Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
2 online now:
Newest Member: popoi
Post Volume: Total: 915,817 Year: 3,074/9,624 Month: 919/1,588 Week: 102/223 Day: 0/13 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Good Calories, Bad Calories, by Gary Taubes
Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 228 of 451 (471456)
06-16-2008 11:27 PM
Reply to: Message 225 by PaulK
06-16-2008 1:58 PM


Re: Insufficiently Supported Dietary Recommendations
PaulK writes:
quote:
1. The obesity epidemic has coincided with increased intake of carbohydrates.
This would be significant (although far from conclusive) if calorie intake had remained the same, with fats replaced by carbohydrates. However, Marantz et al point out that calorie intake increased, with fat consumption remaining about the same in absolute terms.
(It may also be notable that obesity in women seems to have increased more steeply, and women are eating more fat, not less).
This is one of the possibilities that Marantz mentions in his paper, but a simple overconsumption of calories is not the only possibility, and Marantz takes note of this. For example, he quotes from the 2000 Dietary Guideline Advisory Committee where they say about the dietary fat recommendations, "This belief could engender an overconsumption of total calories in the form of carbohydrates, resulting in the adverse metabolic consequences of high-carbohydrate diets."
Marantz is appropriately tentative when he expresses his own opinion on the matter, saying at one point that it "...provides a biologically plausible rationale that the recommendation to choose lower-fat foods could have led to increased energy consumption." This tentative expression is in keeping with his status as an epidemiologist studying disease at the population level, one that wouldn't lend him any particular expertise in forming judgements about underlying metabolic causes.
But I agree that the "too many calories" possibility is plausible. Other possibilities are also plausible, such as the "adverse metabolic consequences" that Marantz mentions in his quote from the guidelines committee, and upon which Taubes focuses so much attention. I've attempted to describe the relevant and significant metabolic processes in this thread.
"A calorie is a calorie" is not about individual differences. The most you can hope to argue there is that individuals react differently to different sources of calories. But that would undermine Taubes' claims about carbohydrates, too.
Oh, okay, I see how you're looking at this. The "a calorie is a calorie" argument is one that metabolic differences don't matter, that individual differences don't matter. Taubes is making the opposite argument, that these metabolic differences between individuals and the different ways they respond to food nutrients argues that how a calorie is experienced is a very personal matter. For some individuals excess caloric intake is harmless, for others it means weight gain.
This means that diet is definitely *not* irrelevant, because food isn't just something that provides energy and does nothing else. The food we eat has a significant impact on body metabolism. As Taubes argues and as Marantz mentions, elevated carbohydrate intake can have adverse metabolic effects, the most significant being elevated insulin levels.
These also seem to undermine Taubes' claims about carbohydrates since they deny a link to diet.
Here you're addressing the observation that tissue metabolism can have a significantly greater influence on obesity than diet, and this is just more evidence for the same argument about the significance of metabolic effects. Belly tissue transplanted to the back of the hand will grow as fat with age as the belly tissue that remained on the belly. What are the metabolic tissue differences that cause this? We don't know. Some individuals are emaciated, in effect starving, in one part of their body, while another part is obese. What are the metabolic causes? We don't know.
But clearly body metabolism is at work. Hormones and other chemicals can make you fat whether you're eating too much or not. Try taking an antipsychotic like Zyprexa for a while and just try to keep the weight off. Can't be done, illustrating that the simple rule of "a calorie is a calorie" is just far too simple a way to think about body metabolism.
So any diet which throws body metabolism out of whack in a certain way can cause adipose tissue to accumulate fat no matter what you do, just like the person whose hand with the transplanted tissue grew fat, and just like the people who can both starve and overfeed the same body on a single diet.
I don't know enough to discuss these points in detail. However they appear too simple to be relied on. If we don't know enough about metabolism to judge then we don't know enough to judge those.
While you can perhaps argue that I oversimplified, the processes I briefly described in points 5 and 6 are not simple. Concerning point 5 about insulin causing the uptake of fat by adipose tissue, this is not in dispute. Concerning point 6 about the progression from normal to metabolic syndrome to type II diabetes, this is much debated, but as the Wikipedia article on metabolic syndrome points out, "The most obvious method of prevention is undoubtedly to reduce the amount of carbohydrates, specifically fast digesting starches and sugars." It isn't fat or protein that puts a strain on the pancreas's production of insulin, it's carbohydrates.
In case you didn't notice, Percy I just mirrored your argument. You didn't refer to studies or take lifestyle into account (or even the details of the traditional Inuit diet).
I used the example of the Eskimos because they're usually a sufficiently familiar example, but we can discuss the Eskimos in more detail if you like.
PaulK writes:
That isn't how I read this statement from Message 220. I'd say that it is quite clearly stating that the best diet has no carbohydrates:
The very complex carbohydrates in starchy foods are preferable to the very simple carbohydrates in sugar. No carbohydrates are even better.
Sorry if I wasn't clear. I still had in mind the context where we were discussing which of the three nutrients, protein, fat or carbohydrates, was inessential.
I've got no quarrels with the first point. But the second seems to be very questionable.
My second point is that Taubes presents a lot of evidence that the carbohydrate hypothesis is a better fit. I suppose you could take issue with whether his evidence is really a better fit, but he does present a lot of evidence.
Aside from the biochemistry arguments (which Molbiogirl disputed - and she likely knows better than either of us) the arguments seem to be very poor, and even inconsistent.
Yes, I can see now why you thought it was inconsistent, hopefully I've made some progress resolving this for you. Regarding Molbiogirl's arguments and research, you might try using them yourself before rendering an opinion.
--Percy

This message is a reply to:
 Message 225 by PaulK, posted 06-16-2008 1:58 PM PaulK has replied

Replies to this message:
 Message 229 by PaulK, posted 06-17-2008 2:01 AM Percy has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 230 of 451 (471499)
06-17-2008 9:00 AM
Reply to: Message 229 by PaulK
06-17-2008 2:01 AM


Re: Insufficiently Supported Dietary Recommendations
PaulK writes:
Of course it only matters to this debate if diet IS relevant. You can't put forward an argument that diet is irrelevant to support the idea that diet IS relevant (but a different component is to blame for ill effects).
Well, it looks like I may not be explaining this very well, let me try again.
Consider the case of women who are emaciated in the upper body and obese in the lower body. Some not yet understood metabolic quality of the lower body fat tissue is causing it to suck up nutritional resources at the expense of the upper body and of overall available energy. The carbohydrate hypothesis is that the adverse metabolic consequences of high-carbohydrate diets can cause adipose fat tissue in otherwise normal people to do the same thing, that is, to suck up nutritional resources at the expense of the rest of the body and of overall available energy.
PaulK writes:
The point is that you demand details that you do not require from our own arguments.
We can discuss this at whatever level of detail you like, but I need something more specific than this to start the ball rolling.
Something in your approach to this discussion leads me to believe that you think stronger claims are being made than is actually the case. Perhaps this Taubes quote will help:
Taubes writes:
I referred to this proposition repeatedly as the "alternative hypothesis", using the word "hypothesis" to imply strongly that it is not a fact but a supposition that should be rigorously tested. (Taubes article in reasononline)
Robustly arguing in favor of a preferred hypothesis should not be interpreted as claiming the currently available evidence is conclusive.
--Percy

