• The biggest increases appeared after 2009 — Researchers found that supplement habits remained relatively stable until the 2009 to 2010 survey cycle, after which use rose sharply. The pattern was even stronger when multivitamin-multimineral products were removed from the analysis. Use of supplements outside these broad formulas rose from 34% to 50%.

Americans increasingly selected separate products rather than depend on a single formula containing numerous nutrients. That distinction matters because adding individual supplements gives you more control over your routine, but it also increases the importance of knowing why you take each product and whether the dose fits your individual needs.

• Older adults recorded the largest increase in supplement use — Age created one of the clearest differences in the data. Among adults age 65 and older, supplement use increased by 16 percentage points, from 62% to 78%. By comparison, use among adults ages 20 to 39 rose from 42% to 46%, while use among those ages 40 to 64 increased from 56% to 62%.

Other groups also recorded substantial changes. Supplement use among adults with less than a high school education climbed from 33% to 48%, while use among Mexican American adults increased from 32% to 49%. Across the entire study period, use remained more common among women, older adults, people with higher incomes and education levels, those with health insurance and non-Hispanic White adults.

• Your supplement cabinet deserves a regular audit — The study found that supplement use differs substantially according to age, income, education and other personal factors. At the same time, researchers emphasized that people often select products for highly individualized reasons. This means there is no universal supplement routine that fits everyone.

You could turn this insight into a simple health challenge. Once or twice a year, list every supplement you take and answer three questions: Why am I taking it? What specific need does it address? Do I still need it? This quick audit helps you move away from collecting popular products and toward a routine based on clear, personal goals.

• The study identified an important gap between popularity and proven results — Researchers pointed out that evidence on the health effects of supplements remains mixed. Some research reports benefits from certain products, while other studies find no benefit or report harm. Evidence about interactions between supplements and medications also remains limited for many products.

Just as important, the study tracked what Americans took, not whether those choices made them healthier. Because this was a repeated cross-sectional analysis, researchers examined different snapshots of the population over time rather than follow the same people for nearly 25 years. As a result, the findings reveal major shifts in behavior but don't prove that greater or more targeted supplement use improved health outcomes.

• More choices make personalized decisions increasingly important — The researchers concluded that supplement use has become more diverse, with Americans increasingly interested in products marketed for specific health concerns.

This shift gives you more ways to tailor your routine, but targeted doesn't automatically mean necessary, safe or effective for your individual circumstances. The data make the trend clear. What they can't tell you is whether your own routine reflects genuine need or accumulated habit. That question is worth answering for yourself.

1. Start with food before reaching for a supplement — Your body needs vitamins, minerals, protein, carbohydrates and fats to produce energy and maintain healthy function. Get as much nutrition as possible from whole, minimally processed foods, then use supplements to address specific needs.

Build your meals around ripe whole fruit, root vegetables, white rice and other carbohydrates you tolerate well, along with quality protein sources such as grass fed ruminant meat, pastured eggs, collagen and grass fed dairy if you tolerate it. Choose fats such as grass fed butter, ghee and tallow instead of seed oils.

2. Make every supplement earn its place — Take out every bottle you use and write down exactly why you take it. Be specific. "For general health" is not a clear goal. If you can't identify the nutritional need or health concern a product addresses, reconsider why it's part of your routine.

I recommend repeating this simple five-minute challenge every few months, especially if you tend to add new products without removing old ones. Working with a knowledgeable holistic health care practitioner can help you identify which supplements are worth keeping in your routine and which are better off avoided.

Magnesium is one example in which reaching the recommended 420 milligrams per day through diet alone is difficult.

Even a healthy diet full of magnesium-rich foods often falls short because intensive farming practices have depleted mineral content in soil over decades. In this case, magnesium glycinate, magnesium L-Threonate, and magnesium malate are the preferred forms — glycinate tends to work well if you’re more sensitive to supplements or want nighttime support, while malate is better suited for muscle and energy needs.

To find your ideal dose, consider starting with magnesium citrate and gradually increasing your intake until stools loosen, then backing off slightly and switching to your preferred form.

Vitamin D is another example. While it’s best to get your vitamin D from sunlight whenever possible, if you don’t get outdoors regularly a vitamin D3 supplement helps bridge that gap. The only way to know if your vitamin D levels are in the optimal range is to get your levels tested. Aim for a vitamin D level between 60 and 80 ng/mL (150 to 200 nmol/L), and test every six months to stay within the optimal range. Talk to your healthcare provider about whether this testing is appropriate for you.

Meanwhile, if you take vitamin D3, pair it with magnesium and vitamin K2 as research suggests these three nutrients work best as a team. In fact, one analysis of health-tracking program data found that people who skip magnesium and K2 need more than twice as much vitamin D to reach the same blood levels as those who take all three together.³

The goal isn't to build the largest supplement collection. It's to help you create the simplest routine that supports your individual needs and fits into your actual life. A well-designed supplement routine needs to work on your busiest days, not just when conditions are perfect. Keep nutritious food at the foundation, use targeted supplements to fill genuine gaps and choose formats simple enough to become a natural part of your day.

3. Choose formats that fit your real life — Even a carefully selected supplement does little good if your routine is too complicated to maintain. Multiple bottles, doses and reminders add friction, while swallowing several capsules at once creates another barrier. That's one reason we're reformulating some of our supplements as powders where the ingredients allow it.

A powder that you stir into food connects supplementation to something you already do every day: eat. Instead of creating a separate ritual that requires you to remember another task, the supplement becomes part of an established daily habit. Taste and texture matter, too. A pleasant, easy-to-use product is far more likely to become part of your routine than something you dread taking.

This food-first format also better reflects my approach to supplementation. Real food remains the foundation, while supplements provide targeted support when your diet doesn't supply enough of a specific nutrient. Supplements don't replace nutritious food or excuse a poor diet. Where appropriate, a powder mixed into a meal keeps that relationship clear by making supplemental nutrition part of how you nourish yourself rather than another medical-style ritual built around bottles and pills.

4. Pay close attention to the form and dose — Two products with similar labels aren't necessarily interchangeable. The ingredients, dose, quality and method of use all matter. For example, a supplement that combines numerous ingredients in small amounts might look more comprehensive, but that doesn't mean it provides the right amount of the specific nutrient you need.

Choose products based on a clearly identified need, then pay close attention to exactly what you're getting and how it fits into the rest of your diet and supplement routine.

5. Look beyond the claims on the front of the bottle — Supplement labels are designed to sell products, but the most important information is often found on the back. Read the full ingredient list rather than relying on claims such as "natural," "immune support" or "healthy aging."

Pay attention to unnecessary additives and other ingredients that don't serve the specific reason you chose the supplement. Look for products with transparent ingredient lists, clearly stated amounts and as few unnecessary additives as possible. Quality matters as much as convenience.

• First, while specific benzodiazepines can be an appropriate treatments for certain types of anxiety, they frequently make the condition worse (e.g., generalized anxiety).

This is particularly important with insomnia, as benzodiazepines (and the related z-drugs like Ambien⁹) do not put you to sleep — rather they are sedatives that sedate (shut down) restorative sleep. As such, patients on sleep pills often suffer the same complications seen with chronic sleep deprivation.

In fact, studies have found sleeping pill users are two to five times as likely to die as non-users,^10,11 and one estimate concluded that in 2010, prescription sleeping pills "may have been associated with 320,000 to 507,000 excess deaths within the USA alone."¹²

Note: I only know of one available sleeping pill¹³ that does not block restorative sleep (along with a far more effective sleep aid the FDA waged an unconscionable war against to keep off the market).

• Second, they frequently create a variety of severe side effects such as:

Sedation, drowsiness, muscle weakness, fatigue, and loss of motor coordination (e.g., studies have found benzodiazepines make you more likely to have an accident than alcohol, and commercial drivers are prohibited from taking benzodiazepines14,15,16).

Dizziness or lightheadedness (e.g., a study of 2,510 nursing home residents found they increased the risk of falls by 44%17).

Causing visual disturbances such as blurred or double vision (e.g., one study found 63.3% of long-term benzodiazepine users reported visual issues18).

Confusion, disorientation, and impairment of cognitive functioning, processing speed, short-term memory, or forming new memories19,20 (e.g., one study21 found 20.7% of long-term benzodiazepine users exhibited significant cognitive impairment across many domains). Note: Many benzodiazepine users I've spoken to have shared that their perception of reality changes and time flashes by so fast. They also shared that it is often quite difficult for them to remember what had happened while they were using these drugs (known as anterograde amnesia — in fact by 1972 it was known that regular diazepam doses reduced recognition memory in 90% of women22).

Increasing the risk of dementia by 51%.23,24 Note: Many of these cognitive side effects are likely due to benzodiazepines blocking restorative sleep (as they mirror those found after sleep deprivation). Since sleep is critical for effective learning (discussed here), I frequently find anxious students need to stop using a benzodiazepine while studying to succeed academically.

Respiratory depression, which can be lethal, especially when combined with other respiratory depressants (e.g., opioids).

Causing many of the conditions they are supposed to treat (e.g., agitation and aggression), especially after the drugs are stopped.25 For example: Additionally, many of these symptoms often last long after the benzodiazepine is discontinued.

• Third, certain groups are particularly at risk of these complications but nonetheless frequently take these drugs.

For instance, nearly 1.9% of pregnant women worldwide report using benzodiazepines despite risks of complications like early delivery, low birth weight, congenital malformations, floppy infant syndrome, and withdrawal symptoms^26,27,28 (e.g., one study found a 41% increased risk of premature birth,²⁹ another found a 69% increase in miscarriages,³⁰ while another found a 145% increase in C-sections, a 241% increase in low birth weights, and a 185% increase in newborns requiring ventilatory support³¹).

Likewise, the elderly are particularly vulnerable to cognitive impairment and falls benzodiazepines cause — particularly since they often have impaired metabolism of the drugs (to the point in 2012 the American Geriatrics Society recommended against giving them to older patients³²), yet benzodiazepine use steadily increases with age.³³

• Finally, they have a high risk of causing overdoses — which is particularly problematic since they are also highly addictive and overdoses keep increasing (e.g., in 2021, there were around 12,499 deaths involving benzodiazepine — a 917% increase over 22 years³⁴).

• Common symptoms — Anxiety, insomnia, irritability, tremors, muscle stiffness and pain, sweating, nausea and vomiting, headaches, panic attacks, dizziness, heart palpitations

• Psychological symptoms — Confusion, memory problems, depression, hallucinations, delusions, paranoia

• Sensory symptoms — Tinnitus, burning sensations, derealization/depersonalization

• Physical symptoms — Seizures, muscle twitches, loss of appetite and weight loss, diarrhea

• Other symptoms — Dry mouth and metallic taste, difficulty swallowing, flushing and skin rashes

• They are used for a short-term period, or only occasionally as needed.

• Care is taken to prevent dependence and monitor for side effects.

• They are used at low doses (whereas in practice excessive doses are often used to counteract tolerance developing to them — which makes it very hard to stop the drugs).

• The patient has a type of anxiety in which benzodiazepines have shown benefit.

• They are used as a support for other therapies that treat anxiety (e.g., effective psychotherapy⁵³) rather than as the primary therapy.

Note: We find initiating the appropriate psychotherapy prior to benzodiazepines dramatically improves therapeutic outcomes.

• Most contaminated meat came from poultry and pork — Poultry appeared to be the primary reservoir for the highest-risk E. coli strains, but all retail meat was heavily contaminated. Chicken and turkey were identified as the top carriers. Of the meat samples carrying strain types associated with meat-linked UTIs, 74% came from chicken (38%) or turkey (36%). Pork and beef also had high contamination rates (54% and 47%, respectively), but accounted for smaller shares of the infection-linked strain types (12% and 14%, respectively).

Contamination rates were as high as 82% in turkey and 58% in chicken purchased from major grocery chains. Researchers identified many of these as extraintestinal pathogenic E. coli (ExPEC) — strains capable of causing infection outside the gut — which suggests that virulent strains originating in food animals were entering the human food chain and causing infections in people’s urinary tracts and bladders.

