What Causes Plaque in Arteries

Insulin Resistance and Atherosclerosis

What’s REALLY Destroying Your Arteries & The New Science of Reversing Plaque | Dr. Anthony Jay

This interview explores Dr. Anthony Jay’s views on insulin resistance, dietary patterns, environmental exposures, and testing strategies that may influence arterial plaque and long-term cardiovascular health.

Dr. Anthony Jay, a biochemist and health consultant, joins host Jesse Chappus to present a metabolic-health-centered interpretation of atherosclerosis. The discussion challenges the idea that LDL cholesterol alone explains cardiovascular risk and instead emphasizes insulin resistance, inflammation, blood pressure, homocysteine, diet quality, physical activity, sleep, stress, and environmental exposures. Viewers will hear claims about ketogenic and low-carbohydrate approaches, fasting, plaque imaging, blood tests, seed oils, microplastics, plant sterols, iron, and supplements. Because several positions in the interview differ from mainstream cardiovascular guidelines, readers should view it as an informed conversation rather than individualized medical advice and discuss any medication or treatment changes with a qualified clinician.

Summary

Insulin resistance and metabolic health: Dr. Jay argues that insulin resistance is a major driver of arterial plaque formation and cardiovascular risk, alongside inflammation, hypertension, elevated triglycerides, poor sleep, stress, smoking, and sedentary behavior.
LDL cholesterol and ApoB: The conversation questions whether LDL cholesterol should be treated as the primary cause of atherosclerosis, describing LDL as a transporter of fats and discussing LDL particle size, ApoB, Lp(a), and the context in which lipid measurements are interpreted.
Fat burning and carbohydrate intake: Dr. Jay promotes metabolic flexibility, lower-carbohydrate eating, intermittent fasting, and fat burning as tools he believes may help improve insulin sensitivity and support plaque reduction.
Plaque assessment: The interview discusses coronary artery calcium scans, CT coronary angiography, soft plaque, calcified plaque, and the importance of measuring meaningful clinical outcomes rather than relying on a single lab value.
Seed oils, animal feed, and microplastics: The discussion raises concerns about seed oils, the fatty-acid profile of animal foods, microplastic exposure, and plant sterols as possible contributors to vascular inflammation or plaque-related risk.
Lifestyle foundations: Topics include fasting, aerobic exercise, resistance training, sleep, stress management, blood-pressure control, and diet quality as potential components of a cardiovascular-health strategy.
Blood tests and risk factors: Dr. Jay highlights insulin resistance markers, triglycerides, HDL, homocysteine, iron status, blood pressure, genetic cholesterol disorders, and plaque imaging as areas to discuss with a healthcare professional.
Supplements: The conversation mentions vitamin K2, berberine, nattokinase, and other supplements. These should not be treated as substitutes for medical evaluation, prescribed therapy, or individualized cardiovascular care.

Important context

The guest’s statements are not a substitute for medical guidance. In particular, the framing that LDL is generally benign or beneficial, and the broader claims about statins, PCSK9 inhibitors, ketogenic diets, fasting, supplements, and plaque reversal, are areas of active scientific debate and may conflict with recommendations from a person’s cardiologist or primary-care clinician. Anyone with chest pain, known cardiovascular disease, diabetes, familial hypercholesterolemia, very high LDL cholesterol, high Lp(a), high blood pressure, or a history of stroke should seek individualized medical care rather than self-treat based on an interview.

Video description

Dr. Anthony Jay is a biochemist, author, and the president of AJ Consulting Company, where he provides personalized DNA analysis and health consulting.

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00:00 – Intro
01:34 – What Actually Causes Arterial Plaque?
10:59 – How Insulin Resistance Really Works
17:20 – Burning Fat to Reverse Arterial Plaque
26:16 – The Positive Role of LDL Cholesterol
34:32 – Does LDL Particle Size Really Matter?
39:15 – Seed Oils Are Good for You?
50:45 – How Animal Feed Changes the Fat You Eat
55:48 – How to Get Seed Oils Out of Your Body
59:02 – Microplastics Are Showing Up in Arterial Plaque
01:05:08 – The Hidden Problem With Plant “Cholesterol”
01:17:38 – Why LDL Gets Trapped in the Artery Wall
01:19:42 – How to Measure Arterial Plaque
01:34:03 – Is Calcified Plaque Really “Healed” Plaque?
01:38:04 – The Diet to Halt Arterial Plaque
01:42:25 – Can High Iron Damage Your Arteries?
01:44:48 – Why High Homocysteine Is Dangerous
01:47:56 – When High Cholesterol Is Actually Genetic
01:52:34 – Berberine & Nattokinase for Arterial Plaque
01:55:27 – The Hidden Cause of High Blood Pressure
01:59:04 – The Blood Tests That Matter Most for Heart Disease
02:01:59 – The Keys to Reversing Arterial Plaque