This message is a reply to:
 Message 229 by PaulK, posted 06-17-2008 2:01 AM PaulK has replied

Replies to this message:
 Message 231 by PaulK, posted 06-17-2008 2:39 PM Percy has seen this message but not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 232 of 451 (471805)
06-18-2008 11:00 AM


The Ketogenic Diet
A ketogenic diet is low in carbohydrates and high in fat. It has been known since the 1920s that such a diet can significantly reduce the incidence rate of epileptic seizures in children.
This came to my attention recently when a friend who works with severely disabled children mentioned a recent Johns Hopkins study showing that a ketogenic diet appears to have long term benefits that persist long after a normal diet is resumed. The article he sent me does not appear to be on-line, so I've uploaded a copy: Ketogenic Diet Reduces Seizures In Many Children, Hopkins Researchers Find
The Wikipedia article on Ketogenic Diet says that the mechanisms by which such a diet reduces seizure events remains a mystery. The Hopkins article echos this, but also says, "a 'flurry of activity' is now under way to reveal the biochemical reasons for the treatment's
success."
This information invites speculation. Is a ketogenic diet generally beneficial with subtle brain effects in normal people not yet noticed? Or does it only benefit epileptic children? Concerning mechanisms, is it that ketone driven brain metabolism is itself beneficial? Or does glucose (carbohydrate) driven brain metabolism carry with it some adverse consequences? Or is it some mix? Or something else altogether?
It's interesting to note that carbohydrate intake is also a key issue with ADHD children. It is widely suspected that the recent ADHD epidemic here in the states is one of over-diagnosis rather than any actual epidemiological change in the American population, but is it possible that high-carbohydrate diets, particularly where refined carbohydrates are a significant component, cause brain chemistry to encourage ADHD-type behaviors, or perhaps even lead to structural changes in the brain that encourage the development of ADHD? The Hopkins data is certainly consistent with the latter possibility.
We likely won't have any answers to such questions for a number of years, but it is interesting that once again carbohydrates are a possible culprit for yet another medical condition.
--Percy

Replies to this message:
 Message 233 by randman, posted 06-19-2008 9:46 PM Percy has replied
 Message 254 by molbiogirl, posted 07-04-2008 12:13 AM Percy has seen this message but not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 234 of 451 (472062)
06-20-2008 7:28 AM
Reply to: Message 233 by randman
06-19-2008 9:46 PM


Re: The Ketogenic Diet
Hi Randman,
Thanks for the attaboy.
It has been a surprising discovery to find that the diet/health research community is in some ways similar to pseudoscientific communities, such as those surrounding UFOs, Bigfoot or ESP. Apparently, because actual real-world relationships between diet and health are so difficult to tease out using traditional research methods, because the existing body of research does not at present point conclusively in any particular direction, this scientific community is far more likely than others to latch onto views that have some kind of appeal unrelated to the quality of the supporting scientific evidence.
Hence you'll find myths being perpetuated that have no scientific support, such as your example that low-carbohydrate diets can cause liver damage. There is no body of research indicating such a risk, not even for no-carbohydrate diets. In cases where there is already significant liver damage, perhaps due to alcoholism, a low-carbohydrate diet might not be recommended because the damaged liver couldn't handle the higher protein load, but lack of carbohydrates seems a very unlikely cause of liver damage.
But I unexpectedly find that I must agree with your comment that "in some fields, science is better than others." In this case it has created irrational fears that low-carbohydrate diets are not only equivalent to quackery, but dangerous. Certainly until recently I, too, believed this to be the case, and it wasn't until I read Taubes book that the science (as well as what I've experienced personally as I grow older regarding diet and weight loss) began to make sense.
--Percy

This message is a reply to:
 Message 233 by randman, posted 06-19-2008 9:46 PM randman has replied

Replies to this message:
 Message 247 by randman, posted 06-24-2008 6:46 PM Percy has seen this message but not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 235 of 451 (472240)
06-21-2008 11:20 AM


Call for a Critical Appraisal
Here's a link to an interesting and easy to understand "statement of position" paper calling for greater emphasis on carbohydrate restriction in the treatment of type 2 diabetes and metabolic syndrome:
The conventional medical wisdom regarding diabetes and dietary fat is difficult to fathom. The American Diabetic Association continues to recommend a diet high in carbohydrates and low in fat. But fat has no direct influence on insulin levels and little indirect influence, and diabetes is a disruption of the body's ability to produce insulin. When considering available mechanisms, it's hard to see a signicant role for dietary fat in diabetes. Eat a cup of grease fat and your insulin levels will barely budge, but eat a candy bar and just watch them soar. Insulin production by the pancreas is extremely sensitive to the presence of glucose, and glucose comes from carbohydrates, not fat.
There is a body of research showing correlations (not causation) between dietary fat intake and insulin resistance (a precursor of type 2 diabetes), but as this article points out, the research is not unambiguous, for as is generally acknowledged, obesity clouds the issue. Whether a person becomes fat by overconsumption of carbohydrate, fat or some combination, obesity carries with it clear risks of diabetes and definitely elevates the indicators of those risks. Concerning this issue the article says:
In our view, inconsistencies in the experimental results with dietary saturated fat arise from a failure to distinguish between replacement by unsaturated fat or by carbohydrate. In the former case, there is usually improvement in CVD risk or outcome (although it is not excluded that this is due to the effect of the unsaturated fat rather than reduction in the risk from the saturated fat). Replacement of saturated fat with carbohydrate, however, is almost always deleterious. Again, the idea that carbohydrate is a control element determining the fate of ingested lipid is overriding.
In other words, a key defect in much dietary research into the causes of diabetes is the extent to which the dietary fat hypothesis is assumed true. The result is insufficient controls on carbohydrate consumption, with the result that the extent of carbohydrate influence is unknown or ambiguous.
This is starting to change. For example, the January, 2008, study, Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation, concludes:
In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.
Those who are old enough probably remember the cholesterol scare of the 80's and early 90's when it was believed that heart disease was influenced by dietary cholesterol. The legacy of this scare is that cholesterol content is still featured prominently on nutritional labels, even though we now understand that dietary cholesterol has only the most indirect of effects upon cholesterol levels in the bloodstream (serum cholesterol), and that serum cholesterol levels are not a significant indicator for heart disease anyway.
The same is true of dietary fat. The levels of various forms of dietary fat (saturated, polyunsaturated, monounsaturated, and there must be others) do roughly translate into blood serum levels, but the effects of these different kinds of fat are multifarious and nowhere near as well understood as mainstream dietary recommendations would have you believe. For example, it is an extremely strong part of conventional dietary wisdom that saturated fat is bad for you, but the research on this is equivocal at best. Teasing out the effect of any particular chemical on the body is complex in the extreme, and the diet/health establishment is performing a serious disservice when it makes dietary recommendations on the basis of ambiguous science.
Here's a rather clear example of the confusion in diet/health research concerning fat. If you search the technical literature about dietary fat and insulin resistance, you'll find many papers that reach the conclusion that dietary fat increases insulin resistance. Yet if you read those papers you'll find that they don't usually control for carbohydrate intake. This muddies the water a great deal, because fat intake just doesn't influence insulin levels very much. Here's a graph of insulin levels plotted against time for both fat and glucose tolerance tests:
What actually may be the case is that carbohydrates act as an amplifier. Dietary fat in the presence of no carbohydrates is relatively harmless, but increasing carbohydrate levels amplify the effects of any dietary fat. This is something that I've been saying all along, that high carbohydrates and high dietary fat are the worst possible combination, and my example is usually Chinese pork fried rice.
So it isn't that dietary fat is harmless. It's that dietary fat is by far the more minor player in this diet/health game. Carbohydrates play a much more significant role, and this makes sense in light of our evolutionary history, where carbohydrates were not a significant contributor to diet until the advent of agriculture.
Here's an interesting fact. When research scientists want to increase the levels of fatty acids in the bloodstream of laboratory rats, you know how they do it? You're probably thinking that they feed them fat, right? And they could do it that way, but that's the hard way. They usually do it by overfeeding them carbohydrates in the form of sucrose (50% glucose and 50% fructose), causing the liver to overproduce fatty acids. In other words, refined carbohydrates are a far more effective way than dietary fats of increasing fatty acid levels in the bloodstream. See, for example, Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats.
Sitting like a big gorilla in the middle of all this dietary research is the simple fact that over the past 30 years during which the dietary fat hypothesis has held sway, western populations have become more obese, more diabetic, and remained just as prone to heart disease as ever.
--Percy
Edited by Percy, : Typo.

