- Dietary saturated fat increases blood cholesterol
- Elevated blood cholesterol increases the risk of having a heart attack
- Therefore, dietary saturated fat increases the risk of having a heart attack
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These studies show that saturated fat increases both LDL cholesterol ("bad cholesterol") and HDL cholesterol ("good cholesterol"), but typically the former more than the latter. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between habitual saturated fat intake and blood cholesterol, it has been very small or nonexistent. Those findings are rarely cited, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments. [UPDATE 4-2012: I did miss several studies, although they're basically consistent with the conclusion I came to here. I plan to update this post with the new references at some point.]
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method is much more accurate than in most observational studies today**. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They analyzed the data every which way, but were never able to squeeze even a hint of an association out of it:
Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:
Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk***.
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends very little support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was roughly 3/4 white rice by calories. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and had a very peculiar and perhaps deficient diet. Also, what is the difference between a diet with 5 and 75 grams of saturated fat per day? Those diets are probably very different, in many other ways than their saturated fat content.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold difference in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's much less influential than other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat a diet that differs in many ways from the diets at the upper end of the range, and other aspects of lifestyle such as physical activity also differ.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol in humans. If it's a factor at all, it must be rather weak. It may be that the diet-heart hypothesis rests in part on an over-reliance on the results of short-term controlled feeding studies. It would be nice to see this discussed more often (or at all) in the scientific literature. It is worth pointing out that the method used to collect diet information in most of these studies, the food frequency questionnaire, is not particularly accurate, so it's possible that there is a lot of variability inherent to the measurement that is partially masking an association. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a modest long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
*** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
**** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators did not attempt to adjust for confounding factors.
116 comments:
You must be mistaken. There are thousands of studies that confirm the saturated diet heart hypothesis. This has been told by our government officials, so this must be true.
Greetings from Soviet-Finland and thanks again for a readable article, even for an engineer.
Thanks Steve. I cross posted this on my blog (www.wmodavis.com)
So what are good predictors of heart disease? oxLDL? Homocysteine?
Oh and thanks for the article; it's always a pleasure to read your blog :)
I know, I am a little picky, but your statement "Just because A causes B, and B causes C, does not mean A causes C." is a little misleading (wrong). 'If A (always) causes B, and B (always) causes C, then A (always) causes C' is completely correct, while 'If A can cause B, and B can cause C, then A can cause C' is unsubstantiated.
Thanks for your blog,
Andrés
All I want is one cardiologist that could explain me this: if high cholesterol and LDL are bad, why patients with CAD have mean TC of 174.4 mg/dl and LDL of 104.9 mg/dl while the general population, at the same time, had a TC of 203 mg/dl and LDL of 123 mg/dl???
http://www.ncbi.nlm.nih.gov/pubmed/16219880
http://www.ncbi.nlm.nih.gov/pubmed/19081406
It's quite fantastic but the first studies incriminating saturated fat didn't even used natural foods with saturated fats, but vegetable oils saturated by hydrogenation (see http://thrivewithdiabetes.com/doc/Cholesterol_was_healthy_in_the_end.pdf ). The analysis of Reiser(1973) on these myths should also not be missed - http://www.ajcn.org/content/26/5/524.full.pdf Some more references here - http://bit.ly/f9kb1E And here are some (actually many!) papers regarding these cholesterol myths - http://bit.ly/hE5HQX
Stephan,
Do you think that increased cholesterol
is the cause for the increase in heart disease and overall mortality, or that it is rather a symptom of something else?
Cholesterol is the precursor of all the protective steroids (pregnelonone, progesterone, DHEA, testosterone) which have been shown to be very protective against all kinds of diseases.
High cholesterol is almost always related to decreased thyroid funticon, which means that less cholesterol is beeing converted into pregnelonone, leading to higher cholesterol levels.
The use of artifically cholesterol lowering statins has been shown to increase overall mortality, which supports the theory that cholsterol is not the cause of the problem, but rather the symptom of another problem.
Mario Renato,
That's a good point. I think that cholesterol is a protective substance.
All substances that lower cholsterol, like statins and PUFAs increase the risk for a heart attack.
Good post Stephan, just a little note regarding the graph you included. The MRFIT study may provide a biased picture because it may reflect the fact that TC is in part of marker of disease.
With data at the individual level (which is good in many respects), one may get the impression that TC causes cardiovascular disease, when in fact it is reflecting other problems that cause heart disease. When you look at averages for populations, you get a different picture.
For example, at relatively low levels TC seems to be protective, and that is not entirely due to HDL, but maybe strongly influenced by the HDL fraction:
bit.ly/bS0wBh
Also, when you look at the full spectrum of TC levels, at the population level, you see U curves all over (not only for overall mortality). The U curves are shifted to the right, when compared to the graph you’ve included in your post:
bit.ly/dK0pFq
Studies that look at individual level data provide new and valuable insights to various phenomena, but they carry potential problems of their own.
Interesting too, that this massive database of heart attack patients (link below) shows a pretty clear association with CAD and low LDL, not high LDL. In fact, if you look at the LDL chart in the upper right corner, you can see very simply that above 160 LDL was the safest place to be, regardless of HDL level. Obviously, the higher the HDL, the better.
Also, look at the 5 bullet points under that same chart. Those type of observations don't exactly line up with what mainstream teaches. One important note to consider is bullet point #5. It seems to me that it's very difficult to acheive a healthy HDL of above 60 (according to them) and simultaneously acheive a 'healthy' LDL below 70 (according to them). Almost as if they are not connecting the dots to understand that the type of foods that give you a healthy and robust HDL don't really result in a super low LDL, save for a very small amount of cases. It’s like a catch 22. It’s like we’re all chasing a phantom.
This makes sense to me too, because I personally saw an increase in LDL and HDL after changing over to a more high fat, moderate protein, lower carb, nutrient dense 'paleo' style diet. So did my wife. But just because the calculated number of your LDL rises, doesn't necessarily mean that your LDL got worse. As Stephan has blogged about here in another post, and as Chris Masterjohn has pointed out, oxLDL and particle type or ‘pattern’ are far more important.
LIPID LEVELS IN CAD PATIENTS
Jack K
Thanks for rounding up all of this evidence, Stephan.
Of course there's also the issue of what kind of LDL saturated fat increases (or doesn't increase, rather). Krauss's studies have shown that replacing saturated fat with carbs increases small, dense LDL, which is more likely to oxidize and is a significantly higher risk factor for CVD than large, buoyant LDL. Carbs also decrease HDL and increase TG, while saturated fat has the opposite effect.
Ned also brings up a good point: TC is not a risk factor for CVD in all populations. The Aboriginal Australians have among the lowest TC levels in the world, and the highest rates of heart disease. The French have high levels of TC, but the lowest rates of CVD in the industrialized world.
Women suffer 300% fewer heart attacks than men, despite having higher average TC levels.
Cholesterol is a risk factor in men under 65 in the U.S., but not in men over 65. In fact, low cholesterol increases mortality risk in the elderly. It's unlikely that a risk factor for a disease stops being a risk factor at the age when that disease kills the greatest number of people.
Post-meal blood sugar is a far more accurate and consistent marker of CVD risk. IMHO we all need to forget about cholesterol and saturated fat and start paying more attention to our blood sugar.
I partially disagree:
If a person is E4 genotype (like me), then I can assure you that saturated fat will dramatically raise their LDL blood cholesterol. I've witnessed it time and again with myself. Genotype deciphers how lipids are metabolized.
People's lipids with E2 or E3 genotypes typically don't usually respond very actively towards saturated fats.
So, if you test a group of people, you must account for this 50% differential, because half the population doesn't have an E4 gene.
That's why the data seems conflicting sometimes.
Hi Stephan
What do you think about the whole large-fluffy vs small-dense thing? It seems to have become kinda gospel on this side of the internet.
I didn’t think LDL was even considered a risk factor at all for certain groups such as Japanese men.
I keep leaning towards becoming a cholesterol denier, in all its incarnations.
Hi Stephen,
You have a geat blog. I am a long time reader and this is my first comment.
I know I am only one example (57 Year old male). In my case, increase saturated fat has increased both my HDL - from low 20s to 40 and - LDL from 130s to 180s. Trigs also came way down from 250 to 90s. My stats have been stable for a couple of years on low carb high fat diet.
