Gary Taubes responds
A couple of weeks ago I posted that Gary Taubes had agree to answer questions from readers of this blog. Over a hundred readers sent in questions through the comment section. Many of these questions were actually multiple questions, so Gary ended up with probably 200+ questions to deal with.
I’ve gone through and compiled a list of the most common questions and presented them to Gary. Here are the questions followed by his responses.
The most commonly asked question was how do Asians and others living a seemingly high-carb existence manage to escape the consequences?
The Asian question first. I do address this in the book and I address it again in the afterward of the paperback. There are several variables we have to consider with any diet/health interaction. Not just the fat content and carb content, but the refinement of the carbs, the fructose content (in HFCS and sucrose primarily) and how long they’ve had to adapt to the refined carbs and sugars in the diet. In the case of Japan, for instance, the bulk of the population consumed brown rice rather than white until only recently, say the last 50 years. White rice is labor intensive and if you’re poor, you’re eating the unrefined rice, at least until machine refining became widely available. The more important issue, though, is the fructose. China, Japan, Korea, until very recently consumed exceedingly little sugar (sucrose). In the 1960s, when Keys was doing the Seven Countries Study and blaming the absence of heart disease in the Japanese on low-fat diets, their sugar consumption, on average, was around 40 pounds a year, or what the Americans and British were eating a century earlier. In the China Study, which is often evoked as refutation of the carb/insulin hypothesis, the Chinese ate virtually no sugar. In fact, sugar consumption wasn’t even measured in the study because it was so low. The full report of the study runs to 800 pages and there are only a couple of mentions of sugar. If I remember correctly (I don’t have my files with me at the moment) it was a few pounds per year. The point is that when researchers look at traditional populations eating their traditional diets — whether in rural China, Japan, the Kitava study in the South Pacific, Africa, etc — and find relatively low levels of heart disease, obesity and diabetes compared to urban/westernized societies, they’re inevitably looking at populations that eat relatively little or no refined carbs and sugar compared to populations that eat a lot. Some of these traditional populations ate high-fat diets (the Inuit, plains Indians, pastoralists like the Masai, the Tokelauans); some ate relatively low-fat diets (agriculturalists like the Hunza, the Japanese, etc.), but the common denominator was the relative absence of sugar and/or refined carbs. So the simplest possible hypothesis to explain the health of these populations is that they don’t eat these particularly poor quality carbohydrates, not that they did or did not eat high fat diets. Now the fact that some of these populations do have relatively high carb diets suggests that it’s the sugar that is the fundamental problem. Ultimately we can only guess at causes using this kind of observational evidence. To know anything with certainty we’d need the kind of randomized controlled trials I yearn for in the epilogue of GCBC.
What is your opinion on leptin in the grand scheme of obesity and fat storage?
I mostly ignore leptin in the book because I think leptin is primarily a signaling molecule and so a downstream effect. In other words, leptin is secreted from the fat cells; it doesn’t regulate directly the amount of fat that accumulates. Moreover, if the primary regulator of fat storage is insulin, which it is, and leptin is secreted in proportion to the amount of fat stored, which it is, then insulin has to regulate leptin.
Where leptin may play a primary role is in the liver. A few years ago Jeff Friedman of Rockefeller University published an article in Science showing that leptin down-regulates SCD-1 in the liver (the only place they looked), which worked in turn to increase oxidation of fatty acids. This makes sense homeostatically: if leptin is released in proportion to the fat accumulated then it is a signal of how much fat we have in reserve. So long as the mitochondria in our lean tissue and organs know that we have fat in reserve, they can continue to burn it without fear of systems failure should they run out of fuel completely. Leptin resistance would then work, like insulin resistance, to make us burn less fat and store more, while the rest of the body would have to rely on carbohydrates (blood sugar) for fuel.
In general, though, I’m interested in the cause of obesity and I don’t think discussing leptin adds much. Here’s what I say about this issue in afterward of the paperback edition of GCBC:
“Another variation on the can’t-possibly-be-so-simple argument that I have heard frequently since Good Calories, Bad Calories was published is the molecular biology theme. The last fifteen years, since the discovery of the hormone leptin in 1994, has seen obesity research become a sub-discipline of molecular biology. As a result, a search of the keyword “obesity” in the National Library of Medicine database will now identify over 100,000 relevant articles in the professional journals (nearly 20,000 review articles alone), a large proportion of which focus on the fruits of molecular biology research and the science of genomics.: It’s a burgeoning field with a cast of thousands, including the role of obesity-related gene variations known technically as polymorphisms, of signaling molecules with names like adiponectin, leptin and grhelin, of the receptors for those signaling molecules and the inhibitors for those molecules and inhibitors of the inhibitors, and so on. The obvious question is how can this research be so extraordinarily fruitful, and yet mostly irrelevant to the cause of obesity? It’s hard to imagine it’s not, and so, as I’ve frequently been told, any discussion of the cause of obesity that doesn’t discuss these molecules, receptors, inhibitors, etc. must be considered amateurish and woefully inadequate. The truth must be complicated.
