Retrospective #61: Stefansson and “The Eskimo Diet”

About 100 years ago a Canadian ethnologist, Vilhjallmur Stefansson, spent 11 years living among the Inuit in the frozen North. For 9 of those years he ate substantially a diet composed of meat (including fish), some organ meats, and fat with just a little carbohydrate (glycogen contained in the muscle tissue and liver). In the summer months he ate a few berries. Upon his return to ‘civilization,’ from his observations of the Inuit with whom he had lived and of his own health, he postulated that such a diet was sufficient for good health. It was, he averred, a complete diet.

Stefansson’s lectures on his experience with an all meat diet drew derision and cries of charlatan from the scientific and medical community. So, to ‘prove’ his hypothesis, he proposed a daring experiment. He offered himself and a colleague, Karsen Andersen, with whom he had shared his experience in the Arctic, as an in vivo experiment (n=2). In 1928, under supervision of doctors at New York’s Bellevue Hospital, they volunteered to live for 1 year on meat and fat alone. The results, which I first read in Gary Taubes’s "Good Calories -- Bad Calories," were fascinating.

Stefansson’s own account of his Arctic adventures was published, for popular consumption, in Harper’s Monthly in November and December 1935. The balance of this blog post will be the report of W. S. McClellan and E. F. Du Bois, the lead investigators of the Bellevue study. Their paper was brought to my attention by Ginny L who was, in 2012 when this was written, a frequent poster and valued resource on Dr. Richard K. Bernstein’s Diabetes Forum.

The paper, “Prolonged Meat Diets with a Study of Kidney Function and Ketosis,” was published July 1, 1930, in the Journal of Biological Chemistry. Herewith, in their entirety, are the conclusions of the previously skeptical doctors:

1. Two men lived on an exclusive meat diet for 1 year and a third man for 10 days. The relative amounts of lean and fat meat ingested were left to the instinctive choice of the individuals.

2. The protein content varied from 100 to 140 gm., the fat from 200 to 300 gm., the carbohydrate, derived entirely from the meat, from 7 to 12 gm., and the fuel value from 2000 to 3100 calories.

3. At the end of the year, the subjects were mentally alert, physically active, and showed no specific physical changes in any system of the body.

4. During the 1st week, all three men lost weight, due to a shift in the water content of the body while adjusting itself to the low carbohydrate diet. Thereafter, their weights remained practically constant.

5. In the prolonged test, the blood pressure of one man remained constant; the systolic pressure of the other decreased 20 mm. and the diastolic pressure remained uniform.

6. The control of the bowels was not disturbed while the subjects were on prescribed meat diet. In one instance, when the proportion of protein calories in the diet exceeded 40 per cent, a diarrhea developed.

7. Vitamin deficiencies did not appear.

8. The total acidity of the urine during the meat diet was increased to 2 or 3 times that of the acidity on mixed diets and acetonuria was present throughout the periods of exclusive meat.

9. Urine examinations, determinations of the nitrogenous constituents of the blood, and kidney function tests revealed no evidence of kidney damage.

10. While on the meat diet, the men metabolized foodstuffs with FA: G ratios between 1.9 and 3.0 and excreted from 0.4 to 7.2 gm. of acetone bodies per day.

11. In these trained subjects, the clinical observations and laboratory studies gave no evidence that any ill effects had occurred from the prolonged use of the exclusive meat diet.

Stefansson was a very colorful character. He was twice president of the prestigious Explorers Club. He lectured in anthropology at Harvard and was Director of Polar Studies at Dartmouth College. His Wikipedia entry concludes: “Stefansson is also a figure of considerable interest in dietary circles, especially those with an interest in very low-carbohydrate diets. Stefansson documented the fact that the Inuit diet consisted of about 90% meat and fish; Inuit would often go 6 to 9 months a year eating nothing but meat and fish—essentially, a no-carbohydrate diet. He found that he and his fellow European-descent explorers were also perfectly healthy on such a diet. When medical authorities questioned him on this, he and a fellow explorer agreed to undertake a study under the auspices of the Journal of the American Medical Association to demonstrate that they could eat a 100% meat diet in a closely observed laboratory setting for the first several weeks, with paid observers for the rest of [the] year. The results were published in the Journal, and both men were perfectly healthy on such a diet, without vitamin supplementation...."

