Guest guest Posted October 5, 2005 Report Share Posted October 5, 2005 Hi All, Another dietary choice may be available, in: http://www.guardian.co.uk/international/story/0,,1584872,00.html Al Pater, PhD; email: old542000@... __________________________________ - PC Magazine Editors' Choice 2005 http://mail. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 6, 2005 Report Share Posted October 6, 2005 Sounds like another politically correct dietitian's low fat diet to me. Another recipe for binging and trouble. I find that a bit more saturated fat (butter from grass fed cows, tallow or coconut oil) in my plate goes a long way to still my hunger and provide the energy substrate one requires if one goes rather low in the carb count. Thus preventing hypoglycemia it seems, as temporaraly more elavated blood lipids are involved in a process which results in a glucose sparing effect through a mild form of insulin resistance. More on this alternative to the perhaps outdated trifty gene theory here: http://jp.physoc.org/cgi/content/full/554/3/595 > Hi All, > > Another dietary choice may be available, in: > > http://www.guardian.co.uk/international/story/0,,1584872,00.html > > Al Pater, PhD; email: old542000@y... > > > > __________________________________ > - PC Magazine Editors' Choice 2005 > http://mail. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 6, 2005 Report Share Posted October 6, 2005 Hi : I am not entirely sure what the health implications of that paper might be for a person on CR. Enlightenment would be appreciated. ty. Second, are you sure that it isn't fat calories that are the most important for people hoping for lifespan extension to restrict? It is beginning to look like carbohydrate calories may be at the bottom, not the top, of the 'calorie types to avoid' list. Third, if coconut oil is not on your 'foods to avoid' list, then do you have anything on it? Coconut oil is, of course, 100% fat; 87% of it saturated; 87% of that is 16:0 or shorter; and 22% of it is myristic. Are you unable to find anything a little more healthy that will satisfy your hunger pains? I haven't checked the numbers, but a couple of bacon double cheeseburgers might be better ; ^ ))) Rodney. > Sounds like another politically correct dietitian's low fat diet to > me. Another recipe for binging and trouble. I find that a bit more > saturated fat (butter from grass fed cows, tallow or coconut oil) in > my plate goes a long way to still my hunger and provide the energy > substrate one requires if one goes rather low in the carb count. Thus > preventing hypoglycemia it seems, as temporaraly more elavated blood > lipids are involved in a process which results in a glucose sparing > effect through a mild form of insulin resistance. More on this > alternative to the perhaps outdated trifty gene theory here: > > http://jp.physoc.org/cgi/content/full/554/3/595 > > > > > --- In , Al Pater <old542000@y...> wrote: > > Hi All, > > > > Another dietary choice may be available, in: > > > > http://www.guardian.co.uk/international/story/0,,1584872,00.html > > > > Al Pater, PhD; email: old542000@y... > > > > > > > > __________________________________ > > - PC Magazine Editors' Choice 2005 > > http://mail. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 6, 2005 Report Share Posted October 6, 2005 Hi : I am not entirely sure what the health implications of that paper might be for a person on CR. Enlightenment would be appreciated. ty. Second, are you sure that it isn't fat calories that are the most important for people hoping for lifespan extension to restrict? It is beginning to look like carbohydrate calories may be at the bottom, not the top, of the 'calorie types to avoid' list. Third, if coconut oil is not on your 'foods to avoid' list, then do you have anything on it? Coconut oil is, of course, 100% fat; 87% of it saturated; 87% of that is 16:0 or shorter; and 22% of it is myristic. Are you unable to find anything a little more healthy that will satisfy your hunger pains? I haven't checked the numbers, but a couple of bacon double cheeseburgers might be better ; ^ ))) Rodney. > Sounds like another politically correct dietitian's low fat diet to > me. Another recipe for binging and trouble. I find that a bit more > saturated fat (butter from grass fed cows, tallow or coconut oil) in > my plate goes a long way to still my hunger and provide the energy > substrate one requires if one goes rather low in the carb count. Thus > preventing hypoglycemia it seems, as temporaraly more elavated blood > lipids are involved in a process which results in a glucose sparing > effect through a mild form of insulin resistance. More on this > alternative to the perhaps outdated trifty gene theory here: > > http://jp.physoc.org/cgi/content/full/554/3/595 > > > > > --- In , Al Pater <old542000@y...> wrote: > > Hi All, > > > > Another dietary choice may be available, in: > > > > http://www.guardian.co.uk/international/story/0,,1584872,00.html > > > > Al Pater, PhD; email: old542000@y... > > > > > > > > __________________________________ > > - PC Magazine Editors' Choice 2005 > > http://mail. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 6, 2005 Report Share Posted October 6, 2005 Lowfat diets are associated with increased rates of depresion, psychological problems, fatigue, violence and suicide. (lancet 3/2/92 v339) Dear Rodney: One major obstacle for understanding the role of saturated fats (not trans fats) in the the diet, yet alone for admitting their importance to the human organism is the hugely succesful barrage of disinformation about fats that has discouraged most people to look beyond what they are told. Yet the empirical evidence (given the faulty science againt them)for their desirability is overwhelming. Does it make sense to be told that coconut oil is unhealthy, a so-called artery clogging fat, when you consider that a large number of those ethnic groups (in thailand before the advent of cheap vegetable oils 20 years ago, in the philippines and Sri Lanka to this day)we recognised as healthy has been using this type of tropical oil for so long? In rather large daily quantities? That it contains roughly 50% lauric acid, (more than human breast milk, the second most important source)a potent anti-bacterial, -viral, -fungal compound very much absent from the SAD? In a letter to the WHO the government of the Philippines congratulated itself upon its succesful AIDS education campaign (that country presenting strikingly low rates of this disease)but those in the know attribute this fact to less idealistic factors... As for the other kinds of saturated fats, what of them? Before 1920 heart disease was relatively rare compared to today, when it is a real epidemic. The sharp rise of coronary disease after this date coincides with decreased consumption of saturated fats such as butter and tallow in favor of increased consumption of their cheaper displacement alternatives, margarine and corn oil boosted by aggressive promotion (interesting to depression era budgets) and later from the early 1950 onwards by a AHA campaign pushing their health virtues on the american public. And what was the irrefutable science behind all this? Experiments which consistent in feeding rabbits (an exclusively herbivorous animal)oxidised cholesterol and noticing how this practice resulted in arterial plaque. The rigorously drawn conclusion was that similar deposits in human arteries were owned to the same foods. Voilà ! the birth of the cholesterol/lipid hypothesis, the basis for the need for cholesterol lowering meds and yet an increasingly discredited theory. It seems that more and more we hear that cholesterol readings do not matter. some studies suggest that the protective, anti-oxydant qualities of cholesterol have been overlooked, and that in many case it is not as accurate a predictor of coronary disease as was previously thought. It seems nomocysteine is much more important. If this is so, what is wrong with saturated fats of animal origin? Could it be that we are turned off by them instinctively because we have been conditioned to do so after being subjected to 60 years of propaganda? Doesn't it strike anybody as odd that oils made up of mostly polyunsaturated fatty acid are advertised as being good for us when you consider the rate at which these very unstable oils oxidise in a bottle and and a highly reactive environment such as the body? Wouln't want to have these messing up my cells! Think of the massive oxidative dammage!There are some studies suggesting more or less persuasively that they are the principal reason behind rising rates of melanomas in australia. Thet are certainly positively linked with macular degeneration. No such association with coconut oil. That stuff can lie in the cupboard for 2 years and not go rancid. In any case it pays to make up ones own mind after careful consideration of the historical facts. http://www.westonaprice.org/knowyourfats/oiling.html To answer your first question Rodney, in evolutionary terms fat consumption was very important for survival. It ensured that man could go a long time without eating and still be able to face the challenges of food gathering in a reasonably fit state. According to Stannard, the author of the article, periods of fasting (and very low carb consumption)possibly triggered a mechanism whereby glucose is spared for brain function by a temporary insulin resistance in muscular tissues. What insures a constant energy substrate in the absence of food are more elevated blood lipids. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 6, 2005 Report Share Posted October 6, 2005 Lowfat diets are associated with increased rates of depresion, psychological problems, fatigue, violence and suicide. (lancet 3/2/92 v339) Dear Rodney: One major obstacle for understanding the role of saturated fats (not trans fats) in the the diet, yet alone for admitting their importance to the human organism is the hugely succesful barrage of disinformation about fats that has discouraged most people to look beyond what they are told. Yet the empirical evidence (given the faulty science againt them)for their desirability is overwhelming. Does it make sense to be told that coconut oil is unhealthy, a so-called artery clogging fat, when you consider that a large number of those ethnic groups (in thailand before the advent of cheap vegetable oils 20 years ago, in the philippines and Sri Lanka to this day)we recognised as healthy has been using this type of tropical oil for so long? In rather large daily quantities? That it contains roughly 50% lauric acid, (more than human breast milk, the second most important source)a potent anti-bacterial, -viral, -fungal compound very much absent from the SAD? In a letter to the WHO the government of the Philippines congratulated itself upon its succesful AIDS education campaign (that country presenting strikingly low rates of this disease)but those in the know attribute this fact to less idealistic factors... As for the other kinds of saturated fats, what of them? Before 1920 heart disease was relatively rare compared to today, when it is a real epidemic. The sharp rise of coronary disease after this date coincides with decreased consumption of saturated fats such as butter and tallow in favor of increased consumption of their cheaper displacement alternatives, margarine and corn oil boosted by aggressive promotion (interesting to depression era budgets) and later from the early 1950 onwards by a AHA campaign pushing their health virtues on the american public. And what was the irrefutable science behind all this? Experiments which consistent in feeding rabbits (an exclusively herbivorous animal)oxidised cholesterol and noticing how this practice resulted in arterial plaque. The rigorously drawn conclusion was that similar deposits in human arteries were owned to the same foods. Voilà ! the birth of the cholesterol/lipid hypothesis, the basis for the need for cholesterol lowering meds and yet an increasingly discredited theory. It seems that more and more we hear that cholesterol readings do not matter. some studies suggest that the protective, anti-oxydant qualities of cholesterol have been overlooked, and that in many case it is not as accurate a predictor of coronary disease as was previously thought. It seems nomocysteine is much more important. If this is so, what is wrong with saturated fats of animal origin? Could it be that we are turned off by them instinctively because we have been conditioned to do so after being subjected to 60 years of propaganda? Doesn't it strike anybody as odd that oils made up of mostly polyunsaturated fatty acid are advertised as being good for us when you consider the rate at which these very unstable oils oxidise in a bottle and and a highly reactive environment such as the body? Wouln't want to have these messing up my cells! Think of the massive oxidative dammage!There are some studies suggesting more or less persuasively that they are the principal reason behind rising rates of melanomas in australia. Thet are certainly positively linked with macular degeneration. No such association with coconut oil. That stuff can lie in the cupboard for 2 years and not go rancid. In any case it pays to make up ones own mind after careful consideration of the historical facts. http://www.westonaprice.org/knowyourfats/oiling.html To answer your first question Rodney, in evolutionary terms fat consumption was very important for survival. It ensured that man could go a long time without eating and still be able to face the challenges of food gathering in a reasonably fit state. According to Stannard, the author of the article, periods of fasting (and very low carb consumption)possibly triggered a mechanism whereby glucose is spared for brain function by a temporary insulin resistance in muscular tissues. What insures a constant energy substrate in the absence of food are more elevated blood lipids. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 Sorry guys I had no idea you felt this way about the WAPF or had negative feelings about the concepts elaborated by the people there. I just thought the link would provide a nice historical exposé of some of the reasons as to why folks react so strongly when confronted with saturated fats and how this reaction of fear has been produced in them. So I will never mention them again. However, none of you or indeed no one who has visited with some regularity the more reputable nutrition sites will deny that the cholesterol hypothesis has come under much questioning in the last 3 or 4 years, most notably in the JAMA last year about that study done with post menopausal women and the effects of saturated fats on CHD incidence in that group. Consuming saturated fats most dedidly negatively corelated with incidence of CHD. Such was the surprise that the study was immediately commented by an editorial note wich tried to be, if not effectively dismissive, than perhaps advising a kind of orthodox caution. There are also quite a number of studies in which serum cholesterol values come out as irrelevant. The exercise study commented a few days ago on this very site shows just that. It would seem that CHD can evolve where cholesterol valus are quite low in the so called healthy range. At this point I'm afraid to refer to the work of K.Mccully (or that of the folks at THINCS) on homocysteine. If his stuff is valid (don't the folks at LEF think so?)it may well mean that eating stuff such as butter may once again be permissible, though for some reason he(not very consequentially)dicourages it. I'm not saying eat a ton of the stuff. In my experince a little bit of butter goes a long way to make eating small quantities of food more satisfying, longer. I do find the Stannard endlessly fascinating. Makes the thrifty gene theory seem rather chronocentric, as did the cholesterol/lipid theory. patrick > Lowfat diets are associated with increased rates of depresion, > psychological problems, fatigue, violence and suicide. (lancet 3/2/92 > v339) > > Dear Rodney: > > One major obstacle for understanding the role of saturated fats (not > trans fats) in the the diet, yet alone for admitting their importance > to the human organism is the hugely succesful barrage of > disinformation about fats that has discouraged most people to look > beyond what they are told. Yet the empirical evidence (given the > faulty science againt them)for their desirability is overwhelming. > Does it make sense to be told that coconut oil is unhealthy, a > so-called artery clogging fat, when you consider that a large number > of those ethnic groups (in thailand before the advent of cheap > vegetable oils 20 years ago, in the philippines and Sri Lanka to this > day)we recognised as healthy has been using this type of tropical oil > for so long? In rather large daily quantities? That it contains > roughly 50% lauric acid, (more than human breast milk, the second most > important source)a potent anti-bacterial, -viral, -fungal compound > very much absent from the SAD? In a letter to the WHO the government > of the Philippines congratulated itself upon its succesful AIDS > education campaign (that country presenting strikingly low rates of > this disease)but those in the know attribute this fact to less > idealistic factors... > > As for the other kinds of saturated fats, what of them? Before 1920 > heart disease was relatively rare compared to today, when it is a real > epidemic. The sharp rise of coronary disease after this date coincides > with decreased consumption of saturated fats such as butter and tallow > in favor of increased consumption of their cheaper displacement > alternatives, margarine and corn oil boosted by aggressive promotion > (interesting to depression era budgets) and later from the early 1950 > onwards by a AHA campaign pushing their health virtues on the american > public. > > And what was the irrefutable science behind all this? Experiments > which consistent in feeding rabbits (an exclusively herbivorous > animal)oxidised cholesterol and noticing how this practice resulted in > arterial plaque. The rigorously drawn conclusion was that similar > deposits in human arteries were owned to the same foods. Voilà ! the > birth of the cholesterol/lipid hypothesis, the basis for the need for > cholesterol lowering meds and yet an increasingly discredited theory. > It seems that more and more we hear that cholesterol readings do not > matter. some studies suggest that the protective, anti-oxydant > qualities of cholesterol have been overlooked, and that in many case > it is not as accurate a predictor of coronary disease as was > previously thought. It seems nomocysteine is much more important. If > this is so, what is wrong with saturated fats of animal origin? Could > it be that we are turned off by them instinctively because we have > been conditioned to do so after being subjected to 60 years of propaganda? > > Doesn't it strike anybody as odd that oils made up of mostly > polyunsaturated fatty acid are advertised as being good for us when > you consider the rate at which these very unstable oils oxidise in a > bottle and and a highly reactive environment such as the body? Wouln't > want to have these messing up my cells! Think of the massive oxidative > dammage!There are some studies suggesting more or less persuasively > that they are the principal reason behind rising rates of melanomas in > australia. Thet are certainly positively linked with macular > degeneration. No such association with coconut oil. That stuff can lie > in the cupboard for 2 years and not go rancid. > > > In any case it pays to make up ones own mind after careful > consideration of the historical facts. > > http://www.westonaprice.org/knowyourfats/oiling.html > > To answer your first question Rodney, in evolutionary terms fat > consumption was very important for survival. It ensured that man could > go a long time without eating and still be able to face the challenges > of food gathering in a reasonably fit state. According to Stannard, > the author of the article, periods of fasting (and very low carb > consumption)possibly triggered a mechanism whereby glucose is spared > for brain function by a temporary insulin resistance in muscular > tissues. What insures a constant energy substrate in the absence of > food are more elevated blood lipids. