Retrospective #80: Calorie Restriction in Humans

Retrospective #79R, “Calorie Restriction and Longevity,” (scroll down to read it), was a rather geeky treatment that dealt with “The Neuroprotective Properties of Calorie Restriction.” I also included in the column several Gary Taubes quotes from “Good Calories – Bad Calories.” Taubes is an award-winning science writer, but that book is also pretty dense.  I call it a “tough slog”, but I underlined about one-third of the 560-page text. It’s a compelling read, and I strongly recommend it to all open-minded and serious readers interested in their metabolic health.

In #79R I took the subject of Calorie Restriction only far enough to establish some of the health and longevity benefits. Unfortunately, they were limited to yeast, worms, fruit flies and mice. And I did not address the “potential pitfalls and health concerns” of calorie restriction in humans. So, in fairness, a little on the pitfalls and concerns.

“CR has many consequences, the majority of which are unknown at this time,” wrote Barbara Hansen in her Journal of Nutrition article, “Calorie Restriction: Effects on Body Composition, Insulin Signaling and Aging” (1995). In it she quotes Bodkin, “Neither the mechanisms by which life extension takes place (in rodents) nor the mechanisms by which the complex features associated with insulin resistance and Metabolic Syndrome are prevented by CR, are understood. Clearly advancements in this area will lead to better understanding of this powerful nutritional tool.”

Quoting Hansen and Bodkin (1993): “CR produces altered pathways of nutrient disposal, including reduced plasma glucose, insulin and leptin levels”; and Hansen (1996): “CR carried out for 10 to 15 years in adult rhesus monkeys has been shown to result in sustained alteration in glycogen metabolism, despite apparent retention of normal insulin-stimulated glucose uptake, normal glucose tolerance and normal fasting glucose and insulin levels.”

Hansen cites another research paper (Ortmeyer, 2000) to demonstrate the effect of CR on insulin action by the “rate-limiting enzyme of glycogen storage, glycogen synthase.” Ortmeyer reported, “CR appeared to unveil a predisposition in approximately one half of the CR monkeys toward metabolic abnormalities in response to insulin.” “Although glycogen content remained normal in all CR monkeys, we suspect that the induction of abnormal insulin action on glycogen synthase by long-term CR may represent a pointer toward the underlying defect that, under ad libitum conditions, would lead to obesity, insulin resistance, and eventually Type 2 diabetes in approximately one half of aging rhesus monkeys.” This is all very important, if it translates from non-human primates to humans.

Two cautions: “Calorie Restriction in Humans: Potential Pitfalls and Health Concerns,” makes two very good points: 1) “In humans, several studies investigating short-term calorie restriction or ‘weight-loss’ programs suggest beneficial outcomes on parameters of cardiovascular disease.” “However, few studies are currently investigating the quality of life and potential pitfalls of long-term calorie restriction in humans.” And 2) “For certain, calorie restriction has a plethora of health benefits in mammals, such as a reduction in age-related diseases such as cancer. However, despite the ‘magic’ of CR, this intervention in humans may present itself with a number of health concerns, which may not be applicable to or impact the life of experimental animals, but may do so in humans.”

Hansen’s 2001 piece above reveals what she regards as a “missed opportunity”: “The power of CR to mitigate, delay or prevent the clinical development of disease, despite the presence of underlying defects in insulin action, points to the critical need for effective CR mimetic approaches to slow or halt the consequences of the underlying genetic predisposition toward obesity and Type 2 diabetes in humans (and in non-human primates).”

That’s a touching sentiment toward her aging rhesus monkey colony, but like a typical laboratory scientist, she calls for a pharmacological approach to address the genetic predisposition to a metabolic disorder of fat regulation affecting perhaps half of humankind who’ve adopted the “Standard American Diet.” A pill to pop! How absurd is this, especially when the solution is staring us all right in the face. Taubes, by the way, calls conventional calorie restricted diets in humans “semi-starvation” diets, which they are! But I am not advocating Calorie Restriction (CR) per se.  That will be clear in Retrospective #81, tomorrow, when I lay out my idea of A NEW DIETARY PARADIGM.

