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Medical Forum / General / Nutrition / November 2004Re: Very low-carb diets work for men and upper body fat
Sorry, exeeds standard guidelines for verity set in this group: "be funded in part by the Robert C. Atkins Foundation, has previously" >http://www.eurekalert.org/pub_releases/2004-11/bc-vld111204.php > >Very low-carbohydrate diets work for men and upper body fat >Scientists say that low carbohydrate diets, like the Atkins and South >Beach Diets, may actually be the best option for men who want to slim. >New research, published this week in the Open Access journal, >Nutrition & Metabolism, shows that over 70% of men lost more weight >and fat on a low carbohydrate diet, despite eating more calories. >Jeff Volek and colleagues, from the University of Connecticut, also >show for the first time that a low carbohydrate diet is much more >effective in losing fat from the stomach and chest. Upper body fat >carries "a greater health risk than fat stored in other regions of the >body," say the authors. They found that fat loss in men was >three-times greater in the trunk area, when they were on a >low-carbohydrate regime compared to the low-fat diet. Nearly all >participants in the study (12 of 15 men and 12 of 13 women) lost more >fat on their upper body on the low- carbohydrate diet. > >Fifteen overweight or obese men, and thirteen women, were randomly >assigned to a very low carbohydrate diet or a low fat diet. After >fifty days, they were switched to the other diet. 11 of the 15 men did >better on the low carbohydrate diet, six lost greater than 10 lbs more >on the low carbohydrate diet, and one subject lost almost 25 pounds >more. Similar results were found for women although the results were >less dramatic. > >Volek and colleagues also looked at whether weight and fat loss were >affected by what order the diets were done in. Their data seem to >favour undertaking a low carbohydrate first, suggesting that those who >have concerns about long term 'low carb' diets could follow a low carb >diet first followed by a low fat diet. > >There is much debate about the health implications of long-term use of >low carbohydrate diets. Volek's lab, whose work is the first-ever to >be funded in part by the Robert C. Atkins Foundation, has previously >shown that low carbohydrate diets improve cardiovascular risk factors. > >For more information about low carbohydrate diets read the review by >well-known endocrinologist, Samy McFarlane, in Nutrition & Metabolism. >Dr McFarlane reviews the new book, 'Atkins Diabetes Revolution', by >Mary C. Vernon, M.D. and Jacqueline A. Eberstein, R.N. McFarlane and >co-reviewer Surender Arora, M.D. found the book "sufficiently >convincing to make us believe that some form of low carbohydrate >intervention is worth investigating and should be considered by >practitioners. The highly negative un-scientific response of critics, >if anything, encourages us in this direction." > >This press release is based on: > >Comparison of energy-restricted very low-carbohydrate and low-fat >diets on weight loss and body composition in overweight men and women >Volek JS, Sharman MJ, G?mez AL, Judelson DA, Rubin MR, Watson G, >Sokmen B, Silvestre R, French DN, and Kraemer WJ. Nutrition & >Metabolism 2004, 1:12 (9 November 2004) > >The article is freely available at >http://www.nutritionandmetabolism.com/content/1/1/12. > >******* > >TC >Sorry, exeeds standard guidelines for verity set in this group: > >"be funded in part by the Robert C. Atkins Foundation, has previously" That's a non-profit foundation endowed by his estated. I suppose we have to throw away all for profit industry funded research we see, too? Not those of us who can *read* study parameters and actually *think* and analyze. Not to mention, you're the last person with any credible claim to veracity. Susan > x-no-archive: yes > [quoted text clipped - 13 lines] > > Susan Yes, I don't take in account biased research whether they come from low carbers, low fatters, meditteranean eaters, paleo dieters, weight watchers, ornish... whatever I would not even care for a biased study on mediterranean diet if I know it is funded by an Foundation pushing meditteranen diet or a programm where you have to buy several meditteranean diet products We shouldn't forget that everything linked with Atkins is money, as you can buy several dietary items with Atkins name in it and this a very profitable market I don't care if they say they're no-profit I know enough no-profit association to know that it doesn't work that way They are not supposed to have a legal profit, but they find the way anyway to earn money illicitly either buy not reinvesting in the Foundation or being payed to promote their marketing items Daniel >Yes, I don't take in account biased research whether they come from low >carbers, low fatters, meditteranean eaters, paleo dieters, weight [quoted text clipped - 12 lines] > >Daniel The only reason you have to worry about all that stuff is if you aren't capable of understanding and evaluating the study design, the data and conclusions on your own. Plus, you're sounding more paranoid than usual. Susan > x-no-archive: yes > [quoted text clipped - 22 lines] > > Susan That's not true I may be able to evaluate the results by myself, but the point is that the results may simple be false or sabotaged It wouldn't be the first time Like studies about longevity and nutrition not taking in account that some of the partecipants where already terminal patients When there's money behind it's easy that someone is payed to have the partecipants results sabotaged or falsified In fact, there were studied in which the partecipants disappeared misteriously after several weeks without mentioning their not adhering to the criteria I'm admit I'm a bit paranoid but I've good reasons to Daniel >That's not true >I may be able to evaluate the results by myself, but the point is that >the results may simple be false or sabotaged >It wouldn't be the first time You completely missed my point. You don't accept the "results" or conclusions of the study, you critique the methodology and evaluate it for omissions, unwarranted inclusions, poor controls of variables, mssing data etc... >Like studies about longevity and nutrition not taking in account that >some of the partecipants where already >terminal patients If that information is included in the study paper, then you decide for yourself if the study is crapola or not. See how it works? You can't just go by headlines and researchers' conclusions that are unsupported by their own data. >When there's money behind it's easy that someone is payed to have the >partecipants results sabotaged or falsified >In fact, there were studied in which the partecipants disappeared >misteriously after several weeks without mentioning their not adhering >to the criteria >I'm admit I'm a bit paranoid but I've good >reasons to Research isn't free, you know, there's always money involved. Shall we just stop trying? I can assure you that you'd have to stand behind me in line at the Medical Science Skeptics Convention. That's why I read research from many countries, some where there is no profit motive or corporate dominance of research. One looks for corroboration of suspicious results across the board. Anyway, the U.S. corporate driven research is pretty transparent; they present data showing one thing, and then write a conclusion deliberately misinterpreting it. This is what's happened with the pharma and sugar industry driven CVD and diabetes diet research. Ignore the conclusions and read the data for yourself. No one is going to spoonfeed you the right answers, you have to work for them. Susan >No one is going to spoonfeed you the right answers, you have to work for them. That's really the point. Unless you have a research qualification and actually work in the field of interest, you are unlikely to be able to see the wood for the trees. You will be unlikely to know all the work going on around the world, and unlikely to be