Cholesterol is Bad For Your Health... Right?

We've heard it a million times before, whether in the news, magazines, on forums, from the doc... cholesterol is bad for your health, right?

Not so fast...

If you've blindly hopped on the band-wagon of dire attempts to lower your cholesterol you may be going about this whole thing the wrong way. And if so, you could be drastically reducing your ability to build muscle and burn fat. If you've always been told cholesterol is bad for you... then you need to read this article first.

LDL, HDL, VLDL, bad cholesterol, good cholesterol… How confusing can this get?

Nearly one half of all deaths in North America and Europe are a result of arteriosclerosis. Is this a serious problem you need to worry about by eliminating cholesterol from your diet? The short answer is ‘No’. Let’s start by explaining what cholesterol really is, how important it is for you, and what you can really do about it.

In general, all lipids can be categorized into three groups:

  1. triglycerides - what you’d probably consider as fat,
  2. phospholipids - the material cell membranes are made out of, and
  3. sterols - compounds with multiple ring structures, the most famous of which is cholesterol.

Because of its ring structure, sterols like cholesterol possess a number of important benefits. It can serve as the starting material for the synthesis of many compounds such as bile, vitamin D, or steroid hormones. It serves a role in aiding fat absorption in the small intestine and it also is stored in cell membranes for a number of important functions including acting as rafts, aiding in membrane transport. More than 90% of all the body’s cholesterol resides in cells as either a tremendous benefit to the cells themselves, or in the production of hormones or other molecules.

Despite popular impressions, cholesterol is not a villain to be found in evil foods. On the contrary, it is a compound the body makes and uses. The only reason that cholesterol has a bad reputation is from the high amounts that can be transported through the bloodstream all at one time. Cholesterol’s harmful effects in the body occur when excess amounts form deposits in the artery walls, ultimately contributing to atherosclerosis, leading to heart attacks and strokes.


The ‘Good’ and the ‘Bad’ Cholesterol

Here is the confusing part: There is really only one type of cholesterol; it’s simply just called cholesterol. What people sometimes get confused about is the distinction between dietary cholesterol from food and the cholesterol that travels in the blood. The ‘good’ or ‘bad’ cholesterol is not a type of cholesterol that can be found in foods, but rather is the name given to the type of carrier molecule that is transporting the cholesterol around the body, and depending how it travels through the arteries determines a lot about the health of those arteries.

Just like how oil will not dissolve in water, lipids cannot dissolve in the bloodstream. For this reason, all lipids need to travel through the bloodstream in a vehicle called a lipoprotein. Lipoproteins are spherical structures where the outside material can mix with blood but the inside material can mix with lipids, making it the perfect vehicle for lipid transport. There are several different types of lipoproteins, differing by its constituents, and as the name suggests, containing some lipids and some proteins. The two major important lipoproteins of popular concern are called low-density or high-density lipoproteins (LDL or HDL respectively). The density of the lipoprotein is a result of how much lipid is contained. The high-density of HDLs are due to the high concentration of protein and relative small amounts of cholesterol or other lipids. Because HDLs are low in cholesterol, among other beneficial features, they are considered the ‘good’ type of cholesterol. LDLs on the other hand are of low-density because they are packed full of lipids, primarily cholesterol, at the expense of proteins and are considered the ‘bad’ type of cholesterol. Your doctor will say it is good to have high amounts of HDL and low amounts of LDL. In a way, having high HDLs relative to LDLs is a way of saying, you have less total cholesterol traveling through your blood, and that is ultimately what makes it ‘good’.


The relative amounts of actual cholesterol contained in an LDL and HDL is not the only functional difference between them. The specific protein populations on each lipoprotein actually signal them to function slightly differently within the bloodstream.