I check your blog at least weekly and recommend it others. Thanks for taking the time to write the blog
Rick
Hey man, great post. Just a quick clarification, although I know what your saying, the way it's written might lead people to misunderstand. If A must cause B and B necessarily causes C then A must lead to C. However, this is a case where we don't know if A cause B or if B causes C. All we have is observed correlations. It might be the case that x causes both A B and C (or at least B and C in this case). Sorry if this is nitpicking; I guess it's just an idiosyncrasy, but the correct way of writing that ** would be to say something like 'it's a logical fallacy to assume that just because we observe B when A is present and we observe C when B is present, that therefore A must cause C. In point of fact X or Y may cause C and A and B may just be correlations or products of X or Y.'
Serdna, thanks for the clarification. You must be a Logic man
Arttu, COme on do you always believe what government officila tell you?? Open your mind man.
Ron Krauss, whose mega-study last year found no relationship between saturated fat intake and heart disease risk, says at the bottom of the following interview that while
high carbs cause a lot of heart disease nowadays, saturated fat intake used to be the main culprit, and people should limit sat fat intake to under 10%. This surprised me, in view of his research, including his research on small dense LDL.
http://www.meandmydiabetes.com/2010/03/26/ldl-cholesterol-ron-krauss-md/
Uffe Ravnskov, MD, PhD wrote a book called
"The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease".
In this book he completely demolishes the diet-heart hypothesis by using all of the studies the establishment uses to promote the idea in the first place. His argument is very well referenced and water tight.
The book is sadly out of print, but if you can find a second hand copy get it and read over and over.
As we now have much more information about cholesterol and heart diseases we should start measuring the quality of LDL (what is the particle size - small or large). Not just HDL and LDL values.
As mentioned it has been shown that SAFA increases both LDL and HDL. LDL increases because SAFA makes LDL particles bigger decreasing the risk.
In the Framingham Heart Study serum cholesterol levels were not associated with heart disease for men aged 50-63 years. This fact is rarely referred at all, because it doesn't fits in the lipid hypothesys. Also, in the Lipid Research Clinic Study, researchers found that when people with established CHD are excluded, the association of cholesterol levels in the general population with mortality becomes very weak. So cholesterol can't probably be a prime mover in CHD, with a causative role. If it is elevated in people with CHD, could it just be the result of the disease process, rather than its cause? About this issue, see pages 181-185 of the book "Vitamin D and Cholesterol", by Dr. David Grimes (online here http://bit.ly/dML4vf )
Rafael B: I think Arttu was speaking with tongue in cheek.
O Primitivo: Your argument is contradicted by the data in Jack's link. Jack links to a summary of one of my favorite studies, Gregg Fonarow's study of the lipid levels of patients admitted to the hospital with heart disease events. The data shows (as Jack points out and ocnsistent with Mario Renato's excellent points) that people going to the hospital for heart disease events have way below average LDL (around 105). Fonarow concludes, preposterously, that the guidelines for LDL lowering are not low enough.
Jack asserts that the study indicates that having high LDL looks favorable for avoiding the dreaded trips to the hospital. Unfortunately, the numbers in the table he points to don't prove that. What is needed is population reference numbers -- which group in the general population is over-represented in the table of those going to the hospital. Oddly, it is not easy to come by good information as to the general population levels that line up with the data in Fonarow's study, but I have tried and can tell you the real disconnect is in the HDL numbers. People with low HDL are way overrepresented in the Fonarow table and those with HDL above 60 are way underrepresented. That may not seem like news, but compare that to the fact that people with low LDL are at least somewhat overrepresnted and those with high LDL at least somewhat underrepresented.
By the way, go look at the actual Fonarow study. The mini-table on the page that Jack links to is only the subset of patients who had known heart disease. Separate information is available for patients admitted with their first heart event (it is pretty much consistent with the table you see in Jack's link).
I could have been a bit clearer. The data in the Fonarow study contradicts O Primativo's point that high LDL may just be a marker of heart disease. The Fonarow data shows that people admitted to the hospital with heart disease events don't even have high LDL. It seems to mark nothing.
By the way, as I recall Fonarow discounts the notion that low LDL in the hospital admittees was significantly affected by statin use, but it may have lowered the LDL numbers a tad (that pesky residual risk of 80%). In any case, the HDL numbers are probably little affected by statin use.
My view is that HDL is very important to prevention, but not focused on because the only drug that works on it (niacin) is a major PITA with its flushing effects. The general advice that exercise helps HDL proved useless to me until I combined a diet with good amounts of fat with resistance training. Resistance training drives up HDL numbers, but the effect is only for a few days so one needs to stick to it. Other forms of exercise never seemed to have much effect for me.
Some posters above make the point regarding age, which I suspect is important to the Fonarow data. After men pass their mid-50s or early 60s, the supposedly higher risk associated with high cholesterol or high LDL flip-flops. Older people have more heart events, and that effect swamps any correlation (if it exists) in the younger folks between high LDL and heart events.
Growing number of researchers have discarded the cholesterol theory completely. Inflammation will cause heart diseases and vein blockages (for example excessive carbohydrates will cause inflammation).
Major question is would the small dense LDL cause the inflammation or is it inflammation in the body that will oxidise the LDL particle.
What do you thin, Stephen?
Yah and that new drug called Anacetrapib is supposed to directly target HDL. It is a CETP blocker. Chris Masterjohn and Dr Davis have written about the dangers associated with that. Getting your HDL up in a healthy range via natural nutrient dense foods with no funny ingredients has been proven. But when we start toying with cholesterol transfers and all kinds of other correctly functioning processes, I see a major red flag.
That chart has some very interesting bullet points. It did note that 21% were receiving lipid lowering drugs prior to hospitalization. And look specifically at the "Conclusions". Am I reading this wrong? To me, these bullet points don't add up.
• In a large cohort of hospitalized CAD patients, almost half have admission LDL levels < 100 mg/dL, whereas less than a quarter of patients have LDL >130 mg/dL. and triglyceride levels over time.
• These findings provide further support for recent guideline revisions with even lower LDL goals.
So 75% of the admitted CAD patients had under 130 LDL, and the goal is to get LDL even lower? I don't get it.
I'm not saying I'm all about high LDL. But I think the LDL markers that we’ve been told are ‘healthy’ may be off by a bit. It seems to me that if you eat a diet rich in high quality fats and have healthy HDL and low trigs, a slightly higher LDL will occur. As we all know, the particle size increase also increases the calculated number, which can be very misleading unless you are "in the know" about the importance of LDL type and oxidation levels.
Picture a swimming pool with a net over it with holes in the net the size of racquetballs. Now place 100 muddy baseballs on the net. These could represent small, dense LDL particles. If any balls fall through the net, it makes the water dirty. Chances are, some baseballs might ‘fall through’ the racquetball sized holes. Now remove 80 of the baseballs and replace them with 130 clean beach balls. Now your LDL count would be 150 (20 baseballs remain), and a whole lot more volume, but did the risk of balls falling through the holes in the net to make the water dirty increase or decrease?
At any rate, fooling around with all these numbers is only going to allow us to get as good a hypothesis as possible, which is why we all do it. But rather than thinking that high LDL 'causes' this or high HDL 'protects' against that, I think it's more appropriate to consider that maybe all these factors are simply markers that tell us a story about what's really going on in the body. And that a high HDL isn't actually what's protecting you from a heart attack, but it's more of a key signal that whatever functions that do protect you from the heart attack are operating well. Does that make sense?
