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Studies Raise Questions About Keto’s Impact on Liver and Heart Health
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/11/18/keto-diet-liver-heart-health-risks.aspx
Analysis by Dr. Joseph Mercola November 18, 2025

Story at-a-glance
- While short-term ketogenic diets may aid weight loss, new research links prolonged ketosis to liver stress, impaired insulin secretion, and cardiovascular problems
- Long-term fat reliance increases circulating free fatty acids, burdening the liver, disrupting glucose regulation, and weakening metabolic flexibility — key factors in overall energy stability and heart health
- Elevated liver enzymes and triglyceride levels on keto indicate hepatic overload. This signals that the body is struggling to manage excess fat turnover and oxidation
- Treat keto as a short-term metabolic intervention, not a lifestyle diet. Gradually reintroduce whole-food carbohydrates to support steady energy, hormonal balance, and overall metabolic health
- To support balanced metabolism and long-term liver and heart health, keep total fat below 30% of daily calories, eliminate seed oils from your diet, and consume sufficient dietary fiber
For several years, I recommended the ketogenic diet as a way to optimize your metabolic and mitochondrial health. Restricting carbohydrates and shifting the body to rely on fat for fuel seemed, at the time, to be a sound strategy for stabilizing blood sugar and enhancing endurance. Backed by a growing body of published research, it appeared to offer a logical and effective route toward better energy regulation and improved metabolic flexibility.
However, after studying the work of the late Ray Peat, Ph.D., my perspective shifted. His insights into the bioenergetic theory of health revealed how carbohydrate availability is tied to your body’s capacity to sustain healthy energy production. The more I examined his work, the clearer it became that long-term carbohydrate restriction could work against many of the very systems it was meant to support.
Your liver and heart appear to be especially vulnerable under the metabolic strain of a high-fat, low-carb diet. That vulnerability has come under closer scrutiny in a recent Science Advances study1 that examined how prolonged adherence to a ketogenic diet affects metabolic balance, insulin regulation, and organ function. Their findings raise important questions about whether keto side effects outweigh its benefits.
Does Keto Raise Liver Enzymes or Cause Fatty Liver?
In the featured study, researchers examined the long-term keto liver effects in mice for nearly a year. The goal was to determine whether a ketogenic diet, often promoted for weight management and metabolic improvement, might instead strain the liver’s ability to process and regulate fat over time and compromise overall metabolic health.2
• Liver distress emerged despite lower body weight — The study found that even though mice on the ketogenic diet gained less weight than those fed a high-fat, high-carb diet, their liver profiles revealed signs of distress. Plasma triglycerides and non-esterified fats (free fatty acids released from stored fat) were significantly elevated, pointing to hyperlipidemia, a state of excess circulating fat in the bloodstream.
Male mice also developed hepatic steatosis (fat accumulation in the liver), along with increased alanine aminotransferase (ALT) activity. ALT is an enzyme concentrated inside liver cells and plays a role in amino acid metabolism. When liver cells are damaged or die, ALT leaks into the bloodstream, raising measurable levels. Elevated ALT directly reflects hepatocellular injury and indicates that the liver is under metabolic or inflammatory stress.
• Broader metabolic stress accompanied liver injury — Mice on the ketogenic diet developed glucose intolerance, meaning their bodies were less able to keep blood sugar stable after eating, and impaired insulin secretion, showing that the pancreas was not releasing enough insulin to regulate glucose. Together, these findings indicate that liver stress was part of a whole-body imbalance.
In particular, the pancreatic β cells (the cells that make and release insulin) showed disruptions in protein trafficking within the endoplasmic reticulum and Golgi apparatus, which fold and package proteins for secretion. This dysfunction resembled what is seen in early diabetes, where the machinery for insulin release becomes compromised.
• Microscopic evidence confirmed cellular damage — Electron microscopy revealed lipotoxic injury in the liver cells. The Golgi apparatus appeared dilated and fragmented, and genes linked to protein stress responses were upregulated. This pattern shows that long-term exposure to high lipid levels not only drives fat buildup but also interferes with protein processing and communication within cells, further aggravating liver dysfunction.
• Animal findings suggest parallels to human liver responses — Although this work was conducted in mice, the core mechanisms involved in fat regulation, glucose control, and protein processing are highly conserved across species. The authors wrote that their findings “have relevant translational ramifications” and “caution against the systematic use of a KD as a health-promoting dietary intervention.” The table below summarizes the animal findings alongside their human relevance:
Liver Outcomes — Enzymes and Steatosis
| Aspect | Preclinical (Science Advances, 2025) |
Human Relevance (as noted by authors) |
|---|---|---|
| Population | Mice | Not studied directly; authors emphasized the need for human research to confirm whether similar effects occur |
| Exposure | Long-term ketogenic feeding (~1 year) | Prolonged high-fat intake under carbohydrate restriction may have comparable metabolic implications in humans, but further trials are required |
| Main signal | Marked hyperlipidemia, hepatic steatosis, elevated ALT, impaired glucose tolerance, and reduced insulin secretion | Findings carry “relevant translational ramifications,” suggesting caution when applying long-term ketogenic diets for metabolic health |
| Interpretation | Chronic ketogenic feeding stresses liver and pancreatic metabolism, indicating risk of liver injury and glucose dysregulation | Authors caution that extended ketogenic use could have harmful effects on metabolic health, especially regarding β-cell function, plasma lipid levels, and liver health |
• Metabolic deterioration extends beyond the liver — In his analysis of the Science Advances study, bioenergetic researcher Georgi Dinkov added that chronic ketogenic patterns not only damage the liver but also suppress overall energy metabolism by reducing lean muscle mass. This has far-reaching metabolic consequences, since muscle is the most metabolically active tissue in the body and a major driver of resting energy use. He explained:
“[T]he resting metabolic rate (RMR) is determined primarily by the ratio of lean mass to fat mass. Thus, as the amount of muscle loss overtakes the amount of fat loss with chronic ingestion of keto diets, the RMR drops significantly. As such, after the person stops the keto diet and goes back to even low-to-moderate carb diets, the formerly keto diet patient rapidly regains the weight lost as a result of the keto diet, and regains it mostly in the form of fat.
Since fat is not nearly as metabolically active as muscle tissue, the newly re-obesified person not only regains all of the lost weight, but almost always exceeds the initial weight before the keto diet was started and finds that they keep gaining weight even if they restrict the calories way below what they used to consume prior to the keto diet.
That is due to the fact that the RMR dropped as a result of the keto diet (and muscle loss) and the regular diet, which the former keto patient used to consume and maintain a stable (though high) weight on, becomes directly obesogenic due to the much lower RMR.”3
These keto side effects often develop silently, without obvious symptoms. If you notice rising liver enzymes or a dull ache under your right rib cage, it may signal that your liver is under stress from the metabolic load. That’s the time to reassess your macronutrient balance before the strain turns chronic.
Why Would LDL Jump on Keto and Who Are ‘Hyper-Responders’?
In a detailed review published in the American Journal of Preventive Cardiology, researchers from the Mayo Clinic examined a striking pattern among people who experience extreme cholesterol elevations while following a ketogenic diet. This group, often referred to as “hyper-responders,” shows a disproportionate increase in low-density lipoprotein (LDL) “bad” cholesterol and apolipoprotein B (apoB), the particles that actually carry cholesterol through the blood.4,5
• LDL levels spiked dramatically in keto followers — The study reviewed clinical records of 17 adults who presented with LDL cholesterol levels above 190 milligrams per deciliter (mg/dL) while adhering to a high-fat, very-low-carb diet. Before starting keto, their mean LDL level was about 129 mg/dL. After roughly 12 months of strict adherence, that value rose by an average of 245%.
• ApoB reflects the number of cholesterol-carrying particles — Each LDL particle contains one molecule of apolipoprotein B (apoB), a structural protein that anchors cholesterol and triglycerides within the particle. ApoB therefore reflects not just how much cholesterol is present, but how many LDL particles are circulating. The more particles you have, the greater the chance they’ll penetrate inflamed artery walls and promote atherosclerosis, or plaque buildup.
• Genetic predisposition amplified the effect — Ten of the 17 patients had family histories of early heart disease or inherited lipid disorders. Five underwent genetic testing, and two carried mutations in the LDL receptor (LDL-R) gene, which impairs the body’s ability to remove LDL from circulation.
This means LDL particles linger in the blood longer, compounding the cholesterol rise. The researchers suggested that both diet composition and genetic background contributed to the extreme lipid response.
• Lean individuals showed the greatest LDL surge — The largest LDL increases appeared in participants with lower body mass index (BMI). The authors proposed that when carbohydrate intake is severely restricted, leaner individuals rely more heavily on fat oxidation, burning fat for fuel.
This shift ramps up production of very-low-density lipoprotein (VLDL) particles, which transport triglycerides from the liver. As VLDL offloads its fat cargo, it converts into LDL and HDL, explaining why even metabolically healthy or athletic people may see dramatic LDL spikes during keto adaptation.
• Stopping keto reversed the effects — In the study, when patients stopped the ketogenic diet, their LDL levels dropped by an average of 220% within nine months. This rebound emphasizes why anyone with a family history of early heart disease, lipid metabolism variants, or an unexplained rise in LDL or apoB while on keto should do so under medical supervision with regular lipid monitoring.
While the authors blamed saturated fats for higher cardiovascular risk among those on a high-fat, low-carb diet, I believe this repeats the same flawed narrative that has misled the public for decades. I’ll expand on this later, but for now, remember that any discussion of keto’s heart effects needs to move beyond the outdated “saturated fat equals heart disease” myth. The issue appears less about saturated fat itself and more about the metabolic overload created by extreme fat consumption.

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Are Heart Palpitations on Keto a Red Flag — or Just Electrolytes?
Keto heart palpitations are among the more common side effects people notice soon after beginning this diet, especially during the first days or weeks of carbohydrate restriction. While mild, short-lived palpitations often resolve, persistent or worsening irregularity can signal deeper strain on the cardiovascular system. Recognizing this connection allows you to support your metabolism without ignoring what your heart is telling you.6,7
• Electrolyte loss drives early palpitations — When carbohydrate intake drops sharply, insulin levels fall and glycogen (stored carbohydrate) is depleted. This shift prompts the kidneys to excrete water along with key minerals, such as sodium, potassium, and magnesium.
These are the body’s electrolytes, which regulate the electrical signals that control heartbeat and muscle contraction. As they drop, the heart’s rhythm can become irregular or faster than usual (tachycardia), especially if hydration is inadequate. Replenishing electrolytes typically stabilizes symptoms within days.
• Fat-based fuel changes cardiac metabolism — Because ketogenic diets push the heart to depend almost entirely on fat oxidation instead of glucose for fuel, this metabolic shift can have unintended effects on cardiac performance, including disturbances in the heart’s electrical rhythm.
Experimental studies in animals also indicate that long-term ketogenic feeding may promote adverse remodeling of the heart muscle — characterized by fibrosis and changes in tissue structure — that can interfere with normal electrical conduction and raise the likelihood of arrhythmias such as atrial fibrillation.8
• When to address symptoms — Occasional palpitations during keto adaptation often resolve with hydration and mineral-rich foods like leafy greens and bone broth. However, ongoing rapid or irregular heartbeats, chest tightness, or palpitations accompanied by dizziness or shortness of breath require prompt evaluation. These may reflect electrical or structural strain on the heart, especially in individuals with high cholesterol, high blood pressure, or pre-existing heart disease.
• Simple checks before medical evaluation — Ensure adequate hydration, avoid caffeine and stimulant intake, and reassess whether palpitations persist once electrolytes stabilize. Thyroid hormone dosing, anemia, and overtraining can also contribute. If the symptoms continue after addressing these factors, a medical evaluation is essential. A basic electrocardiogram (ECG) and blood panel can identify early electrical or metabolic disturbances before they progress.
Learn more about the cardiovascular effects of ketogenic diets in “The Ketogenic Diet Can Put Your Cardiovascular Health at Risk.”
Could a Higher-Carb, Lower-Fat Diet Be Safer for Your Heart and Liver?
The fact is, your body requires glucose to function properly. When carbohydrate intake drops too low for too long, your body compensates by producing glucose from cortisol through a process called gluconeogenesis. This involves breaking down amino acids from muscle tissue to create glucose for essential energy needs.
• Cortisol’s real role in metabolism — Cortisol belongs to a class of steroid hormones called glucocorticoids.9 The prefix gluco refers to glucose (sugar),10 while cortico indicates its origin in the adrenal cortex.11
Although commonly labeled a stress hormone, cortisol’s primary biological purpose is to raise blood sugar when glucose and glycogen (the liver’s stored form of glucose) run low. When this shortage is detected, cortisol activates the PEPCK enzyme, triggering gluconeogenesis.12
• Chronic cortisol elevation signals metabolic imbalance — When cortisol remains elevated due to prolonged carb restriction, it drives inflammation and weakens immune function.13 This persistent stress state undermines long-term metabolic and hormonal health. While low-carb diets may promote short-term weight loss or glycemic control, sustained glucose deprivation pushes the body into a stress-driven, catabolic mode, breaking down tissue to meet energy needs.
• The Randle Cycle explains fat-glucose competition — Insights from Peat’s bioenergetic framework and related metabolic research highlight the Randle Cycle, a cellular “fuel switch” that determines whether your mitochondria burn fat or glucose at a given time. Think of it as a railroad junction — only one train (fuel source) can pass at once.

• For efficient glucose metabolism, the fat load must remain moderate — When dietary fat exceeds about 30% of total calories — lower if you’re overweight — the body shifts toward fat oxidation. This suppresses glucose use inside mitochondria, forcing glucose to remain in the bloodstream and raising blood sugar.
Balancing carbohydrate and fat intake ensures the Randle Cycle stays aligned with energy demand rather than metabolic stress. In a previous interview I had with Dinkov, he explained:
“I’ve noticed that between 15% and 20% [dietary fat] is probably where most people, in their current health state, can metabolize the fat without causing problems for the glucose through the Randle cycle. Especially Type 2 diabetics.
Most of them are overweight or obese, which means they have two sources of fats — one through the diet and the second one from their fatty tissue, because there’s always some lipolysis going on. So for diabetic people, it’s probably a good idea to lower the intake of fat from the diet, because they already have a lot coming from their own bodies.
There’s so many clinics around the world that treat and even cure Type 2 diabetes by putting them on a really restrictive diet until they lose most of their fat. And then suddenly, the metabolism of glucose gets restarted. I think this directly shows you that the problem with glucose wasn’t the glucose itself.
It wasn’t the glucose that was fattening them up. They had too much fat in their bodies, and once you get rid of that fat, no matter how you do it, the problems when metabolizing glucose disappear which, to me, is a great testament to the Randle Cycle.”
Shifting from a chronically low-carb pattern to a more balanced, carbohydrate-inclusive diet is one of the simplest ways to restore metabolic stability. By doing so, you create an internal environment where both your heart and liver can function at their natural pace — energetic, steady, and free of the constant biochemical tension that defines long-term ketosis. For a deeper look at why glucose is the body’s cleanest, most efficient fuel, read “Glucose — The Ideal Fuel for Your Cells.”