• Zoonotic strains were genetically distinct, supporting cross-species transmission — Genetic sequencing revealed that the bacteria in these UTIs carried mobile genetic elements — small packages of DNA — more typical of those found in food animals than in humans. These genetic markers acted like fingerprints, pointing to an animal origin.

Once inside the human body, these animal-derived bacteria can establish themselves in the urinary tract, and because most invasive E. coli infections begin there, they may (in severe cases) progress to the bloodstream. However, note that this featured study examined only community-acquired UTIs, not bloodstream infections. This finding adds to evidence that the food supply is an underrecognized route by which UTI-causing strains reach people.

• Women and older men were most affected — Among the thousands of patients studied, nearly 90% were women, and the average patient age was 50 years old. Among women, 19.7% of E. coli UTIs were zoonotic — more than twice the proportion seen in men (8.5%).

Among men, those with zoonotic infections tended to be older — an average age of 73 years old, compared with 65 years old for men with other E. coli UTIs. These groups may face increased risk due to hormonal, anatomical, and immune differences, though the study did not examine why.

• Socioeconomic inequality was linked to higher risk — Living in high-poverty areas was associated with 1.6 times higher odds that a UTI was zoonotic, compared with low-poverty areas. The researchers proposed several possible explanations, including weaker adherence to food safety rules in resource-poor retail settings, improper storage temperatures, and gaps in food handling and hygiene practices.

In other words, people in poorer neighborhoods may be exposed to more contaminated meat and have fewer resources to lower their risk. The researchers called for stronger measures along the food supply chain — not just personal hygiene — to reduce these risks.

• Antibiotic-resistant bacteria were found in both meat and humans — Some of the E. coli strains isolated from meat showed resistance to commonly used antibiotics, including ampicillin and tetracycline. Resistance was also found in human samples, and antibiotic use in agriculture is one recognized route by which resistance can spread to people — although in this study, multidrug resistance was significantly less common among the meat-linked strains than among other UTI strains.

Some E. coli in the study were also resistant to multiple drug classes, which can limit treatment options. When antibiotic-resistant infections occur, they can require stronger medications and, in some cases, hospital care.

• E. coli from poultry carried the greatest risk of spreading from animals to people — The data showed that chicken and turkey accounted for nearly three-quarters of the meat samples carrying strain types linked to these UTIs. Specific bacterial lineages appeared repeatedly in both meat and human infections.

These included strain types known to cause infections outside the gut. The researchers reported that the highest-risk zoonotic strains were most prevalent among poultry E. coli populations.

• Genetic analysis pointed to where these bacteria came from — The researchers used a statistical model, trained on 17 host-associated genetic markers, to estimate whether a given E. coli genome looked more like one from a human or a food animal source. This allowed them to estimate how many infections likely came from food animals.

They found that nearly 1 in 5 UTI samples in people carried bacteria inferred to be of food-animal origin, while only 0.6% of meat isolates were inferred to be of human origin. This indicates that transmission was happening primarily from animals to people, not the other way around.

• Reducing antibiotic use in livestock may help curb resistance — The researchers noted that after California passed Senate Bill 27 — limiting antibiotic use in farm animals — resistance to two antibiotics targeted by the law, ampicillin and tetracycline, was lower among meat samples than in an earlier study conducted in Arizona.

Tetracycline resistance, for example, was 34.4% in this study, compared with 49.9% in the earlier study. The researchers suggested this may reflect changes in agricultural antibiotic use and called for further research into whether such policies can reduce resistance in human infections. If so, cleaning up the meat supply could help reduce the number of drug-resistant UTIs and other infections.

1. Eliminate CAFO meat from your diet — The single biggest step you can take is cutting out meat from CAFOs. These crowded, industrial farms breed bacteria like E. coli, which end up in your food. I recommend avoiding all conventional chicken, pork, and beef. Choose grass fed beef from regenerative farms instead.

These animals live cleaner lives, without unnecessary antibiotics or unsanitary housing, which may mean their meat carries a lower bacterial load. Note however, the featured study tested conventional retail meat and did not compare farming methods. If you still eat chicken or pork, choose only organic and pasture-raised sources, though I advise avoiding chicken and pork altogether because of their high linoleic acid (LA) content — excess LA has been linked to inflammation and may impair mitochondrial function.

2. Consider methylene blue and cranberries for urinary support — Pharmaceutical-grade methylene blue is one option I’ve found to be helpful, when prescribed by a health care professional. It passes through your kidneys into your bladder, where it is thought to concentrate enough to act against harmful bacteria. By shuttling electrons back and forth, oxidative stress is generated inside bacteria such as E. coli, disrupting their energy production.⁴,⁵ Doctors used it as a urinary antiseptic from the 1890s until the 1930s and 1940s.⁶ For most adults, the dose typically used for acute UTI is one 65-milligram tablet three times a day with water after meals, taken only for a few days.

Use only pharmaceutical-grade methylene blue in capsule or tablet form, prescribed by a health care professional and sourced from a compounding pharmacy. Industrial or aquarium-grade methylene blue is not suitable for human use. Methylene blue isn’t appropriate for everyone, including people taking serotonergic medications such as selective serotonin reuptake inhibitor (SSRI) antidepressants or those with G6PD deficiency, so your prescriber needs to review your medications and health history first.

Whole cranberries or organic cranberry juice — not the sweetened kind — may also help; compounds in cranberries have been studied for their ability to make it harder for bacteria to stick to your urinary tract walls. D-mannose, a naturally occurring sugar found in small amounts in cranberries and other fruits, has also been studied for urinary tract support.

3. Upgrade your kitchen hygiene habits — Even if you eat high-quality meat, handling it carelessly still spreads bacteria. Always wash your hands before and after touching raw meat. Keep cutting boards and knives separate for meats and vegetables. Disinfect countertops with hot water, soap, and vinegar afterward. Cook meat thoroughly as well — the researchers highlight proper cooking, along with handwashing and avoiding cross-contamination, as essential to reducing exposure.

If you use reusable shopping bags, wash them regularly — raw meat packaging often leaks. These habits seem small, but they’re the first defense against infection-causing microbes that would otherwise make their way from your kitchen to your body.

4. Adopt cleaner personal hygiene to block bacteria entry — Many UTIs begin with bacteria traveling from the rectal area to the urethra, especially in women. Always wipe front to back after using the bathroom. I recommend using a bidet for a more thorough clean, particularly if you’re prone to recurring infections or caring for someone who is.

If you’re prone to UTIs, consider showers instead of baths, which may make it easier for bacteria to reach your urethra. Before any sexual activity, wash up — both partners. These habits are simple, free, and may help keep the bacteria that cause UTIs from getting a foothold in the first place.

5. Support your urinary tract and immune health daily — Strengthening your defenses from the inside out helps your body resist infection. Stay well hydrated — let your thirst be your guide and aim for clear, pale-yellow urine throughout the day. Limit processed foods that feed bad bacteria.

Get daily sunlight, which supports immune function through improved mitochondrial energy production. If you’ve been eating a diet high in seed oils, build up exposure gradually — avoid high-intensity sun until you’ve been off seed oils for four to six months, then aim for sun around solar noon. And reduce stress, since chronic stress suppresses your immune system and makes you more susceptible to infections. A strong, well-nourished body is better equipped to resist bacteria — even when exposed.

• Infant formula is full of unhealthy components that promote allergies and obesity (e.g., the first ingredient in formula is often corn syrup and then followed by seed oils — which remarkably federal law requires to be in infant formula due to a law based on flawed nutritional science from the 1960s that was never updated).

• Breast milk was designed to be one of most nutritious foods a developing infant could have and contains many vital components which will never be possible to synthetically replicate.

• Numerous vital growth factors (e.g., ones that facilitate the development of the gastrointestinal tract^2,3,4,5).

• MicroRNA⁶ (which are protected from digestion and hence able to absorb into the body⁷), which guides the development of tissues throughout the body,⁸ regulate critical gene expression,⁹ prevents allergies¹⁰ (e.g., to foods), and produce many critical parts of the developing immune system.¹¹

• A unique set of antibodies and immunoglobulins¹² are produced by the mother to both protect the infant against expected pathogens in the environment¹³ (e.g., what the mother has encountered) while the infant's immune system is still developing, and guide the development of their immune system.¹⁴

• Key cytokines such as TGF-β, IL-6 and IL-10 which also play a critical role in much of the previous (e.g., promoting oral tolerance, supporting immune system development, and enhancing intestinal epithelial proliferation and repair).^15,16,17

Note: A major problem with many vaccines is that they tend to provoke a Th2 response¹⁸ (which eliminates certain extracellular pathogens but also creates autoimmunity) and suppress the Th1 response (which eliminates intracellular pathogens and cancers¹⁹).

Breast milk inhibits immune cells shifting to a Th2 state²⁰ and can change a Th2 response into a more balanced Th1-Th2 response.²¹

• A variety of enzymes that both help the infant's digestive tract break down the ingested milk and release key peptides from breast milk components (that both develop the immune system and directly eliminate pathogenic organisms),^22,23,24 along with many other enzymes and bioactive molecules that inhibit microbial growth (e.g., lactoferrin, lysozymes and mucin, interferon and fibronectin).

• A protein with potent anticancer activity²⁵ (against over 40 types of cancers²⁶) that does not harm normal cells²⁷ and has successfully treated cancer in humans.²⁸ It also has powerful antimicrobial activity²⁹ and enhances bacterial sensitivity to antibiotics.³⁰

• Breast milk contains endogenous cannabinoids that are important for human development (e.g., by affecting appetite, mother-child bonding, immune function, brain development and motor function).^31,32

• Human Milk Oligosaccharides that support the growth of healthy gut bacteria³⁴ (e.g., bifidobacteria and lactobacilli³⁵), reduce inflammation, and contribute to immune system development.³⁶

• Essential fatty acids,³⁷ cholesterol³⁸ (and many other unique lipids³⁹) which are critical for brain development,⁴⁰ eye development,⁴¹ and cognitive function (e.g., academic success⁴²).

These fats are not present in infant formula (or present in relatively low levels — except in animal milk substitutes,⁴³ as it's well recognized copious fats are necessary for their growth) and many experts in the field believe their absence from formula is one of the reasons why breast milk is so much healthier for infants.⁴⁴

Human breast milk also contains bile salt-stimulated lipase,⁴⁵ an enzyme absent in cow's milk and most other commonly consumed milks (e.g., formula) which is specifically adapted to enhance the digestion and absorption of fats and cholesterol in human infants.

Note: Cholesterol is also necessary to produce hormones (e.g., boys undergo a surge of testosterone in the first 1 to 3 months of life⁴⁶ which is pivotal in masculinizing their bodies).

• Highly bioavailable nutrients⁴⁷ (e.g., iron), which allows much lower concentrations of them needed in milk than formula (which then prevents those nutrients from competing with the absorption of other critical nutrients, such as iron added to infant formula interfering with the critical absorption of zinc⁴⁸).

• Lower rates of infections (e.g., pneumonia,⁵⁰ ear infections⁵¹) and lower hospitalization rates⁵² (e.g., for infections).

• Lower rates of gastrointestinal issues (e.g., stomach problems,⁵³ constipation,⁵⁴ gas, diarrhea⁵⁵) and allergies⁵⁶ (e.g., being half as likely to develop asthma⁵⁷).

• Being half as likely to die from Sudden Infant Death Syndrome⁵⁸ (a condition decades of evidence shows is linked to vaccination).

• Being less likely to develop cancers⁵⁹ (particularly leukemia⁶⁰).

• Improved brain development (particularly white matter growth⁶¹).

• Improved cognition (e.g., verbal and spatial skills⁶² or mathematical ability and working memory⁶³). Likewise, breastfeeding for 12 months was associated with a three-point increase in IQ⁶⁴ (along with a 0.8 point increase for each additional month⁶⁵), and higher educational and financial success in life.⁶⁶

• Being significantly less likely to develop autism or ADHD.⁶⁷

• The study revealed just how widespread prediabetes in teens has become — In 2023, 32.7% of adolescents — roughly 8.4 million young people — were living with prediabetes. That means about 1 in 3 U.S. teenagers is already showing early signs of metabolic dysfunction. These figures are based on a nationally representative sample, which makes them a reliable reflection of the population at large.