Show notes: https://jessechappus.com/720

Connect with Dr. Anthony Jay:
AJ Consulting Company – https://link.jessechappus.com/54zHMU8
YouTube – https://link.jessechappus.com/5vYftMN
Instagram – https://link.jessechappus.com/9oW26lS

Get Dr. Jay’s new book, Sugar Beat here: https://link.jessechappus.com/sugar-beat-book

Connect with The Jesse Chappus Show:
Website – https://jessechappus.com
Instagram – https://www.instagram.com/jessechappusshow

Disclosure: Some links above may be affiliate links, which means I may earn a commission if you buy through them, at no extra cost to you.

Disclaimer: The opinions expressed in this video are those of the guest and are presented for informational purposes only. This content is not medical advice. Please consult your healthcare provider regarding any health-related decisions.

Transcript Summary

Opening perspective on plaque

Jesse Chappus opens the interview by asking Dr. Anthony Jay what causes plaque to accumulate in arteries. Dr. Jay says he believes insulin resistance is the main underlying cause. He cites a study involving approximately 28,000 people that he says compared heart-attack risk factors and found a higher hazard associated with insulin resistance than with hypertension, triglycerides, or LDL cholesterol. He argues that focusing exclusively on LDL does not adequately explain why plaque develops.

Dr. Jay says that many adults, including younger adults, may already have insulin resistance. In his interpretation, when tissues become insulin resistant, the heart and arteries do not handle fuel normally. He argues that the body then relies more heavily on fat transport and that LDL particles carry fats through the circulation. He notes that plaque contains cholesterol and other lipids but contends that their presence in plaque does not automatically establish dietary fat or LDL as the root cause.

Sugar metabolism and fat metabolism

Dr. Jay explains that the body predominantly uses glucose and fat as energy sources. He describes glucose as a rapidly available fuel and fat as a slower, more energy-dense source that requires mitochondrial metabolism. He says many cells preferentially use glucose when it is available, while the heart normally has a strong capacity to use fatty acids.

He argues that frequent intake of refined carbohydrates and a lifelong pattern of high carbohydrate exposure can encourage greater dependence on glucose. In his view, this can diminish metabolic flexibility and contribute to insulin resistance. He uses the term “sugar addiction” to describe what he considers an overreliance on carbohydrate-based energy.

Insulin resistance explained

The interview compares insulin resistance with caffeine tolerance. Dr. Jay says repeated stimulation of the insulin pathway can make cells less responsive to insulin, just as repeated caffeine exposure can reduce a person’s sensitivity to caffeine. In this model, glucose remains elevated in the bloodstream while insulin levels also remain high because the body must produce more insulin to obtain the same response.

He describes this as a major metabolic problem and connects it with diabetes risk. The conversation notes that insulin resistance may exist before a person develops clearly abnormal blood-glucose measurements, which makes metabolic health assessment more complicated than simply checking fasting glucose.

Metabolic flexibility and endurance

Dr. Jay discusses endurance athletes and contrasts people who depend heavily on frequent carbohydrate intake with those who have adapted to using fat more effectively during long exercise sessions. He describes the example of an ultrarunner who reportedly completed a 118-mile run without calorie intake after years of low-carbohydrate adaptation.

The broader point is that metabolic adaptation takes time. Dr. Jay says the body’s fuel-use machinery does not switch instantly between sugar and fat. He believes that people can use lifestyle patterns such as lower-carbohydrate meals, intermittent fasting, and exercise to improve their ability to burn fat.

Ketogenic diets and sleep

Dr. Jay says he does not remain in strict ketosis continuously because he finds that very low carbohydrate intake can interfere with his sleep. He describes using a ketogenic lunch, intermittent fasting, and occasional periods of more intensive ketogenic eating, particularly when he wants to support concentration or reduce carbohydrate intake.

He also discusses carbohydrates and sleep, saying that carbohydrate intake can affect serotonin and melatonin pathways and may make some people feel sleepier in the evening. He emphasizes individual variation and says he does not want everyone to copy his personal diet.

