AJKOER
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Thoughts on Chemical Radical Connection Between Alcohol Consumption and Aging
NOTE: Not sure if this forum or Miscellaneous is best for this topic, I have, at least, temporarily re-posted. I would expect, however, somewhat
different comments from each forum.
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It recently occurred to me a possible explanation as to why people who consume excess amounts of alcohol appear to be visually aging more rapidly.
So what is this possible chemical explanation for this hypothetical observation? One path could be that the presence of alcohol in the blood may serve
as a preferable medium to foster the existence and life spans of solvated electrons. The latter, in turn, could promote the creation of so-called free
radical species in the body. For example, in the presence of dissolved oxygen, an electron could potentially produce the superoxide radical anion. The
presence of free radicals, in general, may likely damage DNA with associated acceraled radical activity. This then would lead to elevated oxidative
stress in the body and hypothetically, seemingly an observable accelerated related aging effect.
As to why this hypothesis is not more fully known or has been widely promulgated, likely relates, in my opinion, to human’s entertainment use of
alcohol over recorded time and commercial interests.
Research, for example, brings up this comment at this site https://www.promises.com/addiction-blog/6-ways-alcohol-ages to quote:
“Depletion of vitamin A and other healthy nutrients – Alcohol can impact your nutrition levels by depleting healthy nutrients that help carry
oxygen throughout your body. Alcohol depletes vitamin A levels in particular, and this vitamin is a crucial antioxidant for your skin and body as it
aids in the formation of new cells.”
“If you drink too much or too frequently, you speed up the aging process by accelerating collagen loss. Skin is already delicate and vulnerable to
the elements — wind, smog, smoke and the sun. When you drink, you are hastening the aged, weathered look of your skin.”
I agree with the above, but the explanations presented are not quite as targeted as my thoughts as to the precise initiating radical pathways.
[Edited on 14-8-2021 by AJKOER]
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paulll
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Seems plausible anyway - EtOH also tanks glutathione, which is a pretty important antioxidant.
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Texium
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Quote: Originally posted by AJKOER  | | I agree with the above, but the explanations presented are not quite as targeted as my thoughts as to the precise initiating radical pathways.
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I assume you meant to say, "the explanations presented make a lot more sense than my batshit free radical
proposition."
How does your "explanation" actually add at all to what's already known, beyond wildly speculating about solvated electrons in blood?
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AJKOER
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| Quote: Originally posted by Texium | | Quote: Originally posted by AJKOER | | I agree with the above, but the explanations presented are not quite as targeted as my thoughts as to the precise initiating radical pathways.
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...
How does your "explanation" actually add at all to what's already known, beyond wildly speculating about solvated electrons in blood?
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Texium:
Here is a source https://www.electrochem.org/biology-medicine that you may find interesting, referring to the body’s natural electrical activity, to quote:
"Detecting health problems
Besides treating health problems, electricity can also be used to detect them. Recording devices now turn the body’s natural electrical activity
into diagrams that doctors then use to analyze medical problems. Physicians now diagnose heart abnormalities with electrocardiograms (ECGs), brain
disturbance with electroencephalograms (EEGs), and loss of nerve function with electromyograms (EMGs)."
The presence of electricity likely leads to solvated electrons (especially in an enriched EtOH medium). Then, relating particularly to possible
radical activity:
O2 + e-(aq) = .O2- (aq)
which is the creation of the superoxide radical anion. The latter is well known in the biochemistry literature.
Also, organic chemists work with redox couples adjusted for pH in the presence of alcohol to produce breakdown products (the reaction chain I would
depict as: e-(aq) + H+ = .H the hydrogen atom radical, which further could react as follows: ROH + .H = .R + H2O).
The focus of my thread is the impact of EtOH (and potentially other uncited reagents) on solvated electron concentration in the particular area of
alcohol impacts on the human body with respect to aging.
Note: My suggested (perhaps obvious to some) explanation is more informative than simply stating that, for example, Vitamin A, is somehow destroyed by
alcohol, and the loss of this vitamin produces aging effects.
