The Nutrition Debate #81: Calorie Restriction in Humans

My 12/15/12 column, “Calorie Restriction and Longevity” (#79 here), dealt with one aspect of the first part of a scientific paper, “The Neuroprotective Properties of Calorie Restriction, The Ketogenic Diet, and Ketone Bodies.” This NIH Public Access article published in 2008 is, frankly, very technical, so to make the subject a little more “accessible” (for us both), 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 very compelling read, and I strongly recommend it to all open-minded and serious health readers.

In #79 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. Taubes, by the way, calls conventional calorie restricted diets in humans “semi-starvation” diets, because they are! But I am not advocating Calorie Restriction (CR) per se.  That will be clear next week when I lay out what I think is perhaps a new dietary paradigm. But first, the pitfalls and concerns.

“CR has many consequences, the majority of which are unknown at this time,” wrote Barbara Hansen in The Journal of Nutrition. This now dated 2001 Introduction to “Calorie Restriction: Effects on Body Composition, Insulin Signaling and Aging,” can be seen here. The data she presents, from a 1995 paper by Bodkin, is also dated, but prescient: “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.” Indeed, as we have seen, they did.

Quoting Hansen and Bodkin from 1993: “CR produces altered pathways of nutrient disposal, including reduced plasma glucose, insulin and leptin levels” (emphasis mine); and Hansen et.al. (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” (again, my emphasis). Continuing, “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, of course, it translates from non-human primates to humans.

A cautionary note, though: A 2006 ncbi.nih abstract in PubMed here, “Calorie Restriction in Humans: Potential Pitfalls and Health Concerns,” makes two very good points that illustrate the proper skepticism of the scientific mind. 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. It is likely that some of the physiological and psychological effects of calorie restriction that occur in animals may impact the human life very differently.” 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.” Now this may sound like the perfunctory disclaimer one sees in all ‘objective’ research papers, but it is worth keeping in mind.

The closing paragraph of Hansen’s piece above reveals what she regards as a “missed opportunity.” For me, it reveals the myopic vision of an out-of touch research biologist unable to see a clinical approach informed by nutrition: “The power of CR to mitigate, delay or prevent this 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 it calls for a pharmacological approach to address the genetic predisposition to a metabolic disorder of fat regulation affecting perhaps half of humankind, at least in the context of the Western Diet. A pill to pop! How absurd this is, especially when the solution is staring us all right in the face. It couldn’t be clearer or more apparent to me. If you haven’t figured it out yet, you’ll have to wait ‘til next week for me to spell it out for you.

© Dan Brown 12/29/12

The Nutrition Debate #80: Obesity Caused by Gut Bacterium!

A few days ago, the Health page of the Financial Times online (FT.com here) led with the banner headline, “Scientists Link Obesity to Gut Bacteria.”Call me a skeptic, if you like, or even a “conventional thinker” (pulleesse, don’t call me that!), but I’ll have to “wait and see” on this one. I know, a lot of serious scientists have been talking and writing about this in the blogosphere lately, but this is the first that I have seen it in the “mainstream” media.

So far, I have been dismissing this talk as too “edgy” and too esoteric for my non-scientific brain to wrap around. Besides, I have just gotten comfortable with – in fact, fully embraced Gary Taubes’s alternative Carbohydrate Hypothesis. This theorem places the action – or rather the “broken” action, of the hormone insulin at the center of the obesity epidemic. And now some cutting edge thinkers are moving on to another frontier – the human gut.

I suppose it’s a good thing that science is “advancing” quickly, but scientists would be the first to say that caution is and should be the “order of the day.” And I have no doubt it will. Everything will be “peer reviewed” (for what that’s worth!), and replicated with double-blind, prospective, trials, etc, etc. But journalism is not so constrained, and journalists often get it wrong. And, as a result, so does the public. And then the processed and packaged food industries pick-up on it, and all of a sudden a box of Cheerios cereal is a cholesterol-lowering drug.

But this rant is not about the gut bacterium “discovered” by the Chinese scientists at Shanghai Jiao Tong University, as reported by Professor Zhao Liping in the FT.  It is about the response of Dr. David Weinkove, lecturer in biological sciences at Durham University in Durham, England. Durham, for my non-British readers, is listed third after Oxford and Cambridge in many rankings of institutions of higher learning in the UK. I gave a hearty guffaw when I read his reaction to the news. He said, according to the FT, “If obesity is caused by bacteria, it could be infectious and picked up from some unknown environmental factor, or a parent. IT MIGHT NOT BE BEHAVIORAL AT ALL” (emphasis mine).

I apologize for “shouting” but I just couldn’t believe that he said this. I accept that the vast majority of the lay public believes that nearly 50% of all the adults in the U.S. and the UK are obese because we eat too much and exercise too little. But, for a lecturer in biological science at a leading UK center of research and learning to say it?!! Give me a break!

In an email exchange I had with Gary Taubes on the day before I wrote this, he related to me that he was preparing a rebuttal to the British Medical Journal (BMJ) on a piece they had just published about how low fat diets were associated with weight loss. I read the piece and decided that it was beyond my ken. I replied to him that I would leave the BMJ to him, and I would continue to fight “the good fight” on a different level. But when I am reminded how far we (all of us with an open-minded view of the science) have to “climb” to overcome such ignorance, it is indeed a daunting prospect.

Anyway, if the “gut bacteria” news had escaped your notice by the time this post hits the blogosphere, let me bring you up to speed. Dr. Zhao, the lead scientist and spokesman for the study, asserted, “This is a very important phenomenon. It is the last missing piece of evidence (that) bacteria causes (sic) obesity.” I laughed again at this as I could imagine Dr. Weinkove (of Durham) salivating at the prospect of what that breakthrough news portends. I saw a vision of sugar plums dancing in his head when he said, as the FT reported, “Dr. Zhao’s research paved the way to intervene in obesity and could allow new drugs to be developed for treatment.” It reminded me of the researchers and drug developers who first  came up with the statin compounds to lower LDL lipoproteins, and thus Total Cholesterol (TC,) because LDL was the only sub-component of TC that they could easily and effectively lower with a drug. This led to world-wide sales today of well over $20 billion, and to dubious health benefits and myriad risks. But it was a boon to the bottom line of big pharma.  Billions in profits and decades of grants for the “research community” ensued, both in academia and industry.

