Saturday, January 26, 2013

Ebony - Man fasts 4 months, loses 180 lbs.

Ebony - Google Books

JAMA Network | JAMA | Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal WomenThe A TO Z Weight Loss Study: A Randomized Trial

JAMA Network | JAMA | Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal WomenThe A TO Z Weight Loss Study: A Randomized Trial

Context  Popular diets, particularly those low in carbohydrates, have challenged current recommendations advising a low-fat, high-carbohydrate diet for weight loss. Potential benefits and risks have not been tested adequately.
Objective  To compare 4 weight-loss diets representing a spectrum of low to high carbohydrate intake for effects on weight loss and related metabolic variables.
Design, Setting, and Participants  Twelve-month randomized trial conducted in the United States from February 2003 to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic, premenopausal women.
Intervention  Participants were randomly assigned to follow the Atkins (n = 77), Zone (n = 79), LEARN (n = 79), or Ornish (n = 76) diets and received weekly instruction for 2 months, then an additional 10-month follow-up.
Main Outcome Measures  Weight loss at 12 months was the primary outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and non–high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure. Outcomes were assessed at months 0, 2, 6, and 12. The Tukey studentized range test was used to adjust for multiple testing.
Results  Weight loss was greater for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month weight loss was significantly different between the Atkins and Zone diets (P<.05). Mean 12-month weight loss was as follows: Atkins, −4.7 kg (95% confidence interval [CI], −6.3 to −3.1 kg), Zone, −1.6 kg (95% CI, −2.8 to −0.4 kg), LEARN, −2.6 kg (−3.8 to −1.3 kg), and Ornish, −2.2 kg (−3.6 to −0.8 kg). Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months, secondary outcomes for the Atkins group were comparable with or more favorable than the other diet groups.
Conclusions  In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight and experienced more favorable overall metabolic effects at 12 months than women assigned to follow the Zone, Ornish, or LEARN diets. While questions remain about long-term effects and mechanisms, a low-carbohydrate, high-protein, high-fat diet may be considered a feasible alternative recommendation for weight loss.

Paleolithic diets: Should we eat like our ancestors? | PCC Natural Markets

Paleolithic diets: Should we eat like our ancestors? | PCC Natural Markets

By the time modern humans emerged roughly 50,000 years ago, our ancestors had adopted an omnivorous diet of cooked starches, meats (including organs), nuts, fruit and other plant foods. Although very few hunter-gatherer groups survive today, we know they eat a wide range of diets, from the nut-based diet of the African !Kung, and the palm starch diet of New Guinean hunter-gatherers, to the meat- and fat-rich diet of the Arctic Inuit.

As Michael Pollan writes in "Food Rules," "There is no single, ideal human diet."

Modern hunter-gatherer diets, however, tend to have certain things in common. They don't rely heavily on foods that became dominant after the development of agriculture, including dairy, grains and legumes. Starch comes from root vegetables similar to sweet potatoes, potatoes and taro. But most important, they do not eat industrial, processed foods. Other aspects of lifestyle, such as physical activity, also differ from industrialized populations.
Modern research

A small group of researchers is beginning to test the idea that pre-agricultural "Paleolithic" diets might hold the key to improving modern human health. Dr. Lindeberg and his colleagues have conducted two remarkable clinical trials.

In the first, they recruited diabetic and pre-diabetic volunteers with heart disease and placed them on one of two diets: 1) a "Paleolithic" diet, focused on lean meat, fish, fruit, vegetables, starchy root vegetables, eggs and nuts, or 2) a "Mediterranean" diet focused on whole grains, low-fat dairy, vegetables, fruit, fish, oils and margarine. Over the 12-week study period, the Mediterranean group lost body fat and enjoyed an improvement in markers of diabetes. Of nine participants with diabetic blood sugar levels at the beginning of the study, four had normal levels by the end.

