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Medical Forum / General / Nutrition / October 2006

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Why a "trans fat" hypothesis is required at this point.

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monty1945@lycos.com - 04 Oct 2006 23:59 GMT
"Science" is supposed to be a product of the scientific method, and
this method is not particularly complicated in these kinds of
situations. In essence, any possible causative agent is controlled for
in an experiment, or series of experiments, in order to determine what
is responsible for the phenomenon in question. Today, it is common to
hear people who claim to be "nutritional experts" of one sort or
another to make statements as bold as "trans fat is very unhealthy."
Presumably, the believe that such a statement is scientific; thus, it
is appropriate to ask whether the scientific method was used to arrive
at these kinds of assertions. In this instance, it is at first
necessary to know exactly what the substance called "trans fat" is,
down to the molecular level, which is possible with current technology.
If this is not known, no experiment is can be conducted, and any claim
about "trans fat" is not within the realm of science.

Trans fatty acids are defined and known precisely, and occur naturally
in a number of foods that are very popular in many nations, but in
small amounts. Most "experts" seem to think that the hydrogenation
process is somehow to blame for the "ill health" they believe "trans
fat" causes. This makes experimentation simple; studies can be done on
lab animals commonly used in nutritional experiments of this sort. One
group would be fed a partially hydrogenated fat source (such as corn
oil) at levels considered significant while another group would be fed
a fully hydrogenated oil (such as coconut oil) and a third group would
be fed the oils without hydrogenation. The animals would be allowed to
live out their lives, and any outstanding effects would be noted, along
with the average mortality rates.

However, some on this newsgroup have argued that a fully hydrogenated
fat source can no longer be called a "trans fat." This is because there
are no trans fatty acids present, though the same hydrogenation process
was used. I agree that a distinction should be made, but this is not
what most "experts" are saying - their claim is that hydrogenation is
to blame for the supposed ill effects, and therefore a fully
hydrogenated oil should be at least as "bad" as the partially
hydrogenated oil. This is basic logic and no more needs to be said. The
results of the experiment proposed above should provide good evidence
in this context.

Now let us suppose that the fully hydrogenated oil generates no ill
effects and that the animals live at least as long as is considered
"normal." What, then, is to blame for the supposed ill effects of the
oil that is partially hydrogenated? Some "experts" (such as Mary Enig)
have claimed that the trans fatty acid molecules are "kinked" and cause
some sort of problem having to do with "cell membranes," but this is
speculation. Some make claims based upon various "markers," and not by
observing effects over the course of the lifetime of the animal, along
with recording mortality rates, and so this fails to meet the
requirements of the scientific method. Most of these kinds of
"researchers" simply assume that something that raises cholesterol
slightly, for example, is terribly dangerous, even though the "founding
father" of this notion, Ancel Keys, pointed out that the 200-220 total
cholesterol range was associated with the lowest mortality, and that it
is now known that only oxidized cholesterol is a problem, as AHA
spokesman Dr. Richard Stein pointed out about a year ago. In fact,
today, on sciencedaily.com, there was the following:

It is much more likely that the hydrogenation process destroys the
natural antioxidant protection that exists in the oil, and so is to
blame for the supposed ill effects, if indeed there are any, when
compared to the usual kinds of oils used to make partially hydrogenated
oil products. Therefore, it would make sense to add one more group of
animals to the experiment proposed above - this group would receive its
fat source as an corn oil (or safflower, sunflower, vegetable, etc. -
one typically used for making partially hydrogenated oils), only
instead of feeding it to the animals right from the bottle, it would be
spread thin and exposed to oxygen and sunlight for several days before
it was fed to the animal. In this way, it would not be hydrogenated,
and few trans fatty acids would be created, if any. However, the
antioxidants naturally occurring in the oil would be largely depleted,
and so the researcher would be controlling for the lipid peroxidation
factor in a direct way.

