• There were stark differences in blood structure — According to the researchers, the test samples had far more microclots than healthy controls (a nearly 20-fold difference in the median count), and the clots tended to be larger.

Digging deeper into the data, they discovered that the microclots were intertwined with neutrophil extracellular traps, or NETs. These are sticky webs of DNA and enzymes that neutrophils release when activated. The researchers suggest that NET-rich clots may resist normal breakdown processes, which could leave lingering blockages at the microvascular level.

• The impact of NETs — The researchers reported major increases in several NETs markers — myeloperoxidase, neutrophil elastase, and circulating cell-free DNA — in the long COVID group. These are enzymes and DNA fragments that may act like glue inside the clots. The more NET material the researchers found, the more microclots there were.

• Another noteworthy detail is the size of the structures — Imaging showed that 60% of long COVID patients had the largest microclots (over 1,600 µm²), compared with 13% of healthy controls. Healthy controls also had microclots, but they were fewer and smaller.

Figure 1. People with long COVID had a nearly 20-fold higher median microclot count, and 60% had the largest microclots, compared with 13% of healthy controls.

• How deeply embedded the NET components were within the clots — Microscopy showed DNA and the neutrophil enzyme myeloperoxidase within the microclots, not just around them, although the authors noted this method can't reliably measure what proportion of microclots contain them. This is important because fibrin-based clots normally break down with the help of enzymes like plasmin.

The researchers suggest that when DNA and neutrophil proteins are built into a clot, the breakdown process may become inefficient and slow, which could help explain why long COVID can last for months or even years.

• Microclot size mattered — For example, all three NET markers rose along with microclot counts, and microclots in the 100 to 400 µm² range, the most common size, tracked most closely with them. The authors suggest these markers could one day help diagnose long COVID. It may also help researchers sort patients into subgroups in the future.

• NETs act as scaffolding — When neutrophils eject their DNA and enzymes, they create long, sticky strands designed to trap pathogens. In long COVID, the researchers propose that these strands latch onto fibrin — a protein involved in clotting — and build layered, tangled structures. Once formed, they may float through the bloodstream, lodging in tiny vessels and creating micro-obstructions. The result could be impaired microcirculation and reduced oxygen transfer.

• Another mechanism the researchers proposed involves the resistance of these clots to fibrinolysis — Because NET components may stiffen and reinforce the fibrin structure, the body's usual cleanup systems may struggle to dissolve them. This could lead to chronic retention of microclots, continued vascular stress, and prolonged symptoms.

Figure 2. The researchers propose that NETs bind to fibrin, forming microclots that may resist breakdown and lodge in tiny blood vessels.

• The amount of NET material increased directly alongside the amount of microclots — This suggests the immune and clotting systems may be interacting in a loop, each one pushing the other. Over time, such a loop could drain your energy, stress your cardiovascular system, and keep inflammation alive long after the virus is gone.

• Rates of clotting complications — Deep-vein thrombosis and pulmonary embolism increased dramatically among hospitalized COVID patients, and the researchers reported that in one study, nearly a third of critically ill patients still had blood that clotted too easily even while receiving anticoagulant therapy designed to prevent clots. Even so, another study identified preventive anticoagulant therapy as a “protective factor” against pulmonary embolism.

• What happened after people left the hospital — Extended clotting risk showed up in multiple studies, with patients showing clot formation weeks to months after the initial infection had passed.

• A comparison of clot complications across different groups — The authors noted that those with preexisting cardiovascular disease, diabetes, obesity, or advanced age were more likely to experience severe clotting events. Clotting complications during the acute illness were uncommon in people with mild illness who weren't hospitalized. However, one large study cited in the review found that clot risk was still raised nearly a year later, including in people who were never hospitalized.

• SARS-CoV-2 creates imbalance between clot formation and clot breakdown — Under normal conditions, your body constantly forms tiny clots and dissolves them. But according to the researchers, COVID disrupts this balance by releasing clot-promoting chemicals, damaging vessel walls, and activating platelets at unusually high rates. Once this imbalance begins, your body forms clots faster than it dissolves them.

• Biological mechanisms that tie the processes together — The paper explains how the virus may infect endothelial cells, which are the thin linings inside your blood vessels. When these cells are damaged, they release substances that encourage clotting, narrow the vessel opening, and attract platelets to the injury site.

The result is a chain reaction — damaged endothelium signals inflammation, inflammation triggers platelet activation, and activated platelets send more clotting signals.

Figure 3. In COVID, damage to the vessel lining can set off a chain reaction of inflammation, platelet activation, and more clotting signals.

• The immune system's involvement — COVID-19 stimulates a wave of inflammatory cytokines, which are chemical messengers that tell the body to mount a defense. When these cytokines rise too high, your clotting system receives constant signals to activate.

Some researchers think this may be why some people feel as if their bodies never shut off even after the infection is gone — their inflammatory and clotting pathways may remain switched on, draining energy and straining the heart, lungs, and muscles.

• How platelet behavior changes during and after infection — Platelets are tiny cell fragments that help your blood clot when you're injured. According to the researchers, the SARS-CoV-2 virus drives platelets into a highly activated state where they clump together more easily, interact abnormally with immune cells, and release clot-promoting substances.

Researchers have proposed that this heightened reactivity may not return to normal right away, and that ongoing platelet activation could contribute to lingering symptoms, even when scans or standard tests look fine.

1. Proteolytic enzymes — Whenever I encounter someone who is experiencing long COVID symptoms, one of the first things I suggest is proteolytic enzymes, such as nattokinase, lumbrokinase, and serrapeptase, which may help clear residual spike protein from the body, ease inflammation, and give the brain and tissues space to recover. In a laboratory study, nattokinase broke down the SARS-CoV-2 spike protein in cell cultures,⁶ but this hasn't been tested in people with long COVID.*

These enzymes are best taken on an empty stomach, at least an hour before, or two hours after, consuming protein. If taken with food, they may be diverted into digesting your meal instead of clearing problematic proteins from the bloodstream. Because these enzymes break down fibrin, they may increase bleeding risk. So if you take a blood thinner or antiplatelet medication, have a bleeding disorder, or have surgery scheduled, talk to your doctor before using them.

*These findings are from laboratory or animal research and may not directly apply to human health.

2. Consider the I-RECOVER protocol — The Independent Medical Alliance (IMA), previously known as the FLCCC, offers a detailed plan called the I-RECOVER protocol. It's a detailed guide for addressing post-vaccine and post-infection complications.

It outlines strategies for detoxification, calming inflammation, and restoring mitochondrial function — all foundational steps for improving health after COVID-related injuries. Several of its recommendations involve prescription medications, so work through it with a healthcare provider.

3. Reduce intake of linoleic acid (LA) — Your mitochondria rely on a unique lipid called cardiolipin,⁷ which is located within the inner membrane structures (cristae) where energy is produced. It stabilizes the electron transport chain, maintains the folded cristae structure that expands surface area for energy production, and helps manage proton flow needed to generate ATP.

This is more important than most people realize, as the wrong dietary fats can distort cristae structure and hinder energy production. Roughly 20% of this membrane is composed of cardiolipin, a distinctive phospholipid that contains four fatty acid chains instead of the usual two.

Importantly, cardiolipin requires LA to function properly. The problem begins when excess dietary LA accumulates in the other 80% of the inner mitochondrial membrane — phospholipids that are not designed to carry high LA loads. In those surrounding membranes, LA is highly prone to oxidation.

Figure 4. Cardiolipin makes up about 20% of the inner mitochondrial membrane and requires linoleic acid; excess linoleic acid in the other 80% raises the risk of membrane dysfunction.

Reactive oxygen species (ROS) generated during normal energy production initiate lipid peroxidation, forming toxic aldehydes that bind to respiratory proteins, impair electron transfer, and amplify oxidative stress in a self-perpetuating cycle. When LA in these non-cardiolipin phospholipids exceeds 7% to 8%, the risk of membrane dysfunction increases threefold.⁸

Keeping daily LA intake under 5 grams, and closer to 2 grams when possible, helps limit excess incorporation into these non-cardiolipin membrane compartments. LA is found in excess in seed oils (which are used heavily in ultraprocessed and restaurant foods), condiments, nuts and seeds, adulterated olive and avocado oils, and animal products from grain-fed livestock such as conventional chicken and pork. To track your intake, I recommend downloading my PAX app once it's available.

4. Methylene blue — Some practitioners use this compound for the exhaustion and neurological challenges that linger after COVID infection or getting the shot, although it hasn't been studied for long COVID. It functions as an electron carrier, essentially acting like a rechargeable energy source. Unlike many compounds that perform a similar role, it's less likely to promote harmful oxidative reactions at low doses.

When mitochondrial respiration or oxygen utilization is impaired, methylene blue can reroute electron flow, helping sustain energy production even when normal pathways are blocked. It may also help compensate for reduced blood flow by improving mitochondrial efficiency when tissues aren't receiving enough oxygenated hemoglobin.

Its benefits may extend beyond the time it remains in the body — methylene blue may induce biochemical changes that enhance oxygen-processing pathways and may even promote the formation of new mitochondria over time.

Dosing is hormetic. Low amounts provide benefits that high amounts can negate. Most experts recommend relatively high doses for longer-term treatments, such as 0.5 milligrams (mg) to 1 mg per kilogram of body weight for cognitive support. For a person weighing 150 pounds, that would be a dose of 34 to 68 milligrams. I believe this is excessive and unnecessary.

Doses of more than 3 to 5 milligrams are likely never needed unless you are undergoing treatment for a life-threatening condition such as carbon monoxide or cyanide poisoning. The average dose for most adults that reduces reductive stress is only 5 mg, once a day, regardless of weight. It has a half-life of over twelve hours and will gradually build up if you take it every day, so higher doses are not needed.

Only use pharmaceutical-grade methylene blue in capsule or tablet form, prescribed by a healthcare professional and filled through a compounding pharmacy, as industrial and chemical varieties frequently contain contaminants like heavy metals. Taking it with vitamin C may enhance absorption.

Keep in mind, though, that methylene blue can cause a dangerous reaction called serotonin syndrome when combined with SSRIs and other serotonergic medications, and it isn't safe for people with G6PD deficiency.

To learn more, read "The Surprising Health Benefits of Methylene Blue." It features an interview with methylene blue expert Francisco Gonzalez-Lima, Ph.D., who has spent many years studying this drug.

5. Check your iron levels — Excess iron is another major disruptor of mitochondrial function, and many people — aside from menstruating women or individuals with significant blood loss — tend to accumulate too much. In contrast, copper deficiency may be more common than many people realize. A ferritin blood test shows where you stand; the ideal range is 60 to 75 ng/mL.

Iron and copper need to be in balance because they depend on each other for proper metabolism. Copper is required to move and recycle iron efficiently, so low copper can contribute to iron problems such as anemia, even when iron intake is adequate. Copper is also essential for mitochondrial energy production, detoxification, and overall metabolic health.⁹ You can learn more about this in "The Poorly-Understood Role of Copper in Anemia."

You can increase copper by supplementing with 4 to 10 mg of copper bisglycinate daily or by consuming copper-rich foods like bee pollen, grass fed beef liver, and acerola cherry (which contains the copper-dense enzyme tyrosinase). The upper limit for adults is 10 mg a day from food and supplements combined,¹⁰ so keep your total at or below that and check with your healthcare provider before supplementing.

To reduce excess iron, routine blood donation is a simple and effective method. This usually involves donating two to four times annually, or having smaller amounts removed monthly by a healthcare provider (shown below) if large donations aren't well-tolerated. If you have severe chronic obstructive pulmonary disease (COPD) or congestive heart failure, consult a physician first.

Figure 5. Monthly blood removal amounts by group, for people who don't tolerate large donations well.

• Quercetin strengthens your antioxidant defenses in more than one way — One particularly interesting mechanism involves metal ions such as iron. Under certain conditions, iron drives chemical reactions that generate highly reactive molecules capable of damaging cells. Quercetin binds to iron and reduces its ability to fuel those reactions. It also limits oxidative damage to fats, including fats found in cell membranes and LDL particles.

Another layer involves glutathione, one of your body's major antioxidant defenses. The review describes quercetin's effects on glutathione levels and antioxidant enzymes, along with activation of Nrf2, a protein that switches on genes involved in cellular protection. Think of Nrf2 as part of your cells' internal defense-control system. Quercetin helps activate that system rather than simply neutralizing damaging molecules one at a time.

• Quercetin attacked harmful bacteria through several weak points — Laboratory research reviewed in the paper found activity against pathogens that included E. coli, Staphylococcus aureus, Salmonella and Pseudomonas aeruginosa. The mechanisms were strikingly direct. Quercetin damaged bacterial cell walls and membranes, altered their permeability, interfered with protein production, reduced enzyme activity and disrupted nucleic acid production.

Quercetin didn't attack just one bacterial target. It interfered with several processes microbes need to survive and reproduce. Still, the authors emphasized that antimicrobial research remains incomplete, particularly for fungi, so these laboratory findings don't establish quercetin as a replacement for treatment of bacterial or fungal infections.

• Inflammatory pathways were another major target — The review found that in laboratory and animal studies, quercetin suppressed several chemical signals involved in inflammation, including tumor necrosis factor alpha and certain interleukins. These are signaling molecules your immune system uses to coordinate inflammatory responses. Quercetin also inhibited enzymes involved in producing inflammatory compounds.

That gives you a clearer picture of why quercetin's effects reach across different areas of health. Oxidative stress and inflammation often reinforce each other. The research suggests quercetin acts on both sides of that relationship rather than addressing only one piece.

• Human cardiovascular studies produced measurable changes in blood pressure — Among people with stage 1 hypertension, 730 milligrams (mg) of quercetin taken for 28 days reduced systolic, diastolic and mean arterial blood pressure, according to research summarized in the review. Another study involved 93 overweight or obese adults at high risk for metabolic syndrome.

After six weeks at 150 mg per day, researchers reported significant reductions involving systolic blood pressure and oxidized LDL.

Mechanistically, the paper connects these cardiovascular effects with improved blood vessel function, nitric oxide activity, reduced LDL oxidation, less platelet clumping and lower inflammatory activity. Those processes matter because healthy arteries must remain flexible while resisting oxidative and inflammatory damage.

• Quercetin also helped cells defend themselves against toxic stress — The review examined mycotoxins, toxic compounds produced by certain fungi. Experimental research found that quercetin reduced reactive oxygen species, supported antioxidant enzymes and limited distress inside the cellular structure responsible for processing proteins.

When that stress becomes severe, cells activate apoptosis, a self-destruct sequence that eliminates damaged cells before they cause further harm. Quercetin reduced this chain of damage in experimental cell models.

The evidence has an important boundary. The authors state that quercetin's absorption and metabolism in the human body aren't yet fully understood and that more research is needed before these experimental findings translate into pharmacological uses. That distinction helps you separate promising biological mechanisms from benefits already demonstrated in people.

• The cognitive advantage became clear after 24 weeks — Researchers used several assessments rather than relying on a single measure. The primary test was the Mini-Mental State Examination, or MMSE, which measures abilities such as orientation, memory, attention, calculation and language on a 30-point scale. At 24 weeks, the improvement from baseline was significantly greater in the quercetin-rich onion group than in the placebo group.

