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And here is another one of my responses:
The fact that you do not understand that a formal hypothesis is required in order to make a scientific claim speaks volumes. Even those who make general statements about how "bad" "trans fat" is realize that trace amounts of trans fatty acids are not harmful, as it is basic biochemistry. However, it is obvious to even those very little scientific understanding on this issue realize that since trace amounts will do no harm, there is a need to put forth a claim about the threshold amount that will do harm. This would be included in a formal hypothesis.
Now on to something more important, in my view, which also demonstrates your inability to comprehend the scientifric method:
MattLB stated: QUOTE: How is exposure to sun and oxygen a control for a trans double bond? You're speaking nonsense. UNQUOTE.
Readers of course must judge for themselves, but I will try to "break this down" to the simplest elements, though because the claimants refuse to state a formal hypothesis, I can only assume that what the "nutritional experts" say (most of the time, at least) is what they are in fact asserting:
1. They do not believe that a diet rich in something like canola oil is dangerous in any way (in a common dietary context).
2. They do believe that if canola oil is partially hydrogenated that is then becomes very dangerous (again, in a typical dietary context for nations like the USA).
3. There is a lack of clarity on total hydrogenation (meaning different "experts" are making different claims), though my experimental idea would clear this up, but we will leave this aside here and address your criticism only.
Thus, one group of animals can be fed the partially hydrogenated oil - that is clear. Many researchers would then simply compare this group of animals with one fed canola oil straight from the bottle, but this is an improper control, if it is the only other group. The partially hydrogenated oil will be stripped of natural antioxidants, while the other may still contain much of them (one would have to test the oil first to know). In my design, the oil that is spread thin and allowed to lose its antioxdiants without producing trans fatty acids would act as an excellent control for the notion that the trans fatty acids are to blame for its supposed "ill health effects." If the animals live to about the same ages, then it's clear that the only reasonable explanation is that free radical activity is to blame, not the trans fatty acids. Of course, I would prefer to have several groups of animals: one on a fat free diet, one on a fresh coconut oil diet, one on a canola oil diet (fed straight from the bottle), etc.
In any case, MattLB does not address the obvious question: what if the experiment was conducted according to my design and what if the results were as I expect them to be? Would he then acknowledge that free radical activity is the issue and nothing else? At the very least, it would be interesting to know the answer to this, in terms of how much grasp he possesses on reality.
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And here is a new post, in which I try to simply things to a very basic level ("typo" errors corrected):
Most of you probably don't realize this, but it appears as if no on
point experiment has been conducted. Instead, all the assertions being
proclaimed by various "experts" are based upon "markers." Many of you
are probably unfamiliar with the scientific terminology, and so I will
try to make it easy to understand. One problem is that there is no
"trans fat" hypothesis, and therefore I can only respond to the claims
that are prevelant today in the USA.
1. Canola oil is now being called one of if not the healthiest "all
purpose" dietary oils you can consume.
2. Partially hydrogenated oil, even if it is canola oil, however, would be considered very
unhealthy by the "experts," because it contains what they call "trans
fat," though this is ill-defined (many foods contain trace amounts, for
example, and so at least it would be necessary to state a threshold
amount that is dangerous).
3. A simple experiment could be done to determine what the scientific
reality actually is: one group of animals typically used in these kinds
of experiments would be given diet of 25% canola oil - of the kind that
most Americans are consuming now, while another group would be fed 25%
partially hydrogenated canola oil product - a margarine produced by a
major food company, and purchased from a major supermarket.
4. If the animals fed the margarine live as long or longer, then there
would be direct evidence that demonstrates that this claim about "trans
fat" needs reformulation, at the very least (and is likely to be
nonsense), though it is impossible to discuss it in a truly scientific
context until those making the claim put forth formal hypotheses,
without which there is no way to know what should be tested, because it
is unclear what is being said to be causative, and at what threshold
amount this occurs.
5. Since "saturated fat" is considered "bad" as well, a third group of
animals could be fed fresh coconut oil. This group would likely live
the longest and have the best health. The reason is that the causative agent, as
the molecular-level evidence demonstrates, is free radical mediated
damage and dysfunction, not whether an unsaturated fatty acid possesses
a double bond that has a "kink" in it.
