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The Butyrate-GLP-1 Connection: Unlocking Satiety, Energy, and Inflammation Control
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/09/butyrate-glp-1-connection-natural-weight-loss.aspx
Analysis by Dr. Joseph Mercola March 09, 2026
Story at-a-glance
- Butyrate fuels the gut cells (L-cells) that produce GLP-1, a natural hormone that helps regulate appetite, blood sugar, and metabolism
- Your gut can’t make butyrate without fiber, and modern diets contain far too little — just 16 grams a day compared to 100+ grams in traditional cultures. Low butyrate disrupts the body’s natural hunger regulation system, leading to inflammation, weight gain, mood issues, and metabolic breakdown
- Restoring butyrate is a natural way to activate GLP-1 — no injections or drugs required — by working with your body instead of bypassing it. My new book, “Weight Loss Cure; Melt Fat Naturally With Your Own GLP-1,” provides a step-by-step plan to rebuild butyrate production, restore natural GLP-1 signaling, and correct the root drivers of weight gain
- Pharmaceutical GLP-1 agonists are marketed as breakthroughs, but they’re merely stand-ins for a system your body already perfected: GLP-1 secretion driven by butyrate
- Healing starts with calming the gut using simple carbs like white rice and fruit, then slowly reintroducing fermentable fibers such as resistant starch. Eliminating seed oils, reducing stress, and getting morning sunlight are also key to restoring your gut’s ability to make butyrate and support GLP-1 naturally. Signs that your gut is rebuilding include improved digestion, better mood, reduced cravings, and more stable energy
What if your body already knew how to regulate hunger, burn fat, and keep your metabolism in balance — without injections or synthetic hormones? It does. And it starts with butyrate. This isn’t a biohack. It’s how your metabolism was designed to function.
Butyrate is a short-chain fatty acid (SCFA) made by beneficial gut bacteria when they ferment fiber. It powers the colon cells (L-cells) that produce GLP-1, a natural hormone that helps you feel full, balance blood sugar, and burn energy efficiently.1,2,3,4 The GLP-1 pathway is a built-in system for appetite regulation, blood sugar control, and energy balance, but it only works if your gut bacteria have the right fuel.
The problem? Modern diets have starved your gut’s natural GLP-1 engine. Butyrate production depends on fiber, and the average American gets only about 16 grams a day. In traditional cultures, fiber intake regularly exceeds 100 grams. Hunter-gatherer tribes like the Hadza in Tanzania, for example, eat up to 150 grams of fiber daily.
Human metabolism evolved around the butyrate–GLP-1 connection long before pharmaceutical GLP-1 agonists ever existed. Our ancestors ate diverse plant fibers that fed gut microbes, which in turn churned out butyrate. That butyrate kept the intestinal barrier strong, inflammation low, and appetite hormones in balance.
Today, processed foods and industrial seed oils — especially vegetable oils that are high in linoleic acid (LA) — break that cycle. They damage gut bacteria, slash butyrate output, and disable the L-cells responsible for natural GLP-1 production. The result? We’re tired, inflamed, overweight — and told we need drugs to fix it. But you don’t need to mimic biology with a syringe if you can restore it through your own gut. This is the central topic of my new book, “Weight Loss Cure; Melt Fat Naturally With Your Own GLP-1.”
How Butyrate Fuels Natural GLP-1
Butyrate directly nourishes L-cells in your intestinal lining — the same cells that release GLP-1 after meals. When butyrate is abundant, GLP-1 secretion works the way nature intended:
• It slows gastric emptying, so you feel full longer
• It reduces glucagon, which lowers blood sugar
• It enhances insulin sensitivity and helps your body burn fat
• It sends satiety signals to the brain, curbing cravings and emotional eating
You don’t need a synthetic GLP-1 agonist to access these benefits. You need butyrate. That means giving your gut bacteria the right environment to do their job. This isn’t about overriding your biology. It’s about supporting the natural regulatory loop your gut was built to run. When this system is fueled properly, metabolic balance is the default state.
What Happens When Butyrate Is Low?
Without enough butyrate:
• Your colon cells weaken, leading to “leaky gut”
• Inflammation flares and spreads systemically
• Mood, memory, and stress resilience decline
• GLP-1 production drops, triggering weight gain and blood sugar instability
Conditions like Type 2 diabetes, depression, and Parkinson’s often trace back to this breakdown. The good news? Restoration starts in your gut, and it can begin within days of changing your diet.
Your Gut Bacteria Make SCFAs, but Only if You Feed Them
In my paper, “SCFAs Modulate Gut-Brain Axis Function,”5 I explain how SCFAs, especially butyrate, play a central role in regulating metabolism, appetite, inflammation, and brain function. This happens through the gut-brain axis, where SCFAs produced in the colon influence everything from satiety hormones like GLP-1 to stress resilience and cognitive performance.
Modern diets — low in fermentable fiber and high in inflammatory seed oils — have disrupted this natural metabolic control system. But clinical research shows we can restore it. The figure below summarizes human studies where prebiotic fibers or direct SCFA interventions were used in real-world populations. Key findings include improvements in body fat, satiety, insulin signaling, inflammation, and gut-derived hormone release, which includes GLP-1.
These studies confirm that feeding or restoring SCFA production — especially butyrate — can activate your body’s built-in metabolic and inflammatory controls. That includes the same GLP-1 pathway targeted by weight loss drugs like Ozempic, but without the side effects or dependency. This is your original biology — rebooted through your gut.
But again, to support the butyrate-producing bacteria, you need to feed them the right substrates — fermentable fibers like resistant starch, inulin, and oligosaccharides. If you’re not consuming these regularly, your gut can’t make butyrate. The figure below shows which types of gut bacteria make key SCFAs, what foods they thrive on, and how they help keep your gut healthy and balanced.
Butyrate doesn’t “treat” metabolic dysfunction, per se. It supports normal metabolic function by fueling the mechanisms your body already relies on to support normal appetite, insulin sensitivity, and inflammatory control.
Your Gut Was Built for This: Butyrate and GLP-1 Are the Natural Design
Pharmaceutical GLP-1 agonists are marketed as breakthroughs, but they’re merely stand-ins for a system your body already perfected: GLP-1 secretion driven by butyrate. Your L-cells are engineered to release GLP-1 in response to butyrate. When the gut microbiome is balanced and well-fed with fermentable fiber, GLP-1 production activates after meals to regulate appetite, support insulin release, and promote fat burning — all without a prescription.
This design evolved to work in harmony with ancestral diets rich in whole foods, fiber, and unprocessed carbohydrates. Disruption to this design — whether from ultraprocessed foods, antibiotics, or synthetic additives — breaks the microbial fuel line, not the hormonal hardware. When you restore butyrate production, you remove the blockages and reactivate the normal regulatory feedback loop, which lets your built-in weight regulation system function again, as intended.
How to Restore Butyrate and Unlock Natural Weight Loss
To restore your body’s natural weight management system, you need to restore and support the bacteria in your gut that produce butyrate and other SCFAs. This isn’t about manipulating your biology into doing something unnatural. On the contrary, it’s about rebuilding the internal conditions that allow your body to regulate appetite, metabolism, and fat burning as it was designed to. Here’s how:
1. Start with gut terrain repair — If you’re bloated, constipated, or sensitive to high-fiber foods, you need to calm inflammation before you feed the microbiome. That means:
• Avoiding fermentable fibers at first. When your gut is out of balance, high-fiber foods — even the “healthy” ones — can work against you. Foods like beans, lentils, oats, and raw greens ferment quickly when the wrong bacteria are in control. This creates gas, pressure and inflammation, and worsens gut lining damage.
• Eliminating seed oils (such as soybean, corn, canola, sunflower). LA damages the exact gut microbes you’re trying to support. If your diet includes fried foods, processed snacks, or sauces made with soybean, corn, sunflower, or canola oil, you’re suffocating your good gut bacteria. Replace those fats with ghee, grass fed butter, or tallow — fats your body actually knows how to use. The goal is to shift your internal terrain so your gut bacteria thrive again.
• Using simple carbs like white rice and ripe fruit to stabilize energy without feeding bad bacteria.
2. Add butyrate-promoting foods slowly — Once symptoms ease, introduce fermentable fibers in small amounts. These fibers pass undigested to your colon, where they feed good bacteria that make SCFAs like butyrate:
• Cooked and cooled white potatoes
• Green bananas
Once you tolerate those, add in inulin-rich foods like garlic, onions, and leeks, which feed butyrate-producing bacteria. These fibers bypass digestion in your small intestine and head straight to your colon, where they fuel beneficial bacteria that make butyrate and other SCFAs. Citrus fruits can also be added. They help feed Faecalibacterium prausnitzii, a major butyrate-producer.
3. Support with optional tools — Once your gut begins to stabilize, these targeted tools can help accelerate butyrate production and improve results:
• Akkermansia postbiotics (Phase 1) — Postbiotics are non-living bacterial components that still deliver biological signals. Pasteurized forms of Akkermansia muciniphila contain Amuc_1100, a protein shown to tighten the gut barrier and reduce inflammation. Look for postbiotic formulas with enteric coating or microencapsulation to ensure they survive stomach acid and reach the colon intact.
Without that protection, less than 5% of Amuc_1100 reaches your colon. You could try megadosing to compensate, but that’s expensive and inefficient. Prioritize coated formats to support your gut barrier more effectively.
• Live Akkermansia (Phase 2) — Once your gut lining shows signs of healing (less bloating, more fiber tolerance), you can begin Phase 2. In this stage, introduce live probiotic Akkermansia alongside gentle prebiotics — like small amounts of resistant starch — to support the growth of butyrate-producing strains and reestablish a healthy, oxygen-sensitive microbial environment.
• Fermented foods — Raw sauerkraut, kefir, and other traditionally fermented foods can boost microbial diversity and support butyrate-producing strains. Go slowly — start with small amounts to test tolerance, especially if your gut is sensitive.
• Gut testing — A stool analysis can reveal which bacteria are present, whether your gut is inflamed, and how well you’re producing short-chain fatty acids like butyrate. This can guide food choices and supplementation more precisely.
• Resistant starch — Found naturally in cooked-and-cooled potatoes, green bananas, and legumes — or as supplemental powders — resistant starch bypasses digestion in the small intestine and becomes prime fuel for butyrate-producing bacteria in the colon.
4. Adjust your environment — Your gut doesn’t just respond to what you eat. It’s tuned into your entire lifestyle. Your gut bacteria evolved alongside your daily rhythms, and restoring this alignment is essential to support the normal circadian and hormonal cycles your metabolism depends on. These daily habits help create the internal rhythm your microbiome needs to thrive:
• Sleep — Align your sleep-wake cycle with natural light exposure. Aim for 7 to 9 hours of high-quality sleep and get morning sun to anchor your circadian rhythm. This helps regulate gut motility and microbial repair.
• Stress — Chronic stress alters your microbiome and shuts down butyrate production. Use daily tools like breathwork, walking outdoors, and nervous system regulation practices to calm your hypothalamic-pituitary-adrenal (HPA) axis and support microbial balance.
• Fasting window — Stop eating at least three hours before bed. This gives your migrating motor complex (MMC) — your gut’s internal clean-up crew — time to sweep out bacteria and food debris overnight, reducing fermentation and inflammation.
Signs Your Gut Is Making More Butyrate
These improvements reflect rising butyrate levels and gut healing in real time:
• Bowel movements become regular and well-formed — A sign of improved colonic motility and mucosal integrity.
• Fiber tolerance improves — Less bloating, gas, or discomfort after meals rich in fermentable fiber.
• Hunger fades between meals — As GLP-1 and PYY production increases, satiety naturally extends.
• Mood feels more stable and stress less overwhelming — Butyrate supports BDNF and modulates the HPA axis.
• You lose fat without trying to eat less — Improved metabolic signaling leads to spontaneous caloric reduction.
• Reduced post-meal blood sugar spikes — A measurable effect tied to improved insulin sensitivity and GLP-1 response.
• Lower fasting insulin and triglycerides (if tested) — Both improve with SCFA restoration and microbiome balance.
• Fewer cravings for processed carbs and snacks — Satiety hormones rise while inflammation-driven hunger decreases.
• Less urgency or discomfort with bowel movements — Improved stool consistency reflects stronger gut barrier and reduced inflammation.
•Improved breath or reduction in sulfur/gas odors — Indicates better fermentation profile in the colon (fewer sulfur-releasing or proteolytic bacteria).
Timeline: What to Expect as Your Gut Rebuilds
Your gut already knows how to help you lose weight — by producing butyrate, which fuels the cells that make GLP-1. This is how human metabolism was designed to function. Restore that system, and your cravings shrink, your blood sugar stabilizes, your inflammation calms down, and your body starts releasing excess weight naturally. These shifts are clear signs that your body’s metabolic software is running the way it was meant to.
Your gut doesn’t need to be perfect to start producing butyrate. But there’s a rhythm to recovery, and markers to know it’s working.
| Phase | What happens | Timeframe | Measurable indicators |
|---|---|---|---|
| Terrain repair | Gas, bloating, and sensitivity begin to calm | 1 to 3 weeks | Less urgency, firmer stools, more predictable digestion |
| Fiber reintroduction | Butyrate-producing strains begin to increase | 2 to 4 weeks | Better tolerance of resistant starch, mood uplift |
| GLP-1 response | Appetite regulates, energy improves, cravings decrease | 4 to 8 weeks | Fewer between-meal snacks, better AM energy |
| Metabolic reset | Satiety increases, fat loss begins, blood sugar stabilizes | 6 to 12 weeks | Tighter waistline, reduced post-meal glucose swings |
You can start putting these strategies into practice right now with my new book, “Weight Loss Cure; Melt Fat Naturally With Your Own GLP-1,” which provides a step-by-step plan to rebuild butyrate production, restore natural GLP-1 signaling, and correct the root drivers of weight gain.
