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This is a knowledge network extract, and will likely be somewhat hard to understand

Thoughts

Small amounts, ~ drink per day, at night, to help with waste clearance and fat transport

glymphatic system. researchers have demonstrated through experiments with genetically modified mice that the proper function of the glymphatic clearance system was necessary to remove soluble amyloid-beta from the brain interstitium.

Part of the benefit is from ethanol’s esterfication of cholesterol, which is part of the process by which HDL takes up and transports cholesterol (which is either in excess, being released by adopocytes for energy or is a product of macrophage digestion of oxidized cholesterol). This also appears to have the effect of downregulating the creation of more cholesterol, reducing total cholesterol.

(for others) Check genome SNPs associated with ADH and ALDH.

Notes

  • Don’t mix ethanol with TUDCA

Info

  • Alcohol intake increases HDL-C in a dose-dependent fashion, associated with and possibly caused by an increase in the TR [transport rates] of HDL apolipoproteins apoA-I and -II.

Genes

The main metabolic pathway for ethanol involves the enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).

Selfhacked

Ethanol is metabolized to acetaldehyde by three enzymes: 1. Alcohol dehydrogenase metabolized methanol to acetaldehyde, which is oxidized by acetaldehyde dehydrogenase to acetate. 2. Catalase metabolizes ethanol by utilizing H2O2 supplied by the actionhs of NADPH oxidase and xanthine oxidase. This normally accounts for more than 10% of ethanol metabolism. 3. CYP2E1, is the principal component of the hepatic microsomal ethanol oxidizing system, MEOS) (T10)

Misc

see files: Beneficial effects of low alcohol exposure, but adverse effects of high alcohol intake on glymphatic function _ Scientific Reports.html

Low doses of chronic ethanol intake were associated with a significant decrease in GFAP expression, with little change in the cytokine profile compared with the saline group. These observations suggest that ethanol has a J-shaped effect on the glymphatic system whereby low doses of ethanol increase glymphatic function. [human equivalent of two and half drinks per day]
– showed lower inflammation rates in the brain and a more active glymphatic system that could clear out the inflammatory markers in the brain and reduce inflammation.
– The glymphatic system (or glymphatic clearance pathway, or paravascular system) is a functional waste clearance pathway for the vertebrate central nervous system (CNS)

Pubmed

Sleep and low doses of alcohol.
Stone BM.
Abstract
The effect of 3 doses of alcohol (0.16, 0.32 and 0.64 g/kg) on sleep was studied in 6 healthy young adults. Total sleep time was increased and awake activity was reduced by 0.16 g/kg. The sleep efficiency index was improved by 0.16 and 0.32 g/kg. All 3 doses reduced slow wave sleep, and this was related to the latter part of the night. There was some evidence that REM sleep was delayed, and the REM/NREM ratio reduced. Low doses of alcohol may partially improve sleep, but there are reductions in slow wave activity, and disturbances in REM sleep are likely above 0.32 g/kg.

PMID: 6155259
Low doses of alcohol may partially improve sleep, but there are reductions in slow wave activity, and disturbances in REM sleep are likely above 0.32 g/kg.

Effect of low-dose alcohol use versus abstention on apolipoproteins A-I and B.
Moore RD1, Smith CR, Kwiterovich PO, Pearson TA.
Author information
Abstract
An inverse association between low to moderate alcohol consumption and coronary heart disease has been demonstrated in epidemiologic studies of diverse design. An attempt was made to determine if this association might be due to an effect of alcohol on apolipoproteins A-I and B and to determine if low-dose alcohol intake might have a potentially protective effect by this mechanism in persons at increased risk for coronary heart disease. To address this, an eight-week prospective randomized clinical trial of abstention versus low-dose alcohol consumption, defined as one beverage per day, was conducted in white men, aged 21 to 60 years, most of whom were patients of a preventive cardiology program. Apolipoprotein A-I levels had a mean increase of 9 mg/dl in the 28 participants who drank alcohol compared with a mean decline of 5 mg/dl in the 28 participants who abstained (p less than 0.005). This association was independent of other cardiovascular risk factors. Low-density lipoprotein (LDL)-B levels had a mean increase of 7 mg/dl in both arms of the trial (NS). However, the ratio of apolipoprotein A-I to LDL-B increased by 4 percent in the drinkers and decreased 10 percent in the abstainers (p less than 0.03). No significant changes in mean levels of total high-density lipoprotein (HDL)-, HDL2-, or HDL3-cholesterol were observed with this low dose of alcohol. This effect on apolipoprotein A-I suggests a possible mechanism by which low-dose alcohol may lower the risk of coronary heart disease.