able to evaluate all the different inputs and to know what went before and have your finger on the pulse to have an idea of what is coming in the future. You really need a senior researcher to write a review for the public to get a balanced view of the whole area. Finding a paper that supports your pet theory is probably meaningless, unless you can fit this small piece of the jigsaw puzzle into the overall big picture. A very difficult task, usually. > > x-no-archive: yes > > [quoted text clipped - 37 lines] > > Daniel You people are pathetic. Wake up and face the facts. Restricted carb higher fat diet leads to not just more weight loss but promotes more fat loss especially in vital areas. I do not need a study, weather it is biased or not, to tell me that. I have experienced it personally as have countless others. The only thing that is not resolved here is what inner biases or ideological blocks YOU people have that keep you from accepting reality. This logic applies to many things in life. Some use the "not-tested" approach to live in a pool of whining and complaining. > > > x-no-archive: yes > > > [quoted text clipped - 45 lines] > what inner biases or ideological blocks YOU people have that keep you > from accepting reality. >You people are pathetic. Wake up and face the facts. Restricted carb >higher fat diet leads to not just more weight loss but promotes more >fat loss especially in vital areas. What's pathetic is your reading comprehension, or lack of it. I'm a low carber who relies on her own resesarch, not pronouncements by some a-hole on the internet. Susan >> x-no-archive: yes >> [quoted text clipped - 35 lines] >to the criteria >I'm admit I'm a bit paranoid but I've good reasons to I would have said sceptical, rather than paranoid. Some folk are just busting to find anything that fits their own personal dogma. Not really suitable to a sci group. A person's personal problems and idiosyncracies are not properly aired here. > Sorry, exeeds standard guidelines for verity set in this group: > > "be funded in part by the Robert C. Atkins Foundation, has previously" Yes, biased is an understatement Daniel "70% of men lost more weight and fat on a low carbohydrate diet, despite eating more calories." I'd like to see that!. PR >"70% of men lost more weight and fat on a low carbohydrate diet, despite >eating more calories." > >I'd like to see that!. > >PR Then try it! Susan > x-no-archive: yes > [quoted text clipped - 6 lines] > > Then try it! Good to see you're still around. You seem to have out-lived a complete generation -- or did you bore them to death! Now, why would I try it when a low-fat high-carb diet with a little exercise leaves me in perfect shape. I agree with Daniel though, I would not trust this study, that seems to be able to accept the mythology of a substantial 'metabolic advantage'. 1. 25% fat is not a low-fat diet; 15% would be a better comparison. 2. Alternating diets seems like a very strange methodology for comparing weight loss in individual subjects. 3. If you want me to believe that some men 'ate more' and 'lost more' on low-carb, then you will also believe in fairies and alien abduction -- but then maybe you do. "Actual nutrient intakes from food records during the VLCK (%carbohydrate:fat:protein = ~9:63:28%) and the LF (~58:22:20%) were significantly different. Dietary energy was restricted, but was slightly higher during the VLCK (1855 kcal/day) compared to the LF (1562 kcal/day) diet for men. Both between and within group comparisons revealed a distinct advantage of a VLCK over a LF diet for weight loss, total fat loss, and trunk fat loss for men (despite significantly greater energy intake). " Paul R x-nio-archive: yes >Now, why would I try it when a low-fat high-carb diet with a little exercise >leaves me in perfect shape. How modest. :-) You said you'd like to see it. There's one way to do that. I agree with Daniel though, I would not trust >this study, that seems to be able to accept the mythology of a substantial >'metabolic advantage'. I agree that the advantage isn't what Atkins wrote about. Long term studies find that weight loss is pretty even after 6-12 mos. But lower carb dieters have much better lipid ratios, TGLs and LDL particle size, along with lower BG and HbA1c. All markers for health and longevity. Since insulin is a storage hormone that loves to deposit belly fat, it explains why you see so many otherwise skinny high GL carb eaters (and beer drinkers) with fat, round tummies. >1. 25% fat is not a low-fat diet; 25% is very low fat, by any definition other than the Ornish insanity. 30% is considered too low by most lipid researchers for immune and brain health. > 15% would be a better comparison. No, that's exTREME low fat. Unpalatable and unhealthy. It causes folks' brains to rot so badly that they can't read science or get facts straight. :-) >2. Alternating diets seems like a very strange methodology for comparing >weight loss in individual subjects. Um, you've never heard of crossover studies? Better methodology than a straight comparison. >3. If you want me to believe that some men 'ate more' and 'lost more' on >low-carb, then you will also believe in fairies and alien abduction -- but >then maybe you do. I don't believe in those other things, but I have noted that since fat is hormonally neutral, it takes more fat calories than carb calories to gain or maintain weight. You can look it up. Fat stimulates neither glucagon nor insulin. Only 50% of protein becomes glucose, a signal to store weight, one which is made by 100% of digested carbohydrate. Susan > x-nio-archive: yes > [quoted text clipped - 22 lines] > 25% is very low fat, by any definition other than the Ornish insanity. 30% is > considered too low by most lipid researchers for immune and brain health. By most lipid researchers? Where? Who? How many? I've never heard 30% is considered low In fact, with 30% fact you get all the EFA you need Daniel >By most lipid researchers? >Where? Who? How many? >I've never heard 30% is considered low >In fact, with 30% fact you get all the EFA you need > >Daniel In the scientific literature you so scrupulously avoid reading. We could fill an encyclopedia with what you've never heard nor read. 30% is a widely acknowledged threshold for low fat in most research. Below that is very low fat. Susan > x-no-archive: yes > [quoted text clipped - 11 lines] > 30% is a widely acknowledged threshold for low fat in most research. Below > that is very low fat. The fact that 30% in considered low fat compared with the average amount consumed doesn't mean that many lipid experts says that you get deficiencies by consuming "only" 30% fat A part from rare bizzarre theories there's no study on the scientific literature showing a fat deficiency causing metabolic disfunction when fat intake is 30% Period Daniel > The fact that 30% in considered low fat compared with the average amount > consumed doesn't mean that many lipid experts says that you get > deficiencies by consuming "only" 30% fat This is not about deficiencies, this is about better or worse lipid profile. > A part from rare bizzarre theories there's no study on the scientific > literature showing a fat deficiency causing metabolic disfunction when fat > intake is 30% Well, while it is not clear whether lipid profile has any actuall meaning in this dietary situation, it was clearly shown that decreasing fat below 30% affects lipid profile in a way that would indicated increased risk in persons with normal diet. I hope I wrote that as correct as I could :) Mirek >> The fact that 30% in considered low fat compared with the average amount >> consumed doesn't mean that many lipid experts says that you get [quoted text clipped - 13 lines] > > I hope I wrote that as correct as I could :) Well no, not really <g>. In populations with total cholesterol around 150 or below, cardiovascular disease and heart attacks are very rare -- independent of modest HDL numbers. These levels are never achieved on Atkins diets as far as I know. Diets such as Ornish and