitamin K and vitamin A (in the form of retinoic acid) for their potential to preserve and boost cognitive function, improve neuron development, and reduce dementia risk.

Q: What did scientists discover about vitamin K analogues?
A: A study published in ACS Chemical Neuroscience created modified forms of vitamin K by linking them with a retinoic acid-like side chain. One compound, Compound 7, showed remarkable results. It crossed the blood-brain barrier, converted into MK-4 (the brain’s primary form of vitamin K), promoted neuron growth and differentiation, activated receptors tied to brain signaling, and worked effectively in animal models.

Q: How does vitamin K in the brain influence dementia risk?
A: Research published in Alzheimer’s & Dementia analyzed brain tissue from older adults and found that higher MK-4 levels were linked to a 17% to 20% lower risk of dementia. People with more MK-4 had less Alzheimer’s-type brain damage, fewer tau tangles, slower cognitive decline, and stronger protection in critical brain areas like the midfrontal cortex.

Q: What role does vitamin A’s active form, retinoic acid, play in cognition?
A: Retinoic acid regulates synaptic plasticity, neurogenesis, and memory circuits. Its signaling declines with age and is often disrupted in conditions like Alzheimer’s, depression, and schizophrenia. Supporting retinoic acid pathways helps maintain learning, memory, mood regulation, and neuron survival by influencing gene networks, neurotransmitters like acetylcholine, and key pathways such as mTOR.

Q: How can people optimize vitamin K and A intake for brain health?
A: To support brain health with vitamins K and A, focus on nutrient-rich foods. Good sources of vitamin K2 include natto, fermented cheeses, and grass fed animal products like egg yolks and beef liver. Since K2 is fat-soluble, pair it with healthy fats and other cofactors such as vitamin D3, calcium, and magnesium for better absorption and balance. For vitamin A, leafy greens, carrots, sweet potatoes, tomatoes, eggs, and beef liver are excellent sources, but intake should be moderate to avoid toxicity.

Adults in high-income countries now spend about 11 to 12 hours every day sitting — more than three-quarters of their waking life.1 You might assume a daily workout makes up for all that sitting. It doesn’t. Long, uninterrupted stretches in a chair reduce muscle activity, slow blood flow, and interfere with the normal processes that help regulate blood sugar and fat metabolism. Over time, that pattern is linked to a higher risk of chronic disease, poorer mental health, and earlier death.
The latest research shows, however, that a small intervention can start reversing that damage, with benefits showing up quickly. Researchers recently tested several movement schedules in a real-world setting, not a lab, to see which one people would actually stick with.
The results point to a specific pattern that’s easy to build into an ordinary workday, no gym or extra hours required. Let’s explore exactly what happened when thousands of people put this simple habit into practice and why the results point to one of the easiest health upgrades you can make.

Five-Minute Walks Every Hour Delivered the Best Results

A study published in the British Journal of Sports Medicine investigated whether short walking breaks could fit into everyday life while improving how people feel during the day.2 Researchers followed 19,342 adults who enrolled in a two-week movement challenge connected to an interactive public health podcast. Of those participants, 11,484 completed the baseline period and began the intervention.
Participants selected the walking frequency they believed would fit their own routines: a five-minute walk every 30, 60, or 120 minutes. That design gave researchers valuable insight into what people would actually stick with outside a research setting, making the findings far more relevant to your own daily routine.

• Consistency mattered more than perfection — Participants came from many different backgrounds, occupations, and life situations, including full-time employees, retirees, students, and homemakers. They represented a wide range of ages and professions, allowing researchers to see whether movement breaks remained practical across everyday lifestyles instead of only among highly motivated volunteers.
Every walking schedule produced measurable improvements in how participants felt over the two-week challenge.
Researchers also found that the intervention received high ratings for feasibility, acceptability, and appropriateness, meaning participants generally viewed the habit as realistic, worthwhile, and easy to fit into normal life. Importantly, those positive ratings remained strong regardless of age, employment setting, or other demographic differences examined in the analysis.
• The hourly schedule emerged as the clear winner — At first glance, walking every 30 minutes produced the largest improvements in several measures, but there was an important tradeoff. People found that schedule harder to maintain. The two-hour schedule proved easier to follow, yet it produced smaller improvements. The five-minute walk every 60 minutes struck the best balance between meaningful health improvements and long-term adherence.
Researchers described hourly breaks as offering the best balance between feasibility and effectiveness. If you spend much of your day behind a desk, this finding removes much of the guesswork. Instead of trying to stand every few minutes or waiting until lunch for one long walk, you have a practical target that fits naturally into most workdays.
• More movement didn’t reduce productivity — One of the biggest concerns people have about taking regular breaks is losing valuable work time. This study directly examined that issue. Researchers measured work performance and work engagement throughout the intervention and found no adverse effects from taking regular walking breaks. Participants felt better without sacrificing their ability to perform their jobs.
That matters because fatigue often causes mistakes, slower thinking, and reduced concentration. By interrupting long periods of sitting with short walks, participants lowered fatigue while maintaining their productivity. Instead of viewing movement as time lost, you can begin treating each five-minute walk as an investment that helps you stay mentally sharper throughout the remainder of the day.
• Small improvements accumulated surprisingly quickly — Participants didn’t need months of training before noticing benefits. The intervention lasted only 14 days, yet researchers documented significant improvements across multiple measures of emotional well-being. The changes followed what scientists call a “dose-response” relationship.
This means that the frequency of the walking breaks influenced the size of the improvements. Participants who moved more often generally experienced greater reductions in fatigue and larger increases in positive mood than those who waited longer between walks. The study also tracked how closely people followed their chosen schedules.
As expected, more participants successfully maintained the less demanding two-hour schedule, while fewer fully adhered to the 30-minute schedule. That finding helps explain why the hourly schedule delivered the strongest real-world value: it combined noticeable benefits with a routine that people could realistically continue.
• Your muscles begin working the moment you stand up — The researchers also explained why these brief walks produce such broad effects. Sitting for long periods leaves your large leg muscles relatively inactive. Those muscles normally help regulate blood sugar by pulling glucose from your bloodstream into muscle cells for energy. They also help break down fats and keep blood moving efficiently through your lower body.
Once you begin walking, even at a comfortable pace, those natural processes switch back on. Better circulation also helps prevent blood from pooling in your legs during long periods of sitting. You don’t need an exhausting workout to trigger those benefits. Every five-minute walk acts like pressing a reset button on several important body systems.
As those resets accumulate throughout the day, they help explain why participants reported feeling less drained, more positive, and better equipped to handle everyday demands.

More Daily Steps Lowered Heart Disease and Death Risk

Now that the evidence points to hourly walks as the most practical way to break up sitting, the next question is straightforward: how many total steps does your body actually need each day? For a separate study published in the British Journal of Sports Medicine, researchers analyzed data from the UK Biobank to determine how many daily steps were associated with the lowest risk of death and cardiovascular disease — diseases that affect the heart and blood vessels, including heart attacks and strokes.3
The study included 72,174 adults with an average age of 61 years who wore wrist-based activity monitors for seven days. Researchers then followed participants for an average of 6.9 years, during which 1,633 people died and 6,190 developed cardiovascular disease. Instead of relying on questionnaires, the investigators used wearable devices that continuously measured both daily steps and the amount of time people spent sitting, making the findings more accurate than studies based on memory alone.

• The biggest health gains began well below 10,000 steps — One of the most encouraging findings is that you don’t have to reach an arbitrary 10,000-step goal before your health begins to improve. Researchers found that about 4,000 to 4,500 daily steps represented the “minimal dose” associated with achieving roughly half of the maximum benefit for lowering both all-cause mortality and cardiovascular disease risk.
If you currently average only 2,000 or 3,000 steps each day, adding another 1,500 to 2,000 steps moves you into a range where meaningful health improvements begin. That makes the goal feel much more attainable and gives you an early milestone to celebrate instead of waiting until you hit 10,000.
• Around 9,000 to 10,500 steps produced the lowest risk of death — The researchers also identified what they called the optimal range. Participants who accumulated between approximately 9,000 and 10,500 steps per day experienced the lowest risk of dying during the follow-up period, regardless of whether they spent much of their day sitting. That finding challenges the idea that long hours at a desk automatically erase the value of walking.
Even among adults who sat for at least 10.5 hours each day, increasing daily steps remained strongly associated with lower mortality. If your job requires long periods behind a computer, every additional walk still moves you in the right direction.
• Sitting less still provided an extra cardiovascular advantage — Although daily steps helped everyone, the study found another important difference. Participants who spent less than 10.5 hours sitting each day had about a 10% lower risk of developing cardiovascular disease than equally active participants who remained seated longer, even when both groups accumulated similar numbers of steps.
In other words, daily walking and reducing sitting work together instead of replacing one another. If you already reach your step goal, adding more opportunities to stand, stretch, and move throughout the day gives your heart another advantage.
• Wearable devices make progress easy to measure — Researchers emphasized that step counts offer a simple target because they’re easy to understand and easy to monitor. Unlike exercise prescriptions based on minutes of “moderate intensity” activity, you don’t have to estimate how hard you worked or remember every activity you completed.
Your watch or fitness tracker does the counting automatically. That makes it easier to build confidence over time. If your current average is 5,000 steps, aim for 6,000 next week. Once that becomes routine, move toward 7,000. Those steady improvements help build lasting habits instead of relying on one ambitious goal that feels overwhelming.
• Walking protects your heart through several pathways at once — Regular walking helps improve several major cardiovascular risk factors, including body weight, blood pressure, and cholesterol levels. The paper also explains that prolonged sitting contributes to inflammation — your body’s long-term stress response — oxidative stress, meaning damage caused by unstable molecules called free radicals, and unhealthy changes in the nervous system that regulates your heart and blood vessels.
Walking reverses that pattern by restoring healthy cardiovascular function. The takeaway is simple: every step compounds. The more often you move throughout the day, the more opportunities your body has to protect your heart and blood vessels over the long term.

Make Movement Part of Your Routine

Two habits. Five minutes an hour and a few thousand more steps each day. That’s the core of what the research supports, and neither one requires a gym, special equipment, or an overhaul of your schedule. The key is making both habits so small and so repeatable that skipping them feels harder than doing them. Here’s how to put that into practice.

1. Take a five-minute walk every hour — The strongest real-world evidence showed that a five-minute walk every 60 minutes offered the best balance between health benefits and something people could realistically maintain. Instead of relying on memory, set an hourly reminder. If you work at a desk, treat each movement break like an important meeting that can’t be skipped. Challenge yourself to complete every scheduled break for one week, then pay attention to your energy, focus, and mood.
2. Turn sitting breaks into step opportunities — Standing is a good start, but walking gives your body much more. Walk down the hallway, climb a flight of stairs, circle your office, try walking lunges, or take a quick lap outside. If you have limited mobility, move in whatever way keeps your muscles active, such as marching in place or performing chair exercises. Every step counts toward your daily total while also restoring circulation and helping your body avoid the effects of prolonged sitting.
3. Build movement into the routine you already have — If you lose track of time while working, connect your walks to activities that already happen every day. Walk after every meeting, before checking email, after finishing a focused work session, or whenever you refill your water bottle. Linking movement to existing habits removes the need for constant reminders and makes the routine feel automatic.
4. Increase your daily steps one milestone at a time — If you currently average fewer than 4,000 steps a day, make your first goal 4,000 to 4,500 steps. Research found that this range is associated with a substantial reduction in the risk of death and cardiovascular disease compared with very low step counts.
Once that becomes your normal routine, gradually work toward about 9,000 to 10,000 steps a day, the range associated with the lowest long-term risk. Don’t worry about reaching the final target immediately. Every increase moves you in the right direction.
5. Track both your movement breaks and your daily steps — Most fitness trackers automatically record your steps, making it easy to monitor your progress. Keep a simple checklist of your hourly walks alongside your daily step total. If you consistently complete your movement breaks but your step count remains low, add a short walk after dinner or park farther from the entrance.
Watching both numbers improve creates momentum, builds confidence, and helps turn healthy movement into a lasting habit instead of another short-lived goal.

FAQs About Short Walking Breaks

Q: Why is sitting for long periods harmful even if I exercise regularly?
A: A daily workout is good for your health, but it doesn’t completely offset spending 11 to 12 hours sitting each day. Long periods of sitting reduce muscle activity, slow blood flow, and interfere with normal blood sugar and fat metabolism. Breaking up sitting throughout the day helps restore those natural processes and supports better physical and mental health.

Q: How often should I get up from my desk?
A: The strongest evidence from the featured research points to taking a five-minute walk every hour. Researchers found that this schedule provided the best balance between meaningful health benefits and something people could realistically maintain during a normal workday. More frequent breaks produced slightly greater improvements, but most people found them harder to sustain.

Q: How many daily steps do I really need?
A: You don’t have to reach 10,000 steps before your health improves. The research found that about 4,000 to 4,500 steps a day were associated with substantial reductions in the risk of death and cardiovascular disease compared with very low activity levels. The lowest long-term risk occurred at roughly 9,000 to 10,500 steps per day.

