Guest guest Posted December 13, 2009 Report Share Posted December 13, 2009 Thanks Andre. Good paper. The PubMed ID number is: 19956092 As you note, quite a number of issues are raised by this paper. Much of this work seems to be in agreement with the work being done in Spain on the aging rate of mice by Sanz, Caro, Barja, et al. Their experiments have found that 'protein only' restriction accounts for all the reduction in aging rate produced by CR. But they found mice restricted in 'methionine only' also had a slowed rate of aging, but to an extent less than the mice restricted in all amino acids - not quite the same finding as Partridge's. The conclusion from both data sets (i.e. both Partridge and Barja) seems to be that there are other amino acids (in addition to methionine according to Barja) which participate in the reduced aging rate and increased lifespan. A second question which may be an issue here in distinguishing average lifespan from maximum lifespan. The aging rate studies would appear to be very closely related to maximum lifespan, meaning that the results are likely not just a function of 'rectangularizing' the survival curve by reducing disease incidence. The extended maximum lifespan (in addition to extended average lifespan) is a characteristic usually considered important in CR discussions (Dr. Walford's BT120YD, for example). It is not clear to me whether Partridge's results in this paper apply to both average and maximum lifespan, or just average lifespan. Additionally, the huge reductions in fasting insulin typically seen in humans established on a significant degree of CR, seems to be important. So another issue raised, at least in my mind, by this paper is: " What is it about CR that causes these reductions in fasting insulin? " I suspect the answer to this, whatever it turns out to be, may prove to be very important to health and longevity. And presumably it is restricition of amino acids in some combination that will be found to be the key factor. And while I am on the subject, there is a personal anomaly of mine which may be of interest, and have relevance to this discussion. While, at a BMI of 21, my CRP and fasting insulin are reduced by almost as large an amount as the WUSTL study subjects' averages, my glucose and HbA1c seem to be consistently fairly close to the high end of the currently accepted healthy ranges. Something odd going on here. Might it have to do with the types of protein I eat, I wonder? Of course once all this is sorted out, it could get quite boring around here! Not much else we will need to know after that, maybe? Rodney. > > I would like to point to a very interesting and thorough study that has just been published in the Dec 9 issue of Nature > > R. Grandison, M. Piper and L. Partridge. Amino-acid imbalance explains extension of lifespan by dietary restrictions in Drosophila. > > The study is quite complex but I will try to summarize the main points: > > 1-Background > As all readers of this group already know, dietary restrictions without malnutrition extends lifespan across the board, from yeast to mammals. > An important caveat is that reduction of caloric intake, by itself does not consitently provide life extension in all organisms tested: it appears that the restriction of specific nutrients is the key, more so than low caloric intake. Also, it has been consistently observed that dietary restriction reduces fertility and reproduction rates. This can make sense from a biological and evolutionary perspective. The theory is that during times of food shortage reproduction can be dangerous for the parents and the offspring has low survival rates; mechanisms are then switched on to extend the life of the individuals until food is abundant again and reproduction success can be maximized. > The work of Partridge and colleagues addresses 3 questions: > -are the lifespan and fertility effects of dietary restriction rigorously inversly related, or do specific nutrients affect the two parameters? > -If the two effect can be uncoupled, which nutrients are primarily controlling fertility and which ones are controlling lifespan > -What is the role of glucose metabolism, and in particular, the role of the insulin pathway? > > 2-Findings > At least in Drosophila, it is confirmed that caloric intake per se is a poor predictor of longevity or fertility. When specific sets of nutrients were individually added back to a restricted diet, lipids, charbohydrates or vitamins had no effect (that is, restricted diets with added back lipids or carbs or vitamins, still showed prolonged lifespan and low fertility). However, when a restricted diet was supplemented with all aminoacids, the flies had a short lifespan and high fertility. By testing the effects of individual aminoacids, the Partridge team found that Methionine alone could account for the fertility effect: when Methionine is absent from the diet the fertility is reduced and when Methionine is the only aminoacid in the diet fertility goes back to normal levels. What about longevity? Surprisingly the Methionine effect uncouples reproduction and longevity. Methonine per se can alter fertility but it has no effect on lifespan. Flies on restricted diet live longer and reproduce poorly, flies on restricted diet supplemented with Methionine reproduce normally and still have longer lifespan! Adding back all aminoacids except Methionine