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Specific Fruit Choices Raise Flavanol Intake — and Most Diets Fall Short
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/09/12/fruit-flavonols-heart-health.aspx
Analysis by Dr. Joseph Mercola September 12, 2026
Story at-a-glance
- Previous research, including the large COSMOS clinical trial, found that consuming about 500 milligrams (mg) of flavanols daily was associated with a lower risk of dying from cardiovascular disease and fewer major cardiovascular events. However, note that COSMOS tested a cocoa extract supplement rather than food, enrolled adults aged 60 and older, and the reduction in major cardiovascular events came from a post hoc analysis
- The featured study found following current fruit and vegetable recommendations didn’t provide enough flavanols for most people to reach the intake linked with better heart health, showing that which foods you choose affects flavanol intake more than how many servings you eat. Even then, high-flavanol produce did not reliably reach the 500 mg benchmark in the researchers’ simulations
- Researchers analyzed more than 30,000 people from the U.S. and United Kingdom using objective laboratory measurements instead of relying only on food questionnaires, giving a more accurate picture of real-world flavanol intake
- Apples, blueberries, blackberries, cherries, pears, plums, green tea, and minimally processed cocoa are among the foods that naturally provide higher amounts of flavanols, making them smart additions to a heart-healthy eating pattern
- Instead of simply eating more produce, rotating a wider variety of flavanol-rich fruits and other plant foods into your meals is an easy way to increase these beneficial compounds while enjoying the many other nutrients whole foods provide
For centuries, people have relied on fruits, tea, and cocoa not only for nourishment but also for their health-promoting compounds. Today, researchers have identified one group of those natural compounds — flavanols — as especially important for cardiovascular health. Flavanols are plant compounds found in foods such as apples, berries, pears, beans, tea, and cocoa.
Yet new research published in Food & Function suggests that simply following current dietary guidelines leaves most people well short of the flavanol intake linked with measurable heart benefits.1 That finding deserves your attention because many people assume eating the recommended number of fruit and vegetable servings automatically delivers every beneficial plant compound.
According to this research, that assumption doesn’t hold up well. The gap isn’t mainly about eating more produce — which produce you choose matters more, though as the researchers found, food choice alone doesn’t fully close it either. This is an important distinction because it shifts the conversation away from quantity and toward quality. Once you understand why certain fruits contribute far more of these compounds than others, the results of the study become much easier to act on.
One caveat worth knowing upfront before going into the findings — much of the flavanol evidence base, including the COSMOS trial discussed below, is industry-funded. Two authors of this new paper are employed by Mars, Incorporated — a company engaged in flavanol research and flavanol-related commercial activities — and COSMOS was supported by an investigator-initiated grant from Mars Edge, with study pills donated by Pfizer Consumer Healthcare (now Haleon).2
Healthy Eating Alone Doesn’t Always Deliver Enough Flavanols
Previous research, including the largest clinical trial of flavanols, the COSMOS study, reported that a daily 500 milligram (mg) dose of flavanols — delivered as a cocoa extract supplement to 21,442 U.S. adults (women aged 65 and older, men aged 60 and older) over a median of 3.6 years — was associated with a 27% lower rate of cardiovascular death in intention-to-treat analyses.
Reductions in total cardiovascular events (15%) and major cardiovascular events (16%) came from per-protocol and post hoc analyses, respectively.3 That 500 mg benchmark became the foundation for a follow-up question researchers set out to answer in Food & Function: Do the diets most people actually eat get them anywhere close to that target?4
To answer that question, the researchers analyzed flavanol intake in two large population studies instead of relying on assumptions about what people eat. Both analyses were observational: the COSMOS portion was a cross-sectional analysis of data collected before participants received any supplement, and EPIC-Norfolk is an observational cohort. Neither measured health outcomes — they assessed flavanol intake only.
They used objective laboratory measurements from 6,509 participants in the U.S.-based COSMOS study and 24,154 participants in the U.K.-based EPIC-Norfolk study to determine whether real-world eating habits matched the flavanol intake associated with better heart health. The answer was largely no.
• Eating more produce was only part of the story — In COSMOS, eating more fruits and vegetables came with slightly higher flavanol levels, though the difference was too small to be meaningful. Overall diet quality was the better predictor.
In EPIC-Norfolk, the pattern reversed. Participants with the highest fruit and vegetable intake — and those adhering most closely to U.K. dietary guidance — were slightly less likely to reach 500 mg per day. The researchers described the differences between high and low fruit and vegetable consumers as very modest overall. Either way, most participants failed to reach the estimated 500 mg per day benchmark.
The researchers also note that they deliberately set their biomarker thresholds to overestimate how many people had high intakes, making their figures a best-case scenario, and that COSMOS participants ate considerably better than the general U.S. public — so, the true shortfall is likely larger.*
This matters because it changes how you think about food choices. If your goal is to increase flavanol intake, simply counting servings of fruits and vegetables isn’t enough. Different foods contain dramatically different amounts of flavanols. Choosing foods naturally richer in these compounds has a much larger impact than simply increasing the total number of servings. Think of it like filling a toolbox — adding more tools helps, but adding the right tools makes the biggest difference.
• The researchers tested whether common eating habits could realistically reach the target — To answer that question, they performed thousands of computer simulations using foods commonly eaten in the U.S. Those simulations reinforced the findings from the human studies. Average fruit and vegetable choices rarely produced flavanol intakes near 500 mg per day.
Selecting foods based on their naturally higher flavanol content raised estimated intake — but even then, the probability of reaching 500 mg per day remained below 50%, and the researchers concluded that even five portions of high-flavanol fruits and vegetables did not get simulated diets to the 500 mg mark. That means the quality of your ingredients matters as much as quantity when selecting plant foods — and that closing the gap through ordinary food choices alone is harder than it sounds.
• Objective testing strengthened the findings — Many nutrition studies depend heavily on people remembering exactly what they ate, but memory is imperfect. This investigation added another layer of confidence by measuring flavanol metabolites in urine. Metabolites are the byproducts left in your bloodstream and urine after your body processes what you’ve eaten, measurable chemical fingerprints of your recent diet.
The investigators combined two different biomarkers to reflect different time windows after eating flavanol-rich foods. Because flavanols clear the body quickly, researchers needed two markers with different detection windows to capture intake across an entire day, not just a single meal. The two markers have different estimated systemic half-lives — roughly two hours for one and six hours for the other.
Together, they provided a broader snapshot of daily flavanol intake. Using both measurements also reduced the chance that a single meal would distort the results. One limitation the researchers flagged: there are currently no validated biomarkers for tea-specific flavanols, so tea’s contribution is only partly captured.
• The same shortfall appeared across two different countries — Although people in the U.S. and United Kingdom eat differently, a similarly small share of each population reached the flavanol benchmark. The direction of the diet-quality association, however, differed between the two cohorts, as noted above.
Participants in the United Kingdom consumed much more tea than those in the U.S., yet only 17.9% of EPIC-Norfolk participants reached the estimated flavanol target compared with 19.2% of COSMOS participants.
The researchers also observed several interesting differences between participant groups. Men were more likely than women to reach the estimated flavanol intake in both studies. In COSMOS, normal-weight participants were more likely than participants with obesity to meet the target, while the opposite pattern appeared in EPIC-Norfolk.
Those differences suggest that overall eating patterns, cultural food choices, and lifestyle habits all influence flavanol intake rather than any single factor alone.
• Not every fruit or vegetable contributes equally — One of the most practical lessons from the study is that flavanols are unevenly distributed across foods. The researchers identified apples, berries, stone fruits, beans, tea, and cocoa products as important dietary sources, while many other commonly eaten fruits and vegetables contribute much less.5
That creates an opportunity rather than a challenge. Instead of simply aiming for more produce every day, focus on building meals around foods naturally richer in flavanols. Small upgrades repeated consistently move you closer to the intake levels associated with better cardiovascular health in this research. That approach keeps the goal simple, measurable, and easier to maintain over the long term.
*These findings are from research conducted in clinical settings. Results may not apply to all individuals.
Choose Foods That Naturally Deliver More Flavanols
The research points to a practical conclusion: The foods you rotate through your week matter more than hitting a produce quota. Think beyond counting fruit and vegetable servings and instead focus on foods that naturally supply higher amounts of flavanols. That approach addresses the real issue identified in the research — many healthy diets still fall short because the food choices themselves are too low in these beneficial plant compounds.
1. Choose fruits and vegetables naturally rich in flavanols — If you want to support your heart, make foods like apples (with the peel), blueberries, blackberries, cherries, and plums regular parts of your meals rather than defaulting to lower-flavanol options like bananas or melons. Bananas and melons still provide valuable nutrients and deserve a place in a healthy diet, but when flavanol intake is the goal, every serving works harder when it comes from the right source.
Pairing these foods with green tea is an easy addition, though keep the ceiling in mind. In the U.K. cohort, even the heaviest tea drinkers reached the 500 mg benchmark only about 19% of the time. When possible, choose organic produce to reduce your exposure to agricultural chemicals, and if you have the space, consider growing some of your own fruit. Homegrown berries, cherries, and plums give you fresh, flavorful options while letting you control how they’re grown.
To put the 500 mg daily target in perspective, here are approximate figures reported for select flavanol-rich foods. These come from the News Medical summary of the research rather than from the featured study itself, and the serving sizes are estimates:
• Plums (about 4 medium plums): ~450 mg
• Cranberries (1½ cups): ~300 mg
• Blackberries (1½ cups): ~250 mg
• Green tea (one 8 oz. cup): ~200 mg
• Cherries (about 25 to 30 pieces): ~130 mg
• Apple with skin (one medium apple): ~110 mg
• Strawberries (1½ cups): ~90 mg
• Blueberries (1 cup): ~80 mg
Again, treat these as estimates, not fixed values. The researchers caution that flavanol content varies considerably with cultivar, climate, and growing and harvest conditions. For example, the epicatechin content of a single apple variety can fluctuate more than tenfold, meaning the number of apples needed to reach a given intake could range from 2 to 29.
Green tea’s figure also deserves a mention — the study’s biomarkers do not capture tea-specific flavanols, so how much tea contributes to the intake linked with cardiovascular benefit is not yet established.6
One practical caveat if your gut isn’t in good shape — Large servings of berries and beans add a substantial fiber load, and when the gut microbiome is compromised, fiber can increase endotoxin production. If you notice gas, bloating, stomach pain, diarrhea, or constipation, start with whole fruits and white rice to restore gut function, then work up to larger portions of higher-fiber foods as tolerance improves.
2. Make flavanol-rich foods part of your daily routine — Your body responds to consistent habits, not occasional healthy meals. If you enjoy blueberries with breakfast, an apple as a snack, or a cup of green tea in the afternoon, keep those habits going day after day. Small routines are much easier to maintain than dramatic diet changes.
3. Challenge yourself to add more variety each week — If your shopping cart looks the same every trip, add one flavanol-rich food you don’t normally buy. Try pears, cranberries, red raspberries, black currants, or minimally processed cocoa. Note that black tea’s characteristic flavanols (theaflavins and thearubigins) were not captured by the featured study’s biomarkers, and their contribution to cardiovascular benefit remains to be established.
With cocoa, choose varieties with lower percentages, look for Prop 65 certification and transparent heavy-metal testing, and avoid products containing vegetable oils. A scrutinizing eye keeps meals interesting while expanding the variety of beneficial plant compounds in your diet.
4. Stock your kitchen with intention — Healthy choices become much easier when the right foods are already within reach. Before your next shopping trip, write down three or four flavanol-rich foods you’ll commit to buying that week and treat them as non-negotiables alongside your usual staples.
Small, consistent food choices — an apple instead of a banana, a cup of green tea, a handful of blueberries on the side — are an easy way to raise your flavanol intake. Whether food-based flavanols translate into lower cardiovascular risk has not been tested directly; the risk data available comes from a supplement trial. However, the research does give you a clearer map of where flavanols are concentrated. The next step is simply stocking your kitchen accordingly.
5. Beyond flavanols, build your meals around whole foods — Flavanols are only one part of a heart-healthy diet. Fill your plate with a variety of whole fruits, vegetables, and other minimally processed foods that provide vitamins, minerals, and thousands of other beneficial plant compounds that work together to support a healthy heart.
At the same time, avoid ultraprocessed foods, which are often made with inflammatory seed oils such as soybean, corn, sunflower, safflower, and canola oil. Prepare meals with more stable fats like grass fed butter, ghee, or beef tallow instead. Cutting back on ultraprocessed foods while adding more whole, flavanol-rich foods doesn’t just boost your flavanol intake, it upgrades the entire foundation your heart health is built on.
FAQs About Fruit Choices That Boost Flavanol Intake
Q: What are flavanols, and why are they important for your heart?
A: Flavanols are natural plant compounds found in foods such as apples, blueberries, blackberries, cherries, pears, plums, beans, tea, and cocoa. Previous research, including the COSMOS trial, linked a daily intake of about 500 mg of flavanols with a lower risk of dying from cardiovascular disease and fewer major cardiovascular events.7 COSMOS delivered those flavanols as a cocoa extract supplement to adults aged 60 and older; the major cardiovascular events finding came from a post hoc analysis.
Q: Does eating the recommended amount of fruits and vegetables provide enough flavanols?
A: Not for most people. The Food & Function study found that fewer than 1 in 4 people who followed current dietary recommendations reached the flavanol intake associated with heart-health benefits. The researchers concluded that adherence to current dietary guidelines does not ensure flavanol intake at the level linked with cardiovascular benefit, and that specific dietary reference values for flavanols may still be necessary.
Q: Which foods are among the best natural sources of flavanols?
A: Foods naturally rich in flavanols include apples, blueberries, blackberries, cherries, pears, plums, green tea, black tea, and minimally processed cocoa. Eating a variety of these foods throughout the week is an easy way to increase your flavanol intake while also providing other beneficial nutrients.
Q: Should you stop eating fruits that contain fewer flavanols?
A: No. Fruits such as bananas, melons, and many others still provide vitamins, minerals, fiber, and other beneficial plant compounds. If your goal is to increase flavanol intake, simply include higher-flavanol fruits more often instead of replacing all other fruits.
Q: What is the easiest way to increase your flavanol intake?
A: Focus on food choices instead of simply eating more produce. Stock your kitchen with flavanol-rich fruits, enjoy green tea regularly (black tea also contains flavanols, though not the types this study could measure), rotate different berries and other high-flavanol fruits throughout the week, choose organic produce when practical, and consider growing some of your own fruit if you have the space.
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.
Lower Cholesterol, Naturally and Safely — No Statins Required
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/04/27/lower-cholesterol-naturally-and-safely.aspx
Analysis by Mary Ann Rollano, RN April 27, 2026
Story at-a-glance
- Cholesterol is essential for hormone production, brain function, and cell health, and about 80% of it is made by your body — not consumed in food. High triglycerides, not total cholesterol, pose a stronger risk for heart attack — raising risk by 80% — making triglyceride-to-HDL ratio a better heart disease predictor
- Newer science shows chronic inflammation — not LDL alone — may be the real cause of plaque buildup in arteries, shifting focus to markers like ApoB and CRP
- Natural options like garlic, artichoke, bergamot, plant sterols, green tea, and oats have been shown in clinical studies to lower LDL cholesterol and improve heart markers
- Red yeast rice can lower LDL by up to 33%, but it contains a statin-like compound with the same side effects and potential kidney toxins like citrinin
- Lifestyle changes like cutting sugar, walking daily, and sleeping well can activate the Pareto Principle — where 20% of effort yields 80% of results in lowering cholesterol. Exercise improves five key metabolic biomarkers — glucose, HDL, triglycerides, blood pressure, and waist size — each linked to long-term cardiovascular health
Your body knows how to heal. Think about it — if a poor diet and lifestyle can contribute to an unhealthy body, it stands to reason that a nutrient-rich diet and lifestyle can conversely contribute to a healthy body. That’s not too hard to figure out.
What is hard to figure out is what is bad for your health and what is good. Are statins good or are they bad? Should you take them? Are there alternatives? If so, what are they? There are many conflicting stories because cholesterol metabolism is complex, making it a perpetually confusing topic. You deserve to understand your health before blindly accepting treatments.
I get a lot of questions about cholesterol, statin drugs, and how to lower cholesterol without taking statins. The good news is that certain plants and lifestyles have been scientifically proven to lower cholesterol. So, let’s break it all down. In this post, I cover:
- What is cholesterol, and why do we need it?
- Triglycerides and their relationship to cholesterol.
- How triglycerides and cholesterol interact.
- The Pareto Principle, cholesterol, and statins.
- Herbs and plants with evidence for cholesterol-lowering effects.
- Key metabolic biomarkers.
- With the proper knowledge and approach, you have the power to control your health.
What Is Cholesterol?
Cholesterol is a fatty, waxy substance found in every cell in the body. Roughly 20% comes from dietary sources, while 80% is primarily manufactured in the liver and other cells. Cholesterol metabolism studies show that this ratio can vary slightly depending on individual factors like genetics, diet, and lifestyle.
Excess sugar, particularly artificial sugars, refined carbohydrates, and genetic errors of liver metabolism, are mainly to blame for high cholesterol. Plant fibers can lower cholesterol, so a diet high in fruits and vegetables and whole grains with minimal fats helps maintain normal cholesterol levels.
• Types of cholesterol:
1. Low-density lipoprotein, LDL, is often called bad cholesterol because high levels are theorized to build plaque in the arteries.
2. High-density lipoprotein, HDL, is called the good cholesterol because it helps to remove excess cholesterol from the bloodstream and returns it to the liver for disposal.
3. Very low-density lipoprotein, VLDL, mainly carries triglycerides in the blood and is less commonly measured.
• Why do we need cholesterol? Cholesterol is present in every cell of the human body and is essential for cellular metabolism.
• Cholesterol is essential for several biological functions:1
◦ Cell membrane structure — Cholesterol is a key component of cell membranes, providing stability.
◦ Hormone production — The building block for steroid hormones, including sex hormones (estrogen, testosterone), cortisol, and aldosterone.
◦ Vitamin D synthesis — When the skin is exposed to sunlight, the body uses cholesterol to make vitamin D.
◦ Bile acid production — Cholesterol is converted into bile acids in the liver, which help digest fats.
• Cholesterol and brain health:
◦ Myelin sheath formation — Cholesterol is a major component of myelin, the protective sheath around nerve fibers that speeds up electrical signaling.
◦ Neurotransmitter function — It is involved in the communication between neurons, supporting the function of neurotransmitters like dopamine and serotonin.
◦ Cell signaling — Cholesterol is crucial for forming “lipid rafts,” specialized areas in cell membranes that facilitate cell signaling in the brain.
◦ Learning and memory — Proper cholesterol metabolism in the brain is necessary for synaptic plasticity, learning, and memory.
Triglycerides and Their Relationship to Cholesterol
Triglycerides, another type of fat (lipid) in the blood, come from foods and are synthesized in the liver. Triglycerides also come from extra calories your body does not need right away. Excess calories are converted to triglycerides and stored as fat in the body for later use. While cholesterol is used for structural and hormonal functions, triglycerides serve primarily as an energy source:
• Energy storage — Excess calories from food are converted into triglycerides and stored in fat cells for later use.
• Transport — Triglycerides circulate in the blood within lipoproteins, especially very-low-density lipoproteins (VLDL), which also carry some cholesterol.
How Triglycerides and Cholesterol Interact
• Both are transported in the bloodstream via lipoproteins (VLDL, LDL, HDL).
• VLDL particles mainly carry triglycerides but also transport cholesterol. As triglycerides are removed from VLDL, the particles become LDL, which is richer in cholesterol.
• HDL particles help remove excess cholesterol from tissues and return it to the liver for disposal.
