Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 The studies of CR in primates, so far, show no change in bone density: Exp Gerontol. 2003 Jan-Feb;38(1-2):35-46. Related Articles, Links Calorie restriction in rhesus monkeys. Mattison JA, Lane MA, Roth GS, Ingram DK. Intramural Research Program, Gerontology Research Center, National Institute on Aging, NIH, 5600 Shock Drive, Baltimore, MD 21224, USA. mattisonj@... Calorie restriction (CR) extends lifespan and reduces the incidence and age of onset of age-related disease in several animal models. To determine if this nutritional intervention has similar actions in a long-lived primate species, the National Institute on Aging (NIA) initiated a study in 1987 to investigate the effects of a 30% CR in male and female rhesus macaques (Macaca mulatta) of a broad age range. We have observed physiological effects of CR that parallel rodent studies and may be predictive of an increased lifespan. Specifically, results from the NIA study have demonstrated that CR decreases body weight and fat mass, improves glucoregulatory function, decreases blood pressure and blood lipids, and decreases body temperature. Juvenile males exhibited delayed skeletal and sexual maturation. Adult bone mass was not affected by CR in females nor were several reproductive hormones or menstrual cycling. CR attenuated the age-associated decline in both dehydroepiandrosterone (DHEA) and melatonin in males. Although 81% of the monkeys in the study are still alive, preliminary evidence suggests that CR will have beneficial effects on morbidity and mortality. We are now preparing a battery of measures to provide a thorough and relevant analysis of the effectiveness of CR at delaying the onset of age-related disease and maintaining function later into life. PMID: 12543259 [PubMed - indexed for MEDLINE] On Thu, 28 Oct 2004 15:33:38 -0000, Rodney <perspect1111@...> wrote: > > > Hi folks: > > It has only just occurred to me (I *am* a bit slow, I know) that the > occasional cases of osteoporosis among CRONers might just possibly > result from body fat going too low so that the body starts burning > the protein matrix structure in the bones for energy? > > That way calcium consumption would not matter, as there would be no > place for it to go. > > Is this plausable? (I have no medical qualifications of any kind). > > Rodney. > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 Hi : Thank you. But all that (perhaps?) tells me is that the monkeys are not down to below their danger threshold of body fat. Their diet is, I am sure, VERY carefully regulated with regard to caloric content, protein, fat, calcium etc. My suggestion is that if a CRONer is too enthusiastic, (more so than the experimenters with the monkeys) and drops his body fat below a safe level, bone loss (conceivably) could result. Or do we know for sure that bone matrix is not burned until eveything else is used up first? That is also conceivable of course. And do we understand how the occasional cases of osteoporosis among CRONers occur? And if so, are we sure it was not because of the need to burn the bone protein for fuel? This is pure speculation on my part. As you will realize. I have no answers. Just questions. And the gist of what I am saying may well be totally off base. Rodney. > The studies of CR in primates, so far, show no change in bone density: > > Exp Gerontol. 2003 Jan-Feb;38(1-2):35-46. Related Articles, Links > > > Calorie restriction in rhesus monkeys. > > Mattison JA, Lane MA, Roth GS, Ingram DK. > > Intramural Research Program, Gerontology Research Center, National > Institute on Aging, NIH, 5600 Shock Drive, Baltimore, MD 21224, > USA. mattisonj@m... > > Calorie restriction (CR) extends lifespan and reduces the incidence > and age of onset of age-related disease in several animal models. To > determine if this nutritional intervention has similar actions in a > long-lived primate species, the National Institute on Aging (NIA) > initiated a study in 1987 to investigate the effects of a 30% CR in > male and female rhesus macaques (Macaca mulatta) of a broad age range. > We have observed physiological effects of CR that parallel rodent > studies and may be predictive of an increased lifespan. Specifically, > results from the NIA study have demonstrated that CR decreases body > weight and fat mass, improves glucoregulatory function, decreases > blood pressure and blood lipids, and decreases body temperature. > Juvenile males exhibited delayed skeletal and sexual maturation. Adult > bone mass was not affected by CR in females nor were several > reproductive hormones or menstrual cycling. CR attenuated the > age-associated decline in both dehydroepiandrosterone (DHEA) and > melatonin in males. Although 81% of the monkeys in the study are still > alive, preliminary evidence suggests that CR will have beneficial > effects on morbidity and mortality. We are now preparing a battery of > measures to provide a thorough and relevant analysis of the > effectiveness of CR at delaying the onset of age-related disease and > maintaining function later into life. > > PMID: 12543259 [PubMed - indexed for MEDLINE] > > > > > > On Thu, 28 Oct 2004 15:33:38 -0000, Rodney <perspect1111@y...