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Your stomach cancer risk goes up with one “refreshing” choice

Reproduced from original article:
https://www.naturalhealth365.com/one-refreshing-daily-choice-sharply-raises-stomach-cancer-risk.html

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sugary-drinks(NaturalHealth365)  About two out of three adults in the U.S. drink at least one sugar-sweetened beverage every day.  Whether the drink is a soda with lunch, a lemonade at a backyard party, or a “refreshing” sports drink after exercise, the habit rarely gets a second thought.

Yet fresh findings from two of the country’s longest-running health studies tie that single daily drink to a far higher risk of a cancer than most people would consider significant.

Just one drink separates high risk from low

Researchers at the Mass General Brigham Cancer Institute analyzed 112,284 adults from the Nurses’ Health Study and the Health Professionals Follow-Up Study.  Both studies tracked diet, lifestyle, and health for decades, and 278 participants developed stomach cancer along the way.  After adjusting for other risk factors, the team compared the heaviest and lightest sugary drink consumers.

The difference was significant.  People who drank at least one serving a day had 2.45 times the risk of stomach cancer compared with people who drank less than one serving a month.

Among women who drank more than one sugary beverage daily, the risk climbed to roughly three times higher.

Sugary drinks already carry a long rap sheet

Earlier research has linked sugar-sweetened beverages to colorectal, breast, and liver cancers.  Until now, however, almost nothing connected these drinks to stomach cancer in a population.  According to the researchers, this study is the first to show that link here.

Stomach cancer ranks as the fifth leading cause of cancer death worldwide, so the new link carries real weight.  Additionally, higher total fructose intake tracked with more stomach cancer, too.

Since fructose is the main sweetener in most of these drinks, the pattern points straight at the sugar.

The usual stomach cancer suspect was not behind the link

Infection with H. pylori, a common stomach bacterium, is a well-known driver of stomach cancer.  Naturally, the researchers wondered whether sugary drinks simply went hand in hand with infection.  In a subset of 940 participants with infection data, slightly more than a third showed signs of H. pylori.

Interestingly, sugary drink habits did not track with infection at all.  In other words, the higher cancer risk did not appear to run through the bacterium everyone already blames.  Instead, a daily sugar load seems to matter independently.

Healthy-looking bottles count too

Soda was not the only drink on the list.  The study counted carbonated drinks, punch, lemonade, and sports drinks as sugar-sweetened beverages, and many people consider the last two fairly harmless.  Sadly, a bright label and a fitness image don’t change what’s inside the bottle.

Because the study observed people rather than assigning drinks, the findings show a strong link, not proof of cause.  The team also had limited data on family history, and the number of cancer cases was modest, so larger studies will need to confirm the pattern.  Even so, decades of detailed tracking make the signal difficult to ignore.

Better choices start with what goes in your glass

Swap one sugary drink a day for sparkling water with fresh flavor.  Add a squeeze of lemon or lime, a few crushed mint leaves, or sliced cucumber to plain sparkling water.  The fizz scratches the same itch as soda without the sugar load.  Once one swap feels easy, try a second.

Brew a pitcher of herbal iced tea for the week.  Hibiscus, peppermint, and fresh ginger make bright, refreshing teas that need no sweetener.  Research suggests hibiscus tea supports healthy blood pressure, and ginger has a long history of soothing the stomach.  Keep a pitcher in the fridge so the healthy choice is also the easy one.

Feed your stomach lining with protective foods.  Broccoli sprouts are rich in sulforaphane, and human studies suggest broccoli sprouts can help reduce H. pylori activity in the stomach.  Garlic, cabbage, and fermented vegetables like sauerkraut add further support.  Meanwhile, colorful produce rich in vitamin C helps protect stomach cells from damage.

Read labels before you trust a “healthy” drink.  Look for added sugars listed as cane sugar, high-fructose corn syrup, fructose, or fruit juice concentrate.  For workouts, plain water with a pinch of sea salt handles hydration for most people.

Cancer prevention that starts with the next glass you pour

Few people would ever connect a lunchtime lemonade to stomach cancer, which is exactly why prevention has to begin long before a diagnosis.  If you want to learn more, Jonathan Landsman’s Stop Cancer Docu-Class explores natural approaches to lowering cancer risk, including lab tests that can reveal early warning signs years ahead of a typical diagnosis.

Remember, the small daily choices in this study are just the beginning.

Sources for this article include:

Ghadvances.org
Sciencedaily.com

Unspoken solution for cataracts, macular degeneration and diabetic neuropathy

Reproduced from original article:
https://www.naturalhealth365.com/how-regular-movement-cuts-the-risk-of-three-major-eye-diseases.html

by:  | 
exercise-lower-eye disease-risk(NaturalHealth365)  An estimated 43.3 million people worldwide are completely blind.  Shockingly, another 295 million live with moderate to severe vision impairment.  Behind those numbers are millions of people who can no longer read a prescription label, recognize a grandchild’s face across a room, or drive safely after dark.

As the world’s population continues to age, those numbers are projected to climb even higher in the decades ahead.  Most advice aimed at protecting eyesight focuses on diet, screen breaks, and regular checkups.  But a new UK Biobank analysis of more than 77,000 adults just added a factor almost nobody mentions in the same breath as eye health: how much people move.

The advice gap nobody’s filling

Ask an eye doctor how to protect vision and movement rarely comes up.  The conversation tends to stay inside familiar territory: eat more leafy greens, wear sunglasses, get checked every year.  Useful, but incomplete, and the missing piece turns out to matter more than expected.

Cardiologists talk about exercise constantly.  Eye doctors almost never do, even though the eyes run on some of the smallest, most easily damaged blood vessels in the body.

A massive study, and a split result nobody expected

Researchers tracked 77,644 adults using wrist-worn accelerometers, an objective measure far more reliable than self-reported exercise.  Over a median follow-up of 6.2 years, they recorded new cases of cataract, diabetic retinopathy, age-related macular degeneration, and glaucoma, then compared outcomes against how much moderate-to-vigorous activity each person logged.

Three of the four diseases responded.  Higher activity levels were linked to a meaningfully lower risk of cataracts, the most common cause of treatable vision loss worldwide.

Diabetic retinopathy risk fell sharply as activity climbed toward roughly 250 minutes a week.  Age-related macular degeneration risk dropped too, though more modestly, plateauing once activity reached 300 to 400 minutes weekly.

Glaucoma didn’t move at all.  Statistically, the connection between activity and glaucoma risk was essentially zero.

Why one disease refused to cooperate, and what that reveals

That gap isn’t a flaw in the research, but a clue about how these diseases work.

Cataracts, diabetic retinopathy, and macular degeneration all share a common thread: blood flow, oxidative stress, and the small vessels that feed the eye’s most fragile tissue.

Movement improves circulation and reduces the oxidative damage tied to all three, which lines up with why exercise helped.

Glaucoma operates differently, driven largely by internal eye pressure and by mechanical stress on the optic nerve, a pathway general fitness doesn’t reach the same way.  Whatever protects one part of the eye apparently has little say over another.

Overlooked habits working against healthy eyes

While movement quietly helps three major eye diseases, a handful of everyday habits work just as quietly against all four.

Poorly controlled blood sugar is the single biggest driver of diabetic retinopathy, and the damage accumulates for years before a person notices any change in vision.

Long, uninterrupted stretches of screen time reduce blink rate and dry out the eye’s surface.  That habit often comes paired with the same prolonged sitting already tied to serious cancer risk.

Neither problem made the list of four diseases studied here, yet both compound discomfort and make early symptoms harder to notice.  Skipping regular sleep disrupts the eye’s own repair processes, since much of the fluid clearance and tissue repair inside the eye happens during rest.

Smoking doubles or triples the risk of macular degeneration in most large studies, making smoking cessation one of the most modifiable risk factors that still gets treated as an afterthought.

Eye health deserves a much bigger seat at the table

Vision loss doesn’t only affect what a person sees.  Studies have linked vision loss to higher rates of falls, social isolation, depression, and even faster cognitive decline in older adults.  This is understandable, considering that a huge share of how people navigate the world and stay connected depends on sight.

Three of the four leading causes of vision loss studied here turned out to be at least partly influenced by something as ordinary as a daily walk.  Given the scale of vision loss worldwide, a genuinely modifiable factor like that deserves far more attention than current eye health advice typically provides.

Early signs of eye trouble people tend to explain away

Glaucoma earns a reputation as the sneak thief of sight because the disease rarely causes pain or obvious symptoms until permanent damage has occurred.

Gradually narrowing peripheral vision, often blamed on tiredness or clumsiness, is frequently the first sign of glaucoma damage.  Needing progressively more light to read comfortably, or noticing halos around headlights at night, can point to early cataract formation.

Straight lines that appear wavy or distorted, particularly in central vision, are a hallmark early sign of macular degeneration.  Blurred or fluctuating vision that tracks with blood sugar swings deserves attention as a possible early marker of diabetic retinopathy.

None of these signs confirm a diagnosis on their own, and none replace a dilated eye exam.  Taken together, they’re worth mentioning at the next appointment rather than dismissing as normal aging.

Practical ways to protect vision starting today

Aim for at least 150 minutes of moderate activity weekly, spread across most days.  Brisk walking counts, and the data suggests benefits accumulate well before reaching an elite fitness level.  Pairing that movement with the same recovery habits that reduce muscle damage during other kinds of exercise helps keep a walking routine sustainable long term.

Get blood sugar checked regularly, especially if you have a family history of diabetes.  Diabetic retinopathy develops silently, and catching elevated blood sugar early can protect the eyes years before symptoms appear.

Give screens regular breaks using the 20-20-20 rule.  Every 20 minutes, look at something 20 feet away for 20 seconds, giving overworked eye muscles and a drying ocular surface time to recover.

Treat sleep as part of an eye care routine rather than a separate, unrelated habit.  Consistent, adequate rest supports the overnight repair processes inside the eye that daytime habits alone can’t replace.

What one study can and can’t promise

No single analysis proves that walking more will prevent blindness, and the researchers behind this one were careful to say so.  The data does show that a factor almost never discussed at an eye exam moved the needle on three of the four leading causes of vision loss studied.

Sources for this article include:

NIH.gov
NIH.gov

This Silent Health Crisis Is Now Affecting Nearly 800 Million People


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/08/25/chronic-kidney-disease-worldwide.aspx


Analysis by Dr. Joseph Mercola    August 25, 2026

chronic kidney disease worldwide

Story at-a-glance

  • Chronic kidney disease now affects an estimated 788 million adults worldwide, roughly one in seven adults, making it one of the largest and fastest-growing chronic health challenges on the planet
  • Most people with kidney disease are in the early stages and often have no obvious symptoms, allowing damage to progress silently for years before it’s discovered
  • Kidney disease extends far beyond the kidneys themselves; impaired kidney function contributes to more than one in 10 cardiovascular deaths worldwide by increasing strain on the heart and blood vessels
  • High fasting blood sugar, high blood pressure, and excess body weight were identified as leading contributors to kidney disease-related disability and premature death, highlighting the importance of metabolic health
  • Taking action early by improving blood sugar control, supporting healthy blood pressure, eating potassium-rich whole foods, staying physically active, and monitoring kidney function offers the best opportunity to preserve kidney health long term

Chronic kidney disease is a gradual loss of your kidneys’ ability to filter waste, balance fluids, and regulate the minerals your body depends on. What makes it so dangerous is how quietly it begins. Early on, you may notice nothing at all, or you may shrug off vague signs like fatigue, swelling in your legs or feet, or subtle changes in urination. By the time the damage makes itself obvious, much of it has often already been done.

That silence is exactly what makes a recent global analysis so unsettling. Drawing on health data spanning more than three decades and hundreds of countries and territories, researchers set out to measure how far this condition has actually spread, and what they uncovered suggests it has become one of the most widespread chronic threats to human health, with consequences that reach well past the kidneys and into the heart itself.1

The detail that deserves your attention most, though, isn’t the sheer size of the problem. It’s that the majority of people whose kidneys are already in trouble have no idea, because the early stages do their damage without raising an alarm. That gap, between how common this condition has become and how rarely it gets caught in time, is the real story. And it starts with what this landmark analysis revealed about the true scope of the crisis.

Kidney Disease Quietly Became One of the World’s Biggest Health Threats

Published in The Lancet, this global analysis examined chronic kidney disease trends across 204 countries and territories between 1990 and 2023. Researchers drew on published studies, household surveys, treatment registries, and national health records to determine how many adults were affected, how many died from the condition, and which risk factors contributed most heavily to the burden of disease.2

Their findings revealed that chronic kidney disease is no longer a niche medical problem; it’s become one of the largest health challenges facing adults worldwide.

• The number of affected adults more than doubled in three decades — According to the analysis, 788 million adults were living with chronic kidney disease in 2023, compared to 378 million in 1990. Researchers reported that the global prevalence reached 14.2% of adults, meaning roughly one in seven adults now has some level of kidney damage or impaired kidney function.3

For you, that reframes the question — kidney disease is no longer a problem confined to a high-risk few, which means the odds it’s relevant to you personally are higher than you might assume.

• Most people are stuck in the silent stages — The overwhelming majority of cases occurred in stages 1 through 3. These are the earlier phases of kidney disease, when the kidneys still perform much of their job but damage has already begun. Researchers estimated that stage 1 through stage 3 disease accounted for a combined prevalence of 13.9% of adults worldwide.

This matters because early kidney disease rarely causes obvious symptoms. You can feel completely normal while damage progresses in the background. That creates a challenge, but it also creates an opportunity. If you identify the problem early, you have a much larger window to address the factors that drive further decline.

• Kidney disease reaches far beyond the kidneys themselves — The analysis found that chronic kidney disease ranked as the ninth leading cause of death globally in 2023, accounting for approximately 1.48 million deaths. Researchers also calculated that impaired kidney function contributed to 11.5% of cardiovascular deaths worldwide.

Unhealthy kidneys place extra stress on your entire circulatory system. Your kidneys help regulate fluid levels, blood pressure, and numerous chemical signals throughout the body. As kidney function declines, the strain extends to the heart and blood vessels, increasing the likelihood of serious cardiovascular problems.

• Blood sugar emerged as the biggest contributor to kidney-related health loss — When researchers compared risk factors, high fasting blood glucose accounted for the largest share of kidney-related disability-adjusted life years — a measure that combines years lost to illness and to premature death — at 31.9%. High systolic blood pressure (24.5%) and excess body weight (23.5%) followed closely behind, while dietary factors accounted for 17.6%.

Because these figures come from an observational analysis, they show how strongly each factor is associated with kidney-related health loss — not that any one directly causes it. Even so, improving blood sugar control, maintaining healthy blood pressure, and managing excess weight may help address the factors contributing the greatest share of kidney-related health loss worldwide.

• Age dramatically increased the burden, but the trend affected all adults — Researchers observed that both the prevalence and severity of chronic kidney disease rose steadily with age. More advanced stages became increasingly common among older adults, while the contribution of high blood pressure to kidney-related disease burden also increased with advancing age.