Q: Does walking improve my health if I still have a desk job?
A: Yes. The research found that increasing your daily steps was associated with a lower risk of death even among people who spent much of their day sitting. At the same time, reducing your total sitting time provided additional protection against cardiovascular disease. The greatest benefits came from combining regular walking with fewer uninterrupted hours in a chair.

Q: What’s the easiest way to build these habits into my day?
A: Start small and stay consistent. Set an hourly reminder to take a five-minute walk, connect those walks to routines you already have, such as meetings or water breaks, and gradually increase your daily step count. Tracking both your movement breaks and your daily steps helps you see your progress and makes the habit easier to maintain over time.

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 helps a healthy routine last without relying on willpower?

Stronger motivation each morning
More detailed daily planning
Frequent changes to the routine
Automatic habits linked to daily cues
Habits become easier to maintain when they are tied to regular cues, such as meals, instead of depending on motivation each day. Learn more.

Americans now consume linoleic acid (LA) at levels that would have been unimaginable a century ago — close to 30 grams per day, up from just 2 grams in the 1860s. That’s led to a fundamental change in the way your body operates at the cellular level. This polyunsaturated fat (PUF) was once a minor player in the human diet. You need it, but only in trace amounts. Just 1% to 2% of your daily calories is enough to meet biological needs.

But today, LA makes up more than 15% to 25% of the typical American’s caloric intake. That’s primarily due to processed vegetable oils like soybean, corn, and canola, ingredients you’ll find in nearly every packaged food and restaurant meal. What’s the cost of this overload? Your cells become more vulnerable to oxidative stress. Your mitochondria — the organelles responsible for creating energy — start to break down.

The fat itself transforms into dangerous byproducts known as oxidized linoleic acid metabolites, or OXLAMs, which damage DNA, disrupt energy production, and drive chronic inflammation throughout your body. These OXLAMs have been linked to nearly every chronic disease now plaguing the developed world — heart disease, obesity, Type 2 diabetes, and even neurodegeneration.

And the problem doesn’t resolve quickly. LA embeds in your body fat and stays there for years, continuing to inflict damage even after you clean up your diet. To understand how this happened — and how to reverse it — you need to look at what my paper, published in Nutrients, reveals about the long-term biological effects of this once-essential nutrient turned metabolic disruptor.1

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Chronic low back pain disrupts your life in ways that reach far beyond discomfort. It chips away at your mobility, limits the activities you feel confident doing, and shapes how you move throughout your day. This condition is characterized by stiffness, recurring soreness, and a growing hesitation to bend, lift, or twist, especially when even small motions feel unpredictable.

The video above offers a look at how simple crawling patterns help restore the coordination your spine depends on. These early-life movements reengage stabilizing muscles, ease stiffness and rebuild control — an approach that mirrors the movement-retraining strategies highlighted in recent research.

Left unaddressed, chronic back pain often creates a loop of disturbed sleep, reduced activity, and guarded movement patterns that place even more strain on your spine. Millions of adults fall into this cycle, and many assume their options are limited to rest or short bursts of treatment whenever symptoms flare. What often gets overlooked is how much your daily movement habits influence the path your pain takes over time.

Your body adapts to whatever you repeat, including long periods of sitting, rushed transitions, or stiff, protective motions that keep your spine from moving the way it was designed to move. Research highlights why these everyday patterns matter. Simple changes in how often you move — and how you structure that movement — alter the course of low back pain in meaningful ways.

Whether it’s restoring smoother coordination, increasing your tolerance for activity, or extending the stretches of time you stay pain-free, your habits shape your outcomes. This foundation sets up the deeper insights revealed in the first study, which explains how targeted movement approaches shift the way your body responds to chronic back pain.

Movement Retraining Restores Confidence and Eases Chronic Back Pain

A study published in Musculoskeletal Science and Practice investigated how a 12-week, physiotherapist-led movement program affected people with chronic non-specific low back pain.1 The researchers examined whether retraining basic movement patterns — like rolling, crawling, and squatting — improved function, reduced pain, and helped participants feel more confident in their bodies.

This program, known as Motum, targeted the foundational motor skills your nervous system relies on for coordinated movement, giving participants an accessible framework for rebuilding strength and body awareness. The study population included individuals with chronic back pain lasting longer than three months, a group known to struggle with stiffness, guarded movement, and fear of aggravating their symptoms.

• The program produced strong improvements in fear of movement and balance — Many participants entered the trial with reduced balance, difficulty performing everyday tasks, and growing worry about normal movement. According to the researchers, participants reported that the structure of the classes helped them understand what their bodies needed and how to move with less strain. This clarity mattered because people with chronic pain often lose confidence in their ability to move safely.

The movement program led to a strong drop in fear avoidance, meaning people stopped being so afraid to move and weren’t as worried that a simple motion would set off their pain. Fear avoidance is a major driver of disability because it stiffens your movement and increases stress in your spine. The program also produced a large improvement in balance, a key measure of neuromuscular control, which directly affects how safely you stand, bend, or shift your weight.

• Pain levels and day-to-day function improved in measurable ways — Those in the movement group experienced moderate improvement in pain and functional ability compared to the control group. Even small shifts in daily function create meaningful gains, such as easier transitions from sitting to standing or reduced strain during routine tasks.

• Participants valued individualization, pacing, and real-time corrections — People repeatedly emphasized how helpful it felt to receive personalized corrections during class, allowing them to understand how to position their bodies and avoid harmful compensations.

Participants said the pace felt doable and liked that every movement had easier and harder versions, so they could choose what matched their comfort level. This structure helped them feel in control, increasing the belief that you can perform a task successfully, which is a powerful predictor of long-term improvement.

• Daily life improvement occurred because movements became habits, not one-time exercises — Many participants explained that they used the techniques outside the clinic, applying what they learned when getting out of bed, lifting objects, or adjusting posture throughout the day.

Simple shifts — like rolling more efficiently or engaging your core muscles during transitions — help reduce nighttime discomfort, morning stiffness, and pain during routine tasks. This habit formation aligns with research showing that small, repeatable actions reinforce neural pathways and support long-term change.

• Movement retraining works at the biological level by improving motor control — Chronic low back pain often disrupts your body’s motor control system — the network that coordinates muscle activation, joint alignment, and posture. The paper explains that these disruptions lead to inefficient movement patterns and increased strain on your spine.

Retraining fundamental movements restores smoother motion by teaching the nervous system how to sequence muscles correctly. When motor control improves, your body distributes load more evenly across muscles and joints, lowering stress on irritated structures. That means fewer flare-ups, fewer muscle spasms, and more controlled movement throughout the day.

As movement patterns normalize, your nervous system becomes less reactive and less likely to interpret normal activity as threatening. This reduces pain sensitivity and builds resilience, giving you the confidence to stay active without fear of reinjury.

Walking Reduces the Return of Disabling Back Pain

A study published in The Lancet evaluated whether an individualized, progressive walking intervention paired with education could stop low back pain from recurring after someone had recently recovered.2 This trial aimed to solve a major problem: most people who recover from a flare-up experience another episode within a year. The researchers wanted to know if a simple habit — walking — was strong enough to interrupt that cycle when guided by a physiotherapist.

• Walking kept people pain-free far longer than usual — The study enrolled adults across Australia who had recently recovered from an activity-limiting back pain flare and weren’t walking regularly. Many of them expected another episode because they’d already lived through several cycles of pain.

The walking group stayed pain-free much longer than the control group. That extra time gave them more normal movement, more confidence, and more freedom in their day-to-day life. Physiotherapists delivered the program with a coaching approach, helping participants understand how movement affects the spine and why staying active reduces pain recurrence.

• The walking program nearly doubled the pain-free period for participants — The walking group reached a median of 208 days before experiencing disabling back pain again, compared to only 112 days in the control group. This rate of improvement shows that structured, progressive walking offered a major protective effect.

• Walking improved disability scores and increased overall movement — Disability scores, which measure how pain limits daily function, consistently favored the intervention group throughout the year. These improvements included easier bending, lifting, standing, and daily transitions.

The researchers also noted higher step counts, greater amounts of brisk walking, and more total weekly walking early in the program. These increases show that guided walking not only delayed pain but made people meaningfully more active.

• Participants who followed the walking schedule more closely saw the greatest extension in pain-free days — Even those who walked three to four times per week during the first 12 weeks experienced noticeable improvement. The control group, by contrast, turned to massage, chiropractic care, and physiotherapy more often, showing they struggled more with recurring symptoms. This comparison highlights how walking provided lasting protection rather than short-lived relief.

• Consistent walking restores natural mobility cycles that protect your back — Repeating the walking pattern retrains coordination between your legs, hips, and trunk, reducing the uneven stress patterns that often set off new pain episodes. This restored coordination gives your spine a smoother, more efficient rhythm for everyday movement, lowering your risk of falling back into the old pain cycle.

Reducing Sitting Time Protects Your Back from Worsening Pain

A related study published in BMJ Open investigated whether reducing sedentary behavior would influence back pain intensity, disability scores, and metabolic activity inside the paraspinal muscles that support your spine.3 This trial followed adults for six months to see if small, consistent reductions in sitting time — just one hour a day — would change how their backs felt and functioned.

The study included 64 adults who carried excess weight, had metabolic syndrome, and performed less than two hours of moderate-to-vigorous activity per week while sitting more than 10 hours per day.4 This group represents many people who struggle with low activity levels, long work hours in chairs, and persistent back pain.

One group reduced sitting time using hip accelerometers to monitor movement, while the control group continued their usual routines. The intervention group successfully decreased their sedentary time and increased overall movement, stabilizing their pain instead of watching it intensify.

• Back pain worsened for the sedentary group but stayed level for those who moved more — The control group experienced a significant increase in back pain intensity over six months, while the intervention group showed no rise in pain levels. When you’re living with chronic back issues, not getting worse is a meaningful improvement — especially if your baseline symptoms are already disrupting your life.

• Daily movement increased, sitting time decreased, and these changes shaped pain outcomes — Those assigned to reduce sitting time cut their sedentary hours by an average of 40 minutes per day and increased moderate-to-vigorous activity by roughly 20 minutes per day.

These numbers show that you don’t need heroic exercise sessions to influence your back. Small changes in daily behavior — standing up more often, walking a little extra, breaking up long periods of stillness — alter the trajectory of your symptoms.

• Metabolic activity inside the paraspinal muscles improved with increased steps — The researchers measured insulin sensitivity in the paraspinal muscles using advanced imaging techniques.

While increasing movement didn’t produce major group-level differences in muscle metabolism, an important pattern emerged: across all participants, increases in daily steps were linked to improved glucose uptake in the paraspinal muscles. Improved glucose uptake means those muscles use energy more efficiently, which supports better endurance and spinal stability.

• Consistent light movement prevents back pain from worsening — Investigators concluded that reducing sedentary behavior is a feasible and effective strategy for preventing increases in back pain intensity over time. Even minimal daily improvements protected participants from the upward drift in pain experienced by the control group. This reinforces a powerful message: small, steady actions throughout your day reshape how your back feels in the long run.

Simple Steps Help Your Back Relearn How to Move Safely

Movement retraining and progressive walking rebuild confidence, reduce flare-ups, and help your spine handle daily stress with less strain. Now it’s time to turn that information into steps you can follow. If you struggle with stiffness, recurring soreness, or the fear that one wrong move will trigger another episode, these are the actions that restore control. Your goal is to retrain your body, strengthen the systems that protect your spine, and remove the everyday pressures that keep your back inflamed.

1. Start with basic movement patterns — Reintroducing the movements you learned in infancy — rolling, crawling, kneeling, squatting — restores the coordination your spine depends on. You reclaim smoother movement because these patterns reorganize how your muscles fire.

If you tense up or move rigidly out of fear, these simple drills reset your nervous system and teach your body that movement is safe again. Try practicing short sessions throughout your day to reinforce the patterns without overwhelming your system.

2. Build a consistent walking routine — Walking is one of the strongest tools you have for preventing flare-ups. As shown in the research, individualized, progressive walking nearly doubled the time before back pain returned, giving people months of extra freedom.

If you’ve been largely sedentary or are recovering from a recent episode, start small — even 10 minutes counts — and increase gradually. Your spine thrives on rhythmic movement, and walking delivers exactly that with no equipment, no gym, and no complexity.

3. Break up long sitting periods throughout your day — Long stretches of sitting tighten your spine, reduce blood flow to your supporting muscles, and increase the chances that your back will flare. Even small adjustments — standing every 30 to 45 minutes, walking for two minutes between tasks, or changing your position more often — help stop pain from escalating.

If you spend hours at a desk or in a car, this step gives you immediate leverage: the BMJ Open study showed that cutting sedentary time by roughly 40 minutes a day kept pain from getting worse, while people who stayed sedentary experienced rising discomfort.5 These tiny daily interruptions give your back a break and prevent the slow buildup of strain.