One limitation worth noting: The CDC released this estimate as a short online summary rather than a peer-reviewed paper, and did not publish the underlying data. Outside researchers have said they cannot evaluate it without that data. The figure is the best national estimate currently available, and it should be read as an estimate rather than a settled count.

• This health crisis is not limited to one group — Risk factors like being overweight, having a parent or sibling with Type 2 diabetes, and being physically inactive were strongly tied to prediabetes.² In other words, if you have a family history or live a sedentary lifestyle, your chances of developing prediabetes as a teen are higher.

• The rate of prediabetes is climbing compared to earlier years — When researchers adjusted older data with their updated methods, they found that from 2005 to 2016, the prediabetes prevalence for adolescents would have been 28%. Today, that number has jumped to nearly 33%. Two cautions on reading that as a trend: The comparison spans 2005 to 2016 against 2023. Diabetes researchers who reviewed the figures have said the difference between 28% and 33% is not statistically significant, and that the CDC changed its calculation method without publishing a detailed explanation. So, the direction is worth watching, but the true size of the change is not yet established.

• Teens with prediabetes are already on the path to serious disease — The CDC called prediabetes a “warning sign” because it signals a much higher chance of progressing to Type 2 diabetes, heart disease, and stroke. For parents and young people, that means ignoring these early signals can set the stage for lifelong health struggles.

• Biological mechanisms explain why prediabetes leads to disease — Elevated glucose levels damage the lining of blood vessels, increase oxidative stress, and strain your pancreas as it struggles to produce more insulin. Over time, this wears down your body's ability to manage blood sugar, eventually leading to full Type 2 diabetes. Once that threshold is crossed, your risk of nerve damage, kidney disease, heart disease, and vision loss becomes much greater.

• Prediabetes disrupts your body's energy system through mitochondrial dysfunction — Your mitochondria are the tiny power plants inside your cells that convert glucose into usable energy.

In prediabetes, insulin resistance prevents glucose from entering cells efficiently, and when mitochondria are already damaged, this process breaks down even further. Instead of fueling your cells, sugar piles up in your bloodstream, leaving your body both overloaded and starved at the same time.

This mismatch drains your teen's energy, reduces motivation, and traps them in a cycle of fatigue and poor metabolic health that grows worse without intervention. When mitochondria falter, especially in tissues like your pancreas, liver, and fat cells, the risk of progressing from prediabetes to diabetes rises, because insulin-producing cells work less effectively.

• The scale of the problem is reshaping the health landscape — The CDC reported that adult diabetes diagnoses, which had been declining for more than a decade, are no longer falling. In 2023, about 1.5 million adults were newly diagnosed with diabetes.⁵ This parallel trend suggests that teens with prediabetes today are tomorrow's diabetes patients, adding further strain to families, communities, and health care systems.

• The research underscores the urgency for early action — For your teen, this means understanding that their daily choices — what they eat, how much they move, and how they manage stress — have a direct impact on whether they prevent or improve or slide into diabetes. Framing the challenge as a winnable game is key: track progress, set goals, and celebrate small victories, because each step away from ultraprocessed foods and inactivity is a step toward restoring energy and health.

• Clear vegetable oils and processed snacks from their diet — The first step is to look at the foods most teens eat: fries, chips, packaged snacks, and restaurant meals. Almost all of them contain vegetable oils like canola, soybean, and sunflower oil. These oils are rich in linoleic acid (LA) that in excess is thought to impair mitochondrial function, which may contribute to blood sugar problems.

Replace them with foods prepared at home using butter, ghee, or tallow. For snacks, encourage whole-food options like fruit or grass fed cheese. Think of this as resetting your teen's “energy software” so their body runs on full power again.

• Reintroduce carbohydrates in a smart way — Teens need carbs for energy, especially for growing bodies, busy school days, and sports. The problem is not carbs — it's the wrong kind of carbs. If your teen has gut issues, start with gentle foods like white rice and whole fruit.

As their digestion improves, expand to root vegetables, beans, and whole grains. Carbs fuel the brain and muscles, so the right amount helps them concentrate in class, perform better in sports, and stay in a good mood instead of crashing.

• Reduce exposure to everyday toxins — Your child is exposed daily to plastics, personal care products, and nonstop Wi-Fi. These stressors are among the exposures the bioenergetic framework identifies as working against cellular energy production. Small changes add up: Switch to glass or stainless steel water bottles, avoid microwaving food in plastic, and encourage them to keep their phone out of their pocket and away from their bed at night.

If your teen likes challenges, frame this as a “low-plastic” or “phone-free sleep” experiment — they'll be more likely to stick with it if it feels like a goal instead of a rule.

• Build in regular sunlight for natural energy — Sunlight charges more than vitamin D. It triggers melatonin inside mitochondria, which protects energy production. Encourage sun exposure daily — walking the dog, biking to a friend's house, or sitting outside after school.

If your family has eaten a lot of vegetable oils in the past, give it at least six months of reducing them before getting longer midday sun exposure, because those oils increase the risk of sunburn. Over time, daily sunlight helps improve sleep, mood, and energy regulation in teens.

• Use the HOMA-IR test as a tracking tool — One of the most motivating ways to help your teen is to make progress visible. Recognizing insulin resistance early is essential, as it's a warning sign for your metabolic health — one that often precedes Type 2 diabetes.

The HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) test is a valuable diagnostic tool that helps assess insulin resistance through a simple blood test, so you can spot issues early and make necessary lifestyle changes.

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

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

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

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

• Where you store fat traced different paths in the brain — One of the study's central messages is that two people can weigh the same and share the same BMI while carrying very different risks to the brain. Fat in different regions of the body was associated with distinct patterns of change across separate brain systems — networks tied to movement, emotion, memory, and other functions — and these patterns were not visible from body weight or BMI alone.

Fat in different parts of the body maps out entirely different trajectories of change in the brain, the researchers note. Among all the fat depots the team examined, visceral fat stood apart as the one most consistently tied to trouble.

• Visceral fat showed the strongest association with abnormalities in the brain's white matter — This is the wiring that carries signals between nerve cells. Specifically, higher visceral fat was linked to signs of reduced nerve-fiber density and tissue disorganization in white-matter tracts, while fat in the arms, trunk, and legs was linked to more preserved white-matter structure.

White-matter damage is closely connected to the biology behind small vessel disease and vascular cognitive impairment, conditions that sit upstream of dementia risk.

• The study did not directly test what causes this link, but the researchers offered a plausible explanation — Visceral fat secretes pro-inflammatory signaling molecules, including tumor necrosis factor-alpha and interleukin-6.

The team suggests this may trigger low-grade, body-wide inflammation that spills over into the brain and contributes to white-matter damage — whereas fat in the arms, trunk, and legs releases lower levels of these inflammatory factors. This is presented as a hypothesized mechanism, not a proven chain of events.

• The brain changes are connected to thinking and memory — To link these brain changes to mental performance, the researchers built models that estimate a "brain age gap" (BAG) — the difference between how old a brain looks on a scan and the person's actual age, where a larger gap points to faster-appearing aging.

They found that the brain age gaps from cortical systems (the sensorimotor, limbic, and default mode networks) statistically accounted for part of the relationship between visceral fat and performance on tests of reasoning, executive function, processing speed, and memory. Of all the fat measures studied, visceral fat exerted the most pronounced effect on these outcomes.

• The protein at the center of the findings — The researchers are focusing on a molecular process called K63 polyubiquitination, a kind of chemical tagging inside cells that helps regulate how memories form during learning. In earlier work, the researchers found that K63 activity rises as memory declines: In younger brains, K63 levels drop during learning to help memories form, but in older brains those levels stay too high instead of adjusting normally.

"When you had too much of this protein, we'll call it K63, that you had poorer memory. And what we're actually finding is that with obesity, we're actually seeing an accumulation of this protein," Jarome explained.⁴

• What changed in the obese animals — When the team studied young rats fed a high-fat diet, the animals showed elevated K63 levels comparable to those normally seen in much older rats, and they performed worse on memory tests. The researchers found that the protein accumulated more rapidly in the obese animals than in those undergoing normal aging, appearing at an earlier point in life than it otherwise would.

"What surprised us was we were seeing the same changes in young obese rats that we normally see in much older brains — just on a much faster time scale," Jarome said. This suggested that obesity-induced memory loss and age-related memory loss may be connected through this same pathway.

• The early gene-editing results — In prior research, the team lowered K63 levels using a targeted gene-editing technique and improved memory in older rats. They are now applying that approach to obese animals. Jarome reported that in the old brain the method was able to reduce the protein's levels and restore memory, and the team hopes the same may occur in the obese brain.

"If we can understand the mechanism that connects these two things, then we can start thinking about ways to target it," Jarome said. "My hope is that this will help us better understand what's causing the brain to essentially age faster and make us more likely to have dementia and Alzheimer's disease."⁵

• What higher visceral fat was linked to — Kumar notes aside from cognitive decline and a higher risk of dementia, people with higher visceral fat also have a reduced hippocampal volume (the hippocampus is the brain's memory center). He adds that this association becomes even more pronounced after accounting for a person's age and overall body weight, which is part of why he considers it worth attention.

• The changes may start well before symptoms appear — He emphasizes that the effects on the brain may begin years before dementia becomes obvious. Studies have linked higher visceral fat with smaller overall brain volume, reduced executive function, slower information processing, poorer attention, and lower performance on memory tasks — subtle shifts that may develop gradually.

• Kumar attributes the brain effects to several overlapping biological changes rather than a single cause — He points to chronic low-grade inflammation that can gradually damage brain cells over time, along with insulin resistance (reduced sensitivity to the hormone that manages blood sugar), high blood pressure, unhealthy blood lipids or cholesterol, and damage to the body's smallest blood vessels, all of which can reduce healthy blood flow to the brain.

He adds that hormonal changes tied to visceral fat may further interfere with normal brain function. In his framing, visceral fat actively releases inflammatory chemicals and hormones that can disrupt processes throughout the body. These are described as biologically plausible pathways drawn from existing research, not as proven cause-and-effect in any individual.

• He frames visceral fat as modifiable — Unlike age or genes, visceral fat can often be reduced through healthy lifestyle changes, such as consuming a healthy diet, regular exercise, consuming adequate protein and fiber, getting adequate sleep, and maintaining a healthy body weight.

• Measure the waist, and be skeptical of shortcuts — Kumar cautions readers not to judge their health by the scale alone. He recommends tracking waist circumference and the waist-to-height ratio, suggesting a ratio below 0.5 as a useful target for most adults, because these often reflect visceral fat better than body weight.

He also states plainly that no "fat-burning" supplement has convincing evidence behind it. And he notes that for people already living with diabetes, prediabetes, hypertension, or fatty liver disease, reducing visceral fat may carry added importance for both heart and brain health — saying that what's good for the waist is good for the brain.

• A stronger grip was associated with lower risk — Participants who maintained relatively high muscle strength, measured by their grip, across the study were 26% less likely to develop a neurodegenerative condition. The researchers framed this as a sign that muscle quality may carry more weight than sheer muscle quantity, and that grip strength here serves as a simple, practical stand-in for overall muscle health.

• Where fat sat, not just how much, was associated with risk — The analysis found that people with a higher measure of arm fat compared with leg fat were 18% more likely to receive a diagnosis for a neurodegenerative condition.

The authors are explicit that this does not mean arm fat causes these conditions; it is an association. Instead, they describe fat distribution as at least a signal of underlying health problems that may worsen brain aging — noting, for example, that many of the patients who developed a neurodegenerative condition had a history of heart disease and stroke, both of which have been directly linked to excess fat.

• Belly fat showed a measurable gap in disease rates — Trunk fat was another factor associated with increased risk. Among men with high levels of fat around the trunk, the disease rate was 3.38 cases per 1,000 person-years (a way of counting that combines how many people were studied with how long each was followed), compared with 1.83 cases among men with low belly-fat levels.