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 Sorry guys I had no idea you felt this way about the WAPF or had negative feelings about the concepts elaborated by the people there. I just thought the link would provide a nice historical exposé of some of the reasons as to why folks react so strongly when confronted with saturated fats and how this reaction of fear has been produced in them. So I will never mention them again. However, none of you or indeed no one who has visited with some regularity the more reputable nutrition sites will deny that the cholesterol hypothesis has come under much questioning in the last 3 or 4 years, most notably in the JAMA last year about that study done with post menopausal women and the effects of saturated fats on CHD incidence in that group. Consuming saturated fats most dedidly negatively corelated with incidence of CHD. Such was the surprise that the study was immediately commented by an editorial note wich tried to be, if not effectively dismissive, than perhaps advising a kind of orthodox caution. There are also quite a number of studies in which serum cholesterol values come out as irrelevant. The exercise study commented a few days ago on this very site shows just that. It would seem that CHD can evolve where cholesterol valus are quite low in the so called healthy range. At this point I'm afraid to refer to the work of K.Mccully (or that of the folks at THINCS) on homocysteine. If his stuff is valid (don't the folks at LEF think so?)it may well mean that eating stuff such as butter may once again be permissible, though for some reason he(not very consequentially)dicourages it. I'm not saying eat a ton of the stuff. In my experince a little bit of butter goes a long way to make eating small quantities of food more satisfying, longer. I do find the Stannard endlessly fascinating. Makes the thrifty gene theory seem rather chronocentric, as did the cholesterol/lipid theory. patrick > Lowfat diets are associated with increased rates of depresion, > psychological problems, fatigue, violence and suicide. (lancet 3/2/92 > v339) > > Dear Rodney: > > One major obstacle for understanding the role of saturated fats (not > trans fats) in the the diet, yet alone for admitting their importance > to the human organism is the hugely succesful barrage of > disinformation about fats that has discouraged most people to look > beyond what they are told. Yet the empirical evidence (given the > faulty science againt them)for their desirability is overwhelming. > Does it make sense to be told that coconut oil is unhealthy, a > so-called artery clogging fat, when you consider that a large number > of those ethnic groups (in thailand before the advent of cheap > vegetable oils 20 years ago, in the philippines and Sri Lanka to this > day)we recognised as healthy has been using this type of tropical oil > for so long? In rather large daily quantities? That it contains > roughly 50% lauric acid, (more than human breast milk, the second most > important source)a potent anti-bacterial, -viral, -fungal compound > very much absent from the SAD? In a letter to the WHO the government > of the Philippines congratulated itself upon its succesful AIDS > education campaign (that country presenting strikingly low rates of > this disease)but those in the know attribute this fact to less > idealistic factors... > > As for the other kinds of saturated fats, what of them? Before 1920 > heart disease was relatively rare compared to today, when it is a real > epidemic. The sharp rise of coronary disease after this date coincides > with decreased consumption of saturated fats such as butter and tallow > in favor of increased consumption of their cheaper displacement > alternatives, margarine and corn oil boosted by aggressive promotion > (interesting to depression era budgets) and later from the early 1950 > onwards by a AHA campaign pushing their health virtues on the american > public. > > And what was the irrefutable science behind all this? Experiments > which consistent in feeding rabbits (an exclusively herbivorous > animal)oxidised cholesterol and noticing how this practice resulted in > arterial plaque. The rigorously drawn conclusion was that similar > deposits in human arteries were owned to the same foods. Voilà ! the > birth of the cholesterol/lipid hypothesis, the basis for the need for > cholesterol lowering meds and yet an increasingly discredited theory. > It seems that more and more we hear that cholesterol readings do not > matter. some studies suggest that the protective, anti-oxydant > qualities of cholesterol have been overlooked, and that in many case > it is not as accurate a predictor of coronary disease as was > previously thought. It seems nomocysteine is much more important. If > this is so, what is wrong with saturated fats of animal origin? Could > it be that we are turned off by them instinctively because we have > been conditioned to do so after being subjected to 60 years of propaganda? > > Doesn't it strike anybody as odd that oils made up of mostly > polyunsaturated fatty acid are advertised as being good for us when > you consider the rate at which these very unstable oils oxidise in a > bottle and and a highly reactive environment such as the body? Wouln't > want to have these messing up my cells! Think of the massive oxidative > dammage!There are some studies suggesting more or less persuasively > that they are the principal reason behind rising rates of melanomas in > australia. Thet are certainly positively linked with macular > degeneration. No such association with coconut oil. That stuff can lie > in the cupboard for 2 years and not go rancid. > > > In any case it pays to make up ones own mind after careful > consideration of the historical facts. > > http://www.westonaprice.org/knowyourfats/oiling.html > > To answer your first question Rodney, in evolutionary terms fat > consumption was very important for survival. It ensured that man could > go a long time without eating and still be able to face the challenges > of food gathering in a reasonably fit state. According to Stannard, > the author of the article, periods of fasting (and very low carb > consumption)possibly triggered a mechanism whereby glucose is spared > for brain function by a temporary insulin resistance in muscular > tissues. What insures a constant energy substrate in the absence of > food are more elevated blood lipids. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 >> However, none of you or indeed no one who has visited with some regularity the more reputable nutrition sites will deny that the cholesterol hypothesis has come under much questioning in the last 3 or 4 years, most notably in the JAMA last year about that study done with post menopausal women and the effects of saturated fats on CHD incidence in that group. Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up. Strandberg TE, Strandberg A, Rantanen K, Salomaa VV, Pitkala K, Miettinen TA. Department of Medicine, Geriatric Clinic, University of Helsinki, Finland. timo.strandberg@... J Am Coll Cardiol. 2004 Sep 1;44(5):1002-8. OBJECTIVES: We assessed the impact of serum cholesterol level in early midlife on total mortality during up to 39 years of follow-up and on the quality of life (QoL) in old age. BACKGROUND: Total effects of low serum cholesterol on health have been in dispute, especially in elderly persons, and there are few data on the long-term effects of low cholesterol on QoL. METHODS: The cohort consisted of 3,277 healthy businessmen age 30 to 45 years at baseline (1960s). In addition to baseline, serum cholesterol values were available for part of the cohort in 1974, 1986, and 2000. The QoL was assessed in 80.9% of survivors (n = 1,820, mean age 73 years) with a RAND-36 (SF-36) QoL questionnaire in 2000. Mortality up to 2002 (n = 1,173) was retrieved from national registers. RESULTS: Cholesterol was clearly reduced in survivors during follow-up, except in the lowest baseline serum cholesterol group. Baseline cholesterol predicted 39-year total mortality in a graded manner (p < 0.0001), and a value < or =5.0 mmol/l was associated with a 25% reduction in total mortality. In old age, the physical component summary score of RAND-36 was significantly (p = 0.02) higher (better) in the lowest baseline cholesterol group; no difference was found in the mental component summary score (p = 0.51). CONCLUSIONS: Low serum cholesterol level in midlife predicted not only better survival but also better physical function and QoL in old age, without adversely affecting mental QoL. PMID: 15337210 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 >> However, none of you or indeed no one who has visited with some regularity the more reputable nutrition sites will deny that the cholesterol hypothesis has come under much questioning in the last 3 or 4 years, most notably in the JAMA last year about that study done with post menopausal women and the effects of saturated fats on CHD incidence in that group. Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up. Strandberg TE, Strandberg A, Rantanen K, Salomaa VV, Pitkala K, Miettinen TA. Department of Medicine, Geriatric Clinic, University of Helsinki, Finland. timo.strandberg@... J Am Coll Cardiol. 2004 Sep 1;44(5):1002-8. OBJECTIVES: We assessed the impact of serum cholesterol level in early midlife on total mortality during up to 39 years of follow-up and on the quality of life (QoL) in old age. BACKGROUND: Total effects of low serum cholesterol on health have been in dispute, especially in elderly persons, and there are few data on the long-term effects of low cholesterol on QoL. METHODS: The cohort consisted of 3,277 healthy businessmen age 30 to 45 years at baseline (1960s). In addition to baseline, serum cholesterol values were available for part of the cohort in 1974, 1986, and 2000. The QoL was assessed in 80.9% of survivors (n = 1,820, mean age 73 years) with a RAND-36 (SF-36) QoL questionnaire in 2000. Mortality up to 2002 (n = 1,173) was retrieved from national registers. RESULTS: Cholesterol was clearly reduced in survivors during follow-up, except in the lowest baseline serum cholesterol group. Baseline cholesterol predicted 39-year total mortality in a graded manner (p < 0.0001), and a value < or =5.0 mmol/l was associated with a 25% reduction in total mortality. In old age, the physical component summary score of RAND-36 was significantly (p = 0.02) higher (better) in the lowest baseline cholesterol group; no difference was found in the mental component summary score (p = 0.51). CONCLUSIONS: Low serum cholesterol level in midlife predicted not only better survival but also better physical function and QoL in old age, without adversely affecting mental QoL. PMID: 15337210 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 Dear Jeff: As is usual in this kind of study it begins by pretentiously talking about the effects and impacts of serum cholesterol levels on health and it concludes by talking only of associations. Very weak stuff. Establishing an association does nothing to directly implicate a factor in a pathology. To do so is to highjack science to fit an agenda, an agenda determined in this case by consensus. We know that in most case of CHD cholesterol levels rise. Do we know why? Is it a case of killing the messenger before the message is delivered? What if rising cholesterol is a reaction to developing heart disease? A protective reaction? Could be. Who's to say it isn't. This is something we have to consider. > > >> However, none of you or indeed no one who has visited with some regularity the more reputable nutrition sites will deny that the > cholesterol hypothesis has come under much questioning in the last 3 or 4 years, most notably in the JAMA last year about that study done > with post menopausal women and the effects of saturated fats on CHD incidence in that group. > > > Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up. > Strandberg TE, Strandberg A, Rantanen K, Salomaa VV, Pitkala K, Miettinen TA. > Department of Medicine, Geriatric Clinic, University of Helsinki, Finland. timo.strandberg@h... > > J Am Coll Cardiol. 