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| | From:  rensielk (Original Message) | Sent: 12/22/2007 6:03 PM |
http://www.sciencedaily.com/releases/2007/04/070423083856.htm
Here's an article making the same mistake that Hans makes. They claim a high-fat diet is bad, but compare people eating McDonald's fast food to people eating low-fat foods. They're not controlling for carbohydrates (and calories) in the meals. This is dishonest and unscientific.
http://groups.msn.com/TheScientificDebateForum-/oddsandendspart2.msnw
Here, Hans cites an article on the same site saying that high fat meals of sausage, eggs, and hash browns are bad. They don't consider that the carbs may have been the problem, in accordance with the Scientific Method. Why not get rid of the hash brown and just feed people sausage and eggs cooked in virgin coconut oil. See if it's the fat or the carbs.
Low-carb proponents have been picking apart these stupid "fat is bad" studies for years. But Hans only wants to look at his own theories, like cooked meat and PUFAs. Let's simply consider the hypothesis that the carbs in fatty meals are the problem. The sausage, egg, and hash brown meal was 48g Fat, 33g Protein, and 91g Carbs. That's 47% fat, 14% protein, and 39% carbs. It's high-fat and high-carb, not just high-fat. So, the carbs may be the problem.
http://www.sciencedaily.com/releases/2006/09/060901192519.htm
Actually, there are multiple variables that weren't controlled, like the calories, sodium, cholesterol, etc. It's impossible for someone to conclude based on this study that cooked meat or unsaturated fats or oxidized cholesterol was the problem, but that is exactly what Hans is doing. This is a violation of the Scientific Method. A proper experiment must control all relevant factors - fat, protein, carbs, calories, oils, etc.
Like I said, these studies have been debunked by low-carb sites for years. There are always new studies popping up to say that animal foods are bad, cooked foods are bad, etc. The problem is that they never isolate the other factors like unsaturated oils and carbohydrates added to meals. Maybe the body could protect itself if it wasn't being bombarded by sugars and starches and highly unsaturated oils.
Bruce |
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| Guys, let's be more practical instead of arguing about rejecting posts. Time is running out quickly and we don't have time to wait another 100 years till the scientific method proves carbs are safe or not. Both Hans and Bruce say interesting things so keep the discussion going. Perhaps the most valuable thing we can do is to try actual diets and report the results in most detail possible. IMO both high carb + saturated fat diet as well as low carb + high fat diet (sometimes including more PUFAs in the paleo flavors) seem to work. What really seems bad is high carb + high PUFA diet. One thing which should be controlled for none of you mention is the level of physical activity. Perhaps more active people need more nutrients from the meat and to keep carbs "high" enough just to prevent ketosis. |
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Taka:
You have presented "contrary" evidence here in the past, and it has often been helpful in illuminating nuances, such as the one about Asian vegetarians having less oxidized LDL despite consuming more PUFAs than the meat eaters. However, Bruce is making claims that have a sort of religious certainty about them, yet he won't cite a study so that we can all take a look at it and comment. He also does not make his point clear.
One point I'll mention in this thread (though it's applicable to others) is that there has to be an underlying biochemistry to any nutritional claim, and this is why the molecular-level evidence is so important (especially consdiering how much of it there is now). For example, there is the evidence on cooked meat (HCAs generated, which is even worse if cooked with a PUFA-rich oil), but what is the molecular-level evidence against "simple carbs?" If you want to use such terms or phrases, then you can't turn around and say something like, "well, if you eat too much fructose there is strong molecular-level evidence suggesting that it is dangerous" because that was not your claim - you said "simple carbs," not "high fructose." This is the kind of thing Bruce is doing, and he may not realize it, so that's why I have yet to reject any of his posts. As I've said before, all the evidence is consistent with the general points I've made, and if anyone thinks this is not true, I am very interested to hear what you have to say, but you can't argue the way political pundits do on cable TV news stations - you have to do it in a way that is consistent with basic academic standards. Because not everyone understands that, I have been willing to be patient and hope that Bruce realizes what this means. My patience, however, is not unlimited, because I don't want others to think that this is a site with no standards. |
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Bruce, you posted a link to study showing that there were no ill effects of meat & animal fat only diet for 1 year. I also saw another study of mainly beef & no grain+milk diet for cup of months with positive effect on total cholesterol and allergies. I guess there is a threshold for the dietary HCAs which is not reached if the meat is not burned. HCAs are mutagenic like VitC or green tea catechin if dosed "properly" and combined with things like free iron, PUFAs etc. Sometimes this can stimulate the body defense mechanisms at lower doses.
