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Medical Forum / General / General / May 2005statins do not save lives
Letters about statins and mortality from the Apr 25 issue of the Canadian Medical Association Journal. www.cmaj.ca Women please note: "...no statin trials with even the slightest hint of a mortality benefit in women (JAMA, JACC, BMJ) and women should be told so in the guidelines." E. Vos Dear Editor: I very much enjoyed reading the thoughtful article by Manuel et al (1) in the April 12th issue of CMAJ. They are correct in surmising and demonstrating the wrong-headedness of the present aggressiLve guidelines for the prevention of cardiovascular complications in clinical practice, though not for all the right reasons. What the authors of this article discussed in a sensible, balanced way was the outcomes of reduced CAD events including death. What they did not discuss, and should have, was the adverse outcomes of the medications (primarily statins) used to prevent the CAD events. It was clearly shown that for low risk individuals the benefits of treatment were small (1 death prevented for 1550 patients treated for 5 years). This means that even rare adverse events caused by the treatment will, in comparison, be significant. Even 1 severe rhabdomyolysis event or 1 severe hepatitis event per thousand per year caused by a statin will be significant in these low-risk individuals (more than half a million of whom were recommended for treatment). It is true that cardiovascular mortality has been decreased in primary prevention trials with statins in high risk populations but total mortality has not been significantly decreased, which suggests that the adverse events caused by the treatment have balanced out the positive outcomes attributed to the treatment in the primary prevention group as Vos has documented well in the previous eletter response. It is also true, as Genest et al (2) have pointed out, that the Therapeutics Letter (TL) in Issue 49, (July/Aug/Sept 2003, http://www.ti.ubc.ca/pages/letter49.htm) did show a summary of trials that appeared to show a benefit in terms of overall mortality for statins when used for secondary prevention (i.e., in persons who already have vascular disease) of CAD events. This was not new information to the Therapeutics Letter staff or readership, nor was it a response to pressure from the medical community as suggested by the Genest article. The same information had, in fact, been published in Issue 42, Aug/Sept/Oct 2001 of the TL (http://www.ti.ubc.ca/pages/letter42.htm), prior to their issue demonstrating the lack of overall benefit of statins in primary prevention (Issue 48, Apr/May/June 2003, http://www.ti.ubc.ca/pages/letter48.htm). Genest et al also refer to the Heart Protection Study (3), which showed a reduction in overall mortality for secondary prevention but it also had a 4-6 week pre-randomization period of treatment after which 11,609 (36%) of the study recruits were dropped due to problems related to treatment. We therefore did not get an accurate assessment of the safety and tolerance of this statin dose in the general population. Also, the authors of this study did not report all serious adverse events. This latter fact supports the argument by Vince Bain (4) in his letter to the editor regarding Clinical Trials Registry in this issue of CMAJ in which he correctly states that all data collected in intervention trials should be held by a third party and made accessible to all researchers. This might have prevented needless harm to children treated with ineffective, but harmful SSRI's to which pharmaceutical manufacturers contributed by withholding research data from publication (5). In summary, there is no evidence to show reduced overall mortality with the use of statins for primary prevention of CAD events. There is evidence to show benefit (reduced overall mortality) from the use of statins for secondary prevention of CAD events. From Manuel's data, this secondary prevention group would number approximately 500,000 (Manuel's Tables 3 and 4) out of the total treatable population of 16,000,000 and would number approximately 400,000 out of the 2,530,000 (Manuel's Table 4) for whom statins would be recommended using the 2003 guidelines (or out of the 2,000,000 for whom statins would have been recommended by the 2000 guidelines). It therefore seems to me that, under the 2000 guidelines 1.5 million people would have been recommended statins without evidence of overall benefit, and under the 2003 guidelines, the 'number needed not to treat' would be over 2 million. In order to show benefit, most of the trials ran for 5 years. The approximate cost of 5 years of treatment for the 2 million persons not benefiting from it would be (at $1.65 per dose based on 2003 wholesale cost plus 7%) approximately $6 billion or $1.2 billion per year (a number not dissimilar to those found in Manuel's Figure 1). I'm sure that money could provide more QALY's (Quality Adjusted Life Years) in some other area of healthcare in Canada. References 1. Manuel et al. The 2003 Canadian recommendations for dyslipidemia management: Revisions are needed. CMAJ 2005;172(8):1027-31. 2. Genest et al. The analysis by Manuel and colleagues creates controversy with headlines, not data. CMAJ 2005;172(8):1033-34. 3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin 20536 high-risk individuals: a randomized placebo-controlled trial. Lancet 2002;360:7-22. 4. Bain V. Clinical Trials Registry-Letter to the Editor. CMAJ 2005;172(8):979-80 5. Garland EJ. Facing the evidence: antidepressant treatment in children and adolescents. CMAJ. 2004 Feb 17;170(4):489-91 AND: The look by Manuel et al of the dyslipidemia guidelines is welcome but also overlooks the all-cause mortality issue where statins have essentially failed to deliver. There are no statin trials with even the slightest hint of a mortality benefit in women (JAMA, JACC, BMJ) and women should be told so in the guidelines. Likewise, evidence in over 70 year olds shows no mortality benefit, i.e. the PROSPER trial finds 28 fewer cardiac deaths offset by 24 more cancer deaths. The all-cause mortality failure of statins is possibly best illustrated by atorvastatin (Lipitor): while both trials found cardio 'event' benefit, first ASCOT (placebo vs. 10 mg/d) had the mortality curves effectively touch at mean study end (3.3 years) and now TNT (10 mg/d vs. 80 mg/d) found, on top-dose, 26 fewer CHD [coronary heart disease] deaths offset by 31 more nonvascular deaths at median study end (4.9 years). Incidentally, ASCOT even failed to find cardiac benefit in women and diabetics. It can be said no better than does the ALLHAT study website (accessed 2005-4-11): "...but trials [primarily in middle-aged men] demonstrating a reduction in CHD from cholesterol lowering have not demonstrated a net reduction in all-cause mortality." What is the point lowering 'events' in prevention without lowering mortality from all causes, and increasing harm from 'competing risk factors' related to statin side effects if not to lowered cholesterol itself. The all-cause mortality failing with statins clearly supports the call for more effective approaches, and guidelines should reflect this finding, certain in women, probable in most men with astronomical numbers to treat. Eddie Vos, Sutton (Qc); Colin Rose, cardiologist, McGill University, Montreal (Qc) >>Women please note: "...no statin trials with even the slightest hint of a mortality benefit in women (JAMA, JACC, BMJ) and women should be told so in the guidelines." E. Vos<< COMMENT: Somehow the essential caveat got missed that although there are no purely PRIMARY prevention statin trials with mortality benefits in women, you can't say that about secondary prevention in women. Women did experience a significant *total* decrease in mortality in the 4S trial, as did every other group in that trial. The total mortality (women plus men) was 12% in the placebo vs. 8% in the simvastatin group over 5.4 years median followup, for a decrease of 30% in chance of dying. For women it was less, but still significantly lower. Of course, many of the 4444 participants in the 4S trial had heart disease and knew it. But there are some women with heart disease who will read the "no statin benefits for women" line in the article above, and think it applies to them. It doesn't. Simvastatin significantly decreases risk of dying for all causes, in this group (women with heart disease and high cholesterol). It's outragious to shade the facts so as to (by implication) suggest otherwise. I'm also annoyed at the cancer increase in the