PMID: 3129938
  • low-dose alcohol may lower the risk of coronary heart disease. [defined as one beverage per day]
Effect of alcohol intake on human apolipoprotein A-I-containing lipoprotein subfractions.
Puchois P1, Ghalim N, Zylberberg G, Fievet P, Demarquilly C, Fruchart JC.
Author information
Abstract
High-density lipoprotein comprises two main types of lipoprotein particles: (1) those that contain apolipoproteins A-I and A-II, designated LpA-I:A-II, and (2) those that contain apolipoprotein A-I but not apolipoprotein A-II, designated LpA-I. Both have been extensively studied and are believed to represent distinct metabolic entities that may confer differing protection against coronary artery disease risk. We have previously suggested that LpA-I might represent the antiatherogenic effect, which has been ascribed mainly to its effect on high-density lipoprotein cholesterol; we set out to investigate, in 344 men, the relation between LpA-I:A-II and LpA-I levels and alcohol consumption. As the alcohol intake rose, LpA-I:A-II levels increased, while LpA-I levels fell. On the assumption that LpA-I is the antiatherogenic fraction of high-density lipoprotein, the putative protective action of alcohol consumption against coronary artery disease should be reconsidered.

PMID: 1974416
  • increases LpA-I:A-II ratio, improving cardiovascular system

Changes in serum apolipoprotein and lipoprotein profile induced by chronic alcohol consumption and withdrawal: determinant effect on heart disease? [PMID: 8855152]
– indicates insufficient change in LpA ratio. But, could be propaganda

[The effect of chronic alcohol abuse on the lipids, lipoproteins and apolipoproteins concentrations in the sera] [PMID: 18702334].
The changes in the lipid markers of cardiovascular diseases risk, should not be treated as an explicity favourable, in alcohol abuse patients.
– shows there is indeed a propaganda against alcohol

Alcohol: high density lipoproteins, apolipoproteins.
Cushman P Jr, Barboriak J, Kalbfleisch J.
Abstract
Plasma lipids, including high density lipoproteins (HDL) components, were studied in 26 healthy male alcohol abusers. Age- and gender-matched controls denied the use of substances or behaviors associated with increased HDL. On admission to abstinence treatment, the alcohol abusers' total cholesterol and triglycerides were usually normal. Their HDL-cholesterol levels were high, and fell to normal within 2 weeks of sobriety. Apolipoprotein (APO) AI and AII were high initially and also became normal in 2 weeks. APO A I and II to HDL-cholesterol ratios appeared to change during abstinence, while APO AI/AII did not. APO CIII, high initially, fell during treatment, but was still high after 4 weeks of sobriety. Therefore, alcohol seems to affect several components of HDL and these HDL changes move toward normal at different rates. If alcohol is protective against some cardiovascular disease, it remains to be established whether HDL is involved and which HDL component is most important.

PMID: 3521372
  • intersting study doesn’t state whether APO AI/AII is initially high, just that it didn’t change on abstention
Alcohol consumption raises HDL cholesterol levels by increasing the transport rate of apolipoproteins A-I and A-II.
De Oliveira E Silva ER1, Foster D, McGee Harper M, Seidman CE, Smith JD, Breslow JL, Brinton EA.
Author information
Abstract
BACKGROUND:
Moderate alcohol intake is associated with lower atherosclerosis risk, presumably due to increased HDL cholesterol (HDL-C) concentrations; however, the metabolic mechanisms of this increase are poorly understood.

METHODS AND RESULTS:
We tested the hypothesis that ethanol increases HDL-C by raising transport rates (TRs) of the major HDL apolipoproteins apoA-I and -II. We measured the turnover of these apolipoproteins in vivo in paired studies with and without alcohol consumption in 14 subjects. The fractional catabolic rate (FCR) and TR of radiolabeled apoA-I and -II were determined in the last 2 weeks of a 4-week Western-type metabolic diet, without (control) or with alcohol in isocaloric exchange for carbohydrates. Alcohol was given as vodka in fixed amounts ranging from 0.20 to 0.81 g. kg(-1). d(-1) (mean+/-SD 0.45+/-0.19) to reflect the usual daily intake of each subject. HDL-C concentrations increased 18% with alcohol compared with the control (Wilcoxon matched-pairs test, P=0.002). The apoA-I concentrations increased by 10% (P=0.048) and apoA-II concentrations increased by 17% (P=0.005) due to higher apoA-I and -II TRs, respectively, whereas the FCR of both apoA-I and -II did not change. The amount of alcohol consumed correlated with the degree of increase in HDL-C (Pearson's r=0.66, P=0.01) and apoA-I TR (r=0.57, P=0.03). The increase in HDL-C also correlated with the increase in apoA-I TR (r=0.61, P=0.02).