Functional differences between LDL and HDL

The distinction between LDLs and HDLs has implications for the health of heart and blood vessels. LDLs in the bloodstream are more prone to interact with free radicals with the arterial wall and can cause LDL oxidation. The oxidized LDL then accelerates the formation of artery-clogging plaques. Plaques begin by the deposition of cholesterol into the artery walls left behind by LDLs. In addition, the surrounding tissues proliferate to form larger and larger plaques. With time, these plaques become harder making the arteries stiff and unyielding. Eventually the plaques turn into hard calcifications that make the arteries rigid tubes with an ever-narrowing opening that ultimately becomes a life threat. While LDLs sound really bad for your cardiovascular health, they are necessary for the transport of cholesterol to all the tissues around the body. This is where HDLs come into play. The purpose of HDLs is to circulate around the bloodstream and scavenge any cholesterol left behind by the LDLs to prevent the formation of plaques. It does this by extracting cholesterol from the artery walls and returning them to the liver for appropriate processing and use.

With all that being said, strategies to improve HDL levels are thought to be a highly desirable method to improve cardiovascular health despite high LDL levels. However, the synthesis of HDL is very weakly associated with any dietary interventions, and in fact, the majority of strategies geared to improve HDL levels is quite sparse and frankly, unsubstantiated. Research focused on improving HDL levels has been a hot topic recently but has so far been relatively inconclusive. In reality, it is largely unknown what dictates HDL levels at all. For this reason, the main target to improve cardiovascular health is focused on reducing LDLs (the lipoprotein that carries the majority of cholesterol).

It would be reasonable to assume that if cholesterol levels were too high, one could deduce that reducing cholesterol intake would be a suitable solution. Surprisingly, this is not the case. The cholesterol in the diet actually has quite a minor role in the body’s overall cholesterol level. The liver makes about 800-1500mg of cholesterol per day, from fragments of carbohydrates, protein and fat, thus contributing much more to the body’s total than does diet. In addition, synthesis of cholesterol is tightly regulated. Meaning that when the diet is full of cholesterol, the liver makes less, and when the diet is low in cholesterol the liver makes more. As a result, plasma cholesterol concentration usually is not changed significantly by altering the amount of cholesterol in the diet. Therefore, eating foods high in cholesterol is neither impacting your HDLs nor LDLs.

The dietary exception is that saturated fats and trans-fats are known to increase LDL and is a major contributor to high cholesterol levels. Thus, eating less saturated fat would be one method to lower LDL levels. Alternatively consuming unsaturated fatty acids such as olive oil has been shown to decreases LDL even when energy and fat intakes remain the same. When trying to reduce cholesterol, limiting saturated fat intake is far more effective than actually reducing cholesterol intake, which means there is no great concern about consuming a large quantities of eggs, lean cuts of meat or low fat milk.

Another method to impact overall cholesterol content is through the ingestion of soluble fiber. This works because bile is commonly recycled through the intestines and reused as an emulsifying agent for fat entering the intestine. However, bile can be trapped by dietary fibers in the large intestine and carried out of the body. The chronic loss of bile through excretion forces the synthesis of new bile from existing cholesterol and effectively reduces cholesterol levels. The fibers most effective at lowering blood cholesterol are soluble pectins and gums.

Do you really want to lower cholesterol?

Understanding that cholesterol has important functions in the body is imperative in order to appreciate that reducing cholesterol is not for everybody. Cholesterol levels is typically not a major concern for many young healthy males looking to increase lean body mass. As mentioned above, one of cholesterols major functions is to produce steroid hormones such as testosterone. The Leydig cells in the testes (cells that produce testosterone in men) extract cholesterol specifically from plasma LDLs. Greater testosterone production requires greater cholesterol availability. When the body is sensitized to produce more testosterone, the Leydig cells increase the number of LDL receptors on the cell surface in order to capture LDLs from the blood. Therefore, any male who works really hard to stimulate maximal testosterone production does not want cholesterol levels to be the limiting factor. Ample cholesterol availability is required for maximal testosterone production.