We’re also preparing a butyrate-support product designed to complement these foundational strategies. You can join the waitlist now, and when it becomes available, you’ll receive a $5 off coupon by email.
FAQs
Q: Is butyrate the same as taking a GLP-1 drug like Ozempic?
A: No. Drugs mimic GLP-1 but bypass your gut’s natural system. Butyrate restores the function of the L-cells that make GLP-1, without side effects or dependency.
Q: What are the signs that you’re low in SCFAs like butyrate?
A: If you experience digestive problems, low energy, anxiety, poor stress tolerance, or stubborn weight gain, you’re likely not producing enough SCFAs. These symptoms often overlap with conditions like metabolic syndrome, inflammatory bowel disease, and neurodegenerative diseases.
Q: How do you increase butyrate production naturally?
A: To boost butyrate, you need to feed the gut bacteria that make it. First heal your gut by focusing on easy-to-digest carbs like fruit and white rice. Then, start slowly adding fermentable fibers like resistant starch (found in cooked-and-cooled potatoes and green bananas) and inulin-rich vegetables (like garlic and onions). Cutting out vegetable oils and processed foods is also key to stop disrupting your gut’s microbial balance.
Q: How fast can butyrate production increase?
A: Changes begin within days of dietary shifts, but full restoration of microbial diversity and L-cell function can take weeks to months.
Q: What if you don’t tolerate fiber at all?
A: That’s a sign your gut terrain needs more repair. Start with broth, peeled fruit, and gentle carbs, then gradually work up.
- 1 Signal Transduction and Targeted Therapy, Volume 9, Article Number 234 (2024)
- 2 Int J Obes Relat Metab Disord. 2001 Jun;25(6):781-92
- 3 Adv Nutr. 2018 Feb 9;9(1):21-29
- 4 Pharmacological Research, Volume 160, October 2020, 105174
- 5 Short-Chain Fatty Acids Influence the Gut-Brain Connection by Dr. Joseph Mercola
Block cancer cell development by eating a medicinal herb, study reveals
Reproduced from original article:
https://www.naturalhealth365.com/common-kitchen-herb-blocks-cancer-cell-progression-study-finds.html
by: March 5, 2026
(NaturalHealth365) Most people walk right past parsley at the grocery store. Some buy a bunch, stick the bundle in the fridge, and forget the whole thing ever happened. Others have been cooking with parsley for years without ever realizing what this delicious herb is actually capable of. Parsley – the green that usually ends up as a garnish on the side of your plate – has just become the subject of some very important cancer research.
A new study published in Cancer Letters found that a natural compound in parsley, apigenin, can stop cancer cells from growing and spreading. Researchers tested it against one of the hardest cancers to treat – bladder cancer, which comes back in up to 70% of patients even after treatment. What they found was remarkable.
Apigenin targeted a specific protein that drives tumor growth and slowed cancer growth, all without harming healthy tissue. That last part is worth repeating. No healthy tissue damage. That’s something most cancer drugs cannot claim.
What Western medicine keeps getting wrong about cancer
The cancer industry has spent decades pouring money into expensive drug treatments that often cause serious harm to the very patients they’re trying to help. Meanwhile, natural compounds found in everyday foods have been quietly building a case in the scientific literature – a case that rarely gets the attention it deserves.
Apigenin is a perfect example. Research shows this compound can trigger cancer cell death, slow tumor growth, and block the signals cancer uses to spread through the body. While apigenin works in multiple ways at once, most pharmaceutical drugs target one single pathway. Nature, it turns out, is more sophisticated.
Parsley does far more than fight cancer
The benefits of parsley go well beyond what this one study found. This herb is loaded with vitamins K, C, and A. Vitamin K supports strong bones and healthy arteries, vitamin C powers your immune system and helps your body repair itself, and vitamin A protects your eyes and skin.
Parsley also fights inflammation, the slow, silent process that drives most serious chronic diseases, including heart disease, diabetes, and cancer. Parsley also supports kidney function, helps the body flush out toxins, and delivers a concentrated dose of antioxidants that protect your cells from daily damage.
All of this from a food that many people consider ‘just a garnish.’
Natural solutions: How to actually get enough parsley
Reading about a powerful herb is one thing, but getting enough into your body consistently is another. Here’s how to make parsley a real part of your daily routine:
Fresh juicing – the option most people overlook: Running a generous handful of fresh organic parsley through a juicer is one of the most effective ways to get a concentrated dose of the herb’s active compounds. Add a bunch of parsley to a green juice with cucumber, celery, lemon, and ginger. Many people who focus on natural health skip juicing entirely, and that’s an opportunity they can’t afford to miss.
Add it generously to meals: Don’t treat parsley like a decoration. Throw large handfuls into soups, smoothies, salads, grain bowls, and sauces. Make this herb a real ingredient, not an afterthought.
Parsley tea: Steep a big handful of fresh parsley in hot water for 10 minutes. This is a simple, inexpensive, and easy daily habit to build.
Always buy organic: This matters more than most people realize. Conventionally grown parsley can carry significant pesticide residue. If the goal is to support your health, loading your body with toxic chemicals at the same time defeats the purpose entirely. The same principle applies to your whole diet – organic food reduces the toxic burden your body has to deal with every single day, and that matters enormously for long-term health.
Discover what leading cancer experts already know
Apigenin is just one example of what the natural health world has long said: food and nutrition are serious cancer-fighting tools that Western medicine consistently undervalues. If a compound in a $2 bunch of parsley can stop tumor growth without harming healthy tissue, what else are we missing?
Sources for this article include:
Scientists confirm a shocking brain tumor risk hiding in your home
Reproduced from original article:
https://www.naturalhealth365.com/scientists-confirm-a-shocking-brain-tumor-risk-hiding-in-your-home.html
by: March 7, 2026
(NaturalHealth365) Most families never think twice about one of the most overlooked threats to brain health. For example, the mobile device on the kitchen counter, the “smart” meter attached to many homes, or the wireless router humming in the hallway. Unfortunately, these devices have become a normal part of life.
But a growing stack of peer-reviewed research is raising questions that are becoming very hard to ignore, and the answers affect every person in the household, not just the children.
A new peer-reviewed study published in Environmental Research followed 200 children diagnosed with central nervous system tumors and compared them to nearly 800 healthy children. The findings were sobering. Children exposed to elevated extremely low-frequency magnetic fields (ELF-MF) at levels above 0.4 microtesla faced more than double the risk of developing a brain tumor. Prolonged tablet use, even without internet access, was associated with a risk increase of up to 253%.
What the study found, and why it matters beyond childhood
Researchers measured ELF-MF radiation in children’s bedrooms for 24 hours to capture realistic daily exposure. The source of this radiation comes from power lines, household wiring, and common electrical equipment. More than 5% of the children in the study were already living with ELF-MF levels above 0.3 microtesla, exceeding levels reported in most other populations studied.
Children face heightened risk for clear biological reasons. Their central nervous systems are still developing, their brain tissue is more conductive than that of adults, and their smaller skulls allow radiation to penetrate into deeper brain regions. The International Agency for Research on Cancer has classified both ELF-MF and radiofrequency radiation as possibly carcinogenic to humans, a classification that applies regardless of age.
Adults are not off the hook. Someone who began living near high-voltage power lines in childhood and continues to do so decades later accumulates a lifetime of exposure that no single study can fully capture.
A 2025 systematic review commissioned by the World Health Organization found high-certainty evidence linking wireless radiation to malignant gliomas and nerve tumors in animal studies, tumor types that have also appeared in human research. The 2018 National Toxicology Program study, a $30 million, 10-year effort, found clear evidence of gliomas in rats exposed to cell phone radiation. Adults carrying devices in pockets, sleeping near routers, and working in high-EMF environments are running their own long-term experiment with unknown results.
The exposure nobody is talking about
By September 2021, 96% of U.S. public schools were providing tablets to students. Common Sense Media reported that 40% of children had a tablet by age 2. These devices are now embedded in daily life from toddlerhood through adulthood, yet the radiation they emit – even when not connected to the internet – was significantly associated with increased brain tumor risk in this study.
Western medicine has been largely silent on cumulative EMF exposure as a cancer risk factor, leaving families to navigate this threat without guidance.
Natural solutions to reduce your family’s EMF exposure
Lowering your radiation burden doesn’t require dramatic lifestyle changes, but it does require awareness and a few deliberate habits.
Create distance between your body and devices. Keep tablets and phones at arm’s length whenever possible. Distance dramatically reduces radiation exposure; even a few inches makes a measurable difference. Never place a tablet directly on a child’s lap for extended use, and avoid holding a phone against your head for long calls. Use speakerphone or a wired headset instead.
Reduce bedroom exposure where it counts most. The study measured radiation in children’s bedrooms because that’s where the body does its most critical repair work – during sleep. Remove tablets and phones from bedrooms at night. Turn off Wi-Fi routers before bed, and keep devices unplugged and away from sleeping areas. Adults benefit from these habits just as much as children.
Support your body’s cellular defense systems through nutrition. A strong immune system and efficient DNA repair mechanisms are your best internal defense against environmental carcinogens. Organic cruciferous vegetables, such as broccoli, cauliflower, and Brussels sprouts, activate detoxification enzymes through sulforaphane.
Selenium-rich foods like Brazil nuts support antioxidant pathways that help neutralize oxidative stress caused by radiation exposure. Astaxanthin, one of nature’s most potent antioxidants, has also shown promise in protecting against radiation-induced cellular damage.
Reduce your total toxic load. EMF exposure compounds with other environmental stressors, including pesticides, heavy metals, and inflammatory foods. Eat clean, prioritize filtered water, and support liver and lymphatic function through daily movement and targeted supplementation.
What cancer prevention experts want you to know
The connection between chronic environmental exposures and cancer risk is precisely what Western medicine underestimates, and what holistic health experts have been documenting for years. EMF exposure, oxidative stress, immune suppression, and toxic burden all feed the same underlying processes that allow abnormal cells to escape the body’s surveillance systems.
Sources for this article include:
Chronic Fatigue Syndrome Linked to Energy Metabolism and Immune Dysfunction
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/05/chronic-fatigue-syndrome-energy-metabolism-immune-dysfunction.aspx
Analysis by Dr. Joseph Mercola March 05, 2026
Story at-a-glance
- Myalgic encephalomyelitis, also known as chronic fatigue syndrome (ME/CFS), affects 2 million Americans with debilitating fatigue, post-exertional malaise, and cognitive problems. New research links this condition to mitochondrial dysfunction and impaired cellular energy production
- Studies show ME/CFS patients struggle to produce adequate energy through normal pathways
- The condition compromises immune function by reducing natural killer (NK) cells and dendritic cells, leaving the body with diminished defense capabilities and increased vulnerability
- Blood vessel function suffers when cellular energy drops, causing circulatory problems like poor oxygen delivery, dizziness, and cold extremities that worsen overall fatigue
- Recommended strategies include reducing seed oil consumption, supporting gut health with whole foods, exercising to generate new mitochondria, and prioritizing restorative sleep
Americans report high rates of chronic fatigue, but myalgic encephalomyelitis (ME), also called chronic fatigue syndrome (CFS), represents a distinct, clinically defined disease that affects a small subset of the population rather than a diagnosis that explains widespread tiredness. Around 2 million people currently have ME/CFS, which is characterized by crushing fatigue that does not improve with rest, plus post-exertional malaise, unrefreshing sleep, pain, and cognitive problems, such as brain fog.1
The exact cause of ME/CFS remains unknown. Research suggests that the condition can follow certain triggers, including acute viral infections and severe physical or psychological stress, but no single cause has been identified. In recent years, several studies have reported abnormalities in mitochondrial function and energy metabolism in people with ME/CFS, suggesting a possible role for disrupted ATP production.
Immune Cells Show Clear Signs of Energy Overload
A study published in Cell Reports Medicine examined how ME/CFS is linked to a failure in cellular energy production. For the analysis, the researchers looked at an array of biomarkers, including immune cell metabolism, immune cell composition, and blood makeup.2
The study population included 61 individuals who met strict diagnostic criteria for ME/CFS, meaning they had long-standing fatigue, profound crashes following physical or mental effort, unrefreshing sleep, and cognitive problems.
• There is an ATP imbalance — The study found that adenosine monophosphate (AMP) and adenosine diphosphate (ADP) — two forms of energy molecules that rise when the cell exhausts adenosine triphosphate (ATP) — were elevated in ME/CFS patients. To put that into perspective, ATP is your body’s ideal energy format, whereas ADP and AMP are the substrates for ATP synthesis. If your body begins to use these, the energy you’re using is substandard.
• A theory on how cellular energy production is compromised — The researchers believe that those with ME/CFS have trouble producing enough energy due to an obstacle in the production chain. While their findings aren’t solid enough to propose a definite conclusion, here’s what they theorized:3
“The elevated NAD+ [nicotinamide adenine dinucleotide] levels observed in PBMCs [peripheral blood mononuclear cells], together with the increased AMP and ADP, suggest that NAD+ is not being efficiently reduced to NADH [nicotinamide adenine dinucleotide + hydrogen] to drive ATP synthesis through oxidative phosphorylation.