“Again the counter-argument seems itself simple and straightforward: if you’re hit over the head with a hammer, it will cause both pain and inflammation. The mechanisms of pain and inflammation have also yielded up a wealth of knowledge to the tools efforts of the molecular biologists. These physiological phenomena are understood to be mediated via signaling pathways and molecules (in this case, prostaglandins, tumor-necrosis factors, etc.) that emerge in response to the damage done. The more researchers learn about these responses and the molecules involved, the more complex the pathway from hammer to pain and inflammation to healing will appear. But the relevant fact to all those immediately involved is that both the pain and ensuing inflammation were caused by the hammer and perhaps the person who swung it. Everything else is downstream and may be relevant only to the question of which drugs will best deal with the pain and perhaps accelerate the healing process. “
A number of questioners asked why you think it is more difficult to lose weight the second or third time around on a low-carb diet? And why it seems more difficult to lose on low-carb with increasing age?
I’m curious whether this is in fact true. Another possibility is that it’s more difficult to lose weight on low-carb as we get older; that the carbs effectively do chronic damage to our tissue and so the longer we’ve been overweight or obese, the harder it is to lose weight. I can imagine a scenario in which the fat tissue becomes hypersensitive to the insulin we secrete, or the pancreas becomes hypersensitive to the carbs and secretes even more insulin, or the insulin resistance in the lean tissue becomes less tractable, and so the longer we remain fat, the more our fat tissue compensates when we restrict carbs. It’s also possible that repeated low carb dieting somehow exacerbates this process, but I’d want to see definitive studies (and on all this speculation) before I believed it.
Several people asked for a comment on any important studies that you may have left out of GCBC.
The issue isn’t leaving out studies so much as not wanting to get into the he-said, she-said game of quoting particular studies that support my preconceptions. In this business, you can always find studies that support a particular hypothesis, or at least seem to if you selectively interpret the data. So when I had to make a point about the efficacy of a particular treatment — exercise, for instance, or semi-starvation diets — used meta-analyses or Cochrane Collaboration systematic reviews, which are designed to minimize author bias, to make the general points. When I discussed the saturated fat/cholesterol/heart disease hypothesis in the first few chapters, I did indeed mention virtually every study and certainly every meaningful clinical trial, because I knew if I left anything out I would be accused of cherry picking the data (which, of course, I was anyway). I did omit much of the observational epidemiology on the nature of a healthy diet because I find it meaningless and impossible to interpret correctly, in part for the reasons I discussed above about the Asian diet issue.
When I cut the book down from the initial 400,000 word unfinished draft, a lot of what was removed were indeed the counter- and counter-counter arguments. For instance, obesity researchers will argue that obesity causes hyperinsulinemia, not the other way around. That way they can still say that obesity is caused by over-eating and once we get fat, that causes insulin resistance and jacks up insulin levels. I spent, literally, months writing a lengthy section explaining how this view came about and what the evidence actually did and did not demonstrate. Then when I realized the book had to shrink dramatically, and with the benefit of sage advice from my editor, I decided that it was unnecessary to explain why the mainstream researchers would disagree with my take and then spend yet more space explaining why they were wrong to disagree. One thing I did cut from the book that I regret was a section linking gout to fructose and uric acid, and discussing the history of gout and how it’s frequency in populations and socioeconomic groups paralleled the spread of sugar. Nobody had ever made that point before and I wanted to make it, considering that people have been speculating on what aspect of diet or lifestyle causes gout back to Hippocrates. Still, my friends rightly argued that when your book is a few hundred thousand words long, you can’t afford to keep a section about gout, even if a lot of people get gout these days and, of course, they’re more likely to get it if they’re overweight or obese. Along these lines Dan Harrington asked why his gout goes away on the Atkins diet and that’s my answer: no sugar, primarily, means no fructose and so no fructose-induced hyperuricemia. In other words, fructose raises uric acid levels and gout is caused by the elevated uric acid in the blood stream.
It is true that you can find studies in the literature that seem to contradict the hypotheses in GCBC but are not mentioned in the book, When Gina Kolata reviewed my book in the NY Times, she evoked a study by Jules Hirsch and Rudy Leibel, then both at Rockefeller, suggesting that nutrient composition of the diet has no effect on weight. As I explained in a letter to the Times, the study failed to refute the carbohydrate/insulin hypothesis of weight regulation for a variety of reasons — the subjects, for instance, could have gained as much as 15 pounds a year on one particular diet composition but not another, and the study would not have detected it. And the subjects, almost exclusively, were lean middle-aged individuals. What we’re interested in here, though, is why why people predisposed to obesity get fat, and that may not be something you can study in people who have remained lean into their 40s and 50s. Would Leibel and Hirsch have obtained a different result if they had used, say, obese subjects who had first been slimmed down by some kind of diet (Atkins or a starvation diet)? These types of subjects are considered pre-obese, since they’re so highly likely to go back to being obese. And if Leibel and Hirsch had used them, they might have found that they stay relatively lean on a low carb diet and put on weight easily on a high carb diet. Anyway, rather than get into this kind of too-and-fro in the book, I made the decision not to mention these types of ambiguous studies. I would like to think that had there been a single compelling study refuting the hypothesis — or better yet, two, since you’d like to see things replicated in science — I wouldn’t have written a different book.
What you think of a Slow Burn type of exercise and low-carb dieting? Do you still stand by your notion that exercise doesn’t help people lose weight?
I haven’t looked into the science behind slow burn exercise (although I know Mike has) but I now do it regularly (with Fred Hahn in Manhattan at Mike’s recommendation) and it seems to be helping my lower back pain immensely. I can let you know next spring whether it helps my softball game, where my ability to hit with power has been deteriorating sadly with the advancing years. What fascinates me about it is the weird confluence of the desire for self-improvement with what seems to be deep-set sadomasochistic tendencies. It’s torture when you do it, and then you look forward to going back.