Pritikin achieve this for most people. I am not suggesting one needs to be this low-fat, but to say that a diet with less than 30% fat is somehow deficient is just Atkins hyperbole. I would remind you of this statement from Nathan Pritikin's autopsy in the New England Journal of Medicine, 1985: "At autopsy, the epicardium was smooth with no scars. The coronary arteries were soft and pliable. Several arteries showed some yellow, fat streaks, but no elevated plaques were seen and no reduction of the lumen was found. The absence of atherosclerosis and its effects in a 69-year-old man is remarkable. Hubbard, J., et al, Nathan Pritikin's Heart, NEJM, 52, July 1985." (Yes, I have read the full paper.) Now why did we not see an Atkins' autopsy? Paul R >>> The fact that 30% in considered low fat compared with the average amount >>> consumed doesn't mean that many lipid experts says that you get [quoted text clipped - 18 lines] > independent of modest HDL numbers. These levels are never achieved on > Atkins diets as far as I know. My friend, I was not commenting how rare is CAD in population with TC at 150. Just lipid profile and cardiovascular risk models. Nothing more. Just for record, given all the data I personally _believe_ that all that cholesterol thing works at multiple levels. There is plague buildbup that is probably to some degree caused by small LDL particles. Then there is also reverse cholesterol transport, caused by HDL. Now LDL is really raised by saturated fat, but OTOH LDL particle size and HDL is screwed by high carb, high GI. Under normal circumstances, high LDL is accompanied by higher reverse transport via HDL. All statistic data suggest that really predictive is not TC or LDL alone, but rather LDL/HDL combined with TG. (Note: it is interesting how Kendrick and others Cholesterol sceptics are actually pretty silent about HDL and LDL/HDL ratio :) That is why saturated fat on low-carb diet raises both LDL and HDL - body simply responds to high LDL (or saturated fat?) by increasing HDL. Anyway, throw refined carbs into this process and you will screw this reverse thing. BTW, if would take time to look at that initial Keys study that induced many years later low-fat stupidity, you would find that all countries with high CAD and high fat intake had also high refined carbs consumption. Where glycemic load was low, high-fat was much less problem. To sum it up, it is not unlikely that both ways of CAD diet interventions are valid. You can both affect LDL side of equation, or LDL particle size equation and HDL. You do first by reducing saturated fat, second by reducing refined carbs. Who knows, maybe the best diet is low-carb high sat fat with statins, at least for majority of people able to tolerate them... BTW, I would also like to mention one thing - all the time we are considering diets, we speak only about CAD. But there are other diseases out there that can be affected by diet. And there are e.g. some studies linking higher LDL levels with better immune system, or low LDL levels with aggressive behaviour etc. Mirek >>>> The fact that 30% in considered low fat compared with the average >>>> amount consumed doesn't mean that many lipid experts says that you get [quoted text clipped - 21 lines] > My friend, I was not commenting how rare is CAD in population with TC at > 150. Just lipid profile and cardiovascular risk models. Nothing more. Well I have just showed you one lipid profile risk model with putative dietary fat percentage less than 20% where CAD is low. No, you were saying much more. You were saying that a diet with less than 30% fat produces unhealthy lipid profiles. > Just for record, given all the data I personally _believe_ that all that > cholesterol thing works at multiple levels. There is plague buildbup that [quoted text clipped - 6 lines] > (Note: it is interesting how Kendrick and others Cholesterol sceptics are > actually pretty silent about HDL and LDL/HDL ratio :) HDL, ratios and LDL particle size seem to be more imporant at higher total cholesterol numbers. As you approach 150 (4mmol) and below, this minutiae becomes less important but there may still be a safety threshold, say around 40 (1.1 mmol) for HDL. > That is why saturated fat on low-carb diet raises both LDL and HDL - body > simply responds to high LDL (or saturated fat?) by increasing HDL. Anyway, [quoted text clipped - 12 lines] > sat fat with statins, at least for majority of people able to tolerate > them... There may well be successful dietary approaches to CAD prevention that do not follow the low-fat model, ie, Mediterannean etc, but this is like shuffling the cards hoping to get dealt an ace. For example, we need to know what happens on Atkins type diets for many months after weight loss is stabilised, not during weight loss. In Mediterranean diets is it the wine, the vegetables or n-3 -- ALA or fish oils? How much of any of these factors? What if you slack on one of them? If you have a heart attack, most cardiologists will recommend you get TC down to 150 or below, with or without statins (mostly with). That's the bottom line. Play with it above that if you like, but go and look at the curve. > BTW, I would also like to mention one thing - all the time we are > considering diets, we speak only about CAD. But there are other diseases > out there that can be affected by diet. And there are e.g. some studies > linking higher LDL levels with better immune system, or low LDL levels > with aggressive behaviour etc. You have to distinguish between low cholesterol in healthy and infirm people. The only adverse effect of a low-cholesterol state in healthy people that is in any way supported by reliable ongoing data is haemorrhagic stroke. You will see this with just about any intervention that improves blood flowability, ie, aspirin, fish oil, warfarin etc. This risk is low and is a perfectly acceptable trade-off. Exercise may protect against it. So . . . now do you agree that diets with less than 30% fat are not pathological for EFA or lipid profile? (Not sure why I bother really.) Paul Rogers >Well I have just showed you one lipid profile risk model with putative >dietary fat percentage less than 20% where CAD is low. No, you were saying >much more. You were saying that a diet with less than 30% fat produces >unhealthy lipid profiles. It's an unhealthy lipid profile even with LDL if most of the particles are small, and if the TGLs are above 100-150, a good predictive risk factor. Low fat also tends to create higher HbA1c, a marker even in non-diabetics for higher CVD risk. 150 is arbitrary and unimportant by itself. Ratios and types of particles matter, along with blood glucose along the whole "normal" range being an elevated risk even in the lowest quartiles, the higher it goes. >There may well be successful dietary approaches to CAD prevention that do >not follow the low-fat model, ie, Mediterannean etc, but this is like >shuffling the cards hoping to get dealt an ace. For example, we need to know >what happens on Atkins type diets for many months after weight loss is >stabilised, not during weight loss. I've been on low carb for several years. Many other folks have, too. Once weight loss stops, LDL can creep up, but overall longevity markers are much better on lower carb/low GL. > In Mediterranean diets is it the wine, >the vegetables or n-3 -- ALA or fish oils? How much of any of these factors? >What if you slack on one of them? That's a good question. Some meditteraneans eat very high animal fat/protein. Then you have the French paradox. >If you have a heart attack, most cardiologists will recommend you get TC >down to 150 or below, with or without statins (mostly with). That's the >bottom line. Play with it above that if you like, but go and look at the >curve. Most doctors are really, really dumb. But my relatives who practice cardiology use low carb, as do many endocrinologists for their own health and for patients'. >You have to distinguish between low cholesterol in healthy and infirm >people. The only adverse effect of a low-cholesterol