Now what are the molecular mechanisms behind the deleterious effects of carbs? I agree with Hans that we should make this clear first. I know e.g. that fructose is not metabolized optimally and is stealing phosphorus from ATP. It is also significantly more prone to form AGEs but is normally cleared from the blood stream by liver so the resulting triglycerides may represent a bigger problem if taken in excess. Also the adipocytes may become overloaded with fat resulting from excessive carbs and trigger systemic inflammation but this all happen only when consumed in EXCESS in relation to current needs according to the level of physical activity. Another thing which would deserve closer investigation is that carbohydrates inhibit delta-5-desaturase which is an enzyme required for the synthesis of Mead acid. They also seem to stimulate sex steroid hormones which do the same to desaturases. Some studies suggest that the lack of PUFAs used for controlling the immune response and cell signaling (the "experts" are only aware of AA but the same can be applied to Mead acid) is responsible for diseases like diabetes or atopy. Also insulin accelerates aging but only if elevated continuously - Hans' diet gives just 3 insulin spikes a day what is probably beneficial for tissue rebuilding especially when combined with dietary protein. |
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This is the link Bruce posted - one of the experimental subjects got serious pneumonia after ingesting larger amount of pure glucose for the test. Also meat only diet caused diarrhea but adding animal fat cleared it:
http://www.jbc.org/cgi/reprint/87/3/651.pdf |
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I know that my "GI system" is very sensitive - any little thing can set off problems, so I am very careful about cleanliness and what I eat. Most such studies I've seen look for markers after a few weeks or a couple of months. Keep in mind that I'm not arguing against a meat-rich diet. If you can find high-quality meat (I've seen investigations of supermarkets where they relabel expired meat, for example), then freeze it for a couple of weeks, then cut it up and heat it up on low in a sauce rich in herbs and spices, that seems like it would be much healthier than the "typical American" diet, even if it were low in "carbs," generally-speaking.
However, that is not the way meat is usually eaten these days, and that is not the way meat was eaten until very recently in human history (a few hundred years ago, it was common to put a piece of meat in a fire for a short period time, while other groups of people were still eating it raw (for example, descriptions of native "Eskimo" type peoples by the English explorers). Considering the potential dangers, the cost, the difficulty getting fresh meat and "preparing" it after freezing, I can't say that is what I would consider a "practical" diet, which I do consider mine to be.
Some things to note about a "high carb" diet that is not true of mine (unlike typical "high carb" diets):
My beverages have no calories.
My diet is antioxidant-rich and PUFA-poor.
There is ample fat, but mostly saturated fatty acids.
I only eat three times a day, separated by at least 3.5 hours and with no calorie intake between meals.
My calorie intake is well below average for the "typical American."
I take nutritional yeast in small amounts with each meal (it's rich in B vitamins, but not very rich in folic acid) to avoid the potential problem of flour "fortified" with folic acid (I also take B12 specifically once in a while). It also contains chromium.
I take a little copper each day.
I take magnesium and calcium citrate each day.
For the last few months, I've been eating several bran flakes with each meal.
I eat a little pickled (fermented) cabbage with each meal.
Little or no oxidized cholesterol is consumed.
Small amounts of gelatin are consumed each day.
Now, obviously, there may be other things that don't come to mind right now, but my point is that I'm trying to control for many factors that appear to be significant (long term). Once this is done, studies should be conducted, comparing overall mortality on one diet versus overall mortality on another. Several different animals should be used (dogs, rats, etc.), and if one diet is better than all others with all the animal species, that is likely to be best for humans too. This kind of experiment should have been done long ago, because it would not be very expensive, and this should form the "foundation" of a more useful nutritional science.