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I found a passage in an essay on a popular "alternative" medicine and nutrition site (which is generally good) that totally mistates the issue: QUOTE: Problems with Hydrogenated Oils Many, many diseases have been associated with the consumption of trans fatty acids, such as heart disease, cancer, digestive disorders and degeneration of joints and tendons (which is why we have so many hip replacements today). Trans fats are associated with auto-immune disease, skin problems, growth problems in children and learning disabilities. The only reason that we are eating this stuff is because we have been told that the competing fats and oils--butter, lard, tallow and suet, coconut oil and palm oil--are bad for us and cause heart disease. This message is nothing but industry propaganda to get us to buy substitutes. UNQUOTE. The problem here is obvious: if you totally hydrogenate a fat source, there are no trans bonds present, and all the fatty acids are then saturated. Thus, there may be no problem with hydrogenated fats, so long as there are no unsaturated bonds present ("trans" or "normal"). Of course, there is no fat source in nature that is 100% saturated fatty acids, and I would rather consume fresh coconut oil than coconut oil that is totally hydrogenated, because I don't know what else is in the hydrogenated product, being that it has been subjected to all kinds of processing. Source: http://www.westonaprice.org/modernfood/dirty-secrets.html |
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Here is a statement by the "Chemical & Engineering News" that is about as specific as the "experts" ever get on this issue these days: QUOTE: What are trans fatty acids? Unsaturated fats, found in such foods as avocados and olive and corn oils are heart healthy, but in the air they can go rancid by absorbing oxygen and then decompose, C&EN explains. Manufacturers can stop this process by bubbling hydrogen (hydrogenation) through the fat at a high temperature in the presence of a catalyst like nickel and in the absence of oxygen. The process raises a fat's melting point, turning liquid vegetable oil into products ranging from soft margarine to solid shortening, according to the newsmagazine. When the healthful unsaturated fats are partially hydrogenated, the double bonds are rearranged, converting some to the trans configuration and shifting the double bonds along the chain. Unfortunately, this newly created trans fatty acid is an artery-clogger... UNQUOTE. Note that these claims are mostly based upon terribly flawed statistical correlation ("epidemiological") studies. The most likely explanation is that who are generally least healthy eat the most "trans fat" and so have more heart attacks and that most "trans fat" sources have less antioxidants than unsaturated oils that have not undergone partial hydrogenation. But the claim in the above passage is that the trans configuration is to blame for clogging arteries. How can this possibly be the case? How can the double bond be so different in a cis configuration than a trans configuration, in terms of one causing "heart disease" and the other "protecting" against it? This is an extraordinary claim, and the evidence needs to at least meet the standards of the scientific method, one would think. The idea that polyunsaturated fatty acids are "protective" against heart disease is ludicrous in terms of what is now known on the molecular level (which I've cited on this site in other places), but let us assume that they are unaware of this evidence. Where is the experiment that has shown how a trans fatty acid molecule creates atherosclerotic plaque, and where is the experiment that has shown how a polyunsaturated fatty acid prevents plaque buildup? The best they have to offer are exeperiments in animals that are terribly flawed, and don't show exactly how the molecules supposedly cause the damage. In any case, as I ask people, why don't they just do an experiment on rats or dogs or a species of monkey that doesn't live more than about 15 years, control for all relevant factors (including dietary antioxidants and the amount of oxidized cholesterol in the diet), and see which diet results in the best longevity? Source of the quoted passage: http://www.sciencedaily.com/releases/2003/09/030924055334.htm |
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Here it seems that the 18:2 trans-FA is the problem in CHD. Because it resembles the linoleic acid and they say it accumulates in adipose tissue it confirms that even the normal linoleic acid accumulates in the body fat to significant degree. Such fat stores could be then very dangerous to carry around especially if they get mobilized by e.g. disease or fasting. I can imagine how all kinds of cancers can thrive on such linoleic acid deposits and use it to manufacture AA like we use crude oil to make gasoline or rocket fuel ...
J Nutr. 2003 Apr;133(4):1186-91.
High 18:2 trans-fatty acids in adipose tissue are associated with increased risk of nonfatal acute myocardial infarction in costa rican adults.
Baylin A, Kabagambe EK, Ascherio A, Spiegelman D, Campos H.
Department of Nutrition, Harvard School of Public Health, Boston, MA, USA.