2004 Sep 1;44(5):1002-8. > > OBJECTIVES: We assessed the impact of serum cholesterol level in early midlife on total mortality during up to 39 years of follow-up and on the quality of life (QoL) in old age. > > BACKGROUND: Total effects of low serum cholesterol on health have been in dispute, especially in elderly persons, and there are few data on the long-term effects of low cholesterol on QoL. > > METHODS: The cohort consisted of 3,277 healthy businessmen age 30 to 45 years at baseline (1960s). In addition to baseline, serum cholesterol values were available for part of the cohort in 1974, 1986, and 2000. The QoL was assessed in 80.9% of survivors (n = 1,820, mean age 73 years) with a RAND-36 (SF-36) QoL questionnaire in 2000. Mortality up to 2002 (n = 1,173) was retrieved from national registers. > > RESULTS: Cholesterol was clearly reduced in survivors during follow-up, except in the lowest baseline serum cholesterol group. Baseline cholesterol predicted 39-year total mortality in a graded manner (p < 0.0001), and a value < or =5.0 mmol/l was associated with a 25% reduction in total mortality. In old age, the physical component summary score of RAND-36 was significantly (p = 0.02) higher (better) in the lowest baseline cholesterol group; no difference was found in the mental component summary score (p = 0.51). > > CONCLUSIONS: Low serum cholesterol level in midlife predicted not only better survival but also better physical function and QoL in old age, without adversely affecting mental QoL. > > PMID: 15337210 [PubMed - indexed for MEDLINE] > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 Dear Jeff: As is usual in this kind of study it begins by pretentiously talking about the effects and impacts of serum cholesterol levels on health and it concludes by talking only of associations. Very weak stuff. Establishing an association does nothing to directly implicate a factor in a pathology. To do so is to highjack science to fit an agenda, an agenda determined in this case by consensus. We know that in most case of CHD cholesterol levels rise. Do we know why? Is it a case of killing the messenger before the message is delivered? What if rising cholesterol is a reaction to developing heart disease? A protective reaction? Could be. Who's to say it isn't. This is something we have to consider. > > >> However, none of you or indeed no one who has visited with some regularity the more reputable nutrition sites will deny that the > cholesterol hypothesis has come under much questioning in the last 3 or 4 years, most notably in the JAMA last year about that study done > with post menopausal women and the effects of saturated fats on CHD incidence in that group. > > > Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up. > Strandberg TE, Strandberg A, Rantanen K, Salomaa VV, Pitkala K, Miettinen TA. > Department of Medicine, Geriatric Clinic, University of Helsinki, Finland. timo.strandberg@h... > > J Am Coll Cardiol. 2004 Sep 1;44(5):1002-8. > > OBJECTIVES: We assessed the impact of serum cholesterol level in early midlife on total mortality during up to 39 years of follow-up and on the quality of life (QoL) in old age. > > BACKGROUND: Total effects of low serum cholesterol on health have been in dispute, especially in elderly persons, and there are few data on the long-term effects of low cholesterol on QoL. > > METHODS: The cohort consisted of 3,277 healthy businessmen age 30 to 45 years at baseline (1960s). In addition to baseline, serum cholesterol values were available for part of the cohort in 1974, 1986, and 2000. The QoL was assessed in 80.9% of survivors (n = 1,820, mean age 73 years) with a RAND-36 (SF-36) QoL questionnaire in 2000. Mortality up to 2002 (n = 1,173) was retrieved from national registers. > > RESULTS: Cholesterol was clearly reduced in survivors during follow-up, except in the lowest baseline serum cholesterol group. Baseline cholesterol predicted 39-year total mortality in a graded manner (p < 0.0001), and a value < or =5.0 mmol/l was associated with a 25% reduction in total mortality. In old age, the physical component summary score of RAND-36 was significantly (p = 0.02) higher (better) in the lowest baseline cholesterol group; no difference was found in the mental component summary score (p = 0.51). > > CONCLUSIONS: Low serum cholesterol level in midlife predicted not only better survival but also better physical function and QoL in old age, without adversely affecting mental QoL. > > PMID: 15337210 [PubMed - indexed for MEDLINE] > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 , There is so much confusion in the literature about the role of cholesterol that you can find support for whatever argument you want to make. The relationship between arterial plaque and cholesterol seems to be very well founded. New research also appears to show that low cholesterol is linked to Parkinson's disease, or that muscles cannot grow when cholesterol is low. You have to step back and question why our livers produce cholesterol. There must be some evolutionary advantage. The first question that we should ask is: What cholesterol level is associated with the greatest longevity and health? The current guidelines say that *normal* is: TC<200, LDL<100, HDL 40 to 59, TG<150, but is this optimal? The equations developed by Hegsted, Mensink and Katan provide the blueprint for how cholesterol levels are affected by dietary fat. The equations enable us to modify our cholesterol level through diet, but the question remains: What is optimal? Tony ==== http://www.nlm.nih.gov/medlineplus/news/fullstory_27172.html Low cholesterol linked to Parkinson's in men Huang and colleagues, from the University of North Carolina at Chapel Hill, measured the lipid levels of 124 Parkinson's patients and a group of 112 similar people free of Parkinson's disease. Huang reported that, after adjusting for age, smoking, and use of lipid-lowering agents, men with low total and LDL ( " bad " ) cholesterol levels had an increased risk of Parkinson's. For example, compared to men with LDL cholesterol levels higher than 135, those with levels between 91 and 135 were 6 times more likely to have Parkinson's, and those LDL levels below 91 were 4 time more likely. ========= http://bmj.bmjjournals.com/cgi/content/full/309/6963/1228 Cholesterol and violent death Weidner G, Connor SL, Hollis JF, Connor WE. Improvements in hostility and depression in relation to dietary change and cholesterol lowering. Ann Intern Med 1992;117:820-3. ==== > > Sorry guys I had no idea you felt this way about the WAPF or had > negative feelings about the concepts elaborated by the people there. I > just thought the link would provide a nice historical exposé of some > of the reasons as to why folks react so strongly when confronted with > saturated fats and how this reaction of fear has been produced in them. > > So I will never mention them again. > > However, none of you or indeed no one who has visited with some > regularity the more reputable nutrition sites will deny that the > cholesterol hypothesis has come under much questioning in the last 3 > or 4 years, most notably in the JAMA last year about that study done > with post menopausal women and the effects of saturated fats on CHD > incidence in that group. Consuming saturated fats most dedidly > negatively corelated with incidence of CHD. Such was the surprise that > the study was immediately commented by an editorial note wich tried to > be, if not effectively dismissive, than perhaps advising a kind of > orthodox caution. > > There are also quite a number of studies in which serum cholesterol > values come out as irrelevant. The exercise study commented a few days > ago on this very site shows just that. It would seem that CHD can > evolve where cholesterol valus are quite low in the so called healthy > range. At this point I'm afraid to refer to the work of K.Mccully (or > that of the folks at THINCS) on homocysteine. If his stuff is valid > (don't the folks at LEF think so?)it may well mean that eating stuff > such as butter may once again be permissible, though for some reason > he(not very consequentially)dicourages it. > > I'm not saying eat a ton of the stuff. In my experince a little bit of > butter goes a long way to make eating small quantities of food more > satisfying, longer. > > I do find the Stannard endlessly fascinating. Makes the thrifty gene > theory seem rather chronocentric, as did the cholesterol/lipid theory. > > patrick > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 , There is so much confusion in the literature about the role of cholesterol that you can find support for whatever argument you want to make. The relationship between arterial plaque and cholesterol seems to be very well founded. New research also appears to show that low cholesterol is linked to Parkinson's disease, or that muscles cannot grow when cholesterol is low. You have to step back and question why our livers produce cholesterol. There must be some evolutionary advantage. The first question that we should ask is: What cholesterol level is associated with the greatest longevity and health? The current guidelines say that *normal* is: TC<200, LDL<100, HDL 40 to 59, TG<150, but is this optimal? The equations developed by Hegsted, Mensink and Katan provide the blueprint for how cholesterol levels are affected by dietary fat. The equations enable us to modify our cholesterol level through