reduced the lifespan. since none of the aminoacids was able to decrease lifespan when added alone to the restricted diets, the conclusion is that some combination of the other (non-Met) aminoacids is responsible for the shortening of lifespan. > What about glucose and the insulin pathway? When the experiments where conducted in mutant flies in which the insulin pathway is inactivated, the lifespan reached the highest levels: these mutants lived even significantly longer than normal flies on restricted diet. Interestingly feeding these flies with a restricted diet supplemented with all aminoacids did not reduce their lifespan (which is what happens in the normal flies). Similarly, the deficient insulin signalling, abolished the response of the reproductive system to Methionine. > Very interesting work overall, although it raises lots of questions. One I find particularly intriguing is why carbs have no effect on longevity in Drosophila but the modulation of the insulin pathway is perhaps the strongest predictor of the flies lifespan? Is this true in other organisms and humans? > In summary, protein quality, the precise balance of different aminoacids in the diet and limited activation of the insulin pathway, will likely turn out to be critical. > > Andre > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 14, 2009 Report Share Posted December 14, 2009 This seems to agree with the work of Dr Kenyon and her work with worms Personal diet Kenyon's research prompted her to make personal dietary changes. She stopped eating high glycemic index carbohydrates when she discovered that putting sugar on the worms' food shortened their lifespans.[1] Kenyon follows a low glycemic index diet similar to the Atkins diet[1] and the South Beach Diet[2]. No desserts. No sweets. No potatoes. No rice. No bread. No pasta. When I say ‘no,’ I mean ‘no, or not much,’ she notes. Instead, eat green vegetables. Eat the fruits that aren't the sweet fruits, like melon. Bananas? Bananas are a little sweet. Meat? Meat, yes, of course. Avocados. All vegetables. Nuts. Fish. Chicken. That's what I eat. Cheese. Eggs. And one glass of red wine a day.[3] I have a fabulous blood profile. My triglyceride level is only 30, and anything below 200 is good.[3] You have to eat something, and you just have to make your best judgement. And that's my best judgement. Plus, I feel better. Plus, I'm thin—I weigh what I weighed when I was in college. I feel great —you feel like you're a kid again. It's amazing.[3] In the past, Kenyon had also briefly experimented with a calorie restriction diet for two days, but couldn't stand the constant hunger On 12/13/09 4:51 PM, " perspect1111 " <perspect1111@...> wrote: Thanks Andre. Good paper. The PubMed ID number is: 19956092 As you note, quite a number of issues are raised by this paper. Much of this work seems to be in agreement with the work being done in Spain on the aging rate of mice by Sanz, Caro, Barja, et al. Their experiments have found that 'protein only' restriction accounts for all the reduction in aging rate produced by CR. But they found mice restricted in 'methionine only' also had a slowed rate of aging, but to an extent less than the mice restricted in all amino acids - not quite the same finding as Partridge's. The conclusion from both data sets (i.e. both Partridge and Barja) seems to be that there are other amino acids (in addition to methionine according to Barja) which participate in the reduced aging rate and increased lifespan. A second question which may be an issue here in distinguishing average lifespan from maximum lifespan. The aging rate studies would appear to be very closely related to maximum lifespan, meaning that the results are likely not just a function of 'rectangularizing' the survival curve by reducing disease incidence. The extended maximum lifespan (in addition to extended average lifespan) is a characteristic usually considered important in CR discussions (Dr. Walford's BT120YD, for example). It is not clear to me whether Partridge's results in this paper apply to both average and maximum lifespan, or just average lifespan. Additionally, the huge reductions in fasting insulin typically seen in humans established on a significant degree of CR, seems to be important. So another issue raised, at least in my mind, by this paper is: " What is it about CR that causes these reductions in fasting insulin? " I suspect the answer to this, whatever it turns out to be, may prove to be very important to health and longevity. And presumably it is restricition of amino acids in some combination that will be found to be the key factor. And while I am on the subject, there is a personal anomaly of mine which may be of interest, and have relevance to this discussion. While, at a BMI of 21, my CRP and fasting insulin are reduced by almost as large an amount as the WUSTL study subjects' averages, my glucose and HbA1c seem to be consistently fairly close to the high end of the currently accepted healthy ranges. Something odd going on here. Might it have to do with the types of protein I eat, I wonder? Of course once all this is sorted out, it could get quite boring around here! Not much else we will need to know after that, maybe? Rodney. > > I would like to point to a very interesting and thorough study that has just been published in the Dec 9 issue of Nature > > R. Grandison, M. Piper and