So, while I am skeptical by nature, and that is a good thing both in science and in general, I am still open-minded. I can also hope that this is “a very important phenomenon” and that it is “the last missing piece of evidence” of what causes obesity. And just as cholesterol testing was developed in the 1980s and then evolved beyond LDL, let’s hope that gut bacteria research, whether relevant to obesity of not, evolves as well. After all, as everyone is fond of saying, “there are 10 times more microbes than human cells in our bodies and they can be beneficial.” So, as science advances, particularly with recent progress in the knowledge of the human genome, a “breakthrough” of this magnitude would be welcome. Semi-starvation on a “balanced” diet, and boring daily exercises, don’t work for most people. And my VLC Ketogenic Diet is certainly restrictive and requires discipline. And I like my sugar plums…and Christmas cookies too!

© Dan Brown 12/22/12

The Nutrition Debate #79: Calorie Restriction and Longevity

People often ask me what motivated me to lose so much weight (170 lbs). I tell them: “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 to be older.” I had been gaining weight, and my doctor had been urging me to lose for years. Then, for two visits I was unable to weigh in at his office because his scale 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 said, “Have I got a diet for you!!!” I was motivated.

Of course, as I was losing weight (first on Atkins, and later on Bernstein – for diabetics), I wondered how low I would go. I had the luxury to fantasize about this because I was losing weight easily and without hunger. This will happen when you strictly follow a Very Low Carb (≤20g of carbohydrate a day) Way of Eating. 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 work is a “tough slog” but a “great read” too. Calorie Restriction and its positive association and correlation with longevity are covered in depth 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 online as a NIH Public Access peer-reviewed manuscript here, 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.” And “Calorie Restriction might even reduce disease risk and increase lifespan in normal weight subjects.” Also, “Beneficial effects on mental health have been reported as well, with improved mood following calorie restriction of obese diabetic patients.” Each quote cites a study or studies.

The problem with the preceding paragraph 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 midlife.” “Moreover, age-related deficits in learning and motor coordination are reduced by calorie restriction in rodents.” “Aged mice exhibited similar improvements in learning tasks…” And, “in parallel, calorie restriction also prevented age-related deficits in…a cellular correlate of memory.” “To date, however, clinical trials looking at the effects of calorie restrictions on brain aging and neurological disease have not been performed [on humans],” say the authors.

The authors continue, “the mechanisms that have been proposed to explain the neuroprotective effects of calorie restriction can be grouped into two general categories: 1) improved mitochondrial function, leading to decreased production or reactive oxygen species [free radicals] and increased energy output; 2) regulation of gene expression, resulting in decreased activity of pro-apoptotic factors and increased levels of neuroprotective factors such as neurotrophins.” In addition, “calorie restriction delays age-related oxidative damage to DNA, proteins and lipids” [the ‘antioxidant effect’], thus “decreasing the mitochondrial production of reactive oxygen species” [again,‘free radicals’].

Back to Taubes: “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). I’m thinking, that’s encouraging, and I reasonably conclude from this that it’s what I eat now, not how thin I am, that will (may?) determine my health outcome.

Taubes sums it up nicely this way: “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 lifelong 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 apparently bestows on the organism an enhanced ability to protect against oxidative stress and to ward off other pathogens” (GC-BC pg. 220).

Quoting Taubes again (GC-BC pg. 220): “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 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.” Next week: CR in humans.

 © Dan Brown 12/15/12

The Nutrition Debate #78: Metabolic Syndrome and Risk of Cancer

If you have Metabolic Syndrome there is a greater risk that you will develop certain types of cancer, according to a systematic review and meta-analysis reported in Medscape on November 18, 2012. The retrospective study was performed by a group of physician-researchers and was published in Diabetes Care, the magazine of the American Diabetes Association. To be clear, the study reports an association with cancer risk, not a causal relationship.

If you are unfamiliar with Metabolic Syndrome, it 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. The higher percentage applies if the criterion for inclusion is a smaller waist measurement:  37”vs 40” for men and 31.5”vs 35” for women.

In 1986, when I was first diagnosed as a Type 2 diabetic, I had the full cluster 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, take a look at the specific criteria in Nutrition Debate #9 here.

The results of the study (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.”

The conclusions (pg. 1): “Metabolic Syndrome is associated with increased risk of common cancers; for some cancers the risk differs between sexes, populations and definitions of metabolic syndrome.”

Furthermore detailed conclusions from 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 pretty strong language to be sure. It certainly should give one pause for thought.

Thoughts like, “What can I do about it?” Well, you can change your diet, that’s what. You can lose weight easily and keep it off permanently by eating a Very Low Carb, ketogenic diet. With this diet your blood sugars 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 all the risk factors for Metabolic Syndrome, and they can all go away. You will be free of Metabolic Syndrome. Ipso facto!

© Dan Brown 12/8/12

The Nutrition Debate #77: Low Carb Dieting and Pauline Kale (sic)

My doctor stumbled upon Low Carb dieting on a Sunday morning in early July 2002. He opened The New York Times and saw on the cover of the Magazine a big juicy ribeye steak with a melting lump of butter on top. If his biochemistry is the same as the rest of the human race, his salivary glands began to secrete digestive juices and a signal went from his hypothalamus in the center of the brain to his pancreas to start secreting insulin. There was no olfactory stimulus. The visual image was enough to start this autonomic response. Even the idea of eating will do it. It tells us, “It’s time to eat!”

Of course, my doctor didn’t act on these impulses because another part of his brain told him 1) it’s just a picture and 2) it would be bad for his health to eat so much saturated fat and cholesterol. The rational mind overrode the autonomic. As an internist and cardiologist he had learned in medical school, and had had reinforced in continuing education throughout his professional life, that saturated fat and dietary cholesterol were verboten. They would clog his arteries. He had seen atherosclerotic patients every day in his practice. They were a constant reminder that eating saturated fats and cholesterol would be “the death” of him. We have that message drilled into us constantly as well. The DEATH of us.

