Alcohol Mostly Benign For The Liver, Causing Injury Requires Endotoxin (LPS)

InChristAlone

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Haidut I thought you said this in generative energy:
Screenshot_20171221-221210.png
 

Ritchie

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It's an interesting study, however we know rats have a significantly and markably different digestive system (among other things) to humans, I'm curious as to just how relevant this may be to humans, and how it translates to conclusions that can be confidently drawn from it in regards to people? I would think this study would need to be replicated on actual people to lend any significant weight to the conclusion drawn in the title of this thread, thoughts?
 
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haidut

haidut

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Chronic Ethanol Consumption Same As Chemical Castration

Just found a thread where I asked the exact same question (I'm getting too old for this sh*t:dead:):

Alcohol "addiction" Driven By Endotoxin (TLR4)

and Caffeine for the win:

Caffeine protects the gastric mucosa from NSAIDs and alcohol

Yes, it does have negative effects on NAD/NADH ratio but those effects are also present in any reducing sugar like glucose. I will change the title to say "benign for the liver" to make it more specific.
 
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haidut

haidut

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Haidut I thought you said this in generative energy: View attachment 7656

I did, and I will change the title to "benign for the liver" as that is what the study focused on. The current title implies alcohol is systemically benign, which I did not mean to imply. Interestingly, in lower doses of 1-2 drinks a day it has been shown to dissolve lipofuscin, and is one of the few known chemicals to do that in humans. I think the "safe" amounts will be different for everybody but in people with ALDH deficiency or any other condition leading to buildup of acetaldehyde it will probably be a mostly harmful effect. Long term alcohol consumption has serotonergic effects through 5-HT3 and that is certainly not good, but at the 1-2 drinks daily dose I think most people metabolize it too quickly to cause damage.
Anyways, title changed so it should be clearer now.
 
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InChristAlone

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I did, and I will change the title to "benign for the liver" as that is what the study focused on. The current title implies alcohol is systemically benign, which I did not mean to imply. Interestingly, in lower doses of 1-2 drinks a day it has been shown to dissolve lipofuscin, and is one of the few known chemicals to do that in humans. I think the "safe" amounts will be different for everybody but in people with ALDH deficiency or any other condition leading to buildup of acetaldehyde it will probably be a mostly harmful effect. Long term alcohol consumption has serotonergic effects through 5-HT3 and that is certainly not good, but at the 1-2 drinks daily dose I think most people metabolize it too quickly to cause damage.
Anyways, title changed so it should be clearer now.
Ok thanks. I wonder how would you know if your ALDH is not working?
 
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haidut

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Ok thanks. I wonder how would you know if your ALDH is not working?

If you get a facial and chest flush from 1-2 drinks then there is usually an issue with ALDH not working well.
 

InChristAlone

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Ok great, then mine is definitely working. I had a glass of champagne on Christmas and didn't feel anything.
 

ddjd

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Peat wrote in one of his articles that alcohol is getting a bad reputation for causing all sorts of liver disease and even liver cancer, but alcohol by itself is fairly neutral for the liver and that the role of PUFA, iron and endotoxin is being neglected by mainstream medicine. The study below confirms Peat's statements and shows that by itself alcohol was actually anti-inflammatory even when consumed at a very high daily dose. The only negative effect seen at VERY high level (40% of drinking water, HED is 2L of vodka daily) of alcohol consumption was slight fattening of the liver, which was also seen with sucrose consumption at that level. This highlights the role of inflammation (PUFA) and microbiome in chronic liver disease which medicine likes to blame on genetics and/or "addiction".

Decreased tumor necrosis factor-alpha and interleukin-1alpha production from intrahepatic mononuclear cells in chronic ethanol consumption and upre... - PubMed - NCBI
"...No significant difference in IL-la and TNF-a levels was observed between the two control groups, suggesting that the reduction in these cytokines is due to ethanol consumption. The levels of IL-la and TNF-a production seemed to decline in a time-dependent manner from 4 and 6 weeks, respectively, and remained at stable levels -16 to 20 weeks after ethanol consumption. In marked contrast, IL-6 levels remained unchanged in all groups throughout the time period. There was a decrease in the serum levels of IL-la, but not IL-6, in ethanol-fed rats, whereas TNF-a was undetectable (data not shown)."

"...To determine whether IL-6 and TNF-a production by intrahepatic mononuclear cells is affected by LPS, rats were maintained on 40% ethanol in drinking water, whereas control rats were given sucrose or isocaloric drink. After 8 weeks, all rats were injected with LPS (1.0 pgkg body weight) by the intravenous route. As shown in Fig. 3, 24 hr after injection of LPS, there was a 5-fold increase in the ALT levels that correlated with an increase in the production of IL-6 and TNF-a by cultured intrahepatic cells from ethanol-fed rats, but not control rats (Fig. 4)."

"...After 4 weeks, there was no clear change in the histological pattern in terms of fatty liver score or cellular infiltration in all groups, although fatty liver score was higher in both ethanol and isocaloric groups compared with sucrose-fed group (not shown). In no case was fibrosis seen."
Is there a significant nitric oxide increase from alcohol and would that be one of the key things responsible for the hang over symptoms?
 

Terma

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I ran an experiment on myself last night. I was abstinent from alcohol for 3 months. On Friday I took 5 grams of Phenibut, and during the Phen hangover I decided doing it two days in a row was a bad idea, so instead I purchased 12 tall cans (12x473ml) of the dirtiest beer I like 5.2%, chugged it over approximately 9 hours.

At the very beginning I took ~1 gram Vit C ascorbate, 5g taurine, 2-3g glycine, 2.4g NAC, 300mg theanine, and added small doses of taurine and theanine every few hours.

By the 10th can my intoxication was already starting to fade. After the 12th can I was about as drunk as I usually am on the 2nd can and was considering going back to the store in the morning. I went to sleep at 9am for 4 hours and woke up with a small headache, took 1/4tsp theanine with unpasteurized orange juice, and the headache is leaving. I feel a little cardiac uneasiness but that's it. On the total I likely took about 1g of theanine or less.

It processed 5.676 litres of dirty alcohol like it was nothing. Theanine is pure magic. This is my will and testament.
 

sladerunner69

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you just have to take 2 grams theanine with alcohol + glycine + NAC + and no hangover no nothing no problems it is the theanine.

2 grams of theanine would make me feel like zombified corpse. I take 500 mg of theanine and feel strange sometimes.
 

sladerunner69

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I've always felt this to be the case, but it does increase the intestinal absorption of certain things. As long as people stick to safe and natural foods without too much fat, I don't think they should necessarily be afraid of alcohol. I think the liver's vitamin A level determines part of the response.

And I don't think it 'kills brain cells,' as some grandmothers tell their kids (perhaps to keep them from drinking).

then why is it that you don't drink yourself?
 

Travis

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then why is it that you don't drink yourself?

I don't really object to it, but just not in the habit. I think the 'liver damage' induced by excessive ethanol is equally caused by vitamin A (as the same enzyme metabolizes both). So I think liver damage can be circumvented in those who drink heavily through a low-retinol diet, or conversely by avoiding ethanol for those consuming a high-retinol diet. I think it's the combination of ethanol + retinol that does it, and there are a few articles published that say as much (in more words).

But certainly I think Tanqueray™ is the best, and have liked it ever since my introduction to it.
 

sladerunner69

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I don't really object to it, but just not in the habit. I think the 'liver damage' induced by excessive ethanol is equally caused by vitamin A (as the same enzyme metabolizes both). So I think liver damage can be circumvented in those who drink heavily through a low-retinol diet, or conversely by avoiding ethanol for those consuming a high-retinol diet. I think it's the combination of ethanol + retinol that does it, and there are a few articles published that say as much (in more words).

But certainly I think Tanqueray™ is the best, and have liked it ever since my introduction to it.

Retinol causes liver damage? Or is it the combination of that and ethanol specifically? I have heard of issues with beta carotene but never retinol, and find that a bit implausible to be perfectly honest.

I concur on your choice of gin, nothing beats a cold dirty martini for me.
 

Fractality

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Is there retinol in liver? Where do all the heavy drinkers with the concomitant nutrition issues get retinol from?
 

Travis

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Is there retinol in liver? Where do all the heavy drinkers with the concomitant nutrition issues get retinol from?
The liver has such a high affinity for retinol that you could say that it almost pathologically stores it. The side-effects of excess retinol on the liver have been thoroughly detailed for decades. Let me see how many articles I can find:

Here's one: with a catchy title and free link:


The main problem these days appears to be a few pro-dairy and pro-meat bloggers and overly-optimistic content writers to feel somehow obliged to exaggerate the benefits of all things specific to animal foods while denigrating their precursors specific to plants. Retinol is a big one they latch onto to, and often give a misleading impression of its nature. The failure to specify the danger from high amounts coupled with capitalistic madmen selling 50,000∙IU tablets—and mixed with a dash of naïve 'more is better' psychology—necessarily lead to more-than-a-few people these days still getting liver damage from excessive retinol in spite of all the scientific evidence precisely detailing it. Only just here, on this very forum, I've talked to three cases of high-dose vitamin A induced liver issues. All this is not to say that a reasonable dose couldn't be beneficial, but many people are already getting more-than-reasonable doses from food. Beta-carotene is a precursor whose cleavage is regulated transcriptionally by enteral enzymes in a negative feedback manner, a second form of endogenous retinol control in addition to the tightly-regulated retinol ⟶ retinoic acid activation. Despite sometimes very high levels of liver retinol, serum concentrations remain in a surprisingly-narrow range. I think this could be seen as why liver concentrations can buildup pathologically: to prevent serum retinol overload. We had evolved under conditions that wouldn't allow for frank vitamin A poisoning save for those few cases resulting from eating polar bear liver—as reported in early arctic explorers. But hypervitaminosis A is essentially impossible to induce with natural food otherwise, this being merely a phenomenon of dysregulated supplement salesmen and general fat-soluble vitamin cheerleading.
 
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Fractality

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But hypervitaminosis A is essentially impossible to induce with natural food otherwise, this being merely a phenomenon of dysregulated supplement salesmen and general fat-soluble vitamin cheerleading.

I'm guessing this means that 7-10 oz of beef/calf liver a week wouldn't induce hypervitaminosis A? Would that amount be a problem with chronic drinking (defined as more than 1-2 drinks daily for a male).
 

Travis

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I'm guessing this means that 7-10 oz of beef/calf liver a week wouldn't induce hypervitaminosis A? Would that amount be a problem with chronic drinking (defined as more than 1-2 drinks daily for a male).
I'm not sure, but the carotenes are cleaved as needed and are under yet another regulatory step (the conversion of retinol to retinoic acid is already under three, which keeps blood levels remarkable constant). A vegan may argue that consuming retinol is less natural and its toxicity stems from that; because like heme iron, the body tends to absorb it at a relatively high and constant rate. The amount stored in the liver is highly variable between people and I don't think consuming liver once a week would lead to higher-than-average levels (although a person could argue that even normal levels are high assuming we evolved consuming carotenes).
 
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