Tuesday, March 6, 2012

Do trends in fat intake correlate to changes in heart disease?

Background: This is based on an article published in The British Journal of Nutrion by 13 scientists (Pedersen et al.) and 3 published letters to the editor in response to the article. More detailed background information can be found in an article I described earlier (1).

This part describes the evidence for a link between trends in saturated fat consumption and their correlation to changes in CVD.
Pedersen et al (2) state that:

There have been substantial reductions in mortality from CVD (cardiovascular diseases) in North America, Western Europe and Australasia over the last 30 years that reflect successful national public health policies to reduce the intake of SFA (saturated fatty acids), in addition to promoting smoking cessation and controlling blood pressure.

As they state themselves "in addition to promoting smoking cessation and controlling blood pressure". If these changes occur at the same time, how do we know which change "caused" any possible change in CVD?
In addition, no references were given to back up these "claims".

I did find an article providing data about trends in saturated fat intake in America (3). It showed that the energy% from intake of saturated fat sligtly decreased over time, while the absolute intake increased:
A report from the US Department of Agriculture and the US Department of Health and Human Services states that no reductions were found in the intake of SFA in the American diet over the period 1989–1 to 2005–6(4). Indeed, although the intake of SFA as percentage of total energy (en%) was slightly higher over the first time period (12·3), than over the last three time periods (11·2–11·4), the total amount of SFA in g/d increased slightly over this time (25·7–27·8).
And I gave out the following warning:
More importantly, it is not possible to unequivocally associate changes in SFA intake to changes in CHD mortality over time, since many changes in diet, lifestyle, diagnosis and pharmacological treatments have occurred over the last 30 years.
A bit further in the text, the authors state:
That replacement of SFA by a variety of carbohydrate-containing foods also reduces CHD risk may be inferred from ecological studies, e.g. in Finland. CHD was almost non-existent in rural China when mean cholesterol levels were approximately 3.5 mmol/L  with total fat intakes only about 15% of energy and extremely low intakes of SFA. These observations, replicated in many countries, should not be ignored.

This time, 2 references were given (4, 5). Both referred to "The China Study". But no trends in fat intake were examined in the articles referred to. No references were given that correlated saturated fat intake to heart disease in Finland.

How Pedersen et al. responded to my findings, can be found in their response to my letter (6). They concluded that:
Hoenselaar expresses doubt if a reduction in SFA intake has occurred concurrent with the decline in CHD mortality in developed populations. This is illustrated by citing the small relative reduction of SFA intake in the US population during the period 1990-5/6.
This is an incorrect reflection of the trends in SFA intake I mentioned earlier. As I showed before SFA intake increased from 25.7 to 27.8 g/day. The reason why the relative contribution showed a small decline, is that intakes of energy from other nutrients (in this case carbohydrates) increased even more. Therefore, the strongest change is an absolute and relative increase in carbohydrate intake.

Pedersen et al. continue:
During several decades before the turn of the 20th century, SFA intake declined and PUFA intake increased in the USA. There are also reports of declining SFA intake concomitant with the reduction in CHD mortality in several other populations. In all Nordic countries, SFA intake has decreased compared to the levels in the 1960s. The decline has been particularly noticeable in the Finnish population that has experienced the most rapid fall in CHD mortality in the world.

New Zealand may be cited as another example.
This time the authors refer to 5 articles (7-11). No correlations were made between saturated fat intake and heart disease in any of the articles referred to. What these articles actually described were trends in fat intake over different time periods for three different populations. The rest of my comment was as follows:
Two reports described fat intake in the USA. The changes in SFA and PUFA intake were accompanied by a decrease in MUFA intake. Since these three changes were of equal size and took place at the same time, it will take other data to put them in perspective before they can be possibly directly linked to CHD. Two other reports described fat intake in Nordic countries, with an emphasis on Finland. Again, changes in SFA and PUFA intake took place in the same time frame. This time, these changes were accompanied by a decrease in trans-fat (TFA) intake. The New Zealand report is the only article which might suggest a direct link between SFA and CHD. It shows a trend in decreased CHD rates over time, and (in another part of the text) it is mentioned that SFA consumption decreased over time. However, no direct correlation was examined.
I also showed that both heart disease and stroke mortality are highest in countries with low saturated fat consumption. I described this finding in another article on my blog (12).