The difference was particularly clear when researchers excluded participants who regularly took prescription medications. Among these participants, MMSE scores increased by an average of 1.8 points in the quercetin-rich onion group versus 0.6 points in the placebo group after 24 weeks. This subgroup included 19 people in each group.

• The benefits extended beyond conventional cognitive testing — Researchers also assessed emotional health because mood and motivation influence how well your brain functions in everyday life. On the depression assessment, scores decreased significantly more in the quercetin-rich onion group after 24 weeks, with lower scores reflecting fewer depressive symptoms. Motivation also improved.

That connection matters because cognitive health isn't simply about whether you remember a word or solve a test question correctly. Whether you stay socially engaged, pursue activities you care about and remain mentally active shapes daily function as much as any test score. The researchers proposed that improvements in depression and motivation contributed to the cognitive changes they observed.

• Family members noticed a difference in the burden associated with participants' symptoms — Each participant had a study partner living in the same household who evaluated behavioral and psychological symptoms. After 24 weeks, the burden reported by study partners was significantly lower in the quercetin-rich onion group than in the placebo group.

Not every behavioral measure changed, however. Researchers didn't find a significant difference between groups in the overall severity of neuropsychiatric symptoms. This distinction helps put the findings in perspective: quercetin-rich onion didn't improve every measure tested, but several specific cognitive and emotional outcomes moved in a favorable direction.

• The researchers identified several ways quercetin could support the aging brain — One involves blood flow. Flavonoids such as quercetin affect the vascular system, and changes in blood flow through the brain influence the environment surrounding your neurons. The researchers noted that these vascular effects could support neurogenesis and angiogenesis, the formation of new nerve cells and blood vessels.

Another mechanism involves protection against oxidative injury. Brain cells are particularly vulnerable to this type of damage because they require large amounts of energy to function. The researchers explained that flavonoids support antioxidant defenses that protect neurons from toxic injury, providing a biological explanation for why regular intake could influence cognitive aging.

• The study tested a food-level amount rather than an extreme dose — Participants consumed 11 grams of onion powder each day, equivalent to about 120 grams of raw onion, or roughly half of a medium-sized onion. That provided 50 mg of quercetin daily. The researchers noted that estimated normal dietary intake is approximately 50 to 100 mg per day, placing the study amount within an ordinary dietary range.

No significant differences emerged between groups in body weight, body fat percentage or body mass index, and blood tests related to liver and kidney function showed minimal changes. The practical takeaway is important: the cognitive findings came from consistent intake of a quercetin-rich food over six months, reinforcing the value of obtaining protective plant compounds through whole foods rather than assuming that more from a high-dose supplement is better.

These findings are from research conducted in clinical settings. Results may not apply to all individuals.

1. Eat quercetin-rich foods regularly — Make onions one of your primary food sources of quercetin. Apples, berries, grapes and tomatoes are other useful choices. This gives you quercetin alongside vitamins, minerals and other beneficial plant compounds instead of consuming it in isolation.

Consistency matters. In the 24-week human trial, 50 mg of quercetin per day from quercetin-rich onion improved cognitive function, providing evidence that a food-based amount produces measurable effects.⁴ You don't need to chase unusually high doses to make quercetin part of your health strategy.

2. Use supplemental quercetin thoughtfully — If you want a more concentrated amount than you're getting from food, supplemental quercetin is another option. Research published in Frontiers in Immunology reported a strong safety profile for oral quercetin, with doses up to 1,000 mg per day for three months not producing significant adverse effects.⁵ Intravenous quercetin is different; high IV doses have produced adverse effects and, at still higher doses, kidney toxicity.

More isn't necessarily better. The human study covered earlier used just 50 mg daily from food.⁶ I would use the lowest supplemental amount necessary for your goal rather than viewing 1,000 mg as a target simply because that amount has been studied for safety.

3. Pair quercetin with vitamin C — Vitamin C complements quercetin particularly well. Research has described synergistic effects between the two compounds, meaning their combined activity is greater in certain biological processes than either one alone.⁷ Vitamin C also helps recycle oxidized quercetin back into its active form.

You can increase vitamin C through foods such as citrus fruits, guava, kiwi, bell peppers and other fruits and vegetables. If you're supplementing with quercetin, vitamin C provides a logical companion rather than adding a long list of unrelated supplements.

4. Quercetin's Effects May Extend to Cellular Senescence — Beyond the mechanisms described above, quercetin has also been studied separately as a potential senolytic, a compound researchers are investigating for its ability to help clear senescent cells. These are damaged cells that stop dividing but don't die off, lingering in tissue while releasing inflammatory substances that affect neighboring healthy cells.

This senolytic research is distinct from the human trials discussed earlier in this article, and the specific timing strategies sometimes proposed for it — such as taking quercetin after an extended period without food — have not been directly tested in those trials.

5. Support the same pathways quercetin acts on — Quercetin should be viewed as part of a healthy lifestyle, not a tool to compensate for daily habits that continuously promote oxidative stress and inflammation. Its broad effects make the most sense as one part of a lifestyle designed to protect your cells.

Keep linoleic acid (LA) below 5 grams per day and ideally below 2 grams by eliminating concentrated sources such as seed oils and ultraprocessed foods. Walk for up to 60 minutes daily, add strength training twice a week and break up prolonged sitting. Those habits support metabolic and cardiovascular health while quercetin works through many of the same interconnected systems involved in inflammation, oxidative stress and cellular protection.

• The immediate effect of cancer on families — A single diagnosis forced the Sullivans to pause and raise questions about daily habits that once felt harmless. Food, household products, and everyday exposures were scrutinized heavily.

• Fear turned into action — Instead of staying overwhelmed, Patrick and Ashley focused on what they could control. Food became their starting point because it is a daily choice. They began removing ingredients they no longer trusted and rebuilt meals around simpler, cleaner foods.

• How personal change grew into a larger purpose — Patrick and Ashley channeled what they learned into building a food business with strict rules — simple ingredients, no seed oils, and real flavor. Their story also serves another important lesson — you don't need to experience a life-threatening diagnosis to learn what is in your food and how it's impacting your health.

• The importance of freshness in produce — Consumers and local communities can largely benefit from consistent access to fresh greens, and the key is how they are made. When greens are grown close to where you live, they arrive fresher and last longer.

• Giving back to the community — Good Living Greens is doing a service to their community by offering clean, organic produce from personally vetted farmers. According to co-owner Jill Keefe, less handling and shorter travel time protect freshness as well.

• Keeping it local maintains quality — All Americans deserve access to clean, nutritious produce. However, it's practically impossible for a farmer to follow this practice on a national scale. That's why it's important for local farmers to rise and meet the demand of the community where they live, which may support health outcomes:

"The farmers and the vendors that we work with, none of us have any intention to scale beyond our current size. So, what we need is instead of Big Food and big industries and industrial farming, we need to break that down and federate it and have communities that have their own little ecosystems local retailers, local farmers, local food makers all talking and working with each other about how to meet the needs."

• What you see is what you get — The type of beef by the featured company does not come from large feedlots or anonymous supply chains. Instead, it comes from ranchers who control how animals are raised from start to finish. When cattle are raised on grass rather than industrial feed, the final product is different in quality and texture.

• How inputs shape outcomes — Grass fed cattle graze naturally and are not rushed through growth using industrial shortcuts. This results in beef that is ultimately more nutritious compared to conventionally raised options.

• Transparency benefits your health — The documentary presents a key takeaway regarding the meat you buy. It's important to know where it comes from and who produces it. In addition, local ranchers keep money in the community and offer an alternative to mass-market meat that hides its origins.

• Not all eggs are created equal — The Sullivans also visited Inspire Farms, a business based in Mesa, Arizona that specializes in pasture-raised chickens. Tiffiny Lilley, the owner, tells them that many of her customers are supposedly allergic to eggs, but in her experience, they were allergic to corn — a common chicken feed. Lilley shares:

"So, at 50% of the people come in and tell me they can't eat eggs are also allergic to corn. And I'm like, 'Just buy some of our eggs, try it out and let me know.' And they come back and they're like, 'Holy cow, I can eat eggs because most of the eggs in the market have been fed corn.'"

• Local dairy farmers are trying to survive — The Sullivans also feature Crow's Dairy, a small operation specializing in dairy products made from goat's milk. Wendell Crow, the owner, explains that many of the agricultural rules and regulations in place today are written with big operations in mind, even though small businesses work very differently:

"The USDA does nothing to help the small farmers. Farm Bureau does nothing to help the small farmers. They all think big. The small farmer is providing healthy food ...

But it's just such a conundrum trying to produce a good product and stay in business. I feel bad all the time because there's restaurants who can't afford my cheese, and you have to be really high. And so, I'm only feeding rich people, but I have to charge that to stay in business because I'm small."

• Money is being spent to tell you what to eat — According to Alex Clark, host of the Culture Apothecary podcast, food choices are influenced less by facts and more by what shows up in newsfeeds, ads, and conversations. Culture teaches you what's acceptable to crave and what's worth questioning. For example, when unhealthy food is marketed as fun, easy, and harmless, it becomes part of daily life without much resistance.

Younger generations grew up surrounded by ultraprocessed foods designed to be irresistible and heavily marketed from childhood. This shaped habits early, long before people understood what they were consuming. Big Food has conducted a silent, population-wide experiment where consent was never asked, yet consequences are now apparent.

• Big Food and weight gain — The documentary features Leah Hope, a health transformation coach who was able to break free from Big Food. Throughout her adulthood, she struggled with excess weight linked to ultraprocessed foods.

But at one point, she realized that she was trapped, which caused her to change her habits and lose 190 pounds naturally. By moving toward simpler meals, her body began responding in a healthier way.

Hope did not rely on short-term plans or extreme rules. She focused on habits she could maintain, such as regular exercise. When her diet was no longer designed to encourage overeating, hunger became easier to manage.

• More are joining the cause for a healthier America — One of the experts featured in the documentary is Calley Means, a former DC lobbyist. After realizing the harm he has done, he's now working to change the American food system for the better:

"The fact of the matter is that healthy food is sometimes more expensive because of corrupt government incentives. That is the plane that we're on right now. We need to realize that we are in a terrible situation ...

It is incumbent on each American to shift our diet more to whole foods. This movement of moms, this movement of parents, this movement of farmers, it makes a big, big difference. And getting more involved with this message that we need to reform our agriculture system, that we need to get to root cause of why we're getting sick.

We need to keep that momentum up. When I was sick, I could only think about how much it hurt, how hard life was, and now being healthy. It really means freedom."

• Everyday consumers care about what they eat but lack direct connections to producers — Most people do not have the time or knowledge to search for individual farms. By creating a system like FromtheFarm.Org that brings farmers and customers together in one place, buying real food becomes as easy as buying anything else.

• The advantages of having a digital farmers market — FromtheFarm.org helps small producers reach more people without losing their values. Farmers receive support with marketing, education, and logistics, while you gain access to real food. This structure allows small farms to grow without becoming a large, industrial operation, protecting quality along the way.

• Trust becomes the real product — The film emphasizes that you are not only buying food. You are buying confidence in where it came from and how it was produced. Education from well-intentioned people plays a key role in helping people break free from Big Food.

• American Grassfed Association — The goal of the American Grassfed Association (AGA) is to promote the grass fed industry through government relations, research, concept marketing, and public education.

Their website also allows you to search for AGA-approved producers certified according to strict standards that include being raised on a diet of 100% forage; raised on pasture and never confined to a feedlot; never treated with antibiotics or hormones; born and raised on American family farms.

• EatWild.com — EatWild.com provides lists of farmers known to produce raw dairy products as well as grass fed beef and other farm-fresh produce (although not all are certified organic). Here you can also find information about local farmers markets, as well as local stores and restaurants that sell grass fed products.

• Weston A. Price Foundation — Weston A. Price has local chapters in most states, and many of them are connected with buying clubs in which you can easily purchase organic foods, including grass fed raw dairy products like milk and butter.

• Grassfed Exchange — The Grassfed Exchange has a listing of producers selling organic and grass fed meats across the U.S.

• Local Harvest — This website will help you find farmers markets, family farms, and other sources of sustainably grown food in your area where you can buy produce, grass fed meats and many other goodies.

• Farmers Markets — A national listing of farmers markets.

• Eat Well Guide — Wholesome Food from Healthy Animals — The Eat Well Guide is a free online directory of sustainably raised meat, poultry, dairy and eggs from farms, stores, restaurants, inns, hotels and online outlets in the U.S. and Canada.

• Community Involved in Sustaining Agriculture (CISA) — CISA is dedicated to sustaining agriculture and promoting the products of small farms.

• The Cornucopia Institute — The Cornucopia Institute maintains web-based tools rating all certified organic brands of eggs, dairy products, and other commodities, based on their ethical sourcing and authentic farming practices separating CAFO (concentrated animal feeding operation) "organic" production from authentic organic practices.

• RealMilk.com — If you're still unsure of where to find raw milk, check out Raw-Milk-Facts.com and RealMilk.com. They can tell you what the status is for legality in your state, and provide a listing of raw dairy farms in your area. The Farm to Consumer Legal Defense Fund also provides a state-by-state review of raw milk laws.² California residents can also find raw milk retailers using the store locator available at RAW FARM.³

• Thymic output declines, reducing newly formed T cells — One of the core shifts involves the thymus, the organ that produces naïve T cells. With age, thymic activity declines, leading to fewer newly formed T cells entering circulation. Because naïve T cells are your front-line responders to unfamiliar pathogens, this reduction makes it harder for your immune system to mount strong first-time responses.

• Memory T cells accumulate, limiting adaptability — As naïve T cells drop, memory T cells become a larger share of your immune system. Memory cells help with threats you have already encountered but bring little support when something new appears. This shift helps explain why older adults respond less robustly to vaccines and face more risk from novel infections.

• Inflammaging becomes a defining feature of later life — As immune cell patterns shift with age, the body enters a state of persistent, low-grade inflammation. This phenomenon, known as inflammaging, reflects higher levels of inflammatory mediators circulating at rest and is considered one of the central characteristics of an aging immune system. Learn more about this in "'Inflammaging' Is a Lifestyle Phenomenon, Not a Universal Aging Trait."

• Urolithin A increased naïve-like CD8 T cells — Participants who received urolithin A showed a small but statistically significant increase in naïve-like CD8 T cells, which resemble younger, freshly formed immune cells and carry fewer markers of exhaustion. Alongside this shift, their CD8 T cells became noticeably better at using fatty acids for energy than those in the placebo group, suggesting better metabolic flexibility.

• Some innate immune cell populations increased — Urolithin A supplementation increased CD56dimCD16bright natural killer (NK) cells, the most common NK cell subset in human blood. For context, NK cells help identify and eliminate infected cells, but the researchers note that the functional relevance of this particular shift remains unclear, and NK cell killing activity was not directly measured.*

• Signs of increased mitochondrial biogenesis appeared within CD8 T cells — Participants who took urolithin A showed higher levels of PGC-1α, the protein that guides mitochondrial growth and renewal.

The researchers propose that urolithin A may prompt immune cells to clear out older, less efficient mitochondria and build new ones, strengthening their overall energy system. However, mitophagy itself was not directly measured in participants, and this proposed mechanism rests largely on the team's earlier mouse and laboratory work.