> wrote: > > > > > > Hi folks: > > > > It has only just occurred to me (I *am* a bit slow, I know) that the > > occasional cases of osteoporosis among CRONers might just possibly > > result from body fat going too low so that the body starts burning > > the protein matrix structure in the bones for energy? > > > > That way calcium consumption would not matter, as there would be no > > place for it to go. > > > > Is this plausable? (I have no medical qualifications of any kind). > > > > Rodney. > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 To be sure, human females can go too far with reductions in body fat and BMI, resulting in amenorrhea with hormonal alterations resulting in bone loss. I think bone matrix would be well spared in appropriate CR, given appropriate bone maintaining resistance type stress. On Thu, 28 Oct 2004 16:01:19 -0000, Rodney <perspect1111@...> wrote: > > > Hi : > > Thank you. But all that (perhaps?) tells me is that the monkeys are > not down to below their danger threshold of body fat. Their diet is, > I am sure, VERY carefully regulated with regard to caloric content, > protein, fat, calcium etc. > > My suggestion is that if a CRONer is too enthusiastic, (more so than > the experimenters with the monkeys) and drops his body fat below a > safe level, bone loss (conceivably) could result. Or do we know for > sure that bone matrix is not burned until eveything else is used up > first? That is also conceivable of course. > > And do we understand how the occasional cases of osteoporosis among > CRONers occur? And if so, are we sure it was not because of the need > to burn the bone protein for fuel? > > This is pure speculation on my part. As you will realize. I have no > answers. Just questions. And the gist of what I am saying may well > be totally off base. > > Rodney. > > > > > > > > > > > Hi folks: > > > > > > It has only just occurred to me (I *am* a bit slow, I know) that > the > > > occasional cases of osteoporosis among CRONers might just possibly > > > result from body fat going too low so that the body starts burning > > > the protein matrix structure in the bones for energy? > > > > > > That way calcium consumption would not matter, as there would be > no > > > place for it to go. > > > > > > Is this plausable? (I have no medical qualifications of any > kind). > > > > > > Rodney. > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 Perhaps relevant: Med Sci Sports Exerc. 2004 Sep;36(9):1594-601. Related Articles, Links Bone mineral density of olympic-level female winter sport athletes. Meyer NL, Shaw JM, Manore MM, Dolan SH, Subudhi AW, Shultz BB, JA. The Institute for Sport Science and Medicine, The Orthopedic Specialty Hospital, Murray, UT 84107, USA. tonmeyer@... PURPOSE: To compare areal bone mineral density (aBMD) of female winter sport athletes to healthy controls of similar age and body mass index (BMI). METHODS: Areal BMD (g x cm(-2)) of the whole body, lumbar spine (L2-L4), and right proximal femur were assessed by dual energy x-ray absorptiometry in athletes (N = 40; age: 26.1 +/- 5.7 yr; ht: 165.6 +/- 0.1 cm; wt: 63.0 +/- 6.5 kg; BMI: 23.0 +/- 1.9 kg x m(-2)) involved in speed skating (N = 9), snowboarding (N = 13), freestyle skiing (N = 3), biathlon (N = 8), bobsleigh, skeleton, luge (N = 7), and controls (N = 21; age: 26.0 +/- 5.1 yr; ht: 165.8 +/- 0.1 cm; wt: 62.8 +/- 5.9 kg; BMI: 22.9 +/- 1.3 kg x m(-2)). RESULTS: Using independent t-tests, athletes had lower fat mass, percent body fat, and higher lean mass than controls (P < 0.001). Areal BMD was higher in athletes than controls for all skeletal sites (P </= 0.007). With lean tissue mass as a covariate (ANCOVA), differences in aBMD remained significant for most skeletal sites (P </= 0.016). Menstrual history, mean daily calcium intake, and oral contraceptive use were not associated with aBMD in the athletic group. CONCLUSION: Results show that female winter sport athletes have greater aBMD compared with controls of similar age and BMI. Most aBMD differences remained significant after adjusting for lean tissue mass, and athletes with a history of oligo- and/or amenorrhea had similar aBMD than their eumenorrheic counterparts. This is the first study to examine aBMD in winter sport athletes. The results support the hypothesis that the loading characteristics of intense winter sport participation have osteogenic potential. PMID: 15354043 [PubMed - in process] On Thu, 28 Oct 2004 12:14:27 -0400, Dowling <christopher.a.dowling@...> wrote: > To be sure, human females can go too far with reductions in body fat > and BMI, resulting in amenorrhea with hormonal alterations resulting > in bone loss. I think bone matrix would be well spared in appropriate > CR, given appropriate bone maintaining resistance type stress. > > > > > On Thu, 28 Oct 2004 16:01:19 -0000, Rodney <perspect1111@...