Rebalancing Your Macronutrients for Optimal Metabolism
When it comes to adjusting your macronutrient intake, a sensible approach is needed. The goal is not to fear any one macronutrient but to use each in the right proportion to keep metabolism functioning optimally.
1. Moderate your fat intake — While you need to lessen your fat consumption, that doesn’t mean fats need to be removed from your diet entirely. Make no mistake, fats — especially from clean, stable sources — remain essential for optimal health. The goal is to keep total dietary fat below 30% of your daily calories.
2. Eliminate linoleic acid (LA) from your diet — Common sources include seed oils like soybean, corn, canola, sunflower, and safflower oils, from your diet. Keep your LA intake below 5 grams a day — and if possible, under 2 grams. Replace industrial oils with traditional fats that resist oxidation, such as butter, tallow, and coconut oil.
For decades, government dietary policies encouraged Americans to replace these traditional fats with so-called “heart-healthy” vegetable oils. These guidelines, based on outdated lipid theories, convinced much of the public that seed oils were safer than saturated fats. Yet modern biochemical and clinical evidence shows that LA oxidizes easily, producing toxic byproducts that damage cells, fuel inflammation, and increase oxidative stress.14,15
To help you keep track of your intake, I recommend you download the Mercola Health Coach app, which will be out this year. One of its main features is the Seed Oil Sleuth, which calculates your vegetable oil intake to the tenth of a gram.
3. Choose healthy carbohydrates — Replace refined starches and processed sugars with nutrient-dense, whole-food carbohydrates like ripe fruits, root vegetables, sweet potatoes, and white rice. These restore glycogen stores in your liver and muscles, regulate blood sugar, and reduce the stress-driven glucose production that occurs during low-carb restriction.
Including resistant starches such as green bananas or cooked-and-cooled potatoes also feeds beneficial bacteria, increasing short-chain fatty acids (SCFAs) like butyrate that calm inflammation and protect the gut lining.
4. Consume sufficient dietary fiber — It’s ideal to consume about 30 grams of fiber. However, if your gut is inflamed or imbalanced, increase fiber gradually since pathogenic bacteria can also ferment it, producing endotoxins.
As your gut flora normalizes, aim for 200 to 250 grams of carbohydrates from whole, unprocessed foods to fully support microbial diversity and mucosal healing. For an in-depth understanding of this approach, read “Butyrate — The Metabolic Powerhouse Fueling the Gut and Beyond.”
5. Know when to use keto — While increasing your carb intake can help promote better health, that doesn’t mean the ketogenic diet will never have a place in a wellness regimen. In fact, I still recommend it if you’re just getting your health back on track, as it’s initially useful to help you become more metabolically flexible. But, while short-term keto has several benefits, prolonged ketosis, as discussed throughout this article, can be problematic.
When using keto as a short-term metabolic reset, it’s important to monitor how your body responds. The table below outlines key markers that show whether the diet is supporting recovery or beginning to strain metabolic balance.
Key Markers to Watch on a Ketogenic Diet
When to WorryPractical Levers
| Marker | Typical Keto Effect | ||
|---|---|---|---|
| LDL/apoB | May rise sharply in “hyper-responders,” especially lean individuals | A large or sustained increase from baseline, especially with signs of oxidative stress or inflammation | Eliminate seed oils and other LA sources; prioritize stable fats like butter, tallow, and coconut oil; increase antioxidant-rich foods (vitamin E, polyphenols); optimize thyroid and liver function |
| Triglycerides | Commonly decrease during early keto adaptation | A paradoxical rise, often from excess calories, alcohol, or impaired fat oxidation | Avoid alcohol and reduce total fat intake; include more fiber and whole-food carbohydrates to improve fat clearance |
| HDL | Typically increases modestly | Not a concern unless paired with inflammation or high apoB | Maintain balanced nutrition and oxidative stability; HDL rise alone doesn’t offset metabolic stress |
| Arrhythmia symptoms | Palpitations often tied to electrolyte loss or thyroid shifts | Persistent palpitations, irregular ECG, chest tightness, or dizziness | Rehydrate; restore electrolytes (sodium, magnesium, potassium); address thyroid and adrenal balance; seek medical evaluation if symptoms persist |
Frequently Asked Questions (FAQs) About the Ketogenic Diet
Q: Does keto cause fatty liver or help reverse it?
A: The Science Advances study showed that long-term ketosis elevated free fatty acids, hyperlipidemia, and fat accumulation inside liver cells — classic signs of hepatic steatosis. These changes occurred even without weight gain, showing that fat overload, not calories alone, can injure the liver. In essence, keto may appear helpful early on, but extended use risks shifting the liver from fat-burning to fat-burdened.
Q: Can a ketogenic diet raise LDL even if I’m losing weight?
A: Yes. The Mayo Clinic review documented sharp LDL and apoB increases among “hyper-responders,” many of whom were lean and metabolically healthy. Weight loss itself doesn’t prevent this, because the rise in circulating fats reflects how the body processes fat for fuel under severe carb restriction — not just how much fat it stores.
Q: Why are my alanine aminotransferase (ALT) levels high after starting keto?
A: ALT is an enzyme found primarily in liver cells, and elevated levels usually signal that the liver is under stress. During the early stages of keto, fat breakdown accelerates, flooding the liver with free fatty acids to convert into ketones. This sudden metabolic load can temporarily raise ALT.
However, if levels stay elevated, it may indicate that excess fat is accumulating in liver cells or that oxidative stress is damaging them. Persistent ALT elevation means the liver is struggling to keep up with fat processing — a sign that the diet may be doing more harm than good.
Q: Are heart palpitations on keto normal?
A: Transient palpitations are common during the first days or weeks of carbohydrate restriction because of fluid and electrolyte losses. When glycogen stores drop, the kidneys excrete sodium, magnesium, and potassium — minerals essential for normal heart rhythm. If palpitations persist after hydration and electrolyte restoration, or are accompanied by dizziness or chest tightness, you should seek medical evaluation.
Q: What do U.S. guidelines say about high-fat patterns and heart risk?
A: For decades, U.S. dietary policy has promoted a low-saturated-fat approach for heart health, encouraging Americans to rely on so-called “heart-healthy” vegetable oils like soybean, corn, canola, and sunflower.
However, while moderating overall fat intake is wise, natural saturated fats from traditional sources like grass fed butter, eggs, and meat are not the problem. The real focus should be on eliminating unstable industrial oils and restoring a balanced, nutrient-dense diet that includes whole-food carbohydrates for sustained metabolic health.
- 1, 2 Sci. Adv. 11, eadx2752(2025)
- 3 Haidut, October 3, 2025
- 4 American Journal of Preventive Cardiology Volume 15, Supplement, September 2023, 100548
- 5 Am J Prev Cardiol. 2023 Apr 6;14:100495
- 6 Ketogenic, November 13, 2023
- 7 AFIP Foundation, “Can the Keto Diet Trigger Atrial Fibrillation? Exploring the Science Behind This Diet-Heart Connection”
- 8 Nutrition & Metabolism volume 17, Article number: 91 (2020)
- 9 StatPearls [Internet], Physiology, Cortisol
- 10 Dictionary, gluco-
- 11 Dictionary, cortico-
- 12 StatPearls [Internet], Physiology, Glucocorticoids, Function
- 13 Cleveland Clinic, Cortisol
- 14 Seven Countries Study, About the study
- 15 BMJ 2016;353:i1246
Biotin Is More Than Just a Beauty Vitamin
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/10/18/biotin-vitamin-b7-benefits.aspx
Analysis by Dr. Joseph Mercola October 18, 2025

Story at-a-glance
- Biotin, also known as vitamin B7, is a water-soluble B-vitamin that plays a vital role in converting food into energy and supporting overall metabolic function
- Biotin is widely recognized for its role in supporting healthy hair, skin, and nails by helping the body produce keratin and other structural proteins
- In addition to its beauty benefits, biotin supports nervous system health, blood sugar regulation, and cardiovascular wellness, contributing to overall vitality and well-being
- During pregnancy, biotin needs increase and are essential for normal fetal development, making adequate intake important for expectant mothers
- Your body does not store biotin, so a consistent intake through diet is important. It is naturally present in foods such as eggs, beef liver, salmon, mushrooms, lentils, sweet potatoes, and whole grains
Biotin, also known as vitamin B7, is a water-soluble B-vitamin that plays a vital role in the body’s metabolic processes.1 Naturally found in certain foods such as eggs, mushrooms, sweet potatoes, whole grains, and salmon, it helps convert nutrients into energy, making it essential for overall health.
Its reputation as the “beauty vitamin” stems from its benefits for hair, skin, and nails. Research into its effects on hair dates back to 1965,2 and from there, interest in biotin grew steadily. Today, biotin supplements and personal care products are sold almost everywhere.
However, biotin’s role goes beyond aesthetics. Emerging research hints at deeper health implications, including its roles in neurological function, gene regulation, pregnancy, and chronic diseases. While beauty might be the hook, its real value lies in how it benefits your body from the inside.
Biotin Offers a Balance of Beauty and Wellness
Biotin’s reputation in beauty circles is backed by scientific evidence. Case reports and smaller studies suggest that having adequate levels of this nutrient leads to visible improvements for problems like brittle nails or thinning hair. Here are some of the well-known benefits associated with biotin:3
• Regrows and renews stronger hair follicles — Having adequate biotin levels promotes hair follicle health and growth by supporting the function of keratin, the protein that makes hair strong. Without enough biotin hair becomes brittle, thin, and prone to shedding.4
• Improves nail thickness and strength — In one study published in the journal Cutis, participants who took a daily biotin supplement for six months experienced a 25% increase in nail plate thickness, highlighting its role in strengthening nails and reducing splitting.5
• Supports healthy skin — Biotin contributes to fatty acid metabolism, which is essential for keeping skin hydrated. Deficiency can lead to dry, scaly, red rashes around the eyes, nose, mouth, and perineum.6
Biotin’s Bigger Role in Energy Metabolism
Biotin is also widely recognized for its role in energy metabolism. It supports the function of five enzymes that are essential for breaking down fats, carbohydrates, and amino acids — processes that are fundamental to cellular energy production.7
• Biotin’s influence goes far beyond its enzymatic role — According to a 2024 review published in Nutrients, biotin is “crucial to glucose and lipid utilization in cellular energy production because it modulates the expression of metabolic enzymes via various signaling pathways and transcription factors.”8
• Biotin influences immune signaling pathways — It helps regulate how the body responds to inflammation through certain messenger systems. As noted by the researchers, “Biotin modulates the production of proinflammatory cytokines …”9
• It shows promise in chronic disease management — Animal studies link biotin to reduced inflammation and improved metabolic function.
“It reduced markers of inflammation and modulated immune responses, suggesting potential applications in conditions such as diabetes, multiple sclerosis, and inflammatory bowel disease.”10

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Biotin Promotes Gene Regulation and Supports Nerve Function
Healthy nerve function depends on precise gene regulation and effective cell signaling — two processes influenced by key nutrients. Among these, biotin contributes to gene regulation, shaping how genes are expressed and plays a role in neural communication.11
• Biotin interacts with genetic material to influence the way cells function — According to a 2025 study published in the Journal of Nutritional Biochemistry, biotin directly attaches to histones, which are proteins that wrap around DNA. By doing so, it acts like a dimmer switch that adjusts how strongly certain genes are turned on or off. The research showed that genes linked to DNA repair and protection were more active when biotin was present in sufficient amounts.12
• Histone biotinylation plays a role in gene silencing — This is the deliberate silencing of harmful or unnecessary genes. For example, turning off repetitive DNA sequences, which if left unchecked, can cause instability in the genome. Biotin acts as a safeguard, making sure the body’s genetic library stays organized and free of clutter.
• Biotin also supports neurological function — It helps power up pyruvate carboxylase, an enzyme that fuels nearly one-third of the brain’s main energy cycle, giving neurons and support cells the steady energy they need to function. When biotin is lacking, neurological symptoms like seizures and cognitive problems can appear.
• Biotin also helps regulate signaling messengers — This is vital to ensure clear communication between brain cells.13
Biotin’s Role in Pregnancy and Fetal Development
Biotin needs increase during pregnancy, yet mild deficiency is common among expectant mothers. This is concerning because biotin is essential for embryonic development, and the fetus is entirely dependent on maternal supply.14
• A study investigating fetal biotin status measured plasma biotin levels in 15 pregnant women and their fetuses during mid-gestation — The results showed that fetal biotin levels were significantly higher than maternal levels, suggesting that the placenta actively transports biotin to the fetus, even when maternal levels are low.15
• Sufficient biotin during pregnancy may reduce the risk of preterm labor — A retrospective case-control study published in The Journal of Medical Investigation analyzed serum biotin levels in pregnant women with normal deliveries, preterm births, and small-for-gestational-age (SGA) infants.
The researchers found that maternal biotin levels remained low throughout pregnancy, and those in the SGA group had significantly lower biotin concentrations during the second and third trimesters compared to the normal delivery group.
“This study suggests that maternal biotin deficiency during pregnancy might be the risk of preterm labor or fetal growth restriction. Further studies are required to clarify the roles of biotin in perinatal medicine,” the researchers concluded.16
• A landmark animal study also found that pregnant mice develop marginal biotin deficiency without showing symptoms — Using urinary biomarkers, the researchers concluded that biotin intake during pregnancy may need to be two to three times higher than current recommendations.17
Biotin Is an Alternative for Progressive Multiple Sclerosis Patients
One of the most promising areas of biotin research involves its role in treating progressive multiple sclerosis (MS). Several studies have demonstrated the therapeutic impact of biotin in patients with this challenging form of the disease.
• High-dose biotin proved helpful in MS patients — In a promising French pilot study published in Multiple Sclerosis and Related Disorders, 23 patients with primary and secondary MS were treated with high doses of biotin (100 to 300 mg a day) over an average of 9.2 months. The results were encouraging and suggest that biotin can impact the disability brought about by MS.18
• High-dose pharmaceutical-grade biotin has shown encouraging results in clinical trials — In a randomized controlled study, 13.2% of patients with progressive MS reported improvement after nine months of taking MD1003 — “a pharmaceutical formulation of high-dose biotin” — compared to the placebo group. According to the website Multiple Sclerosis News Today:
“Full results of the MS-SPI study are especially remarkable. This is the first time that a drug has reversed the progression of the disease in a statistically significant proportion of patients.
In addition, if we look at the mean Expanded Disability Scale (EDSS) change, the data compare very favorably with all previous trials that looked at the same endpoint. Almost no progression was observed in patients treated with MD1003 for 24 months, and this has never been observed before …
Results … point to the fact that targeting neuron and oligodendrocyte metabolism represents a promising and novel disease modifying therapy approach in progressive MS, particularly in patients with a not-active progressive disease.”19
This suggests that biotin can support myelin repair and enhance cellular energy production, which may help slow disease progression. Researchers highlight that targeting neuron and oligodendrocyte metabolism through biotin supplementation represents a novel therapeutic approach for patients with MS.20
Biotin Impacts Blood Sugar Regulation in Both Types of Diabetes
Biotin has also been studied for its impact on metabolic health. Research suggests it may help regulate blood sugar levels and improve glucose tolerance.