Type 2 Nutrition #484: "He needs insulin to control his high blood sugar."

In the TV commercial the “wife” says, “He needs insulin to control his high blood sugar.” That’s true. We all need insulin to regulate our blood sugar, so why was I upset to hear her say that? Because of the wife’s misleading message. She was pitching for a drug company that was selling man-made insulin that her “husband” had to inject, after checking his glucose with a finger prick or a continuous glucose monitor.

Everyone needs insulin to control high blood sugar. Everyone’s blood sugar rises after eating, even the healthiest peoples. Carbohydrates, when digested, become glucose.  So do proteins, to a certain extent, in a bit more time. The pancreas secretes insulin which circulates in the blood with glucose to enable the uptake of glucose as energy. In healthy people, the insulin works. The cells open. The circulating blood “sugar” lowers.

Without insulin, either made by the body or injected, a person eventually dies. Until artificial insulin was discovered in 1921, Type 1 diabetics, who had suddenly lost the ability to make their own insulin, did die. Until then, patients (mostly children) were kept alive longer by eating a diet that was about 90% fat. Fat is also a very good energy source that doesn’t require insulin to be used. But with the invention of artificial insulin, the high-fat diet treatment for Type1 diabetics stopped, because it was no longer needed.

So, what’s my beef with a company just trying to sell its product? Answer: The patient in the ad was NOT a Type 1 diabetic who needed insulin to live because his body had stopped making it. He was a Type 2 diabetic whose body had become resistant to taking up glucose because it had too MUCH circulating insulin! Type 2 is a totally different disease from Type 1. Unfortunately, government and Big Pharma doesn’t see it that way.

They want to treat Type 1 and Type 2 diabetes as essentially the same. They want to treat the symptom, a high blood sugar, as if it were caused by the same thing. But Type 1 diabetes is an autoimmune disease where the pancreas suddenly stops making insulin, and Type 2 diabetes is a dietary disease where the cells have, over time, become resistant to taking up glucose because they have long been exposed to too much insulin.

Here’s the irony. When a Type 2 injects insulin, it makes their Insulin Resistance worse! How stupid is that?

It’s frustrating. I don’t have an expensive drug to sell – a drug that misleads you into thinking you’re treating the cause of Type 2 diabetes. Instead, this treatment is just masking the symptom (“high blood sugar”). Insulin Resistance is the cause of Type 2 diabetes. Injecting insulin is making the Type 2 dependent on injected insulin.

I can’t afford to hire an actress to say, “He needs to control his high blood sugar by changing what he eats.” If I had a 30 second TV spot, I would say, “If he eats fewer processed carbohydrates and simple sugars, his pancreas will need to produce less insulin, thus preserving his pancreas. And by having a lower blood insulin, his cells will become more insulin sensitive.” That means they will be less Insulin Resistant and take up more glucose; ie function more normally.

With a 60-second spot, I’d add one of my favorite pitches used by some diabetes drugs: “It might even help you lose weight.” Many T2D drugs use that as a “hook.” But they can’t say that with injected insulin. High levels of insulin in your blood – whether injected, or secreted – cause you to GAIN WEIGHT.

Insulin is the weight storage hormone. Long-acting (24-hour) insulin, by design, keeps your blood insulin high all the time. In Insulin Resistant Type 2s, high blood glucose remains high because of Insulin Resistance. In Insulin Dependent Type 2s, blood insulin is high all the time, so you can’t burn body fat for fuel and YOU MUST EAT WHEN YOU ARE HUNGRY instead of letting your body access its fat stores for energy. 

Think about it! Eating lower carb 1) improves your Insulin Sensitivity naturally, 2) lowers your blood sugar naturally, 3) lowers blood insulin naturally, and thus enables weight loss by letting the body access its fat stores, naturally. Given that, why would any Type 2 diabetic inject insulin to control their blood sugar?