After the experiment was conducted, the results would likely "speak for
themselves." For example, if the fully hydrogenated coconut oil
appeared to be by far the healthiest fat source, then the only
reasonable interpretation would be that lipid peroxidation was the
causative agent.
The ambiguity over the phrase "trans fat" would no longer be
problematic. Instead, what is happening is disturbing; food companies
are creating new concoctions, ones that use fully hydrogenated fat,
which they can claim contains no "trans fatty acids," along with a
cheap and highly unsaturated oil, such as corn, sunflower, vegetable,
safflower, or soybean. If the real problem is not with what is being
called "trans fat," but instead with lipid peroxidation, then these new
fats will cause the same amount of ill health as equivalent "trans fat"
sources. Ironically, the "experts" who claim that the hydrogenation
process is to blame do not tell people to avoid these new concoctions,
which contain large amounts of a totally hydrogenated oil source,
though most if not all of them must be aware of it.

Lastly, I'll point out that one person who posts here as "MattLB"
claims that overall mortality is not especially important. However, if
a particular diet produces a great deal of ill health, the people or
animals consuming it will die at younger ages, so as is often the case
with this individual, his notion is unclear. I do agree that if a diet
is tasteless, unsatisfying, or causes intestinal upset, many people
will not follow it for very long. The diet I recommend, however, would
not fit this description. Moreover, after several years on this diet, I
have seen my "chronic" medical conditions, some of which I've had for
more than a decade, vanish (a tendonosis problem required more
protein). However, this "MattLB" person did not explain exactly what
criteria he/she would use to determine which diet was best, and until
he/she does so, there is no way to respond in a way that is consistent
with the scientific method. This person also claimed that the diet I
suggest is "abnormal," which demonstrates his subjectivity here.
Science is concerned with the results of controlled experiments, not
with what one person decides to classify as "abnormal." In fact, I do
not recommend eating any food that could not have been consumed a
couple of hundred years ago, and so this makes his/her claim
particularly absurd and difficult to comprehend.
monty1945@lycos.com - 05 Oct 2006 00:06 GMT
Correction: Following the sentence that included the name "Richard
Stein," the following passage should have been quoted:

"Oxidation of fats in the blood -- a process akin to rusting -- is
detrimental to health. When the "bad" cholesterol becomes oxidized, it
is more likely to build up and result in arteriosclerosis."

Source:
http://groups.msn.com/TheScientificDebateForum-/nutrition.msnw?action=get_messag
e&mview=0&ID_Message=143&all_topics=0

monty1945@lycos.com - 05 Oct 2006 00:25 GMT
And there was yet another study today on sciencedaily.com that makes
the point about oxidation, not other reasons, for the problems that
lead to "heart disease:"

Antioxidants in the berries inhibit so-called 'bad' LDL cholesterol
oxidisation, which could provide a new weapon to fight cardiovascular
disease. When LDL cholesterol is oxidized, it sticks to the lining of
blood vessels. Consuming the berries in food or drinks is expected to
prevent the arteries from clogging up.

Source: http://www.sciencedaily.com/releases/2006/10/061003143643.htm
Ron Peterson - 05 Oct 2006 05:11 GMT
> Lastly, I'll point out that one person who posts here as "MattLB"
> claims that overall mortality is not especially important. However, if
> a particular diet produces a great deal of ill health, the people or
> animals consuming it will die at younger ages, so as is often the case
> with this individual, his notion is unclear.

Some animals have been fed near starvation diets and survive to a
relatively old age in a lab setting. However, in the wild those same
animals would be particularly vulnerable to predators making the
starvation diet less than optimal.

Signature

  Ron

monty1945@lycos.com - 05 Oct 2006 17:37 GMT
I agree, Ron.  I do not endorse calorie restriction as an end, or at
all, for that matter.  Rather, it is likely that when you restrict
calories substanitally, your body undergoes less oxidative stress than
someone eating a "typical American diet."  As I said, if a diet
satisfies hunger, tastes good, produces no intestinal upset, and
maximizes longevity, why would anyone criticize it?  If one is eating a
"bad" diet, there will be more "disease," resulting in higher mortality
rates.  This odd individual, "MattLB," seems to think that this kind of
diet will result in horrible diseases, and yet mortality will be
higher.  It is typical of his thought process, from what I've read of
his posts, and I just wanted to point out how ludicrous it is.

