Discussion about beer, wine and heart disease

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Discussion about beer, wine and heart disease

 

 

Uffe Ravnskov

Malcolm Kendrick

Herbert Nehrlich

Eddie Vos

Malcolm Kendrick

Herbert Nehrlich

Bogdan Sikorski

Malcolm Kendrick

Leslie Klevay

Joel Kauffman

 

21.7 2003

Uffe Ravnskov

See http://www.realbeer.com/news/articles/news-001922.php?rdf

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!

 

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Malcolm Kendrick

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.

 

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Herbert Nehrlich

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.

 

P.S.: 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.

 

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Eddie Vos

Herbert, 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 statins]

 

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Malcolm Kendrick

Regarding raised HDL. It seems a consistent finding that a raised HDL is usually

found in

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. And high

HDL level is a sign of rapid VLDL metabolism.

 

I await critcism.

 

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Herbert Nehrlich

Good 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.

 

As 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?

 

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Bogdan Sikorski

Malcolm - 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.

 

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Malcolm Kendrick

Bodgan, 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 is)

 

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.

 

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Leslie Klevay

Hello: 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 benefit.

 

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.

 

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Joel Kauffman

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, 2002.

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.

 

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