Does Cholesterol Really Cause Cardiovascular Disease?

Science by HLTH Code Team


For decades, dietary cholesterol has been vilified as a major culprit in the development of cardiovascular disease (CVD). The widely accepted belief was that consuming cholesterol-rich foods, such as eggs and beef, could lead to elevated blood cholesterol levels and increase risk of heart disease. However, recent research has challenged this long-standing dogma, suggesting that the relationship between dietary cholesterol and CVD is far more complex than previously thought. 

In this article, we’ll explore the current scientific evidence regarding dietary cholesterol.

Understanding Cholesterol

Cholesterol is a waxy, fat-like substance that is found in every cell of the human body. It plays essential roles in the formation of cell membranes, the production of bile salts and hormones like estrogen and testosterone, and the synthesis of vitamin D. Cholesterol is necessary for the absorption of fat-soluble vitamins and is crucial for the proper functioning of the immune system, brain, and nervous system. 

The Liver’s Role

The impact of dietary cholesterol has been misrepresented for years. The human body tightly regulates its cholesterol levels. The liver produces most of the cholesterol required for essential bodily functions, and it can adjust its production in response to dietary intake. When dietary cholesterol intake is low, the liver increases cholesterol production to meet the body’s needs. Conversely, when dietary cholesterol intake is high, the liver reduces its own cholesterol production to maintain a balance and stabilize blood cholesterol [1]

Early Assumptions and Dietary Guidelines

Historically, the assumption that dietary cholesterol significantly contributes to CVD was based on limited scientific evidence. Early research suggested that high dietary cholesterol intake was associated with increased blood cholesterol levels, which, in turn, were linked to a higher risk of heart disease. Consequently, dietary guidelines recommended limiting cholesterol intake to 300 milligrams (mg) per day, equivalent to about one large egg.

However, this approach has been challenged by more recent scientific investigations, and even older research. A doctor who specializes in unearthing lost research dug up an NIH-funded study from the 60s and 70s that tested the “diet-heart hypothesis.” 

This hypothesis suggests that the consumption of foods high in saturated fats, such as red meat, butter, and other animal-based products, contributes to increased levels of cholesterol in the bloodstream. Elevated levels of cholesterol, particularly low-density lipoprotein (LDL) cholesterol, were believed to be associated with the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries, leading to increased risk of heart disease.



The hypothesis also emphasized the impact of dietary cholesterol on blood cholesterol levels and consequently on the risk of heart disease. Foods high in cholesterol, such as egg yolks and certain shellfish, were often cautioned against.

As a result of this prevailing theory, public health authorities and medical professionals began advising people to limit their intake of saturated fats and cholesterol-rich foods. This led to the promotion of low-fat diets and the development of dietary guidelines that discouraged the consumption of foods high in these components.

The diet-heart hypothesis influenced dietary recommendations for decades, but this uncovered study had one important conclusion:

The hypothesis failed.

While the records showed that substituting vegetable oils in place of animal fats did lower total blood cholesterol, that lowered cholesterol did not increase longevity [2]. In fact, every 30-point fall increased the risk of dying by 22%. Additionally, lowered cholesterol did not lessen atherosclerosis or decrease risk of heart attacks.  

Modern research continues to cast doubt on the idea that saturated fat and cholesterol lead to cardiovascular disease [3,4]

Cholesterol in the Body

Cholesterol exists in two primary forms: high-density lipoprotein (HDL) and low-density lipoprotein (LDL). HDL cholesterol is often called “good” cholesterol because it helps remove excess cholesterol from the bloodstream, reducing the risk of arterial plaque formation. LDL cholesterol is often referred to as “bad” cholesterol because high levels of LDL are thought to be associated with an increased risk of CVD. 

The reality is that cholesterol–including LDL cholesterol–is quite protective. It is important in helping the body clear pathogens like bacteria during an infection. It does so by physically binding the bacteria and taking it to the liver, where it can then go to the intestines and be eliminated from the body [5,6]

This bears out in human data. People with the lowest LDL cholesterol levels are much more likely to die of serious infections, and they are fifteen times more likely to suffer from blood-based cancers, like leukemia. They also have 5-6 times greater chance of dying from infections. Additionally, people with low LDL cholesterol may simply die more readily [7]. There are compelling studies into human longevity that show that the longest lived humans have the highest cholesterol, including high LDL [8].


The association between dietary cholesterol and cardiovascular disease is a complex and evolving topic. While early assumptions suggested a strong link between dietary cholesterol intake and a risk for heart disease, recent research (and some older research) challenges this notion. The current body of evidence does not support a clear and consistent relationship between dietary cholesterol intake and CVD.

While ongoing research will provide more answers, LDL cholesterol doesn’t appear to be the villain it’s made out to be.





This article is for informational and educational purposes only. It is not, nor is it intended to be substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.