But, that particular Sunday morning my doctor was relaxed at home and engaged in one of his favorite day-off indulgences – putting his feet up and reading his favorite newspaper. Besides, he was intrigued because the title of the cover story was, “What If It’s All Been a Big Fat Lie?” The author, Gary Taubes, is a highly regarded science writer who has won the National Science Writers “Science in Society” award 3 times (and 3 is the limit!) And the New York Times was at that time still “the old gray lady” of print journalism whose motto was “all the news that’s fit to print.” So… my doctor decided to read the story. It was a life-changing event (for me)!

Then, in the noble tradition of medical self-experimentation exemplified by Werner Forssmann, “inventor” of cardiac catheterization in the 1930s, my doctor decided to try the diet that Taubes outlined. And in about 6 weeks, he lost 17 pounds on Atkins Induction! I assume he tested his blood chemistry and lipid panel before and after, and his n=1 self-experiment proved to “do no harm” (and maybe even a little good?). So, soon afterwards, as luck would have it, as I walked into his office, my doctor saw me and said to me, “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. “She is often regarded at the most influential film critic of her day,” according to Harper’s, and she was known for her “witty, biting, highly opinionated and sharply focused” 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 landslide victory in the 1972 presidential election:

“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 and sharply focused,” 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 disparate thought be heresy?

The world of human nutrition today suffers from this same constrained view. “The Nutrition Debate” seeks, in a very modest way, to present another view and to encourage self experimentation. There’s lots of support for this alternative; it just doesn’t get much play in medicine or the media. Of course, there are other forces at work here (big agriculture and big food manufacturers, to name just two of the major stakeholders), but the medical and public health communities are where integrity and professionalism are supposed to mean something. That is where I think we can best make inroads and foment change.

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 the  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 it won’t be as creepy as it was for Pauline Kael in that dark theater in 1972. That’s my hope anyway, and why I keep writing this blog.

 

© Dan Brown 12/1/12

The Nutrition Debate #76: Holiday Indulgences for Low Carbers

If you thought this post was going to be about eating just a smidgen of this and a taste of that, I’m sorry to disappoint. This column is about “commitment,” what it means and how it can come to pass. It is not a lecture, however. This is my experience with “commitment” – both the physical and mental aspects of it – and how it seems to me to be a progressive rather than a “cold turkey” kind of thing, once, that is, you have “committed” to going “all-in” to Very Low Carb eating in the first place.  Of course, as always, YMMV (Your Mileage May Vary) as low carbers are wont to say.

The subject came to mind for me after reading a post on the Bernstein Diabetes Forum the day after Thanksgiving when a Newbie wrote about eating just a smidgen of this and a taste of that from the bounty on the table. Another poster responded rather harshly, I thought at first, coming down pretty hard on the Newbie. He lectured her about “commitment,” albeit with a smiley face postscript. Of course my “take” on this was in the context of someone who has been doing Very Low Carb on and off (at the moment “on”) for over 10 years. I too had been exposed to a bountiful Thanksgiving table, and I had a fasting blood glucose the morning after of 92. So, who better than the self-righteous to express sanctimonious indignation at small indulgences on such special occasions as holiday dinners with family?

I think the problem does not begin with holiday indulgences, however. It begins with the idea of denial and deprivation. Many low carbers try from the beginning, perhaps on being diagnosed a Type 2 diabetic or pre-diabetic, to go halfway instead of “all in.” This approach is understandable and is certainly in keeping with the advice of the vast majority of physicians and diabetes educators. They believe that compliance with major dietary change is difficult. This belief is true even for the enlightened ones who know that a “balanced” diet, containing far too many carbs is “bad medicine” for anyone who can no longer tolerate carbohydrates without doing harm. But the harm is slow, nearly “invisible” and many years in the making. Besides Type 2 diabetes (if you continue to eat moderate amounts of carbohydrate) is regarded by the medical community as a “progressive disease” and as such is treatable with progressively more medications and eventually injected insulin. And that’s all well and good, if you can dodge retinopathy, neuropathy, ED or other forms of autonomic dysfunction. That is, until you die from one of the dreaded complications or a related disease such as heart disease.

But going halfway instead of all-in still leaves a lingering feeling of denial and deprivation, and, if you need to lose weight, as most Type 2 diabetics 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), which becomes glucose through digestion and circulates in the blood. As long as you are a “sugar burner,” you will feel “hungry” at times, and you will continue to retain the idea of being denied and deprived. If you are not hungry, you will feel very differently.  It's a hard thing to describe to someone who’s been hungry for a very long time, as many diabetics and struggling dieters have been.

The best evidence of this is the recipe section on most low carb diabetes websites. It is replete with “substitutes” for desserts and other favorite high-carb dishes. In reality, most of them are reduced carb, but they’re still carbs! People are just not willing to give up dessert! Even I have sometimes written that on special occasions I’ve eaten berries in heavy cream. I’m sure I wrote this because I read in various places that such an “indulgence” was permitted on special occasions. But they are still just carbs (simple sugars actually: sucrose, glucose and fructose), justified by their phytochemicals and fiber, and the idea of a permitted “small indulgence.” If you have eaten a small meal, or even a big plate full of dark meat turkey (no gravy), and cauliflower and Brussels sprouts roasted in olive oil, as I did this year on Thanksgiving, you are no longer hungry and you don’t need dessert! Especially, if you had a few nuts and some cheese (no crackers) before dinner and some wine both before and with dinner. That is a feast meal indeed! Dessert held no interest for me (and 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 used to always 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 I can say I have “commitment.” This is in part due to the example others have shown me on the Internet Forum I visit. There are some stellar examples there who’ve inspired me to think it is possible to have “commitment.” And I now know that it is. I hope I can inspire you to feel that way too.

I feel pretty secure that I am “there” now, but we’ll see. It is now the day after Thanksgiving as I write this and the cookie baking season has begun. 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 types of 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 home-baked cookies. This will be a test. We’ll see if I really do have “commitment” this year.

© Dan Brown 11/24/12

The Nutrition Debate #75: Low Carb Dieting the “Cold Turkey” Way

If you haven’t tried low carb dieting 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” (with respect to eating carbs) is by far the better choice. It has all the advantages of cessation and none of the disadvantages of gradual reduction.