In fact, there are hardly any studies done by American scientists on
people who eat diets very high in saturated fatty acids and very low in
other fatty acids.  Instead, they use something like lard as the
"saturated fat" source, but it is only 39% saturated, not much more
saturated than chicken.  Coconut oil is 92% saturated, and studies of
people on these very high saturated fatty acid diets (and low in
unsaturated fatty acids) demonstrate either that the notion that
"saturated fat" is unhealthy is totally wrong, or that the phrase
"saturated fat" is very misleading and needs to be precisely defined
before scientists use it.  But for whatever reason, "MattLB" thinks
that this kind of diet, enjoyed by millions of Aisans for thousands of
years, and more recently by many French people, deserves to be called
"abnormal."  After years of research on nutritional as well as
psychological issues, I would be more comfortable describing this
individual's thought process as "abnormal" than the diet I follow (that
is, high saturated fatty acid content, low unsaturated fatty acid
content, no oxidized cholesterol, rich in natural antioxidants, etc.).

For those who want to read more about my research, you can go to:

http://groups.msn.com/TheScientificDebateForum-
MattLB - 05 Oct 2006 19:16 GMT
> Rather, it is likely that when you restrict
>calories substanitally, your body undergoes less oxidative stress than
>someone eating a "typical American diet.". As I said, if a diet
> satisfies hunger, tastes good, produces no intestinal upset, and
> maximizes longevity, why would anyone criticize it?

That it maximises longevity is pure speculation on your part.

"Although antioxidants help to control this oxidative stress in cells
in general, they do not decrease the rate of aging, because their
concentrations are lower in long- than in short-lived animals and
because increasing antioxidant levels does not increase vertebrate
maximum longevity."

>From Biol Rev Camb Philos Soc. 2004 May;79(2):235-51.
Aging in vertebrates, and the effect of caloric restriction: a
mitochondrial free radical production-DNA damage mechanism?
Barja G.

>  If one is eating a
> "bad" diet, there will be more "disease," resulting in higher mortality
> rates.  This odd individual, "MattLB," seems to think that this kind of
> diet will result in horrible diseases,

Where did I say that? Cutting out EFA will lead to symptoms of EFA
deficiency which if continued will result in death, but I made no claim
of specific diseases, particularly not "horrible" ones.

> and yet mortality will be
> higher.  It is typical of his thought process, from what I've read of
> his posts, and I just wanted to point out how ludicrous it is.

There are many routes to death and many complex interactions that
occur. Simply measuring mortality gives no information about mechanism
- it's just a marker.

> In fact, there are hardly any studies done by American scientists on
> people who eat diets very high in saturated fatty acids and very low in
> other fatty acids.
> But for whatever reason, "MattLB" thinks
> that this kind of diet, enjoyed by millions of Aisans for thousands of
> years,

Really? What's the fat source that goes with the rice staple?

> and more recently by many French people, deserves to be called
> "abnormal."

I've said nothing of the sort. A "no EFA" diet is abnormal; a high
saturated fat one isn't, as many people eat them.

MattLB
MattLB - 05 Oct 2006 19:44 GMT
> However, some on this newsgroup have argued that a fully hydrogenated
> fat source can no longer be called a "trans fat." This is because there
> are no trans fatty acids present, though the same hydrogenation process
> was used.

Same process, just more thorough.

> I agree that a distinction should be made, but this is not
> what most "experts" are saying - their claim is that hydrogenation is
> to blame for the supposed ill effects, and therefore a fully
> hydrogenated oil should be at least as "bad" as the partially
> hydrogenated oil.

Quote someone who's said that. That's just your twist on things.

