Even though the Wheat Belly approach to health, slenderness, and youthfulness had its origins with efforts to reduce/eradicate risk for heart disease, this is a topic I have not talked about much. So let’s discuss how and why the strategies we use in the Wheat Belly lifestyle are so magnificently effective in managing cardiovascular risk.
We live in a world in which doctors have been brainwashed by the intensive marketing efforts of Big Pharma, persuading them that statin drugs, PCSK9 inhibitors, and other efforts to “reduce cholesterol” are the key to reducing cardiovascular risk. These notions should have been abandoned decades ago, as the science, availability of superior biomarkers, and other strategies have progressed—but are not being passed onto the public, as my colleagues are guilty of willful ignorance and indifference, especially since acute cardiovascular care is so profitable.
Cholesterol is a ubiquitous lipid (fat) in the human body, comprising a major portion of the cell walls in every organ. If we take human plasma and break down the various lipoproteins (fat-carrying proteins) in the bloodstream, we can identify various fractions that vary depending on density, size, protein and fat composition. Many years ago, researchers chose to distinguish various lipoprotein fractions by cholesterol content, leading to breakdown of lipoproteins into high-density (HDL cholesterol), low-density (LDL cholesterol), very low-density (VLDL cholesterol), and all fractions summed up (total cholesterol), forming layers in the sample after being spun in a centrifuge. Cholesterol measurement of the various lipoprotein fractions was therefore intended to be a tool for indirectly quantifying these lipoproteins—but it does not mean that cholesterol causes heart disease. But that is what many doctors perceived, even though using cholesterol as a gauge is hugely overly-simplistic, especially when the technology to categorize lipoproteins by size, triglyceride content, proteins, and other features became available. Yet the silly notion of using cholesterol as an indirect gauge of lipoproteins persists because Big Pharma found a way to exploit this idea.
Throw in the absurd notions of a “heart healthy” diet from agencies such as the American Heart Association (AHA) that still advocates cutting total and saturated fat and increasing whole grains. The evidence supporting this diet is poor, at best, outdated and poorly constructed studies from the 1950s and 1960s, followed by observational studies that showed that greater intake of whole grains was less harmful than intake of white flour—they did not show that cardiovascular risk was reduced or eliminated.
So the conventional management of cardiovascular risk involves:
- Advocating a diet that causes heart disease or at least fails to reduce risk—i.e., a diet low in total and saturated fat and dominated by “healthy whole grains,” an eating pattern associated with insulin resistance, increased measures of inflammation, provocation of small LDL particle formation, increased VLDL particles via increased de novo lipogenesis in the liver, development of fatty liver, increased risk for type 2 diabetes.
- Guesstimating cardiovascular risk using flawed, outdated, and imprecise cholesterol markers while ignoring superior markers of cardiovascular risk
- Prescribing drugs to reduce cholesterol while failing to address small LDL particles, VLDL, postprandial lipoprotein distortions, insulin resistance, endothelial dysfunction, metabolic endotoxemia and other factors.
In short, the modern approach to managing cardiovascular risk is an overwhelming failure. It does not work but allows, by neglect, millions of people to continue to have heart attacks, undergo stent implantation and bypass surgery, and fuel sales of pharmaceuticals and medical devices.
A truly “heart healthy” diet should achieve normalization of the biomarkers associated with cardiovascular risk—SO simple and logical—that go way beyond cholesterol markers, such as:
- Reduction or elimination of small LDL particles—aiming for a small LDL particle count of 200 mol/L or less.
- Reduced fasting and postprandial (after-meal) VLDL particles that initiate the reaction to cause small LDL particles and themselves cause heart disease by gaining entry into the artery wall.
- Drop in triglycerides that parallels the reduction in VLDL particles due to the marked reduction in liver de novo lipogenesis, the liver’s conversion of carbs to triglycerides. Aim to keep fasting triglycerides 60 mg/dl or less and you minimize VLDL particles and their contribution to heart disease.
- Rise in HDL and increased HDL particle size that make them more protective against heart disease—Aim for 60 mg/dl or higher. (Values in the 80,90, or 100 mg/dl are common on this program, unlike the 30-50 mg/dl common among people at risk for heart disease or taking statins.)
- Drop in multiple inflammatory markers such as C-reactive protein to zero or near-zero, an effect apparent on the surface by seeing less skin inflammation and leg edema
- Reduced fasting blood sugar, fasting insulin, and insulin resistance—aiming for fasting glucose of 70-90 mg/dl, fasting insulin of 4 mIU/L or less.
- Reduction in HbA1c and thereby glycation of small LDL particles (glycated LDL particles are more potent causes of heart disease)–You know that glycation has been minimized when your HbA1c is 5.0% or less.
- Rise in RBC omega-3 index due to fish oil supplementation
- Rise in 25-hydroxy vitamin D blood levels due to vitamin D supplementation that yields huge advantages, e.g., reduced inflammation, reduced PTH, normalization of calcium metabolism, reduced insulin resistance, improved endothelial responses (arterial relaxation). We aim for 60-70 ng/ml for maximum benefit.
- Rise in RBC magnesium due to magnesium supplementation that contributes to reduced blood pressure and reduced potential for abnormal heart rhythms
- Optimal thyroid measures—such as a TSH of 2.0 mIU/L or less, free T3 in the upper half of the reference range; iodine supplementation.
- Reduction in endotoxemia, i.e., increased serum lipopolysaccharide (LPS) that originate in disrupted bowel flora and small intestinal bacterial overgrowth (SIBO). This most recent addition to the list is a huge factor in cardiovascular risk.
These are the effects you can achieve simply by engaging in all the strategies in my programs. It helps to have baseline, then follow-up, labs that include a NMR lipoprotein panel; fasting glucose and insulin, HbA1c; 25-OH vitamin D; TSH, free T3, free T4, reverse T3, thyroid antibodies. If you compared the values achieved with these strategies vs. those achieved with a statin drug and a low-fat diet, you would be shocked at the dramatic differences. You will see an astounding amount of persistent abnormalities with conventional efforts, for instance.
Let’s also not forget that statin drugs are responsible for worsening insulin resistance and thereby increasing the potential for type 2 diabetes by more than 30%, are commonly associated with muscle weakness and pain, and disrupt the microbiome by increasing undesirable bacterial species while suppressing healthy species along with a profound reduction in intestinal butyrate that nourishes the intestinal lining and yields numerous health benefits, phenomena that likely hold potential for long-term health disruptions. (The shifts in bowel flora composition that approximates that of a diabetic, along with the considerable reduction in intestinal butyrate likely underlie the increase in insulin resistance and type 2 diabetes with statin drugs.)
Heart disease risk is readily, easily, and effectively addressed using these strategies. Just don’t ask the doctor eager to get you on the cath lab table for answers.