The principal advantages are 1) you won’t feel hungry (because you’re burning fat), 2) you won’t crave snacks (to feed your sugar addiction), 3) you will feel full of energy (because ketosis is ‘the natural state’), and 4) you won’t be thinking about food all the time (because your body is ‘happy’). Of course, if you haven’t tried this before, YMMV (Your Mileage May Vary), and there may be a few bumps in the road until you “get there;” but in a short time (1-2 weeks) you WILL get there, and all these advantages will come to you. They will come if you are disciplined and do not stray from this path.

The disadvantages of gradual reduction are that you will never get to ketosis, and without ketosis you will always be a sugar burner. A sugar burner needs to eat carbs in order to satisfy hunger. If you just eat fewer carbs, gradual reduction translates to gradual starvation. The food you eat is digested for the most part in a few hours. After that your blood sugar, which surged as the digested carbs entered your blood stream, will drop. That elicits a call for more carbs since the insulin that carried the glucose (sugar from digested carbs) to your cells is still in your blood stream (especially if you are already insulin resistant), and it won’t allow the fat you have in storage to supply the energy your body needs.

It tells you to eat more carbs to supply energy. Save the fat. Use carbs which appear to be abundant. Eat more now to prepare for leaner times later. It’s all in your best interest, your body knows this. These primordial mechanisms were developed in our Paleolithic ancestral times. It’s only been a thousand generations and our genes haven’t adapted to the year-round abundance of food we now have, and to all the processed foods that convert to sugar so quickly.

So, if you can’t get to ketosis by reducing 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 “pumped”). All these disadvantages are perpetual. They are with you always, whether you are dieting by gradual reduction of carbs or just eating a normal “balanced” diet, as recommended by our government. That’s because when you are a “sugar burner,” you have to continuously “prime the pump” to keep water (energy) flowing.

In contrast, dieting by going “cold turkey” with carbs is “slow starvation” without any of the disadvantages mentioned above (hunger, craving, volatile blood sugars), and all of the advantages: You quickly (more or less) become a fat burner. You’re not hungry and your body doesn’t crave sugar because it transitioned to burning fat, your body fat, for energy. That is, so long as you don’t feed it too much food – 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 eat (so be careful not to eat too much), then the fat you eat, and then the fat your body stored for just this purpose and time – when it is needed.

Obviously, since your body fat is last in line, as it was designed to be, you’ll have be diligent with respect to the first three sources of energy your body will use. But that’s easier than it looks, if you learn to eat carefully and not too much.  In The Nutrition Debate #69, “In Praise of Small Meals” here, I discuss this in some detail, including describing what I eat. What I didn’t mention there, and I feel may be an important consideration, if you stop eating carbs almost entirely and eat just protein and fat, won’t that increase your food budget? Not really, because you will eat a lot less, honestly.

It’s hard to get used to, having eaten too much for my entire life, but if I listen to my stomach, and monitor my meter and my scale, and think about how my ancestral forbearers lived, and 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 (Type 2 diabetes) and  high blood pressure, I’m very thankful that my doctor found this Way of Eating (after reading Gary Taubes’ “What if It’s All Been a Big Fat Lie”), and suggested more than 10 years ago that I try Atkins Induction (<20g carbs a day). Thanks, doc.

© Dan Brown 11/17/12

The Nutrition Debate #74: No Added Salt? Why?

Why add salt? Well, maybe YOU shouldn’t. Many prepared and processed foods in cans and boxes already have a lot of added salt. It is added to enhance flavor and make the product more palatable. Of course, if you eat mostly real food, i.e., whole foods – the meats and vegetables found in the cases on the perimeter of the supermarket, you may find them tastier if you add salt in their preparation or on the plate. I do. I add lots of salt. I do it because I believe my body has a natural sodium “appetite.” I add salt “to taste.” I believe adding salt to food is a fundamental behavioral response to a primary survival mechanism – to maintain homeostasis and electrolyte balance. I do it so I can live in that healthy state.

 

 So then why is salt restriction universally recommended by the public health authorities and the medical establishment? There is very little evidence (and no “proof”!) that salt “causes” hypertension. It’s another one of those hypotheses that, according to Gary Taubes in his 2007 book, “Good Calories – Bad Calories” (pg. 146), scientists say is based on “biological plausibility – it makes sense and so seems obvious,” like eating fat will make you fat. Taubes first addressed the subject of salt reduction here in his award-winning article “The (Political) Science of Salt,” published in Science on August 14, 1998. He revisited the subject here with “Salt, We Misjudged You,” an op-ed in the New York Times on June 3, 2012.

 

There is also evidence that salt restriction in some populations, among them Type 2 diabetics, may be harmful. On February 2, 2011, Diabetes Care online reported a University of Melbourne study that found “patients with the highest levels of sodium in their urine had the smallest risk of dying over a 10-year period. The study followed “638 people with longstanding Type 2 Diabetes, often accompanied by heart disease and high blood pressure.” The report describes, “At the outset of the study all the patients were in their 60s and nearly half of them were obese.” The researchers reported, “Over the decade the study spanned, 175 patients (27%) died, mostly due to heart disease.  The average amount of sodium in their urine (the ‘gold standard’ for measuring sodium consumption) was 4.2 grams per day. For every extra 2.3 grams of sodium (equivalent to 1 tsp. of table salt) in their urine, their risk of dying during the study dropped by 28 percent.” Doctors who worked on the study said, “It raises the possibility that in people with Type 2 diabetes, low salt intake is not always beneficial.” Boy, those Aussies are cautious (but open-minded) scientists!

 

In his series “Shaking Up the Salt Myth,” Paleo blogger Chris Kresser wrote an article, “The Dangers of Salt Restriction,” in which he reported on a study in JAMA in 2011 that “demonstrates a low-salt zone where stroke, heart attack and death are more likely.” He concludes, “These findings demonstrate the lowest risk of death for sodium excretion is between 4 and 5.99 grams per day” (emphasis mine). The 2010 Dietary Guidelines recommend that Americans “reduce daily sodium intake to less than 2,300 milligrams (1 tsp) and further reduce intake to 1,500 mg among persons who are 51 and older and those of any age who are African American or have hypertension, diabetes, or chronic kidney disease. The 1,500 mg recommendation applies to about half of the U.S. population, including children, and the majority of adults,” the guidelines state (emphasis again is mine). So, the lowest risk of death is associated with consuming from 267% to 399% more sodium than Type 2s or hypertensives or older adults are being “guided” to eat. What a disconnect!