Replies to this message:
 Message 236 by bluegenes, posted 06-21-2008 6:48 PM Percy has seen this message but not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 237 of 451 (472342)
06-21-2008 8:17 PM


Carbohydrates and the Obesity/Diabetes Epidemic
Few would argue that the western world is experiencing an epidemic of obesity and diabetes, but the breadth and depth of the epidemic is often not well understood. This is from the conclusions of Diabetes Trends in the U.S.: 1990-1998:
From 1990 to 1998, the prevalence of diabetes increased by about one-third in the 43 participating states. This increase was observed across all age-groups, races, educational levels, levels of smoking status, weight levels, and nearly all states.
In other words, the increases in diabetes affected everyone everywhere. Whatever the cause, it is prevalent everywhere, it affects everyone, and it obviously can not be anything subtle. The paper The Continuing Increase of Diabetes in the U.S. reports that the rate of diabetes in the U.S. rose from 4.9% in 1999 to 6.6% in 1999. I'm sure more recent data would confirm that the trend continues today. Obesity and diabetes go hand in hand, but just for completeness, here's a paper on the obesity portion of the epidemic:
The Spread of the Obesity Epidemic in the United States, 1991-1998.
Just to be clear, I offer this information not to convince that there's an obesity/diabetes epidemic, for of that there can be little doubt. My purpose is to make clear the huge scale at which this epidemic is taking place.
More and more research is being conducted into the possibility that refined carbohydrates play a significant role, and I today came across this 2004 paper that appeared in The American Journal of Clinical Nutrition: Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment. Its conclusions states:
Increasing intakes of refined carbohydrate (corn syrup) concomitant with decreasing intakes of fiber paralleled the upward trend in the prevalence of type 2 diabetes observed in the United States during the 20th century.
What's extremely interesting about this study is that although only carbohydrates appear in the title, they also looked at dietary fat. Their results showed:
  • That carbohydrates were positively associated with type 2 diabetes (i.e., higher carbohydrate intake, higher risk of diabetes).
  • That dietary fiber was negatively associated with type 2 diabetes (i.e., higher dietary fiber intake, lower risk of diabetes).
  • Protein and fat were not associated positively or negatively with type 2 diabetes (i.e., higher or lower intake of protein or fat, no impact on risk of diabetes).
This is a killer finding. Naturally, like all science, it requires review and replication by the appropriate peer community, and we'll just have to follow developments to see if it becomes accepted.
--Percy

Replies to this message:
 Message 238 by bluegenes, posted 06-21-2008 10:33 PM Percy has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 239 of 451 (472411)
06-22-2008 7:09 AM
Reply to: Message 238 by bluegenes
06-21-2008 10:33 PM