As for exercise, I do not believe that it causes long-term fat loss. I think it might be helpful in a weight loss program only because it gives you a kind of positive feedback that dieting per se does not. You can feel good after a work-out, while it’s hard to feel too good after a meal that didn’t include either the calories or the carbohydrates you preferred. On the other hand, since it does make you hungry — work up an appetite — I worry whether for some or even most people the psychological benefits could be counterbalanced by the drive to consume even more calories than you might have expended during the work-out.
Are you familiar with the work of Dr. Jan Kwasniewski, and, if so, what do you think of it?
I am not.
What kind of response have you gotten from the medical/scientific community about GCBC?
In general, I think it’s safe to say that I’ve been ignored. If obesity researchers have read the book, they haven’t bothered to tell me. When GCBC was published we sent out 150 copies to obesity researchers, authors of obesity task force reports, foundations that fund obesity research, everyone at NIH who funds obesity research, etc. etc. I heard back from 3 or 4 thanking me for sending them the book. Two followed up to tell me they had read it. Some later told me outright that they didn’t have the time to read a 500 page book, and particularly so when they already know what I think because of the 2002 NYT Magazine article and don’t particularly agree. That said, I may be making some progress in getting people to pay attention.
Whenever I do hear from someone who is sympathetic, I ask them to try to set up a lecture at their institution. Often I ask them to contact other researchers they might know and get me lecturers at those institutions. Through this kind of networking, I’ve been invited to lecture at some of the more influential obesity research centers and at least some of those people have taken my arguments seriously. A few months ago, I heard from some contacts at the NIH, that I might be invited down to lecture to the nutrition coordinating committee at NIH, which would be a big step forward, but the fact that I haven’t heard anything since then (August) makes me pessimistic.
When I do give these lectures a common response that I get from nutritionists and obesity researchers, and one that I find profoundly disturbing, is that they find what I say interesting but don’t see it as anything they should think about further. In other words, they have their schtick (as my wife, an almost-academic calls it); whatever research they get their funding to pursue, and even though in theory we’re all in this to cure and prevent obesity and chronic diseases, their schtick may have nothing to do with my schtick. If they’re studying, say, genetic strains of obese rats or questionnaires to improve the accuracy of diet assessment in epidemiologic studies, what does that have to do with my argument that obesity is caused by carbohydrates? So they listen politely, ask a few intelligent questions (in an ideal world) and then go back to their research, because that’s how they make a living. They don’t say to themselves, I’m going to read Taubes’s book and, if I find it compelling, switch my research over to studying the efficacy of carbohydrate restriction. And even if they did, they wouldn’t get funding to do so because they’d have no track record in that field.
So, bottom line, at the moment is that I know of a handful, maybe as many as a dozen researchers, who find the arguments in the book compelling and are doing what they can, in their limited spare time, to help get the message out and maybe get us to the place where the hypotheses are taken seriously and are rigorously tested. The rest either don’t care or don’t know GCBC even exists or just think what I say is wrong and so not worth further discussion, either because they read the book or some of it and think its crap or because they think its crap based solely on what they know about me or heard about the book and so don’t have to read it.
What’s next? Another book?
What am I doing next? As suggested by many readers, I am going to write a short, easy-to-read version of the weight section of GCBC. It won’t be a diet book — no recipes — but it will be far more of a self-help book than GCBC. I might also do a weightier (no pun intended) serious investigation into the sugar and corn syrup industries; their history, political influence, lobbying, etc — that would be interwoven with a more intensive look at the potential health effects of sugar and HFCS and fructose particularly. The first book will definitely be done; the second depends on getting the funding to do so. I’d also like to get back to straight science writing for a while, since I do enjoy writing about good science, which is how I started my career, and it would be a pleasant change from the mainstream nutrition and health nonsense.
How about a blog?
As for a blog, I just haven’t got the time at the moment, although I always hope that that will change in the future.
Many wrote that GCBC had changed their lives. Can you think of a book that has changed your life?
Did any books change my life? Yes, All the President’s Men, by Woodward and Bernstein. I read it in my last year of college or my first year of graduate school and it made me decide that I wanted to be an investigative reporter rather than go to business or law school, which was the direction I seemed to be headed.
What do you know about Dr. Simeon’s HCG protocol?
Mostly nothing.
What led you to the idea that saturated fat doesn’t cause heart disease?
It was a progression of steps. Back in the late 90s, I was reporting a story for Science on the salt-hypertension controversy and one of the worst scientists I ever interviewed (and having written a book about cold fusion, Bad Science, I had interviewed quite a few terrible scientists) took credit not just for getting Americans to eat less salt, but getting them to eat less eggs, meat and butter, too. I literally got off the phone with this guy and called my editor at Science and said, “when I’m done writing about salt, I’m going to do a story on dietary fat. I don’t know what the story is, but if this guy was involved in any substantive way, I know there’s a story to be done.” So that’s what I did. I finished the salt story and then spent a year working on the fat story, which was published in Science.
The story made the point that there was virtually no evidence that a low-fat diet prevented heart disease, but let open a window for saturated fat having some deleterious effect. Then a couple of years later, I was reporting the New York Times Magazine story that would become “What If It’s All A Big Fat Lie?”, when I heard about these five clinical trials comparing low-fat, calorie-restricted diets to Atkins diets. Since the Atkins diet is a high-fat, high saturated fat diet and it improved cholesterol profiles in all these trials, that pretty much clinched it. I’ve been arguing since that these diet trials have to be perceived as tests of the hypothesis that saturated fat is a “bad” fat, although the medical establishment still prefers to ignore that fact.
