Cholesterol and the Carnivore Diet

My cholesterol is high and I likely have the carnivore diet to blame.

Cholesterol is a complex topic. It’s involved in energy metabolism, hormone production, cellular structure, and yes – cardiovascular disease.

Here I want to create a brief resource on cholesterol and review some of the research. I also want to discuss why it’s been vilified for decades, why it might be “high” on a carnivore diet, and what numbers you should actually look out for.

Cholesterol and Clogged Arteries

For over half a century we’ve been told that cholesterol is bad.

If you look in a clogged artery, you find cholesterol. And heart disease is the #1 killer across the board.

Ergo: Cholesterol = Heart Disease = Death

Because of this line of reasoning big pharma developed statins, some of the most profitable drugs in history. They help reduce the amount of cholesterol the body makes.

But are they the miracle drugs that pharma proclaims?

Cholesterol and the Brain

The side effects of statins include memory loss, mental confusion, and people not feeling themselves. Is this really a surprise though?

The brain hogs 25% of all our bodily cholesterol. And it does this for good reason. Cholesterol serves vital functions between nerve endings that conduct electrical impulses that make movement, sensation, thinking, learning, and memory possible.

So it shouldn’t come as a surprise that low cholesterol increases the risk for brain problems like dementia, depression, and Parkinson’s disease.

And it’s not just the nerves in the brain that are affected as low cholesterol has recently been shown to increase the risk for nerve damage (peripheral neuropathy) in diabetics. (r)

Incidentally, big pharma even cautions against statins for the elderly. Why? Because LOW cholesterol is known to be associated with HIGH death rates in older people.

Cholesterol is a repair molecule. And as we age repair becomes increasingly important. And statins interfere with essential repairs and functions.

In fact, research shows that dietary cholesterol (via eating meat-based food as plant-based foods do not provide cholesterol) promotes the repair of demyelinated lesions in the brain. And thus “high” cholesterol helps prevent dementia. (r, r, r, r)

Further, more recent findings show that lowering plasma cholesterol by diet and drugs (i.e. a plant-based diet and statins) increases depressive symptoms. (r, r, r, r, r, r)

Cholesterol Scapegoat

Popular media tells us that cholesterol is bad. Yet cholesterol not only helps prevent dementia, but it protects against infectious disease, has no bearing on heart disease, and even reduces the chance of death from all causes. (r, r, r, r, r)

For decades cholesterol has been vilified – the scapegoat for cardiovascular disease and early preventable death. When really it’s a critical molecule to keeping the brain firing and body fit.

So I think it’s important to highlight some research that seems to get overlooked.

Cholesterol Research

Dangers of Low Cholesterol

• Low cholesterol is associated with decreased life span (r, r, r, r, r)
• Low LDL increases cancer risk (r, r, r, r)
• Low cholesterol increases Alzheimer’s disease risk (r)
• Low LDL increases Parkinson’s risk (r)
• Low cholesterol increases mental health risk (r, r)
• Low cholesterol connected with poorer cognition (r)
• Lowered cholesterol via statins are a failure and dangerous (r)
• Lowered cholesterol via low fat diet does not reduce cardiac events or mortality (r)
• Low LDL and increased risk of stroke (r)
• 75% of heart attack patients have normal or low LDL (r)

Benefits of “High” Cholesterol

• High cholesterol reduces all cause mortality (r, r, r, r)
• High cholesterol reduces risk of dementia (r)
• High cholesterol linked with lower Parkinson’s risk (r)
• High cholesterol lowers the risk of colorectal cancer (r)
• High cholesterol lowers the risk of breast cancer (r, r)
• High cholesterol protects from infections and heart disease (r)
• High cholesterol helps repair brain lesions (r)

Here’s another one: In a Russian study, they found having low cholesterol increased the risk for heart disease. (r) How about that?

From the famous Framingham data set, we can see that low cholesterol combined with obesity quadruples the risk of colon cancer in men. (r) From this same study we see that lower total cholesterol is associated with poorer cognitive performance.

A 2019 study shows that those with the lowest LDL (less than 70) were 2X as likely to die from both heart disease and cancer. (r)

Cholesterol and Heart Disease

But doesn’t high cholesterol result in heart disease?

There are numerous factors that go into heart disease, and singling out total cholesterol or even LDL for that matter is not only a bad idea, but a dangerous one.

Cholesterol and Car Accidents

Imagine you’re driving down the highway. You notice that every time you see an ambulance pulled over with its lights flashing you also see a car that’s been in a serious accident.