Among women, the rate was 2.55 per 1,000 person-years for those with high abdominal fat, compared with 1.39 for those with low amounts. The team notes that targeted efforts to reduce trunk and arm fat while promoting healthy muscle development may be more useful for protection than general weight control — a suggestion about direction for future work rather than a proven strategy.

• The proposed biological explanation — The researchers offer a tentative mechanism while stressing it is not settled. Subcutaneous fat, they explain, can be a sign that the body also has fatty deposits in visceral organs, including within the muscles, which may increase inflammation and impair how those tissues function.

That dysfunction can damage the inner lining of blood vessels — the researchers suspect the same blood-vessel-lining dysfunction may also be involved in neurodegeneration. As they put it, "the underlying mechanisms linking body composition and neurodegeneration have not been fully investigated."¹¹

1. Build and maintain muscle mass through regular strength training — Greater muscle mass is associated with better cognitive resilience and supports insulin sensitivity and overall metabolic health, which is part of why muscle keeps coming up in this research. Aim to work resistance training into your routine, and pair it with daily walks and regular movement throughout your day rather than long uninterrupted stretches of sitting.

2. Track your waist-to-hip ratio instead of relying on weight or BMI alone — This simple measurement gives a clearer picture of visceral fat than the scale does. To find yours, divide your waist measurement by your hip measurement, then check it against the general norms below and watch how it shifts as you adjust your habits.

Waist-to-hip ratio	Men	Women
Ideal	0.8	0.7
Low risk	<0.95	<0.8
Moderate risk	0.96 to 0.99	0.81 to 0.84
High risk	>1.0	>0.85

3. Favor saturated fats from grass fed animal sources and cut processed seed oils — Seed oils turn up in most processed and restaurant foods and are high in linoleic acid (LA), a fat that may contribute to visceral fat accumulation over time. Cooking with stable alternatives such as tallow, grass fed butter, and ghee is a straightforward way to lower your intake, and reading labels on packaged foods helps you spot the seed oils to leave behind.

4. Get enough quality protein, with about a third from collagen — Adequate protein supports muscle maintenance and helps supply the building blocks your body relies on, and getting enough is also linked with keeping visceral fat in check.

A practical target for most adults is around 0.6 to 0.8 grams of protein per pound of ideal body weight, drawing from sources such as ruminant meats, eggs, and low-fat seafood, with roughly one-third coming from collagen-rich sources to round out the amino acids your body uses.

5. Pay attention to your metabolic health, not just your weight — Because insulin resistance and blood-sugar problems repeatedly surface in the discussion of visceral fat and the brain, it can help to keep an eye on the markers that reflect how your metabolism is doing. Tests such as fasting insulin, HOMA-IR, and HbA1c can offer a window into your blood-sugar and insulin health over time.

Talk to your healthcare provider about whether this testing is appropriate for you, and use the results to guide the lifestyle adjustments above rather than chasing the number on the scale alone.

• U.S. patients had worse outcomes — The FDA's analysis revealed that patients in the U.S. had a 27% higher risk of major cardiovascular events when given ticagrelor, the exact opposite of what was seen in Europe and other regions. AstraZeneca argued that high aspirin doses in the U.S. explained this difference, but FDA scientists rejected that explanation as insufficient. This is a regional subgroup finding rather than the trial's primary result, which is why AstraZeneca was able to contest it. Subgroup analyses are normally treated as hypothesis-generating rather than conclusive; what made this one hard to set aside was that the FDA's own reviewers found the sponsor's explanation for it insufficient.

This matters if you were prescribed ticagrelor in the U.S., the region where the drug performed poorly in this analysis. It is worth raising with your cardiologist, who is best placed to weigh it against your own history.

• Lead FDA reviewer sounded the alarm — Dr. Thomas Marciniak, a medical officer at the FDA known for his rigorous reviews, concluded in a 47-page memo that ticagrelor appeared inferior in both safety and efficacy. He described AstraZeneca's submission as “the worst in my experience regarding completeness of the submissions and the sponsor responding completely and accurately to requests.”

His recommendation was to deny approval. Despite this, FDA leadership approved the drug.

• Data monitoring raised red flags — Another alarming detail from the investigation was that AstraZeneca monitored most trial sites themselves, except in four countries where independent organizations oversaw the process. In those four independently monitored countries — including the U.S. — ticagrelor performed worse than clopidogrel.

Where the sponsor oversaw data collection, ticagrelor appeared superior. This inconsistency suggests that oversight and data handling may have shaped the reported outcomes.

• Endpoint adjudication errors — The BMJ also confirmed that adjudicators — those tasked with classifying patient outcomes — correctly added 45 heart attacks (myocardial infarctions) to the clopidogrel group but none to the ticagrelor group. As noted in the BMJ paper:

“In his now unsealed legal complaint from 2012, Victor Serebruany alleged that PLATO’s adjudicators added 45 MIs to the clopidogrel group, ‘and precisely zero additional MIs for . . . ticagrelor.’ The BMJ was able to confirm Serebruany’s numbers. FDA records show that according to site reports there were 504 subjects with MIs on ticagrelor compared with 548 on clopidogrel. Following adjudication, the count increased only for clopidogrel—to 593.

Using trial datasets first obtained from the FDA by Serebruany and subsequently verified through a freedom of information request by The BMJ—which contains both pre-adjudication and post-adjudication judgments—we also found an imbalance among 20 death category decisions that the adjudication committee was in ‘major’ disagreement over and ultimately could not resolve: 17 were in the clopidogrel arm while only 3 were in ticagrelor. The disparity raises questions over the possibility of unblinding.

Despite unresolved disagreements over the 20 deaths, a final post-adjudication cause of death classification was recorded. But in six cases, it flipped whether or not the event met the primary endpoint definition compared with the cause of death attribution provided by site investigators. In every case, The BMJ found the change in attribution favoured ticagrelor.”

• Mechanism of harm tied to bleeding and misclassified events — The trial design used a primary endpoint that combined death from vascular causes, heart attack, or stroke. This meant even small shifts in how events were classified could tip the scales.

• Studies were inaccurately reported, casting serious doubt on AstraZeneca's claims — These trials were central to convincing regulators and doctors that ticagrelor worked better, yet the primary endpoint results were misstated in Circulation, a leading cardiology journal.^8,9

• Participants faced extreme and unusual demands — Patients in these platelet studies, who had stable coronary artery disease, were required to give large amounts of blood — up to 604 milliliters across visits, which is more than a full unit donated at a blood bank. Typically, platelet studies involve just one or two blood draws, but AstraZeneca's required six within a single eight-hour period.

As one trial investigator admitted, only the most committed participants could endure that burden. This unusual setup raises questions about whether the data reflected typical patients or only those willing to undergo intense procedures, which directly impacts whether the results apply to real life.

• Data gaps and missing records weakened credibility — The BMJ investigation found that more than 60 platelet readings were missing from the datasets submitted to the FDA. Even worse, some of the excluded results showed significantly higher platelet activity, suggesting ticagrelor did not inhibit clotting as strongly as advertised.

Implausible readings, such as platelet activity increasing after treatment, were included in final analyses, but instead of being flagged, they were hidden through unpublished “data adjustments.” The findings show that key data was either mishandled or left out.

• Authorship was misrepresented — Several individuals listed as study authors later denied involvement, while others who actively recruited patients were excluded. For example, Tonny Nielsen, identified as a Danish investigator and author, stated outright, “I did not participate in the RESPOND study.” Conversely, a Baltimore physician who enrolled 12 patients wasn't credited.

• Question the strength of the evidence — Before starting any drug, look into whether the key studies supporting it had problems with data accuracy, missing information, or conflicting results. In this case, ticagrelor's studies were riddled with errors and misreporting, and concerns about the data were not secret. Several post-licensure studies have also reported disappointing results. When you ask “What does the cumulative evidence suggest?” you set yourself up for better decisions.

• Reduce your underlying cardiovascular risk — Lowering your cardiovascular risk through diet, movement, and reducing toxic exposures is worth doing on its own terms. (One distinction matters, though: Ticagrelor is prescribed after acute coronary syndrome or a stent, to stop a clot forming on a damaged or stented artery wall. Improving your diet does not remove the need for it.) For general health, cut vegetable oils from your diet, avoid ultraprocessed foods, increase your intake of whole-food carbohydrates, and build strength through daily walking and regular resistance training. These changes support cardiovascular health over the long term.

• Track your progress with the right markers — Instead of relying on outdated measures like total cholesterol, focus on health tests that actually reflect your metabolic health. Monitor your HOMA-IR score to track insulin resistance, check fasting glucose, and keep an eye on your triglyceride-to-HDL ratio.

You can also use a simple blood pressure cuff at home to watch for improvements in circulation. Treat these numbers like checkpoints — improvement is a sign your daily choices are moving in the right direction.

• Stay informed and proactive about drug safety — Don't assume that just because a drug is FDA-approved, it's the best choice. The ticagrelor case shows that approval does not guarantee the underlying evidence was sound. Read investigations, follow updates from independent researchers, and ask yourself whether the benefits outweigh the risks. Knowledge puts you in charge, not the system.

• The researchers assessed both gum health and kidney health — Periodontal disease severity was classified using a standardized staging system, while kidney health was evaluated using estimated glomerular filtration rate (eGFR), a measure of how well the kidneys filter waste, and urinary albumin-to-creatinine ratio (uACR), a marker of protein leakage into the urine. Researchers also measured inflammatory markers, including high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6).

• Inflammation explained only part of the association — Levels of hsCRP and IL-6 increased as both gum disease and kidney dysfunction became more severe. However, hsCRP accounted for only about 35% of the association between severe periodontitis and reduced kidney function and about 10% of the association with albuminuria, a condition where there's an excessive amount of the blood protein albumin into the urine. This suggests other biological mechanisms are involved.

• Severe gum disease became more common as kidney function declined — Severe periodontitis was present in 14% of people with normal kidney function but increased to 36% among those with moderately reduced kidney function.

• Tooth loss and gum tissue damage tracked with worsening kidney health — Measures of long-term periodontal damage, including clinical attachment loss and tooth loss, became more severe across stages of kidney dysfunction.

• Possible pathways connecting the mouth and kidneys — The authors proposed that bacteria from infected gums may spread through the bloodstream and affect distant organs. Other potential mechanisms included endothelial dysfunction, oxidative stress, and metabolic alterations, all of which may contribute to declining kidney health.

• Gum disease and kidney health are closely interconnected — Severe periodontitis was independently associated with reduced kidney function and increased albuminuria, even during the early stages of CKD. The researchers noted that future studies should evaluate whether treating periodontal disease could help preserve kidney function and reduce disease risk.

• How gum disease was measured — To estimate inflammatory burden, the team used a metric called the periodontal inflamed surface area (PISA), which measures the amount of inflamed gum tissue in the mouth.

Using standards developed by the U.S. Centers for Disease Control and Prevention (CDC) and the American Academy of Periodontology (AAP), participants were categorized as having no, mild, moderate, or severe periodontal disease. Overall, 16.3% of participants had severe periodontal disease at the beginning of the study.

• Severe gum disease predicted faster kidney decline — During the follow-up period, 21 participants developed CKD. Researchers found that people with severe periodontal disease had a significantly higher risk of kidney function decline than those with less severe disease. After adjusting for factors such as age, sex, diabetes, hypertension, smoking, and income, severe periodontal disease was associated with a 4.18-fold greater rate of incident CKD.

• Researchers proposed inflammation as one possible explanation — The authors noted that bacteria associated with periodontal disease can enter the bloodstream and trigger immune responses throughout the body. They suggested that chronic inflammation caused by oral infections may contribute to kidney injury and accelerate kidney function decline.

• The study suggests gum disease may be a modifiable risk factor for CKD — The researchers concluded that severe periodontal disease was associated with clinically significant kidney function decline among African American adults. They noted that further research is needed to determine whether treating periodontal disease could slow the loss of kidney function and reduce CKD risk.

