I think that’s a bit unfair. Experiments on humans are kind of frowned upon, and most effects will take a few decades to manifest.
So doctors look at a large group of people with disease X and find a high level of B in the blood. That can be done just looking at existing data. But then the difficult part starts:
Does a high level of B cause X,
does X cause a high level of B,
are they both unrelated,
does a high level of B only cause X in people with a genetic predisposition, but not the rest, and how common is that genetic predisposition in the general population?
Or is a high level of B a consquence of a general unhealthy lifestyle and thus only an indicator, but not a cause?
How can the doctors find the answer to this important question from the data gathered? Answer: they can’t. They need to devise new tests for each seperate hypothesis, assign different groups, and wait (optimally) 20 years before looking at the results.
But in the meantime, to be on the safe side, they recommend that people lower their level of B to avoid X. 20 years later, the doctors find out it’s hypothesis 3, and the real cause is level of C, which they didn’t notice before. So now research starts all over again. And all the people who lowered B think that the doctors are idiots.
But if hypothesis 1 turned out to be correct, the initial recommendation would have saved a lot of lifes, so the doctors did the right thing by playing “better safe than sorry”.
typoink, I’ve got enough peer-reviewed papers like the above, reliable websites, testimonials and personal experience up the wazoo, that by the time I got it organized to post, this thread would be dead and gone. Fat Head is a great start, and he’s got a great blog. He also produced a short DVD series that goes into some more detail on the LH that is available on his blog.
Oh, and I don’t read Weston A Price (raw milk faddists) and certainly not Kevin Trudeau.
Funny you should say that - a later paragraph states “[Statins] decrease the total number of low-density and very low-density lipoproteins in the blood, including the smallest and densest form of LDL, which is now widely believed to be particularly noxious”
I just saw a study yesterday disputing that effect. Taubes, BTW, is an excellent researcher and writer.
I strongly agree with most of the points he makes here. And like most people who eat within the perimeters detailed on his blog, I have seen my HDL climb significantly (and my HDL to LDL ratio get even better) with very high intake of saturated fat.
Angel, I found Weston Price’s *Nutrition and Physical Degeneration *fascinating and a valuable resource, as do many intelligent people with an interest in health and nutrition (including Tom Naughton - who could also be described as a raw milk faddist - and Dr. Kurt Harris). The Weston A. Price Foundation is a totally different creature, but shouldn’t be dismissed out of hand either IMO.
Have none of you guys heard of the hyperlipidemias out there?
Familial Hyperchylomicronemia - autosomal recessive mutation in lipoprotein lipase - causes lipemia retinalis, eruptive xanthomas, hepatosplenomegally, bouts of acute pancreatitis, and heart disease.
Homozygous Familial Hypercholesterolemia - autosomal codominant mutation in LDL receptors - causes childhood heart disease which kills before the age of 10 without a liver transplant.
B-Sitosterolemia - autosomal recessive inability to secrete specific sterols in bile - Tendon xanthomas, and huge risk of coronary artery disease.
Tangiers disease - autosomal recessive inability to make HDL - xanthomas, hepatosplenomegally, neuropathies, coronary artery disease.
You don’t need to do experiments, there are plenty of people with perturbed lipid metabolism that present with terrible disease.
Interesting thread. I have an interest in the topic. Iwonder what heart experts have to say about three data points:
-the inuit/eskimo people. Despite eating a diet of pure fat and meat, they show little incidence of heart disease-why is this?
-the Masia people of east Africa-they live off milk and blood 9from the cos they heard)-they don’t seem to suffer from heart disease.
-the experience of the late Dr. Atkins: Atkins claimed that people who ate his low carbohydrate/high protein diet have a very low incidence of heart diase, and very low cholesteral levels.
Yeah, you’re right, I kind of regretted painting that broad a brush after writing that. I’m not quite convinced about the safety of raw milk yet, but heck, I don’t drink much milk anyway!
The Masai. They have not been seriously studied for a long time now but the understanding was that they get atherosclerosis but that their level of activity protects them:
That noted, the concept that milk might also have some protective effects has been considered as well.
rhub what it has to do with it is considering them as “natural experiments” - disturb lipid metabolism with genetic defects and heart disease increases. Lower cholerstol with statins and heart disease decreases. Is it an absolute slam dunk case? No. Is it very strong evidence? Yes. There is no conspiracy in the medical field (as many of the links proferred claim) to surpress or censor conflicting studies. May the consensus change as more information comes along? Of course. The literature is full of studies debating what balances of fats and sorts of fats may be best and how much the emphasis should be placed decreasing simple carbs and increasing fats from nuts and fish. Science is always a work in progress.
True, LCHF regimens may increase LDL in some cases, but there is a positive change, overall in other lipid markers. So the net effect is an improvement in your ratios, such as TC/HDl and TC/LDL. Here, I’ve got to go run errands, and this is the best I can do right now, but here’s a link and a quote:
In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee
As the title implies, this is a rather frustrated response to the DGAC committee, as much as a published article can be.
It is important to keep in mind the potentially differing effect of cholesterol reduction in those with established coronary heart disease compared to those without it. There are numerous studies, of high ‘quality’, demonstrating that cholesterol lowering (with statins espectially) reduce the recurrence of heart attacks, angina, coronary occlusions, etc.
Here is one representative study - a meta-analysis of 25 studies involving 70,000 individuals. It showed a 20 to 25 percent reduction in ‘bad outcomes’ such as death, heart attacks, etc., in people who already had coronary disease but who then used a statin drug. It is worth emphasizing that meta-analysis of randomized controlled trials, such as that in this study, is the best evidence attainable. Hence, this result (which is typical of other similar studies) should be considered closest to the “truth”.