A logical conclusion might be: these ambulances are very dangerous vehicles causing all these accidents.

On the highway there’s a strong correlation between ambulances pulled over with lights flashing and serious accidents.

But, of course, the ambulances aren’t causing the accidents, they are responding to them. So while ambulances and severe car accidents have a strong correlation, to infer causality would be missing the whole picture.

The whole picture – not a paint stroke.

I think it’s important to consider the human system as a whole, especially when it comes to heart disease and cholesterol. If you just look at total cholesterol, or LDL-P, or just the pattern without including diet/lifestyle, history, and other labs like HDL, triglycerides, insulin, hs-CRP, body composition, blood pressure, CAC score, etc…you’re missing some (a lot!) of the whole picture.

I do think taking a more nuanced look (i.e. evaluating LDL-P and pattern type – which we’ll get to in a second) is a smart idea, and a step in the right direction, rather than just lumping all cholesterol into one big bucket. Because unlike total cholesterol, a high LDL-P is strongly correlated with atherosclerosis risk. But again, I think it’s important to not confuse “risk” with “cause.”

Because what would a high LDP-P mean in the context of a carnivore diet with someone with high HDL, Pattern A LDL, low triglycerides, low insulin, low hs-CRP, and 0% calcification on a CAC scan?

Could LDL-P be inconsequential if it isn’t coupled with the inflammation secondary to a plant-based diet?

In the context of a low carb diet perhaps we should even expect LDL to rise? Both ketone and cholesterol production use the same enzymatic machinery sharing the same precursor molecule. Mechanistically it makes sense that an increase in ketone production would lead to an increase in cholesterol production and the subsequent rise in LDL for transport.

Fatty acids are converted to Acetyl CoA and then to HMG CoA in the liver. From there they are converted to ketones and cholesterol.

This mechanism is highlighted in a study where participants fasted for 7 days and saw a 70% increase in LDL. Fasting shifted these fasters into a fat-based metabolism and the production of ketones which can explain this rise. (r)

These are questions to ask and think about.

Cholesterol: Where did we go wrong?

The “cholesterol is bad” belief is so pervasive you may wonder how it all came to be.

How can all these doctors be wrong?

The Key to the Confusion: The Fat – Cholesterol – Heart Disease Connection

In 1953 a doctor named Ancel Keys manipulated some data to conclude that ambulances (animal fats) were causing the car accidents (to return to our analogy).

I’d argue his research is one of the deadliest “studies” ever done.

Keys published his “research” showing countries with high animal fat intake correlated with a higher risk of heart disease.

This was the catalyst to the low fat, high carb recommendations of the last century – and is one of the biggest contributors to our skyrocketing epidemics of obesity, diabetes, and heart disease.

Meat became bad.

Grains and vegetable oils (“healthy fats”) became good.

What gets lost in history is that Keys excluded 22 other countries from the study that didn’t support his hypothesis.

His conclusions were based on epidemiology (observational studies) and these are limited in many ways even without cherry-picking the data.

Is it really animal fat to blame?

If we just take a quick glance at food consumption data, we start to see another picture:

• In England animal fat consumption was stable between 1920 and 1970 but heart attacks increased 10X.

• In Switzerland, after WWII, the death rate from heart disease decreased yet the intake of animal fat increased 20%

• In Yemen, the people who ate mainly animal fats had little heart disease and diabetes, while in Israel where they ate margarine and vegetable oils had the highest levels of both.

• In Georgia of the former Soviet Union, those who ate the most fatty meat lived the longest.

• In the US, animal fat consumption fell throughout the 20th century while heart disease increased.

Using USDA consumption data, compared to a century ago Americans eat less saturated fat and less red meat (but more poultry). We eat more vegetable oils. A whole lot more grains. In addition, smoking has declined and medical care and technology has improved. Yet these measures have failed to counteract our downward spiraling health trends. In fact, it’s getting worse and worse. (r, r)

Is it really the saturated fat? Could red meat really be to blame?

Today, in Hong Kong, they eat 400% more meat than the national guidelines recommend, but have one of the world’s longest life expectancies. (r)

People in India eat about the least amount of meat in the world. They also have one of the shortest life expectancies (as well as the highest rates of diabetes and depression in the world). Yet, the women in India who eat meat 5 times per week are less likely to suffer from obesity, heart disease, and cancer while having lower rates of insulin resistance and inflammation than non-meat eaters. (r)

This is consistent with the data from FAO that shows as meat-eating increases so does life expectancy.