Conclusion: An international group of scientists states that mortality from cardiovascular diseases has decreased over the past decades. And that this decrease is (partially) caused by a decrease in saturated fat intake. The scientists refer to several articles, none of which examined this correlation. I find it very disturbing that a group of 13 scientists draws firm conclusions, but is not able to find one single study as a base for their findings.
Equally disturbing are their interpretations of simple correlations. If there is a large absolute increase in carbohydrate intakes over the past decades in the USA, the relative contribution of saturated fats will automatically decrease. But this does not mean that saturated fat intakes decreased. In fact, intakes of saturated fats increased from 25.7 to 27.8 g/day! The most obvious conclusion would then be that an increased intake of carbohydrates (or small increase in saturated fat intake) was linked to lower mortality from CVD. Instead, Pedersen et al. suggest that a decrease in saturated fat intake was the cause of lower mortality rates from CVD in the USA.

1) Hoenselaar R. Scientists provide incorrect information (part 1). Natural fats do not negatively influence cholesterol. http://dietanddisease.blogspot.com/2012/03/scientists-provide-incorrect.html
2) Pedersen JI et al. (2011). The importance of reducing SFA to limit CHD. Br J Nutr 106, 961-963. http://www.ncbi.nlm.nih.gov/pubmed/21906408
3) US Department of Agriculture and US Department of Health and Human Services (2010) Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010. http://www.cnpp.usda.gov/DGAs2010-%20DGACReport.htm(accessed 20 September 2011).
4) Campbell TC et al (1998). Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China study. Am J Cardiol. 1998 Nov 26;82(10B):18T-21T. http://www.ncbi.nlm.nih.gov/pubmed/9860369
5) Campbell TC et al (1999). Energy balance: interpretation of data from rural China. Toxicol Sci. 1999 Dec;52(2 Suppl):87-94. http://toxsci.oxfordjournals.org/content/52/suppl_1/87.long
6) Pedersen JI et al (2012). Response to Hoenselaar from Pedersen et al. Br J Nutr 107, 452-454. http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8479188
7)  Committee on Diet and Health (1989) Dietary intake and nutritional status: trends and assessment. In Diet and Health. Implications for Reducing Chronic Disease Risk, chapter 3, pp. 41–84. Washington, DC: National Research Council, National Academy Press.
8) Stephen et al (1990). Trends in individual consumption of dietary fat in the United States, 1920–1984. Am J Clin Nutr 52, 457–469. http://www.ajcn.org/content/52/3/457.long
9) The Project Group: Food Consumption in the Nordic Countries (2001) National, Annual Food Balance Sheets (in Swedish) TemaNord 2001:527. Copenhagen: Nordic Council of Ministers.
10) Valsta LM et al (2010). Explaining the 25-year decline of serum cholesterol by dietary changes and use of lipid-lowering medication in Finland. Public Health Nutr 13, 932–938. http://www.ncbi.nlm.nih.gov/pubmed/20513263
11) Ministry of Health and the University of Auckland (2003). Nutrition and the Burden of Disease: NewZealand 1997–2011. Public Health Intelligence Occasional Bulletin No. 17.Wellington: Ministry of Health. http://www.maorihealth.govt.nz/moh.nsf/
12) Hoenselaar R. Heart disease and stroke mortality are highest in countries with low saturated fat consumption. http://dietanddisease.blogspot.com/2012/03/heart-disease-and-stroke-mortality-are.html 


3 reacties:

Bog said...

But Pedersen et al referred to the IMPACT models done by Capewell. They referred to Finland, USA & New Zealand. These models are similar to those used in econometrics. F.ex out of 80% reduction of age-adjusted CHD mortality in Finland, around 50% is explained by reduction in mean cholesterol levels. Out of this reduction in serum cholesterol, around 80% is explained by reduction in SAFA that occurred during several decades (from 20% of calories to the current 13% of calories). If the intake of SFA did not change in the pre-statin era Finland as you seem to suggest, then what caused such a dramatic reducting in mean serum cholesterol levels in Finland (or in USA)? The fact is that the cholesterol levels in developed nations have dropped significantly already prior to wide-scale statin usage. The conclusions drawn by Pedersen et al are very easy for us to accept.

Moreover, Pedersen et al referred to experimental models showing that elevated LDL alone (in the absence of other risk factors) is sufficient to induce atherosclerosis. The findings from these models are well supported in humans by the large mendelian randomized trials with several hundred thousand of genotypes (Ference et al 2012).

Why have total cholesterol levels declined in most developed countries?

