The idea that abstinence from, or overconsumption of wine or beer or
whatever alcoholic beverage, are bad, whereas a moderate use is
beneficial for the heart and the vessels is yet another
epidemiological bias, repeated again and again in numerous
unimaginative studies. Usually papers from wine-producing countries
stress the benefit of wine whereas studies from beer-producing
countries worship beer-drinking. The confounder is moderation. People
who drink moderately may be moderate in other ways of life, or they
may afford to drink wine every day in moderate amounts and may live in
harmony with alcohol as well as with their family or work or
surroundings with absence of stress or troubles or other factors that
demand heavy drinking or, in the end, total abstinence from it.
That said, please send the wine bottle!
I have looked at many, many studies on the effect of drinking alcohol
on CHD. I think that there is a degree of protection, although I take
Uffe's point that moderate drinkers may well be moderate people in
many other ways.
However, I do think that there is a good biological plausibility
linking alcohol and protection from CHD. Alcohol is a mild
anticoagulant, it also reduces stress, and the level of stress
hormones. There are studies from Italy demonstrating that wine
drinking with a meal has a series of potential
benefits on many of the factors that I believe cause CHD.
In short. I think there could well be a casual link between alcohol
consumption and protection against CHD.
Thank you Uffe, especially for the last comment.I have
noticed a definite increase in elasticity for many years now....
although my pulse rate has been around 48 for quite some time now so I
don't expect any further drop. According to my low pulse and my (perceived)
elasticity plus a respectable blood pressure on those days that my
carbohydrates are kept in limits I may grow to a ripe old age
and will thus be able to learn so many more things through THINCS
members' contributions. If you are ever in Germany you would be
able to test the beer-elasticity-connection easily and enjoyably
yourself: Many German beer breweries have guided tours on certain
weekdays where you observe, listen, perhaps take notes and then retire
to the brewery's Centre for the promotion of Gemuetlichkeit and
more to conduct serious research . All of this needs no funding
whatsoever, all the snacks and the beer is gratis and, after all, it
is all for a good cause.
Any thoughts on which of my two main habits would be more helpful, the
ethanol or the running? At times I do both in moderation.
to increase one's HDL it's alcohol and/or exercise. Balz Frei,
running the Linus Pauling Institute, uses the line in his talks [and
I've modified it and get a laugh every time] about the combination
therapy of "running from bar to bar". This
therapy may convert Cholesterol Skeptics about the role of HDL.
It is interesting that high-dose niacin, alcohol and exercise all
promote flush/blood flow, and that all 3 increase HDL -as opposed to
raised HDL. It seems a consistent finding that a raised HDL is usually
association with lower VLDL. And that if you lower the VLDL, the HDL
goes up? This implies a 'causal' relationship between the levels of
the two substances.
I am working on a conjecture that goes something like this:
When VLDL leaves the liver, HDL transfers apolipoproteins to it. These
allow receptors to recognise the VLDL and thus remove triglyceride
from it using various lipases. When VLDL reduces in size enough, it
becomes LDL, most of which is re-absorbed into the liver. During this
process the apolipoproteins are transferred back to HDL, ready to be
stuck back onto the VLDL that emerges from the liver.
If VLDLs are not being metabolised (probably due to insulin resistance),
there is less LDL to be absorbed, less apolipoproteins to be
transferred back to HDL, and therefore less HDL (measured).
So a low HDL level is actually a result of reduced VLDL metabolism.
HDL level is a sign of rapid VLDL metabolism.
I await critcism.
one Eddie, just don't try to multiply benefits by taking Niacin before
a distance run. Foolishly, I did this before an 'important ' run
thinking of some possible blood sugar boost.The wall of China hit me
at km 4 , to hell with HDL I thought.
to alcohol, I have tried that also as a running aid (copying a famous
octogenarian from California, Wally), ditto with devastating results.
How about combining the three for a 'Poly-effect' ,
although I have a feeling that it may well promote a drastic increase
in intestinal peristalsis (But that would probably be preventable by a
good preventive dose of statins, don't you think?
- Not bad, but why then, some with insulin resistance would have high
or very high LDL Accumulation? - due to unresponsive liver working
hard to get rid of sugar as fat in VLDLs?
After all these people given lots of fat and little sugar reduce their
LDL levels and increase HDL levels rather soon.