We don't have the "luxury" of waiting for scientists to make a definitive statement on diet - we have to eat now. We must make decisions, and what we have is the experimental data that exists and our human reason. I was taught in grad. school not to make "strong" statements if the issue was at all unclear, but after years of nutritional research, there is only one way of viewing the evidence that makes sense, and so that is why I created this site. Interestingly, the kind of experiments I'd like to see where being done in the early days of "nutritional science," for example:
QUOTE: ...This truth will probably be best appreciated by a reference to an experiment carried out in my laboratory some years ago, with the object of determining the relative values of certain national diets of India: Albino rats were employed in this test. The cycle of development in the rat takes place about thirty times as quickly as in man, so that the experiment about to be described, which lasted 140 days, would correspond to the observation of human beings, under the same experimental conditions, for a period of nearly twelve years. Seven groups of twenty young rats, of the same age, sex-distribution and bodyweight, were confined in large, roomy cages under precisely similar conditions of life. To one group the diet as prepared and cooked by the Sikhs, was given; to another that of the Pathans; to a third that of the Mahrattas; and so on through Goorkhas, Bengalis, and Kanarese to Madrassis. The results on the eightieth day of the experiment are shown in Fig. 1; from which it will be seen that the various diets ranged themselves in the following descending order of nutritive value: Sikh, Pathan, Maharatta, Goorkha, Kanarese, Bengali and Madrassi. At the end of 140 days the animals in each group were weighed and an average taken of their aggregate weight. The rat which conformed most closely to the average for its particular group was photographed side by side with the average rats from other groups. The photograph shown in Fig. 1 is the result. From it we see that it conforms to the results of observations made in man himself. In brief, the best diet--that of the Sikhs--contains in abundance every element and complex needed for normal nutrition, the worst diet--that of the Madrassi--has many faults: it is excessively rich in carbohydrates, and deficient in suitable protein, mineral salts and vitamins. Presently we shall see that this difference in the nutritive value of these diets is reflected in the diseases from which the people of the north and south of India suffer... UNQUOTE.
The following passage makes clear the kind of diet considered best by this researcher:
QUOTE: In general the races of northern India are wheat-eaters, though they make use also of certain other whole cereal grains. Now the biological value of the proteins of whole wheat is relatively high; and the wheat is eaten whole, after being freshly ground into a coarse flour (atta) and made into cakes called chapattis. It thus preserves all the nutrients with which Nature has endowed it, particularly its proteins, its vitamins and its mineral salts. The second most important ingredient of their diet is milk, and the products of milk (clarified butter or ghee, curds, buttermilk; the third is dhal (pulse); the fourth, vegetables and fruit. Some eat meat sparingly, if at all... UNQUOTE.
SOURCE: THE CANTOR LECTURES
delivered before
The Royal Society of Arts
1936
by
MAJOR-GENERAL
SIR ROBERT McCARRISON
C.I.E., M.D.; D.Sc., LL.D., F.R.C.P. |
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Low-carb Diet Reduces Inflammation And Blood Saturated Fat In Metabolic Syndrome
ScienceDaily (Dec. 4, 2007) �?Metabolic syndrome is a condition afflicting one quarter to one third of adult men and women and is an established pre-cursor to diabetes, coronary heart disease, and other serious illnesses. Patients have long been advised to eat a low-fat diet even though carbohydrate restriction has been found to be more effective at reducing specific markers, such as high triglycerides, characteristic of the syndrome. Now, a new study indicates that a diet low in carbohydrates is also more effective than a diet low in fat in reducing saturated fatty acids in the blood and reducing markers of inflammation.
While there have been contradictory and confusing messages directed at health conscious consumers about dietary recommendations, most researchers agree on the need to limit inflammatory agents. In a report published in the on-line version of the journal Lipids, researchers at the University of Connecticut with co-authors from SUNY Downstate Medical Center in Brooklyn, the University of Minnesota, and the University of California show much greater improvement in inflammatory markers in patients with metabolic syndrome on a very low carbohydrate approach compared to a low fat diet.
Lead researcher Jeff S. Volek, PhD, RD, associate professor of kinesiology at the University of Connecticut, describes the study as "adding to the evolving picture of improvement in general health beyond simple weight loss in keeping blood glucose and insulin under control." The work is part of a larger study (currently under review) showing numerous improvements in blood lipids. The current work concludes that "lowering total and saturated fat only had a small effect on circulating inflammatory markers whereas reducing carbohydrate led to considerably greater reductions in a number of pro-inflammatory cytokines, chemokines, and adhesion molecules. These data implicate dietary carbohydrate rather than fat as a more significant nutritional factor contributing to inflammatory processes."
Richard Feinman, PhD, professor of biochemistry at SUNY Downstate Medical Center, adds, "The real importance of diets that lower carbohydrate content is that they are grounded in mechanism -- carbohydrates stimulate insulin secretion which biases fat metabolism towards storage rather than oxidation. The inflammation results open a new aspect of the problem. From a practical standpoint, continued demonstrations that carbohydrate restriction is more beneficial than low fat could be good news to those wishing to forestall or manage the diseases associated with metabolic syndrome."