• Biotin supplementation improves blood sugar control in Type 1 diabetes patients — A randomized, double-blind, placebo-controlled clinical trial conducted with 70 participants aimed to determine whether biotin supplementation could improve glycemic control and plasma lipid levels in patients with poorly controlled Type 1 diabetes. The findings were promising:
“Biotin administered as an adjuvant in addition to insulin therapy can improve glycemic control, as well as serum lipids concentrations in Type 1 diabetic patients without any side effects.”21
• Biotin also shows promise in controlling Type 2 diabetes — A 2022 meta-analysis published in Frontiers in Nutrition reviewed five randomized controlled trials, and found that biotin supplementation significantly reduces fasting blood glucose levels. The researchers note that supplementation “could be economical and potentially beneficial to T2DM patients.”22
• Biotin also impacts cholesterol profile — The analysis also reported notable reductions in total cholesterol and triglyceride levels among the participants after 28 to 90 days of use. These findings suggest biotin’s potential as a supportive intervention in metabolic health.
Getting More Biotin in Your Diet
Most of the biotin in your body is found in your liver.23 However, because this nutrient is water-soluble, the body does not retain large amounts of it. Excess amounts of biotin are excreted through your urine, making consistent dietary intake essential.
• So, how much dietary biotin is recommended? The National Institutes of Health (NIH)’s adequate intakes (AIs) for this nutrient depend on your age and gender. For example, babies up to 6 months old are recommended to get 5 micrograms (mcg) per day; for adults above 19 years old, the AI is 30 mcg. Lactating mothers have slightly higher levels, at 35 mcg.24
• Biotin is found in a wide variety of foods — This is why deficiency is rare for people who eat a balanced diet. In food, biotin exists in two forms — free biotin and protein-bound biotin.25
• Free biotin is mostly found in plant sources — This is the active, unbound form of the vitamin that can be directly absorbed in the intestine and used by the body. Some of the top sources include:26,27
◦ Green peas and lentils (40 mcg per 100 grams)
◦ Sweet potatoes (2.4 mcg per ½ cup, cooked)
◦ Spinach (0.5 mcg per half-cup, boiled)
◦ Broccoli (0.4 mcg per half-cup, fresh)
◦ Bananas (0.2 mcg per ½ cup)
◦ Whole grains (0.2 mcg per cup)
• Protein-bound biotin comes from animal foods — This type of biotin is covalently attached to a protein or peptide and needs to first be broken down by enzymes into free biotin before it can be absorbed and used by your body. Below are some of the best sources:28
◦ Eggs — Pastured and organic eggs are one of the richest sources of this vitamin, with one whole egg having 10 mcg. While raw egg whites contain avidin, a glycoprotein that binds to biotin and inhibits absorption, cooking deactivates it. Remember to avoid discarding the yolk as it contains essential fats, cholesterol, and protein.
◦ Grass fed beef liver — Beef liver is among the most concentrated sources of biotin, with 30.8 mcg per 3-ounce serving — over 100% of the daily value (DV).
◦ Raw, organic dairy — Yogurt and milk contain small amounts of biotin (0.2 to 0.3 mcg per cup), while cheddar cheese offers 0.4 mcg per ounce.
◦ Wild-caught Alaskan salmon — It provides 5 mcg per 3-ounce serving. Make sure to get salmon from trustworthy sources, and avoid farmed salmon as much as possible.
Practical Approaches to Support Your Biotin Levels
Supporting your biotin levels doesn’t have to rely on a cabinet full of supplements — There are other simple ways to do this. I’ve already shared plenty of biotin foods you can enjoy, and that’s just the beginning. Here are other ways to keep your biotin levels consistent:
• Know the signs of biotin deficiency — While biotin insufficiency is less common than other nutrient deficiencies, it can still happen. Remember to keep your intake consistent by eating healthy and knowing it’s more available than you think it is. Some signs of deficiency include depression, loss of appetite, nausea, paresthesia, and muscle pain.
• Prioritize your gut health — A healthy gut microbiome contributes to biotin production and absorption. Chronic digestive issues, imbalances in gut bacteria, and excessive antibiotic use can interfere with this. Consuming foods rich in probiotics supports a healthy gut and by extension, more efficient biotin absorption.29
• Take complementary nutrients like zinc and collagen — Biotin doesn’t work in isolation — nutrients like zinc play a key role in supporting hair, skin, and nail health. When combined with a biotin-rich diet, their collective effect can contribute more to comprehensive and lasting health benefits.
Biotin is often celebrated for its role in enhancing hair and nail health. But its benefits go far beyond beauty — it’s a vital nutrient that unlocks energy, helps regulate sugar and lipids, and supports overall wellness.
Before adding biotin supplements to your routine, take a moment to assess your current diet. Prioritize getting this nutrient from whole foods — there are many options that can offer you natural sources of biotin. Supplements complement your effort, but it’s ideal that they’re not your primary source of this nutrient.
Frequently Asked Questions (FAQs) About Biotin
Q: What is biotin and why is it important?
A: Biotin, also known as vitamin B7, is a water-soluble B-vitamin that helps your body convert food into energy. It supports essential functions such as metabolism, healthy hair, skin, nails, and nervous system health.
Q: How much biotin do I need each day?
A: The recommended daily intake for adults is 30 micrograms (mcg), while infants need about 5 mcg. Most people can easily meet these needs through a balanced diet without taking supplements.
Q: How do eggs affect biotin intake?
A: Eggs are among the best sources of biotin. Cooking slightly reduces their biotin content but also deactivates avidin, a protein in raw egg whites that blocks biotin absorption. This makes cooked eggs a safer and more effective way to get biotin, even with minimal nutrient loss.
Q: How is biotin related to multiple sclerosis (MS)?
A: High-dose biotin is being studied as a therapy for progressive multiple sclerosis. Early research suggests that it may help with myelin repair and improve nerve function, which could slow disease progression. These doses are far higher than what’s found in food or standard supplements and should only be taken under strict medical supervision.
Q: Is it possible to take too much biotin?
A: Since biotin is water-soluble, excess amounts are usually excreted in urine. However, very high doses can interfere with certain lab test results, such as thyroid or heart tests. It’s best to follow recommended amounts and talk to a healthcare provider before taking high-dose supplements.
- 1, 25 Wellbeing Nutrition, Biotin: The Beauty Vitamin for Healthy Hair, Skin & Nails
- 2 J Drugs Dermatol, May 2017;16(5):496-500
- 3 Nooria Swiss. Biotin B7 Sublimoor. June 2025
- 4 Maxim Hair Restoration, “Can biotin help restore my lost hair?”
- 5 Cutis. 1993 Apr;51(4):303-5
- 6, 7, 24, 27, 28 Office of Dietary Supplements, National Institutes of Health, January 10, 2022
- 8, 9, 10 Nutrients 2024, 16(15), 2444
- 11, 12, 13 Journal of Nutritional Biochemistry, August 2025
- 14, 15 Biology of the Neonate, 1998;74(1):72–74
- 16 The Journal of Medical Investigation, 2020;67(1.2):170-173
- 17 The Journal of Nutrition Volume 144, Issue 12, December 2014, Pages 1885-1886
- 18 Mult Scler Relat Disord. 2015 Mar;4(2):159-69
- 19, 20 Multiple Sclerosis News Today April 27, 2016
- 21 Oman Medical Journal, 2013;28(3):195-198
- 22 Front. Nutr., October 31, 2022, Sec. Nutrition and Metabolism, Volume 9 – 2022
- 23 National Institutes of Health, January 15, 2021
- 26 LibreTexts, last updated August 13, 2020
- 29 Nutrients, 2023;15(2):264
Bay Leaves Help Lower Blood Sugar and Improve Cholesterol Levels
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/05/19/bay-leaves-lowering-blood-sugar.aspx
Analysis by Dr. Joseph Mercola May 19, 2025
Story at-a-glance
- According to research, consuming as little as 1 gram of bay leaves daily can lower fasting glucose by up to 26% and reduces LDL cholesterol by 40%, offering natural support for metabolic health
- Insulin sensitivity improves with regular bay leaf intake, as studies show it protects pancreatic beta cells and enhances the body’s ability to regulate blood sugar
- Liver and kidney function benefit from bay leaf extract, which reduces inflammation, improves enzyme balance, and prevents diabetes-related organ damage
- Powerful antioxidants in bay leaves fight oxidative stress and inflammation, lowering the risk of metabolic dysfunction, heart disease, and complications linked to diabetes
- Try adding bay leaves to your meals, brewing them into tea, or using them in powdered form to provide an easy, natural way to regulate blood sugar and improve overall health
Bay leaves (Laurus nobilis L.) have been a staple in traditional medicine and cooking for centuries, but modern research now reveals something far more important about this common herb. Studies show that bay leaves significantly lower blood sugar levels and improve cholesterol, making them a powerful tool for managing your metabolic health.
Bay leaves also contain beneficial compounds that help protect cells from oxidative stress, which is one of the key drivers of inflammation and chronic disease. This ability to support both glucose metabolism and lipid balance makes them an overlooked but valuable addition to a health-conscious diet.
Bay Leaves Protect Your Organs While Lowering Blood Sugar
A 2021 animal study published in the Annals of Medicine and Surgery journal1 examined how bay leaf helps mitigate the damage caused by diabetes, particularly in the pancreas, liver and kidneys — organs that are often severely affected by the disease. Over four weeks, diabetic rats were given bay leaf extract, and their blood sugar levels, insulin response and organ function were closely monitored.
- Bay leaf extract led to a significant drop in blood sugar — The rats that received the bay leaf extract experienced a significant drop in blood sugar, bringing their glucose levels much closer to normal compared to diabetic rats that received no treatment.
- Pancreatic beta cells were better preserved — These cells are responsible for producing insulin. In untreated diabetic rats, these insulin-producing cells were severely damaged, leading to insulin dysfunction and uncontrolled blood sugar. In contrast, rats that received bay leaf extract showed stronger insulin production and healthier pancreatic tissue.
- Untreated diabetic rats had severe liver damage — The liver, which helps regulate glucose and lipid metabolism, often becomes inflamed and overloaded with fat in diabetics. The researchers found that rats that didn’t receive bay leaf extract had liver necrosis (cell death), fatty deposits and structural degeneration.
- Bay leaf extract-treated rats had improved liver function — Their liver enzyme (AST, ALT, and GGT) levels, key markers of liver function, improved significantly, suggesting reduced liver stress and better overall metabolic control. Liver enzymes are critical for detoxification and metabolic health, and when elevated, it means the liver is under strain. Bay leaf-treated rats had levels that were closer to those of healthy rats.
- Remarkable improvements were also seen in kidney function — Diabetes causes kidney damage due to high blood sugar and inflammation, often resulting in diabetic nephropathy. In this study, untreated diabetic rats had kidney damage, inflammation, and abnormal structural changes. Bay leaf extract prevented much of the damage, helping reduce cellular stress and maintain normal kidney architecture in the treated rats.2
What Makes Bay Leaves So Powerful?
Bay leaves have a positive effect on insulin signaling, which is one of the key mechanisms behind its antidiabetic effects. Insulin is the hormone responsible for moving sugar from the bloodstream into cells, but when you have diabetes, your cells become resistant to insulin’s effects.
- Bay leaves improve insulin signaling — In the animal study above, bay leaf extract was found to enhance insulin sensitivity. This leads to lower blood sugar levels and improves glucose metabolism, key factors in preventing long-term complications of diabetes.
- Potent antioxidants in bay leaves — 1,8-cineole, α-terpinyl acetate and linalool in bay leaves help reduce oxidative stress, which is a major driver of diabetic complications. High blood sugar generates free radicals, unstable molecules that damage cells and accelerate disease progression. Bay leaf’s potent antioxidants help neutralize free radicals.
- Bioactive compounds in bay leaves help regulate lipid metabolism — In diabetes, cholesterol and triglyceride levels often become dangerously unbalanced, increasing the risk of heart disease. The study showed that rats treated with bay leaf extract had better lipid profiles (reduced LDL cholesterol and triglycerides and increased HDL cholesterol), which helped support heart health and overall metabolic stability.
This research provides compelling evidence that bay leaves are more than just a spice — they’re a powerful tool for metabolic health. “We believe that further preclinical research into the utility of L. nobilis treatment may indicate its suitability as a potential treatment in diabetic patients,” the study authors wrote.3

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Human Research Confirms Results
Previous research has demonstrated these effects in humans as well. A study published in the Journal of Clinical Biochemistry and Nutrition4 examined the effects of bay leaf consumption on blood sugar and cholesterol levels in Type 2 diabetics. Their primary goal was to determine whether bay leaves could naturally help control glucose levels and improve lipid profiles in people who are at risk of diabetes and heart disease.
- Different bay leaf doses were tested over a 30-day period — The study involved 40 participants, all diagnosed with Type 2 diabetes. They were divided into four groups, each receiving a different amount of bay leaves (1, 2 or 3 grams of ground bay leaves in capsule form) or a placebo. After just 10 days, significant changes were already evident in the groups taking bay leaves, and more significant improvements were seen after 30 days.
- Bay leaves help regulate glucose more effectively over time — Participants consuming bay leaves saw fasting blood sugar levels drop by 21% to 26%, with the most significant reductions occurring in those taking 1 or 3 grams daily. Even more interesting, these lower blood sugar levels persisted for 10 days after stopping bay leaf consumption, indicating a lasting effect.
- Cholesterol levels also saw major improvements — Across all bay leaf groups, total cholesterol levels dropped between 20% and 24%, with the biggest reductions seen in LDL cholesterol (“bad” cholesterol). LDL levels plummeted by as much as 40%, a decrease that rivals the effects of some cholesterol-lowering medications.
- Triglycerides decreased significantly — In the 1-gram group, triglycerides dropped by 34%, while the 2-gram group saw a 25% reduction. Even after stopping bay leaf consumption, their levels remained lower than before the study, reinforcing the long-term benefits.
- HDL cholesterol levels soared — The researchers found that HDL “good” cholesterol rose by 19% to 29%, improving participants’ overall heart health. This shift in cholesterol ratios is crucial, as high LDL and low HDL levels are key drivers of heart disease, stroke and other cardiovascular problems.
The researchers noted that none of the participants were taking insulin, and they all continued their usual diabetes medications and diets during the study. This setup allowed them to identify how bay leaves affected the diabetics’ health beyond the effects of their existing treatments.
Another interesting aspect is that the most notable benefits were observed in the 1-gram group. They had the most consistent improvements across blood sugar, cholesterol, and triglycerides. This suggests that even a small daily amount of bay leaves provides meaningful health benefits, making it easy to incorporate into a regular diet.5
What Else Is Bay Leaf Good For?
Bay leaves are an excellent source of vitamins A and C, iron, manganese, copper and calcium — all of these are antioxidants with free radical-scavenging abilities, and positively impact your eyesight, bones, blood and more.6 Below are other health benefits associated with bay leaves.