[Edited on 15-8-2021 by AJKOER]
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Texium
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You’d be dead of alcohol poisoning long before you’d have enough alcohol in your bloodstream to affect its solvent properties. Offering an
explanation that is based solely on speculation is not “more informative,” it’s just connecting dots that likely have no real connection. It’s
not like you’re the first person to ever ponder this. Here’s a paper from 1986 that goes into detail about the underlying mechanisms of various
vitamin deficiencies in alcoholics. And guess what, it doesn’t invoke solvated electrons or radicals (so you probably aren’t interested in reading
it). Additionally, it’s widely agreed that one of the main reasons for vitamin deficiency is simply because alcoholics tend to eat less, since a lot
of their calorie intake is alcohol based, and thus they miss out on all the vitamins and minerals that come with eating a sufficient amount of actual
food. All of your “research” seems to come from pop sci and “health” sites rather than actually digging into the literature…
Attachment: hoyumpa1986.pdf (934kB)
This file has been downloaded 338 times
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andy1988
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I've had my eye on research on 'alcohol induced gut dysbiosis' for a number of months. I started thinking about that after reading on different
species found in the gut, colostrum, and reading about ethanol-tolerant yeast strains. The argument being that the distribution of metabolites
produced by a gut microbiome consistently fed alcohol may be less beneficial than without.
With regards to the alcohol consumption increasing free radical production I think if it exists it would be transient and insignificant compared to a
condition where oxidative stress is persistent. It is hard to reason about relative risk of things. Maybe it could use with some better mathematical modeling?
On the subject of consumption of a beverage and aging, I found this research to be interesting:
| Quote: |
Tucker investigated the relationship between telomere length and both milk intake frequency (daily drinkers vs. weekly drinkers or less) and milk fat
content consumed (whole vs. 2% vs. 1% vs. skim). Telomeres are the nucleotide endcaps of human chromosomes. They act like a biological clock and
they’re extremely correlated with age; each time a cell replicates, humans lose a tiny bit of the endcaps. Therefore, the older people get, the
shorter their telomeres.
And, apparently, the more high-fat milk people drink, the shorter their telomeres are, according to the new BYU study, published in Oxidative Medicine
and Cellular Longevity. The study revealed that for every 1% increase in milk fat consumed (drinking 2% vs. 1% milk), telomeres were 69 base pairs
shorter in the adults studied, which translated into more than four years in additional biological aging.
Somewhat surprisingly, he also found that milk abstainers had shorter telomeres than adults who consumed low-fat milk.
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P.S. On the subject of mathematical modeling in a biological context I found this UoU author's work to be inspiring.
[Edited on 16-8-2021 by andy1988]
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AJKOER
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Upon reviewing Texium cited 1986 work, I quote the following:
"pyrazole, an inhibitor of ethanol oxidation, either alone or with ethanol, abolishes the stimulatory effect of ethanol. "
which suggests to me that pyrazole is a radical (inclusive of the solvated electron) scavenger, and thus would not constitute refuting evidence to my
proposed radical path.
On the reference to telomeres, I find the cited study to be more correlative in nature than causatively suggestive.
Also, thanks for the great references, in particular, per a source provided above (namely, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551541/ ), to quote:
"Exogenous free radical production can occur as a result from exposure to environmental pollutants, heavy metals (Cd, Hg, Pb, Fe, and As), certain
drugs (cyclosporine, tacrolimus, gentamycin, and bleomycin), chemical solvents, cooking (smoked meat, used oil, and fat), cigarette smoke, alcohol,
and radiations [15–25]. "
Did someone else also note the word 'alcohol' above?
So, given the ascribed link between free radical production and alcohol, could someone please postulate a theoretical mechanism (other than my
postulated simple solvated electron augmentation path) that would be significant enough to warrant placing alcohol on the list with cigarette smoke as
cited above?
Thanks
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Honestly, I do not strongly support my position but find other conceivable possibilities to be much weaker!
[Edited on 16-8-2021 by AJKOER]
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