Dr. Anthony Jay talks about the carnivore diet, fat, cholesterol, and heart disease.

Anthony G. Jay, PhD, is a biochemist with a doctorate from Boston University School of Medicine, research experience at Boston University and Mayo Clinic, and publications spanning lipid metabolism, CD36, oxidized LDL, Alzheimer’s disease, and orthopedic research. The discussion covers carnivore dieting, LDL and statins, CAC versus CCTA imaging, insulin resistance, seed oils, and endocrine-disrupting chemicals. His central case is that insulin resistance and metabolic health are more informative for cardiovascular risk than LDL alone, while questioning conventional interpretations of statins and coronary-plaque imaging.

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Carnivore background and Mayo conflict

• A vegan attempt 10–15 years earlier felt terrible, while personal gut problems and a daughter's dairy/gluten sensitivities undermined conventional dietary advice. Paul Saladino, Shawn Baker, and feeling better with more meat moved the diet further toward carnivore.
• Boston University medical training promoted vegan-style eating, low cholesterol, and fiber, and around 1999 a book implying a vegan diet could help cure a father's cancer was passed along. That advice is bad training and propaganda.
• Heart-disease research at Boston University included plaque work around autopsies, followed later by Mayo Clinic research.
• At Mayo, a strict-carnivore telomere study was planned after a study was interpreted as fresh red meat improving telomeres while processed meat did the opposite.[1] Shawn Baker helped publicize the idea, while Mayo HR objected to the carnivore project and to a Twitter post attacking a Mayo "Eat more whole grains" poster and warned that the institution was being tarnished.
• During COVID, Mayo was left after vaccine requirements. Broad masking was also opposed, with free N95s favored for high-risk elderly people while lower-risk people built herd immunity.

Statins, CAC, and CCTA

• Standard-of-care medicine and lawsuit risk push doctors toward statins: failure to recommend them after a high cholesterol result can expose a doctor to litigation if a later heart attack occurs.
• Statins increase calcified plaque, including by more than 10% per year in the cited studies, and re-evaluation of older statin data also found increased coronary calcification.[2] The mechanism is inhibition of cholesterol synthesis along with CoQ10 and vitamin K2 production; K2 normally helps keep calcium out of arteries.
• Coronary artery calcium (CAC) scans are cheap, direct, and repeatable; a personal CAC score was zero despite supposedly high cholesterol. Repeated CAC scans give essentially the same result, while CCTA plaque readings have major scan and reader variability.
• Dave Feldman's KETO CCTA study used AI-based angiography analysis, but the imaging company knew which scans belonged to the keto group and which belonged to controls before analysis, so the AI result is not inherently unbiased.[3]
• Human repeat CCTA work has about ±18.4% interscan variability on newer machines and up to roughly 30% on different or older scanners.[4] Another study using three expert CCTA readers found very poor agreement, around 0.23, or 2.3 out of 10.[5]
• A PLOS ONE study found a strong association between longer statin use and severe coronary calcification; more than 10 years of use corresponds to about a 358% higher risk.[6]
• Relative-risk advertising can make small absolute effects look large. The same relative-risk language is used for statin-associated calcification that drug companies use for statin benefits and COVID-vaccine efficacy, and the explanation that statins merely convert dangerous soft plaque into harmless hard plaque fails because the supporting CCTA evidence is unreliable.

Cholesterol and insulin resistance

• The same institutional resistance seen with the carnivore study occurs when cardiologists and lipidologists attack carnivore because it raises cholesterol. The system makes lower cholesterol synonymous with good and higher cholesterol synonymous with bad without requiring heart-attack or plaque endpoints.
• Smoking, binge drinking, inactivity, stress, trans fats, high iron, dehydration, and sleep deprivation can all raise LDL while harming health, so older population studies can confound LDL with the behaviors producing it. Pharma, guideline pressure, and medical-association funding reinforce the cholesterol model.
• Carbohydrates drive insulin resistance, while carnivore or very-low-carbohydrate eating can drive insulin very low. If glucose stays high on carnivore, more dietary fat can help; exercise also increases glucose uptake independently of insulin. The three foundations for reversing insulin resistance are very-low-carb/carnivore eating with enough fat, exercise, and fasting.
• A newly diagnosed type 2 diabetic with an A1c of 13% can be put on metformin and insulin, then sent to a dietitian whose first lesson is how to keep eating cake while dosing insulin. The diagnosis is the moment for a major lifestyle change, not accommodation of the old diet.
• The surrounding food environment makes that change harder, but travel and convenience do not require returning to high-carbohydrate food; meat-centered options can be carried or ordered.