-Jack Kronk
Barkeater: Some studies show that lipid levels are decreased after acute coronary syndromes, and this fact might probably explain the lower LDL levels found in Fonarow's study. See some references here:
http://www.ncbi.nlm.nih.gov/pubmed/7689082
http://www.ncbi.nlm.nih.gov/pubmed/11111225
http://www.ncbi.nlm.nih.gov/pubmed/18402897
The lipid levels of patients admited to hospital after CVD events, measured some days/weeks/months(?) before those events, are the same as the general population? It depends on the age, older than 50yrs with or without CVD probably have the same TC levels as the LRC-CPPT data show. See http://www.ncbi.nlm.nih.gov/pubmed/2215579
FatFan: Chronic inflammation (and infection) alone will not promote heart disease. The Tsimane indians of Bolivia have huge chronic inflammatory levels (25% of them have CRP above 10mg/dl), and despite of this there is no CVD epidemic:
http://www.ncbi.nlm.nih.gov/pubmed/19668697
http://www.medicalnewstoday.com/articles/160425.php
I wrote about this here (in portuguese): http://bit.ly/g5kA1D Also, CRP lowering was very inefective, as some Jupiter Trail critics wrote in several papers. Some of those papers are referred here http://bit.ly/aMJrLQ
Several unfavourable (and chronic) factors must be present for atherosclerosis to develop: free radical activity (caused by high blood sugars, smoking, alcohol, air pollution, modern vegetable oils), diabetes, inflammation, insulin resistance, obesity, etc. Which of these are the most relevant, and which are not required for CVD progression, is a task for scientists to find out.
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this is so interesting! by the way, here's another similar blog you and others here might like: http://laurasmenus.blogspot.com/
Is there any study that shows that elevated LDL is a risk factor INDEPENDENT of oxLDL? I'll bet not.
Elevated postprandial BG (for get the fasting number) is the fuel for producing oxLDL.
Nice Post Stephan. Sorry about the nitpickers here on the comments forum. It is clear what you you were infering
Would the Helenski study and WHI be relevant to include in a review like this?
I actually found the WHI a bit concerning. I didn't expect the diet intervention to do much good but the fact that the experimental group exercised more and were more likely to quit smoking and still no significant difference...a bit scary
we're not nitpickin bud. this is one of my top favorite blogs.
S.G. is legit.
Stephen,
Have you read Good Calories, Bad Calories by Gary Taubes? If so, what do you think of his crtique of the conventional thinking on cholesterol and heart disease?
lemme try:
after an advanced ketosis molecule glycates, the back end fragment dissipates one time. then, taken into account the flex points of the saturated fat cells, your body will respond by immune system overload.
the good news is that post meal blood sugar regulates into a frequency that never dies. once carb loading commences, carbohydrate molecules will feed the energy levels until satiation. there, in the colon, white rice ferments. oxLDL markers reflective territory for the finite isosceles triangle. no two protons can react without vitamin k2.
all essential organisms can play a role when AGEs occur in dairy products. postprandial oils will never go paleo. inflammation and diabetes epidemics brought on by type 2 meals. the only solution is butter.
O Primitivo
I should have linked the Fonarow study, which can be viewed at
http://www.oxidized-ldl.com/sitebuildercontent/sitebuilderfiles/a2.doc
The study looked at samples taken within 24 hours of admission. I would have thought that Fonarow would have made more out of the theory that lipid levels were in fact affected by the CAD event that led to hospitalization, but he did not. Here is what Fonarow (and other study authors, I should be clear to say) said:
"Although
it has been reported that a decrease in total cholesterol
and LDL takes place during the acute phase of MI, with a
marked fall occurring 24 hours after infarction and lasting
up to 12 days, a recent study found little change in lipid
levels when measured serially in the first 4 days of an acute
coronary syndrome event hospitalization.15 Although the
lipid levels obtained in this study were measured in the
first 24 hours of admission, they may or may not be
entirely reflective of the baseline steady state lipid levels."
Footnote 15 was this:
15. Pitt B, Loscalzo, Ycas J, et al. Lipid levels after acute coronary
syndromes. J Am Coll Cardiol 2008;51:1440-5.
High HDL appears to be associated with much lower risk, but count me also as dubious that jacking it up with something-or-other trapib will be protective. The view that HDL is protective through reverse cholesterol transport is a widely believed tenet of the cholesterol hypothesis, but open to doubt. Chris Masterjohn is a doubter, suggesting that what HDL really does is deliver Vitamin E to prevent oxidation of LDL.
Maybe niacin offers some heart protection through a mechanism linked to HDL, but that too is just a hypothesis.
I do think that if one looks at a their lipid panel, the number to fear more is low HDL rather than high LDL.
It's interesting that the Ogazu peoples ofmthe Orinoco delta, who get 94% of their calories from palm wine and Trader Joe's Ginger Snaps, have exceptionally low LDL's.
Barkeater:
Fonarow's study also available here in PDF:
http://download.journals.elsevierhealth.com/pdfs/journals/0002-8703/PIIS0002870308007175.pdf
http://astute.cardiosource.com/2007/vposters/pdf/275_Fonarow.pdf
I'm aware of that study that found no major difference in the accute phase, its the thrid study I quoted in my last comment and probably the most accurate since it did measured LDL directly.
I agree with you that HDL alone should somehow be a better marker. Even better, perhaps we should focus on the so called Atherogenic Index of Plasma, log (TG/HDL-C):
http://www.ncbi.nlm.nih.gov/pubmed/21122635
http://www.ncbi.nlm.nih.gov/pubmed/11738396
http://www.ncbi.nlm.nih.gov/pubmed/11048517
http://www.ncbi.nlm.nih.gov/pubmed/14578319
http://www.ncbi.nlm.nih.gov/pubmed/15544423
http://www.ncbi.nlm.nih.gov/pubmed/16526201
http://www.ncbi.nlm.nih.gov/pubmed/18719750
How do we lower TG and increase HDL with lifestyle therapeutic changes? Well, just read this amazing blog and you'll get the answers! (Don't try changing the lipids with statins, you will just be treating the symptoms, not the cause).
Hi Stephan,
Tsimane Indian detailed (Sun. 16 Jan.)comment stuck in your email ?
Please post when convenient. Thanx.
Great discussion everyone. O Primitivo brings up a great point, that TC/LDL is only associated with CHD in men under 50 or 55 years old. In older men, and generally in women of all ages, there's no association. That's probably because the early, fatty type of atherosclerosis is more blood lipid dependent than the late, fibrous/calcified type. By the time most Westerners are 60, they have atherosclerosis that's advanced enough that it's no longer very sensitive to blood lipids.
Also, the association between TC/LDL and CHD doesn't apply to all populations, for example the Japanese.
About the 'logical fallacy', imagine a case where A always activates B as well as D. B always activates C, but D always suppresses C. In this situation, A always activates B, and B always activates C, but A does not activate C.
Therefore, just because A causes B, and B causes C, does not imply that A causes C, even if those statements are always true.
In any of these studies, if they didn't measure a baseline 25 Hydroxy D level, then I'm not sure anything is valid.
Steve,
I am completely on board with you regarding the issue of using short term study results and extrapolating them to produce dietary guidelines and to prescribe life long health behaviors. That said, I believe that you need to check on the 1965 study by Hegsted et al titled "Quantitative Effects of Dietary Fat on Serum Cholesterol in Man" from the American Journal of Nutrition. This study (which would not be approved by a current IRB as it was undertaken in a mental institution) was run for 60 months and found that there was a strong correlation not between all saturated fats and serum cholesterol, but mostly from myristic acid (accounting for 67% of change due to saturated fats). This study also displays that the effect of dietary cholesterol on serum cholesterol is significantly less than myristic acid's. Finally, it also shows that polyunsaturated fats (but not monounsaturated fats) lowered serum cholesterol.
Keep up the good work!
Norm
But see that's the thing. Sure myristic acid might raise total cholesterol, but once you get past the idea that it might not be a bad thing, and in some cases, you may actually be in better health with slightly higher total cholesterol if what caused your total to raise is... say a rise in HDL coupled with a shift in LDL pattern type. Chris Masterjohn (and I believe Stephan too) has written about the positive benefits of myristic acid. There are several. I know this... if both butter and coconut oil contain significant amounts of myristic acid, then it's highly likely that it has some strong positive effects overall.
I found this comment in the article Stephan wrote on Palm Oil in July of last year from a guy named Jack C. I do not know if it's all true and correct, but I will post it here anyway with that disclaimer:
Jack C said...
Coconut oil is about 92% saturated, of which 18% is myristic acid. Butter fat contains 12% myristic acid.
Myristic acid has many distinctions, including the fact that it raises LDL cholesterol more than any other fat. It also raises HDL cholesterol an equal percentage.
Saturated fat increase the number of large LDL particles in men. Myristic acid, more than any other saturated fat, increases the preponderance of large LDL particles and decreases the concentration of atherogenic small dense LDL.