4. Pay attention to nutrition and weight control — Excess weight loads your spine the same way carrying a heavy backpack would. Every step, bend, and twist becomes harder. Shifting your diet toward nutrient-dense whole foods and away from ultraprocessed products with seed oils high in linoleic acid (LA) eases that pressure.

In addition to avoiding seed oils, consume enough healthy carbohydrates to support cellular energy. Losing even a modest amount of excess weight lightens the daily load on your back and helps movement feel easier.

5. Practice load management during daily tasks — Your back reacts strongly to how you position your body when you lift, reach, or get out of a chair. Small adjustments, such as tightening your core during transitions or reducing the range of a movement when something feels off, reduce irritation. Rather than pushing through pain, this step teaches you how to adjust instead of aggravate your spine. Your goal is to stay active while avoiding the patterns that trigger inflammation.

FAQs About Movement for Back Pain

Q: How does retraining basic movements help lower back pain?

A: Retraining movements such as rolling, crawling, kneeling, and squatting restores the coordination your spine relies on. These patterns teach your nervous system to move efficiently again, reduce stiffness, improve balance, and lower the fear of triggering pain.

Q: Why is walking such a powerful tool for preventing back pain flare-ups?
A: Progressive walking nearly doubled the amount of pain-free time for people who recently recovered from a flare. It improves mobility, strengthens stabilizing muscles, and creates longer stretches of comfortable, normal movement.

Q: Does reducing sitting time affect back pain?

A: Yes. Even small reductions in sedentary time stop pain from getting worse. In the BMJ Open study, cutting sitting by about 40 minutes a day kept symptoms stable, while people who stayed sedentary experienced increased pain.6

Q: How do daily habits influence chronic back pain?

A: Your back adapts to whatever you repeat. Long sitting periods, stiff transitions, and guarded motion reinforce pain cycles. Frequent movement, smoother mechanics, and mindful posture help reverse those patterns and reduce strain on your spine.

Q: What are the most effective steps I can start today to protect my back?

A: Begin with simple movement drills, build a steady walking routine, interrupt long sitting blocks, shift your diet toward whole foods to reduce spinal load and manage weight, and adjust how you lift and bend. These small, consistent actions work together to ease pain and prevent flare-ups.

When it comes to nutritional supplementation regimens, most research focuses on what’s in the bottle. Far fewer studies investigate the more decisive question: what makes a person actually take it, day after day, long after the initial motivation has faded? Because the finest nutrient ever formulated does nothing if it stays in the bottle.
As it turns out, human behavior has some stubborn patterns worth understanding, because once you see them, the whole arc of starting and quitting a supplement habit suddenly makes sense.

Motivation Is Like Weather

Most of us start a new supplement regimen on a wave of motivation, and we badly overestimate how long that wave will last. The problem is that motivation is like weather — it rolls in, and it rolls out. A routine that depends on you feeling inspired every single morning is built on sand. The first dreary, overscheduled, low-energy day will sap the inspiration right out of you, and before you know it, the habit of taking it every day has evaporated.
This is a well-documented pattern in behavior research: intentions and motivation, on their own, are often weak predictors of what people keep doing over the long haul. What carries a behavior through the flat, uninspired days isn’t a fresh jolt of willpower — it’s automaticity, the state in which an action is taken as if on autopilot.
In one randomized trial, people repeatedly struggled to sustain a new health routine on motivation alone; the approach that helped the behavior persist months later worked by building automaticity, not by trying to keep people perpetually inspired.1 The lesson is both humbling and freeing at once. If your routine collapsed the first hard week, it wasn’t a character flaw. You were merely relying on memory and motivation, which tend to wane over time.

Friction Is Where Habits Die

The second pattern is just as stubborn: we are exquisitely sensitive to friction. Every extra step — another bottle, another decision, another thing to choke down, another schedule to track — becomes yet another reason to skip a dose.
We usually don’t quit a routine in one dramatic moment. We drift, one skipped dose at a time, until the drift becomes the new normal and the bottle migrates to the back of the shelf. The research bears this out plainly.
A systematic review pooling 83 studies of people on daily treatment routines found that the biggest barriers to keeping them up were exactly these: complicated regimens, the sheer difficulty of the daily steps, and simple forgetfulness — while one of the strongest enablers was a simplified routine.2 Make the thing easier and people do more of it. Make it harder and they do less. It really is that simple.

We Are Creatures of Cue and Context

The third pattern explains why some habits survive for years while others never take hold. We are creatures of cue and context. Habits that anchor to something we already do every day — a meal, a morning routine — tend to stick. Habits that float on their own, depending on memory and willpower to summon them out of thin air, tend to evaporate.
This is well established in the science of how habits form. For example, in one randomized study of everyday nutrition behaviors, people who tied a new behavior to an existing daily routine and simply repeated it in the same context built automaticity steadily, with that repeated, cue-linked enactment being the key to making it stick.3 The cue does the remembering for you. When the trigger is already wired into your day, you don’t have to decide to act — the context decides for you, and the behavior follows.
Put the three patterns together and the whole picture sharpens. Motivation fades, friction accumulates, and anything that depends on memory and willpower is an uphill battle. A routine that depends on all three is a routine designed, however unintentionally, to fail.

Two Choices: Discipline or Design

Knowing all of this, there are really only two choices. One is to demand that people become more disciplined. This is the industry’s favorite answer — buy a better pill organizer, set the alarm, try harder — and it quietly blames the customer for a design that rarely works even for the most disciplined among us. It treats a predictable feature of human nature as a personal shortcoming and then sells you tools to white-knuckle your way around it.
The alternative is to design the supplement so it barely asks for discipline at all. We’re choosing the second path, and it now shapes every product formulation decision we make.
When formulating new products, or reformulating old ones, we aim to make them easier to stick with, because friction is where habits die. With that aim in mind, we’re shifting some products from pills or capsules to powders that can be sprinkled on top of food or stirred into beverages.
This food-first format anchors naturally to something you already do — eating — so the cue is built in. The goal is a routine so easy that it survives your worst days, not just your best ones — the overscheduled Tuesday, the bad night’s sleep, the week everything goes sideways.
That is the whole point. A routine that only works when you’re rested, organized, and inspired is not a sustainable one, and nutritional supplements do you no good unless you take them. A routine built around how people actually behave promotes adherence precisely because it doesn’t ask for memory or motivation in the first place.

The Bottom Line

In short, our goal with the redesign of some of the items in our product line is to make consistency so easy that strong will is barely required. Not everything can be turned into a powder, of course. Some nutrients are best delivered in pill or capsule form, and they will stay that way. But for others, a powder is a far better choice, as it allows the nutrient to become part of your meals rather than something you need to remember separately.

Frequently Asked Questions

Q: Isn’t staying consistent just a matter of willpower?
A: It feels that way, but the evidence says otherwise. Motivation and willpower fluctuate for everyone, and routines that depend on them tend to collapse on the first hard day. What sustains a behavior is automaticity — when an action becomes automatic, cued by something you already do on a daily basis, such as eating. The reliable path to consistency is a routine that doesn’t lean on willpower in the first place.

Q: Why do I always start strong and then fade?
A: Because you started on a wave of motivation, and motivation is temporary by nature. The early enthusiasm carries you for a week or two, then ordinary life returns and the routine has nothing left to lean on. It’s not a personal failing — it’s the predictable arc of any habit built on inspiration rather than on cues and ease.

Q: How does anchoring a supplement to a meal help?
A: A meal is a cue you already encounter every day, in a stable context. Tie the supplement to it and you no longer have to remember or decide — the meal triggers the behavior for you. That’s how habits are built to last: through repeated, cue-linked action, not through daily acts of will.

Q: Does “designed to need less discipline” mean it does less for me?
A: No. It means the design is doing work that used to fall on you. A routine engineered around how people actually behave gets followed, and a supplement only helps if it’s taken consistently. Removing the need for willpower is the difference between a routine that lasts and one that quietly fades.

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

The products described are dietary supplements intended to support normal health and wellbeing as part of a food-first lifestyle; they are not intended to diagnose, treat, cure, or prevent any disease, and are not a substitute for a varied diet, a healthy lifestyle, or the advice of your physician.

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 creatine commonly used for?

Improving sleep and reducing stress
Supporting digestion and gut health
Building muscle and improving workout performance
Creatine is a popular sports nutrition supplement that helps support muscle performance and energy during exercise. Learn more.
Lowering blood pressure and supporting circulation

You may know creatine as a supplement for building muscle and improving workout performance. It’s one of the most popular products in sports nutrition, your body produces it on its own, and you take in more of it whenever you eat red meat or seafood. What you likely haven’t heard is that this same compound may play a role in how your immune system defends against cancer.

That possibility comes from a study conducted by researchers at the University of California, Los Angeles (UCLA) and published in iScience.1 Rather than examining creatine’s familiar effects on muscle, the researchers asked whether it helps a specialized set of immune cells do their job inside tumors, a setting where immune defenses often falter and treatments lose their effectiveness.

The answer turns out to hinge on something simple — energy — and on a set of immune cells most people have never heard of. To see why that matters, it helps to follow what the researchers observed inside the immune cells themselves.

Researchers Uncovered a New Role for Creatine Inside the Immune System

For the iScience study, researchers investigated whether creatine influences the activity of dendritic cells, the immune cells responsible for alerting and directing other immune defenders against cancer.2 The researchers focused on tumors because these environments often suppress immune function and make it harder for the body to recognize and attack abnormal cells.
Instead of studying creatine’s effects on muscles or exercise performance, the study examined whether this well-known energy compound helps immune cells maintain the energy required to function effectively inside tumors.

• The study showed that immune cells actively increased their demand for creatine — According to the researchers, dendritic cells inside tumors dramatically increased production of the creatine transporter, a specialized protein that pulls creatine into the cell. When researchers removed this transporter in laboratory mice, the immune cells struggled.
Survival dropped, activation weakened, and the cells lost much of their ability to communicate with cancer-fighting T cells. This finding highlights an important principle: immune defenses require energy just as muscles do. If immune cells can’t access the fuel they need, their ability to coordinate a response declines.
• Creatine supplementation strengthened several measures of immune performance — When researchers added creatine to dendritic cells, the cells survived longer and displayed stronger activation markers on their surfaces. These markers act like identification badges that signal the cells are ready for action.
Creatine-treated cells also produced higher amounts of important inflammatory messenger molecules. While inflammation often receives negative attention, these short-term signals are necessary for a strong immune response against threats. Think of them as emergency alerts that mobilize additional immune resources when danger appears.
• The biggest improvements appeared in the cells’ ability to activate cancer-fighting T cells — Researchers conducted experiments in which dendritic cells interacted directly with T cells. When creatine transport was absent, T cells multiplied less effectively, showed lower survival, and produced fewer immune-defense chemicals.
Those T cells also displayed weaker activation markers, suggesting a less effective response. The study found that creatine helped maintain the communication chain between different branches of the immune system. Much like a coach relaying instructions to players on a field, stronger dendritic cells delivered stronger signals that led to more active T cells.
• Tumor growth slowed when creatine supported the immune environment — In a mouse melanoma model, animals receiving creatine developed more active dendritic cells within their tumors and experienced reduced tumor growth compared to untreated animals. Researchers also found greater numbers of a highly effective subtype of dendritic cell known as cDC1 cells, which specialize in presenting tumor material to T cells.
Single-cell genetic analysis showed increased activity in genes linked to immune activation. At the same time, T cells inside tumors displayed stronger pathways associated with activation and cancer-fighting functions. The results suggest that improving the energy status of one immune cell type created a ripple effect throughout the broader immune response.
• The mechanism centered on adenosine triphosphate (ATP), the body’s cellular energy currency — The researchers discovered that dendritic cells lacking creatine transport had lower levels of creatine, phosphocreatine, and ATP, along with a reduced ability to maintain energy reserves. ATP functions like rechargeable cellular currency that powers nearly every biological task. Creatine acted as an energy buffer, helping cells store and rapidly regenerate ATP when demand increased.
Cells receiving creatine maintained higher ATP levels and lower levels of energy-stress markers. This stronger energy balance activated key immune signaling pathways, including the signaling pathway dendritic cells rely on to mature and switch on their immune-defense genes. Creatine helped immune cells keep their batteries charged. With more available energy, those cells stayed active longer, communicated more effectively, and mounted a stronger response against tumors.

While these findings provide important insight into how creatine influences immune function, the research was conducted in mouse models and in human cells in the lab, not in cancer patients. The human-cell results are encouraging, but clinical trials in people are still needed to know whether these effects improve real-world cancer outcomes.

Note: These findings come from animal and laboratory studies and do not show that taking creatine treats or prevents cancer. Results may not directly apply to human health.

Support Your Immune System’s Energy Supply

The research highlighted a simple but important principle: Immune cells need energy to do their job. When cellular energy falls, immune defenses become less effective. If your goal is to support healthy immune function and a strong foundation for long-term health, focus on the factors that improve cellular energy production rather than chasing quick fixes.