Re: Epidemic? Sure, but is it universal?
bluegenes writes:
Percy writes:
In other words, the increases in diabetes affected everyone everywhere.
No. That's very loose usage of the words "everyone" and "everywhere", (not to mention "affect")
Sorry if I wasn't clear. I didn't intend to say that everyone everywhere is obese and diabetic. But because the obesity/diabetes epidemic acknowledges no boundaries of race, ethnicity, religious affiliation, age, educational level, etc., everyone everywhere in countries with western-style lifestyles is at risk.
Those trying to eat healthy in western-style countries face severe problems because truly healthy food sources are just not available. According to the paper I cited earlier, Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment:
For example, processing whole grains into white flour actually increases the caloric density by > 10%, reduces the amount of dietary fiber by 80%, and reduces the amount of dietary protein by almost 30%.
So the solution would seem to be to make sure the grain products you eat are made with unrefined grain, but unless you grow and mill the grain yourself you're just not going to find such products in western-style countries. I suspect this is a competitive issue, with suppliers of whole-grain products competing to produce the most palatable whole-grain products possible, with the result that whole-grain products are whole-grain in name only. While I don't have hard evidence, I have strong circumstantial evidence that the whole-grain products sold in western-style countries are quite nearly as refined as refined-grain products, and it takes the form of the information on nutritional labels.
Pepperidge Farm 9 Grain Whole Grain Bread, presumably made with unrefined grain, has 20 grams of carbohydrates per slice, 3 grams of which is fiber, and 3 grams of which are sugar. Fiber is indigestible and makes no nutritional contribution, so the net is 17 grams of carbohydrates, of which 3 is sugar, which is usually a 50/50 mix of glucose/fructose.
Pepperidge Farm Hearty White Bread, presumably made with refined grain, has 22 grams of carbohydrates per slice, of which 1 gram is fiber and 4 grams are sugar. The net is 21 grams of carbohydrates, of which 4 is sugar.
So if you eat whole wheat bread instead of white, you'll consume 17 grams of carbohydrates instead of 21 , a rather modest difference. And you'll consume 3 grams of sugar instead of 4, another very modest difference.
If refining grain to white flour actually removes 80% of dietary fiber, as the paper cited above states, then it should be possible to find whole wheat bread with five times the dietary fiber of white bread. You also want no sugar, but no one's interested in making bread that doesn't sell.
There's a lot of built-in confusion in nutritional information about carbohydrates. The fiber portion of carbohydrates is fairly unambiguous. Fiber is carbohydrates that are indigestible and do not contribute to nutrition, but they do moderate the rate of digestion of other food material, such as digestible carbohydrates.
But there's a lot of confusion about what constitutes refined carbohydrates versus complex carbohydrates. The diet/health industry recommends food products high in complex carbohydrates and low in refined carbohydrates, but are refined carbohydrates sugar? Or do refined carbohydrates include bread, pasta and pastry made with refined grains? Is white rice a refined carbohydrate? As near as I can tell, it depends upon context. Sometimes references to refined carbohydrates seem to be focused on sugar, sometimes they're focused on both sugar and refined grain products.
The glycemic index can be very helpful in comparing the quality of carbohydrates in food products that have no sugar or have very low levels of sugar. The reason it can't be used to compare products with sugar is that sugar is only 50% glucose, which is all the glycemic index measures, how rapidly and abundantly the carbohydrate in a food product is broken down into glucose and absorbed by the bloodstream. The other 50% of sugar is fructose, which is metabolized by the liver into fat.
The carbohydrates in non-sugar foods with a low glycemic index are digested and absorbed at a slower rate than those with a higher glycemic index, which is good because blood glucose spikes flood the body with insulin, which is bad for both diabetes and obesity risks.
The increase in diabetes effects the "average" person in sedentary cultures, certainly.
The strongest controlling factors for diabetes risk appear to be obesity and carbohydrate intake. The amount of exercise is also a factor, but it is strongly influenced by whether there is any accompanying weight loss. In other words, if presented with the choice of exercising while maintaining weight versus no exercise but losing weight, the latter choice is much more likely to reduce diabetes risk.
One of the reasons why nutritional advice is so suspect is because when its advice doesn't work the recourse is to blame the victim. If someone gains weight or fails to lose weight while following nutritional advice, then it's the fault of the patient for not properly following the advice. The possibility that the advice is incorrect is rarely considered.
I have lived the reality of both sides of the weight issue. At age 18 I was 5' 10" and 105 pounds. It didn't matter how much I ate, I could not gain weight, and I tried really, really hard in college to gain weight, since I could eat as much as I wanted in the dining hall, plus we usually went out for a late night snack of subs, cheesesteaks or pizza. Participating in varsity and intramural athletics, I was also very active. At the end of 4 years of college I weighed 115, and I believed that anyone who was fat must be incredibly lazy and gluttonous. When I saw fat people I could not understand how they could have allowed it to happen to them.
I gradually put on weight during my 20's and 30's and was gratified to finally take on a more normal appearance. During this period I ate as much as I wanted whenever I wanted, and I apparently put on about two pounds per year. Much of it was muscle, for during this period I was still playing competitive tennis, and for a while I dabbled with running.
My activity level really picked up in my mid-40's when my kids were both finally in school, making available more free time. I began playing tennis at an intense level for at least an hour a day, six or seven days a week. Even in the winter. I was serious about it and eventually became good enough (I was already very good) to be seeded one or two in most tournaments I entered. It was a rare tournament where I wasn't playing on Sunday. During this period my weight reached 180, and it wasn't mostly muscle anymore.
So I went on a diet of about 1600 calories/day and was able to lose about 30 pounds.
Four years later I was back up to 180 pounds, so I went on another diet, but this time discovered I had to drop to 1400 calories/day to lose weight. I again lost about 30 pounds.
Three years later I was up to 190 pounds, so I went on yet another diet, but this time even on 1200/calories day I could not lose weight, and I couldn't go lower because I couldn't stand the hunger. I brought this up with my doctor who told me I must not be keeping track properly. He knew better than to suggest I wasn't exercising enough.
I am still pretty much the same person I was at 20 who could not gain weight no matter what, but now I can't lose weight no matter what. What changed? Am I now lazy and slothful and gluttonous? Is it my fault that I weigh too much? The diet/health establishment would answer yes to these questions. They would say that however little I'm eating, it's still too much, and that however much I'm exercising, it's still too little.
The truth is that it's all a bunch of bull. Thirty years ago I couldn't gain weight on a diet of 3000 calories/day, and now I can't lose weight on a diet of 1400 calories/day, and the reason for the difference is metabolic changes. Metabolic differences also explain why some people are fat and some people are skinny. We still don't know precisely what these changes and differences are, but we're gaining a better understanding with time, especially now that the dietary fat hypothesis is weakening its stranglehold on research.
--Percy

This message is a reply to:
 Message 238 by bluegenes, posted 06-21-2008 10:33 PM bluegenes has replied

Replies to this message:
 Message 241 by bluegenes, posted 06-24-2008 2:14 AM Percy has replied
 Message 243 by Joe T, posted 06-24-2008 2:12 PM Percy has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 240 of 451 (472553)
06-23-2008 9:07 AM


Diet Soda Makes You Fat!
I first heard about this research early this year in the mainstream media, but they didn't explain it very well. Now I've come across the original research paper, and the message, unfortunately, is that diet soda likely makes you fat.
The paper itself (A Role for Sweet Taste: Calorie Predictive Relations in Energy Regulation by Rats) is clear but expressed in technical terms, but here's a well written and short article that explains it pretty well: Do Artificial Sweeteners in Diet Soda Cause Obesity?. Quoting from the article:
We know that just the thought or smell of food triggers a whole set of hormonal and physiologic responses that prepare the body for food.
This pre-digestive response is the key problem. If just the taste of diet soda triggers the release of various hormones, insulin in particular, then all is lost. The increased insulin levels will cause the hormonal balance to shift in the direction of greater production of fat from fatty acids in the bloodstream.
Most diet soda tastes funny to me, but I love orange soda, and I've found this wonderful Sunkist diet orange soda that is indistinguishable from regular orange soda. It has 0 calories and I love it. Unfortunately, my diet experience has led me to suspect that it is somehow just not helping, and this research would tend to confirm this suspicion.
So once again my diet changes: no more diet soda! Ugh, dieting is getting hard.
--Percy
Edited by Percy, : Typo.
Edited by Percy, : 'Nother typo.