Myristic acid stimulates endothelial nitric-oxide synthase (eNOS)more than any other fat. (This is a good thing)
Myristic acid at normal dietary amounts increases tissue content of the omega-3 EPA.
Myristic acid is endoginously synthesized in breast tissue more than any other fat, I suppose for a good reason.
Myristic acid enhances kidney function (per Mary Enig)
Coconut oil does away with skin infections. It makes a good aftershave. (I don't know if myristic acid is responsible or not.)
July 3, 2010 8:31 PM
Likewise, just because polys lower your total cholesterol, does NOT mean that they are healthy to consume. What if poly causes LDL to become small/dense while increasing inflammation and causing more of your cholesterol to become oxLDL? Oh but it lowered the total cholesterol so it must be fine then, no?
If we are going to be honest about what's truly important for good health, then we will not be too concerned with what "improves" the numbers of outdated medical theories that have already been proven to be mostly faulty.
- Jack Kronk
Exactly, Jack! We had a interesting 6 week study last autumn in Finland about replacing butter with rape seed oil. They found that in 6 weeks rape seed oil decreased fibrinogen levels but already in 6 weeks there was additional oxidizing in LDL. Just imagine what the rape seed oil will do in longer perios.
If I eat more saturated fat, both LDL and HDL go up, and if I eat less they both go down. I have no idea how my diet affects my heart disease risk, but the markers do reflect my diet.
Thanks for interesting post. You asked if you missed any prospective long-term studies on the association of saturated fat and LDL-cholesterol. There is a Finnish pediatric study called Strip baby that has shown reduction of LDL-cholesterol by 7 % among boys (but no among girls) in 7 years. The study is even randomized by its nature.
http://circ.ahajournals.org/cgi/content/full/108/6/672
I also checked the effect of low carb vs low fat trials on LDL cholesterol (RCT studies minimum length of 2 years; Cardillo et al. 2006, Shai et al. 2008, Sacks et al 2009 and Foster et al 2010). The effect? Circa -2 % vs - 5 % (low carb and low fat respectively), difference is maximum 0,2 mmol/l
Finnish Strip project is very strange. They suggested and fed rape seed oil (as a prime fat, subsituting also mothers milk for oil) from age 6 month onwards. When we even do not know exactly what is the role of cholesterol in adults how can we know anything about it within infants. Growing child will need proper nutrition. Very brave parents to let their youngster be trialed.
It is very interesting to follow how much this experiment will affect intervention group children in later years.
How do researchers induce cholesterol in lab animals in order to study statins and other medications?
They simply feed them refined sugar (fructose or dextrose) and the protein in cows milk products called casein, or caseinate (excluding butter).
So basically refined sugar and dairy products.
A->B and A->D and B->C and D->!C is a logical fallacy. Just stick to your field ;)
Very good post and discussion!
Keep up the great work!
All the best
Pedro
good grief AL. where in the world do you come up with this stuff man. do you really type all this stuff out. are you like... some crazy scientist living in the mountains who just studies all day? i read a lot of technical mumbo jumbo all the time, but i can only gather bout half what you put out. anyway. carry on, i suppose.
Has research been done on how long it takes for cholesterol levels to respond to a change in diet? I'm not sure what terminology to use. Volatility?
For example, if I normally live on hot fudge sundaes, but switch to a ketogenic diet a week before my HDL and LDL are tested, would the results reflect the long term or the short term?
no. not at all AL. what i'm saying is that you always seem to have some in depth analysis and additional info to add to the articles. i just don't know how the heck you do it. and i definitely don't think i have the smarts for it. my brain hurts when i read some of your commentary. thanks for you contributions!
-jack k
i was just jokin around bud. i don't understand your posts. but i didn't mean to offend. my apologies.
Hi Stephan, It quite catch me the fact that japanese seems to be more prone to a sat.fat -cholesterol association, I am japanese descendant and when I was vegetarian (+ fish) my cholesterol & triglycerides levels were quite low, once I introduce red meat, more eggs, cheese & butter both my trigs & cho./hdl &ldl) increased.
So from my experience I can totally conclude that sat. fat does have a direct effect on cho & trigs levels.
Could my japanese ancestry be the answer to these??
Hi Jaime,
All groups in the Japanese study were of Japanese descent, including those in Hawai'i and California. So I don't think genetic background can account for the finding.
it is very curious that your trigs would increase, unless of course it would be attributable to the idea that chris masterjohn wrote about recently, with respect to a newly increased intake of sat fats may temporarily raise your blood cholesterol levels due to liver cleansing.
Why is my cholesterol so high on this diet?
-jack k
An interesting-sounding book was mentioned in an earlier response:
= = = = =
Stephen said...
Uffe Ravnskov, MD, PhD wrote a book called
"The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease".
In this book he completely demolishes the diet-heart hypothesis by using all of the studies the establishment uses to promote the idea in the first place. His argument is very well referenced and water tight.
The book is sadly out of print, but if you can find a second hand copy get it and read over and over.
January 15, 2011 5:05 AM
= = = = =
Second-hand copies of this book are selling for >$60. Fortunately, the same author has written two more recent books pursuing the same subject.
Fat and Cholesterol are Good for You (Jan 2009)
Ignore the Awkward.: How the Cholesterol Myths Are Kept Alive (Jan 2010)
Both are available from and reviewed on Amazon.
I assume that you are looking for best possible long-term data to refute or support the fat theory.
How about checking the long-term RCT studies in stead of observational studies? One could scrutinize the saturated fat - LDL data in the RCT meta-analyses, like Mozaffarian's meta-analysis (PLOS 2010), for example.
I have available here Finnish Mental Hospital study in which total cholesterol was reduced substantially. SFA diet increased total cholesterol by c. 40-50 mg/ml (c. 1,2 mmol/l) depending on the arm of study protocol. This is pretty impressive in that the patients were institutionlized and thus forced to adopt given diets (feeding study). Follow up six years. I'm aware of the flaws in this study, but ottal cholesterol change was pretty impressive. I guess one could check the equivalent data in other fat replacement studies to get sound results on this.
As ever you have provided a very interesting and well-researched review, Stephan.
I have developed hypertension due to meds and CKD, and have been prescribed an ACE inhibitor. I've also been advised that I should exchange my butter and coconut oil for vegetable and fish oil as "saturated fat raises blood pressure".
Now, knowing the dangers of vegetable oil I don't believe this, but it's very difficult to argue this without good solid evidence to back it up.
I've read your various posts which show that saturated fats are not the devil's work, but I wondered if you had done a review on saturated fats and hypertension, similar to this one on cholesterol?
It is quite interesting that almost all of the studies supporting chlolesterol theory (sat fat is bad and dangerous) are made in suspicious circumstances or by altering studies/data somehow. Examples: Finnish Mental Hospital Study, Finnish North Karelian project,Ancel Keys studies...
Then these studies are used basically in all modern studies as a reference and basis for "the official truth" and new results. We have built a house of cards which is going to crash now.
Over 40 years saturated fat has been studied and "found" guilty. Nevertheless during these 40 years not a single scientific proof or direct evidence has not been found to proof the theory. If the obvious link is there would it be quite simple to prove it?
Hey - Thanks Stephen for more good dissection - one thought - from a layman who doesn't know crap about all the numbers being tossed around (this is really a statistic-nerds blog ;-) )
everyone has data from this hospital or that group of sick already heart-attacky people -
by the time you are admitted to the hospital with your left arm aching and violent arrhythmia, don't you think the majority or these people have been either eating horribly for years, been on a wide variety of meds for probably more than one condition, are emotionally stressed and otherwise significantly physiologically impaired? It seems doctors and researchers then take that data and try to develop theoretical constructs that fit all these technical readings into a nice package - and of course it is impossible and if they do - it is unreliable.
Example is the lower cholesterol levels when someone has certain cancers - and if you look at how convoluted the proposed reasons are - it's all over the board.
perhaps there are so many confounders that depending on the minutia of this or that level observed in deathly sick people, or severely compromised people doesn't give as much insight as we would like into what healthy people's numbers can or should be?
just sayin...