L. Partridge. Amino-acid imbalance explains extension of lifespan by dietary restrictions in Drosophila. > > The study is quite complex but I will try to summarize the main points: > > 1-Background > As all readers of this group already know, dietary restrictions without malnutrition extends lifespan across the board, from yeast to mammals. > An important caveat is that reduction of caloric intake, by itself does not consitently provide life extension in all organisms tested: it appears that the restriction of specific nutrients is the key, more so than low caloric intake. Also, it has been consistently observed that dietary restriction reduces fertility and reproduction rates. This can make sense from a biological and evolutionary perspective. The theory is that during times of food shortage reproduction can be dangerous for the parents and the offspring has low survival rates; mechanisms are then switched on to extend the life of the individuals until food is abundant again and reproduction success can be maximized. > The work of Partridge and colleagues addresses 3 questions: > -are the lifespan and fertility effects of dietary restriction rigorously inversly related, or do specific nutrients affect the two parameters? > -If the two effect can be uncoupled, which nutrients are primarily controlling fertility and which ones are controlling lifespan > -What is the role of glucose metabolism, and in particular, the role of the insulin pathway? > > 2-Findings > At least in Drosophila, it is confirmed that caloric intake per se is a poor predictor of longevity or fertility. When specific sets of nutrients were individually added back to a restricted diet, lipids, charbohydrates or vitamins had no effect (that is, restricted diets with added back lipids or carbs or vitamins, still showed prolonged lifespan and low fertility). However, when a restricted diet was supplemented with all aminoacids, the flies had a short lifespan and high fertility. By testing the effects of individual aminoacids, the Partridge team found that Methionine alone could account for the fertility effect: when Methionine is absent from the diet the fertility is reduced and when Methionine is the only aminoacid in the diet fertility goes back to normal levels. What about longevity? Surprisingly the Methionine effect uncouples reproduction and longevity. Methonine per se can alter fertility but it has no effect on lifespan. Flies on restricted diet live longer! and reproduce poorly, flies on restricted diet supplemented with Methionine reproduce normally and still have longer lifespan! Adding back all aminoacids except Methionine reduced the lifespan. since none of the aminoacids was able to decrease lifespan when added alone to the restricted diets, the conclusion is that some combination of the other (non-Met) aminoacids is responsible for the shortening of lifespan. > What about glucose and the insulin pathway? When the experiments where conducted in mutant flies in which the insulin pathway is inactivated, the lifespan reached the highest levels: these mutants lived even significantly longer than normal flies on restricted diet. Interestingly feeding these flies with a restricted diet supplemented with all aminoacids did not reduce their lifespan (which is what happens in the normal flies). Similarly, the deficient insulin signalling, abolished the response of the reproductive system to Methionine. > Very interesting work overall, although it raises lots of questions. One I find particularly intriguing is why carbs have no effect on longevity in Drosophila but the modulation of the insulin pathway is perhaps the strongest predictor of the flies lifespan? Is this true in other organisms and humans? > In summary, protein quality, the precise balance of different aminoacids in the diet and limited activation of the insulin pathway, will likely turn out to be critical. > > Andre > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 16, 2009 Report Share Posted December 16, 2009 Hi folks: Regarding the previously-mentioned work being done in Spain on macro nutrients and CR the following PMID-listed papers may be of interest: 15692733 16770005 16803986 17136610 17452727 17486421 17716000 18283555 18593280 19039676 19577342 19633937 Rodney. > > > > I would like to point to a very interesting and thorough study that has just been published in the Dec 9 issue of Nature > > > > R. Grandison, M. Piper and L. Partridge. Amino-acid imbalance explains extension of lifespan by dietary restrictions in Drosophila. > > > > The study is quite complex but I will try to summarize the main points: > > > > 1-Background > > As all readers of this group already know, dietary restrictions without malnutrition extends lifespan across the board, from yeast to mammals. > > An important caveat is that reduction of caloric intake, by itself does not consitently provide life extension in all organisms tested: it appears that the restriction of specific nutrients is the key, more so than low caloric intake. Also, it has been consistently observed that dietary restriction reduces fertility and reproduction rates. This can make sense from a biological and evolutionary perspective. The theory is that during times of food shortage reproduction can be dangerous for the parents and the offspring has low survival rates; mechanisms are then switched on to extend the life of the individuals