PROSPER trial being mentioned again and again. From what I can tell, it's an abberation. No other statin trial has seen anything like it. Even the 4S trial when run out open label beyond 10 years (with most of the former placebo group naturally deciding to switch to simvastatin) had a lower cancer mortality after 10 years in the simvastatin group. And total mortality was STILL 414 deaths in the initial statin group vs 468 in the initial placebo group (many of which had been on statins by this time for half the time). SBH There is no evidence of women's benefit from statins outweighing the risk of statin side effects. >>>Women please note: > [quoted text clipped - 34 lines] > > SBH What side effect are you thinking of that is worse than being dead? SBH Points for a catchy response, but nullified by points off for a non sequitur. The rate of serious statin side effects is far higher than the risk of CAD in low-risk and moderate risk women. Also, the total range of choices for increasing heart health is not exhausted by "statins or death." > What side effect are you thinking of that is worse than being dead? > > SBH >>The rate of serious statin side effects is far higher than the risk of CAD in low-risk and moderate risk women. .... Also, the total range of choices for increasing heart health is not exhausted by "statins or death." << COMMENT: Well, you'd think it was, giving how you insist on focusing on mortality. But we're not talking about low and moderate risk women. This thread didn't start out qualifying any group of women. The toral risk of major coronary events in the 4S trial in women was 160 in 827 high risk women over 5 years, which is 19%. That's high, and statins prevented about a third of them. That's in line with other trial results. So what major side effect can you expect from simvastatin which is as serious as a heart attack, and that you can expect at least 7% chance of getting, in 5 years? Since for these women something like 7 in 100 would have a heart attack in the next 5 years, preventable by a statin. That's your benefit. Now, what's the risk which outweighs that? And who says so, and cite the study. SBH :::: The rate of serious statin side effects is far higher than the risk :::: of CAD :::: in low-risk and moderate risk women. .... Also, the total range of :::: choices for increasing heart health is not :::: exhausted by "statins or death." :: Well, you'd think it was, giving how you insist on focusing on :: mortality. [quoted text clipped - 9 lines] :: something like 7 in 100 would have a heart attack in the next 5 :: years, preventable by a statin. Even more lives would have been saved by fish oils and with almost no risk of side effects.  SignatureJuhana "Juhana Harju" <shantigiri@despammed.com> wrote in part: >:::: The rate of serious statin side effects is far higher than the risk >:::: of CAD [quoted text clipped - 18 lines] >Even more lives would have been saved by fish oils and with almost no risk >of side effects. And even more with both statins and fish oil. -- Jim Chinnis Warrenton, Virginia, USA > "Juhana Harju" <shantigiri@despammed.com> wrote in part: > [quoted text clipped - 24 lines] > -- > Jim Chinnis Warrenton, Virginia, USA And probably even more with low GL diet, pantethine and fish oil. With absolutely no adverse reactions, only benefits. Susan Susan <mcfeins@NOgmailNO.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 31 lines] > >Susan Possibly, but the data are a lot skimpier. Pantethine hasn't been shown to reduce mortality or MIs, has it? I do a low-GL diet, but I don't know that the studies really have shown that it will reduce cardiovascular disease or total mortality. (I suspect it does, though.) -- Jim Chinnis Warrenton, Virginia, USA If there is any benefit to statins to which I would readily agree, it is the probable endothelial effect (but that is also achieved to some degree with aspirin, no?). A low GL diet may be great as long as people don't interpret that to mean low carbohydrate, low fibre, and high saturated fat. Zee > If there is any benefit to statins to which I would readily agree, it > is the probable endothelial effect (but that is also achieved to some [quoted text clipped - 4 lines] > > Zee You clearly aren't knowledgable about low carb diets. I eat very low carb, and my diet has more fiber in it than anyone's I know. It's pretty impossible to eat low GL or low carb without eating tons of fiber; you get to eat more carbs when you replace starch with colorful leafy stuff, or very high fiber flax breads, etc. High saturated fat has never been demonstrated as a CVD risk outside of a high GL setting, but it's very easy to avoid eating it for those concerned about it; it may increase insulin resistance in some folks. Susan What I have seen reflected among many who are trying to eat a certain way for cholesterol lowering, or statin injury recovery, is confusion of low GL with low carb and low fibre. I make no such error. Zee > What I have seen reflected among many who are trying to eat a certain > way for cholesterol lowering, or statin injury recovery, is confusion [quoted text clipped - 5 lines] > > Zee I eat very low carb, substantial amount of fat, and my diet is very high in fiber and phytonutrients. Low GL isn't enough to keep my bg and lipids in check. Susan > Susan <mcfeins@NOgmailNO.com> wrote in part: > [quoted text clipped - 36 lines] > Possibly, but the data are a lot skimpier. Pantethine hasn't been > shown to reduce mortality or MIs, has it? It is well demonstrated to bring lipids into desirable ranges and ratios, with absolutely no adverse reactions. Workd for me, while I ate an extremely high fat diet. Sadly, there's no profit to be made by anyone in studies that might demonstrate its effect on mortality. > I do a low-GL diet, but I don't know that the studies really have > shown that it will reduce cardiovascular disease or total > mortality. (I suspect it does, though.) > -- It certainly reduces all the lipid factors that statins are being pushed so hard to act on; and with no risks of adverse reactions. It also can often rid one of the need for diabetes and bp meds. When one looks at the role of glycation in diseases of aging, and one sees that low GL or low carb is the only diet to drop HbA1c low, one can extrapolate. I realize we have no gold standard answer about it. Susan Susan <mcfeins@NOgmailNO.com> wrote in part: >It is well demonstrated to bring lipids into desirable ranges and >ratios, with absolutely no adverse reactions. Workd for me, while I ate >an extremely high fat diet. > >Sadly, there's no profit to be made by anyone in studies that might >demonstrate its effect on mortality. So governments have no research funds? -- Jim Chinnis Warrenton, Virginia, USA > Susan <mcfeins@NOgmailNO.com> wrote in part: > [quoted text clipped - 8 lines] > -- > Jim Chinnis Warrenton, Virginia, USA Yeah, they do. They use them to seed the development of new drugs, then hand over the research to big pharma. Government *could* do this, but they don't. We know how completely in the pockets of industry the NIH researchers are. Now they're saying they refuse to work unless the ethics rules are rolled back and all the conflicts in interest remain firmly in place. Susan Susan <mcfeins@NOgmailNO.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 20 lines] > >Susan You're describing a failure of the governments of the world, or of the citizenry that doesn't care if good research is ever done on diet and supplements. Much of the lack of usable nutrition research predates big pharma. Good work could have been done long ago and wasn't. -- Jim Chinnis Warrenton, Virginia, USA > Susan <mcfeins@NOgmailNO.com> wrote in part: > You're describing a failure of the governments of the world, or of > the citizenry that doesn't care if good research is ever done on [quoted text clipped - 4 lines] > -- > Jim Chinnis Warrenton, Virginia, USA Except for some very good research on pantethine, which I've posted and sent to you before. There's good research on alpha lipoic acid as an insulin sensitizer, but no one's being told by pharma reps or government about that, either. We don't have a mostly sophisticated enough citizenry to understand that profit seeking, not science, directs our research efforts and colors how results are slanted and how data are selectively presented. Look at what happened with the drug Rezulin, when an FDA reviewer thought it was too unsafe to bring to market. He was ostracized, the drug killed folks due to sudden liver failure, and had to be pulled off the market. This due to corporate pressure and gov't regulators in