Retrospective #79: Calorie Restriction and Longevity

When people ask what motivated me to lose so much weight (170 pounds), I reply, “I didn’t want to die; I looked around me and I didn’t see any morbidly obese old people, and I was getting old, and I wanted to live.” As I gained weight over the years, my doctor always urged me to lose. Then, for two visits in a row I was unable to weigh in on his office scale because it only went to 350. So, on the way to work one day in NYC I stopped at the Fulton Fish Market and asked permission to weigh myself on a commercial scale. I was shocked. I weighed 375 pounds. The next week, as I entered my Doctor’s office, he saw me and he said, “Have I got a diet for you!!!” I was motivated.

Of course, as I was losing weight on a Very Low Carb (VLC), NOT low calorie, Way of Eating (WOE), I wondered how low I would go. I had the luxury to fantasize about this because, on VLC, I was losing weight easily and without hunger. This will happen when you strictly follow this WOE. I also remember reading about Calorie Restriction (CR) and longevity in Gary Taubes seminal 2007 book, “Good Calories – Bad Calories” (“The Diet Delusion” in the UK). This defining and authoritative work is a tough slog but life changing. Calorie Restriction and its positive association and correlation with longevity are covered in Chapter 13, “Dementia, Cancer and Aging.” Are you motivated yet?

In 2008 the authors of “The Neuroprotective Properties of Calorie Restriction, The Ketogenic Diet and Ketone Bodies,” published as a Public Access, peer-reviewed manuscript, said, “Obesity is associated with an increased risk of dementia.” They continued, “Low dietary energy intake is associated with decreased incidence of Alzheimer’s and Parkinson’s diseases…and calorie restriction for 6 months improves biomarkers associated with longevity including reduced fasting insulin levels, body temperature and DNA damage. Also, “Beneficial effects on mental health have been reported as well, with improved mood following calorie restriction of obese diabetic patients.”

The problem with the preceding paragraph, alas, is that “all the available information is derived exclusively from animal models. Calorie restriction prolongs the lifespan of yeast, roundworms, rodents and monkeys, even when initiated in mid-life.” they said. That tagged-on last clause was the “pearl” for me. It was a really big takeaway.

I’m thinking, hmmmm, “even when initiated in mid-life.” That’s very encouraging. I can reasonably infer from this: It’s not how thin I AM, but what I eat NOW that will determine my health outcome. IT’S NOT TOO LATE!

“To date, however, clinical trials looking at the effects of calorie restrictions on brain aging and neurological disease have not been performed [on humans],” they said. But, the mechanisms to explain the neuroprotective effects of calorie restriction relate to mitochondrial function, oxidative damage to DNA and regulation of gene expression.

In Taubes’ words: “All this leads us back to the spectacular benefits of semi-starvation on the health and longevity of laboratory animals” (GC-BC: pg. 218). “The calorie-restricted animals live longer because of some metabolic or hormonal consequence of semi-starvation, not because they are necessarily leaner or lighter” (ibid. pg. 219).

Taubes sums it up (ibid. pg. 220): “The characteristics that all these long-lived organisms seem to share definitively are reduced insulin resistance, and abnormally low levels of blood sugar, insulin, and insulin-like growth factor (IGF). As a result, the current thinking is that a reduction in blood sugar, insulin and IGF bestows a longer and healthier life. The reduction in blood sugar also leads to reduced oxidative stress and advanced glycation end-products (AGEs) and all the toxic sequelae that follow. The decrease in insulin and IGF also bestows on the organism an enhanced ability to protect against oxidative stress and to ward off other pathogens.” “The most compelling evidence now supporting this hypothesis has emerged since the early 1990s from genetic studies of yeast, worms and fruit flies, and it has recently been confirmed in mice. In all four cases, the mutations that bestow extreme longevity on these organisms are mutations in the genes that control both insulin and IGF signaling.” 