- Pain relief — In traditional medicine, bay leaves are used for alleviating digestive issues, like ulcer pain, heartburn, gas and colic. It’s also helpful in easing arthritis and headaches.7
- Protects against pathogenic bacteria — A study published in the Journal of Pathogen Research tested the antimicrobial and antioxidant properties of bay leaves against multiple bacterial strains, including Staphylococcus aureus, Escherichia coli (E.coli) and Pseudomonas aeruginosa. The results revealed strong antibacterial effects, particularly against S. aureus and E. coli.8
- Bioactive compounds provide immune support — Researchers attribute these effects to the flavonoids (kaempferol, myricetin and quercetin), polyphenols, and essential oils found in bay leaves, which all have well-documented anti-inflammatory and immune-supporting properties.
- Inhibits bacterial growth — The monoterpenes and sesquiterpenes in bay leaves also disrupt bacterial membranes and inhibit their ability to grow and multiply.9
For more interesting trivia on bay leaves and how they benefit your health, read “Are Bay Leaves Good for You?”
How to Add Bay Leaves to Your Diet
If you’re looking for a natural way to improve your blood sugar levels and cholesterol, adding bay leaves to your diet is one of the easiest steps you can take. The best part? You don’t need much. As the studies above demonstrate, even a small amount daily makes a big difference. Here are tips to get the most out of bay leaves and improve your overall health:
1. Use whole bay leaves in cooking — The simplest way to start using bay leaves is to cook with them regularly. Add a couple of whole bay leaves to soups, stews, rice or slow-cooked meats. The leaves will infuse your food with their beneficial compounds while enhancing flavor. Just remember to remove them before serving, as they are not meant to be eaten whole.
2. Brew bay leaf tea — If you prefer a more direct way to consume bay leaves, make a tea by simmering two or three dried bay leaves in hot water for 10 minutes. This allows the active compounds to extract fully. Drink this tea daily to help regulate blood sugar and reduce oxidative stress. You can also add a squeeze of lemon or a teaspoon of raw honey if you want to enhance the taste.
There are other types of tea that are beneficial for diabetics. Learn more about them in my article, “Study Shows Tea Can Reduce Risk and Progression of Diabetes.”
3. Use ground bay leaves for maximum benefits — If you want a more concentrated effect, use ground bay leaves instead of whole ones. Sprinkle a small amount into sauces, curries or even mix it into a smoothie. This method ensures you consume the beneficial compounds directly without having to remove the leaves later.
4. Combine bay leaves with other antioxidant-rich foods — Bay leaves work even better when paired with other antioxidant-rich foods. Since oxidative stress contributes to insulin resistance and cholesterol imbalances, eating more fresh fruits, vegetables, and healthy fats alongside bay leaves further reduces inflammation and protects your cells.
Adding other herbs and spices to your meals gives you even more metabolic support. One example is cinnamon — read more about it in this article, “Cinnamon — An Ancient Spice That May Be Beneficial for Prediabetics.”
5. Be consistent and give it time — The studies on bay leaves showed significant improvements within 30 days, but these benefits are best sustained through long-term use. Make bay leaves a regular part of your meals and be patient as your body gradually improves insulin sensitivity, lowers LDL cholesterol and balances blood sugar levels. Like any natural approach, consistency is key.
Bay leaves offer a simple, natural way to support metabolic health, and incorporating them into your diet requires minimal effort. Whether you add them to your meals, brew them into tea, or use them as a seasoning, they are a powerful tool for improving glucose regulation and protecting your heart.
If you’re struggling with diabetes, there are other herbs and spices that will help manage your blood sugar levels. Read “These Herbs and Spices Can Help Deter Diabetes” for more information.
Frequently Asked Questions (FAQs) About Bay Leaves
Q: How do bay leaves help lower blood sugar?
A: Bay leaves improve insulin sensitivity, allowing the body to use insulin more effectively. This leads to better glucose control and lower fasting blood sugar levels by up to 26%.
Q: Can bay leaves improve cholesterol levels?
A: Yes, studies show bay leaves reduce LDL (“bad”) cholesterol by up to 40% while increasing HDL (“good”) cholesterol by 19% to 29%, supporting heart health and metabolic balance.
Q: How do bay leaves support liver and kidney function?
A: Research found that bay leaf extract reduces liver inflammation, improves enzyme balance, and prevents kidney damage linked to diabetes, helping protect these organs from long-term deterioration.
Q: What is the best way to consume bay leaves for health benefits?
A: You can use whole bay leaves in cooking, brew them into tea, or take them in ground form. Studies suggest 1 to 3 grams daily for optimal metabolic support.
Q: Do bay leaves have other health benefits beyond blood sugar and cholesterol control?
A: Yes, bay leaves contain powerful antioxidants that fight oxidative stress and inflammation, which helps reduce the risk of heart disease, metabolic dysfunction, and bacterial infections.
Unraveling the Mysteries of Thyroid Health
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/23/unraveling-mysteries-thyroid-health.aspx
Analysis by Dr. Joseph Mercola March 23, 2025
STORY AT-A-GLANCE
- Thyroid health is intricately linked to iodine intake, genetics and overall metabolic balance, challenging the conventional “empty tank” model of treatment
- Autoimmune thyroid disease has a unique mechanism distinct from other autoimmune conditions, primarily driven by your body’s reaction to iodine
- Accurate thyroid testing requires adherence to specific guidelines, including timing, fasting, biotin avoidance, medication timing and consideration of the menstrual cycle
- Gut health, fatty liver and other hormonal imbalances, such as estrogen dominance, are closely intertwined with thyroid function
- A holistic approach, including dietary adjustments, lifestyle changes and careful consideration before relying on hormone therapies, is necessary for optimizing thyroid health
Dr. Alan Christianson is a leading expert in the field of thyroid disorders, and his insights on this topic are invaluable. In fact, his expertise is so insightful that I’ve invited him to be the lead consultant for our upcoming health coaching program. This program will offer comprehensive protocols and practical steps for various health concerns, with a strong emphasis on thyroid health. I want to ensure the information we provide is top-notch, so we’re taking our time to get it just right.
In my previous interview with Christianson, we explored information about excess iodine and thyroid health. These principles are fundamental and will remain relevant for years to come. Before speaking with him, I felt lost when it came to understanding thyroid issues. I knew the conventional approaches, both in conventional and alternative medicine, were missing something important.
They didn’t address the root causes of thyroid problems. It became clear to me that the solutions were much simpler than I had imagined.
I even applied Christianson’s advice to my own health. At the time of our first interview, I was taking a significant dose of thyroid medication, including desiccated thyroid and Cytomel. I was operating under the common misconception that my thyroid issues stemmed from low thyroid hormone production. I was relying on outdated lab tests like thyroid-stimulating hormone (TSH) and basal body temperature.
After understanding the true nature of thyroid autoimmunity, I was able to completely stop all thyroid medications within two weeks. My basal body temperatures are now completely normal 98.4 to 98.8. All my thyroid hormones are normal but my TSH is elevated, which is what you’d expect because my body is now producing its own thyroid hormone and that requires TSH to activate it. It should remain elevated for the next few months.
I’m incredibly grateful for Christianson’s expertise. So, let’s recap some of the key points from our latest discussion. Thyroid problems are incredibly common, and autoimmune thyroid disease is the most prevalent autoimmune condition.
Sadly, thyroid cancers are also on the rise. Conventional and even many natural approaches often assume the problem is simply a lack of thyroid hormone. However, this “empty tank” model doesn’t address the underlying cause. Christianson revealed that thyroid disease is closely linked to an individual’s genetic tolerance to iodine. By managing iodine intake within a safe range, many people actually reverse their thyroid issues.
The Unique Nature of Thyroid Autoimmunity
One of the biggest misconceptions I had before interviewing Christianson was that all autoimmune diseases have the same origin. This is simply not true.
• Thyroid autoimmunity is driven by a different mechanism — While many autoimmune conditions, like rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease, are often linked to a leaky gut, thyroid autoimmunity has a different mechanism. In these other conditions, proteins leak through your damaged gut lining, triggering an immune response.
• The key difference lies in your body’s interaction with iodine — We need iodine for proper thyroid function, but our bodies are adapted to different levels of intake based on our ancestry. People with coastal ancestry generally tolerate higher amounts of iodine, while those with inland ancestry thrive on lower levels. Many people today, even those with inland ancestry, consume too much iodine.
This excess iodine matches the thyroid globulin and distorts the molecule to something your body is not typically expecting. This new protein structure then creates antibodies against it, causing your immune system to mistakenly attack the thyroid tissue.
• The good news is that this process requires an ongoing trigger — By reducing excessive iodine intake, you break this cycle. Your immune system then recognizes that the thyroid is not the enemy, and the autoimmune process often reverses. This reversal often happens surprisingly quickly, within a few months, unlike many other autoimmune conditions that take years to improve. In my own case, I saw significant improvement very rapidly.
While antibody levels are an indicator of thyroid autoimmunity and useful for screening, they don’t always tell the whole story. Some people with autoimmune thyroid disease never have measurable antibodies, while others with mildly elevated antibodies have no thyroid problems at all. Therefore, focusing solely on antibody levels isn’t always the most accurate approach.
The Thyroid-Gut Connection and Other Autoimmune Links
A fascinating connection exists between thyroid disease and certain gut issues. A condition known as thyrogastric syndrome, also called atrophic gastritis or autoimmune gastritis, is found in a significant percentage of people with autoimmune thyroid disease.
• It wreaks havoc on your stomach cells — This condition involves your immune system attacking your stomach’s parietal cells, which leads to poor absorption of important nutrients like iron, B12 and zinc.
• There’s a genetic link to autoimmunity — While this connection isn’t directly related to iodine intake, it suggests a broader genetic predisposition to autoimmunity. It seems that some genes are more specific to thyroid autoimmunity, while others are associated with a general increased risk of various autoimmune conditions. This could explain why people with thyroid disease are more likely to experience other autoimmune problems as well.
• Another common co-occurrence is fatty liver — This is now often referred to as metabolic dysfunction-associated fatty liver disease (MAFLD). Thyroid hormones play a role in regulating liver function, metabolism, body weight, and blood sugar. Therefore, hypothyroidism significantly contributes to the development of fatty liver.

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Understanding Fatty Liver and Metabolic Fuel
My understanding of fatty liver has evolved over time. I previously believed it was primarily caused by an excess of omega-6 fats like linoleic acid (LA). While these fats certainly play a role, Christianson offered a more nuanced explanation.
• Fatty liver is fundamentally a problem of fuel balance within your body — According to Christianson, various fuel molecules, including carbohydrates, fats (like LA), and even alcohol, are processed into acetyl-CoA. When your body exceeds its capacity to use these fuel molecules, it shifts into storage mode.
• Where the body stores this excess fuel varies from person to person — Some people store it primarily as subcutaneous fat, while others accumulate it in their liver. The liver has two main storage compartments: triglycerides and glycogen.
A healthy balance between these two is essential for proper liver function. In fatty liver, the proportion of triglycerides becomes excessively high, creating a vicious cycle that makes it difficult for the liver to reverse the process.
• This explanation helps to understand why alcohol also contributes to fatty liver — Alcohol, like excess fats and carbohydrates, is ultimately converted into acetyl-CoA. Therefore, both excessive consumption of certain fats and alcohol overload your liver’s capacity to process fuel, leading to fat accumulation. This also explains why some people are more susceptible to fatty liver than others.
The Role of Gut Bacteria and Short-Chain Fatty Acids
Our conversation also touched on the crucial role of gut bacteria and short-chain fatty acids, particularly butyrate. Butyrate is often touted as the primary fuel source for colonocytes, the cells lining your colon. However, recent research has revealed a more complex picture.
• Butyrate only makes up about 20% of the short-chain fatty acids produced by gut bacteria — The majority, around 60%, is acetate, a precursor to acetyl-CoA. Propionate makes up the remaining 20%. This raises the question of whether the focus on butyrate has been misplaced. It’s possible that the initial research on short-chain fatty acids created a bias toward butyrate, overlooking the important roles of acetate and propionate.
• Clinically, butyrate is often administered in ways that are ineffective — Oral butyrate is poorly absorbed, and while rectal administration is more effective locally, it doesn’t reach the entire colon.
• A novel, time-release delivery system that effectively delivers nutrients — I’ve developed a novel time-release delivery system that effectively delivers substances, including beneficial bacteria and short-chain fatty acids, directly to the colon. This technology allows us to bypass the stomach’s harsh acidic environment and the small intestine, ensuring targeted delivery to the colon where these substances have the greatest impact.
This new technology opens the door for new research into the optimal ratios of short-chain fatty acids. I plan to explore different combinations, including a formulation with the natural ratio of 60% acetate, 20% propionate and 20% butyrate, to see which approach is most effective.
The Thyroid-Estrogen Connection and the Importance of Prolactin
We also discussed the intricate relationship between thyroid hormones and estrogen. I’ve long believed that testing estrogen levels in the blood is misleading, as estrogen is primarily stored in tissues, not your bloodstream. This leads to inaccurate information and harmful treatment decisions, especially for post-menopausal women.
• Women are incorrectly treated for low estrogen — Christianson notes that women are often treated for low estrogen based on serum levels, even if they are not experiencing symptoms. This approach, based on flawed data, is unlikely to produce positive outcomes. The problem is often not low estrogen, but rather estrogen dominance, which is indicated by elevated prolactin levels.
• Taking exogenous thyroid hormones actually raises prolactin levels — Christianson says that this is due to a feedback loop between the hypothalamus, pituitary gland and thyroid. The same signal that tells your pituitary to produce thyroid hormone also stimulates prolactin production.
This explains why my own prolactin levels increased when I was taking thyroid medication. This information highlights the complexity of hormonal interactions within your body.
• Factors that influence prolactin levels — This led to a discussion of how various factors influence prolactin levels, including hormone replacement therapy, oral contraceptives, xenoestrogens and reactions to thyroid medications.
This highlights the importance of considering the context when interpreting prolactin results. My own experience with progesterone lowering my prolactin levels suggests a clear estrogen connection. The good news is that prolactin testing is relatively inexpensive and accessible, making it a valuable tool for monitoring hormonal balance.
• Further discussions on thyroid health and its implications on metabolic health — As our conversation continued, we further discussed the complexities of thyroid health, the connection between thyroid and other hormones and broader implications for metabolic health.
We also cover information about accurate thyroid testing. As Christianson explained, your body has intricate mechanisms for regulating hormone responses. It adjusts the number and activity of hormone receptors to maintain balance.
However, when you introduce external hormones, you disrupt these finely tuned systems. This is where the wisdom of nature comes into play. When do we support the body’s natural processes, and when do we intervene?
In cases of complete gland removal, like thyroidectomy, intervention is necessary. However, many people have abnormal lab results without a true inability to compensate. It’s important to distinguish between compensation and true dysfunction.
The Five Golden Rules for Accurate Thyroid Testing
Christianson shared five essential rules for accurate thyroid lab testing. These rules are key for obtaining consistent and reliable results but are often overlooked, leading to inconsistent and confusing lab results. Implementing these guidelines significantly improves the accuracy and reliability of thyroid testing.
1. Time of day — Thyroid hormone levels fluctuate throughout the day. The most consistent results are obtained between 6:00 a.m. and 9:00 a.m. Blood spot testing makes it easier to adhere to this timing.
2. Fasting — Fasting status significantly impacts thyroid hormone levels. It’s important to fast before testing.
3. Biotin — Supplemental biotin interfere with lab analyses. It’s recommended to avoid biotin supplements for three days before testing. Surprisingly, this effect is primarily seen with supplemental, not dietary, biotin.