Ravi
Stephen, have you seen this (BMJ 2005):
Effects are modest (if not nill) according to this meta-analysis:
"In free-living subjects the standard step 1 diet of the American Heart Association lowers cholesterol concentration by about 3%, and about another 3% can be achieved with more intensive diet"
http://www.bmj.com/content/316/7139/1213.1.full
Hi stephan, I am not seeking a medical advice, just wanna share my self experiment.
I did a blood panel today and my triglycerides went from 74 to 98
TC from 220 to 277
hdl from 59 to 69
ldl from 146 to 175
vldl is 19.6
Glucose from 87 to 100
and for the first time my liver enzimes (ast-alt) where abnormally high.
All these changes happen in a 8 month period from doing an already "relax" paleo type diet (including kefir, quinoa, some sweet potatoes)to a more strict paleo..read meat at breakfast, more fat etc..no veg oils, wheat, sugar, fructose, grains etc etc etc...
I truly think there is an issue regarding sat fat, maybe is not the fat..maybe is the type of meat (beef?)..thats really the one thing I increased considerably in my diet(from good sources..grass feed)
I think genetics have something to do with it, as half asian I will now go back to my previous diet (were my trigs were in the 40 range, good fasting glucose,etc)
Im leaving paleo principles (and excess fat for now)It was a tasty journey but I just dont feel as good as I used to.
I guess balance is truly the key.
pd:I post a comment earlier asking if japanese ancestry would play a role on results..you disagree but It strongly apply to my case.
Thanks for your work & your care,
"Just because A causes B, and B causes C, does not mean A causes C."
Of course it does, it follows logically from any decent definition of "cause".
One factor almost always missing from lipid studies are macronutrients other than fat and how they affect each other.
"We have proposed the "glucolipotoxicity" hypothesis in which elevated free fatty acids (FFAs) together with hyperglycemia are synergistic in causing islet ĂŸ-cell damage because high glucose inhibits fat oxidation and consequently lipid detoxification." http://endo.endojournals.org/cgi/content/abstract/144/9/4154
"Hyperlipidemia is frequently associated with insulin resistance states as found in type 2 diabetes and obesity. Effects of free fatty acids (FFA) on pancreatic b-cells have long been recognized. Acute exposure of the pancreatic b-cell to FFA results in an increase of insulin release, whereas a chronic exposure results in desensitization and suppression of secretion. We recently showed that palmitate augments insulin release in the presence of non-stimulatory concentrations of glucose. Reduction of plasma FFA levels in fasted rats or humans severely impairs glucose-induced insulin release. These results imply that physiological plasma levels of FFA are important for b-cell function." http://onlinelibrary.wiley.com/doi/10.1002/jcp.10187/abstract
"Therefore, just because A causes B, and B causes C, does not imply that A causes C, even if those statements are always true."
Huh?
If statins always cause muscle aches, and muscle aches always cause random cursing, then statins would always cause random cursing.
You might consider looking at:
1. Pauling, Rath and Apo A or as it's known, lipoprotein(a).
2. University of Michigan study that showed "...no high-quality clinical evidence to support currently proposed treatment goals for LDL cholesterol" (Annals of Internal Medicine, Oct 03, 2006).
3. Ravnskov's study that high cholesterol may actually protect against infections and atherosclerosis (Oxford Quarterly Journal of Medicine, Vol 96, Issue 12, Pp. 927-934).
4. Dr Kilmer McCully's work re homocysteine and infection as a primary cause of atherosclerosis.
I could go on. But I'll stop with this personal experience: I'm 64 yrs old. Last summer I found myself belching, then chest pain (angina) and shortness of breath when doing physical activity. I had quit smoking 5 yrs ago, was on a reduced fat diet plus a daily dose of 10mg of Lipitor. But even though I knew something wasn't right, I didn't run to my doctor, I went to the Internet instead. I found zinc gluconate (google "George Eby angina") and began taking 300 mg per day (split into six 50 mg doses). Six days later I cut the lawn without any pain, without any SOB, without any belching. A week after that I did a 3 hour lawn/weed cutting session for an elderly neighbor and I experienced no pain, no SOB, no belching. Zinc gluconate cured my atherosclerosis. I threw away the Lipitor.
However, high dose zinc can deplete copper stores and that sets you up for an aneurysm. So, more Internet research and I found Pauling. I'm on the Pauling therapy now and never felt better.
Your mileage may vary.
.
I've had a constant high HDL (currently 118) and a
high LDL (can go to 200 w/o statin and to 127 with)
while triglycerides go from 81 w/o statins and about 50 with them. The only way to lower total cholesterol is to try to lower HDL which averages about half the total.
These are numbers after almost 20 years of a low carb diet for a person who has had recent CAD (carotid surgery resulted). I wonder if statins are worth it in these circumstances.
Great post! Keep spreading the news.
x x x
you all are simply confusing yourself. human biology is not simple and loggical nor one's health helped by armchair scientist /bloggist. the facts are people everwhere are living longer[look outside and believe your eyes] and better. this is due primarily to drugs and drug companies and not to natural foods or natural meds. those are the facts. leave the theories to those who have a lifetime to study them.
Glen Lalljie.
Great read - geeks rule. Consider magnesium - essential for over 300 enzymes and vital to active transportation across membranes. It is crucial in production of glycocompounds and is found in many food sources that are also good sources of fiber & essential sugars (mannose, fucose, glucosamine . . .) Imagine a body that is low on magnesium and low on special glycogens and maybe high quality transport devices (HDL's) become sloppier built, falling apart transport devices (LDL's), and eventually VLDL's - crumbling apart and leaving placque debris. High functioning compounds require tools and energy and essential nutrients.
The gallon of milk a day referred to by Mightochondria Al would be a big calcium load and would increase urinary magnesium losses.
We do need magnesium in our water it was regulated out in a 'smart' policy decision in the 20's/30's Pure Water Act. Magnesium isn't even in most brands of "electrolyte" beverages on the market today. I like the Glaceau Smart Water brand.
Early symptoms of magnesium deficiency include anemia, edema, and high cholesterol. Arrthymia's and stroke, osteoperosis and dimentia take a little longer. Statin drugs may reduce cholesterol but they don't reduce all cause mortality, at least for people using it 'preventatively'. Prevent liver problems - don't use statins.
GingerJensdotcom - beginner blog
PS - good predictor of heart disease is waist to hip circumference ratio. -Eat an apple a day to keep the apple waistline away - as well as the doctor. Add a carrot and keep the cancer surgeon away. Both very good foods for building healthy glyoccalyx.
Top researchers have criticised the meta-analysis of prospective studies cited by Stephan showing the relationship between saturated fat acids (SFA) and coronary heart disease (CHD) due to serious flaws and omissions.(1-3) As Katan MB correctly pointed out, “the notion that there exists such a thing as ‘the effect of saturated fat’ is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease and need to be discussed separately.”(2)
Two of the original authors (Sun Q, Hu FB) have since admitted that the conclusions of this meta-analysis were flawed, stating that “in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates, and high intake of refined carbohydrates has been associated with a high risk of CHD.”(3) It would only be expected that a significant association would not be found when replacing SFA with other calorie sources that also have unfavorable effect on serum lipids and associated with an increased risk of CHD. The authors failed to disclose this critical information, just as the senior researcher Krauss RM failed to disclose receiving grants from the National Dairy Council, the National Cattleman’s Beef Association, and the Robert C. and Veronica Atkins Foundation.(2)
This meta-analysis actually included adjustments for serum and dietary lipids, including serum (blood) cholesterol and dietary cholesterol, clear over-adjustments making Stephan’s remarks clearly unfounded in regards as to whether this study supports the relationship between SFA and higher serum cholesterol, and therefore a higher risk of CHD. As Stamler J pointed out in the editorial to this meta-analysis, “Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77—ie, >1.07, which was the estimated CHD RR in the meta-analysis”.(1)
Katan MB pointed out that “About half of the studies used 1 d dietary assessments or some other unvalidated method”.(2) These studies inaccurately measured habitual dietary intake and attenuated the SFA-CHD relationship found in the meta-analysis. Such studies can certainly not be classed as being “high quality”, and as Stamler J stated, “Five [studies] used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids”(1)
Very importantly, saturated fat was associated with an overall 32% increased risk of fatal heart disease despite adjusting for dietary and serum lipids, suggesting that other factors beyond serum lipids may also promote the SFA-CHD relationship.(1)
A pooled analysis of 11 cohort studies showed the relationship of replacing SFA with other macronutrients on the risk of CHD while using consistent adjustments, and limited the inclusion of studies only to those with “availability of usual dietary intake, and a validation or repeatability study of the diet-assessment method used”.(4)
This pooled analysis of actual high quality studies found a significant decreased risk of total and especially fatal heart disease when saturated fat was replaced with polyunsaturated fat, despite adjusting for dietary cholesterol.