Then, Taubes quotes from the cancer researcher J. Michael Bishop’s 1989 Nobel Prize lecture: “When reduced to essentials, the fruit fly and Homo Sapiens are not very different.” Tomorrow’s Retrospective: Calorie Restriction in humans.

Retrospective #78: Metabolic Syndrome and Cancer Risk

If you have Metabolic Syndrome (see Retrospective #9 for the indications) there is a greater risk that you will develop certain types of cancer, according to a systematic review and meta-analysis reported November 2012 in Medscape. The retrospective study was performed by a group of physician-researchers and was published in the American Diabetes Association’s journal, Diabetes Care. The study reports an association with cancer risk, not a causal relationship.

If you didn’t go back to# 9, Metabolic Syndrome is defined by a cluster of risk factors: 1) obesity, particularly central obesity, 2) dysglycemia (i.e. Pre-diabetes or Type 2), 3) elevated blood pressure, 4) and dyslipidemia, specifically high triglycerides and low HDL. Between 35% and 40% of the adult population of the U. S. today has Metabolic Syndrome.

In 1986, when I was first diagnosed as a Type 2 diabetic, I had every one of risk factors for Metabolic Syndrome, but no one told me I had it, or Syndrome X as it was then called. In fact, to this day no one has told me. Why is that, I wonder? Especially since the implications go far beyond cancer risk. The risks of virtually all the so-called Diseases of Civilization (heart disease, stroke, Alzheimer’s, etc.) are associated with a diagnosis of Metabolic Syndrome. Do you have Metabolic Syndrome? If you don’t know or aren’t sure, you really should go back and take a look at Retrospective #9 now.

From the results of the report in Diabetes Care (pg.1): “We analyzed 116 datasets from 43 articles, including 38,940 cases of cancer. In cohort studies in men, the presence of Metabolic Syndrome was associated with liver, colorectal and bladder cancer. In cohort studies in women, the presence of Metabolic Syndrome was associated with endometrial, pancreatic, breast postmenopausal, rectal and colorectal cancers. Associations with Metabolic Syndrome were stronger in women than in men for pancreatic and rectal cancers. Associations were different between ethnic groups: we recorded stronger associations in Asia populations for liver cancer, in European populations for colorectal cancer in women, and in U. S. populations (whites) for prostate cancer.” “Metabolic Syndrome is associated with increased risk of common cancers; for some cancers the risk differs between sexes, populations and definitions of Metabolic Syndrome.”

Additional detailed conclusions from the full text of the report (page 28) drive home the findings: “Our results from meta-analyses of prospective cohort studies indicate that Metabolic Syndrome is consistently associated with an increased risk of several cancers in adults. However, many of the reported associations are small (relative risk between 1.1 and 1.6) and might differ between sexes for some sites and also across populations. In particular, the associations were stronger in women for some cancers (pancreas and rectal), and the magnitude of the association was highest for sex specific cancers (endometrial and breast postmenopausal). Moreover, from analyses in which sufficient datasets existed, the association was stronger for colorectal cancer in European populations (relative risk 1.64).”

And this hit: “Given the widespread diffusion of Metabolic Syndrome and the increased cancer mortality associated with Metabolic Syndrome, the findings of the present meta-analysis may have clinical significance. At least for some common cancer sites (colorectal cancer in both sexes, liver cancer in men, and pancreas cancer in women), we are confident that the results are real, as the grading for study quality was moderate to high and overall risk of bias was low” ( pg. 28).

Finally this blow (pg. 28): “Findings from this meta-analysis, which includes many recently published studies, suggest that Metabolic Syndrome is associated with increased risk of common cancers. The excess risk of cancer conferred by Metabolic Syndrome is low to moderate and in part explained by accompanying obesity and hyperglycemia. Neverthe-less, the increasing prevalence of Metabolic Syndrome worldwide and the high incidence of some malignancies, particu-larly colorectal and breast cancers, imply that every year many cases of cancer are attributable to Metabolic Syndrome” (emphasis mine). Remember, this is a retrospective, meta-analysis – not a prospective double-blind clinical trial, but to use the words “attributable to” is, to be sure, pretty strong language. It certainly should give one pause for thought.