It's exactly because it's NOT fully hydrogenated that's the problem.
It's like not fully cooking a puffer fish - some of the poison is left
behind. In this case what's left behind are unsaturated
trans-isomerized fatty acids.

> Now let us suppose that the fully hydrogenated oil generates no ill
> effects and that the animals live at least as long as is considered
[quoted text clipped - 3 lines]
> some sort of problem having to do with "cell membranes," but this is
> speculation.

Just because you don't understand it (or believe in lipid bilayer
membranes) doesn't make it pure speculation. It's simple physical
chemistry. Linear molecules such as saturated fatty acids and trans
fatty acids pack closely together to make a stiffer membrane. Normal
cis  fatty acids are the ones that are kinked (your error rather than
Enig's I suspect) and can't pack so closely, giving a more fluid
membrane.

> Some make claims based upon various "markers," and not by
> observing effects over the course of the lifetime of the animal, along
> with recording mortality rates

Mortality is a marker and a fairly non-specifc one at that.

>  If the real problem is not with what is being
> called "trans fat," but instead with lipid peroxidation, then these new
> fats will cause the same amount of ill health as equivalent "trans fat"
> sources.

What are you suggesting gets peroxidised in these fully hydrogenated
oils? You're always saying saturated fats don't have that problem.
Fully hydrogenated = saturated.

> Ironically, the "experts" who claim that the hydrogenation
> process is to blame do not tell people to avoid these new concoctions,

Because there aren't any trans fatty acids in fully hydrogenated oils.
Burning food creates a variety of unhealthy chemicals, but if you burn
it so much you're just left with a black ash, it's actually much safer.
It's what's produced in between that's the problem not the two end
points.

> Lastly, I'll point out that one person who posts here as "MattLB"
> claims that overall mortality is not especially important. However, if
> a particular diet produces a great deal of ill health, the people or
> animals consuming it will die at younger ages, so as is often the case
> with this individual, his notion is unclear.

If it simply dies, you don't know the mechanism of action that caused
its death. As I've told you before you'll need to do a dose-response
curve to prove that a particular substance has a particular effect.

> I do agree that if a diet
> is tasteless, unsatisfying, or causes intestinal upset, many people
> will not follow it for very long. The diet I recommend, however, would
> not fit this description.

Nor do most diets.

> However, this "MattLB" person did not explain exactly what
> criteria he/she would use to determine which diet was best,

I did, I told you do do a graded dose-response diet. If EFA are
responsible for ill-health (as you claim) then your experiment would
show increasing health as the EFA content approached zero. If EFA are
in fact essential then you would see decreased health below a certain
threshold, maximised at zero. Note that I am not saying - and have
never said  (despite your imaginings) -  that the more EFA you eat the
better.

> he/she does so, there is no way to respond in a way that is consistent
> with the scientific method.
> This person also claimed that the diet I
> suggest is "abnormal,"

I suggested that the diets you want to use in your experiment are
artifically high (which could be taken as abnormal) in particular fats.
Your diet as posted is unsually restrictive, but not so much that I'd
call it abnormal.

> Science is concerned with the results of controlled experiments, not
> with what one person decides to classify as "abnormal." In fact, I do
> not recommend eating any food that could not have been consumed a
> couple of hundred years ago, and so this makes his/her claim
> particularly absurd and difficult to comprehend.

Stop inventing such absurd claims for me then, and deal with what I
actually say.

MattLB
monty1945@lycos.com - 05 Oct 2006 21:39 GMT
Well, MattLB, you did use the term "abnormal," back in August - I'm
just using your own words.

The reason for the post was to show why a hypothesis is so important in
sicentific claims.  Almost all of the "experts" tell us that
hydrogenation is the problem, but if that is so, then a fully
hydrogenated oil should be at least as bad, and probably worse than the
partially hydrogenated version.  Basic logic.  Whether or not you are
making this claim is not all that relevant, since it's not clear what
you are arguing with respect to "trans fat."  I suggest you put forth a
hypothesis.