until food is abundant again and reproduction success can be maximized. > > The work of Partridge and colleagues addresses 3 questions: > > -are the lifespan and fertility effects of dietary restriction rigorously inversly related, or do specific nutrients affect the two parameters? > > -If the two effect can be uncoupled, which nutrients are primarily controlling fertility and which ones are controlling lifespan > > -What is the role of glucose metabolism, and in particular, the role of the insulin pathway? > > > > 2-Findings > > At least in Drosophila, it is confirmed that caloric intake per se is a poor predictor of longevity or fertility. When specific sets of nutrients were individually added back to a restricted diet, lipids, charbohydrates or vitamins had no effect (that is, restricted diets with added back lipids or carbs or vitamins, still showed prolonged lifespan and low fertility). However, when a restricted diet was supplemented with all aminoacids, the flies had a short lifespan and high fertility. By testing the effects of individual aminoacids, the Partridge team found that Methionine alone could account for the fertility effect: when Methionine is absent from the diet the fertility is reduced and when Methionine is the only aminoacid in the diet fertility goes back to normal levels. What about longevity? Surprisingly the Methionine effect uncouples reproduction and longevity. Methonine per se can alter fertility but it has no effect on lifespan. Flies on restricted diet live longer and reproduce poorly, flies on restricted diet supplemented with Methionine reproduce normally and still have longer lifespan! Adding back all aminoacids except Methionine reduced the lifespan. since none of the aminoacids was able to decrease lifespan when added alone to the restricted diets, the conclusion is that some combination of the other (non-Met) aminoacids is responsible for the shortening of lifespan. > > What about glucose and the insulin pathway? When the experiments where conducted in mutant flies in which the insulin pathway is inactivated, the lifespan reached the highest levels: these mutants lived even significantly longer than normal flies on restricted diet. Interestingly feeding these flies with a restricted diet supplemented with all aminoacids did not reduce their lifespan (which is what happens in the normal flies). Similarly, the deficient insulin signalling, abolished the response of the reproductive system to Methionine. > > Very interesting work overall, although it raises lots of questions. One I find particularly intriguing is why carbs have no effect on longevity in Drosophila but the modulation of the insulin pathway is perhaps the strongest predictor of the flies lifespan? Is this true in other organisms and humans? > > In summary, protein quality, the precise balance of different aminoacids in the diet and limited activation of the insulin pathway, will likely turn out to be critical. > > > > Andre > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 2, 2010 Report Share Posted January 2, 2010 Rod: I have been thinking about this, thus the delayed response. Andre’s paper IMHO does not jibe with the methionine theory (as you seem to mention below) but seems to point to the “insulin” theory (as I mentioned in another post, Dr Kenyon’s work, and her personal diet of avoiding sweets and starches). I remember e-mailing Diane off list and she agreed that this does not agree with the methionine theory. In reading these papers, perhaps we look for the kernel which agrees with our personal biases (?). Even scientists, as we well know, , allow biases to creep into their experiments which may “taint” their results. But if it does, perhaps you can explain? Or anyone? On 12/13/09 4:51 PM, " perspect1111 " <perspect1111@...> wrote: Thanks Andre. Good paper. The PubMed ID number is: 19956092 As you note, quite a number of issues are raised by this paper. Much of this work seems to be in agreement with the work being done in Spain on the aging rate of mice by Sanz, Caro, Barja, et al. Their experiments have found that 'protein only' restriction accounts for all the reduction in aging rate produced by CR. But they found mice restricted in 'methionine only' also had a slowed rate of aging, but to an extent less than the mice restricted in all amino acids - not quite the same finding as Partridge's. The conclusion from both data sets (i.e. both Partridge and Barja) seems to be that there are other amino acids (in addition to methionine according to Barja) which participate in the reduced aging rate and increased lifespan. A second question which may be an issue here in distinguishing average lifespan from maximum lifespan. The aging rate studies would appear to be very closely related to maximum lifespan, meaning that the results are likely not just a function of 'rectangularizing' the survival curve by reducing disease incidence. The extended maximum lifespan (in addition to extended average lifespan) is a characteristic usually considered important in CR discussions (Dr. Walford's BT120YD, for example). It is not clear to me whether Partridge's results in this paper apply to both average and maximum lifespan, or just average lifespan. Additionally, the huge reductions in fasting insulin typically seen in humans established on a significant degree of CR, seems to be important. So another issue raised, at