• Aggressive periodontitis — A rapidly progressing form of periodontal disease that can affect multiple teeth. It often develops at a younger age and occurs in people who do not have an underlying systemic disease.¹²

• Pregnancy gingivitis — Hormonal changes during pregnancy can make the gums more sensitive to plaque, increasing the likelihood of inflammation and bleeding. Dietary changes and shifts in saliva production may also contribute to a higher risk of gingivitis during pregnancy.¹³

• Pericoronitis — Most common in adults ages 17 to 24, this condition develops around a partially erupted tooth.¹⁴ A flap of gum tissue can trap food particles and bacteria, creating an environment where infection can develop. Good oral hygiene can help reduce the risk.

• Desquamative gingivitis — This rare and often painful condition affects the outer layer of the gums, causing redness, irritation, bleeding, and tissue that tears easily.¹⁵ It may be associated with conditions such as mucous membrane pemphigoid, oral lichen planus, and pemphigus vulgaris. Hormonal changes, including those that occur during menopause, may also play a role.

• Atrial fibrillation (AFib) — Oral bacteria that enter the bloodstream through inflamed gums may contribute to the scarring and electrical disruption behind AFib, an irregular, often rapid heartbeat that raises the risk of stroke and heart failure.

A South Korean study of more than 1.2 million adults, published in BMC Oral Health, tracked participants for a median of over 14 years and found that those who developed periodontal disease during course of the study had about a 4% higher risk of developing AFib than those who remained disease-free — a risk that held even after adjusting for smoking, alcohol use, and other health conditions.

Risk was highest among those with chronic, unresolved gum disease, while people whose gum disease resolved had a somewhat lower risk than those with ongoing disease — though still not as low as people who never developed it — suggesting gum health may play a role in cardiovascular risk, though more research is needed to confirm cause and effect.¹⁶

• Mental health disorders — A UK cohort study published in BMJ Open tracked whether a periodontal disease diagnosis preceded higher rates of chronic disease within three years compared to healthy controls. According to the findings, mental ill health rose by 37%, autoimmune disease by 33%, cardiovascular disease by 18%, Type 2 diabetes by 26%, and cardiometabolic disorder by 7%.

Dr. Joht Singh Chandan of the University of Birmingham, one of the study's researchers, explained the significance:¹⁷

"Poor oral health is extremely common, both here in the UK and globally. When oral ill-health progresses, it can lead to a substantially reduced quality of life. However, until now, not much has been known about the association of poor oral health and many chronic diseases, particularly mental ill-health.

We conducted one of the largest epidemiological studies of its kind to date, using UK primary care data to explore the association between periodontal disease and several chronic conditions.

We found evidence that periodontal disease appears to be associated with an increased risk of developing these associated chronic diseases. As periodontal diseases are very common, an increased risk of other chronic diseases may represent a substantial public health burden."

• Chronic illness (multimorbidity) — Gum pain may be an early warning sign of multimorbidity, defined as having two or more chronic health conditions.

An analysis of over 500,000 UK Biobank participants, presented at the EFP's EuroPerio11 congress, found that 57% already had at least two chronic illnesses, and among those reporting gum inflammation symptoms, the risk of multimorbidity jumped by 15% — with pain the strongest predictor, reported by 54% of participants. Lead author Dr. Nisachon Siripaiboonpong of UCL's Eastman Dental Institute explained:¹⁸

"Maintaining good gum health is not just about keeping your teeth, it is about protecting your general health. Preventing or managing gum disease could reduce the risk of multiple long-term conditions and improve quality of life."

• Alzheimer's disease — Porphyromonas gingivalis, the bacteria behind periodontitis, has been found in the brains of people who died of Alzheimer's disease, a progressive neurodegenerative disorder marked by memory loss and cognitive decline.

A 2019 study published in Science Advances identified toxic proteases from the bacteria, called gingipains, whose levels correlated with tau and ubiquitin — both markers of the disease.¹⁹ They also pointed to animal studies showing that oral infection with this pathogen led to brain colonization and increased amyloid beta production:²⁰

Most tellingly, the researchers also found gingipains in the brains of people who had never been diagnosed with Alzheimer's — suggesting that had they lived longer, they likely would have developed the disease.

"Our identification of gingipain antigens in the brains of individuals with AD and also with AD pathology but no diagnosis of dementia argues that brain infection with P. gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease," the authors reported.

• Smoking — This is the most well-established habit-related risk factor for periodontitis. Heavy smokers face up to 7.28 times the odds of developing the disease compared to non-smokers. Smoking also suppresses gum bleeding, a key warning sign, making early damage easier to miss and treatment less likely to succeed.

• Poor oral hygiene — Skipping regular brushing and flossing causes plaque to harden into tartar, which can only be removed by a dental professional and keeps collecting bacteria below the gumline, fueling ongoing inflammation and infection.

• Poor diet — Diets high in ultraprocessed foods and refined carbohydrates feed the bacteria in plaque, increasing the tendency for gums to become inflamed.

• Teeth grinding and clenching — The excess force placed on teeth can speed up the tissue and bone damage periodontitis has already started.

• Chronic stress — Psychological stress has been linked to greater attachment and bone loss, possibly through elevated IL-6 production and a weakened immune response to oral bacteria — though it may also simply make people less likely to keep up with regular oral hygiene.

1. Brush and floss the right way — Brush twice daily with a soft-bristle toothbrush and a nonfluoridated toothpaste, waiting 30 minutes after eating before you brush. Floss at least once a day using a PFAS-free option, and replace your toothbrush every three to four months to keep bacteria from building up.²⁴ For more useful toothbrushing tips, "Poor Oral Health Wreaks Havoc on Your Heart and Brain."

Fluoridated toothpaste, mouthwash, and other harsh antibacterial products can throw off this balance too — biological dentist Dr. Gerry Curatola compares them to a "scorched earth policy" that kills off both harmful and helpful bacteria, making it harder for a healthy oral microbiome to bounce back.²⁵

2. Try oil pulling with coconut oil — This traditional practice involves swishing coconut oil in your mouth for several minutes before spitting it out. Coconut oil's antibacterial lauric acid content has been shown in some clinical studies to help reduce plaque and gum bleeding when used alongside regular brushing and flossing.²⁶ If you want to learn more, read "Why Is Oil Pulling Suddenly All the Rage?"

3. Eat a nutrient-dense, whole-food diet — Fresh vegetables, fruits, healthy fats, and fiber-rich whole foods support a balanced oral microbiome and strengthen your immune defenses. Refined sugar, seed oils, and ultraprocessed foods do the opposite, feeding the harmful bacteria that drive plaque buildup, tooth decay, and gum disease.

4. Support your gums with the right nutrients — Vitamin D deficiency is linked to a higher risk of periodontal disease, while vitamin K2, calcium, and magnesium work together to keep bone strong and prevent harmful calcification.²⁷ A University of Washington-led review also found that low vitamin C levels are tied to bleeding gums.²⁸

5. Quit smoking and vaping — Nicotine restricts blood flow to your gums and masks the bleeding that normally signals inflammation, letting damage progress undetected. Research shows vaping is linked to markedly higher rates of gum disease than not smoking at all, though cigarettes remain the more destructive habit.²⁹

6. Consider seeing a biological dentist — These practitioners take a whole-body approach to oral care, avoiding mercury amalgam fillings and using biocompatible materials that don't add to your body's toxic burden. If you're dealing with persistent gum issues, a biological dentist can help you address the root cause rather than just the symptoms.

• Participants were inactive adults with overweight or obesity — The study included adults who were largely sedentary and had a body mass index in the overweight or obese category. None of them were taking vitamin D supplements, and the study took place during winter — meaning there was virtually no sunlight capable of triggering vitamin D production in the skin. This allowed the researchers to isolate the effect of exercise alone.

• Only the group that exercised preserved their active vitamin D levels — While both groups — those who exercised and those who stayed sedentary — experienced some decline in vitamin D, only the exercise group was able to maintain their levels of the active form that actually affects your health. This is the version that interacts with receptors throughout your body to control calcium balance, immune response and cellular repair.

• Sedentary participants lost 15% of their active vitamin D — The people who didn't move saw a measurable drop in their active vitamin D levels over just 10 weeks. Meanwhile, those who followed a moderate-intensity indoor cycling and resistance training program were able to keep their levels steady, despite not losing any body fat during the study.

• Even with no weight loss, exercise changed vitamin D status — One of the most surprising findings was that participants didn't need to lose fat in order to gain this benefit. This is significant, because obesity is known to trap vitamin D in fat cells and reduce its availability. Yet physical activity appeared to override that effect by improving the body's internal vitamin D regulation.

• The biggest benefits were seen in those who had high fat tissue levels — Researchers found that individuals with the highest fat mass had the most to gain. Their fat tissue was less efficient at converting stored vitamin D to the active form at baseline, but after the intervention, that dynamic shifted. The more a person exercised, the better their conversion rates became, even though the fat tissue volume didn't decrease.

• Two key enzymes controlled how vitamin D was used — Researchers looked at two important enzymes: one that turns vitamin D into its active, usable form, and another that breaks it down. In people who didn't exercise, the helpful enzyme went down while the one that destroys vitamin D went up. But in those who exercised, the body did the opposite — it boosted the enzyme that activates vitamin D and reduced the one that breaks it down.

• Muscle tissue likely plays a supportive role in vitamin D balance — While the study focused on fat tissue, exercise is known to influence muscle metabolism as well. Although researchers didn't measure changes in muscle gene expression directly, the overall improvements in vitamin D activation suggest that better whole-body metabolic health, including muscle function, helps preserve vitamin D during winter.

• Exercise reshapes how your body handles vitamin D — By changing the activity of specific enzymes in fat tissue, regular exercise helped participants maintain more of their active vitamin D, even without losing weight or taking supplements. This challenges the common belief that supplements or sun exposure are the only solutions, offering a new path for people with higher body fat to help maintain their vitamin D levels during the winter.

1. Start moving daily — Aim for regular moderate-intensity exercise and daily movement. The study used indoor cycling and resistance training, but you could use brisk walking, bodyweight circuits or biking. The key is consistency. Your body needs repeated activation to keep converting stored vitamin D into the active form your cells use.

2. Combine moderate cardio with strength training — Don't choose one or the other. Cardio supports circulation and metabolic health, while strength training improves how your muscles handle vitamin D. Together, they reprogram your fat and muscle tissue to activate more vitamin D instead of letting it sit unused. Just don't overdo it.

Too much high-intensity exercise can work against you. Moderate exercise is far more forgiving, though if you have been sedentary or have a health condition, build up gradually and check with your healthcare provider before starting a new program.

Treat the darker months as a window to build your health from the inside out. Most people lose vitamin D between October and March, especially in northern regions. By staying active through this stretch, you may blunt that seasonal drop and give yourself a head start on spring energy, immune strength and metabolic function.

3. Sunlight is the best option to optimize your vitamin D — Remember that your skin is designed to make vitamin D from the sun. So, during the summer months — and winter months if you live in a warm climate — spend time in direct sunlight with bare skin exposed daily.

If you're still using canola, soybean, sunflower or generic "vegetable oil," you're flooding your cells with linoleic acid (LA), a polyunsaturated fat that oxidizes easily, builds up in your skin and increases your risk of skin damage if you get sun exposure during peak hours (10 a.m. to 4 p.m.). Cut these oils from your diet for at least four to six months before getting peak sun exposure.

4. If you supplement, combine vitamin D3 with magnesium and K2 — If you're indoors often or live far from the equator, vitamin D3 supplementation is a reasonable strategy to keep your vitamin D levels optimized in the winter. But vitamin D3 works best when combined with magnesium and vitamin K2. As a guide, aim for 180 micrograms of K2 for every 5,000 IU of vitamin D — K2 helps direct calcium to your bones and away from your arteries.