One of the remarkable effects in the data presented that may have contributed to the results is that despite the three-fold greater saturated fat in the diet for the low carb group, saturated fat in the blood turned out to be higher in the low fat group due to the process known as carbohydrate-induced lipogenesis. Dr. Volek points out that "this clearly shows the limitations of the idea that 'you are what you eat.' Metabolism plays a big role. You are what your body does with what you eat."
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"These data implicate dietary carbohydrate rather than fat as a more significant nutritional factor contributing to inflammatory processes..."
This is only going to happen if the person has AA in their cells.
"...saturated fat in the blood turned out to be higher in the low fat group due to the process known as carbohydrate-induced lipogenesis..."
And this shows how little these "scientists" know, because saturated fatty acids are not inflammatory in any way, and in fact will likely have an "anti-inflammatory" effect in most people. The problem is that they are not eating highly saturated fat sources, like coconut oil, rather than things like canola oil, lard, etc. |
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HSWC, I would like a reference for the refutation of the EFA claim. All I have found is that it was in the 1948 World Book, and the study was conducted by MIT. This is not a reference. Who did the study? What was the title, journal, etc?
My claim is that maybe if we fed people a very low carb diet (0-72g), the "problems" of cooked meat would not occur. As Taka said, the combination of carbs and omega-6 seems to be esp bad. Maybe carbs are fine with high-SFA/low-PUFA, but probably not for all people. You have mentioned how your relatives are overweight and they eat more cooked meat or PUFAs, but they eat more carbs and calories too. You can't blame all problems on PUFAs, esp with simple correlations like what your relatives supposedly eat.
The Western Diet is obviously bad, but you seem to blame a single factor (PUFAs), while I think the high carb diets and/or refined carbs are involved. Agriculture, grains, and sugar did not just come along and improve our health. You can believe the evidence or not, but you can't deny that our diet changed 10,000 years ago and has undergone other radical changes such as the refining of sugar and grains, and the introduction of vegetable oils, hydrogenated oils, etc.
I am not interested in any challenges to put up money for an experiment. That is just hot air, as far as I am concerned. If you want to discuss the evidence and your interpretation of it, fine. But the burden of proof is on YOU to show that meat cooked in any way causes disease in the absence of carbs. If you can't present human studies, you lose.
If you want to propose studies, talk with someone else. I am not a scientist and neither are you. I just think carbs need to be controlled in studies claiming meat or animal foods have harmful effects. Not doing so assumes carbs are harmless, something which should be demonstrated with comparison. Surely you would not be afraid to repeat the sausage, eggs,
and hash brown study WITHOUT hash browns, and using a good coconut oil for all of the cooking. |
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"This is only going to happen if the person has AA in their cells."
I don't see how you can say that in response to every claim, when you haven't proved the absence of AA in your cells.
But to answer Taka's questions, here is the mechanism why carbs and omega-6 are very bad together. The carbs cause small dense LDL and the omega-6 enhance the oxidation of the LDL. Those points should not be controversial, since HS has pointed out studies noting this effect. There may also be other effects whereby carbs derange fat metabolism.
Some things mentioned Gary Taubes's book. He says high carbs (esp refined) cause: high triglycerides, low HDL, high VLDL, small dense LDL (Pattern B), high blood pressure, high insulin and blood sugar, insulin and leptin resistance, glucose intolerance, reactive hypoglycemia, high fibrinogen, high uric acid, high C-Reactive protein, reduced immunity, and high hemoglobin a1c. Many people have lowered these markers on a low-carb or paleo diet. Have you tested all of these, Hans? Are they all in the optimal range?
"saturated fatty acids are not inflammatory in any way"
Perhaps, but that doesn't prove that carbohydrates are safe. Assuming that people have some AA in their cells, including you, maybe carbs cause more to be released. Very few are going to be willing to freeze all their meat and I don't see the rationale for it, except to discourage people from eating any meat. I would use fresh meat and not burn it. |
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I think the relevant passages are quoted on the fish oil and EFA thread, but they did it on rats anyway. The person making the claim has to supply the evidence - I was pointing out that even with rats the "EFA" claim was refuted (and rats seem to be more adapted to these molecules than people, based upon threshold levels for mammary cancers). However, the molecular-level evidence does show that without AA in your cells, your body won't generate the inflammatory molecules that cause all kinds of problems. LTB4 is one example. With Mead acid in your cells, you can only generate up to LTA3 in more than trace amounts. Nobody has proved the presence of any fatty acid in their bodies, with the exception of a small number of studies one can find on pubmed.com. However, I have experienced several effects which are consistent with having the different PUFAs in one's cells (chronic inflammatory problems with AA, improper wound healing with too much omega 3s, and very temporary inflammation with Mead acid).
