MSN Home  |  My MSN  |  Hotmail
Sign in to Windows Live ID Web Search:   
go to MSNGroups 
Free Forum Hosting
 
Important Announcement Important Announcement
The MSN Groups service will close in February 2009. You can move your group to Multiply, MSN’s partner for online groups. Learn More
The Scientific Debate Forum.Contains "mature" content, but not necessarily adult.[email protected] 
  
What's New
  
  Disclaimer: Read this page first.  
  Links  
  Messages  
  General  
  Nutrition  
  "Mission Statement."  
  Why the "germ theory" is not science.  
  The Underlying Cause of "Disease."  
  The Scientific Method.  
  How dangerous are bacteria and viruses?  
  The Contributions of Hans Selye and others.  
  How direct effects are often ignored, and indirect markers used  
  Understanding "disease" at the molecular level.  
  Understanding disease at the molecular level, part II.  
  What the "common cold" can teach us about illness.  
  The AA connection to today's common "diseases."  
  How easy the key experiments would be to do.  
  The best practical diet and the explanation for it.  
  Fish oil quotes you might want to read  
  Where the "immune system" fits into this view of "disease."  
  How many 'scientific studies' violate the scientific method  
  Why you have to be careful with antioxidants.  
  Why Cancers today are more aggressive than those of the past.  
  The Latest Evidence.  
  Some studies worthy of note.  
  HSWC "in action."  
  How language can impede science.  
  How language impedes science, part II.  
  More on why "germs" don't cause "disease."  
  How a latent virus actually causes "disease."  
  A new report that "says it all."  
  The science "show" must go on?  
  Odds and ends  
  Some thoughts on a book by Robert Gallo.  
  Saturated fatty acids are the solution, not the problem.  
  It's stress, not "germs" that causes disease.  
  Epidemiology: Facts versus "factoids."  
  It's stress, not germs, part II.  
  The latest on "inflammation."  
  Why many nutritional claims make no sense  
  The use of hypotheticals in science.  
  What "viral infections" really do to the body.  
  What determines longevity?  
  An example of an anti-"saturated fat" study that is flawed.  
  A Rough Guide to a Gentle Diet.  
  A unified "AIDS" hypothsis without "HIV."  
  A unified "AIDS" hypothsis without "HIV." Part II.  
  Okay, so when is this diet going to kill me?  
  Scientific Debate Forum Pictures  
  The EFA Claim Was Refuted Long Ago  
    
  
  
  Tools  
 
Nutrition : Enig vs. Peat ("EFAs vs. the Mead acid).
Choose another message board
View All Messages
  Prev Message  Next Message       
Reply
 Message 4 of 15 in Discussion 
From: MSN NicknameHansSelyeWasCorrect  in response to Message 2Sent: 2/26/2007 11:07 PM
There were some responses to my original post on sci.med.nutrition. I copied and pasted some of my responses to those responses below. A study that is referenced in my responses is the following:

QUOTE: J Nutr. 1983 Jul;113(7):1422-33.


Role of linoleate as an essential fatty acid for the cat independent of
arachidonate synthesis.


MacDonald ML, Rogers QR, Morris JG.


To determine the essential fatty acid (EFA) requirements of the cat,
specific pathogen-free kittens were fed either a linoleate-deficient
diet or one of two diets containing 5% safflower seed oil (SSO) with or
without 0.2% tuna oil. The diets were fed for 82-101 weeks beginning at
3 months of age. The results showed that linoleate is an essential
fatty acid for the cat. Linoleate deficiency resulted in reduced feed
efficiency (in males), high rates of transepidermal water loss, poor
skin and coat condition, and fatty liver. These manifestations of EFA
deficiency were prevented by SSO. Tuna oil had no additional effect.
Analyses of the fatty acid composition of plasma, erythrocytes and
liver lipids revealed that linoleate deficiency caused changes that
were qualitatively, but not quantitatively similar to EFA deficiency in
the rat. When SSO was provided, linoleate was elongated and desaturated
at the delta 5 position to form 20:2n6 and 20:3(5,11,14). However,
there was negligible conversion of linoleate to arachidonate. These
results indicate that linoleate has specific functions as an EFA,
independent of arachidonate synthesis and prostaglandin formation.
PMID: 6408230 [PubMed - indexed for MEDLINE]
UNQUOTE.