Your statement about "EFA" clearly defies logic, because if UFAs are
the problem, at least in the context of the "typical American diet,"
then a very low fat diet or a high saturated fatty acid diet (where
only coconut oil is used as a fat source) may produce the best health.
However, a very low fat diet might be very unsatisfying, as it was to
me.

I'm all for determining why the lab animals die, and non-traumatic
monitoring of various "markers" deemed of potential significance is a
good idea.  In particular, this approach might demonstrate that many of
the markers thought important only have some value in the context of
the "typical American diet," and not the diet I follow.

In any case, a hypothesis needs to be put forth regarding what "trans
fat" is, and exactly what it is supposed to do. I would like to see an
experiment done that controls for oxidative stress/lipid peroxidation
(providing one group of adult lab animals with a diet rich in coconut
oil, which milliions of humans have consumed for thousands of years),
because when one examines the molecular-level evidence, almost all of
it points to this as the root cause, directly or indirectly (though
sometimes reactive nitrogen species are involoved, rather than ROS).
MattLB - 06 Oct 2006 13:04 GMT
> Well, MattLB, you did use the term "abnormal," back in August - I'm
> just using your own words.

I checked and yes I did:
"No, your experiment tests one thing: how long animals live when given
abnormal diets high in PUFA or coconut oil."

I stand by that, however, as rats or mice would never normally eat such
diets and are not adapted to do so.

> The reason for the post was to show why a hypothesis is so important in
> sicentific claims.  Almost all of the "experts" tell us that
> hydrogenation is the problem, but if that is so, then a fully
> hydrogenated oil should be at least as bad, and probably worse than the
> partially hydrogenated version.  Basic logic.

Simplistic, uninformed logic. I've already told you that full
hydrogenation is the same as saturated, so either you're contradicting
yourself or you just can't comprehend the chemistry.

>  Whether or not you are
> making this claim is not all that relevant, since it's not clear what
> you are arguing with respect to "trans fat."

That it is what is wrong with partially hydrogenated oils. It is not
present in fully hydrogenated oils, so they are safer.

> Your statement about "EFA" clearly defies logic,

Which one?

"If EFA are responsible for ill-health (as you claim) then your
experiment would
show increasing health as the EFA content approached zero."

or

"If EFA are in fact essential then you would see decreased health
below a certain
threshold, maximised at zero."

You believe the first to be true; I the latter. Both are simple
statements that defy no logic and are in fact self-consistently
logical. They are equivalent to:

"Increasing health is seen as the consumption of cyanide approaches
zero."
"Health decreases when you eat less than the RDA for zinc."

You liken EFA to poisons; I liken them to vitamins and minerals.

> because if UFAs are
> the problem, at least in the context of the "typical American diet,"
> then a very low fat diet or a high saturated fatty acid diet (where
> only coconut oil is used as a fat source) may produce the best health.

That's true *IF* UFAs are the problem.

> In any case, a hypothesis needs to be put forth regarding what "trans
> fat" is,

There's no hypothesis needed, it's all there in the name. If you know
what a fatty acid is and you know what a trans double bond is then it's
self-explanatory.

>and exactly what it is supposed to do.

It's not supposed to do anything. It shouldn't exist in the body and
isn't made by the body.

As usual you have failed to answer any questions or provide any
evidence or citations for your claims - hardly a scientific approach.

MattLB
monty1945@lycos.com - 05 Oct 2006 21:48 GMT
As Ling showed, there is no way a structural lipid bilayer is possible.
One can wash off the fatty acids and the cell holds together.  Basic
logic.

Enig's notion predicts that if you fed an animal an animal a diet rich
in partially hydrogenated oil, they will live shorter lives than
another group fed the same oil (such as corn or safflower), because of
the "kinks in the chain."  My experimental idea  controls for this,
because I would spread some safflower oil out on thin sheets and let
the sun shine on it for several hours and for several days (while
exposed to oxygen of course).  My guess is that the partially
hydrogenated oil group would live longer, but certainly would not live
significantly shorter lives, because free radicals are the issue, not
"kinks in the chain."