For example, are you thinking, “What can I do about it?” Well, you could change your diet. You could lose weight easily and keep it off permanently by eating a Very Low Carb ketogenic diet. With this diet your blood glucose will normalize, and with weight loss your blood pressure will come down. And this diet will raise your HDL and lower your triglycerides. These are the indications for Metabolic Syndrome, and they can all go away. You will be free of Metabolic Syndrome. Ipso facto!

Retrospective #77: Very Low Carb and Pauline Kale (sic)

My doctor stumbled upon Very Low Carb one Sunday morning in July 2002. On the cover of the New York Times Sunday Magazine, he saw a big juicy ribeye steak with a lump of butter on top. His salivary glands began to secrete digestive juices and a signal went from his hypothalamus to his pancreas to start secreting insulin. The image alone was enough to start this autonomic process. Even the idea of eating will do it. It told him, “I want to eat that!”

As an internist and cardiologist, however, my doctor learned in medical school, and had reinforced in continuing education throughout his professional life, that saturated fat and dietary cholesterol were verboten. They would clog his arteries. He saw atherosclerotic patients every day. They were a constant reminder that eating so much protein and fat would be “the death” of him. We all get that message drilled into us as well. The DEATH of US.

So, my doctor didn’t succumb to the secretionary impetus because another part of his brain told him 1) it’s just a picture and 2) it would have been bad for his health. The rational mind has learned to override the autonomic.

That particular morning, however, my doctor was relaxed at home and engaged in one of his favorite pastimes – reading the Sunday newspaper. Besides, he was intrigued because the title of the cover story was, “What If It’s All Been a Big Fat Lie?” And the author, Gary Taubes, had won the National Science Writer’s “Science in Society” award 3 times. So, my doctor decided to read the cover story. It was a life-changing event (for me)!

But first, my doctor decided that he would try the diet that Taubes described. It was in the tradition of medical self-experimentation exemplified by Werner Forssmann, “inventor” of cardiac catheterization in the 1930s. And in about 6 weeks, my doctor lost 17 pounds eating just 20 grams of carbs a day. He tested his blood chemistry and lipid panel before and after, and his n=1 self-experiment proved to “do no harm” (even a little good). So, as luck would have it, soon afterwards, when I walked into his office for my appointment, he saw me and said, “Have I got a diet for you!” I needed it too. I had just discovered (on a Fulton Fish Market scale) that I weighed 375 pounds!

So, where does Pauline Kael (correct spelling) come into this picture? According to Wikipedia, Pauline Kael was “a film critic who wrote for The New Yorker from 1968 to 1991.” According to Harper’s, “She is often regarded at the most influential film critic of her day,” and she was known for her “witty, biting, highly opinionated” reviews. I read her every week, but I remember her best for a comment she reportedly made in a lecture to the Modern Language Association in December 1972. It was in the wake of Richard Nixon’s 1972 landslide Presidential election victory.

                “I live in a rather special world. I only know one person who voted for Nixon. Where they are, I don’t know.   They’re outside my ken. But sometimes when I’m in a theater I can feel them.”

I have to admit that that image is pretty funny, and certainly “witty, biting, highly opinionated,” but Wikipedia notes that Kael was widely criticized for this sentiment. It illustrated the isolation in which it is possible to live, if you are surrounded by like-minded people, especially if you think of yourself as being superior in education or intellect. In such cases it extends to beliefs as well. Such elitism is common among the intelligentsia. New York Post writer John Podhoretz once claimed that New Yorkers “can easily go through life never meeting anybody who has a thought different from their own.” Under such circumstances, wouldn’t any non-conforming thought be heresy?

