• Both groups were fed high-fat diets for up to 35 weeks — Some mice received a diet where 10% of calories came from LA using a mixture of soybean oil and coconut oil, while others received a diet based primarily on coconut oil, where only 2% of calories came from LA. A third group ate standard low-fat laboratory chow as a control. The total fat content and total calories were identical between the two high-fat diets.

• Normal mice gained more weight despite identical food intake — Wild-type mice on the soybean oil diet gained 411% of their starting weight compared to 370% on coconut oil. The modified mice, however, gained much less weight on the soybean oil diet than normal mice did, and their weight gain on soybean oil was essentially the same as on coconut oil.

In other words, the researchers found no difference in the number of calories the mice consumed on the different diets, indicating that overeating did not explain the difference.

• Soybean oil raised obesity-linked oxylipins through LA metabolism — A key finding was the sharp contrast in oxylipin production. Oxylipins are oxidized metabolites derived from LA as well as alpha-linolenic acid, another fatty acid in soybean oil. Wild-type mice produced more oxylipins, which have been associated with weight gain, fatty liver disease, and metabolic dysfunction.

The study suggests the issue is not just LA intake but what the body converts it into, since wild-type mice generated more of these obesity-linked oxylipins, while the genetically altered mice produced fewer of these compounds, which the researchers linked to lower levels of key enzyme families responsible for converting LA into oxylipins.

• Only liver oxylipins, not blood oxylipins, matched body weight — The researchers also found that oxylipins in liver tissue, not those in the bloodstream, tracked with body weight. In earlier work, the same team found that blood oxylipin levels in soybean oil-fed mice were no higher than on a low-fat diet, which the researchers say suggests standard blood tests may miss early diet-driven metabolic shifts.

Even the lean modified mice showed elevated levels of the four key oxylipins on a low-fat diet, but without obesity. So, oxylipins looked necessary for weight gain but not sufficient on their own, suggesting that other metabolic factors help determine whether oxylipins translate into visible metabolic harm.

• Partially blocking oxylipin production didn't change weight gain — To narrow down which oxylipins might be driving weight gain, researchers treated wild-type mice on soybean oil with a chemical that blocks a final step in oxylipin production. The treatment shifted some oxylipins, but not the four most tied to obesity.

Those levels stayed high, and treated mice gained as much weight as untreated soybean-oil mice. This supported the idea that these specific oxylipins may be helping to drive soybean oil's fattening effect in mice.

• The findings may help explain why seed oils hit some bodies harder than others — The study points to a mechanism in which weight gain in these mice depended not only on how much fat or how many calories they ate, but on which specific compounds their livers produced from that fat. Because the work was done only in male mice — female mice don't become obese on this diet — and no human trials are planned, it remains to be seen how closely the same process applies to people.^6,7

Researchers are digging deeper to understand how oxylipins promote weight gain and to see if similar effects occur with other LA-rich oils like corn, sunflower, and safflower oils. According to Frances Sladek, a UCR professor of Cell Biology:

"It took 100 years from the first observed link between chewing tobacco and cancer to get warning labels on cigarettes. We hope it won't take that long for society to recognize the link between excessive soybean oil consumption and negative health effects."⁸

• Oxidized linoleic acid metabolites (OXLAMs) can contribute to lasting cellular damage — OXLAMs are created when LA is exposed to oxidative stress. These include reactive aldehydes, such as 4-hydroxynonenal (4-HNE) — the most extensively studied product of LA oxidation — along with other oxidized metabolites such as 9- and 13-HODE. Aldehydes bind to proteins, DNA, and membranes, altering their structure and function.

• LA overload may destabilize cardiolipin and weaken energy production — Cardiolipin is a key fat in the inner mitochondrial membrane that stabilizes energy generation. When LA intake is high, more LA is built into cardiolipin, and LA-containing cardiolipin is especially vulnerable to oxidative damage. Oxidized cardiolipin can disrupt energy production and is involved in the signals that lead cells to clear out damaged mitochondria (mitophagy) or self-destruct (apoptosis).

• High LA intake may disrupt your gut microbiome and weaken the intestinal barrier — In mice, a high-LA soybean oil diet reduced beneficial Lactobacillus bacteria while allowing an adherent, invasive strain of E. coli to expand, making the gut more prone to inflammation. The same research found that the high-LA diet increased the permeability of the intestinal barrier, which can allow unwanted compounds to move into circulation, and raised the animals' susceptibility to colitis.

• Stored LA may keep producing inflammatory signals for years — Once incorporated into your body fat, LA has a long half-life of around two years. This means that even if you stop consuming soybean oil today, your tissues may continue producing inflammatory metabolites for months or even years afterward. This chronic exposure helps explain why LA is considered a persistent metabolic disruptor.

• Phytoestrogens — These compounds mimic estrogen by binding to estrogen receptors in your body. A 2014 commentary published in German Medical Science notes that phytoestrogen intake has been reported to affect fertility and sexual development in animals, and that high doses of isoflavones taken over long periods may stimulate breast and uterine tissue — which is why women treated for breast cancer have been advised to avoid them.¹²

• Phytic acid — A compound that binds to minerals such as calcium, magnesium, iron, and zinc, reducing your ability to absorb them — minerals your body relies on for energy production and many enzyme systems.¹³

Soybeans and soy concentrates are among the richer sources of phytic acid. That said, traditional preparation such as soaking, cooking, sprouting, and fermentation can reduce it considerably, but soy flours, concentrates, and protein isolates used in processed foods can still carry substantial amounts.

• Enzyme inhibitors — These compounds, such as trypsin inhibitors, can interfere with protein digestion by blocking key digestive enzymes, which may limit your ability to access essential amino acids needed for muscle repair, detoxification, neurotransmitter production, and immune health.

• Saponins, soyatoxin, lectins, and oxalates — These are antinutrients that, in sufficient amounts, may irritate the gut lining, increase intestinal permeability, and trigger immune responses. While small amounts may not pose a threat, the widespread inclusion of soy in processed foods means these compounds are consumed far more often than people realize.

• Goitrogens — Substances that can interfere with iodine uptake and thyroid hormone synthesis. Over time, this may disrupt thyroid function, particularly in individuals with borderline iodine status or underlying thyroid issues. Soy isoflavones are among the dietary compounds studied for this effect.¹⁴

In one 2021 case report, a 33-year-old woman developed rapid growth of a multinodular goiter after a weight loss program left her eating 20 to 40 grams of soy protein a day from meal replacement bars, despite reportedly adequate iodine intake. A single case can’t establish cause, but the authors advised caution with high soy protein intake, especially in people at risk for goiter.¹⁵

• GMO and glyphosate exposure — Around 95% of soybeans grown in the U.S. are genetically engineered to tolerate herbicides, most notably glyphosate, the active ingredient in Roundup. Glyphosate use on these crops has risen roughly 15-fold since the 1990s, raising the potential for residues in soy-derived products.¹⁶ Animal research and clinical case reports have linked glyphosate exposure to microbiome disruption, liver toxicity, and possible endocrine effects.¹⁷

1. Eliminate soybean oil from your diet — Cutting down on soybean oil begins with knowing where it shows up. It's not just the bottle in your pantry — refined soybean oil is baked, fried, blended, and sprayed into a wide range of everyday foods. Manufacturers rely on it because it's cheap, shelf-stable, and neutral in flavor.

Labels don't always say "soybean oil" outright. Instead, you'll see vague terms like "vegetable oil," or related soy ingredients such as "soy lecithin," often tucked into products marketed as organic, natural, or "heart-healthy." Unless you check every ingredient list, it's easy to miss. Here's where soybean oil frequently hides in your diet:

Category	Common Products That Contain Soybean Oil
Condiments and dressings	Mayonnaise, salad dressings, marinades, dipping sauces, and sandwich spreads
Packaged snacks	Chips, crackers, popcorn, pretzels, granola bars, and trail mix
Baked goods	Breads, bagels, muffins, cookies, tortillas, and pastries
Frozen and convenience foods	Pizza, microwave meals, frozen dinners, meat substitutes, and non-dairy creamer
Restaurant foods	Fried items, grilled foods, commercial breads and buns, and salad dressings
Pantry staples	Peanut butter, powdered soup mixes, boxed rice, or pasta dishes
Health foods and supplements	Protein bars, energy drinks, plant-based shakes, and soy lecithin in capsules
Infant and toddler products	Baby formula, toddler snacks, and puffed cereals

If you're busy or overwhelmed, use a barcode-scanning grocery app or an AI ingredient checker to flag hidden seed oils fast. To track your intake, I recommend you download my app, Pax, which comes out soon. It has a feature called the Seed-Oil Sleuth, which monitors your LA intake to a tenth of a gram so you can stay in charge of your metabolism.

2. Replace your cooking fats with stable, low-LA options — Use fats like ghee, grass fed butter, beef tallow, or coconut oil for daily cooking. These options are low in linoleic acid and far more resistant to heat damage than vegetable oils. Coconut oil is well-suited for medium-heat cooking and baking, while ghee and tallow offer better stability at high temperatures and add rich flavor to roasted vegetables, stir-fries, and seared meats.

Here's a quick guide to common cooking fats and oils, their typical smoke points, and how they hold up under heat:^18,19,20

Fat/Oil	Typical Smoke Point	Stability/Suitability for Cooking
Ghee (clarified butter)	~ 485°F (≈ 252°C)	Highly heat‑stable saturated fat, good for high-heat cooking and searing
Beef tallow/lard	~ 370 to 420°F (≈ 188 to 216°C)	More stable for roasting or frying than most seed oils; note that lard from conventionally raised pigs can be high in LA
Coconut oil	~ 370 to 420°F (≈188 to 216°C)	Reasonably stable for moderate heat cooking and baking, low in LA
Extra-virgin olive oil (EVOO)	~ 375 to 405°F (≈ 191 to 207°C)	Suitable for low-heat cooking or finishing dishes, but high in MUF
Soybean oil (refined)	~ 400 to 460°F (≈ 204 to 238°C)	Widely used seed oil; high smoke point, but its LA is prone to oxidation and exposes you to a high LA load
Canola oil/generic vegetable oil (seed-oil blend)	~ 400 to 450°F (≈ 204 to 232°C)	Common cooking oil; high LA/PUF load, high smoke point, but contributes to LA overconsumption
Refined sunflower oil	~ 450°F (≈ 232°C)	Another common seed oil high in LA; similar issues as with soybean oil
Peanut oil (refined)	~ 450°F (≈ 232°C)	Frequently used for frying, but still delivers high PUF and LA content

3. Choose low-LA animal proteins and skip high-PUF meats — When buying meat, prioritize grass fed beef, lamb, and bison over chicken or pork. Ruminant animals like cows and sheep metabolize LA differently, as microbes in their rumen convert much of it into more stable saturated fats before it can be stored.

In contrast, poultry and pigs deposit dietary LA directly into their fat and muscle tissue, meaning their meat reflects whatever corn- or soy-based feed they consumed. If you eat eggs, look for pasture-raised options from hens not fed corn or soy. These eggs are typically lower in PUFs and a better match for a metabolically supportive diet.

4. Avoid nuts and seeds, and use olive oil only in moderation — Many popular whole foods are surprisingly high in LA. Almonds, walnuts, pecans, sunflower seeds, pumpkin seeds, and most nut butters are all concentrated sources. If you're regularly snacking on trail mix, blending nut butters into smoothies, or using seed oils in homemade recipes, it's easy to push your LA intake far beyond the 5-gram daily limit.

Even macadamia nuts, though lower in LA, are still rich in oleic acid, a monounsaturated fat (MUF), which is why they're no longer on my recommended list. Large amounts of oleic acid may interfere with glucose metabolism and mitochondrial energy production.

Olive oil, another common MUF source, comes with similar concerns, which is why it's best used only in moderation. The soybean oil vs. olive oil comparison is often used to frame olive oil as the better choice, but that doesn't mean it's ideal. In addition, some commercially sold olive oils have also been found to be diluted or adulterated with cheap, oxidized seed oils, making them far from clean.

5. Choose cleaner sources of seafood and carbohydrates — Flaxseed is often promoted as a plant-based omega-3 source, but in a high-LA environment, it's largely ineffective. Excess LA inhibits the enzymes your body needs to convert plant omega-3s into the usable forms EPA and DHA. Flax is also high in fragile PUFs and contains lignans, which are plant estrogens that can disrupt hormone balance when consumed in large amounts.