Those in the Paleo group fared significantly better. They lost 70 percent more body fat than the Mediterranean group and experienced a remarkable normalization of blood sugar. All 10 participants with diabetic blood sugar levels at baseline reached non-diabetic levels by the end of the study. It's important to note that the volunteers in Dr. Lindeberg's study were mild, early cases of diabetes. A second study of long-term diabetics showed that a Paleo diet did not cure them but it did improve their condition significantly.

Should we all eat a hunter-gatherer diet? Not necessarily. Human evolution did not end with the Paleolithic era. Each person carries a particular set of genetic adaptations that result from the unique dietary environment of his own ancestors, so it's important to emphasize that traditionally prepared grains, legumes and dairy can be healthy foods for many people.

Stephan Guyenet is an obesity researcher at the University of Washington. Visit his blog,, to read more of his writing on nutrition and health.

Stephan is also a big proponent of the palatability school of low carb, and had a big debate with Taubes about that. Taubes focuses mostly on the role of insulin in hunger and fat deposition. Richard at free the animal is eating the potatoes because of (in part) what he learned from Stephan- that we overeat certain foods because they are nutritionally dense and taste good. So when we low carb, we also avoid most of the worst foods like cake and sweets, which we are prone to overeat anyways, because they taste awesome. The low carb diet is blander and less likely to make us binge. But we could achieve a similar effect with a bland yet nutritious food like potatoes. Now whether a starchy vegetable has the same health impact as meat is another question. But I think the ideas of Stephen and Richard are a pushback against the super extreme ketogenic zero carb wing of the low carb movement. So living in fear of healthy carbs is wrong, just as the low fat people, during their age, told us that as long as we cut out fat (the more extremely the better- Ornish), we would have great health and lose weight.

Fat Head - Why We Get Fat: Interview With Gary Taubes

Fat Head Why We Get Fat: Interview With Gary Taubes

Fat Head: Dr. Robert Lustig insists it’s fructose that makes us insulin resistant, not starchy foods. If he’s right, then it was the Coca-Cola and Captain Crunch that turned me into a fat kid, not the mashed potatoes. But as an adult, I’ve avoided sugar yet found that starches most definitely make me gain weight. So assuming for the sake of argument that Lustig is correct, would you say that once fructose has done the damage, we lose our tolerance for carbohydrates in general? If so, why?

Gary Taubes: That’s exactly the possibility I’m discussing. Once you become insulin resistant, your body responds to carbs by secreting more insulin. So it is quite possible — and laboratory work backs this up — that sugar causes the initial insulin resistance because of the effect of the fructose on the liver. So if we never had sugar, we’d be able to eat the other carbs with relative impunity. But being possible doesn’t mean it’s true. I suspect it is, but I’m not sure exactly how this can be tested.

And I agree with you: the world is full of obese and diabetic people who know enough not to eat sugar, but remain obese and diabetic. I could avoid sugar and go back to eating starches and put on 20 pounds of fat effortlessly. I’ve done it in the past — distant past. So I don’t buy the idea that avoiding sugar is enough to make an obese person lean again. And the people I know who believe that all tend to be somewhat plump despite their beliefs. In fact, I recently heard Dr. Lustig give a talk in San Francisco, and he acknowledged that he still has a weight problem, but doesn’t know what to do about it. Hmmm….

Fat Head: Have you come across any evidence that starches can turn people into fat diabetics without fructose being part of the diet?

Gary Taubes: It’s tricky. Typically consumption of sugar, white flour and starchy vegetables all tend to go hand-in-hand. So it’s hard to tease out this one. I suspect beer could, but I don’t know if even beer drinkers who don’t eat sugar tend to become diabetic or not. What we’d need is a population of white-flour eaters who didn’t eat any sugar at all. If we could find such a thing, naturally, then we’d have some idea.