The world of human nutrition today suffers from these same constrained views, but the medical and public health communities are where integrity and professionalism are supposed to mean something. So, when my doctor was willing to try something that goes against the teachings he had practiced and lived by – first on himself (like Forssmann, whose self-experimentation led to his Nobel Prize), and then on his non-compliant, heavily-medicated, morbidly-obese Type 2 diabetic patient (me), I think there’s hope. And if others try it, and it works for them too, maybe the time will come when it won’t be as creepy as it was for Pauline Kael in that dark movie theater in 1972. 

Retrospective #76: Holiday Indulgences for Low Carbers

The subject of this Retrospective came to mind after reading a post on an online forum the day after Thanksgiving 2012. A “newbie” wrote about eating just a smidgen of this and a taste of that from the bounty of the table.

Another poster responded rather harshly, coming down hard on the newbie. He lectured her about “commitment,” albeit ending with a smiley face emoji. My take on this was in the context of someone who had been doing Very Low Carb for over 10 years. I too had been exposed yearly to a bountiful Thanksgiving table. That year I had a fasting blood glucose the morning after of 82mg/dL. Who better than the self-righteous to express sanctimonious indignation at people who enjoy small indulgences on such special occasions as holiday dinners with family?

Upon being diagnosed a Pre-diabetic or Type 2, many low carbers try in the beginning to go halfway instead of “all in.” This is understandable because you begin with the idea that eating Low Carb involves denial and deprivation.

This approach is also the advice given by the vast majority of physicians and diabetes educators. They believe that compliance with major dietary change is difficult. This is true even for the enlightened who know that a “balanced” diet, containing far, far too many carbs, is “bad medicine” for anyone who has a degree of Insulin Resistance and can no longer tolerate carbohydrates. But the harm of diabetes is very slow in coming and invisible for many years.

Besides, in the medical community most physicians and diabetes educations recommend that Type 2 diabetics continue to eat a “balanced” diet. They say Type 2 diabetes is a “progressive disease,” which it will be if you follow their dietary advice. It will be treated with progressively more medications and eventually injected insulin. And that comes along with the Microvascular complications: retinopathy, neuropathy, ED and end-stage kidney disease (with dialysis). That is, unless you die first from one of the Macrovascular complications like heart disease or stroke.

Denial and deprivation, however, are still powerful forces, and going halfway instead of all-in serves as comfort in the sense that you were “good” but still allowed yourself an indulgence. It’s “virtue signaling” to yourself and others. But it leaves you vulnerable. It shows that you are on the fence. You’re wavering. You lack commitment.

Besides, you’re going to take yourself out of “fat burning” status and stall any weight loss you had been working on. If you need to lose weight, as most Pre-diabetics and Type 2s do, it doesn’t get you there. You need to commit “all-in” to Low Carb eating to get to the point where you are not “craving” sugar (all forms of carbohydrate, both simple sugars and complex carbohydrates). They all becomes glucose in your blood. And as long as you are a “sugar burner,” you will be “hungry” at times, and you will continue to feel like you are being denied and deprived.

At our family Thanksgiving dinner that year, before dinner I had nuts and cheese (no crackers) and wine both before and with the meal.  At the table I had a big plate of dark meat turkey (no gravy), and cauliflower and Brussels sprouts roasted in olive oil. That was a feast meal indeed! After all that I was no longer hungry, and dessert held no interest for me. Anyway, I wasn’t even offered any of the homemade pecan or apple pies that were served.

That wasn’t always the case. My wife or my host always used to ask if I wanted dessert. They know not to ask now, and I no longer have to politely decline. I have reached the point where they and I can say I have “commitment.” I like to think they respect me, and I myself, for my commitment. Compare this with the perception of “waffling” and “half in.” When you think of it that way, I hope I can inspire you to feel “commitment” and self-respect too.

I feel pretty secure that I am “there” now, but we’ll see. The days after Thanksgiving are the cookie baking season in our house. There are ten pounds of flour on the counter and five pounds of butter in the freezer. Soon the smell of some of my favorite cookies will be wafting through the house. I have never before been 100% successful in avoiding the feeling of being denied and deprived when it comes to my wife’s home-baked cookies. My mother’s recipe for peanut butter cookies is my favorite. This will truly be a test of my self-respect and commitment. 