Yet the findings were not limited to seniors. The study focused on adults beginning at age 20, highlighting that kidney damage often develops decades before severe symptoms appear. If you think of kidney health as a long-term challenge rather than an old-age problem, you gain a major advantage. Every positive step you take today gives your kidneys a better chance of functioning well years from now.

Support Your Kidney Health and Lower Your Risk

The findings from this global analysis point to a simple reality: Chronic kidney disease rarely begins in the kidneys alone. The biggest contributors were high blood sugar, high blood pressure, and excess body weight. That means the most effective strategy is to address the metabolic and lifestyle factors that place stress on your kidneys year after year.

High blood pressure deserves special attention because it doesn’t just accompany kidney disease — it also contributes to it. Over time, elevated pressure damages the tiny blood vessels inside your kidneys, reducing their ability to filter waste efficiently, while declining kidney function often pushes blood pressure even higher. The earlier you address the factors that strain both your blood vessels and your kidneys, the greater your opportunity to preserve kidney function for decades.

The following strategies are for prevention and early-stage risk reduction; anyone with diagnosed kidney disease should treat potassium, protein, and fluid targets as clinician-directed, because the right numbers flip once function is significantly impaired.

1. Make blood sugar control your first priority — High fasting blood sugar was the largest contributor to kidney disease burden worldwide. When blood sugar remains elevated, excess glucose damages the small blood vessels that allow your kidneys to filter waste effectively. Focus on improving metabolic health with whole foods, adequate protein, and healthy carbohydrates that match your activity level.

For most adults, that means approximately 250 grams of carbohydrates daily, with higher amounts if you’re physically active. Prioritize ripe fruit, root vegetables, and other nutrient-dense carbohydrate sources while eliminating ultraprocessed foods, including seed oils and sugary beverages.

Because protein is essential for maintaining muscle and metabolic health, aim for roughly 0.8 grams of protein per pound (or 1.76 grams per kilogram) of ideal body weight, with approximately one-third coming from collagen-rich sources like slow-cooked meats or bone broth.

2. Improve your blood pressure by improving your metabolism — High blood pressure ranked among the leading contributors to chronic kidney disease worldwide. Yet blood pressure often reflects deeper metabolic problems rather than an isolated condition. Excess weight, poor blood sugar control, chronic stress, and nutrient imbalances all place additional strain on your blood vessels and kidneys.

If you’re carrying excess weight, improving body composition often reduces pressure on both systems simultaneously. Daily movement, strength training, adequate sleep, and stress reduction support healthy blood pressure while helping protect your kidneys from further wear and tear. Even a daily walking routine creates meaningful improvements over time.

3. Restore a healthy sodium-to-potassium balance — Many people focus exclusively on reducing salt, but healthy blood pressure depends heavily on maintaining the proper balance between sodium and potassium. The larger problem is that most dietary sodium comes from ultraprocessed foods that contain very little potassium while delivering excess sugar, phosphate additives, seed oils, and other compounds that increase your kidneys’ workload.

Instead of aggressively restricting salt, focus on removing ultraprocessed foods and replacing them with whole-food potassium sources such as ripe fruit, root vegetables, and well-cooked greens. This strategy supports fluid balance, healthy blood pressure, and kidney function at the same time. It also reduces exposure to additives that place additional stress on kidney tissue.

One important exception: If you already have diagnosed kidney disease, especially stage 3b or beyond, don’t increase dietary potassium without checking with your doctor and knowing your latest labs. Once kidney function is significantly reduced, the kidneys can’t clear potassium efficiently, and too much can become dangerous. The advice to raise potassium applies to prevention and early-stage risk reduction, not to established, more advanced disease.

4. Optimize vitamin D through sensible sun exposure and daily movement — Vitamin D helps regulate the hormonal system that controls blood pressure and fluid balance. When vitamin D levels remain low, that system may become overstimulated, which research has linked to increased tension in your blood vessels and added strain on your kidneys.

Regular sun exposure helps to support vitamin D production, cellular energy generation, and healthy circulation. Aim for a vitamin D level between 60 and 80 ng/mL (150 to 200 nmol/L). If you still consume significant amounts of seed oils and other sources of linoleic acid (LA), avoid intense sun exposure until you have reduced those foods for at least six months.

This is because LA is a polyunsaturated fat that oxidizes easily, builds up in your skin, and increases your risk of skin damage. Pair sunlight with regular movement. An hour of walking, cycling, swimming, or similar activity each day improves circulation, supports healthy blood sugar levels, and reduces pressure on your kidneys’ filtering units. If you’re just getting started, even 10-minute sessions create momentum.

5. Stay hydrated, reduce unnecessary kidney stress, and screen early — For healthy kidneys, hydration helps dilute and remove waste while lowering kidney-stone risk, and thirst is usually a reliable guide. If you’ve been diagnosed with kidney disease, fluid needs can change — sometimes downward — so follow your doctor’s guidance rather than thirst alone.

Pale yellow urine also generally reflects adequate hydration. If you have a history of kidney stones, pay attention to foods high in oxalates, including spinach, sweet potatoes, and figs.

Pairing oxalate-containing foods with calcium-rich foods helps bind oxalates in your digestive tract so fewer reach your kidneys. At the same time, reduce phosphorus from processed foods, colas, and fast-food meats, since excess phosphorus disrupts mineral balance and places additional strain on kidney tissue.

If you have high blood pressure, diabetes, obesity, a family history of kidney disease, or other metabolic risk factors, make kidney screening part of your routine. Ask specifically for two tests: an eGFR (estimated glomerular filtration rate), which estimates how much blood your kidneys filter each minute, and a urine albumin-to-creatinine ratio (uACR), which catches protein leaking through damaged filters — often the earliest warning sign, before eGFR has budged.

Because early-stage kidney disease often produces no symptoms, these simple tests help identify problems long before significant damage occurs.

If you are considering kidney-function or vitamin D testing, talk to your health care provider about whether they’re appropriate for you.

FAQs About Chronic Kidney Disease

Q: What is chronic kidney disease and why is it called a silent health crisis?

A: Chronic kidney disease is a gradual loss of kidney function that often develops without obvious symptoms. Many people remain unaware they have it because early-stage kidney disease rarely causes noticeable problems. By the time symptoms become clear, significant damage has often already occurred.

Q: How common is chronic kidney disease?

A: According to the global analysis published in The Lancet, an estimated 788 million adults were living with chronic kidney disease in 2023. The condition now affects roughly one in seven adults worldwide and has more than doubled in prevalence since 1990.

Q: What are the biggest factors driving chronic kidney disease?

A: The leading contributors identified in the research were high fasting blood sugar, high blood pressure, and excess body weight. These metabolic factors damage the blood vessels that supply the kidneys and increase the strain placed on the kidneys over time.

Q: How does kidney disease affect the rest of the body?

A: Kidney disease affects far more than waste filtration. The kidneys help regulate blood pressure, fluid balance, and numerous chemical signals throughout your body. As kidney function declines, the risk of cardiovascular disease rises substantially. Researchers estimated that impaired kidney function contributes to 11.5% of cardiovascular deaths worldwide.

Q: What are the most important steps to protect kidney health?

A: Focus on addressing the root causes of kidney damage before permanent decline occurs. Maintain healthy blood sugar levels, improve blood pressure through better metabolic health, restore a healthy sodium-to-potassium balance with whole foods, optimize vitamin D through sensible sun exposure and regular movement, stay hydrated, and monitor kidney function early if you have risk factors such as diabetes, obesity, high blood pressure, or a family history of kidney disease.


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

Developing a Fatty Liver Increases Your Risk of Mortality


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/07/28/fatty-liver-disease.aspx


Analysis by Dr. Joseph Mercola       July 28, 2026

fatty liver disease

Story at-a-glance

  • Fatty liver disease affects nearly 25% of adults globally and progresses silently, leading to cirrhosis, heart disease, diabetes, and liver cancer
  • Research shows that fatty liver disease significantly increases mortality risk, especially from endocrine disorders and during the first year after diagnosis
  • Cardiovascular disease ranks as a top threat for people with fatty liver disease, with advanced liver fibrosis substantially increasing the risk of serious adverse events
  • Excessive fructose consumption from processed foods triggers de novo lipogenesis (fat creation) in the liver and promotes insulin resistance, even without alcohol consumption
  • Treatment focuses on addressing root causes through dietary changes, regular physical activity, weight management, muscle-building, and addressing metabolic imbalances like insulin resistance

Fatty liver disease is becoming a widespread condition, affecting nearly 25% of adults globally.1 In other words, about one in every four people around you likely have a fatty liver without even realizing it.

As the name implies, fatty liver is characterized by an abnormal buildup of fat in your liver cells, which triggers inflammation, damages healthy tissue, and eventually leads to permanent scarring known as cirrhosis. Most people living with fatty liver disease don’t experience clear symptoms at first, but as it worsens, fatigue, persistent abdominal discomfort, or unexplained weight loss begin to appear.

Without proper intervention, fatty liver disease progresses to severe liver damage and also significantly raises your risk of heart disease, Type 2 diabetes, and even liver cancer. Even more alarming, research shows that it is directly linked to increased mortality, even in its earlier stages.

Linoleic Acid and Choline Deficiency — A Deadly Combination That Leads to Fatty Liver Disease

In the context of fatty liver disease, excessive linoleic acid (LA) intake is one of the biggest factors because of how it affects your cellular health. Alongside this issue is the lack of choline from your diet. I cover these topics in a study I wrote, which I will share more about in the near future.

• Excess LA creates toxic metabolites — When LA, an omega-6 polyunsaturated fat (PUF), becomes peroxidized, it creates metabolites such as 4-hydroxynonenal (4-HNE), which is a reactive aldehyde known to affect mitochondrial membrane integrity that leads to a buildup of fat in the liver.

As noted in a Nutrients study, “[A] few studies suggested that omega-6 PUFA is related to chronic inflammatory diseases such as obesity, nonalcoholic fatty liver disease and cardiovascular disease.”2

• Choline deficiency contributes to fat buildup — Choline helps maintain cell membrane integrity, and research shows that if there’s a deficiency, fat accumulates in the liver because of impaired very low-density lipoprotein (VLDL) secretion.3

Your liver produces VLDL to transport fat and cholesterol to the cells throughout your body by way of your bloodstream.4 But if there’s not enough phosphatidylcholine (which is synthesized via enough choline intake), fat stays in the liver instead.

• LA and choline deficiency undermine your health — According to independent nutrition researcher Chris Masterjohn, Ph.D., eating foods high in LA while not getting enough choline creates a vicious cycle that ends up with fatty liver disease:5

“I currently believe that dietary fat, whether saturated or unsaturated, and anything that the liver likes to turn into fat, like fructose and ethanol, will promote the accumulation of fat as long as we don’t get enough choline.

Once that fat accumulates, the critical factor igniting an inflammatory fire to this fat is the consumption of too much PUFA (polyunsaturated fat from vegetable and perhaps fish oils).”

Excess Fructose — Another Factor Linked to Fatty Liver Disease

As noted earlier, fatty liver disease is on the rise in America. The original assumption is that alcohol consumption contributed to this pervasive public health issue. However, research shows that you don’t even need to drink to develop fatty liver disease, and another culprit is a common ingredient excessively used in most processed foods — fructose.

• Too much processed fructose harms your liver — Your liver is able to handle modest amounts of fructose by converting it into energy. But when it suddenly receives an influx beyond what is normal (example, when you consume a sweetened drink), your liver undergoes de novo lipogenesis, which means it creates new fat.

• Increased risk of insulin resistance — Consuming high amounts of processed fructose makes your cells more susceptible to insulin resistance. Under normal conditions, insulin helps move sugar from the bloodstream into your cells to be used as energy. But once your cells don’t respond to insulin as they used to, the sugar remains in your blood, causing blood sugar levels to rise and contribute to disease.

• Excess refined sugar shifts your body’s metabolic priorities — To make matters worse, the fructose-driven processes in your liver reduce your body’s ability to burn fat because the bulk of the metabolic effort is aimed at managing the incoming flood of sugar. If this becomes chronic, your body will create more fat that it can comfortably use, increasing your risk of health issues such as heart disease and fatigue.

To be clear, fructose by itself isn’t necessarily harmful. It’s also found in fruits, which contribute to optimal health. The difference is that fruit also contains dietary fiber, vitamins, and other bioactive compounds that slow down fructose absorption. It’s really only processed and refined fructose that is problematic.

So, to protect your liver from developing fatty deposits, even if you’re not drinking alcohol, the solution is obvious — choosing natural sources of sweetness is better compared to processed drinks and foods.

A Deeper Look Into Cause-Specific Mortality Findings

A study published in the Journal of Hepatology6 set out to uncover exactly how fatty liver disease relates to different causes of death. Instead of solely focusing on common cardiovascular or liver-related outcomes, the researchers dug deeper, looking into a wide range of medical issues to show if some conditions were more sharply elevated than others under the influence of fatty liver disease.

• Endocrine-related issues stand out — One noteworthy finding by the study is a noticeable increase in the likelihood of death from endocrine-related causes for people dealing with fatty liver disease.

Endocrine disorders involve hormonal imbalances in organs like the pancreas or thyroid. While you may think of heart or liver complications whenever you hear the phrase “fatty liver disease,” this study showed that hormone-related mortalities were also significantly higher in patients diagnosed with fatty liver disease. Specifically, the risk for these endocrine causes of death are three times more than that of individuals without fatty liver disease.

• Fatty liver disease makes you more susceptible to other chronic conditions — The researchers also addressed deaths attributed to infections, gastrointestinal disease (excluding direct liver conditions), and mental health disorders.

Infections and gastrointestinal problems saw an elevated risk overall, theorizing that fatty liver disease sets off a chain reaction that reduces resilience to certain bacterial or viral threats, as well as creating an environment that is more prone to digestive imbalances.

Furthermore, the researchers noted that the risk of mortality specifically from mental health conditions was not meaningfully increased. However, this is still a noteworthy finding nonetheless.

• Liver cirrhosis causes a cascade of disease — One aspect that deserves mention is the comparison of mortality risk in different subgroups who also suffered from cirrhosis.

Those with advanced cirrhosis showed the greatest vulnerability when it came to non-liver causes of death, even beyond what people usually imagine from hearing “cirrhosis.” Once the liver is significantly compromised, the effects on multiple organ systems become more pronounced.

• The earlier you get treatment, the better the outcome — The research indicated that the mortality hazard was particularly high during the first year after participants received their fatty liver disease diagnosis. That means if you’re diagnosed with this condition, it would be wise to take positive steps sooner rather than later — the health and lifestyle changes you choose will have the biggest impact in those early months.

• Fatty liver disease sets the stage for more severe outcomes — The authors proposed that the metabolic environment surrounding fatty liver disease fosters widespread inflammation and an overload of fatty substances in the bloodstream, which wears down tissues beyond the liver. This chronic state of bodily “alert” reduces a person’s ability to handle secondary complications like infections or hormonal imbalances in the thyroid or pancreas.

