Saturated Fats

General Info | Lipid Hypothesis | Alternative Hypothesis

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Saturated Fats

  • Solid at room temperature
  • Available carbon bonds are occupied by a hydrogen atom
    • All the carbon-atom linkages are filled-or saturated-with hydrogen
  • Found in animal fats
    • meat, dairy, eggs
  • Found in some plant sources
    • cocoa butter, coconut, palm and palm kernel oils
  • Benefits
    • Proper utilization of essential fatty acids.
      • Consumption of Saturated fats may allow for better retention of Omega-3 fatty acids in serum and liver (Garg 1989, 1990)
    • Protect liver from alcohol and possibly other toxins (Cha & Sachan 1994, Nanji 1995)
  • Saturated fatty acids are resistant to heat-induced degradation, unlike Polyunsaturated fats (Grootveld 2001, Halvorsen 2011)


The role of saturated fat in cardiovascular disease has become very controversial.

Lipid Hypothesis

  • Prevailing hypothesis influencing US public policy
    • High Saturated Fat --> High Cholesterol --> Heart Disease
    • Saturated fats can be converted to cholesterol or LDL
      • Main cause of high blood cholesterol, according to American Heart Association

Studies

  • For each 5 percent increase of energy intake from saturated fat, a 17 percent increase in the risk of coronary disease (relative risk, 1.17%; 95 percent confidence interval) as compared with equivalent energy intake from carbohydrates (Hu 1997)
    • Total fat intake was not significantly related to the risk of coronary disease
  • Meta-analysis of randomized controlled trials finds that increasing consumption of polyunsaturated fat as a replacement for saturated fat reduces the risk of coronary heart disease (Mozaffarian 2010).
  • Plasma concentrations of even chain saturated phospholipid fatty acid are positively related to subsequent coronary heart disease risk, whereas, concentrations of omega-6 phospholipid fatty acid are inversely related (Khaw 2012).
    • Interestingly, blood monounsaturated fatty acids, omega-3 poly-unsaturated fatty acids, and trans-fatty acids were not consistently associated with coronary heart disease risk.
    • Authors admit factors other than diet (eg: genetic differences in metabolism) may alter blood fatty acid levels.

Other Studies


Alternative Hypothesis

  • Alternative hypothesis suggests cardiovascular disease is not a result of high saturated fat intakes as once widely believed
    • but instead a biological response resulting in chronic inflammation
    • likely triggered by sedentary lifestyle and other dietary issues including, but not limited to high Linoleic to Linolenic fatty acid ratio and over consumption of sugars.
    • misunderstandings of saturated fats have been attributed to studies design flaws, unethical manipulation of data, and misrepresentation or misinterpreted of findings. (Texon 1989)
      • Others have suggested publication biases favoring studies that continue to reinforce particular political and industrial agendas to influence public policy. (Also see USDA Food Politics)

The Seven Countries Study (Ancel 1953)

  • First landmark study that linked the consumption of dietary fat to coronary heart disease
  • This study served as the basis for nearly all of the initial scientific support for the Cholesterol Theory.
  • It was later discovered that the author unethically selectively analyzed information from only seven countries to prove his correlation
    • rather than comparing all available data from all 22 countries, which it turns out, showed no correlation between dietary fat and heart disease after all.

Framingham Study

  • Began 1948 and involved 6,000 subjects from Framingham, Massachusetts, USA.
  • Identified heart disease risk factors such as smoking, high blood pressure, lack of exercise and high cholesterol.
  • The cholesterol link was weak.
    • Subject who weighed more and had abnormally high blood cholesterol levels were slightly more at risk for future heart disease
  • However, subject who ate more saturated fat, more dietary cholesterol and more calories actually were the most physically active, weighed the least and had lower serum cholesterol levels.
    • Noted by Dr. William Castelli, a former director of the Framingham Heart study (Catelli 1992).

The Cholesterol-heart Disease Hypothesis Critique (Texon 1989)

  • Meyer Texon, MD calls into question the lipid hypothesis propaganda
    • Claims that the American Heart Association and the National Institute of Health misrepresent scientific data.
    • Pointed out abuses of statistical analysis in studies such as the Helsinki Heart Study and the National Heart, Lung, and Blood Institute's multimillion dollar studies.
    • "Thus, after seven years at a cost of $150 million dollars studying 3,806 men, the difference in death was 3 men."
    • Questioned the proposed benefit to cost relationship for attempting to lower cholesterol.
    • Calls for more promising alternative directions for atherosclerosis research.

