Just to make it explicit, although high in ‘animal fat’, the traditional Inuit diet is especially rich in Omega-3 fatty acids. These unsaturated fats, especially prominent in cold water fish, seem to be quite potent in preventing circulatory disease (among a number of things).
Still, few lived to be what we consider “old” today. TimeWinder is correct. Note that today, reaching 100 has almost become unremarkable.
I agree, animal fat isn’t bad for you- taken in moderation. Replacing it with some of the various un-natural things we have does seem to be bad for you. Micheal Pollan makes a point that it’s ONLY the so-called “Western” diet that is bad for normal humans. You can eat Mediterranean, Vegetarian* or even Eskimo and be fine.
I suggest the “Food” diet as Micheal Pollan wrote up.
*rhubarbarin makes an excellent point about the health benefits of Vegetarianism, but many who follow that diet also eschew junk food too.
Yes, this was definately a concern of mine when I started this diet.
I eat large amounts of sardines and anchovies which are high in omega-3s (I feel too guilty eating other seafood) and I also eat mostly grass-fed cow, lamb, and goat, grass-fed cow’s milk products, and pastured fowl and eggs. All have much higher ratios of omega-3s to omega-6s than factory-farmed animals. When I eat non-pastured products I supplement with cod liver oil (high in omega-3s).
Releasing sabre-toothed tigers into Manhattan would, however, increase Animal Planet’s life expectancy–once they made it part of a new reality show. Part Jurassic Park with it’s DNA reconstitution, part Running Man… what’s not to love???
Life expectancy at birth is only 45, but after age 10 life expectancy is similar to Western countries. 6% of the total population of 2300 is 65 and up. Living to the late 90s or triple digits is no rarer than in America.
Kitavans have no access to modern foods, but eat a higher proportion of carbohydrates than most primitive populations studied - from tubers and fruit only. Evidence that one diet does not fit all. Very far from an Inuit diet although they have as much satruated fat in their diet as people in Sweden, from their other staples, coconut and fish.
They have no cardiovascular disease or stroke whatsoever, and apparently no Alzheimers or dementia even in the very elderly.
Omega-3s might possibly explain why the Inuit don’t get heart disease despite their massive amounts of dietary saturated fat, but then what explains the Masai? The French? The Tokelau? Countless others who eat diets high in saturated fats but have lower rates of CVD/CHD than we have in the West?
The answer that you can’t, as long as you accept Western medicine’s belief in the lipid hypothesis, which is based on junk science:
http://www.msnbc.msn.com/id/22116724/ns/health-diet_and_nutrition//
Ancel Key’s study was a scientific fraud, but doctors remain in auto-proctology mode, clinging to this silly belief even when though there are no good studies to support it.
It’s exactly what Feynman was talking about when he lectured on “Cargo Cult Science”:
You know, I don’t disagree with you (I think). My own diet is quite rich in saturated fat and eggs. And, in terms of dietary cholesterol per se, I urge you to read what I said here. Bottom line is that I am not saying you’re wrong, OK?
With that behind us, and as alluded to earlier, if there is a link between saturated fat and vascular health, it may be obscured by the composition of the calories substituted for those of the saturates (or simply by the other dietary constituents). If they’re offset by omega3’s, or CHO, or unsat’d fat, or monounsat’d fat, there may well be very different resultant risks.
To be fair, Key’s seven countries study was not unique in its findings. For example, although I haven’t looked at it for years, I’m pretty sure that the monumental Framingham Study found also that dietary saturated fats were correlated with coronary disease.
By the way, you call the ‘lipid hypothesis’ “junk science”. Are you referring to the ostensible link between dietary lipids and heart disease, between LDL-cholesterol levels and heart disease, or both? I’d be interested to know.
Here’s what some of the key contributors to the Framingham Study:
“The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century.”
–George Mann, ScD, MD, Former Co-Director, The Framingham Study
“In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol. . . we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active.”
–William Castelli, MD, Director, The Framingham Study
http://www.westonaprice.org/Principles-of-Healthy-Diets.html
I’m talking about the former, although the latter may be complete bullshit as well. As I understand, the actual size and density of the LDL particles seem to be the variables that are predictive of CHD/CVD.
Very interesting! I wonder if Castelli was saying that by exercising and being physically fit, and staying slim by doing so, the effects of high dietary saturated fat may be offset. Or he maybe he is saying the whole sat’d fat bit is BS!