At least you've actually cited an experiment. Notice that they said a
linoleate free diet, but they did not tell us if the cats were fed any
fat at all. This is not science, and it makes no sense to compare to
humans anyway. If you think this makes sense, then take me up on my
offer. Cats are rather special mammals in some ways, but dogs, pigs,
monkeys are good for comparison. I'd be willing to do a mouse or rat
experiment, which would be cheaper and easier than the cats. My point:
if you feed these animals fresh coconut oil, or a diet of safflower
oil around 15 to 25%, which is a mimimum of the amount of fat most
Americans have in their diets, the fresh coconut oil animals will live
longer. You can cite all the flawed studies you like, but I will
continue to point out where they are going wrong. You can name-call
all you like, but I will continue to propose on point experiments that
cannont be "massaged" or manipulated. Common sense does not appear to
be your strong suit, so you might as well stick to the cheap insults.



Other worthwhile points to the objective reader who has not read some
of my other posts:


1. Notice they don't tell you which group of cats lived longer.


2. Notice the signs of "deficiency:" "reduced feed
efficiency (in males)" and "fatty liver." These are signs of toxic
exposure, to fumonisins and aflatoxins, probably due to whatever the
alternative feed was. "High rates of transepidermal water loss." This
is interesting, because after being "essential fatty acid deficienty"
for a few years or so, I notice that I drink more water. What this has
to do with health needs to be made clear, but until we know what the
alternative diet actually was, there's no way this study can be
examined scientifically beyond a superficial level. "Poor skin and
coat condition." This is typical "seek and ye shall find" nonsense.
When you look for signs of "deficiency" you find them. This claim is
likely due to researcher bias.


3. Why not feed the cats a diet high in top-quality olive oil as a
control, since then there would be an unsaturated fatty acid control?
This study is actually very good, because it shows once again how much
these "scientists" take for granted and don't know.


4. There is nothing special about linoleic acid. I have never seen a
claim that it is "essential" in and of itself. The claim is always
that it's needed for PG synthesis, even though non-omega 6 PUFAs can be
metabolized into substances that do the same thing, only without the
negative effects of AA. What the "scientists" here are saying makes no
sense at all, but it would be nice if they would mention exactly what
hypothesis they think their results support, because it doesn't even
exist. Again, it is like a claim that linoleic acid has magical
qualities.


5. Thus, I again ask: what is the "essential fatty acid" hypothesis,
exactly? In science, you put forth your hypothesis and you cite the
relveant evidence. With "EFAs" there is no hypothesis, only vague
claims or ones that are undeniably false, along with evidence that
contracts the claim or terribly flawed "studies." This sort of thing
is a mockery or charicature of science.


For those who don't know:

1. "Reduced feed efficiency" means they eat more but don't gain as much
weight, something a lot of Americans would like to have, not avoid.


2. Points about "fatty liver" in humans:


The basic cause of non alcoholic fatty liver disease is insulin
resistance, a condition in which the effects of insulin on cells within
the body are reduced. The most frequent risk factor for insulin
resistance is obesity, especially abdominal obesity.
Fatty liver is itself quite harmless, disappears rapidly with loss of
weight, and infrequently progresses to non alcoholic steatohepatitis,
which is the next stage of non alcoholic fatty liver disease.


http://www.medicinenet.com/script/main/art.asp?articlekey=46582&page=2


And:


Although some drugs or genetic abnormalities can cause NAFLD, the
majority of cases are associated with obesity, insulin resistance, and
type 2 diabetes.


http://www.jci.org/cgi/content/full/115/5/1139


Since we don't know what the cats were fed, there's nothing that can be
said about the experiment. We do know that insulin resistance problems
are nearly unheard of in Asian populations that consume coconut as
their major form of fat. Recently, oxidative stress has been
demonstrated to be the primary cause of "insulin resistance," and since
fresh coconut oil resists oxidative stress, while safflower oil is very
susceptible to it, this is a different way of making a mockery of
scientific understanding.


Let's do the experiment with proper controls and see what happens.


Replies to This Message The number of members that recommended this message.    
     re: Enig vs. Peat ("EFAs vs. the Mead acid).   MSN Nicknametaka00381  2/27/2007 3:05 AM