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How much alcohol can you consume before it starts to kill a single neuron or interfere with proper brain functioning? Does it happen:

  • If you take just a few drops of alcohol?
  • If you drink a rum and coke cocktail?
  • If you get so drunk that you cannot remember what you have done?

I like drinking a bit when I go out to pubs or the like, as I didn't consider that taking a pair of cups approximately once per month could do anything to my brain, but I've reconsidered it, so I'd like to know how much is needed to produce negative effects on the brain. Hope you can guide me with this.

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Median lethal dose (or LD-50) is a useful concept for a question like this. Individual differences are bound to play a role, so I suspect the best way to answer would be to describe the median dose for causing neural damage. BTW FWIW, Kelly Huffman says, "There is no safe level of drinking during pregnancy," but I don't know if that was an opinion or supported by some evidence other than what she would've gotten from the study described here, which doesn't seem suited to produce such evidence. –  Nick Stauner Feb 12 at 5:08
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up vote 9 down vote accepted

There is some debate as to wether alcohol consumption actually destroys brain cells or not. Jensen & Pakkenberg (1993) counted the neurons in the neocortex of deceased acoholics and found that they have the same number of neurons as non-alcoholic men.

Unfortunately the non-alcoholic control group did not consist of teetotallers but only "did not have any history or histological signs of alcohol abuse". It is not unprobable that the brains of people who never drank any alcohol and those of people who drank an amount of alcohol that is merely not considered abusive – a level that is certainly strongly influenced by cultural norms – do differ, so the results of this study have to be interpreted with some caution.

What Jensen and Pakkenberg did find was a reduction of white brain matter to which they attribute the functional deficits that follow alcohol abuse. This brain size reduction is replicated by several other studies, some of which find a reduction in grey matter volume of the frontal lobe as well (Pfefferbaum et al., 1997). For example, Ding et al. (2004) found that the chronic consumption of even smal amounts of alcohol causes brain size reduction. Ding et al. asked 1909 middle-aged adults for their drinking habits, took MRI scans, and found that "each additional alcoholic drink per week was associated with a 0.01 grade greater ventricular size (P=0.03) and a 0.009 grade greater sulcal size (P=0.02) after adjustment for age, sex, race, body mass index, smoking, income, sports index, and diabetes." The ventricles are cavities inside the brain, filled with cerebrospinal fluid, the sulci are the furrows that structure the surface of the brain. What the study found, in other words, was that chronic alcohol consumption enlarged these spaces between brain matter, which means that the brain matter was being reduced in volume.

While Jensen & Pakkenberg (1993) found no difference in the number of neurons of alcoholic and non-alcoholic brains, other studies did find differences, although limited to certain cortical regions. Harper and Kril (1989) found "that alcoholics have reduced neuronal counts in the superior frontal region of the cerebral cortex". That Jensen and Pakkenberg did not find these differences can probably be attributed to a "combined analysis of several cortical regions (Brooks, 2000).

In summary, a combination of neuroimaging and histopathological data indicates that heavy alcohol consumption over a long period of time as occurs in chronic alcoholics can result in the death of neurons in specific regions of the human brain, particularly the frontal cortical regions. Careful selection criterion of subjects, along with unbiased stereological techniques, has provided strong evidence that this neuronal loss in ‘uncomplicated’ alcoholics is due to direct neurotoxic effects of alcohol itself, and not to other factors such as malnutrition or liver disease. (Brooks, 2000; emphasis mine)

The good news is that stopping to drink will have a positive effect (Pfefferbaum et al., 1998):

However, brain atrophy and related neurological deficits induced by chronic alcohol abuse may be partially reversible through sustained abstinence. (Ding et al., 2004)

"Sustained" in this context means that it will take years for the brain to recover, not just the five workdays between weekend drinking bouts ;-)

Apart from neuronal death and brain atrophy directly caused by alcohol, chronic alcohol consumption has many other negative effects on the human organism. For example it damages the blood-brain barrier (Philips, 1982; Kornhuber et al., 1987; Elmas et al., 2001), which is a main factor in the development of neurodegenerative diseases (Singh et al., 2007). Effects on other organs such as the liver or heart can indirectly cause damage to the brain.

I was unable to find any sources that give exact numbers for how much alcohol (in what period of time) destroys how many neurons, directly or indirectly. The only indication I came upon is the correlation between brain volume reduction and drinks per week given in the study by Ding et al. (2004), that I quoted above. This gives some indication at least to the amount of damage, and that every glass per week counts.