Retrospective #75: Going Very Low Carb “Cold Turkey”

If you haven’t tried Very Low Carb (+/- 20g of carbs a day) before, one of the first questions you will ask yourself is, “Do I want to just cut down on carbs gradually, or do I want to go ‘cold turkey’”? For the uninitiated, “cold turkey” refers to a sudden and abrupt cessation rather than a gradual reduction. I make the argument that going “cold turkey” is by far the better way. It has all the advantages and none of the disadvantages.

The principal advantages are 1) you won’t feel hungry, because you’ll be burning body fat for energy, 2) you won’t need snacks, just 2 or 3 small meals a day), 3) you will always, consistently, be full of energy, and 4), because your body is ‘happy,’ you won’t be thinking about food all the time. Of course, there may be a few bumps in the road along the way until you “get there;” but in a short time (just a few days for most people) you WILL get there, and all these advantages will come to you. But you gotta go “whole hog,” be disciplined, and do NOT stray from the path.

The disadvantages of gradual reduction are that you will never get to “fat burner” status, and without that transition, you will continue as a “sugar burner.” A sugar burner doesn’t have access to body fat and needs to eat in order to satisfy hunger. If you just eat fewer carbs, gradual reduction translates to slow starvation. The food you eat is digested for the most part in a few hours. After tha,t your blood sugar, which rose dramatically as the digested food entered your blood stream, will drop. That elicits a call for more food (including the carbs you’re still eating) since the insulin that carried the glucose (from digested carbs) to your cells is still in your blood stream.

This is especially true if you are already Insulin Resistant, as is most likely the case if you are overweight and/or Pre-diabetic or a Type 2. The insulin still circulating won’t allow the fat you have in storage to be the energy source your body needs. That’s why Insulin Resistant people gain weight easily (and become more Insulin Resistant.)

So, if you can’t get to "fat burner" status by curtailing carbs, you’re not going to succeed. Gradual reduction means “slow starvation” with all the disadvantages: hunger, craving, and volatile blood sugars (spikes and dips, leading to feeling tired, sleepy, listless, and then, after you eat again, “pumped”). That’s because when you are still a “sugar burner,” you have to continuously take food by mouth to “prime the pump” and keep energy flowing.

In contrast, ceasing to eat carbs “cold turkey” comes without any of the disadvantages mentioned above (hunger, craving, volatile blood sugars), and all of the advantages: You quickly (usually within a few days) become a “fat burner.” You’ll know it when you’re not hungry and your body doesn’t crave sugar because it transitioned to burning your body fat for energy. The only conditions are that you don’t eat too many carbs, or even too much protein. It will burn the few carbs you eat first, then glucose it makes from some of the protein you ate (so be careful not to eat too much protein), then the fat you ate, and then the fat your body stored for just this purpose.

Obviously, since your body fat is last in line, as biology designed it to be, as described above, you’ll have be diligent with respect to the other sources of energy that your body will use first. But that’s easier than it looks, if you learn to eat carefully and not eat too much.  It’ll be easy because YOU WON’T BE HUNGRY! Scroll down to Retrospective Debate #69, “In Praise of Small Meals,” where I discuss this further, including describing what I typically eat.

Having eaten so much for my entire life, for physiological reasons as described, and for psychological reasons as well, the contrast of eating Very Low Carb is stark. But if I listen to my stomach, and listen for other actual hunger signals, I realize that my body is “happy” when I eat Very Low Carb. I think it’s probably how we all lived just a few generations ago. I also like how good I feel now that my body seems to be very happy not to be fat and heavily medicated and suffering from a “progressive” disease, which is how Type 2 diabetes is still described. I’m very thankful that my doctor found this Way of Eating, tried it himself for a month, and then recommended it to me. I’ve been doing it now for 17 years.