The Truth About Saturated Fat

by Paul Rogers on January 26, 2010

Traditional dietary advice for prevention of heart disease says we should keep our intake of saturated fat low and eat more unsaturated fats like vegetable seed and nut oils and olive oil, which have some saturated fat but are much higher in the polyunsaturated and monounsaturated fats. Although some vegetable oils like coconut and palm oils are high in saturated fat, most saturated fat in the diet comes from animal products like meats and dairy foods.

Unlike essential polyunsaturated fats, we don’t need to eat saturated fat because the body makes it, and stores it, in response to excess food energy intake.

The evidence that saturated fat is involved in heart disease has been challenged recently by an alliance of groups and scientists with various agendas and scientific interests. These range from the low-carb Atkins diet advocates, the Paleo (eat like a cave man) advocates and the Weston Price supporters — people who say that traditional, healthy diets are high in animal foods and saturated fats. All of these groups, in one way or another, tend to say that saturated fats are healthy and don’t have any impact on heart disease, and further, that vegetable oils and fats are the unhealthy ones. Various other so-called natural health and alternative health groups have run with this premise, usually copying and quoting the same ‘evidence’, and I use that term lightly.

What are saturated fats?

I don’t need to go too far into the chemistry of fats other than to say that the various fats take on different properties according to how many carbons and hydrogens are in the fat molecule and where they are positioned. In essence there are many individual ‘fatty acids’ possible both naturally and in manufacture according to this structure. Even saturated fat is not one single fat but many, including lauric, myristic, palmitic and stearic fatty acids. You can read a good summary of fatty acids at Wikipedia.

The evidence on saturated fats and heart disease

As I noted in a previous article about cholesterol, the complexities of nutritional epidemiology are substantial because we don’t just eat one type of food. Various components of a meal may have different impacts on your heart and arteries in relation to the other components of the diet. For example, saturated fat may be less of a problem if you eat a lot of fibre from fruits and vegetables and whole grains, or include plenty of unsaturated fats in the diet. This is possibly why the French seem to have much less heart disease than the Finnish people even though both eat a diet reasonably high in saturated fat. Body weight (BMI) and exercise also have an impact in regulating heart disease. Plucking out one risk factor is inevitably tricky and can produce conflicting results, which the doubters inevitably focus upon.

In any case, the core historical studies looking at heart disease in humans and the risk factors are the Seven Countries study and the Framingham study. The Seven Countries Study has been criticised for various inconsistencies in the original publications, but it is an ongoing study and recent analysis has confirmed how cardiovascular disease and mortality is related to blood cholesterol across various countries. How saturated fat relates to cholesterol and heart disease risk in the Seven Countries studies has been the subject of much discussion and disagreement.

The meta-analysis and saturated fat

However, the inconsistencies across populations in saturated fat consumption and heart disease lead the skeptics to say that saturated fat in the diet has no impact on heart disease. Then, just this month, a new study was published (Siri-Tarino) that merged all previous studies on saturated fat and then tried to find an association with higher or lower intake of saturated fat and heart disease. This type of study is called a meta-analysis and is considered powerful at detecting ‘associations’ if not causal effects.

No ‘association’ with saturated fat and heart disease was found with this study. The authors found essentially no differences in heart disease in people with lower or higher intakes of saturated fat. How could this be after all the advice we have received over 40 years? Yet they also pointed out:

“Inverse associations of polyunsaturated fat and CVD risk have previously been reported. Replacement of 5% of total energy from saturated fat with polyunsaturated fat has been estimated to reduce CHD risk by 42%. Notably, the amount of dietary polyunsaturated fat in relation to saturated fat (ie, the P: S ratio) has been reported to be more significantly associated with CVD than saturated fat alone, with a reduced CHD risk found with P:S ratios of > 0.49 . . .”