Fuel use and plaque reversal

• High cholesterol is contextual. On a low-carbohydrate, high-fat diet, LDL values around 280 or even 380 are not automatically high-risk if triglycerides and the metabolic context are good. LDL is a transporter carrying energy-related cargo, not intrinsically a toxin.
• Mike McKnight's 118-mile/189-km event in 24 hours with zero calories after years of low-carb eating is an example of deep fat adaptation and why calorie-centric assumptions about endurance can fail.
• The heart preferentially burns fatty acids, with the figure put near 95% even in people who eat substantial carbohydrate. Decades of high-carbohydrate eating can make the heart poor at burning fat, then insulin resistance limits glucose use, leaving a "starving heart" that scavenges fatty fuels and contributes to plaque. Carnosine and carnitine are additional fuels, and vegans are low in carnosine.
• In a study of 28,024 women, early-onset coronary risk is linked most strongly to lipoprotein insulin resistance at a hazard ratio around 6.4, hypertension about 2.2, triglycerides about 2.1, and LDL about 1.38.[7] That gap makes insulin resistance the central cardiovascular risk signal.
• ApoB and Lp(a) associations in other studies are usually around 1.6–1.8, still far below 6.4 for insulin resistance.
• Patrick Theut and Dr. Ford Brewer are public examples of lowering CAC after going very low-carb/keto. A private Florida client had CAC fall from about 400 to zero within a year and remain zero on repeat scanning. Because plaque contains lipid, teaching cells to burn fat is the biological route to reversing it; changes can begin in roughly six weeks, while full fat adaptation can take years.

CAC tiers, microplastics, and lipid markers

• CAC severity bands are zero plaque for tier 1; roughly 300–1000 for tier 2, which deserves serious reversal work; and above 1000 for tier 3, where exercise and hypertension require more caution because intense effort could dislodge plaque. Stress itself worsens insulin resistance and plaque risk.
• A microplastics study found plastic particles inside carotid plaque and a large increase in cardiovascular events, with 353% higher heart attacks in people with microplastics in their arteries.[8] This links plaque instability with earlier work on plastics and hormones.
• LDL is not cholesterol itself. Cholesterol is valuable material for steroid hormones and the brain, and the brain is rich in cholesterol and DHA; calling LDL "bad cholesterol" obscures that distinction.
• Ancel Keys helped entrench the cholesterol story. The Seven Countries Study[9] cherry-picked seven countries from a larger set of 22, and the CDC later canonized Keys.
• Thomas Dayspring calling Lp(a) a genetic disorder fits the same pattern: a normal molecule becomes a disease target as new Lp(a)-lowering drugs arrive, after the narrative moves from total cholesterol to LDL, ApoB, particle measures, and Lp(a).
• Recovered Minnesota Coronary Experiment data compared a linoleic-acid/seed-oil diet with a saturated-fat control in a double-blind trial; the reanalysis shows worse heart-disease outcomes in the seed-oil group despite cholesterol lowering.[10]

Medical institutions and endocrine disruptors

• Brown and Goldstein were held up as heroes in medical training for familial hypercholesterolemia and statins. FH moved from an extremely rare disorder to about 1 in 250 as definitions and LDL-receptor variants expanded, allowing a rare-disease model to be generalized to much of the population.
• Doctors often believe they are saving lives because training, licensing, guidelines, and professional associations all reinforce the same model. That institutional behavior is a cult or religion, not open science.
• Earlier plastics and hormone work grew out of laboratory experience, including the Robert Ferrante cyanide-murder case across the hall and the contrast between easy access to toxic chemicals and heavy restrictions on tiny amounts of testosterone for research.
• BPA, parabens, phthalates, atrazine, fragrances, and related chemicals can mimic estrogen, with aggregate exposure linked to low testosterone, male feminization, depression, and other hormone problems. That plastics work later fed into the microplastics concern in the heart-disease book.

