Is the "lipid hypothesis" all hogwash?

[jackdavinci]

@Gary_T

It appears to me the medical profession is unable or unwilling to sort out who would be harmed from these substances from who would not, and defaults to “better safe than sorry” blanket recommendations for everyone to limit their salt intake and keep their cholesterol levels down.

To me it seems the opposite - doctors are pretty lazy and resistant to change or excessive effort. In other words, they won’t bother to start advising their patients about salt, or cholesterol or whatever, unless they are already problematic according to some sort of testing born of symptoms. Generally doctors who have non problematic patients don’t give them much advice.

[rhubarbarin]

jackdavinci, I haven’t had that experience but I suppose it depends on which doctors you’ve seen. I’ve gotten a lot of medical advice that might apply well to the majority population, but is downright BAD advice for someone like me. Being cautioned against gaining more body fat, for instance (I have a bit less than 20% - of course the doctor did not measure it- and while I am healthy, I could do with gaining plenty of fat AND muscle), advised to keep my salt intake low (I have low blood pressure, am very active and tend to have salty sweat - I need to be conscious and add more salt), advised to keep my fat intake low (my cholesterol is TOO LOW, raising it would get me out of high-risk groups for several conditions).

@DSeid

Rhub you can get a mess of calories with nuts, nut butters, avocados, game meats, fish, olive oil and other sources of MUFAs and PUFAs. If you are interested in building strength, then you may appreciate that such is the basis of crossfit’s nutrition advice as well.

I avoid PUFA as much as possible as I think it is unhealthy in any but minimal amounts.

[Grateful-UnDead]

This article should be of interest in the current discussion:

http://www.natap.org/2009/HIV/042209_01.htm

Here is the abstract:

ABSTRACT

Background- Although a wealth of literature links dietary factors and coronary heart disease (CHD), the strength of the evidence supporting valid associations has not been evaluated systematically in a single investigation.

Methods- We conducted a systematic search of MEDLINE for prospective cohort studies or randomized trials investigating dietary exposures in relation to CHD. We used the Bradford Hill guidelines to derive a causation score based on 4 criteria (strength, consistency, temporality, and coherence) for each dietary exposure in cohort studies and examined for consistency with the findings of randomized trials.

Results- Strong evidence supports valid associations (4 criteria satisfied) of protective factors, including intake of vegetables, nuts, and “Mediterranean” and high-quality dietary patterns with CHD, and associations of harmful factors, including intake of trans-fatty acids and foods with a high glycemic index or load. Among studies of higher methodologic quality, there was also strong evidence for monounsaturated fatty acids and “prudent” and “western” dietary patterns. Moderate evidence (3 criteria) of associations exists for intake of fish, marine {omega}-3 fatty acids, folate, whole grains, dietary vitamins E and C, beta carotene, alcohol, fruit, and fiber. Insufficient evidence (²2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; {alpha}-linolenic acid; meat; eggs; and milk. Among the dietary exposures with strong evidence of causation from cohort studies, only a Mediterranean dietary pattern is related to CHD in randomized trials.

Conclusions The evidence supports a valid association of a limited number of dietary factors and dietary patterns with CHD. Future evaluation of dietary patterns, including their nutrient and food components, in cohort studies and randomized trials is recommended.

[Chief_Pedant]

When it comes to “the lipid hypothesis” the sorts of questions we ask are:

1. What is associated with arterial disease?
2. Does what is associated with it cause it?
3. If it does cause it, does altering this putative cause help?
4. If it helps, does it help more than it hurts, and how do we measure the hurt?

You can imagine how complicated it gets to sort those out using real people and real lifestyles.

I think DSeid and others have a reasonable summary of the current consensus: Lipids are associated with arterial disease, they are not the whole story and efforts to alter them help some. Getting off your fat ass and exercising moderately and regularly, along with a significant calorie restriction emphasizing a diet low in certain fats, low in calories overall and low in simple sugars is a great start. Few do that. Statins help statistically; maybe they help as much as they do because the vast majority of the masses don’t do any of the other stuff–or at least enough of it. And I don’t doubt the current statin crop may have long-term untoward effects.

It’s not a shock to medical science to promote the idea that there’s more to the story than just “high lipids mean more heart disease so take statins and you’ll be fine.” That doesn’t make the “lipid hypothesis” all hogwash.