Is Cholesterol Really the Enemy? The Science May Surprise You

Join Dr. James Odell for Season 2 of the Science of Self-Healing Podcast! He's the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years, and he's here to share with you his extensive knowledge of medicine from a different perspective.

The Bioregulatory Medicine Institute

The Science of Self-Healing Podcast

For decades, we've been told that cholesterol is the enemy — a silent threat lurking in our bloodstream, clogging arteries and driving heart disease. But what if that story is incomplete? In this episode, we take a hard look at the science behind the lipid hypothesis, explore what cholesterol actually does in the body, and examine compelling new research that is quietly reshaping how leading cardiologists think about cardiovascular risk. If you've ever been handed a cholesterol number and told to worry — or handed a prescription — this episode is essential listening.

Transcript for: Is Cholesterol Really the Enemy? The Science May Surprise You

Hello, everyone, and welcome to the Science of Self-Healing podcast. For health and wellness knowledge from a different perspective. Produced by the Bioregulatory Medicine Institute, also known as BRMI. We are your source for unparalleled information about how you can naturally support your body's ability to regulate, adapt, regenerate, and self-heal. I'm your host, Dr. James Odell, the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years. And remember, this podcast is for informational purposes only and is not intended to be a substitute for the direct care of a qualified health professional who oversees and provides unique and individual care. The information here is to broaden our different perspectives and should not be construed as medical advice or treatment. Let's get started.

Hello everyone and welcome to another episode of the Science of Self-Healing. In today’s episode, we’re going to challenge the long-held belief that cholesterol is simply the enemy of a healthy heart, explore what it actually does in the body, look at some compelling new research that’s changing the conversation, and finish with practical steps you can take to support your cardiovascular health naturally.

For decades, cholesterol has been portrayed as one of the primary culprits behind heart disease. High cholesterol — especially low-density lipoprotein, or LDL — has been blamed for clogging arteries and causing heart attacks and strokes. As a result, millions of people take cholesterol-lowering medications, and dietary advice for generations has focused on avoiding cholesterol-rich foods and saturated fats.

But a growing number of clinicians and researchers have begun to question whether cholesterol is truly the root cause of cardiovascular disease. Here at BRMI, we’ve contributed to this conversation through research exploring cholesterol from a systems-based perspective — and our position is that cardiovascular disease cannot be reduced to a single laboratory number. Cholesterol must be understood within the broader context of inflammation, metabolic dysfunction, and the body’s natural regulatory processes. Within integrative and bioregulatory medicine communities, cholesterol is increasingly viewed not as a villain but as a necessary biological substance involved in repair, hormone production, and cellular communication.

So let’s start at the beginning — with where the cholesterol-as-villain story actually came from.

The Origins of the Cholesterol Hypothesis

The widespread belief that cholesterol causes heart disease comes from what’s known as the lipid hypothesis, which emerged in the mid-twentieth century. It proposed that high cholesterol leads to the buildup of fatty plaques in the arteries — a process called atherosclerosis — gradually narrowing arteries and raising the risk of heart attacks and strokes. LDL was labeled “bad cholesterol” because it carries cholesterol from the liver to the body’s tissues, while HDL was labeled “good cholesterol” because it carries it back to the liver.

But here’s the thing that often gets overlooked: more than half of people who suffer a heart attack have completely normal cholesterol levels. So if cholesterol were truly the primary driver of heart disease, we wouldn’t expect to see that. And that single fact has quietly driven decades of deeper investigation.

What researchers have found is that the problem is not LDL itself — but what happens when LDL becomes oxidized. Cholesterol is susceptible to oxidation, leading to the formation of what are called oxysterols — think of them as a damaged, chemically altered version of cholesterol — which are associated with cardiovascular disease, eye conditions like cataracts, certain neurological diseases, and some cancers. LDL particles are particularly susceptible to attack by reactive oxygen molecules — free radicals. One key enzyme here is myeloperoxidase— released by white blood cells when the arterial wall is inflamed. It oxidizes LDL, making it atherogenic — meaning it actively promotes plaque formation. The same process also damages HDL, rendering it dysfunctional. The result is inflammation and plaque buildup in the artery wall — a condition called vasculitis.