 

Then there’s the physiological explanation for why Type 2 diabetics who are following a Low Carb or Very Low Carb diet should not restrict their sodium (salt) intake. Michael Eades, M.D., author with his wife Mary Dan Eades, also M.D., of “Protein Power,” blogs about it here in “Tips and Tricks for Starting (or re-starting) Low Carb Part II.” He explains that when your body is depleted of carbs, your blood insulin drops and your insulin sensitivity improves. The excess insulin that made you store fat also drove your kidney to retain fluid. When the insulin level drops on a low carb diet, “the stimulus to the kidneys to retain fluids also goes away.” Dr. Eades says, “The kidneys begin to rapidly release fluid” (urine) and sodium, changing your electrolyte balance. When this happens, “symptoms often occur: fatigue, headache, cramps, and postural hypertension” (light-headedness). “You simply need to take more sodium drink more water,” Dr. Eades says. “You’ve got to start thinking differently.  The low carb diet is one that absolutely requires more sodium. A lot more sodium.” “An easy way to get extra sodium, along with magnesium and potassium, is by consuming bone broth.” “You can also use commercially available bouillon,” he adds, which might help you “get through carb cravings.”

 

In my opinion, the Dietary Guidelines recommendation that salt should be restricted is just bad advice.  And it certainly should not be a universal recommendation. In particular, it should not be applied to Type 2 diabetics who eat a diet of less than 50 grams of carbohydrate a day, aka a Low Carb Diet. This population should eat more salt. This may sound crazy when the “accepted wisdom” of the government “Dictocrats” is that we should eat less; remember, however, that these are the same “experts” who tell us that T2s should be eating a balanced diet containing carbohydrates and sugars.

© Dan Brown 11/10/12

The Nutrition Debate #73: Newly Diagnosed Type 2 or Pre-Diabetic? Scared?

I wasn’t (scared).  And I paid a price. I did just what my doctors told me to do, mostly. I took the pills they prescribed and continued going to see them regularly. I continued to eat the same types of foods I ate before (a “balanced” diet, as they recommended); and I tried to lose weight, as they also recommended. But my body didn’t want to be starved, so the weight loss part didn’t work out so well.

The result: I continued to gain weight and over the years my diabetes got worse. As my blood sugars got worse, I was prescribed more types of oral diabetes medications and larger doses. Eventually, I was maxed out on two types and starting a third. In those days the only option, when the third med failed to control my blood sugar, would have been to inject insulin. I was that close 10 years ago when I found another way. I found a way to both lose weight and manage my diabetes. My doctor suggested I try the Atkins diet.

Today, with a Type 2 diagnosis, if “diet and exercise” doesn’t work after one or two office visits, many physicians prescribe Metformin and then injected insulin as a primary treatment. That may be a good idea if you continue to eat a balanced diet.  It would scare me, nevertheless, knowing that there’s an alternative as I do. You don’t have to do the same old, same old “restricted-calorie balanced diet” in which you starve your body and you are always hungry. It doesn’t work, or at least not for long. If you lose weight, you soon gain it back. And exercise just makes you hungry and justifies eating more as a reward for good behavior. Whew…

 Alternatively, many patients who are newly diagnosed with Type 2 Diabetes go home and immediately go on line to learn for themselves how best to treat their condition. They take charge of their own health. In doing this they avoid expensive medications and manage their diabetes through diet alone. I say “manage” ‘cause ONCE YOUR METABOLISM HAS BEEN DAMAGED BY BETA CELL LOSS AND INSULIN RESISTANCE, YOU WILL BE CARBOHYDRATE INTOLERANT FOR THE REST OF YOUR LIFE. You MUST accept this. If you want to manage this disease without drugs, or with minimum doses), and without the dreaded complications (blindness, amputations and/or end-stage kidney disease), you can do it, but you MUST make VERY dramatic changes in your diet. You must drastically reduce the carbs you eat at every meal.

There is a learning curve to the low and very low carbohydrate Way of Eating, and you will need to keep an open mind and relearn a lot of behaviors if you are going to succeed. There’s lot of help on-line, though, and the best advice I think comes from forums like Dr. Bernstein’s Diabetes Forum (registration required), but there are other good ones as well. I migrated to Dr. B’s forum and have been a regular there for almost 6 years. And over the course of the last 10 years I managed to lose 170 pounds, all without hunger, because I was NOT starving my body. My body was getting the energy it needed from its own fat storage. That’s what it’s there for, in the evolutionary sense, if you think about it.

More importantly, almost as soon as I started eating Very Low Carb (+/- 20 net grams of carbohydrate a day on Atkins Induction), I needed much less medication. I know this because I was getting hypoglycemia (very low blood sugars) from the very beginning. I called the doctor and he told me successively to lower or eliminate all the diabetes meds I was taking. This all happened before I lost weight. And after I lost a lot of weight my blood pressure also improved a lot (on the same meds), and my blood lipids (cholesterol) improved dramatically, especially my HDL and triglycerides.

The key to losing weight without hunger is getting access to your body fat. And the key to that is not eating carbs (both simple sugars and complex carbohydrates), which all convert to glucose. Eating carbohydrates has two effects: 1) they cause the pancreas to secrete insulin which carries the glucose (that the carbohydrates all break down into) to their destination cells. These carbs provide “quick energy.” Our body “craves” them (making us “feel hungry”) if it is in a “glucogenic” state because it relies on glucose as the primary source of energy; and 2) when the body is in a glucogenic state, the insulin blocks fat (both our body fat in storage and that which we eat) from being broken down and used for energy. If we have enough “ready energy” from carbs, we don’t need to use stored energy from body fat. It’s the way our bodies work. Our body fat remains as stored fat, and the fat we eat and the carbs we overeat make more body fat.  Insulin stops our body from being in a “ketogenic” state where it burns both the fat we eat and our body fat for energy.