It is also important to distinguish between attempts at dietary manipulation of cholesterol (and thence heart disease) from drug-based interventions. The former, as pointed out earlier in this thread, seems to be of little or no benefit (at least when employing the traditional, “consensus” type dietary recommendations). OTOH, when used by people at highest risk (i.e. with known heart disease), drug treatment to lower cholesterol (LDL) is of real and significant benefit.
Lawd knows the Atkin’s diet has had its day on these boards. FWIW my personal take on it is that it can be effective to lose weight and that the maintenance phase is fairly consistent with mainstream advice, keeping saturated fat to 10% or less. It does not hold up as evidence that a high saturated fat diet is healthy as it does not advocate high saturated fat long term and the short term high saturated fat phase sacrifices some worsening of vascular compliance and increased inflammation (which as noted may be more important than lipids) in return for the benefits of weight loss, which they then advise maintaining with a low saturated fat diet.
Low carb is the not the question in this thread; high saturated fat and the role of various lipids in atherogenesis pathophysiology is. Indeed there is some good evidence (to my read anyway, including even in the link I just gave) that limiting simple carbohydrates may be of benefit, and that diets higher than the current mainstream recommendations in monosaturated and polyunsaturated fats (MUFA and PUFAs) have significant benefits. That however informs little on the questions asked.
And I note that your response, defending the Atkin diet by pointing out what you see as its other putatively beneficial effect on lipid profiles, implicitly accepts the lipid hypothesis as valid, whereas I was focussed more on the functional effect on blood vessel flexibility and on inflammatory markers, which have independently been correlated with many adverse health outcomes including mortality.
I’m not sure who you’re replying to, but I’ll respond. Not exactly sure where you’re getting that I’m promoting Atkins – I follow more of a “caveman” regimen, but did start on Atkins. Atkins is neither the first nor the only LC diet and I did not have it in mind when I linked the paper. But since you brought it up, I’m not sure you’re correct that it is not high SF long term. Which book are you talking about? The new one? Not saying you’re wrong, I’ll have to go back and check.
Whether the LH is correct or not, its application via public policy to the American public (and other populations) via things like the Food Pyramid has encouraged the consumption of huge quantities of carbohydrates. There is no question to me that this increase in carb consumption has been disastrous.
I agree with you, and venture a guess that most low-carb advocates would agree, that the consumption of saturated fat in the presence of excessive carbs IS harmful. Hence the existence of the dietary philosophy in the first place.
As far as the research papers, you must agree that to isolate the effect of one element (saturated fat) on, say, lipid markers, you must limit the effect of others (carbohydrates). That’s my guess as to why the comparative dietary schemes are labeled “low-carb.” I’m not trying to be a smartass, but how else are you going to do it?
My response was only to your comment about the raising of LDL, not blood vessel flexibility or inflammation, which I have not read enough on yet to address, so I’d be happy to hear more.
Regarding the post topic, I think the OP wanted some verification of some scientific nonsupport of the LH, which I think he got.
Well, I don’t think high saturated fat intake is harmful, regardless of the rest of the diet. My current opinion is that it has an anti-inflammatory, protective effect.
chugs more heavy cream
However more fat in the diet often means more total calories, which often becomes more body fat. I’m not finding the Carbohydrate Hypothesis so convincing these days. Applied to people without borked metabolisms, that is - of which I am one.
I eat loads of that too. Keep in mind that I keenly desire to gain 10-20 lbs, for the sake of vanity and athletic performance. I tried doing it high-carb, and I got really sick (and even large amounts of the carbs that don’t aggravate my digestion and skin, like potatoes and white rice, make my energy levels ‘crash’ so that’s no good either). One can only eat so much protein, and I need a shitload of calories, so I’ve turned to fat by default as it were.
I had responded to a request about what the experts said about the beneficial effects of the Atkin’s diet visavis the lipid hypothesis, and you disputed it.
As far as separating the effect of saturated fat from the effect of carbs, please click on this link already provided. A high saturated fat diet impairs blood vessel flexibility and causes an increase in inflammation markers. A diet high in PUFA or MUFAs does not. A diet high in carbs does not.
I will have to just leave it that I, and Cochrane, and the vast majority of medical scientists, disagree with you about the “scientific nonsupport” for the lipid hypothesis, even though I strongly suspect that lipid levels alone are not the complete story, and even while I agree that the importance of low amounts of simple carbs is underemphasized and that the importance of adequate amounts of PUFAs and MUFAs are just beginning to be understood. Your “caveman diet” has good scientific support and does not conflict with the lipid hypothesis at all. (See this article - “Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet: Health benefits of a Paleo diet” by L A Frassetto, M Schloetter, M Mietus-Synder, R C Morris and A Sebastian in European Journal of Clinical Nutrition 63, 947-955 (August 2009) | doi:10.1038/ejcn.2009.4 - along with other benefits are improved lipids.)
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.
Whoo - I’m all fought out; I’ll have to come back and fight another day yawn
Definitely think/agree the complete story lies not with any one argument, and will probably turn out to somewhere in between. The only thing I will point out is that there is more than one variant of the “caveman” diet - not all stick to lean meat. We generally avoid processed vegetable oils, regardless of MUFA/PUFA content. But again, I’m not well read enough to make an argument re inflammation, although I’ve certainly seen material on that subject.
It’s best to stick with what the original Atkins books say rather than the present Atkins Foundation. They lost trust with the manufacture of fake foods (bars, etc.) You got me curious about the original edition, though. Or I’ll take your word. I’ll check out your latest link soon.Have a good night!