• Laboratory tests showed changes in immune cell activity — When researchers activated T cells in the lab, those from the urolithin A group produced more tumor necrosis factor (TNF), a cytokine that signals rapid immune engagement. Monocytes also demonstrated better uptake of E. coli particles, suggesting an improved ability to recognize and engulf microbial targets under laboratory conditions.*

• Molecular programming shifts within immune cells — Exploratory single-cell analysis suggested that urolithin A shifted inflammatory and metabolic pathways across multiple immune cell types. The researchers caution that these comparisons were exploratory and did not preserve randomization. As they explained:

"Exploratory single-cell RNA sequencing demonstrated urolithin A (UA)-driven transcriptional shifts across immune populations, modulating pathways linked to inflammation and metabolism.

These findings indicate that short-term UA supplementation modulates human immune cell composition and function, supporting its potential to counteract age-related immune decline and inflammaging."⁵

• Muscle strength and endurance — In a randomized, placebo-controlled clinical trial of 66 older adults aged 65 to 90, published in JAMA Network Open, participants were given 1,000 mg of urolithin A or a placebo daily for four months. Urolithin A significantly improved muscle endurance, measured as the number of contractions until fatigue in both hand and leg muscles, compared with placebo.

However, the trial's primary end points — six-minute walk distance and maximal adenosine triphosphate (ATP) production in the hand muscle — did not improve significantly versus placebo. Moreover, the study was funded by the urolithin A manufacturer.**⁷

A separate four-month trial in 88 overweight, untrained adults aged 40 to 64, published in Cell Reports Medicine, found that daily urolithin A supplementation (500 mg or 1,000 mg) improved hamstring muscle strength by about 10% to 12% compared with placebo and produced favorable shifts in several biomarkers associated with mitochondrial health.

Improvements in aerobic endurance and walking distance did not reach statistical significance against placebo, the trial's primary end point (peak power output) was not met, and the study was sponsored by the urolithin A manufacturer.**⁸

• Fatty liver — In a mouse model of fructose-induced fatty liver disease, urolithin A administration reduced hepatic steatosis (fat buildup in the liver) and improved the balance between fat creation and fat breakdown in the liver by impairing lipogenesis and enhancing β-oxidation.⁹ In parallel, a Biomedicines review notes that urolithin A attenuated inflammation in liver tissue in animal models of metabolic disease.¹⁰

• Metabolic disorders — Urolithin A has been studied in laboratory and animal models of obesity, Type 2 diabetes, and metabolic syndrome. In laboratory studies using human fat and liver cells, urolithin A reduced triglyceride accumulation by lowering genes that drive fat creation and activating AMPK, an energy-sensing pathway that shifts cells toward burning stored fat instead of stockpiling it.¹¹

More detailed experiments in mouse preadipocytes (the precursor cells that eventually mature into fat cells) found that urolithin A lowered triglyceride content and suppressed the expression of several key genes that help regulate fat storage, glucose transport, and fatty acid binding, a change that may help limit fat accumulation while still allowing fat cells to form normally.*¹²

Additional research also reported that urolithin A protected mice and rats from high-fat diet-induced obesity and insulin resistance by supporting thermogenesis, increasing browning responses (a shift toward a more metabolically active type of fat cell), reducing oxidative stress, and lowering inflammatory activity within adipose tissue.¹³

• Urolithin A is naturally produced in your body — When you eat foods rich in ellagitannins, a class of polyphenols found in pomegranates and some berries, these plant compounds are first converted into ellagic acid and then transformed into different urolithins depending on which microbial species live in your gut.¹⁴

• Not everyone forms urolithin A efficiently — The ability to generate urolithin A depends on your gut microbiota composition. Factors such as age, diet, medication use, and overall microbial diversity may influence whether the conversion occurs.

According to one review, this conversion is observed in only about 40% of the population, and output varies widely among those who do produce it.¹⁵ This variability is one reason researchers have tested urolithin A directly in clinical trials, including those described above.

• How it's delivered may matter — Because urolithin A acts on mitochondria, some researchers are exploring ways to deliver it more directly to them. Mitochondria are under constant wear, so the body depends on recycling the damaged ones.¹⁶

They contain the furnace of energy production, and because most people consume excess linoleic acid (LA) from seed oils, their mitochondria may be damaged prematurely. These damaged mitochondria need to be recycled; if they accumulate instead, your cellular energy production can decline.

1. Remove processed foods and vegetable oils from your diet — Processed products are typically made with seed oils that contain large amounts of LA, which can interfere with mitochondrial function and reduce your ability to generate energy efficiently.

Nuts, seeds, and most restaurant meals contribute additional LA, since commercial kitchens rely heavily on these oils, so it's best to prepare most of your meals at home. When you do eat out, The Templeton List (templetonlist.com) can help you find healthier restaurants.

Chicken and pork often contain higher levels of LA as well, due to the way they are commonly raised and fed. Center your diet around whole foods and choose low-LA fats such as grass fed butter, tallow, and ghee. Aim to keep your daily LA intake below 5 grams. Use the Seed-Oil Sleuth feature in the upcoming PAX, which can help track the LA in your food.

2. Optimize your carbohydrate intake for cellular fuel — A balanced diet rich in the right carbs and free of ultraprocessed foods feeds your mitochondria with the glucose they're designed to burn. Focus on whole fruits and white rice first, then gradually bring in root vegetables, legumes, and well-tolerated grains as your gut improves. Aim for 250 grams of targeted carbs daily — far more if you're active — to support healthy thyroid function and cellular energy production.

3. Reduce exposure to environmental toxins — Your cells are exposed to synthetic chemicals every day. Substances such as endocrine-disrupting chemicals (EDCs) from plastics, estrogen-mimicking compounds like xenoestrogens, and widespread electromagnetic fields (EMFs) can interfere with how efficiently your mitochondria produce energy. When these exposures accumulate, mitochondrial function can decline.

Taking steps to limit this burden can make a meaningful difference. Choose household items made from natural materials whenever possible, and store food in glass instead of plastic. Creating a low-EMF sleeping environment is also helpful, as it allows your cells to recover overnight with less external stress. Collectively, these changes reduce the strain placed on your body.

4. Get proper sun exposure — Regular sun exposure supports cellular energy by stimulating your mitochondria to produce melatonin — most of your body's melatonin is made in the mitochondria in response to near-infrared light — which provides strong antioxidant protection inside your cells.

However, it's best to avoid direct sun during peak hours (typically 10 a.m. to 4 p.m. in most parts of the U.S.) until you have minimized seed oils in your diet for four to six months, as the buildup of LA in your tissues makes your skin more prone to sunburn. After that, solar noon is the optimal time for sun exposure.

5. Support healthy NAD⁺ levels — Taking niacinamide at a dose of 50 mg three times a day may help raise your NAD⁺ levels, which supports mitochondrial energy production. NAD⁺ also plays a role in normal cell-death signaling and in immune cell function.

• Obese animals were used to mirror real metabolic dysfunction — Male and female mice were fed a high-fat diet for 10 weeks until they developed obesity — a model designed to mirror the stubborn metabolic rigidity people experience in real life. Keep in mind that this was a mouse study reported in a master's thesis, not a peer-reviewed human trial.

Treatment didn't begin until obesity was firmly in place, which makes the findings far more relevant to anyone trying to fix a long-standing weight issue. Once PDH was turned back on with DCA, the animals started losing weight in a favorable pattern: fat dropped, muscle stayed intact. The treated mice also ate and drank less, which may have contributed to the weight loss.

The intervention lasted four weeks after the animals were already obese, suggesting that metabolic repair is still possible even when dysfunction is advanced. If you feel like you've "gone too far" into weight gain or sluggish metabolism, this animal research suggests your energy system is still responsive.

• Fat loss increased without sacrificing muscle, and glucose tolerance improved — Measurements showed that "most of that loss came from fat rather than from muscle."³ That detail is a big deal because muscle is your metabolic engine. Losing it slows energy production and makes every future attempt at weight loss harder. Protecting muscle while losing fat gives you better long-term control over hunger, energy, and body composition.

Blood sugar spikes also dropped and returned to normal faster after treatment in the high-dose group, although insulin sensitivity didn't improve much. Better glucose tolerance means your body is actually using fuel instead of storing it.

• Simple nutrients may support this process without using DCA — DCA itself is an experimental compound that isn't approved for treating obesity, and it has been linked to nerve damage and liver problems at higher doses or with long-term use, so it's not something to try on your own.

Vitamin B1, magnesium, and niacinamide support PDH activity, and Dinkov suggests this combination could have produced effects similar to DCA's, although the thesis didn't test it. B1 and magnesium are cofactors PDH needs, and niacinamide helps raise the NAD⁺/NADH ratio, which may improve how well you burn glucose. This points to a practical, accessible, and nondrug way to support the same beneficial pathway.

• Lowering dietary fat may increase PDH activity — Fat intake directly influences the Randle cycle — the mechanism showing how excess fat blocks glucose oxidation by lowering the NAD⁺/NADH ratio. When your fat intake falls and your carbohydrate intake rises appropriately, PDH can reopen and your metabolism may shift toward higher energy production and easier fat loss.

• Muscle cells behaved very differently based on the fitness and metabolic health of the person they came from — Lean and aerobically fit adults in earlier research showed greater metabolic flexibility: Their muscles relied more on fat during fasting and shifted toward burning glucose when insulin rose. In contrast, obese and sedentary individuals showed a narrow, rigid pattern. In the lab, muscle cells from leaner, more insulin-sensitive men ramped up fat burning more when given extra fatty acids.

In people with obesity, muscles did not shift effectively toward fat during fasting, and they did not shift effectively toward glucose when insulin increased. This locked-in pattern may help explain why some people gain fat even when they're doing everything "right."

• Healthy muscle adapts quickly, while metabolically inflexible muscle does not — Muscle from fit individuals showed a high level of reliance on fat during fasting. When insulin entered the picture, their muscles suppressed fat burning and switched to glucose with ease.

Obese individuals had heavier dependence on glucose at the wrong time. Their muscles also failed to increase glucose oxidation effectively when insulin was present. This mismatch can trap the body in a cycle where fat stays stored and glucose lingers in the bloodstream.

• The presence of excess fatty acids disrupts fuel switching — Elevated fatty acids in the blood can blunt insulin's ability to stimulate glucose oxidation, creating a pattern similar to what is seen in Type 2 diabetes. When muscles face chronically high fatty acid exposure, they become less able to suppress fat burning when insulin rises and less able to burn glucose efficiently.

The body can end up in metabolic deadlock. This suggests dietary choices that increase fatty acid load can interfere with how your muscles manage energy.

• Even triglyceride storage inside muscle varies between individuals — Endurance-trained athletes often have high levels of intramuscular triglycerides, yet they burn through these stores efficiently thanks to superior mitochondrial capacity.

Their muscles treat fat as a high-quality reserve fuel. In contrast, sedentary individuals accumulate fat inside muscle cells but use it poorly, which is associated with insulin resistance. This contrast helps you understand why two people with similar muscle fat levels experience very different metabolic outcomes.

• Mitochondria may be a central player behind fuel choice — The ability to switch between fuels likely depends on how well mitochondria regulate specific enzymes that serve as decision points for glucose and fat entry into energy pathways. When mitochondrial function declines, these switches become sluggish. This suggests that improving mitochondrial performance can improve your metabolic flexibility.

People with metabolically inflexible muscle also show lower oxidative enzyme activity in their muscle tissue, but exercise training can improve this by strengthening mitochondrial performance. This means your muscle doesn't just burn calories; it learns. The more often you move, the more responsive your fuel systems become, reinforcing a virtuous cycle that supports fat loss, stable energy, and metabolic ease.

• The study tested whether improving fitness changes how your body uses fat — Researchers examined how moderate physical activity combined with calorie reduction influenced fat oxidation and insulin-stimulated glucose disposal in obese adults. The goal was to see whether better use of fat during fasting improved insulin sensitivity, which is the body's ability to move sugar out of the bloodstream efficiently.

By isolating both fasting metabolism and insulin-driven metabolism, the researchers identified which changes mattered most for restoring healthier energy balance. The group included 25 men and women with a BMI over 30, all of whom completed 16 weeks of structured physical activity along with reduced calorie intake.

After the intervention, the researchers measured glucose disposal during controlled laboratory conditions to determine how well insulin worked in their muscle tissue. Their findings revealed that these adults improved insulin sensitivity at a meaningful level, and the strongest predictor of that improvement was better fat oxidation during fasting.

• Fat oxidation increased significantly as fitness improved — The researchers reported a rise in fasting fat oxidation from 1.16 to 1.36 milligrams (mg) per minute per kilogram of fat-free mass, which reflects a shift toward using stored fat more efficiently when food intake is low. This shift meant that the proportion of total energy coming from fat increased from 38% to 52% during fasting.

That improvement occurred alongside a 19% increase in VO2 max, a measure of aerobic fitness. The connection between greater fitness and improved fat use suggests that muscles that burn fat more efficiently at the right time also tend to respond better to insulin.

• Insulin sensitivity improved at an impressive rate — Glucose disposal increased from 6.70 to 9.51 mg per minute per kilogram of fat-free mass, representing a 49% improvement in how effectively insulin moved glucose into muscle cells. Participants also lost body fat, but the shift in fat oxidation was the factor most closely tied to the improvement in how their bodies handled glucose.

The study identified enhanced fasting fat oxidation as the single strongest predictor, accounting for 52% of the variance in improved insulin sensitivity. Restoring proper timing and flexibility in fat use may be one path toward better blood sugar control.

• Improved metabolism likely reflects changes inside the muscle itself — Although the study did not provide detailed molecular mechanisms, the pattern of results fits with established physiology: improved aerobic capacity strengthens mitochondrial function, allowing muscle cells to oxidize fat more efficiently during fasting and store glycogen more effectively after meals.

Better mitochondrial performance during exercise also encourages healthier glucose uptake, reinforcing insulin sensitivity. This creates a positive loop where your body becomes better at switching between fuels throughout the day.

Over the 16-week period, repeated aerobic activity appeared to train muscle tissue to prefer fat during fasting and respond more effectively to insulin afterward. This gradual retraining suggests that steady, moderate movement carried out consistently — combined in this study with calorie reduction — can support metabolic repair without extreme restrictions or punishing exercise routines.

1. Lower your dietary fat intake so your cells stop blocking glucose oxidation — If you eat a high-fat diet, especially from seed oils, your system can end up stuck in the Randle cycle, which restricts glucose from entering your energy pathways. By lowering your fat intake and choosing healthy fat sources like tallow, ghee, and grass fed butter, you may help free up PDH to work properly. This shift allows your body to burn sugar cleanly, which may support fat loss.

2. Increase your carb intake to support mitochondrial energy production — If your gut is compromised, start with fruit or white rice before moving into cooked vegetables and other starches as your gut tolerates them. Carbs are protein-sparing and are essential for optimal mitochondrial adenosine triphosphate (ATP) production, your body's energy currency.

Gradually increase your carbs until you reach a stable range that supports your energy — usually around 250 grams per day for most adults. You may notice that your body temperature rises, your mood improves, and your cravings weaken because your cells are getting the fuel they need.

