The Cholesterol Story - Part 1: The Diet-Heart Hypothesis

June 15, 2022

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The cholesterol issue is the most disputed topic in nutrition science, and perhaps all of science. The amount that has been written and published on this issue could fill libraries. In this multi-part blog series though, we are here to write some more. We'll try to cover everything briefly. The entire literature on this topic is so vast, it could take one over a decade to go through it completely. And indeed, investigative health journalist, Nina Teicholz claims it took her 15 years of research to author her groundbreaking book The Big Fat Surprise, which has had a big impact on upending the old paradigm.

What is the “cholesterol issue”? The Diet-Heart hypothesis

Cholesterol is a lipid(a fatty substance) found in our bodies. It is an essential component of our body and serves multiple vital functions. It is involved in the production of vitamin D, bile, and multiple hormones. It is an important component of our cell membranes.

So what’s the “issue” with it? Consider these foods: Red meat, egg yolks, butter, ghee, full-fat dairy and animal fats. These are some of the most nutritious(and delicious) foods on the planet, yet you’ve probably always been told to avoid them. Been told that they’re unhealthy and will give you heart disease. These notions all originate from a single hypothesis that originated in the 1950s in America, called the Diet-Heart hypothesis or the Lipid hypothesis, which proposes the following:

Dietary saturated fat and cholesterol increase blood cholesterol
Elevated blood cholesterol increases the risk of having a heart attack
Therefore, dietary saturated fat and cholesterol increase the risk of having a heart attack

This particular hypothesis has been the biggest bone of contention in nutrition and medical science for the last 70 years. The proposed mechanism behind it is that a higher blood cholesterol level causes the deposition of plaque on the artery wall, leading to atherosclerosis (narrowing of the coronary artery which may lead to heart attacks).

In this article, we are going to unpack this hypothesis and try to ascertain its validity as it stands today.

Starting out, we would like to point out the absurdity of the hypothesis right at its inception. The hypothesis was formulated in the mid-1900s as a response to the rate of heart attacks that started rising very significantly that century. People were confused and looking for answers. And what finally came to be accepted is this theory that basically proposed that the foods Americans had been eating for hundreds of years had suddenly started to kill them for some reason. Red meat, eggs and animal fats like butter, lard and tallow were the staple food over there for hundreds of years until then. After the establishment of this hypothesis, they started to get replaced by unsaturated industrial fats in a major shift.

Validity Of The Hypothesis

Let us go through the 3 points of the hypothesis one by one. In doing so, what you would notice, is that the level of validity decreases with each point. And you can see that it is the third and final point which actually matters. Because that’s the resulting conclusion that serves as a dietary guideline for the public. This, in a nutshell, is why this hypothesis is a failure. The end result is wrong.

Our serum cholesterol levels are measured in 3 main readings: LDL cholesterol, HDL cholesterol and total cholesterol. The cholesterol in our bodies is transported by protein structures in our blood called lipoproteins. As per the existing mainstream paradigm, LDL (low-density lipoprotein) is “bad cholesterol” and HDL (high-density lipoprotein) is “good cholesterol”. Therefore, a low reading of the former and a high reading of the latter is considered good. For total cholesterol also, a low reading is considered optimal.

But it’s the LDL cholesterol reading, specifically, that is the main point of dispute. This is what the existing paradigm focuses on as the main heart disease risk factor and that is what is disputed.

1. Do Cholesterol and Saturated Fats In Our Diet Raise Blood LDL Cholesterol?

Dietary cholesterol, for around 75 per cent of the population, has no effect on blood cholesterol. Around ⅔ of the cholesterol in our bodies is actually produced by the liver and only the remaining ⅓ comes through diet. The liver is very efficient in modulating its cholesterol production according to our intake, which is why we don’t see an effect of dietary cholesterol in blood readings. There are studies showing that when cholesterol is added to the diet of people on cholesterol-free diets, we see a rise in blood readings but not when added to the diets of regular people. The smaller 25 per cent who do see a rise in blood cholesterol with added dietary cholesterol(“hyper responders”) see it to a small extent usually and it’s most often also accompanied by a rise in HDL cholesterol as well, thus lowering the LDL-to-HDL ratio which has also traditionally been considered a key heart disease risk marker.

The USDA guidelines have also, since 2020, dropped their caps on cholesterol, so we don’t need to talk much about this one.

The guidelines have dropped both their low-cholesterol and low-fat diet recommendations. However, the low-saturated fat recommendation is one that still sticks around. And that’s what we’ll discuss primarily in this series.

So coming to saturated fats, do they increase LDL cholesterol? This is still disputed by some experts, but it’s hard to do so. And we don’t intend to argue this point either. Most of the short-term studies do show a rise in LDL with the addition of dietary saturated fat. Longer duration studies are few and the data is conflicted. Even anecdotally, we see a lot of evidence for this: it’s common to see people who go on keto or low-carb diets and start eating a lot of saturated fat to then see a spike in their LDL levels.