This impaired reduction of NAD+ to NADH may also help explain the observed inverse correlation between plasma AMP and PBMC ATP levels, although this finding requires further study.”
• Another major finding involved the natural killer (NK) cells — The researchers also discovered changes in the balance of immune cell types, including a reduction in certain mature dendritic cells and terminal NK cells. These normally help coordinate immune responses and act as a first line of defense.
When the population of NK cells drops, the immune system loses some of its agility and responsiveness. This means the fatigue you’re feeling is not only about energy loss — your immune system shifts into a pattern that reflects reduced readiness.
• Blood tests paint a more complete picture — The team reported higher levels of proteins associated with thrombus formation and altered vascular reactivity in the ME/CFS group. For context, thrombus means blood clot formation, and vascular reactivity reflects how blood vessels respond to signals that regulate tightening and relaxation.
When these protein levels rise, it suggests the lining of the blood vessels is under strain, which disrupts healthy circulation. For someone with ME/CFS, that could mean poor oxygen delivery, dizziness upon standing, and cold extremities.
• The study highlighted where the largest metabolic imbalances appeared — Individuals with the most altered ATP-to-ADP ratios tended to show larger distortions in immune cell composition. That suggests a link between energy depletion and immune exhaustion. If the immune system lacks energy, its cells lose the ability to mature properly or carry out normal defense tasks.
In addition, the vascular protein shifts closely aligned with the energy imbalance. When cellular energy drops, blood vessel function suffers. When this happens, the delivery of nutrients and oxygen is affected. This creates a loop that leaves the entire body underpowered.
• The biological mechanisms behind these findings trace back to disrupted ATP production — Normally, mitochondria generate ATP through oxidative phosphorylation, a process that depends on oxygen, nutrients, and intact cellular machinery.
When ATP falls and ADP or AMP rises, the cell enters a state of metabolic stress. Here, the cell may shift into emergency survival mode instead of normal function. That shift drains resilience, reduces cellular performance, and leaves tissues — especially the immune system and blood vessels — operating at a deficit.
• Another mechanism involves immune maturation — Dendritic cells and NK cells rely on ATP to fuel activation, communication, and response signaling. When ATP drops, these cells lose their functional sharpness. The study found this exact pattern: fewer mature cells and more signs of immune imbalance.
• Mechanistic hallmarks of ME/CFS — Although the paper did not measure symptom improvement over time, it did compare variables to determine which markers best distinguished ME/CFS participants from healthy controls.
A statistical model that incorporated metabolic markers, immune shifts, and vascular proteins reliably separated the two groups. This includes an abundance of AMP and ADP. In addition, the immune system is skewed towards less mature pathogenic fighters, alongside a lower population of NK cells.
Energy Deficits Push the Immune System Toward Burnout
In a related study published in Biomolecules, researchers showed how energy metabolism and immune function interact in ways that worsen symptoms of ME/CFS over time. Here, they used a broad body of evidence to map out how energy shortages inside cells feed directly into immune dysfunction, especially immune senescence and immune exhaustion.4
• Mitochondrial dysfunction stands at the center of this illness — However, the study adds something new to the conversation. In particular, the researchers noted that those with ME/CFS have compromised levels of carnitine, which is needed for fatty acid oxidation and energy metabolism.
Moreover, the researchers noted that this chemical helps maintain integrity of the mitochondria and reduce the production of reactive oxygen species (ROS). The image below provides an overview of their hypothesis:
Source: • The link to viruses — The paper identifies striking parallels between ME/CFS and chronic viral infections. In chronic viral states, the immune system fights for long periods without rest. Over time, some immune cells lose function and responsiveness through a process called cellular senescence, a state in which cells remain alive but no longer divide or respond effectively to threats. And when this reaches a chronic state, ME/CFS pathology occurs.
• Immune function breaks down — The immune system in people with ME/CFS shifts into a dysfunctional state. Similar to the previous study, they have altered NK cell function, changes in cytotoxic T cells, and persistent immune activation patterns that resemble those seen with unresolved infections.
• How energy metabolism and immune regulation are linked — The researchers argue that mitochondrial defects impair the immune system’s internal communication network. In addition, the same dysfunction creates a bottleneck for immune activity itself. In other words, your cells do not produce enough energy to meet the demands of immune signaling, repair, or defense.
• ME/CFS displays patterns of metabolic inflexibility — Cells struggle to switch between energy pathways or ramp up ATP production during stress. When your cells cannot adapt, even minor activity can produce a disproportionate crash. The featured study highlights published literature showing impaired energy production and utilization.
• Immune exhaustion driven by chronic metabolic strain — The paper explains that persistent energy deficits interfere with immune cell communication and their ability to generate powerful responses. When immune cells lack ATP, they lose the ability to proliferate, secrete cytokines, or kill infected targets effectively.
Strategies to Reclaim Your Energy and Live Life to the Fullest
If you’re low on energy, the solution isn’t drinking more coffee or energy drinks. It lies in your mitochondria, which has been compromised to such a point that it can’t function properly anymore. That said, I’ll be releasing a new book soon, “Cancer Cure,” which explores what changes occurred in our society today that resulted in a dramatic rise in metabolic dysfunction among millions of Americans.
The book will also discuss several strategies that can help you regain your cellular energy and improve your quality of life. Here are some of my recommendations:
1. Reduce linoleic acid (LA) intake — One of the reasons why you’re feeling fatigued is excess intake of LA, one of the most prominent toxins in the Western food supply. In fact, I’d go so far as to rank it above refined sugar, although that plays a role, too.
The reason why I’m saying this is because excess LA generates reactive byproducts that eventually suppress immune behavior, as well as damaging your mitochondria. So, get rid of any foods you have that contain LA, which are mainly seed oils — soybean, corn, cottonseed, canola, sunflower, and grapeseed.
In a previous article, I mentioned that modern Western diets now contain 15 to 25 grams of LA daily, which is a far cry from the estimated 2 to 4 grams that pre-industrial populations consumed.
In light of this, I recommend you keep your LA intake below 5 grams a day; if you can keep it below 2 grams, that’s even better. To track the LA in your food, sign up for the upcoming Mercola Health Coach app. It contains a feature called the Seed Oil Sleuth, which calculates daily LA consumption to a tenth of a gram. Swap LA-rich seed oils for healthier saturated fats like grass fed butter, ghee, tallow, and coconut oil.
2. Familiarize yourself about sources of LA — You’ll find LA not just in cooking oil sold in grocery stores. They’re found in most ultraprocessed foods, so it’s important to read through the ingredient list of whatever you’re buying.
In addition, it would be wise to minimize the times you eat in restaurants or order takeout. Unless strictly stated otherwise, it’s safe to assume that all the food cooked in these establishments use seed oils.
LA also is found in conventionally raised chicken and pork due to the ultraprocessed nature of their feed. Prioritize beef, lamb, bison, and other ruminants, which are likely to have lower LA levels.
3. Support your immune cells at the mitochondrial level — When ATP runs low, immune cells can’t communicate, divide, or kill threats efficiently. Several natural compounds have shown promising effects in boosting mitochondrial resilience and NK cell performance:
• Beta-glucans from yeast and mushrooms wake up your immune system by activating macrophages and NK cells.
• PQQ, found in papaya and green tea, sparks the production of new mitochondria and protects them from oxidative wear and tear.
• Urolithin A, a gut-derived compound from pomegranates, recycles defective mitochondria to keep your cellular engines running clean.
• Polyphenols like quercetin, fisetin, curcumin, and resveratrol scavenge harmful free radicals and reduce inflammatory suppression of NK cells.
In preclinical studies, when NK cells were given a combination of these compounds — delivered via nanoliposomes that targeted mitochondria directly—their killing capacity jumped five to tenfold. Instead of exhausting after five to ten kills, these cells could eliminate 30 to 50 targets before tiring out.
4. Repair your gut — Aside from your mitochondria, LA also wrecks your gut microbiome, which plays an extensive role in your health, including energy metabolism.5
Gut repair requires adequate carbohydrate intake to support intestinal cells and microbial balance. Your gut lining relies on glucose as a primary fuel, and insufficient carbohydrate intake can slow repair and weaken barrier integrity. Most adults need at least 250 grams of carbohydrates per day, adjusted for activity level and metabolic status. This intake supports gut repair, thyroid signaling, and overall energy balance.
Begin with well-tolerated carbohydrate sources such as sweet potatoes, carrots, winter squash, ripe fruit, and cooked white rice. These foods supply glucose while being lower in fermentable substrates. Add high-fiber foods slowly if gut health remains poor. Large amounts of fiber can intensify bloating, cramping, and constipation when intestinal permeability or dysbiosis persists. In this phase, prioritize digestible carbohydrates first and increase fiber only in small, gradual steps as tolerance improves.
As epithelial integrity strengthens and immune signaling stabilizes, fiber tolerance will improve as well. At that point, a broader range of fiber-rich foods can support short-chain fatty acid production and long-term resilience.
5. Exercise with restraint and precision — Your immune system relies on cytotoxic T lymphocytes and NK cells to remove damaged or dysfunctional cells. In ME/CFS, immune signaling, mitochondrial output, and energy recovery all falter, which changes how your body responds to physical stress. So, conventional exercise advice does not apply here.
High-intensity or endurance exercise often worsens symptoms and can trigger post-exertional malaise, a hallmark feature of ME/CFS. Rather than restoring immune function, excessive exertion can deepen mitochondrial injury and prolong recovery.
The goal is not fitness training. The goal is cellular signaling without metabolic overload. Most ME/CFS researchers emphasize gentle, low-stress movement that respects your available energy. Appropriate options include slow walking, light stretching, yoga, tai chi, and short bouts of resistance exercise that use body weight or very light loads.
Time and intensity matter more than duration. Many patients tolerate exercise best in intervals lasting seconds to a few minutes, followed by full recovery. Heart-rate monitoring and pacing strategies help you stay below your anaerobic threshold, which lowers the risk of symptom relapse. As mitochondrial function and autonomic balance improve, capacity often expands gradually.
Progress depends on consistency, recovery, and restraint, not intensity. Any program should adapt to daily energy limits rather than fixed schedules or goals.
6. Get restorative sleep — This is another cornerstone of health that’s often overlooked. In the case of people diagnosed with ME/CFS, research shows that sleep habits are often compromised — longer sleep onset latency and reduced sleep efficiency are common occurrences.6
When you get proper sleep, your body undergoes crucial repair processes. In particular, sleep allows your immune system to rest, allowing optimal surveillance in the long run against wayward cells that contribute to fatigue.
If you’re having a hard time sleeping, there are many strategies to help you. Read “Sleep — Why You Need It and 50 Ways to Improve It.” There, I also go over the science on what happens to your body while you rest, as well as the consequences of insufficient sleep.
Frequently Asked Questions (FAQs) About Chronic Fatigue Syndrome and Mitochondrial Function
Q: What is ME/CFS, and how common is it?
A: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) affects approximately 2 million Americans. It’s characterized by crushing fatigue that doesn’t improve with rest, post-exertional malaise, unrefreshing sleep, pain, and cognitive problems like brain fog.
Q: What does new research reveal about the underlying cause of ME/CFS?
A: Research found that ME/CFS patients have elevated adenosine monophosphate (AMP) and adenosine diphosphate (ADP) — energy molecules that accumulate when cells exhaust their primary energy source, adenosine triphosphate (ATP) — suggesting the body struggles to produce adequate cellular energy.
Q: How does ME/CFS affect the immune system?
A: Patients have reduced populations of natural killer (NK) cells and dendritic cells, both critical for immune defense. Because immune cells depend on ATP to function, energy deficits cause immune exhaustion and reduced ability to fight infections.
Q: Why do ME/CFS patients often experience circulatory symptoms like dizziness and cold extremities?
A: Studies found elevated proteins associated with blood clot formation and altered vascular function. When cellular energy drops, blood vessel function suffers, impairing oxygen and nutrient delivery throughout the body.
Q: What lifestyle strategies may help improve cellular energy production?
A: Recommendations include reducing linoleic acid intake (found in seed oils) to below 5 grams daily, optimizing gut health with fiber-rich whole foods, exercising according to ability to stimulate new mitochondria production, prioritizing restorative sleep, and supporting your immune cells at the mitochondrial level with natural compounds such as beta-glucans, PQQ, urolithin A, and polyphenols.
Vitamin E’s Therapeutic Benefits in Bone and Joint Disorders
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/05/vitamin-e-bone-joint-health.aspx
Analysis by Dr. Joseph Mercola March 05, 2026
Story at-a-glance
- Vitamin E is gaining attention in orthopedics because it influences inflammation, oxidative stress, and immune signaling, all of which shape how your bones and joints maintain strength over time
- Osteoporosis develops when bone breakdown outpaces rebuilding, and studies show vitamin E helps suppress this activity, reduce inflammatory cytokines, and support antioxidant defenses involved in bone preservation
- Research also links vitamin E to improved outcomes in osteoarthritis, fracture healing, implant longevity, arthrofibrosis, and osteomyelitis, suggesting broader musculoskeletal relevance beyond bone density alone
- Many people fall short on vitamin E because the most common sources come packaged with high linoleic acid, which raises your antioxidant demand beyond what diet alone typically supplies
- Choosing the right vitamin E supplement matters, since natural full-spectrum forms provide greater biological activity than synthetic versions, especially for bone and joint support
Your bones and joints influence how comfortably you move, how well you recover from physical stress, and how resilient your body remains over time. Many orthopedic conditions develop gradually, shaped by more than calcium intake or bone density alone. Inside your tissues, inflammation, oxidative stress, and immune imbalance can slowly disrupt the processes that maintain bone strength and joint integrity.