pharma's pockets. In the ill fated LymeRix vaccine studies, investigators literally refused to document serious complaints of ill effects reported by enrolled subjects, many of whom went on to be debilitated (as some researchers had predicted) by their participation. There's a lot of good peer reviewed work dating back decades on a drug like Hydergine (now only available as generic due to lack of profit) as being incredibly effective and safe for non Alzheimer's age or vasculitis related dementia but it is virtually never prescribed for this and Novartis stopped manufacturing it. The only money, they explained, was in new drugs for Alzheimers. Even those with non AD dementia are being rx'ed these risky, expensive drugs instead of generic ergoloid mesylates. We have no good, honestly reported, unbiased studies of drugs in the U.S. We won't until researcher's incomes and perks stop being tied to drug manufacturers. Don't take my word for it, reference the NEJM. Susan There are no proponents coming out of medical school. It isn't even covered, and hasn't been for decades. > Susan <mcfeins@NOgmailNO.com> wrote in part: > [quoted text clipped - 31 lines] > -- > Jim Chinnis Warrenton, Virginia, USA No Jim. You cannot say that. Juhana is saying "almost no risk of side effects". That is simply NOT true for statins. Zee :: No Jim. You cannot say that. Juhana is saying "almost no risk of side :: effects". That is simply NOT true for statins. :: :: Zee I agree. If some lipid lowering agents are needed I would combine Polycosanol, Pantethine or Krill oil with fish oils. Those combinations would probably be much safer than statin combined with fish oils and at least as effective in reducing cardiovascular and total mortality. (It is true that there are no studies that would have combined the supplements that I am proposing.) Even better option would be the Portfolio diet combined with fish oils. SignatureJuhana The Portfolio diet may be very difficult for most to follow. And some post-menopausal women might want to avoid phyto-estrogens which are abundant in soy products. Also, some cancers would contraindicate use of soy. This latter is especially ironic in women who took statins for years and now have a diagnosis of ovarian, uterine or breast cancer, but still need to lower cholesterol. Because of the cancer, they want to avoid statins, but must avoid the most successful cholesterol lowering non-drug method to date. Zee > The Portfolio diet may be very difficult for most to follow. And some > post-menopausal women might want to avoid phyto-estrogens which are [quoted text clipped - 7 lines] > > Zee The most successful diet to date for improving lipids and HbA1c (very strong indications that this marker is highly predictive of CVD risk) is low carb, even when high in sat fat. Susan This would be wrong, and possibly deadly, for those with FH. I do concede your suggested dietary approach seems to work for those with diabetes. Zee > This would be wrong, and possibly deadly, for those with FH. I do > concede your suggested dietary approach seems to work for those with > diabetes. > > Zee You're wrong; note below that risks of CVD worsen across the entire "normal" spectrum of glucose tolerance. We already know that low fat diets don't work for CVD prevention, that's why the statin pushers are so firmly behind advocating them. Some cites: J Nutr. 2002 Jul; 132(7): 1879-85. Related Articles, Links A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gomez AL, Scheett TP, Volek JS. Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs 06269-1110, USA. Very low-carbohydrate (ketogenic) diets are popular yet little is known regarding the effects on serum biomarkers for cardiovascular disease (CVD). This study examined the effects of a 6-wk ketogenic diet on fasting and postprandial serum biomarkers in 20 normal-weight, normolipidemic men. Twelve men switched from their habitual diet (17% protein, 47% carbohydrate and 32% fat) to a ketogenic diet (30% protein, 8% carbohydrate and 61% fat) and eight control subjects consumed their habitual diet for 6 wk. Fasting blood lipids, insulin, LDL particle size, oxidized LDL and postprandial triacylglycerol (TAG) and insulin responses to a fat-rich meal were determined before and after treatment. There were significant decreases in fasting serum TAG (-33%), postprandial lipemia after a fat-rich meal (-29%), and fasting serum insulin concentrations (-34%) after men consumed the ketogenic diet. Fasting serum total and LDL cholesterol and oxidized LDL were unaffected and HDL cholesterol tended to increase with the ketogenic diet (+11.5%; P = 0.066). In subjects with a predominance of small LDL particles pattern B, there were significant increases in mean and peak LDL particle diameter and the percentage of LDL-1 after the ketogenic diet. There were no significant changes in blood lipids in the control group. To our knowledge this is the first study to document the effects of a ketogenic diet on fasting and postprandial CVD biomarkers independent of weight loss. The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia. PMID: 12097663 [PubMed - indexed for MEDLINE] > x-no-archive: yes > [quoted text clipped - 27 lines] > fasting and postprandial serum biomarkers in 20 normal-weight, > normolipidemic men. Twelve men switched from their habitual diet (17% > protein, 47% carbohydrate and 32% fat) to a ketogenic diet (30% protein, > 8% carbohydrate and 61% fat) and eight control subjects consumed their > habitual diet for 6 wk. Fasting blood lipids, insulin, LDL particle > size, oxidized LDL and postprandial triacylglycerol (TAG) and insulin > responses to a fat-rich meal were determined before and after treatment. > There were significant decreases in fasting serum TAG (-33%), [quoted text clipped - 7 lines] > There were no significant changes in blood lipids in the control group. > To our knowledge this is the first study to document the effects of a > ketogenic diet on fasting and postprandial CVD biomarkers independent of > weight loss. The results suggest that a short-term ketogenic diet does > not have a deleterious effect on CVD risk profile and may improve the > lipid disorders characteristic of atherogenic dyslipidemia. > > PMID: 12097663 [PubMed - indexed for MEDLINE] I repeat: "low-carb" would be wrong and possibly deadly in context of FH. There is abundant evidence that a high fat (omega 3s; Mediterranean type diet et al) and high complex carb works for FH. But some with very pronounced FH may be counselled to follow low-fat. Those people will also likely be counselled to consider statin therapy. Zee > I repeat: "low-carb" would be wrong and possibly deadly in context of > FH. [quoted text clipped - 5 lines] > > Zee I see you've repeated it. Now produce the studies that found a role for fat in CVD in the absence of high GL. Every good study examining the question has found that GL and fat quality are what's important, and that BG is a major component. CVD risk rises all along the continuum of normal fbg. No more opinions, I want you to cite good science with good data, not unfounded conclusions. *************A recent study involving over 40,000 middle-aged and older American men over a period of six years found that there was no link between saturated fat intake and heart disease in men. It also supported the contention that linolenic acid (a form of fat) is preventive against heart disease. (Ascherio A et. al. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. British Medical Journal, 1996 Jul 13, 313:7049, 84-90.)" "Several studies have shown that high-carbohydrate low-fat diets lead to high triglycerides, elevated serum insulin levels, lower HDL cholesterol levels, and other factors known to raise the risk of coronary artery disease. (See Liu GC; Coulston AM; Reaven GM. Effect of high-carbohydrate low-fat diets on plasma glucose, insulin and lipid responses in hypertriglyceridemic humans. Metabolism, 1983 Aug, 32:8, 750-3. See also Coulston AM; Liu GC; Reaven GM. Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans. Metabolism, 1983 Jan, 32:1, 52-6. See also Olefsky JM; Crapo P; Reaven GM. Postprandial plasma triglyceride and cholesterol responses to a low-fat meal. American Journal of Clinical Nutrition, 1976 May, 29:5, 535-9. See also Ginsberg H et. al. Induction of hypertriglyceridemia by a low-fat diet. Journal of Clin Endocrinol Metab, 1976 Apr, 42:4, 729-35) " "The idea that saturated fats cause heart disease is completely wrong, but the statement has been 'published' so many times over the last three or more decades that it is very difficult to convince people otherwise unless they are willing to take the time to read and learn what...produced the anti-saturated fat agenda." (Dr. Mary Enig, Consulting Editor to the Journal of the American College of Nutrition, President of the Maryland Nutritionists Association, and noted lipids researcher.) "The diet-heart hypothesis [which suggests that high intake of saturated fat and cholesterol causes heart disease] has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century." (Dr. George V. Mann, participating researcher in the Framingham study and author of CORONARY HEART DISEASE: THE DIETARY SENSE AND NONSENSE, Janus Publishing 1993.) High intake of fats from the Omega-3 group increase HDL cholesterol, which is considered protective against heart disease. Obviously it would be difficult to eat an Omega-3 rich diet while following a traditional fat reduced diet, especially if one were following one of the popular American diets that has one eating only 20-30 grams of fat per day. (Franceschini G. et. al. Omega-3 fatty acids selectively raise high-density lipoprotein 2 levels in healthy volunteers. Metabolism, 1991 Dec, 40:12, 1283-6. See also Journal of the American College of Nutrition 1991:10(6);593-601) A recent American study showed that low-fat, high-carbohydrate diets (15% protein, 60% carbohydrate, 25% fat) increase risk of heart disease in post-menopausal women over a higher fat, lower carbohydrate diet (15% protein, 40% carbohydrate, 45% fat). (Jeppeson, J., et. al. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. American Journal of Clinical Nutrition, 1997;65:1027-33) *************The largest and most comprehensive study on diet and breast cancer to date, studying over 5,000 women between 1991 and 1994, showed that women with the lowest intake of dietary fat had a significantly higher incidence of breast cancer than the women with the highest intake of dietary fat. It also found that women with the highest intake of starch had a significantly higher incidence of breast cancer than the women with the lowest intake of starch. The study found no evidence that saturated fat had any effect one way or the other on breast cancer, and that unsaturated fat had a significantly protective effect against breast cancer. (Franceschi S et. al. Intake of macronutrients and risk of breast cancer. Lancet; 347(9012):1351-6 1996) **************** "The commonly-held belief that the best diet for prevention of coronary heart disease is a low saturated fat, low cholesterol diet is not supported by the available evidence from clinical trials. In primary preventions, such diets do not reduce the risk of myocardial infarction or coronary or all-cause mortality. Cost-benefit analyses of extensive primary prevention programmes, which are at present vigorously supported by governments, health departments, and health educationalists, are urgently required....Similarly, diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets for secondary prevention of coronary heart disease but these are not yet sufficiently well defined or adequately tested." (European Heart Journal, Volume 18, January 1997.) "We found no evidence of a positive association between total dietary fat intake and the risk of breast cancer. There was no reduction in risk even among women whose energy intake from fat was less than 20 percent of total energy intake. In the context of the Western lifestyle, lowering the total intake of fat in midlife is unlikely to reduce the risk of breast cancer substantially." (Hunter, DJ et. al. Cohort studies of fat intake and the risk of breast cancer - A pooled analysis. New England Journal of Medicine, 334: (6) FEB 8 1996) 2) Title: DG-DISPATCH - ENDO 99: Diabetics Improve Health With Very High-Fat, Low Carb Diet Doctor's Guide June 15, 1999 By Cameron Johnston Special to DG News SAN DIEGO, CA -- June 15, 1999 -- A very high-fat, low-carbohydrate diet has been shown to have astounding effects in helping type 2 diabetics lose weight and improve their blood lipid profiles. The results of three studies involving such a diet, which is similar to, but has a few key differences from the famous "Dr. Atkins Diet", were presented today at the annual meeting of the Endocrine Society. Dr. James Hays, an endocrinologist and director of the Limestone Medical Center in Wilmington, DE, admitted that the concept of a high-fat diet in people who are already at higher risk of cardiovascular disease might seem incongruous. Nonetheless, this study of 157 men and women with type 2 diabetes showed an impressive benefit in body mass index (BMI) triglycerides, HDL, LDL and HbA1c. Most people are encouraged to reduce the amount of fat in their diets, particularly saturated fats, and diabetics in particular are advised to reduce their overall caloric intake, Dr. Hays explained in an interview in San Diego during the conference. Whereas a normal diet would be in the order of 1800 to 2100 calories, with 60 percent of calories coming from carbohydrates and 30 percent from fat, patients in this diet were restricted to 1800 calories per day and were encouraged to get 50 percent of their caloric intake from fat, and just 20 percent from carbohydrates. The balance of 30 percent would come from proteins. A whopping 90 percent of the fat content in their diets was saturated fat, compared with just 10 percent that was monounsaturated fat. "I think this is at least worth considering for any diabetic," Dr. Hays said in an interview. "The thing many diabetics coming into the office don't realize is that other forms of carbohydrates will increase their sugars, too. Dietitians will point them toward complex carbohydrates ... oatmeal and whole wheat bread, but we have to deliver the message that these are carbohydrates that increase blood sugars, too." Higher-fat diets, on the other hand, seem to make the person feel full faster so they eat less; higher-fat diets also tend to reduce postprandial hypoglycemia so the patients feel better after eating. "Every diabetic comes home from the doctor with instructions as to what their diet should consist of, but they're not getting the information from dietitians about what complex carbohydrates they should eat," Dr. Hays said: "The important thing here is no ketosis. We absolutely don't want people to become ketotic, and so we said they had to have so many exchanges of fresh fruits and vegetables and we specified the ones they could eat." They were able to eat all the meat and cheese they wanted, but as for carbohydrates, they are restricted to eating unprocessed foods, mainly fresh fruit and vegetables, he added. Subjects recruited into the study (84 men, 73 women) were all type 2 diabetics and were required to undergo a standard American Diabetes Association modified diet for one full year before entry into the trial. Over the course of one year, the subjects achieved a mean decline in total cholesterol of between 231 and 190 mg/dl. Triglycerides declined from 229 to 182 mg/dl. Low-density lipoproteins (LDL cholesterol) fell from 133 to 105 mg/dl, while HDL increased from 44 to 47 mg/dl. HbA1c, which at the start of the study averaged 3.34 percent above normal, declined to the point that at one year, the mean was just 0.96 percent above normal. The average weight loss among subjects in the study was in the order of 40 pounds, Dr. Hays said. By the end of the one-year study, he added, 90 percent of the patients had achieved ADA (American Diabetes Association) targets for HbA1c, HDL, LDL and triglycerides. Even among juvenile diabetics, he said, they might not be overweight and they might have more or less normal lipid levels, but when they are on this kind of diet it is possible to treat them with lower doses of insulin and make their lives a little safer, he said. As for the response from cardiologists who see a high-fat diet as anathema to what they have been instructing their patients for years now, Dr. Hays said he has three cardiologist patients who are now on the diet. "If you have a diet that results in weight loss, lower cholesterol, and a better lipid profile, eventually, everybody will be eating that way. It's going to come whether we like it or not." The New England Journal of Medicine -- November 20, 1997 -- Vol. 337, No. 21 Dietary Fat Intake and the Risk of Coronary Heart Disease in Women Frank B. Hu, Meir J. Stampfer, JoAnn E. Manson, Eric Rimm, Graham A. Colditz, Bernard A. Rosner, Charles H. Hennekens, Walter C. Willett ------------------------------------------------------------------------- ------- Abstract Background. The relation between dietary intake of specific types of fat, particularly trans