In fact, an analysis of self-reported data from nearly 3,000 participants in the GrassrootsHealth cohort found that among those reporting no supplemental magnesium or vitamin K2, 244% more supplemental vitamin D was needed for half the group to reach a blood level of 40 ng/mL, compared to those who usually took both. These are observational findings from a self-selected cohort and may not apply to all individuals.⁵

This trio works as a team, improving absorption, reducing arterial calcification and helping your liver process fat more efficiently.

5. Test your vitamin D levels and personalize your approach — Get your vitamin D levels tested at least twice a year and aim for a level between 60 and 80 ng/mL (150 to 200 nmol/L). Vitamin D status has been studied in relation to insulin sensitivity, liver inflammation and immune function, so the target range matters for more than bone health.

Testing gives you a starting point and helps you keep track of your vitamin D levels year-round. Talk to your healthcare provider about whether this testing is appropriate for you.

• Diet is one of the risk factors you can influence — Both Ashamalla and Kumar frame diet as a modifiable factor, meaning it's something within your control, unlike age and genetics. According to a 2004 research review cited in the report, maintaining a healthy diet and lifestyle is associated with lowering cancer risk by roughly 30% to 40%.⁵

Ashamalla is careful to clarify that cancer is not caused by any one food or condiment. Risk builds over time and is shaped by many factors at once, including genetics, age, tobacco use, alcohol use, body weight, physical activity, and environmental exposures. That said, Kumar explains that prevention is rarely about one perfect meal and far more about the patterns you keep for years.

• Processed-meat toppings are the specific condiment flagged — The condiment Kumar says people need to avoid is processed-meat toppings, such as bacon bits, bacon jam, and bacon-based spreads. Again, he reasons that the danger isn't a single serving but repeated, long-term intake of processed meat.

To emphasize the risk to consumers, he notes that processed meat has been classified by the International Agency for Research on Cancer (IARC) as carcinogenic to humans, with the strongest evidence linking it to colorectal cancer.

Nitrites and nitrates are the compounds of concern — The report explains that processed meats, such as bacon, are preserved by smoking, curing, salting, or adding preservatives, and when eaten regularly, they can raise cancer risk because they contain nitrites and nitrates. These are preservative compounds that, according to Dr. Kumar, may form other compounds in the body capable of damaging cells.

• Sugar-heavy barbecue sauce earns a second warning — Beyond bacon-based toppings, Kumar called out sugar-heavy barbecue sauce as another condiment worth minimizing. He observes that many barbecue sauces are essentially sweetened syrup with a smoky flavor, often listing added sugar, corn syrup, or high-fructose corn syrup (HFCS) near the top of the ingredient list.

Again, one spoonful is not the problem. The concern is when sugary condiments become part of a daily pattern of high-sugar, ultraprocessed eating.

Kumar explains that too much added sugar over time can contribute to weight gain, obesity, insulin resistance, and chronic inflammation, and that obesity and inflammation are in turn linked to a higher risk of several cancers, including breast, colon, endometrial, pancreatic, liver, and kidney cancers. Barbecue sauce also tends to appear alongside processed or heavily charred meats.

• The takeaway is about patterns, not perfection — Ashamalla's tip is focusing not on perfection, but on patterns. He describes that your goal needs to be small, repeatable changes, specifically less processed meat, less added sugar, less alcohol, and more toward plant foods, like vegetables and fruits. "Over time, these small substitutions can support a healthier weight, better gut health and a more cancer-preventive eating pattern," he says.

• Most of your nitrate intake comes from vegetables, not meat — While Kumar and Ashamalla's report focused on nitrates found in processed meat, it's also found in plant sources. Interestingly, the nitrates here may support your health.

In the Antioxidants study, vegetables and fruit supply roughly 50% to 75% of your total dietary nitrate intake, and it cites survey data suggesting that around 80% to 85% of human nitrate exposure comes from vegetables. Leafy vegetables such as rucola, lettuce, and spinach carry the highest nitrate levels of all.

Processed meats are a separate and much smaller source, because the meat industry adds nitrates and nitrites during curing, the preservation process that gives cured meat its color, flavor, and shelf life. On the surface, this makes the vegetable numbers look alarming, but the review's point is that raw quantity is not the whole story.

• The chemical reaction is where the risk appears — Nitrates and nitrites are not themselves carcinogenic, according to the researchers. The concern is what they can turn into. Inside the digestive tract, nitrites can react with compounds called secondary amines to form N-nitroso compounds, or nitrosamines, many of which are considered carcinogenic. This conversion is not guaranteed, as it depends on certain conditions.

The acidic environment of the stomach and the presence of iron both push this reaction forward, while antioxidants like vitamin C and vitamin E hold it back. In fact, the authors cite research showing that nitrosamine formation was completely inhibited when antioxidants outnumbered nitrite by a ratio above 2 to 1. It's estimated that this internal, or endogenous, nitrosation produces 45% to 75% of a person's total exposure to N-nitroso compounds.

• Vegetable nitrates appear far less concerning, and processed meat carries an accelerant — This is the pivot on which the whole premise of the featured study rests. Because vegetables are naturally rich in antioxidants and vitamins, the nitrates they deliver come packaged with the very compounds that suppress nitrosamine formation.

The review cited a large meta-analysis of gastric, or stomach, cancer studies in which dietary nitrate intake was associated with a reduction in risk, an effect the authors attributed to those accompanying protective compounds rather than to nitrate itself.

Meanwhile, animal sources tell the opposite story. Processed meat is rich in amines, amides, and heme iron (the iron found in red meat) and this substance is described as a stimulant of endogenous N-nitroso compound formation. The researchers cited findings that nitrates and nitrites from animal sources, including processed meat, were positively associated with renal cell carcinoma, a kidney cancer, whereas overall intake that included plant sources showed no such association.

• The evidence links processed-meat compounds to several cancers, including colorectal cancer — Across the human studies that the analysis looked into, dietary nitrate and nitrite intake has been linked to a higher relative risk of breast, gastric, colorectal, esophageal, thyroid, and other cancers, though the authors are quick to point out that results across the reviewed studies are inconsistent.

The association tends to be weak for dietary nitrate but more noticeable for nitrites. But notably, the researchers pointed out that in 2015, the International Agency for Research on Cancer declared processed meat that had been cured to be a Group 1 carcinogen, its highest classification, based on data related to colorectal and stomach cancer.

• Curing serves real purposes, which is why the problem persists — The review is even-handed about why nitrites are used at all. They develop the characteristic color and flavor of cured meat that consumers are familiar with, act against bacteria, notably Clostridium botulinum, which is the bacterial strain behind botulism. Because no single substitute reproduces all these functions, the authors conclude that nitrates and nitrites should be limited in the meat industry.

The authors note that because of nitrite's multifunctional role, finding a perfect substitute in meat processing remains very difficult.

1. Trade processed-meat toppings for whole-food flavor — Instead of bacon bits, bacon jam, or bacon-based spreads, build savory, smoky depth with roasted mushrooms, caramelized onions, fresh garlic, smoked paprika, herbs, or a homemade salsa or chimichurri.¹⁰ These give you the richness you're after without the cured-meat preservatives, and they turn a passive habit into an active choice you control.

2. Make your own sauces instead of reaching for a ready-made product — Many store-bought barbecue sauces, dressings, and condiments are built on added sugar or high-fructose corn syrup (HFCS), often listed near the top of the label. Whisking together simple, organic ingredients at home lets you skip the sweetened syrups and mystery additives.

In addition, make it a habit to cook at home rather than eating out — hidden seed oils and processed ingredients are hard to avoid in most restaurants and fast food joints.

3. Upgrade the protein and fat you cook with — Center your plate on whole, minimally processed foods like ruminant meats and pastured eggs. Also, reach for stable cooking fats such as tallow, ghee, or grass fed butter rather than industrial seed oils high in linoleic acid (LA). Keeping LA intake low can support better metabolic and cellular health over time.

4. Cut back on refined sugar to protect your metabolic health — Sugary condiments and ultraprocessed foods can nudge you toward weight gain, insulin resistance, and chronic inflammation, and these conditions are linked to a higher risk of several cancers.

5. Optimize your vitamin D, ideally through sensible sun exposure — Sunlight supports cellular energy production and a range of processes tied to overall health, and midday sun is the most efficient way to build your levels naturally. I recommend that you aim for 60 to 80 nanograms per milliliter (ng/mL) of vitamin D in your blood, and the only way to know you're reaching that goal is to get screened regularly. Talk to your health care provider about whether vitamin D testing is appropriate for you.

• Nearly half of participants have nutrient deficiencies — From the data collated, 45.3% of total participants were found to have multiple micronutrient deficiencies.

• Vitamin D, magnesium and vitamin B12 were the most common deficiencies — Vitamin D deficiency was the most widespread, affecting 60.45% of diabetics. The second highest deficiency was magnesium impacting 41.95% of diabetics. The third highest deficiency was vitamin B12, affecting 28.72% of diabetic participants — a group in which metformin use is common.

• Women had a higher rate of deficiency than men — Overall, the data suggests that factors like diet, metabolic dysfunction, and certain medications play a major role in these imbalances, leading to the differences between men and women.

• The link between insulin sensitivity and vitamin D levels — Insulin is the hormone responsible for regulating blood sugar, and without enough vitamin D, insulin sensitivity decreases. As noted in a study published in the International Journal of Molecular Sciences:⁴

"Various pathways suggest that vitamin D directly improves insulin sensitivity and secretion. The level of vitamin D in the body may change the ratio of pro- to anti-inflammatory cytokines, which would impact insulin action, lipid metabolism and the development and function of adipose tissue.

Many studies have demonstrated an inverse relationship between vitamin D concentrations and pro-inflammatory markers, insulin resistance, glucose intolerance, metabolic syndrome, obesity and cardiovascular disease."

• Vitamin D's role in immunity and inflammation — Beyond its role in insulin regulation, vitamin D is also important for immune function and inflammation control, which are relevant to diabetes.⁵

For example, low vitamin D levels have been linked to higher rates of diabetic complications, including diabetic retinopathy (DR), diabetic kidney disease (DKD), and diabetic foot ulcers (DFU).⁶ As noted by the researchers, "DR and DKD are common microvascular complications of diabetes."

• Foot ulcers are another common vascular complication in diabetes — Research has examined whether vitamin D status affects wound healing. According to the researchers:⁷

"Vitamin D is essential in maintaining the normal immune system. Vitamin D could suppress T cell proliferation and inhibit the secretion of T helper type 1 cytokines (e.g., interferon-γ and interleukin-2), while augmenting the production of T helper type 2 cytokines, thereby accelerating wound healing …

Besides, vitamin D may improve wound healing by suppressing endoplasmic reticulum stress, oxidative stress and the NF-κB-mediated inflammatory gene expression. More importantly, vitamin D signaling may be involved in the proliferation, migration, and differentiation of epidermal stem cells and progeny during cutaneous wound repair."

• The link between magnesium deficiency and insulin resistance — According to a study published in Frontiers in Nutrition, "magnesium deficiency can increase insulin resistance, and insulin resistance can also contribute to magnesium deficiency." The researchers succinctly explain its role below:⁹

"Intracellular free magnesium levels are lower in patients with Type 2 diabetes than in nondiabetic individuals. Intracellular magnesium concentrations are essential for optimal insulin receptor bioactivity and downstream signaling events in target cells.

Low magnesium levels contribute to impaired tyrosine kinase activities of insulin receptors, causing altered cellular glucose utilization and eventual insulin resistance."