> wrote: > > > > > > Hi : > > > > Thank you. But all that (perhaps?) tells me is that the monkeys are > > not down to below their danger threshold of body fat. Their diet is, > > I am sure, VERY carefully regulated with regard to caloric content, > > protein, fat, calcium etc. > > > > My suggestion is that if a CRONer is too enthusiastic, (more so than > > the experimenters with the monkeys) and drops his body fat below a > > safe level, bone loss (conceivably) could result. Or do we know for > > sure that bone matrix is not burned until eveything else is used up > > first? That is also conceivable of course. > > > > And do we understand how the occasional cases of osteoporosis among > > CRONers occur? And if so, are we sure it was not because of the need > > to burn the bone protein for fuel? > > > > This is pure speculation on my part. As you will realize. I have no > > answers. Just questions. And the gist of what I am saying may well > > be totally off base. > > > > Rodney. > > > > > > > > > > > > > > > > Hi folks: > > > > > > > > It has only just occurred to me (I *am* a bit slow, I know) that > > the > > > > occasional cases of osteoporosis among CRONers might just possibly > > > > result from body fat going too low so that the body starts burning > > > > the protein matrix structure in the bones for energy? > > > > > > > > That way calcium consumption would not matter, as there would be > > no > > > > place for it to go. > > > > > > > > Is this plausable? (I have no medical qualifications of any > > kind). > > > > > > > > Rodney. > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 While I am on shaky ground here and probably offer more that I don't know than do, I have pondered this for a while. If we accept as a given that CR involves energy restriction below some poorly defined prior equilibrium point ( " set-point " ), a sustained energy deficit will consume energy stores typically adipose. CR involving significant " R " and of adequate duration will not only deplete such energy stores, but at some point also consume LBM. We are aware of cases where improper dieting led to dangerous loss of heart muscle, even properly executed there is expectation that adult onset of significant CR will result in remodeling of LBM. The rat studies we are so fond of involve cages without stairs, or traffic accidents, with minimal exposure to seasons and the flu du annum. What works for hairy rodents in controlled environments may not be a perfect model for big, hairless, mammals. Being formerly obese I have long wrestled with the concept of set point and don't waste much time on it these days. My current thought about CR is that it is likely a combination of multiple effects/mechanisms associated with short term and long term energy restriction. I find it hard to believe that a body during weight loss is even remotely similar to a body after years of equilibrium (at some reduced weight), so to taunt the classic mantra, it's not just calories. Perhaps more accurately it's the calories we eat today, and last week/year too. The body clearly has asymmetrical mechanisms for defending weight since historically running out of energy was a far greater threat than consuming too much. How all these mechanisms interact are surely complex and yet to be fully understood. There is little question that the body discounts adipose stores for driving short term hunger cues. Easy access to these significant energy stores has to impact the reality of dietary energy restriction in real time. I believe the apparent benefits of CR are the product of multiple mechanisms. I would be surprised if low, but adequate %BF is not one such mechanism. While it also appears obvious that adequate raw materials must be ingested to support LBM at whatever equilibrium level after remodeling. If we don't support maintenance and we can't remodel lower, we will suffer systemic failures in bone integrity, organ function, or in extremis life. I recall on CR'd individual who reports losing inches of height. I wouldn't want his bones next time I fall on concrete while playing ball. My impression after all this, is that there is far more that we don't know than what we do. Proceed with caution as we (what you mean we, fat man :-) are in uncharted territory. JR 55YO/22BMI/10%BF -----Original Message----- From: Rodney [mailto:perspect1111@...] Sent: Thursday, October 28, 2004 10:34 AM Subject: [ ] Osteoporosis in CRON Hi folks: It has only just occurred to me (I *am* a bit slow, I know) that the occasional cases of osteoporosis among CRONers might just possibly result from body fat going too low so that the body starts burning the protein matrix structure in the bones for energy? That way calcium consumption would not matter, as there would be no place for it to go. Is this plausable? (I have no medical qualifications of any kind). Rodney. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 I think you're right. If we eat less and waste all the fat we can waste, eventually we start losing muscle and let's say we get to the "nominal" weight and desired BF, etc. At that point, we have to quit losing weight, which means raise energy intake to balance energy output to maintain that desired weight. By that definition there is no such thing as CR, other than the drop from what we were eating at say 200# to that at say 165#. I think we may waste calories in feces at an intake of say 3200 kcals and not waste so much at 165#. But motility requires some wasted calories, IMO. But add to that the drop in body temp MAYBE operating at a different BMR - an unknown. No one has any answers to these things, yet. That is, not for an adult. Regards. ----- Original Message ----- From: Sent: Thursday, October 28, 2004 12:05 PM Subject: RE: [ ] Osteoporosis in CRON While I am on shaky ground here and probably offer more that I don't knowthan do, I have pondered this for a while.If we accept as a given that CR involves energy restriction below somepoorly defined prior equilibrium point ("set-point"), a sustained energydeficit will consume energy stores typically adipose. CR involvingsignificant "R" and of adequate duration will not only deplete such energystores, but at some point also consume LBM. We are aware of cases whereimproper dieting led to dangerous loss of heart muscle, even properlyexecuted there is expectation that adult onset of significant CR will resultin remodeling of LBM.The rat studies we are so fond of involve cages without stairs, or trafficaccidents, with minimal exposure to seasons and the flu du annum. What worksfor hairy rodents in controlled environments may not be a perfect model forbig, hairless, mammals.Being formerly obese I have long wrestled with the concept of set point anddon't waste much time on it these days. My current thought about CR is thatit is likely a combination of multiple effects/mechanisms associated withshort term and long term energy restriction. I find it hard to believe thata body during weight loss is even remotely similar to a body after years ofequilibrium (at some reduced weight), so to taunt the classic mantra, it'snot just calories. Perhaps more accurately it's the calories we eat today,and last week/year too.The body clearly has asymmetrical mechanisms for defending weight sincehistorically running out of energy was a far greater threat than consumingtoo much. How all these mechanisms interact are surely complex and yet to befully understood. There is little question that the body discounts adiposestores for driving short term hunger cues. Easy access to these significantenergy stores has to impact the reality of dietary energy restriction inreal time.I believe the apparent benefits of CR are the product of multiplemechanisms. I would be surprised if low, but adequate %BF is not one suchmechanism. While it also appears obvious that adequate raw materials must beingested to support LBM at whatever equilibrium level after remodeling. Ifwe don't support maintenance and we can't remodel lower, we will suffersystemic failures in bone integrity, organ function, or in extremis life. Irecall on CR'd individual who reports losing inches of height. I wouldn'twant his bones next time I fall on concrete while playing ball.My impression after all this, is that there is far more that we don't knowthan what we do. Proceed with caution as we (what you mean we, fat man :-)are in uncharted territory.JR55YO/22BMI/10%BF Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 Hi : Perhaps relevant. But would not the experience of anorexics be more relevant? Olympic skiers eat large amounts of food and get tons of exercise. Not much like most of us on CRON. Anorexics, by comparison, eat very little food and may or may not get much exercise, just like people on CRON. A search at Pubmed using the words 'anorexia osteoporosis' turns up a large number of studies, and in many cases the introductions state that osteoporosis is commonly asssociated with anorexia. And this even in young people, not just the little old ladies we normally hear about with osteoporosis. PMID 15452690; 15356043; 10776025, are a few examples. A couple of the studies found in that search also appear to discuss a role for fat. None of the studies I have seen seem to tackle the question of exactly what the mechanism/relationship is between the loss of weight associated with anorexia and the deterioration in bone density. But it is a curious coincidence that two types of weight loss - CRON and anorexia - appear to be associated, at least occasionally, with deterioration in bone health. And, where osteoporosis is quite common, in anorexia, the 'disease' is very similar to an extreme version of CR. Which would explain why osteoporosis occurs much less frequently in CRON - because not many people go overboard on CRON, but all