That is where vitamin E has begun to draw more attention. Best known as an antioxidant, it is now being examined more closely for its role in supporting bone and joint tissue, with researchers exploring how it may help preserve the structural strength your musculoskeletal system relies on across many different stages of life.1
Vitamin E Helps Slow the Bone Breakdown That Drives Osteoporosis
Osteoporosis is the most common orthopedic condition affecting older adults, and it develops when bones gradually lose both mass and internal strength. This decline increases the risk of fragility fractures, especially in the hip, spine, and wrist. Among women over 65, about one in four is affected, and lifetime fracture risk in osteoporosis may reach as high as 40%, making it one of the most widespread and serious age-related skeletal conditions.2
• Your bones are not static structures — They are constantly being renewed through a process called bone remodeling. Old or damaged bones are broken down and replaced with new bone to preserve strength and structure over time.
This cycle depends on two main types of cells: osteoclasts, which remove old bone, and osteoblasts, which build new bone in its place. Osteoporosis develops when the breakdown side of this cycle becomes too active, leaving the bone thinner and more fragile.
• Vitamin E interferes with the molecular “on switch” that drives osteoclast formation — A review published in IntechOpen describes a central molecular signaling system that acts like a biological “on switch” for osteoclast formation. When this signaling becomes overactive, the body produces more osteoclasts, and bone loss accelerates.
Vitamin E has been highlighted as a nutrient that interferes with this process by reducing the signals that drive osteoclast development and increasing natural regulators that help keep bone breakdown in check.
• Inflammation also plays an important role in osteoporosis — Inflammatory cytokines act as chemical messengers that can stimulate osteoclast activity. The IntechOpen review reports that vitamin E inhibits cytokines such as TNF-α, IL-1, IL-6, and IL-27, all of which are linked to bone resorption.
• Oxidative stress accelerates osteoclast activity — Vitamin E decreases malondialdehyde, a marker of lipid damage caused by oxidative stress, while increasing antioxidant enzymes such as superoxide dismutase and glutathione peroxidase. These shifts matter because oxidative stress can promote osteoclast activity, and the antioxidant role of vitamin E is tied directly to suppressing bone-resorbing processes.
• Not all forms of vitamin E appear equally active in bone tissue — Vitamin E exists in different forms, including tocopherols and tocotrienols, and these do not always behave the same way in the body. In laboratory models where bone-building cells and bone-resorbing cells interact, tocotrienols reduced the signals that normally tell the body to form more osteoclasts.
Researchers also found that α-tocotrienols lowered c-Fos, an important molecular switch that helps immature cells develop into fully active osteoclasts, while alpha-tocopherol, the form used in most standard supplements, did not show the same effect.3
• Population data links higher vitamin E intake with lower osteoporosis risk — An analysis of data from the U.S. National Health and Nutrition Examination Survey (NHANES) involving 5,800 U.S. adults aged 50 and older found that higher dietary vitamin E intake was associated with lower osteoporosis risk.
Each additional 1 milligram per day corresponded to a 4% reduction in risk, and those in the highest intake group showed substantially reduced odds compared with the lowest intake group. Vitamin E intake also showed a stronger association with lower osteoporosis risk among participants with a history of hormone use, suggesting that hormonal context may shape skeletal outcomes in older adults.4
The rising risk of osteoporosis highlights the importance of maintaining adequate vitamin E levels as a beneficial strategy to support bone health. Learn more in “Hip Fractures from Osteoporosis Predicted to Double by 2050.”
Vitamin E in Other Orthopedic Conditions
Vitamin E’s relevance in orthopedics extends beyond osteoporosis, because many bone and joint problems involve the same internal stressors that wear down tissue over time. A narrative synthesis published in The Indian Journal of Orthopaedics highlights several orthopedic settings where vitamin E appears to influence tissue stability and healing:5,6
• Osteoarthritis — This involves the gradual degeneration of cartilage, the smooth tissue that cushions your joints. Vitamin E’s antioxidant and anti-inflammatory effects may help mitigate cartilage degeneration triggered by mechanical stress or free radical injury. Low vitamin E levels in blood or synovial fluid have also been correlated with more significant osteoarthritis progression.
One study cited in the review involved patients with late-stage knee osteoarthritis, where 400 IU of alpha-tocopherol daily for two months led to reduced pain, stiffness, and functional limitation. These improvements were accompanied by differences in oxidative stress markers in both blood and synovial fluid (the lubricating fluid inside your joints).
• Fracture healing — Bone healing occurs in stages, including callus formation, where temporary scaffolding stabilizes the fracture while new bone is built. A systematic review of animal studies reported that alpha-tocopherol demonstrated a significant positive influence on bone formation during late callus remodeling.
The review also summarizes findings from an osteoporotic fracture model where alpha-tocopherol improved the stage of fracture healing compared with untreated osteoporotic controls. This improvement was accompanied by significantly higher activity of antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase during the early phase of repair.
• Joint replacement and implant longevity — In joint replacement surgery, implant materials slowly experience wear over time. Tiny debris particles can trigger inflammation and bone erosion around the prosthesis, contributing to loosening.
Meta-analyses cited in the review found that when vitamin E is incorporated into highly crosslinked polyethylene liners, a common implant material, it helps improve resistance to oxidative degradation and reduce wear-related bone loss around the implant.
• Post-surgical scar tissue — After orthopedic surgery, some patients develop excessive scar tissue inside the joint, which can restrict movement. This complication is called arthrofibrosis. Vitamin E’s local antioxidant and anti-inflammatory properties were reported to mitigate arthrofibrosis while improving final range of motion and weight-bearing symmetry.
• Osteomyelitis — Osteomyelitis is a serious bone infection, often caused by Staphylococcus aureus bacteria, that can destroy tissue and impair healing. The review highlights an animal study where titanium implants coated with a vitamin E phosphate layer showed lower bacterial levels, higher bone mineral density, and less bone tissue death, compared with uncoated implants.
• Tendon and ligament injuries — Some research suggests vitamin E may reduce swelling and tissue damage after musculoskeletal injury through its effects on inflammatory cytokines. The review notes preliminary suggestions that vitamin E could support healing after anterior cruciate ligament (ACL) tears or sprains by reducing excess scar buildup and protecting collagen fibers.
Across these orthopedic applications, the review presents vitamin E as a promising adjunct, with its consistent effects on inflammation, oxidative stress, and tissue healing.
The Role of Estrogen and Vitamin E in Postmenopausal Bone Health
Estrogen is often presented as a key protector of bone density, especially for women entering menopause. You’ve likely heard that once estrogen production declines, bone loss speeds up — and that’s true to a degree. After menopause, women typically lose bone mass at a faster rate, and this is commonly attributed to lower circulating estrogen levels.
What’s less widely recognized is how estrogen behaves in tissues compared to the bloodstream, and why vitamin E’s antiestrogenic activity may be especially relevant in this context.7,8,9
• Estrogen is not simply low across the board after menopause — Even when blood levels decline, estrogen can remain elevated in fat and other tissues, creating a hormonal environment that still favors estrogenic activity.
The use of hormone replacement therapy (HRT) intensifies this further by increasing estradiol and estrone concentrations within adipose tissue, while also reducing androgens like testosterone. The result is not a clean reversal of deficiency, but rather an increase in estrogen signaling where it already tends to accumulate.
• This is significant for bone health because estrogen affects more than bone density — In excess, estrogen contributes to higher intracellular calcium levels, increased oxidative stress, and suppressed mitochondrial function, which undermine bone regeneration and cellular energy metabolism.
It also fuels inflammatory processes that, over time, damage tissue and disrupt the balance of bone turnover. In this hormonal terrain, bone loss can continue or worsen despite estrogen being present in high amounts at the tissue level.
• Vitamin E helps rebalance the hormonal environment — It acts as a natural estrogen antagonist, blocking receptor activation, limiting estrogen’s stimulatory effects, and inhibiting aromatase, the enzyme that converts androgens into estrogens. These actions help blunt the excess estrogenic activity that accumulates in tissues, particularly in fat.
By doing so, vitamin E helps restore a more stable foundation for bone remodeling, not by increasing estrogen, but by limiting its dominance where it becomes counterproductive.
This perspective challenges the assumption that more estrogen is always better for bones. It also opens a path for targeted nutrient support that doesn’t carry the risks of pharmacological hormone manipulation. For women navigating midlife bone loss, and for anyone experiencing hormone-related disruptions in skeletal health, restoring hormonal balance through vitamin E may offer a safer and more sustainable foundation for long-term skeletal resilience.
Why Many People Don’t Get Enough Vitamin E from Their Diet Alone
Vitamin E exists in many foods, but that doesn’t mean you’re getting enough of it. One reason is that many common vitamin E sources, such as nuts, seeds, and vegetable oils, also come packaged with high amounts of linoleic acid (LA), an unstable omega-6 fat that increases oxidative stress. Instead of correcting a deficiency, these foods increase your demand for antioxidants like vitamin E, so you end up needing more just to keep up with the damage it generates.
• Some plant-based sources contain trade-offs that affect absorption — Beans and other legumes provide small amounts of vitamin E, but they also contain antinutrients such as lectins. In sensitive individuals, these compounds irritate the gut lining and interfere with nutrient absorption, making dietary vitamin E harder to utilize even when intake looks adequate.
• There are better options that provide vitamin E without the drawbacks — These include fresh fruits and vegetables such as pumpkin, asparagus, red bell peppers, tomatoes, kiwi, and mango. Pasture-raised, grass fed meats like beef and bison also contribute meaningful vitamin E, especially when you’re aiming to keep your LA intake low. These foods deliver vitamin E in a form your body absorbs more efficiently, especially when eaten alongside healthy fats.
• Modern diet is dominated by processed foods and industrial seed oils — For every gram of LA you eat, your vitamin E requirement goes up. This means someone eating 20 to 30 grams of LA per day, which is typical on a Western diet, would need far more vitamin E than what food alone can reasonably supply. This is why supplementing is a practical tool to counteract the effects of LA.
• Vitamin E supplementation becomes less necessary as LA burden declines — If you keep your LA intake below 5 grams per day for about three years, you may no longer need vitamin E supplements regularly, or you may only need them occasionally. If you do have a meal high in LA, taking a vitamin E capsule afterward helps protect your body from the effects of that specific meal.
Once your LA levels are lower, you’ll only need around 2 milligrams (mg) of vitamin E for every gram of LA you consume. With a recommended daily LA intake of 5 grams or less, that works out to about 10 mg of vitamin E per day, which is a relatively small amount. For best absorption, it’s ideal to take vitamin E with a healthy fat source, like coconut oil.
How to Choose the Right Vitamin E Supplement
Not all vitamin E supplements are created equal. Many products on the market use synthetic vitamin E, which is less biologically active than the natural form. Synthetic versions are often listed as alpha-tocopherol acetate, and the “acetate” label is a common sign that the product is not the same form of vitamin E found in food.
• Another issue is that many synthetic supplements are racemic — This means they contain a mix of mirror-image forms called isomers, like left and right hands. Your body strongly prefers one “handed” form of vitamin E. Only the “D” isomer provides health benefits, while the “L” isomer does not. In synthetic products, half of the vitamin E comes from this ineffective form, which significantly reduces the supplement’s overall potency.
• That is why label details matter — A high-quality supplement will list d-alpha-tocopherol, which indicates the natural D form. A label that says dl-alpha-tocopherol signals a synthetic mixture.
• Full-spectrum vitamin E provides broader benefits — For the best results, look for a supplement that provides the full range of vitamin E forms, including tocotrienols such as the beta, gamma, and delta types, in the natural D configuration. These different forms of vitamin E work synergistically to provide a wider range of health benefits.
• Choose a clean, food-based supplement without industrial additives — I recommend looking for a food-based supplement that contains all eight forms of vitamin E and avoids soy, soybean oil, and genetically engineered (GE) ingredients. Many lower-quality supplements use GE derivatives from corn, soy, or cottonseed, so choosing a clean, naturally sourced product helps ensure you are getting the highest-quality form available.
Frequently Asked Questions (FAQs) About Vitamin E and Bone Health
Q: What does vitamin E have to do with bone health?
A: Vitamin E influences the biological systems that control how your bones are maintained over time. Research shows it affects the activity of osteoclasts, the cells responsible for breaking down old bone, and helps regulate inflammatory and oxidative processes that accelerate skeletal weakening as you age.
Q: How might vitamin E help with osteoporosis?
A: Vitamin E has been shown to interfere with signals that drive excessive bone breakdown, including pathways involved in osteoclast formation. It also reduces inflammatory cytokines linked to bone resorption and supports antioxidant defenses that help protect bone tissue from oxidative damage, which plays a major role in osteoporosis progression.
Q: Why don’t I get enough vitamin E from food alone?
A: Many foods rich in vitamin E, such as nuts, seeds, and vegetable oils, are also high in linoleic acid (LA), which increases oxidative stress and raises your body’s demand for vitamin E. On a modern diet dominated by processed foods and seed oils, your requirement often exceeds what food alone can realistically supply.
Q: Are vitamin E supplements good for me?
A: Supplementing with vitamin E can be helpful, especially if you have a high LA burden or are trying to support bone and joint health during aging. Vitamin E is fat-soluble and provides antioxidant protection in tissues where oxidative stress contributes to degeneration, although the benefits depend heavily on using the right form.
