Ultimate Guide to Cholesterol and Heart Disease: Dietary Prevention

Heart DiseaseIn part 1 of this series I provided some background information required for the remainder of this series and in part 2 we determined that saturated fat is not associated with negatively altered blood cholesterol or an increased risk of heart disease; thus, the Diet Heart Hypothesis does not hold true.  In part 3, I discussed  some downfalls to traditional blood cholesterol measures as well as some more reliable blood cholesterol measures in the determination of heart disease risk.  In part 3 we ended with the question: If saturated fat and cholesterol don’t cause heart disease, what dietary factors do? Thus, the focus of the 4th and final instalment of this series of posts.


Dietary Prevention of Heart Disease

In light of the above, there is little evidence linking dietary saturated fat and cholesterol to the risk of Heart disease and the question remains as to what dietary factors impact risk.

It is well known that metabolic syndrome is one of the strongest predictors of Heart disease risk (4, 5).  Metabolic syndrome is a clustering of risk factors, such as central obesity, insulin resistance, dyslipidemia and hypertension that together culminate in the increased risk of type 2 diabetes mellitus and cardiovascular disease (6).  Furthermore, the scientific literature consistently finds that people with metabolic syndrome have increased levels of small LDL particles (3) and an increased number of LDL particles, LDL-p/apoB (7-12), one of the best predictors of heart disease risk.  As such, a dietary focus on the reduction of metabolic syndrome would hypothetically be the best measure to reduce the risk of heart disease.

It has been found that saturated fat is not associated with an increased risk of metabolic syndrome, while carbohydrate consumption is.  Specifically, a reduction in carbohydrate consumption and a low carbohydrate diet is more effective at reducing metabolic syndrome than a low saturated or low fat diet (1, 13, 14).  Furthermore, consumption of refined grains such as white rice has been linked to metabolic syndrome (15).  Not surprisingly, high fructose and glucose consumption have also been linked to metabolic syndrome (16, 17).  These findings can be tied together with evidence indicating that both high glycemic index and glycemic load diets are directly associated with metabolic syndrome (18).  Regarding dietary fat; trans fat, excess Omega 6 fat, and high Omega 6:3 ratios have all been linked to metabolic syndrome without a positive link seen with saturated or monounsaturated dietary fat (19-21).  Basically saturated and monounsaturated fats don’t cause heart disease.  Given the fact that majority of fast and packaged foods contain the above noted dietary risk factors for metabolic syndrome, it is no surprise that fast food and processed food consumption is related to metabolic syndrome (22).

The standard America diet is notoriously high in carbohydrate, sugar, and Omega 6 fats and it has been shown that traditional populations consuming a high saturated fat diet, such as the Masai and the Tokelau, begin to develop markers of metabolic syndrome when moving to a contemporary, westernized diet (2, 22, 23).

Heart Disease Cause and Prevention – Final Message

In combination, the Lipid and Diet Heart Hypothesis combine as follows:

  •        Elevated serum cholesterol increases the risk of heart disease
  •        Dietary saturated fat increases serum cholesterol
  •        Dietary cholesterol increases serum cholesterol
  •        Thus, dietary saturated fat and cholesterol increase the risk of heart disease.

However, in order for the above hypotheses to hold true, there must be consistent scientific evidence for each of the above points.  Even though these theories have been utilized to develop public health initiatives and pharmacological treatments there is significant discord in the scientific literature.

Dietary saturated fat and cholesterol have not been consistently shown to be associated with elevated LDL and total cholesterol levels across multiple populations and cohorts, and have also not been associated with an increased risk of heart disease across populations and cohorts.  Therefore, the Diet Heart Hypothesis cannot be considered true.

In its classical form, the Lipid Hypothesis indicates that elevated serum cholesterol and LDL concentrations are a marker for an elevated risk of heart disease; however, this is not consistently shown across all populations and cohorts.  Furthermore, low cholesterol can actually have negative health impacts on all-cause mortality.  Recent scientific evidence still shows a connection to serum lipid markers and heart disease risk indicating that the Lipid Hypothesis may be valid.  However, evidence indicates that the most accurate serum lipid markers for the risk of heart disease are not LDL and total cholesterol concentrations; rather, LDL particle number and apoB appear to be more accurate measures.