Cholesterol is a necessary component to many aspects of human health that should not be universally feared. It’s only the unnaturally high amount of cholesterol that is being produced as a result of a diet high in saturated fat that could lead to severe health problems in the long term. However, if you’re a man looking to boost testosterone levels, a diet containing saturated fat certainly isn’t always a bad thing.

If you want wave good-bye to mountainous biceps peaks and chiseled pecs for string-beans and chubby lumps, continue on with the low cholesterol at any cost craze.

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  1. Brown L. et al. Cholesterol-lowering effects of dietary fiber: A meta-analysis. Am J Clin Nutr 69; 30-42, 1999.
  2. Bruce C, Chouinard RA, Tall AR. Plasma lipid transfer protein, high-density lipoproteins, and reverse cholesterol transport. Annu Rev Nutr. 18; 297-330, 1998.
  3. Choi HY, Hafiane A, Schwertani A, Genest J. High-Density Lipoprotein: Biology, Epidemiology, and Clinical Management. Can J Cariol. 2016.
  4. De Souza RJ, Mentle A, Maroleanu A, Cozma AI, Ha, V, Kishibe Tm Uleryke E, Budylowski P, Schunemann H, Beyene J Anand SS. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ. 2015.
  5. Dubois C, Armand M, Mekki N, Portugal H, Pauli AM, Bernard PM, Lafont H, Lairon D. Effectrs of increasing amounts of dietary cholesterol on postprandial lipemia and lipoproteins in human subjects. J Lipid Res. 35; 1993-2007, 1994.
  6. Duffy, D, Rader DJ. Update on strategies to increase HDL quantity and function. Nat Rev Cardiol. 6; 455-463, 2009.
  7. Hanukoglu I. Steroidogenic enzymes: structure, function, and role in regulation of steroid hormone biosynthesis. J Steroid Biochem Mol Biol. 43; 779-804, 1992.
  8. Glomset JA. The plasma lecithins: cholesterol acyltransferase reaction, J. Lipid Res. 9; 155-167, 1968.
  9. Kris-Etherton PM et al. High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am J Clin Nutr. 470; 1009-1115, 1999.
  10. Lecerf JM, de Lorgeril M. Dietary cholesterol: from physiology to cardiovascular risk. Br J Nutr. 106; 6-14, 2011.
  11. LeeRueckert M, Escola-Gil JC, Kovanen PT. HDL functionality in reverse cholesterol transport—Challenges in translating data emerging from mouse models to human disease.
  12. Lewis GF, Rader DJ. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circ Res. 96; 1221-1232, 2005.
  13. Lichtenstein AH et al. Effects of different forms of dietary hydrogenated fats on serum lipoprotein cholesterol levels. NEJM 340; 1933-1940, 1999.
  14. Mannu GS, Zaman MJ, Gupta A, Rehman HU, Myint PK. Update on guidelines for management of hypercholesterolemia. Expert Rev Cardiovasc Ther. 10; 1239-1249, 2012.
  15. Ohvo-Rekila H, Ramstedt Bm Leppimaki P, Slotte JP. Cholesterol interactions with phospholipids in membranes. Prog Lipid Res. 41; 66-97, 2002.
  16. Olson RE. Discovery of the lipoproteins, their role in frat transport and their significance as risk factors. J Nutr. 128; 439S-443S, 1998.
  17. Payne AH, Hales DB. Overview of steroidogenic enzymes in the pathway from cholesterol to active steroid hormones. Enocr Rev. 25; 947-970, 2004.
  18. Rader DJ, Molecular regulation of HDL metabolism and function: implications for novel therapies. J Clin Invest. 16; 3090-3100, 2006.
  19. Von Schacky C. n-3 Fatty acids and the prevention of coronary atherosclerosis. Am J Clin Nutr. 71; 224S-227S, 2000.
  20. Waters DD, Boekholdt SM. An Evidence-Based Guide to Cholesterol-Lowering Guidelines. Can J Cardiol. 2016.