anorexics go overboard, by definition. Of course it can always be argued that the loss of bone in CRON may simply be the body's response to the fact it weighs less and therefore needs less bone structure as support. Alternatively it could also be argued that it may be the result of nutrient deficiencies in anorexics, which presumably would not apply to us. But it would be unfortunate to be wrong about this if the real cause were to turn out to be the burning of bone protein because of excessively low fat reserves. If that were the case then anyone starting CRON should have that information presented to them front and centre, imo. Rodney. > > > > > > > > > > > > > > > Hi folks: > > > > > > > > > > It has only just occurred to me (I *am* a bit slow, I know) that > > > the > > > > > occasional cases of osteoporosis among CRONers might just possibly > > > > > result from body fat going too low so that the body starts burning > > > > > the protein matrix structure in the bones for energy? > > > > > > > > > > That way calcium consumption would not matter, as there would be > > > no > > > > > place for it to go. > > > > > > > > > > Is this plausable? (I have no medical qualifications of any > > > kind). > > > > > > > > > > Rodney. > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 28, 2004 Report Share Posted October 28, 2004 like popeye " i can't takes it no more " mechanical stresses on bone is primary determinant of bone mass (we're back to exercise) > > > > > > > > > > > > > > > > > > Hi folks: > > > > > > > > > > > > It has only just occurred to me (I *am* a bit slow, I > know) that > > > > the > > > > > > occasional cases of osteoporosis among CRONers might just > possibly > > > > > > result from body fat going too low so that the body starts > burning > > > > > > the protein matrix structure in the bones for energy? > > > > > > > > > > > > That way calcium consumption would not matter, as there > would be > > > > no > > > > > > place for it to go. > > > > > > > > > > > > Is this plausable? (I have no medical qualifications of any > > > > kind). > > > > > > > > > > > > Rodney. > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 29, 2004 Report Share Posted October 29, 2004 Anorexia is not CR. Anorexia is associated with its own metabolic and hormonal derangements unique to its pathology and not concordant with CR, as the primate studies attest. Burning bone protein has naught to do with osteoporosis. " The cellular basis of bone remodelling The changes that occur in osteoporosis can be understood in terms of subtle but important disturbances in bone remodelling. Bone is metabolically active throughout life. After skeletal growth is complete, remodelling of both cortical and trabecular bone continues. This remodelling requires the co-ordinated actions of osteoclasts to remove bone, and osteoblasts to replace it. Osteoclasts are derived from blood (haematopoietic) stem-cell precursors under the direction of essential genes such as src, of signalling proteins such as nuclear factor kB (NF-kB), and many cell-bound and soluble cytokines and growth factors. The so-called RANK/RANK-ligand (receptor activator of NF-kB) system is now known to be one of the dominant regulators of osteoclast development. Osteoblasts differentiate from stromal-cell precursors, and manufacture a complex extracellular matrix, which subsequently mineralizes. Bone formation is regulated by master genes, such as cbfa1, and by growth factors such as members of the transforming growth factor b superfamily, which includes the bone morphogenetic proteins. Apoptosis (programmed cell death) is emerging as a major means of regulating the life span of bone cells of all lineages: osteoclasts, osteoblasts and osteocytes [5]. This may contribute to changes in bone turnover under physiological and pathological conditions. Drugs with adverse effects on bone, such as glucocorticoids, may induce osteocyte apoptosis, whereas therapeutic agents that inhibit bone resorption, including oestrogens and bisphosphonates, may shorten the life span of osteoclasts. Increased apoptosis of osteocytes is a feature seen in fractured femoral necks. The control of calcium metabolism and of skeletal remodelling is achieved by the systemic calcium regulating hormones, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (calcitriol) and calcitonin, acting in concert with local regulatory mediators. There are many ways in which these hormones interact with local mediators and contribute to the physiological regulation of bone metabolism, to the pathogenesis of skeletal diseases, and to the changes that occur with age. Recently, leptin has been identified as another potential systemic regulatory hormone [6]. With loss of oestrogen, there is an increase in remodelling activity in both cortical and trabecular bone. There is a failure for all the bone removed during bone resorption to be replaced by an equivalent amount of new bone. The gradual loss of trabecular and cortical bone, accompanied by deterioration in their structural integrity, leads to impairment of the ability to resist mechanical loading leading to fracture. " http://www.biochemsoctrans.org/bst/031/0462/bst0310462.htm On Thu, 28 Oct 2004 22:37:37 -0000, Rodney <perspect1111@...