Does saturated fat really cause heart disease?

For years we have been told that saturated fat is bad for us and will cause heart disease but is this what the research is currently showing us?

Well, surprisingly no. The idea of saturated fat leading to heart disease is based on the highly controversial lipid-heart hypothesis (or diet-heart hypothesis) whereby serum (blood) “cholesterol” levels are thought to be predictors of adverse cardiovascular outcomes (namely cardiovascular disease). Saturated fat has been shown to elevate LDL-c (which is what doctors lovingly call “bad cholesterol”) in some people (NOTE: not all people) therefore saturated fat is dangerous and will lead to heart disease. The interesting thing is that this line of thought is a logical fallacy (it could possibly come under the banner of a few – association fallacy, non-sequitur fallacy etc.) where saturated fat has been demonised due to an association with “cholesterol” which has an association with cardiovascular disease (CVD). However, there are some significant issues with this:

  1. There is no such thing as good or bad cholesterol. There is only one type of cholesterol and it’s essential for life. You cannot live without it.
  2. LDL is a type of cholesterol transporter called a lipoprotein. It is not cholesterol.
  3. The lipid-heart hypothesis has never been proven and in fact, some pretty significant research in the last few years put that myth to bed 1-2
  4. LDL-c is a measure of the cholesterol content of LDL and it is used as an estimate of your total body cholesterol. It’s not a particularly accurate estimate. 3
  5. The role of dietary saturated fat in LDL-c levels is controversial 4
  6. LDL-c as a singular risk factor (i.e. in the absence of high blood pressure, increased waist circumference, elevated blood glucose etc.) is potentially a poor predictor of cardiovascular disease risk 5
  7. LDL-p shows a higher specificity to cardiovascular disease 6 and is unlikely to be present alone. Triglyceride to HDL ratio can be used as a surrogate for both LDL-p and insulin resistance.

So cholesterol is good, the lipid-heart hypothesis is dead and we can enjoy the fat on our steak. But don’t take my word for it, here’s a couple of significant pieces of research:

  1. Siri-Tarino and colleagues (2010) concluded there was no significant correlation between CVD and saturated fat intake. They also noted that the replacement of saturated fat with carbohydrates increased risk. 1
  2. A Cochrane review in 2015 also concluded that there was no clear benefit in replacing saturated fat with carbohydrate. There are some problems with the study but ultimately it failed to find a correlation with saturated fat and CVD. 2

So if not saturated fat, then what is causing CVD?

You’ve probably heard in recent times that sugar and carbohydrate play a significant role in CVD but how does this happen? Well it’s to do with blood glucose and it’s via a few mechanisms.

  1. Long-term hyperglycaemia (high blood glucose) is very destructive to proteins in our blood, particularly lipoproteins (remember this is a cholesterol transporter). The high blood glucose binds to lipoproteins (this is called glycation) causing the lipoproteins to stay in circulation for too long which, increases plasma concentration. (i.e. elevating the number of circulating LDL). The high glucose also promotes the transfer of cholesterol esters from HDL to apolipoprotein B (apolipoproteins are sort of like a biological barcode which enables the body to recognise what type of lipoprotein it is). Apo-B is significantly correlated to CVD risk so the process of cholesterol transfer is highly atherogenic (plaque promoting). The transfer of cholesterol esters is what leads to the reduction in HDL and promotion of triglycerides. Low HDL and high triglycerides is called dyslipidaemia (disordered blood lipids) and is a significant risk for plaque development. Further exacerbating the situation, hyperglycaemia oxidises LDL (remember there is a lot of LDL floating around) and oxidised LDL plays a pathogenic role in CVD. 7
  2. Another protein damaged by high glucose is haemoglobin. This is the protein responsible for transporting oxygen around the body. The degree of glycation of haemoglobin ultimately determines how efficiently the blood can deliver oxygen. Sustained hyperglycaemia results in significant glycation of haemoglobin which, subsequently impairs oxygen delivery to the body (particularly the extremities). This increases the risk for impaired wound healing, ulcers, circulatory problems and ultimately, CVD. 8
  3. Hyperglycaemia is also toxic to cells (this is called glucotoxicity). The full mechanism is not entirely clear but in part, hyperglycaemia stimulates an overproduction of reactive oxygen species (ROS) by the mitochondria. ROS are highly reactive and in excess, are capable of exerting significant cellular damage (particularly to delicate structures like capillaries and nerve cells). 9-10
  4. Hyperglycaemia also stimulates insulin production and ultimately, sustained hyperglycaemia will lead to hyperinsulinaemia (high blood insulin). Hyperinsulinaemia plays significant roles in both type 2 diabetes and cardiovascular disease. Hyperinsulinaemia is problematic in a number of ways as it promotes fatty acid synthesis, increases blood clotting and adhesion factors (this makes things stick to blood vessel walls), promotes high blood pressure and interferes with nitric oxide secretion from the blood vessel lining. 10 This leads to damage to the blood vessel which, is the first step in the synthesis of endothelial dysfunction (ED) and atherosclerotic lesions (plaque build-up). 11
  5. According to David E. Cohen, MD, PhD, Director of Hepatology at Brigham and Women’s Hospital, director of the Harvard–MIT division of health sciences and technology, and Robert H. Ebert Professor of Medicine at Harvard Medical School; “Insulin resistance appears to be the underlying pathophysiological defect leading to nonalcoholic fatty liver disease (NAFLD).” NAFLD is a significant risk factor for both clinical and subclinical cardiovascular disease. 12-13

I could continue on along these lines of thought for quite some time but it’s pretty clear that if anyone is truly serious about preventing and reversing CVD, then we need to get serious about what’s causing it. It’s well known that dietary fat has little to no effect on blood glucose levels and that dietary carbohydrate has the strongest effect on blood glucose levels. Therefore the focus needs to come away from fat and focus squarely on the role of the role of carbohydrates (namely refined carbohydrates and sugar) in hyperglycaemia and hyperglycaemia in CVD.

1. Am J Clin Nutr. 2010 Mar;91(3):535-46. doi: 10.3945/ajcn.2009.27725. Epub 2010 Jan 13.


3. BMJ 1989; 298 doi: (Published 24 June 1989)


5. Nature Reviews Cardiology 8, 197-206 (April 2011) | doi:10.1038/nrcardio.2010.223

6.  J Clin Lipidol. 2007 Dec 1; 1(6): 583–592.

7. Angiology. 2005 Jul-Aug;56(4):431-8.


9. Free Radic Biol Med. 2010 Mar 15;48(6):781-90. doi: 10.1016/j.freeradbiomed.2009.12.017. Epub 2009 Dec 28.

10. Circ Res. 2010 Oct 29; 107(9): 1058–1070.

11. Int J Biol Sci. 2013; 9(10): 1057–1069.

12. Cohen DE. Pathogenesis and Management of Non-Alcoholic Fatty Liver Disease. Presented at: National Lipid Association Scientific Sessions; May 19-22, 2016; New Orleans.

13. J Hepatol. 2016 Aug;65(2):425-43. doi: 10.1016/j.jhep.2016.04.005. Epub 2016 Jun 1.

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