If you eat seafood, choose wild-caught salmon over farmed varieties, which has a less favorable fat profile. Small, oily fish like sardines, mackerel, and anchovies are also ideal choices. When it comes to carbs, prioritize fruit, root vegetables, and white rice over packaged or fried products.

If your gut is still healing, white rice and whole fruits are the best place to start, and other complex carbs and starches work best once your digestion is functioning well. High-fiber foods, on the other hand, can increase endotoxin when your gut microbiome is compromised, so keep them limited.

6. Limit eating out — Your best option is to prepare most of your meals at home, because most restaurant kitchens default to soybean or canola oil for frying, grilling, baking, and dressings. When you do eat out, check The Templeton List (TempletonList.com), a free directory of restaurants rated on criteria that include healthy oils and real butter, and ask what oils are used and request butter or no added fat when possible.

Grilled foods may seem safe, but they're often marinated or brushed with seed oil blends before hitting the heat. For salads, bring your own dressing or stick to lemon juice, vinegar, and salt. Planning ahead is the most reliable way to stay clear of high-LA cooking oils when you're not in charge of the kitchen.

• Changes in the Earth's tilt relative to the sun — Earth's distance from the sun varies throughout the year, but that isn't what causes the seasons — Earth is actually closest to the sun in early January. Seasons are caused by the 23.5-degree tilt of Earth's axis.² During fall, the Northern Hemisphere is tilting away from the sun, which brings shorter days, a lower sunlight angle, and cooler temperatures. The result? Less UVB reaches your skin, which can lower your vitamin D levels.

• Factors affecting vitamin D production — Ultraviolet B (UVB), the type of sunlight that triggers vitamin D production on your skin, is affected by season, time of day, latitude, clouds, and your skin's melanin concentration.

• Check the daily UV Index (UVI) — This is a forecast issued daily by the National Weather Service and the EPA that tells you how strong the sun's UV radiation is expected to be. Here's a tip — the highest readings occur in the hours around solar noon.⁵

• Consider your Fitzpatrick phototype — It's a guide that describes how certain skin colors react when exposed to sunlight. Thus, it can give you a rough sense of how your skin responds to sun exposure, and how much time in the sun it may need. Here's a chart from DermNet to help you:⁶

Skin Type	Typical Features	Tanning Ability
I	Pale white skin, blue/green eyes, blonde/red hair	Always burns, does not tan
II	Fair skin, blue eyes	Burns easily, tans poorly
III	Darker white skin	Tans after initial burn
IV	Light brown skin	Burns minimally, tans easily
V	Brown skin	Rarely burns, tans darkly easily
VI	Dark brown or black skin	Never burns, always tans darkly

• Have yourself tested first — No matter which strategy you employ — sunlight exposure, food, and supplements — it's always a good idea to have your vitamin D levels tested to know your baseline.

When visiting a lab, ask for a 25-hydroxy vitamin D test. This measures the current vitamin D levels circulating within your body. Conventional guidance, such as that from the Office of Dietary Supplements, considers 20 nanograms per milliliter (ng/mL), or 50 nanomoles per liter (nmol/L), sufficient for most people.³ However, I consider 40 ng/mL (100 nmol/L) the lower cutoff for sufficiency, and even then, I believe even that isn't enough — the real benefits of vitamin D appear when you reach a range between 60 and 80 ng/mL (150 to 200 nmol/L). Note: Talk to your health care provider about whether this testing is appropriate for you.

• Vitamin D2 versus D3 — As noted in my interview with NTD News, vitamin D2 comes from plants, while vitamin D3 comes from animals. If you're going to pick one, I recommend vitamin D3, as it's more effective at raising and maintaining blood vitamin D levels.

One more thing about vitamin D3 — it's a fat-soluble nutrient. This means that it's best absorbed when you take it with meals that include healthy fat, such as pasture-raised egg yolks, tallow, or grass fed butter.

• Supplement interactions — When taking vitamin D3 supplements, remember to increase your intake of magnesium and vitamin K2. Magnesium helps your body convert vitamin D into its active forms, while vitamin K2 helps direct calcium to your bones and away from your arteries. For every 5,000 international units (IUs) of vitamin D you ingest, take around 180 micrograms (mcg) of vitamin K2 in MK-7 form, as well as 400 milligrams (mg) of magnesium. Specifically, glycinate and malate are the preferred forms).

• Medications affecting vitamin D function — Check with your doctor if you're taking medications such as statins and steroids. According to the Office of Dietary Supplements, corticosteroid medications such as prednisone can impair vitamin D metabolism.⁸

• Rechecking interval — Have your blood tested every three to six months. This gives you enough time to see how your levels are responding and whether adjustments are needed.

• The link between sunlight and skin cancer — The fear of increased cancer risk emphasized by dermatologists has some merit, but it's important to understand the nuances. As I mentioned in the interview, frequent sun exposure is associated with a higher risk of squamous cell and basal cell carcinoma. But the good thing is that these are usually caught early and are highly treatable, making mortality risk very low.

Meanwhile, some observational research has linked regular, non-burning sun exposure to a lower risk of melanoma,^{10,11,12,13,14} which is the dangerous type of skin cancer you don't want to get. I suspect a major reason skin is more vulnerable to sun damage today is that many of us eat a diet high in linoleic acid (LA), which is unstable and can form harmful oxidation byproducts when your skin is exposed to sunlight. Thus, reducing the LA stored in your tissues may allow you to enjoy the benefits of sunlight more safely — this process is explained below.

• Avoid excessive use of sunscreens — These products limit vitamin D synthesis. According to the Office of Dietary Supplements, sunscreens with an SPF of 8 or more appear to block vitamin D-producing UV rays.³ Some chemical UV filters, such as benzophenone-3, have also raised concerns about hormone disruption,^{15,16,17,18,19} which is why natural mineral-based sunscreens are preferable to chemical ones.

• Daily base intake — The Office of Dietary Supplements sets a Recommended Dietary Allowance (RDA) of 600 IUs a day for most adults, rising to 800 IUs after age 70.²⁰ However, there is good evidence that this number is far too low.

The RDA was set in 2011 by the Institute of Medicine (IOM), now the National Academies of Sciences, Engineering, and Medicine. It was meant to be the daily intake that would bring 97.5% of people to a blood level of 25-hydroxyvitamin D [25(OH)D] of at least 50 nmol/L (20 ng/mL). In 2014, researchers at the University of Alberta identified a statistical error in how that figure was calculated. The IOM based its estimate on the average 25(OH)D levels reported in each supplementation study, rather than on the variation among the individual participants in those studies.

Individual responses to vitamin D vary far more than study averages do, so this method overstated how many people would actually reach the target on 600 IUs. When the researchers reanalyzed the IOM's data correctly, they estimated that 8,895 IUs a day would be needed for 97.5% of individuals to reach 50 nmol/L.²¹

A separate group of researchers confirmed the error using individual-level data from a different population and estimated the requirement at roughly 7,000 IUs a day.²² A larger follow-up analysis pooled 108 published estimates and arrived at 2,909 IUs a day for healthy adults. The same paper's analysis of nearly 14,000 observations from a health program found that the requirement rose with body weight: 3,094 IUs for normal-weight, 4,450 IUs for overweight, and 7,248 IUs for obese individuals.²³

Depending on the analysis and a person's body weight, these estimates put the requirement roughly five to 15 times higher than the current RDA. Even so, the RDA has not been revised.²⁴

As noted in my interview with NTD News, many adults can take 10,000 IUs a day without problems — although that's well above the 4,000 IU tolerable upper intake level the Office of Dietary Supplements sets for adults.¹⁰ That said, the only way to assess your daily requirement is by checking your levels. It's not the dose that matters but rather your blood level. For general health, a blood level between 60 and 80 ng/mL appears ideal, with a lower cutoff at 40 ng/mL.^25,26,27,28

• Shop smart — Keep fish such as wild-caught Alaskan salmon in your rotation. This variety is a better choice than farmed fish, which have a less favorable fat profile. Similarly, if you consume dairy, look for raw, grass fed varieties rather than commercially pasteurized products.

• Mind your medications — Consult with your doctor to rule out interactions on vitamin D synthesis if you're currently taking medications for a disease.

• Develop your sun sense — Regularly review the UVI reports and be mindful of your Fitzpatrick phototype to make sure you don't get sunburned.

• Test and retest — Take a 25-hydroxy vitamin D test and aim for a range between 60 to 80 ng/mL.

1. Keep LA intake below 5 grams a day — Remove all industrial seed oils (often marketed as “vegetable oils”) from your diet, including soybean, corn, sunflower, safflower, cottonseed, canola, and grapeseed oils. LA is common in ultraprocessed foods, condiments, restaurant meals, and packaged snacks.

High levels of LA also accumulate in the fat of conventionally raised, grain-fed livestock — especially chicken and pork. To minimize exposure, choose pasture-raised or grass fed meat whenever possible.

2. Include C15:0 daily — Use a high-quality pentadecanoic acid powder or a certified butter or ghee concentrate rich in C15:0. Following this habit consistently may support steady uptake into your tissues.

Check your progress every three months — Use a red blood cell test or dried blood spot test to check that your C15:0 levels are at least 0.4% and that LA remains under 5% of your total fat levels. These benchmarks may indicate successful cellular remodeling. (Talk to your health care provider about whether this testing is appropriate for you.)

If your results stop improving, look for unrecognized sources of LA or review your dosing for possible inconsistencies.

3. Encourage fat turnover through healthy lifestyle changes — Boost the clearance of stored LA with time-restricted eating, high-intensity training, and regular heat exposure via sauna sessions or hot baths.

A note on high-intensity training — limit it to 75 minutes or less per week, as longer bouts can hinder recovery and longevity. When it comes to meal timing, avoid chronic or extreme restriction, which can suppress thyroid function and metabolism. Instead, I recommend time-restricted eating (TRE) where you eat all of your meals for the day within a window of 12 to 18 hours — longer in winter, shorter in summer.

4. Build up sun tolerance gradually, especially in the first four to six months after you eliminate seed oils — While LA remains high in your body fat, the skin may be more prone to UV-induced oxidative stress and sunburn. During this period, avoid high-intensity midday sunlight (11 a.m. to 3 p.m.) and go out during early morning or late afternoon instead.

• The study pitted two rodent cell lines against each other — The researchers used WEHI-164 cells, a fibrosarcoma (connective-tissue cancer) line from mice, and L6 cells, a normal muscle-precursor (myoblast) line from rats.

Across the experiments, they tracked cell viability, mitochondrial function, energy production, a cellular cleanup process, cellular aging, and the activity of NF-κB-related genes, then finished with a whole-organism toxicity test. The five plant compounds were each tested at a range of concentrations over 24 and 48 hours.

• Potency alone did not predict selectivity — IC50 values (the concentration of a compound needed to cut cell viability in half) were calculated, wherein a lower number means greater potency. At the 24-hour mark, curcumin and CAPE were preferentially toxic to the cancer line, while biochanin A, berberine, and especially cucurbitacin E were relatively more toxic to the normal muscle cells.

For example, curcumin's 24-hour IC50 was 29.305 micromolar in normal cells versus 14.049 in the cancer cells, indicating it took less to affect the tumor cells. By 48 hours every compound had grown more potent, and the cancer cells proved consistently more susceptible on the delayed measures.

• Energy metabolism was where tumor cells suffered most — The team gauged mitochondrial membrane potential, an indicator of how well the cell's power plants are holding their electrical charge, using a dye called JC-1. All five compounds lowered that charge in the normal muscle cells, with cucurbitacin E and berberine causing the steepest drops.

More telling was adenosine triphosphate (ATP), the cell's energy currency. After 48 hours, it fell by roughly 83% to 92% in the cancer cells versus 23% to 73% in the normal cells, with berberine producing about a 92% reduction in the tumor line. Notably, the loss of membrane charge and the collapse of ATP did not always move in lockstep, which led the authors to conclude that the cancer cells were simply less able to restore their energy balance under sustained stress.

• Cellular aging was pushed hard in the cancer cells — Using a marker called SA-β-galactosidase to flag senescent (permanently non-dividing) cells, the researchers found baseline positivity of about 16.5% in untreated cancer cells. Curcumin drove that to 75.56%, the highest of the group, followed by berberine at 69.68%, CAPE at 68.45%, cucurbitacin E at 66.11%, and biochanin A at 66.02%.

In the normal muscle cells, the increases were more modest, reinforcing the pattern of tumor-preferential stress.

• Two compounds parted ways at the genetic level — In the cancer cells, the team measured messenger RNA for four NF-κB components and PFKFB3, an enzyme that drives glycolysis (a cell's sugar-burning energy route), after treatment with cucurbitacin E and biochanin A.