Probably the most informative paper to date is from the 26 year follow-up of 84,136 nurses, the only major study to show the effect of substituting actual food (containing both macro and micronutrients) and the risk of CHD. This study is inline with the literature and the recommendation to replace foods rich in SFA and cholesterol with unprocessed foods rich in unsaturated fats, fiber and antioxidants.(3)
1. http://www.ajcn.org/content/91/3/497.full
2. http://www.lbs.co.il/showpost.php?p=233292&postcount=7
3. http://circ.ahajournals.org/cgi/reprint/122/9/876.pdf
4. http://www.ajcn.org/content/early/2009/02/11/ajcn.2008.27124.full.pdf
A 1997 meta-analysis included numerous additional observational studies and national statistics publications in regards to the relationship between saturated fat and serum cholesterol that are not mentioned in Stephan’s analysis.(5)
Many of these studies found that either SFA, the SFA/PUFA ratio, Keys score or dietary cholesterol were significantly associated with serum cholesterol, including the Scottish Heart Health Study (8,000+ participants), Caerphilly Prospective Study (653 men), Costa Rica Study (202 M, 174 F), CARDIA Study (depending on age, sex and ethnicity, 4000+ participants), Puerto Rica Study (5803 participants), Ireland-Boston Diet-Heart Study (1001 participants), and the Framingham study (of which a significant amount of information has been published).(5)
The authors discuss the significant limitations of the use of observational studies, concluding that accurate valid and well-standardized methods are required to assess both diet and serum lipids, and single measurements of either diet or serum lipids significantly reduces the true association. Stephan cited several studies that used invalidated dietary measurement methods such as single 24-hour dietary recalls, which poorly measure habitual dietary intake and tend to fail to find a relationship between any nutrient and serum lipids.(5) Nevertheless it appears Stephan favors such studies over dietary experiments conducted under controlled conditions, precisely measuring dietary intake. A meta-analysis of 395 such dietary experiments found a significant relationship between SFA and unfavorable changes to LDL/HDL ratio compared to unsaturated fats.(6)
In regards to the Western Electric Study, there was a non-significant positive relationship between SFA and CHD after adjusting for serum cholesterol (11% increase), indicating the likelihood of a significant relationship in unadjusted results. Also a 200mg/1000kcal decreased intake of dietary cholesterol was associated with a 34% lower risk of all cause mortality.(7)
In the study on Japanese in Japan, Hawaii and California (Ni-Hon-San Study), studied as a group the average cholesterol was 181, 218, and 228 mg/dl for men living in Japan, Hawaii and California, respectively. CHD mortality was 1.7 times higher in Hawaii and 2.8 times higher in California than in Japan, and was associated with an increased intake of SFA.(5)
The Health Professional Follow-up Study does not seem to provide any information in regards to participants SFA intake and serum cholesterol levels, and is definitely not the most recent study. The researchers found a significant relationship between saturated fat and a borderline significant relationship for dietary cholesterol and fatal CHD after maximum adjustment.
A 2007 paper from the EPIC Norfolk Study with 22,915 participants is perhaps the largest observational study examining diet and serum cholesterol, and found a significant relationship between SFA and serum cholesterol.(8) Other studies that have found a positive relationship between SFA and serum cholesterol include the Blue Mountain Eye Study and the Framingham Offspring Study.(9,10)
A new paper published in April from the Whitehall II Study including 4,469 participants found a significant inverse relationship between the PUFA/SFA ratio and LDL cholesterol.(11)
A 2007 review including 10 dietary intervention studies not designed for weight loss and with a minimum follow up of 3 months found a significant relationship between a decreased SFA intake and lower serum cholesterol.(12)
5. http://www.ajcn.org/content/65/5/1597S.full.pdf
6. http://www.bmj.com/content/314/7074/112.abstract
7. http://www.ncbi.nlm.nih.gov/pubmed/3052353
8. http://eurheartj.oxfordjournals.org/content/28/23/2930.full.pdf
9. http://jn.nutrition.org/content/140/1/88.full.pdf
10. http://www.ncbi.nlm.nih.gov/pubmed/8656227
11. http://heart.bmj.com/content/early/2011/04/12/hrt.2010.216309.full.pdf
12. http://www.cfah.org/hbns/archives/viewSupportDoc.cfm?supportingDocID=468
Excellent article, Stephan. I wish the most outspoken doctors who support the lipid hypothesis would admit to the public that no one has a complete understanding of the mechanisms behind the progression of coronary artery disease . To do so would require a complete understanding of human cellular metabolism.
There is far too much dogma in medicine, rather than sceince. I applaud Dr. Ravnskov for questioning this.
Excellent point , Jenny above :)
Take care,
Raz
Hi T,
Let me put this plainly: I have reviewed the observational studies in detail, and you would have to be totally out of your mind to think that overall, they support a SFA-CHD association. Nearly every single one found no association whatsoever. The meta-analysis by Krauss's group only confirmed what was obvious to anyone who had even casually glanced at the studies-- which is a small minority of people.
They way people who have a vested interest in the SFA-CHD story try to get around the lack of association is by moving the goalposts: instead, we'll measure the Keys dietary score, calculate SFA/PUFA ratios, or we'll run mathematical models where we hypothetically substitute one nutrient for another. Here's the logic: since PUFA intake is inversely associated with CHD in many studies, if we make a ratio with SFA, we'll get a significant result that will allow us to indict SFA! Even though the significance comes entirely from the PUFA side of the model and has nothing to do with SFA.
I'm sorry, but that's baloney and it's misleading. That's not how epidemiology works. What you do is you examine if people who eat more SFA have more heart attacks than people who eat less, while controlling for other variables-- and the studies have nearly all found no association. That's how epi works in other disciplines. Moving the goalposts to Keys score, SFA/PUFA ratios and using fancy math to model nutrient substitutions will only fool people who don't know any better or are desperate to believe that there's an association.
The point of my post was to point out that there is no good evidence for a long-term association between SFA intake and serum cholesterol. There was nothing in your comment that challenged that. The meta-analysis you cited in support of the idea that SFA increases serum cholesterol was done using studies with a median length of one month! That's exactly the point of this post-- you can't extrapolate from one month to ten years.
I hadn't seen the EPIC Norfolk data so thanks for pointing that out. They did find a SFA-LDL association, although it was weak. They also found that MUFA intake is associated with higher LDL. Do you believe that MUFA increases LDL?
Your characterization of the health professionals follow-up study is incorrect. After maximum adjustment, there was no association between SFA intake, CHD, fatal CHD or any other CHD-related outcome. This makes it consistent with virtually every other study conducted on the matter. See table 1 for the association between SFA and serum cholesterol (hint: there is none):
http://www.bmj.com/content/313/7049/84.full
Hi T,
I just looked at the Nurse's health study paper you referenced in support of the hypothesis that SFA contributes to CHD, calling it "probably the most informative paper to date". That paper did not even examine the association between SFA and CHD.
Contrary to what you said, the Blue Mountain Eye study did not find any association whatsoever between SFA intake and TC/LDL. What they found was an association between TC/LDL and a CHANGE in SFA intake over time. That result is difficult to interpret due to the fact that in the same study, people who consistently ate more SFA didn't have higher TC/LDL than those who consistently ate less.
You seem to have a tendency to misrepresent findings to support your position. I want to be clear with you, I will not tolerate that on this blog.
The Framingham Offspring study paper you cited appears to support your position. They did find an association between SFA intake and TC/LDL. I'll add that to my post in an update. It's curious that the original Framingham study didn't see that.