Trans-fatty acid intake is associated with coronary heart disease (CHD), but the atherogenic potential of individual trans-fatty acids (FA) from partially hydrogenated oils (18:1 and 18:2) or meat and dairy products (16:1 and 18:1) is unclear. Incident cases (n = 482) of a first nonfatal myocardial infarction (MI) were matched with population controls (n = 482) for age, gender and area of residence, all living in Costa Rica. Trans-FA in adipose tissue samples were assessed by gas chromatography. Odds ratios (OR) and 95% confidence intervals were calculated from conditional logistic regression models. Total adipose tissue trans-fat was positively associated with risk of MI. After adjusting for established risk factors and other confounders, the OR by quintiles of total trans-fat were 1.00, 1.34, 2.05, 2.22 and 2.94 (P-test for trend < 0.01). This association was attributed mainly to 18:2 trans-FA that were abundant in both adipose tissue and in partially hydrogenated soybean oil, margarines and baked products used by this population; OR = 1.00, 0.96, 2.09, 3.51 and 5.05 (P-test for trend < 0.001). Adipose tissue 16:1 trans-FA were also associated with MI; OR = 1.00, 1.57, 1.39, 1.34 and 2.58 (P-test for trend < 0.05). An association with 18:1 trans-FA was not detected. High 18:2 trans-FA in adipose tissue are associated with increased risk of MI. Because the use of hydrogenated oils is increasing worldwide, consumers should be aware of the harmful effects of products containing partially hydrogenated oils.
PMID: 12672941 |
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Med Hypotheses. 1986 Dec;21(4):387-408.
The Eskimo diet. Prophylactic effects ascribed to the balanced presence of natural cis unsaturated fatty acids and to the absence of unnatural trans and cis isomers of unsaturated fatty acids.
Booyens J, Louwrens CC, Katzeff IE.
In addition to the well recognised roles of eicosapentaenoic acid and possibly docosahexaenoic acid, there are two other major important, but unrecognised, features of the traditional Eskimo staple diet namely that it contains the unsaturated fatty acids (UFA) cis oleic, cis linoleic and cis alpha-linolenic as well as their respective C20 and C22 metabolites in physiologically optimal concentrations and, it is virtually totally devoid of unnatural and potentially hazardous trans and cis isomers of these fatty acids. Large quantities of unnatural trans and cis isomers of UFA are found in the Western diet as partially hydrogenated UFA in many foods. These isomers are formed during the manufacture of margarines and related compounds, as food contaminants during excessive heating of cooking oils for deep-frying and other excessive heat-requiring mass food preparation procedures and it is suggested, as the result of excessive feeding with an unnatural diet of ruminants and non-ruminants for increased meat and/or milk production and of poultry for increased egg and/or meat production. These isomers have been shown to display potentially hazardous metabolic effects which include the competitive inhibition of UFA metabolism at various steps and have been causally implicated in the etiology of ischemic heart disease and cancer. It is suggested that the myth of the safety of trans fatty acids arises from misinterpretation of the observation that increasing dietary cis linoleic acid reduces the toxic effects of trans UFA. It is suggested that the decrease of 20% in the ischemic heart disease mortality in the USA during the past two decades is directly related to a shift in the dietary ratio of unnatural trans and cis UFA isomers: cis linoleic acid in favour of the latter. It is predicted that this ratio will be found to correlate with ischemic heart disease patterns in other countries. Eskimos consume the bulk of their food frozen, raw or dried, seldom boiled, but never deep-fried or after exposure to excessive heat. Moreover the proportionality of cis UFA and their metabolites in their traditional staple diet would render gross tissue UFA utilization relatively independent of desaturase enzyme activity. In the Eskimo tissues these enzymes would function to make the minute, critical UFA metabolic adjustments required to ensure the presence of structural UFA in membranes in functionally optimal quantities and, ensure the synthesis of eicosanoids from dihomogamma-linolenic acid, arachidonic acid and eicosapentaenoic acid in balanced, optimal physiological concentrations for the genetic make-up of Eskimos.It is therefore proposed that the composition of the Eskimo diet, specifically with regard to its content of natural cis UFA and of their respective cis longer chain metabolites, could account for its reported prophylactic effects.
It is further proposed that regular dietary supplementation with longer chain UFA metabolites will correct the hazardous metabolic effects caused by the presence of unnatural trans and cis UFA in the tissues of humans chronically consuming a Western diet. By thus mimicking the Eskimo diet, therapeutic and prophylactic effects could be achieved in a wide range of Western degenerative diseases including cardiovascular disease and cancer.
PMID: 3642208 |
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| These are just some vague ideas or "associations." My guess is that this particular fatty acid is just the most common in the usual oils used. Notice that they did not look at AA content. It's already known that PUFAs in LDL make it much more susceptible to oxidation - this is the biggest problem. There could be lesser ones, of course, but you need to think of the evidence more comprehensively, rather than "jumping to conclusions" with this kind of very limited study. |
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J Nutr Sci Vitaminol (Tokyo). 2006 Apr;52(2):83-8.
Dietary hydrogenated soybean oil affects lipid and vitamin E
metabolism in rats.
Naziroglu M, Brandsch C.