Think of this as a daily practice rather than a single intervention. Small actions repeated consistently create the biggest results. While the featured research focused on creatine within a cancer context, that’s certainly not the only or even primary reason for maintaining a steady creatine intake. It plays a role in many aspects of health, from supporting athletic performance and building muscle to boosting brain health and cognition.

This makes sense when you consider its role in energy production, as every cell and tissue in your body needs sufficient ATP for general function. To support healthy energy production for general health, consider the following suggestions:

1. Optimize your creatine intake from whole-food sources first — Creatine occurs naturally in foods such as grass fed beef and lamb. These foods provide not only creatine but also protein, minerals, and other nutrients that support immune function.

If your kidney function is normal, aim for roughly 0.6 to 0.8 grams of protein per pound (or 1.32 to 1.76 grams per kilogram) of ideal body weight, with about one-third coming from collagen-rich sources like slow-cooked meats or bone broth to support overall recovery and resilience.

2. Use creatine strategically and consistently — If you decide to supplement, choose creatine monohydrate. It remains the most studied form and has the strongest research record. Think of creatine as a rechargeable battery. The goal is to steadily maintain your reserves, not flood your system with massive amounts. Most studies that report benefits use consistent daily intake over weeks rather than aggressive loading phases or expensive supplement blends.
For most adults, 3 to 5 grams per day is sufficient. More is not necessarily better. Your muscles and tissues can only store a certain amount, and once those reserves are full, excess creatine is simply eliminated. Higher intakes are more likely to cause bloating, water retention, or digestive discomfort without providing additional benefits.
This step is especially important if you’re vegetarian or vegan because plant foods contain virtually no creatine. People who consume little or no animal protein often start with lower creatine stores and frequently experience the greatest improvements when those levels are restored. Maintaining healthy creatine levels supports energy production throughout the body, including the muscle, brain, and immune systems that depend on a steady supply of cellular fuel.
If you have reduced kidney function or chronic kidney disease, talk with your physician before supplementing. Creatine is converted into creatinine, which can raise the lab values used to assess kidney health, and it should be used under medical supervision in that context.
3. Build stronger cellular energy with enough healthy carbohydrates — Immune cells require energy, and energy production depends heavily on glucose metabolism. Most adults need about 250 grams of healthy carbohydrates daily, adjusting upward if you’re physically active. Focus on ripe fruit, root vegetables, and other easily digested carbohydrate sources that support cellular energy production. Better energy availability helps every system in your body, including your immune system.
4. Use sunlight to strengthen your body’s energy-producing machinery — Healthy immune responses depend on healthy mitochondria, the tiny structures that produce energy inside your cells. Regular sun exposure supports mitochondrial function, vitamin D production, nitric oxide release, and mitochondrial melatonin production. I recommend daily exposure to morning sunlight and sensible midday sun exposure while avoiding excessive sunburn.
If you have consumed large amounts of seed oils, and other sources of linoleic acid (LA), avoid intense midday sun exposure until you have reduced those foods for at least six months. This is because LA is a polyunsaturated fat that oxidizes easily, builds up in your skin, and increases your risk of skin damage.

5. Reduce the four major drains on cellular energy — Beyond creatine itself, the broader principle is supporting cellular energy. Excess LA from seed oils, endotoxins from poor gut health, xenoestrogens from plastics, and excessive electromagnetic field (EMF) exposure all interfere with cellular energy production.

Start with the easiest win: eliminate seed oils, including soybean, corn, sunflower, safflower, canola, and cottonseed oils, and processed foods that contain them. Replace them with traditional fats such as grass fed butter, ghee, and tallow. Every reduction in these energy-draining influences helps create a healthier environment for your immune cells.

FAQs About Creatine in Cancer Immune Defense

Q: What did the UCLA study discover about creatine and the immune system?
A: Researchers found that creatine helps fuel dendritic cells, which are immune cells that coordinate the body’s response to threats. When these cells had access to creatine, they survived longer, became more active, and were better able to activate cancer-fighting T cells. The findings suggest that creatine supports important immune functions beyond its well-known role in muscle performance.

Q: How did creatine affect tumor growth in the study?
A: In a mouse melanoma model, creatine supplementation was associated with slower tumor growth and a stronger immune presence inside tumors. Researchers observed more active dendritic cells, increased activity in genes linked to immune defense, and stronger T-cell responses, suggesting that improved cellular energy helped strengthen the overall immune attack on cancer cells.

Q: Why is ATP important for immune function?
A: ATP is the primary energy source used by cells. The study found that creatine helped dendritic cells maintain higher ATP levels, allowing them to stay active and communicate more effectively with other immune cells. Without adequate ATP, immune cells struggled to perform the energy-intensive tasks required for a strong immune response.

Q: Who might benefit most from paying attention to creatine intake?
A: People who consume little or no animal protein often have lower creatine stores because plant foods contain virtually no creatine. Vegetarians and vegans frequently start with lower levels and may experience greater benefits when creatine stores are replenished. Adequate creatine intake also supports energy production in muscle, brain, and immune tissues.

Q: Does this research prove that creatine prevents or treats cancer?
A: No. The study was conducted primarily in laboratory experiments and animal models rather than in cancer patients. The findings reveal an important biological mechanism showing how creatine supports immune-cell activity, but human clinical trials are needed to determine whether these effects translate into improved cancer outcomes in people.

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.

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What are dihydropyridine calcium-channel blockers (DCCBs) commonly prescribed to treat?

High blood pressure
Dihydropyridine calcium-channel blockers (DCCBs), such as amlodipine, are commonly used to lower blood pressure by relaxing blood vessels. Learn more.
High blood sugar
High cholesterol
Chronic inflammation

Artificial sweeteners are often promoted as smart swaps for sugar, yet they carry consequences that reach far beyond taste or calorie count. What looks like a harmless choice in your morning coffee or afternoon soda interferes with the very systems that keep your brain sharp and resilient.

Cognitive decline is not just about forgetting names or misplacing your keys. It starts with subtle changes in memory, language, and focus that erode your ability to stay independent. Over time, these problems build into serious conditions like dementia, where everyday decision-making and self-care become overwhelming.

Artificial sweeteners such as aspartame, saccharin, and erythritol are hidden in flavored drinks, protein shakes, yogurts, and “diet” desserts. Once you understand how frequently you encounter them, it becomes clear why so many people are unknowingly adding stress to their brain. Choosing these products means you’re exposing your nervous system to chemicals that alter communication between brain cells and strain your gut-brain connection.

Your daily choices about what to eat and drink are not small — they directly influence how well your memory, focus, and language skills hold up as you age. That’s why it’s worth examining the latest research on artificial sweeteners and the surprising way they accelerate brain aging.

Artificial Sweeteners Accelerate Cognitive Decline

Researchers followed 12,772 adults in Brazil for an average of eight years to determine how artificial sweeteners affect thinking and memory skills.1 Participants were civil servants, all age 35 or older at baseline, and they completed detailed food questionnaires and repeated cognitive testing. The study measured consumption of seven common artificial and no- or low-calorie sweeteners.

• Middle-aged adults were the most affected — The average age of participants was 52, and more than half were women. When researchers divided people into groups based on how much of alternative sweeteners they consumed, they found those in the highest group experienced a much faster decline in overall cognition compared to the lowest group. Importantly, this accelerated decline was strongest in people younger than 60, suggesting the risk is magnified during midlife.

• Faster brain aging showed up in specific thinking skills — People in the highest consumption group showed sharp declines in verbal fluency (the ability to think of and say words quickly) and memory. The researchers calculated that this decline was the equivalent of 1.6 years of extra aging in brain function. Even those in the middle consumption group experienced the equivalent of 1.3 years of aging over the study period, which means the risks weren’t limited only to heavy users.

• Diabetes increased the risks even further — Participants living with diabetes were especially vulnerable to the harms of artificial sweeteners. For them, memory and global cognition dropped more rapidly when intake was higher. This is important because people with diabetes are already encouraged to use artificial sweeteners as sugar substitutes, which could worsen long-term brain health. The results suggest that artificial sweeteners are far from a safe alternative for this group.

• Different sweeteners showed different levels of harm — When the researchers analyzed individual sweeteners, they found aspartame, saccharin, acesulfame-K, erythritol, sorbitol, and xylitol were each associated with a faster decline in cognition. Tagatose, however, did not show a clear link to cognitive decline. This suggests not all sugar substitutes carry the same level of risk, but most commonly used artificial sweeteners did.

• More sweetener intake was tied to faster decline over time — Participants were tested at the beginning of the study, again several years later, and at the end of the eight-year period. Those in the lowest group consumed about 20 milligrams (mg) per day, while the highest group averaged 191 mg daily — the equivalent of just one can of diet soda for aspartame.2

People in the higher intake groups showed a quicker drop in memory, verbal fluency, and processing speed compared to lighter users. Importantly, this link was observed in participants younger than 60, but not in older adults.

Artificial Sweeteners Interfere with Brain Signaling and Gut Health

Several of the compounds studied, including aspartame and saccharin, have been shown in other research to affect neurotransmitter activity.3,4 Neurotransmitters are your brain’s chemical messengers, controlling everything from memory formation to verbal processing. Changes in these pathways could explain why verbal fluency and memory were most affected in the study population.

• Metabolic strain is another likely mechanism — Artificial sweeteners are often used by people with diabetes or those trying to manage blood sugar. However, they disrupt your body’s normal insulin response and alter how cells use energy, which increases oxidative stress and harms neurons.5 This is especially concerning because neurons rely on stable energy supply to maintain communication networks required for memory and thinking skills.

• Researchers found brain effects even after accounting for other risks — The team adjusted the data for age, sex, high blood pressure, cardiovascular disease, and other lifestyle habits. Even after these adjustments, the association between sweetener intake and cognitive decline remained strong, showing that the results are not easily explained by other factors. This highlights that the sweeteners themselves are an independent factor in brain health.

• Aspartame harms the good bacteria in your gut — Aspartame disrupts your gut microbiome by depleting beneficial bacteria, weakening your natural defenses, and creating conditions that favor tumor growth.6 These bacteria normally produce protective compounds that help keep your brain and immune system strong. When their numbers drop, harmful microbes gain the upper hand, leaving your body more vulnerable to disease.

• Artificial sweeteners expose your brain to compounds that accelerate cognitive decline — The featured study shows the impact is measurable, long-term, and stronger in people already vulnerable, such as those with diabetes.7 Choosing natural sweeteners allows you to enjoy sweetness while avoiding the brain-aging effects documented in this research.

Simple Steps to Protect Your Brain from Artificial Sweeteners

If you’ve been reaching for diet soda, flavored water, or sugar-free desserts thinking they’re a better option than sugar, you now know they speed up brain aging instead of protecting your health. There are clear steps you can take right now to remove the risk and support your brain’s energy and memory systems. These changes are simple but powerful.

1. Cut out artificial sweeteners completely — Your first step is to stop using products that contain artificial sweeteners like aspartame, sucralose, saccharin, acesulfame-K, and neotame. Look at your flavored water, gum, yogurt, protein shakes, or “diet” snacks. If the label lists any of these names, replace it with something else. Removing these chemicals stops the constant assault on your brain’s memory and verbal fluency.

2. Replace sweetness with whole food alternatives — Instead of “zero calorie” drinks and treats, use real food sources of sweetness. Whole fruits, raw honey, or small amounts of maple syrup provide natural sugars that your body recognizes and uses for fuel.

Fresh fruit makes an easy dessert or snack, honey works well to lightly sweeten tea or drizzle over raw grass fed yogurt, and maple syrup can be added to organic oatmeal. These natural options not only satisfy cravings but also deliver vitamins, minerals, and plant compounds that support steady energy for your brain and body.

3. Support your gut to protect your brain — Your gut and brain communicate constantly. Artificial sweeteners disrupt this connection by altering your gut bacteria. Focus on eating simple, digestible carbs such as ripe fruits, white rice, and root vegetables — once your gut is healed enough to handle them. If your gut is still fragile, focus on fruit and white rice first to fuel your brain without feeding harmful bacteria. Protecting your gut environment directly improves how your brain functions.

4. Choose safer natural sweeteners at home — If you crave something sweet, prepare it yourself with ingredients that support health instead of harming it. Natural stevia from the whole plant, Luo Han Guo (also called monk fruit), and pure dextrose from clean cane sugar are reliable options. Using these alternatives allows you to enjoy sweetness without exposing your brain to the decline linked to artificial sweeteners.

5. Focus on energy, not restriction — Instead of thinking about what you’re giving up, pay attention to what you’re gaining — better focus, stronger recall, and sharper thinking. If you’ve been relying on low-calorie products, it’s time to fuel your body and brain with the right kind of carbohydrates and proteins.

Around 250 grams of carbs each day, combined with quality protein and fats like grass fed butter or ghee, provide the foundation for steady brain energy. Think of this not as a diet but as an upgrade to how your brain runs.