Retrospective #60: Dietary Composition: Dr. Ludwig’s Study

Back in 2012, David S. Ludwig, MD, PhD, and colleagues at New Balance Foundation Obesity Prevention Center (Harvard), and Children’s Hospital, Boston, and Brigham and Women’s Hospital, Boston, and Baylor College of Medicine, Houston, and Vanderbilt University, Nashville, published the results of a well-designed, four-year study in June 27 issue of the Journal of the American Medical Association (JAMA). The purpose was to study “the effect of dietary composition on energy expenditure during weight-loss maintenance “(my emphasis).

Three days later the New York Times published an opinion piece, "What Really Makes Us Fat," loosely based on the study. In it, award winning science writer Gary Taubes, said, “What was done by Dr. Ludwig’s team has never been done before.” He concluded his piece with, “The public health implications are enormous.” (emphasis added)

The study began after all subjects had achieved a 10% to 15% weight loss by a calorie restricted (60%) “run-in” diet. Then, each for 4 weeks, the participants ate three isocaloric (2,000kcal/d) diets: 1) a low-fat diet (60% carbs, 20% fat, 20% protein, high glycemic load); 2) a low-glycemic index diet (40% carbs, 40% fat and 20% protein, moderate glycemic load); and 3) a very-low carb (Atkins) diet (10% carb, 60% fat and 30% protein, low glycemic load).

The JAMA authors concluded: “Our study demonstrates that commonly consumed diets can affect metabolism and components of the metabolic syndrome in markedly different ways during weight-loss maintenance, independent of energy content. The low-fat diet produced changes in energy expenditure and serum leptin that would predict weight regain. In addition, this conventionally recommended diet had unfavorable effects on most of the metabolic syndrome components studied herein. In contrast, the very low carbohydrate diet had the most beneficial effects on energy expenditure and several metabolic syndrome components…” (HDL & triglycerides), emphasis added by me.

Energy expenditure, the primary outcome measure of the study, was measured by state-of-the art stable isotope analysis at Baylor. This outcome was especially stunning: “The results of our study challenge the notion that a calorie is a calorie from a metabolic perspective,” the authors stated. “TOTAL ENERGY EXPENDITURE DIFFERED BY APPROXIMATELY 300 KCAL/D BETWEEN THESE 2 DIETS” (VERY LOW CARB AND LOW FAT), “AN EFFECT CORRESPONDING WITH THE AMOUNT OF ENERGY…EXPENDED IN 1 HOUR OF MODERATE-INTENSITY EXERCISE.”

In other words, as Taubes explained, “…when the subjects were eating low-fat diets, they’d have to add an hour of moderate-intensity physical activity each day to expend as much energy as they would effortlessly on the very-low-carb diet. And this while consuming the same amount of calories. If the physical activity made them hungrier – a likely assumption – maintaining weight on the low-fat, high-carb diet would be even harder,” Taubes wrote.

Taubes then posited, “If we think of Dr. Ludwig’s subjects as pre-obese, then the study tells us that the nutrient composition of the diet can trigger the predisposition to get fat, independent of the calories consumed. The fewer carbohydrates we eat, the more easily we remain lean. The more carbohydrates, the more difficult. In other words, carbohydrates are fattening, and obesity is a fat-storage defect. What matters, then, is the quantity and quality of carbohydrates we consume and their effect on insulin.” These five sentences say it better than a whole book!

Ludwig’s subjects are, frankly, “pre-obese.” As the study states, “only 1 in 6 overweight and obese adults report ever having maintained weight loss of at least 10% for 1 year.” Taubes reasonably says Ludwig’s subjects are “almost assuredly going to get fatter, so they can be research stand-ins for those of us who are merely predisposed to get fat but haven’t done so yet and might take a few years or decades longer to do it.” Does this sound like you?