With respect to LDL particle size, you are right. Small, dense LDL is associated with coronary disease. I’ve even heard it expressed that that may be so because of the enhanced ability of such small particles to enter (damaged) vessel walls, i.e. mechanically easier.
ALthough vastly overstated, it seems pretty clear from good RCTs, that lowering LDL does lead to fewer coronary events. Still, I often think that the LDL is really a surrogate for the more potent causal factor of high apoB levels. It’s hard to lower LDL without lowering apoB. Epidemiologically though, apoB is the more powerful predictor.
I wanted to elaborate that high apoB levels reflect increased LDL particle number. The actual LDL-cholesterol level is less important than the number of LDL particles. This may reflect a bit of a paradigm shift wherein the more LDL particles there are, the more the coronary risk.
Perhaps this is suggesting that an increase in LDL particle number means more LDL particles per LDL-receptor, which means a given LDL particle is less likely to be cleared through that receptor mechanism and therefore have prolonged circulation time. That, in turn, means there’d be more time for the LDL to be chemically modified in the circulation (e.g. glycation, oxidation). Modified-LDL would then be taken up by receptors for modified-LDL such as those found (I think) on both macrophages and endothelial cells. Either way, such a cell, full of LDL-cholesterol, is beginning to sound like a foam cell . . . You get the idea.
Good to know.
By the way, here’s a (somewhat dated) quote I found from Harvard’s Walter Willett, one of the world’s leading epidemiological researchers:
“the focus of dietary recommendations is usually a reduction of saturated fat intake, no relation between saturated fat intake and risk of CHD was observed in the most informative prospective study to date.”
I don’t know about the rest, but here’s a cite showing that the Masai actually had worse atherosclerosis than Westerners; it just happened that their vessels widened more than the plaque could build up, assumed to be due to their exercise regimen.
That’s interesting, dre2xl. Not that it invalidates it, but the linked study is almost 40 years old and probably uses data that’s closer to 50. So, I wondered if more recent investigations confirmed or extended the finding. Interestingly, I could find only a single paper published on the topic of atherosclerosis in the Masai since then (using a simple PubMed search). Basically, it concluded (once more) that the Masai are likely protected from coronary disease, despite their high intake of ‘animal fat’, as a result of their very high levels of physical activity (+/- a genetic component).
As has been pointed out by others here, and something which I am beginning to believe, it may well be that saturated fats have simply been given an unjustifiably bad name.
“Nutrition Action Health Letter” (Center for Science in the Public Interest) states in the Jan/Feb 2010 issue:
I consider (just MHO) CSPI to be hopelessly compromised when it comes to anything to do with dietary fat – they have drunk the “lipid hypothesis” Kool-Aid till the beaker was dry, and can’t be expected to say a single good thing about animal fat. They issued some screed a few years ago saying Americans ate too much cheese. For that, alone, I can never forgive them, and would require some rigorous back-study as to any claims or characterizations they made.
[In the interests of bi-partisanship, I’d have a similar caveat for the cite upthread to the Weston Price people’s website; I sort of agree with much of what the Price crowd says/believes, but IIRC on some subjects, specifically their fairly fanatical support for raw milk, they’ve made claims (cures diabetes, etc.) that I have to cock a sketchy eyebrow at.]
From Quick Studies.pdf:
Here’s the latest blow to the Saturated-Fat-is-Bad-for-You Cargo Cult science, from the European Journal of Clinical Nutrition:
http://www.nature.com/ejcn/journal/vaop/ncurrent/abs/ejcn201045a.html
This was a prospective study with a 14-year follow-up period. They compared people who used full-fat dairy to those that avoided dairy and/or used low-fat dairy products.
The result?
In other words, people who consumed full-fat dairy products were three times less likely to die of heart disease and stroke than those who drank skim milk or avoided dairy, even after adjusting for possible confounds.
Do you have a reference for this? Thanks.
http://www.thepaleodiet.com/articles/AJCN%20PDF.pdf
On average, hunter-gatherers get about 65% of calories from consuming animals, and this is how most humans ate millions of years prior to the dawn of agriculture roughly 10,000 years ago. Agriculture therefore represents about 0.5% of our Environment of Evolutionary Edaptation (EEA).
Yeah, and what was the average life span of those “cavemen”? Most, or all, did not live long enough to develop cardiac diseases or cancers.