Cucurbitacin E kept these genes suppressed over time, whereas biochanin A rebounded after 48 hours and triggered a roughly ninefold jump in PFKFB3. Note that the authors presented this as an observation rather than proof of a mechanism, since they did not directly test what the PFKFB3 surge accomplished.

• The larval safety screen was decisive but deliberately limited — In the Galleria mellonella (wax moth larvae) model, berberine was best tolerated with 9 out of 10 larvae alive, and curcumin caused only mild mortality. CAPE and cucurbitacin E reduced survival more sharply, and biochanin A dropped survival to 2 of 10 within the first day. Berberine and curcumin did not differ significantly from the control solutions, while CAPE, cucurbitacin E, and biochanin A did.

The authors stress this was a preliminary acute-toxicity screen only, not evidence of systemic safety, and they caution that the study compared two different rodent lines, inferred NF-κB activity from mRNA rather than protein, and cannot substitute for mammalian testing.

• Curcumin interacts with many signaling pathways — The review describes how curcumin acts on immune modulators including cytokines, the enzyme COX-2, and reactive oxygen species (ROS), which are unstable oxygen-containing molecules that participate in inflammation and cell signaling. It also reports curcumin's involvement in downregulating growth factors, protein kinases, and signaling pathways such as NF-κB, JNK, and STAT3.

• Curcumin's inhibitory action on NF-κB is a recurring finding — NF-κB is a transcription factor that helps control the expression of proteins tied to both inflammation and cancer progression. According to the review, curcumin has an inhibitory effect on the NF-κB-dependent pathway, which in laboratory models, was associated with suppression of tumor cell growth and induction of apoptosis, the process of programmed cell death.

The review also notes that curcumin can modulate several immune cell types and can suppress activation of the NLRP3 inflammasome, part of the innate immune system, leading to reduced secretion of the inflammatory signal IL-1β.

• The compound has been examined in a wide range of cancers, mostly in cells and animals — The review walks through lung, breast, prostate, brain, pancreatic, gastric, and blood cancers, describing curcumin's multi-target effects in each. In breast cancer cell lines, for instance, curcumin was found to suppress the nuclear translocation of NF-κB, and in lung cancer cells, it acted on the Wnt/β-catenin pathway.

The review is careful to note that most of these findings come from in vitro or animal work, and it repeatedly frames curcumin as a compound under investigation rather than an established therapy.

• Early human trials show activity but remain preliminary — In one phase 2 trial cited by the researchers, 21 patients with advanced pancreatic cancer received 8 grams of curcumin orally per day for 8 weeks. Two patients showed clinical evidence of biological activity, with one maintaining stable disease for more than 18 months and another experiencing a brief but significant tumor regression.

A phase 1 trial combining curcumin with the chemotherapy drug docetaxel in advanced breast cancer reported that 6 grams per day alongside standard docetaxel was feasible and generally well-tolerated; as an early-stage trial, it was designed to assess safety and dosing rather than to establish effectiveness.

The National Cancer Institute (NCI) strikes a similar note of cautious interest. In its review of the evidence, the NCI reports that results from early-phase trials of curcumin in the chemoprevention of colon, oral, and hepatic cancers "appear promising." However, they note that these early trial results "have to be confirmed in well-powered trials evaluating safety and effectiveness as indicated by modulation of clinical outcomes."⁷

The same review is careful to state that the evidence is "currently inadequate to recommend curcumin-containing products for the treatment of cancer."

• The safety profile is generally favorable, with specific cautions — Curcumin has been characterized as "generally safe" by the U.S. Food and Drug Administration (FDA) — a designation that reflects its status as a food ingredient rather than an endorsement as a cancer therapy. With that distinction in mind, dose-escalation studies cited in the review found that consuming up to 12 grams daily produced no damaging effects.

In a separate study of patients with solid tumors, curcumin taken for eight weeks at 900 milligrams (mg) per day was likewise well-tolerated, with mild gastrointestinal upset the only reported effect.

However, the review does flag several caveats. Curcumin has strong iron-chelating activity that produces iron depletion in young mice, it has anticoagulant properties that may increase bleeding time, and it can inhibit certain cytochrome P450 enzymes, meaning it may interact with some treatments. The Mayo Clinic also advises caution when it comes to taking curcumin, as it may affect the efficacy of "certain medications, including some chemotherapy drugs."⁸

• Poor bioavailability is the central obstacle — The review also points out the downsides of curcumin, such as poor water solubility, low absorption, and rapid metabolism, so even at 12 grams per day, its bioavailability remains exceedingly poor.

In one study, free curcumin could be detected in the plasma of only 1 of 12 volunteers after a 10-to-12-gram dose. Researchers have developed formulations — micelles, nanoparticles, and lipid-based carriers — to raise absorption, and the review reports these approaches can help increase plasma levels.

1. Feed your cells their preferred fuel — Glucose, not fat, is the ideal fuel your cells run on most efficiently, and chronically starving your body of carbohydrates can drive reductive stress and lower energy production at the cellular level. Aim for roughly 250 grams of targeted carbohydrates a day if you are a typical adult, and more if you are very active. Whole fruits and well-cooked white rice are a sensible starting point for most people.

2. Cut linoleic acid (LA) and drop the seed oils — Industrial seed oils (also called vegetable oils) are the largest dietary source of LA, an omega-6 fat that accumulates in your tissues over time and may compromise mitochondrial function. Work toward keeping LA intake under about 5 grams a day by cooking with stable saturated fats such as tallow, ghee, and grass fed butter.

It's also important to steer clear of the packaged and restaurant foods where seed oils hide. This one change targets one of the core burdens on cellular energy production.

3. Treat turmeric as a spice, not a high-dose drug — According to MSK's integrative medicine specialist Jason Hou, using turmeric in your cooking is widely considered safe and is a fine way to enjoy it. But on the other hand, concentrated curcumin capsules are a different matter. Hou stresses that they can interfere with certain medications.⁹

Product quality also varies widely, and high intakes have been linked to liver problems in some people.¹⁰ If you are in active cancer treatment or take prescription drugs, talk with your health care provider before adding any curcumin or turmeric supplement.

4. Optimize your vitamin D, ideally through sensible sun exposure — Vitamin D acts as a powerful regulator of gene activity and supports the cellular energy pathways your body relies on. Sensible sun exposure around solar noon is the preferred way to build your levels, with an optimal range of roughly 60 to 80 nanograms per milliliter (ng/mL). Because getting there safely depends on your starting point, talk to your health care provider about whether 25(OH)D testing is appropriate for you.

5. Rebuild gut function so your body can use whole foods — Many people carry a compromised gut microbiome, and jumping straight to high-fiber foods can backfire by raising endotoxin levels. For most people, well-cooked white rice and whole fruits are a sensible first step.

If your gut is more significantly compromised, ease in gradually — starting with gentler options like fruit juice with pulp before progressing to whole fruits and then starches such as white rice as your digestion improves. Pair this with everyday movement, such as aiming for about an hour of walking a day, to further support metabolic health.

• Risk-taking increased gradually rather than all at once — The researchers used a task that required participants to inflate virtual balloons, with each additional pump increasing both the possible reward and the chance that the balloon would burst. Participants could stop and collect their earnings at any point. Both posture groups became more willing to pump the balloons as the experiment progressed, but that increase was noticeably steeper in the expansive group.

That time pattern is important. The groups didn't simply begin the experiment with dramatically different behavior. Instead, their choices separated progressively across repeated decisions. The difference between groups across trials was statistically significant, and a second analysis of how risk-taking changed over time supported the posture effect.

• Greater risk didn't translate into worse performance — Taking more risk sounds negative, but the results were more nuanced. Researchers examined not only how far participants pushed the balloons but also how often balloons burst and how much money participants earned. This allowed them to distinguish greater willingness to accept risk from simple carelessness.

The expansive group earned more overall, while the number of exploded balloons didn't differ between groups. In practical terms, the more upright participants weren't simply clicking recklessly. They accepted more risk without suffering more failures on the task, suggesting that posture influenced the way they balanced risk against reward.

• Actual neck position mattered more than a simple posture label — Mood results also revealed an important distinction. The researchers didn't find a straightforward overall effect in which everyone assigned to the expansive setup automatically felt better. Instead, actual neck angle helped explain changes in pride.

Neck angle also predicted changes in emotional valence — essentially, how positive or negative participants felt. It didn't, however, predict emotional arousal, which reflects how activated or energized a person feels rather than whether those feelings are pleasant or unpleasant.

This tells you why simply commanding yourself to "sit up straight" misses part of the story. People respond differently to the same physical setup. Measuring what the body actually did captured differences that a basic upright-versus-slumped label could overlook.

• The effects remained when people didn't know posture was being tested — Most participants reported little or no awareness that the experiment was altering their posture. Researchers went a step further and repeated their analyses using only participants who reported no awareness whatsoever that tablet position was manipulating how they sat.

The general pattern for mood and risk-taking remained, although the smaller group reduced the statistical strength of some comparisons.

That finding strengthens the real-world relevance of the experiment. You don't have to consciously think, "I'm adopting an expansive posture," for your physical environment to affect how you hold yourself. The researchers specifically noted that common features such as desk height and chair ergonomics could influence mood or behavior through these subtle posture changes.

• The results are useful, but they don't apply equally to everyone yet — The researchers acknowledged several limitations. Participants came mainly from a student population in Canada, most were young women, and the study wasn't preregistered, meaning the research plan and analyses weren't formally recorded publicly before the experiment began.

The authors also noted that posture research has faced replication problems, so these results need to be viewed alongside additional studies rather than treated as definitive proof by themselves.

There was another practical complication: People slump differently. Some participants lowered their heads toward the tablet, while others leaned forward from their hips. Both counted as contracted positions under the study's neck-angle measurement, yet those positions aren't necessarily identical in how they affect you.

1. Raise your screen to support a naturally upright position — Start with the environmental factor tested in the study: screen height. If you spend hours at a computer, position your monitor so you don't have to repeatedly lower your head or bend forward to see it.

Pay attention to what your body actually does after you settle into your normal work. If your head gradually drops or your upper body folds toward the screen, your setup is still encouraging a contracted position. Adjust it until you're able to look forward comfortably without forcing yourself into a rigid pose.

2. Stop working with your laptop or tablet in your lap — A device positioned far below your natural line of sight encourages you to look down. If you regularly work from a couch, bed or chair with your device on your legs, raise it onto a stable surface that allows you to keep your head and upper body more upright.

You don't need to turn good posture into an all-day test of willpower. Make the physical environment do more of the work for you. The study demonstrated that changing tablet height was enough to naturally produce differences in how participants positioned their bodies.

3. Hold your phone at eye level instead of looking down at it — The study tested tablet height, but the same principle applies every time you check your phone. Holding it low, which is what most people do, drops your head forward and loads your neck with significantly more force than a neutral position. When you're reading, scrolling or texting, bring the phone up to your line of sight rather than dropping your chin to meet it.

Better yet, reduce the time you spend on your phone in the first place. Every minute you cut from unnecessary scrolling is a minute your neck and upper body aren't being pulled into a contracted position. It's one of the simplest ways to protect your posture, not by fixing how you hold the device, but by picking it up less often.

4. Adjust your entire workstation instead of focusing only on your neck — Your screen is only one part of the equation. Look at how your desk and chair work together because the researchers identified desk height and chair ergonomics as everyday environmental factors that influence posture.

If you're a desk worker, sit down exactly as you normally would and notice what happens without correcting yourself. Your goal isn't a stiff, exaggerated "power pose." You want a setup that makes an open, comfortable position feel natural rather than something you have to consciously maintain.

5. Stand up and take regular breaks from sitting — Even with a well-designed workstation, you don't want to remain seated in one position for hours. Stand up and take regular breaks from sitting throughout your day. Use natural stopping points — finishing an email, completing a call or wrapping up a task — as cues to get out of your chair.

If you're a desk worker, make these breaks part of your routine instead of waiting until your neck or back feels stiff. Stand, walk around briefly and change your body position before returning to work. This gives your body a simple reset and prevents good posture from becoming another form of prolonged, static sitting.

6. Support your spine while you sleep — Your posture doesn't stop mattering when your workday ends. Your sleep setup gives your spine several hours to recover from the positions you hold during the day, so arrange your bed to keep your neck and spine comfortably supported. If you sleep on your side, place a pillow between your knees. If you sleep on your back, elevate your legs with a wedge to take pressure off your spine.

