Re: Re: insulin and IGF-I, health,

[Guest guest]

That's been my observation, too, but I once lost a discussion about that.

And I can't make myself shorter, gracefully.

Of course we could make our children shorter with less food and a lot of legal fees. Walford suggested "we don't want to raise a generation of short people" (paraphrased).

Still, I don't have or recall articles relating lifespan to pygmies, as we have Eskimos and lifespan, eg.

I also have heard dwarves are short lived, as are giants, but again no articles.

Perhaps the diff, in dwarves as opposed to pygmies, is there is a gene that makes the Pygmies short whereas the dwarves suffer a gene problem, not necessarily transmitted. (just guessing).

In any case, I feel more sure each day that IGF-1 is not the factor that causes cancer any more than any other factor of which a cancer takes advantage.

EG, If I measure my IGF-1and find it higher than average, would I be happy as I would if I measured my bone density and found it above average? Secondly, if I really wanted to lower the system level how would I do that? I could eat less and starve my weight and bone down, but will that make me live longer?

Notice I make a distinction between a "system" level as in changing the thermostat. A lowering by food lowering would not be lowering the system's set value, merely changing the short term IGF-1.

If I went back to eating more food the IGF-1 would come back up to it's system level, unless I triggered an anorexic point.

If we are keeping IGF-1 low by CR, we may be able to live longer, but not if we impact osteo, IMO. Like weight, I want it to be on the low side perhaps, but I think the IGF-1 level will go down with weight loss anyway, because the system is set that way. After all, it is a hormone with a feedback control system, actually two if you include the CNS.

Regards.

[ ] Re: insulin and IGF-I, health,

Hi JW:Oooops, sorry. Correction, shorter people live longer than tall people ........... I believe.Rodney.> > Just a synopsis of IGF-1 from Hadley's endocrinology. (a monogram-> ha)> > > > Hadley describes IGF-I as a molecule that resembles insulin to > which has been added amino acids (pg 259). He suggests the two > evolved from a common molecule that performs the two functions: the > metabolic function of insulin and the growth function of IGF-I.> > It is certain that without IGF-I, humans are smaller (dwarfism) and > too much results in gigantism. (pg 263,4). Pygmies, eg, express lower > levels of IGF-I. (IGF-II does not seem to be involved in growth.)> > Some cells have insulin receptors and some cells have IGF-1 > receptors. Because the molecules are similar, both can share > receptors. "Insulin is more potent in stimulating metabolic effects > than IGF-I and IGF-II. On the other hand, insulin is less potent > stimulating cell proliferation than {IGF-I and IGF-II}."> > > > Pituitary ->somatotropin (STH) -> Liver, other tissues -> > somatomedins, IGF-I, IGF-II> > > > Somatomedin hypothesis: STH stimulates chondrogenesis by way of > somatomedins. STH, not IGF-I, stimulates the multiplication of slowly > cycling cells. IGF-I acts on the proliferation of the resulting > chondrocytes.> > > > Feedback control:> > Pg 262 shows the control from CNS to the hypothalmus which releases > somatocrinin(+) and somatostatin (-) to cause the pituitary to > release STH.> > Feedback control: (pg 261)> > IGF-I stimulates hypothalmic somatostatin release and inhibits > pituitary STH release. > > > > My take:> > If you believe the growth system stays intact, then IGF-1 is lower > for smaller people and falls at age because of less requirement for > bone growth. I suspect driven by some sympathetic nervous system > feedback to the brain. > > If I believe the parts fail due to aging or disease, and I'm sure > they must in some cases, IGF-I might be lower because of less STH, or > liver function failure, but other tissues can generate IGF-I. > > OTOH, higher levels than required at age, might be due to failure > of the feedback control systems. > > > > Pygmies don't live longer.> > > > So what are the cancer implications?> > Look at:> > http://tinyurl.com/8caln> > > > http://jcem.endojournals.org/cgi/content/abstract/73/2/401?> maxtoshow= & HITS=10 & hits=10 & RESULTFORMAT=1 & author2=cohen & title=Insulin-> like+growth+ & andorexacttitle=phrase & andorexacttitleabs=and & andorexactf> ulltext=and & searchid=1125076434843_3264 & stored_search= & FIRSTINDEX=20 & s> ortspec=relevance> > Insulin-like growth factors (IGFs), IGF receptors, and IGF-binding > proteins in primary cultures of prostate epithelial cells> > P Cohen, DM Peehl, G Lamson and RG Rosenfeld > > > > > > And look at the ref articles below it. The abstracts indicate sorta > the history of thought about IGFs, etc in relation to cancer, from > 1996 to 2005.> > > > It seems to me the emphasis shifted from IGF-I, to more complex > things, like IGFBP, receptors.> > > > starting with:> > "A strong positive association was observed between IGF-I levels > and prostate cancer risk. Men in the highest quartile of IGF-I levels > had a relative risk of 4.3 (95 percent confidence interval 1.8 to > 10.6) compared with men in the lowest quartile. This association was > independent of baseline prostate-specific antigen levels. > Identification of plasma IGF-I as a predictor of prostate cancer risk > may have implications for risk reduction and treatment." PMID: > 9438850 > > > > to:> > Interrelation of Energy Intake, Body Size, and Physical Activity > with Prostate Cancer in a Large Prospective Cohort Study > > Although energy intake is known to be imperfectly measured by > questionnaire, we observed a positive association between energy > intake and metastatic or fatal prostate cancer among men who were > leaner, more physically active, younger, and who had a family history > of prostate cancer. Our observations suggest the testable hypothesis > that the elevated risk of clinically important prostate cancer in men > with a high energy intake may be attributable to certain metabolic > profiles that favor enhanced growth factor production over an > increase in adiposity. > > > > including:> > Physical Activity and the Risk of Prostate Cancer in The > Netherlands Cohort Study, Results after 9.3 Years of Follow-up > > Discussion: The results of this current study do not support the > hypothesis that physical activity protects against prostate cancer in > men. > > > > > > Other implications?> > > > The American Journal of Cardiology> > Volume 90 . Number 12 . December 15, 2002> > Effect of congestive heart failure on the insulin-like growth > factor-1 system> > > > "Our study shows that in an elderly population of patients > hospitalized for CHF, there was a significant decrease in total IGF-> 1, a profound decrease in IGFBP-3, and a marked increase in > circulating free IGF-1. The decrease in total IGF-1 was not present > in patients who received angiotensin-converting enzyme inhibitors."