state in healthy >people that is in any way supported by reliable ongoing data is haemorrhagic >stroke. You will see this with just about any intervention that improves >blood flowability, ie, aspirin, fish oil, warfarin etc. This risk is low and >is a perfectly acceptable trade-off. Exercise may protect against it. Well, there's also that pesky suicide risk thing, too. >So . . . now do you agree that diets with less than 30% fat are not >pathological for EFA or lipid profile? (Not sure why I bother really.) > >Paul Rogers I've concluded that brain and immune health aren't well supported by that low a fat %. Also that such low fat is a marker for high GL, which is a marker for increased mortality risk by many diseases, including breast and ovarian cancers. Susan > Well I have just showed you one lipid profile risk model with putative > dietary fat percentage less than 20% where CAD is low. No, you were saying > much more. You were saying that a diet with less than 30% fat produces > unhealthy lipid profiles. It does! Only problem, which you seem to ignore in my post, is that "unhealthy" lipid profile does not mean CAD. It is considered unhealthy only by models. > HDL, ratios and LDL particle size seem to be more imporant at higher total > cholesterol numbers. As you approach 150 (4mmol) and below, this minutiae > becomes less important Perhaps for CAD. But stroke and cancer seems to go up as TC goes down. Well, I of course do know standard explanation for cancer, but other studies showed that persons with cancer showed low TC levels 10 or more years before disease... > but there may still be a safety threshold, say around 40 (1.1 mmol) for > HDL. Well, with HDL at 40, TC 150 and high carb diet (read TG likely to be around 100 or more), your LDL is going to be somewhere around 100, giving excellent LDL/HDL profile. Means ratios are still working... > There may well be successful dietary approaches to CAD prevention that do > not follow the low-fat model, ie, Mediterannean etc, but this is like > shuffling the cards hoping to get dealt an ace. For example, we need to > know what happens on Atkins type diets for many months after weight loss > is stabilised, not during weight loss. I agree. Anyway, that also implies that we will study maintainance phase of diet! Something that was never actually done. Mirek > Perhaps for CAD. But stroke and cancer seems to go up as TC goes down. > Well, I of course do know standard explanation for cancer, but other > studies showed that persons with cancer showed low TC levels 10 or more > years before disease... Mirek, most of the healthy children in the world have cholesterol levels below 150. This is not a 'low' number, this is a healthy number. Are they all at risk from cancer and stroke? Maybe ADHD? <g>. You have been reading too much wacky stuff on the net. Tohoku J Exp Med. 2003 Oct;201(2):75-80. Serum cholesterol, triglyceride, VLDL-c, LDL-c, and HDL-c levels in healthy children. Bahar A, Sevgican U, Karademir F, Gocmen I. Please show me one convincing study that demonstrates that cancer incidence is increased in healthy people with long-term low cholesterol. PR > Mirek, most of the healthy children in the world have cholesterol levels > below 150. This is not a 'low' number, this is a healthy number. Are they > all at risk from cancer and stroke? Maybe ADHD? <g>. You have been reading Well, I do not understand what you want to prove with it... You have agreed that low-TC slightly increases stroke risk. Do you conclude that children are more likely to get stroke? As I am sure that you would not understand what I mean, I will try to be more specific: the most prominent risk factor for all dangerous diseases (cancer, CAD, stroke etc...) is age. Just because young persons with low-TC does not get cancer is irrelevant for age group age high risk. Following is just a speculation, more to explain what I have on mind: Perhaps LDL plays certain role in patching flaws in aging metabolism (as it probaly does with bleeding stroke - here the mechanism is probably apparent - LDL patches veins that are too thin due to aging...). Mirek >> Mirek, most of the healthy children in the world have cholesterol levels >> below 150. This is not a 'low' number, this is a healthy number. Are they >> all at risk from cancer and stroke? Maybe ADHD? <g>. You have been >> reading > > Well, I do not understand what you want to prove with it... That this level of total cholesterol is not hazardous. You will see this in alcoholics and smokers and others in poor health and this probably accounts for much of the excess cancer and other adverse associations. > You have agreed that low-TC slightly increases stroke risk. Do you > conclude that children are more likely to get stroke? Clever response! No I would not expect it. >Perhaps LDL plays certain role in patching flaws in aging metabolism (as it >probaly does with bleeding stroke - here >the mechanism is probably >apparent - LDL patches veins that are too thin due to aging...). I agree that as one ages arterial conditions change -- there is inevitably more plaque, and elasticity declines, more or less for different reasons across the population. TC of 150 is also a difficult number to maintain into older age without a reasonably strict diet and exercise plan. However, the curve (CVD and TC) starts to ascend from this level, and of course you can play with HDL, particle size, homocysteine, fibrinogen, CRP etc above this, but this is difficult for most people as it gets too complex. In my view, the risks of maintaining, long-term, TC of <>150, with exercise, which I suspect provides additional benefits for artery elasticity, far outweigh any excess risk of bleeding stroke. The other risks are negligible and the reduction in CVD risk is somewhat substantial and assured. I don't think we are too far apart on the basics. BTW, here is an interesting study that one could compare with the low-cholesterol scare stories (low-carbers beware!): Circulation. 2000 May 2;101(17):2047-52. Low fasting plasma glucose level as a predictor of cardiovascular disease and all-cause mortality. Wei M, Gibbons LW, Mitchell TL, Kampert JB, Stern MP, Blair SN. "Participants with low fasting plasma glucose levels also had increased risk of all-cause mortality (test for trend P<0.0001). CONCLUSIONS: Participants with low fasting plasma glucose levels had a high risk of cardiovascular disease and all-cause mortality." Cheers, Paul R > In my view, the risks of maintaining, long-term, TC of <>150, with > exercise, which I suspect provides additional benefits for artery > elasticity, far outweigh any excess risk of bleeding stroke. The other > risks are negligible and the reduction in CVD risk is somewhat substantial > and assured. Fair enough. > I don't think we are too far apart on the basics. Not that much. > BTW, here is an interesting study that one could compare with the > low-cholesterol scare stories (low-carbers beware!): [quoted text clipped - 9 lines] > Participants with low fasting plasma glucose levels had a high risk of > cardiovascular disease and all-cause mortality." Could be Mets again, at least initial phase with sort of reactive hypo. Mirek >> In my view, the risks of maintaining, long-term, TC of <>150, with >> exercise, which I suspect provides additional benefits for artery [quoted text clipped - 7 lines] > > Not that much. Here is another recent study. I'm sure you will recognise at least one of the authors (of hunter-gatherer fame): J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. The normal low-density lipoprotein (LDL) cholesterol range is 50 to 70 mg/dl for native hunter-gatherers, healthy human neonates, free-living primates, and other wild mammals (all of whom do not develop atherosclerosis). Randomized trial data suggest atherosclerosis progression and coronary heart disease events are minimized when LDL is lowered to <70 mg/dl. No major safety concerns have surfaced in studies that lowered LDL to this range of 50 to 70 mg/dl. The current guidelines setting the target LDL at 100 to 115 mg/dl may lead to substantial undertreatment in high-risk individuals. In summary, western lifestyles are not conducive to achieving these low LDL numbers without reducing total fat consumption considerably below 30%. Cheers, PR >In summary, western lifestyles are not conducive to achieving these low LDL >numbers without reducing total fat consumption considerably below 30%. > >Cheers, PR That didn't address the more critical issue of particle size, whether it's damaging type or harmless. The number is an artificial target, one that leads away from a more complicated but more effective means of CVD prevention. Susan > x-no-archive: yes >>In summary, western lifestyles are not conducive to achieving these low >>LDL [quoted text clipped - 4 lines] > That didn't address the more critical issue of particle size, whether it's > damaging type or harmless. 