I have been doing my own experiments (on myself), and I have to admit that I feel a bit more confident with this knowing that my great grandparents lived to be 96 and 100 on a similar diet. Again, it's all about the specifics. Someone who eats my diet, but eats every hour and a half, might indeed cause themselves insulin resistance issues at some point, for example. There is much that still needs to be learned, and that is obvious if you read sciencedaily.com each day, as I do. The "trick" is to be able to integrate the existing body of evidence comprehensively. When I began my nutritional research, I was open to everything, and I had no idea where it would lead. I couldn't imagine myself ever eating "junk food," rich in SFAs, as I do now, but that is where the evidence led me. From what I can tell, you don't seem to be able to do this, nor do you seem to understand the molecular-level evidence very well.
For instance, when you talk about the "markers" being in the "optimal" range, you fail to realize that this is based upon epidemiology, but then you criticize epidemiology (even though most of the studies I cited with regard to cooked meat had to do with HCAs, and so are molecular-level). I've told people in the past that if they "normalize" their biochemistry (getting the AA out is one thing that must be done), then they will be able to "cure" themselves. For example, I needed to take stomach acid supplements in large amounts a couple of years ago, but I no longer take any. How did I determine when to take less, then when to take none? I listened to my body. I often try new things, to see how my body responds. I do realize that unless one experiences what I have, it's difficult to believe that one can eat some "junk food," plenty of sugar and salt, etc. I wouldn't have believed myself (if someone told me these things 10 years ago, for example). |
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[Cancer Research 45, 1997-2001, May 1, 1985]
In an attempt to determine the requirement of essential fatty acid for
dimethylbenz(a)anthracene-induced mammary tumorigenesis, rats were fed
diets containing different levels of linoleate: 0.5, 1.1, 1.7, 2.2,
3.5, 4.4, 8.5, or 11.5%. Each diet contained 20% of fat by weight,
with varying amounts of coconut oil and corn oil added to achieve the
desired levels of linoleate. Mammary tumorigenesis was very sensitive
to linoleate intake and increased proportionately in the range of 0.5
to 4.4% of dietary linoleate. Regression analysis indicated that a
breakpoint occurred at 4.4%, beyond which there was a very poor linear
relationship, suggesting the possibility of a plateau. From the
intersection of the regression lines in both the upper and lower
ranges, the level of linoleate required to elicit the maximal
tumorigenic response was estimated to be around 4%. The differences in
tumor yield could not be correlated with changes in prostaglandin E
concentration in the mammary fat pads of normal animals maintained on
similar diets, suggesting that linoleate may act by some other
mechanism to stimulate mammary tumorigenesis.
http://cancerres.aacrjournals.org/cgi/content/abstract/45/5/1997
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This is taken from the Blog you posted, Bruce. It shows that the Kitavan diet is very similar to what Hans is doing - high carb + saturated fat. Both the Kitavans and Hans don't seem to have any problems with the carbs. So it really seems that the PUFAs are the only problem leading to CHD/obesity or the artificial light must play a role since the primitive people are likely to be more synchronized with the seasons.
Living on the isolated island of Kitava
On the island of Kitava there are coconuts, sweet potatoes, yams, a few other starches and fish to eat. This leads to an interesting diet. The estimated percentages of energy from protein, fat and carbohydrates are 10%, 21% and 69% in Kitava. Most of the fat is saturated. Three quarters of the population smoke.
Obviously high carb eating should mean catastrophic blood lipids. You would expect low HDL cholesterol and high triglycerides. And this is exactly what you find. HDL-C down at 1.1mmol/l (some as low as 0.5mmol/l) and triglycerides up at 1.7mmol/l (some up at 3.0mmol/l). Not a good ratio. They smoke too. Must be a hotbed of cardiovascular disease. Especially as some of the total cholesterol readings were up around the (gasp) 7.0mmol/l mark. Pravastatin in the local well water is the obvious answer.
Except they have no heart disease. On a diet of 70% carbohydrate. Life expectancy, ignoring neonatal mortality which appears to be high, is around seventy years. That's without any medical facilities. How do they do it?
BTW there were two amusing comments in the discussion of this paper. The best was:
"Evaluation of TGs and HDL-C as cardiovascular risk factors must thus be restricted to the study population"
I'll rephrase that. In Sweden "bad" lipds (and smoking!) are BAD. Not so in Kitava, here "bad" lipids are not bad. They're a product of diet composition. As there is no heart disease they must be good!