Your pillow matters as well. A cervical pillow designed to support the natural curve of your neck without pushing your head too far forward can help maintain a more neutral posture during sleep. The goal is the same day and night: Shape your environment so your body doesn't have to fight against it.

• The rise of industrialized food production — With industrialization, food production shifted dramatically from traditional methods. This introduced refined sugars, seed oils, fortified grains, and mass-produced convenience foods.

• Modern diets lost their nutritional foundation — Industrialized food production has stripped meals of their original nutritional value and replaced nutrient-dense staples with calorie-rich but micronutrient-poor substitutes.

• The mismatch between biology and diet — Despite your biological need for the same essential nutrients, the modern diet bears little resemblance to the diverse, traditional whole-food-based diets that once sustained human health.

• Organ meats were central to traditional cooking — Historical cookbooks and records from the 1700s to the early 1900s, such as “The Lady's Assistant for Regulating and Supplying the Table” from 1787, highlight the widespread use of organ meats in cooking, as seen in the images below.³

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• Bone broths supported gut, joint, and skin health — Bones were also simmered into broths and soups, which provided collagen and amino acids.^4,5 Today, these have been largely abandoned in favor of boneless, skinless, fat-free cuts that offer far less nutrition.

• Saturated fat was once embraced, not feared — Ancestral diets also included ample amounts of saturated fat, which was not feared but recognized as an essential part of a well-rounded diet. The vilification of saturated fat in the 20th century stemmed from the flawed Diet-Heart Hypothesis by Ancel Keys, which inaccurately linked it to heart disease.

• Seed oils replaced animal fats, but with consequences — This led to the widespread replacement of animal fats with high-PUF (polyunsaturated fats) vegetable oils.⁶

• Debunking the Diet-Heart Hypothesis — Mounting research has challenged Keys' claim. For example, a 2016 re-evaluation of the Diet-Heart Hypothesis found that while replacing saturated fats with vegetable oils lowered cholesterol, it did not reduce the risk of heart disease or overall mortality.⁷

In reality, higher consumption of these oils is associated with an increased risk of Type 2 diabetes.⁸ Explore the full impact of seed oils on your metabolic health in “Linoleic Acid — The Most Destructive Ingredient in Your Diet.”

• Carbohydrates were eaten year-round for steady energy — Carbohydrates were often preserved in the form of jams, jellies, and dried fruits to ensure a steady supply of energy regardless of the season.¹⁰ Winter diets included potatoes, apples, and fermented vegetables, while summer brought fresh berries, melons, and other fruits.

• Ancestral diets maintained macronutrient balance — Unlike modern low-carb diet trends that promote extreme restriction, ancestral diets maintained a balance of macronutrients that supported metabolic health.¹¹

• Whole grains were soaked or fermented for digestibility — Whole grains were a dietary staple, soaked or fermented to improve digestibility and nutrient absorption. They were vastly different from the genetically modified, pesticide-laden varieties that are available today.

• Traditional baking relied on clean, heritage grains — Bread and baked goods were made from non-GMO flours without the addition of synthetic vitamins and minerals, which preserves the integrity of the original ingredients.

• Vegetables were cooked, not eaten raw — Vegetables were another important component of ancestral diets, but unlike the modern trend of raw, fiber-heavy salads, vintage cookbooks consistently showcase recipes that emphasize roasting, steaming, and stewing vegetables. Traditional food preparation methods improved digestibility and reduced antinutrients that interfere with nutrient absorption.¹²

• Sugar was used, but in traditional forms — Sugar, also vilified in modern diet culture, was a regular part of ancestral eating. However, it came in the form of minimally processed cane or beet sugar, honey, and fruit-based desserts rather than artificial sweeteners or high-fructose corn syrup.

• Desserts were homemade with nutrient-dense ingredients — Desserts, such as fruit pies, rice puddings, and custards, were made with whole ingredients like pasture-raised butter, low-PUF eggs, and full-fat dairy, without the industrial additives found in today's processed sweets.¹³

• Three meals a day provided consistent nourishment — Many cookbooks featured meal plans, often referred to as “Bill of Fares,” outlining three daily meals. Below is an example from “The Queen of the Household,” published in 1896.

• Industrially processed foods were absent — Perhaps the most significant contrast between ancestral diets and modern eating habits is the complete absence of industrially processed foods. Everything was made from scratch using whole ingredients, with no reliance on packaged convenience foods.

• Cooking was a daily practice rooted in tradition — Food preparation was not seen as a chore but as a daily rhythm embedded in family life and cultural tradition. Meals were prepared with care, using methods passed down through generations.

• Modern diets have abandoned balance and real food — The modern diet has strayed far from the nutrient-dense, balanced approach that sustained our ancestors for generations, and this has led to the explosion of metabolic dysfunction, obesity, and chronic disease.

• Restoring ancestral principles is essential for health — Without a return to traditional dietary principles built on real food, balanced meals, and nutrient-dense ingredients, these health problems will likely continue to worsen.

• Resting metabolic rate has declined since the 1800s — According to an article published in Current Biology,¹⁴ Americans' resting metabolic rate (RMR) — the total number of calories burned when your body is at rest — has declined by approximately 6% since 1820. This decline translates to roughly 27 fewer minutes of moderate-to-vigorous physical activity per day.

• Lower body temperatures reflect reduced metabolic activity — The study suggests that body temperature, which is directly linked to metabolic rate, has steadily declined over the past two centuries. This serves as a physiological marker of reduction in activity. As physical exertion reduced, metabolism became less efficient, which contributed to the rise of obesity, insulin resistance, and other metabolic disorders.¹⁵

• Occupational shifts drove the loss of daily exertion — Much of this decline is a result of changes in occupational demands. In the 19th century, most jobs required sustained physical effort, with farming, manufacturing, and construction involving prolonged manual labor.

• Work-related energy expenditure dropped sharply — Historical data reconstructed from U.S. Census Bureau statistics show that the average metabolic equivalent of work — measured in METs, a unit representing energy expenditure relative to RMR — has declined by about 25% since 1870.¹⁶ Early industrial workers, for example, frequently performed energy-intensive tasks, whereas modern jobs often involved prolonged sitting with little physical exertion.

• Sedentary lifestyles disrupt metabolic health — The widespread transition to office-based employment and reliance on labor-saving devices has significantly altered how energy is used, shifting populations toward more sedentary patterns that negatively affect metabolic health.

• Loss of outdoor exposure weakened immune resilience — Beyond the loss of movement, this transition has also cut people off from the immune-boosting and anti-inflammatory benefits of exposure to nature.¹⁷ Time spent outdoors has been associated with lower inflammation and better immune regulation.

• Green spaces activate key immune pathways — Without regular interaction with nature, you miss out on key biological stimuli that once conditioned the body for resilience. For instance, research shows that spending time in green environments like forests increases natural killer (NK) cell activity, reduces inflammatory cytokines, and even improves lung function in those with asthma.¹⁸

• Outdoor activity supported optimal vitamin D levels — Daily outdoor activity allowed past generations to naturally produce adequate vitamin D, an important nutrient for bone strength, immune function, and metabolic health.¹⁹ In contrast, modern lifestyles that keep people indoors have led to widespread vitamin D deficiency.²⁰

• Food, water, and air were free from synthetic pollutants — Historically, food was free from synthetic pesticides, herbicides, and chemical preservatives. Water sources were not laced with pharmaceutical residues, chlorine byproducts, or microplastics. Air pollution did not include the modern toxic mix of vehicle emissions, industrial waste, and volatile organic compounds (VOCs) from everyday household products.

• Plastics and chemical disruptors are a modern burden — Plastics, heavy metals, and endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA), phthalates, per- and polyfluoroalkyl substances (PFAS), and dioxins, are modern inventions that have become unavoidable.

Their widespread presence has been linked to metabolic disorders, reproductive issues, and neurodevelopmental abnormalities.²¹ Even infants are now exposed to chemical contaminants from birth.^22,23

• Fortification created hidden health problems — One of the greatest public health deceptions has been the so-called fortification of food with iodine, iron, and fluoride under the guise of disease prevention. Instead of addressing nutrient depletion caused by industrialized agriculture and environmental degradation, these interventions have introduced new health burdens.

• How iodine, iron, and fluoride additives backfired — Iodine, carelessly added to salt, has contributed to autoimmune thyroid disorders and metabolic dysfunction.²⁴ Meanwhile, the indiscriminate addition of iron to processed foods has been associated with iron overload.²⁵ Fluoride, falsely promoted as essential for dental health, has been linked to neurotoxicity and thyroid dysfunction.^26,27

• Chemical treatments accelerate health decline — The modern approach of treating toxic overload with more chemicals and medical band-aids only accelerated our health decline. The solution is not more fortification or synthetic interventions, but rather the removal of unnecessary toxins from our food, water, and air.

• Evening environments supported deep rest — Before electricity, people relied on fire, candles, and oil lamps for illumination, all of which emitted warm, red-toned light that did not interfere with melatonin production. The absence of artificial distractions also encouraged relaxation, storytelling, and social bonding, which reduced stress and prepared the nervous system for deep sleep.

• Daily sunlight exposure included near-infrared light — Natural sunlight contains a full spectrum of wavelengths, including near-infrared (NIR) light. Regular exposure to NIR during daylight hours helped stimulate mitochondrial function and supported melatonin production inside the cells. Mitochondrial melatonin plays a key role in reducing oxidative stress and enhancing the body's repair processes during sleep.

• Blue light disrupts your circadian rhythm — Modern living has introduced technologies like artificial lighting, especially the blue light emitted from screens, which delays melatonin release and disrupts your body's internal clock. Instead of winding down with the setting sun, you remain artificially stimulated late into the night, which leads to poor sleep quality, disrupted hormone balance, and metabolic dysfunction.³⁰

• Electromagnetic fields (EMFs) are a modern threat to restorative sleep — EMFs are another major disruptor of natural rest patterns that previous generations never had to contend with. Wi-Fi routers, smartphones, and other electronic devices now flood the environment with EMFs, which interfere with your body's natural electrical signaling.

• EMF exposure weakens mitochondrial function — Research suggests that exposure to EMFs may suppress melatonin production, disrupt deep sleep cycles, and increase oxidative stress. Over time, this constant exposure has been linked to weakened mitochondrial function, inflammation, and reduced capacity for repair during sleep.³¹

• Modern life has dismantled foundational health habits — Modern conveniences have made daily life easier, but at the cost of the very foundations that sustained human vitality for generations. Diets are now dominated by ultraprocessed foods, movement has been replaced by sedentary habits, and environmental toxins infiltrate every aspect of daily life. These shifts have sabotaged cellular health and fueled an epidemic of chronic disease.

• Reversing decline starts with removing modern disruptors — To reclaim health, you must eliminate harmful influences that didn't exist for past generations and restore the conditions that allow your body to function optimally.

• Ancestral wisdom supports optimal health — By understanding what worked for our ancestors, you can adopt habits that support mitochondrial health and metabolic efficiency instead of relying on a system designed to suppress symptoms rather than prevent illness.

• SSRIs were built on the idea that boosting serotonin would correct depression — Early marketing framed depression as a simple serotonin deficit that medication could normalize by blocking the reuptake of serotonin and raising levels at synapses. This explanation was widely embraced by the public and many physicians because it offered a simple and appealing solution — a chemical imbalance that could be fixed with a pill.

• This theory was never supported by definitive scientific evidence — Diagnoses are based on patient-reported symptoms and clinical interviews, not lab results or brain scans. The prescribing process became driven by checklists and diagnostic criteria, with little room left for nuance or context. Once a patient met enough criteria, a label was applied, and medication was initiated.

• Prozac's launch triggered a fundamental shift in psychiatric practice — Earlier approaches explored personal history, relationships, stressors, and meaning. After SSRIs became the dominant treatment, depression and anxiety were framed almost exclusively as medical conditions requiring pharmacologic correction.

• This change aligned with broader institutional incentives — Drug companies had a clear financial interest in promoting medication as the first and often only treatment option. The push to prescribe was supported by pharmaceutical sales teams, advertising, and continuing medical education courses funded by industry.

• FDA approval was based on short-term trials despite long-term use in practice — Most trials submitted for SSRI approval lasted only six to 12 weeks. These brief studies formed the evidence base for judgments about safety and effectiveness, even though patients in the real world take these drugs for far longer, often for many months, years, or decades.

• Over time, many patients find that the initial effects of SSRIs begin to wear off — When the brain adapts to the presence of the drug, the benefits that were once felt start to fade. This process, known as tachyphylaxis, is common with SSRIs, and Witt-Doerring noted that patients who experience this often return to their doctors reporting that their symptoms have returned.