3. Support PDH with nutrients that activate glucose oxidation — If you've struggled with low energy or slow fat loss, supporting the PDH activity with vitamin B1, magnesium, and niacinamide may help. Vitamin B1 acts as a cofactor for PDH and may also inhibit pyruvate dehydrogenase kinase (PDK), which itself inhibits PDH. Thus, B1 indirectly supports energy production by keeping PDH active.

Niacinamide converts to NAD⁺ in your body, thereby affecting the NAD⁺ to NADH ratio, which is key for metabolic processes. For magnesium, I recommend finding a dose that works for you. Increase magnesium citrate until your stools loosen, then back off slightly and switch to glycinate or malate. This combination may strengthen your ability to burn glucose efficiently.

4. Use movement strategically to reinforce metabolic flexibility — If you're sedentary or only doing high-intensity workouts, shift your strategy. Moderate movement, especially walking and strength training, signals your muscle cells to improve their glucose handling. Aim to walk about an hour a day. Even 20 to 30 minutes of walking after meals can help your mitochondria shift their fuel patterns and may add to the fat loss benefits of better glucose oxidation.

5. Strengthen your metabolic environment so PDH stays active and glucose oxidation remains steady — If your metabolism feels sluggish or your energy dips throughout the day, stabilize your environment in ways that directly support the PDH pathway. A simple starting point is sunlight exposure, which boosts cellular energy production and may help your body shift toward cleaner glucose use.

If you're still eating seed oils, avoid intense midday sun until you've been off them for four to six months. Reduce seed oils aggressively because excess linoleic acid (LA) can interfere with normal mitochondrial function and disrupt your fuel selection signals.

If you still feel stuck after correcting your diet, low-dose pharmaceutical-grade methylene blue from a compounding pharmacy may support mitochondrial energy transfer at just 5 mg once daily. It's essential to emphasize that the appropriate and legal way to use methylene blue is through a prescription from a qualified physician.

If you're contemplating the use of methylene blue for your health, I strongly encourage you to consult with your doctor to determine if it's suitable for your specific needs and circumstances. These steps strengthen the foundational conditions your body needs to keep PDH active and your metabolism flexible, making fat loss easier and more predictable.

• Most successful programs followed a practical, progressive structure — Participants generally trained two or three times per week, completing both upper- and lower-body exercises such as leg presses, chest presses, rows and leg curls. Most programs prescribed two or three sets of eight to 15 repetitions, with resistance equal to about 50% to 80% of the maximum weight a participant could lift once. Sessions generally lasted 40 to 60 minutes.

Progress mattered as much as participation. Loads typically rose about 2% to 10% as participants completed more repetitions, reported less effort or hit their target sets with less strain. Repeating the same easy workout indefinitely stops producing cardiovascular adaptation — your body needs a gradually greater challenge to keep improving.

• Greater training doses were linked to stronger cardiovascular responses — The researchers noted that frequency, total exercise volume and program duration helped explain why cardiovascular improvements differed among studies. Higher weekly exercise doses were associated with greater improvements in hemodynamics — essentially, how efficiently blood moves through your body and how much strain that movement places on your heart and arteries.

Shorter programs or those without adequate progression appeared less likely to provide enough stimulus for meaningful cardiovascular or blood vessel adaptation. This makes consistency a useful target you can track: complete your planned sessions, record your loads and gradually build from there.

• Blood vessels became more flexible and responsive — Thirteen studies examined vascular structure or function. Some reported better endothelial function, improved blood flow, lower resistance in peripheral blood vessels and greater nitric oxide availability. The endothelium is the thin inner lining of your blood vessels, while nitric oxide helps those vessels relax and widen so blood flows more freely.

Several studies also reported decreases of about 0.6 to 0.8 meters per second in pulse wave velocity, a measure of how quickly pressure waves move through your arteries. Slower pulse wave velocity generally reflects less arterial stiffness. A useful comparison: pressure waves travel faster through a rigid pipe than through a flexible hose. Slower velocity tells you your arteries are staying supple.

• Women with greater vascular problems appeared to have more room to improve — The review noted that reductions in arterial stiffness tended to be greater in people who started with higher stiffness or high blood pressure. That's an important practical point: resistance training isn't reserved for people who already have ideal cardiovascular health.

At the same time, vascular results differed across studies, and fewer trials examined these outcomes than blood pressure. The researchers therefore cautioned against treating one specific resistance-training program as the definitive prescription for every woman.

• Strength training changes both blood vessels and nervous system control — Repeated muscle contractions alter blood flow and create shear stress, the gentle friction of blood against vessel walls. This stimulus supports greater nitric oxide availability, less oxidative stress and better vessel dilation. Resistance training also appears to improve the flexibility of vascular smooth muscle and remodel smaller arteries, reducing resistance against which your heart must pump.

Nervous system changes add another layer. Studies of heart rate variability showed shifts toward stronger parasympathetic activity — the calming "rest-and-recover" side of your autonomic nervous system. Together, these vascular and nervous system adaptations help explain why progressive resistance exercise produces benefits that reach well beyond stronger muscles.

1. Make strength training a consistent part of your week — Aim for two to three resistance-training sessions each week. That frequency closely matches the programs examined in the research, which commonly lasted eight to 24 weeks.³ If you're starting from a low activity level, consistency matters more than chasing heavy weights. Build the habit first, then progress.

If you're unsure how to estimate your starting weight, choose a load that lets you complete your target repetitions with good form while the last two or three feel genuinely challenging. That typically lands you in the right intensity range without formal testing.

2. Increase resistance gradually as your body adapts — Progressive overload means slowly asking your muscles to do more. In the studies, resistance commonly increased by about 2% to 10% based on improved performance, completed repetitions or perceived effort. Track your weights and repetitions in a simple log so progress is visible rather than assumed.

3. Consider BFR training if conventional strength training is too demanding — If you're frail, deconditioned or recovering from an injury, BFR training — sold under branded systems such as KAATSU — gives you another way to stimulate your muscles with much lighter loads. BFR uses specialized cuffs to partially restrict blood flow during exercise, allowing low-intensity movements to create a stronger muscular training signal.

Note that BFR training was not part of the cited resistance-training review; this is a separate option worth discussing with a qualified trainer or healthcare provider when heavy lifting isn't appropriate or tolerable.

4. Walk every day and break up long periods of sitting — Strength training is only one aspect of cardiovascular health. Your heart also benefits from frequent, lower-intensity movement throughout the day, which is why I recommend working toward about 60 minutes of walking daily. If that's more than you're doing now, start where you are and add five to 10 minutes per week.

If you spend much of your day seated, stand up and move at regular intervals as well. Walking provides a steady cardiovascular stimulus, while resistance exercise challenges your body in a different way. Together, they create a more complete movement strategy.

5. Lower your LA intake to support cardiovascular and mitochondrial health — Strength training improves how your blood vessels function, but those vessels depend on healthy mitochondria to sustain that function over time. That's why it's important to pair strength training and daily walking with another foundational step: reducing excess LA, the primary polyunsaturated fat found in seed oils. I recommend keeping LA below 5 grams per day, and ideally closer to 2 grams.

The biggest sources include soybean, corn, sunflower, safflower, cottonseed and canola oils. Excess LA becomes incorporated into mitochondrial membranes, where it oxidizes into damaging compounds that interfere with cellular energy production. Reducing these oils while emphasizing fats such as grass fed butter, ghee or tallow addresses cardiovascular health from another direction, by supporting the cellular energy systems your heart and blood vessels depend on.

• The research affirms the short-term benefits — Ketogenic diets produce early improvements in body weight, insulin sensitivity, and glycemic control. However, the literature the researchers reviewed shows that these gains tend to level off after several months, and the sustainability of such changes depends heavily on adherence and nutrient quality.

Several long-term trials included in the paper note that after the first six to 12 months, weight loss plateaus, and metabolic markers may begin to shift in variable directions depending on the composition of the diet and the individual’s baseline metabolic health.*

• One of the recurring themes is that the ketogenic diet’s effectiveness depends on the context — It appears to work particularly well in individuals with insulin resistance or Type 2 diabetes, but the metabolic benefits are less clear in healthy populations.* The study also noted that adherence rates in long-term studies are relatively low, highlighting that maintaining nutritional ketosis over extended periods can be difficult in real-world conditions.

• Long-term safety isn’t fully understood yet — Another important finding is that while ketogenic diets can improve key metabolic markers, they also trigger compensatory changes that blunt or reverse some of those benefits. In fact, certain health problems have already been recorded, as you’ll learn below.

• HOMA-IR and insulin sensitivity — Ketogenic diets have been shown to lower fasting insulin levels significantly, reducing the homeostasis model assessment for insulin resistance (HOMA-IR) index, which measures insulin resistance.

The paper reports that in both obese and diabetic subjects, HOMA-IR improves substantially during the first months of ketosis.* This improvement is largely attributed to the reduction in carbohydrate intake, which minimizes the need for insulin secretion and allows tissues to regain sensitivity to insulin.

However, the paper also warns that this improvement is not uniform across all individuals. In some of the studies reviewed by the team, insulin sensitivity initially improved but later reached a plateau or showed mixed results after extended ketosis. This variability is attributed to physiological adaptation, differences in macronutrient ratios, or the duration of adherence by the participants.

• Fasting glucose — The paper highlights consistent reductions in fasting glucose across several trials. Subjects on ketogenic diets typically exhibit lower baseline glucose values compared to those on higher-carbohydrate regimens.* This effect is particularly strong among individuals with impaired glucose tolerance or Type 2 diabetes.

However, in some long-term interventions, fasting glucose levels tend to stabilize rather than continue to decline, suggesting a new metabolic steady state rather than ongoing improvement.

• Increase in low-density lipoprotein (LDL) occurs — In a case study published in Cureus, a 56-year-old woman had already been on a ketogenic diet for 30 to 40 days (along with regular exercise) before approaching the research team due to fatigue complaints.*⁴ After tests were administered, the team discovered that she had a rapid increase in LDL cholesterol, often referred to as the bad cholesterol.

• Factors contributing to rise in LDL cholesterol — Under the ketogenic diet, the subject lost weight, but the speed at which it happened may have caused unforeseen health problems*:⁵

“The drastic elevation in her LDL-C could also be explained due to the rapid weight loss, as cholesterol in the adipose tissue is known to mobilize as the fat cells shrink. Interestingly, her BMI [body mass index] four weeks after the discontinuation of ketogenic diet did not change despite a marked improvement in her LDL-C.”

• Other studies support the findings — In a 2021 randomized trial published in Nutrients, researchers noted that following a ketogenic low-carbohydrate high-fat diet (LCHF) contributed to a rise in LDL cholesterol in 17 healthy young women. Overall, they described the elevated LDL cholesterol as a cause for concern*:⁶

“The data suggest that feeding healthy, young, normal-weight women a ketogenic LCHF diet induces a deleterious blood lipid profile. The elevated LDL cholesterol should be a cause for concern in young, healthy, normal-weight women following this kind of LCHF diet.”

• Animal data suggest that ketogenic feeding alters lipid metabolism and mitochondrial function — Some rodent studies reviewed in the paper reveal hepatic lipid accumulation, suggesting that long-term ketosis may promote fatty liver changes in certain conditions.* This outcome appears to depend on the fat type and overall energy intake, as not all studies report this effect.

• Changes in gut microbiota composition — In another study, researchers showed that the ketogenic diet altered gut microbial composition in both mice and 17 men with overweight or obesity. Specifically, they noted that Bifidobacterium was affected, which, as I noted in a previous article, is important in maintaining the integrity of mucin in your gut:⁸

“We focused on Bifidobacterium which had a reproducible decrease in abundance during KD consumption in both humans and mice and also with feeding of a synthetic KE in mice. Changes in Bifidobacterium abundance resulted in a significant alteration to intestinal Th17 cell populations …

In humans, both Fusobacteria and Escherichia were significantly enriched on the KD, which have both been implicated in predisposition to colorectal cancer.”

• Nutrient deficiencies — The ketogenic diet requires you to take out many carbohydrate-rich food sources, like whole fruits, vegetables, and certain whole grains, all of which are loaded with vital nutrients your body needs. As noted in a review published in Frontiers in Nutrition:⁹

“Low-carbohydrate diets are often low in thiamin, folate, vitamin A, vitamin E, vitamin B6, calcium, magnesium, iron, and potassium. In the absence of multivitamin supplements, individuals on low-carbohydrate diets are at risk of frank nutritional deficiencies.

Even when consuming only nutrient-dense foods, a 4:1 ketogenic diet is reported to have multiple micronutrient ….”

• Kidney stones — The risk of kidney stones is highlighted as a consistent observation, especially in studies involving long-term ketogenic use. In a 2023 study, for example, 15 out of 88 epileptic children developed renal stones, and 12 of them received medication. Moreover, one of them required surgery.¹⁰

• Bone health and overall fitness — The ketogenic diet also raises concern about bone health. Although the mechanisms are unclear, even a short-term regimen impaired markers of bone health in elite athletes. As noted in a study published in 2020:¹¹

“Our data reveal novel and robust evidence of acute and likely negative effects on the bone modeling/remodeling process in elite athletes after a short-term ketogenic LCHF diet, including increased marker of resorption (at rest and post-exercise) and decreased formation (at rest and across exercise), with only partial recovery of these effects following acute restoration of CHO [carbohydrate] availability.

Long-term effects of such alterations remain unknown, but may be detrimental to bone mineral density (BMD) and bone strength, with major consequences to health and performance.”

• Thyroid function and body weight — In another small pilot trial of 11 healthy adults, following the ketogenic diet for three weeks lowered levels of the thyroid hormone T3, and participants lost more body mass than when they ate a diet high in carbohydrates.¹²

• Short-term keto is still used by some people — In my interview with Georgi Dinkov, we discussed that the ketogenic diet, when followed properly, can be useful for people who are metabolically inflexible. It’s mainly in long-term applications that you’ll run into health problems.

Your body requires glucose and depriving it of this fuel raises cortisol levels. Through a process called gluconeogenesis, cortisol can break down your muscles, bones, and brain to create its own glucose levels — a likely explanation for the changes in bone health markers discussed in the studies earlier.

• Dietary recommendations — If you go on a short-term ketogenic diet, make sure your healthy fats come from nutritious sources, such as pasture-raised eggs, grass fed butter, and wild-caught fish. In addition, minimize your intake of ultraprocessed foods, meats, and snacks.

Talk to your healthcare provider about a high-quality multivitamin supplement, too. As explained earlier, strictly following a ketogenic diet can introduce nutritional deficiencies, and taking a supplement can mitigate these issues down the road.

• Eat more carbohydrates as time goes on — Listen to your body to know when your metabolic flexibility returns. This process can take anywhere from a few weeks to a few months, and when you reach this point, you’ll need to eat more carbohydrates. Again, this goes back to the cortisol-glucose connection.

• However, the long-term picture is more complex — The same mechanisms that drive early benefits — reduced insulin resistance and elevated fat oxidation — can introduce new physiological challenges when sustained indefinitely. Potential risks include nutrient deficiencies, renal strain, thyroid dysfunction, altered gut health, and lower bone mineral density.