Saturated fatty acids (SFA) are associated with excess coronary heart disease (CHD) mortality regardless of whether one uses Krauss’s industry influenced model where the SFA-CHD relationship is intentionally attenuated by comparing SFA primarily to refined carbohydrates, including invalidated dietary measurement methods and adjustments for dietary and serum lipids, or the model of isocaloric substitution with PUFA in the pooled analysis of validated prospective studies. 1 2
It is clear beyond reasonable doubt that a lower intake of any caloric source including SFA implies an increased intake of some other source of calories in order to maintain caloric balance, and that different substitutions for SFA have different effects on CHD risk. Therefore the SFA-CHD relationship can only be appropriately examined by comparing SFA with specific caloric sources, including PUFA and complex carbohydrates. Your claims that there exists such a thing as an independent effect of SFA or PUFA are flawed, and your reviews of epidemiological studies comparing SFA to a baseline diet characterized by processed junk food fails to be very informative.
I consider the paper from the Nurses Health Study the most informative study in regards to the relationship between diet and CHD risk because other studies only focused on substituting macronutrients, whereas this study showed the effect of substituting one serving of food for another and the risk of CHD which is influenced by multiple simultaneous changes of both macronutrients and micronutrients. Although the results of this study cannot show a causal relationship between individual nutrients and CHD, it does indicate an association between, as I worded it “foods rich in” certain nutrients (including SFA) and CHD risk.
The focus of the paper from the Health Professional Follow-up study was the relationship between dietary fat and CHD risk, not the use of a well standardized method to assess the relationship between diet and serum cholesterol. In this study the top vs lowest fifth intake of SFA (a difference of only 16 gm) and dietary cholesterol was associated with a 72% and 25% increased risk of fatal CHD respectively. Also replacing SFA with PUFA was significantly associated with a lower risk of CHD mortality in the longer follow-up of this study included in the pooled analysis.
The primary source of MUFA in Norfolk is undoubtedly meat and dairy (apposed to vegetable oils used in dietary experiments), and therefore MUFA would have strongly correlated with SFA intake and therefore with LDL-C in the Norfolk study. It is notoriously difficult for researchers to compare MUFA with other sources of calories in observational studies due to this limitation, and is indicated as a likely reason why MUFA was associated with an excess risk of CHD in the pooled analysis.
You mentioned virtually nothing about the limited ability to evaluate the validity of dietary data on free-living people, or the high intraindividual variability that results from single measurements of diet and blood cholesterol concentration. Half of the studies you cited used an invalid single 24 hour recall to measure diet, yet you failed to mention this as a possible limitation. Furthermore numerous studies within the two meta-analyses of dietary interventions I previously cited supporting the association between SFA and serum cholesterol were long term lasting up to several years.
A significantly more in depth review of epidemiological studies clearly challenges the content of your post, including a far greater number of studies, and describes the limitations and strengths of various types of studies. It also included studies showing an association between decreases of SFA intake with significant decreases in serum cholesterol and CHD at a population level.
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Hi T,
I object to your suggestion that Dr. Krauss is biased due to his (former) ties to the dairy industry. That is a totally unfounded and unprofessional personal smear that Krauss handily dismissed in his response to Dr. Katan. Did you know that Katan receives funding from Unilever, Nestle, the Olive oil council and other commercial sources with a vested interest in promoting plant oils? Unilever has been a major funding source for Katan. Who represents the "industry influenced model", Krauss or Katan? If you want to criticize people for their industry ties, you have to do it consistently rather than pick and choose, and Katan is certainly more in bed with them than Krauss. I wasn't going to bring it up because I don't think it's that relevant, but people who live in glass houses shouldn't throw stones...
I find it disturbing that you continue to cite the Health Professionals follow-up study to support your position despite the fact that there was no statistically significant association between SFA intake and any measure of CHD after maximum adjustment. If there were really a relationship between the two factors, you wouldn't have to cite non-significant findings to support your position.
The Nurses health study paper you cited is interesting, but they didn't look at SFA. We're talking about SFA here.
What Krauss (and others) have found in their meta-analyses is that SFA consumption isn't associated with CHD risk, but refined carbohydrate is. Others have used mathematical models (which frankly I find questionable since they're purely hypothetical and rest on some big assumptions) to hypothesize that replacing SFA with PUFA would reduce risk. But that makes no sense. If your true goal is to reduce risk, why would you replace something that's statistically harmless (SFA) rather than something that's statistically harmful in the same studies (refined carbohydrate)? Why do they keep focusing on a SFA-PUFA swap when their own models predict that a carb-PUFA swap would be more effective? Answer: because they are desperately wedded to the idea that SFA are harmful, and they will try their best to implicate it even in the absence of evidence to support that position.
I just read the review paper that you lauded at the end of your comment. I can't say it's quite as supportive of your position as you make it out to be. You like good measurement methods, so let's focus on the two studies that did 7-day weighed food records, the Bankers study and the Caerphilly study. The first found no association between animal fat intake and serum cholesterol across a several-fold variation in intake. The second found a significant but extremely weak association between SFA intake and serum cholesterol. "The percentage of variance in the plasma lipid concentrations which could be explained solely by the dietary variables was very small, ranging from 1 to 7 per cent". That sounds quite consistent with the conclusions of my post.
However, there were a few studies in the review article you cited that I missed in my post. I'm going to have to look these up and read them in detail. I may end up re-writing this post if I feel it needs it.
Here's Dr. Martijn Katan's conflict of interest statement from a 2007 paper:
The author has three projects funded by the Wageningen Centre for Food Sciences, an alliance of major Dutch food industries, research institutes, and the Dutch government. None was involved in this editorial. In the past 25 years he has received funding or research materials from Unilever, Nestlé, the Netherlands Dairy Organization, Campina BV, Friesland Foods, the European coffee industry, and the olive oil council, and he has spoken at expenses-paid meetings of these industries, as well as the tea council and the chocolate industry. He sometimes gives unpaid informal advice to colleagues in the food industry. He does not consult or testify for industries, accepts no money or gifts beyond a bottle of wine or book token, and has no stocks or other financial interests in food or beverage companies.
(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1761050/)
Do I discount his research because he's worked extensively with industry? No. I just note it in the back of my mind and consider his papers on their own merit.
Hello, I am 51. I have 2 stents. My first in 2003. I didn't want to believe it was SATFATS, so I found comfort in WAPF and Anthony Colpo. But, here I am, 2011 and I just had another stent put in after a mild MI.
Sure, I ate the butter and steaks BUT and here is where I went wrong since 2003. I ate the white flour, sugar and plant oils.
I am currently following Dr. Esselstyn's program for reversing heart disease. Plants, fruits and whole grains. No oils of any kind. No nuts. No meat. No dairy.
The book says that if I follow this I will CURE my CVD and maybe even reverse some of it.
So far, (1 month) I have lost 15 lbs. I am taking a statin and the usual heart meds.
I miss eating meat. Trust me. I am not doing this because I am against meat and satfats. But, Dr. E makes a great case against satfats and its effects on the endothelium. Damage it enough and the the beginnings of plaques will appear.
I dunno. I am at a loss. I WISH I had not ignored the warnings of PLANT OILS and FLOUR. if I had not consumed those since my first stent, then maybe I would have an argument against satfats in meat.
So here I am a reluctant vegan afraid to eat meat of any kind. What do you folks think? Am I needlessly avoiding meat? Can you recommend I consume meat at this point?
Dave
Hi I've not posted before, but following up on cholesterol being protective.. perhaps we are ingesting chemicals/foods our body has not evolved with and so does not cope with well. To protect the lining of our arteries it produces and lays down cholesteral as a protective mechanism. Too much of this ends up restricting arteries and casugin a problems. So the cause is the foods/chemicals our body does not want (varied and related to genotype), the defense and eventual symptom is excessive colesterol production??
It's clear that cholesterol, HDL mostly, does some protective things. There is some evidence that bacteria and viruses damage or infect the cells in the walls of the artery. Combine that with a high-inflammation, highly-oxidizing American diet and you have the perfect storm.
Just came across this study, thought you might find it interesting.
"Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study"
Petursson, Sigurdsson, Bengtsson, Nilsen, Getz
Journal of Evaluation in Clinical Practice, Volume 18, Issue 1, pages 159–168, February 2012
Another link PubMed
Seems to indicate that for women, there's no such thing as too much total cholesterol for all-cause mortality and overall cardiovascular disease (which I think they are using to include strokes), and only slight ischaemic heart disease detrimental effects from even very high total cholesterol. Even for men, it seems the best range is between 195 and 230 mg/dl.