Fat Head: In Why We Get Fat, you wrote that some people might have to give up dairy products and nuts to lose weight. Dr. Mike Eades has also mentioned that nuts and cheese seem to inhibit weight loss in some low-carb dieters. What is it about those foods that can stall weight loss? Is it just that they’re so calorically dense, or do they produce a higher insulin response than their low carbohydrate content would suggest?

Gary Taubes: I think the caloric density thing is nonsense. Remember, I’m trying to get every last one of us away from thinking in terms of calories as the variable of interest. What we want to know is whether these foods stimulate insulin secretion, or cause insulin resistance, or have some other effect on the storage of fat in the fat tissue or the oxidation of fatty acids by other tissues in the body. So nuts still have carbs in them, and for some people they might contain too many carbs. Same is true for nut butters.

Dairy products can stimulate insulin secretion beyond what you would expect from the carbohydrate content. I don’t know if this is true of cheese because I’ve never seen data on this, but it is possible. And some cheeses could be better than others — hard cheeses, for instance, may be better than soft cheeses.


Fat Head: You wrote something in Why We Get Fat that I think every frustrated dieter needs to hear: the proper diet will help us become as lean as we can be, but not necessarily as lean as we’d like to be. Once we become fat, is there a limit to how much fat we can lose without starving away our lean tissue? If so, what’s the barrier to mobilizing and burning those last 10 or 20 pounds of excess fat?

Gary Taubes: Simple answer, I don’t know. But it’s obvious that not every woman can have the body of an Angelina Jolie, regardless of how few carbs they eat. And not every man can have the body or the body-fat percentage of, I don’t know, a Matthew McConaughey, one of these actors who’s always taking his shirt off in movies.

That’s for starters. Some of us are wired to have more body fat than others from the get-go. Then I think when we grow up in a carb-rich environment, some degree of chronic damage is done to the way we partition fuel. Maybe our muscle tissue never quite loses its insulin resistance, or our fat tissue remains more insulin sensitive than it would be had we never seen carbs. Maybe our pancreas secretes a little too much insulin.

It’s hard to tell, but the way I describe it is this: if I grew up in a hunter-gatherer environment — and my mother did as well, because there are effects that are passed from mother to child through the uterus — I’d probably weigh around 175 pounds, even as an adult. Had I stopped eating carbs in my late teens, I might naturally weigh about 190 or 200, which was my football weight in high school. The fact that I not only kept eating carbohydrates into my forties but gorged on them during the low-fat, you-can’t-get-fat-if-a-food-doesn’t-have-fat-in-it years of the late 1980s and early 1990s means the best I can do now, even eating virtually no carbs at all, is about 220. And there’s nothing I can do to go lower, short of starving myself. Semi-starving myself doesn’t work. I tried that long ago.

Fat Head: So what’s the message for those people? Lose what you can and focus on being healthy, as opposed to obsessing with squeezing into a size-8 dress?

Gary Taubes: Precisely.

Fat Head: One of the anti-Taubes articles going around the internet claims that we don’t need insulin to store fat, and that insulin is an appetite suppressant. Can we store any significant amount of fat without insulin? If so, why do untreated type 1 diabetics waste away?

Gary Taubes: Short answer, probably not. We don’t need insulin to burn glucose for fuel, but if we don’t have insulin, we don’t store fat.

Fat Head: In Why We Get Fat, you also stated that elevated insulin in the brain suppresses appetite. Since so many obese people have high levels of circulating insulin, why aren’t their appetites suppressed? Is there a difference between the effects of insulin in the brain and insulin in the bloodstream?

Gary Taubes: That’s the key point. A few years ago I was interviewing the director of the Joslin Diabetes Center, and I asked him what the role of insulin was in obesity, and he said its role was to suppress appetite in the brain. And it does. Three researchers at the University of Washington spent 10 to 15 years trying to convince people that insulin had this role. They had injected insulin into the cerebral spinal fluid of primates and it did indeed suppress appetite.