So while cholesterol is used for building cell walls, hormone production, and other structural and metabolic functions, triglycerides are used primarily for energy supply and storage.
In a blood test, the total cholesterol level includes LDL, HDL, triglycerides, and sometimes VLDL, and means very little as a combined total. High triglycerides are more concerning because people with high triglyceride levels have an 80% higher risk of having a heart attack compared to people with normal triglyceride levels.2
Inflammation, fibrinogen, triglycerides, homocysteine, belly fat, triglyceride to HDL ratios, and high glycemic levels are the underlying drivers of heart disease.3
“Emerging science is showing that cholesterol levels are a poor predictor of heart disease and that standard prescriptions for lowering it, such as ineffective low-fat/high-carb diets and serious, side-effect-causing statin drugs, obscure the real causes of heart disease.”~ The Great Cholesterol Myth
The Pareto Principle and Cholesterol
The Pareto Principle states that 80% of outcomes often stem from just 20% of causes, also known as the 80/20 rule. While commonly used in business, this principle can be metaphorically applied to biology and health, especially when identifying the key drivers behind complex issues.
As I mentioned, about 80% of the body’s cholesterol is made in the liver, while only 20% comes directly from the diet. Statins target this liver production by blocking the enzyme HMG-CoA reductase, which seems logical on the surface. But this approach overlooks why the liver is overproducing cholesterol in the first place — it treats the symptom, not the cause.
In truth, suppressing that 80% of cholesterol production without addressing the underlying 20% of triggers of metabolic disorders, such as insulin resistance, chronic inflammation, stress, and hormonal imbalances, can be counterproductive.
Even though dietary cholesterol accounts for just 20%, certain foods (like excess sugar, refined carbs, trans fats, and high-fructose corn syrup) can prompt the liver to increase its cholesterol output. A small subset of poor dietary choices may be responsible for most of the problem — a textbook 80/20 scenario.
For many people, small, focused lifestyle changes — such as eliminating processed foods, walking regularly, or improving sleep — can lead to significant improvements in cholesterol levels. Thus, 20% of your effort may yield 80% of the results.
Herbs and Plants with Evidence for Cholesterol-Lowering Effects
Anna McIntyre writes in “The Complete Herbal Tutor”:4
• Antioxidant herbs protect arteries, inhibit the formation of atherosclerotic plaque, lower cholesterol, and help prevent cardiovascular disease.
• Useful herbs include hawthorn, cayenne, amalaki, guggulu, bilberry, elderberry, ginger, turmeric, evening primrose, Chinese Angelica, and licorice.
• Shiitake and reishi mushrooms and oats contain beta-glucans, which help lower cholesterol.
• A clove of garlic a day can substantially lower cholesterol levels.
• Red clover reduces its absorption.
• Artichoke leaves help lower cholesterol by helping the liver’s metabolism of cholesterol.
Some of these herbs and plants studied for their potential to lower cholesterol levels are listed below in more detail. They are the most researched options, with scientific evidence and study findings cited here.5,6,7,8
• Red yeast rice (Monascus purpureus)
◦ Red yeast rice contains monacolin K, a compound chemically identical to the statin drug lovastatin, with all the risks and side effects of taking a statin.9
◦ Multiple randomized clinical trials and systematic reviews have shown that red yeast rice can reduce total cholesterol and LDL cholesterol by 10% to 33%.
◦ It is considered one of the most effective natural products for lowering cholesterol, but quality and safety concerns exist due to variability in monacolin K content and potential contamination with citrinin, a nephrotoxin (kidney-damaging substance).
• Plant sterols and stanols
◦ Found naturally in plant-based foods like fruits, vegetables, nuts, oils, seeds, and grains.
◦ A 2022 network meta-analysis found that plant sterol supplementation leads to modest LDL and total cholesterol reductions.
◦ They work by blocking cholesterol absorption in the small intestine.
• Bergamot (Citrus bergamia)
◦ Bergamot extract and its polyphenols have shown promising lipid-lowering effects.
◦ A 2022 systematic review and meta-analysis found significant decreases in total cholesterol, LDL cholesterol, and triglycerides, and an increase in HDL cholesterol. However, a small number of studies limit the evidence.
• Artichoke (Cynara scolymus)
◦ Randomized trials have shown reductions in total cholesterol by up to 18.5% compared to placebo.
◦ The evidence base is limited but promising, with good safety profiles reported in studies.
• Fenugreek (Trigonella foenum-graecum)
◦ Several trials, mainly from India, have shown reductions in total cholesterol ranging from 15% to 33%.
◦ Some studies also found reductions in LDL cholesterol, though methodological quality varies.
• Guggul (Commiphora mukul)
◦ Some randomized trials have reported 10% to 27% reductions in total cholesterol.
◦ Although results have been inconsistent, and quality concerns exist, it remains one of the more extensively studied herbal options.
• Garlic (Allium sativum)
◦ Ancient history and a wealth of modern research support the use of garlic. More than 3,000 scientific papers cover its chemistry, pharmacology, and clinical uses.10
◦ The therapeutic uses of garlic are extensive, but those specific to the cardiovascular system include reducing elevated cholesterol, preventing atherosclerosis and hypertension, treating poor circulation to the legs, and improving overall blood flow through antiplatelet actions.
• Red clover (Trifolium pratense)
◦ Systematic reviews have found significant reductions in total cholesterol and increases in HDL cholesterol in postmenopausal women, but effects on LDL cholesterol are inconsistent.
• Green tea (Camellia sinensis)
◦ An American Journal of Clinical Nutrition meta-analysis suggests that green tea significantly reduces total cholesterol, including LDL or “bad” cholesterol, to 2.19 mg/dL in the blood. However, green tea didn’t affect HDL, or “good” cholesterol.11
Biomarkers and Blood Work
When examining blood work to evaluate cardiac risk and metabolic health, cholesterol alone is insufficient. These parameters and other risk factors, such as diabetes, cardiovascular issues, and liver function, all need to be considered.
High LDL cholesterol was once thought to contribute to plaque buildup in the arteries, which could lead to the plaque becoming dislodged at some point, leading to a heart attack or stroke. Newer schools of thought don’t point to LDL as causing plaque buildup in the arteries but rather to chronic inflammation as being the cause.12
The newer cardiovascular assessment blood tests measure a specific protein called Apolipoprotein B (ApoB) within the LDL, which directly counts the number of atherogenic (plaque-producing) particles in the blood.
If ApoB is not measured, C-reactive protein (CRP) may be measured. CRP measures overall inflammation in the body and screens for cardiovascular risk. That’s important because many chronic diseases result from chronic inflammation. Metabolic biomarkers are key indicators of overall cellular health and disease risk.
The specific thresholds depend on your risk factors, and each lab has its parameters, but for reference, these are the normal ranges from LabCorp:
• LDL
◦ Optimal — <100 mg/dL
◦ Near-optimal — 100 to 129 mg/dL
◦ Borderline high — 130 to 159 mg/dL
◦ High — 160 to 189 mg/dL
◦ Very high — ≥190 mg/dL
• HDL Cholesterol
◦ Optimal — >39 mg/dL
• VLDL Cholesterol Cal
◦ Optimal — 5 to 40 mg/dL
• Triglycerides
◦ Optimal — 0 to 149 mg/dL
• Apolipoprotein B (ApoB)
◦ Optimal — <130 mg/dL
• C-reactive protein (CRP)
◦ < 1.0 mg/dL or 10.0 mg/L
Relationship of Total Cholesterol to HDL
“Neither type of cholesterol is inherently bad or good. Both are necessary for good health. They need to be balanced in the body. Divide your total cholesterol by your HDL cholesterol. If the resulting number is 4 or less, you are at low risk, regardless what your total cholesterol number is. The ratio of total cholesterol to HDL is a much better predictor of risk than simply your total cholesterol number.13” ~ Christiane Northrup, M.D., The Wisdom of Menopause
Key Metabolic Biomarkers
In her book “Good Energy,” Casey Means, M.D., writes about the five specific biomarkers to evaluate for overall metabolic health.14 Research shows that exercise improves all five of the following basic biomarkers of metabolism:
• Glucose levels above 100 mg/dL — Twelve-week exercise programs of either high-intensity running (40 minutes per week) or low-intensity running (150 minutes per week) both brought participants’ blood sugar from the prediabetic range (100 mg/dL or greater) to the nondiabetic range.
• HDL cholesterol less than 40 mg/dL — A 2019 review of the literature showed that exercise increased HDL cholesterol, “with exercise volume, rather than intensity, having a greater influence.” Meanwhile, “raising HDL levels pharmacologically has not shown convincing clinical benefits.”
• Triglycerides above 150 mg/dL — Numerous studies have demonstrated that physical activity effectively lowers triglyceride levels. In a 2019 study, an eight-week moderate aerobic exercise program significantly reduced triglyceride levels in participants. Furthermore, even a single session of intense aerobic exercise has been found to decrease triglyceride levels the following day.
This positive effect could be due to the increased activity of hepatic lipase in the liver, an enzyme that facilitates the absorption of triglyceride from the bloodstream.
• Blood pressure of 130/85 mm Hg or higher — Research has shown the effects of exercise among populations with high blood pressure were similar to the effects of commonly used medications.
(Note: blood pressure parameters considered high used to be above 140/90 mm Hg. This study15 changed that. The top number (systolic) measures artery pressure during a heartbeat; the bottom (diastolic) measures it between beats. Both are important but know systolic pressure can spike with stress. Blood pressure should be measured in both arms over time — not based on a single reading — especially before starting medication.)
• A waistline of more than 35 inches for women and 40 inches for men — Not surprisingly, regular exercise can help decrease obesity by increasing energy expenditure and promoting weight loss.
Research shows a clear inverse relationship between the amount of movement people do each week and the size of their waistline: more movement, smaller waist circumference. What’s more, lower activity (fewer than 5,100 steps per day) yields a 2.5 times higher risk of central obesity than higher activity (more than 8,985 steps per day).
Key Takeaways
With the proper knowledge and approach, you have the power to control your health.
• Reduce sugar, HFCS, refined carbohydrates, and other highly processed foods.
• Eat a diet high in vegetables, whole grains, especially oats, beans, legumes, pulses (such as beans, lentils, chickpeas), good fats, and oily fish.
• Take regular aerobic exercise and daily walking.
• There is no “one size fits all” diet for heart health. Eat whole foods without preservatives and additives, and concentrate on plant foods.
One important caveat:
• Statins lower LDL cholesterol quickly by blocking an enzyme (HMG-CoA reductase) the liver uses to make cholesterol. Results are often seen in 4 to 6 weeks.
• Diet and lifestyle can be highly effective, but changes may take 3 to 6 months or more. The degree of improvement depends on adherence, genetics, and overall health.
Live life well.
About Author
Mary Ann Rollano is a writer, registered nurse, and award-winning tea specialist with 40 years of experience in health and wellness. Passionate about the four pillars of health — physical, emotional, spiritual, and social harmony — she blends her expertise in tea, herbs, and nutrition to inspire meaningful connections and happier, healthier lives. Connect with her through her Steeped Stories newsletter.
- 1 ScienceDirect. (n.d.). Cholesterol metabolism. In Agricultural and Biological Sciences. Elsevier
- 2, 14 Means, C., & Means, C. (2024). Good energy: The surprising connection between metabolism and limitless health. Avery.
- 3 Bowden, J., & Sinatra, S. T. (2020). The great cholesterol myth, revised and expanded: Why lowering your cholesterol won’t […]. Fair Winds Press
- 4 McIntyre, A. (2019). The complete herbal tutor: The definitive guide to the principles and practices of herbal medicine. Gaia Books
- 5 National Center for Complementary and Integrative Health. (n.d.). High cholesterol and natural products: What the science says. NCCIH Clinical Digest
- 6, 7 J Fam Pract. 2003 Jun;52(6):468-78
- 8 Nutrients 2025, 17(5), 877; doi: 10.3390/nu17050877
- 9 EFSA Journal, 16(8), 5368. doi: 10.2903/j.efsa.2018.5368
- 10 Hoffmann, D. (2003). Medical herbalism: The science and practice of herbal medicine. Healing Arts Press
- 11 The American Journal of Clinical Nutrition Volume 94, Issue 2, August 2011, Pages 601-610
- 12 Circulation, 147(14), 1053-1063. doi: 10.1161/CIRCULATIONAHA.122.061010
- 13 Northrup, C. (2021). The wisdom of menopause: Creating physical and emotional health during the change (4th ed.). Bantam
- 15 NIH, December 13, 2017
What Are Postbiotic Supplements — and Do You Really Need Them?
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/04/02/postbiotic-supplements.aspx
Analysis by Dr. Joseph Mercola April 02, 2026
Story at-a-glance
- Postbiotics are compounds your gut bacteria already produce during digestion, which means they’re a result of gut health rather than a replacement for it
- Most postbiotic supplements deliver isolated compounds and don’t create lasting microbiome changes because they don’t reproduce inside your body
- Research shows postbiotics strengthen gut barrier function, reduce inflammation, and selectively suppress harmful microbes, with the strongest benefits seen when the gut is already compromised
- Whole foods and fermented foods support continuous postbiotic production while also supplying nutrients that supplements can’t replicate
- Supporting your gut environment through diet delivers steady, long-lasting benefits, while postbiotic supplements like heat-killed Akkermansia serve as supportive additions once your gut is healthy
Few people realize that your gut bacteria have produced postbiotics for as long as humans have existed. Long before supplements or wellness trends, these compounds formed naturally every time bacteria in your digestive tract broke down food. Today, postbiotics show up on store shelves as capsules and powders, often marketed as a shortcut to better gut health. But this shift reflects a deeper misunderstanding about how your microbiome actually works.
Postbiotics aren’t bacteria. They’re the compounds bacteria leave behind after digestion — short-chain fatty acids (SCFAs) like butyrate, enzymes, amino acids, vitamins, and fragments of bacterial cell walls. These substances already exist inside you when your gut bacteria function properly, which means postbiotics are an outcome of gut health rather than a replacement for it.
That distinction matters because supplement marketing often skips right past it. The real question isn’t whether postbiotics do useful things in your body — they do. The question is whether buying them in a bottle makes sense when your gut already produces them for free, and what the research actually says about each approach. Let’s look at what the evidence shows.
How Postbiotics Influence Human Health at a Biological Level
A narrative review published in the peer-reviewed journal Biomolecules examined how postbiotics affect your gut and other body systems by analyzing experimental, animal, and human data across multiple research domains.1 The researchers evaluated how different postbiotic components act on tissues, immune responses, and microbial balance.
• Certain postbiotics directly strengthen your gut barrier — When your gut lining develops microscopic gaps, a condition that causes bloating, food sensitivities, and systemic inflammation, specific postbiotics repair the damage by increasing tight junction proteins. These act like mortar between gut cells, creating a selective barrier that lets nutrients pass while blocking toxins, undigested food particles, and bacteria from entering your bloodstream.
When these junctions weaken, unwanted substances slip through your gut lining. Postbiotics helped restore this barrier by increasing protective proteins and reducing inflammatory signals, which directly supports digestive comfort and nutrient absorption.
• Postbiotics directly neutralize the cellular damage caused by oxidative stress — Several postbiotics reduced reactive oxygen species, meaning unstable molecules that damage cells by stealing electrons from healthy structures — like rust spreading through your gut lining. This cellular damage triggers inflammation and impairs your gut’s ability to absorb nutrients.
Excess oxidative stress disrupts digestion and worsens chronic gut conditions. By neutralizing these molecules, postbiotics lowered tissue damage in gut models, which explains why benefits showed up most clearly in inflammatory diseases rather than general wellness settings.
• Antimicrobial effects were selective, not broad spectrum — Certain postbiotic-derived bacteriocins suppressed specific harmful bacteria without wiping out beneficial microbes. This targeted action differed from antibiotics, which disrupt entire microbial communities. Postbiotics influence balance rather than acting as blunt microbial weapons.
However, postbiotics don’t reproduce inside your body. Once intake stops, their effects stop. This explains why they don’t create lasting microbiome changes on their own. It also clarifies why consistent diet and microbial support remain necessary for sustained results.
• The strongest benefits appeared in tissues with barrier functions — Beyond your gut, the review documented improved outcomes in skin wounds, atopic dermatitis, vaginal infections, and oral biofilms. All these tissues depend on tight barriers that keep the outside world outside — whether that’s skin keeping bacteria off your bloodstream or vaginal tissue preventing infections.
• Postbiotics act through signaling, not colonization — Postbiotics interact with receptors on cells, influence immune signaling pathways, and regulate gene expression linked to inflammation and repair. Instead of “taking over” your microbiome, they act as messengers that nudge existing systems toward stability.
Postbiotic Supplements — Breakthrough or Overhyped Shortcut?
An article published in The Conversation examined what postbiotic supplements are and whether people actually need them, noting that most postbiotic research focuses on individual compounds, not full supplements.2 For example, certain postbiotics are linked to better sleep quality, mood, or immune responses, but these effects appear in tightly controlled settings. This means results depend on the exact compound, dose, and population studied, which limits how broadly you can apply them to daily life.
• There’s a gap between lab results and real-world health — Many encouraging results come from cell cultures or animal experiments, such as reduced invasion of colon cancer cells or protection against E. coli in laboratory models. However, these findings don’t translate directly to human outcomes.
• Some heat-killed bacteria showed targeted immune effects in people — The article highlighted a double-blind, placebo-controlled study where a heat-killed strain of Lactobacillus pentosus lowered the likelihood of older adults developing the common cold.3
Another review found that a heat-killed Lactobacillus acidophilus strain reduced both risk and duration of diarrhea in children.4 The strongest clinical support, however, existed for butyrate, an SCFA linked to symptom improvement in people with inflammatory bowel disease in human studies.5
Butyrate doesn’t just feed colon cells — it actually reaches into the cell nucleus and influences which genes get turned on or off, particularly genes controlling inflammation and cellular repair. This epigenetic effect explains why butyrate shows up consistently in research on inflammatory bowel disease.
• Whole foods delivered broader benefits than supplements — Foods like grass fed yogurt paired with fruit provide probiotics, prebiotics, and nutrients together. This combination allows your gut to produce postbiotics naturally while also supplying calcium, protein, potassium, and vitamins. This reinforces that everyday food choices influence gut health more reliably than expensive supplements.
• Cost and payoff rarely favored supplements for the average person — Postbiotics resist heat, oxygen, and time, which makes labels more accurate and storage easier. They also avoid risks linked to live bacteria, which matters for severely immunocompromised individuals. However, supplements often cost more than dietary changes while delivering narrower benefits. As long as your gut is healthy, investing in varied, fiber-rich foods typically produces stronger overall health returns.
How to Support Postbiotic Production the Right Way
Here’s the good news: you don’t need to understand cellular signaling pathways to benefit from postbiotics. Your gut already has the blueprint. Your job is simply to provide the raw materials and get out of the way.
This means if you want the benefits linked to postbiotics, the answer isn’t simply reaching for another bottle on the shelf. The real leverage point is the environment where postbiotics form. Your gut bacteria already produce these compounds when conditions support them. When digestion breaks down, production drops. So, the goal is straightforward — give your gut what it needs and let it do what it already knows how to do.
1. Feed the bacteria you already have before buying bacteria in a bottle — Food comes first because postbiotics form during digestion, not in a capsule. When you eat a range of whole foods that your gut bacteria can break down, your body produces these compounds naturally — alongside minerals, vitamins, and protein. A supplement can’t replicate that full package.
2. Use fermented foods as a daily foundation — If you tolerate fermented foods, make them a regular part of your routine — think sauerkraut with dinner, a spoonful of kimchi at lunch, grass fed kefir in a morning smoothie, or a small serving of miso soup alongside your meal. They supply bacteria that already know how to generate postbiotics once they receive the right fuel. Don’t treat this as a one-time experiment.