• Don’t overdo the ketogenic diet — As I highlighted earlier, it would be wise to view the ketogenic diet as a temporary dietary strategy, not necessarily a lifelong eating pattern. For long-term health maintenance, however, the studies suggest that a high-fat diet isn’t sustainable, and that carbohydrates are needed for a balanced approach that creates metabolic flexibility.

• Physical and psychosomatic symptoms drove most of the gap — Women with Type 2 diabetes or prediabetes reported significantly more symptoms in both the physical and psychosomatic categories than women without diabetes. Physical symptom severity was also significantly higher.

The index covered complaints ranging from hot flashes and night sweats to headaches, fatigue, joint or muscle pain, sleep problems, irritability and difficulty concentrating. The findings suggest that if your blood sugar is impaired, it's worth looking at your symptoms as a pattern rather than dismissing each complaint as an isolated part of getting older.

• The postmenopausal stage showed the strongest separation between the groups — When the researchers divided women according to menopause stage, the statistically significant differences appeared primarily after menopause. They didn't find significant differences between the diabetes and nondiabetes groups during premenopause or perimenopause.

That timing gives you an important clue. The relationship between metabolic health and menopause symptoms wasn't equally apparent at every stage of midlife. Instead, the postmenopausal period stood out as the point when impaired glucose metabolism and greater symptom burden most clearly overlapped in this group of women.

• Blood sugar status still mattered after other health differences were considered — The researchers used additional statistical analysis to account for factors including age, meal frequency, perceived health, weight status, menopause stage and physical activity. Even after those adjustments, having Type 2 diabetes or prediabetes remained significantly associated with both a greater number and greater severity of menopause symptoms.

Several other factors also stood out. Lower self-rated health was associated with more symptoms and greater severity, while overweight or obesity was associated with greater symptom severity. Low physical activity was associated with a greater number of symptoms. These findings give you several areas of health to pay attention to rather than viewing menopause symptoms as something completely outside your influence.

• The study points to an overlap between metabolic health and menopause rather than proving cause and effect — Because this was a cross-sectional study, researchers assessed participants during one period rather than following them for years. That means the findings don't establish that high blood sugar directly caused the additional menopause symptoms, or that more severe menopause symptoms caused impaired glucose control.

The researchers specifically identified obesity, physical activity and psychological stress as factors that deserve further investigation as links between glucose metabolism and menopause symptom burden. The study provides a reason to pay attention to metabolic markers alongside your symptoms rather than assuming menopause alone explains everything you're experiencing.

• The findings have important limits outside the women who were studied — All participants were midlife women living in South Korea, so the results don't establish that women in other countries or populations will experience the same relationship. The researchers also relied on self-administered online questionnaires for symptom reporting, which introduces the possibility of selection and reporting bias.

Central obesity, meaning excess fat concentrated around your waist and abdomen, also wasn't directly measured. That's an important limitation because abdominal fat is closely tied to metabolic health. The researchers called for longer-term studies to clarify how blood sugar regulation, menopause symptoms, body composition, physical activity and psychological stress interact over time.

• Early menopause was consistently tied to greater diabetes risk — The pooled results showed that women who experienced early menopause had 24% higher odds of Type 2 diabetes than women who reached menopause at a typical age. The association remained evident when the researchers looked specifically at studies that tracked participants over time.

In those studies, early menopause was associated with a 31% higher hazard of developing Type 2 diabetes. A hazard ratio compares how quickly an outcome develops in one group relative to another over a follow-up period. Women who reached menopause early were more likely to develop diabetes during follow-up than those who reached menopause at a typical age.

• Late menopause showed a weaker and less consistent relationship — Women who experienced late menopause had 14% higher odds of Type 2 diabetes compared with women who reached menopause at a typical age. However, the results changed when researchers examined diabetes development over time. Late menopause wasn't significantly associated with a higher hazard of developing Type 2 diabetes.

That distinction is important. The researchers described the late-menopause finding as less certain and noted that fewer studies were available for this part of the analysis. They also found moderate differences among the included studies, meaning the studies didn't all produce closely matching results. Early menopause provided the clearer metabolic warning signal.

• The evidence was strong enough to survive several statistical checks — Researchers tested whether publication bias could be distorting the primary findings. Publication bias happens when studies with significant or striking results are more likely to be published than studies finding little or no association. Their statistical test found no evidence of this problem for the outcomes evaluated.

They also repeated the analysis while removing one study at a time. The overall findings remained consistent. Most of the included studies were rated as high quality with a low risk of bias in most areas assessed, adding confidence that the early-menopause association wasn't dependent on one unusually influential study.

• Menopause timing is a useful metabolic clue, not proof of cause — Every study included in the analysis was observational. That means the researchers found relationships between menopause timing and diabetes but couldn't prove that reaching menopause early directly causes Type 2 diabetes. There was also considerable variation in study design and participant characteristics, especially in analyses of diabetes risk over time.

Still, your age at menopause is information worth remembering and sharing with your health care provider. If you reached menopause earlier than expected, the findings give you another reason to pay close attention to metabolic markers rather than waiting for symptoms. The researchers specifically identified menopause age as a factor worth considering when assessing and managing diabetes risk in women.

1. Check HOMA-IR and prolactin for metabolic and hormonal clues — HOMA-IR, or Homeostatic Model Assessment of Insulin Resistance, is a useful way to identify insulin resistance, the underlying metabolic problem that drives Type 2 diabetes. Tracking your HOMA-IR gives you a way to see whether your insulin sensitivity is improving as you make changes to your diet, movement and other daily habits.

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

Prolactin provides another useful clue because estrogen stimulates your pituitary gland to produce this hormone. A standard blood estrogen test measures circulating hormone levels but can miss estrogenic activity happening locally inside your tissues.

Estrogen can be relatively low in your blood while remaining high in your tissues, so an elevated prolactin level can provide additional information about estrogen activity. Thyroid function also matters, making prolactin useful as part of the larger hormonal picture. Talk to your healthcare provider about whether this testing is appropriate for you.

2. Eliminate seed oils to support metabolic and hormonal balance — Start by removing soybean, corn, sunflower, safflower, cottonseed, canola and other seed oils. These oils are major sources of linoleic acid, or LA, a polyunsaturated fat that accumulates in your tissues and interferes with healthy mitochondrial function. Your mitochondria produce most of the usable energy your cells require, making their health central to normal glucose metabolism.

Keep LA below 5 grams per day and ideally below 2 grams. Check packaged-food labels and minimize restaurant foods prepared with seed oils, including dressings and sauces. Choose grass fed butter, ghee and tallow instead. Reducing excess LA also helps address a dietary contributor to excessive estrogenic signaling.

3. Reduce your exposure to estrogen-mimicking chemicals — Your total estrogen burden doesn't come exclusively from hormones made inside your body. Endocrine-disrupting chemicals, including compounds found in plastics, personal care products and household products, interfere with normal hormone signaling. Some mimic estrogen and increase the estrogenic signals your tissues receive.

You have considerable control over these exposures. Store food and beverages in glass or stainless steel instead of plastic, and don't heat food in plastic. Choose personal care products without parabens and phthalates, simplify your household cleaners and filter your drinking water to reduce microplastics and other contaminants. Start with products you use every day, then replace less frequently used items over time.

4. Improve glucose metabolism with adequate carbohydrates and regular movement — If you've been cutting carbohydrates sharply out of concern about blood sugar, the strategy may be backfiring. For most adults, 250 grams of carbohydrates per day supports cellular energy production, though more is needed if you're very active.

If your digestion is healthy, choose whole fruits, root vegetables and other minimally processed carbohydrate sources. If your gut is impaired, start with easier-to-digest choices such as ripe fruit and white rice, then gradually expand your diet as your digestion improves.

Muscle provides a major destination for glucose, making movement another important tool for improving insulin sensitivity. Work toward walking for 60 minutes daily, strength train twice a week and interrupt long periods of sitting with brief movement breaks. Protect your sleep as well. These habits may help your cells use glucose more efficiently for energy and support your body's ability to manage insulin resistance.

5. Reconsider adding estrogen and restore progesterone balance — If you're in perimenopause or menopause, don't automatically assume difficult symptoms mean you need more estrogen. Hormone replacement therapy, estrogen-containing contraceptives and bioidentical estrogen all add estrogen to your total hormonal environment. If excessive estrogenic activity is already part of the problem, adding more estrogen doesn't address that imbalance.

Natural progesterone offers a different approach because progesterone counterbalances many of estrogen's effects. Addressing estrogen dominance and considering natural progesterone rather than adding estrogen helps restore a healthier balance between these hormones.

Combined with lowering environmental estrogen exposure, reducing LA, improving insulin sensitivity and supporting mitochondrial health, this addresses the broader hormonal and metabolic environment associated with menopause.

• People having heart attacks carried far more plastic particles and a greater variety of plastics — Detectable micro- and nanoplastics were found in 84.2% of patients experiencing a STEMI, compared with 40% of patients with chronic coronary syndromes and 31.8% of people whose coronary arteries appeared normal. Researchers also found that heart attack patients carried a median of three different types of plastic, while the other groups typically had none to two.

Polyethylene — the plastic commonly used in grocery bags, food packaging and bottles — appeared in 97% of patients with detectable plastics. Other plastics, including polypropylene, polystyrene, polyethylene terephthalate (PET) and nylon 66, also appeared much more frequently in the STEMI group.

• The highest plastic concentrations appeared exactly where blood flow became blocked — Researchers measured how much plastic was present and where those particles were concentrated. In patients having a STEMI, plastic concentrations were highest in blood collected from the coronary artery just upstream of the blockage, before doctors crossed it with the catheter. Concentrations were lower in blood collected after the blockage and lower still in blood drawn from the arm.

This pattern suggests the particles accumulate where blood flow becomes impaired rather than circulating evenly throughout the body. To strengthen confidence in the findings, the researchers also tested catheters, tubing and other medical equipment for contamination and found no detectable background plastics. In addition, some participants in every study group had no detectable plastics at all, showing the results reflected genuine biological differences rather than contamination.

• Higher plastic levels went hand in hand with stronger inflammation — Patients with the greatest plastic burden also had significantly higher levels of two inflammatory proteins that act as chemical messengers for the immune system. Persistently elevated levels of these proteins are associated with unstable plaque inside the arteries and a greater likelihood of heart attacks.

Rather than appearing as an isolated finding, higher plastic exposure consistently clustered with stronger inflammatory activity throughout the study population.

• Smoking was the strongest predictor of plastic particles in the blood — After accounting for multiple cardiovascular risk factors, smoking history remained the only independent predictor of detectable micro- and nanoplastics, increasing the odds nearly sixfold.

This finding suggests cigarette smoke serves as an important route of exposure or influences how these particles accumulate within the body. For smokers, this means tobacco exposure isn't simply affecting the lungs and blood vessels — it also appears closely linked to the amount of plastic circulating through the coronary arteries.

• Air pollution and plastic exposure appeared to reinforce each other — Researchers also found that patients exposed to PM2.5 concentrations above 15 micrograms per cubic meter were more likely to have detectable plastics in their blood. PM2.5 refers to extremely small airborne particles that are small enough to travel deep into your lungs and enter your bloodstream.

Every participant who both smoked and experienced PM2.5 exposure above that threshold had detectable micro- and nanoplastics in their coronary blood.

Together, these findings suggest environmental exposures don't occur one at a time. Instead, smoking, air pollution and plastic exposure appear to accumulate together, creating conditions associated with more severe cardiovascular disease.

• The smallest plastic particles travel farther and cause greater disruption — Researchers explained that nanoplastics are much smaller than ordinary microplastics, allowing them to pass through biological barriers that normally protect your organs. Once inside the bloodstream, they travel beyond the digestive tract and reach the heart, blood vessels and other tissues.

Their extremely small size also makes them easier for cells to absorb through several transport pathways, allowing them to accumulate inside tissues where they interfere with normal cellular function. The review also notes that plastic particles often carry chemical additives from manufacturing along with pollutants picked up from the environment, exposing your body to far more than plastic alone.

• Plastic particles weaken the protective lining of your blood vessels — Healthy arteries depend on a thin layer of cells called the endothelium, which forms a smooth lining that helps regulate blood flow, blood pressure, clotting and inflammation. According to the review, micro- and nanoplastics injure these cells, reducing their survival and impairing their ability to function normally.

The particles also trigger oxidative stress, meaning harmful unstable molecules overwhelm your body's antioxidant defenses and damage proteins, fats and DNA inside blood vessel cells. At the same time, plastic exposure reduces nitric oxide production. Nitric oxide is a natural signaling molecule that keeps arteries relaxed and flexible. When nitric oxide levels fall, blood vessels become stiffer, circulation declines and conditions become more favorable for cardiovascular disease.

• Chronic inflammation turns your immune system against your arteries — Inflammation normally helps your body fight infection and repair injuries, but the review found that plastic particles keep this response switched on for far too long. Instead of resolving, the inflammatory response stays switched on, with immune cells continuing to release chemical messengers that damage blood vessel tissue from within.

Over time, this ongoing inflammation damages the arteries rather than protecting them, creating an environment that supports cardiovascular disease.

• Immune cells begin building plaque that becomes increasingly unstable — According to the review, chronic inflammation encourages immune cells to absorb cholesterol and transform into foam cells, which are fat-filled cells that accumulate inside artery walls. Foam cells form one of the earliest building blocks of atherosclerotic plaque and continue fueling its growth.

Persistent inflammation also weakens the fibrous cap that covers these fatty deposits. As that protective cap becomes thinner and more fragile, plaque becomes much more likely to rupture, triggering the formation of blood clots that block blood flow to the heart or brain.

• Multiple biological changes work together to increase cardiovascular risk — Rather than causing a single type of damage, micro- and nanoplastics affect several protective systems at once. The review describes injury to blood vessel cells, excessive oxidative stress, reduced nitric oxide production, chronic inflammation, plaque formation and plaque instability as interconnected processes that reinforce one another.

Together, these mechanisms help explain why plastic exposure is associated with progressively worsening cardiovascular health instead of one isolated problem.

1. Start with cleaner drinking water — Your drinking water is one of the most consistent sources of daily exposure, making it one of the smartest places to begin. I recommend installing a high-quality filtration system that's specifically designed to remove microplastics, pharmaceutical residues and other emerging contaminants.

Many standard pitcher filters improve taste and reduce chlorine, but they aren't designed to capture the smallest plastic particles. A properly designed filtration system lowers your exposure every day without requiring you to think about it.

2. Choose fresh, minimally processed foods whenever possible — Highly processed foods typically undergo more manufacturing, packaging and handling, creating additional opportunities for contamination with microplastics. I recommend building your meals around fresh fruits, vegetables, properly raised animal foods and other minimally processed whole foods.

Buying loose produce instead of individually wrapped items also reduces unnecessary plastic exposure before food even reaches your kitchen.

3. Improve the quality of the air you breathe every day — The first study found that higher exposure to fine particulate air pollution occurred alongside greater detection of plastics in coronary blood. If you live near busy roads, industrial areas or regions affected by wildfire smoke, keep your windows closed during poor air-quality days and use a high-quality HEPA air purifier indoors.

If you smoke, quitting is one of the most powerful steps you can take because the research identified smoking as the strongest predictor of detectable plastics in coronary blood.

