Welcome to the Dr. Kumar Discovery Podcast. I’m Dr. Ravi Kumar — a board-certified neurosurgeon — and in this podcast, I aim to challenge medical dogma, cut through bias, and bring clarity to complex health topics.
I believe in questioning everything. It’s something I’ve done throughout my own life and medical career, and it’s something I want to invite you to do with me — because when it comes to your health, knowledge truly is power. The right information can help you make better, more informed decisions — just like it has for me.
Today’s episode tackles a crucial question: Does high LDL cholesterol cause heart disease?
And the reason that question matters is because it leads directly to another — should we be taking medications that lower LDL?
Before we dive in to that, just a quick disclaimer: I am a medical doctor, but I’m not your doctor. This show is for informational purposes only and is not intended to diagnose or treat any medical condition.
I’m here to provide you with information that helps you think more clearly about your health. My goal is to give you the most honest and unbiased perspective I can—so you can take that knowledge, bring it to your own healthcare provider, and figure out the best strategy to accomplish your personal goals.
So let’s get to the question: Does high LDL cholesterol cause heart disease? And should we lower it?
The AHA’s message to the world is simple when it comes to LDL: Lower is better.  For generally healthy adults, they want you to keep your LDL under 100 mg/dL.  If you’ve already had a heart attack or stroke or are deemed high risk, they want your LDL under 70 mg/dL.  There’s no magic cutoff where benefits stop per the AHA—every milligram you shave off helps reduce your risk.  In other words, they want you to drive your LDL as low as you safely can.
But should we actually be doing that?
To answer that, we have to answer our primary question: Does high LDL cholesterol actually cause cardiovascular disease? Because if the answer is yes, then lowering it makes sense. But if the answer is no — or even uncertain — then the idea of medicating millions of people to lower LDL starts to fall apart.
So where do we begin? I think the first step is to look at history. How did we come to believe that high LDL is the driving cause of heart disease?
To really understand this, we have to go back to the 1940s.
At the time, America was in the middle of a cardiovascular disease epidemic. By the mid-20th century, heart disease was responsible for nearly half of all deaths in the United States.
One of its most famous victims was President Franklin D. Roosevelt. Even before his election, his blood pressure was elevated — 140 over 100 — but back then, that was considered normal. Over the course of his presidency, his systolic pressure crept into the 180s, yet his personal physician reassured everyone that it was nothing to worry about.
That changed when his daughter, Anna Roosevelt, insisted on a second opinion. He was taken to Bethesda Naval Hospital, where he was diagnosed with hypertensive heart disease and cardiac failure. At the time, treatment options were limited. He was started on digitalis and told to reduce his salt intake, but his blood pressure continued to rise — eventually reaching 240 over 130.
At the Yalta Conference in 1945 to decide Germany’s fate after the war, Churchill’s physician noted in his diary that Roosevelt looked gravely ill and likely had only months to live. Weeks later, Roosevelt died of a massive cerebral hemorrhage — with a reported blood pressure of 300 over 190.
His death was a turning point. President Truman soon signed the National Heart Act, which created the National Heart Institute and allocated funding for cardiovascular research. Part of that funding launched a 20-year epidemiological study in Framingham, Massachusetts — what we now know as the Framingham Heart Study.
The Framingham Heart Study was a landmark longitudinal cohort study — meaning researchers followed participants over time to track health outcomes. It began in 1948 with 5,209 men and women between the ages of 30 and 62 in Framingham, Massachusetts. The goal was simple but ambitious: to identify the causes of cardiovascular disease.
By 1961, the study had identified three major risk factors for heart disease — high blood pressure, smoking, and high cholesterol. Around the same time, physiologist Ancel Keys was conducting Seven Countries Study and promoting the idea that saturated fat raised cholesterol, which in turn caused heart disease.
Together, these two narratives fueled a decades-long war on cholesterol — especially LDL.
LDL… remember, is the particle that carries cholesterol from the liver to tissues throughout the body for repair and maintenance. A events unfodled in the mid 20th century, LDL became branded as the “bad cholesterol,” turning a critical biological transport system into a public health villain.
