Does Dietary Cholesterol Increase Cardiovascular Disease Risk ?

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There are many myths when it comes to diet and cardiovascular disease, one of these is the much over-stated role that dietary cholesterol is meant to play when it comes to increasing cardiovascular disease risk.

In one corner you have the vegan diet proponents, who often claim that any amount of dietary cholesterol intake from cholesterol-rich foods such as eggs to cause heart disease.

Then in the other corner, we have the Paleolithic diet proponents, many who believe we can consume unlimited amounts of cholesterol-rich foods and have no deleterious effect on heart health.

The truth usually lies somewhere in between, as we will shortly from the scientific research below.

Often the research used to implicate or villainize dietary cholesterol as the “chief” causative factor in heart disease, doesn’t take into account many other diet variables in these studies.

It is clear from the research that it is a type of diet pattern that is associated with an increased risk of developing heart disease, rather than simply consuming cholesterol rich foods alone.

This typical Western diet pattern is characterized by high intake of total fats, most usually high saturated fat, coupled with a low intake of heart-healthy fats such as monunsaturated, PUFA/omega-3 fatty acids and a diet overall low in plant-fiber and plant-foods in general.

Now this is where proponents using this type of dietary research can be disingenuous, because there are many balanced diets which contain cholesterol-rich animal foods that are proven to support heart health and significantly reduce an individuals risk of developing cardiovascular disease.

Two of the diet patterns with the most robust scientific research on their cardiovascular disease benefits are a lacto-ovo vegetarian diet and a traditional Greek Mediterranean style diet.  Yet both of these diets contain foods rich in cholesterol such as animal foods, eggs, red meat and so on, yet clearly don’t have a negative impact on heart health.

The reason why these diets don’t increase the risk of heart disease as vegan proponents like to claim, is because the overall composition of these diets are balanced and predominantly based around plant-foods.

This is often why the research finds very little difference in the health outcome between various health-conscious diets, whether it’s vegetarian to a Mediterranean diet.

Vegan doctors tend to fall into the trap of obsessing over total cholesterol levels and saturated fat, whilst often ignoring many other important cardiovascular disease risk factors such as inflammation, low HDL, hyperhomocysteinemia and hypertriglyceridemia for example.

Atherosclerosis is a multi-factorial, chronic inflammatory disease after all.  Inflammation is now considered to be the true root cause of atherosclerosis and arterial plaque formation according to more current research.

Anyway, let’s take a look at what some of the studies are saying when it comes to dietary cholesterol intake and cardiovascular disease risk.

Does the science support the rigorous stance vegan diet proponents take on dietary cholesterol and often villainizing perfectly healthy foods in moderation.

Or are these vegans just parroting more out-dated and poorly supported science ?

Dietary Cholesterol & Cardiovascular Disease Risk Scientific Research Highlights:

Vegan Diet Cholesterol Heart Disease MythA number of studies have examined and assessed the relationship between dietary cholesterol intake and cardiovascular disease risk.

Despite the ingrained notion in nutrition circles that cholesterol-rich foods cause and/or increase the risk of heart disease, the research isn’t as conclusive or as strong as the vegan diet proponents would like us to believe.

Current research seems to conclude that the role of dietary cholesterol for causing or increasing heart disease risk is minor and may only significantly affect a certain sub-group of individuals at risk for CVD.

The perceived association between dietary cholesterol (DC) and risk for coronary heart disease (CHD) has resulted in recommendations of no more than 300 mg/d for healthy persons in the United States.

These dietary recommendations proposed in the 1960s had little scientific evidence other than the known association between saturated fat and cholesterol and animal studies where cholesterol was fed in amounts far exceeding normal intakes.

In contrast, European countries, Asian countries, and Canada do not have an upper limit for DC. Further, current epidemiologic data have clearly demonstrated that increasing concentrations of DC are not correlated with increased risk for CHD.

Clinical studies have shown that even if DC may increase plasma low-density lipoprotein (LDL) cholesterol in certain individuals (hyper-responders), this is always accompanied by increases in high-density lipoprotein (HDL) cholesterol, so the LDL/HDL cholesterol ratio is maintained. More importantly, DC reduces circulating levels of small, dense LDL particles, a well-defined risk factor for CHD.

This article presents recent evidence from human studies documenting the lack of effect of DC on CHD risk, suggesting that guidelines for DC should be revisited. [1]

Another study from 2005 on the relationship between dietary cholesterol, atherosclerosis and coronary heart disease stated:

The association between dietary cholesterol and CHD risk is, if anything, minor in nature.  This is consistent with the finding that an increase in dietary cholesterol intake results in only a minimal increase in the total/high-density lipoprotein cholesterol ratio.

Taken together these studies suggest that the association between dietary cholesterol and CHD is small, as most subjects can effectively adapt to higher levels of cholesterol intake. [2]

Many vegan diet proponents often refer to very out-dated research on the incorrect association between egg consumption and high serum cholesterol levels.

A study from 2009 published in the International Journal of Clinical Practice stated that it is now acknowledged that the original studies purporting to show a linear relation between cholesterol intake and coronary heart disease (CHD) may have contained fundamental study design flaws, including conflated cholesterol and saturated fat consumption rates and inaccurately assessed actual dietary intake of fats by study subjects.

Newer and more accurate trials, such as that conducted by Frank B. Hu of the Harvard School of Public Health (1999), have shown that consumption of up to seven eggs per week is harmonious with a healthful diet, except in male patients with diabetes for whom an association in higher egg intake and CHD was shown.

The degree to which serum cholesterol is increased by dietary cholesterol depends upon whether the individual’s cholesterol synthesis is stimulated or down-regulated by such increased intake, and the extent to which each of these phenomena occurs varies from person to person.

Several recent studies have shed additional light on the specific interplay between dietary cholesterol and cardiovascular health risk. It is evident that the dynamics of cholesterol homeostasis, and of development of CHD, are extremely complex and multifactorial.

In summary, the earlier purported adverse relationship between dietary cholesterol and heart disease risk was likely largely over-exaggerated. [3]

Lastly the latest systematic review and meta analysis from 2015: Dietary Cholesterol and Cardiovascular Disease concluded that the effect of dietary cholesterol on incident CAD and serum cholesterol outcomes remains unclear.

Intervention trials showed a statistically significant increase in total, LDL, and HDL cholesterol when comparing intervention doses of 500–900 mg/d dietary cholesterol with control doses.

Lower intake of dietary cholesterol has been recommended by some to optimize clinical outcomes or prevent incident CAD; however, there is a lack of longitudinal data (observational or trials) to support such a recommendation.

It is therefore imperative that longitudinal observational studies are conducted with frequent exposure ascertainment and appropriate control for potential dietary confounders. Additional long-term trials should be conducted to examine dietary intake of cholesterol between 300 and 500 mg/d to test the potential role of typical dietary cholesterol intakes on clinical outcomes. [4]

References

[1] Revisiting dietary cholesterol recommendations: does the evidence support a limit of 300 mg/d?

https://www.ncbi.nlm.nih.gov/pubmed/20683785

[2] Dietary cholesterol, atherosclerosis and coronary heart disease.

https://www.ncbi.nlm.nih.gov/pubmed/16596800

[3] Dietary cholesterol and the risk of cardiovascular disease in patients: a review of the Harvard Egg Study and other data.

https://www.ncbi.nlm.nih.gov/pubmed/19751443

[4] Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis

http://ajcn.nutrition.org/content/102/2/276.full

The information in this article has not been evaluated by the FDA and should not be used to diagnose, cure or treat any disease, implied or otherwise.

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