This paragraph reveals the complexity and subtlety of studying mixed diets. You have to ask what happens when you replace saturated fat wtih something else in the diet. If you decrease saturated fat intake and replace it with refined carbohydrates like white bread and sugar for example, you probably won’t find any association of heart disease with saturated fat. If you replace saturated fat with polyunsaturated fats and high-fibre carbohydrates like fruit and vegetables and whole grains, then that makes all the difference as we’ve seen in studies of the Mediterranean diet profile. One reason why refined carbohydrates would not change the outcome when replacing saturated fat is that an excess of this type of carbohydrate gets turned into saturated fat, mostly palmitic acid, by the liver; so it’s no change at all!

Unfortunately, heart associations and the nutritional and dietetics community missed the mark for many years by not advocating that if you lower your intake of saturated fat you must replace it with polyunsaturated fat and high-fibre carbohydrates and not junk carbohydrates like sugars and baked flour goods — or trans fats, the other bad choice.

In any case, the best way to study the effects of nutrition on heart disease is to look at dietary patterns and not artificial indicators of proposed heart health like individual components or blood lipids. It’s clear that the western dietary pattern high in red meat, saturated fat and cholesterol, refined carbohydrates and sugars is unhealthy and that in contast, the Mediterranean pattern low in red meat, saturated fat and cholesterol and high in fresh plant foods is much healthier for the prevention of heart disease and probably cancer.

Blood lipids, diet and risk factors

The low-carb diet advocates like to point to the fact that saturated fat increases the good cholesterol (HDL) even though it also increases the bad cholesterol LDL. In some studies this ratio improves when you replace refined carbohydrates with saturated fat, prompting the claim that low-carb diets are better for heart health. No surprise there because refined carbohydrates and sugars raise circulating fats in the blood as measured by your triglycerides (TG), and lowers HDL at the same time. However, if you  eat a high-carbohydrate diet consisting of plenty of fibre, whole grains, fruit and vegetables, HDL can also be raised and TG lowered, as shown by David Jenkins and others in various studies. The Atkins low-carbers always choose the lowest common denominator to boost the putative value of their diet. It is a false premise.

Is HDL always protective?

The other point to consider, if you like the idea of having very high HDL (high-density lipoprotein), is whether this is always a good thing. High HDLs on a low-carb diet just might invoke a false sense of security because HDLs can turn ‘bad’ under certain circumstances. In a study by researchers at the Sydney Heart Research Institute, this seems to be what happens when you raise HDL with a diet high in saturated fat and low in polyunsaturated fats.

Nicholls SJ, Lundman P, Harmer JA,et al. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006 Aug 15;48(4):715-20. (Heart Research Inst, Sydney)

“CONCLUSIONS: Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.”

Particle number not size

A lot of fat in the diet might raise HDL, but the pro-saturated fat brigade also claim it increases cholesterol particle size of both HDL and LDL (low-density cholesterol), which they claim is heart protective compared to what happens when you eat a lot of refined carbohydrates and sugars that cause small particles sizes of cholesterol. They’re correct that fat produces larger particle sizes when it replaces refined carbohydrates and sugars, but they are wrong that this is necessarily heart protective compared to smaller particles. You shouldn’t be comfortable with LDL of 5 mmol/L  (195 mg/dl) just because it has large particle sizes. A recent meta-analysis looked at the all the studies about particle size and number and found that the only solid information was that particle number and not size was related to heart disease (Ip et al).

This is a little esoteric, but it means that as a long as your LDL cholesterol is low enough (which you get on low saturated fat, high plant food diets), small particle size and HDL have little relevance as long as they are within a certain measure, easily achievable on these diets.  High-fibre diets combined with exercise and the normalisation of weight raise particle size and HDL, so you don’t have to go on a risky low-carb, high saturated fat diet to increase particle size if that’s your goal. When you get your cholesterol low enough with a high-fibre, low saturated fat diet with exercise, you not  only have a smaller number of LDL particles,  but they are also larger in size than if you ate a refined carbohydrate diet, were overweight and did not exercise. It’s complicated, but it is the truth.