1) There's particle size and there's particle numbers. Below 150 TC the micro environment has minimal consequence. 2) The other point is that type B LDL (putative artherogenic, small particle) has not been *independently* associated with CVD other than in conjunction with low HDL, high TG, IR, abnormal BMI etc -- more or less metabolic syndrome. You can correct me on this if you wish, but I would need convincing. > target, one that leads away from a more complicated > but more effective means of CVD prevention. I would suggest 'more complicated, less effective' but perhaps easier to comply with for most people, eg, Mediterranean diet. For lower-carbers (if you must <g>), Atkins is the wrong way to go. Something like South Beach would be a much better option. Paul R >> x-no-archive: yes > [quoted text clipped - 23 lines] > lower-carbers (if you must <g>), Atkins is the wrong way to go. > Something like South Beach would be a much better option. It's easy to be on a Mediterranean diet that's 100% SB compatible for that matter. The question is what constitutes ease. Because of USDA recommendations and the food pyramid, it's easy to find foods labeled "low fat" even if they get pumped up with sugar and smaller amounts of trans fat than the saturated fats that another brand might have. Likewise, with the Atkins popularity, it's easy to find foods in stores and restaurants that are "low carb" but may have too much saturated fat for SB. So when it comes to ease, the best hope is that your diet is becoming popular. Then the "Atkins approved" meal with the bacon on top can be offered with a substitution that's lower in fat, and when you send back the bread, they might offer you something whole grain instead. >It's easy to be on a Mediterranean diet that's 100% SB compatible for that >matter. The question is what constitutes ease. [quoted text clipped - 8 lines] >offered with a substitution that's lower in fat, and when you send back the >bread, they might offer you something whole grain instead. Maybe it's difficult if you don't have a kitchen. I buy meat, fish, poultry, dairy, vegetables and fruit, nuts, oils, etc. Not hard to find what I need at all. Susan >1) There's particle size and there's particle numbers. Below 150 TC the >micro environment has minimal consequence. I disagree, for other reasons. Often, low TC is a marker for liver or other disease or dysfunction. >2) The other point is that type B LDL (putative artherogenic, small >particle) has not been *independently* associated with CVD other than in >conjunction with low HDL, high TG, IR, abnormal BMI etc -- more or less >metabolic syndrome. You can correct me on this if you wish, but I would need >convincing. Here's the thing about letting yourself off the hook if you don't officially qualify for diagnosis with metabolic syndrome: Ann Intern Med 1998 Apr 1;128(7):524-33 Metabolic risk factors worsen continuously across the spectrum of nondiabetic glucose tolerance. The Framingham Offspring Study. Meigs JB, Nathan DM, Wilson PW, Cupples LA, Singer DE Massachusetts General Hospital, Harvard Medical School, Boston University School of Public Health, 02114, USA. jmeigs@sol.mgh.harvard.edu BACKGROUND: Categorical definitions for glucose intolerance imply that risk thresholds exist, but metabolic risk for type 2 diabetes mellitus or cardiovascular disease may increase continuously as glucose intolerance increases. OBJECTIVE: To examine the distributions of the following metabolic risk factors across the spectrum of glucose tolerance: overall and central obesity, hypertension, low levels of high-density lipoprotein cholesterol, and increased triglyceride and insulin levels. DESIGN: Cross-sectional analysis. SETTING: The community-based Framingham Offspring Study. PARTICIPANTS: 2583 adults without previously diagnosed diabetes. MEASUREMENTS: Clinical data; fasting glucose, insulin, and lipid levels; and glucose and insulin levels taken 2 hours after oral challenge were collected from 1991 to 1993. Glucose tolerance was determined by 1980 World Health Organization criteria. Patients with normal glucose tolerance were categorized into quintiles of fasting glucose. The distributions of each metabolic risk factor and the metabolic sum of the six risk factors were assessed across seven categories from the lowest quintile of normal fasting glucose level through impaired glucose tolerance and previously undiagnosed diabetes. RESULTS: The mean age of patients was 54 years (range, 26 to 82 years); 52.7% of patients were women. Glucose tolerance testing found that 12.7% of patients had impaired glucose tolerance and 4.8% had previously undiagnosed diabetes. Multivariable-adjusted mean measures of risk factors and odds ratios for obesity, elevated waist-to-hip ratio, hypertension, low levels of high-density lipoprotein cholesterol, elevated triglyceride levels, and hyperinsulinemia showed continuous increases across the spectrum of nondiabetic glucose tolerance. Although a threshold effect near the upper range of nondiabetic glucose tolerance could not be ruled out for triglyceride levels in men and for insulin levels 2 hours after oral challenge in men and women, no other metabolic risk factors showed clear evidence of thresholds for increased risk. CONCLUSIONS: Metabolic risk factors for type 2 diabetes mellitus and for cardiovascular disease worsen continuously across the spectrum of glucose tolerance categories, beginning in the lowest quintiles of normal fasting glucose level. PMID: 9518396, UI: 98175274 -------------------------------------------------------------------------- ------ Blood Glucose Concentration Linked to>Cardiovascular Risk in Nondiabetic Men> ---------------------------------------------------------------------------- WESTPORT,>CT (Reuters Health) Jan 04 - Increased glycated hemoglobin (HbA1c)>concentrations are predictive of cardiovascular mortality among all men,>not only those with diabetes, according to a report in the British>Medical Journal for January 6. Dr. Kay-Tee Khaw and colleagues, from>the University of Cambridge School of Clinical Medicine, UK, collected>data on all-cause mortality and cardiovascular mortality in 4662 men, 45>to 79 years of age, who participated in the Norfolk UK cohort of the>European Prospective Investigation into Cancer and Nutrition>(EPIC-Norfolk). At baseline, from 1995 to 1997, HbA1c was measured and>the subjects were followed until December 1999. As expected, Dr.>Khaw's group found that diabetic men had increased mortality for all>causes, cardiovascular disease and ischemic disease. They also noted that>HbA1c concentrations were "continuously related to subsequent all-cause,>cardiovascular, and ischemic mortality through the whole population." The>lowest mortality rates were associated with HbA1c concentrations below>5%. Further, the group noted that a 1% increase in HbA1c was>associated with a 28% increased risk of death, which was independent of>age, blood pressure, cholesterol, body mass index and>smoking. "Eighteen percent of the population excess mortality risk>associated with a HbA1c concentration of 5% or more occurred in men with>diabetes, but 82% occurred in men with concentrations of 5% to 6.9% (the>majority of the population)," Dr. Khaw and colleagues point>out. The researchers propose that an elevated concentrations of>HbA1c is a marker for greater absolute risk among all men, and>"preventive treatment with blood pressure- or cholesterol-lowering drugs>should be considered in such patients." They point out that if>the population of nondiabetic men was able to lower its HbA1c>concentration by 0.1%, total mortality could be reduced by 5%, and if the>concentration could be lowered by 0.2%, then total mortality could be>reduced by 10% in this population.  