Gerald Reaven and I at Stanford Faculty Club
Gerald Reaven and I at Stanford Faculty Club


I recently had the opportunity to meet a medical hero of mine at the Stanford University faculty club.  Gerald “Jerry” Reaven is the renown endocrinologist and researcher (pictured with me) who coined the term metabolic syndrome and is author of Syndrome X: The Silent Killer.

I owe Jerry my life given that his metabolic syndrome criteria helped identify my own underlying risk for heart disease and chronic disease.  Something the cholesterol guidelines and archaic Framingham risk calculator would have missed.  Dr.Reaven’s research has also inspired me to devote my medical practice to the care of high risk Asian Indians and now even East Asians who are plagued by an epidemic of insulin resistance characterized by metabolic syndrome.

The LDL Fallacy

Global heart disease is predominantly driven by metabolic syndrome, an insulin resistant condition which has nothing to do with the LDL result you see on a standard lab report.  Metabolic syndrome can cause changes in the LDL particle size (type A versus type B) and number (LDL-P) which do not appear on a standard cholesterol test.

Your basic cholesterol test reports LDL-C, the concentration of cholesterol carried by LDL.  We’ll discuss cholesterol and these LDL nuances in detail on a future post and this is covered in even more detail in my book.  Yet cholesterol guidelines, including the most recently published ones, continue to hyperfocus on a number (LDL-C) that alone has very little value, except to blockbuster statin manufacturers who continue to earn billions from these drugs.

My discussions with many clinicians and researchers such as Jerry who work on the front lines of insulin resistance with no financial ties to statin-producing drug companies, repeatedly reveal the dark truth of how the drug industry has exerted its enormous influence to keep LDL-C in the spotlight while keeping insulin resistance and metabolic syndrome in the background.

One important point Jerry highlighted to me is the fact that LDL-C is predominantly driven by genetics, and lifestyle is relatively ineffective in making significant changes in LDL-C levels.  I’ve seen this time and time again in the clinic.  Many of my patients who have made significant lifestyle improvements notice fairly predictable improvements in their triglycerides, their HDL (good cholesterol), their blood sugar, and their blood pressure, but often the LDL-C is relatively unchanged or may move up or down.

In contrast to LDL-C, LDL size and particle number on the other hand can improve significantly with healthy lifestyle changes. This is another reason why statins are overprescribed.  Patients with elevated LDL-Cs are typically given a 3-4 month trial of lifestyle changes before being put on a statin.  Despite their best efforts and improvements in nearly every other area of heart disease risk, from improving body composition and cardiovascular endurance to reducing inflammation, LDL-C normally budges very little, earning them a lifelong prescription of statins.

If insulin resistant measures were the focus of cholesterol guidelines, especially in susceptible ethnic groups, statin prescriptions would clearly drop.  Now you know why drug companies have worked so hard to keep LDL-C on the pedestal of cholesterol and heart disease risk prediction and treatment guidelines.

What is Metabolic Syndrome?

Metabolic syndrome is a constellation of insulin resistant risk factors and in order to be diagnosed you need to fulfill 3 or more of the following criteria:

  • Central obesity with waist circumference greater than 35 inches (89 cm) for women and 40 inches (102 cm) for men.  See below for ethnic-specific cutoffs.
  • Triglyceride level of 150 mg/dL (1.7 mmol/L) or higher, or you’re receiving treatment for high triglycerides.
  • Low HDL cholesterol (“good” cholesterol) — less than 40 mg/dL (1.04 mmol/L) in men or less than 50 mg/dL (1.3 mmol/L) in women, or if you’re receiving treatment for low HDL, such as taking the drug Niacin.
  • Increased blood pressure, meaning a systolic (top number) blood pressure measurement of 130 mm Hg or more or a diastolic (bottom number) blood pressure measurement of 85 mm Hg or more.
  • Elevated fasting blood sugar (blood glucose) of 100 mg/dL (5.6 mmol/L) or higher, or you’re receiving treatment for high blood sugar.

The IDF (International Diabetes Federation) has a modified version of the metabolic syndrome criteria which includes ethnic specific cut points for waist circumference .  For Asian Indians, East Asians, and Japanese, the waist circumference limits are greater than or equal to 35 in (90 cm) for men and 31in (80cm) for women.  Go here for step-by-step instructions on how to properly measure waist circumference and this post I wrote is really important for understanding different body sizes in diverse ethnic groups.  I also helped create a South Asian body size/BMI page for my medical group’s South Asian website which is worth referencing.

Did you notice something missing from the metabolic syndrome criteria by the way?  LDL-C didn’t make the cut!  Now let’s think about this.  If metabolic syndrome is a major global cause of heart disease acknowledged by most physicians around the world, and our current cholesterol guidelines are supposed to identify heart disease risk in today’s diverse population, why do the cholesterol guidelines continue to worship LDL-C and barely acknowledge metabolic syndrome?  Ask the drug companies.

Making metabolic syndrome a focus of cholesterol and heart disease risk assessment guidelines means diminishing the value of LDL-C , and thus reducing statin prescriptions for a large part of the population who can overcome metabolic syndrome through lifestyle changes.

A quick and dirty measurement of insulin resistance is the triglyceride-to-HDL ratio.  Again thanks goes to Jerry Reaven for this valuable tool. Until we have national standardized assays for insulin levels or more accurate tests available, using this ratio is a good tool for assessing insulin resistance and can predict risk long before your blood sugars start to go up.  Aim for a ratio of less than 3.0.

Keep in mind that many of my high risk Asian Indian and East Asian patients have had their heart attacks before their blood sugars became abnormal.  This ratio has been an indispensable diagnostic tool in my clinic that has revealed significant heart disease risk in patients who otherwise appear normal when applying outdated Framingham and related risk assessments.

In 2009 I personally had a total cholesterol of 154 mg/dL and an LDL of 85 mg/dL, which most docs would have loved  However, my ratio was 11.2 !  By the way I had this ratio despite exercising 4-5 days a week and eating a standard American low-fat, high fiber diet.  Cutting back excess so-called healthy carbohydrates (wheat, oats, grains, etc.) was the key to dropping my ratio down to normal and is a major focus of my book.

Remember, if you are insulin resistant, you are carbohydrate intolerant, and even a small amount of “healthy carbs” can lead to major health complications like obesity,diabetes, and heart disease.  In other words, a bowl of oatmeal for someone highly insulin resistant (aka carbohydrate intolerant) can be harmful, while the same bowl of oatmeal would likely have no adverse effects in someone who is insulin sensitive.  That’s why standard nutrition guidelines fail.  They dish out generic advice to a diverse and metabolically complex population.

So there you have it, physician-driven cholesterol guidelines and USDA-driven nutrition guidelines nearly took my life and I see the adverse metabolic effects of this in my clinic far too often.  We will continue to explore this topic in detail in future postings and you’ll understand clearly how so many of our daily “guideline-recommended” lifestyle choices are contributing to insulin resistance and metabolic syndrome.