Just to make it clear, this is NUANCED, and depends on your gender.

Males: equivalent of 1-2 glasses of wine per day.

Women: equivalent of 1 glass of wine per day AND ONLY IF THEY CONCURRENTLY HAVE @ LEAST 400microg of folate.

All the studies I've seen showed negative effects for women consuming >1 glass per day, and for any amount without proper folate (NOT related to potential for pregnancy).

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Are you saying Jt512 is incorrect on his information, regarding drinking alcohol?

So according to your research it has to be wine, and with folate in the diet, is that correct?

No beer, No scotch, it must be wine for it to be beneficial, is that what you are stating?

Could you be so kind to share this particular research study. ?

Just to make it clear, this is NUANCED, and depends on your gender.

Males: equivalent of 1-2 glasses of wine per day.

Women: equivalent of 1 glass of wine per day AND ONLY IF THEY CONCURRENTLY HAVE @ LEAST 400microg of folate.

All the studies I've seen showed negative effects for women consuming >1 glass per day, and for any amount without proper folate (NOT related to potential for pregnancy).

really dumb question. I know there are studies linking moderate drinking, in general, to better health (in general). Just curious, though, and I'm not even sure how to ask the question clearly, how much of the benefit has to do with the ingredients over the alcohol itself?

In other words, with regards to wine, how much of the benefit is due to the grapes? Would grape juice (not the overly sugared kind) be a better substitute? And with beer, would barley, for instance, be better than beer?

I don't know what goes into other kinds of liquor necessarily, so I can't comment on things like high-quality vodka, whiskey, or pisco, etc..

For one thing, because it increases serum HDL-cholesterol, so it's protective against heart disease. There may be other factors as well. It's not completely understood.

Jay

While it does raise HDL cholesterol, any causal link to reduced heart disease via this mechanism is only hypothesized, not proven.

Nonsense. What paleolithic diet website have you been visiting?

Jay

The studies that I have seen seem to hint at the fact that its something about an "alcoholic drink" in general that confers benefit.

I'm interested to hear what Jay thinks about this, but it's my opinion (decently well supported by the literature) that our use of reductionistic thinking in the realm of food & nutrition is misguided. We (at least many American & European societies) want to know what it is IN PARTICULAR that makes eating X food so beneficial.

Many of the studies I have seen in this light show that each time we find a food that is beneficial, pick (often seemingly at random) a nutrient unique to or at least in abundance in that food, and use it as a supplement, the beneficial results aren't replicated. This suggests that when we derive benefit from a food it isn't due to a single agent but rather to a multifactorial cause.

There are some foods we have identified as beneficial AND have been able to identify a single agent. Often (though not always) these foods were pretty simple to start with- like certain plant oils providing cardio-protective effects. We have replicated these effects with a single substance, omega 3 FA. Great, but the oils weren't exactly a complicated mix to start with.

Nonsense. What paleolithic diet website have you been visiting?

Jay

The studies that I have seen seem to hint at the fact that its something about an "alcoholic drink" in general that confers benefit.

I'm interested to hear what Jay thinks about this, but it's my opinion (decently well supported by the literature) that our use of reductionistic thinking in the realm of food & nutrition is misguided. We (at least many American & European societies) want to know what it is IN PARTICULAR that makes eating X food so beneficial.

Many of the studies I have seen in this light show that each time we find a food that is beneficial, pick (often seemingly at random) a nutrient unique to or at least in abundance in that food, and use it as a supplement, the beneficial results aren't replicated. This suggests that when we derive benefit from a food it isn't due to a single agent but rather to a multifactorial cause.

There are some foods we have identified as beneficial AND have been able to identify a single agent. Often (though not always) these foods were pretty simple to start with- like certain plant oils providing cardio-protective effects. We have replicated these effects with a single substance, omega 3 FA. Great, but the oils weren't exactly a complicated mix to start with.

Interestingly, the converse tends to NOT be true. Typically, foods that we have identified as being HARMFUL to us typically do have ONE causative agent. And removing that agent removes/greatly reduces the harm conferred from that food.

Not in the field myself, but everything I've been taught in pharmacology, physiology and cardio-vascular medicine in the last 3 years supports TarHeel's claim.

Jay, of course that's the mechanism of action for HDL. It's not clear however that a simple absolute rise in HDL represents CAD protection.

The links you provided back this up.

The VA-HIT show that the HDL increase needs to be accompanied by a TG reduction to be cardioprotective.

AFCAPS/TexCAPS showed that HDL BELOW the recommended value has a negative risk associated with it, and that raising the HDL TO THE RECOMMENDED VALUE decreased their risk for CAD. But if I remember that study correctly (haven't read it in ~1 yr), their RR was returned to 1, that is they didn't "gain" cardioprotection, they just returned to normal.

Three years of medical school and partway through an MPH.

The certainty of the claims you're making is vastly overstated.

I would put my "certainty" at about 85%. On the other hand, calling it "only hypothesized" seems to suggest that there is no evidence for it, when, in fact, there is a clear body of consistent evidence from epidemiology, biochemistry, clinical trials, animal studies, and even preliminary studies of infused HDL analogs in humans.

Jay

Mine would be at about 98% for the cardioprotective hypothesis, and about 75% against all comers for HDL and fibrinogen to be the primary mediators.

There's a big difference between 85% and fact.

Care to take a deep breath and reexamine my initial statement?

While it does raise HDL cholesterol, any causal link to reduced heart disease via this mechanism is only hypothesized, not proven.

Are you really saying you disagree with that? Rereading it myself, I probably should have been more clear in saying that I was referring to HDL being the mechanism of risk reduction for alcohol.

I didn't realize you were talking about alcohol. I thought you were talking about HDL-C per se

Right. I never said I was certain. You said I was certain.

I agree that it's not proven, but I think that the phrase "only hypothesized" is misleading.

I'm pretty sure what got me going was the statement "For one thing, because [alcohol] increases serum HDL-cholesterol, so it's protective against heart disease.," since it doesn't necessarily follow that anything that raises HDL is protective against heart disease.

Haha, no. My fault for not being more clear.



I'm pretty sure what got me going was the statement "For one thing, because it increases serum HDL-cholesterol, so it's protective against heart disease.," since it doesn't necessarily follow that anything that raises HDL is protective against heart disease. You did acknowledge that it was more complicated than that, so I probably didn't give you enough credit for nuance.



It depends. I'm ok with saying it, because to me the word hypothesis implies at least a reasonable body of evidence, with many carrying a substantial body of evidence. Different people have different understandings of the term, though, and I suppose RC.com is not a place where you'd assume I was speaking with that understanding.

Kind of a moot point for the topic but since when does a hypothesis imply "a reasonable body of evidence"? It doesn't even depend on you definition of reasonable. The term hypothesis, especially in the scientific field has Zero contingencies on evidence. Really a hypothesis can be a total shot in the dark. A hypothesis can be merely conjecture.
I know its just semantics but you need to be right when you try to take an authoritative position.

Yes, Of course !

Kind of a moot point for the topic but since when does a hypothesis imply "a reasonable body of evidence"? It doesn't even depend on you definition of reasonable. The term hypothesis, especially in the scientific field has Zero contingencies on evidence. Really a hypothesis can be a total shot in the dark. A hypothesis can be merely conjecture.
I know its just semantics but you need to be right when you try to take an authoritative position.

Yes, Of course !