Furthermore, I find it very problematic that failed to take into consideration the experimental evidence showing that dietary cholesterol and saturated fat is a primary cause of atherosclerosis. This line of evidence is so extensive that suggesting that it is somehow irrelevant to humans would require implying that the Darwinian foundation of biomedical research is invalid. Since the breakthrough led by Nikolai Anichkov a century ago, the feeding of cholesterol, and to an extent, dietary fat have been recognized as the sine qua nons for the dietary modification of experimental atherosclerosis, and have been used in thousands of experiments to successfully accelerate the development of atherosclerosis in mammalian, avian and fish species, not only of herbivorous, but also omnivorous and carnivorous nature.This includes the promotion of experimental atherosclerosis in over one dozen different species of nonhuman primates- New World monkeys, Old World monkeys, and great apes including the closest living relative to humans, the chimpanzee (Fig. 1).2 3 12 13 14 15 16 17 18 19 20 21 The atherosclerotic lesions induced by saturated fat and cholesterol feeding, including in the form of fresh eggs yolks in many opportunistic omnivores, such as various species of nonhuman primates, birds and pigs have been shown to closely resemble the disease in humans.1 2 3 4 22 23 24

It has also been observed that the long-term feeding of cholesterol and saturated fat has resulted in heart attacks, sudden death, development of gangrene, softening on the bones and numerous other serious complications in nonhuman primates.2 3 25 26 27 28 For example, it has been shown that when diets rich in cholesterol and saturated fat are fed to monkeys of the genus Macaca, including the rhesus monkey and the crab-eating macaque, they experience heart attacks at approximately the same rate as high-risk populations living in developed nations.3

In species that are unlike humans, very resistant to dietary induced elevations in LDL cholesterol, such as the order of the carnivora, unless LDL-receptor deficient breeds are used atherosclerosis is typically induced by raising serum (blood) cholesterol with a diet with very large amounts of dietary cholesterol, and either containing thiouracil or deficient in essential fatty acids.


Zahc said...

Beware of this Bog guy. He has a habit of posting misleading info in an effort to promote his vegan agenda. Seems that his name is Travis (http://www.drmcdougall.com/misc/2013nl/may/travis.htm) and he runs this blog (http://healthylongevity.blogspot.com/). You may see him posting under various aliases such as "Bog", "Healthy Longevity", "T Warrior" and possibly others.

He was a nuisance on Stephan Guyenet's blog and had to be corrected numerous times for his faulty arguments - http://wholehealthsource.blogspot.com/2012/05/beyond-otzi-european-evolutionary.html. Interestingly in Guyenet's post Bog states:

"while pushing your "appeal-to-tradition"-fallacy you miss an important concept: "correlation does not equal causation". I am sure you've heard the favourite one liner of every fad diet promoter more than once, yet you still fail to comprehend it fully. "

Well, it seems that Bog himself misunderstands the phrase. The correct phrase is "correlation does not IMPLY causation". It's not a favourite one liner of fad dieters but rather a basic statistical principle that is written in just about every statistical text. Just because some people misuse or misunderstand it does not make it any less valid. It equally applies to vegans favourite IMPACT models. While statistical models are useful they cannot establish causation. I suggest you consult with a statistical text to know what models can and cannot do before making claims.

Bog states: "Furthermore, I find it very problematic that failed to take into consideration the experimental evidence showing that dietary cholesterol and saturated fat is a primary cause of atherosclerosis."

That's because the evidence at this point says that dietary cholesterol and saturated fat are not primary causes of atherosclerosis. So yes it is problematic i.e. it is so problematic that all vegans can do is point to animal studies in an attempt to support they case because the human evidence indicates that saturated fat is unlikely to cause anything. The majority of the evidence can be seen on Hoenselaar's website:


Bog will argue that the experiments done on humans were confounded by excess trans fat in the experimental groups. The truth is that the control groups are more likely to be the ones that were disadvantaged by excess trans fat. To anyone who had carefully read Ramsden's paper (http://www.ncbi.nlm.nih.gov/pubmed/21118617) it was explained that n-6 oils not only replaced saturated fat but also a substantial amount of trans fats from margarines and shortenings. In fact, Ramsden states that the trans fat intake in the control groups may have been underestimated so the control groups may have in fact been the ones disadvantaged by trans fat, not the experimental.

The animal argument is another poor one because animal experiments also show that if anything cholesterol plays only a minor role in disease as seen in experiments done with probucol, BHT, DPPD, Taurine, statins, secoisolariciresinol diglucoside, Vitamin E, L-arginine, resveratrol, iron restriction, phycobiliproteins, HBO treatment, exercise etc. which show significant reductions in atherosclerosis independent of cholesterol and in many of them in the presence of severe hypercholesterolemia. Genetic studies are also consistent with role of oxidative stress in disease.

Bog once said to Stephan Guyenet that "You are an intellectual dwarf.... You are cholesterol confusionist....you to spread you pseudoscientific paleo, appeal-to-nature BS." Well Bog, it's time for you to take a good look at yourself in the mirror.

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