FAQs About Artificial Sweeteners and Your Brain

Q: How do artificial sweeteners affect brain health?
A: Artificial sweeteners speed up cognitive decline. A large study found that people who consumed the highest amounts experienced the equivalent of 1.6 extra years of brain aging in memory, verbal fluency, and overall thinking skills.8

Q: Who is most at risk from artificial sweeteners?
A: Middle-aged adults under 60 showed the strongest link between high intake and faster cognitive decline. People with diabetes were also more vulnerable, with sharper drops in memory and global cognition compared to those without diabetes.

Q: What can you use instead of artificial sweeteners?
A: Safer alternatives include whole fruits, raw honey, maple syrup, natural stevia in its plant form, Luo Han Guo (monk fruit), and pure dextrose from clean cane sugar. These options provide sweetness without the brain-aging effects linked to artificial sweeteners.

Q: What steps protect your brain if you’ve been using artificial sweeteners?
A: Eliminate products with artificial sweeteners, switch to whole food sweeteners, support your gut health, try natural substitutes at home, and focus on fueling your body with the right balance of carbs, protein, and healthy fats. These steps restore energy production and protect long-term brain function.

Americans are more stressed than ever — and your gut is likely part of the reason. It’s easy to think of stress as something that lives in your head, but your gut plays a major role in how well, or how poorly, you handle it. When your internal ecosystem is out of balance, even small stressors hit harder. You might find yourself snapping more easily, not sleeping well, or feeling foggy and inflamed without knowing why.

What’s going on inside your gut isn’t just about digestion. It shapes how your body regulates inflammation, hormones, and even your nervous system. And one of the most important factors influencing your gut health is what you eat. The quality of your daily meals affects which microbes thrive, which ones die off, and how effectively your gut communicates with your brain.

If your stress tolerance has dropped or your moods feel unpredictable, consider if your gut is working against you. Fortunately, research is now uncovering which foods help restore microbial balance and which gut bacteria are most closely tied to resilience, calm, and mental clarity. Let’s look at what the latest science reveals about this gut-stress connection and how your food choices could be the missing piece.

High Stress? Your Gut Bacteria Could Be to Blame

A study published in Clinical Nutrition ESPEN analyzed 1,268 healthy Japanese adults to explore how diet, gut microbiota, and stress are interconnected.1 The researchers wanted to understand if the quality of what you eat — not just individual nutrients — has the power to reshape your internal stress response. Using stress questionnaires, food frequency data, and stool sample analysis, the team linked what people ate to what was living in their gut, and how their bodies responded to daily stress.

• Participants were healthy adults, but their stress and diets varied widely — The population included individuals aged 20 to 80, all considered healthy by conventional standards. But when grouped by stress response scores, big differences emerged in gut composition and diet quality.

Those with the highest stress levels consistently ate fewer vegetables and pulses and scored lower on a metric called the Nutrient Rich Food Index 9.3 (NRF9.3). This index rewards diets that are rich in fiber, vitamins, and minerals — and penalizes those with excess sugar and fat.

• The highest-stress group had the worst diet scores and weakest gut defenses — People with the highest stress response had much lower NRF9.3 scores and significantly less Lachnospira, a genus of bacteria linked to short-chain fatty acid (SCFA) production and reduced inflammation. They also had less Ruminococcus_E, another SCFA-producing genus, and more Collinsella, a bacterial genus linked to anxiety and chronic stress.

However, from the perspective of the late Dr. Ray Peat, a biologist and pioneer in bioenergetic medicine and human metabolism, and bioenergetic researcher Georgi Dinkov, whose work is heavily influenced by Peat’s principles, this bacterial profile is less of a cause and more of a consequence of systemic stress.

Rather than trying to boost Lachnospira by eating more fiber, Peat and Dinkov focus on restoring balance in your body — like improving thyroid function and digestion — so harmful bacteria don’t have the chance to grow in the first place.

Beneficial Bacterial Help Your Gut Make Anti-Inflammatory Compounds

Lachnospira ferments fibers and resistant starches to produce SCFAs like butyrate and acetate. These substances feed the cells lining your colon, seal up leaky gut junctions, reduce immune system overactivation, and calm inflammation, especially the kind that worsens under chronic stress.

• SCFAs help calm your brain and gut at the same time — SCFAs don’t just work locally. They travel through your bloodstream, reaching your brain and gut-brain signaling centers. They help regulate your vagus nerve, influence feel-good neurotransmitters like dopamine, and reduce overactivation of the HPA axis — your stress command center.

This process only works well if your gut is already healthy. In a damaged gut, the same fiber fermentation increases toxins, triggers inflammation, and sends the wrong signals to your nervous system — making stress worse, not better. Peat and Dinkov recommend focusing on healing your body first with supportive foods instead of feeding gut bacteria.

• The foods that mattered most weren’t exotic, just overlooked — Researchers identified three key foods that separated low-stress and high-stress individuals: natto, tomatoes, and green peppers. People with the lowest stress scores consistently ate more of these foods, which boosted their NRF9.3 scores and were linked directly to increases in Lachnospira. Natto had the strongest effect, followed by tomatoes and green peppers.

Beans Reprogram Your Gut to Fight Inflammation and Hunger

A 2023 narrative review published in Obesity Reviews looked at how common beans — especially navy, black, and pinto beans — affect your gut microbiome, hunger hormones, and chronic inflammation in both animal and human studies.2 Researchers focused on how beans work inside your gut to change appetite signals and reduce markers linked to metabolic disease.

• Bean-fed animals had better gut bacteria, more gut-friendly compounds, and less inflammation — In multiple mouse studies, adding beans to a high-fat diet boosted microbial diversity and raised populations of beneficial species like Akkermansia and Prevotella. These microbes are known for producing SCFAs, which protect your gut lining and help control inflammation. At the same time, harmful bacteria that thrive on junk food diets dropped in abundance.

• SCFAs increased significantly after bean consumption — SCFAs like acetate, propionate, and butyrate surged in the intestines of animals eating beans. These compounds support colon cells, lower gut permeability, and improve hormone signaling between your gut and brain.

• Appetite hormones shifted in a favorable direction — Mice eating navy or black beans had lower ghrelin (the hunger hormone) and better glucagon-like peptide-1 (GLP-1) responses, which helps you feel full sooner.

Inflammatory markers also dropped across the board. Animals on bean-rich diets had lower levels of inflammatory proteins. Their fat tissues also had less immune cell infiltration, which usually signals metabolic distress. The result: less inflammation, especially in the tissues most affected by obesity.

While these changes might look helpful on the surface, Peat warns they often show up in people with low metabolism and high stress. For example, drugs that raise GLP-1 slow digestion and lower thyroid function. From this view, the effects of beans may not mean your body is healing — they may just be dampening your appetite and stress signals.

• Human data shows similar gut and inflammation benefits — A small study giving 130 grams (g) a day — about 3/4 cup — of pinto beans increased a beneficial SCFA-producing bacteria and led to higher SCFA levels in stool.

Another trial with 35 g per day of navy bean powder in overweight colorectal cancer survivors improved overall gut diversity and decreased a bacterium linked to inflammation. Participants in a mixed-pulse diet trial also had reduced levels of two blood markers tied to chronic disease.

• Beans work by feeding good bacteria and improving gut signaling — Beans are rich in prebiotic fibers and polyphenols — compounds that microbes ferment into SCFAs. These SCFAs strengthen your gut wall, calm immune overactivation, and enhance the release of hormones that tell your brain you’re full.

While some people tolerate small amounts of pressure-cooked beans, resistant starches and fermentable oligosaccharides in beans often increase intestinal gas, raise serotonin, and generate LPS in individuals with sluggish digestion or low bile flow. In that context, beans don’t “heal” your microbiome — they overstimulate it.

For sensitive individuals, Peat and Dinkov recommend alternatives like gelatin, saturated fat, orange juice with salt, and grated raw carrot to nourish the gut barrier without bacterial fermentation.

Diet and the Microbiota-Gut-Brain Axis Sow the Seeds of Good Mental Health

A related review in Advances in Nutrition emphasizes that your gut microbes aren’t just passive bystanders.3 They help regulate inflammation, hormone release, and neurotransmitter production in response to what you eat. These microbes act as middlemen, translating your food choices into signals that either support or sabotage your mental well-being.

• Animal studies show nutrient-driven gut alterations influence behavior and neurochemistry — High-fiber diets or supplementation with prebiotics and fermented foods altered gut bacterial composition and increased beneficial compounds like SCFAs. These shifts boosted brain-derived neurotrophic factor (BDNF), which supports brain plasticity, while lowering inflammation in areas like the hippocampus, helping reduce anxiety and improve memory.

While gut integrity impacts your brain, reducing endotoxin is key to lowering brain inflammation. This again highlights why high-fiber diets often backfire, leading to increased endotoxin unless your gut is healthy. Rather than promoting fermentation to increase BDNF, Peat would recommend reducing endotoxin to protect your brain.

• Human evidence supports the link between stress and your gut — Preliminary trials show that probiotic and prebiotic intake lower cortisol and improve mood and stress perception, particularly in people under chronic stress. However, many of these studies are small, and few have established whether gut microbiota changes are truly driving the improvements or merely occurring alongside them.

• Individual differences matter — What works for one person doesn’t always work for another, because people differ widely in their baseline gut profiles. For example, someone with low microbial diversity could see big changes from a Mediterranean-style diet, while someone with more balanced flora might need more targeted interventions to see mental health benefits.

• Microbiota as mediator vs. moderator — The authors explain two models: in some cases, microbes directly mediate your diet’s impact on your brain, meaning no change happens without them; in others, they moderate the effects — shaping how strongly your body reacts to a food or nutrient. In germ-free mice, for example, certain diets fail to improve behavior at all, proving the microbiota are a required link in that chain.

• Precision nutrition and multi-omics are the future — The review calls for large-scale studies that integrate diet records, gut microbiota analysis, blood metabolite data, and brain imaging to understand how personalized food strategies could support mental health. This could lead to individualized diet prescriptions based on your microbiome’s specific makeup and how it interacts with your nervous system.

How to Rebuild a Healthier Gut and Lower Your Stress Response

If you’re stuck in stress mode and feel bloated, foggy, or inflamed, your gut is a large part of the problem — and the solution. What you eat doesn’t just feed you. It feeds the trillions of microbes inside you, and they play a direct role in how well your body manages stress.

But if your gut is damaged or overrun by the wrong bacteria, even healthy foods backfire. The goal is to rebuild your internal terrain so that the right microbes thrive, inflammation quiets down, and your stress response becomes more resilient. Here’s how I recommend you start taking back control:

1. Start feeding the right bacteria — but don’t rush the fiber — If you’ve got gas, bloating, food intolerances, or loose stools, your gut isn’t just irritated — it’s imbalanced. One of the key stress-fighting bacteria, Lachnospira, thrives on fermentable fibers. But here’s the paradox: fiber is essential, but eating too much too soon when your gut is already inflamed will make symptoms worse.

Start with gentle foods like white rice and fruit. Once your gut stabilizes, slowly add in root vegetables, then green bananas, cooked-and-cooled potatoes, and other fiber-rich options. Only after bowel movements normalize and endotoxin load drops should you consider experimenting with high-fiber foods — and even then, pay attention to your body and back off if bloating or other digestive effects occur.

2. Add foods that grow your gut’s protective shield — Your gut lining has a protective mucus layer, and the bacteria Akkermansia muciniphila helps keep it strong. This species supports the growth of butyrate producers by fortifying your gut’s first line of defense. However, promoting Akkermansia at the expense of metabolic function offers a short-term win with long-term costs.

To nurture it while also supporting your metabolic health, cut out inflammatory vegetable oils, which are high in linoleic acid (LA), and processed foods that break down your barrier, and include polyphenol-rich options like pomegranate, cranberries, and green tea.

3. Upgrade your diet quality — think nutrient density, not calorie counts — The Japanese study found that higher nutrition scores correlated with lower stress levels and better gut balance.4 Your goal isn’t just fiber. It’s total nourishment. That means regularly eating the three foods that stood out in the study: natto (fermented soybeans), tomatoes, and green peppers.

If you’ve never tried natto, it’s sticky and strong-smelling, but packed with fiber, vitamin K2, and resistant starches that feed beneficial microbes. Tomatoes are rich in lycopene and polyphenols, and green peppers offer prebiotic fibers and antioxidants. Rotate these into your meals several times a week.

4. Reset the internal conditions that let harmful microbes take over — Bacterial overgrowth doesn’t just happen — it’s allowed by the terrain. Pathogens thrive when your environment favors them. Factors like estrogen-dominant environments, excess iron, low thyroid function, and constant exposure to vegetable oils and xenoestrogens from plastics create the perfect breeding ground.