4. Thyroid medications — If you take thyroid medication, take your lab tests before taking your medication that day. Testing shortly after taking medication will produce inaccurate results, especially for T3 and T4 levels.
5. Menstrual cycle — For menstruating women, thyroid hormone levels vary throughout the cycle. The most consistent results are obtained during days one to nine and 20 to 28 of the cycle. Testing during days 10 to 19 produces inconsistent results.
Rethinking Thyroid Screening and the Value of Clinical History
Our discussion then turned to the value of conventional thyroid testing, specifically TSH. I expressed my evolving view that TSH is not an effective screening tool. Christianson agreed, emphasizing the importance of considering treatment options.
• Synthetic hormones are not the only solution — In conventional medicine, the primary treatment for thyroid issues is synthetic thyroid medication. However, with the powerful influence of diet and lifestyle, other approaches are available.
• The importance of antibody testing — Christianson emphasized the value of antibody testing as a screening tool, as it’s more predictive of symptoms than TSH. While some individuals with overt hypothyroidism have negative antibodies, antibody testing still provides valuable information. It’s important to remember that normal antibody levels do not necessarily rule out thyroid disease.
This perspective aligns with the approach of clinicians like Broda Barnes, who effectively identified thyroid issues based on clinical history and symptoms, even before the advent of modern thyroid testing. It’s important to remember that while thyroid hormone levels are important, the correlation between those levels and symptoms is much looser than most people realize. In fact, many people with significantly abnormal thyroid hormone levels are surprisingly asymptomatic.
Dietary Considerations for Thyroid Health
We also discussed the importance of diet in thyroid health. I mentioned my red, green and yellow food system from my book, “Your Guide to Cellular Health,” and how it differs from Christianson’s approach in “The Thyroid Reset Diet.” While my system focuses on general metabolic health, Christianson’s is specifically designed for individuals with autoimmune thyroid disease.
• Nuts are not a health food — I expressed concern about some of the “green” foods in Christianson’s diet, such as seasoned nuts. While nuts can be healthy, they’re high in LA and are best consumed in moderation, especially for those with high levels of stored linoleic acid. I also noted that my own food system is not suitable for thyroid health due to the inclusion of high-iodine foods.
Christianson explained that his dietary recommendations are not intended as a universal diet for everyone but rather as a specific tool for a specific situation — autoimmune thyroid disease.
• Modern practices contaminate healthy food sources — He also acknowledged the contamination of otherwise healthy foods, such as raw milk, with iodine due to modern agricultural practices.
The dairy industry commonly uses iodine-based disinfectants to clean teats and equipment. Although a hot water rinse helps mitigate iodine residues, the pervasive use of iodine teat dips introduces an additional, often unnoticed source of iodine into dairy products.
Diabetes and Metabolic Health
We also discussed diabetes, another major endocrine issue. Christianson described diabetes as a problem of fuel partitioning, where excess fuel accumulates in the bloodstream. He cited research showing that even small amounts of fat accumulation in the pancreas significantly impacts diabetes development.
• Glucose as your body’s preferred fuel source — I shared my understanding, influenced by the work of Ray Peat, that glucose is the preferred fuel for most cells, although some cells, like colonocytes and heart cells, primarily use fatty acids.
I also emphasized the dangers of overly restrictive low-carb diets, which trigger the release of stress hormones like cortisol. Christianson agreed, explaining that your body requires glucose and will produce it through cortisol-mediated muscle breakdown if dietary intake is insufficient.
• The ideal daily glucose intake — We agreed that 200 to 250 grams is a reasonable range for most individuals. We also discussed the dangers of excessive cortisol production, whether from dietary restriction or emotional stress, and its impact on sleep and overall health.
• The parathyroid gland — This tiny gland, nestled near your thyroid, plays a role in maintaining calcium balance in your bloodstream. Christianson argues that even slightly elevated calcium levels, especially if recurring, warrant investigation, particularly if accompanied by symptoms like fatigue, anxiety, or joint pain.
He emphasizes that conventionally accepted reference ranges for calcium are overly broad. Further, conventional medicine is limited in addressing parathyroid issues. Surgery is typically the only offered solution and there’s a lack of focus on root causes.
• Hormone replacement therapy — Finally, we touched on hormone replacement therapy, with both of us expressing caution regarding long-term use. Christianson emphasized the importance of considering both the benefits and risks of any intervention, particularly when it involves manipulating hormone levels. He stressed the need for strong evidence of net benefit before recommending such interventions.
Prioritizing Outcomes and Minimizing Harm in Thyroid Health
This in-depth discussion with Christianson illuminates the complex web of factors influencing thyroid health. By understanding the unique nature of thyroid autoimmunity, the importance of accurate testing and the interconnectedness of various bodily systems, we move beyond simplistic solutions and embrace a more holistic and effective approach to thyroid care.
This conversation emphasizes the importance of informed decision-making, prioritizing long-term health outcomes and supporting your body’s innate capacity for healing. By focusing on supporting your body’s natural processes and minimizing harm, you achieve true and lasting improvements in health.
Frequently Asked Questions (FAQs) About Thyroid Health
Q: How does iodine intake affect thyroid health?
A: Iodine plays a crucial role in thyroid function, but excessive intake triggers autoimmune thyroid disease, especially in individuals with lower genetic tolerance. Managing iodine within a safe range helps reverse thyroid issues.
Q: What are the key factors for accurate thyroid testing?
A: Accurate thyroid testing requires:
•Testing between 6:00 a.m. and 9:00 a.m.
•Fasting beforehand.
•Avoiding biotin supplements for three days.
•Taking tests before thyroid medication (if applicable).
•Timing tests with the menstrual cycle (days 1 to 9 or 20 to 28).
Q: How is thyroid autoimmunity different from other autoimmune diseases?
A: Unlike other autoimmune conditions linked to leaky gut, thyroid autoimmunity is primarily driven by an immune response to excessive iodine, which alters thyroid proteins and triggers an attack on thyroid tissue. Reducing iodine intake often reverses the condition.
Q: What is the connection between thyroid health and metabolism?
A: Thyroid function is closely linked to gut health, fatty liver, and metabolic balance. Hypothyroidism contributes to fatty liver disease, while excess fuel intake (from fats, carbs, or alcohol) overwhelms the liver’s storage capacity, leading to metabolic dysfunction.
Q: Why is a holistic approach essential for thyroid health?
A: A comprehensive approach, including dietary adjustments, lifestyle changes, and avoiding unnecessary hormone therapy, is key for optimizing thyroid function. Many thyroid conditions can be improved by addressing root causes rather than relying solely on medication.
High Blood Sugar — Are We Missing Half the Story? The Role of Reductive Stress
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/15/high-blood-sugar-reductive-stress.aspx
Analysis by Dr. Joseph Mercola March 15, 2025
STORY AT-A-GLANCE
- High blood sugar in Type 2 diabetes overwhelms cellular machinery like a chaotic factory, creating not just oxidative stress as previously thought, but also a more fundamental problem called reductive stress. Reductive stress occurs when there’s an oversupply of electron-carrying molecules in cells, creating a “traffic jam” of electrons that can’t be processed efficiently by the mitochondria’s electron transport chain
- While traditional views focused on oxidative stress alone, scientists now understand that reductive stress actually triggers oxidative stress. It’s the initial spark that sets off a chain reaction of cellular damage in diabetic conditions
- When the main pathway for processing glucose becomes blocked due to reductive stress, sugar molecules get diverted into harmful alternative pathways, creating additional toxic byproducts and inflammation
- The combination of reductive and oxidative stress explains many serious complications of diabetes including neuropathy, retinopathy, nephropathy and cardiovascular problems — all stemming from this initial electron overload
- Understanding reductive stress offers new therapeutic possibilities. Instead of just focusing on lowering blood sugar or fighting oxidative damage after it occurs, effective treatments target the electron transport chain efficiency and/or help cells recycle NADH more effectively
Visualize a huge workshop in your body that never stops working. Every second of the day, this workshop — your cells — transforms the food you eat into the energy and building blocks you need to survive. Picture endless supplies of raw materials being delivered to this workshop. When the workshop receives exactly what it needs, it hums along smoothly, producing vital components and discarding waste at a comfortable pace.
But when it is flooded with more resources than it can handle, chaos develops that reminds you of an old “I Love Lucy” episode. Conveyor belts clog, half-finished products pile up and machines begin malfunctioning. That chaos mirrors what happens inside your cells when you have chronically high blood sugar or otherwise known as Type 2 diabetes.
Scientists once focused on how too much sugar in your bloodstream creates damage through something called oxidative stress — an onslaught of destructive, oxygen-containing molecules. While that is important, a more serious stealth problem — reductive stress — turns out to be the main problem.1 For an easy-to-understand overview of what reductive stress is, and how it’s caused, see “Redox Simplified, Part 1.”
Reductive stress was first reported in the literature just before 1990 and is only relatively recently appreciated.2 It is at least as significant as oxidative stress for explaining why your cells lose their balance under conditions of prolonged high blood sugar. Reductive stress is the hidden spark that sets off a harmful chain reaction, eventually leading to severe problems for cells, tissues and organs.
Type 2 diabetes is frequently described as a disease of “overnutrition.” People consume more caloric energy than their bodies know what to do with, so cells try to cope with that oversupply. Insulin is the hormone that helps move sugar from the bloodstream into cells for use or storage.
This sugar is primarily glucose — a simple sugar that is chemically identical to what’s sometimes called dextrose, especially when you find it as a commercially available product in a store or used in IVs. In the early stages of Type 2 diabetes, cells grow resistant to insulin’s signal, making them slow to remove excess sugar from circulation.
However, in the late 1980s, scientists began to understand that there was another, more significant explanation beyond overnutrition. They couldn’t fully explain the observed pathologies solely based on excessive nutrient intake.
While overnutrition can contribute to health problems, more commonly, we see a disruption in the cellular machinery responsible for metabolizing fuel. Essentially, the “furnaces” within cells, the mitochondria, become less efficient at burning fuel. This diminished capacity to use fuel effectively leads to a buildup of harmful byproducts and, ultimately, cellular damage.
Why Overly High Sugar Leads to Reductive Stress
Many researchers once blamed only oxidative stress for the damage caused by chronic elevated blood sugars, but the story is far more complex. A less publicized culprit called reductive stress occurs when there is an oversupply of special electron-carrying molecules in your cells.
• Too much electron-carrying molecules in your cells — One of the key carriers is NADH, which picks up electrons when sugar is broken down for energy. Ordinarily, NADH unloads its electrons in the electron transport chain (ETC) of your mitochondria. When you have too much sugar around, your metabolic pathways generate more NADH than your cells can handle. This oversupply forms a traffic jam of electrons stuck in your mitochondrial ETC.
• The impact of excess NADH — During normal metabolism, oxygen in your mitochondria eventually accepts electrons from carriers like NADH, letting ATP and water form. However, if NADH is piling up too fast or is not being recycled quickly enough, your mitochondria reach a bottleneck and start leaking electrons onto oxygen in erratic ways. That partial reaction creates a reactive oxygen species called superoxide.
• Having excess NADH causes reductive stress — This sets off a cascade that leads to excessive oxidative stress. The two stresses work hand in hand — they both push the system toward an oxidative meltdown. Realizing that they are connected helps explain many of the complications tied to long-term high blood sugar.
Cells also have backup carriers like NADPH and glutathione, which help defend against or fix routine oxidative damage. But when you have high blood sugar, these carriers are also thrown off balance, sometimes contributing further to reductive stress. So, what should be a finely tuned assembly line of electrons becomes a crowded, poorly managed factory.
How Mitochondria and Enzymes Suffer Under Excess Sugar
Under healthy conditions, most sugar flows through glycolysis and then the Krebs cycle in your mitochondria, leading to a steady generation of NADH for ATP production. In a state of chronically high blood sugar, a steady flood of sugar pours in, leading to overly high rates of NADH production.
• Influx of sugar creates electron pressure — Pancreatic beta cells and liver cells are particularly vulnerable because they possess an enzyme called glucokinase, which does not slow down as sugar accumulates. It just keeps stuffing sugar into the mill, generating more pyruvate and acetyl-CoA, and eventually too much NADH.
This leads to what some researchers call electron pressure. Think of it as building water pressure in a dam. The more NADH, the more “water” is pushing against the gates of the electron transport chain. If the gates can’t relieve that pressure quickly enough, water (electrons) spills out in harmful ways, forming superoxide and other reactive oxygen species (ROS).
• Rethinking the accepted causes of oxidative stress — Though we typically consider fat metabolism or the lack of antioxidants to be reasons for oxidative stress, it is actually an overabundance of these electron carriers, like NADH, that triggers these chains of events.
• Low oxygen consumption occurs — Low oxygen usage in cells, sometimes referred to as pseudohypoxia, can also happen under these conditions. Even though oxygen might be physically present, the cell’s ability to use that oxygen effectively stalls when electron carriers accumulate. It’s the same effect as having enough workers on an assembly line but not being able to move products forward because the packaging stations are jammed.

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When Reductive Stress Morphs Into Oxidative Damage
Too much NADH sets the stage for oxidative stress, but how does that transition really happen?
• The process behind excess NADH creation — The mitochondria’s Complex I tries to oxidize NADH — basically convert it back to NAD+ — but an overwhelming influx of NADH leads to partial electron leaks onto oxygen, generating superoxide.
• Superoxide transforms into more harmful substances — The superoxide easily transforms into other even more hazardous molecules, such as hydrogen peroxide or hydroxyl radicals, intensifying the cell’s damage. Hence, reductive stress is the fuse that ignites oxidative stress.
Researchers used to think of oxidative stress and reductive stress as opposites, but in fact, you can’t get a huge wave of oxidative molecules without first bottling up too many electrons somewhere upstream. The meltdown occurs when all these unwanted oxygen-based molecules assault proteins, lipids and genetic material within cells, blocking regular functions and straining the system further.
How Key Enzymes Become Blocked, Triggering Toxic Side Routes
Glyceraldehyde 3-phosphate dehydrogenase, or GAPDH, is an important enzyme in glycolysis. You can think of it as a traffic cop, directing the flow of carbon units down the main route for energy production.
• Reductive stress roadblocks GAPDH — In reductive stress conditions, superoxide and other reactive molecules can chemically inactivate GAPDH, jamming the normal route. That means partially digested sugar fragments accumulate, searching for an escape route. If the main road of glycolysis is blocked, these fragments slip into alternative pathways — often called branching pathways.
• Examples of branching pathways — One of the branches is the polyol pathway, where sugar is first turned into sorbitol and then into fructose. This route increases NADH and drains NADPH, leaving the cell less capable of defending against oxidative threats. Another branch is the hexosamine pathway, which decorates proteins with sugar-like attachments and can promote even more harmful byproducts.
A third branch leads to the creation of advanced glycation end products, lumps of sugar stuck onto proteins that distort them and spark inflammation.
Each of these side roads ends up producing or amplifying reactive oxygen species, so the cell quickly finds itself in an escalating cycle — high sugar leads to reductive stress, which leads to oxidative stress, which damages enzymes, forcing leftover sugar into toxic detours, fueling even more oxidative stress.
