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Let’s start from the beginning. You have been told for years that “saturated fat�?is very unhealthy �?by your teachers, by various “health gurus�?featured on TV news programs, etc. You are now a researcher and you want to look into this claim. You are able to get funding for an experiment, and now you need to consider an experimental design. You decide to use food questionnaires, because it is so common in nutritional studies to do so, and you select a group of healthy adults in their 40s. You will study the “diseases�?they are afflicted with in ten years time, and then try to correlate it with the food they ate, as determined by their answers on the questionnaires. Perhaps they have agreed to fill out the questionnaires every two years, so that you can determine if they have made major changes. Most researchers do not even do this much, actually.
Now let’s get to the results. You find that those who ate more “saturated fat�?had more colon cancer, type II, diabetes, and more “heart disease.�? Of course, you decide what a “statistically significant�?difference is, or else others in your discipline have already decided upon this, and so you must conform to these standards. Here is where things get “tricky.�? The question I ask here is, how was this determination made (and we are assuming that the questionnaires are accurate, which is a big leap of faith, according to studies of this research tool)? There are several possibilities: One is that certain foods are considered “saturated fat,�?such as lard, which is actually only about 39% saturated, and so a decision is made about how many servings of “saturated fat�?per week classifies a person as someone who consumes a lot or a little “saturated fat.�? In this kind of study, the actual amount of saturated fatty acids is not determined, nor is the cooking technique considered.
Another way of determining who ate the most “saturated fat�?involves figuring out how much saturated fatty acids were consumed. In some cases, those who consumed the most saturated fatty acids also consumed the most polyunsaturated fatty acids and cholesterol, and also cooked the food containing these molecules at high temperature while exposed to air. Thus, one would have to study these, and perhaps other factors, as independent variables before the claim that “saturated fat�?causes such-and-such a disease could be made. And yet this is often not the case, though it is an obvious violation of the basic precepts of the scientific method.
Lastly, the researcher might have found that the only variable that appears to be causative is the amount of saturated fatty acids consumed. This was the case in a study of Alzheimer’s Disease, for example. Now let us think about what is actually being eaten by the people, assuming that the questionnaires were accurate. The subjects were people on “typical�?American diets. None were eating large amounts of coconut, for example. In addition, even if some were eating large amounts of butter, for example, we are not told if they ate the butter raw, or cooked it (which would oxidize the cholesterol in it, unlike margarine, which does not contain cholesterol). In general, food that contains the highest levels of saturated fatty acids also contain the most cholesterol, the notable exception being eggs, which don’t contain many fatty acids of any type, relative to other high protein foods Americans usually eat. Using a control group that used a fat source such as coconut oil, which contains no cholesterol, would be necessary for this kind of study to meet the standards of the scientific, along with other taking other possibly relevant factors into account. For example, it is also generally true that the food that contains the most saturated fatty acids are also very rich in iron, again unlike coconut oil. It is also possible that food that contains the most saturated fatty acids is more likely to be cooked at high temperatures while exposed to air, which would make the unsaturated fatty acids, cholesterol, and iron in it into a very dangerous concoction. The saturated fatty acids, though, would pose no immediate biochemical hazard. And as I am trying to make clear here, until the research is conducted properly, there is no reason to fear saturated fatty acids at this point. Rather, the “findings�?suggesting that “saturated fat�?is unhealthy are based upon poorly conducted and misinterpreted studies, such as I’ve described above.
None of this excuses the researcher from being unfamiliar with various studies of those who eat large amounts of coconut product, as well as the raw demographic data, compiled by the World Health Organization and other agencies. If the researcher had done some research of the literature (with an open mind) he or she would realize that something is amiss, and hopefully design a new experiment in a more intelligent way, and in a way that is consistent with the scientific method. To date, there are few studies that demonstrate that the researchers have come to this realization.
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My point in the above post is supported by the following kinds of evidence:
http://www.sciencedaily.com/releases/2007/08/070801161507.htm
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=502446
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch
=6138545&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Here's a new report of an experiment that did not control for different kinds of dietary fatty acids:
"...Because the differences among the groups of rats could be traced to the amount of fat, and no anti-rejection drugs had been given, the results validate their theory that fat was the culprit in killing the beta cells, Dr. Unger said..."