least in my mind, by this paper is: " What is it about CR that causes these reductions in fasting insulin? " I suspect the answer to this, whatever it turns out to be, may prove to be very important to health and longevity. And presumably it is restricition of amino acids in some combination that will be found to be the key factor. And while I am on the subject, there is a personal anomaly of mine which may be of interest, and have relevance to this discussion. While, at a BMI of 21, my CRP and fasting insulin are reduced by almost as large an amount as the WUSTL study subjects' averages, my glucose and HbA1c seem to be consistently fairly close to the high end of the currently accepted healthy ranges. Something odd going on here. Might it have to do with the types of protein I eat, I wonder? Of course once all this is sorted out, it could get quite boring around here! Not much else we will need to know after that, maybe? Rodney. > > I would like to point to a very interesting and thorough study that has just been published in the Dec 9 issue of Nature > > R. Grandison, M. Piper and L. Partridge. Amino-acid imbalance explains extension of lifespan by dietary restrictions in Drosophila. > > The study is quite complex but I will try to summarize the main points: > > 1-Background > As all readers of this group already know, dietary restrictions without malnutrition extends lifespan across the board, from yeast to mammals. > An important caveat is that reduction of caloric intake, by itself does not consitently provide life extension in all organisms tested: it appears that the restriction of specific nutrients is the key, more so than low caloric intake. Also, it has been consistently observed that dietary restriction reduces fertility and reproduction rates. This can make sense from a biological and evolutionary perspective. The theory is that during times of food shortage reproduction can be dangerous for the parents and the offspring has low survival rates; mechanisms are then switched on to extend the life of the individuals until food is abundant again and reproduction success can be maximized. > The work of Partridge and colleagues addresses 3 questions: > -are the lifespan and fertility effects of dietary restriction rigorously inversly related, or do specific nutrients affect the two parameters? > -If the two effect can be uncoupled, which nutrients are primarily controlling fertility and which ones are controlling lifespan > -What is the role of glucose metabolism, and in particular, the role of the insulin pathway? > > 2-Findings > At least in Drosophila, it is confirmed that caloric intake per se is a poor predictor of longevity or fertility. When specific sets of nutrients were individually added back to a restricted diet, lipids, charbohydrates or vitamins had no effect (that is, restricted diets with added back lipids or carbs or vitamins, still showed prolonged lifespan and low fertility). However, when a restricted diet was supplemented with all aminoacids, the flies had a short lifespan and high fertility. By testing the effects of individual aminoacids, the Partridge team found that Methionine alone could account for the fertility effect: when Methionine is absent from the diet the fertility is reduced and when Methionine is the only aminoacid in the diet fertility goes back to normal levels. What about longevity? Surprisingly the Methionine effect uncouples reproduction and longevity. Methonine per se can alter fertility but it has no effect on lifespan. Flies on restricted diet live longer! and reproduce poorly, flies on restricted diet supplemented with Methionine reproduce normally and still have longer lifespan! Adding back all aminoacids except Methionine reduced the lifespan. since none of the aminoacids was able to decrease lifespan when added alone to the restricted diets, the conclusion is that some combination of the other (non-Met) aminoacids is responsible for the shortening of lifespan. > What about glucose and the insulin pathway? When the experiments where conducted in mutant flies in which the insulin pathway is inactivated, the lifespan reached the highest levels: these mutants lived even significantly longer than normal flies on restricted diet. Interestingly feeding these flies with a restricted diet supplemented with all aminoacids did not reduce their lifespan (which is what happens in the normal flies). Similarly, the deficient insulin signalling, abolished the response of the reproductive system to Methionine. > Very interesting work overall, although it raises lots of questions. One I find particularly intriguing is why carbs have no effect on longevity in Drosophila but the modulation of the insulin pathway is perhaps the strongest predictor of the flies lifespan? Is this true in other organisms and humans? > In summary, protein quality, the precise balance of different aminoacids in the diet and limited activation of the insulin pathway, will likely turn out to be critical. > > Andre > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 3, 2010 Report Share Posted January 3, 2010 Hi Francesca: [i have written this rather in haste so I regret there may be some repetition which I have not edited out.] To try to answer your question: IMO there is a great deal more that we do not know about nutrition than we do know. This CERTAINLY extends to understanding precisely how it