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 242 of 451 (472699)
06-24-2008 10:01 AM
Reply to: Message 241 by bluegenes
06-24-2008 2:14 AM


Re: Epidemic? Sure, but is it universal?
bluegenes writes:
Your own case does seem unusual.
Actually, my case is typical. The typical experience as one ages is greater and greater difficulty keeping off the pounds. The only thing unusual about me is that I'm probably much more active than your average 56 year-old.
There was a time when I was happy with my weight, and when I blamed overweight people for their own weight problem. I remember my smugness and self-satisfaction very well because it was only a year ago. After all, I had twice successfully lost weight. Then I began the 3rd diet of my life and hit a brick wall. I couldn't lose weight no matter what.
So I have now, in effect, walked a mile in the shoes of the obese, and it has been eye opening. Blaming the obese for their obesity makes no sense. Being overweight carries with it a host of social, employment and medical problems, and if it were easy to lose weight then few would be fat. The fact of the matter is that mere willpower is no match for metabolism.
It goes like this. The first week you're on your diet and you go to bed hungry you're fine with it, because the early weight lose is significant and easy. The second week of hunger is fine, too, because you're still optimistic. And the third week of hunger is okay, and maybe the fourth, and maybe for weeks and weeks more. It all depends upon how many diets you've been on before, how many nights of hunger you've already had to endure. At some point you just break down, you say the heck with it, and you go downstairs, open the fridge and just gorge. The next day you castigate yourself and vow to be stronger, and the cycle of hunger wearing down willpower begins again. Eventually willpower is defeated and docile and you put the weight back on and then some.
I'm not trying to be dramatic. Anyone who has battled obesity through their life will confirm that this is true, and many just become resigned to their obesity, especially since increasing age brings with it metabolic and lifestyle changes that make weight loss increasingly difficult.
There are certainly metabolic (and other) differences that make some people tend to be fatter than others, and those differences have always existed. They don't explain large scale increases in the average weight of whole populations though, do they?
You're right, they don't. These metabolic differences are not being introduced into the discussion as the explanation for the obesity/diabetes epidemic. But given the same diet/exercise regimen, metabolic differences cause different people to have different weight gain/loss experiences, and elevated levels of carbohydrate intake cause metabolic changes in the direction of obesity/diabetes. This underlying principle of Taubes argument is just that simple.
Naturally the metabolic processes and pathways are very complex, it's just the basic principle that is simple, just as simple as the dietary fat hypothesis that it seeks to replace.
Consider this:
Countries Compared by Health > Obesity. International Statistics at NationMaster.com
The four countries at the bottom have an average per capita income higher than the average of the four at the top, and there's no reason why the top four shouldn't have statistics like those of the bottom four (which have the minor obesity problems we had here in the U.K. 20 to 40 years ago - and I don't think we've mutated genetically a great deal since then!).
I think it might be better to consider diet versus obesity, not average per capita income versus obesity. In particular, national figures on fat and carbohydrate consumption would be very helpful. Also, there's a confounding issue when comparing different countries, because their statistic gathering techniques and criteria can differ a great deal.
Anyway, good luck with the diet.
Thanks, and speaking of the diet, it continues to go well, but very slowly. We (my wife and I) had gradually worked in higher proportions of foods with carbohydrates (still no sugar carbohydrates), causing us to both plateau for a few weeks. A week or so ago we reduced the proportions of these foods again and weight loss resumed. I'm now down 13-1/2 pounds and just this week had to take my belt in a notch. Weight loss is very slow, but for me it has to be. If I diet too aggressively I find I run out of energy quickly during exercise.
--Percy

This message is a reply to:
 Message 241 by bluegenes, posted 06-24-2008 2:14 AM bluegenes has replied

Replies to this message:
 Message 244 by bluegenes, posted 06-24-2008 4:36 PM Percy has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 248 of 451 (472839)
06-25-2008 6:53 AM
Reply to: Message 243 by Joe T
06-24-2008 2:12 PM


Re: Epidemic? Sure, but is it universal?
Hi Joe,
It sounds like you could tell that the heart of my dieting dilemma is choosing the right foods that have carbohydrates. I'm encountering two problems:
  1. Labeling. Labels do not describe carbohydrates beyond breaking it down into fiber, sugar and alcohol sugar (whatever that is). I assume that the sugar portion is roughly 50/50 glucose/fructose and the fiber is indigestible and can be ignored when considering contributions to nutrition. But what is the nature of the remaining carbohydrates? Using my wheat-bread/white-bread example, is the 17 grams of carbohydrates in wheat bread of a better nature than the 21 grams of carbohydrates in white bread? Does the additional mere gram of fiber in wheat bread really provide any measurable advantage? It seems to me the glycemic index would be very informative in this regard, but it isn't included on the label.
  2. What is a refined carbohydrate? I know you addressed this concerning white rice, but it seems to me there's a spectrum of carbohydrate complexity ranging from the very simple to the very complex. Simplest is sugar, which is 50/50 glucose/fructose. Ignoring fructose, all other carbohydrates are sugars that are broken down into glucose in the digestive system. The more work the digestive system has to do to break a carbohydrate down into glucose, the better that carbohydrate is for you. In other words, the more complex the carbohydrate, the more healthy it is judged to be.
    So even though white rice and white bread and regular pasta are made from refined carbohydrates, they are still more complex than glucose. The question is, how much more complex than glucose are they? Once again I think the glycemic index would be helpful here.
Unfortunately the glycemic index for a specific type and brand of food often isn't available. What you can find is generic measures for glycemic index at websites, which for things like broccoli and potatoes are probably pretty accurate, but for things like whole grain bread and pasta is very likely extremely brand/product dependent. So in the grocery store, how do you know (I mean actually *know*, not guess and hope) which carbohydrate foods to buy?
--Percy

This message is a reply to:
 Message 243 by Joe T, posted 06-24-2008 2:12 PM Joe T has not replied

Replies to this message:
 Message 250 by randman, posted 06-25-2008 2:30 PM Percy has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 249 of 451 (472843)
06-25-2008 7:50 AM
Reply to: Message 244 by bluegenes
06-24-2008 4:36 PM


Re: Epidemic? Sure, but is it universal?
bluegenes writes:
What I thought was unusual was your extreme light weight for someone of average height when you were young, and then battling with being overweight (not obese) when a full 75 lbs heavier. You would have been one of a small minority who could have put on 50 lb in adult life without being overweight!
More than 50. Not so long ago I was within shouting distance of double my age-18 weight of 105.
(At 5'10", you would have to be 209 lbs to be considered obese in that survey - you've never been there, from what I understood).
By that measure that takes into account height, weight and waist measurements, I was obese, but I think that says more about the limited application of this type of measure than anything else. This is going to sound kind of trite, but I hate clothes shopping, and one of my motivations for reducing weight is so that I don't have to buy more clothes, because the ratio of those that fit to those that didn't was getting scaringly small for a while. I like to tell myself that this is the most minor of my reasons for wanting to lose weight, but sometimes I'm not sure I'm being honest with myself.
Concerning an increasingly obese population and looking at it in terms of addiction, when such a huge proportion of the population has the same problem, then I think it might more accurately be considered as being within the normal range of behavior.
--Percy

This message is a reply to:
 Message 244 by bluegenes, posted 06-24-2008 4:36 PM bluegenes has not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 251 of 451 (472985)
06-26-2008 9:44 AM
Reply to: Message 250 by randman
06-25-2008 2:30 PM


Re: Epidemic? Sure, but is it universal?
It sounds like your conclusions about this are pretty similar to mine, especially the "no bread, rice, pasta, potatoes" part. I haven't had any problems so far when on the road or eating at other people's houses, usually I just stick to the meat or vegetable dishes. Of course, they could serve spaghetti with a rich tomato sauce and garlic bread, and then I'd have no options.
--Percy

