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Medical Forum / General / Cardiology / February 2006

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high fat/high carbohydrate diet induces aortic valve disease

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Jim Chinnis - 25 Feb 2006 16:08 GMT
I found this new study abstract interesting, but don't have the full paper
yet. I'm left wondering what a pure HF or pure HC diet would do and why a
HF/HC diet isn't called a low-protein diet. --Jim

J Am Coll Cardiol. 2006 Feb 21;47(4):850-5. Epub 2006 Jan 26. Related
Articles, Links  


A high fat/high carbohydrate diet induces aortic valve disease in C57BL/6J
mice.

Drolet MC, Roussel E, Deshaies Y, Couet J, Arsenault M.

Groupe de recherche en valvulopathies, Institut de cardiologie de Quebec,
Quebec, Canada.

OBJECTIVES: The purpose of this study was to compare aortic valve function
and morphology in adult wild-type (WT) mice and in low-density lipoprotein
receptor-deficient (LDLr-/-) mice fed or not fed a
high-fat/high-carbohydrate (HF/HC) diet. BACKGROUND: Observations suggest a
link between degenerative aortic valve stenosis (AS) and atherosclerosis.
Aortic valve stenosis has been successfully induced in animal models of
extreme hypercholesterolemia, but these models are less relevant to humans.
It is not known if a proatherogenic HF/HC diet without added cholesterol
could have the same negative impacts. METHODS: Forty C57BL/6J mice were
divided into four groups: WT + normal diet, WT + HF/HC diet, LDLr-/- with a
normal diet, and LDLr-/- with a HF/HC diet. Aortic valve function and
histology were evaluated by echocardiography after four months. RESULTS:
Wild-type mice on a HF/HC diet became mildly hypercholesterolemic, obese,
and hyperglycemic. As expected, LDLr-/- mice became severely
hypercholesterolemic. Both WT and LDLr-/- mice on a HF/HC diet displayed
smaller valve areas and higher transvalvular velocities (p < 0.01) after
four months. Aortic valve leaflets were thicker and infiltrated with lipids
and macrophages in both HF/HC groups. CONCLUSIONS: A HF/HC diet in mice
results in significant aortic valve abnormalities. Putting WT mice on a
HF/HC diet reproduced a combination of atherogenic factors (obesity, mild
dyslipidemia, and hyperglycemia) more commonly encountered in humans than
isolated severe hypercholesterolemia. Severe hypercholesterolemia was not a
prerequisite in our model. This experimental model suggests that AS
development is multifactorial and that hypercholesterolemia should not be
the only target in this disease.

PMID: 16487855
--
Jim Chinnis   Warrenton, Virginia, USA
montygram - 26 Feb 2006 03:31 GMT
I guess you have not read my previous posts (search the group for
montygram if you want to read some).  Saying "high fat" means nothing,
as each individual fatty acid has a particular physiological efffect.
Moreover, oils can be "refined" and thus lose their natural antioxidant
cover.  Then there are synergistic effects with the other food one
eats.  So to say "high fat" is to basically say that you have abandoned
science in favor of the witchcraft that passes for "nutrition" these
days.
nospam@aol.com - 26 Feb 2006 04:00 GMT
Rear back,  Monty.  When omegas become a religion, contradictions become holy
and nutrition becomes witchcraft, it is time to pull back and examine where your
ideas are coming from.

Ora

>I guess you have not read my previous posts (search the group for
>montygram if you want to read some).  Saying "high fat" means nothing,
[quoted text clipped - 4 lines]
>science in favor of the witchcraft that passes for "nutrition" these
>days.
montygram - 26 Feb 2006 06:44 GMT
Cite the evidence and we can have an intelligent scientific debate (I
hope).  When you make a scientific claim, you cite the evidence for it.
There is a near mountain of evidence against dietary omega 3 and 6
PUFAs, but no evidence for them (with the exception of the temporary
interference with arachidonic acid metabolism that some omega 3s
accomplish - at the expense of dangerous omega 3 metabolites being made
instead).  If you are an intelligent, non-biased individual, let us
have a debate.  If you prefer a moderated debate, I can arrange that.
If you read my old posts, you can see my argument in detail.  How such
dangerous molecules ever came to be called "essential" by "scientists"
may be likened to witchcraft, in that things are perceived that really
are not there, but most people never question such assertions.  The
comparison is apt, but I prefer to simply examine the evidence.  My
detractors cannot even present their claims as a basic scientific
hypothesis.  Wouldn't someone claiming that something is witchcraft
also refrain from doing so?  They also will not debate me in a
moderated forum, and won't even negotiate with me on any of my
experimental offers.  However, if you just feed a dozen mice a diet of
30% fish and canola oil and compare their life spans to another dozen
fed 30% fresh coconut oil (with only trace amounts of fat from other
foods), you will understand why I am so concerned about thee
witchcraft, or whatever you wish to call it.

