2013: Blood Lipids and Risk Assessment

Dietary fats and cardiovascular disease: a 2013 update

 

Quick Take:  What the lipid panel means: Total Cholesterol is no longer considered a strong risk factor, since a high HDL fraction is actually desirable, so therefore the Total/HDL ratio is a more significant metric. Serum triglycerides is also a strong measure for CHD risk, as it reflects both the circulating fats and carbohydrate in serum. LDL cholesterol metric does not discern particle types, which, if they are small, pose a CHD risk, and when they are large and “fluffy”, they do not.  apo B and C reactive protein can sort that out.

Refined carbohydrate and high glycemic foods are now seen as having equal risk as saturated fat

Although research dating back to the 1950’s have associated dietary fat and particularly saturated fat with risk of coronary heart disease, more recent epidemiological evidence has been challenging these findings.  In 1961, the American Heart Association first published guidelines to limit saturated fat and total fat, and these guidelines were further embraced in the 1970s.

However, large clinical trials have been disappointing.

The dyslipidemia guidelines of the European Society of Cardiology and the European Atherosclerosis Society treatment targets for 2011 were adopted by South Africa in 2012.  They are:   The LDL-C goal is 1.8 mmol/l for the very high-risk group (>30%), 2.5 mmol/l for the high-risk group (15-30%), and 3 mmol/l for those below 15% risk.

In recent years, important issues have emerged about the role of SFA in CHD risk.

  • How do SFAs  compare with trans fats or highly processed refined carbohydrates in affecting CHD risk.
  • Do specific SFAs have different relations with CHD risk
  • Should dietary advice focus more on major food sources of SFAs because they may contain high amounts of protein, calcium, and other components that also influence the risk of CHD, so the effect of particular foods on CHD cannot be predicted solely by their content of SFAs
  • Has there been an adverse effect to CVD risk as SFAs have been increasingly replaced by carbohydrate as populations have become more obese
  • Are there similar health risks with intake of SFAs or its major food sources and risks of other diseases, including stroke and cancer, which should be considered in making dietary recommendations
  • Important observational studies used to guide the development of the lipid hypothesis, such as the seminal Seven Countries Study by Ancel Keys in 1980, have been now considered biased and with several confounding variables.

 

An expert panel looked at evidence from epidemiologic/observational,clinical/interventional, and mechanistic studies, and provided an extensive review of current dietary recommendations.  They concluded:

“1) The risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2–3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index.

2) Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs.

3) No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown.

4) The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD.

5) The effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.”

 

Although LDL cholesterol has been the most widely accepted lipid biomarker for CHD risk,

…”there is now convincing evidence from the Prospective Studies Collaboration meta-analysis that supports the ratio of total cholesterol to HDL cholesterol as a powerful predictor of CHD (27) and that this ratio is more predictive than is LDL cholesterol. Apolipoprotein B and non-HDL cholesterol are also biologically important markers and play roles in clinical risk assessment, particularly in individuals with the metabolic syndrome. There is growing evidence of the relation of specific LDL particle subclasses to CHD risk, but their levels tend to be correlated with other lipid measures (28). Triglyceride concentrations, both fasting and more importantly nonfasting (2930), are also relevant as indicators of CVD risk in the metabolic syndrome and insulin resistance. Lipoprotein(a) is a well-established marker of genetic predisposition to CHD, but uniform standards for clinical assays have not been established (31).”

However, other biomarkers that explain CVD risk are desirable. Single risk factors have limitations when considered on their own because the effects of diet on CVD risk are mediated by many pathways, with blood lipids being only one. Although elevated LDL cholesterol is one of the major risk factors known, there is still a need for clinical endpoints for assessing the effects of diet on CVD risk. Also, we must consider the type of CVD—sudden death is different from stable plaque. A comprehensive risk score made up of multiple biomarkers of CHD risk, including total and HDL cholesterol, blood pressure, body fatness, glucose tolerance, and inflammatory markers, can substantiate the effects of diet on CHD risk, but the risk score should be consistent with other evidence. The effect of diet on a single biomarker may be insufficient evidence to assess CHD risk.

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