Consuming small amounts of fermented foods daily compounds over time and builds a more resilient gut environment. Aim for 2 to 4 tablespoons of fermented vegetables daily, or 4 to 8 ounces of grass fed kefir or yogurt. If you’re new to fermented foods, start with 1 teaspoon and increase gradually over two to three weeks to avoid digestive upset.
If fermented foods consistently cause bloating, headaches, or digestive distress even at tiny doses, you may have small intestinal bacterial overgrowth (SIBO), histamine intolerance, or bacterial overgrowth. In these cases, address the underlying condition first with a qualified integrative practitioner before reintroducing fermented foods.
3. Pair foods instead of isolating nutrients — Combine foods that contain live bacteria with foods that feed them. For example, pairing yogurt with berries or kimchi alongside a fiber-rich meal gives your gut bacteria both the microbes and the fuel they need to generate postbiotics on their own. This keeps postbiotic production running without the mental load of tracking compounds or counting doses. Just meals that work together instead of in isolation.
4. Consider a postbiotic Akkermansia supplement — but prepare your gut first — A key gut bacterium called Akkermansia muciniphila, which I call Akker, lives in your gut’s mucus layer, where it helps produce SCFAs and repairs the barrier that protects you from toxins. Your gut’s mucus layer acts as a buffer zone between bacteria and your intestinal cells.
When this layer thins — from stress, poor diet, or medications — bacteria migrate closer to the gut wall, triggering inflammation. Akkermansia specializes in mucus metabolism, continuously renewing this protective barrier while generating SCFAs as byproducts. You can take pasteurized, “heat-killed” Akker — a postbiotic form — but timing matters.
As I explain in my new book, “The Weight Loss Cure,” instead of colonizing your gut, postbiotics deliver targeted molecular signals that help strengthen your gut barrier and reduce inflammation. They’re also shelf-stable, acid-resistant, and easy to tolerate, which makes them an excellent addition to a gut-healing strategy alongside probiotic-rich foods and other microbiome-supporting nutrients.
But the key word is “addition” — make sure your gut terrain is healthy before layering in a supplement. Akkermansia thrives in a low-inflammation environment. If your cells are still saturated with linoleic acid (LA) from years of seed oil consumption, supplementing won’t help. Give your body at least six months to clear stored LA by eliminating soybean, corn, sunflower, and other seed oils.
This allows your cellular membranes and mitochondria to rebuild with stable fats, creating the conditions where Akkermansia — and its postbiotic products — can actually function.
This means eliminating soybean, corn, cottonseed, sunflower, safflower, and other vegetable oils — the oils hiding in salad dressings, mayonnaise, restaurant food, and processed snacks. Cook with grass fed butter, ghee, or tallow instead. Read ingredient labels obsessively for the first month until you know which products to avoid.
5. Trust your gut instead of chasing labels — Pay attention to digestion, energy, bowel regularity, and comfort. A short daily check-in tells you more than any marketing claim. For instance, keep a simple daily log for two weeks tracking:
• Bowel movements — Aim for one to two formed stools daily without straining
• Energy — Note mid-afternoon crashes or brain fog
• Bloating — Rate on a scale of zero to 10 after meals
• Sleep quality — Note how often you wake at night
Improvements in two or more categories within three to four weeks suggest your approach is working. If it’s not, adjusting food choices — like focusing on easy-to-digest carbs including fruit and white rice — usually delivers more progress than adding another product to the rotation. Supporting the system that produces postbiotics delivers steadier results than trying to replace it.
FAQs About Postbiotics
Q: What exactly are postbiotics?
A: Postbiotics are the compounds your gut bacteria produce after digesting food, including SCFAs like butyrate, enzymes, amino acids, vitamins, and bacterial cell fragments. They aren’t live bacteria and are created naturally when your gut microbiome functions well.
Q: Do you need postbiotic supplements to get these benefits?
A: Only if your gut isn’t producing enough on its own. Your gut already produces postbiotics when it receives the right food. Supplements deliver isolated compounds, while whole foods support the entire system that generates postbiotics naturally and consistently.
Q: What health effects do postbiotics actually have?
A: Research shows postbiotics strengthen gut barrier integrity, reduce inflammation and oxidative stress, and selectively suppress harmful microbes without disrupting beneficial ones. The strongest benefits appear in people with gut or barrier-related problems rather than in already healthy individuals.
Q: Why don’t postbiotic supplements create lasting changes?
A: Postbiotics don’t reproduce or colonize your gut. Once intake stops, their effects stop. Lasting improvements depend on restoring the gut environment that produces postbiotics continuously through digestion.
Q: What’s the most effective way to support postbiotic production?
A: Focus on food first. Regularly eating whole foods, pairing fermented foods with the fibers that feed bacteria, avoiding gut-disrupting fats like LA in vegetable oils, and tracking digestion and energy signals support steady postbiotic production without relying on supplements. Once your gut is healthy, pasteurized, “heat-killed” Akker provides additional support.
The Butyrate-GLP-1 Connection: Unlocking Satiety, Energy, and Inflammation Control
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/09/butyrate-glp-1-connection-natural-weight-loss.aspx
Analysis by Dr. Joseph Mercola March 09, 2026
Story at-a-glance
- Butyrate fuels the gut cells (L-cells) that produce GLP-1, a natural hormone that helps regulate appetite, blood sugar, and metabolism
- Your gut can’t make butyrate without fiber, and modern diets contain far too little — just 16 grams a day compared to 100+ grams in traditional cultures. Low butyrate disrupts the body’s natural hunger regulation system, leading to inflammation, weight gain, mood issues, and metabolic breakdown
- Restoring butyrate is a natural way to activate GLP-1 — no injections or drugs required — by working with your body instead of bypassing it. My new book, “Weight Loss Cure; Melt Fat Naturally With Your Own GLP-1,” provides a step-by-step plan to rebuild butyrate production, restore natural GLP-1 signaling, and correct the root drivers of weight gain
- Pharmaceutical GLP-1 agonists are marketed as breakthroughs, but they’re merely stand-ins for a system your body already perfected: GLP-1 secretion driven by butyrate
- Healing starts with calming the gut using simple carbs like white rice and fruit, then slowly reintroducing fermentable fibers such as resistant starch. Eliminating seed oils, reducing stress, and getting morning sunlight are also key to restoring your gut’s ability to make butyrate and support GLP-1 naturally. Signs that your gut is rebuilding include improved digestion, better mood, reduced cravings, and more stable energy
What if your body already knew how to regulate hunger, burn fat, and keep your metabolism in balance — without injections or synthetic hormones? It does. And it starts with butyrate. This isn’t a biohack. It’s how your metabolism was designed to function.
Butyrate is a short-chain fatty acid (SCFA) made by beneficial gut bacteria when they ferment fiber. It powers the colon cells (L-cells) that produce GLP-1, a natural hormone that helps you feel full, balance blood sugar, and burn energy efficiently.1,2,3,4 The GLP-1 pathway is a built-in system for appetite regulation, blood sugar control, and energy balance, but it only works if your gut bacteria have the right fuel.
The problem? Modern diets have starved your gut’s natural GLP-1 engine. Butyrate production depends on fiber, and the average American gets only about 16 grams a day. In traditional cultures, fiber intake regularly exceeds 100 grams. Hunter-gatherer tribes like the Hadza in Tanzania, for example, eat up to 150 grams of fiber daily.
Human metabolism evolved around the butyrate–GLP-1 connection long before pharmaceutical GLP-1 agonists ever existed. Our ancestors ate diverse plant fibers that fed gut microbes, which in turn churned out butyrate. That butyrate kept the intestinal barrier strong, inflammation low, and appetite hormones in balance.
Today, processed foods and industrial seed oils — especially vegetable oils that are high in linoleic acid (LA) — break that cycle. They damage gut bacteria, slash butyrate output, and disable the L-cells responsible for natural GLP-1 production. The result? We’re tired, inflamed, overweight — and told we need drugs to fix it. But you don’t need to mimic biology with a syringe if you can restore it through your own gut. This is the central topic of my new book, “Weight Loss Cure; Melt Fat Naturally With Your Own GLP-1.”
How Butyrate Fuels Natural GLP-1
Butyrate directly nourishes L-cells in your intestinal lining — the same cells that release GLP-1 after meals. When butyrate is abundant, GLP-1 secretion works the way nature intended:
• It slows gastric emptying, so you feel full longer
• It reduces glucagon, which lowers blood sugar
• It enhances insulin sensitivity and helps your body burn fat
• It sends satiety signals to the brain, curbing cravings and emotional eating
You don’t need a synthetic GLP-1 agonist to access these benefits. You need butyrate. That means giving your gut bacteria the right environment to do their job. This isn’t about overriding your biology. It’s about supporting the natural regulatory loop your gut was built to run. When this system is fueled properly, metabolic balance is the default state.
What Happens When Butyrate Is Low?
Without enough butyrate:
• Your colon cells weaken, leading to “leaky gut”
• Inflammation flares and spreads systemically
• Mood, memory, and stress resilience decline
• GLP-1 production drops, triggering weight gain and blood sugar instability
Conditions like Type 2 diabetes, depression, and Parkinson’s often trace back to this breakdown. The good news? Restoration starts in your gut, and it can begin within days of changing your diet.
Your Gut Bacteria Make SCFAs, but Only if You Feed Them
In my paper, “SCFAs Modulate Gut-Brain Axis Function,”5 I explain how SCFAs, especially butyrate, play a central role in regulating metabolism, appetite, inflammation, and brain function. This happens through the gut-brain axis, where SCFAs produced in the colon influence everything from satiety hormones like GLP-1 to stress resilience and cognitive performance.
Modern diets — low in fermentable fiber and high in inflammatory seed oils — have disrupted this natural metabolic control system. But clinical research shows we can restore it. The figure below summarizes human studies where prebiotic fibers or direct SCFA interventions were used in real-world populations. Key findings include improvements in body fat, satiety, insulin signaling, inflammation, and gut-derived hormone release, which includes GLP-1.
These studies confirm that feeding or restoring SCFA production — especially butyrate — can activate your body’s built-in metabolic and inflammatory controls. That includes the same GLP-1 pathway targeted by weight loss drugs like Ozempic, but without the side effects or dependency. This is your original biology — rebooted through your gut.
But again, to support the butyrate-producing bacteria, you need to feed them the right substrates — fermentable fibers like resistant starch, inulin, and oligosaccharides. If you’re not consuming these regularly, your gut can’t make butyrate. The figure below shows which types of gut bacteria make key SCFAs, what foods they thrive on, and how they help keep your gut healthy and balanced.
Butyrate doesn’t “treat” metabolic dysfunction, per se. It supports normal metabolic function by fueling the mechanisms your body already relies on to support normal appetite, insulin sensitivity, and inflammatory control.
Your Gut Was Built for This: Butyrate and GLP-1 Are the Natural Design
Pharmaceutical GLP-1 agonists are marketed as breakthroughs, but they’re merely stand-ins for a system your body already perfected: GLP-1 secretion driven by butyrate. Your L-cells are engineered to release GLP-1 in response to butyrate. When the gut microbiome is balanced and well-fed with fermentable fiber, GLP-1 production activates after meals to regulate appetite, support insulin release, and promote fat burning — all without a prescription.
This design evolved to work in harmony with ancestral diets rich in whole foods, fiber, and unprocessed carbohydrates. Disruption to this design — whether from ultraprocessed foods, antibiotics, or synthetic additives — breaks the microbial fuel line, not the hormonal hardware. When you restore butyrate production, you remove the blockages and reactivate the normal regulatory feedback loop, which lets your built-in weight regulation system function again, as intended.
How to Restore Butyrate and Unlock Natural Weight Loss
To restore your body’s natural weight management system, you need to restore and support the bacteria in your gut that produce butyrate and other SCFAs. This isn’t about manipulating your biology into doing something unnatural. On the contrary, it’s about rebuilding the internal conditions that allow your body to regulate appetite, metabolism, and fat burning as it was designed to. Here’s how:
1. Start with gut terrain repair — If you’re bloated, constipated, or sensitive to high-fiber foods, you need to calm inflammation before you feed the microbiome. That means:
• Avoiding fermentable fibers at first. When your gut is out of balance, high-fiber foods — even the “healthy” ones — can work against you. Foods like beans, lentils, oats, and raw greens ferment quickly when the wrong bacteria are in control. This creates gas, pressure and inflammation, and worsens gut lining damage.
• Eliminating seed oils (such as soybean, corn, canola, sunflower). LA damages the exact gut microbes you’re trying to support. If your diet includes fried foods, processed snacks, or sauces made with soybean, corn, sunflower, or canola oil, you’re suffocating your good gut bacteria. Replace those fats with ghee, grass fed butter, or tallow — fats your body actually knows how to use. The goal is to shift your internal terrain so your gut bacteria thrive again.
• Using simple carbs like white rice and ripe fruit to stabilize energy without feeding bad bacteria.
2. Add butyrate-promoting foods slowly — Once symptoms ease, introduce fermentable fibers in small amounts. These fibers pass undigested to your colon, where they feed good bacteria that make SCFAs like butyrate:
• Cooked and cooled white potatoes
• Green bananas
Once you tolerate those, add in inulin-rich foods like garlic, onions, and leeks, which feed butyrate-producing bacteria. These fibers bypass digestion in your small intestine and head straight to your colon, where they fuel beneficial bacteria that make butyrate and other SCFAs. Citrus fruits can also be added. They help feed Faecalibacterium prausnitzii, a major butyrate-producer.
3. Support with optional tools — Once your gut begins to stabilize, these targeted tools can help accelerate butyrate production and improve results:
• Akkermansia postbiotics (Phase 1) — Postbiotics are non-living bacterial components that still deliver biological signals. Pasteurized forms of Akkermansia muciniphila contain Amuc_1100, a protein shown to tighten the gut barrier and reduce inflammation. Look for postbiotic formulas with enteric coating or microencapsulation to ensure they survive stomach acid and reach the colon intact.
Without that protection, less than 5% of Amuc_1100 reaches your colon. You could try megadosing to compensate, but that’s expensive and inefficient. Prioritize coated formats to support your gut barrier more effectively.
• Live Akkermansia (Phase 2) — Once your gut lining shows signs of healing (less bloating, more fiber tolerance), you can begin Phase 2. In this stage, introduce live probiotic Akkermansia alongside gentle prebiotics — like small amounts of resistant starch — to support the growth of butyrate-producing strains and reestablish a healthy, oxygen-sensitive microbial environment.
• Fermented foods — Raw sauerkraut, kefir, and other traditionally fermented foods can boost microbial diversity and support butyrate-producing strains. Go slowly — start with small amounts to test tolerance, especially if your gut is sensitive.
• Gut testing — A stool analysis can reveal which bacteria are present, whether your gut is inflamed, and how well you’re producing short-chain fatty acids like butyrate. This can guide food choices and supplementation more precisely.
• Resistant starch — Found naturally in cooked-and-cooled potatoes, green bananas, and legumes — or as supplemental powders — resistant starch bypasses digestion in the small intestine and becomes prime fuel for butyrate-producing bacteria in the colon.
4. Adjust your environment — Your gut doesn’t just respond to what you eat. It’s tuned into your entire lifestyle. Your gut bacteria evolved alongside your daily rhythms, and restoring this alignment is essential to support the normal circadian and hormonal cycles your metabolism depends on. These daily habits help create the internal rhythm your microbiome needs to thrive:
• Sleep — Align your sleep-wake cycle with natural light exposure. Aim for 7 to 9 hours of high-quality sleep and get morning sun to anchor your circadian rhythm. This helps regulate gut motility and microbial repair.
• Stress — Chronic stress alters your microbiome and shuts down butyrate production. Use daily tools like breathwork, walking outdoors, and nervous system regulation practices to calm your hypothalamic-pituitary-adrenal (HPA) axis and support microbial balance.
• Fasting window — Stop eating at least three hours before bed. This gives your migrating motor complex (MMC) — your gut’s internal clean-up crew — time to sweep out bacteria and food debris overnight, reducing fermentation and inflammation.
Signs Your Gut Is Making More Butyrate
These improvements reflect rising butyrate levels and gut healing in real time:
• Bowel movements become regular and well-formed — A sign of improved colonic motility and mucosal integrity.
• Fiber tolerance improves — Less bloating, gas, or discomfort after meals rich in fermentable fiber.
• Hunger fades between meals — As GLP-1 and PYY production increases, satiety naturally extends.
• Mood feels more stable and stress less overwhelming — Butyrate supports BDNF and modulates the HPA axis.
• You lose fat without trying to eat less — Improved metabolic signaling leads to spontaneous caloric reduction.
• Reduced post-meal blood sugar spikes — A measurable effect tied to improved insulin sensitivity and GLP-1 response.
• Lower fasting insulin and triglycerides (if tested) — Both improve with SCFA restoration and microbiome balance.
• Fewer cravings for processed carbs and snacks — Satiety hormones rise while inflammation-driven hunger decreases.
• Less urgency or discomfort with bowel movements — Improved stool consistency reflects stronger gut barrier and reduced inflammation.
•Improved breath or reduction in sulfur/gas odors — Indicates better fermentation profile in the colon (fewer sulfur-releasing or proteolytic bacteria).
Timeline: What to Expect as Your Gut Rebuilds
Your gut already knows how to help you lose weight — by producing butyrate, which fuels the cells that make GLP-1. This is how human metabolism was designed to function. Restore that system, and your cravings shrink, your blood sugar stabilizes, your inflammation calms down, and your body starts releasing excess weight naturally. These shifts are clear signs that your body’s metabolic software is running the way it was meant to.
Your gut doesn’t need to be perfect to start producing butyrate. But there’s a rhythm to recovery, and markers to know it’s working.
| Phase | What happens | Timeframe | Measurable indicators |
|---|---|---|---|
| Terrain repair | Gas, bloating, and sensitivity begin to calm | 1 to 3 weeks | Less urgency, firmer stools, more predictable digestion |
| Fiber reintroduction | Butyrate-producing strains begin to increase | 2 to 4 weeks | Better tolerance of resistant starch, mood uplift |
| GLP-1 response | Appetite regulates, energy improves, cravings decrease | 4 to 8 weeks | Fewer between-meal snacks, better AM energy |
| Metabolic reset | Satiety increases, fat loss begins, blood sugar stabilizes | 6 to 12 weeks | Tighter waistline, reduced post-meal glucose swings |
You can start putting these strategies into practice right now with my new book, “Weight Loss Cure; Melt Fat Naturally With Your Own GLP-1,” which provides a step-by-step plan to rebuild butyrate production, restore natural GLP-1 signaling, and correct the root drivers of weight gain.
We’re also preparing a butyrate-support product designed to complement these foundational strategies. You can join the waitlist now, and when it becomes available, you’ll receive a $5 off coupon by email.
FAQs
Q: Is butyrate the same as taking a GLP-1 drug like Ozempic?
A: No. Drugs mimic GLP-1 but bypass your gut’s natural system. Butyrate restores the function of the L-cells that make GLP-1, without side effects or dependency.
Q: What are the signs that you’re low in SCFAs like butyrate?
A: If you experience digestive problems, low energy, anxiety, poor stress tolerance, or stubborn weight gain, you’re likely not producing enough SCFAs. These symptoms often overlap with conditions like metabolic syndrome, inflammatory bowel disease, and neurodegenerative diseases.
Q: How do you increase butyrate production naturally?