Taubes then concludes, “From this perspective, the trial suggests that among the bad decisions we can make to maintain our weight is exactly what the government and medical organizations like the American Heart Association have been telling us to do: eat low-fat, carbohydrate-rich diets, even if those diets include whole grains and fruits and vegetables.” NOTE BENE: “…EVEN IF THOSE DIETS INCLUDE WHOLE GRAINS AND FRUITS AND VEGETABLES.”

Your choice: Eat Very Low Carb, or eat whole grains, fruits and vegetables and exercise 1 hour a day to burn them off.

Retrospective #59: The VLCKD: What I Eat and Why

I eat a Very Low Carbohydrate Ketogenic Diet (VLCKD) because I want to lose weight. And I want to do it in a healthy way, and because I want it to be easy (of course) and not involve hunger. I also want to eat in a way that achieves good blood glucose control (I’ve been a Type 2 diabetic for 33 years), and I want to continue to maintain the huge improvements in blood lipids (cholesterol), and blood pressure, and inflammation that I’ve seen since before I lost 170 pounds.

When I started to eat Very Low Carb, I didn’t know that I had a medical condition called Metabolic Syndrome. I had all five indications: central obesity, T2DM (or pre-diabetes), hypertension, elevated triglycerides and low HDL. After a period of time on the VLCKD, all five of these indications were mediated by this diet.

I know I have sufficiently restricted my carbohydrate intake to be in ketosis by testing my blood glucose in a fasting state (before eating breakfast). My body always has a little glucose available for energy, either in the form of glycogen in the liver or muscle cells, or from amino acids stored in the liver from eating too much protein. The liver will make glucose from these glucogenic amino acids through a process called gluconeogenesis. Since I am a Type 2 diabetic with impaired glucose tolerance and insulin resistance, if I eat too many carbohydrates, my fasting blood sugars will rise above ‘normal’ for me. When I return to dietary ketosis, my fasting blood glucose drops to the mid- 80s, with Metformin. That’s me. Your Mileage May Vary. We’re all different.

My pancreatic function and other aspects of my metabolism are broken and have been for many years. Like many Type 2s and even pre-diabetics (diagnosed and undiagnosed!), to maintain healthy blood sugar levels, I cannot tolerate more than very small amounts of carbs, low GI or otherwise. I must accept that I will never be able to do so without blood glucose “excursions” (dangerously high levels of “sugar” circulating in my system. Inevitably, that will lead either to diabetic complications (eye, nerve or kidney disease), or one of the Macrovascular complications that are strongly associated with Type 2 diabetes, such as cardiovascular disease, hypertension, and various cancers. So, what do I need to eat to remain continuously in a mild state of ketosis?

Breakfast and lunch are easy for me because, as Richard K. Bernstein, MD, recommends in his book, “The Diabetes Solution,” I eat the same thing every day. Breakfast is two fried eggs, two strips of bacon and 12 oz of coffee with 1 ½ oz of heavy whipping cream and 1g of pure stevia powder. K:G ratio = 1.88:1.

For lunch, (when I remember to eat it – I’m really not hungry, so I’m not “reminded”), I eat a can of Mediterranean style Brisling sardines in olive oil. I drink the oil in the can too (about 1 Tbs). Lunch K:G ratio = 2.93:1. I sometimes wash it down with diet iced tea (sweetened with liquid stevia). Of course, water would be a better choice.

For dinner, we eat a medium portion of protein (with skin and/or fat on) and a portion of vegetables with melted butter or olive oil. Sometimes, with salmon for example, we use a sauce made with crème fraiche. We like roasted meats, including chicken, spare ribs, lamb chops, short ribs or a petite filet (with a single 8oz filet shared by the 2 of us). We also like to rub our cuts of meat with herbs and olive oil before roasting. We sometimes roast the vegetables too, after tossing them in olive oil and sea salt. Cauliflower, Brussels sprouts and asparagus are especially good this way. We avoid the sugary vegetables (carrots, peas, beets and corn) and of course all the starchy root vegetables. And we do not eat bread at home. (I sometimes cheat with bread in a restaurant.)