Insulin resistance, seed oils, and soy

• Gil Carvalho's advice favoring oats, soy, canola oil, more fiber, and statins, and Muhammad Alo's statement that insulin resistance affects under 10% of people, embody the dietary and cardiology consensus. That consensus is wrong.
• An NHANES analysis found insulin resistance in roughly 44% of U.S. adults under about age 40 by the cited medical criteria.[11] Another national cardiometabolic-health study used by Ben Azadi puts metabolic dysfunction closer to 93%.[12] Either way, carbohydrate-heavy advice is inappropriate for a population with widespread insulin resistance.
• Fat cells turn over slowly: bomb-pulse carbon-14 work puts average adipocyte age near 10 years.[13] A six-week seed-oil intervention cannot erase years of stored fatty acids or adequately test long-latency cardiovascular outcomes.
• Modern seed-oil studies rarely measure heart attacks, strokes, or plaque over the decades needed. Omega-6 fats are highly oxidizable without the resolvin/protectin pathway associated with omega-3s, so saturated fat is better than high omega-6 intake.
• Soy is estrogenic through isoflavones such as genistein and daidzein. Short U.S. soy trials can show little difference because background endocrine-disruptor exposure is already high, while a European randomized crossover study in men found six weeks of soy-flour supplementation lowered serum testosterone.[14] Soy therefore adds another estrogenic exposure.

References

1. [03:20] Processed Meat, but Not Unprocessed Red Meat, Is Inversely Associated with Leukocyte Telomere Length in the Strong Heart Family Study — https://doi.org/10.3945/jn.116.234922
2. [07:31] High dose and long-term statin therapy accelerate coronary artery calcification — https://doi.org/10.1016/j.ijcard.2015.02.072
3. [11:44] Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial — https://doi.org/10.1016/j.jacadv.2024.101109
4. [13:17] Coronary CT Angiography: Variability of CT Scanners and Readers in Measurement of Plaque Volume — https://doi.org/10.1148/radiol.2016161670
5. [14:15] Interobserver variability among expert readers quantifying plaque volume and plaque characteristics on coronary CT angiography: a CLARIFY trial sub-study — https://doi.org/10.1016/j.clinimag.2022.08.005
6. [16:53] Long-term statin therapy is associated with severe coronary artery calcification — https://doi.org/10.1371/journal.pone.0289111
7. [34:13] Association of Lipid, Inflammatory, and Metabolic Biomarkers With Age at Onset for Incident Coronary Heart Disease in Women — https://doi.org/10.1001/jamacardio.2020.7073
8. [43:05] Microplastics and Nanoplastics in Atheromas and Cardiovascular Events — https://doi.org/10.1056/NEJMoa2309822
9. [45:51] Seven Countries Study — https://www.sevencountriesstudy.com/about-the-study/
10. [47:21] Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) — https://doi.org/10.1136/bmj.i1246
11. [58:10] Insulin Resistance and Cardiometabolic Risk Profile Among Nondiabetic American Young Adults: Insights From NHANES — https://doi.org/10.1210/clinem/dgab645
12. [58:39] Trends and Disparities in Cardiometabolic Health Among U.S. Adults, 1999-2018 — https://doi.org/10.1016/j.jacc.2022.04.046
13. [59:26] Dynamics of fat cell turnover in humans — https://doi.org/10.1038/nature06902
14. [62:25] Dietary supplements of soya flour lower serum testosterone concentrations and improve markers of oxidative stress in men — https://doi.org/10.1038/sj.ejcn.1601495 :::