A: To boost butyrate, you need to feed the gut bacteria that make it. First heal your gut by focusing on easy-to-digest carbs like fruit and white rice. Then, start slowly adding fermentable fibers like resistant starch (found in cooked-and-cooled potatoes and green bananas) and inulin-rich vegetables (like garlic and onions). Cutting out vegetable oils and processed foods is also key to stop disrupting your gut’s microbial balance.
Q: How fast can butyrate production increase?
A: Changes begin within days of dietary shifts, but full restoration of microbial diversity and L-cell function can take weeks to months.
Q: What if you don’t tolerate fiber at all?
A: That’s a sign your gut terrain needs more repair. Start with broth, peeled fruit, and gentle carbs, then gradually work up.
- 1 Signal Transduction and Targeted Therapy, Volume 9, Article Number 234 (2024)
- 2 Int J Obes Relat Metab Disord. 2001 Jun;25(6):781-92
- 3 Adv Nutr. 2018 Feb 9;9(1):21-29
- 4 Pharmacological Research, Volume 160, October 2020, 105174
- 5 Short-Chain Fatty Acids Influence the Gut-Brain Connection by Dr. Joseph Mercola
The Real Reason Your Arteries, Kidneys, and Bones Age Too Fast
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/01/28/phosphate-additives-health-risks.aspx
Analysis by Dr. Joseph Mercola January 28, 2026
Story at-a-glance
- Modern diets hide excessive phosphate additives in ultraprocessed foods, which are absorbed rapidly and efficiently, disrupting natural mineral balance and overwhelming organs far more severely than refined sugar
- Industrial phosphate additives enhance texture, flavor, and shelf life, increasing total intake by 40% or more compared to natural sources, leading to widespread hidden overconsumption
- Chronic phosphate overload hardens arteries, stresses kidneys, elevates blood pressure, and accelerates aging, even when blood tests appear normal or phosphate levels stay within conventional ranges
- Elevated phosphate triggers excess fibroblast growth factor-23 (FGF-23), harming the heart, hormones, and metabolism, while weakening bones and increasing fracture risk through calcium imbalance
- Avoiding ultraprocessed foods and choosing whole, natural ingredients lowers phosphate load, improves cardiovascular and kidney function, restores mineral balance, and promotes long-term health and vitality
Most people have learned, one way or another, to be cautious about refined sugar. They know it drives insulin resistance, weight gain, inflammation, and fatty liver disease. They also know fructose is especially dangerous when separated from the fiber and nutrients found in whole fruit. Refined sugar has become a known villain because it’s obvious and measurable and tied to cravings we recognize immediately.
But the modern diet contains something far more elusive, a compound that quietly weaves itself through the food supply and affects the body in deeper, more systemic ways than people realize. That compound is phosphate — specifically, the industrial phosphate additives added to processed foods.
The challenge is that added phosphate doesn’t register in the mind the way sugar does. It doesn’t taste sweet, spike cravings, or create the obvious sensation of “I probably shouldn’t be eating this.”
And because manufacturers aren’t required to list the amount of inorganic phosphate, only the ingredient name, consumers never know how much phosphate they’re ingesting. They also don’t know how it behaves once it enters the bloodstream, or how dramatically it differs from the natural phosphorus found in real whole foods.
How Processing Changed the Way Humans Encounter Phosphorus
For most of human history, dietary phosphorus arrived through traditional foods like meat, fish, eggs, dairy, nuts, seeds, and plants. In these forms, phosphorus is absorbed slowly and incompletely.1 Plant sources often bind it in phytate, which humans don’t digest efficiently. As a result, your body only absorbs around 60% of the phosphate found in real, whole foods.2
• Animal foods contain bioavailable phosphorus — However, the presence of fat, protein, and other minerals slows the rate at which it appears in the bloodstream. This slow, steady pattern mirrors the body’s natural design and allows the kidneys, bones, and hormones to maintain equilibrium without effort.
• The industrial food system changed the phosphorus dynamic almost overnight — Manufacturers discovered that phosphate additives were incredibly useful for preserving moisture, improving texture, adjusting acidity, stabilizing mixtures, and extending shelf life.3 They injected these additives into deli meats, marinated chicken, processed cheeses, canned soups, protein drinks, powdered creamers, and nearly every cola on the market.4
In fact, research shows that if you eat a diet that’s mainly comprised of ultraprocessed ingredients, your phosphate intake goes up by 41% above the normal range.5
• Modern humans routinely absorb two or three times more phosphate than their bodies were built to handle — Again, phosphate is hidden, and it also dissolves rapidly and is absorbed with near-perfect efficiency. This unnatural speed and completeness of absorption overwhelm the regulatory systems designed to maintain mineral balance. Eventually, health problems arise.
What Excess Phosphate Does to Your Arteries
The blood vessels are one of the first places phosphate begins to exert its effects. When phosphate levels rise too often, the arteries respond by absorbing calcium into their walls, forming microscopic deposits that grow over time. This process is called vascular calcification, and it turns soft, flexible blood vessels into stiffer, more rigid tubes.6
• Your heart suffers as a result from excess phosphate intake — It needs to work harder to push blood through the vessels; as a result, blood pressure rises, and the risk of heart attack and stroke increases long before a person notices anything is wrong.
According to a 2024 study, high serum phosphate levels increase your risk for cardiovascular death by as much as 44%. The same increased odds are also seen with coronary atherosclerosis.7
• Testing for phosphate levels can be hard — The most troubling part is that these changes can occur even when phosphate levels remain within the “normal” range on a blood test. Clinical norms are based on overt deficiency and kidney disease thresholds, not on the subtle long-term effects of chronic overload. As explained in one study, diagnosis remains to be a complicated matter due to the presence of various hormones, minerals, and cofactors that influence serum phosphate levels.8
• Excess phosphate ages your body faster — A diet high in phosphate additives can push the body into a state of accelerated aging without ever tripping a diagnostic alarm. This is why phosphate overload is so dangerous — it leaves almost no trace until the damage is already advanced.
How does high phosphate intake cause advanced aging? While there’s no solid evidence yet, researchers theorize that it creates cytotoxic effects in multiple organs. In addition, apoptosis is triggered, causing unwanted cell death, which accelerates aging.9
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The Hidden Burden on the Kidneys
Your kidneys are your body’s primary phosphate regulators. Their job is to remove excess phosphate from the blood and maintain stable levels throughout the day through a complex interaction with other organs such as your intestines, bones, and several endocrine factors.10 But kidneys evolved under conditions in which phosphorus arrived slowly, bundled inside complex foods. The sudden, repeated surges created by phosphate additives place a burden on them they were never meant to carry.
• Excess phosphate weakens kidneys over time — This constant strain can impair filtration, contribute to kidney tissue damage, and increase the risk of chronic kidney disease11 even in individuals who have never had high blood sugar, high blood pressure, or any other classic risk factor.
• The damage slowly creeps up on you — Phosphate overload has quietly become one of the most under-recognized kidney stressors in the modern diet. In fact, the American Kidney Fund classifies it as a symptom, rather than a cause of kidney damage.12
And because the early stages of kidney dysfunction are nearly impossible to feel,13 many people don’t realize the connection between their food choices and their kidney health until they are already experiencing measurable decline.
• Processed beverages harm your kidneys — In particular, cola consumption has been repeatedly linked to increased kidney risk. Even diet colas — those with zero sugar — deliver phosphoric acid directly into the bloodstream, creating a phosphate load similar to what occurs when someone consumes fast food or processed meats.
The lack of calories does nothing to protect the kidneys. In fact, many people unknowingly consume more phosphate after switching to diet soda, believing they have made a healthier choice.
A Hormonal Disturbance Few People Have Heard Of
When phosphate rises beyond what the kidneys can eliminate easily, the bones step in by releasing a hormone called fibroblast growth factor-23 (FGF-23).14 Its purpose is protective — it tells the kidneys to excrete more phosphate and helps prevent dangerously high levels from circulating in the blood.15
• When FGF-23 stays chronically elevated, it becomes harmful in its own right — Research links high FGF-23 to left ventricular hypertrophy, vascular dysfunction, and disordered mineral metabolism.16 It’s also been associated with other conditions, such as end-stage kidney disease, cardiovascular mortality, and all-cause mortality.17
What makes this finding important is that FGF-23 reacts primarily to dietary phosphate, especially phosphate additives. People who eat mostly whole foods have dramatically lower levels.18 However, those who regularly consume processed foods, frozen meals, convenience meats, and sodas often have chronically elevated FGF-23 without knowing it, even if they’re generally healthy.19
This chronic elevation acts as an internal stress signal, a sign that the body is constantly fighting to keep up with an unnatural mineral load.
• Testing for FGF-23 isn’t mainstream — Most doctors never test for FGF-23, and most patients never hear the term. Yet it may be one of the most important biomarkers of long-term health in a world saturated with processed food.20
The Surprising Impact on Bone Health
People often associate phosphate with bone strength because of its role in bone formation, but the relationship becomes distorted when intake is excessive. Bones rely on a careful balance between calcium and phosphate, and when phosphate intake rises too high, the body pulls minerals from the skeleton to compensate. This imbalance can contribute to lower bone density and a greater risk of fractures over time.21
• Soda consumption weakens your bones — Studies consistently show that heavy cola consumption is associated with weaker bones, especially in women.22 Again, this effect appears even with diet colas, confirming that it’s not sugar — but phosphoric acid — that drives the mineral imbalance.23 Over decades, this cumulative stress weakens the skeleton in ways people rarely associate with their beverage choices.
Colas sit at the center of the phosphate problem not just because of sugar, but because of their phosphate content. The tangy, biting flavor people recognize comes directly from phosphoric acid, one of the most absorbable forms available. A single soda can deliver a phosphate load equivalent to an entire day’s worth of natural phosphorus from whole foods. And because sodas are consumed quickly and often without food, the impact is even more pronounced.
• This creates a perfect storm — Sugar damages the liver and metabolism, while phosphate damages the heart, kidneys, and bones. Diet soda removes one of these threats but leaves the other fully intact. Many people who avoid sugar still harm their vascular and kidney health every day through phosphate exposure alone.
Why This Problem Is So Invisible
One reason phosphate overload has gone unnoticed for so long is that it doesn’t trigger immediate symptoms. There is no energy crash, no digestive discomfort, no jittery feeling.24 Unlike sugar or caffeine, you can’t feel phosphate as it enters your bloodstream. You only feel it years later when your blood pressure is higher, your kidney function is lower, or your arteries show signs of calcification.
• Phosphate is rarely listed on food labels — Nutrition facts panels almost never list the amount of phosphorus or phosphate in a product. The only clues appear in the ingredient list as chemicals with the term “phos” in their names.
Some foods contain five or six different phosphate additives, each contributing to the overall load. Most consumers have no idea how to interpret these words, and many assume they are harmless because they appear in foods marketed as healthy or low-fat. As noted in one study:25
“The USDA [United States Department of Agriculture] Branded Foods Products Database (BFPD) contains label information about food and beverage content for foods sold in the U.S. Picard et al. reported that of the 3,466 foods in the BFPD, 52% contained inorganic and organic phosphate additives, but only a small fraction listed phosphate content on the label.”
• Inorganic phosphate is hidden everywhere — Even people who avoid junk food often consume phosphate through items like flavored yogurts, nut milks, deli meats, vegan cheeses, and protein powders. The modern food system has found a way to slip phosphate into nearly every category, and the cumulative effect is what accelerates aging.
The Path Back to Balance
Reducing phosphate overload doesn’t require elaborate strategies or precise counting. It simply requires shifting more of the diet toward real, whole foods and away from products whose ingredient lists sound like chemistry sets.
• Dietary suggestions — Look for organic fresh meats instead of injected or marinated meats. Other changes you can make include choosing grass fed whole dairy instead of processed cheeses or creamers, and water or tea instead of sodas. In the video above, bioenergetics expert Georgi Dinkov provides some recommendations, specifically when it comes to choosing cuts of meat.
• Health improvements can be rapid — When people shift away from ultraprocessed food (especially sodas), their kidneys begin to recover, their blood pressure often improves, and their arteries experience less mineral stress. FGF-23 levels also fall. The body moves closer to the mineral environment it was designed to thrive in.
• Understanding phosphate isn’t about fear — Ultimately, it’s about awareness. Once people know where it hides and how it behaves, they naturally begin choosing foods that support long-term health rather than undermine it.
The Final Word on Phosphate
Phosphate overload is one of the most significant, least-discussed drivers of premature aging in the modern diet. Unlike sugar, which people can taste and measure and resist, phosphate sneaks in through everyday foods people never think to question. It stiffens arteries, stresses kidneys, disrupts hormones, weakens bones, and raises blood pressure — all quietly, without obvious symptoms.
Once you recognize this, your relationship with food changes. You start noticing the patterns. You start seeing the “phos” ingredients for what they are. And you gain the ability to protect your long-term health in a way most people never will.
Frequently Asked Questions (FAQs) About Phosphate on Bone Health
Q: What makes phosphate additives more harmful than natural phosphorus found in whole foods?
A: Industrial phosphate additives are absorbed almost completely and rapidly, unlike natural phosphorus from meats, plants, or dairy, which is digested slowly. This rapid absorption overwhelms the body’s natural mineral regulation systems, leading to long-term harm.
Q: How does excess phosphate affect the heart and arteries?
A: Chronic phosphate overload causes calcium deposits to form in artery walls (vascular calcification), stiffening blood vessels and increasing blood pressure. Research links high phosphate levels to a 44% higher risk of cardiovascular death and accelerated aging.
Q: In what ways does phosphate harm the kidneys and bones?
A: Phosphate surges strain the kidneys’ filtration capacity, contributing to chronic kidney disease, even in healthy individuals. High phosphate also disrupts calcium balance, weakening bones and increasing fracture risk, especially among heavy soda drinkers.
Q: Why is phosphate overload so hard to detect?
A: Phosphate doesn’t produce immediate symptoms and isn’t fully measured on standard nutrition labels or blood tests. Most ultraprocessed foods and drinks contain hidden phosphate under ingredients with “phos” in their names.
Q: How can people reduce phosphate intake and protect their health?
A: Choose whole, unprocessed foods — fresh meats, whole dairy, and water or tea instead of sodas. Reducing phosphate-rich processed foods lowers blood pressure, supports kidney recovery, improves mineral balance, and slows premature aging.
- 1 NIH, Phosphorus
- 2 Semin Nephrol. 2013 Mar;33(2):180–190
- 3, 22, 25 Nutrients. 2023 Aug 9;15(16):3510
- 4, 5 J Ren Nutr. 2013 Feb 8;23(4):265–270.e2
- 6 Circ Res. 2011 Sep 2;109(6):697-711
- 7 Arterioscler Thromb Vasc Biol. 2024 Mar;44(3):584-602
- 8 Nutrients 2023, 15(5)
- 9 FASEB J. 2010 Sep;24(9):35623571
- 10 Vitamins and Hormones Volume 120, 2022, Pages 47-78
- 11 National Kidney Foundation, Kidney Failure Risk Factor: Serum Phosphorus
- 12 American Kidney Fund, High Phosphorus (Hyperphosphatemia)
- 13 Cleveland Clinic, Kidney Failure
- 14 Int. J. Mol. Sci. 2020, 21(22), 8810
- 15 Kidney International (2009) 76 (Suppl 114), S34–S42
- 16 J. Vasc. Dis. 2025, 4(4), 39
- 17 Hypertension. 2020 Jul;76(1):236-243
- 18 Physiol Rev. 2012 Jan;92(1):131-155
- 19 J Ren Nutr. 2014 Jan;24(1):10.1053/j.jrn.2013.09.003
- 20 J Nephrol. 2020 Mar 4;33(3):509-527
- 21 Oregon State University, Bone Health in Brief
- 23 Nutr J 20, 41 (2021)
- 24 Nutrients. 2023 Feb 28;15(5):1236
Unraveling the Mysteries of Thyroid Health
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/23/unraveling-mysteries-thyroid-health.aspx
Analysis by Dr. Joseph Mercola March 23, 2025
STORY AT-A-GLANCE
- Thyroid health is intricately linked to iodine intake, genetics and overall metabolic balance, challenging the conventional “empty tank” model of treatment
- Autoimmune thyroid disease has a unique mechanism distinct from other autoimmune conditions, primarily driven by your body’s reaction to iodine
- Accurate thyroid testing requires adherence to specific guidelines, including timing, fasting, biotin avoidance, medication timing and consideration of the menstrual cycle
- Gut health, fatty liver and other hormonal imbalances, such as estrogen dominance, are closely intertwined with thyroid function
- A holistic approach, including dietary adjustments, lifestyle changes and careful consideration before relying on hormone therapies, is necessary for optimizing thyroid health
Dr. Alan Christianson is a leading expert in the field of thyroid disorders, and his insights on this topic are invaluable. In fact, his expertise is so insightful that I’ve invited him to be the lead consultant for our upcoming health coaching program. This program will offer comprehensive protocols and practical steps for various health concerns, with a strong emphasis on thyroid health. I want to ensure the information we provide is top-notch, so we’re taking our time to get it just right.
In my previous interview with Christianson, we explored information about excess iodine and thyroid health. These principles are fundamental and will remain relevant for years to come. Before speaking with him, I felt lost when it came to understanding thyroid issues. I knew the conventional approaches, both in conventional and alternative medicine, were missing something important.
They didn’t address the root causes of thyroid problems. It became clear to me that the solutions were much simpler than I had imagined.
I even applied Christianson’s advice to my own health. At the time of our first interview, I was taking a significant dose of thyroid medication, including desiccated thyroid and Cytomel. I was operating under the common misconception that my thyroid issues stemmed from low thyroid hormone production. I was relying on outdated lab tests like thyroid-stimulating hormone (TSH) and basal body temperature.
After understanding the true nature of thyroid autoimmunity, I was able to completely stop all thyroid medications within two weeks. My basal body temperatures are now completely normal 98.4 to 98.8. All my thyroid hormones are normal but my TSH is elevated, which is what you’d expect because my body is now producing its own thyroid hormone and that requires TSH to activate it. It should remain elevated for the next few months.
I’m incredibly grateful for Christianson’s expertise. So, let’s recap some of the key points from our latest discussion. Thyroid problems are incredibly common, and autoimmune thyroid disease is the most prevalent autoimmune condition.
Sadly, thyroid cancers are also on the rise. Conventional and even many natural approaches often assume the problem is simply a lack of thyroid hormone. However, this “empty tank” model doesn’t address the underlying cause. Christianson revealed that thyroid disease is closely linked to an individual’s genetic tolerance to iodine. By managing iodine intake within a safe range, many people actually reverse their thyroid issues.
The Unique Nature of Thyroid Autoimmunity
One of the biggest misconceptions I had before interviewing Christianson was that all autoimmune diseases have the same origin. This is simply not true.
• Thyroid autoimmunity is driven by a different mechanism — While many autoimmune conditions, like rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease, are often linked to a leaky gut, thyroid autoimmunity has a different mechanism. In these other conditions, proteins leak through your damaged gut lining, triggering an immune response.
• The key difference lies in your body’s interaction with iodine — We need iodine for proper thyroid function, but our bodies are adapted to different levels of intake based on our ancestry. People with coastal ancestry generally tolerate higher amounts of iodine, while those with inland ancestry thrive on lower levels. Many people today, even those with inland ancestry, consume too much iodine.
This excess iodine matches the thyroid globulin and distorts the molecule to something your body is not typically expecting. This new protein structure then creates antibodies against it, causing your immune system to mistakenly attack the thyroid tissue.
• The good news is that this process requires an ongoing trigger — By reducing excessive iodine intake, you break this cycle. Your immune system then recognizes that the thyroid is not the enemy, and the autoimmune process often reverses. This reversal often happens surprisingly quickly, within a few months, unlike many other autoimmune conditions that take years to improve. In my own case, I saw significant improvement very rapidly.