• Diabetes is the result — The cyclical meltdown causes the hallmark problems of diabetes — nerves lose function (neuropathy), eyes develop vision problems (retinopathy), kidneys fail (nephropathy) and blood vessels clog or weaken (leading to strokes, heart attacks and amputations). It’s a chain reaction that starts from too much sugar and too many electrons in the wrong place at the wrong time.
The following graph, Figure 4 from Liang-Jun Yan’s paper, “Pathogenesis of chronic hyperglycemia: from reductive stress to oxidative stress,”3 published in the Journal of Diabetes Research in 2014, illustrates this process.

Consequences for People with Diabetes and Recommended Solutions
As chronic hyperglycemia persists, cells get battered by waves of destructive molecules. This environment disrupts insulin secretion, lowers insulin sensitivity and robs tissues of normal functioning. Measuring such damage often shows high levels of oxidative stress in people with poor sugar control, reinforcing that the end result of reductive stress — excess electron carriers — translates into extensive oxidative harm.
• There is a glimmer of hope — If the fundamental problem is that NADH builds up too fast, then reducing or balancing that electron overload might prevent later catastrophes.
• Addressing the root problem of diabetes — While many diabetes treatments focus on lowering blood sugar in general, or on cleaning up ROS after they form, what we really need are strategies to either curb the production of extra NADH or help cells recycle NADH back to NAD+ more efficiently.
• Other strategies that help manage diabetes — Some researchers suggest that strengthening the electron transport chain, or using dietary or pharmaceutical interventions that enhance NAD+ regeneration, can short-circuit the entire cascade before oxidative stress goes wild.
In simpler language, controlling reductive stress means improving the traffic flow of electrons in the cell, ensuring they don’t stack up to dangerous levels. If you manage the electron flow at the front end, you reduce the chance of harmful chain reactions downstream.
Putting It All Together — Why Reductive Stress Matters So Much
Prolonged high blood sugar is definitely toxic to cells, but we now see that the toxicity operates through a two-phase process — first, reductive stress (an electron overload), then oxidative stress (excess oxygen-based radicals) finalizes the damage.
• Oxidative stress is just one piece of the puzzle — The statement above modifies the classic narrative that only oxidative stress is to blame. Recognizing how reductive stress kindles oxidative stress helps us see that lowering sugar might not be enough; we also need to keep watch on the entire electron-handling machinery within cells.
• Reductive stress must be detected earlier — One of the big questions is why reductive stress has been overlooked for so long if it’s so central. Part of the answer is that oxidative stress is easier to detect with standard lab tests and known chemical markers, whereas reductive stress is more subtle, only revealing itself in how the electron carriers build up.
Also, reductive stress was first documented decades ago and then largely forgotten, overshadowed by the simpler story of oxygen-based radicals. Only with improved technologies and a deeper dive into electron transport chain dynamics did researchers rediscover how an oversupply of NADH or NADPH can disrupt everything.
In everyday life, the main message remains consistent — keep blood sugar under control to protect your cells from a damaging cascade.
• Strategies to address reductive stress — Good nutrition, exercise and regular medical check-ups all form part of the frontline in preventing reductive stress from flaring into full-blown oxidative chaos.
• The importance of studying reductive stress — Long term, the real advantage in understanding reductive stress is that it offers a new angle — one that goes beyond the usual talk of high sugar and ROS. By targeting the earliest link in the chain, you can knock out multiple problems at once, safeguarding insulin production, reducing inflammation and preserving healthy organ function.
Supplements That May Help Address Reductive Stress
Several nutritional supplements can be helpful in this regard, including the following:
• Coenzyme Q10 (CoQ10) / Ubiquinol:
◦ Mechanism — CoQ10 is a vital component of the ETC in mitochondria. It acts as an electron shuttle, helping to move electrons along the ETC and facilitate ATP production. In its reduced form, ubiquinol, it can also act as an antioxidant.
◦ Relevance to reductive stress — By improving the efficiency of the ETC, CoQ10 may help to prevent the buildup of NADH and the subsequent leakage of electrons that leads to reductive stress.
• Alpha-lipoic acid (ALA):
◦ Mechanism — ALA is a potent antioxidant that can also regenerate other antioxidants, such as vitamin C and glutathione. It also plays a role in mitochondrial energy metabolism.
◦ Relevance to reductive stress — ALA’s antioxidant properties can help to mitigate the oxidative damage that results from reductive stress. It may also indirectly support the ETC by regenerating other antioxidants involved in the process.
◦ Note — ALA exists in two forms (R-lipoic acid and S-lipoic acid), and the R form is generally considered more biologically active.
• Methylene blue:
◦ Mechanism — Methylene blue acts as an alternative electron acceptor in the ETC, effectively bypassing Complex I and III. It can cycle between its oxidized and reduced forms, shuttling electrons directly to cytochrome c and oxygen, improving mitochondrial function even when the standard electron transport chain is impaired.
Methylene blue’s ability to accept electrons makes it particularly useful in conditions where the standard ETC is overwhelmed or dysfunctional.
◦ Relevance to reductive stress — By providing an alternative route for electron flow, methylene blue helps relieve the electron congestion that characterizes reductive stress. It effectively acts as an “electron pressure release valve,” helping to prevent the buildup of NADH and reducing the likelihood of electron leakage and subsequent oxidative damage.
• Pyrroloquinoline quinone (PQQ):
◦ Mechanism — PQQ is a potent antioxidant that has been shown to stimulate mitochondrial biogenesis (the creation of new mitochondria).
◦ Relevance to reductive stress — By increasing the number of mitochondria and improving their function, PQQ enhances the cell’s overall capacity to handle electron flow and reduce the likelihood of reductive stress.
• Riboflavin (B2), niacinamide (B3) and thiamine (B1):
◦ Mechanism — B vitamins play essential roles as coenzymes in various metabolic pathways, including those involved in energy production and the ETC. Riboflavin is a precursor to FAD, and niacin is a precursor to NAD. Both are electron carriers.
◦ Relevance to reductive stress — Adequate levels of B vitamins are essential for the proper functioning of the ETC and may help to prevent the buildup of reducing equivalents.
Frequently Asked Questions (FAQs) on Reductive Stress and Type 2 Diabetes
Q: What is reductive stress, and how does it relate to Type 2 diabetes?
A: Reductive stress occurs when cells accumulate too many electron-carrying molecules, such as NADH, due to prolonged high blood sugar levels. This overload creates a bottleneck in the mitochondria, leading to an imbalance that ultimately triggers oxidative stress. In Type 2 diabetes, excessive sugar intake overwhelms the metabolic system, causing a cascade of harmful effects that damage cells, tissues and organs.
Q: How does reductive stress contribute to oxidative stress and cellular damage?
A: When NADH builds up in cells, it overwhelms the electron transport chain (ETC) in mitochondria, leading to electron leakage. These leaked electrons react with oxygen to form harmful reactive oxygen species (ROS) like superoxide and hydrogen peroxide. This oxidative damage disrupts cellular processes, impairs insulin function and contributes to complications like neuropathy, retinopathy and kidney disease.
Q: Why is reductive stress often overlooked in diabetes research?
A: Traditionally, scientists have focused on oxidative stress as the primary cause of cellular damage in diabetes. However, newer research shows that reductive stress precedes oxidative stress and acts as the initial trigger. The difficulty in measuring reductive stress and its more subtle effects led to its underappreciation for decades, but advances in mitochondrial research have revived interest in its role.
Q: What strategies can help manage reductive stress in Type 2 diabetes?
A: Managing blood sugar levels through a healthy diet and exercise supervision is key to preventing reductive stress. Additionally, certain supplements, such as coenzyme Q10 (CoQ10), alpha-lipoic acid (ALA) and methylene blue may help manage reductive stress and prevent oxidative damage.
Q: How do supplements like CoQ10 and alpha-lipoic acid help with reductive stress?
A: CoQ10 improves mitochondrial function by facilitating electron transfer in the ETC, reducing the buildup of NADH. Alpha-lipoic acid (ALA) acts as an antioxidant and helps regenerate other protective molecules like glutathione. Both supplements aid in restoring cellular balance, reducing oxidative stress and improving insulin sensitivity in people with diabetes.
Ozempic Linked to 19 Adverse Health Events
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/22/ozempic-linked-to-19-adverse-health-events.aspx
Analysis by Dr. Joseph Mercola February 22, 2025
STORY AT-A-GLANCE
- GLP-1 receptor agonists like Ozempic and Wegovy, originally intended as diabetes medications, have gained popularity for weight loss, leading to global shortages despite having modest benefits
- Research shows these drugs reduce seizures and substance addiction risks, but they increase the likelihood of 19 other health conditions, including fainting, kidney problems and pancreatic issues
- Common side effects include nausea, diarrhea, vomiting and abdominal pain, with potential risks of acute pancreatitis and thyroid cancer, making the trade-off dangerous for users
- Ozempic’s manufacturer Novo Nordisk reported $40.6 billion in revenue, highlighting how the “magic pill” mentality and ultraprocessed food consumption create a profitable cycle for pharmaceutical companies and food manufacturers
- Instead of relying on weight loss drugs, focus on optimizing cellular energy production through dietary changes, avoiding vegetable oils and supporting your gut and mitochondrial health
By now, most people around the world have heard of Ozempic and Wegovy, which are GLP-1 receptor agonists. These drugs, originally made for treating Type 2 diabetes, cause rapid weight loss, thus attracting individuals who have been struggling to lose weight for a long time. In fact, the effectiveness of these drugs has led to a global shortage.1 However, as with many other drugs that promise immediate results, there’s a catch.
Ozempic Hailed as a ‘Miracle Drug,’ but the Downsides Are Sinister
A report from The Epoch Times2 covered a study published in Nature Medicine,3 showing the impact of certain GLP-1 receptor agonists, sold under brand names such as Ozempic and Wegovy. As noted by The Epoch Times, “The media, patients, and even some doctors have dubbed the medications ‘miracle drugs’ because of their profound weight-loss effects.”4
In addition to weight loss, the study also noted that these drugs also lower the risk of “seizures and addiction to substances such as alcohol, cannabis, stimulants and opioids.”5 It’s believed that these drugs affect the brain’s neurological pathways related to reward and impulse control, explaining how these changes in behavior occur.6
Despite these benefits, the researchers caution potential, as there’s a dark side to these drugs that mainstream media and Big Pharma do not want you to see. According to the report, Ozempic increases your risk of developing a slew of other serious health conditions:7
“Researchers warn that these benefits come with an increased risk of 19 health conditions, such as syncope (fainting), arthritic disorders, and kidney and pancreatic problems.”
Similarly, a 2022 study found that commonly reported problems include nausea, diarrhea, vomiting and abdominal pain. An increased risk for acute pancreatitis and thyroid cancer was also noted.8 Meanwhile, Nature Medicine claims the benefits are “modest” at best:9
“While GLP-1RA drugs display effectiveness against a wide array of health problems, the magnitude of associated benefits is modest — about a 10% to 20% reduction for most outcomes.”
A Closer Look at the Research
The Nature Medicine study analyzed 215,970 diabetics using GLP-1 receptor agonists and compared them to multiple control groups: 159,465 taking sulfonylureas, 117,989 using DPP-4 inhibitors, and 258,614 on SGLT2 inhibitors. An additional control group of 536,068 used all three medications, while a separate baseline group of 1,203,097 received only standard care.10
They then produced a master list of health outcomes related to GLP-1 agonist receptor usage. As noted by The Epoch Times, while these drugs produced benefits, there were also significant adverse health outcomes:11
“Compared to usual care, GLP-1RA use was associated with a reduced risk of substance use and psychotic disorders, seizures, neurocognitive disorders (including Alzheimer’s disease and dementia), coagulation disorders, cardiometabolic disorders, infectious illnesses and several respiratory conditions.
There was an increased risk of gastrointestinal disorders, hypotension, syncope, arthritic disorders, nephrolithiasis, interstitial nephritis and drug-induced pancreatitis associated with GLP-1RA use compared to usual care. The results provide insights into the benefits and risks of GLP-1RAs and may be useful for informing clinical care and guiding research agendas.”
In a report by GoodRx, Stacia Woodcock, PharmD., outlines the mechanisms that lead to weight loss and other supposed benefits related to taking these drugs:12
• They signal your pancreas to release more insulin — After a meal, your blood glucose levels go up. Usually, the pancreas releases insulin when this happens to lower blood glucose levels. But in Type 2 diabetics, the body doesn’t always release enough. Incretin mimetics work on the pancreas to help raise insulin levels after you eat, which then lowers your blood glucose level.
• They increase your body’s sensitivity to insulin — Your body may also not respond as well to insulin if you’re diabetic. Incretin mimetics help increase insulin sensitivity, so your body can respond better to insulin when it’s released.
• They tell your liver to stop making glucose — This helps stop the production of new glucose to keep blood levels down.

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The Cycle of Ultraprocessed Food and Ozempic Wrecks Public Health
As the weight-loss effects of GLP-1 receptor agonists gained widespread attention, Big Pharma’s profits in this market skyrocketed. According to The New York Times, Novo Nordisk, the maker of Ozempic and Wegovy, reported $40.6 billion in revenue in 2024; this figure is expected to jump by 16% to 24% in 2025.13
In the Tucker Carlson Show interview featured above, Dr. Casey Means, a Stanford-educated surgeon now focusing on functional medicine, expounds on the idea that a “magic pill” that causes weight loss and other supposed benefits appeals to millions of users:14
“I think it’s very dark. It’s a stranglehold on the U.S. population. Almost like solidifying this idea that there is a magic pill — I mean, literally, the book by Johann Ari is called ‘Magic Pill’ — and convincing us that, you know, salvation from our chronic health issues is going to be found in a shot when we are living in a toxic stew that’s destroying our cellular biology.”
Elsewhere in the interview, Means shares how ultraprocessed food contributes to obesity, thus cycling back to taking drugs that cause weight loss. In the end, only Big Pharma and Big Food are the real winners here, as millions of adults struggle with the damage they cause:15
“We are the only species in the world that has an obesity and chronic disease epidemic, the only species in the world that has a chronic disease and obesity epidemic because of ultraprocessed food.
You think about every other animal in the wild — they’re eating real, natural foods except for domesticated animals, which are also getting chronic diseases just like humans because they’re eating our food. But every other animal, they’re able to regulate their satiety. They’re not eating themselves to death like we are. We’re literally eating ourselves to death …
This could be on track to be the most profitable medication ever in human history. It will be if the powers that be let it. And what the unfortunate part is that it doesn’t take our bodies out of the toxic stew that’s crushing our biology. Yes, we may melt some fat and muscle without changing any of the other levers that we just talked about that are crushing our biology. So, this is not the public health solution.”
Practical Ways to Address Underlying Metabolic Challenges
I believe the key to maintaining a healthy weight is optimizing your cellular energy production. This requires a multifaceted approach that takes effort to implement, but it leads to safer, healthier results — something GLP-1 receptor agonists don’t offer. With that in mind, here are my recommendations:
1. Avoid Ozempic and other GLP-1 agonist receptor drugs — The most obvious strategy is avoiding GLP-1 agonist receptors in the first place. If you’re tempted to start, you owe it to yourself to read the study to understand the dangers.