Q: What should I look for in a high-quality vitamin E supplement?
A: Look for a natural form labeled d-alpha-tocopherol, not synthetic dl-alpha-tocopherol or acetate-based products. The best supplements include the full spectrum of vitamin E compounds, especially tocotrienols, and avoid soy, seed oils, and genetically engineered additives for cleaner, more effective support.
- 1, 5 JOIO 59, 1364–1380 (2025)
- 2, 3 IntechOpen, November 6, 2023
- 4 Front Endocrinol (Lausanne). 2024 Oct 21:15:1410581
- 6 Indian Journal of Orthopaedics 59(9) June 2025
- 7 J Clin Endocrinol Metab. 2024 Jul 10;110(2):511–522
- 8 Biomedicine & Pharmacotherapy June 2018, Volume 102, Pages 403-411 (Archived)
- 9 To Extract Knowledge from Matter February 9, 2025
Newly Discovered Coffee Compounds Outperform Diabetes Drug
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/06/coffee-compounds-outperform-diabetes-drug.aspx
Analysis by Dr. Joseph Mercola March 06, 2026
Story at-a-glance
- Scientists identified six previously unknown compounds in roasted Arabica coffee beans, and three of them slowed carbohydrate digestion more effectively in lab tests than the diabetes drug acarbose
- These coffee compounds work by blocking the same digestive enzyme that turns starch into glucose, helping sugar enter your bloodstream more gradually instead of spiking sharply after meals
- The discovery shows your daily cup of coffee contains measurable bioactive molecules that directly interact with blood sugar metabolism
- Lab testing confirmed consistent enzyme-blocking effects, strengthening the evidence that these compounds are biologically active rather than random plant chemicals
- Long-term blood sugar control still depends on correcting insulin resistance and restoring cellular energy production, not relying on coffee alone
Scientists recently discovered new compounds in roasted coffee beans — and in lab tests, some of them outperformed a common diabetes medication at slowing down carbohydrate digestion. The drug they compared it to, acarbose, works by blocking an enzyme in your gut that breaks starch down into sugar. The enzyme is called alpha-glucosidase — it sits in the lining of your small intestine and snips complex starches into simple glucose molecules.
When that enzyme is slowed, sugar enters your bloodstream more gradually after a meal instead of all at once. That’s a big deal for anyone dealing with blood sugar issues. What makes this finding stand out is that these aren’t compounds scientists already knew about.
The research team identified six previously unknown molecules in coffee, isolated three of them, and put them to the test. The results were striking enough to warrant a closer look at what’s actually going on inside your morning cup — and what it means for blood sugar management.
Scientists Found New Coffee Compounds That Slow Sugar Spikes
In the study published in Beverage Plant Research, scientists didn’t just separate coffee into random chemicals and hope something worked.1 They first tested roasted Arabica coffee extracts to see which parts actually slowed the enzyme that breaks down carbohydrates. Then they focused only on the parts that showed real effects. That matters because it means these compounds were selected based on performance, not chance.
• They split coffee into pieces and tested each one — The researchers divided a concentrated coffee extract into 19 different parts and tested each part to see if it could slow the sugar-releasing enzyme. Only a small group showed strong activity. Instead of wasting time on inactive parts, they zoomed in on the ones that clearly made a difference. Think of it like testing 19 keys and quickly figuring out which few actually open the lock.
• They discovered three completely new coffee compounds — From the most active group, the team isolated three brand-new natural compounds that hadn’t been described before. They named them caffaldehydes A, B and C. Each one was carefully tested to see how strongly it slowed the enzyme that breaks starch into sugar.
All three new compounds shared the same main structure, but they had slightly different fatty acid “tails” attached. The version with the longer fatty acid tail showed the strongest enzyme blocking — think of it like a longer key that fits more snugly into the enzyme’s active site, making it harder for starch molecules to get in. That shows how even small chemical differences change how powerfully a natural compound works in your body.
• All three compounds outperformed a common diabetes drug — The scientists compared the three newly identified coffee compounds to acarbose, a medication used to slow carbohydrate digestion. In lab testing, each of the three compounds blocked the enzyme more effectively than acarbose under the same conditions. In simple terms, it took less of each coffee compound to achieve the same level of enzyme slowdown as the drug, with one compound showing the strongest effect of all.
• They found three more hidden compounds without fully isolating them — After identifying the main three, the researchers used advanced scanning technology to search for similar compounds in the rest of the coffee extract. They identified three additional new compounds that looked structurally related to the first group. These were found even though they were present in much smaller amounts. This tells you coffee contains more active molecules than previously recognized.
• They confirmed how these compounds work in the body — The targeted enzyme sits in your digestive tract and helps turn complex carbohydrates into glucose. When this enzyme slows down, sugar enters your bloodstream more gradually instead of flooding it all at once. The study clearly states that the three main compounds were responsible for this enzyme-blocking effect in the tested extract.
The researchers ran the enzyme tests multiple times and reported consistent results. The numbers stayed close across repeated experiments, which means the effect was reliable in the laboratory setting.
How to Fight Diabetes at the Source
You just learned that specific compounds in roasted Arabica coffee block the same enzyme targeted by a common diabetes drug. That matters. But isolated lab findings are only part of the picture. Enzyme-blocking is one layer of blood sugar control. The deeper question is why your cells aren’t handling glucose properly in the first place. If you want steady blood sugar, you have to correct the root problem: impaired glucose handling driven by mitochondrial dysfunction and insulin resistance.
Your mitochondria are the energy generators inside every cell — when they work well, they efficiently convert glucose into adenosine triphosphate (ATP), the molecule your cells actually run on. Focus first on restoring cellular energy production, because when your cells burn fuel efficiently, glucose doesn’t linger in your bloodstream and cause damage. Here are six direct steps you can take.
1. Get more from your coffee by drinking it clean — The compounds in this study came from roasted Arabica beans, which means regular brewed coffee is a natural source. But how you prepare and drink it matters. Choose organic, single-origin Arabica beans to minimize pesticide exposure. Grind them fresh and brew with filtered water.
Skip artificial creamers, flavored syrups, and sugar — these add inflammatory ingredients that work against the very blood sugar benefits you’re trying to gain. If you use a creamer, opt for grass fed dairy, including whole milk or cream. Black coffee or coffee with clean fats keeps those bioactive compounds front and center without sabotaging your metabolism.
2. Increase carbohydrates strategically — Most adults need 250 grams of carbohydrates daily for optimal cellular energy, and more if you’re physically active. If you restrict carbohydrates long term, you drive reductive stress — an excess of electrons that jams up your mitochondria’s energy-producing machinery — and impair mitochondrial ATP production.
Start with easily digested carbs like fruit and white rice, especially if your gut health is compromised. Then, gradually add in root vegetables, non-starchy vegetables, starchy vegetables like squash or sweet potatoes, beans and legumes, and finally minimally processed whole grains — only if your gut can handle them. Gradual increases restore metabolic flexibility.
3. Remove seed oils completely and replace them with stable fats — Excess linoleic acid (LA) from seed oils disrupts mitochondrial energy production and promotes insulin resistance. That’s a root driver of unstable blood sugar.
Eliminate seed oils, including corn, soybean, canola, sunflower, and safflower oils, along with commercial salad dressings, packaged snacks like crackers, and most restaurant foods. Replace them with grass fed butter, ghee or tallow. Lowering tissue LA over time improves cellular energy efficiency and reduces oxidative stress.
4. Build muscle with adequate protein and collagen — Muscle tissue absorbs glucose directly from your bloodstream — the more lean mass you carry, the more capacity your body has to clear excess blood sugar without relying heavily on insulin. Aim for 0.8 grams per pound of ideal body weight, or 1.76 grams per kilogram.
One-third of that intake should come from collagen sources, like bone broth. This supports structural integrity and metabolic resilience. If you’re over 40, this step becomes even more important because muscle loss accelerates insulin resistance.
5. Use sunlight and targeted movement to improve glucose handling — Daily sun exposure enhances mitochondrial function and nitric oxide production. Morning light sets your circadian rhythm and improves metabolic signaling. Combine that with one hour of walking daily — start gradually with 15 minutes and work your way up — and progressive strength training. Movement improves insulin sensitivity immediately.
Sunlight amplifies cellular energy production. If you’ve been regularly consuming seed oils, avoid midday sun exposure (10 a.m. to 4 p.m.) for at least the first six months after eliminating them, as LA stored in skin tissue increases your risk of sunburn.
6. Know Your HOMA-IR score — a simple test for insulin resistance — Recognizing insulin resistance early is essential, as it’s a warning sign for your metabolic health — one that often precedes Type 2 diabetes. The HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) test is a valuable diagnostic tool that helps assess insulin resistance through a simple blood test, so you can spot issues early and make necessary lifestyle changes.
Created in 1985, it calculates the relationship between your fasting glucose and insulin levels to evaluate how effectively your body uses insulin. Unlike other more complex tests, HOMA-IR requires just one fasting blood sample, making it both practical and accessible. The HOMA-IR formula is as follows:
HOMA-IR = (Fasting Glucose x Fasting Insulin) / 405, where
• Fasting glucose is measured in mg/dL
• Fasting insulin is measured in μIU/mL (microinternational units per milliliter)
• 405 is a constant that normalizes the values
If you’re using mmol/L for glucose instead of mg/dL, the formula changes slightly:
HOMA-IR = (Fasting Glucose x Fasting Insulin) / 22.5, where
• Fasting glucose is measured in mmol/L
• Fasting insulin is measured in μIU/mL
• 22.5 is the normalizing factor for this unit of measurement
Anything below 1.0 is considered a healthy HOMA-IR score. If you’re above that, you’re considered insulin resistant. The higher your values, the greater your insulin resistance. Conversely the lower your HOMA-IR score, the less insulin resistance you have, assuming you are not a Type 1 diabetic who makes no insulin.
Interestingly, my personal HOMA-IR score stands at a low 0.2. This low score is a testament to my body’s enhanced efficiency in burning fuel, a result of increased glucose availability. By incorporating additional carbohydrates into my diet, I provided my cells with the necessary energy to operate more effectively.
This improved cellular function has significantly boosted my metabolic health, demonstrating how strategic dietary adjustments lead to better insulin sensitivity and overall metabolic performance.
If you drink coffee daily, recognize that it contains bioactive compounds that interact with glucose metabolism. But don’t rely on coffee alone. Real metabolic recovery requires correcting insulin resistance, restoring mitochondrial energy production, and removing the environmental stressors that sabotage your cells. When you address the root, the numbers follow.
FAQs About Newly Discovered Coffee Compounds
Q: What did scientists discover in coffee beans?
A: Researchers identified six previously unknown natural compounds in roasted Arabica coffee beans. Three of these were isolated and tested in the lab, where they slowed the same digestive enzyme targeted by the diabetes drug acarbose. The coffee compounds worked more strongly than the drug under identical lab conditions.
Q: How do these coffee compounds affect blood sugar?
A: They slow down an enzyme in your digestive tract that breaks starch into glucose. When that enzyme is slowed, sugar enters your bloodstream more gradually after a meal instead of spiking quickly. Slower absorption helps reduce sharp blood sugar swings.
Q: Does this mean coffee cures diabetes?
A: No. The study was done in a laboratory setting, not in human clinical trials. It shows that roasted Arabica coffee contains bioactive compounds that influence carbohydrate digestion. It doesn’t prove that drinking coffee alone reverses diabetes. Blood sugar control depends on overall metabolic health.
Q: Why is insulin resistance the real issue to address?
A: Insulin resistance means your cells don’t respond properly to insulin, forcing your body to produce more of it to manage blood sugar. Over time, this leads to chronically elevated insulin and glucose levels. Measuring your HOMA-IR score gives a clearer picture of how well your body handles glucose and whether you’re improving.
Q: What practical steps support healthy blood sugar regulation?
A: Choose clean, organic Arabica coffee without added sugars or artificial creamers. Eliminate seed oils to reduce metabolic stress. Eat adequate carbohydrates to support cellular energy, especially from whole fruits and digestible starches. Build muscle with sufficient protein, including collagen. Get daily sunlight and consistent movement to improve mitochondrial function and insulin sensitivity.
Oxidative Stress and Oral Bacteria Help Set the Stage for Stomach Cancer
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/06/stomach-cancer-prevention-oxidative-stress.aspx
Analysis by Dr. Joseph Mercola March 06, 2026
Story at-a-glance
- Stomach cancer develops silently over decades, with early biological damage occurring long before obvious symptoms like indigestion or anemia appear
- Oxidative stress leaves distinct DNA damage in stomach cells, allowing abnormal cells to survive instead of being removed
- Harmful bacteria from your mouth can migrate into your stomach, where they drive chronic inflammation and weaken local immune defenses
- Age-related immune decline makes it harder for your body to control damaged stomach cells and invading microbes
- Reducing oxidative stress, protecting oral health, avoiding seed oils, and strengthening immune coordination early helps interrupt the process that leads to stomach cancer
You might dismiss persistent heartburn as “just stress” or blame your upset stomach on last night’s dinner. But inside your stomach lining, a different story might be unfolding — one that began years ago, long before you felt anything was wrong.