Yes this is epidemiology, and I just mentioned how these data sets come laced with flaws and limitations, but that doesn’t mean these findings should be ignored. They should be further investigated. Especially as research is showing red meat intake to be inversely associated with cardiovascular disease and cancer – two of the leading causes of death. (r)

The Big Fat Mistake

Clinical trials in the 70s, following Keys’s theory, showed that eating saturated fat raises LDL cholesterol. This added fuel to the flame.

NOTE: Since these initial studies in the 70s – better research has shown that increased saturated fat consumption is only weakly associated with increased cholesterol. (r)

Keys linked animal fat to heart disease. Researchers linked fat to increased cholesterol levels. Combine these observations with what you find when you look in a clogged artery (cholesterol…) and we arrive at the pervasive conclusion that persists today: fat is bad (it raises cholesterol) and cholesterol is bad (it clogs arteries).

Fat Redemption

This logical train of thought where fat increases cholesterol and cholesterol is found in clogged arteries and thus leads to heart disease and death has one problem. It’s a house of cards built on a cracked foundation. The house crumbles under scrutiny.

The good news is that researchers started to realize Key’s false conclusions.

In 1998 a detailed study looked at the effect of fats in cardiovascular disease and found that Key’s conclusions failed. There was no evidence to link saturated fat to heart disease. (r)

In 2010 the search continued to justify the “fat is bad” doctrine of the previous decades. But a massive study published in “The American Journal of Clinical Nutrition” which included nearly 350,000 people concluded “dietary intake of saturated fat does not increase the risk of cardiovascular disease or coronary heart disease.” (r) And another that year with nearly 60,000 people arrived at the same conclusion, but instead found an inverse relationship with stroke (i.e. the more fat consumed, the less likely one was to suffer a stroke). (r)

In 2014, Dr. Chowdhury led a study which was published in the”Annals of Internal Medicine” and found “no evidence that eating saturated fat increased heart attacks and other cardiac events.” As Dr. Chowdhury put it: “It’s not saturated fat that we should worry about.” Instead, research shows that replacing saturated fat with vegetable oils increases the likelihood of death and heart disease (62% and 70% respectively). (r, r)

In a review of the research from 2010 to 2021, researchers found, “there is no scientific ground to demonize SFA as a cause of CVD.” (r)

Slowly but surely, we’re starting to get there.

Cholesterol: The Turning Tide

“Good” and “Bad” Cholesterol

Ok, maybe it’s not the fat, but could it be the cholesterol?

Just like “fat was bad,” so too was cholesterol. Egg yolks became dangerous. Egg white omelettes became the health food.

However, a substantial amount of research suggests that dietary cholesterol has little impact on total blood cholesterol levels. The body maintains cholesterol levels via a negative feedback loop. The more you eat, the less your body will make and vice versa.

Eat all the egg yolks you want and your blood total cholesterol likely won’t change much if at all.

But other experiments (like ones Dave Feldman is conducting) show that what you eat does influence cholesterol levels in a very dramatic and dynamic way.

So while dietary cholesterol may not be contributing to “high” blood cholesterol, the kind of foods you eat can. Further, diet not only influences total cholesterol in this way, but also the kinds of cholesterol transporters (lipoproteines) circulating in the blood.

There are some very smart doctors who think specific kinds of LDL (the “bad” cholesterol) are to blame (like LDL-P and Pattern B subtypes) for heart disease.

LDL – The “Bad Cholesterol”

Pattern A vs B

Not all LDL is the same. There is a big fluffy kind (“Pattern A”) that is thought to be harmless even by the lipidologist who stand behind the LDL-P hypothesis.

Then there is the small, dense, more worrisome version of LDL (“Pattern B”).

Eating saturated fat tends to increase the big fluffy, Pattern A, benign LDL.

Eating sugar and carbs tend to increase the smaller, scarier, Pattern B, LDL. (r)

(In fact, it’s been shown that if you replace fats with carbs it tends to increase fasting triglycerides as well. Not good.)

So it’s important to understand that even if you have a high total LDL-C (concentration) that doesn’t tell you if you are Pattern A or Pattern B.

LDP-C vs LDL-P

So we have different LDL patterns (A vs B) and we also have different LDL quantity measurements (concentration vs particle number).

LDL-C is your total concentration of LDL. This is the number you generally get in a blood test. It’s also the less important one.