This menu usually adds up to about 1,200 calories a day, which is at least 1,000 less that I probably use. The balance of energy comes from my fat stores, as long as I am in dietary ketosis and my blood insulin level is low. That only occurs because my carbohydrate intake is very low, and protein moderate, allowing my dietary and body fat to break down for fuel. This diet is about 5% carb, 20% protein and 75% fat. The K:G ratio of most meals is >1.5. This is a Very Low Carb Ketogenic Diet (VLCKD).                   

Type 2 Nutrition #481: “I’ve lost 30 pounds!” (Tim Cook, Apple CEO)

If you Google “Tim Cook ‘I’ve lost 30 pounds,’” you'll find several pages touting Cook’s boast about how he used his iWatch to lose weight. Of course, he was mainly promoting the utility of a prospective Apple iWatch app in conjunction with emerging medical technology to help manage health conditions and make our lives better.

The quote appears at about the 8:15 mark in this May 2017 video interview with CNBC’s Jim Cramer. Cramer was trying to get Cook to reveal the next “new” product from Apple. Cook smiled and at first resisted, saying, “I can’t tell you” [about new products]; and then… [here’s where it sounded a bit scripted]:

Cramer, eggs him on with, “Health?”

Cook replies, “You know, this, the watch, has been an incredible move into health, in the wellness and fitness piece.”

Cramer: “You too?” [more script]

Cook: “Yes, I’ve lost 30 pounds, partly [due] to my watch.”

Cramer: [prompting Cook] “…because it prompts us.”

COOK: [finally getting to his pitch] “BECAUSE IT MOTIVATES YOU. IT CONSTANTLY GIVES YOU FEEDBACK. IT CONSTANTLY GIVES YOU REWARDS, AND THIS MAKES A DIFFERENCE…OVER TIME.”

What Cook and Cramer were talking about is an Apple iWatch app in development that tracks blood sugar continuously from a sensor attached to the upper arm just below the surface of the skin. The sensor captures the rise and fall of blood “sugar” in response to several factors, but predominantly to food that is eaten.

If you eat something that causes a large increase, you know that that it will shut down any fat burning your body is doing to supply energy while the “sugar” (glucose from any type of carb) is burned off first. You learn that if you want your body to stay in fat burning mode, instead of glucose mode, you should avoid those foods.

Cook’s pitch and Cramer’s interest are all about business, specifically the conjunction of health science and technology. It’s a crowded field. Scores of innovators are operating under the radar, clamoring to get on the bandwagon for a piece of the mass-market. The early birds certainly have an advantage, but…over time, as technology advances, the products will become commodified, and competition will bring costs down.

In the 2017 interview, Cook was certainly aware that a “high cost” solution was on the market. By March 2018 the FDA had approved the Dexcom 6 Continuous Glucose Monitor (CGM). It costs about $5,000 a year and includes an integrated mobile app which automatically downloads results to a Bluetooth-enabled device.

Then in August 2018 the FDA approved the new Freestyle Libre CGM (about $1,620 a year). It does not have an integrated mobile app yet, but a startup, Ambrosia, has a workaround called BluCon to download results.

Metronic is in the race too but lags at this writing. Stay tuned, though. By the time you read this, who knows?

Medical insurance, including Medicare and “Supplemental,” will only pay for this durable medical equipment and supplies. at the current time. if you are an insulin-dependent diabetic who injects MEALTIME insulin. The government’s policy is designed to help patients avoid life-threatening hypos (hypoglycemia), which, for some diabetics, is an all-too-common and sometimes life-threatening occurrence, often requiring hospitalization.

But Tim Cook’s market is “the wellness and fitness piece” – i.e., the entire rest of the world – who will benefit from an inexpensive app and an affordable sensor that can be integrated with the latest Apple iWatch… BECAUSE IT MOTIVATES YOU. IT CONSTANTLY GIVES YOU FEEDBACK. IT CONSTANTLY GIVES YOU REWARDS, AND THIS MAKES A DIFFERENCE. And almost everyone could stand to lose 30 pounds. Lots of us, even more!