So, by eating a VERY LOW CARB diet, and losing a lot of weight, all these good things happen. My body is happy. My DOCTOR is happy. I have lots of energy, and I am much healthier today in every sense (BS, cholesterol, BP) than I was when I was fat and heavily medicated. All I had to do was take charge of my own health and use the internet, my meter and my scale to figure out what to do. Your meter and your scale will give you the feedback you need too, if you decide not to be scared and to take control of your own health and what you put into your body. It’s your life, after all.             

© Dan Brown 11/3/12

The Nutrition Debate #72: How to “Fix” Your Cholesterol

Physicians all over the world want to “fix” your “cholesterol.” They’re well meaning, and they know there is a small benefit, probably due to a reduction in inflammation, associated with a reduction in the LDL lipoprotein component of your Total Cholesterol, all other components being equal. They know that by lowering your LDL, your Total Cholesterol will be lowered by the same amount. And they know they can do that with a pill. They can get it to within the range recommended by the “standard of practice” by prescribing a statin drug: Crestor or Lipitor or Zocor or another brand, or one of the generics, commonly simvastatin. So, what’s wrong with that? The answer: it’s not enough!

In the first place, lowering LDL Cholesterol is by far the most common intervention for which your doctor can write a “script” (prescription).That’s why they do it. It must be frustrating for them though since “high cholesterol” (meaning both Total Cholesterol and LDL) is almost always associated with low HDL and high triglycerides. They are all so common in the population, and they are seen in the same patient. The result, however, is that sales of statins in the U.S. alone passed $20 billion a few years ago, but since HDL and triglycerides are more difficult to “treat,” they remain unchanged.

It must be doubly frustrating that “high cholesterol” is commonly associated with hypertension (high blood pressure) and obesity. Collectively these indications are called Metabolic Syndrome. See The Nutrition Debate #9 here for the indications and ranges. The particular cholesterol markers associated with Metabolic Syndrome are, interestingly, low HDL lipoproteins and high serum triglycerides. This is why in medical terms this cholesterol condition is called “dyslipidemia,” which means dysfunctional blood lipids (fats).

Although progress is being made in treating high triglycerides, unfortunately there is no pill to beneficially raise HDL. But dietary intervention works for both of these. See The Nutrition Debate #67 “HDL Cholesterol and the Very Low Carb Diet” here, #68, “Triglycerides, Fish Oil and Sardines” here, and then #27, “…the strongest predictor of a heart attack” (the Trig./HDL ratio) here for evidence of the CVD benefits of dietary intervention from both HDL and triglycerides.

Of course, hypertension can be treated with medications, usually a “cocktail” of two or three, but obesity stubbornly resists medical interventions. It is up to the patient, the doctors say, and the doctors usually report the patient is “non-compliant.” That is to say, the patient either cannot lose weight on the recommended restricted calorie balanced diet, or the patient who does lose weight soon gains it all back and often “then some.” Hunger wins out. The body doesn’t want to be starved even with fat reserves. It tells you to eat lots of glucose (carbs) for quick energy, even between meals.

So “high cholesterol” and hypertension, seen together, are still the targets most doctors treat together. The problem is: Total Cholesterol is an antiquated and almost useless term. It is only used because it can be easily measured and the calculated component lowered to the standard-of-practice range by statins. HDL and triglycerides remain unchanged. But, a Total Cholesterol that would be “too high,” because of its LDL component, would be perfectly okay with your doctor if the LDL were the same but the HDL was much higher and the triglycerides much lower. See The Nutrition Debate #25, “Understanding Your Lipid Panel” here, for two identical Total Cholesterols with different components.

The reason for this is evident from the formula used for the lab test of your cholesterol. It is called the Friedewald formula. In it, Total Cholesterol and HDL and triglycerides are assayed (actually measured), but the LDL value is calculated, thusly: LDL = T.Chol – HDL – TG/5 (where triglycerides/5 are a surrogate for VLDL within a wide range).

So, the best way to truly “fix” your cholesterol is to significantly raise your HDL and lower your triglycerides. And if you follow my “prescription” for doing that, by following a restricted-calorie Very Low Carbohydrate diet, you will also lose weight without hunger, because your body will be free to burn your body fat. And as a result, you will get control of your blood sugar (if you need to), and lower your blood pressure. Your Type2 diabetes (if you have it, or you are pre-diabetic) will go into remission and you will have no clinical signs of dysglycemia. Your Metabolic Syndrome will go undetected because the indications will have abated. Your doctor can’t do that. You can. But first you have to know your cholesterol – not just your Total Cholesterol and LDL, but also your HDL and triglycerides. Take charge of your health and find out!

 

© Dan Brown 10/27/12

The Nutrition Debate #71: Weight Loss Maintenance

After losing 170 pounds on a Very Low Carb diet (first with Atkins and then Bernstein), I later regained 72. And although I still ate Very Low Carb most of the time, and always at breakfast and lunch, and most dinners, I occasionally “binged,” and I routinely ate too much dinner. I also sometimes snacked after dinner even though I was not hungry.

 Altogether, it was more than my body needed to maintain my weight, and it ultimately led to the loss of blood sugar control that I enjoyed while I was eating “strictly according to plan.” My A1c went from 5.4 to 6.3. And my blood pressure went back to 130/90 (with the same meds) from 110/70. My HDL and triglycerides were still very much improved, but my LDL had also begun to creep up. And my doctor was urging me to start statins again.

So, that is how I regained weight: Too much food, snacking after dinner, and occasional binging. It didn’t take “much” (the way I saw it), but it was enough. It took almost four years to regain the weight, with a few ups and downs along the way, and I’ve finally decided “enough is enough.” It’s time to turn it around again. About a month ago I set a goal to lose 55 pounds: 30 (to get to 247) by the end of the year (4 months’ time) and then 25 more (to get to 222) “eventually.” It’s my “let’s see how it goes approach.” Thereafter, I will strive to keep my weight within 5 pounds of 225.