So whenever I hear claims that a natural part of our biology — like LDL — is inherently harmful, I want to step back and ask: What’s the evolutionary context? Why would we have created a system that is inherantly harmful. And.. What was the natural state of cholesterol in humans before industrialization?
To answer that, we need to look at historical cholesterol numbers. But.. Our ability to measure cholesterol is relatively recent advancement. In the 1920s, we had only crude tools. It wasn’t until 1949 that ultracentrifugation allowed scientists to separate different lipoproteins like LDL and HDL. Then, in the 1970s, the Friedewald formula was developed — finally giving us a practical way to estimate LDL cholesterol from total cholesterol, HDL, and triglycerides.
Due to this technological lag in cholesterol measurement, we don’t have good data from before the 1950s on what human cholesterol levels looked like in the US and much of the developed world. — and by that time, modern diets had already taken hold and likely skewed our natural lipid physiology. But what we can do… is look at traditional populations, largely untouched by modern society, that have had their cholesterol levels measured. These groups offer a window into how human physiology functions in more ancestral conditions.
In studies of traditional societies — like the Tsimane of Bolivia, the !Kung of the Kalahari, the Maasai of Tanzania, the Greenland Inuit, the Siberian Yupik, and the Tokelauans of the South Pacific — total cholesterol levels range from around 247 to 120 mg/dL, and LDL levels from about 170 to 75 mg/dL.
And What stands out is that none of these groups — despite being largely free of ischemic heart disease — have ultra-low cholesterol. And I say this jokingly,None of these groups appear to be following the AHA guidelines.
And there’s a reason for this. Cholesterol is essential. It’s used for cellular repair, hormone production, and immune defense. In fact, people with very low cholesterol often have chronic illness, and in environments where infection risk is high, cholesterol plays a protective role. Cholesterol, inherently, is a survival molecule.
So based on evolutionary biology and observational data from traditional cultures, it’s clear that extremely low cholesterol is not a natural or necessary condition for human health. In fact, in some of these groups — like the Greenland Inuit — total cholesterol levels around 247 and LDL around 170 are perfectly normal, and not associated with ischemic heart disease.
Now that we’ve seen how wide the natural range of cholesterol is in traditional populations, the next question is this: Is modern life pushing cholesterol levels higher — and is that what’s causing disease?
To explore that, we need to look at epidemiological data of modern societies. And just to remind you, epidemiology can’t prove causation — it shows patterns and associations. But it’s still a powerful tool to generate hypotheses and uncover trends worth investigating further.
One notable example is NHANES III — this is the third National Health and Nutrition Examination Survey — a large, US study that looked at over 14,000 adults aged 18 and older. Researchers measured participants’ LDL cholesterol levels and tracked outcomes like cardiovascular death, stroke, and overall mortality.
What they found was very surprising. - People with LDL levels below 70 mg/dL actually had higher mortality rates: 45% higher all-cause mortality, 60% higher cardiovascular mortality, And most strikingly, a 400% increase in stroke mortality — that’s four times the risk of death from stroke in those with very low LDL. And of note, pushing LDL below 70 mg/dL, the exact same level that is associated with increased mortality in this group,  is the target recommended by the American Heart Association for people at high risk.
Now, on the other end of the spectrum, the NHANES study ALSO found that individuals with LDL levels above 190mg/dL showed a 49% increase in cardiovascular mortality, and a 63% increase in coronary heart disease mortality… But — and this is key — there was no statistically significant increase in stroke mortality or all-cause mortality among those with high LDL.
So… This throws a wrench into the idea that high LDL is universally harmful. Because if very low LDL — below 70 mg /dL — is associated with higher rates of death from stroke, heart disease, and all causes, we need to seriously question the wisdom of aggressively driving LDL so low in the general population. And it definitely challenges the idea that “Lower is better”
Even more interesting — the range of LDL that seemed safest in this study, roughly 70mg/DL to 190mg/dL, overlaps almost perfectly with the range we saw in traditional, non-industrialized populations. That’s a pretty compelling observation.
Another important study looked at over 68,000 people over the age of 60 and found something striking:
LDL cholesterol was inversely associated with all-cause mortality.