4. Support your blood vessels by lowering chronic inflammation — The studies showed that higher plastic exposure was associated with inflammatory activity that damages blood vessels. You help counter that by building your diet around foods that actively support your blood vessels — leafy greens, berries, pasture-raised eggs and grass fed butter — while maintaining healthy blood sugar, getting regular movement, sleeping well and spending time outdoors.

These habits strengthen the cells lining your arteries and reduce many of the same biological processes linked to cardiovascular disease. Another important step is avoiding excess linoleic acid (LA), the polyunsaturated fat found in seed oils such as soybean, corn, sunflower, safflower and canola oil.

When LA becomes damaged through oxidation, it produces harmful compounds that injure cell membranes and activate inflammatory pathways throughout your body, including your blood vessels, liver and nervous system. Reducing your intake of these oils removes a persistent source of chronic inflammation and helps protect the arterial lining that micro- and nanoplastics are actively working to damage.

5. Reduce unnecessary plastic contact throughout your home — Small changes add up over time. Choose wooden, stainless steel or glass kitchen tools instead of plastic whenever practical. Store leftovers in glass containers, avoid heating food in plastic and replace worn plastic cutting boards and scratched food containers that shed more particles as they age.

If you're just getting started, pick one room in your home each month and gradually replace plastic items with safer alternatives. That steady approach makes lasting progress much easier than trying to change everything at once.

• Study participants taking vitamin D2 experienced a sharp drop in their vitamin D3 levels — Across the combined data, those who took vitamin D2 had about 18 nanomoles per liter (nmol/L) lower concentrations of vitamin D3 (measured as 25-hydroxyvitamin D3; 95% confidence interval, 10 to 26 nmol/L) than participants in control groups who took a placebo or nothing. In other words, people trying to boost their vitamin D by taking D2 ended up lowering the circulating form that actually powers their immune, hormonal, and metabolic systems.*

• Healthy adults were most commonly studied, but the results were mostly consistent across age and gender — Most trials included healthy men and women, and one involved both young and older males, though only the younger group’s results were included.

Across age and sex groups, the same trend appeared — vitamin D2 supplementation triggered a measurable decline in vitamin D3 status. Even when doses and study durations varied widely, from a few weeks to several months, the downward effect on vitamin D3 levels appeared in most trials.

• The drop wasn’t a random fluctuation — it may reflect how the body regulates vitamin D metabolism — Researchers believe that vitamin D2 activates an enzyme that accelerates the breakdown of vitamin D3.

Specifically, D2 appears to stimulate a protein responsible for dismantling both D2 and D3 into inactive fragments for excretion. When this enzyme becomes more active, your vitamin D3 doesn’t just fade — it’s chemically destroyed faster, leaving you with less of the form that supports bone, heart, and immune health.

• Vitamin D3 may be superior in supporting immune and metabolic functions — Vitamin D3 altered genetic pathways that control inflammation and immune function in a human gene-expression study, while D2 altered them differently.

In earlier research cited by the authors, only D3 was associated with increased activity of interferons — immune molecules that help your body recognize and fight infections* (in a blood gene-expression study of white European women, but not South Asian women).² D2 not only failed to produce this effect but also appeared to suppress the immune response in some cases.

• The findings suggest why supplement quality matters more than quantity — Many people buy vitamin D2 because it’s cheaper, vegan-friendly, and widely added to processed foods. Yet this review notes that choosing D2 for cost or convenience could work against your health goals. If your goal is to support energy, immune function, and mood or hormone balance, D3 — not D2 — is the form that your body recognizes and uses efficiently.

• A clinical trial found that vitamin D3 raises blood levels faster and more efficiently than D2 — In an open-label randomized controlled trial conducted in the Middle East, 250 adults with vitamin D deficiency or insufficiency were assigned to take either vitamin D2 or D3 once a week for 12 weeks.³ Each capsule contained 50,000 international units (IU) — a dosage often prescribed in cases of deficiency.

After just eight weeks, those taking vitamin D3 showed an average increase of 18.74 nanograms per milliliter (ng/mL), compared to only 5.88 ng/mL in the D2 group. By week 12, the gap had widened even more, with the D3 group averaging an increase of 20.76 ng/mL while the D2 group rose only by 7.93 ng/mL.*

• Deficiency risk is especially high for certain groups — Worldwide, about 1 billion people are vitamin D deficient, with 50% having vitamin D insufficiency.⁴ However, in some groups the prevalence is even higher. If you have darker skin, excess body fat, or take medications that speed up vitamin D metabolism (like certain anticonvulsants or steroids), your vitamin D stores drop faster.

Those who wear protective clothing, spend little time outdoors, or live in institutions are also vulnerable. Chronic gut conditions such as inflammatory bowel disease and celiac disease compound the problem by reducing nutrient absorption. For these individuals, choosing D3 is not a matter of preference — it’s a matter of effectiveness.

• For those unable to get consistent sun exposure, D3 supplementation fills the gap efficiently — If you live in a region with long winters or simply can’t be outdoors often, vitamin D3 supplementation is often necessary. Its chemical structure matches what your skin naturally produces, ensuring your body recognizes and uses it efficiently.

If your goal is to raise low vitamin D levels, D3 raised blood levels more than D2 in that trial, even at the same dose. Whether you’re restoring low levels after a long winter or maintaining your levels year-round, D3 gives your body what it already knows how to use.

• The first hydroxylation happens in your liver — This converts vitamin D3 into 25-hydroxyvitamin D — the form measured in standard blood tests. But this intermediate form still can't activate your cells.

The real work begins when 25-hydroxyvitamin D enters your cells and encounters an enzyme called CYP27B1, which adds the second hydroxyl group to create 1,25-dihydroxyvitamin D — the only form that can bind to vitamin D receptors and trigger the genetic changes that support immunity, calcium regulation, and metabolic health.

• Here's the problem: some people may have impaired CYP27B1 activity — This means their cells struggle to complete this final activation step. You could have perfectly normal 25-hydroxyvitamin D levels on paper yet still experience symptoms of vitamin D deficiency because your cells can't convert it into the active form that does the actual work.

• Currently, no commercial test measures intracellular 1,25-dihydroxyvitamin D levels — This leaves this conversion problem invisible to most doctors and patients. Emerging research is exploring ways to deliver the active form directly into cells, bypassing the need for oral vitamin D3 entirely and reducing overdose risk through natural cellular feedback mechanisms that shut down production when adequate levels are reached.

1. Get your vitamin D from the sun whenever possible — Your skin is designed to make vitamin D3 when exposed to direct sunlight. Aim for regular exposure on large areas of skin — such as your arms and legs — without sunscreen daily. It’s important to monitor your skin when you’re out in the sun, keeping an eye out for redness or burning — a simple “sunburn test” that accounts for the season and your skin type. If your skin remains free of pinkness, your sun exposure is likely safe.

2. Cut out seed oils before getting sun exposure during peak hours — If you’re still using canola, soybean, sunflower, or other types of “vegetable” oil, you’re flooding your cells with linoleic acid (LA) — a polyunsaturated fat that oxidizes under UV light and can damage your skin from within. This buildup makes you more prone to sunburn and skin damage, especially during peak hours of 10 a.m. to 4 p.m.

Switch to stable animal fats like tallow, ghee, or grass fed butter instead of seed oils. Avoiding seed oils for at least six months gives your skin time to shed stored LA, which may help you tolerate midday sun safely and produce vitamin D naturally again.

3. If you supplement, use vitamin D3 — not D2 — and pair it with magnesium and K2 — Vitamin D3 is identical to the form your skin makes from sunlight, while D2 may interfere with your natural balance and lowers your D3 levels. When you take D3, include magnesium and vitamin K2 for better absorption and safer calcium regulation.

These three nutrients work together — magnesium activates vitamin D in your body, while K2 directs calcium into your bones instead of your arteries. In an observational analysis of about 3,000 participants, people not taking these cofactors needed 244% more vitamin D for half of them to reach 40 ng/mL, so combining them may lower the amount of vitamin D needed.⁵

4. Test your vitamin D levels twice a year to personalize your plan — Testing your blood levels is the only way to know where you stand. Aim for a range between 60 and 80 ng/mL (150 to 200 nmol/L). If your levels are low, focus on daily sunlight and consistent D3 supplementation to restore them.

Tracking your levels every six months helps you see how your efforts are working, so you and your healthcare provider can adjust dosage, diet, or lifestyle before problems develop. Treat it like a progress check — a simple way to measure how well your body is converting your efforts into results.

5. Exercise may help activate and protect your vitamin D during the winter — When sunlight fades in the colder months, your body’s ability to make vitamin D drops sharply — especially if you live in northern regions or carry extra body fat. That doesn’t mean you’re powerless. A 10-week randomized controlled trial found that regular exercise alone, without supplements or dieting, helped overweight adults maintain healthy vitamin D activity even when their sun exposure was minimal.⁶

Physical movement changes the way your fat tissue handles vitamin D. It may stimulate key enzymes that convert stored, inactive vitamin D into its usable form while slowing down the rate at which it’s broken apart. The people with the most fat tissue saw the biggest improvements, suggesting your body can train itself to use vitamin D more efficiently through consistent activity.

If you struggle to get enough winter sun, make exercise your built-in vitamin D activator — walk briskly outdoors, do strength training, or take a daily movement break to support your energy, mood, and immune function all season long.

• Three major effects that Ozempic users aren't being told about — According to Bikman, Ozempic leads to long-term effects such as loss of muscle and bone, dulled emotional response that could lead to depression, and rapid rebound weight gain that leaves patients with a worse fat-to-muscle ratio than before.

• You lose not just fat, but lean muscle mass, too — The article notes one clinical trial on semaglutide,⁴ wherein 140 participants (95 of them on semaglutide) were tracked over 68 weeks and found that while those on semaglutide lost 23 pounds of fat, they also lost 15 pounds of lean mass, which includes muscle along with water and organ tissue.

That's nearly 40% of their total weight loss coming from tissue the body relies on. Because they lost even more fat, the share of their body made up of lean mass actually rose slightly.

• "Frail people are much more likely to die young" — Bikman notes that having low muscle mass and fragile bones especially among seniors, not only puts you at risk of injury from falls; it also weakens your immune system, compromising your body's ability to handle infections, which is also a common health concern among the elderly.

• GLP-1 drugs are associated with an increased risk of depression — He highlights one study⁶ wherein people with obesity taking GLP-1 drugs (semaglutide or liraglutide) had a 195% increased risk of major depression and over 100% greater risk of suicidal behavior compared to those not taking these drugs. Because it was an observational study, it shows an association, not cause and effect. According to the researchers:

"These findings underscore the critical need for physicians to thoroughly assess patient history before prescribing GLP-1 RAs and highlight the urgent requirement for further prospective clinical trials to fully understand the implications of GLP-1 RA use on mental health in the obese patient population."⁷

• Reports of suicidal thoughts are higher than expected — Bikman also notes additional findings from a World Health Organization (WHO) database⁸ that revealed suicidal thoughts were reported about 45% more often with semaglutide than expected, compared with all other medications.

This kind of database analysis flags a possible safety signal, though it can’t show that the drug causes these thoughts. In clinical trials, rates of depression and suicidal behavior didn’t differ from placebo, but most of those trials excluded people with a history of either.⁹

• Why does Ozempic affect your mental state? Basically, the drug's main component targets GLP-1 receptors — these are present not just in your digestive tract but also in critical brain areas. These regions, such as the lateral septum and hypothalamus, are essential for managing emotions, reward systems, and appetite control.

• Particularly noteworthy is its influence on dopamine — This neurotransmitter is closely associated with mood regulation and reward perception. Early research suggests that stimulating GLP-1 receptors may enhance dopamine transporter expression, leading to decreased free dopamine levels in specific brain regions. This shift in dopamine signaling could affect your mood, motivation levels, and even how you experience pleasure.

• Government agencies insist there's "no direct link" — Although the U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA) later concluded there wasn't enough evidence to confirm a direct causal link, these early signals are hard to ignore.

• So why do you regain fat after stopping Ozempic? Simply put, when you've been taking Ozempic and suddenly stop, the hunger cues it had suppressed come raging back — this causes you to revert to unhealthy eating, which causes the weight to return.

To put it simply, the muscle and bone mass you lost while using this drug don't return naturally; however, fat comes back easily and quickly. Bikman also suggests semaglutide may trigger the formation of new fat cells.

"This becomes a problem because when a person start[s] to regain fat mass after stopping Ozempic, with more fat cells comes a greater potential to gain more fat. 'As a result, even though a person may still weight less than they did before starting the drug, they may be fatter, with a higher percentage of body fat,'" he said.¹²

• Other "health benefits" also disappear when you stop using it — Ozempic is said to help reduce blood pressure, but this could bounce back when you discontinue using the drug. There's evidence that certain positive cardiometabolic effects persist; however, the gains are modest.

• Bikman believes patients should plan to come off the drug — During this time, they need to assess their cravings for carbohydrates. "Ideally, a person has learned how to eat better and control carb cravings and their weight loss can be sustained in the long run," Bikman said. Any plan to stop should be made with the prescribing physician; the trial’s authors concluded that ongoing treatment may be needed to maintain the benefits.

• Ozempic interferes with normal digestion (and not just in minor ways) — While nausea, vomiting, constipation, and diarrhea are the most commonly reported digestive side effects, these symptoms could snowball into dangerous, even life-altering complications, according to health experts.

• Digestive side effects are common — In some cases, these escalate into serious health concerns. Kiran Jones, a clinical pharmacist at Oxford Online Pharmacy, says the most worrying among them is stomach paralysis, or "gastroparesis." This condition means food moves extremely slowly — or not at all — through the stomach. Left untreated, it causes persistent vomiting, malnutrition, and long-term digestive distress.

• GLP-1 receptor agonists intentionally slow digestion — This design aims to suppress your appetite and keep you feeling full longer. However, when overactivated, this same mechanism can throw your whole digestive system out of balance.

• Chronic digestive issues have a major impact on your mental health — Constant nausea, bloating, or pain disrupts your sleep, affects mood, and increases anxiety. Over time, your confidence in your body erodes.

• There are other rare but severe side effects linked to these drugs — Some users have experienced acute kidney injury (often linked to dehydration from vomiting or diarrhea), pancreatitis, and gallbladder problems, and the drugs carry a boxed warning about thyroid tumors seen in rodent studies.¹⁴

I wrote an article about the many damaging effects linked to these medications, even though they only lead to "modest benefits." Read "Ozempic Linked to 19 Adverse Health Events" for more information.

• Nearly 75% of the adverse events occurred after 2022 — Around 46,000 adverse event reports coincide with the increased availability and marketing of these drugs.

• FAERS has recorded 10,000 "serious" reactions to these drugs — These are events that result in hospitalization or life-threatening conditions. These aren't just minor inconveniences; they're significant medical events that could have long-lasting impacts on your health.

• There were also 162 reported deaths in people taking these weight loss drugs — According to a Daily Mail article, the reported deaths increased by 40% in just six months. For more information, read "Ozempic and Other Weight Loss Drugs Linked to 162 US Deaths."

1. Think carefully before starting Ozempic and other GLP-1 agonist receptors — These medications initially seem efficient in eliminating excess fat. However, their benefits are usually short-lived and, as mentioned above, the side effects (many of which are still unknown) are damaging. If you’re already taking one, talk with your prescribing physician before stopping or changing your dose — stopping can raise blood sugar if you have Type 2 diabetes.

