Type 2 Diabetes, a Dietary Disease #334: A Unifying Hypothesis of Chronic Disease: Part 1

I don’t remember how I landed on South African blogger Marika Sboros’s site, FOODMED.NET; but I love it, and I have signed up for regular delivery. Her blog’s subtitle is “Let food be your medicine,” so you can readily see my affinity. I first read a post in the “Managing Your Blood Sugar” series titled NOAKES: "IT'S THE FATTY LIVER DISEASE, STUPID' PART 2, tagged “LCHF.” Interestingly, Marika explains, LCHF in her lexicon means “Low Carb Healthy Fats.” I like it. It’s time to take on the PUFAs!

The author of this particular post is world-renowned scientist and University of Cape Town Professor Emeritus Dr. Tim Noakes. Noakes introduces his subject via the misunderstood term “risk factors” as taken from epidemiology and “observational” or “associational” studies. He delves briefly into “hazard ratios” (HRs), relative and absolute risk, and related subjects to show how data is commonly manipulated and abused.

“This is intellectually absurd,” Noakes says. “How can everything be a risk factor for everything else?” he asks. He answers, “The answer can be found in the ignored work of Dr. Gerald Reaven, Emeritus Professor of Medicine at Stanford University.” “Reaven has spent the past 60 years studying the condition that intellectually he now owns, insulin resistance.”

Reaven’s interest in insulin resistance was piqued by the distinction between Type 1 and Type 2 diabetes. Type 1 is characterized by the total absence of endogenous insulin; Type 2, insulin resistant diabetes, by “abnormally high amounts [of insulin] because the target cells on which the insulin normally acts are resistant to its action; hence the condition of insulin resistance or carbohydrate intolerance. Persons with insulin resistance have blood insulin concentrations that are elevated most of the time, a condition known as hyperinsulinemia.”

Noakes says, “Reaven’s great contribution has been to show this persistent hyperinsulinemia in insulin resistance, whether or not associated with T2DM, produces a collection of grave secondary consequences.”

“But Reaven’s greatest (and bravest) intellectual contribution is to suggest that insulin resistance and hyperinsulinemia are the necessary biological precursors definitely for four and perhaps for all six of the most prevalent chronic conditions of our day: 1) Obesity; 2) Arterial disease (local: heart attack or stroke; disseminated: T2DM; 3) High blood pressure; 4) Non-Alcoholic Fatty Live Disease (NAFLD); Cancer; and Dementia (Alzheimer’s Disease, also known as Type 3 Diabetes).”

Reaven gave the  keynote Banting lecture at the 1988 American Diabetes Association annual meeting. His talk explained the underlying factor for a constellation of abnormalities: glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension.  He named it “Syndrome X; it was also given the moniker Reaven’s syndrome. Today it is simply called Metabolic Syndrome.

“The key finding from Reaven’s work,” Noakes says, “is that these conditions are not separate – they are different expressions of the same underlying condition. Thus a patient should not be labeled as having high blood pressure or heart disease or diabetes or NAFLD (or perhaps even cancer or dementia).”

“Instead,” Noakes continues, “the patient should be diagnosed with the underlying condition – insulin resistance – with the realization that the high blood pressure, the obesity, the diabetes, the NAFLD, or the heart attack or the stroke are simply markers, symptoms if you will, of the basic condition.”

“And that basic condition,” Noakes concludes, “is insulin resistance which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates eaten each day. “

Thus we have it: Reaven’s unifying hypothesis of chronic disease: “One disease, one cause, many symptoms.” Tune in next week for a glimpse at the profound implications of this fundamental advance in medical science.