In other words, the higher a person’s LDL, the lower their risk of death — the exact opposite of what the traditional cholesterol hypothesis would predict.
This challenges the long-standing belief that high LDL leads to early death. Instead, the data suggest that in older adults, higher LDL may actually be protective — and that lower LDL is associated with a higher risk of death.
Now, after hearing that, take into account this bit of information: an NHANES study from 2011–2012 showed that over 70% of adults over 65 were taking statins to lower their cholesterol — they may be literally taking an anti-longevity drug based on what we’ve learned.
Of course, correlation doesn’t prove causation. And Some critics argue this is a case of reverse causation — that people don’t die because their cholesterol is low, but rather that their cholesterol drops because they’re dying, possibly from cancer or other terminal illnesses.
But this study addressed that concern. In five of the studies included in their review, participants with low LDL had been screened to rule out terminal disease at baseline — meaning they were healthy at the time their cholesterol was measured and determined to be low.
This pattern — low cholesterol predicting higher mortality in older adults — has now been observed across multiple studies and seems to be a consistent trend.
But here’s the real kicker.
Remember the Framingham Heart Study — the same study that helped launch the decades-long push to lower cholesterol in the name of preventing heart disease?
Well, that study didn’t stop in the 1960s. It continued for decades, tracking participants over the long term. And in 1987, researchers published a 30-year follow-up on those original participants.
What they found was surprising.
In people over the age of 50, for every 1 mg/dL drop in total cholesterol, there was: an 11% increase in overall mortality and a 14% increase in cardiovascular death over the next 18 years
Let me say that again: a tiny drop in cholesterol was associated with incremental higher risk of dying, from both heart disease and all causes, in adults over 50.
So the same study that initially linked high cholesterol to heart disease, later showed that, after age 50, lower cholesterol was associated with worse outcomes.
In that context, higher cholesterol actually appeared protective.

Interlude
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So now we’ve seen that traditional populations — untouched by modern life — have a wide range of total cholesterol and LDL levels, from low-normal to fairly high. And across that range, they’re largely free of heart disease. 
We also have epidemiological studies showing increased risk at both extremes — especially with very low cholesterol — including higher rates of cardiovascular death and all-cause mortality.
So between the traditional cultures and modern observational data, we have a pretty good idea of where humans naturally fall on the cholesterol spectrum.
But we need more clues still.  Which means we need to ask more question that get us closer to making some type of conclusion:
And here’s one:
Are there modern populations with naturally high cholesterol who also live in industrialized societies?
And if so, are they all dying of heart attacks?
If that were the case — if high cholesterol in a modern lifestyle reliably caused early death — that would support the argument that high LDL is dangerous.
Well, we actually do have such a population: people with familial hypercholesterolemia, or FH — a genetic condition that causes very high LDL levels from birth.
One study looked at 4,688 men and women with FH and found that they did have higher rates of cardiovascular death — but only up until the age of 70. After that, the association between high cholesterol and mortality disappeared.
So what does that tell us?
It suggests that high LDL may increase cardiovascular risk earlier in life, but that relationship fades — or even reverses — with age.
It’s another clue in a complex picture. Still not proof of causation, but it helps us understand that the relationship between cholesterol and health may not be as simple as “lower is better.”
But like everything in human biology, the story is rarely simple.
The body is incredibly complex — a dynamic interplay of systems, pathways, and feedback loops. So anytime we reduce it to something like “high LDL equals heart disease,” we risk missing the bigger picture.
So if we have these patients with FH that have high LDL and high rates of heart disease, can we find a populations of people living in modern society who also have high LDL — but have no evidence of heart disease?
And the answer is… Yes we do.m A very interesting group of studies explored this concept using a tool called the coronary artery calcium scan. This is a type of CT scan that images the arteries feeding the heart — the coronary arteries — and looks specifically for calcified plaque.
Here’s how it works: you’re connected to an EKG machine that tracks your heartbeat, and the CT scan takes synchronized snapshots of your heart at the same point in each cardiac cycle. This creates a clear, stable image of the coronary arteries, allowing the scanner to detect and measure calcium buildup — which is a marker of atherosclerotic plaque.