Note:

When you read scientific studies about the effects of alcohol, you must consider the author's affiliation. Many studies are financed by the beverage industry and may be biased. For example, a study that found that alcohol protected against diabetes was financed by the Alcohol Task Force of the foundation International Life Sciences Institute, in which Moët & Chandon, Allied Domecq, Brasseries Kronenbourg, Heineken und Diageo are members (Exler, 2007). Studies that show that consumption of red wine reduces the threat of cardiovascular diseases, were forged (Jaslow, 2012).


Sources:

  • Brooks, P. J. (2000). Brain atrophy and neuronal loss in alcoholism: a role for DNA damage?. Neurochemistry international, 37(5), 403-412.
  • Ding, J., Eigenbrodt, M. L., Mosley, T. H., Hutchinson, R. G., Folsom, A. R., Harris, T. B., & Nieto, F. J. (2004). Alcohol Intake and Cerebral Abnormalities on Magnetic Resonance Imaging in a Community-Based Population of Middle-Aged Adults The Atherosclerosis Risk in Communities (ARIC) Study. Stroke, 35(1), 16-21. doi:10.1161/​01.STR.0000105929.88691.8E
  • Elmas, I., Küçük, M., Kalayci, R. B., Çevik, A., & Kaya, M. (2001). Effects of profound hypothermia on the blood–brain barrier permeability in acute and chronically ethanol treated rats. Forensic Science International, 119(2), 212-216.
  • Exler, A. (2007, March 7). Vom Wein beseelt. Die Zeit. http://www.zeit.de/2007/11/Weinlobby
  • Harper, C., & Kril, J. (1989). Patterns of neuronal loss in the cerebral cortex in chronic alcoholic patients. Journal of the Neurological Sciences, 92(1), 81-89.
  • Jaslow, R. (2012, January 12). Red wine researcher Dr. Dipak K. Das published fake data: UConn. CBS. http://www.cbsnews.com/news/red-wine-researcher-dr-dipak-k-das-published-fake-data-uconn/
  • Jensen, G. B., & Pakkenberg, B. (1993). Do alcoholics drink their neurons away?. Lancet, 342(8881), 1201-1204.
  • Kornhuber, J., Kaiserauer, C. H., Kornhuber, A. W., & Kornhuber, M. E. (1987). Alcohol consumption and blood-cerebrospinal fluid barrier dysfunction in man. Neuroscience Letters, 79(1), 218-222.
  • Pfefferbaum, A., Sullivan, E.V., Mathalon, D.H., & Lim, K.O. (1997). Frontal lobe volume loss observed with magnetic resonance imaging in older chronic alcoholics. Alcoholism: Clinical and Experimental Research, 21, 521–529.
  • Pfefferbaum, A., Sullivan, E. V., Rosenbloom, M. J., Mathalon, D. H., & Lim, K. O. (1998). A controlled study of cortical gray matter and ventricular changes in alcoholic men over a 5-year interval. Archives of General Psychiatry, 55(10), 905-912.
  • Phillips, S. C., & Cragg, B. G. (1982). Weakening of the blood-brain barrier by alcohol-related stresses in the rat. Journal of the Neurological Sciences, 54(2), 271-278.
  • Singh, A. K., Jiang, Y., Gupta, S., & Benlhabib, E. (2007). Effects of chronic ethanol drinking on the blood–brain barrier and ensuing neuronal toxicity in alcohol-preferring rats subjected to intraperitoneal LPS injection. Alcohol and Alcoholism, 42(5), 385-399.
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Thanks a lot for your answer, you have seriously made a lot of research to answer my question properly. –  user2643593 Feb 12 at 13:03
    
Love the point about affiliation biasing too...Damn them crooked corporate hacks! Er, wait a sec...do you mean to say the theory that small amounts of red wine improve cardiovascular health was a hoax? I'm somewhat afraid to know the truth! –  Nick Stauner Feb 13 at 8:52
    
How this "to the amount of damage, and that every glass per week counts" is compatible with positive correlation of (moderate) alcohol consumption and intelligence? Also: Online games offer trove of brain data and cited therein The largest human cognitive performance dataset reveals insights into the effects of lifestyle factors and aging - esp Fig 2. –  Piotr Migdal Feb 26 at 19:47
    
Moderate drinking is (on average) associated with a more active social life. This in turn may correlate with better social skills, higher intelligence, better health etc., which all affect cogntive performance. Alcohol consumption may just be an indicator, not a cause, here. The authors explain: "... there may be other related but unobserved variables that explain some of the effects of alcohol consumption ... the apparent cognitive advantage for those who report moderate alcohol intake may be in part due to increased social and cognitive engagement ..." –  what Feb 27 at 7:35
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