Thanks for the response. I know you closely monitor your biomarkers, and your RHR would be enviable even in a nondrinker. You may be a rare specimen whose health is at least partially immune to the effects of alcohol. Just like many posters here seem to be age-defiant, I hope you can continue to defy the conventional wisdom that says drinking is bad for you.

I don’t think my health is immune to the effects of alcohol. I think I am doing sufficient with the biochemistry with a limited amount of exercise and some focus on sleep that even with the effects of alcohol (reduced by my biochemical approach to it) my health is good enough that I don’t think I should stop entirely. When I do drink it is not a trivial quantity.

I wonder sometimes if I stopped drinking entirely whether HbA1c and ALP would both go up. They are both reduced by alcohol. My last results were 4.8% and 43IU

These figures are both known to be reduced by alcohol. In theory lower is better (up to a point), however. This is what I mean by pleiotropic.

I do not recommend anyone else follows my approach with alcohol. I may test a few weeks off it, however.

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How is your liver doing, have you measured it comprehensively with tests from different perspectives?

Last week ALT 19.5, ALP 43. AST 26.5, GGT 27.4, Bilirubin 9.34 mcmol/l.
Generally around these.

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Is that enough to check for possible cumulative damage to liver, regarding like liver cirrhosis?
What I mean with that, how does the numbers change when the liver doesn’t function properly?

Might it be a sudden change and thus you didn’t prevent it? (Is there other tests?)

Remember I have these figures for pretty well every week over the last two years.

Yes but I was wondering if they could measure relevant possible alcohol related changes to the liver or if it’s too late when if or when it happens. I’m not implying I have the answer implicitly, just wondering.

They are what people use to track these things. Also MCV. MCV is still a bit elevated, but was a lot more elevated.

Here’s what Perplexity thinks:

There are several methods used to measure and detect alcohol-related changes to the liver before significant damage occurs:

  1. Alcohol biomarkers: Certain biomarkers in the blood can indicate excessive alcohol consumption and potential liver injury. These include:
  • Gamma-glutamyl transferase (GGT): Elevated levels suggest heavy alcohol use and early liver damage.[1][2]
  • Carbohydrate-deficient transferrin (CDT): Increased levels indicate sustained heavy drinking over the past 2-3 weeks.[2]
  • Phosphatidylethanol (PEth): Levels above 80 ng/mL indicate at least 4 drinks per day over the past 2-4 weeks.[2]
  1. Liver function tests: Blood tests like alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin can detect early liver inflammation or injury from alcohol.[1][3]

  2. Imaging tests: Ultrasound, CT, or MRI scans can detect fatty liver (steatosis), which is often the earliest stage of alcohol-related liver disease. These imaging modalities can also assess liver stiffness, indicating fibrosis.[4]

  3. Transient elastography (FibroScan): This non-invasive technique uses ultrasound to measure liver stiffness, which correlates with the degree of fibrosis or scarring in the liver due to alcohol exposure.[5]

  4. Liver biopsy: Although invasive, a liver biopsy can provide a definitive diagnosis of early alcohol-related liver disease, such as steatohepatitis (inflammation and fat accumulation), before cirrhosis develops.[1][3]

Early detection of alcohol-related liver changes is crucial, as abstaining from alcohol at this stage can potentially reverse the damage and prevent progression to more severe forms of liver disease like cirrhosis.[1][3]

Citations:
[1] https://www.msdmanuals.com/home/liver-and-gallbladder-disorders/alcohol-related-liver-disease/alcohol-related-liver-disease
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9666811/
[3] Alcohol-related Liver Disease > Fact Sheets > Yale Medicine
[4] Alcohol-related liver disease - Diagnosis - NHS
[5] Alcohol-related liver disease (ARLD) - British Liver Trust

What about MRI, ultrasound, FibroScan, possible liver biopsy (risks with these)?

If 10 is damage enough to be detected in blood test, you’d probably want to see on the scale of 1-10 when it is 3, then going to 4, and then 7, etc, is my point. Could the imaging tests do that? Or is just damage on blood tests enough?

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@John_Hemming

Besides the liver, a recent study in the BMJ showed that even moderate drinking–8 to 12 drinks a week–shrinks the hippocampus, and the shrinkage increases over time.

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I take the view if the blood tests put me in the “good” territory and are consistently there (and in fact have improved over the testing period) I am not inclined to look further.