Overall, these findings shed light on how fatty liver disease escalates health risks in ways that go well beyond heart or cancer concerns. By uncovering which conditions spike the most, medical professionals and affected patients will be able to adopt a more targeted approach to prevention and eventual healing.

Additional Insights Into Fatty Liver Disease-Related Mortality

A supporting study published in Clinical Molecular Hepatology7 focused on the different ways fatty liver disease impacts a person’s survival. Similar to the Journal of Hepatology study, the researchers assessed which ailments hit hardest, investigating the relative importance of heart complications, cancer, liver failure, and diabetes-related deaths. In addition, they analyzed how those risks shift when fatty liver disease progresses and interacts with other conditions.

• Cardiovascular disease ranks as a top threat — This finding is not just in terms of incidence, but also how often it resulted in mortality for people with fatty liver disease. This challenges the assumption that liver complications always dominate the list, hinting that heart health could be even more urgent for this group.

The team also looked at extra-hepatic cancers, which means cancers that develop outside the liver. According to their findings, extra-hepatic malignancies rose markedly in fatty liver disease patients, intensifying the likelihood of fatal outcomes in that population compared to those who don’t have it.

• A big part of the puzzle is advanced fibrosis — For some people, fat accumulation gradually causes a chain reaction, scarring the liver extensively. This reduces the organ’s ability to detoxify and regulate essential metabolic processes.

The researchers observed that, once the scarring reaches a certain threshold, the risk of serious complications — heart attacks, strokes, and aggressive cancer developments — increases even more than expected from fatty liver disease alone. They also highlighted that metabolic factors, such as high blood sugar or lipid abnormalities, further compound these dangers.

• Certain genetic and hormonal factors influence risk of complications — Carrying variants of the PNPLA3 gene ramps up the severity of fatty liver disease and speeds up its progression. For context: PNPLA3 is involved in how the liver handles fats, so if the gene is slightly altered, fat piles up more rapidly, leading to extra stress on the body.

Another point the researchers stressed involves thyroid function — having low thyroid hormone levels or even borderline levels heighten the all-cause mortality risk in fatty liver disease cases. That link is rooted in how thyroid hormones help control metabolism. If your metabolism slows or becomes erratic, more fat accumulation occurs, fueling inflammatory processes that eventually jeopardize your health.

• Sarcopenia also increases mortality — Muscle tissue is metabolically active, so losing it not only slows metabolism but also undermines the body’s ability to process glucose, regulate insulin, and maintain robust immune defenses.

By tracking patients who had both fatty liver disease and significant muscle loss, the researchers found a higher death rate that extended beyond liver issues alone. This finding shows that maintaining healthy muscle mass — through strength training or adequate protein intake — will be beneficial for those who already have a compromised liver profile.

• Healthy lifestyle adjustments protect your liver — Losing weight was deemed hugely impactful, specifically when people combined healthy eating with consistent physical activity. Essentially, when you burn excess body fat, the inflammatory load on the liver drops.

Less stored fat means less likelihood of insulin resistance, which the study pinpointed as a driver of advanced disease. Meanwhile, the researchers observed that people who followed a healthy diet noticed sharper reductions in their overall mortality risk.

• Chronic inflammation is a central factor — Fatty deposits, once they accumulate enough, trigger inflammatory cells to release substances that undermine vascular integrity, hamper immune responses, and encourage unchecked cell growth. Over time, that escalates everything from minor arterial plaque formation to the emergence of malignant tumors.

Practical Strategies to Fight Fatty Liver Disease

If you’re dealing with fatty liver disease, addressing the core reasons behind it is important to achieve lasting improvement. No one-size-fits-all approach exists, but committing to different targeted, meaningful lifestyle shifts will set you on a path toward healing. Here are my recommendations:

1. Improve your diet — The most immediate way to tackle the root cause of fatty liver is by switching to a healthy diet. Focus your meals on whole, unprocessed foods, especially vegetables, fruits, lean proteins, and healthy carbohydrates. Remember to boost your choline intake as well, which is found in pastured egg yolks, arugula, and grass fed beef liver.

Lastly, remove ultraprocessed foods and anything that contains high-fructose corn syrup and other added sugars.

2. Prioritize physical activity — Exercise is one of the best things you can do for your health. Aim for at least 30 minutes of moderate-intensity activity most days of the week, such as brisk walking, cycling, or swimming.

Increased physical activity helps your body burn off excess fat stores, especially around your liver, and boosts insulin sensitivity, directly reducing the inflammatory cycle caused by fatty liver disease.

3. Actively manage your weight — In relation to the previous point, excess body weight is a culprit in fatty liver development. Losing even a modest amount — around 7% to 10% of your total body weight — has dramatic benefits.8

If you’re obese or overweight, set achievable, incremental weight goals rather than extreme dieting. Steady, consistent reduction is the most effective way to reverse liver fat accumulation.

4. Build and maintain muscle mass — Muscle isn’t just for strength — it’s crucial for metabolism. Engage in resistance training at least twice weekly to build and preserve your muscle mass. This boosts your body’s ability to process sugar, regulate insulin, and reduce harmful fat deposits. Essentially, healthy muscle mass directly supports liver function by lowering systemic inflammation and improving overall metabolism.

5. Address underlying metabolic imbalances — If you’re diabetic, pre-diabetic, or insulin-resistant, improving your blood sugar control is essential. Pay close attention to your carbohydrate intake, choosing complex carbs (like white rice) over simple sugars. To understand the impact of carbohydrates on your metabolic health, read the article “The Hidden Health Benefit of Carbohydrates.”

6. Consider citicoline supplementation — As noted earlier, choline deficiency creates fatty deposits in your liver because the organ is not able to send the produced VLDL throughout your body. To boost your intake, consider taking supplements. However, not just any choline supplement will do — I recommend citicoline because most forms of choline supplements have poor availability.

Citicoline is the immediate precursor for the synthesis of phosphatidylcholine, and increased intake helps your fat to be transported out of your liver. Formulations differ depending on the manufacturer, ranging from 500 to 2,500 mg per day. To find out your ideal dose, consult with your health care provider because choline toxicity, while rare, is a real condition.9

Frequently Asked Questions About Fatty Liver Disease and Chronic Disease

Q: What exactly is fatty liver disease, and why is it a concern?

A: Fatty liver disease occurs when excess fat accumulates in liver cells, leading to inflammation, damage, and eventually, cirrhosis. It significantly increases risks for health complications such as heart disease, Type 2 diabetes, liver cancer, and endocrine disorders. This leads to higher overall mortality rates.

Q: What are the common signs of fatty liver disease?

A: Initially, fatty liver disease usually shows no clear symptoms, making early detection challenging. As it advances, symptoms like fatigue, persistent abdominal discomfort, and unexplained weight loss appear. Early screening and proactive treatment will greatly improve outcomes.

Q: How does fatty liver disease affect health beyond liver damage?

A: Beyond liver damage, fatty liver disease significantly elevates the risk of cardiovascular diseases, endocrine-related deaths, gastrointestinal issues, infections, and extra-hepatic cancers. The chronic inflammation associated with fatty liver disrupts multiple organ systems, leading to heightened vulnerability to other health problems.

Q: What lifestyle factors contribute most to fatty liver disease?

A: Dietary factors, especially excessive fructose from sugary foods and drinks, play a major role. High fructose intake triggers fat creation in the liver, promotes insulin resistance, and reduces fat-burning capacity, exacerbating liver fat accumulation. Other critical factors include obesity, physical inactivity, and loss of muscle mass (sarcopenia).

Q: What are the best ways to treat or reverse fatty liver disease?

A: Fatty liver disease can be effectively treated or reversed by adopting a healthy diet rich in whole foods, engaging in regular physical activity, losing excess body weight, maintaining muscle mass through resistance training, and addressing underlying metabolic conditions, such as insulin resistance or diabetes. Early intervention significantly improves prognosis.

What berberine does to your metabolic health in 12 weeks

Reproduced from original article:
https://www.naturalhealth365.com/why-berberine-may-be-the-most-underrated-metabolic-health-tool-most-people-have-never-heard-of.html


by:  | berberine-lowers-blood-sugar(NaturalHealth365)  Berberine has been used in traditional medicine for over 3,000 years.  In fact, natural healing experts knew the value of this substance long before understanding the dangers of any metabolic issue.

What makes berberine unusual among natural compounds is that the modern clinical literature has largely confirmed what traditional practitioners already observed.  For example, a major meta-analysis published in Frontiers in Pharmacology in July 2025 provides the most comprehensive summary to date of how berberine affects key markers of metabolic disease.

Researchers synthesized results from multiple randomized placebo-controlled trials examining berberine’s effects on metabolic syndrome.  Metabolic syndrome is the cluster of conditions that includes high blood sugar, elevated triglycerides, excess abdominal fat, and abnormal cholesterol.

What berberine does to blood sugar and cholesterol

The results across outcomes were consistent and statistically significant.  Berberine reduced fasting plasma glucose meaningfully.  The effect on two-hour glucose tolerance was even more pronounced, with a reduction of 1.606 mmol/L.  That is a clinically relevant shift in one of the markers most closely linked to the progression of type 2 diabetes.

On the lipid side, LDL cholesterol decreased by an average of 0.495 mmol/L, and total cholesterol decreased by 0.451 mmol/L.  Triglycerides, which many functional medicine practitioners consider a more sensitive marker than LDL, declined by 0.367 mmol/L.  Waist circumference, a direct measure of visceral fat, shrank by an average of 3.27 centimeters.

Why berberine works so well

Berberine activates an enzyme called AMPK, which functions as a master metabolic switch inside cells.  When AMPK switches on, cells become more responsive to insulin.  Fat burning increases, glucose production in the liver slows, and cholesterol synthesis decreases.  That simultaneous effect across multiple pathways explains why berberine tends to improve several markers at once.

Berberine also modulates the gut microbiome in ways that improve metabolic function independently of AMPK.  This adds a second layer of benefit that most pharmaceutical metabolic drugs lack.  The compound’s ability to shift gut bacterial populations toward healthier strains links the metabolic and digestive benefits through a single mechanism.

How holistic healthcare providers use berberine

Many holistic physicians have used berberine for blood sugar support, cholesterol management, and gut health for decades.  Many practitioners consider berberine the most clinically validated botanical compound for metabolic support available without a prescription.

Several head-to-head trials have found comparable blood glucose reductions between berberine and Metformin, the most widely prescribed diabetes drug in the world.  Berberine, however, has a significantly different side-effect profile.

Holistic practitioners also use berberine for gut infections caused by bacteria and parasites, for small intestinal bacterial overgrowth, and as support for insulin resistance related to PCOS.  The antimicrobial properties are well documented.

The compound’s ability to shift the gut microbiome composition toward healthier populations links these digestive and metabolic uses to the same underlying mechanism.

How to use berberine effectively

The standard amount is 500 mg taken two to three times daily with meals, not all at once.  Taking berberine with food improves absorption and reduces the mild digestive discomfort some people experience with higher single amounts.

Most clinical trials showing significant improvements in blood sugar and lipid levels lasted 8 to 12 weeks of consistent daily use.  Berberine requires sustained use to produce meaningful change rather than offering immediate effects.

Combining berberine with specific nutrients amplifies the metabolic benefit.  Berberine absorption improves when taken with fat-containing foods, since the compound is fat-soluble.

Milk thistle, specifically the compound silymarin, supports liver function alongside the metabolic improvements.  Alpha lipoic acid, a well-researched antioxidant for insulin sensitivity, pairs naturally with berberine for people focused on metabolic health.

Quality sourcing matters for a compound this potent.  Berberine is available in capsule, tablet, and liquid extract form from dozens of online and health food store suppliers.  Products standardized to 97% berberine hydrochloride provide the form used in most clinical trials.

Berberine also occurs naturally in goldenseal root, barberry bark, and Oregon grape.  All three are widely available as dried herbs and tinctures for people who prefer whole-plant preparations.

What the evidence adds up to

Few natural compounds have the depth of clinical trials that berberine has accumulated.  The 2025 meta-analysis synthesized dozens of randomized controlled trials and found statistically significant improvements across every major metabolic marker except blood pressure.  That breadth of effect, at amounts most adults tolerate well, is why berberine has earned a central place in holistic medicine.

Practitioners managing metabolic health without pharmaceutical dependency increasingly reach for berberine first.

What most people do not realize is that chronically elevated blood sugar, triglycerides, and insulin resistance are the primary drivers of fatty liver disease.  These are the exact same markers that berberine addresses most directly.  Fatty liver now affects an estimated 30% of adults worldwide, and most cases develop silently through the same metabolic dysfunction that berberine’s clinical data targets at the root.

Sources for this article include:

Frontiersin.org
Frontiersin.org

Insulin Resistance Is Driving 12 Types of Cancer, Researchers Say


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/04/14/insulin-resistance-cancer.aspx


Analysis by Dr. Joseph Mercola     
April 14, 2026

insulin resistance cancer

Story at-a-glance

  • Machine learning research shows insulin resistance is linked to higher risk across at least 12 cancer types, positioning metabolic dysfunction as an early warning signal rather than a late-stage problem
  • Insulin resistance often develops years before diabetes, meaning symptoms such as fatigue, abdominal weight gain, and unstable blood sugar reflect deeper changes that influence long-term disease risk
  • Metabolic health predicts cancer risk more accurately than body weight alone, highlighting the importance of tracking markers like HOMA-IR instead of relying on the scale
  • High insulin levels and chronic inflammation create conditions that favor abnormal cell growth, explaining how disrupted energy metabolism contributes to cancer development across multiple organs
  • Removing seed oils, supporting steady carbohydrate intake, restoring gut health, reducing environmental stressors and tracking HOMA-IR improves insulin sensitivity and gives you measurable control over your long-term metabolic risk

Insulin resistance — a metabolic condition characterized by fatigue, abdominal weight gain, brain fog, and unstable blood sugar — now sits at the center of cancer research. Unlike a single blood test result, insulin resistance reflects how your cells respond to insulin over time.

This means glucose struggles to enter cells efficiently. Your mitochondria — the thousands of tiny power plants inside each cell that convert food into usable energy — lose their steady fuel supply, and energy production becomes erratic.

From a clinical perspective, insulin resistance often develops years before diabetes appears, which explains why many people live with symptoms without recognition. When insulin signaling breaks down, chronic inflammation and elevated insulin levels create biological signals that encourage abnormal cell growth and disrupt normal cellular repair.

Now, a large-scale analysis has used machine learning to connect this metabolic dysfunction directly to cancer incidence — revealing which cancers are most affected, why body weight alone misses the real risk, and how insulin resistance acts as an early warning signal across multiple organs.1

AI Model Reveals Insulin Resistance as a Cancer Risk Signal

For a study published in Nature Communications, researchers built a machine-learning model that predicts insulin resistance before diagnosable disease develop.2 Instead of relying on one lab test, the model looked at everyday health data — things like age, blood sugar, and triglycerides.