These factors weaken your defenses and invite invaders. To create lasting change, start by cleaning up your environment, balancing your iron and hormones, and supporting your thyroid. A healthy environment makes it harder for pathogens to thrive. This is Peat’s terrain theory in action. Rather than “fighting” bad microbes, you outcompete them by restoring metabolic function. The cleaner your environment, the less food you need to fight with.

5. Go slow and track your results — This process is about healing, not rushing. Use a food and symptom journal to track what works and what doesn’t. Look for signs like less bloating, more regular bowel movements, deeper sleep, and a calmer mood. These are your green lights. The more your system calms, the more you’ll be able to reintroduce higher-fiber foods without discomfort. Long term, the goal is microbial diversity and a strong gut lining, but you have to earn it by going at your body’s pace.

When your microbiome is balanced, your brain feels clearer, your stress responses become less extreme, and your whole system works more efficiently. You’re not broken. You’re just out of balance. And balance can be rebuilt, one smart step at a time.

FAQs About Gut Bacteria and Stress

Q: How do gut bacteria affect stress levels?

A: Certain gut bacteria help produce SCFAs, which reduce inflammation, seal your gut lining, and regulate brain chemistry. People with more Lachnospira and other SCFA-producing bacteria show lower stress levels and better emotional resilience. However, making too many SCFAs can give the illusion of healing while actually raising stress chemicals like serotonin and cortisol. In this view, a healthy gut comes from fixing your metabolism — not by trying to change your gut bacteria directly.

Q: Which foods help grow stress-lowering gut bacteria?

A: Foods high in fermentable fiber and polyphenols, such as natto, tomatoes, green peppers, beans, and root vegetables, help feed beneficial microbes like Lachnospira and Akkermansia, but only if your gut is already healthy. If your digestion is compromised, these foods trigger gas, bloating, and stress reactions until your gut barrier is restored.

Q: What is the fiber paradox, and why does it matter?

A: The fiber paradox refers to the fact that while fiber is essential for feeding good bacteria, people with gut imbalances feel worse if they eat too much too soon. Starting slowly with easily digestible carbs like fruit and white rice and gradually increasing fiber allows your gut to heal first.

Q: How do beans improve gut health and reduce inflammation?

A: Beans are rich in prebiotic fibers and polyphenols that fuel SCFA production. In a healthy gut, this supports colon health, improves hunger signals, reduces inflammation, and helps regulate stress-related hormones and immune activity in your gut. However, in an unhealthy gut, beans raise endotoxin and suppress thyroid function. Only eat beans if your gut is healthy and digestion is robust — and even then, eat pressure-cooked beans only.

Q: What lifestyle factors make gut imbalances and stress worse?

A: Diets high in vegetable oils, refined sugar, and processed foods promote harmful bacteria. Environmental factors like hormone imbalance, excess iron, and exposure to xenoestrogens in plastics also weaken gut defenses. Cleaning up these variables helps restore microbial balance and stress resilience.

Small intestinal bacterial overgrowth, or SIBO, is more than just a gut imbalance — it’s a sign your digestive system has lost its rhythm. While most people think of it as a bacterial problem, it’s really a deeper issue with energy, motility and terrain. In other words, SIBO shows up when your gut slows down, your defenses weaken and bacteria migrate into areas they don’t belong.

The symptoms, like bloating, gas, constipation or diarrhea, and even food intolerance, are frustrating enough. But what’s worse is how often the condition gets misdiagnosed, mismanaged or misunderstood altogether.

Too often, the focus is on wiping out bacteria rather than asking why those bacteria took over in the first place. Antibiotics are handed out as first-line treatment, yet they often leave patients feeling worse — triggering yeast overgrowth and further disrupting the gut ecosystem.

What many practitioners miss is that SIBO tends to develop in people with low stomach acid, sluggish gut motility or thyroid-related slowdowns that let things stagnate. Add metabolic stress, iron overload or hormone imbalances to the mix, and you’re dealing with a perfect storm, not just of bacteria but of terrain gone haywire. That’s why short-term strategies don’t work. They treat symptoms while the root causes remain.

A real-world study out of Valencia, Spain, offers something different.1 Instead of relying solely on lab markers, the researchers asked a better question: How do people actually feel after treatment? And that’s where the answers start to get interesting.

Recognizing SIBO as a Real, Treatable Condition Improves Outcomes

A clinical study published in Nutrients examined how a comprehensive treatment approach improved the lives of people diagnosed with SIBO.2 The researchers focused on whether patients felt better after 90 days, not just whether their lab tests changed.
They assessed both breath test results and self-reported health scores. Breath tests are commonly used to detect abnormal gas levels, like hydrogen and methane, that signal bacterial overgrowth in the small intestine. This was one of the largest studies of its kind, specifically analyzing real-life patient experiences.

• The study followed adults with confirmed SIBO — The 179 patients had a confirmed diagnosis of hydrogen- or methane-dominant SIBO. Most were middle-aged (average age 45.7) and 82.7% were women. All participants received tailored treatment involving medication, herbs, probiotics, and a nutritionist-guided diet. The researchers wanted to see how this multi-layered approach impacted not just test outcomes, but people’s day-to-day quality of life.

• Over 70% of patients felt better by the end of treatment — More than 7 in 10 patients — 72.6% — reported significant improvements in symptoms after three months. In contrast, only 41.3% had “normalized” breath test results. People felt relief from bloating, pain, stool issues and digestive distress even if gas levels remained elevated.

• Changes were seen quickly and continued to improve over time — Many patients started feeling better within 30 days, but the most consistent progress happened between 30 and 90 days. This suggests that healing your gut and rebalancing your microbiome takes time. It also reinforces the need for consistent follow-through. People who stuck with the protocol saw the greatest improvements by the three-month mark.

• SIBO with constipation showed slightly stronger symptom relief — People with methane-type SIBO, which is often associated with constipation, tended to respond slightly better than those with hydrogen-dominant SIBO, which usually causes diarrhea and gas.

While both groups improved, 73.2% of methane SIBO patients saw relief, compared to 71.4% in the hydrogen group. The treatment’s ability to restore more regular bowel patterns played a major role in this improvement.

Multi-Pronged Strategies Improved Digestion, Mood, and Resilience

Patients reported better emotional balance, mental clarity, sleep quality and energy following treatment. Key gut symptoms, including bloating, constipation, diarrhea, urgency, and post-meal fullness also improved, and better function in areas like mobility, self-care, and participation in normal daily activities was reported. Stool quality improved as well. Many shifted from hard or loose stools to more normal stool consistency by day 90.

• Higher initial self-rated health predicted better outcomes — Patients who believed they were in better health at the start had a much higher chance of seeing significant symptom improvement. That finding speaks to the power of self-perception and mindset in recovery. When you trust your body and feel capable of getting better, your odds go up.

• SIBO treatment linked to brain and mood improvements — People often report better mood and fewer symptoms of anxiety and depression after SIBO treatment. This is tied to the gut-brain axis, the communication highway between your gut and brain. Inflammation, poor motility and stress disrupt this pathway, so restoring gut health naturally supports mental clarity and emotional stability.

• Treatments likely worked by restoring gut barrier and microbial balance — Researchers believe that using glutamine, probiotics, and prebiotics supported gut barrier integrity and reduced inflammation. Herbal antimicrobials (like berberine, peppermint, and oregano oil) targeted overgrowth without destroying beneficial species. These mechanisms help reshape the ecosystem of your small intestine, allowing good bacteria to thrive and limiting the survival of problematic ones.

• The gut’s healing process took time and multiple strategies — This wasn’t a one-size-fits-all or quick-fix model. Each patient received guidance from a nutritionist, along with clinical supervision. Diet was customized, herbs were chosen based on gas type and reintroduction phases were paced gradually. This multi-layered approach allowed for better tolerance and more lasting results.

Why Cutting Carbs and Using Antibiotics Often Make SIBO Worse

If you’ve been told to cut carbs to control bacterial overgrowth, it’s time to rethink that approach. Starving your gut reduces symptoms for a while, but it won’t fix the problem — and in the long run, it will slow your metabolism, impair gut motility and shrink your food tolerance. That’s not healing. That’s trading one form of dysfunction for another.

• SIBO isn’t caused by eating carbs — It’s a metabolic breakdown. When your digestive system is underpowered — when your thyroid is sluggish, your stomach acid is low or your gut motility is compromised — bacteria that should stay in your colon creep into your small intestine and multiply. That’s when symptoms like bloating, discomfort, gas and constipation take over.

• Antibiotics aren’t the solution — If you’ve already been through a round of antibiotics like rifaximin for SIBO, you could be dealing with something else, too — candida overgrowth. Western medicine often overlooks the fact that antibiotics don’t just kill bacteria. They disrupt your entire gut ecosystem.

Yeast like Candida albicans are left behind, untouched and ready to spread. They move fast. And when you’ve cut carbs in the hopes of “starving” the bad bacteria, candida doesn’t die. It adapts. It transforms into an invasive, aggressive form that damages your gut lining and creates a second layer of dysfunction — fungal overgrowth layered on top of bacterial imbalance.

How to Fix SIBO Naturally

To truly recover, you need to address both problems — SIBO and candida overgrowth — at the same time, and you need to start by rebuilding your metabolism and immune defenses. Here’s where I would start:

1. Avoid fiber and complex carbs until your symptoms ease — If you have SIBO, your gut is often overwhelmed by bacteria that have migrated into your small intestine, where they don’t belong. Many healthy foods — especially those rich in fiber or starch — become problematic in this state. That’s because they ferment too quickly or aren’t broken down properly, which feeds the overgrowth and leads to gas, bloating, discomfort and inflammation.

Different types of carbs affect your gut differently. Soluble fibers, for instance, are typically tolerated better than insoluble ones. Soluble fiber ferments more slowly, giving your digestive system more time to process it. But if you’re dealing with active symptoms, even these make things worse. Insoluble fibers are often especially irritating — they bulk up stool and speed up digestion, which exacerbates symptoms like diarrhea, urgency or cramping.

Your best strategy early on is to limit trigger foods. Focus on those that are easiest to digest and least likely to fuel bacterial overgrowth. This includes soft fruits without skins and well-cooked white rice.

Avoid beans, raw greens, whole grains, and fibrous fruits or vegetables until your system stabilizes. As your digestion improves, you’ll gradually regain tolerance. The key is listening to your body and expanding your diet slowly. Move from simple, low-fiber carbs to more fibrous whole foods once your gut is calm.

2. Feed your gut cells without feeding harmful bacteria — Your small intestine is designed for absorption — not fermentation. But when bacteria overgrow in this area, even nutritious carbs become fuel for the wrong microbes. That’s why choosing the right carbohydrates is essential, especially during early recovery.

Simple carbs that are rapidly absorbed in your upper intestine tend to be better tolerated by those with SIBO. These carbs don’t reach your colon, so they’re less likely to feed harmful oxygen-tolerant bacteria that produce toxins like endotoxin. In fact, by avoiding fermentation, they help lower endotoxin exposure and reduce inflammation throughout your gut lining.

At the same time, this approach gives your cells a clean source of energy to repair tissue and improve motility. Start with carbs like white rice, fruit juices with pulp or whole fruits. Once your symptoms improve and your digestion stabilizes, begin introducing gentle complex carbs like well-cooked squash or peeled potatoes. From there, gradually reintroduce more fibrous options like root vegetables, and finally beans and whole grains.

The goal isn’t to restrict carbohydrates forever. It’s to give your gut time to rebuild and your mitochondria the energy they need to repair digestive tissues. As your gut health improves, your ability to digest and benefit from more complex carbs will return — without flaring symptoms or fueling overgrowth. Ultimately, instead of restricting carbs, focus on eating 250 grams of the right types daily.

3. Address the terrain that allowed overgrowth in the first place — SIBO and candida don’t happen in a vacuum. They show up when your body becomes a safe haven for them. Candida, for instance, thrives in estrogen-dominant environments. It also feeds on excess iron.

Balancing hormones, avoiding xenoestrogens in microplastics and keeping your iron levels in check are all part of this healing equation. And if your thyroid is underactive, everything — from motility to immune defense — slows down. That’s why I often recommend checking thyroid function if you’ve been stuck in the SIBO-candida loop.

4. Monitor your body temperature to keep candida in check — Low body temperature gives candida exactly what it wants — a cooler, more hospitable environment where it can spread. Fungal pathogens like candida thrive when your temperature dips below normal while higher body temperatures help suppress fungal growth and keep your internal defenses strong. If your daytime temp consistently falls below 98.6 degrees F, you’re giving candida room to take hold and multiply.

5. Stop treating symptoms in isolation and start rebuilding your inner environment — You don’t need a low-carb protocol or a long course of antibiotics. You need a metabolic foundation strong enough to resist bacterial and fungal overgrowth in the first place.

That means fueling consistently with the right healthy carbs, avoiding environmental chemicals, lowering stress and giving your body the raw materials it needs to keep your gut ecosystem stable. Once your terrain improves, the bad bacteria stop thriving — without you needing to attack them head-on with antibiotics.