There is no doubt that continually drinking is worse than having breaks.

Hence I am well aware when I am drinking and what effect that has on biomarkers. I have found it interesting that the biomarkers are now suffering less from drink than they were doing. I also record in some detail what I drink.

My advice to others is that if you drink make sure you have some days ideally in sequence when you take no alcohol at all.

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My observation of relatives and friends who regularly drank a lot is that there is a genetic factor involved. Some seemed to be immune to developing cirrhosis of the liver while others developed it at a fairly young age. Also, I know drinkers that never seem to have a “hangover” from drinking.

“The development of cirrhosis is a complex process influenced by various factors, and not all heavy drinkers will necessarily develop the condition. Early recognition and abstinence from alcohol are crucial in preventing progression to advanced liver disease.”

I am a believer that life is more than being health conscious.
I rarely drink just because I don’t like the effects that even a moderate amount of alcohol has on me. It interferes with my sleep and I can have a hanger from just a few beers.

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Some good news on Melatonin and AMD:

Question What is the association between melatonin use and the development and progression of age-related macular degeneration (AMD)?

Findings In this cohort study of 121 523 patients with no history of AMD aged 50 years or older, taking melatonin was associated with a decreased risk of developing AMD. Likewise, among 66 253 patients with preexisting nonexudative AMD, melatonin supplementation was negatively associated with the rate of progression to exudative AMD.

Meaning These findings provide a rationale for expanding clinical research on the potential therapeutic efficacy of melatonin in preventing AMD development or its progression.

Source: Melatonin and Age-Related Macular Degeneration Risk

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Interestingly high dose melatonin on Reddit (not the font of all wisdom) is thought to be 30mg. This survey probably only has people in the 0.3-20mg range.

It would be interesting to find out what the effects are of dosing say over 0.5g per night.

I think the main mechanism of action of melatonin is the protection of mitochondrial DNA from damage. There do seem to be other links to things like autophagy, but I think the main mechanism is reducing deterioration.

The bodies other systems then can work on improving mitochondria.

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If you mega dose, take it two hours before bed. You’ll feel better in the morning.

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Its probably an HPA cycle issue where you need to take it one or two cycles before bed. More recently I have been experimenting with melatonin during the day. However, I am avoiding having it in the HPA cycle before going to bed.

I tried dissolving some in whisky. That did not work that well, but I swigged about a gram of melatonin around midday in some whisky. This did cause me to require about a 15 minute nap.

I will drink the rest of the melatonin powder I tried to dissolve in alcohol in the near future, but I am trying to work out the effects on a multi day basis. I also have a couple of gigs (one was today at 5pm) and I need to plan around those.

Melatonin is a bit soluble in alcohol. Reading up on it it is perhaps more soluble in DMSO. However, I am more tempted by drinking whisky than DMSO. However, science may require a swigging of melatonin dissolved in DMSO.

One thing I have noticed since I have started taking melatonin prior to drinking is that my MCV which is a bit high because of my drinking has been going gently down. Still above 90 femtolitres, however.

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Everyone responds a little differently. When I take it 2 hrs before bedtime I have trouble staying awake until bedtime. I take it ~1 hour bfbt.
I am currently taking 500 mg when I get up in the morning. It does not affect my daytime sleepiness.

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https://www.melatonin-research.net/index.php/MR/issue/archive

Lots of research on melatonin here. Sorry if already posted.

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https://onlinelibrary.wiley.com/doi/10.1111/jpi.12782

“Overall, there has been limited adverse events reporting from high-dose melatonin studies. Based on this limited evidence, melatonin appears to have a good safety profile. Better safety reporting in future long-term trials is needed to confirm this as our confidence limits were very wide due to the paucity of suitable data.”

“Randomised controlled trials investigating high-dose melatonin (≥10 mg) in human adults over 30 years of age were included.”

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Melatonin: a multitasking molecule

“…by virtue of its ability to detoxify free radicals and related oxygen derivatives, melatonin influences the molecular physiology of cells via receptor-independent means. These uncommonly complex processes often make it difficult to determine specifically how melatonin functions to exert its obvious actions. What is apparent, however, is that the actions of melatonin contribute to improved cellular and organismal physiology. In view of this and its virtual absence of toxicity, melatonin may well find applications in both human and veterinary medicine.”

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