It calculated whether someone’s Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) score crosses a level that signals meaningful insulin resistance. HOMA-IR is a simple score calculated from fasting blood sugar and insulin levels that estimates how resistant your cells have become to insulin. The model was applied to the UK Biobank, which tracks long-term health data from adults ages 40 to 69.3

Among the 372,395 people who didn’t have cancer at the start, 51,193 were diagnosed during follow-up. Individuals flagged as insulin resistant consistently showed higher rates of diabetes, heart problems, and several cancers. This tells you risk builds years before diagnosis — which means prevention is still possible.

• Certain cancers showed stronger links to insulin resistance — Researchers reported connections to 12 cancer types overall, with the largest increases seen in uterine cancer (about 134% higher risk), kidney cancer (about 56% higher risk) and esophagus cancer (about 46% higher risk).

Pancreatic cancer risk rose roughly 29%, colon cancer 18%, and breast cancer 13% — all in individuals flagged as insulin resistant. Insulin resistance was not tied to one organ — it appeared across multiple systems, shifting it from a blood sugar issue into a whole-body metabolic warning signal.

• Metabolic health mattered more than body weight alone — People with higher body weight but no insulin resistance didn’t show the same risk pattern. Meanwhile, those with insulin resistance did — even when body weight looked similar. This means your metabolic function — how your body handles energy — provides more meaningful information than the number on a scale.

The connection between insulin resistance and cancer showed up in younger adults and older adults alike. The effect also stood out in people with a history of smoking, especially former smokers, where insulin resistance amplified risk. Your past exposures and current metabolic health interact, which explains why risk looks different from one person to another.

• Insulin resistance showed clear early disease timelines — Over several years of follow-up, people flagged as insulin resistant developed diabetes far more often, with more hospital admissions related to metabolic disease. One analysis showed more than seven-fold higher odds of developing diabetes during follow-up. That timeline highlights something important: insulin resistance shows up long before major disease, giving you measurable signals to act on.

• High insulin acts like a growth signal inside your body — When cells stop responding well to insulin, your body releases more of it to compensate. Elevated insulin then interacts with growth pathways that control how cells divide and survive. When that signal stays high for years, it creates conditions where abnormal cells gain an advantage — one of the earliest steps in tumor development.

Specifically, elevated insulin activates the IGF-1 (insulin-like growth factor) signaling pathway, which tells cells to grow and divide faster — and suppresses the normal “self-destruct” signals that clear out damaged cells before they become dangerous.

• Ongoing inflammation creates a favorable environment for tumors — Insulin resistance often exists alongside chronic low-grade inflammation. This type of inflammation changes the environment around cells so damaged cells persist longer than they should. Metabolic stress and cancer risk move together because they share the same biological environment.

• Machine learning creates a practical “digital biomarker” for early action — Researchers described the concept of AI-derived insulin resistance as a digital biomarker — a single score that combines multiple metabolic signals into one risk indicator.

Instead of waiting for disease, this approach allows earlier monitoring and more targeted screening. That makes insulin resistance something visible and measurable over time, giving you a clearer way to track improvement rather than guessing about your metabolic health.

How to Remove the Drivers of Insulin Resistance

The research makes the risk clear — but it also reveals something empowering: insulin resistance is measurable and reversible. Insulin resistance develops when your cells struggle to receive glucose and mitochondria — the part of your cells responsible for producing energy — lose steady fuel. The priority is removing what blocks insulin signaling. When cellular energy production recovers, the entire disease trajectory shifts — including cancer risk.

As metabolic function improves, your cells produce more ATP (adenosine triphosphate) — the energy currency that powers virtually every cellular process — inflammatory signals drop and the reinforcing cycle between insulin resistance and mitochondrial dysfunction begins to reverse. The following steps address the root cause.

1. Remove damaged fats that disrupt insulin signaling — Vegetable oils — including soybean, corn, and canola — are loaded with linoleic acid (LA), a polyunsaturated fat that damages your mitochondria. Over time, excess LA disrupts metabolism and fuels inflammation. The biggest sources to eliminate first are vegetable oils, salad dressings, fast foods, and processed snack foods — most of which rely heavily on soybean and canola oil.

Replace those oils with stable, nourishing fats such as grass fed butter, ghee, or tallow. Aim to keep daily LA intake under 5 grams, ideally closer to 2 grams. When my Mercola Health Coach app launches, the Seed Oil Sleuth feature will help you track this down to the tenth of a gram.

2. Consume carbohydrates your gut tolerates well — Most adults need around 250 grams of carbohydrates daily to support cellular energy, and steady glucose availability reduces metabolic stress that drives insulin resistance.

However, if you’re bloated, constipated, or gassy, jumping straight into high-fiber foods feeds certain gut bacteria that release endotoxins — inflammatory fragments that slip through a weakened gut lining into your bloodstream. This increased endotoxin load triggers systemic inflammation and worsens insulin signaling. Gentle carbohydrates such as whole fruit and white rice deliver reliable glucose without overwhelming digestion.

3. Progress slowly toward microbiome-supportive carbohydrates — After digestion stabilizes, introduce resistant starch foods such as cooked-and-cooled potatoes or green bananas, then foods like onions, garlic and leeks that feed butyrate-producing bacteria. Short-chain fats such as butyrate help colon cells maintain an oxygen-free environment that supports insulin sensitivity and metabolic stability.

4. Reduce environmental stressors that block metabolic recovery — Plastics release hormone-disrupting chemicals that interfere with metabolic signaling, so shift food storage toward glass or stainless steel to lower exposure. Limiting unnecessary electromagnetic field (EMF) exposure by increasing distance from devices and turning them off when not in use reduces ongoing cellular stress.

Keep your phone out of the bedroom at night, use speaker mode for calls, avoid working with a laptop directly on your body, and turn off your home Wi-Fi at night. When these exposures decline, cells regain the stability required for efficient glucose use.

5. Use movement to clear glucose and retrain insulin response — Regular movement — especially walking and strength training — drives muscle cells to pull glucose from your bloodstream without large insulin spikes. This lowers insulin demand and improves sensitivity. Consistent movement expands mitochondrial capacity, helping break the cycle where insulin resistance and low cellular energy reinforce each other.

6. Track HOMA-IR — a simple test for insulin resistance — Recognizing insulin resistance early is essential, as it’s a warning sign for your metabolic health — one that often precedes Type 2 diabetes. The HOMA-IR test is a valuable diagnostic tool that helps assess insulin resistance through a simple blood test, so you can spot issues early and make necessary lifestyle changes.

Created in 1985, it calculates the relationship between your fasting glucose and insulin levels to evaluate how effectively your body uses insulin. Unlike other more complex tests, HOMA-IR requires just one fasting blood sample, making it both practical and accessible. The HOMA-IR formula is as follows:

HOMA-IR = (Fasting Glucose x Fasting Insulin) / 405, where

• Fasting glucose is measured in mg/dL

• Fasting insulin is measured in μIU/mL (microinternational units per milliliter)

• 405 is a constant that normalizes the values

If you’re using mmol/L for glucose instead of mg/dL, the formula changes slightly:

HOMA-IR = (Fasting Glucose x Fasting Insulin) / 22.5, where

• Fasting glucose is measured in mmol/L

• Fasting insulin is measured in μIU/mL

• 22.5 is the normalizing factor for this unit of measurement

Anything below 1.0 is considered a healthy HOMA-IR score. If you’re above that, you’re considered insulin resistant. The higher your values, the greater your insulin resistance. Conversely the lower your HOMA-IR score, the less insulin resistance you have, assuming you are not a Type 1 diabetic who makes no insulin.

Interestingly, my personal HOMA-IR score stands at a low 0.2. This low score is a testament to my body’s enhanced efficiency in burning fuel, a result of increased glucose availability. By incorporating additional carbohydrates into my diet, I provided my cells with the necessary energy to operate more effectively.

This improved cellular function has significantly boosted my metabolic health, demonstrating how strategic dietary adjustments lead to better insulin sensitivity and overall metabolic performance.

FAQs About Insulin Resistance and Cancer

Q: What is insulin resistance and why does it matter for cancer risk?

A: Insulin resistance happens when your cells stop responding well to insulin, which forces your body to release more of it. Over time, high insulin and chronic inflammation create biological signals that support abnormal cell growth. Research shows insulin resistance is linked to higher incidence of multiple cancers, making it an early metabolic warning sign.

Q: Which cancers are most strongly linked to insulin resistance?

A: The strongest links appeared with uterine, kidney, and esophagus cancers, with elevated risk also seen for pancreas, colon, and breast cancers. This shows insulin resistance affects the entire body rather than a single organ system.

Q: Why is metabolic health more important than body weight alone?

A: Body weight doesn’t fully explain risk. People with higher weight but healthy insulin sensitivity didn’t show the same risk pattern, while individuals with insulin resistance did. This means how your body handles energy provides more useful insight than the number on a scale.

Q: How does insulin resistance contribute to disease over time?

A: Insulin resistance often develops years before diabetes and other chronic diseases appear. During that time, mitochondria receive inconsistent fuel, inflammation increases, and cellular repair declines. This long timeline creates an opportunity to detect and reverse metabolic dysfunction early.

Q: What steps improve insulin sensitivity and lower long-term risk?

A: Key strategies include removing seed oils and other damaged fats, consuming carbohydrates that support steady cellular energy, restoring gut health gradually, reducing environmental stressors such as plastics and EMFs, moving regularly to clear glucose, and tracking HOMA-IR to measure progress. These steps improve mitochondrial energy production and restore healthy insulin signaling.

– Sources and References

Insulin Resistance — What It Is and How to Fight It


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/01/insulin-resistance-what-it-is-how-to-fight-it.aspx


Analysis by Dr. Joseph Mercola     
March 01, 2026

Story at-a-glance

  • Insulin resistance occurs when cells don’t respond properly to insulin, causing elevated blood sugar and increased insulin production that leads to diabetes, heart disease, and cancer
  • Diet significantly impacts insulin sensitivity, with processed foods containing linoleic acid (found in seed oils) promoting inflammation and worsening insulin resistance
  • Mitochondrial dysfunction plays a key role in insulin resistance, as these cellular “power plants” become less efficient when overloaded with linoleic acid and refined sugars
  • Doctors measure insulin resistance using HOMA-IR (a simple blood test) or, less commonly, the more expensive hyperinsulinemic-euglycemic clamp method
  • Improving insulin sensitivity involves eating whole foods, consuming 200 to 350 grams of healthy carbohydrates daily, avoiding processed foods, choosing healthy fats and exercising regularly

Have you ever wondered why some people gain weight easily or struggle with high blood sugar? It could involve insulin resistance. This happens when your body’s cells don’t respond well to insulin, a hormone that controls your blood sugar. If left unchecked, it leads to serious issues like Type 2 diabetes, heart disease, and even some cancers.

In the video above, Dr. Peter Attia, who received his medical degree from Stanford and completed surgical residency at the eminent Johns Hopkins Hospital, interviews Dr. Ralph DeFronzo, a distinguished diabetes researcher and clinician.1 They discuss what insulin resistance is and how it impacts specific organs — along with how to accurately check if you have it. But here’s the good news: you can improve your insulin sensitivity with simple changes, especially to your diet.

What Is Insulin Resistance?

Insulin is like a key that unlocks your cells so they can take in sugar (glucose) from your blood. When you eat, your body turns food into sugar, which enters your bloodstream. Insulin then moves that sugar into your cells to give you energy. But when you have insulin resistance, your cells don’t respond well to insulin.

It’s like the locks on your cells are rusty — the key doesn’t work right. As a result, sugar builds up in your blood, and your body pumps out more insulin to try to fix it. Over time, this leads to high blood sugar and too much insulin, which isn’t good for you.

• Why should you care? Insulin resistance isn’t just a small problem — it’s linked to serious health risks. If your cells can’t use insulin properly, you could face:

◦ Type 2 diabetes — Too much sugar in your blood damages your body over time.

◦ Heart disease — High insulin levels harm your blood vessels.

◦ Certain cancers — Some studies suggest insulin resistance might increase cancer risks, like breast or colon cancer.

The bright side? You can fight back by understanding what’s going on and making smart choices, like tweaking your diet.

• How does diet improve your insulin sensitivity? What you eat has a significant impact on how well your body uses insulin. Let’s break it down and see how your diet either helps or hurts your insulin sensitivity.

• What’s the deal with linoleic acid (LA)? One important thing to watch is a fat called linoleic acid (LA). You find it in seed oils that are common in processed foods like chips, fried snacks, and baked goods. A little LA is OK, but too much harms your cellular energy production and causes inflammation — think of it as your body getting irritated inside.

This irritation makes insulin resistance worse. To help your body out, cut back on these processed foods and go for healthier fats instead, like ghee, tallow, and grass fed butter.

• How does redox balance fit in? Another piece of the puzzle is something called redox balance. Imagine it as a seesaw in your cells that keeps everything working smoothly. When this seesaw tips out of balance, it interferes with how your cells use insulin. Eating foods packed with antioxidants — like colorful fruits and veggies — helps keep that seesaw steady and supports your insulin sensitivity.

Insulin Resistance — A Problem with Your Cells’ Energy Factories

Now, let’s dig a little deeper. Insulin resistance isn’t just about sugar — it’s tied to how your cells make energy. Here’s what you need to know.

• What causes insulin resistance? Your cells have tiny power plants called mitochondria that turn sugar into energy. When these power plants don’t work right, it’s called mitochondrial dysfunction. Think of it like a factory with broken machines — it can’t keep up. This interferes with how your cells use insulin, leading to insulin resistance.

Seed oils play a big role here, as LA is a mitochondrial poison that compromises your cellular energy production. Once rare, seed oils are now everywhere in processed foods — like baked goods, frozen meals, and salad dressings. Refined sugar also plays a role.

Unlike natural sugars in fruits that come with fiber and nutrients, refined sugars offer no nutritional benefits and significantly increase health risks. Eating too much refined sugar overworks your mitochondria, making them less efficient. Over time, this tips your body toward insulin resistance.

• How does redox imbalance make it worse? There’s also something called redox imbalance. Inside your cells, there’s a balance between helpful and harmful particles. Too much refined sugar or unhealthy fats (like LA) throw this off, creating stress that damages your mitochondria. It’s like overloading a circuit — things start to break down. This stress makes it harder for insulin to do its job, pushing you closer to insulin resistance.

• Why does this matter for your health? When your mitochondria struggle, insulin resistance leads to bigger problems:

◦ Type 2 diabetes — Your blood sugar stays high because cells can’t use it.

◦ Heart issues — Damaged energy production affects your heart and vessels.

◦ Brain health — Some experts even call Alzheimer’s “Type 3 diabetes” because of insulin resistance in the brain.

The fix? Diet and lifestyle changes help your mitochondria work better and improve your insulin sensitivity.

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Using HOMA-IR to Spot Insulin Resistance Early

One of the simplest and most reliable ways to gauge how well your body handles insulin is through a test called HOMA-IR, short for Homeostatic Model Assessment of Insulin Resistance.