Institute of Nutritional Sciences, Martin-Luther-University of Halle-
Wittenberg, Halle/Saale, Germany. [email protected]
Fatty acids containing stearic acid, which are found in hydrogenated
fat, may have a detrimental effect on the cholesterol and
triacylglycerol (TAG) content of plasma lipoproteins, and on the
absorption of fatty acids and fat-soluble vitamins. The aim of our
study was to examine the tissue concentration of lipids and vitamins A
and E after feeding a hydrogenated soybean oil (HSO) diet to rats.
Twenty male Sprague-Dawley rats were randomly divided into two groups,
fed on coconut oil (control) and HSO, respectively in amounts
corresponding to 15% of the total feed. Plasma total cholesterol,
VLDL- and LDL-cholesterol, lipid peroxidation and daily excretion of
the TAG and cholesterol in feces were higher in the HSO than in the
control group. TAG values in plasma and liver, and HDL-cholesterol
levels in plasma were lower in the HSO than in the control group. The
same was true for phospholipids in plasma and for saturated fatty
acids, mono- and polyunsaturated fatty acids levels in the liver and
vitamin E in plasma, LDL and adipose tissue. The results of this study
provide new evidence concerning the effect of dietary hydrogenated fat
on lipid, TAG and vitamin E status, which are important for
maintenance of good health. Consumption of dietary HSO may be
associated with cardiovascular disease. |
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| The abstract in the post above is (or at least it was at one time) available online. If you read it, you will learn that that the "hydrogenated " soybean oil used was hard and solid, but in Table 2, they show the actual fatty acids in this concoction, and it contains about 40% MUFAs and 3% PUFAs. It is hard because it contains a lot of long-chain SFAs. This is very important, because when someone talks about a totally hydrogenated oil or fat, he/she apparently means that it was hydrogenated until it was solid, not that all the fatty acids were turned into saturated ones, though this makes a lot more sense. Thus, a totally hydrogenated oil is not necessarily all SFAs, and so this would have to be controlled in order to determine if the number of double bonds, which can participate in lipid peroxidation reactions (known to be potentially very dangerous), is the most important factor in determining how potentially dangerous a fat source is (at least if the source is refined, and contains few of its natural antioxidant protection). However, you will rarely, if ever, find a study of "hydrogenated" fat sources that controls for the number of double bonds. |
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Wikipedia provides some explanations about trans- and interesterified-fats and their history:
http://en.wikipedia.org/wiki/Trans_fat
http://en.wikipedia.org/wiki/Interesterified_fat |
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The second site you cited had a link to this study:
Nutrition & Metabolism 2007, 4:3 doi:10.1186/1743-7075-4-3.
On the internet: http://www.nutritionandmetabolism.com/content/pdf/1743-7075-4-3.pdf
The researchers found: "Conclusion: Both PHSO and IE fats altered the metabolism of lipoproteins and glucose
an unmodified saturated fat when fed to humans under identical circumstances."
The problem is that we don't know why this occurs? It is due to the structure of the fatty acid, the antioxidant content (or lack theerof), or something else? With my diet, even if you ate a small amount of such food, there would be much more fat from cheese and dark chocolate, and so I don't think such effects would occur, and so it's not really an issue for me. The problem, as I see it, is that some people will eat a huge amount of prepared foods and not realize what might happen to them if they eat a huge amount of food with interesterified fatty acids in it, for instance. |
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| I should have mentioned that the study I quoted in the post above was short term, and so it's possible that there would have been no long-term change in the markers they decided to examine. |
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I posted the following on another newsgroup. It is the kind of study I would do if I were given funding at some point:
QUOTE: Abstract: "Offspring of long-lived individuals are a useful model to
discover biomarkers of longevity. The lipid composition of erythrocyte
membranes from 41 nonagenarian offspring was compared with 30 matched
controls. Genetic loci were also tested in 280 centenarians and 280
controls to verify a potential genetic predisposition in determining
unique lipid profile. Gas chromatography was employed to determine
fatty acid composition, and genotyping was performed using Taqman
assays. Outcomes were measured for erythrocyte membrane percentage
content of saturated fatty acids, monounsaturated fatty acids,
polyunsaturated fatty acids (omega-6 and omega-3), geometrical isomers
of arachidonic and oleic acids, and total trans-fatty acids. Also,
allele and genotyping frequencies at endothelial-nitric oxide synthase
and delta-5/delta-6 and delta-9 desaturase loci were considered.