Source: http://www.sciencedaily.com/releases/2007/08/070828084431.htm
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An interesting article about saturated fat entitled "What if Bad Fat is Actually Good for You?":
http://tinyurl.com/3dsuv8 |
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| But notice the picture on the first page; they are showing butter in the context of being fried. It's amazing how so many really "smart" people can't figure out that there are several factors at work. |
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I wrote up a post for another newsgroup about this article, copied and pasted below:
An article with this title appeared on the site: http://www.menshealth.com/
in the health section.
Here is a passage:
QUOTE: "The message isn't that you should gorge on butter, bacon, and
cheese," says Volek. "It's that there's no scientific reason that
natural foods containing saturated fat can't, or shouldn't, be part of
a healthy diet." UNQUOTE.
Relative to overall calories, there are probably only a few people in
the USA who eat more saturated fatty acids than I do each and every
day. However, I do not eat bacon, and I only eat butter and cheese if
they are not cooked (sometimes I use butter in sauces at low settings
on the stove top, but not very often). Eggs seem to be a bit more
resistant to high heat cooking, but I only eat lightly boiled eggs
(this is a cholesterol issue, not an SFA one, but it's often brought
up by the "experts" in this kind of discussion). And obviously,
almost all foods with a fat content have some SFAs, so this passage
needs clarification. I do consume some gelatin, which is derived from
animals but contains no fat (I do this not because I'm concerned with
"animal fat" - as I point out below, such phrases are misleading a
good deal of the time).
Apparently, the idea is that the nutritionists' classification scheme
of "saturated," "monounsaturated," and "polyunsaturated" fat sources
is accurate. The scientific reality is that it is a misleading and
purely semantic construct. The problem is that nutritionists have
created a "science" that is often not consistent with actual
scientific evidence. An obvious example is to talk about
"cholesterol," when they may be referring a substance that has all
kinds of other molecules that have been modified by free radicals (and
which can be very dangerous, unlike non-modified cholesterol). They
often say "saturated fat" when referring to lard in an experimental
context, but lard is about 40% SFAs, and of course it makes much more
sense to refer to it as a "mixed fat," though this still does not
address the point that all molecules have to be accounted for if the
scientific method is to be followed. Obviously, few people eat diets
that are so specific, and thus this line of thinking can lead to all
kinds of claims that are unfounded. Lard contains cholesterol, which
may or may not be oxidized, for example. Coconut oil is about 92%
SFAs, but it contains larger amounts of shorter chain SFAs, which are
easier for the body to use (and so extracts of coconut oil are used
for people who have people with dietary fats). Some fat sources are
rich in powerful antioxidants (keeping free radical activity down),
whereas others have none (like lard). Again, all these factors need
to be taken into account before a scientific claim similar to the
usual ones made by nutritionists is made.
Is there an alternative that can lead to practical solutions?
Fortunately, yes. It involves understanding biochemistry, and
abandoning the nutritional dogma (so as to conduct an investigation
without bias). If you listen to nutritionists, you probably think
there is very little biochemistry evidence, yet what I found is that
there is so much (and it is so good, in general) that there is really
no need for qualified statements such as the one I quoted. The
evidence is strong enough now for an overall framework to be
constructed (and which allows one to formulate a practical, tasty,
inexpensive, healthy, and satisfying diet), without worrying about the
nutritionists' classification schemes (and also the failure of some of
them to act like the scholars they present themselves as). If you
want to know what this new framework is like, you can visit my free
web site:
http://groups.msn.com/TheScientificDebateForum-
Don't expect to understand everything within a few minutes. Take some
time, and read the essays that you find most interesting first. Don't
worry about the technicalities in the evidence I quote - you can
always ask questions in the two newsgroup forums on the site. |
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Here comes a claim that saturated fat as well as trans-linoleic acid hamper oxygen transport throughout the body. I think that erythrocytes may also incorporate Mead acid and no one has looked at its oxygen-transport properties yet ...
http://www.brianpeskin.com/soapr07-2-4-pgs-1.pdf |
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Here are two reports that appear to support the notion that it's the PUFA-rich "modern diet" that is to blame for various "chronic diseases," but because the researchers don't control for fatty acids (for example, one group of people should be fed a diet rich in fresh coconut oil but ingest no other major source of fat), most people think that "fat" is "bad," and will often say that "saturated fat" is "really bad," when the evidence supports the opposite (if "saturated fat" is defined in a reasonable way):
http://www.sciencedaily.com/releases/2008/01/080103153217.htm
http://www.sciencedaily.com/releases/2008/01/080102083757.htm |
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Here's a relevant abstract, which contradicts "mainstream advice:"
J Nutr. 2003 Jan;133(1):78-83.