• The role of magnesium in the context of insulin management — In a 2020 animal study, researchers noted that increasing magnesium levels helped enhance insulin sensitivity while decreasing insulin resistance. Furthermore, boosting magnesium intake helped protect against pancreatic cell injury — an important organ that helps produce insulin and glucagon to keep blood sugar levels at a normal range.¹⁰

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

• Magnesium deficiency among diabetics is a vicious cycle — A low intake of magnesium from foods increases the risk of developing diabetes. And when diabetes does develop, more magnesium is lost via urination. And similar to the other studies mentioned, this particular study noted that magnesium deficiency "is associated with poorer glycemic control and greater insulin resistance in patients with [Type 2 diabetes]."¹¹

• Vitamin B12 deficiency affects your nervous system — Among those taking metformin, 28.72% had a vitamin B12 (cobalamin) deficiency. This is concerning because vitamin B12 is essential for nerve health. Without enough vitamin B12, nerves can be damaged, producing symptoms such as numbness, a tingling feeling in the hands and feet and fatigue.¹³

• The widespread deficiency is accepted as normal — Metformin is one of the most ubiquitous medications related to diabetes management. According to Harvard Health Publishing, ever since its approval by the U.S. Food and Drug Administration (FDA) in 1995, "It has since become the most widely prescribed medication for people with diabetes who cannot control their blood sugar through diet and exercise alone."¹⁴

Despite the popularity of metformin, research has shown that it has been strongly linked to vitamin B12 deficiency,¹⁵ and the risk rises as the dosage increases.¹⁶ In fact, such is the prevalence of vitamin B12 deficiency among metformin users that the U.K. government has acknowledged it "to be a common side effect."¹⁷

• How does metformin cause a vitamin B12 deficiency? Right now, there's no clear and definite answer, but there are some theories. According to a study published in the World Journal of Diabetes:¹⁸

"The most accepted theory is that metformin antagonizes the calcium cation and prevents the calcium-dependent IF-vitamin (intrinsic factor) B12 complex from binding to the ileal cubilin receptor and consequently will reduce the endocytosis process of vitamin B12."

• The highest rates were reported in the Americas — It's estimated that 54.04% of diabetes patients in this region had at least one micronutrient deficiency. Other regions, including Southeast Asia, Europe and Eastern Mediterranean, also showed increased rates of deficiencies, but not to the degree of the Americas.

• Beware how your sociocultural traditions influence your risk of diabetes — According to the researchers, "cultural practices may contribute to geographic variations in micronutrient deficiency."¹⁹ So, be sure to consider the cultural makeup of your diet, then make the appropriate adjustments wherever possible while still adhering to your beliefs.

1. Discuss metformin’s B12 effect with your prescriber — As mentioned earlier, metformin is associated with lower vitamin B12 levels, and B12 deficiency can cause nerve damage, fatigue, and cognitive problems. If you have been taking metformin for a while, ask your clinician about B12 monitoring. Do not stop or reduce metformin on your own — discontinuing it without supervision can cause blood sugar to rise to dangerous levels.

Focus on eating healthy carbohydrates to support your mitochondrial function instead of ultraprocessed foods and drinks. According to a 2024 prospective cohort study, those who consumed refined sugar and artificially sweetened drinks have a 29% higher relative risk of diabetes compared to controls.²¹

2. Increase your vitamin B12 levels — I recommend you consume high-quality animal foods like eggs, raw grass fed dairy and ruminant meats, as these are the best natural sources of B12. Eliminate alcohol, too — it interferes with B12 absorption (as well as other important nutrients) and increases oxidative stress in your body.²²

3. Get more vitamin D from sunlight — Vitamin D deficiency is the most common micronutrient problem among diabetics, and low vitamin D status is associated with reduced insulin sensitivity.

Ideally, spending time outside in natural sunlight, especially around midday when UVB rays are strongest, is the best strategy. However, this is only applicable if you've been minimizing your intake of vegetable oils for four to six months. That's because vegetable oil is high in linoleic acid (LA), a polyunsaturated fat that is prone to oxidation and accumulates in skin tissue, increasing susceptibility to sunburn.

Until then, I recommend spending time outdoors only in the early morning or late afternoon. Also, make sure to have your vitamin D levels tested regularly. The recommended range for optimal health is between 60 and 80 ng/mL. Talk to your healthcare provider about whether this testing is appropriate for you.

4. Boost your magnesium intake — As mentioned earlier, magnesium is required for proper insulin function, energy production and nerve health. In addition, it's also important to more than 300 enzymatic processes.

I generally advise getting nutrients from whole foods, but magnesium is a rare exception. Most people are deficient and meeting the recommended daily intake of 400 mg through diet alone can be difficult.

One key reason is soil depletion. Modern farming practices have significantly reduced the mineral content of soil, so even magnesium-rich vegetables contain much lower levels than they once did. This means that even if you follow a plant-based, whole-food diet, you may still fall short.

Another challenge is that some of the best dietary sources of magnesium — nuts and seeds — are also high in linoleic acid, an omega-6 fat. Since most people already consume excessive linoleic acid from vegetable oils, eating large amounts of these foods can contribute to inflammation and mitochondrial dysfunction. Balancing magnesium intake while avoiding excess omega-6 fats can be tricky.

For these reasons, supplementing with magnesium is often a wise choice. I prefer magnesium glycinate and magnesium malate, as they are well-absorbed and easy on the digestive system. To find your ideal dose, start with magnesium citrate and increase gradually until your stools loosen, then back off slightly — that level is your ideal dose. You can then switch to glycinate or malate.

5. Remove the root causes of nutrient deficiencies — If you're constantly losing key nutrients, you must repair and rebuild your cellular health, which requires a multifaceted approach:

“I'm very affected by my upbringing,” he says. “It's my framework. I was also taught to never go to the doctor, ever, for my whole life. And also, no foreign chemicals. If I take two Advil right now, I'm unconscious.

Whether it's the foods, or the things you put into your body, or how you interact with nature. I also remember my family being weird — or so I thought as a kid in the 80s in America.

We'd go to Sandy Hook, the beach, and my family would immediately run in and grab sand from the bottom of the ocean and scrub their faces with it. The other thing, literally anytime I wasn't feeling well, for the first 15 years of my life, my mom or my grandma would say ‘Drink some tea and go to sleep ...’

If you asked 18-year-old me in 1993, ‘Talk about medicine,’ my initial answers would be ‘ginger, cinnamon, mint, red beets.’ When I used to have a chest cold, my mom would put vodka on a rack and heat it up and put it on my chest. Not Vicks VapoRub. Just real ancient, historical ways of doing stuff ...

I just remembered something I haven't thought about 30 years. I used to think of my body like a superhero. If the superhero character got their thumb cut off, the thumb would just grow back in. I literally grew up thinking that if I did nothing, that it would fix itself.

Three weeks ago, I jammed my thumb playing basketball very badly. My friends were like, ‘Let's put some ice on it.’ It swelled up. I didn't do it.

A week later, my trainer said, ‘You know, it's interesting that you didn't do the ice thing, because I've been reading a lot about how the body naturally does it. It swells up to protect you. It's a natural cast.’ It was just interesting the way he was talking about it. And he said, ‘Some people are now debating that you're actually better off not icing it.’”

“I believe my optimistic point of view on everything has an incredible impact on my life,” Vaynerchuk says. “So, it goes both ways. I grew up in my dad's liquor store, and so, I got into very bad habits and really hurt my back. My QL.

But I would say soft tissue and fascial work has given me a new lease on life. I've always felt healthy. But I definitely had aches and pains and mobility issues until I got serious about that seven, 10 years ago.”

“One of the great things that happened to me was I was born in the Soviet Union, but I grew up in America. So, propaganda was something I thought about all the time. Like when Reagan was president, I could sense that he was doing a good PR job. At 10, I understood.

I was also very entrepreneurial, and very quickly, in my early 20s, I'm like ‘Everything is business.’ We now talk about Big Food, Big Pharma. It was very, very intuitive to me in my 20s. And so, I've lived my adult life taking everything with a grain of salt.

I feel like that's becoming a more modern conversation as people are trying to figure out east-west, historical versus modern. And you know, I do think people overcorrect the other way.

I've got personal [friends] who so have demonized modern medicine that they are no longer with us, because they didn't do some things that they should have that probably could have helped them. So, I think a lot about finding the middle.”

“I think what I've done well is communicate to people about incredible truths [that] in marketing ... have been fruitful. I think people are getting a lot more alternative knowledge from the way the internet works and things of that nature. But I think I'm incredibly practical.

It's funny, I think about business and marketing the way that you and I are discussing health right now. If you're worried about your body, why on earth would you not listen to your body? I find something very interesting about the medical industry, which is they like to fight each other on who's right.

And I see it in marketing. I tell a lot of marketing ideological professors or pontificators who also write books like I do — ‘Wait a minute, if you're so good at marketing, why doesn't your book sell?’ I grew up learning marketing by trying to help my father's liquor store do more business, because that's what you do for your family business.

And so, since I was 6 years old, I've been obsessed with attention. Let me explain what I mean. What I find amazing about what you and I are doing right now is we couldn't do this 40 years ago. Humans that have passion or expertise for things couldn't get into the world. We needed to have a gatekeeper say that we'll interview you or will give you three minutes on this show.

But no one had platforms. And so, I've been focused on attention my whole life. And now, every platform allows for attention. That is a remarkable change in the world. So, for example, I believe that what I was doing at 6, which was paying attention to what the cars that were driving by my lemonade stand would most likely look at to see that my lemonade was 25 cents.

From that day on to today, I spend all of my time trying to understand where consumer attention is. What are they paying attention to? What do they look at? Which platforms? Is it direct mail? Is it Google? Is it YouTube? Is it TikTok? And so, my great passion is understanding where attention is and then communicating in practical, optimistic terms what we are talking about.”

“One, I was deeply knowledgeable and passionate about wine at that point, and I spoke about wine in a way that no one had ever spoken about it before. Wine was put on a very elitist pedestal. And as you probably know, through your life, people are intimidated by wine, right? ...

So, I wanted to make it less intimidating. I spoke about it in very casual terms, and I would compare it to things that people knew. Instead of talking about a wine tasting like ‘an esoteric cassis from the south of France,’ I would say, ‘You know that grape Jolly Rancher you loved as a kid?’ I made it relatable.

And finally, I used a new medium. I was able to use YouTube when it first came out when nobody really knew how big it was going to be to reach a lot more people than, let's say, The New York Times' dining section.

I believe the framework that I started for wine is what I do now. I have a marketing company called VaynerMedia that works with the biggest companies in the world to do their marketing and social and traditional channels. But I feel passionate for the people that are listening that are entrepreneurial.

I just wrote a new book called ‘Day Trading Attention,’ which is really my thesis. I couldn't explain to everyone here how great of an opportunity everybody has to reach an audience for the first time, really, in the history of distribution, [in a way that's] immediate and creative.

For the first 15 years, it was email marketing. You would have to amass a lot of followers, and then you would post and a percentage of them would see it. We now live in a new era where it's really profound.

Every individual piece of content on LinkedIn, on YouTube, on Instagram, has the potential to reach a very broad audience based on the quality of the piece of content, not on how many followers you have.

This is a level of meritocracy of information and entertainment that we have never seen in the history of the world. And I could not recommend more for people to get very serious about organic social media, meaning you just post — you don't even have to run media ads on it — for you and your platform.”

“I turned on Netflix the other night and saw a documentary about gut health trending in the top 10. I was happy to see that. I'm personally fascinated by intuition and the fact that — I believe — the gut is your primary brain, and your brain is second.”

“Patience is [among] my top five favorite traits in a human being,” he says. “However ... a lot of people, when they hear me talking about patience, think that I'm talking about non-action, or that I'm talking about laziness. And I keep telling people, there's a reason that there are separate words. Laziness and patience are not the same ...

I created V Friends, it's my Sesame Street-meets-Pokémon, to help kids and parents finally find the middle, because everything can be great and balanced, and most things aren't, really, where they're at.”

• The strongest results occurred in participants who already had more advanced disease — The study found that the greatest benefit occurred in people with intermediate AMD or advanced AMD in one eye. For this group, the combination of antioxidants and zinc reduced the risk of progressing to advanced AMD by about 25% and lowered the risk of vision loss by about 19%.

Those percentages are relative, meaning they describe how much lower the risk was in the treated group compared with the placebo group — not a 25% chance of holding on to your vision. They also apply only to people who were already at high risk when the study began.*

In contrast, participants with no AMD or only early disease didn't experience the same measurable benefit. These findings positioned the AREDS formula as a targeted intervention for people at highest risk, not a preventive supplement for the general population.