So what's happening? Do horrible triglycerides block to your arteries like hot beef fat blocks a cold sewer in Sweden, but then by magic they become non sticky in Kitava? Go figure. Hint, maybe it's not the lipids that trigger the blocked arteries.
Second comment was
"our findings lend no support to the concept that a very high intake of carbohydrates (>60% of energy) increases the risk of cardiovascular disease"
ie living on low fat doughnuts is safe for everyone. Everyone. No suggestion that you have to live in Kitava for this to be the case. So if you eat a junk diet in Sweden and get Kitava lipids in Sweden plus smoke Kitava cigarettes, will you be OK? Somehow I doubt it!
So why are the Kitavans free of heart disease?
Their average fasting glucose is 3.7mmol/l and their fasting insulin 4.0 microU/ml. They do not have any features of metabolic syndrome! Except the lipids of course. Despite eating appalling quantities of carbohydrate. If we define metabolic syndrome as carbohydrate intolerance how do the Kitavans manage this?
I think that this goes back to the main limit on population growth, which is food. Daniel Quinn is the best source of information on this subject. As the Kitavans live with minimal Western food it seems they must be living within the food production capacity of their island. The basic principle is that populations grow to the limit set by their food supply. On Kitava you cannot make babies out of thin air. No extra yams means no extra people. The fluctuations in food and population must mean there are fluctuations in hunger and plenty, but if populations really do expand to the limits of food supply, the island location must ultimately apply calorie restriction. On average.
Ad lib food on a global basis has resulted in a population explosion. On an individual basis it results in a waistline explosion. As carbohydrate is cheap, addictive and hunger generating it is what usually fuels the metabolic syndrome, hence "bad" lipids are associated with metabolic syndrome as carbohydrates are the usual tool of excess calorie intake.
Calorie restriction, intermittent fasting and once daily eating all limit the development of insulin resistance and hyperglycaemia, pretty well independent of macro nutrient ratio. On Kitava there must be accidental calorie restriction as the population is in equilibrium with with a fixed food supply, hence no metabolic syndrome. Despite the "bad" lipids, which merely reflect the composition of their restricted diet.
Can we all do the same? Probably yes, but having read about life on the calorie restricted optimal nutrition (CRON) diet this is definitely not for me. Licking the plate clean because the sauce is delicious is one thing. Doing it because you are starving is quite another! No, there does appear to be a better way.
Eating a ketogenic diet appears to mimic calorie restriction. Ketosis limits appetite so allows modest calorie restriction without any hunger. Forget any drug which may be developed to mimic eating a high fat diet. Better pile on the lard, dump the "healthy" carbohydrate and generate a few ketone bodies. Enough to keep your energy intake reasonable without that desperate dreaming of food which is reputed to go with CRON.
Or you can starve on a balanced diet.
SOURCE:
http://high-fat-nutrition.blogspot.com/search/label/Living%20on%20Kitava |
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An interesting paper from the other forum. It suggests that carbohydrates/sugar stimulate chronic inflammation in the body by increasing the oxidation of AA into pro-inflammatory mediators. They say like if you go very low carb your AA increases while inflammation/X-syndrome goes down. AA increases because it is not being oxidized into the pro-inflammatory mediators. If it is used for energy instead the very low carb diet would be a good strategy to safely switch from AA to the Mead acid ...
Lipids. 2008 Jan;43(1):65-77. Epub 2007 Nov 29.
Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation.
Forsythe CE, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM, Kraemer WJ, Feinman RD, Volek JS.
Department of Kinesiology, University of Connecticut, 2095 Hillside Road, Unit 1110, Storrs, CT, 06269-1110, USA.
Abnormal distribution of plasma fatty acids and increased inflammation are prominent features of metabolic syndrome. We tested whether these components of metabolic syndrome, like dyslipidemia and glycemia, are responsive to carbohydrate restriction. Overweight men and women with atherogenic dyslipidemia consumed ad libitum diets very low in carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks. In comparison to the LFD, the VLCKD resulted in an increased proportion of serum total n-6 PUFA, mainly attributed to a marked increase in arachidonate (20:4n-6), while its biosynthetic metabolic intermediates were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid ratio also increased sharply. Total saturated fatty acids and 16:1n-7 were consistently decreased following the VLCKD. Both diets significantly decreased the concentration of several serum inflammatory markers, but there was an overall greater anti-inflammatory effect associated with the VLCKD, as evidenced by greater decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.
PMID: 18046594
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