Retrospective #58: What is Dietary (Nutritional) Ketosis?

Fasting ketosis occurs “after a few days of fasting…when liver glycogen stores are depleted” and “the body shifts from a glucose-based metabolism to a fat-based one,” Lucas Tafur explained in 2012 on his now defunct website. It is a physiologic state that the ketone expert, Dr. Richard Veech at The National Institutes of Health, calls “the normal state of man.” But Tafur avers, “It can either be triggered by fasting or by diet.” Therein lies the message.

Dietary ketosis is the adaptive response, or “acquired evolutionary mechanism, [that] shifts [the body] from a glucose-based metabolism to a fat-based one,” Tafur explains. This shift occurs when the carbohydrates are unavailable for fuel. The enzymes that break down fat for energy are controlled by insulin which is very responsive to the presence of carbohydrate. Dietary ketosis is achieved by the sustained and sharply curtailed intake of carbohydrates. How sharply? It varies. Your mileage may vary (YMMV), but for me it’s 20 to 30g of carbs a day.

What is the mechanism and how does it work? (Sorry, but I think some of my readers will find the science both useful). A part of everything we eat becomes fuel. Carbohydrates break down to mostly glucose. That’s good because glucose quickly converts to energy, and the body (the brain, especially) needs a little glucose, NOT carbs – about 30-35 grams a day, either directly as glucose or in a form (e.g. ketone bodies) that substitutes for it perfectly.

Fat (both body fat and ingested) are triglycerides, made up of 3 fatty acid molecules and 1 glycerol molecule. Note the stem ‘gly.’ When each triglyceride molecule is broken down into free fatty acids for fuel, it leaves a glycerol molecule to join with another to make glucose. Thus, about 10% of ingested or stored body fat becomes glucose.

When protein is digested into its component amino acids and is taken up by the body, what is left over goes to the liver. There, when the body needs glucose, the liver makes glucose from those stored amino acids by a process called gluconeogenesis (“glucose-new-creation”). About 54% of the protein we eat is glucogenic, i.e. can become glucose, especially if we eat too much at any one meal. It is stored and then reconstructed and utilized as glucose!

Carbohydrates – almost all of them, from simple sugars to complex starches – digest to glucose. Some starches digest slowly, but simple sugars and highly processed carbs (in products sold in boxes and bags) break down fast to the single-cell sugars glucose, fructose or galactose. In the case of fructose, they are shunted directly to the liver to protect your body from them. Your liver will convert fructose to glucose to glycogen to store in the liver, but if the liver is already full of glycogen, it will convert the fructose to fat by a process called de novo lipogenesis.

The way to achieve the condition called dietary ketosis is this: eat a very low carbohydrate, moderate protein and high fat diet. Expressed as a formula – sorry, again – where K = ketogenic molecules and G = glucose molecules.

 K/G ratio = (0.9*FAT+0.46*PRO)/ (0.1*FAT+0.54*PRO+1*CHO.)

The fat, protein and carbohydrates (CHO) are all entered in grams (weight). A ketogenic ratio of numerator (K) to denominator (G) is >1.5. Thus, the ratio should be at least 1.5 to 1, stated >1.5:1, in each meal, every day.

Because this dietary regimen is very high in fat and very low in carbs, you will not be hungry between meals, so long as you don’t eat carbohydrates. You will be satisfied because fat is satiating and protein digests slowly. But all carbs break down to glucose, and circulating glucose will raise you blood insulin levels and take you out of ketosis.

Once you are in dietary (nutritional) ketosis, fatty acids and ketone bodies are used as the major sources of fuel. But, the “balanced diet” establishment says, this could cause a problem for the brain because fatty acids do not cross the blood-brain barrier. Fortunately, the liver uses the fatty acids from the breakdown of triglycerides (both body fat and ingested fat) to make ketone bodies which enter the brain and substitute for glucose. Ketone bodies are actually a more efficient fuel for the brain than glucose. Ketones as brain fuel are also a desired alternate to glucose if the brain has started to develop Insulin Resistance (aka “Type 3” Diabetes). Increasingly, the ketogenic diet is being used as a therapeutic diet for Mild Cognitive Impairment (MCI), aka early-stage Alzheimer’s Disease.