• Escalation becomes the default response, leading to widespread polypharmacy — Instead of questioning the treatment itself, the usual response is to increase the dose, switch to a different drug, or add another medication. The assumption is that the illness has progressed, rather than the drug having lost its effect or causing a physiological dependency. This escalation leads to polypharmacy, a situation where multiple psychiatric drugs are prescribed at once.

• Long-term use often turns numbness into despair — Patients who remain on SSRIs for years report low energy, cognitive dullness, and difficulty feeling bonded to others. Witt-Doerring described his own patients who feel hollowed out and unable to reconnect with who they were before medication.

• Sexual function is especially vulnerable to these effects — According to Witt-Doerring, one of the most disturbing yet underrecognized side effects of these medications is post-SSRI sexual dysfunction (PSSD), a state in which patients experience persistent genital numbness, inability to feel pleasure, and persistent loss of sexual sensation even after discontinuing the drug.

• PSSD distorts a person's relationship to sexuality and identity — Witt-Doerring also shared that he sees patients who begin questioning their orientation not because their attractions have changed but because the ability to experience arousal or pleasure has vanished. This is especially confusing for those placed on SSRIs during adolescence when sexual identity is still forming.

• Despite international recognition, PSSD remains invisible in U.S. medicine — The European Medicines Agency requires SSRI labeling to state that sexual dysfunction can continue after treatment stops, yet the condition has no formal recognition in the United States.

Witt-Doerring noted that most physicians have never heard of PSSD, and those who have often avoid discussing it. Patients searching for answers are dismissed or misdiagnosed, leaving them without guidance, validation, or support.

• SSRI exposure during pregnancy has been linked to developmental risks — According to the interview, about 9% to 10% of pregnant women in the U.S. are taking antidepressants, often without being informed of the impact on their child. Animal studies, and some human studies, have reported altered sensory processing, changes in social behavior, and disrupted neurodevelopment in children exposed to SSRIs in utero.

• “The suicide rates are out of control in this population” — Witt-Doerring has spoken with families and individuals whose lives were devastated by SSRI-induced harm, including cases of suicide linked to PSSD and emotional blunting. Yet these deaths remain uncounted and unacknowledged, attributed instead to mental illness rather than to the medications.

• The interview also raised psychiatric drug effects as a factor in mass shootings — Witt-Doerring explained that SSRIs can trigger paradoxical side effects, in which the drug produces the opposite of its intended effect. Instead of reducing distress or calming the patient, these reactions may induce agitation, mania, aggression, or even suicidal thoughts and behaviors.

• The system doesn't meaningfully track these outcomes — Manufacturers submit adverse event reports to the FDA, yet many receive no individual follow-up. The evidence of drug-induced suicidality or violence often ends up buried in surveillance files or written off as anecdotal. With no follow-through, red flags go unaddressed, public warnings never materialize, and the same patterns repeat without correction or accountability.

• Tennessee makes a move to track the link between psychiatric drug use and school shootings — Tennessee has instituted a new law mandating post-incident reviews of whether the shooter was using antidepressants, stimulants, antipsychotics, or related medications.

These data have historically been withheld or redacted, making it impossible to study drug-related contributions to violence. This approach represents the first attempt to publicly track these links and prevent them from being buried.

• Benzo withdrawal often lasts far longer and cuts far deeper than SSRI withdrawal — Unlike SSRIs, which are usually tapered over weeks or months, benzodiazepine withdrawal can stretch on for years. Witt-Doerring treats patients experiencing protracted withdrawal syndromes marked by burning nerve pain, electric shock sensations, and intense physical discomfort.

Many develop akathisia, an inner restlessness so severe that patients describe it as psychological torture. The longer the exposure, the harder the withdrawal becomes.

• Benzo withdrawal has been linked to suicides — As the nervous system becomes profoundly dysregulated, basic functioning breaks down. The ability to return to baseline after stress collapses, leaving patients unable to work, sleep, or interact normally. Many become disabled during this process and require long-term, specialized care that is rarely available.

• Misdiagnosis during withdrawal deepens the injury — Prescribers frequently fail to recognize benzodiazepine withdrawal symptoms and often interpret them as a return of the original anxiety or panic disorder. Instead of supporting a careful taper, they restart the benzo or add new medications. This prolongs the neurological damage, extends dependence, and traps patients in a cycle that becomes harder to escape with each intervention.

• Even when the taper is successful, full recovery is uncertain — Witt-Doerring describes cases in which patients experience persistent cognitive deficits, emotional blunting, or physical pain long after the drug has left their system. The nervous system may eventually recalibrate, but for some, the damage appears to linger indefinitely.

• The severity of benzo-related harm remains largely hidden from public view — Despite the widespread focus on opioids, the suffering Witt-Doerring sees in patients withdrawing from benzodiazepines is equally severe. These are individuals who followed medical instructions as directed, yet ended up physically and neurologically altered by drugs they believed were safe.

• Stimulant use in school-aged children has become normalized and often encouraged — Many parents feel pressured to medicate their children after teachers report concerns about behavior or performance. Instead of examining root causes such as sleep quality, nutrition, home environment, or normal neurodevelopmental variability, the system suppresses outward behaviors with medication.

The result is short-term compliance in classrooms rather than true understanding or support of a child's needs.

• Tolerance, side effects, and medication escalation often follow — Children and adolescents frequently become tolerant to their prescribed dose, prompting dose increases or switches to other stimulants. This pattern is similar to the escalation seen with SSRIs and benzodiazepines, where the initial intervention sets off a cascade of further treatments. Many remain on stimulants for years despite minimal long-term benefit.

• Attention problems often stem from metabolic and lifestyle factors — Adults labeled with ADHD frequently show signs of insulin resistance or unstable blood sugar. Diets high in processed carbs can impair glucose delivery to the brain, leading to brain fog, irritability, low energy, and poor focus.

These issues are not typically explored in clinical settings, and patients are placed on amphetamines with no evaluation of metabolic health or nutritional status. For many, improving metabolic function and removing processed foods has a far greater impact on focus and mood, yet these interventions are seldom considered.

• Modern cannabis contains far higher THC levels than historical varieties — The cannabis of the past had much lower concentrations of THC, the psychoactive compound responsible for its intoxicating effects. Commercial growers and corporate cannabis interests have now pushed THC concentrations to levels that dramatically increase the risk of psychosis, mania, and paranoia.

• High-THC products can trigger first episodes of psychosis — Many of the patients Witt-Doerring treats for schizophrenia, bipolar disorder, or severe mood disturbances had their first break immediately after using potent cannabis. These episodes are often misdiagnosed as primary psychiatric illness rather than drug-induced reactions.

• Misdiagnosis leads to long-term psychiatric labeling and medication — Once a patient is hospitalized after a cannabis-related psychotic event, the role of cannabis is rarely revisited. Instead, they are placed on antipsychotics and other psychiatric drugs, often for life, based on a diagnosis that never acknowledges the trigger.

• Financial incentives push the FDA toward rapid drug approval rather than public protection — Witt-Doerring, who worked inside the FDA's Division of Psychiatry, saw firsthand how this dynamic influenced decision-making.

• Academic psychiatry has been drawn into the same system of influence — Leading journals, university researchers, and prominent clinicians often maintain close financial ties to pharmaceutical companies through grants, consulting fees, and speaking honoraria.

As Witt-Doerring noted, industry shapes what gets studied, what gets published, and what messages reach clinicians and the public. When academia adopts industry framing rather than challenging it, it abandons its duty to question assumptions and protect patients from harm.

• Direct-to-consumer platforms have widened access to SSRIs with minimal oversight — Companies like Hims and Hers now prescribe psychiatric drugs online after brief questionnaires. These services began as lifestyle brands offering treatments for issues like erectile dysfunction or hair loss. However, they now distribute mind-altering medications with no live consultation, a questionnaire in place of a clinical interview, and minimal follow-up.

The result is an easy-entry pipeline into psychiatric drug use for people who have never received formal mental health care.

• Government policies are expanding psychiatric labeling and drug access for children — Illinois recently passed a law requiring statewide mental health screenings beginning in third grade. Witt-Doerring pointed out that such policies accelerate the pathologizing of everyday childhood behaviors.

1. Reduce linoleic acid (LA) in your diet — This polyunsaturated fat (PUF) accumulates in your tissues, damages mitochondria, and disrupts mood regulation. It's found in vegetable oils, such as soybean, corn, and sunflower oil, as well as ultraprocessed foods. Swap out these items with real, whole foods, as well as saturated fats like grass fed butter, ghee, or tallow when cooking.

Keep your LA intake between 2 and 5 grams a day. To track your intake, I recommend you sign up for Pax. It has a feature called the Seed Oil Sleuth, which monitors your LA intake to a tenth of a gram so you can stay in charge of your metabolism.

2. Rebuild your gut to support mood and immunity — Your gut and brain are deeply connected, and when your gut microbes are out of balance, inflammation rises, worsening symptoms of depression. To keep your cells producing energy efficiently, your body needs about 250 grams of carbohydrates each day. If you're active, you need even more. However, loading up on fiber too quickly can overwhelm your gut, trigger endotoxin release, and make things worse.

Start with easy-to-digest carbs like fruit and white rice. As your digestion improves, gradually add root vegetables and well-cooked legumes. Once your gut is more stable, you can introduce whole grains that you tolerate well.

3. Move regularly, gently, and consistently — Physical activity helps regulate neurotransmitters and improves energy production. One umbrella review of 97 meta-analyses found physical activity reduced symptoms of depression and anxiety, with effects comparable to or slightly greater than those reported separately for medication and psychotherapy.¹⁷

Prioritize daily walking and light strength training to support circulation, oxygenation, and lymphatic flow. Even 20 minutes outside makes a difference. Gradually work your way up to one hour daily for best results.

4. Get daily sun exposure to power your mitochondria — Morning sunlight stimulates your mitochondria to produce adenosine triphosphate (ATP), the energy your body runs on, while reinforcing your circadian rhythms. Expose your skin and eyes to early daylight each day. Avoid midday sun exposure until you've eliminated seed oils for at least six months. This gives your skin time to rebuild its resilience and reduce oxidative stress.

5. Support recovery with rest and routine — Your body handles stress and repairs better when your days are steady. Keep consistent sleep and meal times to stay aligned with your circadian rhythm. In the evening, dim lights after sunset and avoid screens close to bedtime to support high-quality sleep.

6. Increase your GABA levels safely — If you're considering supplements, GABA may be one option to explore. Unlike psychiatric drugs that interfere with complex brain chemistry, GABA works with your body's existing calming pathways. Doses around 100 milligrams have been the most studied for anxiety and sleep, with one insomnia trial using 300 milligrams daily.

A systematic review of the human trials describes the evidence as limited.¹⁸ Combining GABA with L-theanine, an amino acid that raises GABA levels, can further enhance these effects. To learn why GABA offers a safer and more effective path than SSRIs, read “SSRI Drugs Can Cause Chronic Fatigue Syndrome.”

1. Prioritize vitamin K2-rich foods — Incorporate natto (fermented soybeans), by far the richest source of the MK-7 form of K2, which remains in your body for extended periods. Most other fermented vegetables contain much smaller amounts.

Certain cheeses, including Brie, Munster, and Gouda, also provide vitamin K2. If you’re getting these products, make sure they’re certified raw-milk cheeses made with animal rennet. Grass fed organic animal products, including egg yolks, liver, butter, tallow and raw dairy products, are also good sources of vitamin K2.

2. Align K2 intake with healthy fats — As vitamin K2 is fat-soluble, it should be consumed alongside healthy fats such as grass fed butter or tallow to enhance absorption. This may help your body make better use of this nutrient for bone and cardiovascular health.

3. Harmonize K2 with complementary nutrients — Vitamin K2, vitamin D, magnesium, and calcium work together as an interconnected system in calcium metabolism. Calcium is the main structural mineral of bone. The active form of vitamin D, 1,25-dihydroxyvitamin D, is the primary hormone controlling how much dietary calcium the intestine absorbs.⁵⁰ Magnesium supports this process upstream, because the liver and kidney enzymes that convert vitamin D into its active forms use magnesium as a cofactor.⁵¹ In a randomized trial, magnesium supplementation changed blood vitamin D levels in a pattern that depended on participants’ starting vitamin D status.⁵² Vitamin D also increases production of vitamin K–dependent proteins, including osteocalcin in bone and matrix Gla protein (MGP) in blood vessel walls, and these proteins need vitamin K to become biologically active.⁵³ Activated MGP is a key natural inhibitor of calcification in soft tissues, and mice lacking MGP develop severe arterial calcification.⁵⁴ In human trials, vitamin K2 supplementation consistently increases MGP activation, shown by lower circulating levels of its inactive form.⁵⁵,⁵⁶

4. Choose supplements carefully — If you choose to use supplements, look for those containing the MK-7 form of K2. There is no official recommended daily intake for vitamin K2; a practical guide is about 180 micrograms of K2 for every 5,000 IUs of vitamin D3 you take. Take supplements with meals that include healthy fats to support absorption. Again, if you take warfarin or another blood thinner, check with your doctor first.

