You've probably heard the hype about Human Growth Hormone supporting muscle mass. Well, it does help muscles to heal from exercise. But there's a big down side.

I never used Human Growth Hormone directly, but for years I've been using bovine colostrum. It contains insulin like growth factor 1. My endocrinologist explained that human growth hormone works by making insulin like growth factor 1, and that it increases insulin resistance.

For over a year I've been reading that longevity is improved by inhibiting insulin like growth factor 1. But I imagined that by taking colostrum to help heal the tiny tears due to weight training, I was exchanging length of life for quality of life.

Reading "The Pathway of Youth" in the Jan 2012 issue of Scientific American, made me rethink colostrum use.

"... the capacity for growth, which seems the very essence of youthfulness, drives us into the grave later in life."

Research into TOR (target of rapamycin receptors) has lead to a new explanation, based on a theory by evolutionary biologist George Willimas.

"... aging is cause by two-faced genes that are beneficial early in life but harmful later on. Such 'antagonistic pleiotropic genes' are favored by evolution..."

In effect the TOR pathway behaves very much like an aging program even though it was built to aid early development.

The bottom line is that while colostrum facilitates muscle mass it

* promotes cell senescence, which "damages nearby cells and saps tissues' regenerative capacity"

* "contributes to the accumulation of aggregation-prone proteins and of dysfunctional mitochondria, which spew free radicals"

* "contributes to the accumulation of degredation-resistant proteins in neurons, a process that plays a part in Alzheimer's and other forms of neurodegeneration"

* "abets proliferation of smooth muscle cells in arteries ( a key step in atherosclerois)"

* promotes insulin resistance

* promotes fat accumulation

* multiplies osteoclasts that break down bones, and

* promotes tumors.


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Replies to This Discussion

Yes, the TOR pathway.

The mammalian target of rapamycin (mTOR) also known as mechanistic target of rapamycin or FK506 binding protein 12-rapamycin associated protein 1 (FRAP1) is a protein which in humans is encoded by the FRAP1 gene.[1][2] mTOR is a serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, and transcription.[3][4] mTOR belongs to the phosphatidylinositol 3-kinase-related kinase protein family.

mTOR integrates the input from upstream pathways, including insulin, growth factors (such as IGF-1 and IGF-2), and amino acids.[3] mTOR also senses cellular nutrient and energy levels and redox status.[5] The mTOR pathway is dysregulated in human diseases, especially certain cancers.[4] Rapamycin is a bacterial product that can inhibit mTOR by associating with its intracellular receptor FKBP12.[6][7] The FKBP12-rapamycin complex binds directly to the FKBP12-Rapamycin Binding (FRB) domain of mTOR.[7]

mTOR is the catalytic subunit of two molecular complexes.[8]

mTOR stands for mammalian Target Of Rapamycin and was named based on the precedent that Tor was first discovered via genetic and molecular studies of rapamycin-resistant mutants of Saccharomyces cerevisiae that identified FKBP12, Tor1, and Tor2 as the targets of rapamycin and provided robust support that the FKBP12-rapamycin complex binds to and inhibits the cellular functions of Tor1 and Tor2.

Decreased TOR activity has been found to slow aging in S. cerevisiae, C. elegans, and D. melanogaster.[32][33][34][35] The mTOR inhibitor rapamycin has been confirmed to increase lifespan in mice by independent groups at the Jackson Laboratory, University of Texas Health Science Center, and the University of Michigan.[36]

It's hypothesized that some dietary regimes, like caloric restriction and methionine restriction, cause lifespan extension by decreasing mTOR activity.[32][33] But infusion of leucine into the rat brain has been shown to decrease food intake and body weight via activation of the mTOR pathway.[37]

Brown EJ, Albers MW, Shin TB, Ichikawa K, Keith CT, Lane WS, Schreiber SL (June 1994). "A mammalian protein targeted by G1-arresting rapamycin-receptor complex". Nature 369 (6483): 756–8. doi:10.1038/369756a0. PMID 8008069

"based on a theory by evolutionary biologist George Willimas"

I assume you're referring to George C. Williams?




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