2. Eliminate seed oils from your diet — If you regularly consume ultraprocessed foods, I recommend stopping right now and replacing them with real, whole foods. Processed foods contain linoleic acid (LA)-rich seed oils that can disrupt your metabolic pathways and alter how your body stores fat. Instead, cook your meals using tallow, grass fed butter, or coconut oil.

3. Shift your carbohydrate sources gradually — Avoid making sudden dietary changes that will shock your system. If your gut is compromised, start by introducing easily digestible carbohydrates like whole fruit or white rice before incorporating more complex carbs. If you have severe gut issues, sip dextrose water to provide your cells with a steady source of easy-to-digest, healthy carbohydrates for energy.

4. Consider your protein and collagen intake — I suggest aiming for 0.8 grams of protein per pound of your ideal body weight and balancing that amount so that about one-third comes from collagen. This will help support muscle maintenance, tissue repair, and hormone balance.

If you exercise frequently, you might need to slightly increase your intake. My suggestion is to take it slow and listen to how your body responds. Stable protein intake is foundational for regulating cravings and stabilizing energy.

5. Support your mitochondrial health with other healthy habits — Getting daily sun exposure is one example; however, if you're still consuming seed oils, make sure to avoid intense midday sun for at least six months.

The LA in these oils migrate to your skin and oxidize under sun exposure, causing skin damage. Get enough sleep at night, minimize your stress, and incorporate moderate-intensity movement, such as walking about an hour a day, in your lifestyle — these strategies will support your cellular energy production and aid in weight management.

• Many people lack Akkermansia due to various reasons — One reason is having impaired mitochondrial function or an environment that is inhospitable to beneficial gut bacteria. Ideally, Akkermansia should comprise 3% to 5% of your total gut microbiome and it plays many different roles aside from promoting GLP-1.

• Akkermansia has the ability to produce mucin — This thick, gel-like substance protects the gut lining from harmful pathogens, irritation from stomach acid and enzymes, as well as mechanical damage. Moreover, mucin helps nourish the gut bacteria already existing in your gut.

• Certain foods may help boost your Akkermansia levels — Polyphenol-rich fruits like berries and inulin-rich foods such as garlic, asparagus, bananas, and leeks may help increase your Akkermansia levels.

Note, however, that if your gut health is currently out of whack, introducing high amounts of dietary fiber in your system all at once could worsen your gastrointestinal symptoms. So, work on healing your gut first, then gradually increase fiber intake.

• Supplements are also available — Start with a pasteurized Akkermansia postbiotic, then move to live Akkermansia once bloating is minimal, your stools have been consistent for at least a week, and you can tolerate more fiber. Ideally, look for Akkermansia products that use timed-release capsules or microencapsulation technology to ensure it reaches your colon effectively. Here's how to make sure Akkermansia reaches your colon.

• Microbiota transfer tested in controlled conditions — To reduce the effect of the mice’s own microbial background, the researchers first depleted their intestinal bacteria with a two-day course of antibiotics and antifungals. They then introduced a pooled mixture of gut microbes via FMT from healthy adults who had not taken antibiotics or probiotics for at least six months and who ate a regular diet that included meat daily.*

• Performance tested with standard strength measures — Over the next three months, the mice were evaluated using two established methods. The Rotarod test measured how long they could balance on a rotating rod, while the wire suspension test assessed how long they could hold onto a thin wire using their front paws. These tools are typically used to gauge motor coordination, balance, and grip strength.*

• Microbial transplants led to varied outcomes — Some mice improved their strength and endurance, others showed little change, and some declined. By grouping the animals into “strengthened,” “unchanged,” and “weakened” categories, the team linked these differences to the microbial communities that had established in their intestines.*

• Gut samples revealed more microbial diversity than stool — Species richness, a measure of how many different types of bacteria are present, rose in all groups after FMT. When the researchers analyzed contents from the intestinal tract rather than stool alone, they found greater microbial diversity and clearer differences between the strengthened, unchanged, and weakened groups.

This broader microbial variety allowed them to identify specific bacteria that were closely linked to muscle improvements. Stool alone, they found, did not capture the full picture of microbial diversity in the gut.*

• Three species consistently linked to strength — Across both motor tests, mice with better performance carried higher levels of Lactobacillus johnsonii, Limosilactobacillus reuteri, and Turicibacter sanguinis. Their abundance followed a stepwise pattern — the more of these microbes present, the greater the improvements in muscle performance.*

• Direct probiotic supplementation boosted muscle function — To confirm the effect, the researchers introduced L. johnsonii and L. reuteri into a new group of 40 older (12-month-old) female mice — 10 per group — which better represented aging physiology. Over three months, both strains enhanced grip and coordination, while the combination produced the largest gains.*

• Muscle tissue confirmed structural and growth benefits — In the dual-strain group, muscle weight increased by 157% compared with controls. Microscopic analysis showed larger fibers in the gastrocnemius, soleus, and extensor digitorum longus muscles, which was consistent with the strength gains seen in testing.

Growth-related markers supported these findings. Gene activity for follistatin, which counteracts myostatin to promote muscle development, nearly doubled in the L. johnsonii group, while gene activity for insulin-like growth factor 1 (IGF-1) increased most in mice receiving both strains together.*

• The microbial effects extended to metabolism and inflammation — Mice that received both strains together had lower triglycerides, total cholesterol, and LDL cholesterol compared with controls. Inflammatory signaling also shifted.

Levels of interleukin-6 (IL-6) were elevated in the L. johnsonii group but reduced in the group that received both strains, suggesting that the combination may help ease systemic inflammation — though the authors note that these inflammatory responses need further study.*

• A 2019 study in Science Translational Medicine established the foundation — Researchers compared mice raised without any gut microbes (germ-free) to mice that had a normal, healthy microbiome. The germ-free mice had smaller muscles, less strength in their grip, and changes in the activity of genes that normally control muscle growth and breakdown.⁴

They also showed signs of weaker communication between nerves and muscles, including lower blood levels of choline — the building block of acetylcholine, the chemical messenger that nerves use to signal muscle fibers — and reduced activity of genes needed to assemble the junction where nerves meet muscle. Moreover, they exhibited disrupted energy metabolism with reduced mitochondrial function and an unusual buildup of glycogen, the form in which muscles normally store sugar for fuel.

• Short-chain fatty acids (SCFAs) protect muscle from wasting — When gut bacteria ferment dietary fibers, they produce acetate, propionate, and butyrate, which can serve as an energy source and, in laboratory experiments, boosted the activity of genes involved in mitochondrial function.

The researchers found that giving germ-free mice SCFAs in their drinking water partly reversed their muscle impairments, improving strength, nudging muscle mass upward, and lowering the atrophy marker atrogin-1, though not every marker improved.

In other animal research, butyrate helped preserve muscle mass in aging female mice, increased mitochondrial proteins, and improved glucose tolerance, while SCFAs more broadly have been shown to stimulate IGF-1 production. Acetate promoted glucose uptake and glycogen storage in rabbit muscle, further stabilizing energy supply in muscle tissue.

Together, these findings suggest that a diet that feeds SCFA-producing bacteria may have meaningful consequences for your muscular resilience.⁵

• A 2023 Gut Microbes review extended these insights across species — Drawing on both animal and human research, the review concluded that gut microbes appear to be closely involved in maintaining muscle and metabolic health as people age. The authors described how certain bacteria produce SCFAs when they break down dietary fiber. These SCFAs may serve as fuel for muscle cells and support healthy mitochondrial function.⁶

The review also noted that age-related shifts in the microbiome reduce diversity, make the gut lining more permeable, and allow bacterial molecules such as lipopolysaccharides (LPS) to enter circulation. This process promotes inflammatory chemicals, including TNF-α and IL-6, which have been linked to disrupted muscle-building pathways and faster muscle loss.

• Probiotics showed benefits for muscle mass and function in animals — Strains such as Lactobacillus plantarum TWK10, L. paracasei PS23, L. reuteri, and Bifidobacterium longum improved muscle mass, endurance, and strength in animal studies.

However, human evidence was more mixed — in the trials and meta-analysis cited by the featured review, some strains improved endurance, body composition, or muscle mass and strength, but the said meta-analysis found no benefit for total lean body mass, and some studies in older adults found little or no effect on muscle.⁷

• Prebiotics and lifestyle factors further supported the gut-muscle axis — Oligosaccharide supplementation reduced inflammation and increased muscle mass in animal models. The review also noted that vitamin D and calcium intake improved gut barrier function and microbial diversity, while physical activity increased the abundance of beneficial taxa such as Bacteroides and improved musculoskeletal health.⁸

• Fiber-rich foods — Whole plant foods provide the fibers that feed gut microbes, supporting a more diverse and balanced microbiome. Examples include broccoli, Brussels sprouts, cauliflower, and leafy greens. These deliver a broad range of fibers that different microbes use to thrive, creating a more resilient gut ecosystem.

However, if your gut is compromised, introducing large amounts of fiber too quickly can worsen symptoms like bloating, discomfort, and irregularity. A disrupted microbiome may not yet have the capacity to process fiber efficiently, which means even healthy foods can trigger negative reactions.

My recommendation is to first work on restoring balance by removing dietary disruptors, such as seed oils high in linoleic acid (LA), ultraprocessed foods, and excess sugars, while also minimizing unnecessary antibiotics and other substances that disrupt the microbiome.

At the same time, focus on supporting your gut lining with gentler carbohydrates like white rice or whole fruits to let your gut adjust without causing trouble. As your gut improves, add more veggies to your meals. Resistant starches like cooked-then-cooled potatoes or green bananas, in particular, can also help fuel butyrate production.

• Polyphenol-rich fruits and vegetables — Polyphenols from colorful plants, including berries, grapes, apples, and leafy greens, may encourage the growth of beneficial gut bacteria. The researchers noted:

“[P]olyphenols accumulated in the large intestine have been found to modulate the microbiome composition through antimicrobial effects or prebiotic-like action of metabolites generated through polyphenol metabolism in the colon.

For instance, the intake of diets rich in anthocyanin and procyanidin B2 is known to increase butyrate-producing bacteria and alleviate age-associated changes in aging rodent models.

Furthermore, a polyphenol-rich diet, supplemented with specific probiotics, was found to alleviate chronic low-grade inflammation, thereby reducing biological inflammaging, accompanied by an increase in probiotic bacteria and SCFAs in the gut microbiome of adults aged 50 years and older.”¹⁰

• Red ginseng — The review highlighted red ginseng as an antioxidant-rich herb that may confer antiaging effects by reducing oxidative stress, promoting the growth of healthy gut bacteria, and supporting the intestinal barrier. According to the researchers:

“Studies with specific probiotic-fermented ginseng interventions have also demonstrated antiaging properties attributed to upregulation of specific genes linked to antioxidant activity and positive modulations in gut microbiome communities.”¹¹

• Polyunsaturated fats (PUFs) — The review lists PUF-rich diets among its microbiome-based strategies and credits diets rich in mono- and polyunsaturated fats with lasting health benefits. However, other research suggests that excess PUFs, especially omega-6 LA from seed oils, may damage mitochondrial function and drive oxidative stress. Oils such as soybean, corn, safflower, and sunflower should be avoided. Omega-3s, while beneficial, need to be consumed in moderation as well.

• Certain nuts and seeds — Although the featured review doesn’t single out nuts and seeds, they are common sources of the PUFs fats it favors, and many of them are high in LA. Peanuts, sunflower seeds, and similar varieties contribute to the very imbalance I warn against.

• Olive oil — Often promoted as a healthier alternative to seed oils, olive oil is high in monounsaturated fat, mainly oleic acid. A 2025 study in Cell Reports found that oleic acid was the only dietary fat that drove the formation of new fat cells in mice at typical dietary levels — olive oil diets included.

Moreover, higher blood levels of monounsaturated fats were associated with obesity in a large U.K. cohort. Excess oleic acid has also been proposed to disrupt mitochondria and slow energy production. While olive oil’s polyphenols may offer some protection, they may not fully offset these effects.¹³

When olive oil is exposed to heat, it can oxidize, and some store-bought versions have been found to be diluted with cheaper seed oils. If you choose to include it in your diet, use only small amounts, unheated, and in high-quality cold-pressed varieties. Stable saturated fats such as grass fed butter, ghee, tallow, or coconut oil are more reliable sources of fat.

• Probiotics — The researchers noted that specific probiotics may help restore gut barrier integrity, lower inflammatory markers, and support healthier metabolism, based largely on studies in aged mice. However, they stressed that larger trials in older adults are still needed, given how widely microbiome responses vary from person to person.*

Some of the strains that were noted as beneficial in aging mouse studies include B. longum, L. paracasei, L. rhamnosus, L. plantarum, and L. fermentum. For guidance on selecting probiotic supplements and using them effectively, check out “The Science of Probiotics — How Beneficial Bacteria Support Health.”

• Prebiotics — Prebiotics such as galactooligosaccharides (GOS) were reported to improve mucus thickness, enhance epithelial integrity, and increase SCFA production. These changes supported both microbial diversity and intestinal resilience. However, it’s important to first optimize your gut health before taking prebiotics to keep them from nourishing harmful microbes instead of the beneficial ones.*

• Synbiotics — Combinations of probiotics and prebiotics, known as synbiotics, improved blood metabolite profiles, including high-density lipoprotein (HDL) cholesterol, and overall bowel health in older women in one clinical study. The review emphasized their role in promoting synergy between microbial growth and beneficial fermentation processes.*

• Next-generation probiotics — Species such as Akkermansia muciniphila and Faecalibacterium prausnitzii were identified as promising “next-gen” probiotics. In one mouse study, giving both species eased features of muscle atrophy by lowering myostatin, an inhibitor of muscle growth. Both are believed to play a role in mitigating age-related degeneration.

If you’ve been following my articles, you know I’ve previously underscored the importance of these microbes, particularly Akkermansia, as keystone species for gut health. In a small pilot clinical trial of 40 overweight or obese adults with insulin resistance (32 completed it), three months of pasteurized Akkermansia helped improve insulin sensitivity by about 29% and lowered total cholesterol compared with placebo, and also reduced blood levels of LPS, a marker of gut barrier leakage.

Reductions in body weight and fat mass were small and did not reach statistical significance. A follow-up analysis of the same volunteers identified related shifts in blood metabolites.*^15,16

If you’re considering Akkermansia, I recommend a two-phase approach. Start with a pasteurized Akkermansia postbiotic in an enteric-coated or microencapsulated format, so more of it reaches the colon intact. Introduce live Akkermansia, alongside gentle prebiotics like small amounts of resistant starch, only once bloating is minimal or absent, your stool form has stayed consistent for at least seven days, and you can tolerate more fiber without symptoms returning.

Learn more about the benefits of Akkermansia, how to choose a high-quality supplement, and the dietary steps that help it thrive in “Gut Microbes Influence How You Handle Stress.”

• FMT — In the research highlighted above, FMT served as a way to test what happens when an entire community of gut microbes from a healthy donor is introduced into another host. This method involves transferring stool, with all of its living bacteria, into the recipient’s gut to reestablish microbial balance.

