It is interesting that the MRI findings on brain recover modestly in the first week of abstinence, then from 1 week to 1 month more recovery happens and by ~7 months a very substantial recovery of brain thinning.
The areas that repair in the first month, and especially the first week of abstinence have to do with areas that will have you want to drink more alcohol. So making it through a week of abstinence is a lot of work - then by a month, probably easier to maintain.
Anyway - I doubt that the brain effects that may be negative are mitigated by other chemicals. Along with that …. People have to live and have fun. If this is part of someone’s quality of life and enjoyment … go to it, as long as it is bringing good things to you.
For many it doesn’t, but for some it does. I’d guess it does uniformly decrease life and healthspan … but for some not drinking decreases quality of life …
I have found it interesting recently that my MCV has been going down even though I have been drinking a bit more than normally. (although the last couple of days have been on the wagon). I think that is because I have been taking melatonin before drinking.
I’d make sure iron studies are stable, as generally the opposite is the case with alcohol as it suppresses hepcidin and has you absorb more iron and due to multiple mechanisms should drive your MCV up or keep it stable.
A dropping MCV can be an early sign of occult blood loss … and I’d generally think looking at Ferritin, Transferrin Sat, Serum Fe and make sure nothing has happened to suggest some losses … just as a precaution — if you’ve not already done that … as you monitor everything very thoroughly.
It depends if Ferritin and Transferrin sat coming down - that can be worrisome for blood loss … Iron studies are complicated and as much as Ferritin in a situation of inflammation can elevate— a dropping ferritin can be due to dropping iron stores.
More information from the UK Biobank on the impact of alcohol on organ aging. The impact seems to be almost as bad as smoking, at least for some organs (though red wine seems to get a pass).
We’re back to Tony Wyss-Corsay and colleagues with a recent preprint of their study of 44,000 UK Biobank participants, 3,000 plasma proteins, for 11 organ-specific clocks. This work fully replicated their earlier publication but again there were a notable extension of findings.
Seen below is the relationship of various interventions including smoking, alcohol, moderate or vigorous exercise, foods on organ-specific age gaps.
I love LDN, I started it while in fertility treatment (not in treatment anymore) and continue 4.5mg now. A warning is if you are hypothyroid esp Hashimoto get everything retested after 4-6 weeks.
Why many studies wrongly claim it’s healthy to drink a little alcohol
It is becoming clear that any amount of alcohol is harmful, so why do so many studies claim that moderate drinking could help you live longer?
Drinking even small amounts of alcohol reduces your life expectancy, rigorous studies show. Only those with serious flaws suggest that moderate drinking is beneficial. That’s the conclusion of a review of 107 studies looking at how drinking alcohol affects people’s risk of dying from any cause at a particular age.
“People need to be sceptical of the claims that the industry has fuelled over the years,” says Tim Stockwell at the University of Victoria in Canada. “They obviously have a great stake in promoting their product as something that’s going to make you live longer as opposed to one that will give you cancer.”
While the risks of moderate drinking are small, people should be told that it isn’t beneficial, says Stockwell. “It’s maybe not as risky as lots of other things you do, but it’s important that consumers are aware,” he says. “I think it’s also important that the producers are made to inform consumers of the risks through warning labels.”
But he points out that it doesn’t consider the social aspects of moderate drinking. “It is healthier to socialise without the need for alcohol, but the benefits of spending time with others is still likely to be greater than the risk from the consumption of one to two units of alcohol,” he says. “The challenge being perhaps limiting alcohol intake in this way.”
Why Do Only Some Cohort Studies Find Health Benefits From Low-Volume Alcohol Use? A Systematic Review and Meta-Analysis of Study Characteristics That May Bias Mortality Risk Estimates
Oddly enough studies seem to concentrate on coming to a conclusion in the round about alcohol rather than looking at mechanisms to reduce the harm from alcohol. (other than abstinence).
Alcohol consumption can have significant negative effects on the brain, but it does not directly “kill” brain cells in most cases. Rather, alcohol can damage neurons and disrupt brain function through various mechanisms.
