I heard that there is some old (circa 1960-19070) and well known research showing that alcohol causes red blood cell
to agglutinate into big "lamps" (tens or even hundreds in a lump). Apparently these lumps are clearly visible in eye capillaries if I were to use a microscope.
Some people say that agglutinated red cell can't get
through small capillaries of the brain to reach neurons and as a result we get a high similar
to what we get if we go too high on a hot air balloon without an oxygen mask.
I'd really like to know if all above is true/partially true/all
wrong as it looks to me as a very likely explanation of how alcohol actually works.
Even before I started looking for information on Google I was sceptical, if only because so many people drink so much alcohol for so many years and don't die from oxygen starvation of the brain. I know some very intelligent alcoholics and I'm sure the booze doesn't improve them, but they don't show much sign of suffering a stroke - which is what your question basically suggests.
There's a paper at this address. Apparently drunk rats didn't suffer brain damage (but the research was sponsored by a brewer).
Try searching for blood-sludging to find out more.
<<There's a paper at this address. Apparently drunk rats didn't suffer brain damage (but the research was sponsored by a brewer).>>
Sorry - link does not work.can you mention the site name and keywords instead, please?
Anyway I am not suggesting a full stroke - blood apparently still flows through bigger cappilaries but red cells clamps can't go through smallest cappilaries - some neurons probably do die - how one would know they did not? Say 0.01% of neurons died as a result of a drink - is there any way at all to check this?
To rephrase - I think I heard somewhere that about a third of your neurons dies by the time you hit 65 or 70 years old. One can hardly notice it, I guess? I don't think there is a way of checking a state on a single neuron yet?
See my later reply to myself on page 2 here for details of the research I think I originally heard about!
I would never beleive anything a brewer (or anyone dependednt on one) says about alcohol - would you? :-) They keep saying for years that alcohol is a miracle medicine... :-)
I eventually tracked down the paper in question via the hosting website and the link was still broken. The abstract reads as follows:
After 3 weeks of alcohol intoxication, the brains of rats were searched with light-and electron
microscopy for degenerating nervous tissue and agglutination of
erythrocytes in the blood vessels.
There was
no sign of degeneration of nerve cells or synapses in the cerebral
cortex, hippocampus, cerebellum, midbrain or hindbrain. No histological
sections showed blood vessels with erythrocytes inside them.
It is concluded that the agglutination of red blood cells seen in the conjunctivae of intoxicated human alcoholics is not
necessarily an indication that vascular congestion is also occurring in
the brain of such patients, nor that this is the primary mechanism of alcohol-related brain damage.
If you want to track down the whole thing look for this: Journal of the Neurological Sciences Volume 72, Issue 1, January 1986, Pages 43-48
*This work was supported financially by the Australian Associated Brewers.
Oh well... Did not bother buying the article for thie reason - it is not really impartial - or is it?
2)Not sure what they mean by
"No histological sections showed blood vessels with erythrocytes inside them."
I mean blood vessels should have erythrocytes in them - unless you drain all blood before starting looking??? Or may be they were all bloked by sludge so no red cells made into them for 3 weeks???
Details for people wha may be interested:
Does alcohol-induced blood cell agglutination cause brain damage?
Stephen C. Phillips
aDepartment of Anatomy, Monash University, Clayton, Victoria 3168 Australia
*This work was supported financially by the Australian Associated Brewers.
I took a Physiology for BioEngineers class in Grad School, taught by a PhD in Medicine from Harvard Medical School, and he said that drunk behavior was simply hypoxia caused by the effect of alcohol on hemoglobin's ability to function.
He mentioned nothing about brain damage or blood clots, just that the brain wasn't getting enough oxygen due to the change in blood chemistry caused by alcohol on hemoglobin.
If you've ever seen "An Officer and a Gentleman", you may remember David Keith's portrayal of someone who didn't recognize his own symptoms of hypoxia in the altitude chamber - he acted drunk. The movie's technical advisor no-doubt told him that hypoxia results in "drunken" behavior.
The only physiological affect of alcohol (at concentrations you would survive) are a very small increase in the size of RBA and a very slight reduction in flexibility. Neither of these would produce the type of effect you are describing and, if they did, it would affect capillaries in all parts of the body, not just the brain
My understanding is that alcohol - like other neurotoxins - produces most of its effects by interfering with neurotransmitters.
If drinking starved the brain of oxygen then excessive and long-term alcohol abuse would cause permanent brain damage which would be manifested in a similar way to having a stroke. This isn't the case as far as I know.
It has been suggested that the brain can become slightly "pickled" by long-term alcoholism - e.g. shrinking and hardening - but the liver causes much bigger health problems when you're at that advanced stage.
I am no expert in the pharmacokinetics of ethanol, but I hardly believe a word of it.
Red cells have tendencies to attract each other harmlessly, often in neat stacks like coins, but the effect has to be quite pronounced to cause any harm. Actual clotting is a far more specific process; it certainly is promoted by stacking and pooling, but you can have a lot of erythocyte crowding withiut the slightest clotting, harmless or otherwise. Generally all that happens is that they crowd through the capillaries in greater concentrations. I would require actual physiological measurements to convince me that the effect of a blood concentration of say 0.2% would cause any serious anoxia in a healthy person, and it takes a pretty good binge to exceed that!
As for real clotting, alcohol actually slows clotting time as well as clot solution. It might perhaps lead to the release of clots and atheromas adhering to blood vessel walls, which really can be dangerous, but that is another matter.
As for the effect of anything short of near-lethal drunkenness amounting to shortage of oxygen supply to the brain, I hear a deafening flutter of horse feathers. Plenty of small organic molecules interfere with the function of the CNS. We call them anaesthetics. And would you believe it? Those silly anaesthesiologists keep looking for more and more sophisticated anaesthetics, when now it seems that they could simply smother the patient with a pillow to achieve any desired degree of anoxia, letting a bit of air through whenever his ears turn too cyanotic! Tsk!
Actually, ethanol is itself a pretty good anaesthetic, especially taken intravenously. (DON"T try this at home folks!!! The main reason that it is a poor anaesthetic per os, is that the difference between the lethal and the anaesthetic dose of ethanol is uncomfortably small, and that control of the effective oral dose absorbed from the gut is unreliable. Mainlining otoh offers so many options for amateurs to kill themselves, that it deserves an honorable mention on the Darwin Awards site.) Like other volatile anaesthetics such as ether, chloroform, cyclopropane etc, the main anaesthetic effect of ethanol is directly on the nerves. It affects the cell surface and the propagation of the impulses. Pete mentioned neurotransmitters, and faik he might be right too.