With this in mind, attention has fallen on a rare human lineage with a growth hormone receptor mutation that produces dwarfism, the Laron syndrome population. Unfortunately it isn't yet possible to say whether or not these individuals have any advantage over the rest of us when it comes to longevity. They do appear to be resistant to cancer and type 2 diabetes, though the evidence in support of that conclusion isn't completely iron-clad at this point. People with Laron syndrome and, separately, people who practice calorie restriction for its health benefits can be compared with the same processes operating in mice. When doing so, we can see that human longevity is not enormously changed, while mouse longevity does increase by up to 70% for growth hormone disruption, and up to 40% for calorie restriction. That degree of gain is certainly not the case in humans. Evolution has delivered a much more plastic life span to short-lived mammals, responsive to environmental circumstances, and with a biochemistry capable of these large changes in the pace of aging.
Putting growth hormone signaling to one side for the moment, considerable effort has been devoted over the years to the broader search for human genetic variants that are associated with longevity. The consensus on genes and longevity is that individual variations in your genome have little influence over aging until later life, and from that point forward, the older and more damaged you get the more that genetic variation matters. Nonetheless, the search has found very few compelling associations. There is solid evidence for variants in APOE and FOXO3A, and less solid evidence for a few other variants such as in TXNRD1, but these are not large effects. Beyond this there are scores of other associations that are never replicated, showing up in only one study or one population, and again with small effects - by which I mean maybe you have a 1.5% chance of living to 100 instead of a 1% chance if you held one of these variants. The big picture is of hundreds or thousands of individually tiny effects; which of these genes and variants are more or less relevant varies widely between populations and individuals, and is very dependent on environmental factors.
That said, there are genetic variants with sizable effects on resistance to specific age-related disease, such as those in ASGR1 or ANGPTL4, both of which reduce blood cholesterol and cardiovascular disease risk. Nothing is published on their effects on longevity at this time, but give it time. Should we believe that there are human genetic variants that meaningfully increase life expectancy in the carriers based on what we've seen to date? The association studies with their poor catch of results suggest no. The existence of the variants mentioned above suggest maybe, but equally it is the case that aging has many facets. Being resistant - or even immune - to one thin facet, such as cardiovascular disease, is thought unlikely to do a great deal to overall longevity. It just means that something else gets you in the end, perhaps a couple of years later.
Returning to growth hormone metabolism, I see that researchers are claiming that a common human gene variant of growth hormone receptor, per their statistics, may result in a ten year difference in life expectancy. This is replicated in multiple study populations, but the effect appears only in men. It is interesting, but there is every reason to be cautious with this sort of very statistical genetic association study. I'd say read the paper and put it aside until someone replicates the result. Would a ten year gain from a growth hormone signaling genetic variant be surprising if this turns out in fact be the case? Maybe not, given what we know about the relative sizes of effects in mice and humans. Ten years is about on the outside end of variations that can plausibly exist in some numbers and yet blend in with broader population data, and the effects in mice are considerably larger on a relative basis.
https://www.fightaging.org/archives/2017/06/common-human-growth-hormone-receptor-variant-associated-...
Common Human Growth Hormone Receptor Variant Associated with Greater Longevity
The longest lived laboratory mice, more than a decade after the creation of the first lineage, are still those with impaired growth hormone signaling. That record has yet to be overtaken, and I suspect that it may well stand unbroken until the development of rejuvenation therapies based on damage repair is further advanced, and senescent cell clearance is joined by other types of therapy, their effects adding together. Thus growth hormone and growth hormone receptor genes in humans are one of the places to look for variants and mutations that might improve our understanding of how metabolism influences aging, and as a bonus for those interested in pharmacological or genetic adjustment of metabolism, may lead to ways to modestly slow aging.
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