LDL-P is a measure of total particles, not just concentration. It’s this absolute particle number that worries many lipidologists. And LDL-C and LDL-P don’t always move in the same direction. (r)

Your LDL-C could be “high” but your LDL-P could be “low” and vice versa (called discordance).

Further, evaluation of apoB (or LDL particle number) to assess cardiovascular/mortality risk is limited because:

• ApoB does not always associate with risk.
• ApoB does not improve prediction and is not better than many other risk markers.
• ApoB particles in themselves do not cause atherosclerosis.

Here are 71 papers on apo B and cardiovascular events / mortality, demonstrating that it’s not a superior risk marker.

Lastly, standard blood work doesn’t go into this detail. In most cases you’d need your doctor to order a fractionated lipid panel, which isn’t routinely done as it can be expensive, and if it’s not a superior marker of risk, why do it?

HDL – The “Good” Cholesterol

High HDL, the so-called “good” cholesterol, is thought to be protective against heart disease. It’s even been shown to be more predictive than LDL-C for cardiovascular risk.

A review of 60 clinical trials found that “the ratio of total to HDL cholesterol is a more specific market of CAD (coronary artery disease) than is LDL cholesterol.”

And what’s the best way to raise HDL? Saturated fats. (r, r, r)

People who adopt carbohydrate-restricted diets especially a meat-based diet like the carnivore diet tend to see triglycerides go down and HDL go up. 

According to Drs. Phinney and Volek:

“The triglyceride/HDL ratio provides a broader assessment of risk, and its relationship with insulin resistance makes it far superior to LDL-C.  And how best to improve your triglyceride/HDL ratio?  The striking reductions in plasma triglycerides and consistent increases in HDL-C in response to low carbohydrate diets are unparalleled by any other lifestyle intervention, or even drug treatment, and therefore represents the most powerful method to improve this ratio.”

The Art and Science of Low Carbohydrate Living

If we just broadly look at cholesterol or LDL, the research is quite clear – it doesn’t cause heart disease. (r) Looking at more specific numbers like HDL/Triglycerides as well as LDL-P and Pattern type give a better assessment of risk. And while I think looking at these detailed risk assessors are steps in the right direction, I also think one needs to be careful to look at these in the context of the whole picture.

Cholesterol and the Carnivore Diet: Meat-Eating Epidemiology

Because of the decades of false alarms sounding about fat and cholesterol, we now have even worse issues with epidemiological nutrition research.

These observational studies get tangled with a “healthy user bias.“

Since fat, cholesterol, and therefore red meat, has been vilified for decades, the kinds of people who eat it are the same kinds of people who don’t listen to other health warnings (i.e. like smoking). And on the flip side, people who do listen to health warnings, and hence eat less meat, are also more likely to eat less of other foods that ARE actually bad like sugar, trans fats, and processed foods. These people also tend to have healthier lifestyles – for example – they are more active and less likely to smoke and drink alcohol.

This healthy user bias underpins many false conclusions against meat-eating – which warrants the question – after all this – could it be that meat (fat and cholesterol ) was healthy in the end?

The evidence is compelling. (r)

Further, the Lipid Energy Model, a new theory that explains why LDL cholesterol may elevate in lean people who restrict carbohydrates, combines epidemiological observations with mechanistic support to hypothesize why these elevations in cholesterol could be normal, healthy physiology. (r, r)

The Lipid Energy Model suggests that lean people on a low carbohydrate diet require a much higher dependance on fat as fuel. Therefore, they have an increase in fatty acids released from adipose and these get taken up by the liver where they are packaged into VLDL to ship fat to the rest of the body. As VLDL drop off fatty acids to peripheral tissues, they become LDL and components from the breakdown process are passed to HDL particles.

This results in a lipid profile of high LDL and high HDL cholesterol, and low triglycerides, aka LMHR “Lean Mass Hyper Responders.“

If you are a LMHR and worried about elevated LDL, by simply eating 50-100g carbohydrate/day you can dramatically decrease this elevation. But I would make sure you know the pros/cons of carbs as well as which are the best ones.

NOTE: it appears you can also predictably decrease LDL on a low carb/high fat short term by overfeeding on fat, a potentially useful tool…

Measuring What Matters

One of the most challenging obstacles in health science is measuring what matters. 

For example, drugs are often developed to reduce the risk of heart attack or stroke with a goal of long term survival. These are hard to measure without long-term clinical outcomes. So instead, pharmaceutical companies use indirect “surrogate” or “proxy” measures.

