Circulating Insulin-like Growth Factor-I Concentrations and Risk of 30 Cancers: Prospective Analyses in UK Biobank
Anika Knuppel, Georgina K. Fensom, Eleanor L. Watts, Marc J. Gunter, Neil Murphy, Keren Papier, Aurora Perez-Cornago, Julie A. Schmidt, Karl Smith Byrne, Ruth C. Travis and Timothy J. Key
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DOI: 10.1158/0008-5472.CAN-20-1281 Published September 2020
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Abstract
Circulating insulin-like growth factor I (IGF-I) is positively associated with the risks of colorectal, breast, and prostate cancer, but evidence for other less common cancers is limited. In this study, we investigated associations between serum IGF-I concentrations and incidence of less common cancers in the UK Biobank study. To enable comparison of effect estimates, and as positive controls, both common and less common cancer sites (total 30) were included in an outcome-wide analysis. Data from 394,388 cancer-free participants in the UK Biobank study were analyzed. Multivariable adjusted Cox proportional hazards models were used to determine associations between baseline serum IGF-I concentrations and cancer incidence, using repeated IGF-I measurements from up to 14,149 participants to correct for regression dilution bias. Higher IGF-I concentration was associated with increased risks of thyroid cancer [HR per 5 nmol/L higher concentration 1.18; 95% confidence interval (CI), 1.01–1.37] in addition to colorectal (HR, 1.08; 95% CI, 1.03–1.13), breast (HR, 1.11; 95% CI, 1.07–1.15), and prostate cancer (HR, 1.08; 95% CI, 1.05–1.12), and reduced risks of ovarian and liver cancer. Mean follow-up was 6.9 years and the possibility that the observed associations may be influenced by reverse causality bias cannot be excluded. Additional nominally significant associations with malignant melanoma, multiple myeloma, oral cancer, and esophageal squamous cell carcinoma did not survive correction for multiple testing. Studies with longer follow-up and pooled analyses are needed to further assess how broad the role of IGF-I is in cancer development.
Significance: The results from this outcome-wide analysis are consistent with a positive association of IGF-I with cancers at several sites.
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Graham49
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IGF-I levels are not related to dietary glucose/insulin levels, as far as I know.
It has long been recognized that the IGF-axis is altered in PCa. Unfortunately, the study did not look at IGF binding proteins. In PCa, not only may IGF-I be elevated, but IGFBP-3 & others may be reduced - increasing IGF bioavailability.
One way of inhibiting IGF-I is by restricting fully-formed protein & selectively restricting an essential amino acid.
That is a good choice. The tricky part is to limit homocysteine recycling back to methionine. That requires restricting methyl donors (folate or folic acid normally), or one of the necessary cofactors (B12 is my preference.)
Here are the 5 PubMed hits for <"Selective amino acid restriction">:
The relative roles of growth hormone and IGF-1 in controlling insulin sensitivity
David R. Clemmons
Additional article information
Abstract
IGF-1 and growth hormone (GH) interact with insulin to modulate its control of carbohydrate metabolism. A new study (see the related article beginning on page 96) shows that blocking the effect of GH in the presence of low serum IGF-1 concentrations enhances insulin sensitivity.
Understanding the relative roles of peptide hormones in modulating responsiveness to insulin presents a major challenge because of the adaptability of the growth hormone/IGF-1/insulin system. Changes in glucose and insulin secretion result in counter-regulatory responses, and modifications in growth hormone (GH) and IGF-1 function alter insulin’s ability to maintain normal carbohydrate homeostasis. Historically, this problem has been analyzed in both human and rodent hormone-deficiency models (e.g., GH deficiency) in which the hormone of interest is replaced and the metabolic consequences are determined (1). The recent development of tissue-selective knockout animal models has brought new insights to our understanding of the relative roles of these hormones in carbohydrate homeostasis. In this issue of the JCI, Yakar et al. address the relative roles of GH and IGF-1 in regulating insulin sensitivity in mice (2). The authors created an animal model in which IGF-1 synthesis in the liver is eliminated and then crossed these animals with mice that overexpress a mutant form of GH that prevents GH activation of its receptor. The authors conclude that GH is a major determinant of insulin resistance in these IGF-1–deficient animals, since, in the presence of low concentrations of serum IGF-1, blocking the action of GH results in a major improvement in insulin sensitivity.
"Insulin-like growth factor 1, also called somatomedin C, is a hormone similar in molecular structure to insulin which plays an important role in childhood growth, and has anabolic effects in adults"
I guess that makes sense. HGH probably would produce a similar effect.
So how might this research inform our behavior and or decisions?
Far back, I had read that HGH can be sold to elder people as self production of this hormone diminishes with age. Otherwise, it is tightly controlled for being a dopping substance for athletes.
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