Unlike other cumbersome procedures, HOMA-IR only requires two basic blood tests done first thing in the morning before you eat: one for fasting glucose and one for fasting insulin levels. These tests are relatively affordable and widely available at most labs. Armed with those numbers, you then plug them into a straightforward formula to get your HOMA-IR score:

HOMA-IR = (Fasting Glucose in mg/dL × Fasting Insulin in μU/mL) / 405

The goal is to see just how hard your body is working to keep your blood sugar in check. If your HOMA-IR is higher than 1.0, it’s generally a warning sign that you might be edging into insulin resistance territory. The lower your score, the better your insulin sensitivity, so even values that hover around 1.0 deserve some attention if you’re looking to optimize your health.

The beauty of HOMA-IR lies in its simplicity. You don’t have to schedule multiple visits or endure complicated test procedures. You wake up, don’t eat or drink anything other than water, head to the lab for a quick blood draw, and get your results shortly after. Alternatively, Mercola Labs has a dried blood spot card that allows you to prick your finger after you get up and put drops of blood on a card and mail it in, which is far more convenient and less expensive.

It’s a far cry from the gold-standard research method known as the euglycemic hyperinsulinemic clamp, introduced by DeFronzo in 1979, where participants are hooked up to an IV for hours. In the clamp procedure, researchers administer insulin and glucose simultaneously, measuring exactly how much glucose is needed to keep blood sugar at a steady level when insulin is being pumped in.

Although extremely accurate, this process is time-consuming and inconvenient, making it unfeasible for routine monitoring in a clinical or everyday setting. It’s also pricey, costing an average of $1,000 for a single test. Consequently, it’s primarily confined to research settings.

That’s why HOMA-IR remains such a powerful tool in both scientific research and personal health management: it balances accuracy with practicality. It’s not a perfect snapshot — no single test can capture the full complexity of your metabolic health — but it’s solid enough to highlight when your body starts resisting insulin’s signals.

I found it shocking that both DeFronzo — who invented the euglycemic hyperinsulinemic clamp test — and Attia, one of the smartest biohackers out there, failed to acknowledge that the HOMA-IR test is the pragmatic, simple, inexpensive way to measure insulin resistance, as opposed to the test that DeFronzo invented.

By using the HOMA-IR test and catching those early warnings, you can make diet and lifestyle tweaks long before you slip into more serious issues. For most people, if your HOMA-IR creeps above 1.0, it’s time to pay closer attention to factors like sugar intake, seed oils, plastic exposure, and gut health.

Over time, as you dial in these elements of your routine, you can retest HOMA-IR and see if your score drops. That direct feedback can be a potent motivator to keep you on track toward a healthier, more energetic life.

Practical Tips to Boost Your Insulin Sensitivity

Ready to make some changes? Here’s how to improve your insulin sensitivity through diet:

1. Eat more whole foods, including healthy carbs — Carbohydrates play a key role in supporting your mitochondrial function. Glucose, derived from carbohydrates, serves as your cells’ preferred fuel source for energy production. Instead of restricting carbs, focus on eating 200 to 350 grams of the right types, such as whole fruits, root vegetables and well-tolerated whole grains. If you have dysbiosis, avoid fiber until your gut is healed.

2. Cut back on processed foods — Avoid processed foods — they’re full of LA-rich seed oils and refined sugars that drive inflammation and worsen insulin resistance.

3. Pick healthy fats — Swap out canola, corn, and soybean oil for healthy fats like grass fed butter, tallow, and ghee.

4. Move your body — Exercise isn’t food, but it helps your cells use insulin better. A daily walk does wonders.

Small steps like these help your body respond to insulin again and lower your health risks. Start small: swap store-bought baked goods for fresh fruit or take a daily walk outside. You can make a big difference in your health with these positive changes.

FAQs — Your Top Insulin Resistance Questions Answered

Q: What foods help insulin sensitivity?

A: Prioritize healthy carbohydrates like fruit and root vegetables, and avoid seed oils high in linoleic acid. Skip processed foods high in refined sugar and unhealthy fats.

Q: How do doctors check for insulin resistance?

A: They often use HOMA-IR, a simple test that involves fasting blood sugar and insulin levels. While the hyperinsulinemic-euglycemic clamp is considered the gold standard, HOMA-IR is less expensive and more practical for routine use.

Q: Can exercise fix insulin resistance?

A: Yes, moving your body helps your cells use insulin better. Even daily walks help improve insulin sensitivity.

Q: What are the long-term health risks associated with insulin resistance?

A: Insulin resistance is linked to serious conditions like Type 2 diabetes, heart disease, and even some cancers. Addressing insulin resistance through diet and lifestyle changes is important for preventing these chronic illnesses.

Are Processed Plant-Based Foods Bad for Your Heart? Here’s What Research Says


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/02/03/processed-plant-based-foods-heart-disease-risk.aspx


Analysis by Dr. Joseph Mercola     
February 03, 2026

processed plant based foods heart disease risk

Story at-a-glance

  • Not all plant-based foods support heart health — ultraprocessed items may actually increase cardiovascular risk despite their “vegan” label
  • A large French cohort study of over 63,000 adults found an approximately 40% reduction in cardiovascular disease risk when participants ate minimally processed, nutrient-rich plant foods
  • There was also a 38% increase in overall cardiovascular disease risk when diets were dominated by ultraprocessed, low-quality plant-based foods, even if they appeared “healthy”
  • Key red flags include: high sodium in vegan meats and deli slices, seed oils that damage mitochondrial function, refined starches/sugars, and gut-disrupting additives like methylcellulose and gums
  • The most protective plant-based diets are built from whole foods with minimal processing, like legumes, vegetables, fruits, and whole grains

You ordered the Impossible Burger. You’ve swapped whole milk for oat milk. You even started reading labels — so why did your latest blood work show warning signs your doctor didn’t expect?

Many health-conscious people assume a plant-based diet automatically protects their heart. They then turn to vegan or vegetarian products sold in supermarkets, including fake meats, nut milks, and packaged snacks. But watch out — some of these plant-based foods can actually do more damage to your health. Let’s dive into the reasons why most highly processed plant-based foods are bad for your heart.

What Do Recent Studies Say About Processed Plant-Based Diets and Heart Disease?

A large French study published in The Lancet found that it’s not just about what you eat — how your food is made matters just as much. The research, which was conducted as part of the large-scale, web-based NutriNet-Santé project, followed 63,835 adults for nearly a decade. The study authors wanted to answer an important question: Which plant-based diets actually protect against heart attacks and strokes and which ones don’t?1,2

What made this study different from most is that it didn’t just look at whether people ate more plants or less meat — it also looked at the nutritional quality of the plant-based foods. Most importantly, it looked at how processed those foods were. In other words, a diet made up of frozen veggie nuggets, flavored soy drinks, and processed plant-based snacks might be plant-based, but is it heart-healthy?

• The participants’ diets were evaluated — Through online questionnaires, participants provided detailed records of what they ate and drank over a period of at least three days. The researchers then categorized their diets by the proportion of plant- versus animal-based foods, while also factoring in nutritional quality and the degree of food processing.

• How the diets were scored — To analyze the data, the researchers used four different types of plant-based diets:

◦ Healthy plant-based and unprocessed (hPDI-UnPF) — Fresh veggies, fruits, legumes, etc.

◦ Healthy plant-based and ultraprocessed (hPDI-UPF) — Packaged “healthy” snacks and plant-based frozen meals

◦ Unhealthy plant-based and unprocessed (uPDI-UnPF) — Sugary drinks and white bread (but not heavily processed)

◦ Unhealthy plant-based and ultraprocessed (uPDI-UPF) — Sweets, chips, and sugary plant-based products

They then tracked the participants’ health over time to see which diet types led to more or fewer heart problems.

• The study revealed a clear pattern — The researchers found that the people who mostly consumed nutritious plant-based, minimally processed foods (hPDI-UnPF) had 44% lower risk of coronary heart disease and 32% lower risk of overall cardiovascular disease.

On the other hand, the uPDI-UPF diet was the worst for heart health. People who ate high amounts of unhealthy and heavily processed plant foods had a 46% higher risk of heart disease and 38% higher risk of overall cardiovascular disease.3

What Is an ‘Unhealthy’ Plant-Based Diet (UPDI), and How Is It Different from a Healthy One?

To put it simply, an Unhealthy Plant-Based Diet Index (uPDI) refers to a plant-based diet that includes mostly low-quality plant foods that are heavily processed or high in added sugars and refined carbs. While these foods technically come from plants, they don’t offer the same health benefits as whole, nutrient-rich plant foods.

A separate U.S. study, published in the American Journal of Preventive Cardiology, reinforced these findings — with an even more alarming twist. Conducted by researchers from Johns Hopkins Bloomberg School of Public Health and the University of Washington, the research took a deep dive into how plant-based diets relate to silent, early signs of heart disease.4,5

• Gathering the data — Between 1999 and 2004, researchers looked at data from 7,708 adults who participated in the National Health and Nutrition Examination Survey (NHANES), a large, nationally representative health study in the U.S. They took note of what the people ate over a 24-hour period.

• The diets were grouped into three plant-based indices — These were categorized based on how plant-based the diets were and whether the plant foods were mostly healthy or unhealthy:

◦ Overall Plant-Based Diet Index (PDI) — The total amount of plant foods eaten.

◦ Healthy Plant-Based Diet Index (hPDI) — Diets rich in whole plant foods like fruits, vegetables, whole grains, legumes, and nuts.

◦ Unhealthy Plant-Based Diet Index (uPDI) — Diets high in sugary drinks, sweets, refined grains, and fried starchy foods (like fries) and white bread.

• Measuring heart health — Instead of looking at full-blown heart attacks or disease, the researchers focused on “subclinical cardiovascular disease,” which are early signs of heart trouble that don’t yet cause symptoms but can be detected through biomarkers in the blood. Using blood samples from the participants, the researchers tested for:

◦ Cardiac Troponin I (cTnI), a marker for subtle heart muscle damage.

◦ Cardiac Troponin T (cTnT), another protein released during heart strain.

◦ NT-proBNP, a protein that is released when the heart is under stress, and is often used to detect or predict heart failure.

Elevated levels of these biomarkers suggest that the heart may be under strain — even if a person feels perfectly fine.

• What the study findings revealed — The results were stark: People whose diets were mostly made up of unhealthy plant foods had 65% higher odds of having elevated troponin I — the same biomarker of damage that doctors look for after a heart attack. Think of troponins like a smoke alarm for your heart — when heart muscle cells are stressed or damaged, they release these proteins into your bloodstream. Even small increases can be signs of subclinical (hidden) heart disease.

“Up to 50% of individuals with no apparent history of cardiac issues have subclinical levels of troponins. While these levels are not of immediate concern, they may be interpreted as a warning sign of potential future issues,” Medical News Today reports.6

On the other hand, people who had higher hPDI scores had a much lower risk of having elevated cTnI levels. Those in the highest group for healthy plant eating had about 50% lower odds of heart stress compared to those in the lowest group. This table summarizes these findings:

Index Focus Examples Health impact
hPDI Nutrient-dense, minimally processed plant foods Lentils, chickpeas, berries, and leafy greens Supports lower cardiovascular risk
uPDI Ultraprocessed, low-nutrient plant-based foods Vegan pastries, sweetened plant milks, sugary cereals, fake meats Linked to higher cardiac biomarkers
NOVA 4 Industrially processed (UPFs) across all categories Vegan nuggets, ready-to-eat meals, plant-based sodas, additive-laden bars Strongly linked to chronic disease risk

Take note that the table also includes the NOVA classification — a global system that sorts foods by their level of industrial processing. But why does this matter? Simply put, NOVA Group 4 is where most “plant-based” convenience foods live — and where the highest cardiovascular risks hide.

NOVA group 4 includes ultraprocessed foods (UPFs), which often carry the biggest risk due to added sugars, preservatives, emulsifiers, and other synthetic ingredients. Many uPDI-scoring foods fall into this group and both the French and U.S. studies back up this distinction.

The common thread between these two studies is simple but often missed: Eating “plant-based” doesn’t automatically protect your heart. It depends on what kind of plant-based foods you’re eating, how they’re made, and what else comes along with them. So what exactly is in these foods that makes them so harmful? Let’s break down the four biggest culprits.

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Why Processed Vegan Foods Raise Cardiovascular Risk

The problem with many processed vegan foods isn’t that they’re plant-based — it’s how they’re made. The packaging might look clean and green, but what’s inside tells a different story. Excessively high sodium, polyunsaturated fats (PUFs), refined starches, and chemical additives all stack up to create a metabolic mess that quietly damages your heart.

• Let’s start with sodium — Although conventional medical advice recommends limiting sodium intake, the fact is you still need it to support various physiological functions, including helping generate and conduct the electrical signals that control your heartbeat. Hence, instead of completely limiting it, it’s best to acquire it from natural, unprocessed food sources and is balanced by a high potassium intake — this supports healthy physiology.

Unfortunately, most ultraprocessed, plant-based foods, such as meat substitutes in particular, have excessively high amounts, disrupting your sodium-to-potassium ratio. According to Dr. Jayne Morgan, a cardiologist at Hello Heart:

“Many plant-based meats are heavily seasoned to mimic meat flavors. This often means very high sodium levels, which is a major contributor to hypertension,” she said. “A plain chicken breast might have 70 mg of sodium [in four ounces of chicken], while a processed plant burger could have 400–600 mg of sodium!”7

• Linoleic acid (LA) is another major red flag — Many processed plant-based foods — especially vegan dressings, cheese alternatives, and “healthy” snacks — are made with seed oils like sunflower, safflower, or canola. These oils are extremely high in linoleic acid (LA), a polyunsaturated omega-6 fat that, in excess, disrupts mitochondrial function.

Your mitochondria are the energy factories inside every cell. When excess linoleic acid accumulates, it interferes with how these factories burn fuel — like putting the wrong gasoline in your car. The result is sluggish energy production and cellular debris that triggers inflammation.

Your body stores LA in fat tissue, where it gradually degrades into harmful byproducts. These compounds inflame blood vessel walls and sabotage your cells’ ability to produce energy efficiently. Most modern plant-based processed foods are loaded with LA, making them a hidden metabolic threat — even when labeled “heart-healthy.”

• Refined starches and sugars add another layer of concern — Packaged vegan pastries, sweetened plant drinks, and “healthy” granola bars spike blood sugar and insulin levels. Over time, this worsens triglyceride profiles and contributes to metabolic dysfunction (a state where your body struggles to properly regulate blood sugar, fat storage, and energy production), especially in people with poor gut health or underlying insulin resistance.

• And then there are the additives — Ingredients like methylcellulose, carrageenan, gums, and modified starches are often used to thicken, bind, or stabilize processed vegan products. There’s emerging evidence suggesting these compounds may disrupt the gut lining, alter the microbiome, and trigger inflammation, all of which contribute to cardiovascular stress over time.