Mechanisms of Alcohol-Induced Brain Damage
Disruption of Calcium Homeostasis
Alcohol causes a rapid, dose-dependent increase in intracellular calcium levels in neurons
This sustained increase in calcium may be a key factor in alcohol-induced neuronal death ([1])
Oxidative Stress and Inflammation
Alcohol increases oxidative stress and proinflammatory proteins in the brain
These factors contribute to neurotoxicity and neurodegeneration ([2])
Blood-Brain Barrier Dysfunction
Excessive alcohol consumption can damage the blood-brain barrier
This may lead to changes in endothelial cell tight junctions and white matter thickness ([3])
This leads to increased expression of TRAIL death receptors and neuronal apoptosis ([4])
Effects on Brain Structure and Function
Brain Atrophy
Chronic alcohol abuse can lead to loss of both gray and white matter volumes ([5])
Neuronal Loss
Specific brain regions, particularly corticolimbic areas, are sensitive to alcohol-induced neurodegeneration
This can result in cognitive deficits and learning impairments ([2])
Impaired Neurogenesis
Alcohol can inhibit the formation of new neurons in the hippocampus
This may contribute to cognitive and memory deficits ([2])
Long-Term Consequences
Fetal Alcohol Spectrum Disorders (FASD)
Alcohol exposure during pregnancy can cause massive neuron death in the developing fetal brain
This leads to permanent structural and functional damage ([6])
Chronic Neurologic Effects
Long-term alcohol abuse can result in cerebellar ataxia, peripheral neuropathy, and Wernicke-Korsakoff encephalopathy ([7])
Potential for Recovery
Brain regeneration may occur during abstinence from alcohol
This includes the proliferation of new cells in multiple brain regions, including new neurons in the hippocampus ([2])
Conclusion
While alcohol does not directly “kill” brain cells in most cases, it can cause significant damage to neurons and disrupt brain function through various mechanisms. Chronic alcohol abuse can lead to lasting structural and functional changes in the brain, but some recovery may be possible with abstinence.
References
Intracellular calcium plays a critical role in the alcohol-mediated death of cerebellar granule neurons. (Journal of neurochemistry, 2013)
Mechanisms of neurodegeneration and regeneration in alcoholism. (Alcohol and alcoholism (Oxford, Oxfordshire), 2009)
Effect of alcohol on the central nervous system to develop neurological disorder: pathophysiological and lifestyle modulation can be potential therapeutic options for alcohol-induced neurotoxication. (AIMS neuroscience, 2021)
TRAIL Mediates Neuronal Death in AUD: A Link between Neuroinflammation and Neurodegeneration. (International journal of molecular sciences, 2021)
Brain atrophy and neuronal loss in alcoholism: a role for DNA damage? (Neurochemistry international, 2000)
Alcohol and the Developing Brain: Why Neurons Die and How Survivors Change. (International journal of molecular sciences, 2018)
Chronic Neurologic Effects of Alcohol. (Clinics in liver disease, 2019)
Parental Alcohol Exposures Associate with Lasting Mitochondrial Dysfunction and Accelerated Aging in a Mouse Model
We find that even in middle life (postnatal day 300), the adult offspring of alcohol-exposed parents exhibited significant increases in markers of stress-induced premature cellular senescence in the brain and liver, including an upregulation of cell cycle inhibitory proteins and increased senescence-associated β-galactosidase activity. Strikingly, in the male offspring, we observe an interaction between maternal and paternal alcohol use, with histological indicators of accelerated age-related liver disease in the dual-parental offspring exceeding those induced by either maternal or paternal alcohol use alone. Our studies indicate that chronic parental alcohol use causes enduring mitochondrial dysfunction in offspring, resulting in a reduced NAD+/NAHD ratio and altered expression of the NAD±dependent deacetylases SIRT1 and SIRT3. These observations suggest that some aspects of FASDs may be linked to accelerated aging due to programmed changes in the regulation of mitochondrial function and cellular bioenergetics.
“While no associations were found for low- or moderate-risk drinking patterns vs occasional drinking among individuals without socioeconomic or health-related risk factors, low-risk drinking was associated with higher cancer mortality”