SignatureThe only dietary intervention proven to lower these risks is lower carb. >I would suggest 'more complicated, less effective' but perhaps easier to >comply with for most people, eg, Mediterranean diet. For lower-carbers (if >you must <g>), Atkins is the wrong way to go. Something like South Beach >would be a much better option. This is stunningly ignorant remark, suggesting no variation in individual clinical needs. Atkins is completely healthy, as much as South Beach. Different folks have different tolerances. I remained severely IR and hypoglycemic on the Zone, became hypothyroid on Atkins induction, and do best on 50% fat, 30% protein, 20% carbs, for now. Everyone's needs are different; making a sweeping recommendation as you just did is, well, dumb. Susan >Paul R > >--- > >Checked by AVG anti-virus system (http://www.grisoft.com). >Version: 6.0.796 / Virus Database: 540 - Release Date: 13/11/2004 >This is stunningly ignorant remark, suggesting no variation in individual >clinical needs. Atkins is completely healthy, as much as South Beach. For whom? Why are Australia's medical authorities warning against the long term dangers of Atkins? >Different folks have different tolerances. But normal folks (the vast majority of humans on the planet (not just North America and Australia) lie within a fairly narrow range. >I remained severely IR and >hypoglycemic on the Zone, became hypothyroid on Atkins induction, and do best >on 50% fat, 30% protein, 20% carbs, for now. Everyone's needs are different; >making a sweeping recommendation as you just did is, well, dumb. You keep claiming to be "normal" with just biological variation. Sorry, from what you have told us and hinted at, you are far from normal, and any dietary requirements you have are irrelevant to normal folk. > BTW, here is an interesting study that one could compare with the > low-cholesterol scare stories (low-carbers beware!): [quoted text clipped - 11 lines] > > Cheers, Paul R Do you have any links about low cholesterol? About 4 years ago I tested slightly above 100. Last week I got pretty much near the same results: Total: 109 Triglycerides: 44 HDL: 54 LDL: 46 Eric >> Circulation. 2000 May 2;101(17):2047-52. >> Low fasting plasma glucose level as a predictor of cardiovascular disease [quoted text clipped - 10 lines] >> >> Cheers, Paul R Low glucose is usually a result of hyperinsulinemia, which leads to insulin resistance, to higher cancer and CVD risks. Susan >x-no-archive: yes > [quoted text clipped - 15 lines] >Low glucose is usually a result of hyperinsulinemia, which leads to insulin >resistance, to higher cancer and CVD risks. Why? Wouldn't it be more likely starvation? (hunger?) Hyperinsulinaemia is usually a result of insulin resistance, surely, and so the glucose is likely to be higher than normal. >>Low glucose is usually a result of hyperinsulinemia, which leads to >>insulin resistance, to higher cancer and CVD risks. > > Why? Wouldn't it be more likely starvation? (hunger?) Very unlikely until starvation is really advanced (so advanced that electrolyte deficiencies would probably kill you first). Your liver can keep your glucose in the normal range even if you have to break down muscle protein to get alanine for hepatic gluconeogenesis to do it. > Hyperinsulinaemia is usually a result of insulin resistance, surely, > and so the glucose is likely to be higher than normal. In the early stages of the type 2 diabetic progression, the pancreatic beta cells lose their first-phase insulin secretion but maintain their second-phase secretion. In normal glucose metabolism, IIRC, first-phase secretion involves quick release of a quantity of insulin that doesn't really depend on the glucose level (just on the fact that the level rose) whereas second-phase secretion is sensitive to the actual level. The result is that (when first-phase secretion is lost), consumption of substantial amounts of carbohydrate results in a large increase in blood glucose, followed later by a much higher than usual level of insulin secretion, which often "overshoots," resulting in low BG. Essentially you've got a feedback loop which is "ringing" (going into oscillation). Thus reactive hypoglycemia is often an early symptom of DM2. >>>Low glucose is usually a result of hyperinsulinemia, which leads to >>>insulin resistance, to higher cancer and CVD risks. [quoted text clipped - 5 lines] >keep your glucose in the normal range even if you have to break down >muscle protein to get alanine for hepatic gluconeogenesis to do it. Of course. Doh! I was thinking too hard that hyperinsulinaemia is not likely to be causing low glucose. >> Hyperinsulinaemia is usually a result of insulin resistance, surely, >> and so the glucose is likely to be higher than normal. [quoted text clipped - 11 lines] >you've got a feedback loop which is "ringing" (going into oscillation). >Thus reactive hypoglycemia is often an early symptom of DM2. Aha! That makes it clearer. Thanks for that. The system is not intuitive on first blush. Much more to know about :-) > I agree that the advantage isn't what Atkins wrote about. Long term > studies [quoted text clipped - 8 lines] > drinkers) > with fat, round tummies. Lower TG in non-exercisers on Atkins I will accept; all others still up for grabs long-term compared with high-fibre low-GI, low-fat diet. >>1. 25% fat is not a low-fat diet; > [quoted text clipped - 7 lines] > brains to rot so badly that they can't read science or get facts straight. > :-) Well, mine is not quite as low as that, more like 20%. However, we need to compare extreme with extreme here. Atkins ketosis is extreme, Ornish is extreme (more like 10% fat though.) >>2. Alternating diets seems like a very strange methodology for comparing >>weight loss in individual subjects. > > Um, you've never heard of crossover studies? Better methodology than a > straight comparison. See other response to Mirek. >>3. If you want me to believe that some men 'ate more' and 'lost more' on >>low-carb, then you will also believe in fairies and alien abduction -- but [quoted text clipped - 7 lines] > one > which is made by 100% of digested carbohydrate. It also takes some energy to store carbohydrates as fat; and in ketosis there are probably some overheads as well but we are not talking about a modest thermic advantage here. The significant differences that this study purports to show are in the 'first law'category ;-). Also, it does not seem to me to be biologically plausible for there to be a substantial thermic advantage in ketosis. This is, after all, a starvation metabolic state. The evolutionary tendency would be for the opposite. Cheers, Susan, Paul R >Lower TG in non-exercisers on Atkins I will accept; all others still up for >grabs long-term compared with high-fibre >low-GI, low-fat diet. They're not up for grabs in the comparisons in the scientific literature, but you can believe whatever floats your boat. >Well, mine is not quite as low as that, more like 20%. However, we need to >compare extreme with extreme here. Atkins ketosis is extreme, Ornish is >extreme (more like 10% fat though.) Both are extremes. But only one is unhealthy for everyone, and that's Ornish. On 20% fat, my TGL (excellent marker for development of CVD) was about 300. On high fat, it's 100-126. On low fat, my HDL was 34. On high fat, it's 70. My LDL is down to 126, and the particle size is large and fluffy, the non-damaging type. I no longer have labile