diet, but the question remains: What is optimal? Tony ==== http://www.nlm.nih.gov/medlineplus/news/fullstory_27172.html Low cholesterol linked to Parkinson's in men Huang and colleagues, from the University of North Carolina at Chapel Hill, measured the lipid levels of 124 Parkinson's patients and a group of 112 similar people free of Parkinson's disease. Huang reported that, after adjusting for age, smoking, and use of lipid-lowering agents, men with low total and LDL ( " bad " ) cholesterol levels had an increased risk of Parkinson's. For example, compared to men with LDL cholesterol levels higher than 135, those with levels between 91 and 135 were 6 times more likely to have Parkinson's, and those LDL levels below 91 were 4 time more likely. ========= http://bmj.bmjjournals.com/cgi/content/full/309/6963/1228 Cholesterol and violent death Weidner G, Connor SL, Hollis JF, Connor WE. Improvements in hostility and depression in relation to dietary change and cholesterol lowering. Ann Intern Med 1992;117:820-3. ==== > > Sorry guys I had no idea you felt this way about the WAPF or had > negative feelings about the concepts elaborated by the people there. I > just thought the link would provide a nice historical exposé of some > of the reasons as to why folks react so strongly when confronted with > saturated fats and how this reaction of fear has been produced in them. > > So I will never mention them again. > > However, none of you or indeed no one who has visited with some > regularity the more reputable nutrition sites will deny that the > cholesterol hypothesis has come under much questioning in the last 3 > or 4 years, most notably in the JAMA last year about that study done > with post menopausal women and the effects of saturated fats on CHD > incidence in that group. Consuming saturated fats most dedidly > negatively corelated with incidence of CHD. Such was the surprise that > the study was immediately commented by an editorial note wich tried to > be, if not effectively dismissive, than perhaps advising a kind of > orthodox caution. > > There are also quite a number of studies in which serum cholesterol > values come out as irrelevant. The exercise study commented a few days > ago on this very site shows just that. It would seem that CHD can > evolve where cholesterol valus are quite low in the so called healthy > range. At this point I'm afraid to refer to the work of K.Mccully (or > that of the folks at THINCS) on homocysteine. If his stuff is valid > (don't the folks at LEF think so?)it may well mean that eating stuff > such as butter may once again be permissible, though for some reason > he(not very consequentially)dicourages it. > > I'm not saying eat a ton of the stuff. In my experince a little bit of > butter goes a long way to make eating small quantities of food more > satisfying, longer. > > I do find the Stannard endlessly fascinating. Makes the thrifty gene > theory seem rather chronocentric, as did the cholesterol/lipid theory. > > patrick > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 Dear Tony: The fact that there is so much confusion in the literature is good reason to proceed with caution and not be too hasty in drawing conclusions about cholesterol. The attempt to lower serum cholesterol values is, I think, just such a hasty conclusion. For all we know it might just play a protective role in the body. For evidence which establishes associations to mean anything definetely does depend upon your way to look at it, I agree with you there. So it seems that it is associated with a lower rist of Parkinson's disease. It does not say that the absence of cholesterol causes Parkinsons, only that its presence is associated with a lower risk. This does suggest a protective function doesn't it? It is no new concept that the stuff my protect against other neurological diseases. This possibility is one more reason not to be too hasty in our conclusions. We might regret it. > > > > Sorry guys I had no idea you felt this way about the WAPF or had > > negative feelings about the concepts elaborated by the people there. I > > just thought the link would provide a nice historical exposé of some > > of the reasons as to why folks react so strongly when confronted with > > saturated fats and how this reaction of fear has been produced in them. > > > > So I will never mention them again. > > > > However, none of you or indeed no one who has visited with some > > regularity the more reputable nutrition sites will deny that the > > cholesterol hypothesis has come under much questioning in the last 3 > > or 4 years, most notably in the JAMA last year about that study done > > with post menopausal women and the effects of saturated fats on CHD > > incidence in that group. Consuming saturated fats most dedidly > > negatively corelated with incidence of CHD. Such was the surprise that > > the study was immediately commented by an editorial note wich tried to > > be, if not effectively dismissive, than perhaps advising a kind of > > orthodox caution. > > > > There are also quite a number of studies in which serum cholesterol > > values come out as irrelevant. The exercise study commented a few days > > ago on this very site shows just that. It would seem that CHD can > > evolve where cholesterol valus are quite low in the so called healthy > > range. At this point I'm afraid to refer to the work of K.Mccully (or > > that of the folks at THINCS) on homocysteine. If his stuff is valid > > (don't the folks at LEF think so?)it may well mean that eating stuff > > such as butter may once again be permissible, though for some reason > > he(not very consequentially)dicourages it. > > > > I'm not saying eat a ton of the stuff. In my experince a little bit of > > butter goes a long way to make eating small quantities of food more > > satisfying, longer. > > > > I do find the Stannard endlessly fascinating. Makes the thrifty gene > > theory seem rather chronocentric, as did the cholesterol/lipid theory. > > > > patrick > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 Dear Tony: The fact that there is so much confusion in the literature is good reason to proceed with caution and not be too hasty in drawing conclusions about cholesterol. The attempt to lower serum cholesterol values is, I think, just such a hasty conclusion. For all we know it might just play a protective role in the body. For evidence which establishes associations to mean anything definetely does depend upon your way to look at it, I agree with you there. So it seems that it is associated with a lower rist of Parkinson's disease. It does not say that the absence of cholesterol causes Parkinsons, only that its presence is associated with a lower risk. This does suggest a protective function doesn't it? It is no new concept that the stuff my protect against other neurological diseases. This possibility is one more reason not to be too hasty in our conclusions. We might regret it. > > > > Sorry guys I had no idea you felt this way about the WAPF or had > > negative feelings about the concepts elaborated by the people there. I > > just thought the link would provide a nice historical exposé of some > > of the reasons as to why folks react so strongly when confronted with > > saturated fats and how this reaction of fear has been produced in them. > > > > So I will never mention them again. > > > > However, none of you or indeed no one who has visited with some > > regularity the more reputable nutrition sites will deny that the > > cholesterol hypothesis has come under much questioning in the last 3 > > or 4 years, most notably in the JAMA last year about that study done > > with post menopausal women and the effects of saturated fats on CHD > > incidence in that group. Consuming saturated fats most dedidly > > negatively corelated with incidence of CHD. Such was the surprise that > > the study was immediately commented by an editorial note wich tried to > > be, if not effectively dismissive, than perhaps advising a kind of > > orthodox caution. > > > > There are also quite a number of studies in which serum cholesterol > > values come out as irrelevant. The exercise study commented a few days > > ago on this very site shows just that. It would seem that CHD can > > evolve where cholesterol valus are quite low in the so called healthy > > range. At this point I'm afraid to refer to the work of K.Mccully (or > > that of the folks at THINCS) on homocysteine. If his stuff is valid > > (don't the folks at LEF think so?)it may well mean that eating stuff > > such as butter may once again be permissible, though for some reason > > he(not very consequentially)dicourages it. > > > > I'm not saying eat a ton of the stuff. In my experince a little bit of > > butter goes a long way to make eating small quantities of food more > > satisfying, longer. > > > > I do find the Stannard endlessly fascinating. Makes the thrifty gene > > theory seem rather chronocentric, as did the cholesterol/lipid theory. > > > > patrick > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 A response to a similar article about the relationship between saturated fat, cholesterol and CVD. The response below was written to someone who basically asked the same question you do and raised the same issue. They used a different study that the one in the JAMA last year and also raised the issue that Dr Castelli is often quoted as saying " The more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower peoples' serum cholesterol. we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active. " -- Dr. Castelli, Director of the prestigious Framingham Study It seems about once a year, someone joins the list and raises this issue. Welcome aboard. Jeff PS I left the names to indict the guilty! Hi Logan: Do you remember the quotation you supplied (attached below, between the '=============' lines), attributed to Dr. Castelli? Since you made that post I have contacted Dr. Castelli to inquire about the circumstances in which those comments were made. Here is what he told me about it: He says he was observing that in one of the first dietary history studies done at Framingham a data set was used which showed that those who ate the most saturated fat had the lowest cholesterol readings. That seemed surprising at the time. But even more surprising, the same data also indicated that those in the group who ate the most calories weighed the least. Since eating more and weighing less appeared contradictory, this raised questions. They