• Healthy young adults completed exercise sessions before testing the meals — The study involved 16 healthy, physically active adults (average age of 25 years old) who performed a single bout of leg resistance exercise before consuming their assigned meal, with each pork meal providing 20 grams of protein.² Participants then underwent repeated blood draws and muscle biopsies, giving researchers detailed data on real-time muscle repair responses.

• Low-fat pork produced the strongest improvement in muscle-building activity — The low-fat pork meal triggered a sharper rise in myofibrillar protein synthesis, which is the process your body uses to repair and build muscle tissue after you train.

In contrast, the high-fat pork meal muted this muscle-building response so much that it was not statistically different from the carbohydrate drink, even though it still raised muscle-building activity above resting levels. That suggests the fat in the meal can blunt how strongly your muscles respond to the protein you just ate, even if the amount of protein is identical.³

• The most meaningful improvement was the faster leucine surge — Researchers reported that the low-fat meal produced a higher peak in essential amino acids and a faster, higher peak in leucine, compared to the high-fat meal.

Leucine is thought to act like an ignition switch for muscle repair — the researchers refer to this as the "leucine trigger" hypothesis — and in this featured study, higher peak leucine levels were moderately linked to a larger rise in muscle-building activity. With the high-fat meal, this leucine rise was delayed and smaller, which may have weakened the muscle-building signal. Notably, the total amount of amino acids that reached the bloodstream over five hours was similar for both pork meals, so the difference appears to lie in how quickly and how high amino acids peaked rather than in how much protein was absorbed.

• Slower digestion is the researchers' leading explanation — The researchers did not measure digestion directly, but they point to earlier published literature showing that fat slows gastric emptying, meaning food leaves the stomach more slowly, which would delay amino acid delivery into your bloodstream. In this featured study, leucine peaked at about 129 minutes after the high-fat meal versus about 90 minutes after the low-fat meal. If you train hard, that potential timing mismatch is worth keeping in mind when you plan your post-workout meal.

• Signaling pathway data did not explain the difference — In an additional analysis that was not part of the study's preregistered plan, the researchers measured signaling proteins involved in muscle repair. A key marker rose after exercise regardless of which meal was eaten, and the other markers varied without a consistent advantage for the low-fat meal. The authors concluded that this signaling data "provided very little mechanistic insight" and that differences in blood amino acid levels were most likely the main factor behind the stronger response to the low-fat meal.

• Most of the research involved healthy, physically active adults — The body composition section focused on people who had been training regularly for more than three months, mostly healthy young adults doing resistance or endurance training, although the review also drew on studies in physically active older adults and adolescent athletes.

Results varied across studies. Several trials found greater gains in lean mass or greater fat loss with higher protein intake, while others found no added benefit, and a few showed favorable changes in markers of bone turnover. Taken together, the authors concluded that a high-protein diet "appears to increase muscle accretion and fat loss and may have beneficial effects on bone when combined with exercise."*

The Recommended Dietary Allowance (RDA) is set at 0.8 grams of protein per kilogram of body weight, but many of the beneficial outcomes appeared at intakes two to three times higher. But, in my view, most adults actually need about 0.8 grams of protein per pound of ideal body weight (or about 1.76 grams per kilogram).

• The clearest benefits involved lean mass and body fat — The review found that eating more protein tended to produce greater gains in lean mass, meaning participants often added more muscle tissue when they trained with higher protein intake. The authors described the overall effect on lean mass as "small but beneficial," and cited a meta-analysis of 49 studies with 1,863 participants in which protein supplementation significantly increased "fat-free body mass" across a range of training programs.

In several trials, fat mass also fell more in the higher-protein groups, although the authors note that the evidence for fat loss is more limited. They point to possible mechanisms that include higher resting and sleeping energy expenditure and increased thermogenesis. For those unfamiliar, thermogenesis refers to your body's ability to generate heat by burning calories, including during digestion.

• Effects on strength and recovery were less consistent — Most of the trials that were reviewed found no added strength gains from higher protein intake. Results for protein eaten before sleep were also mixed — in one 12-week trial involving recreationally active young men who trained in the evening, a pre-sleep protein drink led to greater gains in strength and muscle size, while several other trials found no difference. In another study of professional soccer players, pre-sleep protein improved muscle soreness and other recovery measures after night matches.

The review notes that pre-sleep protein "seems to improve recovery from late-evening exercise," although the authors also say its role "is not entirely understood" and that it may help mainly by adding to your total daily protein intake. If you train in the evening, one strategy worth considering is using pre-sleep protein to "extend" your anabolic window.

• Protein feedings raise muscle protein synthesis, including overnight — In theory, these repeated rises can support greater muscle building over time, although the authors caution against extrapolating these short-term "snap-shot" findings to long-term results. Protein also enhances nitrogen balance, which reflects how effectively your body retains amino acids for tissue repair.

Nitrogen balance improves when you consume enough protein to exceed the amount your body breaks down. That said, a positive balance is generally considered a sign that your body is in a state that favors building and repairing tissue.

• Protein's thermic effect may play a role in fat loss — Higher protein intake elevates diet-induced thermogenesis, meaning your body expends more energy digesting protein than digesting fat or carbohydrates. This effect may support fat loss by modestly increasing total daily energy expenditure.

1. Choose lean, low-LA protein within an hour after training — If you want to support recovery, choose protein sources that are both low in fat and naturally lower in LA. As mentioned earlier, I do not recommend pork or chicken, as both tend to accumulate high levels of LA. High-fat meals may also slow digestion and delay amino acid delivery, which, in the featured The American Journal of Clinical Nutrition study, was linked to a weaker muscle-building response.

Lean, low-LA options such as grass fed beef, bison, or a high-quality whey isolate can give your muscles rapid access to the amino acids they need while helping limit the oxidative stress associated with excessive LA intake.

2. Get enough high-quality protein — and balance it with collagen-rich sources — If you deal with tightness, stiffness, or slow recovery, increasing your protein intake gives your body the raw materials it needs for both muscle repair and connective tissue support. Most adults do best with about 0.8 grams of protein per pound of ideal body weight (about 1.76 grams per kilogram).

Red meat provides excellent complete protein, but muscle meat alone is relatively low in certain amino acids important for tendon, ligament, cartilage, and fascia health.

To fill this gap, make sure roughly one-third of your protein comes from collagen-rich sources such as bone broth, pure gelatin powder without additives, oxtail, shanks, or grass fed ground beef that includes connective tissue. These foods supply glycine, proline, and hydroxyproline — amino acids that serve as building blocks for connective tissue and have been studied for their roles in joint health, inflammatory balance, and sleep quality.

3. Spread your protein evenly across your day — If most of your daily protein ends up at dinner, shifting toward even distribution may help your body stay in repair mode for longer. Some research suggests that your muscles may respond more effectively when amino acids arrive in regular intervals rather than in one large meal, although the review cited above notes it is not yet clear how much protein timing matters for body composition. By having balanced portions at breakfast, lunch, your post-exercise meal, and dinner, you may support steadier energy, stronger recovery, and higher training output.

4. Use protein before sleep if your goal is faster progress — with one important caveat — If you're training intensely or feeling sore longer than you'd like, a small early-evening protein serving may support overnight repair. I normally advise avoiding food for at least three hours before bed, because late eating disrupts metabolic rhythms and interferes with natural nighttime repair. That remains the preferred rule.

If you want the added recovery benefit, finish this serving two to three hours before bed so digestion is complete before you lie down. Grass fed, raw yogurt or pure gelatin powder stirred into warm herbal tea can supply a steady drip of amino acids into the night. This may help you wake up less sore and more ready for training — without disrupting your circadian rhythm.

5. Keep your post-workout meal simple so your body absorbs amino acids without competition — If you load your plate with large, complex meals after training, your digestive system has more to process at once, which may slow how quickly amino acids reach your bloodstream. Many people find that a streamlined, easy-to-digest post-exercise meal works best.

• Adult stress switched genes on differently in primed animals — Researchers compared mice whose brains had been experimentally primed during development with control mice after both groups experienced stress as adults. In the control mice, adult stress generally reduced gene activity in the VTA. In the primed mice, many genes that stress normally quieted became more active instead.

These genes were involved in several basic cell functions, including controlling other genes, sending signals between cells, supporting the material surrounding cells and regulating immune activity. Early-life stress, in other words, didn't simply make the brain "more stressed." It changed how brain cells were prepared to respond when another stressful event arrived.

• The heightened stress response affected social behavior — Researchers then exposed both groups of mice to a relatively mild social stressor in adulthood to see whether the earlier priming made a measurable difference. Social interaction declined specifically among the mice whose brains had been primed earlier in life.

Stress also increased the number of these mice classified as vulnerable to stress and reduced the number classified as resilient. The same pattern wasn't found in the control mice.

Both male and female mice showed this greater sensitivity. That suggests the effect wasn't limited to one sex in this experiment. However, these behaviors are laboratory measures of stress sensitivity in mice and aren't the same as diagnosing anxiety or depression in people.

• Stress also changed how freely the mice explored — Researchers placed the mice in an unfamiliar open space and measured their behavior. After adult stress, the primed mice spent less time exploring the center of the space, while control mice didn't show the same change.

Combined with the social-interaction results, this showed that heightened stress sensitivity appeared in more than one type of behavior. Even a relatively mild adult stressor produced clearer behavioral changes when the animals had already been primed during development.

• Dopamine-producing brain cells became easier to activate after stress — Researchers also measured the electrical activity of dopamine neurons. After adult stress, dopamine neurons in the primed mice shifted to a hair-trigger state, sitting closer to the firing threshold, so less stimulation was needed to set them off. Stress made these brain cells easier to activate.

Importantly, the neurons weren't constantly overactive beforehand. The difference became apparent after the animals encountered stress. This helps explain the idea of priming: An earlier experience prepared the brain to react more strongly, but a later stressful event was needed to bring that heightened response into view.

• Reducing the molecular change weakened the heightened response — Researchers then tested the process in reverse. In mice exposed to early-life stress, they reduced the activity of the enzyme responsible for one of the key molecular changes identified in the study. Doing so prevented the exaggerated stress response in dopamine neurons. In normally raised mice, the same intervention didn't significantly change the neurons' basic activity.

Testing the pathway in both directions strengthened the evidence that it played a direct role. Increasing the molecular change made later stress responses stronger, while reducing it weakened effects associated with early-life stress. Still, the researchers emphasized that this pathway represents only one part of the brain's much broader response to early adversity, and further research will determine how closely these findings translate to humans.

The mouse study traced one molecular pathway in one brain region. But human research paints a broader picture of what early adversity can set in motion, and the range of health consequences it's been linked to extends well beyond the brain's stress circuitry.

• Childhood adversity is linked to serious health risks later in life — Prolonged stress has consequences that extend far beyond how you feel in the moment. Adverse childhood experiences, or ACEs, include psychological, physical or sexual abuse; domestic violence; neglect; parental separation or divorce; early death of a parent; and living with household members affected by substance abuse, mental illness, suicidal behavior or incarceration.

In a large retrospective study of more than 9,500 adults, a higher number of adverse childhood experiences was associated with a graded increase in risk for nicotine, alcohol and drug abuse, depression, suicide attempts, heart disease, cancer, chronic lung disease and liver disease later in life.³

In other words, severe or repeated childhood stress doesn't simply affect emotional well-being. The biological changes set in motion during this key window of development have been linked to lasting effects on both physical and mental health well into adulthood.

1. Reduce chronic stress before it becomes your normal — Everyone benefits from identifying persistent sources of stress, regardless of what happened earlier in life. Identify the pressures that repeatedly leave you tense or on edge — a demanding schedule, a toxic relationship, financial strain you've been ignoring — and address the ones within your control.

The study reinforces why this matters: Repeated exposure to stress affects how the brain responds to future challenges. Reducing unnecessary stress gives your brain and body more opportunities to recover instead of moving continuously from one stressor to the next.

