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| Old Order Amish, evolving - naturally |
Shocking news for creationists yesterday!
Fundamentalist Christian creationists have been caught evolving and breaking one of the sacred creationist dogmas - that all mutations are harmful and degenerative. This was discovered in a group of appropriately-named Old Order Amish from Indiana, USA.
Due to a mutation, they are living 10% longer compared to those members of the same Amish group without the mutation.
This was discovered by researchers led by Sadiya S. Khan, Sanjiv J. Shah and Douglas E. Vaughan, et al, from Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
The first genetic mutation that appears to protect against multiple aspects of biological aging in humans has been discovered in an extended family of Old Order Amish living in the vicinity of Berne, Indiana, report Northwestern Medicine scientists.
An experimental “longevity” drug that recreates the effect of the mutation is now being tested in human trials to see if it provides protection against some aging-related illnesses.
Indiana Amish kindred (immediate family and relatives) with the mutation live more than 10 percent longer and have 10 percent longer telomeres (a protective cap at the end of our chromosomes that is a biological marker of aging) compared to Amish kindred members who don’t have the mutation, reports the new Northwestern study.
Amish with this mutation also have significantly less diabetes and lower fasting insulin levels. A composite measure that reflects vascular age also is lower — indicative of retained flexibility in blood vessels in the carriers of the mutation — than those who don’t have the mutation, the research also found.
The paper was be published Nov. 15 in the journal Science Advances.
These Amish individuals have very low levels of PAI-1 (plasminogen activator inhibitor,) a protein that comprises part of a “molecular fingerprint” related to aging or senescence of cells. It was previously known that PAI-1 was related to aging in animals but unclear how it affected aging in humans.
“The findings astonished us because of the consistency of the anti-aging benefits across multiple body systems,” said Dr. Douglas Vaughan, the lead author of the paper who has been studying PAI-1 for almost 30 years.
Their findings are published open access in ScienceAdvances.
Abstract
Plasminogen activator inhibitor–1 (PAI-1) has been shown to be a key component of the senescence-related secretome and a direct mediator of cellular senescence. In murine models of accelerated aging, genetic deficiency and targeted inhibition of PAI-1 protect against aging-like pathology and prolong life span. However, the role of PAI-1 in human longevity remains unclear. We hypothesized that a rare loss-of-function mutation in SERPINE1 (c.699_700dupTA), which encodes PAI-1, could play a role in longevity and metabolism in humans. We studied 177 members of the Berne Amish community, which included 43 carriers of the null SERPINE1 mutation. Heterozygosity was associated with significantly longer leukocyte telomere length, lower fasting insulin levels, and lower prevalence of diabetes mellitus. In the extended Amish kindred, carriers of the null SERPINE1 allele had a longer life span. Our study indicates a causal effect of PAI-1 on human longevity, which may be mediated by alterations in metabolism. Our findings demonstrate the utility of studying loss-of-function mutations in populations with geographic and genetic isolation and shed light on a novel therapeutic target for aging.
Sadiya S. Khan, Sanjiv J. Shah, Ekaterina Klyachko, Abigail S. Baldridge, Mesut Eren, Aaron T. Place, Abraham Aviv, Eli Puterman, Donald M. Lloyd-Jones, Meadow Heiman, Toshio Miyata, Sweta Gupta, Amy D. Shapiro and Douglas E. Vaughan
A null mutation in SERPINE1 protects against biological aging in humans
Science Advances 15 Nov 2017: Vol. 3, no. 11, eaao1617, DOI: 10.1126/sciadv.aao1617
Copyright © 2017 The Authors
Published open access
Reprinted under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0)
Biologically, this is interesting in so far as it looks like a single mutation has produced three different beneficial conditions all associated not only with longevity but also with health in old age. The protective telomeres on the end of chromosomes is 10% longer with the mutation; fasting insulin levels are lower, reducing the incidence of diabetes, and the blood vessels remain soft and flexible. All three of these are regarded as indexes of ageing.
The findings astonished us because of the consistency of the anti-aging benefits across multiple body systems. For the first time we are seeing a molecular marker of aging (telomere length), a metabolic marker of aging (fasting insulin levels) and a cardiovascular marker of aging (blood pressure and blood vessel stiffness) all tracking in the same direction in that these individuals were generally protected from age-related changes. That played out in them having a longer lifespan. Not only do they live longer, they live healthier. It’s a desirable form of longevity. It’s their ‘health span.’
So here we have an example of a mutation which is undoubtedly beneficial to the carrier. Whether it translates into a benefit to the mutant alleles itself is another matter because it is unlikely to contribute directly to more surviving offspring - the real test of biological 'fitness'. However, having longer-lived grandparents might well be beneficial to the next generation. But that's not the point here; the point is that this mutation can't be regarded as harmful.Dr. Douglas Vaughan, corresponding author
Irving S. Cutter Professor and chairman of medicine
Northwestern University Feinberg School of Medicine and Northwestern Medicine.
Irving S. Cutter Professor and chairman of medicine
Northwestern University Feinberg School of Medicine and Northwestern Medicine.
The problem is that creationist dogma says that all mutations are harmful and therefore evolution can't progress by a process of selecting for a new mutation that conveys some new or improved attribute. This comes from their equally dogmatic and evidence-free claim that somehow information theory means no new information can be created but is can be lost and that mutation is a loss of information.
It should follow then that the new information which causes telomere length to reduce more lowly, for fasting insulin levels not to rise and for the blood vessels not to harden just can't be there.
And yet it is. And it is there in a population of people who don't believe in it - by religious dogma. The dogma is refuted by the observable evidence.
Of course, regardless of the absurdity of insisting that no new information can arise when gene duplication is a well attested occurrence and even whole genome duplications are not unknown, what we have here is not new information but a change in existing information. The only thing to be said for the claim that information theory forbids this is that either information theory has been misunderstood or misapplied, or it is wrong. Given creationists propensity for misrepresenting scientific theories, the probability lies with the former - they've lied about it again.
Now we have living, walking and slowly ageing creationist to prove it for us.
I love these little ironies!
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