hypertension. I don't believe the Atkins induction period is at all necessary for low carb success, though it's very important to some morbidly obese folks for whom it represents the first and only intervention to help them control appetite and overeating. >>>2. Alternating diets seems like a very strange methodology for comparing >>>weight loss in individual subjects. [quoted text clipped - 3 lines] > >See other response to Mirek. I saw it. I agree that a washout period, if there was one, would be an important factor. OTOH, by crossing over, you're still comparing two groups of possibly plateauing weight losers, so differences may be construed to be the diet. >It also takes some energy to store carbohydrates as fat; and in ketosis >there are probably some overheads as well but we are not talking about a >modest thermic advantage here. The significant differences that this study >purports to show are in the 'first law'category ;-). Doesn't apply to highly variable human metabolism. We're not machines. We have endocrine stuff (highly scientific term). :-) Also, it does not seem >to me to be biologically plausible for there to be a substantial thermic >advantage in ketosis. This is, after all, a starvation metabolic state. The >evolutionary tendency would be for the >opposite. It takes more energy to metabolize protein, for one thing, plus less of it turns to storage stimulating insulin. I agree that the metabolic advantage is only present in the short term studies; so much water is lost early on, conserving lean body mass, and the groups even out in long term studies. But the low carbers are healthier, or at least have better serum markers for longevity. The insulin resistant ones, like me, can eat a lot more on low carb to maintain or lose, but I suspect this advantage is less pronounced in those with normal, healthy carb metabolism. I maintained scrupulous (read obsessive) fitday records of my eating when I began gaining weight on low fat. At 800 calories per day, I was maintaining! I was measuring and recording every bite of food immediately, BTW, not trying to recall it later. On low carb, I still have to eat very low calorie, but it's more like 1200 cal per day to maintain. Susan Susan >Cheers, Susan, > [quoted text clipped - 4 lines] >Checked by AVG anti-virus system (http://www.grisoft.com). >Version: 6.0.791 / Virus Database: 535 - Release Date: 8/11/2004 >It takes more energy to metabolize protein, for one thing, plus less of it >turns to storage stimulating insulin. <*sigh*> ...less of it turns to storage stimulating glucose. Sheesh. Susan > 2. Alternating diets seems like a very strange methodology for comparing > weight loss in individual subjects. Actually, that is pretty standard method in any nutritional research - not only weight loss. Mirek Sure, I can understand crossovers when looking at lipid differences with diet or behaviour in children on food additives, for example -- or perhaps even in group weight-loss comparisons over sustained periods, but with weight loss measurement in individuals, particularly over an interval as short as 30-50 days, one then has to account for how weight loss in the primary regimen might affect the following regimen. For example, weight loss could slow afer an initial 50 days and provide a poor comparison for the dietary change in the next fifty. Seems to be a significant confounder to me. However, we don't have the complete paper yet from what I read at the site. Paul R >> 2. Alternating diets seems like a very strange methodology for comparing >> weight loss in individual subjects. [quoted text clipped - 3 lines] > > Mirek > "70% of men lost more weight and fat on a low carbohydrate diet, > despite eating more calories." > > I'd like to see that!. Caloric intake by itself is irrelevant. Caloric intake compared to calories expended is what's relevant. It's theoretically simple to change from a diet rich in simple carbohydrates that break down easily and quickly into sugars to a diet with other foods that are marginally higher in calories, but also cause the body to expend more calories breaking the food down, resulting in a net loss when subtracting calories expended from calories consumed compared to the previous diet, even though the previous diet may have had fewer calories consumed. I'm not saying that it's typical, but it's certainly possible. The reality is that the fat consumed will increase satiation, and also slow down the sugar intake. This will result in lower cravings, and possibly lower consumption of food (and calories too, of course.) The difference is that while the person may be lowering calories, it's not being done at the expense of hunger or reactive hypoglycemia, compared to a diet high in carbs and junk food where the dieter is trying to reduce calories by cutting down on consumption alone, and possibly causing a shift in metabolism to go with it. The down side is that followers of Atkins type diets tend to be off it within nine months anyway, perhaps due to boredom or missing certain types of food, and then their diet becomes whatever they feel like eating. Another problem is that since saturated fats are not controlled, one Atkins dieter could end up with a significantly different diet from another follower merely based on personal preference. I don't know about the studies, but anecdotal evidence has shown me that some people go on Atkins, eat as much as they want, and end up losing weight and lowering their cholesterol. But others go on it and end up with even higher cholesterol. If the only variable being controlled for is whether the person is "on Atkins" or "not on Atkins," I can't say that the study can rule out that it's possible to have an Atkins compliant diet that is healthful, or one that is compliant and unhealthful depending on the choices made. > I don't know about the studies, but anecdotal evidence has shown me that > some people go on Atkins, eat as much as they want, and end up losing [quoted text clipped - 7 lines] > choices > made. Very correct observation. Mirek >> "70% of men lost more weight and fat on a low carbohydrate diet, >> despite eating more calories." [quoted text clipped - 4 lines] > calories > expended is what's relevant. . . . [snip more obvious stuff]. Of course it is, but you missed the point. There is no way around the first law of thermodynamics. By now, most rational scientists and observers (even Susan) agree there is no significant metabolic advantage to low-carb diets. They either make you eat less -- or to satisfy you, they make you exercise more. (I don't think so.) If the numbers in this study say they ate more than the control *and* lost more weight, then either the diet measurement was wrong or they exercised more! Get it? BTW, most studies show protein is more satiating than fat. Paul R >more weight, then either the diet measurement was wrong or they exercised >more! Get it? No, Paul, it's because in short term studies, the low carbers lose a very fast 10lbs of water in the first two weeks. In longer studies, this rapid whoosh is no longer a factor. You overreach in imagining what things must mean. >BTW, most studies show protein is more satiating than fat. > >Paul R And that protein and fat together are the most satiating. Susan > x-no-archive: yes > [quoted text clipped - 8 lines] > > You overreach in imagining what things must mean. Susan, not going back to look at it again, but I thought water loss (of which I am quite aware) was accounted for in the study -- ie, that they actually measured fat loss, muscle gain/reduction. You are correct though. (Good to see you are doing well on your current regimen.) PR >Susan, not going back to look at it again, but I thought water loss (of >which I am quite aware) was accounted for in the study -- ie, that they >actually measured fat loss, muscle gain/reduction. Not in most of the comparison studies. LBM preservation is measured, relative to weight loss. Obviously, those whose initial weight loss is mostly water have preserved more LBM initially. >You are correct though. (Good