tyw
Member
I think the centarians and thyroid is essentially a look at thyroid levels near the end of life,they are close to death regardless of being a centarian,they are winding down metabolically.
Could we not construe the study as high RT3 as pushing them closer to death.
Lower active thyroid hormone Its protective to a certain point ,beyond this point is dangerous as with RT3 having a protective effect to a certain point.
I think we would need a full thyroid work up from 80 years old and on to deduce anything from this.
See Mittirs post here on the okinawan diet and longevity,it's an interesting angle,Peat mentioned it before and other have also,the Japanese are notorious for lying about older people's age,some were dead already for 20 years as their children kept collecting their pension and pocketing it.
One example of pension fraud .Sogen Kato - Wikipedia
Mittirs post Epidemiological Evidence?
The amount of Thyroid related hormones is a fine balancing act. And just like my comments with Vit A, D, and Calcium, what is "high Thyroid" for one person is not necessarily considered "high" for another person.
The second paper I quoted showed analysis for Askenazi Jew showed normal T4 and a lot more TSH compared to aged matched subjects. ie: this was not just "at the end of life", and the patterns were observed even 30-40 years prior to death.
These people are different, and what consists "hypothyroid" to the mainstream establishment is not pathological to them.
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There are enough cases of legitimately verified centenarians on Okinawa to rightfully say that it is an anomaly in terms of greater longevity.
Why? All we can say right now is that they are that way because they are born that way.
Sure, we don't know with certainty but don't you think we have enough evidence pointing in the same direction? Aspirin and caffeine may not be enough as examples but there are others that added up together to paint pretty much the same picture.
Pregnenolone Increases Maximum Lifespan By 60% (animal Model)
Inhibiting Serotonin During Protein Feeding Doubles Maximum Lifespan
Blocking Serotonin Extends Lifespan By 40%, Triples Youthspan
Serotonin Antagonists Extend Lifespan, SSRI Dramatically Shorten It
[INSERT HERE ALL THE STUDIES ON LIFESPAN EXTENSION BY RESTRICTING TYPROPHAN/METHIONINE/CYSTEINE]
So, I am not asking for a definitive answer as I know there is none currently. But when you have all of these chemicals extending maximum (and sometimes average) lifespan the question naturally arises - assuming they all work (and it is a big assumption until more is known) what is the common mechanism behind them. Is there a least common denominator of action so to speak? Well, there may be more than one but the one we do know about is that these all have the effect of increasing RMR. So, if you know of another plausible explanation (even though it may be speculative) please share it as I would like to follow up on it. My post is not so much about "hey these things work" as it about "IF these things work, what else other than metabolism can you suggest as a mechanism".
So, happy to hear your comments on that one.
These are not necessarily mechanism that involve Metabolism, and definitely not about mechanisms that support the idea of increasing metabolism.
Firstly, I will caution against almost any study that is not a human study when discussing human longevity. We are so different to the rest of the animals out there (even primates), that any such comparison is either not very significant, or invalid.
If one really wants to see how complicated the field of Human Longevity is, I have recommended the book 'Human Longevity' by Dave Valentine before. It is expensive, but it will give a full picture about how everything from PUFA regulation to ROS regulation to oxygen restriction to select tissues, are adaptations that humans have geared towards longevity.
Another one of the reasons why I am so against animal studies, is because the Aging process has so many dependent variables depending on the organism in question.
There are the extremes of organisms that start aging the moment they are sexually mature, and then there are Humans, for which aging is controlled largely by the brain (unless there is sudden trauma to other parts of the body).
This isn't a universal mechanic, since you will find similar levels of PUFA in the brain of long-lived pigeons, and short-lived rats -- The Long Life of Birds: The Rat-Pigeon Comparison Revisited .... in other words, the brain does not set the pace of aging for Birds.
The human brain is unlike any other brain, and the regulatory mechanisms that provide for all this hormone regulation must work in concert with the rest of the body in very complex ways that we do not understand.
That is to say, the healthy aged person's brain is able to maintain their "youthful hormonal profile".
Can you replace this using exogenous means? Maybe, but there will be a lot of tweaking required, and there is risk of a hard dependency on exogenous compounds (by shutting down endogenous production or feedback pathways).
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Unfortunately, there is no single theme that any of the mechanisms described above are converging upon.
Even something like serotonin is subject to regulation by so many uniquely-human factors, that it isn't just a simple matter of "reduce incoming serotonin from food and gut bacteria" (which doesn't answer "how do the serotonergic neurons in the CNS respond to this negative feedback")
Even something like brain responsiveness is not just about energetics, and even if it were just about "more energy is better", then one has to explain all the various mechanisms that the brain has to restrict oxygen and substrate use, and rely heavily on lactate for fuel, and then come to a conclusion as to which regions of the brain should be given more energy, at what times, for how long, etc, etc ....
The only unifying factor that I see in all this study, is "Efficiency" -- energy used when it needs to be used, just enough to deal with the incoming stimulus, and while producing as little waste products (including heat) as possible.
We see this in mitochondria, where those of the longest lived organisms are those which manage to produce little ROS (through whatever means). We see this is the brain, where the most responsive to stimuli are those that are able to relax nervous system potentials and fire them very quickly at will, vs the "always on, high metabolic rate, high waste product" schizophrenic brain:
- Molecular Psychiatry - Mitochondrial dysfunction in schizophrenia: evidence for compromised brain metabolism and oxidative stress
- http://www.sciencedirect.com/science/article/pii/S0925492705002052
We have no idea how to achieve this in a generalised manner . All useful strategies are purely defensive strategies, used to avoid damaging stressors when the body is not ready or able to handle them.
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