[Guest guest]

That's been my observation, too, but I once lost a discussion about that.

And I can't make myself shorter, gracefully.

Of course we could make our children shorter with less food and a lot of legal fees. Walford suggested "we don't want to raise a generation of short people" (paraphrased).

Still, I don't have or recall articles relating lifespan to pygmies, as we have Eskimos and lifespan, eg.

I also have heard dwarves are short lived, as are giants, but again no articles.

Perhaps the diff, in dwarves as opposed to pygmies, is there is a gene that makes the Pygmies short whereas the dwarves suffer a gene problem, not necessarily transmitted. (just guessing).

In any case, I feel more sure each day that IGF-1 is not the factor that causes cancer any more than any other factor of which a cancer takes advantage.

EG, If I measure my IGF-1and find it higher than average, would I be happy as I would if I measured my bone density and found it above average? Secondly, if I really wanted to lower the system level how would I do that? I could eat less and starve my weight and bone down, but will that make me live longer?

Notice I make a distinction between a "system" level as in changing the thermostat. A lowering by food lowering would not be lowering the system's set value, merely changing the short term IGF-1.

If I went back to eating more food the IGF-1 would come back up to it's system level, unless I triggered an anorexic point.

If we are keeping IGF-1 low by CR, we may be able to live longer, but not if we impact osteo, IMO. Like weight, I want it to be on the low side perhaps, but I think the IGF-1 level will go down with weight loss anyway, because the system is set that way. After all, it is a hormone with a feedback control system, actually two if you include the CNS.

Regards.