unsaturated fat, and the risk of coronary disease remains unclear. We therefore studied this relation in women enrolled in the Nurses' Health Study. Methods. We prospectively studied 80,082 women who were 34 to 59 years of age and had no known coronary disease, stroke, cancer, hypercholesterolemia, or diabetes in 1980. Information on diet was obtained at base line and updated during follow-up by means of validated questionnaires. During 14 years of follow-up, we documented 939 cases of nonfatal myocardial infarction or death from coronary heart disease. Multivariate analyses included age, smoking status, total energy intake, dietary cholesterol intake, percentages of energy obtained from protein and specific types of fat, and other risk factors. Results. Each increase of 5 percent of energy intake from saturated fat, as compared with equivalent energy intake from carbohydrates, was associated with a 17 percent increase in the risk of coronary disease (relative risk, 1.17; 95 percent confidence interval, 0.97 to 1.41; P = 0.10). As compared with equivalent energy from carbohydrates, the relative risk for a 2 percent increment in energy intake from trans unsaturated fat was 1.93 (95 percent confidence interval, 1.43 to 2.61; P<0.001); that for a 5 percent increment in energy from monounsaturated fat was 0.81 (95 percent confidence interval, 0.65 to 1.00; P = 0.05); and that for a 5 percent increment in energy from polyunsaturated fat was 0.62 (95 percent confidence interval, 0.46 to 0.85; P = 0.003). Total fat intake was not significantly related to the risk of coronary disease (for a 5 percent increase in energy from fat, the relative risk was 1.02; 95 percent confidence interval, 0.97 to 1.07; P = 0.55). We estimated that the replacement of 5 percent of energy from saturated fat with energy from unsaturated fats would reduce risk by 42 percent (95 percent confidence interval, 23 to 56; P<0.001) and that the replacement of 2 percent of energy from trans fat with energy from unhydrogenated, unsaturated fats would reduce risk by 53 percent (95 percent confidence interval, 34 to 67; P<0.001). Conclusions. Our findings suggest that replacing saturated and trans unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake. (N Engl J Med 1997;337:1491-9.) Source Information >From the Departments of Nutrition (F.B.H., M.J.S., E.R., W.C.W.), Epidemiology (M.J.S., J.E.M., E.R., B.A.R., W.C.W.), and Biostatistics (B.A.R.), Harvard School of Public Health; and the Channing Laboratory (M.J.S., J.E.M., E.R., G.A.C., B.A.R., C.H.H., W.C.W.) and the Division of Preventive Medicine (J.E.M., C.H.H.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School -- all in Boston. Address reprint requests to Dr. Hu at the Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115. 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 Susan Susan <mcfeins@NOgmailNO.com> wrote in part: >Now produce the studies that found a role for >fat in CVD in the absence of high GL. Not fair! You don't think that nutritionists have ever independently varied fats and GL to see what's what do you?! -- Jim Chinnis Warrenton, Virginia, USA > Susan <mcfeins@NOgmailNO.com> wrote in part: > [quoted text clipped - 5 lines] > -- > Jim Chinnis Warrenton, Virginia, USA Actually, I believe they have, but I don't know how many, if any, I hve in my archives. I do know that many studies I've viewed have concluded that fat quality, not quantity, was far more critical in preventing CVD. This means either no trans fats, low sat fat, or more oil from olives, fish, nuts and avocados and less from vegetable/canola, etc. Still, the point is, one cannot conclude anything at all about the role of saturated fat in CVD when the other variables aren't removed. We do know that the oldest experiment on Arctic explorers who ate nothing but meat for a year showed improved cholesterol and, I think, liver tests. The mentally ill man who ate nothing but 25 eggs per day was in extraordinarily good CVD health. Just to cite two extremes. Susan > x-no-archive: yes > [quoted text clipped - 17 lines] > > No more opinions, I want you to cite good science with good data, not > unfounded conclusions. > [quoted text clipped - 252 lines] > Frank B. Hu, Meir J. Stampfer, JoAnn E. Manson, Eric Rimm, Graham A. > Colditz, Bernard A. Rosner, Charles H. Hennekens, Walter C. Willett ------------------------------------------------------------------------- > ------- > [quoted text clipped - 119 lines] > > Susan I think you have not read carefully what I have said. And in the conclusion above, what I have said is corroborated by this which you posted "...metabolic risk fators for type 2 diabetes..." zee > I think you have not read carefully what I have said. And in the > conclusion above, what I have said is corroborated by this which you > posted "...metabolic risk fators for type 2 diabetes..." > > zee LOL! That's what you picked up from all that research? It just boggles the mind. Susan > x-no-archive: yes > [quoted text clipped - 11 lines] > > Susan :: I repeat: "low-carb" would be wrong and possibly deadly in context of :: FH. [quoted text clipped - 5 lines] :: :: Zee IMHO, Susan is partly right here. Your suggestion to follow Mediterranean diet and complex carbs is OK, but in addition to that, someone with insulin resistance should reduce the intake whole grains as well (and cut all refined grains, of course). SignatureJuhana > :: I repeat: "low-carb" would be wrong and possibly deadly in context of > :: FH. [quoted text clipped - 10 lines] > resistance should reduce the intake whole grains as well (and cut all > refined grains, of course). Except for whoe rye kernels, whole grains aren't good for those who are IR, either. Glucose meters tell the tale. Susan :: x-no-archive: yes :: Juhana Harju wrote: ::: IMHO, Susan is partly right here. Your suggestion to follow ::: Mediterranean diet and complex carbs is OK, but in addition to [quoted text clipped - 3 lines] :: Except for whoe rye kernels, whole grains aren't good for those who :: are IR, either. Glucose meters tell the tale. I thought that whole barley and whole grain pasta have a low glychemic index also, but I am not a diabetic, so I might be wrong. :-) SignatureJuhana > :: x-no-archive: yes > :: Juhana Harju wrote: [quoted text clipped - 3 lines] > ::: that, someone with insulin resistance should reduce the intake > ::: whole grains as well (and cut all refined grains, of course). One study posted did corroborate what I said in its conclusion statement; consider "metabolic syndrome" ie) insulin resistance. Not all complex carbs (with good protein and high fibre preferably) will be grains. Consider channa dal. A little study on nutrition would go a long way here.... Zee > :: Except for whoe rye kernels, whole grains aren't good for those who > :: are IR, either. Glucose meters tell the tale. > > I thought that whole barley and whole grain pasta have a low glychemic index > also, but I am not a diabetic, so I might be wrong. :-) > One study posted did corroborate what I said in its conclusion > statement; consider "metabolic syndrome" ie) insulin resistance. Not [quoted text clipped - 3 lines] > > Zee You're a cherry picker, looking for a point rather than taking in information. Estimates of IR in the general population range from 25 - 40%. Over 40 that's way higher. I researched diet and CVD for many months before determining the best nutritional approach and my entire family is healthier for it. Some folks can eat lentils, many who are IR can't. I eat black soybeans, which are almost completely made up of protein and fiber. But I also eat animal protein of some sort at least once or twice every day. I didn't need a statin to cut my CVD serum risk profile by over 50%. And I eat about 50% of calories from fat, about 1/4 or 1/3 of it saturated. Red meat has more mono and poly fat than saturated fats in it, BTW. Especially trimmed. Susan > I eat black > soybeans, which are almost completely made up of protein and fiber. Any pointers on how to fix them? I'd like to give them a try. >> I eat black soybeans, which are almost completely made up of protein >> and fiber. > > Any pointers on how to fix them? I'd like to give them a try. Any way you use other beans. I used them for chili. I also make a salad with some chopped red onion, cumin, lime juice and olive oil. Susan > x-no-archive: yes > [quoted text clipped - 13 lines] > > I researched diet and CVD for many months before determining the best > nutritional approach and my entire family is healthier for it. > [quoted text clipped - 11 lines] > > Susan > I thought that whole barley and whole