Is there anything new or updated in the paperback version of GCBC or is it the same as the hardback?
It’s the same as the hardback, but there is a 3000 word (or thereabouts) afterward that’s worth reading.
I tried to come up with a selection of questions that represented the majority of questions asked. I know that some went unanswered, but when Gary agreed to do this I promised him that he wouldn’t have to answer an exhaustive list that would require days of time. So, I’m sorry if any specific question went unanswered, and I hope you understand. Thanks to everyone for the terrific response.
Hello all: This is off topic but just my 2 cents opinion related to eating a lot in this society. I once saw the pastor Joel Osteen critisizing the american diet, and the way people treat food in this society. Pastor Joel Osteen said that there are people in this country that even carry jelly fish, snacks and M & Ms in their pockets or take it to work so that they can snack on something all day. And there is an addiction to food in this society indeed. The only addictions we hear on mainstream media is drug, and alcohol addiction, but, he said that there is an insulin reaction, when people drive around a fast food restaurant and smell french fries. So that’s another cause of weight gain in this society, the anxious addiction toward food. And then there are the holidays coming up which is a *threat* to people of concious eating. I think that the solution for many problems of this society like drug addiction, crimes, obesity, is not only a lifestyle change in the way people eat and live, but also a less isolationist, individualist lifestyle and with a lot more social-relations. Because loneliness, leads to depression and anxiety, and depression and anxiety leads to snacking and compulsive eating in order to fill that *existential vaccum* created by this individualist, lonely way of life.
Here is an article about Holidays Weight-Gain:
Holiday Weight Gain Slight, But May Last A Lifetime
http://www.nichd.nih.gov/news/releases/holidayweightgain.cfm
A new study suggests that Americans probably gain about a pound during the winter holiday season-but this extra weight accumulates through the years and may be a major contributor to obesity later in life.
This finding runs contrary to the popular belief that most people gain from five to ten pounds between Thanksgiving and New Year’s Day.
This conclusion was reached by researchers at the National Institute of Child Health and Human Development (NICHD) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The results of their study appear in the March 23 New England Journal of Medicine. “These findings suggest that developing ways to avoid holiday weight gain may be extremely important for preventing obesity and the diseases associated with it,” said NICHD Director Duane Alexander, M.D.
According to government statistics, more than half of all adult Americans are overweight, as defined by body mass index, said Jack A. Yanovski, M.D., Ph.D., the study’s principal investigator and head of NICHD’s Unit on Growth and Obesity. Body mass index is a mathematical formula used to correct body weight to account for a person’s height. According to Dr. Yanovski, the latest national surveys show that 54.9 percent of Americans have a body mass index of 25 or more and are overweight, while 22.3 percent are considered obese, with a body mass index of 30 or more.
“The prevalence of obesity in the U.S. has increased dramatically over the past decade,” Dr. Yanovski said. “Weight gain during adulthood may contribute to heart disease, diabetes, and other serious health problems.”
“Because losing weight is so difficult, it is important to learn when and why people gain weight so that effective strategies to prevent obesity can be developed, ” said study co-author Susan Z. Yanovski, M.D., Executive Director of NIDDK’s National Task Force on the Treatment and Prevention of Obesity.
Previous studies suggested that Americans gain an average of 0.4 to 1.8 pounds each year during their adult lives, Dr. Yanovski said. It was unknown, however, if people gained weight at a steady rate throughout the year, or just at certain times, such as during the winter holiday season. To find out just how much of this weight increase occurred over the holidays, Dr. Yanovski and his colleagues measured weight and collected other health information from 195 volunteers. These volunteers worked at, or lived near, the NIH campus in Bethesda, MD. The group was racially, ethnically, and socioeconomically diverse. The study’s participants ranged in age from 19 to 82 years, and in weight from 95 to 306 pounds. In all, 51 percent were women, and 49 percent were men. The percentage of volunteeers who were at a healthy weight, were overweight, or were obese was similar to that of the U.S. adult population. All 195 were weighed at six-week intervals before, during, and after the winter holiday season; 165 returned for additional measurements in June and in September, one year after the study began.
Compared to their initial weight in late September or early October, the volunteers gained just over a pound (1.05 lb) by late February or early March. Most of that weight gain (0.8 lb) occurred during the six-week interval between Thanksgiving and New Year’s Day. The researchers asked the volunteers about several factors that might influence weight change, such as stress, hunger, activity level, changes in smoking habits, or number of holiday parties they attended. The researchers found that only two factors influence weight gain: level of hunger and level of activity. Volunteers who said they were much more active or much less hungry since their last clinic visit were the least likely to gain weight over the holidays, and some even lost weight. Those who reported being less active or more hungry had the greatest holiday weight gain.
“The finding that study volunteers reporting more physical activity had less holiday weight gain suggests that increasing physical activity may be an effective method for preventing weight gain during this high-risk time,” Dr. Yanovski said.
The researchers also found that study volunteers believed that they had gained much more weight than they actually had over the holidays, overestimating their weight gain by slightly more than 3 pounds. Fewer than 10 percent of subjects gained more than 5 pounds over the holiday season. However, Dr. Yanovski added, overweight and obese volunteers were more likely to gain five pounds than were those who were not overweight, which suggests that the holiday season may present special risks for those who are already overweight.