The problem is these people succeeded so well in their crusade that the rest of the community — this guy at the Joslin among them — simply forgot about what insulin does in the body, which is to promote fat accumulation and energy storage. And it makes perfect sense that a hormone that responds to eating will work to store fuel in the body while it also works, secondarily, to tell the brain that fuel is coming in and eating can cease in a bit. That’s the kind of feedback loop you find all over homeostatic systems. But the fundamental issue is that in the body, insulin promotes fat accumulation and that’s where the problem is.

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets1,2,3

Carol S Johnston,
Sherrie L Tjonn,
Pamela D Swan,
Andrea White,
Heather Hutchins, and
Barry Sears

+ Author Affiliations

1From the Department of Nutrition, Arizona State University, Mesa, AZ (CSJ, PDS, and AW); Conscious Cuisine, Scottsdale, AZ (SLT); and Inflammation Research Foundation, Marblehead, MA (HH and BS)


Background:Low-carbohydrate diets may promote greater weight loss than does the conventional low-fat, high-carbohydrate diet.

Objective:We compared weight loss and biomarker change in adults adhering to a ketogenic low-carbohydrate (KLC) diet or a nonketogenic low-carbohydrate (NLC) diet.

Design:Twenty adults [body mass index (in kg/m2): 34.4 ± 1.0] were randomly assigned to the KLC (60% of energy as fat, beginning with ≈5% of energy as carbohydrate) or NLC (30% of energy as fat; ≈40% of energy as carbohydrate) diet. During the 6-wk trial, participants were sedentary, and 24-h intakes were strictly controlled.

Results:Mean (±SE) weight losses (6.3 ± 0.6 and 7.2 ± 0.8 kg in KLC and NLC dieters, respectively; P = 0.324) and fat losses (3.4 and 5.5 kg in KLC and NLC dieters, respectively; P = 0.111) did not differ significantly by group after 6 wk. Blood β-hydroxybutyrate in the KLC dieters was 3.6 times that in the NLC dieters at week 2 (P = 0.018), and LDL cholesterol was directly correlated with blood β-hydroxybutyrate (r = 0.297, P = 0.025). Overall, insulin sensitivity and resting energy expenditure increased and serum γ-glutamyltransferase concentrations decreased in both diet groups during the 6-wk trial (P < 0.05). However, inflammatory risk (arachidonic acid:eicosapentaenoic acid ratios in plasma phospholipids) and perceptions of vigor were more adversely affected by the KLC than by the NLC diet. Conclusions:KLC and NLC diets were equally effective in reducing body weight and insulin resistance, but the KLC diet was associated with several adverse metabolic and emotional effects. The use of ketogenic diets for weight loss is not warranted. I've been reading Phinney's books on ketogenic diets for weight loss and athletic performance. Also reviewing the A to Z study in which Atkins beat out Barry Sears The Zone diet, which allows more carbs. This study seems to exonerate the Zone approach, allowing more carbs. I suspect each of us, for genetic reasons, or because of our current state of health, has different requirements or tolerances for, carbohydrate. I have also been thinking about the Lustig/Taubes combo, that perhaps glucose ain't so bad, until the fructose damages our liver and makes us insulin resistant. If so, some of us with bad IR, diabetes or heart failure may be unable to tolerate carbs well at all. The original Atkins diet had the right idea, perhaps. Drastically cut carbs to 20g a day until you lose the weight you want (or can reasonably expect) to lose, then slowly add carbs to find the level at which you start to add weight.

I also find myself finding more truth in the "calories DO count" school of thought. Insulin probably does encourage fat deposition. It definitely increases hunger. But study after study also shows that free feeding of protein and fat causes people to voluntarily eat less. If that's the beginning and end of what low carb can do, that's pretty damn good, especially if you add in the other positive health benefits. We've gone to far if we suggest unlimited amounts of fat and protein can be consumed with no weight gain. Still putting all the pieces together and learning new things about low carb, even after first doing it 15 years ago!