The result is a score: 0 means no detectable calcium — and by extension, no measurable arterial disease. 1–99 suggests mild plaque. 100–399 indicates moderate atherosclerosis. 400 and above means significant plaque burden and higher risk.
Now, here’s where it gets interesting.
A Danish study looked at 23,132 patients who underwent CAC scans — and it also measured their LDL cholesterol levels. What they found was striking:
Patients with a CAC score of 0 had extremely low cardiovascular risk — even if their LDL was over 193 mg/dL.
Let me repeat that: individuals with very high LDL levels — well above the conventional risk threshold — but a CAC score of 0 had negligible risk of heart attack.
So what does this tell us?
It tells us that LDL is not the whole story.
Because if high LDL alone were enough to cause heart disease, these patients — with LDLs over 190 — should have had significant plaque buildup. But they didn’t. They had clean arteries.
That’s powerful evidence that atherosclerosis isn’t just about LDL. There are other factors at play — inflammation, oxidative stress, endothelial injury — and simply lowering LDL may not be the magic bullet.
And this more recent data from CAC scoring is actually supported by several older studies — particularly autopsy studies — that looked directly at the relationship between serum cholesterol and atherosclerosis.
One study, conducted in India in 1961, examined 500 individuals who had recently died from causes unrelated to cardiovascular disease. Shortly after death, their cholesterol levels were measured — and important to this study is that postmortem cholesterol levels closely mirror those taken just before death.
Researchers then performed autopsies to assess the degree of atherosclerosis in their arteries.
The results?
There was no correlation between blood cholesterol levels and the extent of atherosclerosis.
In fact, they found people with very low cholesterol who had severe atherosclerosis, and others with very high cholesterol who had very little arterial disease.
This kind of evidence adds yet another layer of complexity. It challenges the assumption that cholesterol levels alone drive plaque buildup, and it forces us to rethink the simplicity of the “cholesterol equals atherosclerosis” model.
So here’s the next logical question:
What about the people actually having heart attacks?
If high LDL truly causes heart disease, then you’d expect most heart attack patients to have high cholesterol, right?
Well, several studies have looked at this — including one particularly large analysis involving 115,492 patients who were admitted to the hospital with acute myocardial infarction, or heart attack.
Researchers measured their cholesterol levels at the time of admission and grouped them into quartiles. The lowest quartile was defined as having LDL levels below 77 mg/dL.
And here’s what they found: Patients with the lowest LDL levels had the highest amount of myocardial necrosis — meaning larger areas of heart muscle had died. These same patients also had the highest rates of adverse cardiovascular events after admission. And perhaps most telling: in-hospital mortality — the risk of dying while hospitalized — was highest in those with the lowest cholesterol.
So in this massive group of real-world patients who had just suffered heart attacks, the ones with the lowest LDL were least likely to survive.
That’s not what you’d expect if high LDL were the primary driver of heart attacks. If anything, this study suggests that very low cholesterol may be a marker of vulnerability, not protection.
Another study looked at cholesterol levels in patients admitted with NSTEMIs — that stands for non-ST elevation myocardial infarctions.
To clarify, an NSTEMI is a type of heart attack where the coronary artery is partially blocked, meaning the heart muscle is deprived of oxygen and nutrients, but not completely cut off. The tissue is injured but still alive. In contrast, a STEMI involves a full blockage and usually results in permanent heart muscle death.
In this study, about 500 patients with NSTEMIs were evaluated. They were split into two groups: One group had LDL levels below 105 mg/dL. The other had LDL levels above 105 mg/dL
Researchers followed both groups for three years after admission. And here’s what they found:
Patients with lower LDL levels had higher all-cause mortality. Specifically, those with LDL below 105 had over a 100% higher relative risk of death over the three-year period compared to those with higher LDL. Low LDL was linked to a significantly higher chance of dying, even years after the heart attack.
So let’s take a step back and summarize what we’ve covered so far.
We started with the history — how cholesterol became public enemy number one in the world of cardiovascular disease. It began with the Framingham Heart Study, launched shortly after the death of President Franklin D. Roosevelt from cardiovascular disease. That study showed a positive association between higher total cholesterol and cardiovascular events, setting off decades of focus on cholesterol reduction.