“Although an average holiday weight gain of less than a pound may seem unimportant, that weight was not lost over the remainder of the year,” Dr. Yanovski said. When 165 of the study volunteers were weighed a year after the study began, they had not lost the extra weight gained during the holidays, and ended the year a pound and a half heavier (1.4 lb) than they were the year before.
“This is a ‘good news/bad news’ story,” said Dr. Yanovski. “The good news is that people don’t gain as much weight as we thought during the holidays. The bad news is that weight gained over the winter holidays isn’t lost during the rest of the year.”
The knowledge that people actually accumulate a large proportion of their yearly weight gain over the winter holiday season, the researchers added, may prove useful in treating overweight and obesity.
“?the cumulative effects of yearly weight gain during the fall and winter are likely to contribute to the substantial increase in body weight that frequently occurs during adulthood,” the researchers wrote. “Promotion of weight stability during the fall and winter months may prove useful as a strategy to prevent age-related weight gain in the United States.”
The NICHD and NIDDK are two of the Institutes comprising the National Institutes of Health, the Federal government’s premier biomedical research agency. NICHD supports and conducts research on the reproductive, neurobiological, developmental, and behavioral processes that determine and maintain the health of children, adults, families, and populations. The NICHD website, http://www.nichd.nih.gov/, contains additional information about the Institute and its mission.
The National Institute of Diabetes and Digestive and Kidney Diseases supports and conducts research on many of the most serious diseases affecting public health, such as diabetes and other endocrine disorders, inborn errors of metabolism, digestive diseases, obesity, nutrition, urology and renal disease, and hematology. For additional information, see http://www.niddk.nih.gov.
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just wanted to comment on the rawmeatybones thing… the raw food diet for dogs is a funny little parallel to the low carb diet for humans. Most Vets and popular opinion are dead set against it, meanwhile science and common sense point in the complete opposite direction.
We ignored our vet’s dire warnings against going raw (we also ignored the science diet crap they sell there), and our 11 mo. old pug is probably the healthiest, strongest, leanest pug on the planet.
It’s always seemed bizarre to me that vets would recommend what are basically high-carb diets for animals that are clearly carnivorous. But they do. I guess vets are as susceptible to the idiocy of the low-fat crowd as anyone else. Very strange.
Thanks for all of your insight and helpful information for me to learn from. I’m listening. I do believe that it’s a result of the low calories that is the reason for the weightloss…but what the hcg is doing is ALLOWING me to not care about food, while I’m doing this. I can’t imagine trying to white knuckle a 500 calorie diet on ‘just’ a placebo of water. I appreciate whatever the hcg is doing to suppress the appitite. Which is, I believe, one of the main reasons why it’s prescribed.
For me, whatever it is about the hcg, even if it’s JUST psychological, it’s what I needed. If I can take off chunks of it at a time and then maintain on low carb in between I can’t SEE how it’s not a benefit? I tried Atkins at one point, I got nothing much. I faithfully followed PP and got somewhere slowly, but because I have so much, and it takes longer, I’d lose interest. I need the psychological results of the loss to keep me motivated. When you have 250 pounds to lose…and it comes of slowly….dang, it’s overwhelming.
My thinking is now that if I can get it off…and maintain on a PP lifestyle then that’s something I CAN sign up for.
Thanks for letting me talk and taking the time with me to help me also understand.
I’m glad it’s working for you. Keep me posted on your success.
Low-Carber,
I have come to vehemently reject the idea of compulsive or addictive eating. I think half of it is related to insulin issues, and the other half is related to mood/neurotransmitter issues.
Since going low carb, I resolved almost all problems with eating.
Since addressing my neurotransmitter problems, any lingering food issues have almost entirely vanished. When I am energetic and optimistic because my neurotransmitters (dopamine esp) are working, I have no problems at all with food. I can even eat carbohydrates, and unless I consume a tremendous quantity, nothing bad happens. I find it much more difficult to gain weight, I do not as easily become tired after meals, I have heaps of energy, etc.
I think abnormal patterns of sleep and sunlight are a major cause of neurotransmitter imbalances in our society. Vitamin D plays a *huge* role. I was a staunch denier of the importance of supplements, but since taking considerable doses of D3, calcium, combined with st johns wort and 5-htp, my chronic dysthmia has abated and I am almost always energetic and optimistic.
Food fixation is just a symptom of some underlying abnormality. Food is not an addictive substance, even candy and cookies… it’s just not.
It’s actually proven in research that dopamine/melatonin balance controls seasonal fattening in animals. Dopamine blocking medications invariably cause the metabolic syndrome in humans. Prior to the low carb diet I was a picture of dopamine-blocking medication side effects. PCOS, hypoglycemia, hypersomnia, anergia and lack of motivation…
The reason low carb helped with everything so much isn’t just because of lower glucose, but because lower glucose actually changes neurotransmitters via the hypocretin system in the brain. When glucose is elevated, hypocretin tells your brain to turn off the lights. Symptoms of SAD result (in my case, were not seasonal but chronic). Sleep deprivation reduces glucose metabolism in the brain and a stimulant effect is observed in many people.
Vitamin D3 has a significant role in dopamine metabolism. St johns wort and calcium also affect neurotransmitters and keep them elevated.