grain pasta have a low glychemic index > also, but I am not a diabetic, so I might be wrong. :-) They do have a theoretical lower GI, and barley contains chromium, I believe, which should help, but... The more they're cooked, the higher the GI. They rocket my BG as fast and as high as table sugar. Even undercooked. Surely you're aware of studies demonstrating that GI is not a good predictor of individual results, or of insulin index? Susan :: x-no-archive: yes :: Surely you're aware of studies demonstrating that GI is not a good :: predictor of individual results, or of insulin index? Do you mean that glycemic load is more important or what? SignatureJuhana > :: x-no-archive: yes > > :: Surely you're aware of studies demonstrating that GI is not a good > :: predictor of individual results, or of insulin index? > > Do you mean that glycemic load is more important or what? That's part of it, but it's also that individual response to GI vary a great deal. And some very low GI foods have a high insulin release. Susan :: And some very low GI foods have a high insulin release. Like which and why? SignatureJuhana 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. :: x-no-archive: yes :: :: Blood Glucose Concentration Linked to>Cardiovascular Risk in :: Nondiabetic Men> :: [...] I agree that blood glucose and insuline levels are important risk factors. But your claim that low carb diet would be the best to lower lipids is simply not true. Limiting carbs within the context of traditional Cretan Mediterranean diet would probably be the best policy for anyone with high cholesterol and high blood glucose (metabolic syndrome). SignatureJuhana > :: x-no-archive: yes > :: [quoted text clipped - 5 lines] > But your claim that low carb diet would be the best to lower lipids is > simply not true. Well, yeah, it is true, quite a bit of research demonstrates it, particularly with HbA1c, which I believe will become an important benchmark for CVD risk widely used in the non-diabetic population. Only low carb lowers it a LOT and keeps it low. > Limiting carbs within the context of traditional Cretan Mediterranean diet > would probably be the best policy for anyone with high cholesterol and high > blood glucose (metabolic syndrome). You know, there is no such thing as a one size fits all diet. I have to eat lower carb than some other folks do. I do better if I limit sat fat, some folks do fine eating nothing but. The notion that you can ignore every other aspect of environment and lifestyle and just adopt a particular diet as ideal for everyone is ridiculous. Susan :: x-no-archive: yes :: [quoted text clipped - 13 lines] :: benchmark for CVD risk widely used in the non-diabetic population. :: Only low carb lowers it a LOT and keeps it low. No research demonstrates that low carb is effective in reducing cholesterol. Just compare it to the Portfolio diet. Low carbers often eat a lot of red meat. Red meat, high heme iron and high ferritin has been shown to increase the risk of diabetes and CVD. ::: Limiting carbs within the context of traditional Cretan ::: Mediterranean diet would probably be the best policy for anyone [quoted text clipped - 5 lines] :: that you can ignore every other aspect of environment and lifestyle :: and just adopt a particular diet as ideal for everyone is ridiculous. 'Ridiculous' is a strong word here. Actually the Mediterranean diet has been transferred to different populations and it has been shown to work everywhere. There are studies about Mediterranean diet trials in India, Austalia etc. Still I do agree that people with high blood glucose should limit even whole grains. The advantage doing it within the context of Mediterranean diet is that then you get proteins in a healthy package (from beans and fish) in addition to safe and heart healthy fats (from olive oil, nuts and fish). SignatureJuhana > No research demonstrates that low carb is effective in reducing cholesterol. Very wrong. It invariably raises HDL, dramatically lowers the independent and highly predictive TGL, and VLDL. Even when LDL goes up temporarily, it's less likely to be damaging, VLDL and less likely to be oxidized or cause endothelial damage due to lower glucose. > Just compare it to the Portfolio diet. Low carbers often eat a lot of red > meat. Red meat, high heme iron and high ferritin has been shown to increase > the risk of diabetes and CVD. There are no such studies that control for the crap that many heavy red meat eaters eat with it, or the quality of the red meat. Fries and coke, cure meats are likely the culprits. > 'Ridiculous' is a strong word here. Actually the Mediterranean diet has been > transferred to different populations and it has been shown to work > everywhere.t That doesn't mean something else, such as low carb doesn't work. Further, if you look at just lowering cholesterol, you're missing the big picture. I lowered my TC on Ornish, but I had extremely low HDL and sky high TGL and developed IR, PCOS and labile hypertension on it. But, hey, my TC dropped. Not as much as on low carb, though. My TC dropped by 100 points, and my HDL doubled from a decade long 34 up to 70. My TGL dropped by almost 200 pts. It is ludicrous to propose that everyone, everywhere, in every health status, activity level, etc... should be eating the same food. That's the wrongheaded type of thinking that has the ADA pushing cereal and bread to diabetics, who have to take a boatload of pills to tolerate them. here are studies about Mediterranean diet trials in India, > Austalia etc. Still I do agree that people with high blood glucose should > limit even whole grains. The advantage doing it within the context of > Mediterranean diet is that then you get proteins in a healthy package (from > beans and fish) in addition to safe and heart healthy fats (from olive oil, > nuts and fish). Most low carbers learn more about healthy EFAs, GL, the role of fiber and antioxidant rich foods than low fat dieters. Starches are frankly impoverished of nutrients when compared to colorful, leafy plant foods. Susan :: Most low carbers learn more about healthy EFAs, GL, the role of fiber :: and antioxidant rich foods than low fat dieters. Starches are :: frankly impoverished of nutrients when compared to colorful, leafy :: plant foods. Personally I am no dieter. I have always been lean and I don't have any need to follow any weight control, cholesterol lowering or glycemic control diet. Still I have a healthy diet. My TC is 4 and the ratio of LDL to HDL is good. No problem with triglyserides either. I have always wondered why low carbers pay attention only to the quality of carbs, but not to the package in which protein comes nor to the quality of fats. For me it is obvious that one should aim to eat the healthiest foods from each of the macronutrient groups. SignatureJuhana > Personally I am no dieter. I have always been lean and I don't have any need > to follow any weight control, cholesterol lowering or glycemic control diet. > Still I have a healthy diet. My TC is 4 and the ratio of LDL to HDL is good. > No problem with triglyserides either. Good for you! I was lean (I couldn't stand to eat anymore on Ornish) too, when I developed PCOS and severe IR and learned it was caused by a low fat, high carb diet. > I have always wondered why low carbers pay attention only to the quality of > carbs, but not to the package in which protein comes nor to the quality of > fats. For me it is obvious that one should aim to eat the healthiest foods > from each of the macronutrient groups. That's just a faulty and unsubstantiated assumption on your part. I learned about the importance of the CLA, omega 6/3 content and arachidonic acid content in feedlot beef as a health risk from low carb resources. When red meat is studied using feedlot beef rather than grass fed free range beef, the results indict agribusiness practices, not beef. Low carb reading is where I also learned only to buy wild, not farm raised fish, and why. Susan :: x-no-archive: yes ::: I have always wondered why low carbers pay attention only to the ::: quality of carbs, but not to the package in which protein comes nor [quoted text clipped - 8 lines] :: practices, not beef. Low carb reading is where I also learned only :: to buy wild, not farm raised fish, and why. Not so unssubstantiated. I have been following the comments and discussions of low carbers here in Finland where I live and the ignorance is enormous. I do agree that there are also some low carbers who are quite knowledgeable. When it comes to CLA, please notice that not all evidence is positive. Also the high heme iron is likely to