is that CR works. Everyone who has looked at the thousands of studies available at PubMed on this subject agrees that significant restriction of total calories substantially improves health, and sizeably extends both average and maximum lifespan, in every species (dozens, I believe) that has been tested. But all sources I am aware of agree that we do not know how it works and scientists in many places are working to try to figure out what the mechanism is. It is still not clear how CR works or, put another way, which nutrient component(s) it is, the restriction of which explains the increased lifespan. There is not, as far as I am aware, a " methionine theory " as you suggest. There is simply scientific research much of which has been posted here. Most of the experiments which have varied macronutrient content of CR diets seem to be in agreement (those that I have seen) that higher levels of total protein result in measurably faster aging rate, and account for all, or nearly all, the lifespan extension observed in CR. Some experiments restricted just fat calories, others just carb calories and both found NO EFFECT from the restriction of either of these two macronutrients. (As I had noted in a previous post attached below, I believe, and provided the references.) But experiments which restricted only protein showed substantial aging rate benefits. So it does seem that it is some aspect of protein restriction that is the issue. The results of experiments where specific amimo acid intakes were restricted are very very new and are not in full agreement (surprise, surprise!). Some have found that MET restriction seems to explain a high proportion of the effects. Others do not. But they all, as far as I can recall, agree that there are other aspects of protein intake besides MET that, in addition to any effects of MET, it appears must also be a factor. So, quite clearly the jury is still out on this - as it is on so many aspects of nutrition. Further research will, in due course, enlighten us better. It SEEMS to me that it is reasonably clear, based on the (very recent) science I have seen, which has been posted here, that protein restriction slows the aging rate. If this is confirmed then it seems likely it will result in extended maximum lifespan - a very important aspect of genuine CR. But again, it is early days. This has yet to be confirmed by other investigators. But as has been pointed out here before, including by me, methionine does NOT seem to explain ALL of the faster-aging effects evidently attributable to total protein. So most of the information I am aware of suggests that there must be other amino acids, higher amounts of which also increase the aging rate. But we do not know this anywhere even close to 'for certain'. And we will not until there is a lot more reseach published about it. These results - from varying different macronutrient components - have been published only within the last two to five years. And methionine, while probably at or very near the top of many people's list of suspects, has yet to be charged and convicted. I do not recall any study which has named another specific amino acid as explaining an appreciable amount of CR effects. (If anyone knows of such a study please post about it). But it certainly seems that there must be some others involved. And if so then they will be found. As for Kenyon ..... please correct me if I am wrong, but from reading what I have seen posted here, it appears she is on an Atkins diet? And she pursues such a diet simply because when she supplemented her nemotodes with pure sugar they didn't live as long? If, as it was reported, this is her reason then my take is that this hardly seems to qualify as science. Is there published research to support this? Is she saying that the benefits of CR result from the absence of sucrose in the diet? The Atkins diet makes no sense at all to me. Its originator and promoter died almost certainly of a massive stroke, and at the time of death weighed 270 pounds. This is a " diet " ? As for insulin .......... very low fasting insulin is certainly a predictor of lifespan (the lower the better it seems) in multiple species. Indeed CR is *famous for* dropping fasting insulin by, IIRC, almost 80%. (Take a look at the fasting insulin data in the WUSTL study). Indeed, in my case where, even at a BMI of 21 - not fully CRed, IMO - my fasting insulin is almost as low as those of the WUSTL subjects. So, since I am not aware that many (if any?) of the WUSTL subjects are on the Atkins 'diet', I do not see how going on an Atkins diet is necessary, or desirable, or even works, for reducing fasting insulin. But I have not seen published fasting insulin data for an appeciably-sized group on an Atkins diet. (Please post if anyone knows of such data from a reliable source.) And it seems strange to me that Kenyon would condemn ALL carbohydrates (isn't that what the Atkins diet is all about?) because her nemotodes do not respond well to sucrose supplementation. This hardly qualifies as news. Most people here would agree that sucrose is simply a source of empty calories. When most here are interested in the opposite - a small number of calories accompanied by large amounts of important micronutrients. So I do not see why avoiding sucrose would be considered remarkable. Most people on CR already do the same. Or so I thought. And the Atkins