This approach is slow, steady and rooted in repair, not restriction. If you’ve been caught in the cycle of antibiotics, antimicrobials and elimination diets, it’s time to shift your strategy. You’re not broken; you’re just under-fueled and over-stressed. Start by fixing your metabolism, and your gut will follow.

If you’re dealing with both SIBO and candida, the solution isn’t to pick one to battle — it’s to shift the terrain they’re living in. A well-fed, high-functioning gut doesn’t allow overgrowth to take hold. That’s the real goal here. And it’s absolutely within your reach.

FAQs About SIBO

Q: What is SIBO and why is it often misdiagnosed?

A: SIBO happens when bacteria that belong in your colon migrate into your small intestine. This leads to bloating, gas, abdominal pain and irregular bowel habits like constipation or diarrhea. It’s frequently misdiagnosed because many of its symptoms mimic other digestive disorders, and standard breath tests often give inconsistent results.

Many doctors treat it as a simple bacterial problem, when in reality, it’s a sign of metabolic and digestive dysfunction that allows overgrowth to happen in the first place.

Q: What makes this study’s findings so important for people with SIBO?

A: The Nutrients study redefines what success looks like in SIBO treatment. Instead of chasing perfect lab results, it focused on whether people actually felt better after individualized treatment, including diet changes, herbs, probiotics, and medication. And they did — more than 70% of participants experienced relief from bloating, stool issues, fatigue, and digestive distress, even if their breath tests still showed elevated gas.

Q: Why do antibiotics and low-carb diets often make SIBO worse?

A: Antibiotics like rifaximin temporarily reduce bacterial overgrowth but often cause collateral damage by disrupting your gut’s microbial balance. This opens the door for fungal pathogens like candida to take over. Meanwhile, cutting carbs in an effort to “starve” bacteria weakens your metabolism, slows gut motility and stresses your immune defenses — conditions that make both SIBO and candida worse, not better.

Q: What’s the link between SIBO and candida overgrowth?

A: When antibiotics knock out bacteria, yeast like Candida albicans thrive in the disrupted environment. Candida becomes more aggressive under stress, especially when carbs are restricted. It shifts into an invasive form that damages your gut lining and worsens inflammation. Many people unknowingly end up with both SIBO and candida — two overlapping imbalances that require a dual approach to resolve.

Q: What’s the best way to heal from SIBO and candida overgrowth long-term?

A: Lasting recovery starts by restoring your metabolic health and internal terrain. The goal isn’t to fight microbes — it’s to make your gut a place where overgrowth can’t take hold. That includes:

• Supporting gut repair with simple carbs like whole fruit and white rice before gradually reintroducing more fiber

• Avoiding hormone, low body temperature and iron imbalances that feed candida

• Ditching elimination diets in favor of nutrient-dense, metabolism-supporting foods

• Improving thyroid function to activate gut defenses

Colorectal cancer is one of the most prevalent types of cancer today, particularly in Western countries where modern, processed-food diets have become the norm. Every year, 1.2 million cases of colorectal cancer are diagnosed worldwide, and around 930,000 people succumb to this disease.1 It’s the second most common cancer affecting men, and ranks as the third most common cancer in women.2

Some of the early symptoms of colorectal cancer include abdominal discomfort, blood in the stool, fatigue, and unexplained weight loss. However, these symptoms are usually dismissed until the disease has progressed, and it’s too late.

Now, research has highlighted a powerful yet often overlooked factor that will help protect against this lethal disease — vitamin D.

Data Shows Vitamin D Plays a Bigger Role in Colon Cancer Prevention

A comprehensive analysis published in the journal Nutrients in April 2025 has discovered a fascinating but substantial link between vitamin D and colorectal cancer (CRC). The researchers reviewed and analyzed data from 50 separate studies involving over 1.3 million participants to determine how much vitamin D impacts your risk of developing colorectal cancer.3

• This large-scale review looked at diverse populations — The data covered various groups and nationalities, including women in the U.S. Midwest, Danish adults with a family history of cancer, and Canadians living in high-altitude areas. The participants had different health statuses as well — some had colorectal cancer, or a documented vitamin D deficiency. Others were also given a vitamin D supplement.

• While the participants varied in health status and genetic risk, a consistent pattern emerged — The researchers found that the lower your vitamin D levels, the higher your risk of developing colon cancer. On the flip side, people with adequate or optimal levels of vitamin D had dramatically lower rates of cancer.

“Maintaining optimal vitamin D levels and adequate dietary intake is crucial in preventing CRC and improving patient prognosis,” the researchers said.

• Unfortunately, majority of people today have very low levels of this vital nutrient — A study that looked at the vitamin D status of more than 5,600 adults found that 37.6% had vitamin D insufficiency (blood levels between 20 and 30 ng/mL), while 42% were severely deficient (blood levels lower than 20 ng/mL) in this nutrient.4

Mónika Fekete, Ph.D., a professor in the Institute of Preventive Medicine and Public Health at Semmelweis University and the study’s lead author, commented:

“While vitamin D is not a substitute for screening or a healthy lifestyle, it is an important and relatively modifiable factor worth paying attention to — especially in individuals at higher risk of deficiency, such as older adults, people with limited sun exposure, those with darker skin, or individuals with chronic illnesses.”5

More Notable Highlights from the Featured Study

This research makes it clear that if you’re not paying attention to your vitamin D status, you’re missing out on one of the simplest and most powerful tools available to reduce your risk of colon cancer. Below are some of the compelling findings from the featured analysis that point to vitamin D as a key factor in reducing your risk of colorectal cancer.

• A landmark 1996 study found that women with the highest vitamin D intake had a 58% lower risk than those with the lowest intake.6

• A 2021 meta-analysis found a 39% lower risk of colorectal cancer in people with higher blood levels of vitamin D. The researchers also noted that when vitamin D levels were monitored over time, those who maintained higher levels had a 20% lower chance of developing colorectal cancer down the line.7

• A Canadian study found that supplementing with vitamin D reduced the incidence of precancerous polyps — by 33% for all polyps and 43% for high-risk ones. These polyps often go on to become cancer if not addressed early, so this kind of intervention has massive implications.8

• The Iowa Women’s Health study found that women who took vitamin D with calcium saw a 15% drop in colorectal cancer risk compared to those who didn’t take any supplements.9

• The Danish “Diet, Cancer and Health” study (one of the major ones included) found that vitamin D offered even stronger protection in people with a high genetic risk of colon cancer. That means if you’ve got a family history of this disease, optimizing your vitamin D status isn’t just helpful — it could be life-saving.10

How Does Vitamin D Affect Your Colorectal Cancer Risk?

Vitamin D is a fat-soluble nutrient your body naturally synthesizes when your skin is exposed to sunlight. As I’ve noted in previous articles, it plays an essential role in your bone health, immunity, and brain function, including mood regulation.

• Vitamin D’s role in cancer protection — Vitamin D acts by attaching to vitamin D receptors (VDR) found in your cells, including your colon cells. When this occurs, a series of signals are released that affect how your cells grow, develop, and survive.11 However, having poor vitamin D levels weakens these protective effects, allowing abnormal colon cells to survive and multiply instead.12

• Another vital purpose of vitamin D — Animal studies have also found that vitamin D helps delay some age-related changes by activating another important pathway via the vitamin D receptor. This pathway involves a molecule called Nrf2, which plays a crucial role in protecting your body from oxidative stress and DNA damage — two factors that are commonly linked to the development of cancer.13

• Vitamin D also supports the health of your intestinal lining — The colon is constantly regenerating itself, and this requires precise communication between your cells. Vitamin D ensures that this process runs smoothly. According to one research:

“Vitamin D and its nuclear receptor (VDR) regulate intestinal barrier integrity, and control innate and adaptive immunity in the gut. Metabolites from the gut microbiota may also regulate expression of VDR, while vitamin D may influence the gut microbiota and exert anti-inflammatory and immune-modulating effects.”14

Vitamin D Has Protective Effects Against Other Cancers, Too

In general, cancer now ranks as the second-leading cause of death worldwide, after cardiovascular disease.15 As the featured analysis and the supporting studies it investigated discovered, it’s clear that optimizing your vitamin D levels is a key strategy to reduce cancer deaths. However, health officials rarely acknowledge its importance. In fact, there are multiple ways by which vitamin D helps protect against cancer, such as:16

• Inhibiting cancer cell growth — It targets different stages of cancer development and progression. This includes the initiation, growth, and spread of cancer cells.

• Preventing cancer spread — It has antimetastatic effects, meaning it stops cancer cells from spreading from the original tumor site to other areas of the body. This is useful for improving survival rates, as metastasis is often responsible for many cancer fatalities.

• Stopping tumor formation — Vitamin D is anti-tumorigenic; it helps prevent tumors from forming or growing by inducing cancer cell death, blocking cell cycle progression, or blocking pathways that trigger tumor growth.

A 2023 review published in the Journal of Steroid Biochemistry and Molecular Biology highlighted some of the types of cancer that vitamin D could help prevent, such as:17

Breast
Prostate
Bladder
Glioblastoma
Melanoma

Squamous cell carcinoma
Ovarian
Multiple myeloma
Osteosarcoma
Head and neck

The study also highlighted the role of genetic differences in the VDR that could influence breast cancer risk. Read more about the findings here — “More Evidence Showing Vitamin D Combats Cancer.”
Sunlight — Mother Nature’s Vitamin D Factory

While some amounts of vitamin D are found in foods like fatty fish, liver, and egg yolks, the ultimate way to boost your levels of this nutrient is through mindful and appropriate sun exposure.

• When sunlight hits your skin, it produces a type of vitamin D called cholecalciferol — It’s far different from vitamin D2, which is what you get from plant sources like mushrooms and yeast. D3 is actually more effective at increasing blood levels. On a typical sunny day, your body may produce up to 25,000 international units (IU) of vitamin D.18

• How much sun is enough? Ideally, you need to expose your bare skin to direct sunlight daily. Gauge how long to stay under the sun safely by doing this simple test — Pay close attention to your skin for any sign of pinkness. The goal is to stay just below the point where your skin starts to turn slightly pink. If your skin turns red, it’s a sign of damage, not benefit — get out of the direct sun immediately.

• Your body cannot get too much vitamin D from sun exposure — Your body stops making vitamin D when you’ve got enough, so you can’t overdo it from sunlight alone. However, if you have darker skin, you’ll need to spend more time in the sun to produce the same amount of vitamin D as someone with lighter skin.

• An important caveat about sun exposure — If you’re still consuming a processed food diet loaded with vegetable oils or seed oils, then sun exposure will work against you. This is because seed oils are packed with linoleic acid (LA), which then accumulates in your skin.

When the LA in your skin interacts with the UV rays from the sun, it triggers inflammation and DNA damage. To avoid this, I recommend avoiding direct sunlight during peak hours until you’ve eliminated seed oils for at least six months.

• Additional reminders on sun exposure — In some cases, it’s impossible to completely avoid peak sunlight during the period when you’re purging LA from your diet. If this is the case, it’s best to follow protective measures:

◦ Take 12 milligrams of astaxanthin daily — This will enhance your skin’s UV resistance.

◦ Apply niacinamide (vitamin B3) cream before and after sun exposure.

◦ Take a baby aspirin — This will help prevent LA from converting to harmful oxidized linoleic acid metabolites (OXLAMs). Ideally, take the aspirin 30 minutes to one hour before sun exposure.

• A strategy to speed up LA removal from your skin — One interesting discovery I made was that there’s a way to quicken up the pace by which your body purges LA embedded in your skin. This is by ingesting a special fat called pentadecanoic acid or C15:0, found in raw, grass fed milk.

I recommend getting at least 2 grams of C15:0 per day, which will significantly speed up LA clearance from your body from two to three years to 12 to 18 months. My article, “The Fast-Track Path to Clearing Vegetable Oils from Your Skin” will give you more insightful details about C15:0.

However, not everyone has access to sunlight at all times. For example, people who live in far northern regions have very few months of peak sunlight. In this case, a vitamin D3 supplement is the best alternative.

Get Tested to Ensure You’re Meeting the Ideal Levels for Cancer Prevention

Measuring your vitamin D level, ideally twice a year, is the only way to determine if you’re getting enough sun exposure and/or taking the right amount of vitamin D3 supplement.

• What’s the optimal level for cancer prevention? Ideally, you need to aim for between 60 ng/mL and 80 ng/mL. The cutoff for sufficiency is around 40 ng/mL. In Europe, the measurements you’re looking for are 150 to 200 nmol/L and 100 nmol/L, respectively.

• Adjust your levels depending on your test results — Once you’ve confirmed your vitamin D levels via testing, adjust your sun exposure and/or vitamin D3 supplementation accordingly. Then, remember to retest in three to four months to make sure you’ve reached your target level.

• Optimize other nutrients to help meet your levels — Remember to balance your vitamin D3 with calcium, magnesium, and vitamin K2 through your healthy diet.