2. Remember that your stress response isn't set in stone — One of the most encouraging findings was that the earlier changes didn't leave brain cells constantly overactive. Instead, differences became apparent when the animals encountered stress again. If you had a difficult childhood, your past isn't your destiny.

Focus on what you can change now — your environment, daily routines and exposure to unnecessary stress — rather than assuming early adversity permanently determines how you'll respond.

3. Protect your sleep from stress — Stress and poor sleep reinforce each other, leaving you less prepared to handle the next challenge. Protect a consistent sleep schedule, keep your bedroom dark and quiet, and avoid stimulating activities close to bedtime. When you're well-rested, you're better equipped to deal with everyday pressures without every problem feeling overwhelming.

4. Build periods of recovery into your day — Stress becomes harder to manage when one demand runs directly into the next. Give your body regular opportunities to shift out of that heightened state. If you're under heavy pressure, create quiet periods without work demands, upsetting news or other avoidable stimulation. Even the simple habit of protecting time for recovery helps you stop treating nonstop stress as your normal baseline.

5. Strengthen the relationships that help you handle stress — Strong social connections give you another layer of support when life becomes difficult. Make regular contact with people who leave you feeling supported and secure, whether that's family, close friends or others you trust.

When something difficult happens, talk it through instead of automatically withdrawing or carrying the entire burden yourself. Building reliable social support gives you a practical resource to draw on when unavoidable stress hits.

• The cells responded to erythritol by activating their antioxidant defenses — One revealing detail was what happened after oxidative stress increased. Two antioxidant proteins, superoxide dismutase-1, or SOD-1, and catalase rose by about 45% and 25%, respectively. Think of these proteins as part of the cell's cleanup crew. SOD-1 helps convert a highly reactive molecule called superoxide into hydrogen peroxide, while catalase then helps convert hydrogen peroxide into water.

At first glance, higher antioxidant activity sounds beneficial. In this case, however, researchers interpreted it as a compensatory response; the cells were boosting their defenses because they were under greater oxidative pressure. Those defenses weren't enough to neutralize the rise in reactive oxygen species, unstable molecules that damage cells when they accumulate.

• Erythritol changed the molecular switches that control nitric oxide production — The researchers found an important detail behind the drop in nitric oxide. The total amount of endothelial nitric oxide synthase, or eNOS, didn't significantly change. Instead, erythritol altered chemical switches that control whether this enzyme works efficiently.

One activating signal was about 35% lower, while an inhibitory signal was about 40% higher. In simple terms, the cells still had the nitric oxide-making machinery, but the switches shifted toward "off." Nitric oxide production consequently fell by about 20%. This matters because eNOS also helps regulate brain blood flow, limit platelet clumping and control inflammation and clot formation.

• The constriction signal rose without an increase in the enzyme that processes it — Erythritol-treated cells produced more of the precursor your cells use to make endothelin-1. Yet endothelin-converting enzyme, which helps process that precursor, didn't significantly differ between treated and untreated cells.

That finding adds detail to the mechanism. Erythritol didn't simply increase every component of the pathway. Instead, it selectively altered parts of a system that controls blood vessel constriction, ultimately producing substantially more endothelin-1.

• Erythritol weakened the cells' response when clot-clearing help was needed — Under normal resting conditions, erythritol didn't significantly change t-PA, a substance your blood vessels release to help break down blood clots. The problem appeared when researchers exposed the cells to thrombin, which signals that clotting is taking place.

Untreated cells responded by releasing about 25% more t-PA, increasing from 90.1 to 110.2 picograms per milliliter. Erythritol-treated cells barely responded, rising from 87.4 to only 87.6 picograms per milliliter. The cells still had their clot-clearing defense, but erythritol interfered with their ability to activate it when it was needed.

• The experiment identifies a mechanism, but it doesn't prove erythritol causes strokes in people — The researchers specifically acknowledged that an isolated cell experiment can't establish clinical risk. They also tested an acute exposure, so the study doesn't reveal what repeated erythritol consumption does over months or years.

Still, the model has value because these human brain microvascular endothelial cells are used to study how brain blood vessels function. The researchers also noted that erythritol crosses the blood-brain barrier, meaning it reaches and interacts with the brain's vascular environment. These results provide biological evidence of vascular disruption under laboratory conditions, while long-term human studies are still needed to determine what those changes mean for actual stroke risk.*

1. Remove products with added erythritol from your routine — Start by checking ingredient lists on foods and drinks marketed as sugar-free, low-sugar or keto-friendly. Erythritol is often used as a bulk sweetener, so these products expose you to amounts far beyond the tiny quantities naturally present in some foods.

Also be aware that erythritol shows up in products you might not associate with sugar-free sweeteners, including protein bars, flavored waters, chewable supplements and even some toothpastes and mouthwashes.

If you regularly add erythritol to coffee or homemade foods, or eat packaged products containing it, removing those concentrated sources is the simplest place to start. You're eliminating the trigger studied by the researchers rather than trying to compensate for its downstream effects.

2. Don't replace erythritol with another artificial sweetener — Swapping erythritol for another artificial sweetener doesn't address the larger problem of relying on highly processed substitutes for sweetness. Instead, retrain your palate by making naturally sweet whole foods your first choice.

Fresh fruit is one of the easiest options. You could have berries, an apple or an orange for dessert, for example. When you want an added sweetener, small amounts of raw honey or maple syrup are other options. Raw honey works well in tea or with grass fed yogurt, while maple syrup adds sweetness to oatmeal and other whole-food meals.

3. Choose natural carbohydrates instead of sugar-free processed foods — Your body needs carbohydrates for energy, so avoiding erythritol doesn't mean avoiding carbs. Whole fruits such as oranges, apples, berries and ripe bananas provide natural sugars along with other nutrients. Sweet potatoes and other root vegetables are additional options.

I generally recommend about 250 grams of healthy carbohydrates per day for most adults, adjusted for your activity level and individual needs. White rice is another useful source, particularly if you don't tolerate large amounts of fiber well. Building your carbohydrate intake around these foods reduces the need for artificially sweetened products in the first place.

4. Choose simpler sweeteners when you make foods at home — If you still want extra sweetness beyond whole foods, making your own meals and desserts gives you much more control. I favor natural stevia from the plant and Luo Han Guo, also known as monk fruit. Pure dextrose derived from clean cane sugar is another option.

Check the ingredient list even when the front label says "stevia" or "monk fruit," many of these products use erythritol as a bulking agent. Look for a product without erythritol or other unwanted sweetener blends so you're actually making the substitution you intended.

5. Retrain your taste buds to need less sweetness — If nearly every snack, drink or meal tastes intensely sweet, your palate becomes accustomed to that level of sweetness. Instead of focusing only on finding the perfect replacement for erythritol, gradually make your foods and drinks less sweet overall.

Try cutting the amount of sweetener you add to coffee, tea, yogurt or homemade foods in half for one week. Once that tastes normal, cut it in half again. Within a few weeks, you'll notice that fruit, roasted sweet potatoes and other whole foods taste sweeter than they used to. Over time, this helps you break the cycle of constantly seeking intensely sweet flavors, so avoiding erythritol and other processed sweeteners becomes easier rather than feeling restrictive.

• The “Disease of the Digital Age” — The One Name project says this condition is “characterized by a wide range of symptoms linked to electromagnetic radiation (EMR) emitted by modern technologies such as cell towers, smart meters, Wi-Fi networks, Bluetooth devices, and smart technologies.” According to their press release:

“For those affected, even minimal exposure to EMR can trigger severe reactions, e.g., headaches, dizziness, fatigue, heart palpitations, tinnitus, sleep disturbances, ADHD and other cognitive impairments — leaving them unable to tolerate many modern environments and, in extreme cases, isolated from technology and society.”

• EMF-sensitive individuals have been ignored for a long time — For many years, individuals suffering from symptoms linked to wireless radiation exposure have faced skepticism and dismissal. Many have been called “sensitive,” and their struggles invalidated — they're told that their problem is more psychological than physiological, and that it's “all in their head.”

• By contrast, “EMR Syndrome” directly attributes the illness to electromagnetic radiation exposure — It shifts the focus to the cause rather than the individual's reaction to it. Organizing committee member Kent Chamberlin, Ph.D., said, “This decision was the result of a truly collaborative process. We've not only created a unified identity for this condition but also a renewed sense of hope for those living with it.”³

• Advantages of this new terminology — By formally establishing a single, clear term to identify this looming health condition, those who suffer from the adverse effects of wireless technology will have better clarity in diagnosis. It will also help streamline research efforts and open the door for policy changes that prioritize human health over unchecked technological advancements. Dr. Sharon Goldberg, an integrative physician, comments:

“The name EMR Syndrome not only reflects the reality of the condition, but also serves as a call to action for awareness, funding, and innovation to help those affected reclaim their lives.”⁴

• Many were involved in the name-selection process — They conducted an online public forum for over four months, collecting input from patients, researchers and safe technology advocates. Their initial goal was to identify the most important criteria for a new name rather than simply picking one based on personal preference.⁵

• A special committee made the final decision — After gathering data, a decision-making committee composed of 11 medical professionals, engineers, and safe technology leaders was tasked with making the final decision. Their goal was to find a term that was both scientifically accurate and widely understandable.

• After multiple discussions, “EMR Syndrome” was chosen — This new name struck a balance between credibility in research, accessibility for the general public and effectiveness in advocacy.

“This balance was paramount to the process,” Pam Wallace, an organizing committee member who directs SafeTech Forward in Michigan, said. “It's the reason we had professionals from the medical, scientific, legal and educational communities on the Decision-Making Committee.”⁶

• Dealing with EMFs is an everyday struggle for many sensitive people — For these individuals, every day is a constant battle filled with pain, discomfort, and other symptoms that take an extreme toll on their lives.⁹ Jennifer Wood, one of the individuals with EMR Syndrome featured in the documentary, shares her ordeal:

“[S]ome places are worse than others. When I'm in a crowd of people that are using a lot of cell phones or Wi-Fi, it gets much more intense. It's the same feeling. You feel pins and needles in your head and a metallic bar in the forehead. It's a kind of nausea that you can't describe.

It's not the kind of nausea I used to feel if I got sick from food or the flu or something. It's a kind of poisonous nausea that's impossible to describe.”¹⁰

• How does EMR Syndrome develop? In some cases, individuals have reported becoming suddenly sensitive to EMFs after an illness or a significant exposure event. Others develop symptoms gradually over time as their bodies accumulate exposure. Prof. David O. Carpenter, director of the Institute for Health and the Environment, says:

“There were a number of reports that have been published where military people involved in radar work got in the radar beam and got an excessive exposure. And there's some 10 or 12 reports of individuals perfectly healthy before that sudden exposure.

After that exposure, [they] suffered from constant headaches, from photophobia. They couldn't stand to be in the presence of light. They felt their brain wasn't working right. It's classic electrohypersensitivity.”¹¹

• EMF sensitivity had a significant effect on their lifestyle — Many of these individuals have resorted to extreme measures to reduce the impact of EMFs on their health, making significant adjustments to their lifestyle habits and living space to minimize their exposure.

• Individuals with EMR Syndrome experience a wide range of unpleasant symptoms — While they vary from one person to another, there are commonly reported indicators, such as:

◦ Skin itch/rash/flushing/burning and/or tingling — A “burning pins and needles” kind of pain, especially in the head and chest area

◦ Confusion/poor concentration and/or memory loss

◦ Fatigue and muscle weakness

◦ Headache

◦ Chest pain and heart problems

• Other reported symptoms associated with EMFs — In some cases, EMF-sensitive individuals also experience ear pain, insomnia, tinnitus (ringing in the ears), paralysis, panic attacks, seizures, feeling a vibration in the body, and unrelenting dizziness.

• EMF symptoms are often met with skepticism — Because the conventional medical community doesn't recognize this condition, those who suffer are often met with skepticism. After being subjected to various lab tests and examinations, many end up being dismissed by their conventional physicians.

• EMFs are severely damaging your mitochondria — One of the things that catalyzed me to write this book was my deep appreciation of the impact of mitochondrial function in health and disease. Once I realized that EMFs cause massive mitochondrial dysfunction, the danger our wireless society poses became very clear to me.

• Having fewer mitochondria has detrimental effects on your health — The fewer mitochondria you have, and the more dysfunctional they are, the faster you'll age and the more prone you'll be to chronic degenerative diseases. By inducing mitochondrial dysfunction, the wireless world we're living in is driving us all into an early grave. Through “EMF*D,” I hope to help more people understand this biological threat.