Synthesis: Low-Carb and Food Reward/Palatability, and Why Calories Count | Free The Animal

Synthesis: Low-Carb and Food Reward/Palatability, and Why Calories Count | Free The Animal

What's the distinction? Food Reward & Palatability is the short answer. Again, I'll get to that in more depth later. First, let me ask you a few questions, aimed at LC/Paleo, or Plain Vanilla LC.

Do you find it pretty easy to draw a distinction between say, a free range, organically fed whole turkey you bake in the oven, and supermarket turkey franks with a side helping of "animal by-products," hormones, fillers, texture enhancers, preservatives, nitrites, added sodium, coloring, and cruelty...that you nuke?
Additionally, do you find it easy to draw a distinction between say, leaf lard from a pastured pig that gets lots of time in the sunshine, and industrially processed, extracted, heated, churned, & turned, deodorized and left out to dry soy a plastic container?
Yes and yes? OK, then how come you find it so difficult to draw a distinction between a loaf of Wonder Bread in a wrapper, and 5 pounds of potatoes straight & dirty from your organic farmer's your door?

So have I abandoned low-carb? Not exactly. Do I think it's effective? Yes, in a limited capacity for some...even most who are substantially overweight or obese, or where otherwise, it just fits with any individual's lifestyle of work & play and they feel great and have good results naturally (I'm leaving diabetics out of this post as outliers). Do I think it's the best approach for fat loss? It depends on the individual. Why does it depend? Food Reward/Palatability shakes out individually, likely on a Bell Curve distribution, that's why.

Here's how I think it works in general.

You're fat. You go low carb per se. You lose water weight because liver and muscle glycogen is being depleted. This is very motivational; or, rewarding, even "palatable." So you continue on. By virtue of blanket LC, you're excluding highly rewarding and palatable fast food, pizza, pasta, ice cream, sugar drinks, Hot Pockets, and all the other crap in favor of meat, veggies, nuts, cheese, and maybe some LC junk food if that's your thang. Yea, it's great to eat red meat again, and while some can pack away 16oz ribeye steaks one after the other, most can't. They're satisfied, and satisfied sooner, with less caloric intake, more often. It subtracts down. They lose weight. Was LC effective? Yes. Why? Food reward/palatability. And because calories count.
The problem is that while a few get all the way to ripped leanness this way, huge numbers don't (including me), and that's why LC and LC/Paleo have not only to recruit the new and uniformed (do keep it going, Jimmy & Co.), but have growing numbers amongst adherents who range from slightly disillusioned to royally pissed off...because they can't get rid of that last 10-20 pounds...or more, in some cases.
In various degrees of frustration and despair, you console yourself with the various cheats—from foods you love and have missed—that got you fat before. But you're smarter this time around, see? You don't toss the baby out with the bathwater. Rather, you "cover" or redeem your indiscretions at the drive through and freezer section with bouts of zero to very low carb over days, and manage to eek out some sort of a homeostasis—maintaining your moderately overweight composition. Or, in many cases, LC as you practice it ceases to be effective in shedding any more fat—even without drive through, freezer section, or Jamba Juice excursions.
This is not necessarily an altogether bad thing. Better than really fat or obese.

So how do we take the next step, beyond the huge value LC had been to get off that initial 40, 50, 60, 80, 160, 320 pounds (60 in my case)? We recognize that it wasn't really any magic about LC that got us there. LC simply, effectively, lowered our food reward/palatability and as a consequence, we spontaneously lowered our average daily intake of calories.

Calories count.

Richard is eating 400 calories of potatoes a day as part of his latest challenge. Bland yet nutritious. Always new ideas in the paleo world, hard to keep up sometimes.

