Dr. Richard David Feinman, PhD

Richard David Feinman ("the other Feinman") is Professor of Cell Biology (Biochemistry) at the State University of New York (SUNY) Downstate Medical Center  in Brooklyn, New York. Dr. Feinman’s original area of research was in protein chemistry and enzyme mechanism, particularly in blood coagulation and related processes.

Dr. Feinman has worked in several scientific areas including animal behavior and he has had a previous life in the visual arts. His friends consider him a Renaissance Man but he has made peace with the term dilettante.

His current interest is in nutrition and metabolism, specifically in the area of diet composition and energy balance. Work in this area is stimulated by, and continues to influence, his teaching in the Medical School where he has been a pioneer in incorporating nutrition into the biochemistry curriculum.   Dr. Feinman is the founder and former co-Editor-In-Chief (2004-2009) of the journal, Nutrition&Metabolism. Dr. Feinman received his BA from the University of Rochester and he holds a PhD in chemistry from the University of Oregon.

Richard Feinman is principal author of the 26-author comprehensive review “Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base.”

His recent book “The World Turned Upside Down - The Second Low Carbohydrate Revolution” describes how “How the science of carbohydrate restriction arising from a rag‑tagcollection of popular diets defeated the powerful low‑fat army and became the default approach to health.”

Books by Dr. Richard Feinman, PhD

Video Presentations of Dr. Richard Feinman, PhD

An Interview with Prof. Richard Feinman, PhD (Parts 1-3)

In early August I had the pleasure of being welcomed by Richard at his home in Brooklyn, NY. He was a most gracious host, and I felt privileged to enjoy a discussion with one of the technical leaders in the movement.  Our conversation centred on something huge and inexorable that will stem the epidemic of 'diabesity' in our world; that's right folks - we were talking about the Second Low Carbohydrate Revolution.

It is finally upon us, riding on a tide of emerging science. And it is long, long overdue.

On Keto, LCHF and Cancer with Prof. Richard Feinman, PhD

"Ketogenic Diet and Diabetes" - Dr. Richard Feinman, PhD

Nutrition in Crisis - with Dr. Richard Feinman, PhD (Full Interview)

Scholarly Articles from Dr. Richard Feinman, PhD

Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction - Nutrition & MetabolismMetabolic Syndrome (MetS) represents a constellation of markers that indicates a predisposition to diabetes, cardiovascular disease and other pathologic states. The definition and treatment are a matter of current debate and there is not general agreement on a precise definition or, to some extent, whether the designation provides more information than the individual components. We consider here five indicators that are central to most definitions and we provide evidence from the literature that these are precisely the symptoms that respond to reduction in dietary carbohydrate (CHO). Carbohydrate restriction is one of several strategies for reducing body mass but even in the absence of weight loss or in comparison with low fat alternatives, CHO restriction is effective at ameliorating high fasting glucose and insulin, high plasma triglycerides (TAG), low HDL and high blood pressure. In addition, low fat, high CHO diets have long been known to raise TAG, lower HDL and, in the absence of weight loss, may worsen glycemic control. Thus, whereas there are numerous strategies for weight loss, a patient with high BMI and high TAG is likely to benefit most from a regimen that reduces CHO intake. Reviewing the literature, benefits of CHO restriction are seen in normal or overweight individuals, in normal patients who meet the criteria for MetS or in patients with frank diabetes. Moreover, in low fat studies that ameliorate LDL and total cholesterol, controls may do better on the symptoms of MetS. On this basis, we feel that MetS is a meaningful, useful phenomenon and may, in fact, be operationally defined as the set of markers that responds to CHO restriction. Insofar as this is an accurate characterization it is likely the result of the effect of dietary CHO on insulin metabolism. Glucose is the major insulin secretagogue and insulin resistance has been tied to the hyperinsulinemic state or the effect of such a state on lipid metabolism. The conclusion is probably not surprising but has not been explicitly stated before. The known effects of CHO-induced hypertriglyceridemia, the HDL-lowering effect of low fat, high CHO interventions and the obvious improvement in glucose and insulin from CHO restriction should have made this evident. In addition, recent studies suggest that a subset of MetS, the ratio of TAG/HDL, is a good marker for insulin resistance and risk of CVD, and this indicator is reliably reduced by CHO restriction and exacerbated by high CHO intake. Inability to make this connection in the past has probably been due to the fact that individual responses have been studied in isolation as well as to the emphasis of traditional therapeutic approaches on low fat rather than low CHO.We emphasize that MetS is not a disease but a collection of markers. Individual physicians must decide whether high LDL, or other risk factors are more important than the features of MetS in any individual case but if MetS is to be considered it should be recognized that reducing CHO will bring improvement. Response of symptoms to CHO restriction might thus provide a new experimental criterion for MetS in the face of on-going controversy about a useful definition. As a guide to future research, the idea that control of insulin metabolism by CHO intake is, to a first approximation, the underlying mechanism in MetS is a testable hypothesis.