So the story isn’t simply “LDL bad.” It’s “oxidized LDL, in an inflamed environment, is dangerous.” That’s a meaningfully different picture — because it shifts the question from how much cholesterol you have, to what’s causing it to behave badly. And to answer that, we first need to understand why our bodies make so much cholesterol in the first place.

Cholesterol’s Essential Biological Functions

What often gets left out of the cholesterol conversation entirely is this: cholesterol is not inherently harmful. It is essential for human survival.

Cholesterol is a structural component of every cell membrane in the body, helping maintain stability and fluidity. It’s the raw starting material — the precursor — for steroid hormones such as estrogen, progesterone, testosterone, and cortisol, which regulate everything from reproduction and stress response to immune function and metabolism. It’s required for vitamin D synthesis, and the liver converts it into bile to digest dietary fats and absorb the fat-soluble vitamins A, D, E, and K.

And here’s a fact I want you to really sit with: cholesterol is a major component of the brain. I’ll say that again — it is a major component of the brain. It’s found in the myelin sheaths — the protective insulating layer around nerve fibers — and in the synapses, the tiny gaps between nerve cells where signals pass from neuron to neuron. Myelin allows electrical impulses to travel quickly and efficiently. If it’s damaged, those signals slow down. Cholesterol keeps it intact, and also supports the formation of synapses themselves, so your neurons can communicate at all.

The liver produces most of the cholesterol in our bodies, carefully regulating output based on the body’s needs. This tells us that cholesterol is not a dietary accident — it’s a tightly controlled biological resource. Which raises an important question: why does the medical community still focus on a single cholesterol number as the primary measure of cardiovascular risk? That’s what we’ll explore next.

Beyond LDL: What ApoB Tells Us

Here’s where even mainstream cardiology has quietly shifted away from the simple “good cholesterol, bad cholesterol” framework.

Researchers have increasingly focused on a protein called apolipoprotein B — or ApoB. Think of LDL particles as tiny delivery vehicles transporting cholesterol through the bloodstream. Each vehicle has a single ApoB protein on its surface — like a license plate. When you measure ApoB, you’re not measuring cholesterol content — you’re counting the number of those potentially harmful vehicles.

The National Lipid Association published a formal consensus in 2024 stating that ApoB more accurately reflects cardiovascular risk than LDL cholesterol alone. A systematic review that same year, covering over 593,000 participants, concluded that ApoB should be the primary clinical measure — because a standard LDL number is not a sufficient substitute.

Two people can have identical LDL readings but very different ApoB levels — meaning very different numbers of atherogenic particles. The person with more particles is at greater risk, but the standard test won’t show that. This is a deeply bioregulatory insight: context matters more than any single number. We’ll come back to just how far that insight goes when we look at the LMHR study shortly. But first — it’s not just how many LDL particles you have, it’s also what kind they are.

Not All LDL Is Created Equal: The Particle Size Story

Some LDL particles are large and buoyant — big, fluffy particles that float relatively harmlessly through the bloodstream. Others are small and dense — compact particles far more likely to penetrate the arterial wall, oxidize, and trigger inflammation. Research clearly shows that small, dense LDL is far more atherogenic than the large, buoyant kind.

A standard cholesterol panel doesn’t tell you which type you have. Two people can have the same LDL number but very different risk profiles depending on particle size. A 2025 paper in the Journal of Clinical Cardiology concluded that smaller, denser LDL may contribute far more to atherosclerosis than traditional lipid measurements indicate, and that clinical guidelines need to catch up.

What drives small, dense LDL? Largely the same things we’ll keep returning to: excess refined sugar, processed carbohydrates, insulin resistance, and chronic inflammation. These conditions cause the body to produce more of the dangerous particles — even when the total LDL number looks normal.

So we have a particle count problem with ApoB, and a particle quality problem with LDL size — both pointing to the same conclusion: the number on the standard test tells only a fraction of the story. With that in mind, let’s look at what bioregulatory medicine considers one of the most compelling perspectives on cholesterol — the idea that it may not cause arterial disease at all, but respond to it.

Cholesterol as a Response to Vascular Damage

At BRMI, one of the ideas we find most compelling is that cholesterol may act as part of the body’s natural repair system. The inner lining of blood vessels — called the endothelium — is constantly exposed to stress, toxins, and metabolic disturbances. When it becomes damaged, lipoproteins carrying cholesterol are recruited to help reinforce the tissue. Cholesterol may function like a biological patch — its presence in arterial plaque representing the body’s attempt to stabilize an injury, not the cause of it.