Most people don't realize that such experiments have yet to be
conducted.  They believe, as I did, that researchers with scientific
credentials would have enought sense to control for anything that the
evidence suggest might be a causative agent.  Instead, most researchers
seem more interested in designing experiments so that the results
appear to correspond with textbook claims, rather than following the
scientific method.
MattLB - 06 Oct 2006 13:47 GMT
> As Ling showed, there is no way a structural lipid bilayer is possible.

How did he show it?

>  One can wash off the fatty acids and the cell holds together.

What do you mean by "hold together"? The soluble components of the
cytoplasm will be lost with a detergent wash. It's done deliberately
when doing investigations of cytoskeletal protein networks.

> Basic logic.

Another term for which you evidently have your own peculiar definition.
The two statements aren't logical consequences of each other.

> Enig's notion predicts that if you fed an animal an animal a diet rich
> in partially hydrogenated oil, they will live shorter lives than
> another group fed the same oil (such as corn or safflower), because of
> the "kinks in the chain."

No, because of a lack of kinks in the chain.

> My experimental idea  controls for this,
> because I would spread some safflower oil out on thin sheets and let
> the sun shine on it for several hours and for several days (while
> exposed to oxygen of course).

How is exposure to sun and oxygen a control for a trans double bond?
You're speaking nonsense.

MattLB
monty1945@lycos.com - 06 Oct 2006 19:32 GMT
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:

> How is exposure to sun and oxygen a control for a trans double bond?
> You're speaking nonsense.

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.
MattLB - 09 Oct 2006 17:11 GMT
> The fact that you do not understand that a formal hypothesis is
> required in order to make a scientific claim speaks volumes.

A claim is a thesis; a hypothesis is speculation (informed speculation
perhaps, but speculation nonetheless).

>  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.

Yet you rage against unsaturated fats in exactly the same way.

> However, it is obvious to even those very
> little scientific understanding on this issue realize that since trace
> amounts will do no harm,

Says you.

> 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.

You would have to have a hypotheis that there was a threshold first and
do that experiment.

> > How is exposure to sun and oxygen a control for a trans double bond?
> > You're speaking nonsense.
>
> 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

Which lets you make any argument you want. Try offering evidence.

> 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).

Unlike you most scientists wouldn't be so absolute in their
pronouncements.

> 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).

Becomes more dangerous, certainly. It's gone from being full of
molecules found in nature, to containing ones alien to the human body.

> 3. There is a lack of clarity on total hydrogenation (meaning different
> "experts" are making different claims),

The lack of clarity is entirely of your own making.

> 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,

Rubbish. A control should be identical except for the *one* thing you
change  - in this case what they eat. If a difference is seen, then you
can adapt the experiment to try and work out why.

> if it is the only other group.  The partially
> hydrogenated oil will be stripped of natural antioxidants,

Why/how do you know?

> 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."

It's not a control and if you can't see that everything you say about
the scientific method is just hot air. If it is your hypothesis that
the antioxidants are gone from the partially hydrogenated oil then the
correct control would be to simply remove the antioxidants from the
normal oil, leaving everything else the same. Otherwise you're adding
in the effect of a light and oxygen exposure that the partially
hydrogenated didn't get.

>  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.

No, your experimental design tells you nothing about the effect of
trans fatty acids, just the effect of antioxidant meddling. If instead
you were to add the antioxidants you claim were lost from the partially
hydrogenated back to it, then the only possible negative effect would
be the the fault of the trans fatty acids.

> 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?

No, because you haven't controlled for the variables properly.
Suggesting that exposing oil to light and sun will have exactly the
same effect and magnitude on the antioxidants as (you claim)
hydrogenation is very naive.

>  At the very least, it
> would be interesting to know the answer to this, in terms of how much
> grasp he possesses on reality.

More on both science and reality than you.

MattLB
 
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