Re: insulin and IGF-I, health,

[Guest guest]

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]

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. "