This shifts the focus to the underlying conditions that damage blood vessels in the first place — chief among them, chronic inflammation. And that idea got powerful scientific support from a landmark study published just this year.

New Research: The LMHR Study

In April 2025, researchers from the Lundquist Institute at Harbor-UCLA published a study in the Journal of the American College of Cardiology that directly challenges the idea that high LDL, on its own, drives heart disease.

They studied 100 metabolically healthy adults who had followed a long-term ketogenic — very low carbohydrate — diet for an average of five years. These individuals, known as Lean Mass Hyper-Responders, were lean and metabolically healthy but had very high LDL levels. Conventionally, every one of them would likely have been placed on a statin.

Using advanced CT imaging of the coronary arteries, researchers looked for plaque at the start of the study and again one year later. There was no correlation between high LDL or high ApoB and plaque presence or progression. The single best predictor of future plaque accumulation was whether plaque was already there at the start — not the cholesterol number.

The authors called for more individualized approaches to cardiovascular risk assessment. But the message is clear: in metabolically healthy people, high LDL alone does not appear to drive plaque progression. And notice — the study found no correlation with high ApoB either. This takes the argument a step further than simply saying LDL is an imperfect marker. It suggests that even ApoB — the more sophisticated particle count we discussed earlier — may lose its predictive power when metabolic health is good. Which tells us the most important variable isn’t which particle you’re counting. It’s the metabolic environment those particles are operating in. Strip away that context, and no cholesterol number fully tells the story. And that metabolic context — especially the role of chronic inflammation — is what we need to look at next.

The Role of Inflammation and Metabolic Dysfunction

Inflammation is a necessary short-term response to injury or infection. But when it becomes persistent and systemic — quietly ongoing throughout the body — it damages tissues everywhere, including the delicate lining of our arteries.

Several factors common in modern life contribute to this. Diets high in processed foods and refined sugars disrupt metabolic balance and increase inflammatory signaling. Environmental toxins — glyphosate, pesticides, heavy metals — add to the oxidative burden. Chronic psychological stress, poor sleep, and sedentary behavior all keep inflammatory pathways activated.

Metabolic dysfunction deepens the problem. Conditions like insulin resistance — where cells stop responding properly to insulin — and metabolic syndrome alter how the body handles fats and carbohydrates. This leads to elevated blood sugar, higher triglycerides — another fat in the blood — and more of those small, dense, oxidized LDL particles we discussed earlier. These disturbances damage blood vessels and fuel the inflammatory cycle. Within this framework, elevated cholesterol often reflects deeper metabolic imbalances rather than being their cause.

So if inflammation and metabolic dysfunction are the real drivers, what has conventional medicine been doing about it? Largely, prescribing statins. And that approach deserves a closer look.

Rethinking Statin Therapy

Statins work by blocking an enzyme the liver uses to produce cholesterol, and they quickly became some of the most widely prescribed medications in the world — sometimes even for people whose cholesterol is already within the normal range. But statins don’t just block cholesterol production. They block an entire biochemical pathway called the mevalonate pathway, which produces a whole family of important molecules.

The most critical is coenzyme Q10 — CoQ10 — produced inside our mitochondria, the energy factories of our cells. CoQ10 is essential for producing ATP, the basic unit of cellular energy that every cell in your body runs on. When statins inhibit CoQ10 synthesis, cells struggle to generate energy. This explains why so many statin users experience muscle pain, fatigue, and weakness. The side effects of CoQ10 deficiency include muscle wasting, severe back pain, heart failure of the heart muscle itself — striking, given that statins are supposed to protect the heart — neuropathy, and tendon inflammation sometimes leading to rupture. Other documented effects include cataracts, gastrointestinal problems, reproductive effects, and gynecomastia — abnormal breast tissue development in men. The FDA has also issued a formal warning that statins may cause cognitive impairment in some individuals, particularly the elderly.

And the cost is significant — between $900 and $1,400 per year — making statins the most widely sold pharmaceutical drug in the world, generating 12.5 billion dollars in annual revenue. None of this is to say statins have no place in medicine. But it does raise a genuine question: if we’re treating a number rather than a root cause, are we really solving the problem?