"The serum LDL/HDL cholesterol ratio is influenced more favorably by
exchanging saturated with unsaturated fat than by reducing saturated
fat in the diet of women."
Müller H, Lindman AS, Brantsaeter AL, Pedersen JI.
University College of Akershus, Bekkestua, Norway.
We compared the effects of a high fat diet [38.4% of energy (E%) from
fat; HSAFA diet, polyunsaturated/saturated fatty acid (P/S) ratio =
0.14], a low fat diet (19.7 E% from fat; LSAFA diet, P/S = 0.17), both
based on coconut oil, and a diet with a high content of mono- and
polyunsaturated fatty acids (PUFA; 38.2 E% from fat; HUFA diet, P/S =
1.9) on serum lipoproteins. The 25 women studied consumed each diet
for 3-wk periods in a crossover design. The two high fat diets were
identical except for the quality of the test fat. The LSAFA diet was
identical to the HSAFA diet except that half the fat was replaced by
carbohydrates. Serum total cholesterol, LDL cholesterol and apoB
concentrations did not differ between the HSAFA and the LSAFA diet
periods. Total cholesterol, LDL cholesterol and apoB were lower when
women consumed the HUFA diet than when they consumed the other two
diets. HDL cholesterol and apoA-I were 15 and 11%, respectively,
higher when women consumed the HSAFA diet than when they consumed the
LSAFA diet; HDL cholesterol and apoA-I were lower when women consumed
the HUFA diet than when they consumed the HSAFA diet, but not the
LSAFA diet. The LDL cholesterol/HDL cholesterol and apoB/apoA-I ratios
were higher when women consumed the LSAFA diet than when they consumed
the HSAFA diet. The LDL/HDL cholesterol ratio was higher when women
consumed either the LSAFA or the HSAFA diet than when they consumed
the HUFA diet, whereas apoB/apoA-I was higher when women consumed the
LSAFA diet than when they consumed the HUFA diet. Triacylglycerol and
VLDL cholesterol were higher when women consumed the LSAFA diet than
when they consumed either the HSAFA or the HUFA diet. We conclude
that, to influence the LDL/HDL cholesterol ratio, changing the
proportions of dietary fatty acids may be more important than
restricting the percentage of total or saturated fat energy, at least
when derived mainly from lauric and myristic acids, both of which
increase HDL cholesterol. |
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Yet another report that does not distinguish between different kinds of fat (and of course, by "high fat," they really mean a historically high PUFA diet):
QUOTE: Men who eat a diet low in fat and red meat but high in vegetables and lean protein and who drink alcohol in moderation may not just be doing their hearts a favor. A new study shows that such a heart-healthy diet may also be good for the prostate... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/02/080213102841.htm |
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And another report about how bad "fat" is, when they are really demonstrating how bad a PUFA-rich diet is, relative to a "low fat" (that is, a low-PUFA) diet. If this was not the case, then people eat fat-rich but low-PUFA diets would also have these problems (such as the Amish and Asians eating coconut-rich diets). The researcher, however, talks about "saturated fat" rather than the PUFA content:
Title: "Low-fat Diets More Likely To Reduce Risk Of Heart Disease Than Low-carb Diets."
Source: http://www.sciencedaily.com/releases/2008/02/080229141756.htm |
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Chris Masterjohn of the Weston A. Price Foundation argues that a low-fat diet will only provide benefits insofar as it's also low in PUFAs. The carbs will be converted to saturated fatty acids, making low-fat a high-SFA diet too.
"...when [SFA] intake was analyzed as a continuous variable, each [5%] of calories from [SFA] produced a 0.16-millimeter lessening of atherosclerotic progression. The effect changed from a slowing of progression to a reversal at about [13%] of calories from [SFA]...