My point is this; if someone is preoccupied with food, this is not a cause of obesity but a sign of some sort of metabolic problem. The moral overtones of Joel Osteen’s analysis of our “social problem” of chronic snacking are nothing new. The only thing different about our society is that we spend all our time working in doors and sleep about 6 or 7 hours a night and are detatched from family/friends an unusually high amount and are not free to pursue pleasurable human activity like creating and communicating. This affects metabolism, which affects how we perceive food.
I’m finding this all extremely interesting – I’ve only considered in passing the idea of feeding my cat raw meat. As a kitten I fed him on organic bones both raw and cooked, and meat also. He can still reduce a t-bone to nothing in a matter of seconds. However, he has suffered various injuries (falling off a 6-storey balcony was the first), and in my fear of him repairing thoroughly I’ve followed vet orders on the dry food. I do still give him bones occasionally. I suppose I should have known better, given that I advise humans on why not to eat carbs!
Here is my question –
My cat, Arnie, has recently suffered from a recurring urinary infection. It causes a blockage in his urethra, which could, of course, cause death, I’ve had to rush him to animal emergency several times recently. He has been put on a special diet (CD dried food) to help break up the crystals causing this, and it seems to be working as he hasn’t had a problem since starting this diet. For that reason I’d be scared to change what he is eating.
Any comments?
*PS – funny how this comment section has turned into an animal advice column of sorts!
It has, and I’m staying out of the debate because what I know about feeding cats (other than that they are carnivores) could be written on the head of a pin with room left over for the Lord’s Prayer.
Kathy from Maine commented about the W2W site: “Isn’t this what the Women to Women Center is Maine is pushing? Human growth hormone (nasal spray in their case), a cyclic approach to calories (though VERY low most times), and promoted by Gary Trudeau?”
~ I don’t know because I don’t know these things, BUT isn’t Hgh (Human Growth Hormone) different from Hcg (Human Chorionic gonadotropin). I found, online, WHERE I GET MOST INFORMATION!! (EEEEEEKKK) something called GNRH in a nasal spray. I hadn’t heard of Hcg as a nasal spray though. Only in shots, or something called Releana, an oral liquid.
I don’t know specifically anything about W2W.
ItsTheWooo wrote: “You know, one thing I didn’t consider is this: hCG is related to morning sickness and food aversion. In the first trimester the fetus is most sensitive to toxins and pathogens, and this is when hCG would be highest. hCG and high estrogen in the first trimester makes pregnant women very nauseated and adverse to food, especially meat. The magic in the hCG shot is that it might allow someone to not want to eat… the weight loss is simply a byproduct of consistent under eating, which lowers insulin and allows for weight loss.
Not all women get morning sickness, so I suppose the ones who find the hCG helps are the ones who would hypothetically have very bad morning sickness if pregnant, whereas the ones who find it worthless would be less prone?”
This is why on Hcg you do it for only ‘short’ periods of time, 23 -40 days, or it loses it’s effect on you. You body, so it states, becomes immune to it, you take a break, and then your able to do it again and it will have the same effect. I’ve never been pregnant, so I don’t know if I’d have had bad morning sickness?
And, if I may ask It’sTheWooo, what is the leptin replacement called? I read about leptin and it’s inablity to cross the brain blood barrier for some of us, and have even asked my Dr. to order my leptin levels, and we have, but unsure as to what they mean. Could this hcg stuff help with that BBB?? Seems as though that leptin, bbb subject was talking about the hypothalamus, if I recall. Again, I’m just a basic ‘Joe”….well “Jospehine”. Just not a plumber. lol Even though I happen to live NEAR THAT plumber…lol.
All I can report is that the fat is coming off differently.
“Can you imagine the dire economical effect of everyone realising that processed carbs are bad for health? The millions upon millions of people that are in the carb industry whether it is production, marketing, processing, retail. ”
I can imagine a very different economy with a different way of building wealth, but by no means worse than the mess we have now. Perhaps the transition would be messy.
Perhaps if we consumed more locally produced foods our local and regional economies would be much stronger (not to mention the food supply would be safer and less vulnerable to widespread food-borne illness and bioterrorism), instead of sending our capital out of the region to stockholders of grocery store retailers and multinational corporations like Archer Daniels Midland, ConAgra, and Monsanto.
Regarding vets and their objections to feeding cats and dogs real food, low fat might be part of their mindset, but I don’t think it is the major objection (though the “weight control” dry kibble foods are lower in fat and higher in carbs & fiber, so the pet food companies certainly think along those lines and that may dribble down to vets).
My vet’s objections to feeding a more natural carnivorous diet (raw meat and bones) were these:
a) feeding raw food to the cats would increase the risk that the human family members would somehow get sick ourselves from the raw food – perhaps a valid concern – but it hasn’t happened in nearly three years of regularly making and feeding raw food – and one cat likes to lick our hands when she sits in our laps. I employ normal kitchen hygiene when preparing the food and I guess we wash our hands enough after handling the cats. I’m sure my son doesn’t wash his hands enough, though no raw pet food induced illness has occurred.
b) cats especially, being obligate carnivores, have extremely specific nutrient requirements that must be met to avoid poor health, malnutrition, and even premature death. She’s right about the important nutrient balance, but not about it being to hard to achieve. Her view was that most pet caregivers don’t have the ability to get the nutrients balanced and that 60 + years ago before commercial pet food was available, many cats and dogs were malnourished because of the “unbalanced” table scraps fed to them. Perhaps so. People certainly didn’t pamper their pets the way they often do now, but at the same time, some of the current “spoiling” is literally sickening those beloved pets (cats and dogs are now getting the same chronic illnesses that humans get, primarily caused by a lifetime of eating crap, as well as exposure to tobacco smoke). My guess is in the past cats were fed scraps obtained from the butcher more than scraps from the table, and were also likely to have access to the outdoors, where they caught their “daily vitamins & nutrient supplements” (yes, sadly, that might include songbirds). But they also lived shorter lives due to cars and diseases caught in the wild. My cats are great at catching small rodents and lizards, even the older fat, slower cat. Since transitioning to raw food, they now sometimes eat the mice they catch, especially the heads.
