Re: OT Missing five years

Hi Michelle:

I am going back to your post again because I thought of some threads I
had posted over some of the past 4 years.

I'm interested in how people draw conclusions. Are you suggesting low
fat is basically a winner ... if people start early enough?

Actually no. I think the answer is probably more complicated than
that.

First of all, not all fats are created equal. We're all familiar with
the research that indicates the monosaturated fats are not only not
harmful, but actually protective in preventing stroke.

Quentin is a big fan of monounsaturated fats and posted quite a bit on
the value of extra virgin olive oil. Likewise he has said much about
the omega 3 fatty acids as well as the ratio of the omega 6 to omega 3
fatty acids. I have also found support for fatty acid choices in the
thread Maximizing the "incretin effect" through diet and supplements #1
was focused on dietary fatty acids - http://tinyurl.com/72m9e.

Secondly, there is the question of genetic predisposition.

Agreed. We inherit our mitochondria at least primarily from our mothers.
The mitochondria are our energy engines. They also are the largest
producers of oxidative stress. There is the balance between pro-oxidant
and antioxidants (the natural antioxidants glutathione, catalase, and
superoxide dismutase.) Then we could go off on muscle fiber composition
which is effected by both genetics and exercise type. Nuclear factor
kappa B (NFkappaB) is involved in the inflammation process when things
get out balance, COX-2 gets generated as well as various cytokines
especially in fat tissue (adipose). The viscous cycle of this stuff
comes into play.

The flip side is that the study shows there is not much point stressing about reducing fat intake later in life.
Put simply it puts the lie to the notion that people only survive when they are in the hands of professionals. The
professional counseling made no difference.

Good observations.

Plaque formation isn't that well understood. People on statins which
dramatically reduces cholesterol apparently still have increases in
plaque


Yes, I've read several articles for laypeople (no scientific studies)
that state researchers are wondering if statins work not because they
lower cholesterol, but because they reduce inflammation.

C. Inflammation:
Inflammation markers are a more recent analytic tool.
Tumor necrosis factor-alpha (TNF-a [Greek symbol], interleukin-1 & 6
(Il-1 & 6), C-reactive protein, high white cell count, and the ratio of
APO-B to APO-A1 are some of these markers.

Definitions:
"Apolipoprotein. Lipoprotein refers to the whole particle.
Apolipoprotein means just the protein part of the lipoprotein. The
prefix apo comes from the Greek 'separated from.' There are many
different types of apolipoproteins. For example, apolipoprotein A (often
called just apoA) is associated with HDL, and apolipoprotein B (apoB) is
associated with LDL. Sometimes people call the apolipoproteins just
apoprotein. Lipoprotein(a). Just to make things more confusing, there's
a special kind of LDL called lipoprotein(a), or just Lp(a). This LDL is
attached to an extra glycoprotein (a protein containing some sugar)
called apolipoprotein(a). It's not the same as apolipoprotein A, which
is associated with HDL The amount of Lp(a) seems to depend primarily on
your genetic background, although trans fats may increase it, and high
levels are associated with increased cardiovascular risk." (source:
Gretchen Becker) http://tinyurl.com/ckz8t.

A rare kind of HDL - http://tinyurl.com/9ver6 (genetic aspect)
Conclusions A recombinant ApoA-I Milano/phospholipid complex (ETC-216)
administered intravenously for 5 doses at weekly intervals produced
significant regression of coronary atherosclerosis as measured by IVUS.
Although promising, these results require confirmation in larger
clinical trials with morbidity and mortality end points." Source: Effect
of Recombinant ApoA-I Milano on Coronary Atherosclerosis in Patients
With Acute Coronary Syndromes -
http://jama.ama-assn.org/cgi/content/abstract/290/17/2292
Articles that cite this article:
http://jama.ama-assn.org/cgi/content/abstract/290/17/2292#otherarticles

... Dr. Nissen concluded that
the patients who die of a plaque rupture when they are 45 years old
probably have had the disease since they were teenagers.

Very interesting, Frank. I know the emphasis in medicine is in
extending life, particularly the quality of extended life, but I doubt
that given the relationship between increasing age and increasing
coronary artery disease, this is something that can be avoided
altogether.

I do think endothelial function can be improved through diet and
exercise, yet not swiftly.

The link for the following is good as of a few moments ago.
http://www.clinicalcardiology.org/productcart/pc/index.asp

But URLs I had for the topics below are not functioning:
Endothelial Dysfunction, the Renin-Angiotensin System, and Nitric Oxide:
Impact on Coronary Artery Disease and Therapeutic Interventions This is
a set of lengthy articles and quite technical.

Biology of Endothelium
Endothelial Function and Oxidant Stress
The Homeostatic Balance Between Angiotensin II and Nitric Oxide
Endothelial Dysfunction in Essential Hypertension
Endothelial Function, Fibrinolysis, and ACE Inhibition
Plaque Disruption and Cornary Thrombosis:New Insight into Pathogenesis
and Prevention
Theapeutic Interventions in Endothelial Dysfunction: Endothelium as a
Target Organ
Growth Factors as Potential New Treatment for Ischemic Heart Disease
Potential Role of ACE Inhibition in Myocardial Ischemia

Others put their success compared to say India with having an ultra
low fat diet with something like 80% carbohydrate by calories.

This reminds me of my army days. I went from 153 to 182 pounds in less
than 3 months after induction. I found that I could control my weight by
varying the amount of potatoes I ate. A good proportion of that weight
gain was muscle and some was water retention due to increased salt
intake. We put salt tablets in our canteens and there were salt tablets
in the mess hall. My waist size went from 29 to 33 inches as well. By
the time I reached 65 years of age my waist was 38 and then diabetes DX.
I had weighed ~195 lbs. for much of 30 years. My weight has stabilized
at about 159-162 through multiple therapies including calorie restriction
and metformin. In recent years my body fat percentage has ranged less
than 1%, i.e., 17.3-17.8%. Carbohydrates have been greatly reduced,
especially for breakfast and lunch.

Maybe the point is to pick your diet--either high carb or high fat--but
not mix the two. ;-)

I don't know about that. ;) I definitely increased protein through
whey protein consumption and changed the mix of fats toward more
monounsaturated fats, less saturated and trans fats, and a lower omega 6
to omega 3 ratio. This ratio was reduced by reducing omega 6s and
increasing omega 3s, especially EPA and DHA from fish oil. I don't come
close to knowing the proportions of macronutrients in my diet.

Back to good blood glucose control:
http://circ.ahajournals.org/cgi/content/full/107/7/1017
High Glucose Causes Upregulation of Cyclooxygenase-2 and Alters Prostanoid
Profile in Human Endothelial Cells
Role of Protein Kinase C and Reactive Oxygen Species

Frank
.

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