"Additionally, every [5%] increase in the percentage of calories from [PUFA] was associated with a 0.17-millimeter worsening of atherosclerotic progression."
http://www.cholesterol-and-health.com/Campbell-Masterjohn.html#context
So, the evidence is clear. Low-fat diets are only beneficial in that they are low in PUFAs and the carbs are converted into saturated fat, making low-fat diets high-SFA and low-PUFA, by default. Saturated fatty acids reverse atherosclerosis and PUFAs cause it to progress. So, lard may be very bad, while beef fat or butter or coconut oil won't be. |
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Look at the Japanese Sumo wrestlers. They don't have any higher rates of atherosclerosis while getting fat on purpose by consuming a lot of carbohydrates in the form of rice and of course some real fat from meat. I cannot speak of my arteries but after the 4-years on flax/fish oil I ended up with a billiary polyp (a kind of gall bladder stone) which shrank to its half after 1 year of stopping any PUFA supplementation and replacing vegetable oils with meat fat and butter as much as practical. Gall bladder is the organ which removes/detoxify PUFA-derived lipid peroxides from the body. The high SFA regime also got my cholesterol way up but that's not enough to force me changing the diet again especially when I feel considerably better now.
One thing about the carbs which makes me wonder is that the low carb people don't seem to suffer from the excessive PUFA consumption - see e.g. the Cordain site www.thepaleodiet.com. After watching the Gary Taubes lecture about the obesity epidemic (http://webcast.berkeley.edu/event_details.php?webcastid=21216 ) it seems to me that in the absence of carbohydrates the body cannot store the dietary PUFAs and therefore burns them for energy right away before they can cause any substantial damage. Even for the flax oil in paintings it takes some time to oxidize so the problem may arise only when you have the PUFAs wondering around in your body fat stores. |
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I don't think that low-carb will fully protect you from high-PUFA. Here is a study I found a while ago comparing a low-carb diet high in SFAs (60%) to a low-carb diet high in PUFAs (60%). MUFAs were kept constant at 25% of fat.
http://jcem.endojournals.org/cgi/reprint/89/4/1641.pdf
These diets were 70% fat, 15% carbs, and 15% protein. The authors noted some problems with the high-PUFA diets, like nausea, which was "significantly higher in the POLY group." They also found that PUFAs caused more severe symptoms of ketosis, which they concluded was good. (I disagree with them.) If I was eating low-carb, I would focus on beef (raw or rare), cheese, butter, coconut oil, macadamia oil, 85% dark chocolate or cocoa butter, and other fats that are very low in PUFAs. This study tells me that PUFAs don't burn clean and they generate more toxic byproducts than SFAs.
Bruce |
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On another newsgroup, one person claimed that Malaysians had high rates of heart attacks even though they at a lot of coconuts. It turned out that this was a recent development, and that most Malaysians had switched over to a diet rich in highly unsaturated fat sources:
"...This region is undergoing unprecedented economic growth, rapid
technological changes, urbanization, and major changes in lifestyle.
The very high CHD death rates in Singapore (the most economically
developed country in the region), which are similar to those of the
United States and Australia, provide a warning that Asia may expect a
surge in CHD..."
Source: Circulation. 1996;94:2671-2673.
© 1996 American Heart Association, Inc.
http://circ.ahajournals.org/cgi/content/full/94/11/2671 |
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New Report: "To Block The Carcinogens, Add A Touch Of Rosemary When Grilling Meats."
Source: http://www.sciencedaily.com/releases/2008/05/080521184129.htm
QUOTE: ...J. Scott Smith found out about rosemary’s strength against the compounds while researching ways to reduce them as part of a long-term Food Safety Consortium project at Kansas State University. Smith, a KSU food science professor, has been looking into the carcinogenic compounds known as HCAs (heterocyclic amines)...
The presence of HCAs is a potential problem in cooked beef. The likelihood of their presence is influenced by cooking time and temperature. Previous studies showed that meat products cooked below 352 degrees Fahrenheit for less than four minutes had low or undetectable levels of HCAs. The HCAs would increase as temperature and cooking time increased... UNQUOTE.
Of course, there is no mention of how dietary PUFAs seem to enhance this HCA problem significantly (as I found evidence for, and posted on this site).
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