This message is a reply to:
 Message 250 by randman, posted 06-25-2008 2:30 PM randman has not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 252 of 451 (473711)
07-02-2008 7:26 AM


More About Fructose
A recent New Scientist article describes research finding that fructose causes "alarming changes in body fat and insulin sensitivity that do not occur after eating glucose" (Is fructose fuelling the obesity epidemic?, requires a subscription to read the whole article on-line).
As described in this thread, the highest sources of fructose by far are sugared products. Table sugar, sucrose, is a 50/50 mix of fructose and glucose. High-fructose corn syrup (HFCS), the sweetener of choice in soft drinks, is a 55/45 mix of fructose/glucose. Sugar and HFCS are by far the highest sources of fructose in our diet. For comparison, a 12 ounce can of Coca-Cola contains 22 grams of fructose, while a cup of grapes contains only 2.
The study found that in obese subjects who consumed a diet where 25% of energy came from either fructose or glucose that:
In those given fructose there was an increase in the amount of intra-abdominal fat, which wraps around internal organs, causes a pot belly and has been linked to an increased risk of diabetes and cardiovascular disease. This did not happen with the group who consumed glucose instead, even though both gained an average 1.5 kilograms in weight.
As the article goes on to relate, more study is required to understand the relationship and interactions between glucose and fructose, but Peter Havel, the lead researcher from the University of California, Davis, says that those with metabolic syndrome might be wise to avoid consuming too much of HFCS products. Interestingly and unsurprisingly, PepsiCo funded the research and disagreed with this conclusion.
The yet-to-be-published paper was presented at the meeting of the Endocrine Society in San Francisco that took place in mid-June, and Havel's talk is listed in the conference program (Endocrine & Metabolic Effects of Consuming Beverages Sweetened with Fructose & Glucose).
--Percy

Replies to this message:
 Message 255 by molbiogirl, posted 07-04-2008 1:03 AM Percy has seen this message but not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 256 of 451 (474039)
07-04-2008 6:08 PM