A large body of literature indicates that metabolic syndrome is one of the best predictors of heart disease risk, which is concurrent with finding that LDL particle number and apoB are consistently elevated in this population.  Thus, dietary advice for reducing heart disease should be in line with that which reduces metabolic syndrome.  Such a diet includes mainly whole foods, limited fast/processed food, a reduction in glycemic index and load, a reduction in fructose, removal of trans fat, achieving an appropriate Omega 6:3 ratio, low inflammatory food intake, and limited refined grains.

Therefore, it is suggested that a new Lipid and Diet Heart Hypothesis be put forward as follows:

  •         Elevated serum LDL particle number/apoB increase the risk of heart disease
  •         High glycemic index/load diets increase LDL particle number
  •         High fructose and glucose diets increase LDL particle number
  •         Dietary trans-fat increase LDL particle number
  •         An Omega 6:3 ratio above 2:1 increase LDL particle number
  •         Thus, high glycemic load, high glycemic index, high fructose, high glucose, high Omega 6:3 ratio, high refined grain, and trans-fat containing diets increase the risk of cardiovascular disease.

However, even this is a simplified version of the complex interaction between food, serum lipid measures, and cardiovascular disease risk as it does not include other risk factors such as chronic system inflammation, oxidative stress, immune system dysregulation, activity level, food sensitivity, appropriate vitamin and mineral intake, chemical food additives, pesticide exposure, etc.  It is certain that as more research is published, further connections will be discovered.

In the end, I hope you have found this series of posts helpful in whatever you may be looking for, any comments you have are welcome below.


The Barefoot Golfer



  1.  http://www.ncbi.nlm.nih.gov/pubmed/21978979
  2.  http://www.ncbi.nlm.nih.gov/pubmed/?term=J.+Chron.+Dis.+34%3A45.+1981
  3.  http://www.ncbi.nlm.nih.gov/pubmed/24558110
  4.  http://www.ncbi.nlm.nih.gov.libaccess.lib.mcmaster.ca/pubmed/10842650
  5.  http://www.ncbi.nlm.nih.gov.libaccess.lib.mcmaster.ca/pubmed/20164784
  6. http://www.ncbi.nlm.nih.gov.libaccess.lib.mcmaster.ca/pubmed/25407540
  7.  http://www.ncbi.nlm.nih.gov/pubmed/16380547
  8.  http://www.ncbi.nlm.nih.gov/pubmed/22211563
  9.  http://www.ncbi.nlm.nih.gov/pubmed/22674204
  10.  http://www.ncbi.nlm.nih.gov/pubmed/20213498
  11. http://www.ncbi.nlm.nih.gov/pubmed/21960651
  12. http://www.ncbi.nlm.nih.gov/pubmed/21138461
  13.  http://www.ncbi.nlm.nih.gov/pubmed/25415333
  14.  http://www.ncbi.nlm.nih.gov/pubmed/23035144
  15. http://www.ncbi.nlm.nih.gov/pubmed/24200655
  16. http://www.ncbi.nlm.nih.gov/pubmed/24042453
  17. http://www.ncbi.nlm.nih.gov/pubmed/23594708
  18. http://www.ncbi.nlm.nih.gov/pubmed/21111092
  19. http://www.ncbi.nlm.nih.gov/pubmed/21228440
  20. http://www.ncbi.nlm.nih.gov/pubmed/24496399
  21. http://www.ncbi.nlm.nih.gov/pubmed/?term=Dietary+Fats+and+Health%3A+Dietary+Recommendations+in+the+Context+of+Scienti%EF%AC%81c+Evidence
  22. http://www.ncbi.nlm.nih.gov/pubmed/24193228
  23.  http://www.ncbi.nlm.nih.gov/pubmed/4103135?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


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