> wrote: > > > Hi : > > Perhaps relevant. But would not the experience of anorexics be more > relevant? Olympic skiers eat large amounts of food and get tons of > exercise. Not much like most of us on CRON. Anorexics, by > comparison, eat very little food and may or may not get much > exercise, just like people on CRON. > > A search at Pubmed using the words 'anorexia osteoporosis' turns up a > large number of studies, and in many cases the introductions state > that osteoporosis is commonly asssociated with anorexia. And this > even in young people, not just the little old ladies we normally hear > about with osteoporosis. PMID 15452690; 15356043; 10776025, are a > few examples. A couple of the studies found in that search also > appear to discuss a role for fat. > > None of the studies I have seen seem to tackle the question of > exactly what the mechanism/relationship is between the loss of weight > associated with anorexia and the deterioration in bone density. But > it is a curious coincidence that two types of weight loss - CRON and > anorexia - appear to be associated, at least occasionally, with > deterioration in bone health. And, where osteoporosis is quite > common, in anorexia, the 'disease' is very similar to an extreme > version of CR. Which would explain why osteoporosis occurs much less > frequently in CRON - because not many people go overboard on CRON, > but all anorexics go overboard, by definition. > > Of course it can always be argued that the loss of bone in CRON may > simply be the body's response to the fact it weighs less and > therefore needs less bone structure as support. Alternatively it > could also be argued that it may be the result of nutrient > deficiencies in anorexics, which presumably would not apply to us. > > But it would be unfortunate to be wrong about this if the real cause > were to turn out to be the burning of bone protein because of > excessively low fat reserves. If that were the case then anyone > starting CRON should have that information presented to them front > and centre, imo. > > Rodney. > > > > > > > > > > > > > > > > > > > > Hi folks: > > > > > > > > > > > > It has only just occurred to me (I *am* a bit slow, I > know) that > > > > the > > > > > > occasional cases of osteoporosis among CRONers might just > possibly > > > > > > result from body fat going too low so that the body starts > burning > > > > > > the protein matrix structure in the bones for energy? > > > > > > > > > > > > That way calcium consumption would not matter, as there > would be > > > > no > > > > > > place for it to go. > > > > > > > > > > > > Is this plausable? (I have no medical qualifications of any > > > > kind). > > > > > > > > > > > > Rodney. > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 29, 2004 Report Share Posted October 29, 2004 Hi : Thanks. That is reassuring. Do we know what the cause of the osteoporosis is in the occasional CR practitioner who suffers from it? If we did it might help us to take actions that would ensure that each of us fail to qualify for it. Rodney. > > > > > > > > > > > > > > > > > > > > > Hi folks: > > > > > > > > > > > > > > It has only just occurred to me (I *am* a bit slow, I > > know) that > > > > > the > > > > > > > occasional cases of osteoporosis among CRONers might just > > possibly > > > > > > > result from body fat going too low so that the body starts > > burning > > > > > > > the protein matrix structure in the bones for energy? > > > > > > > > > > > > > > That way calcium consumption would not matter, as there > > would be > > > > > no > > > > > > > place for it to go. > > > > > > > > > > > > > > Is this plausable? (I have no medical qualifications of any > > > > > kind). > > > > > > > > > > > > > > Rodney. > > > > > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 29, 2004 Report Share Posted October 29, 2004 > > like popeye " i can't takes it no more " > > mechanical stresses on bone is primary determinant of bone mass (we're > back to exercise) > I found the following abstract pertaining to " mechanical stresses on bone is primary determinant of bone mass " via Google, " Long-term potentiation in bone--a role for glutamate in strain-induced cellular memory? " Spencer GJ, Genever PG. Biomedical Tissue Research, Department of Biology, University of York, York, YO10 5YW, UK. gjs6@... BACKGROUND: The adaptive response of bone cells to mechanical strain is a primary determinant of skeletal architecture and bone mass. In vivo mechanical loading induces new bone formation and increases bone mineral density whereas disuse, immobilisation and weightlessness induce bone loss. The potency of mechanical strain is such that a single brief period of