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[h=1]Fot those arent sure what telomeres are, its highly recommended you research them. Then you'll better understand why IGF-1 lr3 is touted as the fountain of youth, and why so many claims have been made as to how well IGF-1 works in reversing the aging process. Yes Reversing, Not just slowing down the aging process, but literally reversing it.

Pubmed on IGF-1 and Telomeres!

Higher circulating levels of IGF-1 are associated with longer leukocyte telomere length in healthy subjects.[/h][h=3][/h]

[h=3]Abstract[/h]
<abstracttext>Mutations that inhibit the insulin-like growth factor-1 (IGF-1) extend the lifespan of worms, flies and mice. However, it appears that relatively low circulating levels of IGF-1 in humans are associated with aging-related diseases and diminished longevity. As leukocyte telomere length (LTL) is ostensibly a biomarker of human aging, we examined the relationship between LTL and blood IGF-1 in a healthy cohort. Our sample comprised 476 healthy, unrelated Caucasians (208 men and 268 women), aged 16-104 years, living in the West Coast of Southern Italy. We measured LTL by Southern blots and IGF-1 by enzyme-linked immunoassay. Both IGF-1 and LTL diminished with age (IGF-1, r=-0.601, P<0.001; LTL, r=-0.706, P<0.001). Age-adjusted LTL was positively associated with IGF-1 level throughout the age range of the cohort (r=0.270, P<0.001). IGF-1 accounted for about 10% of the inter-individual variation in LTL over and above the effect of age. Our findings suggest that both circulating IGF-1 and LTL are indices of healthy aging in humans. Further research will be necessary to establish whether LTL will ultimately be used in clinical settings as an index of healthy aging.</abstracttext>

 
[h=1]Insulin-like growth factors and leukocyte telomere length: the cardiovascular health study.[/h][h=3]Author information[/h]

[h=3]Abstract[/h]<abstracttext>The insulin-like growth factor (IGF) axis may affect immune cell replicative potential and telomere dynamics. Among 551 adults 65 years and older, leukocyte telomere length (LTL), insulin-like growth factor-1 (IGF-1), and insulin-like growth factor-binding proteins 1 and 3 (IGFBP-1, IGFBP-3) were measured. Multivariate linear regression was used to model the association of LTL with IGF-1 and IGFBPs, while controlling for confounding and increasing precision by adjusting for covariates. We observed a significant association between higher IGF-1 and longer LTL after adjustment for age, sex, race, smoking status, body mass index, hypertension, diabetes, and serum lipids. The results suggested an increase of .08 kb in LTL for each standard deviation increase of IGF-1 (p = .04). IGFBP-1 and IGFBP-3 were not significantly associated with LTL. High IGF-1 may be an independent predictor of longer LTL, consistent with prior evidence suggesting a role for IGF-1 in mechanisms relating to telomere maintenance.</abstracttext>

 
[h=1]Telomeres and endocrine dysfunction of the adrenal and GH/IGF-1 axes.[/h][h=3]Author information[/h]

[h=3]Abstract[/h]<abstracttext>Telomeres, located at the end of linear chromosomes, are essential to maintain genomic stability. Telomere biology has recently emerged as an important player in the fields of ageing and disease. To maintain telomere length (TL) and reduce its degradation after mitosis, the telomerase enzyme complex is produced. Genetic, epigenetic, hormonal and environmental factors can regulate telomerase function. These include stress hormones such as cortisol and growth factors. The hypothalamic-pituitary-adrenal (HPA) axis has been evaluated in psychiatric diseases where hypercortisolism and oxidative stress are often present. Some researches have linked TL shortening to increases in stress-related cortisol, but others have not. The effects of cortisol on the telomere system are complex and may depend on the intensity and duration of exposure. On the other hand, low levels of IGF-1 are associated with inflammation and ageing-related diseases (ischaemic heart disease, congestive heart failure). Both IGF-1 and TL diminish with age and are positively and strongly correlated with each other. It is not clear whether this positive correlation reflects a single association or a cause-effect relationship. Further research will ideally investigate longitudinal changes in telomeres and both these hormonal axes. To our knowledge, TL dysfunction has not been described in either endogenous hypercortisolism (Cushing's syndrome) or acromegaly where excessive amounts of GH and consequently IGF-1 are produced. This review focuses on the possible relationships between telomere dysfunction and the hypothalamic-pituitary-adrenal (HPA) axis and GH-IGF-1 system.</abstracttext>

 
found another great article last night on igf and telomeres, i will try finding it again and posting it here
 
I keep finding this article in 4th position on google while researching "igf-1 lr3 and congestive heart failure".
 
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well I wouldn't be using IGF-1 lr3 for congestive heart failure problems, or at least I hope your not
 
Are there any article that indicate a dosages used for IGF long term for the anti aging community. I know in the body building field some guys stay on forever, but for the most part many cycle the product. I am assuming that IGF is like HGH (BB dose 6iu+, and the anti aging crowd is more of a 2iu dose) and is a dose effective thing, correct?

Hopefully I am making sence.
 
Yes, it would be dose dependent. There probably aren't any official studies that show what an anti-aging dose would be for IGF, but for as much as I've used it, I would make an educated guess that around 40-60mcg/day would be a starting point going up to 80-100mcg/day on the high end. If I was rich or better to say WHEN I get rich, I'm going to get myself on IGF year round. I've always felt better, slept better, and had better built muscle while on MC's IGF.
 
I keep finding this article in 4th position on google while researching "igf-1 lr3 and congestive heart failure" for my mom. I'm working on finding her something to help her quality of life with CHF and COPD.

What did you find out about this?
 
Telomere length is genetic. You would have to make a change on the genetic level. If it does regenerate telomere strands in humans then they need to be using it on rapidly aging children.
 
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