By all accounts in the literature, my situation is very common. Many of those who find it easy to lose weight on a Very Low Carb eventually relapse and tumble into the same pitfall. Most gain back most of the weight they lost, especially if they abandon the principles of Very Low Carb eating. That’s a “fatal flaw” of any diet. But I didn’t, really (I tell myself). Why therefore did I fail? Everyone wants to know why they failed. And everyone wants to tell you. But nobody really knows for sure. Until now, maybe.

Before I share with you what I intend to do to maintain my weight loss (once I attain my goal weight of 225lbs.), I need to describe the diet I am using to lose weight again. I call it a Restricted Calorie Very Low Carb Ketogenic Diet.  It has 3 components: 1) Restricted Calorie: you need to have a calorie deficit to burn body fat; 2) Very Low Carb (VLC): you need to eat VLC to allow insulin to NOT BLOCK the breakdown of body fat in storage; and 3) Ketogenic: you need to supply ketone bodies from both dietary and body fat breakup, and glycerol and amino acids from fat and protein, to provide alternate fuels (e.g., ketone bodies) and mechanisms (gluconeogenesis) for synthesizing glucose for your central nervous system and other cells that require them. These processes and mechanisms are called “complementary pathways.”

For me this diet is 1,200kcal/day comprised of 5% (20g) of carbohydrate, 25% (75g) of protein and 70% (90g) of fat. This formulation produces a ketogenic/glucogenic (K/G) ratio of 1.66, and should produce a weight loss of 2 pounds per week. A 1,000 kcal/day calorie deficit x 7 days = 7,000 kcal/wk = 2 lbs., since there are 3,500 kcal/pound.

The way I propose to maintain my goal weight is described in “The Art and Science of Low Carbohydrate Living” by Jeff Volek and Stephen Phinney.  This is a very good book, but there are lots of good books out there about the Low Carb way of eating. However, none that I have read specifically describes in terms of macronutrients WHAT TO DO, once you have reached your “goal weight,” in order to maintain it. This book does, and it explains why. It describes the mechanisms and processes the body goes through ESPECIALLY WHEN YOU ARE CARBOHYDRATE INTOLERANT.  The authors use this new “buzz” phrase repeatedly. Accept it. It applies to all Type2 diabetics, pre-diabetics, and the majority of overweight, obese and morbidly obese people, as well as those who have Metabolic Syndrome. That means you.

The following excerpts from Chapter 16, “The Importance of Dietary Fat in Long-Term Maintenance,” outline Volek and Phinney’s rationale. The authors reason that “long term adherence to carbohydrate restriction is an important issue, and capturing the benefits of a low carb diet for the management of chronic conditions associated with insulin resistance requires that we address this challenge. Given the dramatic improvements in the dyslipidemia associated with metabolic syndrome, and the marked improvement in diabetes management when adequate carbohydrate restriction is sustained” (pg. 205), they conclude that dietary carbohydrate intake cannot be increased in weight maintenance. So, the need “…to feed the post-weight loss patient adequate energy for weight stability, while maintaining the degree of carbohydrate restriction necessary to sustain the diet’s benefits” (pg. 206), as carb intake must remain flat, then only protein and fat remain. And if about half of protein is glucogenic (can convert to glucose in a secondary process in the liver called gluconeogenesis), the amount of protein in the maintenance diet can only increase slightly and then only as an equal percentage of total energy intake in the maintenance diet as it was in the weight loss diet. Thus, the macronutrient that must increase in the maintenance diet, both as a percentage of total intake and in absolute calories, is fat.  I’m thinking ghee and coconut oil.  And maybe snacks of nuts and cheese once in a while. Wheeeeee...                                                    

 © Dan Brown 10/20/12

The Nutrition Debate #70: LDL Cholesterol and Statins

My doctor is hinting that I should start taking statins again. Knowing that I know a little something about lipid health, and that I have “taken charge” (in a sense) of my own healthcare, I expect he knows he has to tread softly with me on the subject of statins. He also knows that I respect his knowledge (he is an internist and cardiologist), and he has worked well with me for over 20 years.

After failing to get me to lose weight on a balanced diet, under his nutritionist’s supervision, in August 2002 my doctor suggested I try Atkins. It worked. In 9 months I lost 60 pounds, and a few years later after gaining back 12 pounds I started on Bernstein and lost 100 more in less than a year and then later another 22 (170 total). Upon starting Atkins I immediately needed to greatly reduce and/or eliminate all three classes of oral diabetes medications I had been taking. (I have been a Type 2 diabetic for 26 years.) By my lowest weight my blood pressure had also gone from 130/90 to 110/70 on the same BP meds.

In addition, my lipid health completely turned around. My HDL Cholesterol more than doubled from 39 to 81 (averages), and my triglyceride averages went from 137 to 49. (For details of the HDL story go here and for the triglycerides go here.) But, you may ask, how did my LDL Cholesterol fare during this transformational period? At a glance it appears to me that it did pretty well, but bear in mind that LDL Cholesterol is a calculated number (not an assayed value). Also, statins lower LDL very effectively.

Between 1992 and August 2002, when my doctor suggested I try Atkins, my LDL had been tested 12 times. The average was 142mg/dl. For reference, from 130 to 159mg/dl LDL is considered “borderline high.”Over the next 16 months, while I was on the Atkins diet and losing weight, it was tested 16 more times, and the average was 125. The clinical guidelines consider under 130 “near/above optimal.”  But, for patients who have either hypertension, Type 2 diabetes or are obese, the guidelines suggest <100, and if the patient presents with more than one of these conditions, the guidelines are <70mg/dl.

So, since I was obese, hypertensive and a Type2 diabetic, in December 2003 my doctor suggested I start on a statin: I started on 80mg of Lipitor, as I recall, and it definitely lowered my LDL Cholesterol. Over the next 5 years the average of the 21 LDLs taken was 60! I was lucky. I had no side effects that I can recall (but maybe cognition was one of them – LOL). And, soon after starting them I switched to a generic (Simvastatin,) and over a period of time took less and less until my doctor finally took me off them completely in December 2008.