Correcting Misinformation
Molbiogirl has returned to this thread and resumed her campaign of ridicule, character assassination, error, and misinformation. I guess there's something about the carbohydrate hypothesis that causes irrational and emotional knee-jerk objections, which is no way to contribute to a dispassionate scientific discussion. For Molbiogirl, science and research papers are just a backdrop upon which to paint her canvas of mudslinging and fallacies. There's really no way a rational dialogue can take place while Molbiogirl maintains this malevolent and emotional approach, and so all I can do is correct any misinformation I find in her three recent consecutive messages, Message 253, Message 254, and Message 255.
First, from Message 253:
Molbiogirl in Message 253 writes:
I finally settled on some really obvious flaws (no "temporary fat storage in the liver" after carb digestion, no "elevated VLDL levels" after carb digestion, etc.) to try and drive the point home ... no dice.
Taubes never says anything about "temporary fat storage in the liver". What he says is that the liver produces triglycerides (molecules containing three fatty acids) for temporary storage, and it was me who assumed that storage was in the liver. Molbiogirl corrected me, but since then has continued repeating the false claim that this is something Taubes said, something she knows isn't true since she has Taubes' book in her possession.
Moving on to Message 254:
Molbiogirl in Message 254 writes:
What you have failed to mention is that the reduction in epileptic seizures is accompanied by over 1/3 of the children suffering significant cognitive impairment.
Which you would have known had you watched the Charlie Rose interview (Taubes/Dr. Howard/Dr. Ornish) that I linked earlier in the thread.
Taubes tried to throw the ketogenic diet/epileptic seizure connection in Dr. Howard/Dr. Ornish's face and got a thorough dressing down -- with the facts.
The same mechanism for eliminating the seizures is apparently responsible for seriously degrading cognitive processes.
Molbiogirl misremembers the Charlie Rose nutrition panel discussion (YouTube Video), and this is wrong on two levels. First, it is actually Dr. Barbara Howard who introduces the topic, not Taubes. Second, Dr. Howard, a representative of the American Heart Association which is irrationally opposed to low carbohydrate diets, makes a series of claims that aren't supported by the research, even though she says they are:
Dr. Barbara Howard on the Charlie Rose show at 19:40 writes:
I would challenge Gary strongly about the accuracy of the Atkins data because it is well known that if a person eats very high protein and a lot of fat you become ketotic. As soon as you become ketotic you lose fluid and you lose your appetite, so of course you get a short term weight loss. But no one has ever shown even in a non-randomized trial that that can be sustained. What has been shown is that high protein, the levels of protein that they include in that diet, are absolutely detrimental, to the kidney and to the liver. They cause bone loss, very worrisome for a post menopausal woman, and those diets have been used in children for many years who have epilepsy, and those children show definite cognitive dysfunction."
Notice that Dr. Howard does not say what Molbiogirl claims she did, about "over 1/3 of the children suffering significant cognitive impairment." Dr. Howard mentions no such figures. As to the rest of the claims, it appears that Dr. Howard is confusing ketosis, a normal metabolic process, with ketoacidosis, which is indeed dangerous but has other causes unrelated to low carbohydrate diets.
On this panel, Dr. Barbara Howard and Dr. Dean Ornish are both arguing as if there existed conclusive evidence showing that not only are low carbohydrate diets ineffective, they are dangerous. But the research that actually exists is not consistent with such conclusions, as much as they might wish it were.
Concerning whether a ketogenic diet (a diet high in fat and low in carbohydrates) causes cognitive impairment in children with severe epilepsy, I could not find research studies showing this connection, which is not to claim it doesn't exist, I just couldn't find it, though I did find some urban legend-style misinformation out there on the Internet. And I also found a review study (Ketogenic Diet for the Treatment of Refractory Epilepsy in Children: A Systematic Review of Efficacy) from the journal Pediatrics (published by the American Academy of Pediatrics) that concludes:
"Although controlled trials are lacking, the evidence is sufficient to determine that the ketogenic diet is efficacious in reducing seizure frequency in children with refractory epilepsy."
And about cognitive impairment it says:
Poorly controlled epilepsy has been associated with higher rates of mortality, unemployment, and cognitive impairments.
Possibly Dr. Howard is confusing the remedy with one of the symptoms of refractory childhood epilepsy.
Moving on to Message 255:
Molbiogirl in Message 255 writes:
First, let me say that the New Scientist link you provide is referencing a 2001 paper by Havel. That's kinda funny, donchathink? A 2008 article discussing 7 year old findings?
The article is not about "a 2001 paper by Havel." As it clearly states, "Havel presented the results at a meeting of the Endocrine Society in San Francisco last week." By "last week" they mean mid-June of this year, just a few short weeks ago, not 2001. I can't imagine how Molbiogirl could make such a serious mistake, especially since she actually quotes the article in its entirety (here's the link to the article again: Is fructose fuelling the obesity epidemic?).
So when Molbiogirl goes on to ask:
Second, let me ask: Have you read the full Havel paper?
The answer is, of course, no. This was a presentation at a very recent conference, and the paper hasn't yet been published to my knowledge.
Fourth. I have read the 2001 Havel article.
Except that no "2001 Havel article" is mentioned in the New Scientist article. From the quotes Molbiogirl provides I was able to track the paper down. It is Fructose, weight gain, and the insulin resistance syndrome, and it is a November, 2002 (not 2001), paper that appeared in the American Journal of Clinical Nutrition. I don't know what it was in the New Scientist article that led Molbiogirl to this paper, but it looks very interesting and I will give it a read.
Problem No. 1. The obesity epidemic started long before HFCS was a staple of the American diet. HFCS wasn't developed until 1957. Obesity was already a problem. Remember the Pima!
Obesity has a long history, but the obesity epidemic that affects the entire western world across all religions, races and income categories is considered to have begun in the 1980s. This link contains a series a slides showing the increasing obesity rates by state from 1985 to 1999: The Worldwide Obesity Epidemic. Just start at slide 10 for 1985 and keep clicking for the next slide to see the US turn from mostly non-obese to mostly obese as the years click by. It makes for dramatic watching.
Glycogen. Not fat! (A reminder for those who haven't read the entire thread -- carbs are metabolized into glycogen -- a form of energy that is stored in the muscles and liver that isn't fat.)
This is so oversimplified as to be wrong. Both glucose and fructose are carbohydrates, and fructose is primarily transformed into triglycerides (fatty acids) by the liver. There are also metabolic pathways by which glucose can be transformed into triglycerides. Just baldly stating that "carbs are metabolized into glycogen" is very misleading.
Also, by the way she presents this point Molbiogirl may give some the impression that Taubes in some way claims that it is carbohydrates being digested into fat that causes obesity. Rest assured that this is not part of Taubes argument. While there are indeed metabolic pathways by which carbohydrates can be transformed into fatty acids, Taubes hypothesis is that it is elevated insulin levels caused by the intake of refined carbohydrates that make us fat, because elevated insulin levels increase the update of fatty acids by adipose tissue (fatty tissue).
Huh. Fructose is good for Type 2 diabetics. Taubes would have a fit.
Most components of diet have both positive and negative effects, and fructose is no exception. One of the negative effects of fructose described by Taubes is that because sustained intake at elevated levels (e.g., several cans of HFCS-sweetened beverage per day) can reduce the ability of the liver to transform glucose into glycogen (it's busy transforming fructose into triglycerides), thereby causing glucose to remain at higher levels in the bloodstream which in turn causes the pancreas to churn out more insulin, which causes increased insulin resistance, one of the primary symptoms of metabolic syndrome and diabetes. Molbiogirl can find this on page 200 in Taubes book.
De novo lipogenesis does not increase in response to eucaloric glucose ingestion (31).
Translation of biochem speak: de novo lipogenesis = making new fat. Taubes kinda missed this fact in his "exhaustive" studies.
This contains two errors, the first of which is not Molbiogirl's fault. First, the Havel paper is stating this a bit more strongly than the paper they reference (Regulation of hepatic de novo lipogenesis in humans), which says in the abstract:
The enzymatic pathway for synthesis of fatty acids from acetyl-coenzyme A, or de novo lipogenesis (DNL), is present in human liver and, to a lesser extent, in adipose tissue. Although the molecular and enzymatic regulation of the components for DNL are well characterized, the quantitative importance of the assembled pathway and its physiologic functions have remained uncertain.
The abstract does not describe the results, and the paper is only available for pay, but I did find a very similar paper (De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women) which concludes, "De novo lipogenesis increases after overfeeding with glucose and sucrose to the same extent in lean and obese women but does not contribute greatly to total fat balance."
Of course, we knew already that this was not a primary metabolic pathway for triglyceride production, but the Havel paper is clearly overstating the case to say that, "De novo lipogenesis does not increase in response to eucaloric glucose ingestion." I think all he was trying really to say is that it is not a primary contributor and need not be given much consideration when identifying sources of triglyceride production sufficiently significant to contribute to obesity. And, of course, Taubes describes these issues correctly in his book.
(In one of the 3 studies) body weight increased in a group of 14 middle-aged men, 11 with type 2 diabetes mellitus and 3 with type 1 diabetes mellitus, who incorporated 50-60 g fructose/d into their diets for 24 wk (38).
14 guys! Most of whom had diabetes. I'm serious. Somebody call the Nobel committee.
Molbiogirl is in a biology PhD program and is well aware of how small the number of subjects is in most studies. Limited sample size is extremely common in the field of diet/health research. There have been some large gold-standard studies, but they are extremely expensive (the country studies cost hundreds of millions of dollars 40 years ago and would cost billions today), so most studies are small. Small sample size will be true of much research literature cited in support of either side of the dietary fat hypothesis.
But one wonders why Molbiogirl is trying to discredit a paper she's using to support her position?
Fructose, unlike glucose, does not stimulate insulin secretion from pancreatic cells (40, 41). ... Although high-carbohydrate meals stimulate leptin production in humans relative to high-fat meals (80), if the carbohydrate provided in this study had been fructose rather than glucose, the results would probably have been different because of the dissimilar effects of the 2 sugars on insulin secretion. To compare the effects of glucose and fructose on leptin production, plasma leptin concentrations were measured in rhesus monkeys after intravenous infusion with saline, glucose, or fructose. Glucose infusion markedly increased plasma glucose and insulin concentrations and progressively increased plasma leptin 4-8 h into the infusions. In contrast, an intravenous infusion of the same amount of fructose only modestly increased plasma glucose and did not stimulate insulin secretion or increase circulating leptin concentrations over an 8-h period (65).
There goes yet another of Taubes' pet theories. He thinks insulin is the driving force behind obesity.
The conclusion that insulin is not a driving force behind obesity does not follow from the quoted passage. Indeed, it doesn't address the causes of obesity at all. This is a frequent occurrence in Molbiogirl posts, to quote something, almost anything it sometimes seems, then claim it somehow supports her position no matter how irrelevant.
Another puzzle for Taubes. How on god's green earth is hyperinsulemia induced without insulin?
As mentioned earlier, this is described on page 200 in Taubes' book.
An increased supply of nonesterified fatty acids in the liver also leads to an increase in the production of VLDL triacylglycerol (102).
Aha! Elevated VLDL correlated with fat! Poor old Taubes. He's getting a licking in this paper.
This requires a little translation. "Non-esterified fatty acids" are free fatty acids. "Triacylglycerol" is the technical term for what is more commonly called triglycerides, which are three fatty acids bound together into a single large molecule for transport around the body in the bloodstream.
The passage Molbiogirl quotes is saying that increasing the supply of free fatty acids to the liver can lead to an increase in the production of VLDL triglycerides, which isn't inconsistent with anything Taubes says. Where Taubes writes about this process in his book he's talking about coronary heart disease, not obesity.
The combination of the high-fat diet with fructose resulted in increased circulating triacylglycerol, and fructose with copper deficiency resulted in significant increases in blood cholesterol.
Uh oh. Looks like one needs both fat and fructose to elevate TAGs. More bad news for Taubes.
Fat plus fructose is only one of the many metabolic pathways that can elevate triglyceride levels.
Hyperlipidemia did not develop when starch was combined with a high-fat diet (110).
Translation of biochem speak: hyperlipidemia = putting on too much fat aka getting pudgy.
And starch = carbs. Nail in the coffin for Taubes, if you ask me.
In other words, this passage says that high levels of triglycerides did not result when starch (carbohydrates) was combined with a high fat diet. This is rather inconclusive, as what's truly significant is insulin levels. The more complex the carbohydrate, the less insulin is released to transform triglycerides into fat, and the passage gives no indication of the degree of complexity of the carbohydrate.
Hellerstein (111) showed that there is little de novo lipogenesis from glucose under eucaloric conditions in humans.
Yet another study Havel mentions that completely destroys Taubes' central argument.
Taubes position is definitely not that "de novo lipogenesis" from glucose is the cause of obesity. Again, where Taubes talks about the liver producing triglycerides from glucose it was in the context of coronary heart disease.
This concludes the correction of errors and misinformation provided by Molbiogirl in her three messages. Molbiogirl is operating under the supposition that the evidence disproving the carbohydrate hypothesis already exists, but it doesn't. And the evidence conclusively supporting the dietary fat hypothesis doesn't exist either. It is this paucity of evidence that Taubes decries most.
Whether the carbohydrate or dietary fat hypotheses are right or wrong will be shown by scientific research and discourse, not by whatever it is Molbiogirl is doing. In other words, in a scientific discussion you have to say things that are about the hypothesis rather than about the people backing the hypothesis, and more importantly, when finally addressing the topic you have to say things that are actually true.
--Percy