Saturated fat carcinogenic for the small intestine

Fat, up until now, has generally not been shown to cause cancer at any particular body site even though suspicions have been held for breast and colon, but obesity is related to breast and colon cancer. Red meat and processed meat is reasonably well established as a risk factor for cancer of the colon (large bowel) and rectum. The small intestine (small bowel) has not been studied as much, so a group of researchers decided to see if there was an associated increase in risk for meat eating and small intestine cancer. While they did not find any association with meat eating, they did find a significant link with consumption of saturated fat (Cross).

“In contrast, we noted a markedly elevated risk for carcinoid tumors of the small intestine with saturated fat intake in both the categorical (highest versus lowest tertile: HR, 3.18; 95% CI, 1.62-6.25) and continuous data (HR, 3.72; 95% CI, 1.79-7.74 for each 10-g increase in intake per 1,000 kcal). Our findings suggest that the positive associations for meat intake reported in previous case-control studies may partly be explained by saturated fat intake.”

I should explain that  this study is not conclusive, but it certainly does suggest the carcinogenicity of saturated fat for the small intestine. The point is that it adds to the logical evidence for reducing saturated fat intake as part of healthy eating. In my article: What You Don’t Know About Saturated Fat That Could Harm You, I explained why saturated fat in excess is not healthy for reasons other than a direct association with heart disease or cholesterol — insulin resistance, inflammation, cognitive decline — all these things have reasonable scientific evidence in support.

The truth about saturated fat

The truth is that diets relatively low in saturated fat and higher in polyunsaturated and possibly monounsaturated fat and comprising an abundance of plant foods including whole grains, nuts, seeds and beans, fruits and vegetables, low to moderate in meat and low in added sugars are the diets for which there is the best evidence of cardiovascular risk reduction and general long-term protection from chronic disease (Sofi).

This is the Mediterranean, plant-food dietary pattern. The high animal-food dietary pattern of Atkins low-carb, Paleo and associated diet agendas are pure propaganda with an absence of evidence of long-term safety, efficacy or scientific substantiation.

References

– Verschuren WM, Jacobs DR, Bloemberg BP, et al. Serum total cholesterol and long-term coronary heart disease mortality in different cultures. Twenty-five-year follow-up of the seven countries study. JAMA. 1995 Jul 12;274(2):131-6.
— Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Jan 13.
— Jenkins DJ, Kendall CW, Faulkner D, et al. A dietary portfolio approach to cholesterol reduction: combined effects of plant sterols, vegetable proteins, and viscous fibers in hypercholesterolemia. Metabolism. 2002  Dec;51(12):1596-604.
— Turley ML, Skeaff CM, Mann JI, Cox B. The effect of a low-fat, high-carbohydrate diet on serum high density lipoprotein cholesterol and triglyceride. Eur J Clin Nutr. 1998 Oct;52(10):728-32.
— Ferdowsian HR, Barnar ND. Effects of plant-based diets on plasma lipids. Am J Cardiol. 2009 Oct 1;104(7):947-56. Review.
— Waldmann A, Ströhle A, Koschizke JW, Leitzmann C, Hahn A. Overall glycemic index and glycemic load of vegan diets in relation to plasma lipoproteins and triacylglycerols. Ann Nutr Metab. 2007;51(4):335-44.
— Ip S, Lichtenstein AH, Chung M, Lau J, Balk EM. Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes. Ann Intern  Med. 2009 Apr 7;150(7):474-84. Review.
— Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer DS. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006 Aug 15;48(4):715-20. (Heart Research Inst, Sydney)
— Navab M, Reddy ST, Van Lenten BJ, et al. The role of  dysfunctional HDL in atherosclerosis. J Lipid Res. 2009 Apr;50 Suppl:S145-9. Review.
— Sofi F, Cesari F, Abbate R, Gensini GF, Casini A. Adherence to Mediterranean diet and health status: meta-analysis. BMJ. 2008 Sep 11;337:a1344. Review.
— Cross AJ, Leitzmann MF, Subar AF, et al. A prospective study of meat and fat intake in relation to small intestinal cancer. Cancer Res. 2008 Nov 15;68(22):9274-9.

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