Another point you may want to consider: we are told that "saturated fat
is bad," or something similar.  Can you tell me what "saturated fat"
is?  I have reviewed hundreds of studies that use this phrase, but is
is NEVER defined.  How is that scientific?  On food in a supermarket,
the label will give the saturated fatty acid content as "saturated
fat," and that is fine (though again, each fatty acid type has unique
effects on the body), but in studies, lard and coconut oil, for
example, are both used as the "saturated fat" fed to one group of
animals, but chicken is not called a "saturated fat."  Yet lard's
saturated fatty acid content is MUCH closer to chicken than to coconut
oil, as it is to the fat in a Brazil nut.  Who decided that this was
acceptable?  It never was, officially, and appears to be based on
commonly-held notions that developed over time.  It is clearly
illogical, unless someone can demonstrate that a threshold amount of
saturated fatty acid content is somehow significant.  This has been
done in the case of the most common omega 6 PUFA, linoleic, which at
4-5% of overall calories (in a diet that supplies at least a minimum
amount of calories needed for energy) will raise your risk of the
"common cancers" significantly (see "Diet and Health" by the National
Research Council for a review of the studies which made this finding).
Instead, we have the raw demographic data, showing the incredibly low
rate of "chronic disease" in peoples who eat large amounts of coconut
products.  Again, read my old posts and you can get all the details.
Alf Christophersen - 26 Feb 2006 15:00 GMT
>Cite the evidence and we can have an intelligent scientific debate (I
>hope).  When you make a scientific claim, you cite the evidence for it.
> There is a near mountain of evidence against dietary omega 3 and 6
>PUFAs, but no evidence for them (with the exception of the temporary
>interference with arachidonic acid metabolism that some omega 3s

What people disagree with you is your saying that omega-6 and omega-3
are not needed at all. Using AA as an example why no PUFA should be
taken.

You are just overdoing things.

There are many researchers who agree that ideally, diet contain no AA
at all. Why? Because liver make whatever AA it needs as long as there
are linoleic acid available in diet.

Only linoleic and alpha-linolenic acid is needed basically. Period.

Why then take EPA ??

That's because most peoples diet DO contain AA, and EPA concur with AA
if infections occure etc. about the active site of COX I and COX II
plus all the lipoxygenases responsible for producing the general class
of lipoxides. Another way to produce lipoxides that activate COX-I
(and start stimulating body to produce more COX-II) is free radical
attack of other PUFA, but also cholesterol and many other compounds.

Another aspect of EPA intake is to inhibit excess AA production in
liver if we live on a diet overall at a omega-6 to omega-3 ratio in
excess of 20 (typical US diet) becase industry by purpose remove
omega-3 from food to increase shelf time. Omega-3 acids concur also
with the delta-5 desaturase responsible for making AA from omega-3
precursor C20:3 n-6 (the molecule that form PG-1 series by COX)

In  normal people AA is mostly immediately broken down in peroxisomes
into acetyl-CoA and is the preferred substrate for beta-oxidation.
But, some people has reduced capability for that and then AA start to
do trouble, partly by being oxygenated non-enzymically and ring split
at the O2 insertion point, forming two keto-groups (aldehydes) that
are extremely reactive and crosslink fats and proteins, fats and DNA
and proteins and DNA or proteins to proteins. Several of these are
found in plaques as shown in articles I have cited before on
isolevuglandins (isolevuglandines do not trigger any article at all in
PubMed)
mattlb@angelfire.com - 27 Feb 2006 12:11 GMT
> Cite the evidence and we can have an intelligent scientific debate (I
> hope).  When you make a scientific claim, you cite the evidence for it.

A pity you don't.

>  There is a near mountain of evidence against dietary omega 3 and 6
> PUFAs, but no evidence for them

Here's just one of many:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16251608&query_hl=4&itool=pubmed_docsum


It shows that EPA,DHA and AA all increase levels of the LDL receptor
thereby lowering blood LDL levels. That's good news for avoiding
atherosclerosis.

>   If you are an intelligent, non-biased individual, let us
> have a debate.  <snip>  How such
> dangerous molecules ever came to be called "essential" by "scientists"
> may be likened to witchcraft,

This is you being an intelligent, non-biased individual is it?

> are not there, but most people never question such assertions.  The
> comparison is apt, but I prefer to simply examine the evidence.  My
> detractors cannot even present their claims as a basic scientific
> hypothesis.

You've never presented yours.

>  but in studies, lard and coconut oil, for
> example, are both used as the "saturated fat" fed to one group of
> animals, but chicken is not called a "saturated fat."

Because it's not just fat.

>  It is clearly
> illogical, unless someone can demonstrate that a threshold amount of
> saturated fatty acid content is somehow significant.

You seem to think so. You're always going on about how high in
saturated fatty acids coconut oil is.

MattLB
 
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