Re: Not exactly new news

Randy Wrote:
The Med diet had the Same amount of carbs as the low fat diet.
The difference was a Little more fat (mono) Less protein and More
fiber in the Med group.

Quentin Wrote:
I'm interested in what  "a Little more fat" translates to in actual
numbers.  Other wise we are dealing with opinions.  Valuable as they
are they don't encourage anyone to change their minds about what did
and didn't happen.  Randy,  I'd find this discussion more beneficial
if we had the numbers.  I'm sure others would also.

Randy Replies:
All my data came from the paper. Please refer to the paper!
http://content.nejm.org/cgi/content/full/359/3/229

Here are the numbers:

Med group - 50.2% Carbs, 18.8% Pro, 33.1 Fat
Low Fat - 50.7% Carbs, 19.0% Pro, 30 Fat
Low Carb - 40.4% Carbs, 21.8% Pro, 39.1 Fat

The Med group was the only one that increased fiber intake. The other
groups decreased fiber slightly.


Randy Wrote:
Fasting Glucose change: -32 for Med, +1.2 for Low Carb
Fasting Insulin:  -4 for Med, -2.2 for Low Carb
Insulin Resistance change: -3.3 for Med, -1 for Low Carb

Quentin Wrote:
I looked at those and thought what a pity they didn't report the more
meaningful post prandial figures.  Post prandial levels relates much
more closely to damage being done.  

Randy Replies:
If the improvment in the Med group was only fasting bgs, your case
would be much stronger.
But the Med group had a fasting bg drop of 32 points, a decrease in
fasing insulin of 90% and a >300% increase in Insulin Sensitivity.
Thats not a pattern for large PP swings! Thats a pattern all around
for much greater glycemic control.
Thats why I contend that something is askew with their numbers.

Here a recent Low Fat (<20%) High Carb (70%), High fiber (>40 grams)
diet done under tightly controlled condition that improved IS 30% in
21 days (and improved a bunch of other stuff as well). Also, this
study had very little weight loss to futher strengthen the results:

Full paper here: http://jap.physiology.org/cgi/content/full/100/5/1657

Randy

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Effect of a short-term diet and exercise intervention on oxidative
stress, inflammation, MMP-9, and monocyte chemotactic activity in men
with metabolic syndrome factors
Christian K. Roberts,1 Dean Won,1 Sandeep Pruthi,1 Silvia Kurtovic,1
Ram K. Sindhu,2 Nosratola D. Vaziri,3 and R. James Barnard1
1Department of Physiological Science, University of California, Los
Angeles; 2Division of Endocrinology, Metabolism and Molecular
Medicine, Charles R. Drew University, Los Angeles; and 3Division of
Nephrology and Hypertension, Department of Medicine, University of
California, Irvine, California

Submitted 6 October 2005 ; accepted in final form 14 December 2005


ABSTRACT

The present study was designed to examine the effects of lifestyle
modification on key contributing factors to atherogenesis, including
oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese
men (n = 31), 15 of whom had metabolic syndrome, were placed on a high-
fiber, low-fat diet in a 3-wk residential program where food was
provided ad libitum and daily aerobic exercise was performed. In each
subject, pre- and postintervention fasting blood was drawn for
circulating levels of serum lipids, glucose and insulin (for
estimation of insulin sensitivity), oxidative stress-generating enzyme
myeloperoxidase and marker 8-isoprostaglandin F2, the inflammatory
protein C-reactive protein, soluble ICAM-1 as an indicator of
endothelial activation, sP-selectin as a marker of platelet
activation, the chemokine macrophage inflammatory protein-1, and total
matrix metalloproteinase-9. Using subject sera and human aortic
endothelial cell culture systems, we measured VCAM-1 cell surface
abundance and monocyte chemotactic protein-1, nitric oxide,
superoxide, and hydrogen peroxide production in vitro by fluorometric
detection. Also determined in vitro was serum-induced, monocyte
adhesion and monocyte chemotactic activity. After 3 wk, significant
reductions (P < 0.05) in body mass index, all serum lipids and lipid
ratios, fasting glucose, insulin, homeostasis model assessment for
insulin resistance, myeloperoxidase, 8-isoprostaglandin F2, C-reactive
protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory
protein-1, and matrix metalloproteinase-9 were noted. In vitro, serum-
stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1
production, and fluorometric detection of superoxide and hydrogen
peroxide production decreased, whereas a concomitant increase in NO
production was noted (all P < 0.01). Additionally, both monocyte
adhesion (P < 0.05) and MCA (P < 0.01) decreased. Nine of 15 were no
longer positive for metabolic syndrome postintervention. Intensive
lifestyle modification may ameliorate novel coronary artery disease
risk factors in men with metabolic syndrome factors before reversal of
obesity.

atherosclerosis; lipids; cell adhesion molecules; nitric oxide; matrix
metalloproteinase-9



--------------------------------------------------------------------------------
ATHEROSCLEROTIC DISEASE IS the leading cause of mortality in developed
countries, with coronary artery disease (CAD) being the number one
killer of both men and women. Early epidemiological and clinical
studies established a link between dietary saturated fat and
cholesterol, serum cholesterol, and CAD mortality (28). The Framingham
Heart Study and Multiple-Risk Factor Intervention Trial Study
emphasized the relationship between serum cholesterol, especially low-
density lipoprotein cholesterol (LDL-C), and CAD (9). Although serum
lipid levels have been the focus to explain the incidence of
atherosclerosis, other risk factors such as oxidative stress,
inflammation, endothelial cell activation, platelet activation, and
plaque stability are important. For example, levels of the oxidative
stress markers 8-isoprostaglandin F2 (8-iso-PGF2) (42) and
myeloperoxidase (MPO) (7), inflammation-associated proteins C-reactive
protein (CRP) and soluble intracellular adhesion molecule (sICAM)-1
(48), soluble P-selectin (47), and the matrix metalloproteinase MMP-9
(17) all independently predict early risk of cardiovascular disease or
myocardial infarction.
Diet and exercise modifications have been documented to ameliorate the
classic CAD risk factors, including hyperlipidemia, hypertension, and
insulin resistance (49). The clustering of multiple CAD risk factors
in the same individual, commonly referred to as the metabolic
syndrome, is extremely prevalent in Westernized societies, affecting
23% of the population and 43% of those above 60 years of age (20).
Accordingly, the examination of the effect of modifying environmental
influences (e.g., diet, physical activity, cigarette smoking) is
warranted. The present study was designed to investigate the
hypothesis that a combined intervention consisting of a high-fiber,
low-fat diet and physical activity confers reductions in oxidative
stress, inflammation, and monocyte-endothelial interactions in obese
men at high risk for CAD and related clinical outcomes.





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