While FMT is still in the experimental stage, early evidence, mostly from animal studies, links it to improvements in gut health, immune function, and aspects of aging — though in the featured mouse study, transplanted microbes strengthened some animals and weakened others. Learn more about this emerging therapy in “‘Crapsules’ — The Latest Feces Transplant Pill.”

• What the reanalysis uncovered — In this study, the team reviewed the raw trial data — not just published outcomes — and reaudited everything using the original study protocol. They applied the RIAT model (Restoring Invisible and Abandoned Trials) to see what the results would look like if all the data were handled transparently and analyzed according to the original protocol.

What they found turned the original TADS conclusion on its head — the team found "little support to justify the routine use of fluoxetine as treatment for adolescent depression."⁵ On top of that, over two-thirds of all serious adverse events (22 of 32) happened in kids who took fluoxetine.

• Fluoxetine's benefits were inconsistent — The reanalysis found that fluoxetine's advantage over placebo depended on how it was measured. Specifically, on the main outcome measure — the Children's Depression Rating Scale-Revised (CDRS-R) — the difference between fluoxetine and placebo was statistically insignificant.

Fluoxetine did produce more treatment responders than placebo on the second main measure, the Clinical Global Impression-Improvement scale (64% vs. 39%), but it beat placebo on only two of 11 secondary measures — both rated by clinicians who weren't blinded.

What's worse, the original study authors had emphasized suicidal thoughts and behaviors as rare. But the reanalysis team identified 11 additional suicide-related events that weren't reported in the official TADS reporting.

They also documented 10 suicide attempts in 10 participants — nine of whom were taking fluoxetine — compared with the seven attempts reported in the original paper. There were no completed suicides. That's a major correction to the record and shifts the risk-benefit picture.

• Adverse events were abundant — The reanalysis noted that 369 adverse events occurred for 171 participants, and 66% of those occurred in participants taking fluoxetine. These weren't limited to suicide-related episodes.

Some events appeared in the trial's records but not in the published papers, including two hospitalizations that should have been classified as serious adverse events, and three suicide attempts that were logged in the study's attrition-prevention records but not in its adverse event database. The original reports also left out events that occurred in fewer than 2% of participants and adverse events in participants whose treatment was ended early.

• Even the combination of CBT with fluoxetine was misleading — While it did show the strongest symptom drop, the reanalysis points out a problem — those therapy sessions weren't blinded. Therapists and participants both knew who was receiving treatment.

That opens the door for expectancy bias, meaning they expected themselves to improve, so they reported feeling better, regardless of whether the drug helped. That calls into question how much of that symptom improvement came from the medication itself.

• Statistical shortcuts flattered the results — The reanalysis also pointed to flaws in the original statistical analysis. In the original trial, multiple comparisons were made between groups without correcting for how that inflates the chance of false positives.

Essentially, the more statistical tests you run, the higher the odds you'll find something significant just by chance. The RIAT team corrected for this. After the correction, fluoxetine alone still didn't outperform placebo on the main depression scale, while its edge on the responder measure held.

• Possible reason why side effects occur — The reanalysis didn't examine how fluoxetine causes side effects, but the theory behind selective serotonin reuptake inhibitors (SSRIs) raises questions of its own.

SSRIs are thought to work by increasing serotonin levels in the brain, which is linked to mood. But that theory doesn't explain why some teens on fluoxetine experience agitation or insomnia, both of which were noted in the early TADS reports.

• Complete disclosure is required for the public's safety — The study called for full access to clinical trial data moving forward, and concluded that fluoxetine's "inconsistent benefits do not outweigh the harms identified in this study" and that the increase in harms "warrants further circumspection when prescribing it to adolescents." As summarized by the team's closing words:⁶

"Our reanalysis confirms the original reported findings that superiority over placebo was not demonstrated for fluoxetine. Contrary to original TADS Team's reporting, we have uncovered a higher, clinically significant level of harm, including 11 additional suicide-related adverse events."

• The side effects of fluoxetine are downplayed — While previous reports have mostly emphasized fluoxetine's effects on depressive symptoms, the BMJ Open team turned the spotlight to what was missing. For example, well-known SSRI side effects such as weight and appetite changes and sexual problems were never mentioned in TADS-related publications, and others, such as insomnia, dropped out of the reports after the first 12 weeks.

Only suicidal behavior was consistently tracked through the 36-week period, leaving out a wide array of common and distressing adverse experiences that could have shaped treatment decisions for families and clinicians.

• A misleading classification was flagged — Nine cases of suicidal behavior were reported in the placebo group even though those teens were taking fluoxetine at the time and the placebo period had already ended.

As the reviewers explain, the risk of suicidal behavior won't appear higher for fluoxetine than for placebo if teens taking fluoxetine are counted in the placebo group, which made the drug's safety profile look cleaner than it was.

• Another issue was the reporting threshold itself — The researchers noted that the TADS team only counted events that caused clinically significant interference with functioning, required medical attention or led to a new medication. Milder events weren't counted as adverse events:⁸

"In the TADS, adverse events were defined as an unfavourable medical change that occurred after beginning or during the study that might or might not be related to or caused by the study drug or CBT treatment.

This was further specified as any medical event that caused clinically significant interference with functioning (e.g., headache that caused school absence or otherwise caused clinically significant activity restriction), any event that required medical attention, and any medical event associated with impairment in functioning and induced the patient to take a concomitant medication.

Conditions that did not lead to clinically significant interference with functioning or did not require medical attention were not defined as adverse events."

• The threshold kept milder problems off the record — The reviewers couldn't find published versions of the questionnaires used to collect side effect data, so it's unclear which symptoms were specifically asked about. They also noted that the threshold likely reduced the number of side effects reported:⁹

"The TADS protocol included a threshold limit on what would be considered an adverse event, specifying that the event must cause clinically significant interference with functioning, require medical attention or cause a need to take medication. As an example, emerging mania was not recorded unless symptoms exceeded this threshold.

It must be assumed that this reduced the number of reported adverse effects, which may not have been severe enough to reduce daily functioning or cause a need for additional treatment."

• There's also the issue of long-term follow-up — Even though the TADS trial lasted for 36 weeks, most publications only focused on the 12-week acute treatment phase. After that, side effect reporting all but disappeared:¹⁰

"Due to its long duration (36 weeks) and follow-up (1 year), the TADS could have provided valuable information on the long-term occurrence of adverse effects both in frequency and severity. The adverse effects profile of FLX [fluoxetine] in the TADS has only been reported in detail for stage 1, where approximately 200 patients received FLX for 12 weeks."

1. Strengthen your gut health — Improving your digestive health is a foundational step toward better mental well-being due to the gut-brain axis. To nurture this relationship further, incorporating homemade probiotic-rich foods and steering clear of ultraprocessed foods high in linoleic acid (LA) may support communication between your gut and brain.

Excess LA may harm your gut health. I recommend keeping your intake between 2 and 5 grams a day from all sources — LA is still an essential fat, so don't aim for zero. To help you monitor your intake, download the upcoming PAXapp. It has a feature called the Seed Oil Sleuth, which calculates the LA in your food to a tenth of a gram.

In addition, limiting processed foods and reducing exposure to antibiotics and agricultural chemicals can further protect your gut microbiome. A nutrient-rich diet fuels cellular energy and supports metabolic functions — both of which may help support a stable mood.

2. Embrace a lifestyle that supports mental resilience — Support your mental health through regular exercise and quality sleep. Physical activity enhances mitochondrial health and boosts natural energy levels. Even simple habits like walking about an hour each day and keeping a consistent sleep routine can help lift your mood.

3. Try non-pharmaceutical methods — Examples include counseling, talk therapy, and cognitive-behavioral therapy (CBT). These methods empower you to develop coping strategies, confront root causes of distress, and build mental resilience without depending on medications.

Another promising option is the Emotional Freedom Techniques (EFT), a form of psychological acupressure that some small studies suggest may help ease anxiety and depressive symptoms.¹¹

4. Prioritize healthy vitamin D levels — Ensuring your body has adequate vitamin D through safe sun exposure may support your mood. As noted in a previous article, research has linked low vitamin D to a higher risk of depression. Thus, increasing your levels naturally by spending time outdoors may help support emotional well-being.

However, it's not advisable to get out in the sun right away, especially if you've been eating a diet high in LA. When sunlight hits your skin, the LA embedded there may oxidize and promote inflammation.

To protect your health, it's advisable to avoid midday sunlight, especially between 11 a.m. and 3 p.m. for about four to six months after you cut out seed oils, then gradually build up exposure around solar noon. To hasten the process, I recommend getting C15:0 (pentadecanoic acid) from full-fat grass fed dairy.

Most people get only about 100 to 200 milligrams of C15:0 per day. I personally take 2 grams daily. At that level, research suggests your keratinocytes — the skin cells in your outermost layer — may start incorporating C15:0 in place of LA. For an in-depth guide on this process, read "The Fast-Track Path to Clearing Vegetable Oils from Your Skin."

5. Foster honest dialogue with the youth — When supporting a young person's mental health, creating a safe, non-judgmental space for open communication is important. Encouraging them to express their emotions and concerns helps them feel heard and understood. This approach also aids in detecting any early signs of distress, which can lead to timely, effective support or intervention.

6. Explore these other natural strategies — For those seeking natural relief from stress and anxiety, gamma-aminobutyric acid (GABA) supplements may be one option to explore. GABA is your brain's main calming neurotransmitter, and a systematic review of placebo-controlled human trials found limited evidence that oral GABA helps with stress.¹² Talk with your health care provider before trying it, especially if you take medication for anxiety, sleep, or mood.

Methylene blue supports mitochondrial energy production, and in one small 3-week trial in adults with severe depression, it outperformed placebo.¹³ It should only be used in pharmaceutical-grade form prescribed by a health care professional, and never alongside antidepressants that act on serotonin, since case reports have linked the combination to serotonin syndrome.¹⁴

• Americans moved away from broad multivitamins and toward targeted nutrients — Conventional multivitamin-multimineral products steadily lost popularity while individually selected vitamins and minerals became much more common. Multivitamin use declined from 35% of adults in 1999-2000 to 31% in 2021-2023, while use of individual nutrients continued to climb.

Instead of buying one product that contained dozens of ingredients, more Americans chose supplements designed for specific goals. That trend suggests consumers increasingly wanted personalized nutritional support instead of blanket coverage. It's worth asking whether each supplement in your routine fills a genuine nutritional need or whether it landed in your cabinet because of clever marketing.

• Vitamin D, zinc and several individual nutrients experienced the strongest growth — When researchers excluded multivitamins and focused only on individually purchased nutrients, vitamin D showed one of the largest increases in the entire study, rising from 5.1% of adults to 29%. Zinc more than doubled, increasing from 4.6% to 11%. Researchers also documented substantial increases in vitamin K, vitamin B12, biotin, magnesium, potassium, copper, and iron.*

At the same time, several older specialty minerals, including nickel, tin, silicon, vanadium, chromium and boron, became less common. Those shifting patterns show consumers gravitating toward nutrients tied to specific health concerns rather than broad-spectrum coverage.

• Consumers increasingly purchased supplements for specific health goals rather than general wellness — The researchers found growing use of products such as collagen, hyaluronic acid, ashwagandha, elderberry and prebiotic or probiotic supplements. Many of these products were uncommon when the study began but became increasingly popular during the later survey years.

The fastest-growing categories centered on immune health, digestive health, skin health, joint support and healthy aging. Those purchases reflect changing consumer priorities, but the researchers emphasized that popularity alone doesn't establish effectiveness. Choosing a supplement based on evidence instead of advertising remains one of the smartest decisions you can make.

• Supplement habits changed gradually over many years rather than overnight — Statistical analyses showed that many supplement categories remained relatively stable until roughly 2009 through 2012 before increasing much more rapidly.* That means today's supplement marketplace reflects a long-term shift in consumer behavior rather than a short-lived fad.

Researchers also observed additional increases during the COVID-19 pandemic, particularly for vitamins, minerals and products commonly promoted for immune health, including zinc and elderberry. Rather than creating entirely new trends, the pandemic accelerated purchasing habits that were already developing.

• The study revealed who buys supplements but not whether the supplements improved health — The researchers carefully documented which supplements Americans used and how those choices changed over time, but they didn't evaluate whether those products prevented disease, improved health or increased longevity. That difference matters because widespread use doesn't automatically prove effectiveness.

The researchers specifically noted that continued studies are needed to determine which supplements truly deliver meaningful health benefits.

• The findings encourage you to evaluate every supplement with a clear purpose — The study paints a detailed picture of how Americans think about supplementation. Consumers increasingly select products aimed at specific goals instead of relying on one-size-fits-all multivitamins, showing that people are becoming more intentional with their choices.

This is a positive direction, provided those decisions are grounded in science instead of marketing. Before adding another supplement to your routine, identify the nutritional gap you're trying to fill and look for solid evidence that the ingredient addresses that specific need.

1. Start with food and sunlight whenever possible — I view supplements as exactly what their name implies — additions to an already healthy lifestyle, not replacements for one. Nutrient-dense foods provide vitamins, minerals and thousands of beneficial compounds that work together in ways isolated nutrients can't. In the case of vitamin D, regular, sensible sun exposure remains the ideal source.

Build your meals around high-quality protein, whole fruit and other minimally processed foods first, then use supplements to address nutrients that remain difficult to obtain.

2. Supplement the nutrients that are hardest to get from modern diets — Magnesium is one of the clearest exceptions to the food-first approach because decades of intensive farming have reduced the amount available in many foods. Even if you eat well, it's difficult to get enough from diet alone. That's why I often recommend magnesium glycinate or malate.

Glycinate tends to suit magnesium-sensitive individuals and support nighttime recovery, while malate is better suited to muscle function and energy production.

3. Choose supplements that solve your problem instead of following the latest trend — The study found that Americans increasingly purchase supplements for immune health, gut health, skin, joints, and healthy aging. That doesn't mean every popular product belongs in your routine. Before buying another supplement, identify the nutritional gap or health goal you want to address.

If you aren't sure where your biggest nutritional gaps lie, working with a knowledgeable holistic health practitioner helps you identify the nutrients that best fit your individual needs. A supplement deserves a place in your routine because it meets a genuine need, not because it dominates social media or advertising.

4. Make your supplement routine almost effortless — Even the highest-quality supplement offers little benefit if your routine is too complicated to maintain. Multiple bottles, handfuls of capsules, and staggered dosing schedules create friction that quietly erodes consistency. That's one reason many supplement makers are reformulating their products as powders wherever the ingredients allow it.

Mixing a powder into a homemade smoothie or another meal you already eat ties supplementation to a habit you already perform every day. Instead of creating another pill-taking ritual, you simply make targeted nutrition part of your daily meals.

5. Fix the foundations that no supplement can replace — Before spending another dollar on a new supplement, ask whether the basics are in order. Poor sleep can undermine magnesium retention, disrupt blood sugar regulation and accelerate the very aging processes people try to address with supplements.

Sedentary habits can blunt nutrient absorption and reduce circulation to the tissues where vitamins and minerals do their work. A diet built on processed food tends to create deficits faster than any capsule can fill them.

Supplements generally perform best when the body receiving them is already functioning well. Prioritize consistent sleep, daily movement, and meals built around whole foods first — those three changes alone can resolve many of the gaps people try to supplement their way around.