Retrospective #57: What is Ketogenic Nutrition?

In mid-2012, on her now defunct blog “Weight Maven,” Beth Mazur introduced me to Lucas Tafur whose domain has also since expired. Lucas Tafur is an interesting story. Before he created the Lucas Tafur site, his blog was called, ahead of its time, “Ketogenic Nutrition.”  It provided me with a nostalgic look back at what proved for me to be a very effective way to lose 170 pounds. Tafur quotes one of the world’s leading experts on ketone bodies, Dr. Richard L. Veech of the National Institutes of Health: "Doctors are scared of ketosis. They're always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man.”

Put into context, in the continuum of our day-to-day existence, we’re either in a fed or a fasting state. The fed state begins with eating and continues until the food has been digested and absorbed. The fasting state then begins and continues until we eat again. When fasting, the body is said to be in ketosis, a normal physiological state.

When we are in a fed state, we derive our energy largely from glucose. This is called a glycogenic state. When we are in a fasting state, the body derives its energy from our fat stores from our adipose (fat) tissue, which breaks down by lipolysis. Who can doubt that it has been that way for thousands of generations? We were hunters and gatherers, not grazers. That is the way we were “designed” and evolved until, with the “invention” of agriculture about 500 generations ago, and domestication of animals, and foods that could be stored, we became Neolithic.

In just the last few few generations, we have gone further astray, with disastrous consequences. Of course, what has happened in these last few generations is not an evolutionary adaption; it is but an aberration. It is also a completely reversible change once we come to see and accept what “we” (complicit with our agricultural/industrial enterprise and the associated medical, “public health” and media establishments) have done to ourselves. We can return to a fed and then fasting Way of Eating in which ketosis is once again “the normal state of man.”

The old scenario: We hunted, we ate and we were satisfied. After our meal was digested and absorbed, we entered a fasting period, a period of ketosis, as Dr. Veech said, “the normal state of man.” The body used its fat stores, broken down to fatty acids, a glycerol molecule, and ketone bodies, for energy. But, as Tafur then points out, ketosis can “either be triggered by fasting or by diet.” Therein lies the point to which Lucas Tafur was leading us.

The rest of this column is excerpted from Lucas Tafur’s defunct “Ketogenic Nutrition” website. “Fasting ketosis develops after a few days of fasting, when liver glycogen stores are depleted. The body, as an acquired evolutionary mechanism, shifts from a glucose-based metabolism to a fat-based one.” “Studies have shown that the adaptive response to fasting is regulated not by energy restrictions per se, but by carbohydrate restriction. This is because the rate limiting enzyme of ketogenesis…is controlled by insulin levels.” (Emphases added by me.)

“The body’s main energy store is adipose tissue. Fat is more calorie-dense, meaning that it yields more energy per gram than glucose. Fat is the body’s preferred fuel, ketones being a “super fuel” that can be used by some tissues that haven’t evolved to use free fatty acids (FFA) such as the brain. Ketone bodies help the body spare amino acids by reducing the need for glucose. This way muscle mass is maintained…. Without ketosis, body protein stores would be cannibalized…. “

“The body stores fat primarily as saturated fat because it is metabolically more efficient than glucose and produces less toxic residue when metabolized. Exogenous glucose is the first substrate to be used because it is toxic to the body. It produces metabolic disregulation caused by hyperglycemia, which triggers an inflammatory and autoimmune response. Ketosis represents the opposite scenario; it protects the body during a life-threatening situation like starvation.” (end quote)

Lucas Tafur, and Beth Mazur, and Kurt Harris (see Retrospectives #18 & #19), were all ahead of their time and have all since disappeared from the scene. They all made contributions to my understanding of nutrition and human metabolism, including Tafur’s description of fasting ketosis. But what is dietary ketosis? See the next Retrospective.

