2018 – The Year of Low Carb

Low Carb Revolution

Share This Post

Share on facebook
Share on linkedin
Share on twitter
Share on email

Interview with Dr. Richard Feinman, Professor of Cell Biology,

Richard Feinman, PhD, is a cell biologist who is widely credited with doing some of the first serious scientific research on the Atkins Diet.  His career has spanned decades as low fat diets waxed and waned in public health recommendations. While he emphasizes not being an ”advocate,” he has continued to argue for the importance of  low carbohydrate diets as the first line of defense against diabetes, metabolic syndrome, and obesity.

Cronometer.com’s April Wilson Smith interviewed Dr Feinman of Suny Downstate, Brooklyn, New York


Question:  Who are you and what do you do?


I’m Richard Feinman, and I identify myself as Richard Feinman, The Other because I’m often confused with the physicist and Nobel prize winner Richard Feynman.  I’ve been a Professor of Cell Biology at SUNY Downstate in Brooklyn, New York for many years.  I’m originally trained as an enzyme chemist and have worked in several fields, including behavioral neuroscience.  My main research interest rests with the application of ketogenic diets for cancer. Currently I’m also interested in the philosophy of science and how it applies to the accuracy and reliability of what is published in medical literature.


Question: How did you get interested in low carb diets?


I’ve always known about low carb diets because I’ve always been fighting fat.  Judging from old photographs, I was never fat as a child, but I always had what they describe as a poor body image.  I recognized by observation early on that the things that increased my weight were carbohydrates.  Generally I knew what to eat, but like everyone with a weight problem I didn’t always eat those things.


Low carb diets became a professional issue for me when I began teaching metabolism to medical students.  Metabolism is the science of how your food is transformed to provide energy to cellular material.  The problem is that the interconversions of the substances derived from food (metabolites) is complicated.  So the old idea that “you are what you eat” is not really right because right after you’ve eaten it it’s immediately turned into something else.  You are what your metabolism does to what you eat.  Does your metabolism turn what you eat into fat, or does it burn it right away?

In order to provide some kind of consistent theme to relate all the different parts of metabolism I use low carb diets as a model because low carb diets are the easiest way to illustrate how metabolism is controlled by a large number of different enzymes and hormones.  Primary among them is insulin and the major source of insulin is carbohydrates, either dietary carbohydrates or carbohydrates from other substances in metabolism.  Insulin is not the only important hormone, but I usually describe it as analogous to the role of the quarterback in American football.  There are at least twenty two different things happening on the field at once, but you can understand things reasonably well by focusing on the quarterback.  Insulin doesn’t explain everything in metabolism, but like the quarterback, watching its role gives you a pretty good idea of what’s going on.


Question: So what does insulin do, and why is it such a major player in diabetes, metabolic syndrome and obesity?


Insulin is primarily an anabolic hormone, which means it builds things up.  It will increase storage of fat and glycogen (where we store carbohydrate) and protein synthesis.  Normally when you eat a meal, insulin goes up, the ingested fat is stored in the fat cells, and protein is used to make new cell material.

Metabolism has two goals: provide energy and keep glucose levels relatively constant. The first is not a major problem in that almost all of us have stored enough fat to live for weeks or even months in the absence of food. If you’re on a starvation diet, your body stops storing fat and burns fat for energy, but what about regulating glucose?  The brain, central nervous system and red blood cells require glucose, and insulin regulates glucose.  Unlike our fat stores, we maintain very limited accumulation of carbohydrate and to meet the second need, so you must make the glucose from something else.  That’s mostly protein.   Under those conditions, the body starts to consume its own protein for gluconeogenesis (new making of glucose). If you are without food or carbohydrate for very long, you have the danger of muscle wasting.  However, with a low carbohydrate diet, you have decreased insulin so decreased fat storage and increased burning of fat, but you also consume adequate protein so the body can create glucose without burning its own muscle tissue.

That is why the Atkins diet and other low carbohydrate diets are so effective at helping people lose weight without losing muscle.  The insulin lowering effect of the low carb diet also suggests it as the first line of treatment for metabolic syndrome and obesity.