to see you are doing well on your current >regimen.) > >PR I can't lose weight without cutting to 1000 cal per day or less, so I don't know if you can call that doing well. But I have cut my cholesterol 100 pts, all from LDL, with a doubling of my HDL. No meds, no exercise for the past two years due to illness. Pantethine supplementation did prove to be an enormous help. Cut my CVD serum profile risk from average (it used to the the highest) to below average. Susan >>> "70% of men lost more weight and fat on a low carbohydrate diet, >>> despite eating more calories." [quoted text clipped - 6 lines] > > Of course it is, but you missed the point. What point was that? > There is no way around the > first law of thermodynamics. Did I say otherwise? > By now, most rational scientists and > observers (even Susan) agree there is no significant metabolic > advantage to low-carb diets. What's a "rational scientist?" Is that one who agrees with you? This sounds like the basis for a circular argument. What's important is that the studies stand up to peer review, and I agree that generally agreed upon research does not eschew carbs in general. Refined foods and grains, or certain starches such as potatoes are not the best thing for you, but it's not that carbs are bad across the board. > BTW, most studies show protein is more satiating than fat. And low carb diets tend to encourage protein, hence the satiation can result in lower caloric intake. > And low carb diets tend to encourage protein, hence the satiation can > result > in lower caloric intake. Yes, and to return to my original point. There is no 'metabolic' advantage of low-carb diets only, perhaps, greater satiation and less food intake -- and as Susan pointed out, more initial water loss. This study suggests that more weight was lost even though more calories were consumed compared to a low-fat diet. If we exclude excess water loss, I am saying this is bunkum. If you agree with me why don't you say so? If you believe in magic, please confirm. Paul R >There is no 'metabolic' advantage >of low-carb diets only, perhaps, greater satiation and less food intake -- [quoted text clipped - 3 lines] >consumed compared to a low-fat diet. If we exclude excess water loss, I am >saying this is bunkum. Well, yes and no. While the advantage Atkins touted isn't all he cracked it up to be, my own experience, and that of many others, along with the literature suggests that all calories count, but different macronutrient calories count differently. We are a dynamic metabolic system, one that responds differently to different fuels. Some calories are more likely to reduce appetite, some are less likely to stimulate glucagon and insulin, some do both (fat). For this reason, it's possible for someone to eat more calories on low carb than low fat for the same result. What I said was that neither diet was superior in lbs lost in the long term _among those who maintain compliance._ >If you agree with me why don't you say so? If you believe in magic, please >confirm. > >Paul R It's not magic, Paul, it's science. I believe in healthy doses of skepticism, and in skipping right past the hype for the medical research, but not in arguing against new concepts. Susan >> And low carb diets tend to encourage protein, hence the satiation can >> result [quoted text clipped - 10 lines] > If you agree with me why don't you say so? If you believe in magic, > please confirm. I've told you when I've agreed with you. As to metabolic advantage, if you mean what I think you mean, then I agree. But I also think that satiation is a relevant factor. Many high carb foods are simple carbohydrates that cause sugar to get absorbed quickly, and ultimately leave a person with an elevated insulin level and an increased appetite. But you are right, it's not a "low carb" thing. It's a "bad carb" thing. >d >appetite. But you are right, it's not a "low carb" thing. It's a "bad carb" >thing. For some of us, regrettably, it's both. Susan >x-no-archive: yes > [quoted text clipped - 3 lines] > >For some of us, regrettably, it's both. Sheesh. When are you going to realise that you are ill? Very abnormal. Your requirements are irrelevant to normal folk, Cherry picking studies that claim you are just on some "normal continuum" are perhaps comforting to you, but not at all helpful to newbies here. The "standard guidelines for verity in this group" is not just being funded by industry but, much more importantly, not HIDING THE FACT that the study is being funded by industry. You yanks do not seem to have any basic understanding of the simple concepts of conflicts of interests. If the conflict of interest is stated up front, you can then assume some modicum of honesty and forthrightness on the part of the researchers and then can evaluate the science on the basis of the science. Conversely, if the authors and researchers fail to declare (repeatedly) their financial interests, or, as is more typical, take steps to hide (repeatedly) any financial interest, then their basic honesty amd integrity as humans and scientists are under question, it becomes very difficult to get past that and actually consider the science being presented. For supposedly educated people, why do you have such blatant blindspots when it comes to conflicts of interest? I don't understand how you guys have such a poor understanding of corruption and conflicts of interest. Unless you just use it for convenience, as a point in an argument that you know you cannot win otherwise. Failing to find fault in the science you grab at any convenient reason, valid or not, to dispute the validity of a study, therefore you can pretend to be able to win the argument. Cherry picking. Hardly the high road in a scientific debate. TC > Sorry, exeeds standard guidelines for verity set in this group: > [quoted text clipped - 61 lines] > > > >TC The "standard guidelines for verity in this group" is not just being funded by industry but, much more importantly, not HIDING THE FACT that the study is being funded by industry. You yanks do not seem to have any basic understanding of the simple concepts of conflicts of interests. If the conflict of interest is stated up front, you can then assume some modicum of honesty and forthrightness on the part of the researchers and then can evaluate the science on the basis of the science. Conversely, if the authors and researchers fail to declare (repeatedly) their financial interests, or, as is more typical, take steps to hide (repeatedly) any financial interest, then their basic honesty amd integrity as humans and scientists are under question, it becomes very difficult to get past that and actually consider the science being presented. For supposedly educated people, why do you have such blatant blindspots when it comes to conflicts of interest? I don't understand how you guys have such a poor understanding of corruption and conflicts of interest. Unless you just use it for convenience, as a point in an argument that you know you cannot win otherwise. Failing to find fault in the science you grab at any convenient reason, valid or not, to dispute the validity of a study, therefore you can pretend to be able to win the argument. Cherry picking. Hardly the high road in a scientific debate. TC > Sorry, exeeds standard guidelines for verity set in this group: > [quoted text clipped - 61 lines] > > > >TC > The "standard guidelines for verity in this group" is not just being > funded by industry but, much more importantly, not HIDING THE FACT [quoted text clipped - 94 lines] > > > > > >TC The answer is simple. It is because it has become so prevalent and widespread, so institutionalized in every single aspect of US government and corporate sector and that it has become so common place and a such a standard practice of operation that it is not even considered unethical or immoral. Sad considering this very situation is the number one reason that has allowed the theft of our democracy, economy, environment, and health. |
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