While antibody levels are an indicator of thyroid autoimmunity and useful for screening, they don’t always tell the whole story. Some people with autoimmune thyroid disease never have measurable antibodies, while others with mildly elevated antibodies have no thyroid problems at all. Therefore, focusing solely on antibody levels isn’t always the most accurate approach.
The Thyroid-Gut Connection and Other Autoimmune Links
A fascinating connection exists between thyroid disease and certain gut issues. A condition known as thyrogastric syndrome, also called atrophic gastritis or autoimmune gastritis, is found in a significant percentage of people with autoimmune thyroid disease.
• It wreaks havoc on your stomach cells — This condition involves your immune system attacking your stomach’s parietal cells, which leads to poor absorption of important nutrients like iron, B12 and zinc.
• There’s a genetic link to autoimmunity — While this connection isn’t directly related to iodine intake, it suggests a broader genetic predisposition to autoimmunity. It seems that some genes are more specific to thyroid autoimmunity, while others are associated with a general increased risk of various autoimmune conditions. This could explain why people with thyroid disease are more likely to experience other autoimmune problems as well.
• Another common co-occurrence is fatty liver — This is now often referred to as metabolic dysfunction-associated fatty liver disease (MAFLD). Thyroid hormones play a role in regulating liver function, metabolism, body weight, and blood sugar. Therefore, hypothyroidism significantly contributes to the development of fatty liver.
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Understanding Fatty Liver and Metabolic Fuel
My understanding of fatty liver has evolved over time. I previously believed it was primarily caused by an excess of omega-6 fats like linoleic acid (LA). While these fats certainly play a role, Christianson offered a more nuanced explanation.
• Fatty liver is fundamentally a problem of fuel balance within your body — According to Christianson, various fuel molecules, including carbohydrates, fats (like LA), and even alcohol, are processed into acetyl-CoA. When your body exceeds its capacity to use these fuel molecules, it shifts into storage mode.
• Where the body stores this excess fuel varies from person to person — Some people store it primarily as subcutaneous fat, while others accumulate it in their liver. The liver has two main storage compartments: triglycerides and glycogen.
A healthy balance between these two is essential for proper liver function. In fatty liver, the proportion of triglycerides becomes excessively high, creating a vicious cycle that makes it difficult for the liver to reverse the process.
• This explanation helps to understand why alcohol also contributes to fatty liver — Alcohol, like excess fats and carbohydrates, is ultimately converted into acetyl-CoA. Therefore, both excessive consumption of certain fats and alcohol overload your liver’s capacity to process fuel, leading to fat accumulation. This also explains why some people are more susceptible to fatty liver than others.
The Role of Gut Bacteria and Short-Chain Fatty Acids
Our conversation also touched on the crucial role of gut bacteria and short-chain fatty acids, particularly butyrate. Butyrate is often touted as the primary fuel source for colonocytes, the cells lining your colon. However, recent research has revealed a more complex picture.
• Butyrate only makes up about 20% of the short-chain fatty acids produced by gut bacteria — The majority, around 60%, is acetate, a precursor to acetyl-CoA. Propionate makes up the remaining 20%. This raises the question of whether the focus on butyrate has been misplaced. It’s possible that the initial research on short-chain fatty acids created a bias toward butyrate, overlooking the important roles of acetate and propionate.
• Clinically, butyrate is often administered in ways that are ineffective — Oral butyrate is poorly absorbed, and while rectal administration is more effective locally, it doesn’t reach the entire colon.
• A novel, time-release delivery system that effectively delivers nutrients — I’ve developed a novel time-release delivery system that effectively delivers substances, including beneficial bacteria and short-chain fatty acids, directly to the colon. This technology allows us to bypass the stomach’s harsh acidic environment and the small intestine, ensuring targeted delivery to the colon where these substances have the greatest impact.
This new technology opens the door for new research into the optimal ratios of short-chain fatty acids. I plan to explore different combinations, including a formulation with the natural ratio of 60% acetate, 20% propionate and 20% butyrate, to see which approach is most effective.
The Thyroid-Estrogen Connection and the Importance of Prolactin
We also discussed the intricate relationship between thyroid hormones and estrogen. I’ve long believed that testing estrogen levels in the blood is misleading, as estrogen is primarily stored in tissues, not your bloodstream. This leads to inaccurate information and harmful treatment decisions, especially for post-menopausal women.
• Women are incorrectly treated for low estrogen — Christianson notes that women are often treated for low estrogen based on serum levels, even if they are not experiencing symptoms. This approach, based on flawed data, is unlikely to produce positive outcomes. The problem is often not low estrogen, but rather estrogen dominance, which is indicated by elevated prolactin levels.
• Taking exogenous thyroid hormones actually raises prolactin levels — Christianson says that this is due to a feedback loop between the hypothalamus, pituitary gland and thyroid. The same signal that tells your pituitary to produce thyroid hormone also stimulates prolactin production.
This explains why my own prolactin levels increased when I was taking thyroid medication. This information highlights the complexity of hormonal interactions within your body.
• Factors that influence prolactin levels — This led to a discussion of how various factors influence prolactin levels, including hormone replacement therapy, oral contraceptives, xenoestrogens and reactions to thyroid medications.
This highlights the importance of considering the context when interpreting prolactin results. My own experience with progesterone lowering my prolactin levels suggests a clear estrogen connection. The good news is that prolactin testing is relatively inexpensive and accessible, making it a valuable tool for monitoring hormonal balance.
• Further discussions on thyroid health and its implications on metabolic health — As our conversation continued, we further discussed the complexities of thyroid health, the connection between thyroid and other hormones and broader implications for metabolic health.
We also cover information about accurate thyroid testing. As Christianson explained, your body has intricate mechanisms for regulating hormone responses. It adjusts the number and activity of hormone receptors to maintain balance.
However, when you introduce external hormones, you disrupt these finely tuned systems. This is where the wisdom of nature comes into play. When do we support the body’s natural processes, and when do we intervene?
In cases of complete gland removal, like thyroidectomy, intervention is necessary. However, many people have abnormal lab results without a true inability to compensate. It’s important to distinguish between compensation and true dysfunction.
The Five Golden Rules for Accurate Thyroid Testing
Christianson shared five essential rules for accurate thyroid lab testing. These rules are key for obtaining consistent and reliable results but are often overlooked, leading to inconsistent and confusing lab results. Implementing these guidelines significantly improves the accuracy and reliability of thyroid testing.
1. Time of day — Thyroid hormone levels fluctuate throughout the day. The most consistent results are obtained between 6:00 a.m. and 9:00 a.m. Blood spot testing makes it easier to adhere to this timing.
2. Fasting — Fasting status significantly impacts thyroid hormone levels. It’s important to fast before testing.
3. Biotin — Supplemental biotin interfere with lab analyses. It’s recommended to avoid biotin supplements for three days before testing. Surprisingly, this effect is primarily seen with supplemental, not dietary, biotin.
4. Thyroid medications — If you take thyroid medication, take your lab tests before taking your medication that day. Testing shortly after taking medication will produce inaccurate results, especially for T3 and T4 levels.
5. Menstrual cycle — For menstruating women, thyroid hormone levels vary throughout the cycle. The most consistent results are obtained during days one to nine and 20 to 28 of the cycle. Testing during days 10 to 19 produces inconsistent results.
Rethinking Thyroid Screening and the Value of Clinical History
Our discussion then turned to the value of conventional thyroid testing, specifically TSH. I expressed my evolving view that TSH is not an effective screening tool. Christianson agreed, emphasizing the importance of considering treatment options.
• Synthetic hormones are not the only solution — In conventional medicine, the primary treatment for thyroid issues is synthetic thyroid medication. However, with the powerful influence of diet and lifestyle, other approaches are available.
• The importance of antibody testing — Christianson emphasized the value of antibody testing as a screening tool, as it’s more predictive of symptoms than TSH. While some individuals with overt hypothyroidism have negative antibodies, antibody testing still provides valuable information. It’s important to remember that normal antibody levels do not necessarily rule out thyroid disease.
This perspective aligns with the approach of clinicians like Broda Barnes, who effectively identified thyroid issues based on clinical history and symptoms, even before the advent of modern thyroid testing. It’s important to remember that while thyroid hormone levels are important, the correlation between those levels and symptoms is much looser than most people realize. In fact, many people with significantly abnormal thyroid hormone levels are surprisingly asymptomatic.
Dietary Considerations for Thyroid Health
We also discussed the importance of diet in thyroid health. I mentioned my red, green and yellow food system from my book, “Your Guide to Cellular Health,” and how it differs from Christianson’s approach in “The Thyroid Reset Diet.” While my system focuses on general metabolic health, Christianson’s is specifically designed for individuals with autoimmune thyroid disease.
• Nuts are not a health food — I expressed concern about some of the “green” foods in Christianson’s diet, such as seasoned nuts. While nuts can be healthy, they’re high in LA and are best consumed in moderation, especially for those with high levels of stored linoleic acid. I also noted that my own food system is not suitable for thyroid health due to the inclusion of high-iodine foods.
Christianson explained that his dietary recommendations are not intended as a universal diet for everyone but rather as a specific tool for a specific situation — autoimmune thyroid disease.
• Modern practices contaminate healthy food sources — He also acknowledged the contamination of otherwise healthy foods, such as raw milk, with iodine due to modern agricultural practices.
The dairy industry commonly uses iodine-based disinfectants to clean teats and equipment. Although a hot water rinse helps mitigate iodine residues, the pervasive use of iodine teat dips introduces an additional, often unnoticed source of iodine into dairy products.
Diabetes and Metabolic Health
We also discussed diabetes, another major endocrine issue. Christianson described diabetes as a problem of fuel partitioning, where excess fuel accumulates in the bloodstream. He cited research showing that even small amounts of fat accumulation in the pancreas significantly impacts diabetes development.
• Glucose as your body’s preferred fuel source — I shared my understanding, influenced by the work of Ray Peat, that glucose is the preferred fuel for most cells, although some cells, like colonocytes and heart cells, primarily use fatty acids.
I also emphasized the dangers of overly restrictive low-carb diets, which trigger the release of stress hormones like cortisol. Christianson agreed, explaining that your body requires glucose and will produce it through cortisol-mediated muscle breakdown if dietary intake is insufficient.
• The ideal daily glucose intake — We agreed that 200 to 250 grams is a reasonable range for most individuals. We also discussed the dangers of excessive cortisol production, whether from dietary restriction or emotional stress, and its impact on sleep and overall health.
• The parathyroid gland — This tiny gland, nestled near your thyroid, plays a role in maintaining calcium balance in your bloodstream. Christianson argues that even slightly elevated calcium levels, especially if recurring, warrant investigation, particularly if accompanied by symptoms like fatigue, anxiety, or joint pain.
He emphasizes that conventionally accepted reference ranges for calcium are overly broad. Further, conventional medicine is limited in addressing parathyroid issues. Surgery is typically the only offered solution and there’s a lack of focus on root causes.
• Hormone replacement therapy — Finally, we touched on hormone replacement therapy, with both of us expressing caution regarding long-term use. Christianson emphasized the importance of considering both the benefits and risks of any intervention, particularly when it involves manipulating hormone levels. He stressed the need for strong evidence of net benefit before recommending such interventions.
Prioritizing Outcomes and Minimizing Harm in Thyroid Health
This in-depth discussion with Christianson illuminates the complex web of factors influencing thyroid health. By understanding the unique nature of thyroid autoimmunity, the importance of accurate testing and the interconnectedness of various bodily systems, we move beyond simplistic solutions and embrace a more holistic and effective approach to thyroid care.
This conversation emphasizes the importance of informed decision-making, prioritizing long-term health outcomes and supporting your body’s innate capacity for healing. By focusing on supporting your body’s natural processes and minimizing harm, you achieve true and lasting improvements in health.
Frequently Asked Questions (FAQs) About Thyroid Health
Q: How does iodine intake affect thyroid health?
A: Iodine plays a crucial role in thyroid function, but excessive intake triggers autoimmune thyroid disease, especially in individuals with lower genetic tolerance. Managing iodine within a safe range helps reverse thyroid issues.
Q: What are the key factors for accurate thyroid testing?
A: Accurate thyroid testing requires:
•Testing between 6:00 a.m. and 9:00 a.m.
•Fasting beforehand.
•Avoiding biotin supplements for three days.
•Taking tests before thyroid medication (if applicable).
•Timing tests with the menstrual cycle (days 1 to 9 or 20 to 28).
Q: How is thyroid autoimmunity different from other autoimmune diseases?
A: Unlike other autoimmune conditions linked to leaky gut, thyroid autoimmunity is primarily driven by an immune response to excessive iodine, which alters thyroid proteins and triggers an attack on thyroid tissue. Reducing iodine intake often reverses the condition.
Q: What is the connection between thyroid health and metabolism?
A: Thyroid function is closely linked to gut health, fatty liver, and metabolic balance. Hypothyroidism contributes to fatty liver disease, while excess fuel intake (from fats, carbs, or alcohol) overwhelms the liver’s storage capacity, leading to metabolic dysfunction.
Q: Why is a holistic approach essential for thyroid health?
A: A comprehensive approach, including dietary adjustments, lifestyle changes, and avoiding unnecessary hormone therapy, is key for optimizing thyroid function. Many thyroid conditions can be improved by addressing root causes rather than relying solely on medication.
New Year, Real You — The Secret to Lasting Change and a Happier Metabolism
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/01/14/sustainable-weight-loss.aspx
Analysis by Ashley Armstrong January 14, 2025
STORY AT-A-GLANCE
- Quick-fix diets often fail to address the root causes of weight struggles, leading to frustration and rebound weight gain
- Preparing your metabolism before fat loss ensures lasting results and prevents unnecessary setbacks
- A maintenance phase boosts metabolism, repairs your relationship with food, and sets the stage for future success
- A healthier metabolism allows you to eat more while maintaining your weight and makes fat loss easier
- Combine strength training and daily movement to build lean muscle and support metabolic health
Is “New Year, New You” on your mind? Let’s talk about sustainable change. We’ve all been there — January rolls around and suddenly our social media feeds are flooded with miracle diets and quick-fix weight loss solutions. That fresh-start energy is powerful, and there’s absolutely nothing wrong with wanting to make positive changes to your health and body composition. In fact, it’s completely natural and admirable to set new goals for yourself.
But here’s the real talk: Those trending “rapid weight loss” programs that promise to transform you in weeks? They’re often like using a Band-Aid to fix a leaky pipe — it might look good for a moment, but it’s not addressing what’s really going on underneath.
Think about it this way: Your body is like a sophisticated engine. Before you start pushing it to perform differently, wouldn’t it make sense to first ensure it’s running at its best? This means focusing on foundations first — optimizing your metabolic health and building sustainable daily habits. It’s like tuning up your car before a long road trip, rather than just hoping for the best.
The truth is, successful, lasting weight loss isn’t about quick fixes or extreme measures. It’s about creating a framework that supports your goals long-term. After all, what’s more frustrating than losing weight only to find yourself back at square one (or even further back) a few months later?
If you’re thinking about starting a weight loss journey this year, remember: There’s no shame in wanting to change your body composition. The key is doing it intelligently, with intention, and with your long-term well-being in mind. Ready to make real, lasting changes? Let’s start by building the right foundation for your success.
Do This Before Fat Loss
In 2024, I went through my own fat loss journey, dropping 17 pounds. But here’s what matters: Over four months later, I’m maintaining those results while eating a generous 2,600 calories daily (and still slowly increasing my calories). For reference, I am 5’, 4.5” and now weigh ~130 lbs.
No rebound, no constant hunger, just sustainable results. But I’ll let you in on something crucial — the real work happened before I even started thinking about fat loss. You see, most people are stuck in a frustrating cycle: jumping from one restrictive diet to another, hoping something will finally stick. It’s like trying to sprint on an empty tank — it just doesn’t work.
The game-changer? Spending most of your year in what we call a “maintenance phase,” focusing on optimizing your metabolic health. Think about it — you can’t effectively start a fat loss phase when you’re already eating minimal calories. Your body needs a strong foundation first.
This is where a “Reset” phase comes in — a 2 to 12 month period where you gradually increase your calorie intake and work on improving your day to day habits in order to boost your metabolism.
It might sound counterintuitive, but by taking the time to improve your metabolic rate, something amazing happens: your body becomes more efficient at burning calories. This means you can eat more food while maintaining your weight. (Yes, really!)
When you finally transition into a fat loss phase after this metabolic preparation, the process becomes strategic and efficient — no more endless struggling or metabolic damage that often comes with traditional dieting approaches.
The key takeaway? Before jumping into another diet, give your body time to build a stronger metabolic foundation. Your future self will thank you for it.
Why Metabolism Matters
A better metabolic rate means your body will function better systemically, you will have more energy, you will think better, sleep better, and function better overall. A better metabolic rate also makes fat loss a whole lot easier.
Following the Law of Thermodynamics (energy cannot be created or destroyed) — you must be in a caloric deficit to lose weight (calories in < calories out). Yes, there is of course nuance as there are MANY factors that impact the “Calories Out” side of the equation, but we must create an energy deficit which depends on a number of variables. The balance between your energy intake and energy expenditure overtime will determine whether you maintain, lose or gain weight.
Your energy intake (calories in) equates to all of the calories you consume from food and liquids. Your energy expenditure (your ‘calories out’) is the sum of:
1. Your basal metabolic rate (BMR), which refers to the energy required for your body to maintain basic function. This includes breathing, digesting food, pumping blood throughout the body, maintaining strong hair and nails, the generation of energy, etc.
This accounts for 65% to 70% of your total daily expenditure — making it the largest contribution to the energy expenditure equation. Increasing your metabolic rate is one of the best ways to make weight loss and maintenance more sustainable in the long run. You can increase your BMR and this is advantageous for weight loss!
2. Nonexercise activity thermogenesis — NEAT (body movements outside of planned exercise, like fidgeting, doing laundry, etc.). Calories burned from NEAT will vary A LOT. More active individuals (higher daily step counts) will burn more calories due to higher levels of NEAT. Dr. Levine has shown that NEAT can vary by up to 2,000 calories per day between two individuals of the same size!
3. Exercise, the energy your body uses for planned physical activity, whether that is strength training, playing sports or a cardio session. You actually don’t burn many calories during a strength training session — and the goal isn’t to burn calories. The goal is to elicit a muscular adaptation to then increase the amount of lean mass (muscle) you have, and thus increase your metabolism.
4. Thermic effect of food (TEF) — The amount of calories your body uses to digest the food you consume.
There’s been a lot of debate about the “calories in vs. calories out” model for weight loss, and for good reason. Dr. Fatima Cody Stanford, an obesity specialist and professor at Harvard Medical School, shared this powerful critique:
“This idea of ‘a calorie in and a calorie out’ when it comes to weight loss is not only antiquated, it’s just wrong,” says Dr. Fatima Cody Stanford, an obesity specialist and assistant professor of medicine and pediatrics at Harvard Medical School.
“The truth is that even careful calorie calculations don’t always yield uniform results. How your body burns calories depends on a number of factors, including the type of food you eat, your body’s metabolism, and even the type of organisms living in your gut. You can eat the exact same number of calories as someone else, yet have very different outcomes when it comes to your weight.”
She’s absolutely right — there’s nuance here! Factors like your metabolism, hormones, and even gut health all play a major role in how your body uses energy. The types of foods you eat can even influence how many calories your body burns.
But here’s the key takeaway: While energy balance isn’t as simple as “just eat less, move more,” it still does apply. Extra energy (calories) that your body doesn’t need doesn’t just disappear — it’s stored as fat. This is why understanding your metabolism is so important.