Martin Pall, Ph.D., is one of the experts who helped me understand the mechanisms of EMFs and how they harm people, animals and plants. Pall has a bachelor's degree in physics from Johns Hopkins and a Ph.D. in biochemistry and genetics from Caltech.

He has also published research on EMFs,^13141516 making him uniquely qualified for this type of research. For nearly two decades, Pall has been scouring the medical literature, integrating and drawing parallels between work done by others to shed light on this issue.

• Why do EMFs lead to chronic illnesses? To put it simply, the primary danger of EMFs — and what drives the processes of chronic disease — is the mitochondrial damage triggered by peroxynitrites, one of the most damaging types of reactive nitrogen species.

Low-frequency microwave radiation activates the voltage-gated calcium channels (VGCCs) in the outer membrane of your cells, causing them to open, thus allowing an abnormal influx of calcium ions. This activates nitric oxide, which reacts with superoxide and forms peroxynitrite.¹⁷

• Peroxynitrites are potent reactive nitrogen species — They are associated with an increased level of systemic inflammation and mitochondrial dysfunction — they are thought to be a root cause for many of today's chronic diseases. Some of the common risks associated with EMFs include:

◦ Open the blood-brain barrier, allowing toxins to enter your brain.¹⁸

◦ Fragment DNA — Studies have shown EMFs cause DNA fragmentation.^19,20 Significant oxidative stress from peroxynitrites may also result in single-strand breaks of DNA.²¹

◦ Raise the risk for abnormal cell growth and cancer, including leukemia and cancer of the brain, acoustic nerve, salivary gland, eyes, testes, thyroid, and breast — As early as 2011, the evidence was strong enough for the International Agency for Research on Cancer, the cancer research arm of the World Health Organization, to declare cellphones a Group 2B “possible carcinogen.”²²

Since then, multiple studies have found support for EMF having carcinogenic potential, including the U.S. National Toxicology Program's cell phone radiofrequency radiation study.²³²⁴

• Has neurological effects — Studies show how EMFs can lead to massive changes in the structure of neurons, including cell death and synaptic dysfunction.^25,26

• Contributes to reproductive problems in both sexes — For example, prenatal exposure to magnetic fields can nearly triple a pregnant woman's risk of miscarriage.²⁷ In men, studies show EMF radiation from cellphones and laptops reduces sperm motility and viability, and increases sperm DNA fragmentation.²⁸²⁹

• Alters your microbiome — It turns what might otherwise be beneficial microbes pathogenic. This has far-ranging health effects, since your gut microbiome plays an important role in health.³⁰

• Connect your desktop computer to the internet via a wired connection and be sure to put your desktop in airplane mode — Avoid wireless keyboards, trackballs, mice, game systems, printers, and house phones, and opt for the wired versions.

• Turn off your Wi-Fi when not in use, especially at night when you are sleeping — Ideally it is best to work toward hardwiring your house so you can turn off the Wi-Fi at all times. If you have a notebook without any Ethernet ports it is easy to purchase a USB Ethernet adapter that will allow you to connect to the internet without a wireless connection.

• Shut off the electricity to your bedroom at night — This typically works to reduce electrical fields from the wires in your wall unless there is an adjoining room next to your bedroom. If that is the case, you will need to use a meter to determine if you also need to turn off power in the adjacent room.

• Use a battery-powered clock, ideally one without any light — I use a talking clock that I merely press a button to determine the time and never see any light at night.

• If you still use a microwave oven, consider replacing it with a steam convection oven — It will heat your food as quickly and far more safely. Next to induction stovetop burners, microwave ovens are likely the largest EMF polluters in your home.

• Avoid using “smart” appliances and thermostats that depend on wireless signaling — This would include all new “smart” TVs. They are called smart because they emit a Wi-Fi signal and, unlike your computer, you are unable to shut the Wi-Fi signal off. Consider using a large computer monitor as your TV, as they don't emit Wi-Fi.

• Refuse smart meters as long as you can — You can also add a shield to an existing smart meter.³¹

• Considering moving your baby's bed into your room instead of using a baby monitor, or use a hard-wired monitor — In any case avoid any baby monitor that is wireless. There are some wired options available.

• Replace CFL bulbs with incandescent bulbs — Ideally remove all fluorescent lights from your house. Not only do they emit unhealthy light, but more importantly they will actually transfer current to your body just being close to the bulbs.

• Avoid carrying your cellphone on your body unless it is in airplane mode — Never sleep with it in your bedroom unless it is in airplane mode (and especially not under your pillow). Even in airplane mode it emits signals, which is why I put my phone in a Faraday bag.

• When using your cellphone, use the speaker phone and hold the phone at least 3 feet away from you — Seek to radically decrease your time on the cellphone. I probably am down to below 30 minutes a month on my cell, mostly when traveling. Instead use VoIP software phones that you can use while connected to the internet via a wired connection.

• Researchers specifically looked at antidepressant exposure over time — People were considered “exposed” to antidepressants if they had filled at least two prescriptions within one year, at any point during the 12 years leading up to the study. That exposure was then divided into two categories: short-term (one to five years) and long-term (six or more years).

• Risk increased the longer people stayed on antidepressants — Compared to people who had never used these drugs, those on antidepressants for one to five years had a 56% higher risk of sudden cardiac death.

But the danger didn't plateau. It escalated. Individuals who had been on antidepressants for six or more years had more than double the risk of sudden cardiac death — specifically, a 2.2 times greater likelihood of dying suddenly from heart-related causes.

• Risk levels were lower but still elevated in people over 70 — In those aged 70 to 79, taking antidepressants for one to five years was associated with an 83% increase in sudden cardiac death risk. With six or more years of use, the risk rose to 2.2 times higher than in people not using antidepressants.

Interestingly, for the youngest group (18 to 29) and the oldest group (80 and up), the data didn't show a statistically significant increase, though the sample size may have been too small to detect it.

• The study showed a clear dose-response relationship with time — The longer you stay on antidepressants, the more likely you are to die suddenly from a heart-related cause. For instance, in people aged 40 to 49, those with six or more years of use had a 70% higher risk compared to those with one to five years. The pattern continued:

• Biological and behavioral factors are driving this connection — Study co-author Dr. Jasmin Mujkanovic from Copenhagen University Hospital explained that there are multiple possible reasons for the higher risk. One factor is direct drug effects. Some antidepressants alter how electrical signals travel through your heart, which could trigger fatal rhythm disturbances.

Another possibility is that antidepressant use is a marker of more severe psychiatric illness, which itself is known to increase cardiovascular risks. Depression is also linked to delayed medical care, unhealthy behaviors, and poor heart health.

• Heart rhythm disruption is a likely mechanism of action — Many antidepressants, especially selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs), affect ion channels in the heart.

• Symptoms like sadness or anxiety are your body's way of signaling that something needs attention — Feeling emotionally low isn't always a disorder. It's often a sign your system is under stress. You could be low in important nutrients or getting too little sunlight or too much blue light.

You could also be disconnected from your purpose, your relationships, or your body. In any of these cases, masking the symptoms with medication ignores the deeper message — and leaves the root problem untouched.

• Two-thirds of people taking antidepressants don't get any real benefit — Even though antidepressants are routinely offered as the go-to solution for depression, the success rate is low. About 66% of people prescribed these medications do not experience meaningful symptom relief.² And the side effects include increased risk of Type 2 diabetes,³ dementia,⁴ and even suicide.

• A 2022 review showed antidepressants only work for a tiny group of people — Researchers from the U.S. Food and Drug Administration (FDA) conducted the largest-ever review of antidepressant studies.⁵

They analyzed data from 232 randomized, double-blind, placebo-controlled trials submitted to the FDA between 1979 and 2016, including unpublished trials that drug companies never released. In total, the data covered 73,388 patients with diagnosed depression.

• Only 15% of patients benefited beyond the placebo effect — The analysis found that antidepressants outperformed placebo in just 15% of patients. The authors did not find that benefit confined to the most severe depression; their conclusion was that the advantage of antidepressants over placebo is best understood as affecting a minority of patients, and that lower-risk treatments might be preferable to start with in mild to moderate depression.

• Use trusted resources to educate yourself and plan a slow taper — You need a clear strategy. That's where books like “Psychiatric Drug Withdrawal: A Guide for Prescribers, Therapists, Patients and Their Families” by Dr. Peter Breggin and “The Antidepressant Solution: A Step-by-Step Guide to Overcoming Antidepressant Withdrawal, Dependence, and Addiction” by Dr. Joseph Glenmullen come in.

These guides walk you through the process, explain what to expect, and offer real-life strategies to manage symptoms. The goal is to support your nervous system during the transition so you don't rebound or crash. Once you've got the right support in place, taper gradually. Your doctor should know the safest dosing schedule based on your medication.

• Help loved ones build momentum when they can't do it alone — If you have a friend or family member struggling with depression, the best thing you can do is show up — literally. Invite them outside. Offer to cook. Take a walk together. Depression makes basic decisions feel overwhelming. But the presence of another person, especially someone gently nudging them toward light, movement, and connection, is often enough to change the trajectory of their day.

• In a true crisis, act fast and get help immediately — If you're in a place where you're not just sad but desperate — or thinking about ending your life — this isn't the moment to map out a supplement plan or search for a new doctor. You need to get to safety first. Call the 988 Suicide & Crisis Lifeline or 1-800-273-TALK (8255), or head straight to your nearest emergency room. Stabilize now. The healing comes after.

1. Move your body in ways that support your brain:

2. Adjust your diet to reduce inflammation and stabilize mood:

Nutrients to prioritize:

3. Get real sunlight, not just vitamin D pills:

4. Use tools that regulate your nervous system without side effects:

5. Clean up your environment and reset your nervous system:

• Consumers for Dental Choice

• Dental Amalgam Mercury Solutions (DAMS) — Email them here or call 651-644-4572 for an information packet

• Huggins Applied Healing

• Holistic Dental Association

• International Academy of Biological Dentistry & Medicine (IABDM)

• International Association of Mercury Safe Dentists

• Talk International

• High blood sugar levels and diabetes — The protective glycocalyx layer is made of proteins and sugars — High blood sugar damages the glycoprotein layer, thinning it down in a measurable way. High blood sugar can reduce the glycocalyx layer by about half.¹ This, in turn, exposes the endothelial cells to the bloodstream and anything else damaging that might be there.

The damage to the glycocalyx is one reason why diabetics are prone to both arterial and capillary (small vessel) disease. You can't get atherosclerosis in the capillaries, as there's no room. Instead, the capillaries become broken down and destroyed. This in turn can cause ulcers, due to poor circulation in the skin of your legs and feet.

Peripheral neuropathy can occur as the ends of nerve cells are deprived of oxygen. It can also contribute to visual problems (diabetic retinal damage) and kidney damage. Blood pressure may also become elevated as your heart has to work harder to push blood through a network of damaged/missing small blood vessels.

• Heavy metals such as aluminum and lead.

• High blood pressure, as it puts stress on the endothelium — Atherosclerotic plaque (atherosclerosis) doesn't occur in low-pressure vessels, such as veins, unless the pressure is raised, adding biomechanical stress.

• Avoid unnecessary use of nonsteroidal anti-inflammatories (NSAIDs) such as ibuprofen and naproxen — While they effectively inhibit inflammation, they can promote platelet aggregation by blocking COX-2. In other words, they can activate your blood clotting system, making blood clots more likely.

• Get plenty of sensible sun exposure — Sun exposure triggers NO that helps dilate your blood vessels, which may help lower your blood pressure. NO also protects your endothelium, and sunlight's near-infrared light increases mitochondrial melatonin to improve cellular energy production.

• Avoid seed oils and processed foods — Seed oils are a primary source of the omega-6 fat called linoleic acid (LA), which I believe may be far more harmful than sugar. Excessive intake is associated with most chronic diseases, including high blood pressure, obesity, insulin resistance, and diabetes.

LA gets embedded in your cell membranes, contributing to oxidative stress, and can remain there for up to seven years. Oxidative linoleic acid metabolites (OXLAMs) are thought to be causing the primary damage, including endothelial damage.

• Lower your insulin and blood sugar levels — Simple strategies to accomplish this include avoiding ultraprocessed foods and artificial sweeteners, keeping your LA intake within 2 to 5 grams per day, and getting regular exercise.

• Address chronic stress, which can raise both blood sugar and blood pressure, promote blood clotting and impair your repair systems. Cortisol, a key stress hormone, may reduce endothelial cell production.

• Quit smoking.