But when we looked beyond that, things got more complicated.
We examined traditional cultures, largely untouched by modern lifestyles, and found that cholesterol levels varied widely — from nearly 250 mg/dL in the Inuit of Greenland, to around 120 mg/dL in the !Kung of the Kalahari — and yet, these populations had very little ischemic heart disease.
Then we looked at epidemiological studies. These showed that very low LDL cholesterol — under 70 mg/dL — was consistently associated with higher all-cause mortality, higher cardiovascular mortality, and in some studies, a dramatically higher risk of stroke. While high LDL — over 190 — was also associated with increased cardiovascular risk, it wasn’t linked to higher overall mortality.
Next, we looked at people with familial hypercholesterolemia — a genetic condition that causes extremely high LDL levels. These individuals did show a higher risk of heart attacks at younger ages — but that risk disappeared after age 70, suggesting the relationship changes over time.
We also discussed the coronary artery calcium (CAC) scan, a modern imaging tool that looks directly for calcified plaque in the coronary arteries. What we found was that individuals with very high LDL levels but a CAC score of zero had negligible cardiovascular risk. In other words, even with “very high” cholesterol, if there’s no plaque, the risk of cardiovascular disease was minimal.
Finally, we reviewed studies of patients actually having heart attacks — both STEMIs and NSTEMIs — and found that those with lower cholesterol at the time of admission had worse outcomes, both in the hospital and over the long term. That’s despite not having high cholesterol to begin with.
So when you put it all together, it appears that cholesterol has some duality.  On one hand it is essential to life and strongly associated with survival and longevity.  On the other hand it appears it can become ensnared in the disease process of atherosclerosis.
Its relationship to cardiovascular disease is very complex and nuances — shaped by age, context, underlying health, and many other factors. And in some cases, low cholesterol may actually be a risk, not a protection.
So how do we make sense of all this?
It’s complicated — and frankly, the literature is massive and often contradictory. Debating cholesterol and heart disease can feel a lot like talking about religion or politics — people are entrenched, and opinions vary wildly.
But in situations like this I like to take a step back and ask: What does common sense and real-world evidence tell us?
We know from traditional cultures that a broad range of cholesterol levels — both high and low — can exist in healthy, heart-disease-free populations.
We know that people with very high LDL can have minimal cardiovascular risk if their coronary artery calcium score is zero.
We know that very low cholesterol can be harmful, especially in older adults.
And we know that very high LDL may pose more risk earlier in life, but that link seems to weaken — or disappear — as people age.
So why is the correlation between LDL and heart attacks so inconsistent?
Well, one idea that helps make sense of it is something called the Injury Response Hypothesis.
This theory suggests that atherosclerosis doesn’t begin with cholesterol — it begins with damage to the endothelium, the delicate inner lining of blood vessels.
And when that injury occurs — from things like high blood pressure, smoking, toxins, inflammation — the body sends LDL cholesterol to the site to help repair it.
But in the process, LDL can get trapped, oxidized, and inflamed, becoming part of a plaque that builds up over time. So LDL ends up at the crime scene, but that doesn’t mean it caused the crime.
If you’ve listened to previous episodes, you’ll remember we talked about linoleic acid — the omega-6 polyunsaturated fat found abundantly in seed oils. When you consume high amounts of linoleic acid, your LDL particles become highly oxidizable. They essentially turn into oxidative bombs — primed to go off in the right (or wrong) environment.
Now remember: the role of LDL is not to cause damage. Its job is to deliver cholesterol to tissues for repair and maintenance, including to sites of endothelial injury. That’s a normal, healthy function.
But here’s where things can go wrong.
Let’s say you’re living in a state of chronic endothelial injury. Maybe you smoke or are frequently exposed to secondhand smoke. Maybe you have high blood pressure pounding on your arteries. Or diabetes, where high blood sugar leads to glycation and oxidative stress. Maybe you’re dealing with chronic infections, air pollution, or you drink alcohol in excess — all of which increase oxidative stress.
In this setting, your endothelium is constantly calling for help — and LDL is the first responder.
Now, normally this situation would likely still be salvageable from a healing standpoint, but when you add seed oils to the mix you are loading your LDL particles with oxidizable fats.