CONCLUSIONS:
Alcohol intake increases HDL-C in a dose-dependent fashion, associated with and possibly caused by an increase in the TR of HDL apolipoproteins apoA-I and -II.

PMID: 11067787
  • Alcohol intake increases HDL-C in a dose-dependent fashion, associated with and possibly caused by an increase in the TR [transport rates] of HDL apolipoproteins apoA-I and -II.
Effect of ethanol on cholesterol and bile acid metabolism.
Lefevre AF, DeCarli LM, Lieber CS.
Abstract
Ethanol feeding increased significantly levels of hepatic esterified cholesterol and serum free and esterified cholesterol in rats. Incorporation of intraperitoneally administered [(14)C]acetate into cholesterol was significantly increased. Labeling of cholesterol was also enhanced in liver slices from animals pretreated with ethanol and incubated with [(14)C]-acetate. Ethanol consumption prolonged the half-excretion time of labeled cholic or chenodeoxycholic acids, increased slightly the pool size, and decreased daily excretion. By contrast, supplementation of the diet with cholesterol shortened the half-excretion time, did not modify pool size, and increased daily excretion. When ethanol and cholesterol feeding were combined, the effects of ethanol prevailed and there was suppression of the adaptive changes in bile acid metabolism induced by cholesterol feeding. There was also a greater accumulation of esterified cholesterol in the liver than that produced by cholesterol alone, ethanol administration alone, or the summation of both effects. Thus, cholesterol accumulation produced by ethanol feeding is associated with both enhanced cholesterogenesis and decreased bile acid excretion. Both mechanisms may play a role, but the latter is probably predominant in these studies in which cholesterol accumulation was markedly enhanced by the addition of cholesterol to the ethanol-containing diet.

PMID: 5059198
  • Ethanol feeding increased significantly levels of hepatic esterified cholesterol and serum free and esterified cholesterol in rats.
  • Thus, cholesterol accumulation produced by ethanol feeding is associated with both enhanced cholesterogenesis and decreased bile acid excretion
    • would appear the decreased free cholesterol explains the decrease in bile acid secretion
Hepatic cholesterol synthesis and esterification in rats after chronic ethanol feeding.
Venkatesan S1, Simpson KJ, Peters TJ.
Author information
Abstract
1. Chronic (5 weeks) alcohol-fed and isocaloric glucose pair-fed control rats had similar body weights, liver weights and liver protein contents. 2. Hepatic esterified cholesterol and triacylglycerol levels were two- to three-fold higher in alcohol-fed rats than in controls. 3. Hepatic cholesterol synthesis rates measured in vivo with 3H2O were significantly reduced in alcohol-fed rats. 4. Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (NADPH) (EC 1.1.1.34) activity was increased and the apparent Km for 3-hydroxymethyl-3-glutaryl-CoA was decreased in alcohol-fed rats. 5. Hepatic acyl-CoA:cholesterol acyltransferase (cholesterol acyltransferase; EC 2.3.1.26) activity was significantly increased in alcohol-fed rats. 6. These results indicate that there is no direct relationship between 3-hydroxy-3-methylglutaryl-CoA reductase activity and sterol synthesis in liver of alcohol-fed rats.

PMID: 3356114
  • Hepatic acyl-CoA:cholesterol acyltransferase (cholesterol acyltransferase; EC 2.3.1.26) activity was significantly increased in alcohol-fed rats
  • cholesterol synthesis rates measured in vivo with 3H2O were significantly reduced in alcohol-fed rats.
    • my guess here is that because cholesterol transport rate/efficiency increased, this serves as a downregulation signal on the need for cholesterol, reducing its synthesis

Misc

see files : PIIS0928468003000518.pdf
Acetaldehyde is a product of oxidative metabolism of ethanol occuring mainly in the liver .... acetaldehyde-modification of apolipoprotein B has been shown to increase the catabolism of LDL particles

Sources

Vodka

Luksusowa: Coming from the Polish word meaning "luxurious," from distilled potatoes and has a fairly smooth finish, Fairly sweet, with what I would probably call an almost creamy finish
New Amsterdam: five times distilled and then filtered twice for a smooth, clean finish
Monopolowa: potato from Austria it’s as crisp and clean

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