realized something must be awry, so they set out to determine what it was. The answer turned out to be that in this particular group of subjects those who ate the most saturated fat also had the highest energy expenditure. So that, although they ate more, they weighed less because they were burning a lot more calories. Also relevant was the fact that exercise appreciably reduces blood cholesterol in the very short term. So, in order to figure out whether it was eating saturated fats that was lowering cholesterol, or the exercise instead, they investigated further. Specifically, a direct quote cut-and-pasted from Dr. Castelli's recent communication: " .... how do you know that eating cholesterol and saturated fat raise your serum cholesterol? You have to do a metabolic ward study. Being on a metabolic ward is like being in prison and the two best studies were done in Minneapolis (Dr. Ancel Keys) and Boston (Mark Hegsted). They would increase the cholesterol and saturated fat in your diet, controlling for everything else and showed the more cholesterol you ate, or the more saturated fat you ate, the higher you serum cholesterol went. " In other words it was the higher physical activity that had accounted for the lower blood cholesterols of the subjects in the earlier study - exercise was the confounder that had not been controlled for. Further, he goes on: " Virtually all the early diet trials were based on removing saturated fat and cholesterol from you diet and lowering your serum cholesterol. They also showed that the better they did this, the better was the fall in coronary heart disease. " So, Dr. Castelli is saying, not only did lowering saturated fat intake drop cholesterol, it also reduced heart disease. And further, Dr. Castelli says: " ....... the latest diet data from Framingham showed that the women of Framingham who ate a high fat, low calorie diet doubled the deposits in their carotid arteries compared to women on a heart healthy diet. " And still further he notes that the impact on lipids of a high saturated fat diet is even greater than that measured by standard cholesterol tests. This is because the tests are normally done after an eight to ten hour fast. But the atherogenic effects (chylomicron remnants) peak around the time the meal is eaten and then diminish dramatically as the hours go by. So they are much greater in the period immediately following a high fat meal than when the tested blood is normally drawn many hours later. ------------------- So the actual views held by the source you provided to support your arguments about the causes of heart disease, ARE THE OPPOSITE of what you would have us believe them to be. You quoted the first part of the story, then for some reason omitted the rest - that is, by far the most important part. In my opinion, that was less than helpful. Rodney. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 A response to a similar article about the relationship between saturated fat, cholesterol and CVD. The response below was written to someone who basically asked the same question you do and raised the same issue. They used a different study that the one in the JAMA last year and also raised the issue that Dr Castelli is often quoted as saying " The more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower peoples' serum cholesterol. we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active. " -- Dr. Castelli, Director of the prestigious Framingham Study It seems about once a year, someone joins the list and raises this issue. Welcome aboard. Jeff PS I left the names to indict the guilty! Hi Logan: Do you remember the quotation you supplied (attached below, between the '=============' lines), attributed to Dr. Castelli? Since you made that post I have contacted Dr. Castelli to inquire about the circumstances in which those comments were made. Here is what he told me about it: He says he was observing that in one of the first dietary history studies done at Framingham a data set was used which showed that those who ate the most saturated fat had the lowest cholesterol readings. That seemed surprising at the time. But even more surprising, the same data also indicated that those in the group who ate the most calories weighed the least. Since eating more and weighing less appeared contradictory, this raised questions. They realized something must be awry, so they set out to determine what it was. The answer turned out to be that in this particular group of subjects those who ate the most saturated fat also had the highest energy expenditure. So that, although they ate more, they weighed less because they were burning a lot more calories. Also relevant was the fact that exercise appreciably reduces blood cholesterol in the very short term. So, in order to figure out whether it was eating saturated fats that was lowering cholesterol, or the exercise instead, they investigated further. Specifically, a direct quote cut-and-pasted from Dr. Castelli's recent communication: " .... how do you know that eating cholesterol and saturated fat raise your serum cholesterol? You have to do a metabolic ward study. Being on a metabolic ward is like being in prison and the two best studies were done in Minneapolis (Dr. Ancel Keys) and Boston (Mark Hegsted). They would increase the cholesterol and saturated fat in your diet, controlling for everything else and showed the more cholesterol you ate, or the more saturated fat you ate, the higher you serum cholesterol went. " In other words it was the higher physical activity that had accounted for the lower blood cholesterols of the subjects in the earlier study - exercise was the confounder that had not been controlled for. Further, he goes on: " Virtually all the early diet trials were based on removing saturated fat and cholesterol from you diet and lowering your serum cholesterol. They also showed that the better they did this, the better was the fall in coronary heart disease. " So, Dr. Castelli is saying, not only did lowering saturated fat intake drop cholesterol, it also reduced heart disease. And further, Dr. Castelli says: " ....... the latest diet data from Framingham showed that the women of Framingham who ate a high fat, low calorie diet doubled the deposits in their carotid arteries compared to women on a heart healthy diet. " And still further he notes that the impact on lipids of a high saturated fat diet is even greater than that measured by standard cholesterol tests. This is because the tests are normally done after an eight to ten hour fast. But the atherogenic effects (chylomicron remnants) peak around the time the meal is eaten and then diminish dramatically as the hours go by. So they are much greater in the period immediately following a high fat meal than when the tested blood is normally drawn many hours later. ------------------- So the actual views held by the source you provided to support your arguments about the causes of heart disease, ARE THE OPPOSITE of what you would have us believe them to be. You quoted the first part of the story, then for some reason omitted the rest - that is, by far the most important part. In my opinion, that was less than helpful. Rodney. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 " Virtually all the early diet trials were based on removing saturated fat and cholesterol from you diet and lowering your serum cholesterol. They also showed that the better they did this, the better was the fall in coronary heart disease. " Jeff, I have seen this mentioned a number of times, but do you or any body know what replaced the saturated fats and cholesterol, was it foods that would be expected to reduce heart disease risk and cholesterol (fruit, veg, fiber) or did they just eat low-fat junk food instead ? - thanks. ___________________________________________________________ Unlimited Tiscali Broadband from 14.99! http://www.tiscali.co.uk/products/broadband/ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 7, 2005 Report Share Posted October 7, 2005 " Virtually all the early diet trials were based on removing saturated fat and cholesterol from you diet and lowering your serum cholesterol. They also showed that the better they did this, the better was the fall in coronary heart disease. " Jeff, I have seen this mentioned a number of times, but do you or any body know what replaced the saturated fats and cholesterol, was it foods that would be expected to reduce heart disease risk and cholesterol (fruit, veg, fiber) or did they just eat low-fat junk food instead ? - thanks. ___________________________________________________________ Unlimited Tiscali Broadband from 14.99! http://www.tiscali.co.uk/products/broadband/ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 9, 2005 Report Share Posted October 9, 2005 Hi : Well where should I start? LOL I could address each of the points in your post, item by item. However, on reflection, there is a limit to how much time I am prepared to spend going over stuff again that has been extensively discussed here a number of times in the past. So I think it might be better, instead, just to make two general points. But before doing so, let me say that I assume, I certainly hope, that everyone here, including me of course, is open minded to new information and is prepared to change their minds about important things when information suggests that is advisable. But the new information has to be persuasive, and it is apparent that different people are persuaded by different types of information. In this regard, my opinion is that one of the most outstanding aspects, among many, of Dr. Walford's 'Beyond the 120-Year Diet' is the section dealing with the different types of evidence and, especially, which of those one should pay very close attention to, and which are almost invariably best ignored. This has relevance to some of the discussions here during the past week or two. Anyone who hasn't read the book needs to do so. And anyone who doesn't remember the content of the section about types of evidence would do well to read it again, imo. I believe it starts on page 22. That said, let me get on to my first point. It seems, , you believe there is a conspiracy among medical researchers and physicians to bamboozle the public into believing the causes of heart disease are saturated fat consumption, and consequent higher cholesterol levels when, according to you, they really aren't ............ " .......................hugely successful barrage of disinformation ......... faulty science .............. 