Muscle Soreness

When people start an exercise program, they are sometimes discouraged, and sometimes concerned about muscle soreness that builds for a few days after exercise, and can last up to a week.  The process is called “delayed onset muscle soreness” (DOMS), and is a normal process for most of us, especially when we are not well exercise acclimatized.  A thorough 2013 review is here.

 

 

The Skinny on Dietary Fats

The Quick Take On Total Dietary Fat: Although a low total fat diet was first promoted by the American Heart Association in 1961, with an upper limit of 30% of calories, by the 1980s, many higher fat diets (the Mediterranean Diet, and many traditional diets) have since been shown to be healthful, and so the upper fat limit was removed in 2001, as the healthfulness of polyunsaturated fatty acids (PUFAs) has been clarified. Even whole food, pure vegan diets, with an emphasis on various nuts and seeds, some oils, avocado, olives and coconut are approximately 30% of their calories as fats.

On Dietary Saturated Fats: Although saturated fats (SFAs–long chain FAs with no double bonds) continue to be identified as being associated with increased LDL levels and CHD risk, unlike PUFAs, their risk is thought to be equal to the effect of refined or higher glycemic carbohydrate foods (which they are often replaced by in some foods).  Although there is a family of saturated fats normally eaten in the Western diet (C:12 lauric, C:14 myristic, C:16 palmitic, and C:18 stearic), they have been shown to have varying degrees of atherogenicity, although the significance of this becomes confusing when it is realized that these SFAs are never eaten in isolation.

It is hard not to be confused about this topic, but this is, in part, because the biologic effects of fatty acids is complex and constantly evolving.  For decades, it has all seemed straight forward: total fats, especially saturated fats, and trans fats were targeted for reduction, while unsaturated fats, such as mono- (MUFAs) and poly-unsaturated fatty acids (PUFAs, such as omega-3 and omega-6 fatty acids (FAs)) were considered heart-healthy.  In recent years, however, the suspected primary dietary contributors (especially SFAs) to coronary vascular disease are being re-examined,  because, “In truth, there was not very good epidemiological evidence in the beginning.”

First, shortly after World War II, when for the first time, dietary excesses were thought to be more relevant than dietary deficiencies, biochemist Ancel Keys first suspected that dietary fat was linked to heart disease (he would later publish his seminal, but now, controversial, Seven Countries Study, which appeared to give strong observational evidence that dietary fat and heart disease were directly correlated).  By 1961, he was directing American Heart Association nutritional guidelines to eat less fat and less meat, no more than three times a week, and the low fat movement was born. By 1977, nine years after the bipartisan, non-legislative Select Committee on Nutrition and Human Needs under George McGovern was formed, official recommendations for the US population included the need to reduce dietary fat from 40% to 30%, relying heavily on the opinions of another low fat proponent, nutritionist Mark Hegsted of Harvard University.  Dietary guidelines have  have been encouraged to eat a low fat diet for health.  At the time, not much distinction was made between kinds of fats.  Research like Dr. Dean Ornish’s program for reversing heart disease established a 10% low fat diet as part of a comprehensive lifestyle approach in a landmark study that demonstrated reversal of advanced coronary disease on PET scans after just one year. 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.

Fats from fish have increasing been thought of as healthful.  A comprehensive review on the health benefits

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.”

References:

Dietary Monounsaturated Fatty Acids Appear Not to Provide CardioprotectionChiara Degirolamo and Lawrence L. Rudel Curr Atheroscler Rep. 2010 November; 12(6): 391–396.doi:  10.1007/s11883-010-0133-4

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.