Erythrocyte membranes from nonagenarian offspring had significantly
higher content of C16:1 n-7, trans C18:1 n-9, and total trans-fatty
acids, and reduced content of C18:2 n-6 and C20:4 n-6. No association
was detected at endothelial-nitric oxide synthase and delta-5/delta-6
and delta-9 desaturase loci that could justify genetic predisposition
for the increased trans C18:1 n-9, monounsaturated fatty acids and
decreased omega-6 synthesis. We concluded that erythrocyte membranes
derived from nonagenarian offspring have a different lipid composition
(reduced lipid peroxidation and increased membrane integrity) to that
of the general population."
Source: Rejuvenation Res. 2007 Dec 26 [Epub ahead of print].
Title: Fatty Acid Profile of Erythrocyte Membranes As Possible
Biomarker of Longevity.
Note: Nonagenarians are those between the ages of 90 and 99.
Commentary (by me): This does not mean you should go out and eat food
rich in trans fatty acids, because as the researchers point out, their
findings are consistent with a lipid peroxidation hypothesis for
longevity. However, this is consistent with what I do, and that is to
look for food that is over 50% SFAs, low in cholesterol, and if this
is the case, I don't worry if there are any trans fatty acids at that
point, since it's going to be a stable item and generate little if any
lipid peroxidation (still should not eat it if it has any hint of
rancidity to it). Also, note how they totally contradict the notion
that "trans fat" will cause some sort of structural harm to cells. In
fact, the opposite appears to be the case, and I've pointed out how
ridiculous the anti-"trans fat" claims were for a long time (on
several different levels). Instead, it would make more sense to test
the food item to see how quickly it goes rancid, and there are a few
tests that can be used (Rancimat and ORAC, as examples). However,
will you hear about this study in the "mainstream media?" Or will you
hear yet another report about how "bad" "trans fats" are, with either
no evidence cited or else an "epidemiological" study cited that did
not control for lipid peroxidation (in other words, what most likely
happens when "trans fat" appears to be unhealthy is that those who ate
the most TFAs also ate the most PUFAs and/or had a diet significantly
lower in antioxidant-rich foods). UNQUOTE.
It's also true that since cooked meat and a PUFA-rich diet seem to be a terrible combination, those consuming the most TFAs may also have more dangerous molecules being generated by the cooke meat/PUFAs combination. |
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Wow, first paper of this kind in humans !!! This has been reported in many animal species, even in the same genus such as bees - the long lived queens increase oleic acid at the expense of PUFAs. I am not sure whether the trans-configuration is important but this clearly contradicts the other "correlation" studies citing high oleic acid in membranes and low PUFAs linked to obesity, insulin resistance, syndrome X etc.
If they find the mutation (or is it a behavioral trait e.g. that the PUFAs just taste bad to these people?) responsible for such difference they may directly test this hypothesis in a transgenic mouse ... |
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Trans fatty acids are said to inhibit tumor growth here:
J Nutr Biochem. 2007 Oct;18(10):637-49. Epub 2007 Apr 5.
Dietary factors and growth and metabolism in experimental tumors.
Sauer LA, Blask DE, Dauchy RT.
Bassett Research Institute, Cooperstown, NY 13326, USA. [email protected]
Development of a diet that provides adequate nutrition and effective cancer prevention is an important goal in nutrition and cancer research. A confounding aspect of dietary control of tumor growth is the fact that some nutrients may up-regulate tumor growth, whereas other nutrients and nonnutrients down-regulate growth. Both up- and down-regulators may be present in the same foodstuff. Identification of these substances, determination of their mechanisms of action and potencies, as well as the interactions among the different mechanisms are topics of ongoing research. In this review, we describe results obtained in vivo or during perfusion in situ using solid tissue-isolated rodent tumors and human cancer xenografts in nude rats. Linoleic acid (LA), an essential n-6 polyunsaturated fatty acid (PUFA), was identified as an agent in dietary fat that is responsible for an up-regulation of tumor growth in vivo. Tumor LA uptake, mediated by high intratumor cAMP, stimulated formation of the mitogen, 13-hydroxyoctadecadienoic acid (13-HODE) and also increased ERK1/2 phosphorylation, [(3)H]thymidine incorporation and growth. A mechanism for control of this growth-promoting pathway was revealed during studies of the effects of dietary nutrients and nonnutrients known to inhibit tumor growth. These included four groups of lipophilic agents: n-3 fatty acids, melatonin, conjugated LA isomers and trans fatty acids. Each of these agents activated an inhibitory G protein-coupled receptor-mediated pathway that specifically suppressed tumor uptake of saturated, monounsaturated and n-6 PUFAs, thereby inhibiting an early step in the LA-dependent growth-promoting pathway.
PMID: 17418560
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