Question: Can you say more about low carb diets for metabolic syndrome and diabetes?


Dr. Gerald Reaven, an endocrinologist who died just this past February, derived the concept of metabolic syndrome, which he first referred to as “Syndrome X.”  Toward the end of his career her preferred the term “insulin resistance syndrome.”  He observed that central obesity (being “apple shaped”), high blood pressure and diabetes all have two common causes: insulin resistance and impaired glucose tolerance.   Now we’re used to the idea of metabolic syndrome, but at the time it was a radical insight.

Diabetes is the classic insulin-controlled disease.  In the 1920s, it was discovered that the defect in Type 1 diabetes was an inborn lack of insulin and you could treat Type 1 by administering insulin.  Before that time it was treated with a low carb diet.  When insulin was discovered you could now actually provide a cure for the Type 1 diabetes patient.  The trouble is several fold.  At that time the difference in Type 1 and 2 was misunderstood.  Type 1 was seen as a hormone deficiency disease and you could replace the missing hormone with insulin and then you could eat carbs because all you had to do was pair the carbs with insulin.

Diabetes is a hormone deficiency disease, but that’s not the whole story.  It’s a systems disease.  It’s a breakdown in control due to the absence of insulin.  By trying to regulate insulin externally, you get much greater fluctuations than you would have by regulating it with diet.  For people with Type 1 diabetes, external insulin will always be necessary, but the systems disease can be improved with a low carb diet.  There is no question that low carb diets should be the primary treatment for Type 2 diabetes.  There are a large number of people who essentially are cured, and maintain insulin and blood sugar control as long as they remain on a low carb diet.


Question: All this makes sense, but the medical establishment has been negative about low carb diets for years.  Why is that, and what’s changing? 


Years ago, probably starting in the 1960’s, the nutrition establishment became obsessed with fat and the idea that fat was the cause of heart disease.  The idea might come from the fact that arteriosclerosis plaques have fat in them, but it’s a big jump to say that fat is the key player in heart disease.

This hypothesis was tested in the Framingham Study, which began in 1948 with just over 5,000 participants in the small town of Framingham, Massachusetts and is now on its third generation.  The study participants recorded what they ate, what their activity level was, and other things.  The goal was to tabulate all this information, look at rates of heart disease, and ask the question: what is the relationship between dietary factors and heart disease.  But the experimenters weren’t asking that question at all: what they were really asking is, “Can I prove the Diet Heart Hypothesis?” – the hypothesis that dietary fat causes heart disease.

It turned out that there was no relationship between fat, saturated fat, cholesterol or heart disease.  Early results showed that high fat diets increased cholesterol, but later results showed differently.  For the past 30 years all of the tests of the Diet Heart hypothesis have been ambiguous at best.  Where you find low fat diets providing benefit is also where the carbs are low – in overall low calorie diets.  Most people feel that that a high saturated fat diet if it were also high carbohydrate might be a risk for heart disease (because glucose via insulin is catalytic and effects other nutrients) but it is hard to show even that.

Resistance to low carbohydrate diets as a first line of treatment for diabetes, obesity and metabolic syndrome has come from the Diet Heart Hypothesis and the assumption that people would replace carbs with saturated fat.


Question: So what’s changed? Why do you call 2018 the Year of Low Carb?


While the tests of the Diet Heart Hypothesis have consistently failed, studies on low carb diets for diabetes have consistently shown improvement.  A real breakthrough paper came out this year by Dr. Sarah Hallberg and colleagues of Ohio University, working with Dr. Jeff Volek, a long term researcher in low carb diets and a powerlifter, both academically and personally.  The paper, entitled, “Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study,” showed that of over 300 patients with Type 2 diabetes who were put on a ketogenic diet along with continuous remote medication monitoring from a machine that provided feedback to care providers on patients,  94%  were able to eliminate or reduce the use of artificial insulin. Patients on the ketogenic diet also lowered their HbA1C (a measurement of blood sugar levels over time) from 7.6% to 6.3% and lowered their body weight by 12%.  The 87 patients in the control group who received the usual care from their doctors and a diabetes education program experienced no changes in medication needs, weight or HbA1C.  Meanwhile, no one in the ketogenic diet group had any adverse effects from the diet – there was no downside, only improvement.