The conversation also references therapeutic ketogenic diets used in certain medical settings, including epilepsy. Dr. Jay describes a child with severe seizures whose symptoms improved on a medically supervised high-fat ketogenic diet, while acknowledging that such restrictive approaches are not appropriate or necessary for most people.

Plaque reversal and fat burning

Dr. Jay argues that a fat-burning metabolic state may be useful for people who want to reduce plaque. His reasoning is that plaque contains lipids, so improving the body’s ability to use fat as fuel may help address the metabolic environment associated with plaque accumulation.

He criticizes approaches that judge interventions mainly by whether they lower cholesterol. He says that, in his view, more meaningful outcomes include changes in plaque imaging, diabetes risk, cardiovascular events, stroke risk, cognitive outcomes, and overall health. This is a central theme of the interview.

LDL as a fat transporter

Dr. Jay says LDL should be understood as a particle that transports fats, not simply as “bad cholesterol.” He argues that LDL may rise in people who consume fewer carbohydrates and rely more on fat as a fuel source. The interview refers to the “Oreo Cookie Treatment Lowers LDL More Than High-Intensity Statin Therapy” case report, which described a large reduction in LDL cholesterol after a ketogenic participant ate Oreo cookies for a limited period.

The speakers interpret the case report as an illustration that LDL may decline when the body shifts from fat metabolism toward carbohydrate metabolism. However, a reduction in an LDL value after adding ultra-processed foods does not establish that those foods improve cardiovascular health, and no individual should use this example as dietary guidance.

Cholesterol context and confounding factors

Dr. Jay says that high LDL may occur in different contexts. He distinguishes between a person with higher LDL who is physically active, metabolically healthy, and using fat as fuel, and a person with higher LDL associated with smoking, trans fats, heavy alcohol intake, stress, poor sleep, inactivity, or metabolic dysfunction.

He argues that population studies can be difficult to interpret because LDL levels may be influenced by many variables at once. He says that a single cholesterol result should be interpreted within a broader picture that includes insulin resistance, triglycerides, HDL cholesterol, blood pressure, inflammatory factors, lifestyle, family history, and imaging when clinically appropriate.

Lp(a), ApoB, and the changing focus on markers

The interview discusses Lp(a), ApoB, LDL particle number, and LDL particle size. Dr. Jay says Lp(a) and LDL have related structures and suggests that both may have roles in immune response. He describes increases in LDL and Lp(a) during illness as possible evidence of this function.

He is critical of the tendency to treat individual lipid markers as isolated targets. He contends that scientific and medical attention has shifted over time from total cholesterol to LDL cholesterol, ApoB, particle number, and particle size. He argues that insulin resistance and broader metabolic dysfunction should receive greater emphasis.

Medications and clinical endpoints

Dr. Jay expresses skepticism about lipid-lowering medications, including statins and PCSK9 inhibitors, and says that studies should focus on clinical outcomes rather than only changes in cholesterol values. He raises concerns about diabetes risk and drug-industry influence.

These statements reflect the guest’s perspective and should be interpreted cautiously. Statins and other lipid-lowering therapies have substantial bodies of clinical research, and their risks and benefits depend on a person’s overall cardiovascular risk, medical history, LDL level, genetic factors, and treatment goals. Patients should not stop or change prescribed medicines without speaking to the clinician who manages their care.

Seed oils and dietary fat quality

The interview turns to seed oils and claims that commonly consumed industrial seed oils may contribute to metabolic dysfunction, oxidative stress, or inflammatory processes. Dr. Jay also discusses how animal feed can alter the fatty-acid composition of animal foods.

The discussion encourages viewers to pay attention to food quality and to limit highly processed foods. However, the broader question of which dietary fats best reduce cardiovascular risk is scientifically complex. A practical evidence-oriented focus is to minimize trans fats and highly processed foods, prioritize minimally processed plant and animal foods according to personal preferences and health needs, and work with a clinician or registered dietitian when managing cardiovascular risk.

Microplastics and plant sterols

Dr. Jay raises concerns about microplastics detected in arterial plaque and discusses potential effects of environmental exposures on inflammation and vascular health. He also discusses plant sterols, sometimes called phytosterols, and argues that excessive accumulation could be problematic for some people.

These are emerging and complex areas of research. Readers should avoid overinterpreting early or observational findings as proof that a particular exposure directly causes plaque in an individual person. Reducing unnecessary plastic exposure and emphasizing whole, minimally processed foods can be reasonable general strategies, but they do not replace established prevention and treatment approaches.