Stomach cancer still ranks among the world’s most lethal malignancies, yet it rarely receives the attention its death toll warrants. In 2020 alone, it accounted for roughly 769,000 deaths worldwide, placing it fourth among all cancer-related causes of death.1
Stomach cancer develops slowly, often over decades, without clear warning signs early on. By the time symptoms such as ongoing digestive discomfort, unexplained weight loss, nausea, or anemia appear, damage is already underway. Many people, understandably, write these signals off as stress, aging, or routine stomach trouble.
Even when doctors detect early changes in your stomach lining, they face an unsettling reality: they can’t reliably predict whose damaged tissue will become cancer and whose will remain stable. That uncertainty leaves you monitoring and waiting, knowing something’s wrong but unable to quantify your actual risk. Recent large-scale research shifts that picture.2
Instead of viewing stomach cancer as a sudden event, the data show a slow accumulation of biological stressors that leave detectable traces long before cancer appears. If you assume cancer only becomes visible once symptoms begin, that assumption no longer holds. The most important clues emerge earlier, embedded in subtle changes inside your stomach itself.
How Oxidative Stress and Oral Bacteria Push Stomach Cells Toward Cancer
A study published in Cancer Discovery looked at more than 1,500 samples of damaged stomach tissue from people in six different countries with very different stomach cancer rates. The researchers focused on intestinal metaplasia — think of it as your stomach lining forgetting its original job and trying to become intestine instead.
This identity crisis happens after years of irritation, and while it’s not cancer yet, it’s a warning that the protective barrier is breaking down. This condition raises cancer risk, but not everyone with it develops stomach cancer. The researchers wanted to understand why some people progress to cancer while others do not.
Many of the tissue samples came from older adults, smokers, or people living in regions where stomach cancer is more common. These groups already face higher risk, yet doctors often can’t tell who will get worse.
The study revealed that danger emerges not from any single factor, but from a perfect storm: ongoing cell damage overwhelms repair mechanisms while a weakening immune system fails to clear the damaged cells, and bacteria from your mouth colonize the wounded tissue, driving relentless inflammation.
• Repeated DNA damage showed up inside precancerous stomach cells — Researchers found damage in 47 different genes inside intestinal metaplasia tissue. One gene, called ARID1A, stood out because damage to it was strongly linked to higher cancer risk and poorer outcomes.
Think of ARID1A as your cell’s quality control inspector. It checks for DNA damage and, when it finds too much, triggers the cell’s self-destruct sequence. When this gene is damaged, it’s like the inspector went home — broken cells that should die instead stick around, accumulate more damage, and eventually turn cancerous.
• A clear signal of oxidative stress appeared in damaged tissue — The study identified a specific DNA damage pattern. Think of this as a fingerprint that shows what harmed the cell. The pattern points to oxidative stress, which is damage caused by unstable oxygen molecules that build up during poor metabolism or toxin exposure.
This pattern showed up in precancerous tissue but not in healthy stomach cells. Smoking made this damage much worse, showing how daily habits speed up injury inside the stomach lining.
• Aging blood cell mutations weakened immune protection — As you age, some blood stem cells accumulate mutations that give them a growth advantage — they’re like weeds in your bone marrow garden, crowding out the healthy plants. These mutated stem cells then churn out immune cells that don’t function properly. It’s not that you have fewer immune cells; you have the wrong kind, and they can’t effectively patrol your stomach lining for damaged cells.
• Bacteria from the mouth moved into the stomach — Researchers found higher levels of mouth bacteria, especially Streptococcus, inside stomach tissue from high-risk patients. These bacteria belong in your mouth, not your stomach. Their presence signals that your stomach’s protective barrier has broken down. Your stomach is supposed to be nearly sterile — its harsh acid environment is designed to kill most microbes.
When mouth bacteria survive there, it signals two disasters at once: your protective acid barrier has failed, and foreign invaders are now permanently camped in territory they shouldn’t be able to access. It’s like finding ocean fish swimming in your freshwater lake — the ecosystem has fundamentally broken.
While oral bacteria like Streptococcus are now a recognized threat, the more famous stomach bacterium H. pylori remains important. However, this research reveals that H. pylori isn’t working alone — your oral microbes interact with damaged tissue and weakened immunity to amplify risk.
• Immune weakness and bacteria fed off each other — The study showed that weakened immune defenses allowed mouth bacteria to survive in the stomach. Those bacteria then increased inflammation, which caused even more cell damage. This created a vicious cycle where damage, inflammation, and immune failure reinforced each other over time.
• Damage also disrupted the stomach’s microbial control system — Mutations appeared in a gene that helps regulate how the stomach manages bacteria. When this system breaks down, harmful bacteria persist while protective responses fade. Combined with oxidative stress, this turns your stomach lining from a protective barrier into a chronic inflammation zone.
Here’s what makes this research genuinely hopeful: every mechanism the scientists identified is modifiable. You don’t need expensive tests or experimental treatments. The biological processes that set the stage for stomach cancer respond to straightforward interventions — some as simple as what you eat for breakfast or how you care for your teeth. The key is acting now, while those early changes are still reversible.
Steps That Reduce the Drivers of Stomach Cancer Risk
The research makes one point clear: stomach cancer doesn’t begin as a sudden event. It grows out of long-term biological stress that wears down stomach tissue year after year. Oxidative damage, mouth bacteria that drift into your stomach, and gradual immune weakening create the conditions where abnormal cells survive instead of being cleared. The steps below focus on interrupting those processes early, when change still matters.
1. Lower oxidative stress where it starts — If you smoke, experience chronic inflammation (arthritis, autoimmune disease, inflammatory bowel issues), or battle persistent fatigue, oxidative stress is already damaging your stomach lining — even if you feel no digestive symptoms. Tobacco exposure directly drives the DNA damage pattern linked to stomach cancer, which makes complete avoidance essential. Energy balance matters just as much.
Chronic carbohydrate restriction weakens mitochondrial energy production and increases reductive stress, which raises internal damage. Adequate carbohydrate intake — about 250 grams daily — keeps your cellular energy production running smoothly, like a well-tuned engine that produces power instead of smoke. When carbs are too low, your mitochondria struggle and sputter, creating the very oxidative stress you’re trying to avoid.
2. Protect oral health as a first line of stomach defense — If gum bleeding, bad breath, frequent cavities, or dental inflammation show up regularly, harmful mouth bacteria are already thriving. Research shows these bacteria migrate into your stomach and fuel chronic inflammation there.
Careful brushing along the gumline, consistent flossing, and a diet low in refined sugar and processed foods help optimize your oral health. A healthier mouth directly lowers inflammatory pressure inside your stomach.
Practical implementation: Brush for two minutes twice daily using a soft-bristled brush angled at 45 degrees toward your gumline — this targets the bacterial buildup where gums meet teeth. Floss before brushing at night to dislodge debris that bacteria feed on.
If you see blood when you floss, you likely have gum inflammation; continue daily flossing and the bleeding should stop within one to two weeks. If it doesn’t, schedule a dental cleaning with a biological dentist.
3. Minimize linoleic acid-rich seed oils to protect mitochondrial function — Inside each mitochondrion there’s a highly specialized structure called the inner mitochondrial membrane — the surface where energy production takes place. Roughly 20% of this membrane is composed of cardiolipin, a distinctive phospholipid that contains four fatty acid chains instead of the usual two.
Cardiolipin stabilizes the electron transport chain, maintains the folded cristae structure that expands surface area for energy production, and helps manage proton flow needed to generate ATP.
Importantly, cardiolipin requires linoleic acid (LA) to function properly. The problem begins when excess dietary LA accumulates in the other 80% of the inner mitochondrial membrane — phospholipids that are NOT designed to carry high LA loads. In those surrounding membranes, LA is highly prone to oxidation.
Reactive oxygen species (ROS) generated during normal energy production initiate lipid peroxidation, forming toxic aldehydes that bind to respiratory proteins, impair electron transfer, and amplify oxidative stress in a self-perpetuating cycle. When LA in these non-cardiolipin phospholipids exceeds 7% to 8%, the risk of membrane dysfunction increases threefold.
Keeping daily LA intake under 5 grams, and closer to 2 grams when possible, helps limit excess incorporation into these non-cardiolipin membrane compartments. This means minimizing seed oils hidden in packaged foods, sauces, dressings, and restaurant meals, and choosing more oxidation-resistant fats such as tallow, ghee, or grass fed butter.
The Mercola Health Coach app, which will be available soon, includes a feature called the Seed Oil Sleuth. It makes tracking your LA intake easy — calculating it down to a tenth of a gram.
4. Remove habits that accelerate immune decline with age — Your immune system doesn’t simply “get worse with age” — it changes, and certain habits accelerate its dysfunction. After 40, blood stem cell mutations become more common, but lifestyle factors determine whether these mutations dominate your immune system or remain in check.
Alcohol undermines mitochondrial energy production and weakens immune signaling in your gut, which raises long-term risk. Protecting sleep timing and getting morning sunlight support circadian rhythm, the system that coordinates immune defense. A more responsive immune system clears damaged stomach cells before they accumulate additional mutations.
Protect your circadian rhythm by maintaining consistent sleep/wake times within a 30-minute window, even on weekends. Get 10 to 15 minutes of outdoor morning sunlight within one hour of waking — no sunglasses — to set your circadian clock. Dim indoor lights after sunset and avoid screens in the hours before bed. Aim for sleep between 10 p.m. and 6 a.m. when immune repair functions peak.
5. Pay attention to early warning signs, not just symptoms — If a family history of stomach cancer, long-term smoking exposure, or chronic gut issues are part of your background, silence does not equal safety. Signals such as unexplained anemia, persistent stomach discomfort, appetite changes, or sudden shifts in oral health reflect deeper changes in immunity and bacterial balance. These signs appear long before cancer develops and offer a window to act early, while prevention still works.
Together, these steps slow the biological wear that allows stomach cancer to take root. Lower oxidative stress, healthier oral bacteria, protected mitochondrial structure, stronger immune coordination, and a calmer stomach lining change the trajectory long before disease becomes visible.
FAQs About Stomach Cancer
Q: What makes stomach cancer so dangerous compared to other cancers?
A: Stomach cancer develops over many years and often causes few clear symptoms early on. By the time warning signs such as persistent indigestion, anemia, nausea, or unexplained weight loss appear, significant damage to your stomach lining has already occurred. This slow, silent progression is a major reason it remains one of the leading causes of cancer-related death worldwide.
Q: What early changes increase the risk of stomach cancer?
A: Three mechanisms conspire to create cancer risk: oxidative stress that damages DNA faster than cells repair it, age-related immune dysfunction that fails to clear damaged cells, and oral bacteria that colonize damaged stomach tissue and drive chronic inflammation. When all three are present simultaneously, risk multiplies exponentially. These factors leave detectable biological damage long before cancer forms, even when a person feels mostly well.
Q: How does oxidative stress contribute to stomach cancer risk?
A: Oxidative stress damages DNA inside stomach cells. Over time, this damage allows abnormal cells to survive and multiply instead of being removed. Smoking, poor metabolic health, and unstable dietary fats like LA accelerate this process, increasing the likelihood that precancerous changes progress.
Q: Why does oral health matter for stomach cancer prevention?
A: Certain mouth bacteria, especially those linked to gum disease, can move into your stomach when natural defenses weaken. Once there, they drive chronic inflammation and interfere with immune signaling. Maintaining good oral hygiene reduces the bacterial load reaching your stomach and lowers long-term inflammatory pressure.
Q: What practical steps lower long-term stomach cancer risk?
A: Key actions include eliminating smoking, supporting steady cellular energy with adequate carbohydrates, avoiding seed oils high in LA, protecting sleep and circadian rhythm, limiting alcohol, and paying attention to early warning signs such as anemia or persistent stomach discomfort. Addressing these root causes early changes the biological conditions that allow stomach cancer to develop.
The Humble Fruit That Delivers 10 Powerful Health Benefits — and Most People Aren’t Eating Enough of It
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/06/watermelon-health-benefits.aspx
Analysis by Dr. Joseph Mercola March 06, 2026
Story at-a-glance
- Eating 2.5 to 3 pounds of watermelon daily provides 51 to 80 mg of lycopene — well above the 10 to 30 mg therapeutic threshold linked to reduced cancer risk, cardiovascular protection, and skin defense against UV damage
- Watermelon is 92% water, delivering roughly 1 liter of slow-absorbing, electrolyte-accompanied hydration that your body retains more efficiently than plain drinking water
- The citrulline in watermelon converts to arginine, boosting nitric oxide production for improved blood flow, lower blood pressure, and enhanced exercise performance
- Fruit is one of the most important ways to get potassium into your body, and watermelon is one of the easiest and most practical vehicles for doing so consistently
- From kidney support and gut health to eye protection and muscle recovery, watermelon stacks an impressive number of therapeutic benefits into a single, widely available whole food
Most people think of watermelon as little more than a summer treat — something you slice up at a barbecue and eat while the juice drips down your chin. But this humble fruit, a member of the Cucurbitaceae family that traces its origins back 5,000 years to ancient Egypt, may be one of the most therapeutically valuable whole foods you can add to your daily routine.
I’m not speaking theoretically here. I’ve been eating approximately 2.5 to 3 pounds of watermelon every single day for the last five years. Not seasonally. Not occasionally. Every day. And the cumulative benefits I’ve experienced have only reinforced my conviction that this is one of the most underutilized health strategies available. What I want to share with you today are 10 research-backed reasons why I believe this practice is worth adopting — and why I have no intention of stopping.