• Combining antioxidants with zinc worked better than using either treatment alone — Researchers compared four treatment strategies and found a clear pattern. Zinc on its own did show a benefit, but only in the group at highest risk — and even there, the finding was borderline. Antioxidant vitamins, on their own, never produced a result the researchers could separate from chance.

The combination of antioxidants and zinc consistently produced the greatest benefit, outperforming either approach by itself.

Participants receiving the combined formula had the lowest likelihood of progressing to advanced AMD, while those receiving the placebo had the highest risk. The results led the researchers to recommend the combination rather than either component alone. The trial was not designed to formally test how the nutrients interact with one another.

• The researchers tested one precise formula instead of general vitamin use — The benefits came from a carefully standardized combination consisting of 500 milligrams (mg) of vitamin C, 400 international units of vitamin E, 15 mg of beta-carotene, 80 mg of zinc as zinc oxide, and 2 mg of copper as cupric oxide.

That zinc dose is far above ordinary intake — the Recommended Dietary Allowance (RDA) is 11 mg daily for men and 8 mg for women, and the Tolerable Upper Intake Level for adults is 40 mg daily.⁴ It was a deliberately high research dose given under trial supervision, not a general intake recommendation.

Copper was included as a precaution, because high-dose zinc can interfere with copper absorption. In AREDS, annual blood sampling in a subset of participants showed no increased risk of copper-deficient anemia in those assigned to zinc.

The study also found that nearly two-thirds of participants already took a daily multivitamin, yet those at high risk still received additional protection from the AREDS formula beyond what a standard multivitamin provided. Because the multivitamin offered in the trial also contained 15 mg of zinc, some participants were taking as much as 95 mg of zinc daily.

• The study also clarified what the formula didn't accomplish — Although the nutrient combination slowed progression to advanced AMD, it didn't restore vision that had already been lost. The researchers also evaluated cataracts and found that participants taking zinc alone, antioxidants alone, or the combined formula developed cataracts at approximately the same rate as those taking the placebo.

These findings narrowed the role of the formula to one specific purpose — slowing progression to advanced AMD in people already at elevated risk.

• Long-term treatment proved generally safe but still required important precautions — Researchers monitored participants throughout the seven-year study for adverse effects and reported relatively few serious problems overall.

However, about 7.5% of participants receiving zinc-containing treatments experienced urinary tract conditions requiring hospitalization compared with 5% of those who didn't receive zinc. That difference was statistically significant , and it was larger among men considered alone (8.6% versus 4.4%).

Mild anemia also occurred somewhat more often in participants taking zinc, although laboratory testing didn't show meaningful differences between treatment groups. The researchers also highlighted an important safety concern regarding beta-carotene, noting its association with increased lung cancer risk in smokers. That finding eventually led to updated AREDS2 formulations that replaced beta-carotene with lutein and zeaxanthin.

In AREDS2, current smokers were excluded from beta-carotene randomization, and the excess lung cancers that were observed occurred mostly in former smokers (23 cases versus 11 cases).

• A follow-up trial updated the original formula based on what the first study revealed — The AREDS2 study, completed in 2013, made three key changes.⁵ Researchers replaced beta-carotene with 10 mg of lutein and 2 mg of zeaxanthin, two carotenoids that naturally concentrate in the macula. They also tested whether reducing the zinc dose from 80 mg to 25 mg affected the formula's effectiveness and found that the lower dose provided similar protection against progression to advanced AMD.

There was no statistically significant difference between the two doses, and the review authors note that this raises a reasonable question about whether the higher dose is still warranted.⁶

The study also evaluated omega-3 fatty acids but found they didn't provide additional benefit when added to the formula. Today, most eye health supplements sold as "AREDS" formulas are based on the AREDS2 formulation, making it the version most people are likely to encounter.

• The retina naturally contains some of the highest zinc concentrations in the body — Researchers explained that the retinal pigment epithelium and choroid — the layers that nourish and support the retina — contain the greatest concentrations of zinc anywhere in the eye. These tissues do far more than store the mineral. Concentration is not the same as quantity, though.

The review's own accounting places the eye at under 0.01% of total body zinc, with most of the body's supply held in skeletal muscle and bone.

Zinc supports hundreds of enzymes along with protein production, cell repair, communication between retinal cells, and the activity of protective enzymes that defend eye tissue against everyday damage. The review is careful to note that zinc is not an antioxidant per se — it does not participate in redox reactions directly, but stabilizes and supports the enzymes that do.

The review also noted that scientists still don't fully understand every molecular pathway through which zinc protects retinal cells, making it one of the most actively studied nutrients in vision research.

• Zinc deficiency affected eyesight long before permanent damage became obvious — The review described several situations in which inadequate zinc disrupted normal vision. People with acrodermatitis enteropathica — a rare inherited disorder that impairs intestinal zinc absorption — develop eye abnormalities that are largely front-of-the-eye problems, including blepharitis, conjunctivitis, and corneal opacities.

In Crohn's disease, reduced retinal zinc has been implicated in a bilateral maculopathy with vision impairment that was responsive to zinc supplementation.

Long-term intravenous nutrition has likewise been associated with impaired visual function and low plasma zinc, though the review does not report reversal with zinc replacement in that group. These are rare, severe systemic deficiency states, not conditions the review extends to well-nourished people.

Researchers also reported that zinc deficiency often reduced the eye's ability to adjust from bright light to darkness, a process called dark adaptation. The clinical evidence here comes largely from people with alcoholism and hepatic cirrhosis, and the mechanism is indirect — zinc is a cofactor for the enzyme that converts vitamin A to retinal — so, these cases often require both zinc and vitamin A to improve.

When dark adaptation slows, driving at night or walking through dimly lit areas becomes much more difficult. Animal studies further showed that severe post-weaning zinc deficiency damaged photoreceptors — the specialized cells that detect light — along with the retinal pigment epithelium, although the same review notes that postnatal zinc deficiency on its own produced functional changes without visible structural damage.

The picture is not one-directional — in one rodent experiment, rats fed a low-zinc diet showed less light-induced retinal damage than those on regular or high-zinc diets.

• More zinc didn't produce better results — One of the review's clearest messages is that healthy vision depends on maintaining zinc within a normal range rather than consuming as much as possible. Laboratory studies showed that excessively high zinc concentrations triggered harmful chemical reactions inside retinal tissue by increasing reactive oxygen species, unstable molecules that damage proteins, fats, and DNA.

These were in vitro experiments on isolated retinal tissue exposed to zinc concentrations of 500 micromolar or more, which is far above anything produced by ordinary dietary intake, and not directly comparable to an oral supplement dose.

High zinc levels also reduced the activity of important antioxidant enzymes, weakening the eye's natural defense systems. To prevent both deficiency and overload, the body relies on specialized transport proteins that continually move zinc into and out of cells to maintain a healthy balance.

• The foods you choose influence how much zinc your body actually uses — Researchers emphasized that eating zinc and absorbing zinc are not the same thing. Animal foods such as red meat and shellfish provide zinc in a form your body absorbs more efficiently than many plant foods. In contrast, phytates — compounds naturally present in whole grains and legumes — bind to zinc in the digestive tract and reduce the amount your body absorbs.

The review also found that dietary protein and natural organic acids such as citric acid improve zinc bioavailability, meaning they increase the percentage of zinc your body absorbs and puts to use. Because the body has no specialized storage system for zinc, maintaining a steady dietary intake helps support healthy zinc levels in the eyes and throughout the rest of the body.

• Your body carefully regulates zinc every day without you noticing it — The review explained that only a tiny fraction of your body's approximately 2 to 3 grams of total zinc circulates in the bloodstream at any given time. Most of it is stored inside muscles, bones and other tissues where it performs essential biological functions. Specialized transport proteins in the intestines increase zinc absorption when dietary intake falls, conserving tissue zinc.

When intake is high, however, the review reports that the body compensates mainly by increasing how much zinc it excretes in stool rather than by absorbing less. So, a large supplemental dose is not automatically self-limiting.

At the same time, the digestive tract, liver and other organs continually recycle and redistribute zinc to maintain stable levels. This tightly regulated system helps ensure that delicate retinal cells receive the zinc they need while protecting them from the harmful effects of excess exposure.

• Researchers discovered that excess zinc released after nerve injury speeds optic nerve cell death — Research from a completely different corner of eye science reinforces why zinc balance matters so much. Scientists at Boston Children's Hospital and Harvard Medical School were studying retinal nerve damage in glaucoma when they made an unexpected discovery about zinc itself.^8,9

They found that after an acute optic nerve injury in mice, zinc flooded out of neighboring amacrine cells — specialized retinal nerve cells that communicate with retinal ganglion cells — within about one hour of the injury. Surprisingly, the zinc didn't come from the damaged ganglion cells themselves.

Instead, excess zinc spread from surrounding cells and contributed to the death of retinal ganglion cells, the neurons that form the optic nerve and carry visual information from your eye to your brain. In laboratory mice, researchers removed excess zinc using a process called chelation, which binds and removes specific metals.

Ganglion cells survived longer and even regenerated after treatment, and the protective effect remained even when treatment was delayed for several days because zinc toxicity developed gradually instead of immediately.

These findings suggest that maintaining normal zinc balance is just as important as preventing zinc deficiency and raise the question of whether limiting excess zinc could help protect the optic nerve in diseases such as glaucoma. Note that this work has only been demonstrated in laboratory animals so far and has not been tested in people.

1. Build your meals around foods that naturally provide zinc first — Your body absorbs zinc from foods such as oysters, grass fed beef, lamb, and other animal foods more efficiently than from many plant sources. If you regularly eat these foods, you give your eyes a steady supply of the mineral they need every day instead of relying entirely on supplements. It's usually best to meet your nutritional needs through whole foods whenever possible because they provide many nutrients that work together.

Next, understand the participants the studied formula was tested on. The research evaluated one specific combination of antioxidant vitamins and zinc in people who already had a high risk of progressing to advanced AMD. No benefit was observed in people with healthy eyes or early-stage disease.

The formula uses zinc at a dose well above the general upper intake level and was given under clinical supervision, so whether it is appropriate for you is a decision for your eye care provider based on your disease stage — not something to start on your own.

2. Avoid thinking that more zinc is always better — Your retina depends on balanced zinc levels. Too little interferes with normal eye function, while too much also disrupts healthy retinal cells. Stay within the recommended daily intake that was referenced earlier — 11 mg a day for men and 8 mg for women, with an upper limit of 40 mg for adults — unless your eye care provider has specifically recommended the AREDS formula based on your disease stage.

Higher doses aren't automatically better; as the research in this article shows, excess zinc can damage the very cells you're trying to protect. It is also worth knowing that when AREDS2 compared 80 mg of zinc against 25 mg, it found no significant difference in protection.

3. Help your body absorb the zinc you eat — If you eat large amounts of whole grains or legumes, remember that they contain natural compounds called phytates that reduce zinc absorption. Eating zinc-rich animal foods as part of a balanced meal helps improve the amount your body actually uses. Making small adjustments to your daily meals often produces more lasting results than focusing only on pills.

• The right fuel sources — glucose — “You need the right fuel sources and you certainly can produce energy from fat … We all utilize fat all day long, but certainly when your body's under stress or the needs go up, then glucose is going to be your primary because you can just utilize it faster. It kind of goes through the entire cycle faster,” Deering says.³

• Optimal oxygen production — Oxygen is vital for energy metabolism. It is the final electron acceptor in the electron transport chain. And when O2 isn't available in your cell, your cell then uses the far more inefficient glycolytic pathway (fermentation) for energy production more than necessary.

• Proper thyroid function — High intake of omega-6 polyunsaturated fat like linoleic acid can have a detrimental impact on your thyroid and metabolic health by affecting cells' use of thyroid hormones. A carb-rich low-PUFA diet will support thyroid health by balancing estrogen levels, ensuring glucose availability and safeguarding your cells' ability to use active thyroid hormone.

• Sunlight exposure — The fourth requirement to produce energy effectively, according to Deering, is regular sunlight exposure. “I also like to add in sun because we need sun for life and to produce energy,” she says.