U.S. Multiple Risk Factor Intervention Trial (MRFIT)

  • Sponsored by the National Heart, Lung, and Blood Institute
  • Compared mortality rates and eating habits of over 12,000 men
  • Men with "good" dietary habits (reduced saturated fat and cholesterol, reduced smoking, etc.)
    • Demonstrated marginal reduction in total coronary heart disease.
    • Demonstrated higher overall mortality from all causes.
      • increase in deaths from cancer, brain hemorrhage, suicide, and violent death.
    • After 10 years, no significant difference in death from heart disease or total death.

The South Carolina Experience (Lackland 1990)

  • A survey of South Carolina adults found no correlation of blood cholesterol levels with consumption of nine fat intake habits, including the consumption of red meat, fat on meat, fried fish/chicken, butter, eggs, whole milk, bacon/sausage, cheese, and the use of solid fats when cooking vegetables.

Post-mortem Autopsies (Felton 1994)

  • Comparisons of aortic plaques with serum and adipose tissue imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation.
  • No associations were found with saturated fats
  • Arterial plaque is primarily composed of unsaturated fats, particularly polyunsaturated fats.

Review of Literature (Ravnskov 1998)

  • Reviewed studies examining direct link between dietary fats and atherosclerotic vascular disease in humans.
  • The review included ecological, dynamic population, cross-sectional, cohort, case-control studies, and controlled, randomized trials of the effect of fat reduction alone.
  • He concludes that there is little evidence that Saturated Fatty Acids as a group are harmful or that Polyunsaturated Fatty Acids as a group are beneficial.

Meta-analysis (Siri-Tarino 2010)

"A meta-analysis of the prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increase of risk of CHD or CVD."

Review of Literature (Hoenselaar 2011)

  • Results and conclusions about saturated fat intake in relation to cardiovascular disease from
    leading advisory committees, do not reflect the available scientific literature.


References

Anonymous (1982). Multiple Risk Factor Intervention Trial; Risk Factor Changes and Mortality Results. JAMA. 248:12:1465

Castelli WP (1992) Concerning the Possibility of a Nut.... Arch Intern Med. 152(7):1371-1372

Cha YS, Sachan DS (1994). Opposite effects of dietary saturated and unsaturated fatty acids on ethanol-pharmacokinetics, triglycerides and carnitines. J Am Coll Nutr. 13(4),338-43.

Eberly LE, Neaton JD, Thomas AJ, Yu D, et al (2004). Multiple-stage screening and mortality in the Multiple Risk Factor Intervention Trial. Clin Trials. 1(2):148-61.

Enig M, Fallon F (1999). Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats, 5-6.

Felton CV, Crook D, Davies MJ, Oliver MF (1994). Dietary polyunsaturated fatty acids and composition of human aortic plaques. The Lancet. 344(8931), 1195 - 1196.

Garg ML, Wierzbicki AA, Thomson AB, Clandinin MT (1989). Dietary saturated fat level alters the competition between alpha-linolenic and linoleic acid. Lipids. 24(4),334-9.

Garg ML, Thomson ABR, and Clandinin MT (1990). Interactions of saturated, n-6 and n-3 polyunsaturated fatty acids to modulate arachidonic acid metabolism. J. Lipid Res. 31, 271-277.

Grootveld M, Silwood CJL, Addis P, Claxson A, Serra BB, Viana M (2001). Health effects of oxidized heated oils. Foodservice Research International 13: 41–55.

Hoenselaar R (2011). Saturated fat and cardiovascular disease: The discrepancy between the scientific literature and dietary advice. Nutrition 28: 118–123.

Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Rosner BA, Hennekens CH, Willett WC (1997). Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med. 337(21):1491-9.

Khaw KT, Friesen MD, Riboli E, Luben R, Wareham N (2012). Plasma phospholipid fatty acid concentration and incident coronary heart disease in men and women: the EPIC-Norfolk prospective study. PLoS Med. 2012;9(7):e1001255.

Lackland DT, Wheeler FC (1990). The need for accurate nutrition survey methodology: the South Carolina experience. J Nutr. 120 Suppl 11:1433-6.

Mozaffarian D, Micha R, Wallace S. (2010) Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 23;7(3):e1000252

Nanji AA, Sadrzadeh SM, Yang EK, Fogt F, Meydani M, Dannenberg AJ (1995). Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Gastroenterology. 109(2),547-54.

Ravnskov U (1998). The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol. 51(6),443-60.

Siri-Tarino PW, Sun Q, Hu FB, Krauss RM (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 91(3):535-46.


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