2. Do High LDL Levels Mean You’re At a High Risk Of Heart Disease?

This, particularly, is the most heavily contested point of the diet-heart hypothesis. Most credible experts on either side of the debate don’t hold a very strong opinion on this. The data on this (which is very, very vast) does not present any strong conclusion either way.

The key point here though, we think, is that looking at the LDL-heart disease correlation is a ridiculous practice. It may have made sense in the mid-1900s when we didn’t have more data. But in 2022, it hardly even matters. It’s just the old paradigm that’s still managed to stick around. There are huge vested interests in both Big Pharma and Big Food that benefit from it.

LDL Cholesterol Can Be Protective

While there are studies showing an association between high LDL and heart disease and ones that show no association, there are also some studies actually showing a protective effect of higher LDL. That is lower mortality and disease in the high LDL cohort.

And we do also see a temporary rise in LDL levels in people when they suffer from an injury or get an infection, thus further supporting the protective effect characteristic.

High LDL cholesterol is known to have immune-boosting effects also (probably why we see it rise during infections). Familial hypercholesterolemia- which is considered a genetic disorder today causing very high levels of LDL cholesterol has actually been hypothesised to serve as an advantage during evolutionary times, allowing individuals who have the condition to be more resilient to infections.

Children born with a genetic disorder involving abnormally low serum LDL levels are susceptible to very severe infections and need to be supplemented with cholesterol as a remedy.

“I Have High Cholesterol. What Do I Do?”

The million-dollar question. What do you do when you have high LDL cholesterol and should you worry about it. The standard medical treatment is to aggressively treat it of course. Most allopathic doctors will give you statin drugs to lower your LDL and ask you to cut out all saturated fats from your diet strictly. But even among more holistic alternative practitioners who don’t buy the LDL-heart disease hype, there is some hesitation to go ahead and inform a patient to not worry about their high LDL levels at all. Often some general tips to reduce LDL are doled out to patients if they do wish to lower their levels. These include replacing some of their saturated fat intakes with unsaturated fats like olive oil, eating more fibre, eating less and getting more exercise.

The Correct Functional Medicine Approach

As we mentioned above, the approach of focusing on LDL cholesterol in isolation does not make sense. We need to look at a lot of other markers that are much better predictors of heart disease and do a comprehensive evaluation.

The general functional medicine approach is to check everything, even beyond cardiovascular and lipid markers and work on them. This is what we do with all patients for all issues actually: extensive testing and root cause analysis. What we find in most cases, is after our holistic treatment, where we fix the root cause issues, the high LDL cholesterol automatically reverses. This also ties in with what we mentioned earlier about how high LDL cholesterol may be protective and spikes when the patient suffers from an infection or injury. Meaning that after the treatment of the underlying issue, the high LDL reverses.

Common underlying conditions observed with high LDL cholesterol (treatment of which reverses the high LDL) are:

metabolic dysfunction
gut dysbiosis
chronic infections
subclinical thyroid dysfunction
toxin overload
genetic cause (familial hypercholesterolemia)

It’s also important to look at all other lipid and cardiovascular markers which are known to be better predictors of heart disease either on their own or in conjunction with others and monitor them. This include:

Triglyceride levels. Triglycerides are large particles of fat circulating in our bloodstream and serve as the main storage of fat in our blood.
Lipoprotein-a, a specific LDL lipoprotein that has been found to be a very effective predictor of heart disease
HDL cholesterol, and HDL-to-LDL and HDL-to-triglycerides ratio. Dave Feldman(more on him below) actually offers a bounty reward for anyone who can produce any data showing that people with the following trio: high LDL, low triglycerides, and high cholesterol are at a higher risk of heart disease
CRP(C-Reactive Protein) which is a key inflammation marker
Homocysteine
LDL particle size (it's the smaller denser particles which actually deposit on the artery walls and cause blockage and not the larger fluffier ones. We can control particle size very effectively through diet and lifestyle. Read below)
Oxidative stress, and oxidised vs. non-oxidised cholesterol. The former contributes to a much greater degree to artery wall blockage
Fasting insulin, which is the most reliable marker for general metabolic health. Poor metabolic health has been identified as a big risk factor for heart disease.

Apart from blood markers, we also, of course, have tests to directly measure the level of atherosclerosis progression, by measuring the level of artery blockage, if any. Used for high-risk patients, these include a CAC (coronary artery calcium) test and CIMT(carotid intima-media thickness test). These tests are critical because atherosclerosis very often does not present any symptoms until directly causing a heart attack.

We have attempted to list everything here, but most practitioners have their own protocol which includes a specific set of tests only.

A High LDL Reading Only In a Specific Setting Is The Problem

“Increased LDL doesn't operate in a vacuum, inflammation must first increase endothelial permeability, which then causes LDL to create a build-up of plaque in the inner membrane of the arteries”

We mentioned in the above list of markers, CRP which is a key inflammation marker.

Thus we see the root of the problem appears to be inflammation, and the arterial plaque buildup is a response to the same. Inflammation or autoimmune conditions are the root cause or at least a big driver for the majority of chronic health issues today. It develops most commonly due to a leaky gut (leaky gut syndrome) and a leaky blood-brain barrier allowing for food sensitivities to develop, and pro-inflammatory foods worsen this condition

This can be reversed very easily in most cases by a holistic functional medicine approach which aims to address the root cause of inflammation in your body and reverse it. As we mentioned above, after doing this the high LDL usually reverses too. This is the reason.