JAMA Network | JAMA Internal Medicine | Therapeutic Fasting in Morbid ObesityLong-term Follow-up

JAMA Network | JAMA Internal Medicine | Therapeutic Fasting in Morbid ObesityLong-term Follow-up


The weights of 207 morbidly obese patients were reduced via prolonged fasting. Half the patients fasted for close to two months, losing a mean of 28.2 kg; one fourth fasted for less than one month; and the other fourth fasted for more than two months, with a mean 41.4-kg loss. This latter group was heavier initially, and more than 50% attained near-normal weight. Patients with onset of obesity in childhood had the lowest tolerance for fasting and the lowest success rate in attaining normal weight. Over a 7.3-year follow-up period in 121 patients, the reduced weight was maintained for the first 12 to 18 months. Subsequently, regain proceeded equally in all groups irrespective of length of fast, extent of weight loss, or age at onset of obesity. Regain to original weight occurred in 50% within two to three years and only seven patients remained at their reduced weights. Regain to greater than original weight was more common in childhoodonset obesity.

(Arch Intern Med 137:1381-1382, 1977)
Daisie Johnson; Ernst J. Drenick, MD

Influence of fasting and refeeding on Body Composition

Article by Dr. Drenick on the patients he fasted. Take away, muscle was lost in small amounts, but obese people have more muscle to begin with to support their large frames, so protein loss is not a burning issue.

LIFE - Google Books The zero calorie diet- a 315lb patient eats nothing for 117 days

LIFE - Google Books

Page 105, the zero calorie diet. Article about Dr. Drenick fasting patients in 1968. "The zero calorie diet- a 315lb patient eats nothing for 117 days"

Friday, January 11, 2013

DNA pioneer James Watson takes aim at cancer establishments and antioxidants

DNA pioneer James Watson takes aim at cancer establishments | Reuters

One such commonality is oxygen radicals. Those forms of oxygen rip apart other components of cells, such as DNA. That is why antioxidants, which have become near-ubiquitous additives in grocery foods from snack bars to soda, are thought to be healthful: they mop up damaging oxygen radicals.

That simple picture becomes more complicated, however, once cancer is present. Radiation therapy and many chemotherapies kill cancer cells by generating oxygen radicals, which trigger cell suicide. If a cancer patient is binging on berries and other antioxidants, it can actually keep therapies from working, Watson proposed.

"Everyone thought antioxidants were great," he said. "But I'm saying they can prevent us from killing cancer cells."


Research backs him up. A number of studies have shown that taking antioxidants such as vitamin E do not reduce the risk of cancer but can actually increase it, and can even shorten life. But drugs that block antioxidants - "anti-antioxidants" - might make even existing cancer drugs more effective.

Anything that keeps cancer cells full of oxygen radicals "is likely an important component of any effective treatment," said cancer biologist Robert Benezra of Sloan-Kettering.

Sunday, January 06, 2013

Profits over your dead body | Ars Technica

Profits over your dead body | Ars Technica:

Profits over your dead body
Health regulatory and advocacy groups are deliberately corrupted.

Now, the conspiracy minded among you might be thinking of cartoon villains covering up dastardly poison pills, but this is not actually the case. Ben Goldacre, a physician who writes the Bad Science blog, has now made a comprehensive catalog of these practices published in a book called Bad Pharma. In examining the healthcare industry, he paints a complicated picture in which almost all the actors are both bad guys and good guys. It can be read as a stinging rebuke, but more than anything it's criticism from someone who appreciates everything modern medicine has done—but wants to see it do even better.

Thursday, January 03, 2013

Appetite Heightened By Ingestion Of Fructose - Health News - redOrbit

Appetite Heightened By Ingestion Of Fructose - Health News - redOrbit

A new study from Yale University School of Medicine examines possible factors regarding the association between fructose consumption and weight gain.

The researchers used brain magnetic resonance imaging, which indicated that ingestion of glucose but not fructose reduces cerebral blood flow. Activity in brain regions that regulate appetite was also reduced. The participants reported an increase in feeling sated and full from the ingestion of glucose but not fructose.

“Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance. Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety,” according to the authors. “Thus, fructose possibly increases food-seeking behavior and increases food intake.”