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 258 of 451 (475707)
07-17-2008 4:01 PM
Reply to: Message 257 by Joe T
07-17-2008 1:57 PM


Re: A New Study
Hi Joe, thanks for posting this MSNBC article (Low-carb beats low-fat in diet duel). There's a few things I want to comment on, but first a short personal report.
Concerning the state of my diet, I'm now down 15 pounds. I'm losing weight very slowly, and as I've mentioned, I have to do it that way. If I lose weight too fast then I lose stamina, which I can't afford to do. Today the temperature is around 90, and in an hour or so I have to play some tennis, which I do around three times a week. If I eat too little I get too tired too quickly.
Concerning the state of my health, a few weeks ago I had my annual checkup, which includes blood work. My triglycerides, cholesterol, HDL and LDL levels have never been better. They're way better, in fact, best they've ever been in the last 20 years. Before that I have no data.
Now a few comments about the article.
First, here's a link to the actual study itself in the New England Journal of Medicine: Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet. I actually have to leave in a few minutes and can't read it right now.
msnbc writes:
The low-fat diet ” no more than 30 percent of calories from fat ” restricted calories and cholesterol and focused on low-fat grains, vegetables and fruits as options.
If the low-fat diet this study used is typical of modern low-fat diets, then anachronistically enough the low-fat diet still features cholesterol restriction when it's been known for at least 20 years that dietary cholesterol does not become blood cholesterol. Dietary cholesterol is broken down by the digestive system before it reaches the bloodstream. Dietary cholesterol is not the source of blood cholesterol.
The Mediterranean diet had similar calorie, fat and cholesterol restrictions, emphasizing poultry, fish, olive oil and nuts.
So the main difference between the low-fat and the Mediterranean diets used in this study is that the low-fat diet included more carbohydrates. Of the three diets in the study, the low-fat had the highest carbohydrate content and the worst performance for weight loss.
"So not a lot of butter and eggs and cream," said Madelyn Fernstrom, a University of Pittsburgh Medical Center weight management expert who reviewed the study but was not involved in it.
Since Madelyn Fernstrom reviewed the study, she has knowledge of details that may not have been mentioned in the article, but I should mention that butter and eggs contain very little carbohydrates and would not normally be restricted in any way on a low carbohydrate diet. Proportionally cream contains far higher levels of carbohydrates than butter or eggs, but one doesn't normally drink much cream, anyway. Certainly a couple of teaspoons of cream in a cup of coffee is going to contribute negligibly to carbohydrate intake, definitely less than a single gram. Cream or milk in products like ice cream is another matter, since the sugar in such food products results in high carbohydrate levels, including fructose.
More surprising were the measures of cholesterol. Critics have long acknowledged that an Atkins-style diet could help people lose weight but feared that over the long term, it may drive up cholesterol because it allows more fat.
This should come as a surprise only to members of the American Heart Association and the American Diabetes Association, which for reasons known only to themselves choose to ignore the decades of research clearly showing that increased intake levels for fat and protein do not correlate with cholesterol levels. Or with obesity. Or with heart disease, for that matter. Or with diabetes, either.
As far as the American Heart Association goes, I hope its members think of it in the same way American Catholics think about the Pope. It's a good and important organization, it fills an important organizational role, but by and large they're not actually going to follow its dietary advice.
I also wanted to comment on a couple things you mentioned:
Joe T writes:
Note that the fats consumed by the low carb peoples were vegetable based so this probably doesn’t do anything one way or another to settle the Taubes/Atkins claims (as I understand them) that saturated animal fats are not a health issue.
If I could clarify Taubes position on saturated fats (which may or may not be the same as Atkins, I don't know - I don't have the book with me right now, but I don't recall Atkins mentioned in much more than a historical role), he's not saying saturated fats are not a health issue. What he's saying is that they aren't the health issue that the American Heart Association says they are, and there are already many completed research studies calling their position on saturated fats into question. Like most components of diet, saturated fats carry both benefits and risks. High intake levels of saturated fats correlate with higher risk of coronary heart disease (this correlation should not be mistaken for causation, which hasn't been established), while low intake levels correlate with even higher rates of rectal cancer (again, no causation established). Pick your poison. By the way, the risk of death from rectal cancer is higher than that for coronary heart disease.
Taubes also describes some positive dietary contributions of saturated fats. I don't recall the details, and as I said, I don't have the book with me right now.
3. Diabetics only lowered their blood sugar on the Med diet.
This finding is the only one I find surprising. It will be interesting to read the study when I get a chance to see if it contains any speculation about why higher fat intake might boost blood sugar levels.
By the way, the article contains a link to a Newsweek article about the same study (The Never-Ending Diet Wars) by Dean Ornish, who says the study has some serious flaws. Dr. Ornish's name might be familiar to some, he has his own diet called The Ornish Diet, which is a low-fat diet, so naturally he's unhappy with the study's results. I don't have time to give this much of a look right now, either, I'll have to comment later.
--Percy
Edited by Percy, : Clarification in next to last para.
Edited by Percy, : Spelling in last para.
Edited by Percy, : Fix minor grammar mistake.

This message is a reply to:
 Message 257 by Joe T, posted 07-17-2008 1:57 PM Joe T has not replied

Replies to this message:
 Message 259 by Percy, posted 07-19-2008 9:48 AM Percy has seen this message but not replied

Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024