Since that time my LDL has been tested 11 times for an average of 123, and that includes the last two: 146 and 149. This 123 average is virtually the same average as my first year on Atkins (125). It is also under the 130 “near/above optimal” value, and I still weigh today more than 100 pounds less than when I started Atkins.

However, my weight, blood pressure, fasting blood sugars and A1c’s have been creeping up a bit recently. So I find myself at a crossroads: Either I stick closely to my Very Low Carb Restricted Calorie diet (as I have been for the last 6 weeks) to lose weight, improve my BP, A1c and LDL Cholesterol, or I start to take a low dose statin again (for the LDL only). My doctor wants me to look into pitavastatin. So I did. It did well recently in a prospective, randomized, double blind, double-dummy trial reported on PubMed.com here. A minimum dose of 2mg had a 39% reduction of LDL compared to a 35% reduction of LDL for a minimum 20mg dose of Simvastatin. I didn’t check out the side effects or “adverse incidents.”

I think my approach (should the subject arise at my next office visit) will be to say “no” to starting on a statin again so long as I am making improvements in my weight, BP, A1c and LDL Cholesterol. (See, your subtle approach worked, doc.) If I can consistently keep my LDL between 100 and 130 without a statin, and lose weight again, and improve my BP and A1c and FBG entirely through my Very Low Carb Restricted Calorie diet, I think I can keep the doctor off my back. Let’s see, after he reads this, if he will agree with this plan.

© Dan Brown 10/14/12

The Nutrition Debate #69: In Praise of Small Meals

Like many Americans and increasingly people around the world who have eaten a “Westernized” diet, I succumbed to one of the ubiquitous Diseases of Civilization: Metabolic Syndrome. See The Nutrition Debate #9 here for the symptoms. The major signs are obesity, hypertension (high blood pressure) and dyslipidemia (especially high triglycerides and low HDL). It is also nearly synonymous with Type 2 diabetes. I don’t have to tell you: Obesity and T2 diabetes are epidemics of “epic” proportions (pun intended).

Many have already discovered an effective treatment for Metabolic Syndrome – one that can reverse virtually all of the symptoms and avoid further damage to organs and arteries (endothelial dysfunction). Lose weight. And in a way that is without hunger, using the Very Low Carb (VLC) restricted calorie diet advocated in this blog. The benefit of the VLC restricted calorie diet is that it will ameliorate all the symptoms of Metabolic Syndrome: the obesity, the hypertension, the dyslipidemia and dysglycemia (pre-diabetes or even full T2 diabetes).

You can lose weight without hunger. I lost 170 pounds.  Your high triglycerides will plummet and your HDL can soar. For evidence of my own improvement in these areas, see the Nutrition Debate #67, “HDL Cholesterol and the Very Low Carb Diet,” and #68, “Triglycerides, Fish Oil and Sardines.” In addition your blood pressure will likely improve. Mine did. I went from 130/90 (with medications) to 110/70 (with the same medications). Finally, and this is the best news of all: your blood sugars will greatly improve, eliminating or substantially reducing the need to take oral diabetes medications.

In addition, if strictly adhered to, a Very Low Carb diet will put your T2 diabetes in full remission with no clinical signs of disease. Mine is. And once you have reached your goal weight, all of your gains will be retained so long as you continue to eat Very Low Carb. So long as you keep the weight off, and continue to eat VLC, you will have “normal” blood sugars and lower A1c’s, great lipids, especially triglycerides and HDL, and improved blood pressure. But, you can’t go back. You must keep the weight off. And you must continue to eat VLC. Very Low Carb must become your Way of Eating for life (double entendre intended).

 This Way of Eating is very effective for weight loss and weight maintenance because if you aren’t hungry, you should not eat as much. You can eat a small meal and be satisfied. Not sensing hunger, that is, by eliminating the biological imperative your body senses to eat to survive to avoid starvation, you will not want to eat between meals and at every opportunity, and you will not have the desire to scarf down more food than you need when you do sit down to eat.

But hunger is not the only driver of eating. Another force/response that I discuss in the Nutrition Debate #63 here is Impulse Control. Thinking about food, or seeing food, even a visual image on TV, is a stimulus. It induces a hormonal response. Insulin and other hormones start to flow. The stimulus could be one of those Red Lobster TV commercials that depicts an “endless shrimp” dinner. Delicious! Or it could be just the thought of that “half-gallon” of ice cream you know is in the freezer. Resisting this impulse requires self-control: you must deny this biological imperative/response too.

A similar type of behavior modification is involved in proactively understanding that 1) if a small VLC meal satiates your hunger, you should be satisfied and thus learn to eat it and no more. Similarly, if you are not hungry for 5 or 6 hours after a small VLC meal, 2) you should learn that you do not need to eat a between-meal snack. I have learned these two lessons during 10 years of eating VLC and found it easy to apply them. Small meals and no snacks. Let me illustrate:

For 10 years I have been eating a breakfast of 2 fried eggs, 2 strips of bacon and a cup of coffee with half and half and artificial sweetener. It is about 6 grams of carbohydrate (2 eggs = 1, 2 Splenda = 2, and 2oz H&H = 3). It is mostly protein and fat (21g protein; 27g fat). Total calories: about 350. Believe it or not, this small meal is good for 6 or 8 hours!

However, for lunch I have a can of sardines eaten from the can: 13g protein, 24g fat and zero (0) grams of carbohydrate. Calories, including the olive oil in the can: 270. If I have a beverage, it is either a glass of water or diet ice tea. I eat this meal approximately 5 hours after breakfast not because I am hungry (I am not), but because I want to eat some protein (with some fat) at lunchtime to prevent my muscle protein from being used for energy. Because I am not eating carbohydrates for energy, none are stored and dietary protein and fat are needed with each meal as energy sources.

Dinner is likewise mostly protein and fat; however, it is still just a “smallish” serving of protein plus a non-starchy vegetable (carb) tossed in butter or roasted in olive oil (fat). Alternately, I sometimes eat a salad with vinaigrette dressing. Together, the three meals combined are about 1,200 calories, 75g protein, 90g fat and 20g of carbohydrate. This meal plan is about 25% protein, 70% fat and 5% carbohydrate. And all of these meals are small and very satisfying. © Dan Brown 10/7/12