A Bioregulatory Approach to Cardiovascular Health

At BRMI, our approach is to restore the body’s natural regulatory capacity rather than suppress individual markers. Health is a dynamic balance between the immune, hormonal, nervous, and metabolic systems. When these function together harmoniously, the body maintains resilience and the ability to repair itself. When they’re disrupted — by inflammation, toxins, poor nutrition, chronic stress, or metabolic dysfunction — chronic disease can develop.

For cardiovascular health, that means reducing inflammatory burden, supporting detoxification pathways, improving mitochondrial function — remember those cellular energy factories — reducing oxidative stress, and optimizing nutrition with whole foods rich in antioxidants and healthy fats. It also means regular movement, restorative sleep, stress management, and time in natural environments. All of these contribute to the body’s ability to regulate inflammation and maintain vascular health. Which brings us to the most practical part of today’s episode.

What You Can Do: Practical Steps to Maintain Lipid Balance

To maintain a healthy lipid balance, consider the following:

Take antioxidants to prevent cholesterol from oxidizing. Vitamin C, vitamin E, and CoQ10 are particularly important — and if you’re currently on a statin, CoQ10 supplementation is especially worth discussing with your doctor, since statins deplete it.

Avoid trans-fats, found in many processed and fried foods, which are known to drive inflammation.

Avoid excess sugar, especially refined fructose, and artificial sweeteners like aspartame. These promote blood platelet clumping, which means increased clotting risk, and drive the production of small, dense LDL particles.

Take cod liver oil or algae oil — excellent sources of anti-inflammatory vitamin A, vitamin D, and omega-3 fatty acids EPA and DHA.

Consider evening primrose, borage, or black currant oil. These provide GLA — gamma-

linolenic acid — which the body converts into anti-inflammatory prostaglandins, internal signaling molecules that help regulate inflammation.

Eat copper-rich foods — shellfish, nuts, seeds, and dark leafy greens. Copper deficiency is linked to clot formation and arterial inflammation.

Avoid reduced-fat milk and powdered milk products like powdered whey. They contain oxidized cholesterol, shown to irritate the arterial wall.

Eat sulfur-rich foods: garlic, onions, and cruciferous vegetables like broccoli, kale, and cabbage. When the diet has sufficient sulfur and adequate cholesterol, sunlight catalyzes the formation of cholesterol sulfate — a water-soluble form of cholesterol that travels freely in the blood without needing to be packaged in an LDL particle. It reduces red blood cell clumping, prevents clots, improves blood flow, and supports cell repair. It’s a perfect example of the body using cholesterol intelligently — when given the right conditions.

Closing Thoughts

The real danger isn’t LDL cholesterol — it’s oxidized LDL operating in an inflamed, metabolically disrupted environment. Cholesterol is an essential molecule the body produces deliberately, for critical purposes in every cell, in the brain, in the hormonal system, and in the arteries themselves when repair is needed. A standard LDL test doesn’t tell you about particle size, oxidation, your ApoB count, your inflammatory markers, or your metabolic health. It tells you one number.

As the 2025 LMHR study showed — published in one of the most respected cardiology journals in the world — in metabolically healthy individuals, high LDL doesn’t predict plaque progression. The cholesterol number, without metabolic context, is not the full story. It never was.

A holistic approach that reduces inflammation, restores metabolic function, and supports the body’s own regulatory systems offers a far more effective path toward long-term cardiovascular wellness than chasing a single number on a blood test.

Well, that’s all for this episode. Please tune in in two weeks for another episode of the Science of Self-Healing. Till then — be well.

Bioregulatory medicine is a total body (and mind) approach to health and healing that aims to help facilitate and restore natural human biological processes. It is a proven, safe, gentle, highly effective, drugless, and side-effect-free medical model designed to naturally support the body to regulate, adapt, regenerate, and self-heal. BRMI is a non-commercial 501(c)(3) foundation and will expand and flourish with your support. Our goal is to make bioregulatory medicine a household term.

This article is for informational purposes only and is not intended to be a substitute for the direct care of a qualified health practitioner who oversees and provides unique and individualized care. The information provided here is to broaden our different perspectives and should not be construed as medical advice, diagnosis, or treatment.