If your metabolism isn’t functioning optimally — due to poor habits, chronic dieting, or hormonal imbalances — your calorie-burning capacity will be significantly lower. And that means weight loss becomes much harder, even if you’re eating “healthy” foods.
So, what’s the solution? You have to meet your metabolism where it’s currently at. Instead of slashing calories or overtraining, focus on gradually improving your metabolic health over time. This patient, intentional approach helps your body adapt and become more efficient at burning energy, setting you up for sustainable success.
Food doesn’t just “poof” into thin air — it’s either used as energy, stored for later, or helps rebuild and repair your body. The key is to optimize how your body processes that energy, so you can feel great and achieve your goals without constant frustration.
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Understanding Your Metabolism — A Game-Changing Perspective
Picture this: You’re planning to drive cross-country. Would you start that journey with a car that’s barely running, or would you first make sure your engine is in top condition? When it comes to fat loss, your metabolism is that engine — and its condition makes all the difference. Let me paint you a picture with a real-world scenario:
Meet Anna. She’s maintaining her weight at 1,600 calories daily. To lose weight, she’d need to drop to ~1,200 calories — that’s less than what most children need! It’s like trying to run a marathon on an empty stomach.
Not only is it unsustainable, but it’s also setting yourself up for a cycle of restriction, binge eating, and frustration. Sound familiar? Now, let’s flip the script.
Instead of jumping straight into restriction, Anna decides to invest 3 to 6 months in boosting her metabolism. Through strategic changes in her lifestyle and nutrition (more on these amazing tricks coming up!), she gradually increases her maintenance calories to 2,300 per day. That’s right — she’s now maintaining her weight while eating 700 more calories daily!
Your maintenance calorie intake is not a set number, it is a range of calories. Below the bottom end of that range, you lose weight, above the top end of that range, you gain weight. But again, the cool thing is that you can shift that range up by improving your metabolism!
Here’s where it gets exciting: When Anna decides to start her fat loss journey from this higher maintenance calorie intake, she can eat at a much more reasonable calorie level. No more surviving on lettuce leaves and coffee! She can enjoy satisfying meals while still making progress toward her goals.
Think of it like upgrading your body’s engine. By improving how your metabolism and thyroid system function, you’re essentially turning your body into a more efficient calorie-burning machine. The result? When you do decide to lose fat, you can do it while eating more food, feeling more energized, and actually enjoying the process.
Remember: Your body is incredibly adaptable, but it needs time and patience. The journey from Point A to Point B isn’t a sprint — it’s a strategic process that sets you up for lasting success. Ready to learn how to make this transformation happen? Let’s dive into the exact steps you need to take.
Boosting Your Metabolism — Your Step-by-Step Guide
Now that you understand why improving your metabolism is so crucial, you’re probably wondering: “Okay, but how exactly do I do this?” Let’s break down the process of increasing your BMR (basal metabolic rate) — or in simpler terms, how to rev up your body’s natural calorie-burning engine.
What I’m about to share with you is a proven roadmap that has worked not just for me, but for countless others in our course, Rooted in Resilience.
Here’s the key: Think of these steps as building blocks. Just like you wouldn’t put the roof on a house before laying the foundation, each step builds upon the last. Master one before moving to the next — this isn’t a race, it’s about creating lasting change. Let me walk you through these five game-changing steps:
• Step 1: Break free from the quick-fix trap — Let’s talk about something we’ve all been tempted by — those alluring quick-fix diets that promise dramatic results overnight. You know the ones: “Cut all carbs and watch the pounds melt away!” But here’s what those flashy promises don’t tell you.
Sure, eliminating carbs might show you a lower number on the scale initially. But here’s the reality check: what you’re mostly losing is water weight from dropping stored glycogen, and sometimes even precious muscle mass (definitely not what we’re aiming for!). It’s like cleaning your house by shoving everything into a closet — it looks good temporarily, but you haven’t solved the real problem.
I’ve seen this pattern hundreds of times in our course. The story usually goes something like this: “I tried keto and lost weight quickly … but then I gained it all back, plus some extra pounds.” These aren’t isolated cases.
When you restrict entire food groups, you’re not just affecting your weight — you’re disrupting your hormones, slowing down your metabolism, and worst of all, setting yourself up for an exhausting cycle of restriction and binging.
Here’s a truth that might surprise you: Cutting carbs isn’t some magical key to fat loss. Yes, some people lose weight on low-carb diets, but that’s simply because they’re eating fewer calories overall — not because carbs are the enemy.
Your body is perfectly capable of burning fat while enjoying carbohydrates. In fact, a balanced approach that includes all macronutrients often leads to better, more sustainable results.
Remember this: Your body is smarter than any trending diet. Instead of looking for the next quick fix, let’s focus on what really works — building a stronger metabolism and creating healthy, sustainable habits that stick around long after the latest fad diet has faded away.
• Step 2: Know your numbers — they tell your story — You’ve heard the saying “what gets measured, gets managed,” right? Well, when it comes to improving your metabolism, this couldn’t be more true. Think of it like trying to follow a map without knowing your starting point — pretty tricky, right?
This is why your first crucial step is simple but powerful: Start tracking your weight and food intake. Consider this your metabolic GPS — it tells you exactly where you’re starting from and helps guide your journey forward. Why is this so important? Because without knowing your baseline:
◦You can’t accurately gauge your maintenance calorie needs
◦You won’t know if you’re making real progress or just seeing normal fluctuations
◦You might be eating far less (or more) than you think
◦You’ll miss important patterns in how your body responds to different foods and portions
The easiest way to get started? Download an app like Cronometer and begin logging your meals. Don’t worry about changing anything just yet — simply observe and record. Weigh yourself consistently (ideally first thing in the morning) and track these numbers too.
Remember: This isn’t about judgment or restriction — it’s about gathering information. Think of yourself as a scientist collecting data about your own body. This baseline data will become your roadmap for making informed decisions about your nutrition and metabolism going forward.
• Step 3: Become the chef of your metabolic success — Want to know one of the most powerful ways to boost your metabolism? It’s simpler than you might think: Start cooking your own meals. This isn’t just about saving money or knowing what’s in your food (though those are fantastic bonuses!) — it’s about giving your body the precise fuel it needs to fire on all cylinders.
Think of your metabolism like a high-performance engine. Sure, it might run on regular gasoline, but it performs best with premium fuel. When you cook your own meals, you’re in control of that fuel quality.
Restaurant meals and processed foods often come with a hidden metabolic cost: they’re typically loaded with both carbs and fats (think french fries — high carb and deep fried), rich in inflammatory PUFAs (processed vegetable oils), and surprisingly low in the micronutrients your body craves.
But here’s the good news: You don’t need to become a gourmet chef or never eat out again. Even cooking most of your meals at home (while still enjoying the occasional restaurant meal) can make a huge difference. Why? Because you’re:
◦Avoiding those sneaky preservatives, gums, and fillers that can wreak havoc on your gut health
◦Controlling your ingredients to support energy production
◦Choosing foods that help balance your hormones
◦Building a foundation for a stronger metabolism
Remember, every meal you cook is an investment in your metabolic health. Start simple, focus on whole foods, and watch how your body responds when you fuel it with care. Your metabolism will thank you!
• Step 4: Develop a well-rounded exercise and movement routine — Here’s the thing: you don’t need to go overboard with exercise to improve your metabolism, but staying active is essential. Humans are built to move! Regular activity isn’t just about burning calories — it supports a healthy metabolic response, helping your body function at its best.
Science backs this up. Studies show that people who move consistently throughout the day — not just during a quick workout — maintain better body composition and higher metabolic rates than those who are more sedentary.
In fact, sitting all day after a workout can cancel out some of the health benefits of that workout. Yup, even if you crushed it in the gym, being sedentary the rest of the day means your body isn’t reaping the full rewards, like improved fuel utilization. So, what’s the sweet spot?
◦ Strength train 2 to 3 times per week — Why? Muscle is the most metabolically active tissue in your body. Building and maintaining muscle helps boost your metabolism long-term.
◦ Aim for 8,000 to 12,000 steps per day — Think light walks, active breaks, or just incorporating more movement into your daily routine.
The goal is to blend intentional workouts with regular movement throughout the day. This balanced approach maximizes the benefits of exercise, promotes fat loss, and supports overall health — without the burnout of overtraining. Let’s keep it simple: Move more. Lift weights. Feel amazing. You’ve got this!
• Step 5: Gradually increase your calorie intake — Now that you’ve spent a few weeks learning how to track and understand your calorie intake, it’s time to take the next step — slowly increasing your calories. Why? Gradual increases help your body adapt, improving your metabolism without unwanted weight gain. Here’s how to do it:
◦ Split your calories into 3 balanced meals per day (breakfast, lunch, and dinner), plus a snack if needed.
◦ Start small — Increase your daily calories by just 10 to 30 calories per week. For example, if you’re starting at 1,800 calories in week one, aim for 1,820 to 1,830 in week two, and so on.
◦ Track bodyweight trends — Weigh yourself 3 to 7 times per week and compare weekly averages. The goal is to increase calories while keeping your weight stable. A small bump at the beginning is normal, but we don’t want to see a continuous upward trend.
Why so slow? This gradual approach gives your body time to utilize the extra energy effectively, boosting your metabolic rate (a.k.a. improving your “calories out”) without storing it as fat. Think of it as training your metabolism to work smarter, not harder. What’s the payoff?
After just 3 months of small weekly increases, you could be eating 240 to 360 more calories per day! That’s extra fuel for your body without sacrificing progress. Many people can continue to increase for several more weeks (since most people have severely downregulated their metabolisms due to years of restrictive diets!)
But remember: You can’t increase calories indefinitely. At some point, you’ll reach the upper end of your maintenance calorie range, where adding more calories leads to weight gain. If that happens, adjust slightly down and stay at that sweet spot. The longer you maintain at the upper end of your calorie window, the better your body will adapt.
This is about more than calories — it’s about building a stronger, more efficient metabolism while giving your body the fuel it needs to thrive.
Summary
And that’s a wrap, folks — five steps to improve your metabolism! Taking time to focus on a maintenance phase can do wonders for your body and mind. Dieting endlessly wears down your metabolism, leads to mental fatigue, and makes it harder to stick with any plan. When you’re constantly bouncing in and out of dieting cycles, it’s easy to lose the belief that you can actually succeed at sustainable fat loss.
Here’s the good news: eating at maintenance can reset your metabolic baseline, restore your mental energy, and build the momentum you need to crush your future fat loss goals. And for some people, these changes alone — better habits and a stronger routine — can even lead to weight loss as their “calories out” increases, creating a natural calorie deficit.
But the benefits don’t stop there. A maintenance phase can also repair your relationship with food. Long-term dieting often damages our hunger cues, makes it harder to trust our instincts, and turns eating into a mental battle. Imagine a life without constant food anxiety, restrictive rules, or fear of eating “too much.”
Instead, picture yourself eating with satisfaction and abundance, free to focus on your passions and goals. Resetting your metabolism isn’t just about physical health — it’s about creating the freedom to live fully, without the weight of dieting holding you back.
Transform Your Health — One Step at a Time
Ashley and her sister Sarah have put together a truly groundbreaking step-by-step course called “Rooted in Resilience.” They have compiled what clearly is the best application of Dr. Ray Peat’s work on Bioenergetic Medicine that I have ever seen.
It is so good that I am using the core of their program to teach the many Health Coaches that I am in the process of training for the new Mercola Health Clinics I am opening this fall. It took these women working nearly full-time on this project for a year to create it.
This has to be one of the absolute best values for health education I have ever seen. If you want to understand why you struggle with health problems and then have a clear program on how to reverse those challenges, then this is the course for you.
It is precisely the type of program I wish I would have had access to when I got out of medical school. I fumbled around for decades before I reached the conclusion they discuss in the course and share with you so you can restore your cellular energy production and recover your health.
| Use reverse dieting to increase your calories without gaining weight and tanking your metabolism, all while improving your energy levels |
| Select and eat the right foods to heal your metabolism and improve glucose utilization |
| Balance your hormones to help reduce anxiety, weight gain and sleep disturbances |
| Heal your gut for proper immune function, mood and weight management |
| Tweak your diet and lifestyle habits to improve your mindset and mental health |
| Crush your fitness goals with ease and get your life back on track |
| Master the most essential habits for health with bonus guides, including tons of meal plans to take the stress out of meal time planning and shopping, and so much more! |
Learn more about Rooted in Resilience here.
About the Author
Ashley Armstrong is passionate about helping educate and inspire others to improve their metabolic health. She and her sister run the “Strong Sistas” social media account, and have free information and courses on their website centered around improving metabolism.
Ashley is also passionate about improving the food system and providing food products that support thyroid and metabolic health. Ashley is a regenerative farmer, and co-founder of Angel Acres Egg Club, which specializes in low-PUFA (polyunsaturated fat) and low phytoestrogen eggs that are shipped to all 50 states, and Nourish Cooperative which ships low-PUFA chicken and pork, beef, cheese, A2 dairy and traditional sourdough to all 50 states.
How to Stay Healthy and Happy Through Menopause
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/01/13/menopausal-health.aspx
Analysis by Dr. Joseph Mercola January 13, 2025
STORY AT-A-GLANCE
- Menopause typically occurs between ages 45 and 55, causing hormonal changes that lead to symptoms like hot flashes and night sweats, significantly impacting daily life and well-being
- Research shows diets rich in healthy carbohydrates reduce hot flashes by 88%, with participants experiencing better overall physical and emotional well-being
- Low-carbohydrate diets likely harm postmenopausal women by increasing bone breakdown markers and inflammation, while decreasing bone formation, raising osteoporosis risk
- Contrary to common belief, low estrogen isn’t the main menopause issue; studies suggest low progesterone causes night sweats and excess estrogen is problematic
- Natural progesterone supplementation may effectively manage menopausal symptoms and support overall health; natural remedies like ashwagandha root extract, daily sauna use and cognitive behavioral therapy are also useful
Menopause is a natural phase in a woman’s life, marking the end of menstrual cycles and reproductive years. Typically occurring between ages 45 and 55, menopause is confirmed after 12 consecutive months without a menstrual period. This transition triggers fluctuations in estrogen and progesterone levels, leading to physical and emotional changes.
While menopause is a natural process, its symptoms may significantly impact your daily life and overall well-being. Common experiences during the menopausal transition include irregular periods, night sweats, mood swings and sleep disturbances. Among these, vasomotor symptoms like hot flashes and night sweats may be particularly challenging.
These sudden waves of heat last from a few seconds to several minutes, occurring multiple times a day or night. The unpredictability and frequency of hot flashes often lead to discomfort, interrupted sleep and a diminished quality of life. Fortunately, there are many effective strategies to stay healthy and happy during this transition.
The Impact of Diet on Menopausal Symptoms
Your diet plays a key role in managing menopausal symptoms and maintaining overall health. Research highlights the connection between dietary habits and the severity of vasomotor symptoms, offering promising strategies for natural symptom relief.
Diets rich in healthy carbohydrates have been associated with a lower prevalence of hot flashes, especially in regions like Japan and China, where traditional diets emphasize rice, vegetables and other plant-based foods.1
One study, published in Menopause journal, demonstrated that greater increases in carbohydrate and fiber consumption were directly associated with reductions in severe hot flashes experienced by menopausal women.2
Specifically, the more you incorporate healthy carbs into your diet, the more you may alleviate the intensity and frequency of these distressing symptoms. Conducted over 12 weeks, this randomized, controlled trial involved 84 women experiencing at least two moderate-to-severe hot flashes daily.
Participants were divided into two groups: an intervention group and a control group maintaining their usual diet without specific changes. The intervention focused on minimizing oil and fatty foods while increasing the intake of whole grains, fruits and vegetables. Weekly virtual meetings provided support and guidance, helping participants adhere to the dietary changes.
Increasing Carbohydrate Intake Reduced Hot Flashes
Using a mobile application, participants tracked their hot flash frequency and severity, alongside completing the Menopause-Specific Quality of Life (MENQOL) questionnaire to assess broader impacts on their well-being. This comprehensive approach evaluated both the direct and holistic effects of dietary modifications on menopausal symptoms.
The study yielded impressive results. Women in the intervention group experienced an 88% reduction in moderate-to-severe hot flashes over the 12-week period, compared to a 34% decrease in the control group. Remarkably, by the study’s end, half of the participants in the intervention group reported being free of moderate-to-severe hot flashes entirely, a stark contrast to the control group, where such occurrences remained virtually unchanged.
Beyond hot flash reduction, the dietary intervention led to significant weight loss, with participants shedding an average of 7.9 pounds (3.6 kilograms). Improvements were also noted across various domains of the MENQOL questionnaire, particularly in vasomotor, physical and sexual health.
These enhancements suggest that the benefits of a healthy carbohydrate-rich diet extend beyond symptom relief, contributing to overall physical and emotional well-being. According to the study, “[T]he greater the reduction in fat intake and the greater the increases in carbohydrate and fiber consumption, the greater the reduction in severe hot flashes.”3
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The Role of Carbohydrate Quality in Menopausal Health
The quality of the carbohydrates you consume is important for managing menopausal symptoms. Research conducted in Tehran, Iran, highlighted the significance of the Carbohydrate Quality Index (CQI) in alleviating both somatic and psychological symptoms of menopause.4
CQI assesses the quality of carbohydrates in your diet based on factors such as dietary fiber intake, glycemic index (GI) and the ratio of solid carbohydrates to total carbohydrates. Higher CQI scores indicate a diet rich in high-fiber, low-GI foods, which help maintain stable blood sugar levels and reduce inflammation.
The study, involving 393 postmenopausal women, found a strong inverse relationship between CQI and the severity of menopausal symptoms. Women with higher CQI scores experienced fewer total menopausal symptoms, including hot flashes, mood swings and sleep disturbances.
In other words, the quality of your carbohydrate intake — not just the quantity — plays an important role in enhancing your menopausal experience. By choosing carbohydrates that are nutrient-dense, you support your body’s hormonal balance and reduce the frequency and intensity of uncomfortable menopausal symptoms.
On the other hand, eating a diet high in refined carbohydrates, such as sweetened beverages and other ultraprocessed foods, is linked to depression in postmenopausal women5 and may have a similar affect during perimenopause. This is because processed foods commonly contain seed oils, rich in polyunsaturated fatty acids (PUFAs) like linoleic acid, which mimic estrogen, contributing to estrogen dominance. As a result, PUFAs disrupt hormonal balance and mitochondrial function.
Low-Carbohydrate Diets Harm Bone Health in Postmenopausal Women
Adopting a low-carbohydrate, high-fat (LCHF) diet might offer short-term weight loss benefits, but research raises concerns about its impact on bone health, particularly for postmenopausal women. A study on athletes revealed that a short-term ketogenic LCHF diet impaired markers of bone formation and increased markers of bone resorption.6
Specifically, participants on the LCHF diet showed elevated levels of C-terminal telopeptide of type I collagen (CTX), a marker indicating increased bone breakdown, alongside reduced levels of procollagen 1 N-terminal propeptide (P1NP) and osteocalcin (OC), which are essential for bone formation and metabolism.
For postmenopausal women, who are already at an increased risk of osteoporosis, these findings are particularly relevant. Chronic bone resorption without adequate formation leads to decreased bone mineral density, increasing the risk of fractures and osteoporosis.
Cutting carbohydrates through a low-carb diet may also have unintended consequences on your immune system. Research shows that LCHF diets led to increased levels of interleukin-6 (IL-6) and cortisol post-exercise.7 IL-6 is a cytokine involved in inflammation, and elevated levels indicate an inflammatory state that compromises immune function.