Proxies help get drugs to market as fast as possible.

Blood Sugar and Death

For example, the drug Avandia is good at controlling blood sugar. Since blood sugar is easy to measure it was used as the proxy for this diabetic medication.

The problem is that 2 out of 3 diabetics suffer heart complications. So, one of the main goals of diabetic treatment is to reduce the risk of heart problems.

But what happened with Avandia is that although it helped control blood sugar, that proxy measurement got confused by what actually matters – death. And in Avandia’s case it increases the risk of heart attack, stroke, and death. (r, r, r, r, r, r, r)

The proxy (blood sugar) didn’t correlate with the outcome (mortality).

This happens all the time.

Cholesterol Proxy

Statins are prescribed to lower cholesterol. Cholesterol is a proxy. There are drugs like Vytorin and Zetia which are great at lowering cholesterol. But they have no evidence of lowering heart disease or stroke. But lots of evidence of adverse side effects. (r)

So what numbers matter?

When it comes to cardiovascular disease and risk there are a few numbers that I would pay special attention to, remembering to keep the whole picture, all the context, in mind.

• Particle size pattern (r, r, r)
• Remnant cholesterol (it may be higher in a HFLC diet because the higher proportion of distribution by VLDLs)
• Triglycerides (<150 mg/dL) and especially Trigs/HDL ratio (the closer to 1.0 the better – mine were actually under 1) (r)
• Inflammation – hs-CRP (< 1.0 mg/L)
• Blood sugar, HbA1c and insulin
• Blood pressure
• Body composition (maintaining muscle mass and limiting excess fat) as well as waist to height ratio (r, r, r, r)
• CAC scans (r, r, r)

If you look at all these numbers together you can start putting the puzzle pieces together. You can start seeing a more clear and complete picture of actual risk.

Cholesterol and the Carnivore Diet: Conclusion

What led me to the carnivore diet was a search for brain health. I wanted to get rid of the fog that was clouding my thinking. I wanted to find a level of mental performance that could drive me through the day in high gear.

I found it in a meat-based carnivore diet.

And while stable blood sugar levels, the removal of phytotoxins, and complete nutrition from a meat-based diet all played a role in recovering my inherent brain performance, I believe, the increased dietary cholesterol was a significant piece of the puzzle as well.

Plants do not provide any cholesterol. Only animal-sourced food provide cholesterol. But cholesterol is so important that the body will make it regardless if you eat it or not.

However, research suggest that if you aren’t helping your body out by consuming cholesterol in the diet, there are consequences. And we see many of these ramifications highlighted in decreasing brain and mental health.

Further, we see that it’s not so much dietary cholesterol that impacts one’s lipid profile, rather it is carbs/sugars that tend to worsen risk factors (like elevating the triglyceride to HDL ratio and LDL-P).

If Fat and Cholesterol are OK – then why are we so sick?

Humans evolved over millions of years as meat-eaters. Then overnight (in the evolutionary time scale) it became the cause of heart disease, obesity, diabetes, and the chronic diseases of modern society.

Heart disease didn’t start to take off in the 1920s. How can a modern disease be related to an old-fashioned food?

What’s really to blame?

Could it be that our diet that has radically diverged from what we are designed to eat?

Could all the sugars, grains and flours, processed vegetable oils (plant-based foods that continued to get more and more transformed via science and technology) cause inflammation in blood vessels that invite the artery clogging plaques to form in the first place?

The Lazy River

For millions of years cholesterol floated down the lazy river (blood vessels) on tubes (lipoproteins). The shore was smooth. These tubes (carrying cholesterol) would float against the shore and bounce right off to continue their journeys down the river on their way to deliver essential services downstream.

But in the last century the shores have changed. The onslaught of sugars, grains, and oxidized vegetable oils were like dumping debris into the river. It damaged the shores. They became rugged, jagged, and sticky.

In this condition some tubes pull off onto the shore to try and help clear the debris. But their helpful hands get overwhelmed by the non-stop debris dumped into the river meal-after-meal, day-after-day.

With greatly damaged shores tubes get stuck on the jagged-shore lined with sticky debris. The lazy river narrows (plaque formation). It starts flowing at higher speeds (high blood pressure). The once lazy river turns into dangerous white water rafting with an ever-shrinking bottleneck.

The river gets clogged, and the ride comes to an end.

If you’d like to learn more about how to go about a meat-based diet and what you should look out for, I’d highly recommend watching the Meat Health Masterclass: