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victoria1

Alcohol

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After reading around in this forum I got the impression that most people doing CR is against alcohol and never touch it. So I wonder, do any of you drink alcohol while doing CR?

 

Let me just say that I've read studies done on alcohol and the effect it has on the human body, and I know it is not good for you overall. But I still sometimes make room for some wine and champagne in my daily calorie "allowance". I don't know how much of an impact this will have in the long run in regards to longevity, but I feel like the amount I consume is ok. 

 

What's you opinion on alcohol? And what do you think about the resveratrol found in red wine?

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My opinion on alcohol is that in principle it should be avoided but some times we can indulge in it with moderation and other times it may have a medicinal effect.

 

I noticed that some most wines and liquors are able to improve digestion if the stomach is bloated from the meal. It is sufficient a very moderate amount.

 

The USDA recommends a threshold of no more than 1 standard drink per day for women. That means the content of a glass of wine or equivalent. Pls read here for other typical standard drinks. By the way, the above USDA recommendations are consistent with the max amounts given by medical people here in Italy when I asked and by nutrition experts with credentials.

 

When in weddings or other social events (very rarely now), I'll drink some wine but in moderation and among servings, or at the start but diluted with much water.

 

Resveratrol content in red wine is not high, from 2 to 7 mg/liter on average

 

A typical quantity contained in a supplement capsule is 500 mg; this would mean that, on average, it would take about 100 liters of red wine to reach such dosage. In US units it's 100 quarts or 200 pints or 25 gallons.

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I agree with McCoy, and only use that brain poison to get totally roasted at friends' weddings (poor things) or occasional slutty nights in New Orleans.

 

But I think the idea that red wine (or any alcohol) is a health food is the bonkers propaganda of the massive alcohol lobby. Maybe humans began alcohol consumption back during times when ancestors rightly determined that ground water was Savannah-poisoned by wildebeest poop? When I want the healthy benefits of red wine, I eat some grapes then watch helplessly as my blood glucose rises, so I eat edibles and chill. Marijuana is a way healthier alternative to, what Matt Groenig (Homer Simpson) said: "To alcohol! The cause of... and solution to... all of life's problems."

 

Fire away.

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38. Costanzo S, Di Castelnuovo A, Donati MB, Iacoviello L, de Gaetano G. Wine, beer or spirit drinking in relation to fatal and non-fatal cardiovascular events: a meta-analysis. Eur J Epidemiol. 2011 Nov;26(11):833-50. doi: 10.1007/s10654-011-9631-0. Epub 2011 Nov 11. PubMed PMID: 22076059

 

Got this from Michael Rae post on his supplement regimen a few years back. It indicates that very low doses of red wine 3oz daily have some relatively profound effects, but of course its epedemiolgy alas.

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We know that alcohol is carcinogenic, and brest tissues are one of the most vulnerable ones. However, I have seen studies that red wine is not associated even with breast cancer. Similar to high phenolic EVOO, maybe red wines are not unhealthy due to the fact that protection of high flavonoids content trumps hazard of alcohol. Still though, one should avoid alcohol or only drink red wine in moderation.

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[Wine is typically about 12% or 12 g/100g alcohol, so: "We decided to consider as light, moderate and heavy drinking every interval whose midpoint was respectively ⩽12.5, ⩽50 and >50 g per day of alcohol."

Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis.

Bagnardi V, Rota M, Botteri E, Tramacere I, Islami F, Fedirko V, Scotti L, Jenab M, Turati F, Pasquali E, Pelucchi C, Galeone C, Bellocco R, Negri E, Corrao G, Boffetta P, La Vecchia C.

Br J Cancer. 2015 Feb 3;112(3):580-93. doi: 10.1038/bjc.2014.579.

PMID: 25422909 Free PMC Article

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4453639/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4453639/pdf/bjc2014579a.pdf

Abstract

BACKGROUND:

Alcohol is a risk factor for cancer of the oral cavity, pharynx, oesophagus, colorectum, liver, larynx and female breast, whereas its impact on other cancers remains controversial.

METHODS:

We investigated the effect of alcohol on 23 cancer types through a meta-analytic approach. We used dose-response meta-regression models and investigated potential sources of heterogeneity.

RESULTS:

A total of 572 studies, including 486 538 cancer cases, were identified. Relative risks (RRs) for heavy drinkers compared with nondrinkers and occasional drinkers were 5.13 for oral and pharyngeal cancer, 4.95 for oesophageal squamous cell carcinoma, 1.44 for colorectal, 2.65 for laryngeal and 1.61 for breast cancer; for those neoplasms there was a clear dose-risk relationship. Heavy drinkers also had a significantly higher risk of cancer of the stomach (RR 1.21), liver (2.07), gallbladder (2.64), pancreas (1.19) and lung (1.15). There was indication of a positive association between alcohol consumption and risk of melanoma and prostate cancer. Alcohol consumption and risk of Hodgkin's and Non-Hodgkin's lymphomas were inversely associated.

CONCLUSIONS:

Alcohol increases risk of cancer of oral cavity and pharynx, oesophagus, colorectum, liver, larynx and female breast. There is accumulating evidence that alcohol drinking is associated with some other cancers such as pancreas and prostate cancer and melanoma.

Edited by AlPater

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Even the AHA does not recommend drinking alcohol for health benefits.

"How alcohol or wine affects cardiovascular risk merits further research, but right now the American Heart Association does not recommend drinking wine or any other form of alcohol to gain these potential benefits...the American Heart Association cautions people NOT to start drinking ... if they do not already drink alcohol."
 
Source:  http://www.heart.org/HEARTORG/HealthyLiving/HealthyEating/Nutrition/Alcohol-and-Heart-Health_UCM_305173_Article.jsp#

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I started consuming alcohol on a regular basis back when there was a lot of research seeming to point to possible benefits vs all cause mortality, and especially CV health. Always in pretty small amounts - 0.5-1 drink equivalents 4 times a week, 99% of the time red wine. Eventually the research became a hopeless muddle, but I kept up my drinking routine out of inertia and besides, I enjoy the taste. However, these days it seems research is tilting more and more toward alcohol in any amount being a net negative - should this solidify into greater consesus, I will stop drinking altogether. For now, I'm carrying on my very, very modest drinking.

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AHA is not, and should not be, recommending alcohol use since alcohol abuse threatens beyond the person itself. People can use these kind of information to justify their bad behavior.

 

I don't buy alcohol has a j shape mortality curve because there are other common factors that light drinkers share i.e. healthy awareness and don't forget that CVD and stoke are top killers which alcohol can help a little to prevent.

 

It is good to see people trying to avoid bad stuff but every time you inhale you introduce new carcinogenics to your body from air. But I also believe the idea that "what doesn't kill you makes you stronger", so very little bad stuff that your body can handle increase your ability to fight. Again, this should not be an excuse for bad habits.

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Several months ago I read some media reports about this study: "Alcohol consumption as a cause of cancer" by Jennie Conner.

 

Here is one good media report on it: "Alcohol is a direct cause of seven forms of cancer, finds study"

 

I am in no way qualified to think critically about this research and all of the other mixed research out there on alcohol, but at the moment I tend to think this is probably right. What is most interesting to me about Conner's take on all of this is that she is thinking very practically about how her research should be applied to public health and that instead of focusing on heavy drinkers and try to convince them to stop or moderate their drinking, it would prevent more cancer if we focused on convincing moderate drinkers to eliminate drinking all together.

 

Even moderate amounts of alcohol cause an increase in cancer in pretty much every part of the body that the alcohol comes in contact with.

 

I know that there are some people who practice CR who do drink moderately, or at least used to. I'm curious what they would make of Conner's work.

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I've just listened to a presentation by Dr. Franco Berrino, coauthor of Dr Luigi Fontana in writing the book on longevity: "The great way".

 

Interestingly, he says that alcohol intake is correlated to breast cancer because it stimulates the production of testosterone in women.

 

Guys: probably it is a function of moderation. CDC's 2 glasses a day of wine might be too much. Also, I expect that more concentrated alcoholics like whiskey may be more harmful to esophagus and stomach.

Edited by mccoy

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“The highest risks are associated with the heaviest drinking but a considerable burden is experienced by drinkers with low to moderate consumption, due to the distribution of drinking in the population,” Connor said

 

https://www.theguardian.com/society/2016/jul/22/alcohol-direct-cause-seven-forms-of-cancer-study

 

How does the "distribution of drinking in the population" turn low to moderate alcohol consumption into a considerable cancer-risk burden?

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“The highest risks are associated with the heaviest drinking but a considerable burden is experienced by drinkers with low to moderate consumption, due to the distribution of drinking in the population,” Connor said

 

https://www.theguardian.com/society/2016/jul/22/alcohol-direct-cause-seven-forms-of-cancer-study

 

How does the "distribution of drinking in the population" turn low to moderate alcohol consumption into a considerable cancer-risk burden?

 

 

I presume the sentence should have gone like this: "distribution of tolerance to alcohol in the population". To the less metabolically tolerant, even a moderate amount may result in a significant cancer hazard. 

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It seems that some (maybe most) of the health benefits of alcohol drinking come from preventing AGE formation in the body. First study is the direct one:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC26793/

 

The other two are the comparison between alcohol drinkers vs. non-drinkers for erectile dysfunction and diabetes prevalence:

 

https://www.ncbi.nlm.nih.gov/pubmed/27788774

https://www.ncbi.nlm.nih.gov/pubmed/22445622

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All roads lead to TOR?

---------------------------------------

 

Reduced mortality and moderate alcohol consumption

The phospholipase D-mTOR connection

 

Abstract

Many studies have suggested that moderate alcohol consumption reduces mortality. There is also substantial evidence that lifespan is extended with suppression of TOR (target of rapamycin). It was reported recently that rapamycin is able to extend the lifespan of a mammal—implicating the mammalian TOR (mTOR). mTOR has a requirement for the lipid second messenger phosphatidic acid (PA), which is generated by phospholipase D (PLD). Therefore, in principle, suppression of PLD would be similar to treatment with rapamycin. Significantly, PLD utilizes ethanol preferentially over water in the hydrolysis reaction that ordinarily generates PA. In the presence of ethanol, phosphatidyl-ethanol is generated at the expense of PA leading to the suppression of mTOR. This reaction, known as the transphosphatidylation reaction, provides a mechanistic basis for the reduced mortality observed with moderate consumption of alcohol—that being the suppression of mTOR.

 

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957519/

PMCID: PMC2957519
Edited by Sibiriak

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mccoy: I noticed that some most wines and liquors are able to improve digestion if the stomach is bloated from the meal.

 

 

Perhaps there is something to be said for bittersweet digestifs (amari) or  aperitifs such as campari?

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Is it just polyphenols which you could get elsewhere without alcohol?

-----------------------------------------
 

Alcohol: Friend or Foe? Alcoholic Beverage Hormesis for Cataract and Atherosclerosis is Related to Plasma Antioxidant Activity

Results:

One drink of red wine, lager beer, or stout (5% alcohol v/v, and alcohol-free) significantly increased the average antioxidant activity in plasma samples obtained from volunteers averaged over 240 min. Three drinks of red wine, lager beer, or stout (5% alcohol v/v, and alcohol-free) significantly increased the average pro-oxidant activity in plasma samples obtained from volunteers averaged over 360 min. For a solution of alcohol, three drinks resulted in pro-oxidant plasma on average, whereas while one drink did not significantly affect the plasma oxidative status. A preliminary experiment in which two volunteers showed a significantly increased time to metabolize ethanol after ingestion resulted in elevated antioxidant activity in plasma for lager beer and red wine.

 

Conclusions:

One drink of red wine, beer, or stout provided equivalent increases in plasma antioxidant activity. Three drinks of red wine, beer, or stout provided equivalent increases in plasma pro-oxidant activity. This may explain, at least in part, the decreased risk of cataract and atherosclerosis from daily consumption of one drink of different types of alcoholic beverages as well as the increased risk from daily consumption of three drinks of alcoholic beverages. The plasma pro-oxidant activity appears to be due to ethanol metabolism, whereas the antioxidant activity may be due to the absorption of polyphenols in the beverages.

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2657506/

PMCID: PMC2657506
 
Wine, beer, alcohol and polyphenols on cardiovascular disease and cancer.

Epidemiological and clinical studies have pointed out that regular and moderate wine consumption (one to two glasses a day) is associated with decreased incidence of cardiovascular disease (CVD), hypertension, diabetes, and certain types of cancer, including colon, basal cell, ovarian, and prostate carcinoma. Moderate beer consumption has also been associated with these effects, but to a lesser degree, probably because of beer's lower phenolic content. These health benefits have mainly been attributed to an increase in antioxidant capacity, changes in lipid profiles, and the anti-inflammatory effects produced by these alcoholic beverages. This review summarizes the main protective effects on the cardiovascular system and cancer resulting from moderate wine and beer intake due mainly to their common components, alcohol and polyphenols.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407993/

PMCID: PMC3407993
 
Is a cardioprotective action of alcohol a myth?

CONCLUSION

Taken together, recent data strongly suggest that the protective effect of alcohol against CVD might have been overestimated because of uncontrolled confounding.

 

[...]No data are currently available to support a causal relationship between alcohol intake and CHD. In the absence of well-conducted randomized
trials assessing the causal role of alcohol in cardioprotection, future epidemiological studies evaluating the relationship between alcohol and CHD
should very carefully choose the covariates to be included in a multivariate analysis. We believe that careful consideration of possible bias should
be taken into account before advancing or advocating health claims to the general population.

https://www.researchgate.net/publication/230632657_Is_a_cardioprotective_action_of_alcohol_a_myth

Edited by Sibiriak

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European Journal of Clinical Nutrition (2007) 61, 147–159. doi:10.1038/sj.ejcn.1602507; published online 2 August 2006

 

Nutritional Hormesis

 

Hormesis, the biological and toxicological concept that small quantities have opposite effects from large quantities, is reviewed with emphasis on its relevance to nutrition.

 

The review of Pohorecky (1977) provides strong psychological, behavioral and biochemical evidence for alcohol (ethanol) affecting the experimental behavior of animals and humans in a biphasic dose–dependent manner, with low-doses being excitory and high-doses depressant. For non-human mammalian biological end points (including, amongst others, the liver, kidney, heart, spleen, endocrine, embryonic development and birth weight), Calabrese and Baldwin's (2003c) assessment of the toxicological and pharmacological literature demonstrated ethanol-induced biphasic dose responses over a wide range. In most cases, the low-dose hormetic responses were judged to be statistically significant and reliable. They observed striking similarities across studies in both hormetic dose-ranges and hormetic dose–response magnitudes, with the maximum hormetic response approaching two-fold but was usually 25–40% greater than the control value. Furthermore, the maximum hormetic response was generally within a factor of 2–4 of the estimated NOAEL. They argued against a common explanatory mechanism, and for a diverse plethora of underlying mechanisms. They also stated that regardless of actual response mechanisms, the similarity of dose–response characteristics likely reflected an important overall regulatory strategy built into the framework of a homeostatic control system. Calabrese and Baldwin (2003c) further noted that these collective findings closely resembled the biphasic hormetic responses to a wide range of toxic chemical agents that they had previously reported (Calabrese and Baldwin, 1997).

 

While there are a considerable number of published investigations suggesting that chronic alcoholics have an increased susceptibility to infectious diseases (in particular pneumonia), Hallengren and Forsgren (1978) have presented evidence that at low to moderate blood alcohol concentrations there is an increased adherence, phagocytosis and chemotaxis of human polypmorphonuclear leucocytes. The magnitude of the detected response is consistent with that seen for hormetic responses, with the hormetic concentration range being about four-fold. It would appear that these results have important ramifications for biomedical researchers and clinicians.

 

Human health benefits of regular light-to-moderate alcohol consumption vis-à-vis abstinence include decreased risks of dementia, diabetes, osteoporosis, and cardiovascular disease and death (Standridge et al., 2004). Both case–control and cohort epidemiological studies have consistently shown that light-to-moderate drinkers are at lower risk of cardiovascular disease and death than nondrinkers, although heavier alcohol consumption can negatively affect the neurologic, gastrointestinal, hematologic, immune, psychiatric and musculoskeletal organ systems.

 

The hormetic biphasic effects of alcohol consumption on total human mortality is a well studied and documented phenomenon with the basic J-shape of the dose–response curve confirmed in the vast majority of studies and being remarkably stable and independent of assessment measure (Gaziano and Buring, 1998; Rehm, 2000). For example, Gronbaek (2004) cited 19 separate epidemiological studies conducted over the last three decades that describe the impact of alcohol on total mortality as J-shaped, with a beneficial effect of regular light-to-moderate intake (10–40 g per day, or one to three alcoholic beverages), and a detrimental effect of both lower and higher intake. These studies have been reported by a large number of different research teams, with the effects observed in populations of different genders, races and nationalities. The total mortality risk reduction at light-to-moderate levels is likely due to lower risk of fatal cardiovascular disease without dramatic increases in other causes of death.

 

Rehm (2000) notes that the J-shape results mainly from the beneficial effect of moderate alcohol consumption on ischemic cardiovascular conditions coupled with the detrimental effects of drinking on other health conditions. While the risk curves of detrimental effects may vary between linear, exponential or threshold effects, they always seem to be monotonic: the more consumption, the higher the disease-specific mortality risk. Rehm further notes that this means that the J-shaped curve should not be expected and cannot be found in populations with no or few coronary heart disease (CHD) deaths, for example, in some developing countries or in younger age groups.

 

Epidemiological studies indicate that all types of alcoholic beverages are associated with increased cancer risk at higher drinking levels, suggesting that ethanol itself causes the detrimental effect rather than any particular type of beverage. A great deal of recent research has focused on the possible benefits of specific alcoholic beverages. Some have postulated that wine's polyphenolic antioxidants including resveratrol and proanthocyanidin reduce risk of cardiovascular disease. Resveratrol has been shown to exert its effects on cells by inducing a stress response mediated by the sirtuin protein family (Tissenbaum and Guarente, 2001; Howitz et al., 2003).

 

At this point in time the totality of evidence suggests that the major beneficial component of alcoholic beverages on cardiovascular mortality is in fact ethanol per se rather than some other component (Rimm et al., 1996). Gronbaek (2004) states that it is likely that any apparent additional beneficial effect of wine on health in addition to the effect of ethanol itself is a consequence of confounding.

 

Several plausible mechanisms for the cardioprotective effect of light-to-moderate alcohol intake have been suggested (Korthuis, 2004; Standridge et al., 2004). One is its role in increasing plasma HDL cholesterol concentrations and in reducing low-density lipoprotein (LDL) cholesterol concentrations. Such changes have been suggested to account for approximately half of alcohol's protective effect against CHD. (Commonly referred to as the good cholesterol, HDL binds with cholesterol and brings it back to the liver for elimination or reprocessing, thereby lowering total cholesterol levels in body tissues and its build-up on arterial walls, and in a sense reversing the atherosclerotic process.) Free radical scavenging and inhibition of LDL oxidation by free radicals have also been proposed as mechanisms; as well as reduction/inhibition of platelet adhesion and aggregation, clotting factor concentrations, vascular smooth muscle cell proliferation and migration, and inflammation involving monocytes and T lymphocytes.

 

Of particular interest in light of previous reference to hsps heat shock proteins are animal studies showing that oxidative stress from low dose alcohol consumption induces several heat shock and antioxidant proteins, which may serve as cardioprotective proteins in hearts subsequently exposed to ischemia/reperfusion (I/R) injury (Sato et al., 2004). Also of interest is the surprising finding that alcoholics had significantly less DNA damage than controls and demonstrated higher capacity for DNA repair, possibly because excessive ethanol rather than damaging DNA (it is not genotoxic) induces antioxidant and repair enzymes (Pool-Zobel et al., 2004).

 

http://www.nature.com/ejcn/journal/v61/n2/full/1602507a.html#Hormetic-alcohol-ethanol

Edited by Sibiriak

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I resuscitate this thread since there is another ongoing thread on the potential detrimental effects of alcohol.

 

Interestingly, Sibiriak mentioned one article where alcohol is believed to potentially exhibit an hormetic effect by interfering with the phosporylation of mTOR hence causing a downregulation of it → CR mimetics

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