Arterial plaque deposition is influenced by LDL particle size too. The smaller particles are able to pass through the damaged artery endothelium and deposit.

Oxidation levels affect the rate of plaque deposition very significantly as well. Oxidised cholesterol deposits at higher rates as plaque. Maintaining a good ratio of omega-3/omega-6 in the body (avoid high-omega 6 refined seed oils) and eating more antioxidants helps with this. There is a good amount of direct data to support Omega 3 intake leading to better cardiovascular health. This is why omega-3 supplements are very popular for heart health.

Low-carb Diets and “Lean Mass Hyper Responders”

From the above, it might appear as though a high serum LDL is reflective of an inflammatory condition and poor health in the body. But this may not always be the case, especially in the case of low-carb diets. As we said, a high LDL alone does not necessarily indicate a problem.

Ketogenic and low-carb diets have drastic effects on the body because they shift the primary fuel source of the body from sugar to fat. Your mitochondrial function is altered and this affects the functioning of every single cell in your body. Naturally, this affects your metabolic and lipid markers as well. But mainstream medicine still fails to recognise this and evaluates blood reports from low carb (or “fat adapted”) individuals through the same lens as they do for regular people on a carbohydrate-based diet. This is a rudimentary error.

On a low-carb-high-fat diet, LDL tends to become very high for some people. And it’s mostly very lean and healthy people in which this is observed- “lean mass hyper responders”. These people tend to be very healthy otherwise, as indicated by other blood markers. And this is very common with high functioning low-carb athletes.

This phenomenon has sparked a lot of interest and research. Dave Feldman and his team at cholestrolcode.com and the guys over at dietdoctor.com have researched and posted extensively about it, if you wish to learn more.

Dave Feldman, a citizen scientist, has become very popular in this field due to his very meticulous scientific experiments with this. One of the most interesting things he initially observed was that after being on a ketogenic diet, his LDL shot up whenever he fasted and it went down when he ate a lot. This is completely contrary to the current mainstream understanding which says that eating less and exercising lower your LDL. Dave has summarised his theories on cholesterol and fat metabolism in low-carb individuals into what he calls the Lipid Energy Model, which he presented at Stanford University and has published about in multiple medical journals.

The theories behind this can be a little complicated to understand and have not yet been widely verified. But the basic crux of it is this: On a low carb high-fat diet, the body is actively using fats (as fatty acids and ketones) from both your diet and your fat tissues for energy at a very high rate. This requires a high rate of transportation of fat stores through the bloodstream. The resulting mechanism for this can cause a greater residue of LDL particles in your blood.

But these are always the larger fluffier LDL particles that don’t usually deposit on your arteries. This can be confirmed by an LDL particle size test. And if your cholesterol oxidation levels are low and other blood markers are sound, then you can be assured you are not at risk.

In the large majority of cases of LDL rise in low-carbers, we also see drastic improvements in metabolic markers, and most of the other lipid and cardiovascular markers which we listed above. Indicating improvements in cardiovascular risk, despite the LDL rise.

3. Do Saturated Fats and Dietary Cholesterol Increase The Risk Of Heart Disease?

This is where the diet-heart hypothesis comes crashing down when reviewed against the literature. Since the introduction of the hypothesis in the 1940s, scientists across the world have run many direct experiments to test if saturated fats cause/aggravate heart disease. And if we look at the randomized-controlled clinical trials, in particular, they have just drastically failed to verify this final and key point of the hypothesis. It has thus been successfully disproved.

The following is from a recent 2020 paper in the Journal of American Cardiology that reviewed all the literature on saturated fat intake. And this is from some of the most established and prominent scientists in the field:

“The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke.”

Almost all the data linking saturated fats to heart disease is epidemiological and many reports have accurately pointed out how the data has selection bias. The most popular epidemiological study that commenced with the inception of the hypothesis in 1947, the Seven Countries Study, has been criticized for leaving out the countries for the study that would contradict the hypothesis.

Some of the other very popular observational studies cited to support the SFA and heart-disease link involve food-frequency questionnaires that are known to be very inaccurate.

Conclusion

To conclude we would just like to highlight once again how wildly outdated the one-size-fits-all approach of mainstream medicine is. To just blindly focus on the singular LDL cholesterol marker and lower it with no consideration for why it may be rising in the first place. And completely ignoring so many of the other more reliable data we have at our disposal today.

If the impact of pushing this hypothesis just meant replacing saturated fats with some of the natural traditional unsaturated fats like olive oil then there wouldn’t be as much of an issue. But what transpired was the widespread adoption of industrially refined seed oils high in omega-6. This has been a huge public health catastrophe.

In the next article in this series, we will be talking about the history of the diet-heart hypothesis and all the cholesterol science, how the existing paradigm has managed to stay on despite so much evidence to the contrary, the vested interests behind it and the impact it has had on our culture and health both globally as well as in India.

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