• If you’re supplementing with vitamin D3, here’s a tip — Take it with a meal that has some healthy fat, like grass fed butter or tallow. Since vitamin D is fat-soluble, this will help your body absorb it.

Your Gut Health — Another Vital Factor to Reduce Your Colon Cancer Risk

Vitamin D, or the lack of it, is indeed a key factor that increases your risk of colon cancer, but there’s another major aspect that many people are ignoring until it’s too late — their gut health.

There’s actually a significant connection between the state of your gut microbiome and colorectal cancer risk, particularly the composition of the food you eat. Your gut is a fascinating, complex ecosystem teeming with trillions of bacteria, both helpful and harmful. These tiny residents play a crucial role in digestion, nutrient absorption, and even your immune system.

But when you consume a poor, nutritionally deficient diet loaded with ultraprocessed junk foods high in vegetable oils and LA, not only are you hampering the growth of good bacteria, but you’re also nourishing the pathogenic bugs. This disruption in the gut microbiome leads to an inflammatory environment, increasing the risk of colon cancer.19

Hence, you need to take the necessary steps to protect your gut health. Read my article “Unveiling the Link Between Ultraprocessed Foods and Colon Cancer” for more information.

Frequently Asked Questions (FAQs) About Vitamin D for Colorectal Cancer Prevention

Q: How does vitamin D help protect against colorectal cancer?

A: Vitamin D plays a direct role in cell regulation. It slows the growth of abnormal cells, encourages unhealthy cells to die, reduces inflammation in the gut, and helps maintain the health of the intestinal lining — all of which are key in preventing cancer from developing or progressing.

Q: What vitamin D level is considered protective against colon cancer?

A: For cancer prevention, aim for blood levels of 60 to 80 ng/mL. Levels below 30 ng/mL are considered low, and anything under 20 ng/mL is classified as deficient. Most adults fall below these thresholds, putting them at unnecessary risk.

Q: Does vitamin D reduce the risk of colon polyps, too?

A: Yes. One Canadian study found that supplementing with vitamin D reduced all colon polyps by 33%, and high-risk polyps by 43%. These types of growths are often precursors to cancer, so reducing them is a major step in prevention.

Q: Is sun exposure enough to meet my vitamin D needs?

A: Sunlight is the most effective way to make vitamin D naturally, but only if you’re not loaded with seed oils, which cause skin damage. If sun exposure isn’t possible — due to location, skin tone, or season — a vitamin D3 supplement is recommended.

Q: Who is most at risk for vitamin D deficiency and colorectal cancer?

A: Older adults, people with darker skin, those with chronic illness, or anyone with limited sun exposure are more likely to be deficient. If you have a family history of colorectal cancer, optimizing your vitamin D levels becomes even more important.

Diabetic kidney disease, characterized by gradual damage to the kidneys caused by persistently elevated blood sugar, often develops silently for years before obvious symptoms appear. Early warning signs include swelling in the feet and ankles, fatigue, changes in urination, and rising blood pressure. Left unchecked, it can progress to kidney failure that requires dialysis or a transplant.

Because high blood pressure speeds that decline, controlling it is considered a cornerstone of treatment, which is what makes research presented at the European Renal Association Congress so unsettling.1 Among adults with Type 2 diabetes who were already taking medications meant to preserve their kidneys, one widely prescribed class of blood pressure medication was linked to worse kidney outcomes rather than better ones.

That result defied what the researchers expected to find. These modern therapies were thought to protect the kidneys well enough to offset any downside of adding another blood pressure drug. Instead, the added risk held, even in patients receiving the very treatments designed to slow kidney decline.

The explanation appears to lie not in the bloodstream at large but inside the kidney’s own filtering machinery, where a medication meant to ease pressure within blood vessels may do the opposite. Understanding how that happens reveals why a drug trusted to protect the circulation can behave so differently once blood reaches the kidney.

Common Blood Pressure Drugs Were Linked to a 33% Higher Risk of Kidney Decline

The study investigated whether dihydropyridine calcium-channel blockers (DCCBs) — a group that includes amlodipine, the most commonly prescribed, along with nifedipine and felodipine — remained safe for people with Type 2 diabetes who were already receiving the newest kidney-protective treatments.2

Researchers analyzed data from 31,031 adults treated between 2016 and 2021. Every participant was already taking both renin-angiotensin system (RAS) inhibitors and sodium-glucose cotransporter-2 (SGLT2) inhibitors, which are considered standard therapies for protecting kidney function in diabetic kidney disease. The researchers wanted to determine whether adding DCCBs influenced long-term kidney outcomes.

• The study compared two large treatment groups — Among the participants, 12,172 people (39.2%) were taking DCCBs while 18,859 people (60%) were receiving other blood pressure medications. Patients were followed for a median of roughly 3.5 years, giving researchers a substantial window to observe changes in kidney health.

For readers already managing diabetes, this makes the findings particularly relevant because DCCBs are commonly prescribed as a second-line treatment when blood pressure remains elevated despite other medications.

• The difference in kidney outcomes was significant — After adjusting for differences in age, health status, and other baseline factors, researchers found that DCCB use was associated with a 33% higher risk of major adverse kidney events (RR 1.33, 95% CI, 1.03-1.73) compared to alternative blood pressure treatments.

The researchers defined these events as either a decline of 40% or more in estimated glomerular filtration rate (eGFR) — the standard test used to measure how efficiently your kidneys filter waste from your blood — or progression to end-stage kidney disease requiring dialysis or a kidney transplant. If you already have diabetes and kidney concerns, those outcomes represent some of the most serious complications physicians try to prevent.

• The findings challenged expectations about modern therapy — According to lead researcher Dr. Timna Agur, the research team originally expected that the kidney-protective effects of SGLT2 inhibitors would offset any concerns associated with DCCBs. Instead, the elevated risk remained. That observation suggests newer therapies did not fully erase the difference researchers observed between treatment strategies.

• Changes in blood flow through the kidney’s filtering structures are a likely mechanism — In diabetic kidney disease, those filters already operate under excessive strain. Researchers believe DCCBs relax the vessel carrying blood into each filtering unit more than the vessel carrying blood out — the reverse of how RAS inhibitors work, which ease pressure by relaxing the outflow vessel. This may result in pressure building inside an already overworked filter.

Imagine increasing water pressure entering a garden hose while partially restricting the exit point. Pressure builds inside the system. Researchers suggest a similar process could occur within the kidney’s delicate filtration network, exposing those structures to greater mechanical stress over time.

• The results raise practical questions about treatment choices — The authors emphasized that this was an observational study, meaning it can’t prove that DCCBs directly caused the poorer outcomes. Other factors could contribute to the differences observed between groups. Even so, Agur noted that “given how commonly these medications are prescribed, any increase in kidney risk could have important implications for large numbers of patients with DKD [diabetic kidney disease].”

For someone living with diabetes, this research highlights the value of understanding not only whether blood pressure is controlled, but also how different treatment approaches affect long-term kidney health. It also creates a simple challenge you can discuss with your physician: review your medication list and ask how each drug fits into your overall kidney-protection strategy rather than assuming all blood pressure medications influence the kidneys in the same way.

How to Lower Blood Pressure Without Adding More Stress to Your Kidneys

High blood pressure doesn’t just affect your heart. Over time, it places tremendous strain on the tiny filtering units inside your kidneys, gradually damaging the structures responsible for removing waste from your blood. While the study itself only compared blood pressure drugs, it’s a reminder that the most durable strategy is to address what drives high blood pressure in the first place.

Because diabetes and high blood pressure frequently develop together, improving blood sugar control often may help improve blood pressure as well. When you combine better metabolic health with proper mineral balance, stress reduction and regular movement, you may help reduce the pressure that contributes to kidney strain and the need for more aggressive treatment. Here are five practical ways to start.

1. Fix your sodium-to-potassium balance with whole foods — The real issue isn’t the salt shaker on your table. It’s the ultraprocessed food that dominates the modern diet. Packaged snacks, fast food, processed meats, and convenience meals deliver large amounts of sodium while providing very little potassium.

Potassium may help relax blood vessels, support healthy fluid balance and make it easier for your body to maintain normal blood pressure.

Important: if your kidney function is already reduced, do not increase potassium without your physician’s guidance — damaged kidneys may not clear it safely, especially alongside RAS inhibitors, and excess potassium can affect heart rhythm. As your diet shifts toward real food, the sodium-to-potassium ratio naturally moves in the right direction, helping reduce strain on both your blood vessels and your kidneys.

2. Stop chasing low-salt numbers and improve diet quality instead — Many people are told that severe salt restriction is the answer to high blood pressure. Aggressively cutting salt can increase stress hormones, raise insulin levels, and make blood pressure regulation more difficult.

Rather than obsessing over sodium numbers, remove the foods that contribute most of the problem: ultraprocessed products loaded with refined carbohydrates, phosphate additives, seed oils, and excess sodium. A diet built around nutrient-dense whole foods may support healthier blood pressure while helping reduce the workload placed on your kidneys every day.

3. Lower the stress signals that keep blood pressure elevated — Your nervous system plays a major role in blood pressure control. When your body remains locked in a chronic stress response, blood vessels constrict and pressure rises. One simple tool is box breathing.

Breathe in for four seconds, hold for four seconds, exhale for four seconds, and hold again for four seconds. Repeat the cycle for 10 minutes daily. Combined with adequate sleep, regular outdoor time and daily movement, this may help calm your nervous system and reduce one of the most overlooked drivers of elevated blood pressure.

4. Optimize vitamin D to support healthy blood vessel function — Vitamin D plays a role in regulating the renin-angiotensin system, one of the primary hormone networks involved in blood pressure control. When vitamin D levels remain low, this system becomes overactive, increasing pressure throughout the vascular system and adding stress to kidney tissue.

Regular sun exposure may support vitamin D production, circulation and cellular energy generation. Aim for a vitamin D level between 60 and 80 ng/mL (150 to 200 nmol/L).

If you still consume significant amounts of seed oils and other sources of linoleic acid (LA), avoid intense sun exposure (10 a.m. to 4 p.m.) until you have substantially reduced those foods for four to six months because stored LA may increase susceptibility to sun-related skin damage. Talk to your healthcare provider about whether vitamin D testing is appropriate for you.

5. Move enough to make your blood vessels healthier — Physical activity remains one of the most effective ways to improve blood pressure naturally. Movement may help improve circulation, support insulin sensitivity, reduce stress, and help maintain a healthy body composition.

If you’re already active, work toward an hour of walking, cycling, swimming, or similar movement most days. If you’re starting from scratch, focus on consistency rather than intensity. Even a 10-minute walk after meals may help improve blood sugar control and support healthier blood pressure.

If you have Type 2 diabetes and currently take a DCCB, the European Renal Association findings make it worthwhile to review your treatment plan with your doctor. Don’t stop any prescribed medication on your own. Instead, discuss whether your current approach remains the best fit for your kidney health and what additional lifestyle changes could help improve blood pressure control over time.

*These findings are drawn from an observational, real-world clinical study. Results may not apply to all individuals, and the study cannot establish that DCCBs directly cause poorer kidney outcomes.

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 Blood Pressure Medications and Kidney Health in People with Type 2 Diabetes

Q: What did the study find about common blood pressure medications and kidney health?
A: Researchers found that people with Type 2 diabetes who took DCCBs had a 33% higher risk of major adverse kidney events (RR 1.33, 95% CI, 1.03-1.73) compared to those using other blood pressure medications. This increased risk remained even though all participants were already taking modern kidney-protective therapies.

Q: Why might these medications increase the risk of kidney damage?
A: Researchers believe DCCBs may alter blood flow inside the kidneys in a way that increases pressure within the kidneys’ filtering units. Over time, that extra pressure could place additional stress on structures that are already vulnerable to damage from diabetes, which may accelerate the loss of kidney function.

Q: Does this study prove that DCCBs directly cause kidney disease?
A: No. The study was observational, meaning it identified an association rather than proving cause and effect. Other factors could have contributed to the differences seen between treatment groups. However, the findings are important because DCCBs are widely prescribed and the study involved more than 31,000 adults with Type 2 diabetes.

Q: What can I do to lower blood pressure while supporting kidney health?
A: Focus on the factors that drive high blood pressure in the first place. Improving blood sugar control, eating potassium-rich whole foods, reducing ultraprocessed foods, managing stress, maintaining healthy vitamin D levels, and staying physically active all may help support healthier blood pressure and reduce strain on your kidneys.

Q: What if I have Type 2 diabetes and currently take a DCCB?
A: Don’t stop your medication on your own. Instead, review the study findings with your doctor and discuss how your current treatment plan fits into your long-term kidney-protection strategy. Ask whether your blood pressure is being managed in the most kidney-friendly way possible and whether additional lifestyle changes could help reduce your need for more aggressive treatment.

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Which of these vitamins helps support healthy bone remodeling?

Vitamin A
Vitamin C
Vitamin E
Vitamin K
Vitamin K helps coordinate the ongoing process of removing old bone and building new bone, which is important for maintaining bone strength. Learn more.