be a problem even if red meat is from pasteurizing cattle. Fatty fish has healthier lipids than red meat, even if the cattle has been fed with grass. SignatureJuhana > Not so unssubstantiated. I have been following the comments and discussions > of low carbers here in Finland where I live and the ignorance is enormous. I > do agree that there are also some low carbers who are quite knowledgeable. All the low carb plans emphasize food quality and fat quality. Every one. > When it comes to CLA, please notice that not all evidence is positive. Also > the high heme iron is likely to be a problem even if red meat is from > pasteurizing cattle. Fatty fish has healthier lipids than red meat, even if > the cattle has been fed with grass. Not so, there's absolutely no good evidence finding any unhealthy role for naturally grass fed red meat in the human nutrition. There's no evidence at all, actually, because variables have not been controlled for. Susan :: x-no-archive: yes :: [quoted text clipped - 7 lines] :: All the low carb plans emphasize food quality and fat quality. :: Every one. Well, people have different understanding what food and fat quality actually means. Many people think that it is healthy to eat anything that is organic. Personally I think that it is healthier to eat some healthy non-organic foods than to eat unhealthy organic foods. There is also a wide range of low carbers. Many of them start a diet high in red meat not knowing that it is important to eat a lot of veggies, too. I have red many messages of low carbers who have not red a single book presenting a diet plan. There are also wide range of low carb plans. Some earlier plans of Atkins are very different from the latest. And so on. ::: When it comes to CLA, please notice that not all evidence is ::: positive. Also the high heme iron is likely to be a problem even if [quoted text clipped - 5 lines] :: There's no evidence at all, actually, because variables have not :: been controlled for. Some variables are known. EPA, DHA and phospholipids are healthy variables, heme iron and saturated fat are unhealthy variables, at least in excess. SignatureJuhana > Well, people have different understanding what food and fat quality actually > means. Many people think that it is healthy to eat anything that is organic. > Personally I think that it is healthier to eat some healthy non-organic > foods than to eat unhealthy organic foods You seem to work from the inside out; you decide what it is that you like about a diet philosophically, then you seek to buttress that by claiming scientifically unfounded faults with foods you don't want folks to eat. Kind of like Dean Ornish leaving very heart healthy fish off his original diet plan because he's a vegetarian, screw the patients' health and the science. >There is also a wide range of low > carbers. Many of them start a diet high in red meat not knowing that it is > important to eat a lot of veggies, too. I don't know many of those. I doubt they last long without a well developed eating plan and knowledge. Low carbers as a group are so knowledgable, in fact, that they're not buying the artificially sweetened, trans fat laden mass market low carb Frankenfoods that are languishing on store shelves. >I have red many messages of low > carbers who have not red a single book presenting a diet plan. > > There are also wide range of low carb plans. Some earlier plans of Atkins > are very different from the latest. And so on. Atkins hasn't made any changes of significance in the plans, just the new ownership is marketing it more deftly. > ::: When it comes to CLA, please notice that not all evidence is > ::: positive. Also the high heme iron is likely to be a problem even if [quoted text clipped - 8 lines] > Some variables are known. EPA, DHA and phospholipids are healthy variables, > heme iron and saturated fat are unhealthy variables, at least in excess. Saturated fat has not been proven unhealthy, not witout fries or a baked potato. We need heme iron, it's the best absorbed. What we don't need is excess, or supplemental iron subject to oxidation. Low carbers are encouraged by all plans to get high EPA and DHA, from food and, if needed, from supplements. All low carb plans emphasize fats from healthy sources. Sirloin beef has more mono fat than any other, BTW. Susan Is this the kind of thing you were asking for reviewing pantethine, with citations? http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/pan_0195.shtml Susan :: x-no-archive: yes :: :: Is this the kind of thing you were asking for reviewing pantethine, :: with citations? http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/pan_0195.shtml Thanks, that is a good one, I found it too. :-) SignatureJuhana :: x-no-archive: yes ::: 'Ridiculous' is a strong word here. Actually the Mediterranean diet ::: has been transferred to different populations and it has been shown [quoted text clipped - 3 lines] :: Further, if you look at just lowering cholesterol, you're missing the :: big picture. [...] There is mounting evidence for the Mediterranean type of diet. Just have a look at the Lyon Heart Study. I am not looking just lowering cholesterol. I am also looking at reducing cardiac arrythmias, reducing the risk of thrombosis, increasing insulin sensitivity, increasing antioxidants, increasing nutrient density, reducing inflammation and CRP, reducing homocysteine... SignatureJuhana > :: x-no-archive: yes > [quoted text clipped - 12 lines] > increasing nutrient density, reducing inflammation and CRP, reducing > homocysteine... Yabbut, your eyes are closed to any evidence of that which you do not already believe. Susan :: x-no-archive: yes :: [quoted text clipped - 19 lines] :: Yabbut, your eyes are closed to any evidence of that which you do not :: already believe. I don't think so. I am always ready to learn more. SignatureJuhana > I don't think so. I am always ready to learn more. Good! You should start by trying to find any good controlled studies finding fault with dietary saturated fat not eaten with carbs. All I've ever found was a suggestion that *might* be true about saturated fat *perhaps* making cell walls less permeable and therefore less sensitive to insulin, but it's far from being established as fact. Susan "Juhana Harju" <shantigiri@despammed.com> wrote in part: >I agree. If some lipid lowering agents are needed I would combine >Polycosanol, Pantethine or Krill oil with fish oils. Those combinations >would probably be much safer than statin combined with fish oils and at >least as effective in reducing cardiovascular and total mortality. (It is >true that there are no studies that would have combined the supplements that >I am proposing.) There are also no studies showing any outcomes improved with most of the *individual treatments*, such as policosanol and pantethine and krill oil. >Even better option would be the Portfolio diet combined with fish oils. Maybe. -- Jim Chinnis Warrenton, Virginia, USA > "Juhana Harju" <shantigiri@despammed.com> wrote in part: > [quoted text clipped - 14 lines] > -- > Jim Chinnis Warrenton, Virginia, USA We have no objective outcomes reported on statins, IMO, with researchers all having financial stakes in the drugs when they study them. If the lipid targets are an issue, then we know pantethine is effective, that fish oil, too, will lower TGLs, dramatically with high doses. I don't know of anyone who's gotten any of the alleged benefits of policosanol or guggulipid, but I got exactly what the research results were using pantethine, added to my low carb diet, which had already improved my lipid profile a great deal. Susan Susan <mcfeins@NOgmailNO.