loading at physiological strain magnitude is able to induce a long-lasting osteogenic response that lasts for days. Although the process of mechanotransduction in bone is incompletely understood, observations that responses to mechanical strain outlast the duration of stimulation necessitate the existence of a form of cellular memory through which transient strain episodes are recorded, interpreted and remembered by bone cells. Recent evidence supports the existence of a complex multicellular glutamate-signalling network in bone that shares functional similarities to glutamatergic neurotransmission in the central nervous system. In neurones, these signalling molecules coordinate synaptic communication required to support learning and memory formation, through a complex process of long-term potentiation. PRESENTATION OF THE HYPOTHESIS: We hypothesise that osteoblasts use a cellular mechanism similar or identical to neuronal long-term potentiation in the central nervous system to mediate long-lasting changes in osteogenesis following brief periods of mechanical strain. TESTING THE HYPOTHESIS: N-methyl-D-aspartate (NMDA) receptor antagonism should inhibit the saturating response of mechanical strain and reduce the enhanced osteogenicity of segregated loading to that of an equivalent period of uninterrupted loading. Changes in alpha-amino-3-hydroxy-5-methyl-isoxazole propionate (AMPA) receptor expression, localisation and electrophysiological responses should be induced by mechanical strain and inhibited by modulators of neuronal long-term potentiation. IMPLICATIONS OF THE HYPOTHESIS: If true, this hypothesis would provide a mechanism through which the skeleton could be pharmacologically primed to enhance or retrieve the normal osteogenic response to exercise. This would form a basis through which novel therapies could be developed to target osteoporosis and other prevalent bone disorders associated with low bone mass. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd= Retrieve & db=PubMed & list_uids=12892570 & dopt=Abstract http://snipurl.com/a5e2 Back to the weights for me. Aequalsz PS Actually you may have already presented this, or you may have a somewhat stilted way of writing. :-) If so am sorry. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 29, 2004 Report Share Posted October 29, 2004 Greetings! No, I hadn't posted this study but i do like it a lot! I particularly like studies like this one that confirm what i already 'know'.. go figure :-B The body is an amazing protean adaptive system and virtually ALL aspects are subject to remodelling in the face of mechanical stresses and strains. i don't think the important roles that these mechanical stresses play in life and longevity is appreciated by most on this list! Thanks for the nice study ! > > > > like popeye " i can't takes it no more " > > > > mechanical stresses on bone is primary determinant of bone mass > (we're > > back to exercise) > > > > > I found the following abstract pertaining to " mechanical stresses on > bone is primary determinant of bone mass " via Google, > > " Long-term potentiation in bone--a role for glutamate in > strain-induced cellular memory? " > > Spencer GJ, Genever PG. > > Biomedical Tissue Research, Department of Biology, University of > York, York, YO10 5YW, UK. gjs6@y... > > BACKGROUND: The adaptive response of bone cells to mechanical strain > is a primary determinant of skeletal architecture and bone mass. In > vivo mechanical loading induces new bone formation and increases bone > mineral density whereas disuse, immobilisation and weightlessness > induce bone loss. The potency of mechanical strain is such that a > single brief period of loading at physiological strain magnitude is > able to induce a long-lasting osteogenic response that lasts for days. > Although the process of mechanotransduction in bone is incompletely > understood, observations that responses to mechanical strain outlast > the duration of stimulation necessitate the existence of a form of > cellular memory through which transient strain episodes are recorded, > interpreted and remembered by bone cells. Recent evidence supports the > existence of a complex multicellular glutamate-signalling network in > bone that shares functional similarities to glutamatergic > neurotransmission in the central nervous system. In neurones, these > signalling molecules coordinate synaptic communication required to > support learning and memory formation, through a complex process of > long-term potentiation. PRESENTATION OF THE HYPOTHESIS: We hypothesise > that osteoblasts use a cellular mechanism similar or identical to > neuronal long-term potentiation in the central nervous system to > mediate long-lasting changes in osteogenesis following brief periods > of mechanical strain. TESTING THE HYPOTHESIS: N-methyl-D-aspartate > (NMDA) receptor antagonism should inhibit the saturating response of > mechanical strain and reduce the enhanced osteogenicity