The U-shaped graphs seemed different than the red-yellow-green table, however, so I am not sure I am interpreting the study correctly, since the table seems to indicate that men, too, have the best outcomes for any total cholesterol over 214 mg/dl (5.5 mmol in their chart), while the graphs seemed to indicate men had an upper limit beyond which their risk increased.
I believe the basis for the idea that saturated fat increases blood cholesterol is the role bile acids play in fat catabolism. Though cholesterol catabolism is mediated largely through the bile acid pathway, it is theorized that when there is excess triglyceride consumption, cholesterol is overproduced by the liver, overshooting the amount of cholesterol that will be degraded to form bile acids to catabolize (or really transport and make soluble for catabolism) these aforementioned triglycerides.
I'm writing a series on avoiding atherosclerosis and this is actually one of the questions I encountered in my research.
The study stephen points to in 2010 in footnote # 3 regarding saturated fat not leading to heart disease did not take into account if the group(s) of people studied were on statin drugs or not. one of its authors Krauss has had money support from the Atkins diet group & the meat industry. That study therefore is null. Scientists & the medical community at large acknowledge saturated fat does cause a increase in ldl.Of course if diet involves a lot of fibre(fruits,vegetables,whole grains like oatmeal,legumes) a lot of ldl can be absorbed in the intestinal track should one eat large amounts of sat. fat & thus eliminated away as waste when you go to the washroom.Love those carbs !
Hi Steven,
Thanks for your great summary. I have to agree with Davide Palmer. I'd love to see a reanalysis based on APOE4 genotype because of its role in cholesterol transport. It may also be important to look at APOE2 as well.
There may also be other important interactions, perhaps gender, age other genes or lifestyle factors that need to be more thoroughly examined. The problem is most epidemilogical studies is that sample sizes are often not large enough to support the variety possible interactions that can occur.
Dr., if you get aroudn to following this up - here is a review of control trials:
http://www.ncbi.nlm.nih.gov/pubmed/12716665
Perhaps you'd include your rationale to exclude these results - 12-91 day feeding trials.
Hi Steven,
Yes, I do not dispute the results of short-term trials, although the trials have not always supported the SFA-blood cholesterol link. See for example this large controlled study (LIPIGENE) that showed that large differences in SFA intake had no impact on LDL in overweight people:
www.ncbi.nlm.nih.gov/pubmed/20938439
My rationale for not including short-term trials in this discussion is that they're short term. I don't dispute the fact that SFA can impact blood cholesterol in the short term, but the question I'm asking is "does this effect persist in the long term"? Hence my interest in observational studies that look at the relationship between SFA intake and cholesterol over several years.
Good to see this blog still valid after 2 years.
I am interestes to find out more on the fake SFA'a used in experiments designed to make SFA's the preferred culprit re ill health.
There are some links in the responses but none of them open for me. Maybe some updates resources?
It's important to be able to show people how their opinions have been manipulated.
Currently here in OZ a university etc funded blog called "The Conversation" is discussing fats etc. so it's worth reading.
Aneurysms, herniated discs, hemorrhoids, high cholesterol, and emphysema are among the most destructive, painful, and numerous diseases in our society. Slipped or herniated discs are estimated to cost 200 billion dollars directly and indirectly each year in the USA alone ]. Four to six of 100 Americans autopsied died of a ruptured aneurysm. 3.6 to 6 percent of those examined had non ruptured brain aneurysms [Renkel]. Each year, 16,000 Americans die due to a ruptured aortic aneurysm. Of the 200,000 strokes that occur each year in the USA, 20% are aneurysms in the brain. I suspect that copper deficiency status is the most important parameter affecting them. For instance, aneurysms are produced in turkeys by depleting copper [Guenther]. Copper deficiency causes blood vessels to become weak and is probably the chief cause of hemorrhoids and varicose veins. Restoring copper during those diseases is imperative.
That copper is below optimum in a large number of people is virtually certain from current evidence. Keep in mind that the MDR is designated too low to start with, as is the RDR. Young adult American women average 1.16 mg per day [Murphy] and men about 1.5. The difference between the sexes is no doubt primarily due to women eating less food than men. People in Belgium average 1.5 +/- 0.4 mg per day ]. Adolescent males, both incarcerated and free, are below the RDA [Gans] which has been set at 2.0 but should be at least 3.0. Porto Rican school lunches are below the federal RDR [Preston]. Hemodialysis patients have low copper and zinc serum levels [Komindr]. Even so, a full blown copper deficiency takes several months to develop in people with an injured digestive system, much longer than for zinc . This is because the liver stores large amounts of copper Emphysema [Soskel], premature gray hair [Wu], blood clotting [Milne 1896], slow healing bone breaks [Dolwet], diabetes enhancement [Cohen 1982] and anemia are such symptoms. The median layer of the blood vessel (where the elastin is) is thinner from a deficiency but its elastin copper content is the same as normal men. The overall thickness is not different [Senapati, et al]. Elastin is about as flexible as a rubber band and can stretch to two times its length [Carnes 1977]. The 39 or more different kinds of collagen are about 1000 times stiffer. A healthy artery requires about 1000 mm of mercury or 10 times the normal mean blood pressure in order to rupture [Shadwick]. Therefore keeping strength of arteries up would seem to be even more important than keeping blood pressure down although not necessarily so far as kidney glomeruli are concerned. However a copper deficiency coupled with high sodium (or high chloride?) causes disruption of the glomeruli basement membrane resulting in acute kidney failure [Moore].
Copper nutrition is very important in herniated discs, hemorrhoids and aneurisms because copper is essential for lysyl oxidase, which enzyme cross links the elastin tissue. Cross linking is especially crucial for elastin tissue because elastin gets all of its strength from cross linking. The strength of collagen is not as badly affected because of the long length of collagen molecules. However inadequately cross linked collagen is subject to creep.
The articles starting at; http://charles_w.tripod.com/copper.html would be useful to you, especially copper from food in http://charles_w.tripod.com/copper3.html
A copper deficiency also produces high cholesterol [Klevay 1978] [Reiser]. Copper supplements would be infinitely superior to and safer than statin drugs for lowering cholesterol or eating low cholesterol food [Couzin]. However adding copper without zinc can actually make that situation worse [Festa]. Copper is also essential for an adequate immune system [Prohaska 1981] [Percival]. Premature babies can have too little copper. However babies should be supplemented with extreme care because they can not excrete copper, which is excreted with the bile in adults. This care includes not making formula out of water from copper pipes.
My comment is quite late, but I'm trying to talk to my md sister about butter and couldn't resist reacting to the study done in Japan, Hawaii, and California. I lived in Hawaii as a child in the late 50s/early 60s, and fresh food was actually quite unusual -- everything was shipped in except lettuce, since pineapple and sugar cane were the primary industries (at that time, tourism came in third). California was lush with fresh fruits and vegetables. I think a follow-up on overall dietary habits of the three locations would reveal a lot.
Thank you for this blog.
Great article Stephan. Could you please reply to the comments about E4 and E2 genotypes? As I don't know my genotype, and I haven't seen a response, these comments worry me somewhat. Thank you.
I relied heavily on articles such as this reporting on studies that found no association between saturated fat and cholesterol. I also thought the low carb, low insulin route was the way to go.
I went three years on a very low carb, very high saturated fat diet.
LDL went from 105 to 305. Particle size tests were not great either. I repeated the test to be sure and got a similar result, I went on a very low fat diet for a month and my LDL dropped to 105. In both tests my insulin, sugar, triglycerides were low
I was told by some low carb/palio authorities that in about a third of the people saturated fat will stimulate cholesterol production and by some that very low carb is not good; some insulin may play a role in cholesterol metabolism. Another low carb doc says that high cholesterol in the absence of insulin resistance is meaningless; its all about low insulin
I just switched to a balanced diet, real food only and have not rechecked.
Does it make a difference why you cholesterol is high? For instance, someone who has high cholesterol even on a low fat diet, because they can't metabolize it vs someone who has high cholesterol because they eat tons of fat?
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