My vet is right in that there *is* a lot of varying and sometimes confusing information on pet diets online and in print, some good and some awful advice, with inclusion or exclusion of plant foods being the most controversial, so if choosing this raw meat & bones route, it is important to “get it right” to provide all the essential nutrients. But domesticated cats have been around a long time (though they often were “companion workers”, meant to keep the rodents population down and out of the grain stores, therefore self-feeding); somehow humans have managed to keep cats all these nearly 10,000 years, so it isn’t rocket science as long as one keeps their natural predator diet of small animals in mind. Cats and dogs certainly need more than muscle meat to eat – they also need the minerals in bones and organ meat, especially liver. Cats in particular, also need heart muscle for a certain delicate amino acid (heat sensitive) – taurine, though it can also be provided with taurine supplements. But of course, the full complement of nutrients in the whole food is preferable. And feeding real food is a bit more expensive and more work than cheap kibble, but it saves time and and potentially a lot of money at the vet, which isn’t a small consideration at all (some might think that is the primary reason for the typical vet advice against raw food, but I really don’t think that is the case, I think they are well-meaning but just brainwashed by the pet food companies from vet school to the company reps that frequently visit, just like many physicians are heavily influenced by big pharma).
c) She wouldn’t recommend anything that wasn’t back up by peer-reviewed vet journals. So until it is officially sanctioned in “the literature”, no matter how many clients have great success preventing and reversing disease with real food from raw meat & bones, she won’t recommend it to her clients. Well, hell with probably freeze over before that happens, because the pet nutrition research and education is primarily sponsored and funded by pet food companies, creating a huge conflict of interest and certain slant. Commercial pet food, even the “premium” stuff is made from the dregs of the food processing industry, formulated with a very “reductionist” view of nutrition and the low price and convenience of commercial pet food will continue to win over pet caregivers, as they are conditioned to only think of commercial feeding options and cost/convenience factors.
So I think this movement towards feeding real food will be primarily driven by a few (the the number is increasing) smart pet care givers who can see the connection to poor pet health and commercial pet foods, with some breeders and a few enlightened independent-minded vets chiming in.
Bringing this study to your attn, in case you hadn’t seen it:
http://www.naturalnews.com/024887.html
The abstract:
http://cancerres.aacrjournals.org/cgi/content/abstract/68/22/9274
“[W]e noted a markedly elevated risk for carcinoid tumors of the small intestine with saturated fat intake in both the categorical (highest versus lowest tertile: HR, 3.18; 95% CI, 1.62–6.25) and continuous data (HR, 3.72; 95% CI, 1.79–7.74 for each 10-g increase in intake per 1,000 kcal). Our findings suggest that the positive associations for meat intake reported in previous case-control studies may partly be explained by saturated fat intake.[Cancer Res 2008;68(22):9274–9]”
A couple of things. First, this is an observational study (of tiny numbers), and as such, can’t be used to determine causality. Second, there are numerous observational studies out there – some show a positive correlation between meat eating and various cancers, other show no correlation, and others yet show a negative correlation. This gives people a choice of studies to rely on to substantiate their own bias.
@ Anne & Mr. Freddy,
I hope your trainer has you doing squats or something else remotely functional as a primary lower body movement. While it is great to progress in certain movements, I would rather people be able to execute a proper squat without weight than 1000 lbs leg press. I would advise staying clear of any machine you could fall asleep on : ) Squats help promote stabilization in the trunk and are vastly superior in terms of their cross-over benefit to daily movement. At least you aren’t doing leg extensions… if so, hopefully not regularly.
I would advise mixing it up, too – perform leg movements in varying planes, playing around with the volume, repetition speed (yes, it is advisable to lift weights fast, too) and implements (dumbbells, barbells, cables). I highly recommend reading the methods of Chad Waterbury, Mark Ripptoe, Eric Cressey and Tony Gentilcore – they are true masters of performance enhancement and lifting.
Missy, you still haven’t read reference [12]
Perception of hunger is one of the things the study measured, and there was no significant difference between the mean hunger ratings of the HCG and placebo groups. Although, in this case, the full distributions were at least interesting! They used a 5-category self-reported hunger scale (“none”, “little”, “some”, “much”, and “uncontrollable”), and twice as many people in the HCG group rated hunger as “none” than in the placebo group. However, that was /also/ true of people rating their hunger as “uncontrollable” (again the HCG group was the higher one). See Table 3 for the full story.
But again, if it worked for you, that’s great.
Hi Missy,
The leptin I was taking is not commercially available. I was taking it as part of a clinical research study for women who fit a certain profile (infertile due to specific hormonal aberrations, including severely low leptin).