• Processing also strips away fiber — While whole plant foods like legumes, vegetables, and fruits are naturally rich in fiber that supports digestion, satiety, and blood sugar balance, most processed vegan products strip that fiber out. When manufacturers refine grains, extract plant proteins, or create meat substitutes from isolates, they remove the fiber that feeds your gut bacteria and helps stabilize metabolic health.

What’s left is often a fast-digesting, low-fiber food that spikes blood sugar and leaves you hungrier sooner. Over time, a diet low in fiber and high in ultraprocessed foods contributes to microbiome imbalance, insulin resistance, and inflammation, which quietly accelerate cardiovascular disease.

Together, these factors paint a clear picture: Processed vegan foods often mimic the nutrient profile of ultraprocessed junk food. They’re marketed as healthy alternatives, but functionally they deliver the same metabolic and cardiovascular consequences as the products they aim to replace.

How Can You Spot Ultraprocessed Vegan Foods at the Store?

It’s easy to get fooled by packaging that screams “plant-based” or “100% vegan.” But beware, because many of these prepackaged foods are ultraprocessed — and that’s something you can’t spot from the front of the box. You’ve got to flip it over and read the label.

• Start with the ingredient list — A good rule of thumb is this: The longer it is, the more processed the food probably is. Look for short lists with five or fewer recognizable, whole-food ingredients. When you see words like methylcellulose, gums, carrageenan, or “natural flavors,” be cautious. These are often used in plant-based meats, cheeses, and snacks to create texture or enhance flavor and they indicate a high degree of industrial processing.

• Check the sodium content — A heart-healthy food ideally stays under 300 mg of sodium per serving. Many vegan deli slices, burgers, and cheese alternatives blow past that — some reaching 500 to 600 mg or more per serving. If you eat these items daily, your sodium intake can spike fast, especially if you’re stacking them with sauces or condiments that also pack a salty punch.

• Beware of seed oils — If you see sunflower oil, soybean oil, or safflower oil high on the ingredient list, that’s a sign to put the item back. Even if the front of the package says “plant-based” or “cholesterol-free,” these oils silently sabotage your cardiovascular health behind the scenes. Even in your home, consider eliminating all seed oils and switching to healthier fats instead like coconut oil, ghee, or grass fed butter.

• Don’t forget to look at sugars and starches — A surprising number of plant-based snacks are just refined carbs in disguise — vegan cookies, “clean” energy bars, sweetened nut milks, and grain-based cereals with added sugar. These products spike blood glucose and increase triglyceride levels over time.

Who Should Be Most Cautious with Processed Plant-Based Foods?

If you’re dealing with high blood pressure, heart failure, or chronic kidney disease (CKD), continuing to eat ultraprocessed vegan foods is a risky bet. The excessive sodium packed into vegan deli slices, faux meats, and convenience meals puts additional strain on your blood vessels and kidneys — systems that are already compromised in these conditions. Even “healthier” plant-based frozen meals can push your sodium intake well beyond safe daily limits, especially if you’re relying on them multiple times a week.

People with high LDL cholesterol, or those with a family history of cardiovascular disease, also need to read the fine print. Hydrogenated seed oils are routinely added to vegan cheeses, spreads, and mock meats to simulate richness or texture. But these oils aren’t neutral. They interfere with cholesterol metabolism and promote plaque buildup inside your arteries.

The same goes for athletes and highly active individuals who rely on convenience foods. You might assume that you’re making clean choices by going plant-based, but many of those grab-and-go options are metabolic landmines. High refined carb loads, low-quality protein blends, and oxidized fats found in bars, shakes, and prepackaged “performance” snacks can impair recovery and fuel systemic inflammation. If you’re training hard, your cells need clean-burning fuel — processed vegan snacks won’t give you that.

Even if you’re metabolically healthy, eating ultraprocessed plant-based foods daily carries risks that compound over time. The harm isn’t always immediate. Elevated cardiac biomarkers, insulin resistance, and triglyceride spikes (which cause plaque buildup) can build silently, especially when meals are built around processed items instead of whole, nourishing foods.

What to Eat Instead — A Whole-Food Plant-Forward Plan

If your goal is to eat in a way that supports your heart, metabolism, and long-term energy, then it’s time to move away from the processed plant-based hype and build meals around simple, whole ingredients. This doesn’t mean you need to give up on plant-forward eating — it just means you need to get smarter about which plants you’re eating and how they’re prepared.

Here’s what a single day of eating might look like if you’re focusing on nutrient-dense, minimally processed, low-PUF plant-forward meals (If you’re vegan, you can skip the eggs and dairy):

• Breakfast — Well-cooked rice porridge, topped with fresh berries and a drizzle of raw honey or maple syrup. Add a boiled egg or a slice of raw cheese for balanced protein.

• Lunch — Lentil and well-cooked vegetable bowl (carrots, squash, and greens) tossed in coconut oil, and served with sourdough bread. Sprinkle with fresh herbs for added flavor and color.

• Snack — An in-season piece of fruit with a drizzle of honey, paired with a cup of warm herbal tea.

• Dinner — Braised lentils or mung beans slow-cooked with caramelized onions, carrots, and fresh herbs, served over a bed of well-cooked root vegetables like turnips, beets, or sweet potatoes. Pair this with a side of sautéed dark leafy greens (such as collards or mustard greens) cooked gently in coconut oil, grass fed ghee, or butter for digestibility and better fat profile.

This type of eating plan emphasizes low-inflammatory fats, stable blood sugar, and digestible starches to support your mitochondria, gut lining, and cardiovascular system. There’s no reliance on fake meat, emulsified cheeses, or ultraprocessed snacks — just real food in real form, prepared in a way your body actually recognizes.

Frequently Asked Questions (FAQs) About Ultraprocessed Plant-Based Foods and Heart Health

Q: Are processed vegan foods bad for heart health?

A: Many are. Processed vegan foods often contain high amounts of sodium, polyunsaturated fats from seed oils, and inflammatory additives such as gums and emulsifiers. These compounds contribute to elevated blood pressure, impaired cholesterol profiles, and early cardiac stress markers. Even though they’re free from animal products, that doesn’t make them heart-safe.

Q: Is a whole-food plant-based diet good for your heart?

A: Yes — when built around minimally processed, nutrient-dense ingredients like legumes, leafy vegetables, fruit, and tubers. The NutriNet-Santé study showed a nearly 40% lower risk of cardiovascular disease in people who consistently ate high-quality, low-processed plant foods.

Q: Do plant-based meats have too much sodium?

A: Absolutely. Many meat alternatives contain 400 to 600 mg of sodium per patty, compared to around 70 mg in plain cooked chicken. That sodium load adds up quickly and can disrupt your sodium-to-potassium ratio, particularly if you’re eating these products more than once per day.

Q: What is the unhealthy plant-based diet index (uPDI)?

A: The uPDI is a research-based scoring system that classifies plant-based diets based on food quality. Diets high in ultraprocessed plant products like sweetened beverages, packaged snacks, and refined grains score higher on the uPDI and are associated with increased cardiovascular risk. In contrast, healthy versions (hPDI) emphasize whole, nutrient-dense foods and show protective effects.

Q: What processed foods count as plant-based?

A: Think: vegan nuggets, faux cheeses, snack bars, sweetened oat or almond milks, instant noodles labeled “plant-based,” and prepackaged deli slices. These may be meat-free but are still loaded with additives, unhealthy oils, and refined starches. Their level of industrial processing, not the absence of animal products, determines the risk.

Q: What are the risks of plant-based meats?

A: Beyond sodium and seed oils, these products often include inflammatory ingredients like methylcellulose and carrageenan. Over time, regular consumption raises your risk of heart disease, metabolic dysfunction, and digestive issues.

Q: Do processed plant-based snacks spike blood sugar?

A: Yes. Many vegan snack bars and cereals are built on refined grains and added sugars, which digest quickly and spike glucose levels. This contributes to insulin resistance and increased triglycerides — two key drivers of cardiovascular disease.

Q: Are plant-based burgers safe to eat daily?

A: They’re not ideal for everyday meals. Most are loaded with sodium, seed oils, and binding agents. Occasional use might be manageable, but a daily habit increases your intake of harmful fats and additives that undermine cardiovascular and metabolic health.

Alternative Sweetener Sorbitol Drives Hidden Liver Fat Buildup


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/01/15/sorbitol-liver-damage.aspx


Analysis by Dr. Joseph Mercola     
January 15, 2026

sorbitol liver damage

Story at-a-glance

  • Sorbitol, a common sugar alcohol in sugar-free and “diet” products, drives liver fat buildup even when your gut bacteria are healthy, making it a hidden contributor to fatty liver disease
  • When your microbiome is weakened from antibiotics, stress, or ultraprocessed foods, sorbitol slips through your gut unchanged and reaches your liver, where it triggers rapid fat production
  • Sorbitol is converted into fructose inside your liver, bypassing normal metabolic controls and overwhelming your ability to process sugar safely
  • Strengthening your gut bacteria, eliminating vegetable oils and alcohol, and increasing choline-rich foods help protect your liver from sorbitol-driven damage
  • Simple daily steps — removing sorbitol-containing products, restoring gut balance, supporting vitamin D metabolism, and using whole-food carbs — give you direct control over your liver health

Fatty liver disease has become a major metabolic threat, and it often develops quietly while you feel nothing more than fatigue or vague abdominal discomfort. Fat starts building inside your liver long before symptoms feel serious, and if nothing interrupts that process, the damage moves toward inflammation, scarring, and even liver failure. Many people discover the problem only after it has already progressed.

A study published in Science Signaling points to an unexpected driver hiding in everyday foods.1 Sorbitol shows up in sugar-free gums, flavored waters, low-calorie snacks, and countless “diet” products many assume are safe, but the evidence shows this sweetener places significant strain on your metabolism.

Sorbitol shifts your internal chemistry quickly once it enters your system. Your gut and liver work together to handle sugar exposure, and when that balance breaks down, your metabolism changes. This turns hidden artificial sweeteners into a much bigger issue and highlights how strongly your gut health shapes your liver health. Once you see how sorbitol behaves inside your body, you can start using strategies that protect your liver instead of overwhelming it.

Sorbitol Overload Rewires Your Liver Within Days

The Science Signaling study investigated how sorbitol behaves inside the body and why it triggers fatty liver changes when gut bacteria fail to break it down.2 The researchers used adult zebrafish because these animals absorb sugar alcohols directly through their intestines, allowing scientists to watch sorbitol move through the gut-liver pathway in real time.

• High sorbitol intake triggers liver fat even with a healthy microbiome — The fish had intact metabolisms before the experiment, which allowed the team to isolate how sorbitol exposure altered liver function. They found that even standard diets triggered liver fat when gut microbes were removed via antibiotic treatment.

However, fish given high sorbitol doses developed the same fat buildup, even when their microbiome was still present. This means sorbitol exposure overwhelms your system enough to bypass normal defenses.

• The loss of gut bacteria caused sorbitol to build up rapidly in the intestines and bloodstream — Antimicrobial-treated fish showed a “substantial accumulation of lipid” in the liver after only seven days, indicating fatty liver.

Without microbiota, the intestine produced sorbitol from glucose and left it untouched, allowing it to move directly into the bloodstream. This means imbalanced gut microbiota or frequent antibiotic exposure increases your vulnerability to sorbitol-driven liver fat.

• The liver converted excess sorbitol into fructose, which triggered metabolic stress — Sorbitol overloaded the liver’s fructose-processing pathway and activated an enzyme called glucokinase, which accelerates glucose breakdown and fat production. Sorbitol tricks your liver into behaving as if you consumed a large dose of fructose, even if you didn’t. This increases the risk of liver fat accumulation, especially if you already deal with metabolic challenges.

• Sorbitol-derived fructose reached unusually high levels when gut bacteria were missing — Metabolic tracing revealed that fructose created from sorbitol was roughly 15 times higher in microbiome-depleted fish compared to controls. That means your gut bacteria act like a metabolic shield. When that shield weakens, sorbitol slips through and forces your liver into fat-storage mode.

• Excess sorbitol also pushed the liver to store more glycogen and create more fat — Sorbitol-driven activation of glucokinase boosted glucose storage and pushed remaining glucose into pathways that produce fatty acids and triglycerides. They measured increased expression of fat-production genes, confirming that sorbitol accelerates the exact biochemical steps that worsen liver disease.

How Sorbitol Overload Disrupts Metabolism

The study showed that an enzyme in your intestine turns glucose into sorbitol. Under normal conditions, your gut bacteria break down that sorbitol before it goes anywhere important. But when those bacteria are missing or weakened, the sorbitol slips through untouched and travels straight to your liver. Once it gets there, another enzyme turns it into fructose. This is a problem because fructose skips your body’s usual safety checks and pushes your liver to create fat very quickly, leaving it overloaded.

• Sorbitol flips a switch inside your liver that speeds up fat production — After sorbitol turns into fructose, a molecule called fructose-1-phosphate signals your liver to activate glucokinase, an enzyme that makes your liver process sugar faster and turn more of it into fat. This is why even short bursts of sorbitol exposure trigger noticeable changes in liver fat.

•The microbiome proved to be the deciding factor for protection — When the team reintroduced sorbitol-degrading Aeromonas bacteria into microbiome-depleted fish, liver fat storage decreased dramatically. This means your microbiome determines how well you handle sorbitol.

If your gut bacteria break it down, your liver stays protected. If they don’t, sorbitol reaches your liver and fuels fat accumulation. This gives you a powerful, actionable insight: protecting your gut diversity is one of the best defenses against hidden metabolic stressors like sorbitol.

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Steps to Protect Your Liver from Sorbitol Overload

Your first priority is to stop the flood of sorbitol before it reaches your liver. The research shows that the real problem starts in your gut, not your liver, which means your daily choices determine whether sorbitol is broken down safely or whether it slips through and triggers fat buildup.

If you already struggle with bloating, irregular digestion, sugar cravings, fatigue, or a history of heavy antibiotic use, you’re more vulnerable to sorbitol escaping your gut and overwhelming your liver. The following steps help you remove the stressors creating the damage instead of simply working around the symptoms.

1. Reduce or eliminate sorbitol-containing processed foods — If you rely on sugar-free gum, flavored waters, low-calorie snacks, or “diabetic-friendly” packaged foods, you’re likely taking in more sorbitol than your system can handle. Removing these products lowers the strain on your microbiome and stops excess sorbitol from reaching your liver. You protect yourself immediately by choosing whole foods rather than processed ones with hidden artificial sweeteners.

2. Strengthen your gut bacteria so sorbitol breaks down before it reaches your liver — Your microbiome acts as your internal sorbitol filter, and when it’s depleted, sorbitol slips past your gut defenses. If you notice digestive issues, use antibiotics, or have a history of restrictive diets or ongoing stress, assume your gut bacteria need rebuilding.

Start by avoiding ultraprocessed foods, including vegetable oils, which are high in linoleic acid (LA), a polyunsaturated fat that oxidizes and injures your mitochondria. If your diet is filled with ultraprocessed foods, your gut microbes will be skewed toward the harmful strains.