10 Research-Backed Reasons Watermelon Deserves a Daily Spot in Your Diet
1. A lycopene powerhouse that outperforms tomatoes — When most people think of lycopene, they think of tomatoes. But cup for cup, watermelon actually delivers comparable, and in many cases superior, levels of this key carotenoid antioxidant, particularly in its more bioavailable cis-isomeric form — a molecular shape your intestines absorb more readily than the form found in raw tomatoes.
• My daily 2.5 to 3 pounds of watermelon provides approximately 51 to 80 milligrams (mg) of lycopene — To put that in perspective, the majority of clinical studies demonstrating significant health benefits — including reduced risk of prostate cancer, lower LDL oxidation, and improved arterial function — have used doses in the range of 10 to 30 mg per day.
I’m getting double to triple the therapeutic dose from watermelon alone, and I’ve been doing so consistently for five years.
• Lycopene’s role in cardiovascular protection is particularly well documented — It helps prevent the oxidation of LDL cholesterol, which is one driver in the formation of arterial plaque.1 It also helps lower blood pressure and reduces overall oxidative stress throughout your body.2,3
2. Superior hydration your body actually retains — We’ve been conditioned to believe that drinking eight glasses of water a day is the gold standard of hydration. But there’s growing recognition that how you take in water matters just as much as how much you consume.
• Watermelon is approximately 92% water — This means my daily intake delivers roughly 1 liter or more of fluid. But here’s what makes it different from simply drinking a liter of water: the water in watermelon is absorbed more slowly and steadily because it’s bound within the cellular matrix of the fruit, accompanied by natural electrolytes like potassium and magnesium, along with natural sugars that facilitate absorption.
• This is essentially nature’s electrolyte drink — But without the artificial colors, flavors and excessive sugars found in commercial sports beverages. After five years of this, I notice a clear difference — the hydration from whole-food water sources feels more sustained than what I get from drinking water alone.
3. Citrulline: The amino acid your cardiovascular system is craving — One of the most underappreciated compounds in watermelon is citrulline, a nonessential amino acid that your kidneys convert into arginine. Arginine, in turn, is the precursor to nitric oxide — a molecule that is absolutely crucial for vascular health.4
• Nitric oxide relaxes and dilates your blood vessels — This improves blood flow, reduces blood pressure and decreases the workload on your heart.5 Think of it as the difference between pushing water through a narrow garden hose versus a wide-open pipe — your heart has to work significantly harder when vessels are constricted.
A study published in the American Journal of Hypertension found that watermelon extract significantly improved arterial function and lowered aortic blood pressure in participants with prehypertension.6
• The implications extend beyond heart health — Improved nitric oxide production supports everything from cognitive function to sexual health to exercise endurance. And I’m getting this from a whole food every single day, not a supplement.
4. One of the most important ways to get potassium into your body — This is a point I want to emphasize because I believe it’s widely underappreciated: fruit is one of the most important ways to get potassium into your body.7 Most Americans are chronically deficient in this essential mineral, and the consequences — elevated blood pressure, muscle cramps, irregular heart rhythm, impaired nerve function — are far more serious than most people realize.
• The recommended daily intake ranges from 2,600 to 3,400 mg — Yet the average American gets barely half that. My daily 2.5 to 3 pounds of watermelon delivers approximately 640 to 840 mg of potassium — roughly 20% to 30% of my daily requirement from a single food source. And it arrives in a highly bioavailable form, accompanied by water and other electrolytes, which optimizes absorption in a way that supplements simply cannot replicate.
• There’s a reason potassium occurs naturally inside hydrating, mineral-rich fruit — not in isolated tablets — The delivery system matters. The co-factors matter. And watermelon is one of the most practical and enjoyable vehicles for consistent potassium intake I’ve ever found — which is exactly why I’ve maintained this practice for five years running.
When you combine potassium’s blood pressure benefits with citrulline’s vasodilatory effects, watermelon is doing double duty on cardiovascular health through two entirely different mechanisms.
5. A potent anti-inflammatory food — Chronic, low-grade inflammation is at the root of virtually every modern degenerative disease, from heart disease and diabetes to Alzheimer’s and cancer.8,9 Lycopene, along with other bioactive compounds in watermelon like cucurbitacin E — a triterpene compound found in members of the gourd family — has been shown to reduce systemic inflammatory markers, including C-reactive protein.
• This isn’t a subtle effect — Research consistently shows that individuals with higher lycopene intake demonstrate measurably lower levels of inflammation. Given that my daily intake provides well above the therapeutic threshold — and has done so consistently for five years — I’m delivering a meaningful anti-inflammatory intervention with every serving.
6. Gut health and digestive ease — Watermelon is one of the gentlest foods on the digestive system. Its high water content — combined with approximately 3 to 5 grams of fiber per 2.5 to 3 pounds — supports healthy digestion and regular bowel movements without the bloating or discomfort that higher-fiber foods sometimes cause.
• Watermelon offers a way to nourish your body without taxing your gut — This is especially important for individuals dealing with digestive sensitivities or recovering from gastrointestinal issues. The water content also helps keep things moving through your intestinal tract efficiently, which supports the elimination of waste and toxins. In five years of daily consumption, I can attest that this is one of the easiest foods to digest consistently.
7. Eye health protection — Watermelon provides beta-carotene, which your body converts to vitamin A — a nutrient essential for maintaining healthy vision and supporting your retina. A daily serving of 2.5 to 3 pounds contributes meaningfully toward your daily vitamin A needs.
• Watermelon contains small but relevant amounts of lutein — This is a carotenoid that concentrates in the macula of the eye and is associated with reduced risk of age-related macular degeneration — one of the leading causes of vision loss as we age.10 While watermelon alone won’t replace dedicated lutein-rich foods like leafy greens, it adds another layer of protection as part of a whole-food diet.
8. Kidney support and detoxification — Your kidneys are your body’s primary filtration system, and they thrive on adequate hydration. The high water content in watermelon helps flush your kidneys naturally, supporting the elimination of waste products and reducing the burden on this key organ system.
• Watermelon goes beyond simple hydration — The citrulline it contains plays a direct role in the urea cycle — the metabolic pathway your body uses to convert toxic ammonia into urea for safe excretion. Every time your body breaks down protein, ammonia is produced as a byproduct.
Your liver and kidneys need to convert that ammonia into urea so it can be safely excreted in urine. Citrulline is a key player in that conversion process. By supporting this biochemical process, watermelon is actively assisting your body’s detoxification capacity at the cellular level.
• Watermelon is ideal for individuals concerned about kidney stone risk — The combination of increased fluid intake and potassium from watermelon helps reduce the concentration of stone-forming minerals in the urine.
9. Muscle recovery and exercise performance — If you exercise regularly — and I hope you do — watermelon should be on your post-workout menu. Research published in the Journal of Agricultural and Food Chemistry found that citrulline from watermelon juice significantly reduced muscle soreness in athletes after intense exercise.11
• Watermelon is a remarkably complete recovery food — The natural sugars in watermelon help replenish glycogen stores after physical activity, while the water and electrolytes support rehydration. Watermelon combines anti-inflammatory compounds, amino acid precursors, natural sugars, and hydration in a single package.12
• You don’t need an expensive recovery supplement — Nature already designed one. I’ve relied on this for the past five years and my recovery after physical activity remains excellent.
10. Weight management made effortless — Here’s where the math becomes extraordinary. A full 2.5 to 3 pounds of watermelon contains only about 350 to 420 calories. That’s an enormous volume of food — enough to genuinely fill your stomach and satisfy your desire for something sweet — at a caloric cost that most people can easily accommodate.
• High glycemic index on paper, but modest blood sugar impact in practice — While watermelon does have a relatively high glycemic index, its glycemic load is actually quite low because it’s composed almost entirely of water. Glycemic index measures how fast a food raises blood sugar per gram of carbohydrate, while glycemic load accounts for how much carbohydrate you’re actually eating.
Because watermelon is mostly water, a large serving contains relatively little sugar in absolute terms. This means that for most people without blood sugar disorders, the impact on blood glucose is minimal relative to the volume consumed.
• The satiety factor cannot be overstated — When you’re full on 350 to 420 calories of watermelon, you’re far less likely to reach for processed snacks, sugary desserts or other processed foods that drive weight gain. It’s a strategy of displacement — filling your body with nutrient-dense, low-calorie whole food so there’s simply less room for the things that harm you.
5 Years and Counting — with an Honest Caveat
I want to be transparent about something. Eating 2.5 to 3 pounds of watermelon every single day, year-round, is not something that would have been possible for any of our ancestors. Historically, watermelon was a seasonal fruit, available for a few months at most.
No traditional culture consumed it 365 days a year. Our grandparents certainly didn’t. The very fact that I can walk into a grocery store in January and buy a ripe watermelon is a modern convenience that has no precedent in human dietary history. And I think that’s worth acknowledging.
There’s a reasonable argument to be made that our bodies evolved eating foods in seasonal rhythms — periods of abundance followed by periods of absence — and that eating any single food every day of the year, no matter how beneficial, departs from that ancestral pattern. Some would argue that seasonal rotation gives the body metabolic variety and prevents overexposure to any one set of compounds. I take that point seriously. It’s a fair critique.
But after weighing it carefully over the past five years, I’ve concluded that the sheer density of therapeutic benefits — the lycopene, the citrulline, the potassium delivered through whole fruit, the superior hydration, the anti-inflammatory effects, the cardiovascular support, the kidney and gut benefits, the muscle recovery, the eye protection and the effortless weight management — stacks up to a case that, in my judgment, clearly outweighs the theoretical downside of departing from a seasonal eating pattern.
• We live in a world that our ancestors didn’t — We’re exposed to environmental toxins, chronic stress, processed food and sedentary lifestyles they never faced. The argument that we should only eat what was historically available doesn’t account for the fact that our bodies are also dealing with challenges that are historically unprecedented. In that context, I believe leveraging a food this nutrient-dense and this therapeutically versatile on a daily basis is a rational and well-supported choice.
• Is it perfectly natural in the strictest ancestral sense? No. Do I believe the benefits far outweigh any concerns about year-round consumption? After five years of personal experience backed by a substantial body of research — yes, I do. Very few whole foods deliver this breadth of therapeutic value at such a low caloric cost and with such ease of consumption. You don’t need to cook it. You don’t need to prepare it in a special way. You just eat it.
• My recommendation — Consider making 2.5 to 3 pounds of ripe, deep-red watermelon a daily habit — not just a summer treat. Choose seedless varieties when possible, as research suggests they contain higher lycopene levels. And choose melons with deep red flesh — the deeper the color, the higher the lycopene concentration.
Start with 1 to 1.5 pounds daily for the first week, split between morning and afternoon. Increase to 2.5 to 3 pounds as your digestion adjusts. Eat it fresh rather than juiced to preserve fiber. Choose whole melons with a deep yellow ground spot and a hollow sound when tapped. Pre-cut watermelon can be refrigerated for up to three days.
I started this five years ago as an experiment. It has since become one of the most consistent and rewarding health practices in my daily routine. As always, I encourage you to take control of your health through informed choices grounded in real science. Sometimes the most powerful interventions are the simplest ones — and they’ve been sitting on your kitchen counter all along.
FAQs About Watermelon’s Health Benefits
Q: How much watermelon is needed to get meaningful health benefits?
A: Consuming about 2.5 to 3 pounds of watermelon daily provides substantial amounts of lycopene, citrulline, and potassium — levels that align with amounts used in research on cardiovascular health, inflammation, and metabolic support.
Q: Does watermelon support heart and blood vessel health?
A: Yes. Watermelon delivers lycopene and citrulline, which help support nitric oxide production, improve blood flow, reduce arterial stiffness, and contribute to healthier blood pressure and cholesterol markers.
Q: Is watermelon a good way to stay hydrated?
A: Watermelon is about 92% water and provides hydration alongside electrolytes and natural sugars that support fluid absorption, helping your body retain hydration more effectively than water alone.
Q: Will watermelon spike my blood sugar because of its sweetness?
A: Although watermelon has a high glycemic index, its glycemic load is low due to its high water content, meaning the real-world blood sugar impact is modest for most people without blood sugar disorders.
Q: What makes watermelon useful for recovery, digestion, and weight management?
A: Watermelon combines hydration, natural sugars, fiber, and citrulline, which support muscle recovery, digestive comfort, and satiety, allowing large portions to be consumed with relatively low calorie intake.
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Exploring the Link Between Niacin and Fatty Liver Disease
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/02/24/niacin-choline-fatty-liver-disease.aspx
Analysis by Dr. Joseph Mercola February 24, 2026
Story at-a-glance
- Fatty liver disease is the most common liver disorder, driven by obesity, Type 2 diabetes, and insulin resistance. It often progresses silently for years before symptoms appear
- Niacin helps your body use energy better. It turns down a molecule called microRNA-93, which normally blocks two key proteins that help your cells make energy and burn fat. By restoring those proteins, niacin helps your mitochondria work more efficiently. This shift supports fat burning in your liver instead of fat storage
- Higher niacin intake has been linked to reduced liver fat, lower inflammation, improved insulin sensitivity, better cholesterol levels, and reduced long-term mortality in fatty liver patients
- Niacinamide is the better choice compared to niacin because of its function as an NAD+ precursor. The ideal dosage is 50 milligrams three times a day, ideally in powder form for precise intake. Niacinamide also doesn’t cause skin flushing
- Increasing choline intake is the best way to manage fatty liver disease. Research shows it helps transport fat out of the liver. While there are several types of choline supplements available, citicoline is the preferred one because of its high bioavailability
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 Mercola Health Coach app once it becomes available. It will contain 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.