60 years of propaganda ............ " . Well let me say that there is no shortage of places on the net where everyone is welcome to expound on their latest pet conspiracy theory, where people who by the nature of their discussions give all the appearances of being nucases, rant to (at?) each other twenty four hours a day, 365 days a year, with everyone automatically agreeing with everyone else, with nothing more to be said other than to repeat it, sometimes ad nauseam. Now there is no reason at all why someone who believes there is some kind of serious health conspiracy should not express such a view at . But there is one HUGE difference between this site and the multitudes of conspiracy websites. That difference is that here there is a requirement for EVIDENCE. And the more remarkable the claim, the more remarkable the evidence needs to be to support it ............. if any reader here is going to take it seriously. So what does this site generally expect members to provide in the way of evidence, or be able to provide if asked, when they make unusual or important claims? The answer can be found on the home page of this site, where it says, among other things: " We value published, peer-reviewed, mainstream scientific sources .............................. " [And as you may have noted we do not always automatically accept published studies as being the last word either. If the logic, or the data analysis in a study appears faulty, or if there is good reason to suspect bias because of financial or other interests the authors may have, some members here are not beyond, occasionally, where considered appropriate, direct criticism of a published, peer- reviewed paper. For example, some cantankerous OF here did that the other day, about a study which seemed to be touting the ludicrous proposition that exercise is the only way to avoid accumulation of adipose tissue.] The people who spend a few minutes here each day to find health information choose this place rather than somewhere else because they very much like the principles on which this site was originally set up by its founder. The requirement for serious scientific evidence being perhaps the single most important of those principles. So my question for you is: " what serious evidence do you have to support your assertion that such a conspiracy exists? " What is your evidence, in other words, for the " disinformation " , " faulty science " , " propaganda " ............ to which you refer? Quoting someone no one has heard of, who expressed an opinion to this effect with great enthusiasm on his, or someone else's, website is not regarded as serious evidence here. Indeed not evidence at all, let alone serious evidence. My second point to you is in a similar vein, but with a slightly different slant. It relates to a conversation you had with Jeff about the link between saturated fats and heart disease. Let me summarize what I believe happened in that interaction: 1) You asserted (post # 21,009) that there was a conspiracy to wrongly blame saturated fats for heart disease. You did not provide any evidence to support this claim. 2) Jeff responded (post # 21,019) by posting the abstract of a September 2004, forty year, prospective study, of thousands of subjects, with over 1000 reported deaths from the group, which examined this issue and concluded: " CONCLUSIONS: Low serum cholesterol level in midlife predicted not only better survival but also better physical function and QoL in old age, without adversely affecting mental QoL. " Jeff even provided the PMID # so that you could easily reference it should you wish to. 3) Your reaction (in post # 21022) was first to say, in short, the following: " .......... pretentious .......... talking only of associations ....... weak stuff ........... highjack science to fit an agenda .............. " etc.. You then continued by saying, in effect, that it might not be the cholesterol that is the problem, it might be something else, it might be X, or it might be Y or Z, who knows ............. and you provided NOTHING that would qualify as evidence to support any of this. What is more you seem to say this in a manner which suggests you believe that these intuitive assertions made by you while offering no supporting evidence, should cause us all to write off the forty year prospective study Jeff had posted (as well as the other huge, carefully structured and very long established studies which have come to similar conclusions) as garbage, and take ***YOUR*** word for it!!!!!!!!!!!!!!!!!! Can you be serious? Well sorry . That kind of discussion may float at other places you frequent on the net or elsewhere, but it doesn't float here for the reasons I have outlined above. If you want to convince people here about this issue, or any other issue, the only way you are going to succeed is by presenting some serious supporting evidence. That is: published, peer reviewed, papers, preferably done by investigators at institutions that are very well known for zealously guarding their reputation for excellence and disinterest (in the real meaning of that word) in health research. But for me, I am not personally interested in DISCUSSING the issue further. There are only 24 hours in the day and this is something that has been extensively discussed here many times previously. The archives are available to be searched by anyone who wishes to do so. If you were to post the abstracts of some studies you believe support your position I will certainly read them. But for rants making all kinds of claims without providing support, I have a very short attention span. Indeed do not be surprised if a moderator with a similarly short fuse discards them without posting them ......... it has happened before here to this kind of post. Serious evidence is the only thing that has a chance of changing my views on this issue. And in my opinion - and much more important it is something that has been continuously emphasized by the founder of this site - that is the way it ought to be. Final point. Apparently you entirely misunderstood my post about my communications with Dr. Castelli. In no way did he contradict other published findings of the Framingham studies. Quite the contrary, what he said fully supported those findings. Which, if you re-read it, I think you will realize. Hope this explains my position on this stuff. All the best, Rodney. > > Dear Jeff: As is usual in this kind of study it begins by > pretentiously talking about the effects and impacts of serum > cholesterol levels on health and it concludes by talking only of > associations. Very weak stuff. Establishing an association does > nothing to directly implicate a factor in a pathology. To do so is to > highjack science to fit an agenda, an agenda determined in this case > by consensus. > We know that in most case of CHD cholesterol levels rise. Do we know > why? Is it a case of killing the messenger before the message is > delivered? What if rising cholesterol is a reaction to developing > heart disease? A protective reaction? Could be. Who's to say it isn't. > This is something we have to consider. > > > > > > --- In , " Jeff Novick " <jnovick@p...> wrote: > > > > >> However, none of you or indeed no one who has visited with some > regularity the more reputable nutrition sites will deny that the > > cholesterol hypothesis has come under much questioning in the last 3 > or 4 years, most notably in the JAMA last year about that study done > > with post menopausal women and the effects of saturated fats on CHD > incidence in that group. > > > > > > Low cholesterol, mortality, and quality of life in old age during a > 39-year follow-up. > > Strandberg TE, Strandberg A, Rantanen K, Salomaa VV, Pitkala K, > Miettinen TA. > > Department of Medicine, Geriatric Clinic, University of Helsinki, > Finland. timo.strandberg@h... > > > > J Am Coll Cardiol. 2004 Sep 1;44(5):1002-8. > > > > OBJECTIVES: We assessed the impact of serum cholesterol level in > early midlife on total mortality during up to 39 years of follow-up > and on the quality of life (QoL) in old age. > > > > BACKGROUND: Total effects of low serum cholesterol on health have > been in dispute, especially in elderly persons, and there are few data > on the long-term effects of low cholesterol on QoL. > > > > METHODS: The cohort consisted of 3,277 healthy businessmen age 30 to > 45 years at baseline (1960s). In addition to baseline, serum > cholesterol values were available for part of the cohort in 1974, > 1986, and 2000. The QoL was assessed in 80.9% of survivors (n = 1,820, > mean age 73 years) with a RAND-36 (SF-36) QoL questionnaire in 2000. > Mortality up to 2002 (n = 1,173) was retrieved from national registers. > > > > RESULTS: Cholesterol was clearly reduced in survivors during > follow-up, except in the lowest baseline serum cholesterol group. > Baseline cholesterol predicted 39-year total mortality in a graded > manner (p < 0.0001), and a value < or =5.0 mmol/l was associated with > a 25% reduction in total mortality. In old age, the physical component > summary score of RAND-36 was significantly (p = 0.02) higher (better) > in the lowest baseline cholesterol group; no difference was found in > the mental component summary score (p = 0.51). > > > > CONCLUSIONS: Low serum cholesterol level in midlife predicted not > only better survival but also better physical function and QoL in old > age, without adversely affecting mental QoL. > > > > PMID: 15337210 [PubMed - indexed for MEDLINE] > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 9, 2005 Report Share Posted October 9, 2005 Hi : Well where should I start? LOL I could address each of the points in your post, item by item. However, on reflection, there is a limit to how much time I am prepared to spend going over stuff again that has been extensively discussed here a number of times in the past. So I think it might be better, instead, just to make two general points. But before doing so, let me say that I assume, I certainly hope, that everyone here, including me of course, is open minded to new information and is prepared to change their minds about important things when information suggests that is advisable. But the new information has to be persuasive, and it is apparent that different people are persuaded by different types of information. In this regard, my opinion is that one of the most outstanding aspects, among many, of Dr. Walford's 'Beyond the 120-Year Diet' is the section dealing with the different types of evidence and, especially, which of those one should pay very close attention to, and which are almost invariably best ignored. This has relevance to some of the discussions here during the past week or two. Anyone who hasn't read the book needs to do so. And anyone who doesn't remember the content of the section about types of evidence would do well to read it again, imo. I believe it starts on page 22. That said, let me get on to my first point. It seems, , you believe there is a conspiracy among medical researchers and physicians to bamboozle the public into believing the causes of heart disease are saturated fat consumption, and consequent higher cholesterol levels when, according to you, they really aren't ............ " .......................hugely successful barrage of disinformation ......... faulty science .............. 60 years of propaganda ............ " . Well let me say that there is no shortage of places on the net where everyone is welcome to expound on their latest pet conspiracy theory, where people who by the nature of their discussions give all the appearances of being nucases, rant to (at?) each other twenty four hours a day, 365 days a year, with everyone automatically agreeing with everyone else, with nothing more to be said other than to repeat it, sometimes ad nauseam. Now there is no reason at all why someone who believes there is some kind of serious health conspiracy should not express such a view at . But there is one HUGE difference between this site and the multitudes of conspiracy websites. That difference is that here there is a requirement for EVIDENCE. And the more remarkable the claim, the more remarkable the evidence needs to be to support it ............. if any reader here is going to take it seriously. So what does this site generally expect members to provide in the way of evidence, or be able to provide if asked, when they make unusual or important claims? The answer can be found on the home page of this site, where it says, among other things: " We value published, peer-reviewed, mainstream scientific sources .............................. " [And as you may have noted we do not always automatically accept published studies as being the last word either. If the logic, or the data analysis in a study appears faulty, or if there is good reason to suspect bias because of financial or other interests the authors may have, some members here are not beyond, occasionally, where considered appropriate, direct criticism of a published, peer- reviewed paper. For example, some cantankerous OF here did that the other day, about a study which seemed to be touting the ludicrous proposition that exercise is the only way to avoid accumulation of adipose tissue.] The people who spend a few minutes here each day to find health information choose this place rather than somewhere else because they very much like the principles on which this site was originally set up by its founder. The requirement for serious scientific evidence being perhaps the single most important of those principles. So my question for you is: " what serious evidence do you have to support your assertion that such a conspiracy exists? " What is your evidence, in other words, for the " disinformation " , " faulty science " , " propaganda " ............ to which you refer? Quoting someone no one has heard of, who expressed an opinion to this effect with great enthusiasm on his, or someone else's, website is not regarded as serious evidence here. Indeed not evidence at all, let alone serious evidence. My second point to you is in a similar vein, but with a slightly different slant. It relates to a conversation you had with Jeff about the link between saturated fats and heart disease. Let me summarize what I believe happened in that interaction: 1) You asserted (post # 21,009) that there was a conspiracy to wrongly blame saturated fats for heart disease. You did not provide any evidence to support this claim. 2) Jeff responded (post # 21,019) by posting the abstract of a September 2004, forty year, prospective study, of thousands of subjects, with over 1000 reported deaths from the group, which examined this issue and concluded: " CONCLUSIONS: Low serum cholesterol level in midlife predicted not only better survival but also better physical function and QoL in old age, without adversely affecting mental QoL. " Jeff even provided the PMID # so that you could easily reference it should you wish to. 3) Your reaction (in post # 21022) was first to say, in short, the following: " .......... pretentious .......... talking only of associations ....... weak stuff ........... highjack science to fit an agenda .............. " etc.. You then continued by saying, in effect, that it might not be the cholesterol that is the problem, it might be something else, it might be X, or it might be Y or Z, who knows ............. and you provided NOTHING that would qualify as evidence to support any of this. What is more you seem to say this in a manner which suggests you believe that these intuitive assertions made by you while offering no supporting evidence, should cause us all to write off the forty year prospective study Jeff had posted (as well as the other huge, carefully structured and very long established studies which have come to similar conclusions) as garbage, and take ***YOUR*** word for it!!!!!!!!!!!!!!!!!! Can you be serious? Well sorry . That kind of discussion may float at other places you frequent on the net or elsewhere, but it doesn't float here for the reasons I have outlined above. If you want to convince people here about this issue, or any other issue, the only way you are going to succeed is by presenting some serious supporting evidence. That is: published, peer reviewed, papers, preferably done by investigators at institutions that are very well known for zealously guarding their reputation for excellence and disinterest (in the real meaning of that word) in health research. But for me, I am not personally interested in DISCUSSING the issue further. There are only 24 hours in the day and this is something that has been extensively discussed here many times previously. The archives are available to be searched by anyone who wishes to do so. If you were to post the abstracts of some studies you believe support your position I will certainly read them. But for rants making all kinds of claims without providing support, I have a very short attention span. Indeed do not be surprised if a moderator with a similarly short fuse discards them without posting them ......... it has happened before here to this kind of post. Serious evidence is the only thing that has a chance of changing my views on this issue. And in my opinion - and much more important it is something that has been continuously emphasized by the founder of this site - that is the way it ought to be. Final point. Apparently you entirely misunderstood my post about my communications with Dr. Castelli. In no way did he contradict other published findings of the Framingham studies. Quite the contrary, what he said fully supported those findings. Which, if you re-read it, I think you will realize. Hope this explains my position on this stuff. All the best, Rodney. > > Dear Jeff: As is usual in this kind of study it begins by > pretentiously talking about the effects and impacts of serum > cholesterol levels on health and it concludes by talking only of > associations. Very weak stuff. Establishing an association does > nothing to directly implicate a factor in a pathology. To do so is to > highjack science to fit an agenda, an agenda determined in this case > by consensus. > We know that in most case of CHD cholesterol levels rise. Do we know > why? Is it a case of killing the messenger before the message is > delivered? What if rising cholesterol is a reaction to developing > heart disease? A protective reaction? Could be. Who's to say it isn't. > This is something we have to consider. > > > > > > --- In , " Jeff Novick " <jnovick@p...> wrote: > > > > >> However, none of you or indeed no one who has visited with some > regularity the more reputable nutrition sites will deny that the > > cholesterol hypothesis has come under much questioning in the last 3 > or 4 years, most notably in the JAMA last year about that study done > > with post menopausal women and the effects of saturated fats on CHD > incidence in that group. > > > > > > Low cholesterol, mortality, and quality of life in old age during a > 39-year follow-up. > > Strandberg TE, Strandberg A, Rantanen K, Salomaa VV, Pitkala K, > Miettinen TA. > > Department of Medicine, Geriatric Clinic, University of Helsinki, > Finland. timo.strandberg@h... > > > > J Am Coll Cardiol. 2004 Sep 1;44(5):1002-8. > > > > OBJECTIVES: We assessed the impact of serum cholesterol level in > early midlife on total mortality during up to 39 years of follow-up > and on the quality of life (QoL) in old age. > > > > BACKGROUND: Total effects of low serum cholesterol on health have > been in dispute, especially in elderly persons, and there are few data > on the long-term effects of low cholesterol on QoL. > > > > METHODS: The cohort consisted of 3,277 healthy businessmen age 30 to > 45 years at baseline (1960s). In addition to baseline, serum > cholesterol values were available for part of the cohort in 1974, > 1986, and 2000. The QoL was assessed in 80.9% of survivors (n = 1,820, > mean age 73 years) with a RAND-36 (SF-36) QoL questionnaire in 2000. > Mortality up to 2002 (n = 1,173) was retrieved from national registers. > > > > RESULTS: Cholesterol was clearly reduced in survivors during > follow-up, except in the lowest baseline serum cholesterol group. > Baseline cholesterol predicted 39-year total mortality in a graded > manner (p < 0.0001), and a value < or =5.0 mmol/l was associated with > a 25% reduction in total mortality. In old age, the physical component > summary score of RAND-36 was significantly (p = 0.02) higher (better) > in the lowest baseline cholesterol group; no difference was found in > the mental component summary score (p = 0.51). > > > > CONCLUSIONS: Low serum cholesterol level in midlife predicted not > only better survival but also better physical function and QoL in old > age, without adversely affecting mental QoL. > > > > PMID: 15337210 [PubMed - indexed for MEDLINE] > > > Quote Link to comment Share on other sites More sharing options...
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