Leptin deficiency is only likely to be a problem AFTER considerable weight loss. If you are still obese or morbidly obese it is unlikely you have leptin deficiency. Genetic abnormalities in leptin synthesis are exceedingly rare, there is only a handful of people in the world and they are almost all part of the same inbred family… although mutations in receptors are somewhat more common in obese people.
Leptin deficiency will make someone chronically prepubertal. Women will not ovulate and men cannot produce mature sperm, which is why deficiencies of synthesis are almost unheard of except in heavily inbred families who have a recessive trait (otherwise you can’t pass that gene, can you?)
I know leptin cannot effectively cross the BBB if triglycerides are high, which is another way of saying that leptin signaling in the brain is blocked if you have really high insulin and are building fat like a mofo.
I do not know if hCG has any effect on the BBB. The primary role of hCG in the body is to support the placenta until it is mature enough to produce enough progesterone of its own to keep it alive.
I know that morning sickness and food aversion in pregnancy is very strongly related to high hCG combined with high estrogen. I know hCG makes estrogen, like LH would (LH being the estorgen-making hormone dominant during fertility and hCG stepping up after implantation and pregnancy).
Intuitively I doubt that hCG works via leptin at all… leptin is mostly relevant AFTER weight loss, when cells are hypotrophic and insulin is low. Leptin is only dominant when body fat/insulin is relatively deficient, because leptin will never be deficient unless all of those are.
If hCG works at all besides placebo I would expect it to work somehow via estrogen, testosterone, and whatever neurotransmitters/hormones affect the phenomenon of morning sickness.
Thanks Tim Peters. I, BECAUSE of YOUR wink….lol..went and made SURE to reread it. I know what it says, but I know what I feel. For me, my feelings trump the study. It is working, for me, and I hope it continues. I really do appreciate your feedback.
Wooo, I learned today that I’m not deficient in leptin. Just went to my Dr today and that’s one thing we’ve monitored. He is going to have me ‘test’ for it at the end of my next weightloss cycle though. Thanks for sharing more with me as well!
No problem missy,
I hope you have really good insurance… I’ve been told that the diagnostic test for leptin level is pretty expensive. It isn’t worth monitoring unless you have symptoms of deficiency… and even then it isn’t really worth it other than to confirm suspicions (there is no way to treat leptin deficiency in 2008, unless you’re a gabillionaire or part of a research study). It’s extremely unlikely anyone with a very high BMI is going to be leptin deficient, anyway, even if they’ve lost a bit of weight. If you are still near 400-300 pounds leptin isn’t something you’re even going to have to even think about until you’re at least in the 200s probably.
The leptin deficiency post weight loss/maintenance is related to the former obese individual having hypotrophic (small) fat cells that are hyperplastic (numerous). Even the most obese individuals only have 3xs the amount of fat cells as a normal weight person, which approximately means that leptin deficiency shouldn’t even begin to be an issue until fat mass has been diminished to a level that is no greater than 3 times the amount of an average non-obese individual. If you’re more than 100 pounds over ideal weight, it probably isn’t a n issue.
Wooo, lol, when I go to the hospital to get blood drawn, ‘they’ don’t even know what vial to use for it. LOL There is always a delay, I’ve noticed, till they ‘check’ with someone. lol It’s just good to have a baseline. I doubt we’ll test it again till much further down. I’ve got good insurance. Thanks!
“It’s always seemed bizarre to me that vets would recommend what are basically high-carb diets for animals that are clearly carnivorous. But they do. I guess vets are as susceptible to the idiocy of the low-fat crowd as anyone else. Very strange.” (MRE)
I’m more cynical. I think they know that it would be bad for business if people fed their cats and dogs raw meaty bones. The animals would be healthier than eating the high-carb rancid garbage filled with corn and soybeans. And the vets would be out of business. That’s why the majority of them tell people to feed their animals processed chow filled with rancid fats and grains. For the same reason, the manufacturers of the food sell “weight loss formula” which is lower in fat and higher in carbs and fiber, the exact opposite of what a carnivore needs. The people are all very shrewd and they know what they are doing, just like the cardiologists who tell their patients to eat grains and vegetable oils. They have a good racket. They don’t want anyone rocking the boat by pointing out that cats are carnivores and have no need for corn, rice, soybeans, vegetable oils, and fiber – nor do humans for that matter.
Hello,
I am new to this blog — just found it today. I see that the last post was last January, so I’m not sure if this is being read anymore.
My personal experience with the relationship between weight loss and low carbs occured by accident in 2003. I was extremely busy working and preparing for the wedding of my eldest daughter. I often skipped “regular meals” and ate on the fly. Recognizing that I became hungry less frequently if I ate protein/high fat foods, I always kept them available in the refrigerator and in my car. I always had nuts on hand and would eat a few periodically to stave off hunger pangs. I did eat vegetables and fruits in small quantities. In five months I went from a size 18 to a size 12. Surprised at the ease and efficiency of the “diet,” I continued it for the next seven months during which I went from a size 12 to a size 4. I lost a total of 50 pounds without any loss of energy. Now, five years later, I have maintained my weight loss.
I eat all fruits and vegetables. I avoid fast food and most processed foods, but I do eat too many sweets (chocolate, ice cream, etc.). Now that I have some understanding of the impact of carbs/sugar on general health, I believe I need more information about improving my diet to avoid the chronic, degenerative illnesses related to high-carb consumption.
Can someone tell me where I can get specific information and guidelines to use to help me modify my diet?
Hmmm. Don’t know what you found, but there have been numerous posts since January. Many about what to do to modify your diet.