Re: newbie question on fat ratios

[Guest guest]

>>You speak of the dilating of vessels and influence of NO2.. is this

the improvement in endothelial dysfunction and myocardial perfusion that

I have been reading about?

Its all a fairly new area of research but I think we are on the same

page. Below are two abstracts on it.

BTW, This is also how Viagra works. Viagra increases the production of

NO in the vessels, increasing dilation and blood flow to the area. So,

while it wont get someone aroused, once aroused, it will make sure the

blood flow stays in the area. Which, also relates to another area and

that is that a high percentage of impotence in men over 40 is caused by

the same conditions that cause CVD and Atherosclerosis. Its not just

the arteries in the heart that are getting blocked and having impaired

endothelial function. And, of course, the same lifestyle strategies

that have been shown to reverse this in the heart (ornish, pritikin)

will also reverse the condition in other areas, improving flow and

function, and improve impotence and ED in men. Now, maybe we cant get

guys to eat better so that one day in the future they may not have heart

disease, but if they only knew how it could impact their sexual vitality

in the short term, we would have them all fighting their way to the

salad bar. Some times our male guests find them self feeling like

a teenager again.

Can J Cardiol. 2004 Aug;20 Suppl B:7B-15B.

The pivotal role of nitric oxide for vascular health.

Cooke JP.

The endothelium is a single cell layer that lines all blood vessels.

This tissue produces an impressive array of paracrine factors that

maintain vascular homeostasis. One of these factors is the potent

vasodilator endothelium-derived nitric oxide (NO). Impairment in the

synthesis or bioactivity of NO, as manifested by reduced

endothelium-dependent vasodilation, has been shown to be an independent

risk factor for major adverse cardiovascular events. The linkage between

endothelium-derived NO and cardiovascular health is likely due to the

pleiotropic effects of NO on the vessel wall. NO inhibits the

proliferation of vascular smooth muscle cells, the aggregation of

platelets, and the adherence and infiltration of inflammatory cells.

Thus, an impairment of NO bioactivity or synthesis will reduce its

braking effect on processes involved in atherogenesis. New insights have

been made regarding the mechanisms by which NO bioactivity becomes

impaired. Cardiovascular risk factors induce vascular oxidative stress,

which accelerates the degradation of NO. In addition, oxidative stress

causes the accumulation of asymmetric dimethylarginine (ADMA). ADMA is

an endogenous inhibitor of NO synthesis. Elevation of ADMA appears to be

a common mediator by which cardiovascular risk factors impair NO

synthesis. Elevation of plasma ADMA has been linked to impaired

endothelium-dependent vasodilation, carotid intimal thickening and

adverse cardiovascular events. A number of modern therapies directed

against atherosclerosis also improve the function of the NO synthase

pathway. New agents that specifically target the NO synthase pathway

have been developed, and represent a new front on the war against heart

disease.

Prev Cardiol. 2001 Winter;4(1):28-37. Related Articles, Links

Maintaining the endothelium: preventive strategies for vessel integrity.

Lissin LW, Cooke JP.

Division of Cardiovascular Medicine, Stanford University Medical Center,

Stanford, CA.

The endothelium is a diaphanous membrane, only one cell layer thick,

that lines all of our blood vessels. Despite its apparent fragility, it

exerts profound control over vascular tone, structure, and intersection

with circulating blood elements. One of the factors that the endothelium

synthesizes is nitric oxide, which is the most potent endogenous

vasodilator known. In addition to its blood flow regulating effects,

nitric oxide also inhibits key processes in atherosclerosis, including

monocyte adherence, platelet aggregation, and proliferation of vascular

smooth muscle cells. Nitric oxide synthesis is impaired, and its

degradation is accelerated, in many of the conditions associated with

atherosclerosis, including hypercholesterolemia. Restoration of nitric

oxide synthesis and activity in these disorders can improve blood flow,

relieve symptoms, and perhaps reduce the progression of

atherosclerosis.© 2001 by CHF, Inc.

>>When you say " stabilization " are you referring to stopping progression

of plaque or somthg else?

Again, its all new, but yes, and also that there is less chance that the

soft plaque is likely to rupture, which is now seen as the cause of many

MIs.

Here is some of our recent published studies on the NO issue. I can

post more info on them if anyone wants.

, C.K., N.D. Vaziri, R.K. Sindhu and R.J. Barnard. A high-fat,

refined carbohydrate diet affects renal NO synthase protein expression

and salt sensitivity. J Appl. Physiol 94:941-946,2003

, C.K., N.D. Vaziri, R.J. Barnard. Effect of diet and exercise

intervention on blood pressure, insulin oxidative stress, and nitric

oxide availability. Circulation 106:2530-2532,2002

Also, in response to the conversation a few weeks ago on the 2005 USDA

Dietary Guidelines, and their comments on low fat diets like Pritikin

being low in Vit E,and EFAs,.... I posted the corrected info here and

links to CEU courses discussing our position on the issues and a copy of

the letter we wrote the committee. I have a conference call with the

USDA committee chairs tommorrow to correct the mis-information, the

quote and I will let you know the end result.

It's a great example of why the details are so important beyond

executive summaries, abstracts and headlines. The reference they use to

show we are low in EFAs and Vit E, actually says the exact opposite and

includes nutritional analysis of our menus and states that we are

" nutritionally adequate " .

Oy Veh!

Thanks for your comments

Jeff