diet (presumably high protein) flies in the face of just about all of the CR experiments that have looked at restricting different components of the various macronutrients as noted above. Does Kenyon restrict calories? Does her body mass index reflect a suitably modest caloric intake? Does she track her nutrient intake and make sure she gets the RDAs for all the micronutients. A few months ago I posted that I had analyzed the nutient intake of someone on a 3000+ calorie Atkins Diet. He was deficient more than half the micronutrients listed at CRON-o-Meter, and in some cases substantially so. In the meantime, until we get a lot more results from macronutrient restriction experiments we each place our bets. IMO, FWIW protein restriction seems to be very important. As usual, I reserve the right to change if better - serious scientific - evidence emerges that suggests I should. Rodney. > >> > > >> > I would like to point to a very interesting and thorough study that has > >> just been published in the Dec 9 issue of Nature > >> > > >> > R. Grandison, M. Piper and L. Partridge. Amino-acid imbalance explains > >> extension of lifespan by dietary restrictions in Drosophila. > >> > > >> > The study is quite complex but I will try to summarize the main points: > >> > > >> > 1-Background > >> > As all readers of this group already know, dietary restrictions without > >> malnutrition extends lifespan across the board, from yeast to mammals. > >> > An important caveat is that reduction of caloric intake, by itself does not > >> consitently provide life extension in all organisms tested: it appears that > >> the restriction of specific nutrients is the key, more so than low caloric > >> intake. Also, it has been consistently observed that dietary restriction > >> reduces fertility and reproduction rates. This can make sense from a > >> biological and evolutionary perspective. The theory is that during times of > >> food shortage reproduction can be dangerous for the parents and the offspring > >> has low survival rates; mechanisms are then switched on to extend the life of > >> the individuals until food is abundant again and reproduction success can be > >> maximized. > >> > The work of Partridge and colleagues addresses 3 questions: > >> > -are the lifespan and fertility effects of dietary restriction rigorously > >> inversly related, or do specific nutrients affect the two parameters? > >> > -If the two effect can be uncoupled, which nutrients are primarily > >> controlling fertility and which ones are controlling lifespan > >> > -What is the role of glucose metabolism, and in particular, the role of the > >> insulin pathway? > >> > > >> > 2-Findings > >> > At least in Drosophila, it is confirmed that caloric intake per se is a > >> poor predictor of longevity or fertility. When specific sets of nutrients > >> were individually added back to a restricted diet, lipids, charbohydrates or > >> vitamins had no effect (that is, restricted diets with added back lipids or > >> carbs or vitamins, still showed prolonged lifespan and low fertility). > >> However, when a restricted diet was supplemented with all aminoacids, the > >> flies had a short lifespan and high fertility. By testing the effects of > >> individual aminoacids, the Partridge team found that Methionine alone could > >> account for the fertility effect: when Methionine is absent from the diet the > >> fertility is reduced and when Methionine is the only aminoacid in the diet > >> fertility goes back to normal levels. What about longevity? Surprisingly the > >> Methionine effect uncouples reproduction and longevity. Methonine per se can > >> alter fertility but it has no effect on lifespan. Flies on restricted diet > >> live longer! and reproduce poorly, flies on restricted diet supplemented with > >> Methionine reproduce normally and still have longer lifespan! Adding back all > >> aminoacids except Methionine reduced the lifespan. since none of the > >> aminoacids was able to decrease lifespan when added alone to the restricted > >> diets, the conclusion is that some combination of the other (non-Met) > >> aminoacids is responsible for the shortening of lifespan. > >> > What about glucose and the insulin pathway? When the experiments where > >> conducted in mutant flies in which the insulin pathway is inactivated, the > >> lifespan reached the highest levels: these mutants lived even significantly > >> longer than normal flies on restricted diet. Interestingly feeding these > >> flies with a restricted diet supplemented with all aminoacids did not reduce > >> their lifespan (which is what happens in the normal flies). Similarly, the > >> deficient insulin signalling, abolished the response of the reproductive > >> system to Methionine. > >> > Very interesting work overall, although it raises lots of questions. One I > >> find particularly intriguing is why carbs have no effect on longevity in > >> Drosophila but the modulation of the insulin pathway is perhaps the strongest > >> predictor of the flies lifespan? Is this true in other organisms and humans? > >> > In summary, protein quality, the precise balance of different aminoacids in > >> the diet and limited activation of the insulin pathway, will likely turn out > >> to be critical. > >> > > >> > Andre > >> > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
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