I think what happens with a high (saturated) fat diet is that most of
the fat is carried by chylomicrons directly from the gut to the fat
stores. The fat doesn't pass through the liver, or get converted to
triglyceries in the liver - so it never gets measured, as this process
occurs in the
post-prandial period, and no-one (hardly anyone) measures lipoproteins
in the post-prandial period.
On the other hand you eat a low fat, high carb/sugar diet, the excess
sugar is converted to triglyderides in the liver, and is then sent out
within VLDL. This process takes more time, so VLDL levels are found to
be higher (in the fasting period).
What we are seeing with high carb diets (high VLDL, low HDL) is
exactly what you would expect to see (I believe), and vice-versa.
The biggest problem, in this whole area, is that no-one ever seems to
consider that with lipid/fat/carb metabolism we are looking at a
highly dynamic process. We take fasting (static) measurments, and then
claim to understand what is going on. This is like trying to work out
the plot of a movie from looking at a single frame.
There is plenty of research to show that the fasting state and the
prandial/post-prandial state are completely different worlds. People
with normal fasting blood sugars can demonstrate a whole spectrum of 'spikes'
and other abnormalities after eating. (People with measurable CHD that
There is a study from Mexico which found a group of men with severe
CHD andno risk factors: no raised blood sugar, normal HDL, normal VLDL,
normal BP, not overweight, non-smokers etc. etc. However, when their
metabolisms were stressed with an OGTT they demonstrated insulin
resistance, hyperinsulinaemia and hyperglycaemia. Not detectable in
the fasting state.
Enough, perhaps. But I shall lay my cards on the table and state that
I believe plaques develop in the post-prandial period. This is when
the levels of all pro-atherogenic substances reach their peak.
Measuring things in the fasting state isn't going to give us more than
a very opaque view of the real processes going on.
Beer mitigates some effects of copper deficiency in rats. So we
titled our paper (Am J Clin Nutr 51:869, 1990) in which we reviewed
all the epidemiology to date along with the history of beer and per
capita beer consumption.
Because of numerous similarities between animals deficient in copper
and people with ischemic heart disease we did five experiments.
Rats that drank beer lived 6 times as long as rats that drank water
and had lower cholesterol, less heart damage and better utilization of
dietary copper. Similar amounts of alcohol in water had no
We also suggested that increased beer consumption may explain why
average cholesterol concentrations fall in summer. It is
important to emphasize that the epidemiology relates to the
consumption of alcoholic beverages, not of alcohol.
Recommendations for alcohol consumption in
books by diet experts and “experts” vary from nearly none to
several glasses daily of red wine only, to 1.5 drinks of any variety
(20 mL of ethanol daily) daily, all based on the long-known protection
from CVD. In fact, there is no significant difference in
all-cause death rates between non- and moderate drinkers (Theobald et
al, 2001; Malyutina et al., 2002), who showed that the CVD protection
is balanced by more stroke and cancer. None is proper for those
with the “leaky gut” syndrome (Braly et al., p150; Smith, p148-9).
For the carb-sensitive only the carb content matters, so ales and
stouts with up to 18 g/355 mL should be avoided in favor of diet beers
with ¾ 5 g/355 mL. Low-sugar red wine such as pinot noir at ¾
150 mL per day or champaigne brut naturale is equivalent, but
those interested in the antioxidants in wine can obtain them by eating
grapes and berries (Smith, p149).
References Dangerous Grains: Why
Gluten Cereal Grains May be Hazardous to Your Health, by James Braly,
MD & Ron Hoggan, MA. New York, NY:Avery/Penguin Putnam,
Malyutina, S., Bobak, M., Kurilovitch, S., Gafarov,
V., Simonova, G., Nikitin, Y. & Marmot, M. (2002).
Relation between heavy and binge drinking and all-cause and
cardiovascular mortality in Novosibirsk, Russia: a
prospective cohort study. The Lancet, 360, 1448-1454.
Going Against the Grain: How Reducing and
Avoiding Grains Can Revitalize Your Health, by Melissa Diane Smith,
Chicago, IL:Contemporary Books, 2002.
Theobald, H., Johansson, S., Bygren, L. &
Engfeldt, P. (2001). The Effects of Alcohol
Consumption on Mortality and Morbidity: A 26-Year Follow-Up Study.
The Journal of Studies on Alcohol, 62(6), 783-789.