The fact is your body fundamentally requires glucose to operate effectively. When you don’t consume enough carbohydrates for an extended period, your body begins to produce glucose from cortisol through a process called gluconeogenesis.8 In this process, cortisol breaks down amino acids, including those present in your muscles.
Cortisol is part of a group of steroid hormones known as glucocorticoids. The prefix “gluco” refers to glucose (sugar), while “cortico” indicates its origin from the adrenal glands. Although commonly recognized as a stress hormone, cortisol’s primary role is to raise blood sugar levels when glucose is scarce and your liver’s glycogen stores are depleted.
When your body senses low glucose levels, cortisol triggers the expression of the PEPCK enzyme, initiating gluconeogenesis.9 However, if cortisol levels remain persistently high due to inadequate carbohydrate intake, it leads to increased inflammation and eventually weakens your immune system. This scenario is clearly undesirable. I used to advocate for a low-carb diet, but I now understand that it is not the best strategy for achieving optimal health.
Which Carbs Are Best?
To fuel your body during perimenopause and menopause, your body needs to meet a certain carbohydrate threshold, approximately 250 grams a day, to support metabolic functions. Healthy gut bacteria play an important role in breaking down the beneficial fibers present in nutritious carbohydrates such as fruits, vegetables and whole grains.
Unfortunately, many individuals lack an optimal balance of these beneficial microbes. When this equilibrium is disturbed, consuming these otherwise wholesome foods leads to a disease in your health. This occurs because harmful bacteria proliferate, releasing toxic endotoxins that significantly disrupt mitochondrial function.
If you’re struggling to digest healthy carbohydrates, consider incorporating pure glucose, also known as dextrose, into your diet for a few weeks. This strategy is especially useful if your digestive system is severely impaired and you find it difficult to consume any carbohydrates.
Sipping dextrose water can add a safe form of carbohydrates that do not increase endotoxin production. This allows you to gradually reintroduce a broader range of carbohydrates into your meals. Over time, this gradual reintroduction supports the restoration of your mitochondrial function.
For those with particularly compromised gut health, begin with dextrose water, sipping it slowly throughout the day. As your tolerance builds, transition to consuming fruit juice with pulp or whole fruits. Ultimately, as your gut health strengthens, you will be able to incorporate more fiber-rich fruits, vegetables and starches into your diet, enhancing your overall well-being and carbohydrate tolerance.
My newest book, “Your Guide to Cellular Health: Unlocking the Science of Longevity and Joy,” goes into this topic in detail. By categorizing carbs into a traffic light system of green, yellow and red, it provides a practical framework for you to identify and incorporate beneficial carbohydrates into your diet.
Why Boosting Estrogen Isn’t the Answer
Low estrogen levels are frequently identified as a key feature of menopause and addressed with hormone replacement therapy that includes estrogen — a treatment I advise against. In our interview, bioenergetic researcher Georgi Dinkov explained that estrogen is both carcinogenic and antimetabolic.
It significantly hampers your mitochondria’s ability to produce cellular energy in the form of ATP by relying on aerobic glycolysis (known as the Warburg effect), which severely disrupts oxidative phosphorylation. This disruption further enhances estrogen’s carcinogenic effects.
Moreover, Dinkov emphasizes that estrogen production typically does not decrease with age, suggesting that administering estrogen is not the universal solution for relieving menopausal symptoms as it is often portrayed.10 Despite this, estrogen is conventionally used to reduce hot flashes, even though this is problematic. Research shows that it’s low progesterone — not low estrogen — that’s linked with night sweats.
In one study, progesterone supplementation significantly improved night sweats and sleep quality among perimenopausal women.11 Further, blocking estrogen and/or taking dehydroepiandrosterone (DHEA) prevents many menopausal symptoms and related conditions, including obesity and insulin resistance.12
Unfortunately, many people believe they are low in estrogen due to bloodwork, when they actually have high levels in their organs. This is because serum estrogen levels are not representative of estrogen that’s stored in tissues. Estrogen can be low in plasma but high in tissues. Prolactin levels serve as a reliable indicator of estrogen activity, as estrogen directly stimulates your pituitary gland to produce prolactin.
When prolactin levels are elevated, it signals increased estrogen receptor activation, whether from the body’s own estrogen production or environmental exposures like microplastics. This relationship is particularly significant when combined with low thyroid function, making prolactin an important marker for identifying hormonal imbalance.
Progesterone and Other Natural Strategies for Menopause Symptom Relief
Many natural therapies provide relief from menopausal symptoms. Ashwagandha root extract may relieve mild to moderate menopausal symptoms in women who are perimenopausal.13 Additionally, therapies such as hypnosis and cognitive behavioral therapy have been effective in easing vasomotor symptoms, sexual dysfunction and sleep disturbances associated with menopause.14
To further support mental and emotional well-being during this transitional phase, incorporating relaxation practices and mindfulness-based stress reduction techniques is recommended.15 Daily sauna use may also help menopausal women avoid weight gain by improving insulin sensitivity and fat metabolism.16
That said, for perimenopausal and menopausal women, natural progesterone, which is an estrogen antagonist, may be especially useful. Its benefits extend far beyond menopause, effectively modulating your stress, supporting neurological health and reducing allergic responses, making it a hormone I believe nearly every adult could benefit from.
- 1, 2, 3 Menopause, 30(1):p 80-87, January 2023
- 4 Maturitas. 2021 Aug:150:42-48. doi: 10.1016/j.maturitas.2021.05.006. Epub 2021 May 29
- 5 Am J Clin Nutr. 2015 Aug;102(2):454-63. doi: 10.3945/ajcn.114.103846. Epub 2015 Jun 24
- 6 Front Endocrinol (Lausanne). 2020 Jan 21;10:880, doi: 10.3389/fendo.2019.00880
- 7 Med Sci Sports Exerc. 2022 Mar 1;54(3):377-387
- 8 StatPearls [Internet], Physiology, Fasting, Cellular Level
- 9 StatPearls [Internet], Physiology, Glucocorticoids, Function
- 10 Youtube, Dr. Mercola, What You Need to Know About Estrogen and Serotonin – Interview with Georgi Dinkov
- 11 Scientific Reports, Volume 13, Article number: 9082 (2023)
- 12 To Extract Knowledge from Matter, May 9, 2023 (Archived)
- 13 J Obstet Gynaecol Res. 2021 Dec;47(12):4414-4425
- 14, 15 J Evid Based Integr Med. 2019; 24: 2515690X19829380, Conclusions
- 16 American Society for Nutrition, July 1, 2024
Understanding the Root Causes of Dyslipidemia in Atherosclerotic Cardiovascular Disease
Reproduced from original OMNS article (OrthoMolecular News Service):
http://orthomolecular.org/
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Orthomolecular Medicine News Service, January 10, 2025
Richard Z. Cheng, M.D., Ph.D., Thomas E. Levy, M.D., J.D.
Highlights
A paradigm shift from the cholesterol-centric focus on symptom management to addressing the root causes of ASCVD has demonstrated potential for prevention and reversal, as shown by our recently reported 10 ASCVD reversal cases (1).
Abstract
Dyslipidemia has long been the primary target for atherosclerotic cardiovascular disease (ASCVD) treatment. However, we have recently presented compelling evidence demonstrating that dyslipidemia is an intermediary mechanistic step, not a root cause of ASCVD, and that the American Heart Association’s decades-long cholesterol-centric dogma is both unreasonable and potentially unethical, bordering on criminal negligence (2).
In our international consultation services, we have shifted from this outdated paradigm to an orthomolecular medicine-based integrative approach, focusing on restoring biochemical balance (between nutrients and toxins) and physiological harmony (among various hormones). Using this approach, we recently reported a series of 10 successful ASCVD reversal cases (1).
This paper explores the multifactorial root causes contributing to dyslipidemia, including dietary factors, nutritional deficiencies, infections, physical inactivity, and hormonal imbalances. Special attention is given to the roles of high-carbohydrate diets, ultra-processed foods, seed oils (containing high amounts of omega-6 PUFA), and high-fructose consumption. The effects of micronutrient deficiencies, such as those of vitamins B, C, D, E, and magnesium, are examined in the context of lipid metabolism. Additionally, the paper highlights the impact of chronic infections, sedentary lifestyles, and hormonal dysregulation on lipid abnormalities.
Understanding these key root causes provides a foundation for more effective prevention and treatment strategies (3). In future papers, we plan to explore these topics in greater detail, advocating for a paradigm shift from cholesterol-centric management to addressing the underlying causes of dyslipidemia and ASCVD.
Introduction
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of morbidity and mortality worldwide. For decades, cholesterol and dyslipidemia have been central to ASCVD management strategies. However, our prior critiques of the cholesterol-centric paradigm have underscored that dyslipidemia is not the root cause but rather an intermediary mechanism of ASCV (2). Here we explore the multifactorial root causes underlying dyslipidemia, and advocate for prevention and treatment strategies that address these root causes. We focus here on categorizing the primary root causes contributing to ASCVD through dyslipidemia. More comprehensive discussions on these root causes will be presented where appropriate in subsequent papers in this series.
1. Dietary factors and dyslipidemia
- High-carbohydrate diets have been strongly associated with dyslipidemia, particularly characterized by increased triglycerides and decreased HDL cholesterol levels (4–6). This effect is especially pronounced with high glycemic index carbohydrates (5). The mechanism may involve reduced clearance of LDL particles and increased production of their precursors (7). Carbohydrate-induced hypertriglyceridemia occurs when dietary carbohydrate exceeds 55% of energy intake, despite reduced dietary fat (8). This paradoxical effect may be due to enhanced intestinal de novo lipogenesis and mobilization of stored lipids (9). However, the impact of carbohydrates on lipid metabolism is complex, with some studies suggesting that low-carbohydrate diets may have beneficial effects on atherogenic dyslipidemia (10).
- Low-carbohydrate ketogenic diets (KDs) have shown promising effects in improving metabolic disorders, particularly dyslipidemia. KDs can lead to significant reductions in triglycerides, total cholesterol, and LDL cholesterol, while increasing HDL cholesterol (11,12). These diets have been found to improve insulin sensitivity, reverse atherogenic dyslipidemia, and reduce inflammatory biomarkers associated with cardiovascular disease (13,14). KDs have also demonstrated benefits in managing obesity, metabolic syndrome, and type 2 diabetes (15,16). Studies have shown that KDs can decrease fasting serum insulin concentrations, improve LDL particle size, and reduce postprandial lipemia (11,12). While the optimal carbohydrate proportion and diet duration require further investigation, KDs appear to be a safe and effective approach for treating metabolic disorders (17,18).
- Ultra-processed foods and dyslipidemia. High consumption of ultra-processed foods (UPF) has been shown to be associated with an increased risk of dyslipidemia and other cardiometabolic disorders. Multiple prospective cohort studies have found that individuals with higher UPF intake have significantly greater odds of developing hypertriglyceridemia, low HDL cholesterol, and hypercholesterolemia (19,20). This association has been observed in both adults and adolescents (21,22). Systematic reviews and meta-analyses confirm these findings, reporting consistent positive associations between UPF consumption and increased risk of dyslipidemia, as well as diabetes, hypertension, and obesity (23,24). Longitudinal studies in children have also shown that higher UPF intake is associated with elevated total cholesterol and triglyceride levels (25). Proposed mechanisms include altered food matrix, toxicity from additives, and processing-induced contaminants affecting lipid metabolism, gut microbiota, and inflammatory pathways (26).
- Seed oils (rich in omega-6 PUFA) and dyslipidemia. Research suggests that high intake of omega-6 polyunsaturated fatty acids (PUFAs) from seed oils may contribute to inflammation, oxidative stress, and atherosclerosis (27). Despite recommendations for omega-6 PUFA consumption, some studies indicate potential long-term side effects, including hyperinsulinemia and increased cancer risk (28). Flaxseed and its oil, rich in omega-3 fatty acids, have demonstrated positive impacts on cardiovascular risk factors and dyslipidemia (29,30). Adjusting the omega-6 to omega-3 PUFA ratio may be crucial in managing chronic diseases (30). During cooking, both omega-3 and omega-6 high PUFA seed oils are readily oxidized, become rancid, and may produce harmful trans-fats (72).
- High fructose (found in HFCS and fruits). Research suggests that high fructose consumption, particularly from high-fructose corn syrup (HFCS), may contribute to dyslipidemia and other metabolic disorders. Studies have shown that fructose intake can increase postprandial triglycerides, LDL cholesterol, and apolipoprotein B levels (32,33). Fructose consumption has also been linked to visceral adiposity, insulin resistance, and hepatic de novo lipogenesis (fatty liver disease) (34,35). The metabolic effects of fructose differ from glucose due to its rapid hepatic conversion and extraction (36). While some studies found no significant metabolic differences between HFCS and sucrose (37), others suggest that HFCS consumption at 25% of energy requirements can increase cardiovascular disease risk factors comparably to fructose (32). Recent research emphasizes the synergistic effects of glucose and fructose on lipid metabolism, supporting public health efforts to reduce sugar intake (38,39).
2. Nutritional deficiency and dyslipidemia
Many vitamins and micronutrients play critical roles in lipid and energy metabolism, and deficiencies—whether isolated or combined—can lead to metabolic disturbances. Below are some key examples:
- B vitamins. Niacin and vitamin B6 have shown significant potential in managing dyslipidemia and associated cardiovascular risks. Niacin supplementation can lower triglycerides, LDL, and VLDL levels while increasing HDL (40). B vitamin supplementation improves lipid metabolism and reduces inflammation in patients with stable coronary artery disease (41). Animal studies have demonstrated antihyperlipidemic and hepatoprotective effects of vitamin B6 (42). Deficiencies in vitamins B6 and B12 are frequently reported in hyperlipidemic patient (43). Higher dietary niacin intake is associated with a reduced risk of dyslipidemia (44).
- Vitamin C and dyslipidemia. Research demonstrates that vitamin C supplementation can improve lipid profiles by lowering total cholesterol, LDL cholesterol, and triglycerides, particularly in individuals with hypercholesterolemia or diabetes (45–47). Some studies also report increases in HDL cholesterol (48,49). Beneficial effects of vitamin C have been observed across diverse groups, including diabetics, hemodialysis patients, and oil workers exposed to petroleum fumes (50,51). A meta-analysis of 13 randomized controlled trials confirmed that vitamin C supplementation significantly reduces LDL cholesterol and triglycerides in hypercholesterolemic individuals (46). The effects of vitamin C vary depending on dosage, duration, and individual health status (47). Dr. Linus Pauling’s pioneering work on vitamin C and cardiovascular disease laid the foundation for understanding its role in vascular health, indirectly linking it to lipid metabolism. We plan to dedicate a paper to further explore Pauling’s insights and their relevance to dyslipidemia and ASCVD. One of us (TEL) discusses vitamin C’s role in improving lipid profiles, combating oxidative stress, and supporting vascular health in the books Primal Panacea (52) and Stop America’s Number One Killer (53).
- Vitamin D and dyslipidemia. Vitamin D deficiency is significantly associated with dyslipidemia. Studies reveal that individuals with lower serum 25-hydroxyvitamin D levels are more likely to exhibit abnormal lipid profiles, including elevated total cholesterol, LDL, and triglycerides, and decreased HDL (54–57). This relationship persists even after adjusting for confounding factors. Vitamin D deficiency is linked to alterations in metabolomic profiles, particularly sphingolipid pathway (58). Interactions with other micronutrients, such as vitamin A, zinc, and magnesium, may influence vitamin D’s impact on lipid metabolism (59). Our recent comprehensive review of vitamin D demonstrates that maintaining optimal serum levels above 40 ng/mL reduces the risk of cardiovascular disease incidence and mortality (60) (accepted for publication by Nutrients).
- Vitamin E and dyslipidemia. Vitamin E has shown anti-atherosclerotic properties (61). Research on vitamin E and dyslipidemia shows mixed results. Some studies suggest that vitamin E supplementation can improve lipid profiles in dyslipidemic patients, reducing total cholesterol, LDL-C, and triglycerides (62,63). Higher serum vitamin E levels have been associated with a more favorable lipid profile (64). Vitamin E supplementation has been shown to suppress elevated plasma lipid peroxides and increase serum antioxidant activity (65). The impact of antioxidative vitamins on lipid profiles varies based on dosage, duration, and individual health status (47).
- Magnesium and dyslipidemia. Hypomagnesemia has been linked to metabolic abnormalities and dyslipidemia (66–70). Studies report negative correlations between serum magnesium and triglycerides, LDL, and total cholesterol, while positive correlations are observed with HDL cholesterol (70,71).
3. Infections and dyslipidemia
- Infections promote dyslipidemia. Dyslipidemia is a common complication in HIV-infected patients and those with COVID-19, associated with increased severity and mortality (72). It is characterized by elevated total cholesterol, LDL, and triglycerides, with decreased HDL (73,74). The pathogenesis involves inflammation, oxidative stress, and lipid peroxidation (75). These lipid abnormalities may increase cardiovascular risk in HIV patients (76,77). Research suggests a significant association between oral infections, particularly periodontitis, and systemic metabolic disturbances. Periodontitis has been linked to increased risk of cardiovascular diseases and dyslipidemia (78,79). Studies have found higher levels of total cholesterol, LDL cholesterol, and triglycerides, along with lower HDL cholesterol, in individuals with periodontitis (80,81). Chronic oral infection with Porphyromonas gingivalis, a key periodontal pathogen, has been shown to accelerate atheroma formation by altering lipid profiles in animal models (82). The relationship between periodontitis and hyperlipidemia appears bidirectional, with elevated triglycerides potentially modulating inflammatory responses to periodontal pathogens (83). The underlying mechanisms involve systemic inflammation, metabolic endotoxemia, and genetic factors that influence both oral infections and cardiometabolic diseases (84). These findings highlight the complex interplay between oral health and systemic metabolism.
- Infection control improves dyslipidemia. Periodontal treatment has been shown to improve lipid control (85). Eradication of Helicobacter pylori infection may decrease the risk of dyslipidemia (86).
4. Physical inactivity and dyslipidemia/high cholesterol
Research consistently shows an inverse relationship between physical activity (PA) and dyslipidemia. Higher PA levels are associated with increased HDL-C and decreased triglycerides in both men and women (87,88). Sedentary behavior increases the risk of dyslipidemia, while moderate-to-vigorous PA (MVPA) may reduce this risk (89,90). The prevalence of dyslipidemia is high in some populations, with limited awareness and treatment (91). Individuals meeting PA guidelines have lower odds of dyslipidemia, even with poor diet quality (91). However, adults with hypercholesterolemia are less likely to meet PA recommendations compared to those without (92). PA patterns, including timing and intensity, may influence lipid profiles differently (90). Overall, habitual PA is associated with more favorable lipid profiles and reduced cardiovascular disease risk (93,94).
5. Hormonal imbalance and dyslipidemia/high cholesterol
- Thyroid dysfunction, particularly hypothyroidism, is strongly associated with dyslipidemia and increased cardiovascular risk (95,96). Both overt and subclinical hypothyroidism can lead to elevated total cholesterol, LDL cholesterol, and apolipoprotein B levels, while potentially affecting HDL cholesterol and triglycerides (97,98). These lipid abnormalities are primarily due to reduced LDL receptor activity and altered regulation of cholesterol biosynthesis (99). Thyroid hormone replacement therapy has been shown to improve lipid profiles in overt hypothyroidism, but its benefits in subclinical hypothyroidism remain debated (99,100). Recent studies have also highlighted the role of thyroid hormones in regulating HDL function and cholesterol efflux (98). Given the prevalence of thyroid dysfunction and its impact on lipid metabolism, screening for thyroid disorders is recommended in patients with dyslipidemia (101).