- 1 AASLD, New MASLD Nomenclature
- 2 Mayo Clinic, Fatty Liver Disease
- 3 Cleveland Clinic, Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
- 4 Diabetes Obes Metab. 2022 May 19;24(8):1553-1564
- 5 UNIST, April 12, 2025
- 6, 10 Metabolism, Volume 169, August 2025, 156266
- 7, 11 JAMA Netw Open Published Online: February 1, 2024 2024;7;(2):e2354277
- 8 Ther Adv Chronic Dis. 2022 Feb 23;13:20406223221077958
- 9 Jinfiniti, December 21, 2024
- 12, 14, 16, 17, 18 Office of Dietary Supplements, Niacin
- 13 J Clin Lipidol. 2019 Nov-Dec;13(6):873-879
- 15 Journal of Investigative Medicine High Impact Case Reports Volume 12: 1–3
Human Hearts Can Regrow Some Muscle Cells After Severe Damage
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/02/25/human-heart-muscle-cell-regrowth.aspx
Analysis by Dr. Joseph Mercola February 25, 2026
Story at-a-glance
- Heart attacks occur every 40 seconds in America, affecting a total of 805,000 people annually. It is characterized by blocked coronary arteries that starve cardiac muscle of blood flow
- Australian researchers found human hearts can regenerate muscle cells after heart attacks, with preserved cardiac tissue showing 7% to 8% mitosis rates (a measure of cell regeneration activity), though 25% to 50% is needed for full repair
- Hypoxia, which is the oxygen-deprived state during heart attacks, may also trigger regeneration, similar to how fetal hearts produce new cells in the low-oxygen womb environment
- Advanced heart failure reduces heart muscle cell renewal dramatically, but patients with mechanical heart pumps showed regeneration rates of 3.1% annually — six times higher than healthy hearts
- Prevention remains crucial. Strategies such as minimizing linoleic acid consumption, monitoring body fat percentage, engaging in moderate resistance training, and learning to recognize heart attack warning signs increase outcomes
According to the U.S. Centers for Disease Control and Prevention (CDC), a heart attack occurs every 40 seconds throughout America. This totals to around 805,000 people every year — 605,000 of them experience it for the first time, while the remaining 200,000 are repeat cases. Moreover, 1 in 5 people don’t know they’ve already had a heart attack.1
But what exactly happens when you have a heart attack? Simply put, blood flow to the heart becomes severely restricted usually due to a buildup of plaque in the coronary arteries. Once a complete blockage occurs, cardiac muscles die as they also don’t get blood flow. From here, symptoms such as chest pain, cold sweats, fatigue, nausea, and shortness of breath manifest.2
Treatment is centered on restoring blood flow as soon as possible to prevent further tissue death. Here lies a question that has bothered researchers for years now — once a heart attack occurs, can cardiac tissue regenerate on its own and achieve optimal function again? New evidence shows that there’s a sliver of hope, but it needs to be fleshed out further.
The Human Heart Can Regrow Cardiomyocytes After a Heart Attack
Experts have long been aware that certain animals can regrow their own heart cells after a heart attack. One example is zebrafish, which can actually do a complete regrowth. Meanwhile, mice have shown the ability to induce mitosis (dividing and multiplying of cells) in the affected area.
The human heart, on the other hand, was believed to be different. According to Sean Lal, Ph.D., a professor of clinical and molecular cardiology at the University of Sydney and coauthor of the featured study, medical students are generally taught that the number of heart cells you’re born with remains the same throughout your lifespan or until you suffer a heart attack.3
Now,4 a team of Australian researchers found that this may not be the case. Their study, published in the journal Circulation Research, made a big breakthrough that deepens the understanding of what we know about the human heart. Specifically, they discovered how it can regenerate new heart muscle cells (cardiomyocytes).5
To test their hypothesis, the researchers used a heart that sat in storage for almost two decades. It was donated by the family of a 48-year-old man who suffered from a severe heart attack. He was brain-dead and on life support, but the damaged heart couldn’t be transplanted into someone else.
The heart was preserved and frozen in liquid nitrogen to preserve tissue quality. “Essentially, the tissue and cells were ‘frozen in time,'” according to lead researcher Rob Hume, Ph.D.6
• Analysis of the heart — Using an array of analytical techniques, the researchers were able to determine how the heart underwent mitosis. According to Lal, the samples they collected from the donor heart showed a mitosis rate of 7% to 8%. But to be able to repair the heart back to its optimal state, the mitosis rate should ideally be 25% to 50%.
In the image below, you can see that the pink area is where a cardiomyocyte is regenerating. This was triggered by adding certain antibodies into the tissue, which attached to proteins that are expressed during mitosis:
• A theory on why regeneration happens — Lal explained that hypoxia could be the factor that triggers mitosis in the heart muscles. Basically, the very same oxygen-deprived environment caused by a heart attack also triggers regeneration in the affected area. This supports his initial theories regarding fetal hearts, noting that, “Fetal hearts make tonnes of new heart cells in utero, which is an oxygen-low environment.” He connects this to his research about adult hearts:7
“It’s almost like the heart has some inbuilt memory. Maybe when you have low oxygen after a heart attack, you reprogram your heart cells to make new cells like you did when you were in utero. That is what we are exploring.”
While the experiment shows promise, the researchers acknowledge that their findings still won’t be able to prevent a heart attack. However, they do hope to continue following up on their findings to create therapies that can promote better mitosis in heart cells.8
Heart Muscles Turn on Renewal Switches Under the Right Conditions
A related study published in Circulation also looked at how your heart can make new muscle cells. The study tracked DNA signatures inside cardiomyocytes to measure actual new cell formation, not just cell enlargement.9
According to the researchers, the goal was to determine whether the adult human heart has what they called a “latent cardiomyocyte regenerative potential” and whether certain conditions activate it. The findings? Your heart’s ability to replace lost cells varies dramatically depending on your physiological state, with some patients showing dramatic surges in renewal when conditions improve.
• Framework of the analysis — A group of patients with advanced heart failure provided the data for this analysis. The study compared their heart tissue with healthy adult hearts and then separated those who received left ventricular assist device (LVAD) support — a mechanical pump that takes workload off the heart — to see how different environments affected cardiomyocyte renewal.
• The enormous contrast between healthy and failing hearts — In a normal adult, cardiomyocyte turnover sits at about 0.5% per year, meaning a small but steady replacement of muscle cells. This results in an almost 40% replacement during the entire lifespan of a human — a contrast to the theory proposed in the earlier featured study, wherein the number of cardiomyocytes remains the same.
In end-stage heart failure, that renewal rate collapses. The study reports that cardiomyocyte generation drops 18 to 50 times lower compared with healthy controls. This means once heart failure advances, your heart’s natural repair machinery slows to a crawl, making recovery harder unless something shifts the internal environment dramatically.
• A deeper look at the data — In failing hearts, renewal fell to 0.03% per year for nonischemic cardiomyopathy and even to 0.01% per year in ischemic cardiomyopathy — the type tied to heart attacks. This corresponds to the lower rate of regeneration mentioned earlier.
Everything changes, however, in patients whose hearts recovered function with LVAD support. Among those individuals, cardiomyocyte renewal rose dramatically to 3.1% per year. This means some hearts aren’t only stabilizing under better conditions — they are rebuilding themselves at a faster rate than healthy hearts normally do.
• What’s happening inside heart muscle cells — The researchers documented that in the worst heart failure cases, DNA synthesis inside cardiomyocytes mostly produced polyploidy — extra DNA copies inside the same cell — rather than creating entirely new muscle cells.
In other words, your heart might look active at the molecular level even while failing, but the activity is misdirected. Instead of replacing lost cells, the damaged heart tends to enlarge existing cells or add extra nuclei, a process that does not restore lost pumping strength.
• A roadblock to regeneration — The researchers mentioned cytokinesis (the final step in cell division where one cell splits into two) as a key chokepoint. This means that many heart cells are already entering the repair cycle, but they fail to complete it. They copy DNA, they prepare to divide, but they do not finish the split. Your ability to rebuild heart muscle depends on helping cells complete that final step.
• Suggestions for future studies — While the researchers were able to detect the regenerative rate in cardiomyocytes, they didn’t go deep into solutions. However, they did offer suggestions that can be used as a launching pad for other experts and expand known facts in this field:10
“[M]echanical unloading might reverse metabolic cascades that increase reactive oxygen species production. This, in turn, can reduce oxidative DNA damage and activation of the DNA damage response pathway that causes cell cycle arrest in cardiomyocytes. Indeed … a successful approach for cell replacement strategies could be to selectively stimulate cytokinesis in already cycling cardiomyocytes.”
Don’t Wait for a Heart Attack to Happen — Boost Your Cardiovascular Health Now
As I often say, it’s better to prevent a disease from happening in the first place instead of treating it, and this also applies to heart attacks. That said, here are my recommendations to keep your heart in top shape:
1. Minimize your intake of linoleic acid (LA) — In 2025, I published a paper in the World Journal of Cardiology regarding the health effects of excess LA consumption on cardiovascular health. In it, I describe how LA becomes integrated into the cardiolipin in your mitochondrial membranes, where it becomes a substrate for lipid peroxidation. This causes harmful reactive oxygen species (ROS) that eventually results in clogged arteries.
In light of this information, cutting back on LA is one of the smartest things you can do for your cardiovascular health, not to mention your overall well-being. I recommend keeping your intake below 5 grams a day, but if you can keep it below 2 grams, that’s even better.
As much as possible, avoid all ultraprocessed foods, as they are cooked in LA-rich vegetable oils, such as soybean, corn, safflower, and cottonseed. To help you monitor your intake, sign up for the upcoming Mercola Health Coach app. It contains a feature called the Seed Oil Sleuth, which will track the LA in your food to a tenth of a gram.
2. Track your weight — Even if your body mass index (BMI) is in a supposedly healthy range, that doesn’t mean you’re in the clear. As I noted in my previous article, intermuscular fat eventually promotes inflammation, which increases your risk for heart attack, as well as heart failure.
Instead of relying on BMI, it’s better to track your overall body fat percentage. You can use body fat calipers, which gives you a hands-on approach by measuring skinfold thickness in key areas throughout your body. When used consistently, they are reasonably accurate.
You can also use smart scales, which work by using bioelectrical impedance analysis (BIA) to measure body fat. While your current hydration levels can affect the results, they’re also generally helpful for getting an overall picture of your body fat composition. But the better approach here is combining the two methods for even better tracking accuracy.
3. Start building muscle — Now that you’ve gotten an idea on your current fat levels, how do you lower it? One effective method, which you can start doing right away, is resistance exercise or strength training.
Research shows that consistent resistance exercise decreases fat infiltration in your muscles. In addition, the eventual increase in your overall muscle density is linked to better cardiovascular health and longevity.11,12
However, take care when it comes to lifting weights — it would be wise to keep it in moderation. In my interview with Dr. James O’Keefe, he noted that 130 to 140 minutes of strength training per week makes you lose the longevity benefits of exercise. Based on our conversation, the sweet spot for lifting weights is 40 minutes once a week, or 20 minutes twice a week on non-consecutive days.
4. Know the signs of a heart attack — Even if you do everything correctly, it’s still wise to familiarize yourself with the signs of a heart attack. This will allow you to get proper help right away.
For more in-depth information on this topic, read “How to Spot and Treat a Heart Attack.” It contains other helpful tips that can help reduce tissue damage once a heart attack occurs, such as keeping methylene blue and sublingual melatonin close to you.
Frequently Asked Questions (FAQs) About Cardiomyocyte Regeneration After a Heart Attack
Q: Can the human heart regenerate after a heart attack?
A: Yes, research shows the heart has regenerative capacity, albeit limited. Australian scientists found 7% to 8% of heart muscle cells actively going through mitosis in damaged cardiac tissue, though full repair would require 25% to 50%. Low oxygen during heart attacks may trigger this regeneration.
Q: How does heart failure affect the heart’s ability to repair itself?
A: Heart failure dramatically reduces regeneration. Healthy hearts replace about 0.5% of muscle cells yearly, but advanced heart failure drops this to 0.01 to 0.03%, which is up to 50 times lower than normal.
Q: Can mechanical heart pumps improve cardiac regeneration?
A: Yes. Patients using left ventricular assist devices (LVADs) showed renewal rates of 3.1% per year — six times higher than healthy hearts. Based on the findings, reducing the heart’s workload allows natural repair machinery to function better.
Q: Why do heart cells fail to complete regeneration?
A: The main roadblock is cytokinesis, which is the final step where one cell splits into two. Many heart cells copy DNA but cannot complete division. Future therapies may target this chokepoint.
Q: What can I do to prevent heart attacks?
A: Minimize linoleic acid (LA) intake (below 5 grams daily) by avoiding ultraprocessed foods, track body fat percentage, engage in moderate resistance training (40 minutes weekly), and learn to recognize heart attack warning signs.
- 1 Centers for Disease Control and Prevention
- 2 Mayo Clinic, Heart Attack
- 3, 6, 7 The Age, January 18, 2026
- 4 Circ Res. 2026 Jan 16;138(2):e327486
- 5 Indica News, January 20, 2026
- 8 Medical Xpress, January 19, 2026
- 9, 10 Circulation. 2025 Jan 21;151(3):245-256
- 11 European Heart Journal January 20, 2025
- 12 The Journal of Gerontology Series A: Biological Sciences and Medical Sciences. 2015 Apr 2;70(9):1133–1140