In addition, your body’s preferred energy source is glucose, and that comes from carbs. Aim for a steady intake of around 250 grams of healthy carbs from fruit and rice to restore gut balance. Later, once your digestion is stronger, add root vegetables, legumes and well-tolerated whole grains.

3. Remove the major stressors that injure your liver in the first place — If your liver isn’t working the way it should, the goal is not just symptom relief — it’s removing what caused the damage. Your liver handles detoxification, hormone processing, and fat metabolism, and when it’s overloaded, everything else falls behind. The two biggest stressors are vegetable oils and alcohol. The LA in vegetable oils like soybean, canola, corn, sunflower, and generic “vegetable oil” is a mitochondrial poison.

Alcohol adds another layer of damage by breaking down into substances that injure liver cells directly. Alcohol and LA follow the same toxic pathway in your liver, creating harmful aldehydes that cause mitochondrial damage and fatty liver disease. Give your liver breathing room by removing both. For cooking, switch to grass fed butter, ghee, tallow, or coconut oil.

4. Move out liver fat by increasing choline intake — Your liver relies on choline to package and move fat out of its cells. Without enough choline, fat piles up inside the liver and triggers dysfunction. Pastured egg yolks and grass fed beef liver offer the highest levels. If you rarely eat these foods, assume your liver is working without enough support.

FAQs About Sorbitol and Your Liver

Q: What makes sorbitol harmful to your liver?

A: Sorbitol disrupts your metabolism by slipping past your gut bacteria and reaching your liver unchanged. Once there, your liver converts it into fructose, which triggers rapid fat creation and glycogen buildup. Even short-term exposure pushes your liver into fat-storage mode.

Q: Why does gut health determine how your body handles sorbitol?

A: Your gut bacteria normally break down sorbitol before it enters your bloodstream. If your microbiome is depleted from antibiotics, stress, restrictive dieting, or ultraprocessed foods, sorbitol passes through untouched and overwhelms your liver.

Q: Can sorbitol cause liver fat even if my gut bacteria are healthy?

A: Yes. High doses of sorbitol overwhelm your microbiome’s protective capacity. The study found that even fish with intact gut bacteria developed significant liver fat when sorbitol intake was high.

Q: What steps help protect my liver from sorbitol-driven damage?

A: You lower risk by removing sorbitol-containing products, rebuilding gut bacteria with balanced carbs and whole foods, eliminating vegetable oils and alcohol, increasing choline-rich foods, and supporting metabolic repair through sunlight and proper vitamin D balance.

Q: Why is sorbitol riskier than most people realize?

A: Sorbitol looks harmless on labels, but your gut and liver treat it very differently. When it bypasses your microbiome, your liver converts it into fructose and rapidly stores fat. This hidden metabolic load makes sorbitol far more damaging than many people expect.

– Sources and References

A Surprising Reason Why You May Need More Carbs in Your Diet


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/12/28/surprising-reason-why-you-may-need-more-carbs.aspx

Analysis by Dr. Joseph Mercola     December 28, 2025

Story at-a-glance

  • A ketogenic diet can be very useful initially when transitioning people who are metabolically inflexible. However, continuing in ketosis long term can lead to problems, including stubborn weight gain or the inability to lose unwanted weight
  • The reason for this has to do with cortisol. Your body needs glucose, and when deprived for too long, your body will release cortisol to stimulate the production of glucose by your liver. Cortisol also promotes inflammation and central obesity, so you don’t want chronically elevated cortisol levels
  • Your metabolic rate is strongly affected by the type of sugar you consume. High-fructose corn syrup promotes ill health while whole fruit, raw honey, and pure organic cane sugar are readily metabolized without promoting weight gain
  • When adding in more carbs, you also need to reduce your fat intake to avoid elevating your triglycerides
  • Restricting dietary fat and/or blocking the oxidation of fat inside of the cell have strong therapeutic effects against cancer by forcing the cell out of its excessive fatty acid oxidation state

In this interview, Georgi Dinkov and I continue our discussion about diet, diving into some of the finer details that can make or break your health. Dinkov is a student of Ray Peat, who passed away around Thanksgiving 2022, leaving behind a legacy of iconoclastic wisdom on how to optimize biological health.

For example, a ketogenic diet can be very useful initially when transitioning people who are metabolically inflexible, which is about 95% of the population of the United States. So, in the short term, the vast majority of people can benefit from going keto. However, if you continue in ketosis long term, you’re going to run into problems.

Elevated Cortisol Leads to Central Obesity

As just one example, while weight loss is a typical response when going on a ketogenic diet, months later, maintaining that weight loss often becomes a struggle again. Dinkov experienced this firsthand. Once he started following Ray Peat’s recommendations, he lost the weight again and kept it off.

“My take is it’s an endocrine problem,” Dinkov says. “So if you’re struggling with weight you cannot lose, I think it’s a good idea to do a blood work [panel] for the steroids … Every single person that has been struggling with excessive weight that has emailed [me] their blood results, without exception, their cortisol is either high-normal or above the range, both the AM and the PM value.

Their thyroid is less than optimal, in fact, pretty bad for most people … They’re at the upper limit of normal. A very large number of people are basically hypothyroid … I think we are eating foods that are lowering our metabolic rate. We’re living an excessively stressful lifestyle.

That’s probably not a surprise for anybody. Many people think, well, stress is good for you. It’s good as a hormetic response in an acute situation, but not when you have chronically elevated cortisol. Every doctor will tell you if you have a chronic elevated cortisol, you will develop the so-called spectrum of Cushing syndrome …

One of the defining features of elevated cortisol is that you have central obesity. So that, to me, is really the problem. We have higher than desirable levels of stress, suboptimal diet, and we’re surrounded by a number of different endocrine disrupters which are now proven to reliably cause obesity in animal models, even in very small amounts. Most of those are found in plastics.”

Why I Changed My Mind About Low-Carb Diets

One of the foundational concepts of health that I’ve had to radically revise my thinking on, based on the work of the late Ray Peat and his student Georgi Dinkov, is the idea that eating a low-carb diet long-term is the best way to optimize your metabolic and mitochondrial health.

I now realize that this was misguided, and the reason for that has to do with the fact that your body requires glucose and if you aren’t eating it you will go into a hypoglycemic coma and die. Obviously, your body has safeguards to prevent that and the major one is the hormone cortisol.

In medical school, we learned that cortisol is a glucocorticoid. Gluco means glucose (sugar) and cortico means it comes from the adrenal cortex. It’s also another word for steroid. We were told that cortisol is responsible for maintaining glucose homeostasis but led to believe its primary purpose was for inflammation.

Well, that’s just not true. While cortisol certainly contributes to glucose balance, its primary purpose is to raise your blood sugar when it is too low and you don’t have enough glycogen reserves in your liver.

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How Does Cortisol Work?

But just how does cortisol increase your blood sugar? It does it by breaking down your muscles, bones, and brain. It sacrifices your lean muscle mass to release amino acids that your liver converts to glucose in a process called gluconeogenesis.

So, ultimately, cortisol also is going to cause inflammation and impair your immune function. And it increases food cravings. So, you do not want your cortisol to be elevated. For a long time, I was a proponent of a low-carb diet, but now I realize that chronic low-carb is not a good idea.

As a fuel, glucose is vastly superior to fat, and this was something I simply got wrong. The same thing goes for fasting. Both low-carb and fasting are great interventions in the short-term for those who are overweight and metabolically inflexible.

However, once you’ve regained your metabolic flexibility, it is important to revise your strategy and add healthy carbs back in, or else these strategies will backfire and lead to decreased metabolic health, compromised mitochondrial function, and impaired metabolism.

Cortisol happens to be the primary aging hormone. If it is chronically elevated, you simply will die prematurely as it is highly catabolic, meaning it will break down your body tissues. To stay healthy as you age, you need to be anabolic and build healthy tissues like muscle and mitochondria. Elevated cortisol will seriously impair those efforts.

Important Cautions Before You Increase Carbs

So, it is clear that you need to be doing everything you can to keep your cortisol levels and chronic inflammation low. But it would also be a major mistake to increase your carb intake if you are still on a high-fat diet. I did this experiment in the mid-80s after I read the book by the Diamonds called Fit for Life.

They suggested having fruit only for breakfast which I tried. Then I did my lab work and found my fasting triglycerides and lipoprotein profiles had exploded for the worse. I prematurely concluded that a high fruit diet was nonsense and remained relatively low carb for nearly four decades.

This was until I encountered Ray Peat’s work and reevaluated my initial impression. I now understand that I was missing important parts of the strategy. And now I eat 3 to 4 pounds of watermelon (without the rind) virtually every morning at 5:30 as my first meal, followed by three eggs and eight ounces of white rice and two ounces of maple syrup 1 to 2 hours later.

That sounds like a lot of carbs, and it is. I have additional fruits later in the day and now my carb intake is about 475 grams a day and comprises about 60% of my daily calories. You might wonder what has happened to my weight and blood sugar with all these extra carbs.

Well, I thought my weight was good at 192 as I increased my muscle mass, but it has decreased by ten pounds to 182 with no change in muscle mass. My fasting blood sugar has dropped ten points. So far it seems to be working for me.

The Vital Metabolic Switch You Need to Understand

This is one of the most important principles in food science that I never learned or understood until later. My strong guess is that this is also true for most natural medicine clinicians. Low-carb diets have helped at least tens of millions of people improve their health for a very good reason and that is there is a stealth switch that controls what fuel your mitochondria can burn as they can only burn one fuel at a time, either fat or glucose.

The switch has been given the name the Randle Cycle, but it is more helpful to visualize it as a railroad switch that changes the tracks of the train, and the train can only travel down one track not both. This is because only one type of fuel can be burned at a time.

The best-case scenario is you metabolize, or burn, glucose in your mitochondria without any reductive stress (a term I will explain in my upcoming interview with Georgi Dinkov). When you do this, you will only generate 0.1% reactive oxygen species (ROS).

Not only does this route generate less ROS but is also incredibly efficient at energy production by creating 36 to 38 ATP for every molecule of glucose that is metabolized. It will also generate metabolic water and carbon dioxide which are also important for your health.

For this to occur you will need to consume less than 30% of your calories as fat. When you consume significantly more than that amount the switch changes to burn fat in your mitochondria and you will not be able to burn glucose until your fat decreases to less than 30% of calories.

Since glucose is unable to be shuttled into the mitochondria to burn it winds up backing up into your blood stream raising your blood sugar. This is a major contributor to diabetes. What little glucose is burned for fuel is done by using glycolysis which is a primitive pathway that bacteria and cancer cells use.

It is great we have this pathway as you absolutely need it for quick fuel when you are activating your type II muscle fibers. But if this is the primary way you burn glucose you are in a catastrophic metabolic state as you are creating loads of lactic acid as a waste product instead of healthy CO2, and you are only generating 2 ATP for every molecule of glucose, which is 95% less energy.

Lactic acid increases reductive stress, which causes reverse electron flow in the mitochondria and causes reductive stress which increase the ROS to 3% to 4% which is 30X to 40X more than when glucose is burned efficiently in the mitochondria. You likely don’t yet understand reductive stress, the opposite of oxidative stress, but will have done an interview with Georgi on this and will be posting it later this month.

How High-Fructose Corn Syrup Causes Disease

One factor that makes a big difference in your metabolic rate is the type of sugar you consume. Contrary to popular belief, there’s a dramatic difference between high-fructose corn syrup and cane sugar. They’re really two different foods. If the high-fructose corn syrup is properly processed to remove all starch, then it’s very similar to cane sugar because it’s about 55% fructose and 45% glucose.

However, studies have shown beverages sweetened with high-fructose corn syrup contain a tremendous amount of starch, which isn’t accounted for in the calories listed on the label. Once the starch is factored in, the caloric content of many sodas can easily quadruple that on the label, so you’re getting FAR more calories than you think.

Additionally, because the starch is made up of such tiny particles, they can enter your blood circulation unprocessed via your digestive system, causing an allergic reaction.

They can also trigger a low-grade inflammatory reaction, which will trigger the release of histamine, nitric oxide, and serotonin. As noted by Dinkov, if you’re sneezing and have itchy eyes even though it’s not allergy season, you may well be having a reaction to something you ate or drank, and high-fructose corn syrup may be the culprit.

Starch particles also serve as fuel for pathogenic bacteria in your gut, and the endotoxins from these bacteria contribute to inflammatory conditions. Small intestine bacterial overgrowth (SIBO) is one example of what can happen, especially if you’re on a proton pump inhibitor, as these drugs decrease the amount of stomach acid you’re producing. Stomach acid is there not only to help with digestion but also to keep bacteria in check.

“If you’re not producing a sufficient amount of acid, you’re going to get bacteria colonizing your small intestine, either from food or creeping up from the large intestine. And that’s not a good thing. Basically … the portion of the intestine that is supposed to be clean and just focused on absorbing food is now harboring a microbiome.

And then, if you give it any kind of a food that the bacteria can process, you’re increasing the turnover [which] result in the endotoxemia that is now accepted to cause a large number of diseases, especially cardiovascular disease, obesity, and neurological disease.

Alzheimer’s has been conclusively tied to chronic low-grade endotoxemia. They’re still claiming there’s a genetic component to it, but they’re now admitting that endotoxin is a causative factor in Alzheimer’s disease,” Dinkov says.

Can Cane Sugar Be Part of a Healthy Diet?

Most people who embrace natural health believe sugar is a pernicious evil, but Peat’s and Dinkov’s position is that the negative effects are primarily caused by high-fructose corn syrup, and that pure cane sugar can actually be a useful strategy to counteract some of the challenges that people can get into when on a strict low-carb diet. Dinkov explains:

“Cane sugar, if it’s pure, has a very different overall systemic health effect than high-fructose corn syrup … I think most of the sugar sold in the crystal form, especially organic ones, is pretty safe. Heavy metal contamination used to be a problem in sugar distillation but it looks like most of the western countries have sorted this out …

Now, some people that have an issue with sugar are saying, ‘Well, it’s just empty calories and whatnot.’ Multiple studies demonstrated that honey, which is very similar in composition to plain white sugar, does not trigger the normal hyperglycemic response that most of the other simple carbohydrates do. In fact, it improves the hyperglycemia in Type 2 diabetic patients despite being pure sugar.

I think that’s the greatest confirmation that we have that sugar is not evil. It depends how you’re getting it and in what form. One animal study demonstrated that rats, when given free access to [Mexican] Coke sweetened with cane sugar, they were eating the equivalent of 8,000 calories daily … without gaining an ounce of fat.

So sugar is not dangerous. It’s perhaps the only nutrient that we evolved to metabolize for fuel. But the other two micronutrients, even though we can metabolize them as fuel, come with a lot of strings attached …

If you’re oxidizing PUFA, then all hell breaks loose. If you’re oxidizing saturated fats, it’s far less dangerous. But in the long run it still puts you, due to the Randle cycle, into the semi-diabetic state because it decreases your insulin sensitivity.