of segregated > loading to that of an equivalent period of uninterrupted loading. > Changes in alpha-amino-3-hydroxy-5-methyl-isoxazole propionate (AMPA) > receptor expression, localisation and electrophysiological responses > should be induced by mechanical strain and inhibited by modulators of > neuronal long-term potentiation. IMPLICATIONS OF THE HYPOTHESIS: If > true, this hypothesis would provide a mechanism through which the > skeleton could be pharmacologically primed to enhance or retrieve the > normal osteogenic response to exercise. This would form a basis > through which novel therapies could be developed to target > osteoporosis and other prevalent bone disorders associated with low > bone mass. > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd= > Retrieve & db=PubMed & list_uids=12892570 & dopt=Abstract > > http://snipurl.com/a5e2 > > Back to the weights for me. > > Aequalsz > > PS Actually you may have already presented this, or you may have a > somewhat stilted way of writing. :-) If so am sorry. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 29, 2004 Report Share Posted October 29, 2004 Hi Freebird: Of course you do not have to answer (I recognize it is none of my business) but, assuming you are male, is there a history among the males in your family of osteoporosis? For most of us it isn't a problem for males. But there are exceptions of course. No one here as far as I know advocates a complete absence of exercise. The issue (imo) is how much is adequate. Rodney. > > > > > > like popeye " i can't takes it no more " > > > > > > mechanical stresses on bone is primary determinant of bone mass > > (we're > > > back to exercise) > > > > > > > > > I found the following abstract pertaining to " mechanical stresses on > > bone is primary determinant of bone mass " via Google, > > > > " Long-term potentiation in bone--a role for glutamate in > > strain-induced cellular memory? " > > > > Spencer GJ, Genever PG. > > > > Biomedical Tissue Research, Department of Biology, University of > > York, York, YO10 5YW, UK. gjs6@y... > > > > BACKGROUND: The adaptive response of bone cells to mechanical strain > > is a primary determinant of skeletal architecture and bone mass. In > > vivo mechanical loading induces new bone formation and increases bone > > mineral density whereas disuse, immobilisation and weightlessness > > induce bone loss. The potency of mechanical strain is such that a > > single brief period of loading at physiological strain magnitude is > > able to induce a long-lasting osteogenic response that lasts for days. > > Although the process of mechanotransduction in bone is incompletely > > understood, observations that responses to mechanical strain outlast > > the duration of stimulation necessitate the existence of a form of > > cellular memory through which transient strain episodes are recorded, > > interpreted and remembered by bone cells. Recent evidence supports the > > existence of a complex multicellular glutamate-signalling network in > > bone that shares functional similarities to glutamatergic > > neurotransmission in the central nervous system. In neurones, these > > signalling molecules coordinate synaptic communication required to > > support learning and memory formation, through a complex process of > > long-term potentiation. PRESENTATION OF THE HYPOTHESIS: We hypothesise > > that osteoblasts use a cellular mechanism similar or identical to > > neuronal long-term potentiation in the central nervous system to > > mediate long-lasting changes in osteogenesis following brief periods > > of mechanical strain. TESTING THE HYPOTHESIS: N-methyl-D-aspartate > > (NMDA) receptor antagonism should inhibit the saturating response of > > mechanical strain and reduce the enhanced osteogenicity of segregated > > loading to that of an equivalent period of uninterrupted loading. > > Changes in alpha-amino-3-hydroxy-5-methyl-isoxazole propionate (AMPA) > > receptor expression, localisation and electrophysiological responses > > should be induced by mechanical strain and inhibited by modulators of > > neuronal long-term potentiation. IMPLICATIONS OF THE HYPOTHESIS: If > > true, this hypothesis would provide a mechanism through which the > > skeleton could be pharmacologically primed to enhance or retrieve the > > normal osteogenic response to exercise. This would form a basis > > through which novel therapies could be developed to target > > osteoporosis and other prevalent bone disorders associated with low > > bone mass. > > > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd= > > Retrieve & db=PubMed & list_uids=12892570 & dopt=Abstract > > > > http://snipurl.com/a5e2 > > > > Back to the weights for me. > > > > Aequalsz > > > > PS Actually you may have already presented this, or you may have a > > somewhat stilted way of writing. :-) If so am sorry. Quote Link to comment Share on other sites More sharing options...
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