[ ] Re: insulin and IGF-I, health,

Hi JW:Oooops, sorry. Correction, shorter people live longer than tall people ........... I believe.Rodney.> > Just a synopsis of IGF-1 from Hadley's endocrinology. (a monogram-> ha)> > > > Hadley describes IGF-I as a molecule that resembles insulin to > which has been added amino acids (pg 259). He suggests the two > evolved from a common molecule that performs the two functions: the > metabolic function of insulin and the growth function of IGF-I.> > It is certain that without IGF-I, humans are smaller (dwarfism) and > too much results in gigantism. (pg 263,4). Pygmies, eg, express lower > levels of IGF-I. (IGF-II does not seem to be involved in growth.)> > Some cells have insulin receptors and some cells have IGF-1 > receptors. Because the molecules are similar, both can share > receptors. "Insulin is more potent in stimulating metabolic effects > than IGF-I and IGF-II. On the other hand, insulin is less potent > stimulating cell proliferation than {IGF-I and IGF-II}."> > > > Pituitary ->somatotropin (STH) -> Liver, other tissues -> > somatomedins, IGF-I, IGF-II> > > > Somatomedin hypothesis: STH stimulates chondrogenesis by way of > somatomedins. STH, not IGF-I, stimulates the multiplication of slowly > cycling cells. IGF-I acts on the proliferation of the resulting > chondrocytes.> > > > Feedback control:> > Pg 262 shows the control from CNS to the hypothalmus which releases > somatocrinin(+) and somatostatin (-) to cause the pituitary to > release STH.> > Feedback control: (pg 261)> > IGF-I stimulates hypothalmic somatostatin release and inhibits > pituitary STH release. > > > > My take:> > If you believe the growth system stays intact, then IGF-1 is lower > for smaller people and falls at age because of less requirement for > bone growth. I suspect driven by some sympathetic nervous system > feedback to the brain. > > If I believe the parts fail due to aging or disease, and I'm sure > they must in some cases, IGF-I might be lower because of less STH, or > liver function failure, but other tissues can generate IGF-I. > > OTOH, higher levels than required at age, might be due to failure > of the feedback control systems. > > > > Pygmies don't live longer.> > > > So what are the cancer implications?> > Look at:> > http://tinyurl.com/8caln> > > > http://jcem.endojournals.org/cgi/content/abstract/73/2/401?> maxtoshow= & HITS=10 & hits=10 & RESULTFORMAT=1 & author2=cohen & title=Insulin-> like+growth+ & andorexacttitle=phrase & andorexacttitleabs=and & andorexactf> ulltext=and & searchid=1125076434843_3264 & stored_search= & FIRSTINDEX=20 & s> ortspec=relevance> > Insulin-like growth factors (IGFs), IGF receptors, and IGF-binding > proteins in primary cultures of prostate epithelial cells> > P Cohen, DM Peehl, G Lamson and RG Rosenfeld > > > > > > And look at the ref articles below it. The abstracts indicate sorta > the history of thought about IGFs, etc in relation to cancer, from > 1996 to 2005.> > > > It seems to me the emphasis shifted from IGF-I, to more complex > things, like IGFBP, receptors.> > > > starting with:> > "A strong positive association was observed between IGF-I levels > and prostate cancer risk. Men in the highest quartile of IGF-I levels > had a relative risk of 4.3 (95 percent confidence interval 1.8 to > 10.6) compared with men in the lowest quartile. This association was > independent of baseline prostate-specific antigen levels. > Identification of plasma IGF-I as a predictor of prostate cancer risk > may have implications for risk reduction and treatment." PMID: > 9438850 > > > > to:> > Interrelation of Energy Intake, Body Size, and Physical Activity > with Prostate Cancer in a Large Prospective Cohort Study > > Although energy intake is known to be imperfectly measured by > questionnaire, we observed a positive association between energy > intake and metastatic or fatal prostate cancer among men who were > leaner, more physically active, younger, and who had a family history > of prostate cancer. Our observations suggest the testable hypothesis > that the elevated risk of clinically important prostate cancer in men > with a high energy intake may be attributable to certain metabolic > profiles that favor enhanced growth factor production over an > increase in adiposity. > > > > including:> > Physical Activity and the Risk of Prostate Cancer in The > Netherlands Cohort Study, Results after 9.3 Years of Follow-up > > Discussion: The results of this current study do not support the > hypothesis that physical activity protects against prostate cancer in > men. > > > > > > Other implications?> > > > The American Journal of Cardiology> > Volume 90 . Number 12 . December 15, 2002> > Effect of congestive heart failure on the insulin-like growth > factor-1 system> > > > "Our study shows that in an elderly population of patients > hospitalized for CHF, there was a significant decrease in total IGF-> 1, a profound decrease in IGFBP-3, and a marked increase in > circulating free IGF-1. The decrease in total IGF-1 was not present > in patients who received angiotensin-converting enzyme inhibitors."