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 19 lines] >We have no objective outcomes reported on statins, IMO, with researchers >all having financial stakes in the drugs when they study them. Well, you're right that if we throw out all the statin trials because of conflicts of interest, then there are no data to show that they have an effect on outcomes, either. The current system for reporting research is a poor one, but I don't think everything has to be thrown out, just taken with a grain of salt. Hopefully, some of the nonsense is coming to an end. Some of the statin trials had their designa and hypotheses published in advance of the studies. That';s a great start on a good system, IMO. >If the lipid targets are an issue, then we know pantethine is effective, >that fish oil, too, will lower TGLs, dramatically with high doses. If the lipid targets are the real targets. Lipid targets are themselves rather complex when all aspects are considered. If agent X changes lipids in a way the reduces LDL and mortality, that doesn't mean that reducing LDL with agent Y will reduce mortality. >I don't know of anyone who's gotten any of the alleged benefits of >policosanol or guggulipid, but I got exactly what the research results >were using pantethine, added to my low carb diet, which had already >improved my lipid profile a great deal. > >Susan We all have to work with what we can and balance the risks. -- Jim Chinnis Warrenton, Virginia, USA > We all have to work with what we can and balance the risks. > -- > Jim Chinnis Warrenton, Virginia, USA Exactly. With my extremely lethal lipid profile and family history of early death from CVD, and my perfectly healthy mother's debilitation by statins, I've decided to do a lot of homework. I've found that low carb, high pantethine works for me. My CVD serum lipid risk profile is down from 9.5 to 3.5, on paper, as a result. I emphasize naturally raised meat, with it's favorable fat content, and wild fish in my diet, and organic produce. I probably eat more veggies, salad and fiber than any one here, except maybe you. ;-) Susan High-Grain Diet May Increase Risk of Cardiovascular Disease American Journal Clinical Nutrition January 2003 77: 43-50 When humans consume more carbohydrates than can be stored, the excess carbohydrate energy is converted to fat by the liver. This process may maintain blood sugar control and prevent diabetes in the short-term, however it may also increase triglyceride concentrations, which may increase the risk of cardiovascular disease. In the last decade, researchers established that fat production by the liver varies depending on dietary habits and health status. The typical Western diet has a high fat content, which means that only a limited amount of carbohydrates are available for liver fat production, and liver fat production tends to be very low among individuals who eat this type of diet. However, when too many carbohydrates were consumed, both liver fat and sugar production were increased. A very low-fat (10 percent of energy) and very high-carbohydrate (75 percent of energy) diet also leads to increased liver fat production, with the increase being even more pronounced when more than half of the carbohydrate was consumed as simple sugars. This points to the importance of carbohydrate quality, as another study using 68 percent of energy from complex carbohydrate resulted in minimal liver fat production. However, it was found that obese individuals with high insulin levels who consume a high-fat (40 percent of energy) diet had a liver fat production rate three to four times higher than that of lean individuals with normal insulin levels. But, both normal and high insulin groups had lower liver fat production on the high-fat diet than on a low-fat, high-carbohydrate diet. Moreover, the low-fat, high-carbohydrate diet caused an increase in triglyceride concentrations, a risk factor for coronary heart disease, which was associated with the liver fat production in both normal and high-insulin individuals. Researchers concluded that the low-fat, high-carbohydrate diet might not be ideal, as it can induce liver fat production and insulin resistance. This is especially true when most of the carbohydrate is in the form of simple sugars. -- 1: Am J Clin Nutr 2003 Jan;77(1):43-50 Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets. Schwarz JM, Linfoot P, Dare D, Aghajanian K. Department of Nutritional Sciences and Toxicology, University of California, Berkeley (J-MS and KA), and the Department of Medicine, University of California, San Francisco (J-MS, PL, and DD). BACKGROUND: Hypertriglyceridemia is associated with increased risk of cardiovascular disease. Until recently, the importance of hepatic de novo lipogenesis (DNL) in contributing to hypertriglyceridemia was difficult to assess because of methodologic limitations. OBJECTIVE: We evaluated the extent of the contribution by DNL to different conditions associated with hypertriglyceridemia. DESIGN: After 5 d of an isoenergetic high-fat, low-carbohydrate diet, fasting DNL was measured in normoinsulinemic (/= 115 pmol/L) obese (n = 8) subjects. Fasting DNL was measured after a low-fat, high-carbohydrate diet in normoinsulinemic lean (n = 5) and hyperinsulinemic obese (n = 5) subjects. Mass isotopomer distribution analysis was used to measure the fraction of newly synthesized fatty acids in VLDL-triacylglycerol. RESULTS: With the high-fat, low-carbohydrate diet, hyperinsulinemic obese subjects had a 3.7-5.3-fold higher fractional DNL (8.5 +/- 0.7%) than did normoinsulinemic lean (1.6 +/- 0.5%) or obese (2.3 +/- 0.3%) subjects. With the low-fat, high-carbohydrate diet, normoinsulinemic lean and hyperinsulinemic obese subjects had similarly high fractional DNL (13 +/- 5.1% and 12.8 +/- 1.4%, respectively). Compared with baseline, consumption of the high-fat, low-carbohydrate diet did not affect triacylglycerol concentrations. However, after the low-fat, high-carbohydrate diet, triacylglycerols increased significantly and DNL was 5-6-fold higher than in normoinsulinemic subjects consuming a high-fat diet. The increase in triacylglycerol after the low-fat, high-carbohydrate diet was correlated with fractional DNL (P < 0.01), indicating that subjects with high DNL had the greatest increase in triacylglycerols. CONCLUSIONS: These results support the concept that both hyperinsulinemia and a low-fat diet increase DNL, and that DNL contributes to hypertriglyceridemia. PMID: 12499321 [PubMed - in process] http://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract http://www.mercola.com/2003/jan/8/high_grain_diet.htm :: x-no-archive: yes :: [quoted text clipped - 3 lines] :: :: [...] Well, to have a more balanced view, lets have a look at this review (the full study is also available): American Journal of Clinical Nutrition, Vol. 70, No. 3, 451S-458S, September 1999 © 1999 American Society for Clinical Nutrition Supplements Cereals, legumes, and chronic disease risk reduction: evidence from epidemiologic studies1,2,3 Lawrence H Kushi, Katie A Meyer and David R Jacobs, Jr 1 From the Division of Epidemiology, University of Minnesota School of Public Health, Minneapolis. There is growing evidence that cereals and legumes play important roles in the prevention of chronic diseases. Early epidemiologic studies of these associations focused on intake of dietary fiber rather than intake of grains or legumes. Generally, these studies indicated an inverse association between dietary fiber intake and risk of coronary artery disease; this observation has been replicated in recent cohort studies. Studies that focused on grain or cereal intake are fewer in number; these tend to support an inverse association between intake of whole grains and coronary artery disease. Studies on the association of dietary fiber with colon and other cancers have generally shown inverse relations, but whether these relations are attributable to cereals, other fiber sources, or other factors is less clear. Although legumes have been shown to lower blood cholesterol concentrations, epidemiologic studies are few and inconclusive regarding the association of legumes with risk of coronary artery disease. It has been hypothesized that legumes, in particular soybeans, reduce the risk of some cancers, but epidemiologic studies are equivocal in this regard. Overall, there is substantial epidemiologic evidence that dietary fiber and whole grains are associated with decreased risk of coronary artery disease and some cancers, whereas the role of legumes in these diseases appears promising but as yet inconclusive. http://www.ajcn.org/cgi/content/abstract/70/3/451S SignatureJuhana > :: x-no-archive: yes > :: [quoted text clipped - 44 lines] > -- > Juhana Montreal cardiologist and McGill University professor Colin Rose: CAD caused by atherogenic diet, not a deficiency of statins. As usual...Rose nails it. ~~~~~~~~~~~~~~~~~~~~~~~~~ "If there are any lipid experts left with no connection to the drug industry let them appoint themselves to a 'working group' and write a consensus opinion. If they don't want to appoint themselves I can try to arrange for them to be appointed. Until then I will use statins only for patients with severe, symptomatic, congenital lipid problems. Dr. Dobson wonders what I would 'explain to grieving family members that he failed to prescribe a statin for someone who was unable to control their LDL with diet and who went on to suffer a fatal heart attack'? Well, I am glad he asked. I would tell them that a hear |
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