- Cortisol imbalance significantly contributes to dyslipidemia, high cholesterol, and increased cardiovascular risk. Excess cortisol, such as in Cushing’s syndrome, is associated with elevated triglycerides, total cholesterol, and LDL cholesterol levels (102). Similarly, stress-induced cortisol elevation disrupts lipid metabolism, promoting atherogenesis and increasing the risk of atherosclerosis (103). Conversely, patients with metabolic syndrome and low cortisol levels exhibit less pronounced lipid disturbances (104). Elevated basal cortisol levels and reduced circadian variability have been linked to unfavorable lipid profiles, particularly in individuals with depressive and anxiety disorders (105). Additionally, the cortisol-to-DHEA ratio has been positively correlated with atherogenic lipid profiles in HIV patients with lipodystrophy (106). Glucocorticoid therapy, a common cause of cortisol excess, can lead to dyslipidemia and hypertension, further heightening cardiovascular disease risk (107). Excess cortisol is also strongly associated with obesity, hypertension, and metabolic syndrome (108,109). Furthermore, studies have found that elevated long-term cortisol levels, as measured in scalp hair, are linked to a history of cardiovascular disease (110). In obesity, higher cortisol concentrations are directly correlated with an increased risk of cardiovascular comorbidities (111). These findings highlight the multifaceted role of cortisol in dyslipidemia and emphasize the need to manage cortisol levels to mitigate cardiovascular risks effectively.
- Estrogen imbalance significantly impacts lipid metabolism and cholesterol levels. During menopause, estrogen deficiency leads to increased total cholesterol, LDL cholesterol, and triglycerides, while decreasing HDL cholesterol (112). High maternal estradiol levels can induce dyslipidemia in newborns by upregulating HMGCR expression in fetal hepatocytes (113). Estrogen administration in premenopausal women increases VLDL and HDL constituents, enhancing VLDL apoB and HDL apoA-I production (114). In postmenopausal women, estrogen therapy lowers LDL cholesterol levels (115). Estrogen treatment in cholesterol-fed rabbits attenuates atherosclerosis development by modulating lipoprotein metabolism (116,117). Endogenous sex hormones play a role in regulating lipid metabolism in postmenopausal women, with SHBG associated with a more favorable lipid profile (118). Estrogen administration in postmenopausal women decreases LDL cholesterol and hepatic triglyceride lipase activity while increasing HDL cholesterol (119).
- Progesterone imbalance can significantly impact lipid metabolism and cholesterol levels. Progesterone administration in rats led to increased hepatic triglycerides and cholesterol esters, while decreasing plasma cholesterol levels (120). In cultured cells, progesterone inhibited cholesterol biosynthesis (121). Dyslipidemia affected ovarian steroidogenesis in mice through oxidative stress, inflammation, and insulin resistance (122). In premenopausal women, ovarian lipid metabolism influenced circulating lipids (123). Estrogen plus progesterone replacement therapy in postmenopausal women lowered lipoprotein[a] levels and improved overall lipid profiles (124). High-dose medroxyprogesterone decreased total, LDL, and HDL cholesterol in postmenopausal women (125). In children, progesterone/estradiol ratios were associated with LDL-cholesterol levels (126). Female runners with menstrual irregularities showed altered steroid hormone and lipid profiles compared to eumenorrheic counterparts (127).
- Testosterone imbalance can significantly impact lipid metabolism and cholesterol levels. Research suggests a complex relationship between testosterone and lipid profiles. Low testosterone levels are associated with adverse lipid profiles, including higher total cholesterol and triglycerides, and lower high-density lipoprotein (HDL) cholesterol (128,129). Conversely, higher testosterone levels correlate with increased HDL cholesterol in men, particularly those with cardiovascular disease (130,131). Testosterone deficiency may contribute to hypercholesterolemia through altered expression of hepatic PCSK9 and LDL receptors (132). The effect of testosterone on lipids varies with age, gender, race/ethnicity, and menopausal status (133). Exogenous testosterone administration in hypogonadal men may improve lipid profiles by decreasing LDL and total cholesterol, although it may also decrease HDL cholesterol (134). While testosterone’s influence on lipids is evident, its overall impact on cardiovascular disease risk remains unclear and requires further investigation (134,135).
Conclusion
Dyslipidemia, long regarded as a primary target in ASCVD management, is increasingly understood as an outcome of complex, multifactorial root causes. These root causes include dietary factors, such as high-carbohydrate diets, ultra-processed foods, seed oils, and high-fructose consumption, which significantly influence lipid metabolism. Nutritional deficiencies, including vitamins B, C, D, and E, and magnesium, further exacerbate dyslipidemia, while chronic infections and physical inactivity compound cardiovascular risk. Hormonal imbalances, including dysfunctions in thyroid hormones, estrogen, progesterone, testosterone, and cortisol, also play a pivotal role in lipid abnormalities.
Addressing these underlying factors presents an opportunity to move beyond the traditional cholesterol-centric paradigm. Strategies such as dietary modifications, increased physical activity, infection control, and optimization of nutritional and hormonal balance can significantly improve lipid profiles, reduce cardiovascular risk, and even reverse ASCVD in some cases, as we have demonstrated in our recent report (1).
By focusing on the root causes of dyslipidemia, healthcare providers can offer more personalized and effective interventions, shifting the emphasis from symptom management to true disease prevention and reversal. This approach has the potential to improve not only ASCVD outcomes but also overall cardiovascular health and longevity. Future studies should prioritize the integration of these multifaceted strategies into clinical practice, emphasizing the importance of addressing the root causes of dyslipidemia for sustainable cardiovascular health.
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Proteins Linked to Alzheimer’s Disease Now Observable in Real Time
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/31/proteins-linked-to-alzheimers-disease.aspx
Analysis by Dr. Joseph Mercola December 31, 2024
STORY AT-A-GLANCE
- Nearly 7 million Americans currently have Alzheimer’s disease. Projections show this number will increase to 13 million by 2050, according to the Alzheimer’s Association
- A study used liquid-based atomic force microscopy to visualize beta-amyloid protein development in real-time, identifying “superspreader” fibrils that accelerate disease progression across brain tissue
- Three major toxins that damage mitochondrial function are excessive linoleic acid (LA) intake, endocrine-disrupting chemicals from microplastics and electromagnetic field (EMF) exposure from electronic devices
- Certain pathogenic bacteria strains like Collinsella, Lachnospira, and Veillonella increase Alzheimer’s risk, while probiotic strains like Eubacterium nodatum produce protective benefits through short-chain fatty acids
- Prevention strategies include optimizing vitamin D levels, maintaining low fasting insulin, avoiding gluten and casein, exercising regularly and challenging your mind with new skills
According to the Alzheimer’s Association, nearly 7 million Americans are currently diagnosed with Alzheimer’s disease, the most common type of dementia. Furthermore, the situation is expected to worsen — by 2050, around 13 million Americans are projected to be diagnosed with this neurodegenerative disease.1
Alzheimer’s disease remains challenging for modern medicine to diagnose and treat. However, a recent study2 has made a breakthrough in understanding how the disease progresses, creating a foundation for future clinicians and researchers to build upon to create better treatment plans.
A Breakthrough in Observing Alzheimer’s Disease Progression
In a study3 published in Science Advances, researchers were able to visualize the development of amyloid-beta proteins to see how Alzheimer’s disease spreads. Beta-amyloid proteins have been observed using a variety of methods, several of which were reviewed in the study:
“Methodological advances have been able to resolve the ultrastructure of Aβ and tau protein aggregates formed along the primary nucleation pathway using cryo-electron microscopy (cryo-EM) and solid-state nuclear magnetic resonance spectroscopy.
Likewise, the aggregation kinetics and toxicity of these proteins have been investigated using ultrasensitive fluorescence-based assays, nanopore devices, and circular dichroism.
Details on the morphology, on-surface assembly, and chemical structure of Aβ and tau protein aggregates have also been made accessible using standard atomic force microscopy (AFM), video-rate AFM, and infrared spectroscopy.”
For context, beta-amyloid proteins aggregate in the brain, and they’re suspected of playing a key role in the development of Alzheimer’s. Hence, they’re what researchers usually focus on to find therapeutic solutions.4 Previous staining methods used for observational analysis distort the protein structures.
To find new ways to analyze the mechanisms of Alzheimer’s disease, the team used liquid-based atomic force microscopy (AFM). As explained by the authors:5
“Building on the observations from previous secondary nucleation studies, we postulated that it should be feasible with a high-resolution AFM to record elementary information such as oligomer size, shape, and adsorption site on individual fibrils with sub-10-nm diameter. Operating the AFM in an aqueous solution medium would allow the diffusion of oligomers on the fibril surface.”
Tracking the Progression of Alzheimer’s Disease in Real Time
Once the team settled on the methodology, they moved onto testing. To start, they agitated beta-amyloid samples for 30 minutes at room temperature. Then, they set up different experiments to observe the growth and progression protein aggregates from 30 seconds to 250 hours:6
“Nanoscale imaging supported by atomic-scale molecular simulations tracked the adsorption and proliferation of oligomeric assemblies at nonperiodically spaced catalytic sites on the fibril surface. Upon confirming that fibril edges are preferential binding sites for oligomers during embryonic stages, the secondary fibrillar size changes were quantified during the growth stages.”
From their observations of protein fibril development in real time, they were able to classify some of them as “superspreaders” based on their surface anatomy. Specifically, these superspreaders “feature highly active edges and surfaces where new protein molecules accumulate, eventually forming longer fibrils that may spread across brain tissue.”
As they spread, more protein aggregation occurs, effectively progressing the hallmarks of Alzheimer’s disease. Ultimately, the research team hopes that this breakthrough in fibril analysis will be able to help improve the diagnosis and monitoring of neurodegenerative diseases. “This work brings us another step closer to better understanding how these proteins spread in brain tissue of Alzheimer’s disease,” says Peter Nirmalraj, one of the authors of the study.7
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Mitochondrial Dysfunction Is at the Heart of Alzheimer’s Disease
As researchers continue to come up with new tools to help diagnose and treat Alzheimer’s better, following a healthy lifestyle is important to reduce your risk. Prevention is by far your best option. I believe addressing mitochondrial dysfunction is key to protecting cognitive function, which is achieved by improving your cellular health.
The first thing to address is your diet. A study published in Neurology noted that eating an inflammatory diet raises your risk of dementia.8 In addition, I believe that there are three major toxins damaging your mitochondrial function by affecting intracellular calcium, which subsequently impacts cellular health.
Essentially, when calcium within your cells increase, your body produces superoxide and nitric oxide. These two combine to form peroxynitrite, a potent reactive oxygen species that contributes to poor health. Three pervasive toxins that raise intracellular calcium levels and drive peroxynitrite formation include:
1. Excessive linoleic acid (LA) consumption — LA is an omega-6 polyunsaturated fat (PUFA) found most abundantly in seed and vegetable oils and processed foods. I believe it is one of the most pernicious toxins of the Western diet, driving inflammation and chronic diseases among the populace.
Overconsumption negatively impacts your metabolic rate and gut microbiome, which are key factors for optimal health. To protect your health, I recommend keeping your LA intake below 5 grams a day.
Note that it’s virtually impossible to avoid LA, as most foods inherently have them, and your body does need some of it. The key is to avoid excess.
2. Endocrine-disrupting chemicals (EDCs) — Microplastics are so prevalent in our environment that humans ingest approximately a credit card’s worth of plastic every week.9 These microplastics contain endocrine-disrupting chemicals (EDCs), particularly phthalates and bisphenol A (BPA).
When these substances enter the body, they activate and overstimulate estrogen receptors. This increased estrogen activity raises intracellular calcium levels, which in turn leads to peroxynitrite formation.
To reduce your exposure, the first line of defense is minimizing your dependence on plastic products, such as bottled water and single-use food containers. Bringing a glass container and reusable tumbler for your water when going outside will significantly cut down your plastic usage. For additional strategies, read my article “How Microplastics Affect Your Reproductive Health.”
3. Electromagnetic field (EMF) exposure — The devices you use every day emit EMFs that activate voltage-gated calcium channel (VGCC) receptors within your cells. This triggers calcium influx, catalyzing peroxynitrite production.10
Major sources of EMFs include your cellphone, Bluetooth devices, wireless computer accessories and smart appliances that connect to your home’s Wi-Fi. For practical strategies on protecting yourself from EMFs, read my article “Study: Phone Radiation Kills Cheek Cells.”
Keep Your Gut Flora Healthy to Protect Cognitive Function
Your gut microbiome is one of the most crucial aspects for achieving optimal health. Research11 has shown that it plays a role in various functions, such as modulating the immune system, glucose metabolism and reducing insulin resistance. In addition to these findings, a study12 published in Scientific Reports showed that certain bacterial strains in the gut increased the risk of Alzheimer’s disease.
In the study, the researchers singled out strains such as Collinsella, Lachnospira and Veillonella as contributors to the risk of Alzheimer’s disease. According to the study authors:13
“In our analyses, Collinsella from the phylum Actinobacteria was identified as a risk factor for AD (Alzheimer’s disease) in both the discovery and replication samples … Importantly, an increased abundance of this genus has also been observed in AD transgenic mice and AD patients. Our findings provide evidence at the human genome-wide level of a connection between Collinsella and AD that supports previous observational studies …
In addition, we identified two Firmicutes genera as risk factors for AD (Lachnospira and Veillonella), with Veillonella being validated in the replication sample. Recently, it was reported that AD patients have an abundance of Veillonella in their oral microbiome. In the gut, it has been shown that an overabundance of species like V.parvula promotes intestinal inflammation …
The dual association of oral and gut abundance of Veillonella with disease points to this genus as a target for therapeutics and a potential bridge between conditions like gut inflammation and periodontitis with AD.”
The researchers also identified strains that provide protective benefits against Alzheimer’s disease, such as Eubacterium nodatum and Eisenbergiella. These produce short-chain fatty acids (SCFAs), particularly butyrate, from dietary carbohydrates.14
Butyrate nourishes your colonic epithelial cells, reinforcing the intestinal barrier. SCFAs also stimulate mucin production, creating a protective shield against harmful bacteria. Akkermansia also produces SCFAs, and research has shown that Alzheimer’s patients tend to have very low levels of this important keystone species.15
Carbohydrates Help Support Your Gut Health
Nurturing oxygen-intolerant beneficial bacteria, including Akkermansia, will strengthen your intestinal lining to create an environment that promotes overall wellness. On the other hand, low levels of oxygen-intolerant bacteria will lead to increased intestinal permeability, also known as leaky gut.
This causes openings in the intestinal barrier, allowing toxins, undigested food particles and harmful microbes to enter your bloodstream, resulting in systemic inflammation and chronic health issues.
To create an environment that allows your gut microbiome to thrive, increasing your intake of carbohydrates is a priority. Ashley Armstong provides some good recommendations for gut-friendly carbs, which include:
- Well-cooked white rice
- Sourdough bread
- Root vegetables like potatoes and sweet potatoes
- Fresh, ripe fruits
- Masa harina, or traditionally made tortillas
Also remember to include fermented foods. I’m a big believer of making your own fermented vegetables at home because they’re both simple and cost-effective to prepare. I don’t recommend buying commercially prepared fermented vegetables, as they often contain artificial sweeteners and additives, negating the benefits of fermented foods in the first place.
Additional Strategies to Prevent Alzheimer’s Disease
Aside from optimizing your gut health and mitochondrial function, there’s a plethora of helpful Alzheimer’s prevention strategies, several of which are outlined below:
| Avoid gluten and casein (primarily wheat and pasteurized dairy, but not dairy fat, such as butter) — As noted in a 2022 study,16 your blood-brain barrier is negatively affected by gluten. When bacteria enter your blood stream, the risk of Alzheimer’s disease increases. Other cognitive disorders are linked to a weakened blood-brain barrier as well, such as Parkinson’s disease, anxiety and depression. |
| Make sure you’re getting enough animal-based omega-3 fats — Omega-3 fats, namely EPA and DHA, help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression and lowering your risk of developing the disorder. That said, omega-3s are PUFAs, so don’t overdo it. |
| Optimize your vitamin D level with safe sun exposure — Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. In a 2023 study,17 increasing vitamin D reduced dementia risk by 40%.
The best way to get vitamin D is through sensible sun exposure, aiming for a blood level between 60 ng/mL and 80 ng/mL. However, you need to purge seed oils from your body before going into the sun at solar noon. The LA in your skin oxidizes when exposed to sunlight, causing inflammation and skin damage. To protect your skin, avoid sun exposure during solar noon for four to six months as you work on removing LA from your body. Stick to sunlight during early morning and late afternoon in the meantime. For additional skin defense, your can take astaxanthin, a low-dose aspirin or molecular hydrogen. Niacinamide cream will also lower your risk of skin damage. |
| Keep your fasting insulin levels below 3 — Insulin resistance is linked to accelerated brain aging, as well as neurodegeneration.18 |
| Eat a nutritious diet, rich in folate — Vegetables, without question, are your best form of folate. Avoid supplements like folic acid, which is the inferior synthetic version of folate. Research shows that folate is a protective factor against Alzheimer’s disease.19 |
| Avoid and eliminate mercury and aluminum from your body — Dental amalgam fillings, which are 50% mercury by weight, are one of the major sources of heavy metal toxicity. Make sure you use a biological dentist to have your amalgams removed. Sources of aluminum include antiperspirants, nonstick cookware and vaccine adjuvants. |
| Make sure your iron isn’t elevated and donate blood if it is — A study20 published in Aging Medicine shows that excess iron increases your risk of Alzheimer’s disease by initiating the Fenton reaction, leading to increased oxidative stress. |
| Exercise regularly — Exercise triggers beneficial changes that support cognitive function. Particularly, it’s been shown to improve blood flow to the brain, leading to an increase in biomarkers related to improved neuronal plasticity and better cell survival.21 |
| Eat blueberries and other antioxidant-rich foods — Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against neurological diseases. |
| Challenge your mind daily — Mental stimulation, such as learning to play a musical instrument, is associated with a decreased risk of Alzheimer’s.22 |
| Avoid anticholinergics and statin drugs — Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence and certain narcotic pain relievers.
Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of CoQ10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein. |
- 1 Alzheimer’s Association, “Facts and Figures”
- 2 Science Advances, Vol 10, Issue 43, October 25, 2024
- 3 Science Advances, Vol 10, Issue 43, October 25, 2024, Introduction
- 4 News-Medical.net, October 28, 2024
- 5, 6 Science Advances, Vol 10, Issue 43, October 25, 2024, Abstract
- 7 Wiley Analytical Science, October 29, 2024
- 8 Neurology. 2021 Dec 14;97(24):e2381–e2391, Abstract
- 9 World Wildlife Fund, Assessing Plastic Ingestion from Nature to People
- 10 Open Journal of Veterinary Medicine, 11, 57-86, Abstract
- 11 Gut Microbes. 2024 Jan 4;16(1):229786, Diet with Probiotics and Their Impact on Gut Health
- 12, 13, 14 Scientific Reports volume 13, Article number: 5258 (2023), Discussion
- 15 Critical Reviews in Microbiology, 2023, 49(2), 151-176
- 16 Am J Lifestyle Med. 2022 Jan 11;16(1):32–35, Abstract
- 17 Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404, Highlights
- 18 Int J Mol Sci. 2021 Sep 15;22(18):9987, Abstract
- 19 Front Neurosci. 2021 Apr 14;15:661198, Abstract
- 20 Aging Med (Milton). 2024 Oct 22;7(5):649–667, Iron Overload/Accumulation and Increase Risk of AD
- 21 Front Aging Neurosci. 2023 Aug 4;15:1243869, Conclusion
- 22 Aging Ment Health. 2021 Apr;25(4):593-601, Abstract