Retrospective #55: Homage to Gary Taubes

I’ve just read Gary Taubes’s “The Soft Science of Dietary Fat,” published in Science (2001). It’s an early look into a subject that’s since come a long way. I believe it was a foundational piece that was the impetus for his later work.

I read it looking for a way to understand why a friend who has been a Type I diabetic for over 70 years “believes absolutely” that saturated fat and dietary cholesterol are bad for our health and should be avoided.  I’m not trying to change her beliefs. She’s a survivor and an expert on how to manage her disease. I just want to understand why.

Taubes doesn’t need me to defend him either. He “studied applied physics at Harvard and aerospace engineering at Stanford (MS, 1978,”) and then “took his master’s degree in journalism at Columbia University in 1981.” “He has won the Science in Society Award of the National Association of Science Writers three times.” After “The Soft Science of Dietary Fat,” he came to the public’s attention with his blockbuster July 7, 2002 New York Times Sunday Magazine cover story, “What If It’s All Been a Big Fat Lie?” It was the “2^nd coming” of the low carb era.

After 5 years of research and writing Taubes went on in 2007 to publish his magnum opus, “Good Calories – Bad Calories” (“The Diet Delusion” in the UK). In an “Afterwords” in the paperback edition, Taubes admits that this epic tome had less impact on the medical establishment than he would have liked. A more accessible book, “Why We Get Fat: And What to Do About It,” came out in 2010. In 2011 he was back on the cover of The New York Times Magazine with “Is Sugar Toxic,” and in 2016, he published, “The Case Against Sugar,” another NYT best seller.

Many physicians and researchers have attributed to Taubes the inspiration for their career direction. He certainly has inspired me. He’s responsible, indirectly I suppose, for the name of this blog, “The Nutrition Debate.” As a “nutrition groupie,” I bundle my own experience with ideas I’ve had and those of experts I read daily to put it “out there” for the world to consider. If the light level behind the mirror of conventional thinking is raised, perhaps the world will come to see the “alternate hypothesis” that Taubes describes in “Good Calories – Bad Calories.” Perhaps, the silver lining of the mirror will dissolve and be transparent. The following is excerpted from Taubes’s 2001 essay.

“The original simple story in the 1950s was that high cholesterol levels increase heart disease risk. The seminal Framingham Heart Study, for instance, which revealed the association between cholesterol and heart disease, originally measured only total serum cholesterol. But cholesterol shuttles through the blood in an array of packages. Low-density lipoprotein particles (“bad” cholesterol) deliver fat and cholesterol from the liver to tissues that need it, including arterial cells, where it can lead to atherosclerotic plaques. High-density lipoproteins (“good” cholesterol) return cholesterol to the liver. The higher the HDL, the lower the heart disease risk. Then there are triglycerides, which contain fatty acids, and very low-density lipoproteins (VLDLs), which transport triglycerides.”

“All of these particles have some effect on heart disease risk, while the fats, carbohydrates, and proteins in the diet have varying effects on all these particles. The 1950s story was that saturated fats increase total cholesterol, polyunsaturated fats decrease it, and monounsaturated fats are neutral. By the late 1970s – when researchers accepted the benefits of HDL – they realized that monounsaturated fats are not neutral. Rather, they raise HDL, at least compared to carbohydrates, and lower LDL. This makes them an ideal nutrient. Furthermore, saturated fats cannot be quite so evil because, while they elevate LDL, which is bad, they also elevate HDL, which is good. And some saturated fats – stearic acid, in particular, the fat in chocolate – are at worst neutral. Stearic acid raises HDL levels but does little or nothing to LDL. And there are trans fatty acids, which raise LDL, just like saturated fat, but also lower HDL. Today, none of this is controversial, although it has yet to be reflected in any Food Guide Pyramid.”

Well, the Food Pyramid is gone, only to be replaced by “My Plate,” arguably a worse representation of a healthy eating pattern. But the modern movement that Gary Taubes spawned has gained enormous momentum. Today, it is a legacy to the work begun by Gary Taubes and his seminal piece, “The Soft Science of Dietary Fat?”