Pills and injections offer short-term relief, but they often mask deeper imbalances in how your cells produce and use energy. Real improvement happens when you remove the factors that strain your metabolism rather than rely on a drug to force quick weight loss.
2. Remove vegetable oils from your diet — If you regularly consume ultraprocessed foods, I recommend stopping right now and replacing them with real, whole foods. Processed foods contain linoleic acid-rich vegetable oils that disrupt your metabolic pathways and alter how your body stores fat. Instead, cook your meals using tallow, grass fed butter or coconut oil.
To protect your health from further damage, limit your intake of linoleic acid to less than 5 grams per day from all sources. I recommend using Cronometer, an online food tracker, so you don’t go over this recommended range.
3. Shift your carbohydrate sources gradually — Avoid making sudden dietary changes that can shock your system. If your gut is compromised, start by introducing easily digestible carbohydrates like whole fruit or white rice before incorporating more complex carbs.
For severe gut issues, sip dextrose water throughout the day as a temporary aid to support healing, but limit its use to about two weeks. The goal is to provide your cells with a steady source of easy-to-digest, healthy carbohydrates for energy.
4. Consider your protein and collagen intake — I suggest aiming for 0.8 grams of protein per pound of lean body mass and balancing that amount so that about one-third comes from collagen. Doing this supports muscle maintenance, tissue repair and hormone balance.
If you exercise frequently, you would probably do well with a higher intake, but take it slow and listen to how your body responds. Stable protein intake is foundational for regulating cravings and stabilizing energy.
5. Support your gut and mitochondrial health with other healthy habits — I recommend getting daily sunlight exposure while being mindful of timing. If your diet previously included vegetable oils, avoid intense midday sun for at least six months to reduce the risk of sunburn and skin damage. Additionally, grounding in low-EMF environments can be beneficial if available — oceans, particularly in North America, tend to be the safest option.
In addition, moderate-intensity movement, such as walking, supports cellular energy production and aids in weight management. Gradual, consistent effort in these areas strengthens your metabolism and leads to lasting health improvements. I believe this approach is far superior to relying on a so-called “magic” drug like Ozempic.
Boost Your GLP-1 Naturally with Akkermansia
The idea of a quick-fix pill may be tempting, but it comes at a long-term cost to your health. A better approach is to naturally boost your GLP-1 levels by supporting Akkermansia, a beneficial gut probiotic that produces a GLP-1-inducing protein. As noted in one study:16
“A. muciniphila increases thermogenesis and glucagon-like peptide-1 (GLP-1) secretion in high-fat-diet (HFD)-induced C57BL/6J mice by induction of uncoupling protein 1 in brown adipose tissue and systemic GLP-1 secretion.”
Many people lack Akkermansia due to various reasons, such as impaired mitochondrial function or an environment that is inhospitable to beneficial gut bacteria. Ideally, Akkermansia should comprise 3% to 5% of your total gut microbiome and it plays many different roles aside from promoting GLP-1.
For example, Akkermansia has the ability to produce mucin, which is a thick, gel-like substance that protects the gut lining from harmful pathogens, irritation from stomach acid and enzymes, as well as mechanical damage. Moreover, mucin helps nourish the gut bacteria already existing in your gut.
To boost Akkermansia naturally, eat plenty of berries and inulin-rich foods such as garlic, asparagus, bananas and leeks. Note, however, that if your gut health is currently out of whack, introducing high amounts of dietary fiber in your system all at once can worsen your gastrointestinal symptoms. So, work on healing your gut first, then gradually increase fiber intake.
- 1, 15 JAMA Netw Open. 2024 Aug 20;7(8):e2423385
- 2, 4, 5, 6, 7 The Epoch Times, January 28, 2025
- 3, 10, 11 Nat Med. 2025 Jan 20
- 8 Front Public Health. 2022 Oct 20;10:996179
- 9 WashU Medicine, January 20, 2025
- 12 GoodRX, October 2, 2023
- 13 The New York Times, February 5, 2025
- 14 YouTube, Tucker Carlson, August 17, 2024
- 16 Nature Microbiology volume 6, pages 563–573 (2021)
Glucose — The Ideal Fuel for Your Cells
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/19/glucose-mitochondria.aspx
Analysis by Dr. Joseph Mercola February 19, 2025

STORY AT-A-GLANCE
- Glucose is the most efficient fuel source for cellular energy production, generating more ATP (energy) per oxygen molecule compared to fats, making it especially valuable during low-oxygen conditions like intense exercise
- Unlike fats, glucose can produce energy even without oxygen through a process called glycolysis. This serves as a crucial backup energy system during high-intensity activities when oxygen is limited
- Glucose serves as a versatile building block in the body, participating in essential pathways like gluconeogenesis (creating new glucose from proteins) and the pentose phosphate pathway, which produces crucial components for DNA and RNA
- Your body stores excess glucose as glycogen in the liver and muscles, creating readily available energy reserves that can be quickly accessed between meals or during exercise
- While fats are excellent for long-term energy storage, they require more oxygen to break down and can produce more harmful reactive oxygen species (ROS) compared to glucose during energy production
Cells contain specialized organelles called mitochondria that are responsible for cellular energy production. Mitochondria generate adenosine triphosphate (ATP), which functions as the primary energy molecule used by cells to power essential biological processes,1 including muscle contraction and nerve signal transmission.
Mitochondria can metabolize both glucose and fats to produce ATP through a series of biochemical reactions. However, research indicates that glucose serves as the most efficient and versatile substrate for mitochondrial ATP synthesis, as the metabolic pathways involving glucose yield more ATP per molecule of oxygen consumed compared to fatty acid oxidation.2,3,4,5,6,7,8,9,10
To understand why glucose shines so brightly as a fuel source, it helps to zoom in on a few key concepts: how glucose delivers energy, why its metabolic “exhaust” tends to be less stressful on your cell’s machinery, and how relying on other fuels like fats can introduce imbalances and potential harm. By the end, you’ll see that glucose provides a balanced and high-yield form of energy production, effectively preventing certain risks that come with over-reliance on other fuels.
Why Glucose Is the Best Fuel
First, glucose enters your cell and gets broken down into smaller pieces outside the mitochondria, in the main part of the cell. This is like preparing the ingredients before cooking a big meal — you’re chopping up the vegetables before you start cooking. This step produces a little bit of energy, but not much. It’s like a small spark before the fire really starts.
These smaller pieces, the chopped-up glucose, then enter your mitochondria, where the real action begins. They go through a cycle of changes, a bit like a series of dance steps or a recipe with multiple steps. This is where the main process of breaking down glucose happens. This process creates special “energy carriers” that are like delivery trucks ready to transport energy to where it’s needed in your cell.
Finally, these energy carriers go to a special area in your mitochondria, which you can imagine as a power plant’s control room or a generator. They deliver their “energy cargo” through a chain of events like an assembly line in a factory. As the energy cargo moves along this line, it creates a flow of power that spins a tiny “turbine” or a water wheel. This spinning generates the main energy currency of your cell, ATP.
This whole process can create significant energy from one molecule of glucose, much like getting a lot of mileage from a full tank of gas. Glucose is a such a great fuel because it creates more of these special “energy carriers” early on, compared to other fuels like fats. These carriers are very efficient at delivering their energy to create ATP. This makes glucose the star of the show when it comes to powering your cells, ensuring they have the energy they need to function properly.
Why Fat Isn’t Always the Best — The Reductive Stress Angle
We often hear about fats as a super fuel because they hold large amounts of stored energy. Imagine a huge barrel of oil that can power a city for days. It sounds great — until you discover that extracting energy from that oil might require more oxygen, produce more damaging fumes, or strain the city’s power lines with surges and brownouts.
In a similar way, while fats can give your mitochondria plenty of stored energy, they are not always the easiest or safest fuel to burn.11,12,13,14,15,16,17
Here’s the main difference: fats and glucose produce different types of “energy carriers” during their breakdown. These carriers transport electrons, which are tiny particles with a negative charge, to your cell’s mitochondria. One type of carrier is called FADH2, and the other is called NADH. Think of FADH2 and NADH as different models of delivery trucks, each designed to carry electrons but using slightly different routes and having slightly different efficiencies.
When fats are broken down, they tend to create more FADH2 than NADH. The problem is that FADH2 enters the energy production process, called the electron transport chain (ETC), at a later stage (Complex II).18 It’s like a delivery truck that takes a longer, less efficient route. Because of this later entry point, fewer ATPs are made.
Another issue with relying heavily on fats for energy is the risk of something called reductive stress. Reductive stress happens when there are too many electrons (negative charges) flooding your system. Imagine an electrical circuit in your house: if you plug in too many high-powered appliances at once and overload the circuit, you risk sparks, short circuits, or even a power outage.
Similarly, in your cell, this overload of electrons leads to the formation of harmful molecules called reactive oxygen species (ROS).19 These ROS are like the “sparks” in our overloaded circuit analogy. They can damage important parts of the cell, such as proteins and DNA, similar to how sparks can damage your home’s wiring.20
A surplus of negative charge from the electrons that are not handled in an organized manner is called reductive stress. This is a relatively recent concept and was not discovered until 1989.
On the other hand, when glucose is broken down, it produces mostly NADH. NADH is like a more efficient delivery truck that takes a direct route, entering the electron transport chain at the very beginning (Complex I).21 This allows for more ATP production because the electrons have a longer runway as they enter the electron transport chain much earlier. This also tends to produce fewer harmful ROS “sparks.”
Furthermore, glucose has another advantage: it can still be used to produce some energy even when oxygen levels are low, a process called glycolysis.22,23 Fats can’t do this efficiently. So, if you’re doing intense exercise like sprinting or are in an environment with less oxygen, your cells can still partially rely on glucose to generate ATP,24 even if it’s not as much as when oxygen is abundant.
It’s like having a backup generator that can still provide some power even if the main power source is low.
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Glucose in Day-to-Day Life — More Than Just Energy
Glucose is much more than just a source of immediate energy for your cells; it plays a central role in a wide variety of other essential processes that keep your body functioning smoothly. You can think of glucose as a central hub connected to many different metabolic “side roads” that allow your cells to store energy, build necessary molecules, and recycle components as needed.25,26 These pathways are important for maintaining the body’s overall metabolic balance.
One of these important pathways is called gluconeogenesis.27 This Latin term, “gluconeogenesis,” simply means that your body can create new glucose from existing fuel sources in your body, primarily from protein.
While this ability to make glucose from non-carbohydrate sources is a magnificent backup system, ensuring the body has a supply of this essential fuel during times of need, relying on it as a primary source of energy can have powerfully destructive consequences, such as muscle wasting.
Another crucial pathway is glycogenesis. This process is like the body’s way of storing extra glucose for later use. When there’s an abundance of glucose, such as after a meal, the body converts it into a storage form called glycogen, primarily in the liver and muscles.28 Glycogen is like a quick-release fuel reserve that can be rapidly broken down back into glucose when energy demands increase, such as during exercise or between meals.
Then there’s the pentose phosphate pathway. This pathway is less about generating ATP (the cell’s main energy currency) and more about producing other important molecules, namely NADPH and ribose-5-phosphate.29 NADPH is a crucial molecule that acts as a reducing agent, meaning it donates electrons when your body needs them to run other metabolic processes.
The pentose phosphate pathway is a special process in your cells that doesn’t focus on making energy (ATP) directly, but instead creates other essential building blocks. You can think of it as a side road in your cell’s metabolic network, branching off from the main energy production route.
One of the key products of this pathway is NADPH. As mentioned before, NADPH is a molecule that acts like a delivery truck for electrons. It carries electrons and donates them in various cellular reactions. Why is this important? Well, many reactions in your body require electrons to proceed, and NADPH provides them.
The other important product of the pentose phosphate pathway is ribose-5-phosphate. This is a type of sugar molecule, but not the kind you eat. Ribose-5-phosphate is an essential component for building the genetic material of your cells, specifically DNA and RNA.30
DNA carries the instructions for building and operating your entire body, while RNA helps carry out those instructions. So, ribose-5-phosphate is essential for creating new cells, repairing damaged tissues, and generally keeping your body functioning properly. It is a five-carbon sugar that is essential for building the framework of DNA and RNA.
Glucose Is an Essential Building Block
Because glucose is involved in all these interconnected pathways, including gluconeogenesis, glycogenesis, and the pentose phosphate pathway, it acts as a truly versatile building block that can be used in many ways. Unlike fat, which is primarily an energy storage molecule, glucose can be readily converted into other essential molecules, used for immediate energy, or stored for later use.
It’s not just a quick source of energy; it’s also a fundamental component that helps maintain your body’s overall metabolic balance, ensuring that your cells have all the resources they need to function, grow, and adapt to changing conditions.
Only glucose can perform the miracle of being created from non-carb sources, a process called gluconeogenesis, highlighting its unique and indispensable role in the body. It’s like a universal puzzle piece that can fit into many different slots, making it an essential player in the complex network of cellular processes.
This ability to be interconverted between different forms and to participate in diverse pathways makes glucose, and not fat, the essential metabolic player it is. It’s not merely a short-term energy fix; it helps maintain your body’s broader metabolic balance, something that fat cannot achieve.
What Happens When There’s Too Much Glucose?
Glucose may be the ideal fuel, but your body prefer a “just right” approach. If glucose levels become chronically high — whether because of poor dietary habits, stress, or insufficient insulin action — your cells will suffer. One major problem is glycation, where glucose sticks to proteins, forming advanced glycation end products (AGEs) that can accumulate like sticky residue in a machine.31,32
Over time, these AGEs can degrade the function of tissues, triggering inflammation or stiffening blood vessels.
Excess sugar in your bloodstream also prompts more ROS production. While some ROS are part of normal cell signaling, too many damage mitochondria themselves, leading to even less efficient energy production.33,34
In that sense, flooding your system with glucose is like sending too many packages through a conveyor belt: at first, everything hums along, but eventually, congestion and accidents happen. Balancing glucose is key to letting the mitochondria work optimally, free from the chaos that extremes in sugar can create.
Type 2 diabetes offers a prime illustration of how essential glucose balance is. In diabetes, cells no longer respond properly to insulin, which normally helps cells take in glucose. Despite high blood sugar, many cells starve for energy, and mitochondria become less effective at generating ATP.35
Over time, tissues and organs suffer: small blood vessels deteriorate, nerves may be damaged, and the risk of heart disease climbs. This meltdown highlights how simply flooding your bloodstream with sugar isn’t enough; glucose must reach your mitochondria in a controlled way.
The heart and brain, known for their heavy energy demands, also show how valuable glucose can be. During a heart stress event or intense mental task, glucose provides far quicker energy per oxygen molecule than fat.36 This is particularly important if oxygen supply is in short supply — like a clogged artery in the heart or a momentary oxygen drop in the brain.
Summary — Why Glucose Earns the Title ‘Ideal Fuel’
So, in summary, glucose provides your cells with a highly efficient and adaptable way to generate energy and perform other essential functions. One of its key advantages is that it offers a high ATP yield per oxygen molecule used. ATP is the primary energy currency of your cells, like the electricity that powers your house.