In late August, a meeting of researchers studying low carbohydrate diets for obesity, diabetes, neurological diseases such as epilepsy (for which ketogenic diets have long been one of the most effective treatments) and even cancer convened at Ohio State.  There is much momentum for moving ahead with low carbohydrate diet research.


Question: What happened next?


And then there was the wet blanket.  Just as we were leaving the meeting, the Lancet Public Health published an article saying that low carb diets would increase all-cause mortality.  There were, however, no low carb diets. In fact, there were no diets at all in the sense of telling people what to eat, monitoring their response and evaluating pre-set hypotheses. The authors made up their own definition of a low-carb diet. They applied this to a previously published paper that was not intended to study low-carbohydrate diets (the name Arteriosclerosis Risk in Communities tells you what it was about).  Patients were asked to estimate their food intake based on a food frequency questionnaire (FFQ), in itself is highly problematic methodology, as food recall is notoriously bad and biased, especially over long periods of time.  Quick, what did you have for lunch last Monday?  What about how frequently you ate any given group of food over the last few years? The data for each patient were responses to these FFQ’s for two visits, six years apart. Some wit on the internet (maybe that was me) said it was a great project for a graduate student; you take a point every six years.  It is obvious that this is not sophisticated research. You may well ask, “How could such a thing get into a major medical journal?” I asked the editor and we’ll see what she says.

A final problem is that the definition researchers used as a low carbohydrate diet was 40% carb or less.  That’s not what most people in the field would call low carb.  In fact, it is clear that although this paper was about low-carbohydrate diets, nobody with real experience of low-carbohydrate diets reviewed the paper or was consulted in any way.

When you look at the actual results in the analysis, both those on what the researchers defined as “low carb” (40% or less) or high carb (70% or more) diets had a higher risk of all-cause mortality, but not by much.

Finally, this study has redefined a “moderate” carbohydrate consumption level as 50% – which is what we have now, in the midst of an epidemic of obesity and diabetes.

Low carbohydrate diets have been proven to successfully treat diabetes, yet The Lancet is telling people that they kill you.  This is what turned me into a whistleblower: I’m reacting not just as a scientist, but as a citizen.


Question: What do you mean by being a whistleblower?


I wrote an article critiquing this paper to The Lancet.  They rejected it and said to write a letter to the editor.  This isn’t just bad science, it’s a danger to real people.  In this part, I’m a citizen.  I’m not a health care provider but I do interact with many people with diabetes.  What I see is parents with kids with Type 1 diabetes.  The kids have to inject insulin and if they go on low carb they have much better control, need less insulin, and avoid the highs and lows that make life so difficult. And the parents avoid calls from school because the kid is in crisis and miserable.  These guys who wrote The Lancet study are telling parents not to do what helps kids.  That’s unconscionable.


Question: What are your next moves in getting the word out there?


A new edition of my book: The World Turned Upside Down: The Second Low-Carbohydrate Revolution, is coming out soon.  Meanwhile, I’m working with groups of people with diabetes and others to spread the word to people who want to know what works.

I told the publisher of my book that what I had to offer was the credentials of a practicing biochemist.  I joked that I’m almost the only biochemist dumb enough to stay in nutrition and she asked, “Why do you do it?”   There are two reasons.  First, the biochemistry is beautiful.  It is still the power of science.  Second, the Feinman family fault is righteous indignation: It’s a terrible problem and we shouldn’t let it persist.



April Wilson Smith holds a Master of Public Health from Thomas Jefferson University and is a long time tracker of all things health and wellness.  She has been vegan, low fat, low carb, a calorie restriction practitioner, serious Zen student, and yoga enthusiast.  She is now a freelance writer based just outside Philadelphia, Pennsylvania.

Share This Post

Share on facebook
Share on linkedin
Share on twitter
Share on email

Recommended Reads

Track your food, exercise and health metrics with our app.