So pure sugar is what we are meant to oxidize for fuel. If you get it from ripe fruit, great. If you can get it from [raw unadulterated] honey, probably just as good if not even better. But if not, then the pure white variety, preferably organic, that you get from the store, I think is a very good source of most of the carb calories that you intend to eat throughout the day.”

The Glucose-Cortisol Link

In my book “Fat for Fuel,” I argued that healthy saturated fats generate fewer free radical species in the electron transport chain than sugar. However, I’m starting to revise my views on this, based on Peat’s work.

The problem is that if your glucose level is low because you’re on a low-carb diet, your body is going to compensate by self-generating glucose, and that stimulus to make glucose is part of the obesity puzzle, because one of the ways in which your body produces glucose is by secreting cortisol.

And, as explained by Dinkov, if your cortisol is chronically elevated, you end up with central obesity and chronic inflammation, which clearly isn’t good. So, you’ve got to have a certain amount of glucose, and it’s best to get it from your diet rather than forcing your liver to make it, as cortisol is then also being churned out. Dinkov explains:

“If glucose is oxidized properly going through the Krebs Cycle and electron transport chain, it generates more carbon dioxide per molecule of glucose oxidized than do fats.

Now, carbon dioxide has this kind of controversial role in medicine. It used to be considered a metabolic byproduct that could be dangerous. People with chronic obstructive pulmonary disease have higher than normal levels of carbon dioxide in the blood.

But then, medicine started to look into this more closely, I think, over the last 10 years, outside of Dr. Pete’s research, and said, ‘Hm. Carbon dioxide seems to have a lot of positive effects in the body.’ One of them is vasodilation.

So basically, if your metabolism is not working properly, if you’re not oxidizing glucose properly, you’re not going to produce sufficient amounts of carbon dioxide. What happens then? Vasoconstriction. And since that is actually a problem, it raises blood pressure and all kinds of other things; all hell breaks loose. The body then releases an emergency vasodilator, known as nitric oxide. And that is now acquiring a bad reputation.

Even in mainstream medical circles, they’ve started seeing that people who are taking the drug nitroglycerin, which used to be the mainstream drug for angina — chest pain — for cardiovascular disease and blood pressure.

With nitroglycerin, you’ll quickly lower blood pressure. But over time, the inflammatory nature of nitric oxide ensures that these people actually get worse. And, in fact, most people who take nitroglycerin on a long-term basis die from a heart attack or ischemic stroke.

So, if you’re not eating enough glucose, your body will make it. And, in fact, the primary evolutionary role of cortisol, the acute role, is actually preventing blood glucose from dropping too low, because that will put you into a hypoglycemic coma.

In the longer run its secondary role is to dampen down inflammation. So really, the acute, the lifesaving role of cortisol on a daily basis, is to prevent you from dropping into a coma because your blood glucose went too low.

But we don’t want that process because it’s going to get the glucose from the tissues. So, we need glucose [in our diet]. I think even the ketogenic proponents are now getting to the point of saying, ‘We cannot be always in ketosis.’ In the long term, it’s not good.”

Will Sugar Feed Cancer?

Ketogenic diets have also been hailed for their ability to prevent and treat cancer, but even this may turn out to be a misunderstanding in the end.

“I think some of the ideas around glucose feeding cancer stem from two basic misunderstandings,” Dinkov says. “One is that cancer is an evil cell, genetically mutated, and that your only chance is to kill all of those cells because they’re not going away by themselves.

First of all, that’s not true. Spontaneous remissions of cancer are known, and they vary depending on the cancer. Prostate cancer has a pretty high rate of spontaneous remission … A paper that came about five years ago … from the MD Anderson Cancer Center in Texas … said it’s always been the position of medicine that cancerous mutations [happen] and after that, the cell becomes metabolically deranged.

But it looks like we’ve had it backwards. It’s the metabolic derangement that happens first, and, over time, this triggers the genetic mutations, because the cell, being in an energetic deficiency, cannot properly maintain its structure. That was a huge admission …

So what we need to be doing here is not trying to kill the cancer cell, because it is not a cancer cell. It is actually a normal cell that is metabolically deranged.

If we could compare it to anything, it’d be a diabetic cell [and] diabetes is now known to be caused by hyperlipidemia — too much fat in the body, too much fat in the blood. Basically, the cells are getting stuck in oxidizing fats, due to the Randle cycle.

And then, the glucose that’s floating around in diabetes, a good portion of it — because it cannot be metabolized — is being peed out … or you’re converting it into lactic acid. This [MD Anderson] paper said the exact same thing is happening in cancer.

We are seeing an abnormal rate of fatty acid oxidation, because the cell is stuck in the cycle due to oversupply of fat.

The glucose, the ‘cancer cell’ cannot actually metabolize it, but because the cell needs its glucose for a variety of purposes — not just synthesizing energy, but also synthesizing DNA and RNA, and those two … can only be synthesized from glucose, not from fats — the cancer cell says, ‘Oh, I’m in a state of extreme deficiency of glucose. Give me more.’

So, it increases the synthesis of these glucose transporters known as GLUT1 through GLUT4. Basically, that’s why when you give a patient with cancer a little bit of radioactive sugar, it accumulates mostly into the tumor, because the tumor has a much higher capacity for uptake of sugar.

However, and this is the key difference, it has a much lower capacity for oxidizing that sugar. So, you’re going to see a lot of radioactive sugar accumulation in the tumor, but most of it will get converted to lactic acid. So this paper that came out said, ‘We need to do something that gets the cell out of its stressed state.’

And I think we already agreed that excessive oxidation of fat is a stress state. Right? We don’t want to produce lactic acid, and as long as we are over-oxidizing fat, we will be producing lactic acid, and we will be uptaking more glucose …

Several studies have come out since then … and they said, ‘OK, how can we restrict the supply of fat?’ assuming the fat is the problem. There’s only really two macronutrients that can go to the cell. Assuming cancer is a metabolic disease, and assuming a cell can only oxidize fat or sugar, then if it’s not the sugar, it’s got to be the fat. There’s nothing else.

And if it’s not the mutations, if the mutations are secondary to the metabolic derangement, it’s got to be one of these two macronutrients that we can manipulate to actually try to cure the cancer. They already tried glucose restriction … That did not cure cancer. It did have a sensitizing effect to chemotherapy, but it did not result in actual cancer remission.

So now we’re back to the other micronutrient, restricting the supply of fat. Multiple studies … I have at least 30 on my blog … have shown that restricting lipolysis by administering the beta blocker propranolol … lowers lipolysis.

The way [propranolol] lowers blood pressure is by blocking adrenaline. If you’re blocking adrenaline, you’re also lowering lipolysis, because adrenaline is the primary activator of the hormone-sensitive lipase enzyme. Basically, you’re going to be restricting the supply of fat from your own tissues to the tumor.

What else can be done? Well, that’s not the only source of fat. You’re also getting it through the diet. Other studies have tried doing low-fat diets for cancer, and are getting actually good results. Not cure, but good results. The propranolol induced full remission in the cancer.”

Summary

Dinkov also cites research in which the beta oxidation inhibitor etomoxir, prescribed for heart disease, induced full remission in neuroglioblastoma, which is thought to be incurable. So, in summary, either restricting dietary fat or blocking the oxidation of fat inside the cell appears to have strong therapeutic effects against cancer by forcing the cell out of its excessive fatty acid oxidation state.

“And, once you do that, there’s no metabolic damage preventing the cell from oxidizing glucose,” Dinkov says. “It’s all functional. If you flood the cell with fat then, basically, that’s what the cell will oxidize, because it’s overabundant relative to the glucose that is getting to the cell. If you stop that process, or at least greatly restrict it, the cell starts oxidizing glucose again.”

The Devil in the Details

Here, I’d like to share a personal story. In an effort to adopt this new knowledge, I increased my carbohydrate intake to about 250 grams to 300 grams, depending on the day and the fruit availability. When I got my blood work back, I was surprised to find my triglycerides were in the low triple digits, just over 100, which is abnormal.

Normally, I’m closer to 50. In my clinical experience, elevated triglycerides is almost always related to excessive carbohydrate intake, which seems to conflict with what Dinkov just explained. But here’s the key: When you increase carbohydrates, you also have to lower fat. If you don’t, you could end up with complications, as just happened to me. So, now I’m lowering my fat intake. Dinkov confirms my experience:

“Most of the animal studies say, ‘High sugar diet causes this. High sugar diet causes that.’ But if you look at their diets, these animals are already on a high-fat diet. All they did was add more sugar on top of it. Well, of course, in a situation like that, you’re going to have an increase in the triglycerides, increase in LDL cholesterol, because the body can synthesize cholesterol from the sugars.

So, you’re going to get these biomarkers associated with cardiovascular disease to increase, but it’s actually not really a fair comparison. What you should be doing is keeping the diets isocaloric, the same. And also, not increase the total amount of calories, just replace some of that fat with sugar …

Another thing that is probably important is that since there’s always some baseline lipolysis going on, when you’re increasing the carbohydrate intake, the excess that cannot get metabolized will get converted to triglycerides and then stored.

When you are increasing the carbohydrate intake, you should be decreasing the amount of fat. If you’re not, then at least you should be taking something that stimulates the oxidation of carbohydrate so that it doesn’t result in the raising of triglycerides.

Aspirin, caffeine, especially vitamin B-3 niacinamide, all of these are known to lower triglycerides and, by now, the consensus mechanism of action is that all three of these components are increasing the oxidation of carbohydrates.

So, if you’re increasing carbohydrates and you’re getting an increase in triglycerides, two things, either you’re eating too much fat or your baseline metabolic rate is not where it should be, so you can use some metabolic stimulation from these substances.”

In addition to increasing the oxidation of glucose as fuel, aspirin, caffeine, and niacinamide may also inhibit the oxidation of fatty acids, specifically linoleic acid, and the most foundational strategy that anyone could implement to improve their health is to lower their linoleic acid, the omega-6 intake. These supplements will also lower inflammation, which in turn will lower your baseline cortisol.

The metabolite of aspirin, salicylic acid, also has an inhibitory effect on the enzyme 11-beta-hydroxysteroid dehydrogenase Type 1. This enzyme synthesizes active cortisol from the inactive precursor cortisone.

“So, aspirin will actually lower your synthesis of cortisol directly, not just by lowering inflammation, but also lowering the actual synthesis of cortisol,” Dinkov explains. “A study demonstrated that baby aspirin, 81-100 milligrams daily, decreased fatty acid oxidation by about 30% …

Aspirin also has an anti-lipolytic effect, not as strong as niacinamide, but it’s got these three different things that are basically helping to lower both the supply of fat to the cell and excessive oxidation of fats even at these tiny dosages.”

Be mindful about the aspirin you use, though. Immediate-release aspirin made with cornstarch is the preferred version that is now hard to find. Extended-release aspirin is not recommended due to the additives they put in it. Your best option would be to use a salicylic acid or willow bark supplement.

Benefits of Vitamin E

Dinkov also reviews the benefits of other supplements, such as vitamin E, which inhibits lipolysis, improves glucose metabolism, acts as an estrogen antagonist and helps counteract much of the damage caused by linoleic acid and other polyunsaturated fats (PUFAs).

According to Dinkov, research suggests your need for vitamin E can be directly calculated by your PUFA intake. You need about 2 milligrams of vitamin E from all sources per gram of PUFA that you’re eating. So, if you’re eating 50 grams of PUFA daily — which is about 10 times what you should be getting — you need about 100 mg of total tocopherol.

Importantly, PUFAs aren’t just the omega-6s. It’s also omega-3. In the interview, Dinkov goes into detail as to why omega-3 supplements such as fish oil are mostly garbage and shouldn’t be used. I also wrote an article about this very topic.

Whole food, in this case, small fatty fish and wild-caught Alaskan salmon are really your best bet. It’s virtually impossible to find fish oil that’s not rancid. So, to review, when you’re calculating your PUFA intake you also need to include your omega-3s. Ideally, your daily PUFA intake would be below 10 grams.

Dinkov’s Dietary Suggestions

In closing, Dinkov reviews some of his top dietary recommendations for optimal health. No. 1 is keeping PUFA intake below 10 grams; below 5 grams would be even better. No. 2 is to avoid high-fructose corn syrup when adding carbs. Stick with the simple sugars from ripe fruit, raw honey (make sure it’s not adulterated with high-fructose corn syrup, as many are) and/or pure organic cane sugar.

As for the macro composition of your diet, equal amounts of fat, healthy carbs, and protein seem to be best for otherwise healthy individuals, so he recommends getting one-third or 33% of your daily calories from each. If you have metabolic problems or some kind of inflammatory disease, he recommends cutting down on fats.

Lower fat intake will also allow your body to digest protein better, as bile acids are released in response to fat, and bile interferes with the absorption of protein. Next, he recommends adding:

  • Vitamin E, based on your PUFA intake (as detailed above)
  • Aspirin or willow bark extract
  • Niacinamide at a dose of 50 mg to a max of 100 mg, three times a day. In addition to antiobesity effects, niacinamide will also help synthesize NAD+, which has important health benefits
  • Caffeine — BC powder, sold as a headache remedy, contains both aspirin and caffeine. According to Dinkov, research has shown that taking caffeine with aspirin increases the blood concentrations of both and prolongs their effects. Taking 50 mg of aspirin with 50 mg of caffeine can raise your metabolic rate by about 7% and keep it elevated for up to 12 hours
  • Copper — Copper is the rate limiting factor for cytochrome c oxidase (Complex 4). With aging, the amount of copper in that enzyme decreases while iron increases, and the less copper you have, the lower your metabolic rate. Ideally, get your copper from whole foods such as liver, oysters, shrimp, or acerola cherry. If using a supplement, bisglycinate is a good option with high bioavailability

How to Apply This When Using Time-Restricted Eating (TRE)

If you’re using time-restricted eating, or considering starting, then this final side note will be important. If you’re metabolically inflexible, insulin resistant, and unable to easily switch between burning sugar and fat as your primary fuel, then a TRE program, such as that described by Dr. Mindy Pelz in my interview with her, may be quite beneficial, and this is true whether you’re eating a ketogenic diet or not.

However, once you regain your metabolic flexibility, which can take anywhere from a few weeks to a few months, you will need to increase your eating window. The reason for this goes back to the glucose-cortisol connection, Dinkov explains in this interview. Your body needs glucose, and if you deprive it for too long, it will produce cortisol to stimulate your liver to make it.

This increased cortisol can contribute to chronic inflammation and cellular damage. Therefore, once you are no longer insulin resistant, it is best to vary your eating window between eight and 12 hours, and avoid going lower or higher than that window. It is also best to avoid eating before sunrise or after sunset and at least three hours before bedtime.

More Information

To learn more, be sure to listen to the entire interview, as we dive into far greater detail than what I’ve summarized here. Georgi is an absolute fire hydrant when it comes to biochemical details.

Also check out Georgi’s blog at www.haidut.me or follow him on Twitter. You can also obtain a major sampling of Ray Peat’s work for free by going to these two sites: wiki.chadnet.org/Ray-Peat and RayPeat.com.