When your cells break down glucose, they produce more ATP for every molecule of oxygen they consume compared to when they break down fat. This is especially important for tissues that sometimes experience low oxygen levels, such as your muscles during intense exercise. Think of it as getting more energy output for the same amount of input — glucose is simply a more efficient fuel in this regard.
Furthermore, glucose has the remarkable ability to generate energy even without oxygen. During short bursts of high-intensity activity, like sprinting, your muscles might need energy faster than your body can deliver oxygen. In these situations, your muscle cells can still produce ATP through a process called glycolysis, which breaks down glucose without needing oxygen.
Fat breakdown, on the other hand, always requires oxygen, so it can’t provide this emergency energy boost.37 It’s like having a backup generator that can kick in when the main power source is unavailable. Glycolysis is unique in that it does not require oxygen to proceed.
So, to reiterate, glucose isn’t just about providing energy; it’s also incredibly flexible in how it can be used by the body. It participates in various metabolic pathways, allowing for the creation of many necessary compounds.
For instance, glucose metabolism helps produce NADPH, a molecule that acts like a delivery truck for electrons, which are needed for various cellular processes, including building and maintaining your body’s antioxidant defenses. These defenses protect your cells from damage caused by ROS. In addition, your body can store extra glucose as glycogen, primarily in your liver and muscles.38,39
Glycogen is like a reserve tank of fuel that can be quickly tapped into when your body needs a rapid energy supply, such as between meals or during exercise.
Why Glucose Beats Fat for Everyday Energy Needs
Finally, when glucose is broken down, it mainly produces NADH, another type of electron carrier. NADH enters the cellular energy production machinery to the electron transport chain in your mitochondria, at the very beginning (Complex I), which helps maintain a smooth and efficient “electron flow,” like a well-regulated electrical current.
Relying too much on fat for energy can lead to an overproduction of FADH2, a different type of electron carrier that enters the machinery later (Complex II). This disrupts the electron flow, creating reductive stress.40,41 Reductive stress is like an overloaded electrical circuit, where too much negative charge builds up, increasing the risk of producing those harmful “sparks” called ROS, which can damage your cells. Maintaining a balance of electrons is essential.
Some people might point out that humans evolved to store a lot of fat for a reason, and that’s true. Fat is an excellent long-term energy reservoir, crucial for surviving periods of famine or prolonged food scarcity. However, in everyday situations, especially those involving physical activity or fluctuating oxygen levels, glucose offers a far more versatile and efficient way to meet your body’s energy and metabolic needs. It can be used to produce energy quickly even without oxygen.
It can generate important molecules needed to maintain your cellular health and regulate electron flow to prevent damage, and also be used to create other molecules in essential processes. So, while fat is a vital energy reserve for long-term survival, glucose is the preferred fuel for optimal performance in most day-to-day activities and plays a much broader role in supporting overall metabolic health.
Balancing Glucose for Optimal Mitochondrial Function
From top to bottom, glucose shows itself to be the “special sauce” for keeping your mitochondria humming along at peak capacity. Its biochemical pathways are poised to spin out large amounts of ATP, carefully managing the electron flow to avoid redox chaos.
While glucose is clearly a vital fuel for the body, it’s important to understand that it’s not a free pass to consume excessive amounts of sugar. Your body thrives on balance, and just like with anything else, too much glucose is detrimental. Excess glucose leads to harmful processes like glycation, where sugar molecules bind to proteins and impair their function, and oxidative stress, an imbalance between free radicals and antioxidants that can damage cells.42,43,44
Chronically elevated blood sugar levels can contribute to serious health problems, including Type 2 diabetes, heart disease, and even cognitive decline.45,46,47,48,49,50,51
One of the marvels of your biology is that maintaining moderate glucose levels, coupled with good insulin sensitivity, allows your cells to enjoy the best of both worlds. Insulin sensitivity refers to how effectively your cells respond to insulin, a hormone that helps regulate blood sugar. When insulin sensitivity is high, your cells can efficiently take up glucose from the bloodstream and use it for energy or store it for later use.
This allows cells to reap the benefits of glucose as a fuel source while avoiding the negative consequences of both excessive sugar intake and an overreliance on fat for energy.
A crucial piece of this complex equation is understanding your current state of metabolic health. Factors like your exposure to mitochondrial poisons and gut health status play major roles in determining how your body processes glucose and what your optimal carb sources are. In short, your individual metabolic health determines which carbohydrates will support your health and which will be detrimental — and this can change over time.
Future articles will delve deeper into the fascinating interplay between metabolic health, individual variations, and personalized approaches to optimizing glucose metabolism.
- 1, 12 Khan Academy, Cellular Respiration
- 2, 11, 18, 22, 24 Osmosis, Cellular Respiration — What Is It, Its Purpose, and More
- 3, 35, 45 Physiology, Glucose Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; January 2025
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- 5 Lift Glucose, August 22, 2024
- 6 Libre Texts Biology, 5.9: Cellular Respiration
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- 15, 20, 43 PLoS One. 2023 Sep 21;18(9):e0289475
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- 19 Eurasian J Med. 2018 Oct;50(3):193–201
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- 37 Clin Sci (Lond). 1980 Dec;59(6):469-78
- 40 Antioxid Redox Signal. 2020 May 14;32(18):1330–1347
- 41 Antioxid Redox Signal. 2020 Jun 26
- 46 Int. J. Mol. Sci. 2023, 24(5), 4394
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How Meal Timing Impacts Your Blood Sugar Levels
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/01/23/meal-timing-and-blood-sugar-control.aspx
Analysis by Dr. Joseph Mercola January 23, 2025

STORY AT-A-GLANCE
- Your body has an internal clock (circadian rhythm) that affects various functions, including your sleep patterns, hormones and digestion
- The circadian rhythm also affects how your body processes food. Your metabolism, the process of turning food into energy, follows this daily rhythm
- A recent study found that “late eaters” (those who consume 45% or more of calories after 5 p.m.) had poorer blood sugar control, regardless of weight or diet
- Eating later in the day disrupts your body’s natural ability to metabolize glucose due to reduced insulin secretion and sensitivity at night
- Consuming a healthy breakfast, avoiding late-night snacks and distributing carbohydrates throughout the day are key strategies for managing blood sugar
Have you ever felt that afternoon slump after a big lunch or found yourself wide awake after a late-night snack? These experiences aren’t random. Your body operates on an internal clock, much like a built-in schedule, called the circadian rhythm, and it affects everything, including your sleep patterns, hormones and digestion.
A recent study demonstrates another area that the circadian rhythm controls, particularly your blood sugar levels. It provides an interesting insight — it’s not just what you eat that matters; when you eat your meals do too, meaning that timing your meals based on your circadian rhythm significantly impacts your glucose levels and, ultimately, your overall health.1
‘Late Eaters’ Have Higher Glucose Levels and Are More Prone to Weight Gain
A study published in the journal Nutrition & Diabetes found that people who tend to eat later in the day have a higher risk of problems with blood sugar control. This means their bodies have a harder time regulating glucose, the main sugar found in the bloodstream.2
The researchers studied 26 people between the ages of 50 and 70 who were either overweight or obese and had either prediabetes or Type 2 diabetes. They divided the participants into two groups based on when they ate their meals — “early eaters” who ate most of their calories before evening and “late eaters” who ate almost half (45% or more) of their calories after 5 p.m.
To make sure the comparison was fair, both groups ate the same types and amounts of food. The only difference was their eating schedule. Participants used a mobile app to record all their meals.
The study’s key finding was that people who ate more later in the day had more trouble managing their glucose tolerance — their body’s ability to absorb glucose and use it for the brain and tissues — no matter their weight or what kinds of foods they ate. These “late eaters” also tended to eat more carbohydrates and fats in the evening. According to the researchers:
“Adding to previous findings on the detrimental effect of late eating on BMI [body mass index] and metabolism and its association with poorer diet, we now observed that the association of LE [late eaters] with poorer glucose tolerance is independent of greater body weight, fat mass, calorie amount, or poorer diet composition.”3
Dr. Diana Díaz Rizzolo, a member of the Faculty of Health Sciences, UOC and the study’s lead author, explained:
“The body’s ability to metabolize glucose is limited at night, because the secretion of insulin is reduced, and our cells’ sensitivity to this hormone declines due to the circadian rhythm, which is determined by a central clock in our brain that is coordinated with the hours of daylight and night.”4
Our Inner Timekeeper — The Circadian Rhythm and Your Metabolism
Think of your body as a finely tuned orchestra. Each organ and system have a role to play, and the circadian rhythm is the sync over a 24-hour period. Just like a conductor uses a baton, our bodies use light conductor, keeping everything in and darkness to stay on schedule.
Sunlight signals our bodies to release hormones like cortisol, which helps us feel alert and gives us energy. When darkness falls, our bodies produce more melatonin, a hormone that promotes relaxation and prepares us for sleep.5
This internal clock also affects how our bodies process food. Our metabolism, the process of turning food into energy, follows this daily rhythm. For example, our bodies are usually better at using insulin — a hormone that helps move sugar (glucose) from our blood into our cells for energy — in the morning.6 Insulin acts like a key that unlocks the door to your cells, allowing sugar to enter and provide energy. This is why our bodies handle sugars more efficiently earlier in the day.
This brings us to an important area of research called chrononutrition, which looks at how our eating patterns line up with our internal clock.7 As the featured study illustrates, consistently eating at times that don’t match our natural rhythms, like frequently eating late at night, throws off our metabolism.8
This is especially relevant for shift workers who often have irregular sleep and eating schedules and are more likely to experience metabolic problems.9 When your circadian rhythm is disrupted, it leads to insulin resistance. This makes it harder for sugar to get into your cells, leading to high blood sugar levels and increasing the risk of Type 2 diabetes.10
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When You Eat Matters — Meal Timing and Blood Sugar Control
Now that we understand how our internal clock affects metabolism, let’s look at how the timing of our meals specifically impacts blood sugar control. Here’s how breakfast, late-night eating, how often you eat and even intermittent fasting affect your blood sugar:
• Skipping breakfast — Skipping breakfast could set you up for blood sugar problems throughout the day. Research shows that people who skip breakfast often have bigger blood sugar spikes after lunch and dinner.11 It’s as if skipping breakfast makes your body less efficient at handling sugar later on, creating a ripple effect throughout the day.
• Night owl nibbling — Late-night snacking is a common culprit when it comes to blood sugar issues. Your body is like a factory that powers down at night. Just like a factory slows its operations, your body’s ability to process sugar also slows down in the evening.
Eating late at night is like asking the factory to suddenly ramp up production when it’s already winding down. This leads to weight gain and increases the risk of Type 2 diabetes. Considering that our ancestors likely ate most of their food during daylight hours when they were active, aligning our eating habits more closely with this natural pattern is beneficial.
• Spreading the carb load — The frequency of your meals also plays an essential role in blood sugar management. Instead of eating three large meals, try spreading your carbohydrate intake throughout the day with smaller, balanced meals and snacks.
This helps avoid high blood sugar spikes that happen after eating a lot of carbs at once. It’s like giving your body small, manageable doses of fuel instead of one big overload, allowing it to process the sugar more steadily.
• Intermittent fasting — Another approach to consider is intermittent fasting (IF), which involves cycling between periods of eating and fasting. Some studies suggest IF improves how well your body uses insulin and helps lower blood sugar levels.
There are different ways to do IF, such as the 16/8 method (eating within an 8-hour window and fasting for 16 hours) or the 5:2 diet (eating normally for five days and restricting calories for two).
Implement Healthier Habits with These Strategies
Now that you understand how meal timing affects your blood sugar, below are some easy-to-follow tips to improve your eating habits:
• Make breakfast a priority — Think of breakfast as the first log you put on the fire of your metabolism each day. It gets things going and sets the tone for your blood sugar control. When you skip breakfast, it’s like trying to start a fire with damp wood — it just doesn’t work as well.
Instead of sugary cereals or pastries, which cause a quick spike and then a crash in your blood sugar, try these simple swaps:
◦ Yogurt with ripe fruit — Yogurt made from raw, grass fed milk is packed with protein to keep you feeling full and satisfied. Adding fruit gives you vitamins, fiber and natural sweetness. A sprinkle of cinnamon might even help with blood sugar control.
◦ Whole-wheat toast with an organic pasture-raised egg — This simple meal provides a good mix of healthy fats, protein and complex carbohydrates.
• Avoid late-night snacks — Remember the campfire analogy? Eating late at night is like throwing logs on a dying fire. Your body isn’t as efficient at processing food late in the day, so you’re more likely to have excess sugar in your bloodstream. To avoid late-night eating:
◦ Set a regular dinner time — This helps regulate your hunger cues. Aim to eat dinner a few hours before bedtime to give your body time to digest.
◦ Eat without distractions — When you eat while watching TV or using your phone, it’s easy to overeat. Try to create a calm environment for meals.
◦ Establish a relaxing bedtime routine — Sometimes, late-night cravings are due to boredom or habit. A relaxing routine, like reading or taking a warm bath, helps you avoid the urge to snack. If you still feel hungry, try a glass of water or herbal tea. For more useful strategies to help you get high-quality sleep, read “Top 33 Tips to Optimize Your Sleep Routine.”
• Distribute your carbs wisely — Carbohydrates are your body’s main source of energy, but some carbs are digested faster than others. Think of it like different types of fuel — some burn quickly, causing a sudden burst of energy followed by a crash, while others burn slowly and provide steady energy. To distribute your carbs wisely:
◦ Choose whole grains — Whole grains have more fiber, which helps regulate blood sugar.
◦ Eat plenty of ripe fruits and well-cooked vegetables — These are packed with vitamins, minerals and fiber, which helps slow down the absorption of their natural sugars.
◦ Watch your portions — Even healthy carbs raise blood sugar if you eat too much at once. Balance your meals with protein and healthy fats. Include at least 0.8 grams of protein per pound of lean body mass, and ensure one-third of your protein intake is collagen-based.
As for healthy fats, choose grass fed beef tallow, ghee and coconut oil for cooking and eliminate vegetable oils that are loaded with linoleic acid (LA). Avoid processed foods and restaurant meals, which are often loaded with these oils.
• Small changes make a big impact — Making big changes to your diet is tough, so start small and make gradual, sustainable changes. Remember, consistency is key. Here are some easy ideas to get you started:
◦ Focus on one meal — Start by improving one meal, like breakfast, and then gradually work on other meals.
◦ Set realistic goals — Set small, achievable goals, like eating breakfast every day for a week or swapping sugary drinks for water.
◦ Track your progress — A food journal or app will help you stay motivated and see how far you’ve come. My Mercola Health Coach App has a Food Buddy feature to help guide your food choices and keep track of your health goals. It’s coming out very soon, so stay tuned.
- 1, 2, 3, 8 Nutrition & Diabetes, 2024, volume 14, Article number: 90
- 4 News Medical Life Sciences, November 20, 2024
- 5 Johns Hopkins Medicine, Sleep/Wake Cycles
- 6 Nature, 2010, 466(7306), 627-631
- 7 Nutrients. 2022 Feb 16;14(4):823
- 9 Advances in Nutrition, March 2023, Volume 14, Issue 2, Pages 295-316
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