What happens next?
These LDL particles arrive to help — but instead of aiding repair, they act like Trojan horses.
Once inside the damaged endothelium, their linoleic acid content oxidizes rapidly, turning them dysfunctional and toxic. Macrophages rush in to clean up the mess, engulf the oxidized LDL, and transform into foam cells.
That debris accumulates, scars over, and eventually calcifies — and now you’ve got an atherosclerotic plaque.
So in that context — where there’s chronic injury and your LDL particles are highly oxidizable — LDL loses its innocence. It becomes part of the pathology.
And I think this is when a coronary artery calcium (CAC) scan becomes a powerful tool. If you have high LDL and you’re living a high-risk lifestyle, a CAC score can tell you if the damage has already begun.
If your score is not zero, that’s a sign that LDL is playing a pathological role — and in that case, lowering your LDL may be a good idea. It gives you time to make a change.
You can stop injuring your endothelium. You cut out seed oils and replace them with monounsaturated fats like olive oil or saturated fats from grass-fed butter, ghee, or coconut oil. You start addressing the root causes.
But here’s the thing: if you’ve already accumulated injury — if you’ve got existing atherosclerotic lesions — your body is still in a vulnerable state.
In that case, it may still make sense to go on a medication to lower your LDL while you work on reversing the damage. You’re giving your arteries a break while the healing process begins. And once you’ve fixed those causative factors and your overall risk improves, you can revisit the idea of stopping the medication — in partnership with your doctor.
This is where allopathic medicine, which I was trained in as a neurosurgeon, can play an important role. Allopathic medicine which is the style of medicine an MD practices is designed to treat disease — but it doesn’t always address the root cause.
I often use this analogy: imagine your sink is overflowing. The water’s spilling onto the floor, and instead of fixing the clog, we just keep mopping the floor.
That’s what we often do in modern medicine — prescribe statins, antihypertensives, or perform surgeries. We’re managing the damage, but the root problem — the clogged drain — remains.
Eventually, no amount of mopping will keep up. That’s when chronic illness overwhelms the system.
So my approach is: yes, mop the floor if you need to. That’s where medications might help — temporarily managing risk while you work on the real fix. You have to pull the plug — remove the clog — and solve the underlying problem.
Now lets, talk about a different scenario.
 Let’s say,  you’re already observing a health lifestule — if you don’t smoke, your blood pressure is under control, you’re not flooding your system with seed oils, and you’ve got a balanced omega-6 to omega-3 ratio — then your LDL particles likely aren’t oxidizing, and they aren’t a problem. They show up to areas of infrequent endothelial injury, deliver cholesterol to aid in repair, and then move on.  Your body is functioning like it is supposed to.
But your LDL is high and your doctor is telling you you should go on a medication. You can get a coronary artery calcium scan. This will definitively guide you and put your mind at ease.
Because if your CAC score is zero, you’ve just reassured yourself in the clearest, most evidence-based way we currently have — that your cardiovascular risk is essentially negligible.
So where does that leave us?
Well, it doesn’t leave us with a definitive answers — but that’s okay.
Because in medicine, definitive answers are rare. What we can do is gather the best available evidence, strip away the bias, and use common sense to guide our decisions.
If you’re getting information from a pharmaceutical company that makes statins — or from a hospital system that profits from disease management — you’re likely not always getting objective advice. Not necessarily due to bad intentions, but because subconscious bias is everywhere.
That’s why it’s so important to get your information from sources that prioritize clarity over agenda. Then, run it through your own common sense algorithms, and make prudent, personalized choices based on your risk, your values, and your health.
Now, some of you may already be on a statin — or your doctor may have recommended one.
And you might be wondering: What should I do?
Should I stay on it? Should I start it? What are the risks and benefits?
That’s exactly what we’ll explore in the next episode.
We’ll talk about what to do if you’re already on a cholesterol-lowering medication, or you’re being told to start one — but you’re not convinced by the standard narrative.
Because the story doesn’t end here — it continues.
Thank you so much for joining me on this journey of discovery.
I’m Dr. Ravi Kumar.
See you next time — Cheers.