Why LDL may become trapped

The speakers discuss possible reasons that LDL particles become retained in artery walls. The conversation connects this issue to endothelial function, inflammation, oxidative stress, insulin resistance, high blood pressure, and the condition of the arterial lining.

Dr. Jay argues that the arterial environment matters as much as, or more than, a circulating LDL value. He uses this framework to support his emphasis on addressing metabolic dysfunction, blood pressure, inflammation, and lifestyle rather than focusing on a single lab number.

Measuring arterial plaque

The interview discusses coronary artery calcium, often called a CAC score, and coronary CT angiography, or CCTA, as tools that may help assess calcified and noncalcified plaque. Dr. Jay says he favors looking at actual plaque burden and changes over time rather than assuming risk solely from cholesterol values.

These imaging tests are not appropriate for everyone and involve clinical decisions about age, symptoms, radiation exposure, insurance coverage, and what a result would change. People considering imaging should discuss whether it is useful for their personal situation with a clinician.

Calcified plaque and healing

The speakers discuss the idea that calcified plaque may represent a more stable form of plaque compared with softer, more vulnerable plaque. Dr. Jay questions whether calcification should automatically be described as “healed” plaque and argues that the larger goal should be preventing or reducing harmful plaque burden.

The clinical meaning of calcium scores, soft plaque, calcified plaque, and plaque stabilization is nuanced. A CAC scan can be useful in certain risk discussions, but it should be interpreted alongside symptoms, family history, blood pressure, diabetes status, smoking history, laboratory findings, and other risk factors.

Diet to halt plaque progression

Dr. Jay advocates a lower-carbohydrate, metabolically focused eating pattern. He emphasizes reducing refined carbohydrate intake, avoiding frequent eating, supporting fat burning, and using fasting strategically. He also discusses the potential value of high-quality animal foods, minimizing ultra-processed foods, and adjusting diet based on individual response.

For readers, the more durable takeaway is that cardiovascular nutrition should prioritize sustainable habits. These generally include replacing ultra-processed foods with minimally processed foods, emphasizing fiber-rich plant foods where tolerated, selecting adequate protein, supporting a healthy body composition, avoiding tobacco, moderating alcohol or avoiding it, and choosing a dietary pattern that a person can maintain safely over time.

Iron, homocysteine, and genetics

The interview addresses high iron and homocysteine as potential contributors to vascular risk. Dr. Jay suggests that elevated iron levels may contribute to oxidative stress in certain circumstances and describes high homocysteine as a concern for vascular health.

He also discusses genetic causes of high cholesterol and says that people with unusually high levels may need a different evaluation from those whose lipid patterns are related primarily to lifestyle or metabolic health. This is an important distinction because familial hypercholesterolemia and other inherited lipid disorders require medical assessment and may substantially change treatment decisions.

Berberine and Nattokinase

Dr. Jay discusses berberine and nattokinase as supplements that some people use for metabolic or cardiovascular support. He presents them as possible adjuncts within a broader lifestyle strategy.

Supplements can interact with medicines, affect blood sugar or blood clotting, and vary substantially in quality and dose. People taking blood thinners, diabetes medications, blood-pressure medications, or multiple prescriptions should consult a pharmacist or clinician before using berberine, nattokinase, vitamin K2, or similar products.

Blood pressure and stress

The speakers describe high blood pressure as an important cardiovascular risk factor and connect it with chronic stress, poor sleep, insulin resistance, inflammation, diet, and inactivity. Dr. Jay emphasizes the importance of managing stress and improving lifestyle conditions that may influence blood pressure.

A practical point for readers is that blood pressure should be measured accurately and discussed with a clinician if readings are persistently elevated. Lifestyle measures can help, but some people also need medication to reduce their risk of heart attack, stroke, kidney disease, and other complications.

Core message

The interview’s central message is that arterial plaque and cardiovascular risk are complex. Dr. Jay argues that insulin resistance, inflammation, fuel metabolism, lifestyle habits, environmental exposures, and the health of the arterial wall deserve more attention than LDL cholesterol alone.

For readers, a balanced approach is to use the video as a conversation starter. Consider discussing personal risk factors with a qualified clinician, including blood pressure, glucose and insulin status, triglycerides, HDL cholesterol, LDL cholesterol, ApoB, Lp(a), family history, smoking, sleep, exercise, diet quality, and whether cardiovascular imaging is appropriate.