Soy protein diet improves endothelial dysfunction in renal transplant
patients.
Cupisti A, Ghiadoni L, D'Alessandro C, Kardasz I, Morelli E, Panichi V,
Locati D, Morandi S, Saba A, Barsotti G, Taddei S, Arnoldi A, Salvetti
A
Nephrol Dial Transplant. 2006 Sep 23;

BACKGROUND: Since it has been demonstrated that soy diet can improve
endothelial function, in the present study we evaluated the effect of
dietary substitution of 25 g of animal proteins with soy proteins on
endothelial dysfunction in renal transplant patients. METHODS: In 20
renal transplant patients (55 +/- 11 years, serum creatinine 1.7 +/-
0.6 mg/dl), brachial artery flow mediated dilation (FMD) and
endothelium-independent vasodilation (sublingual nitroglycerine, 25
microg) were measured at baseline, after 5 weeks of a soy diet and
finally after 5 weeks of soy wash-out. Changes in plasma lipids,
markers of oxidative stress (lipid peroxides, LOOH) and inflammation
(C-reactive protein), isoflavones (genistein and daidzein), asymmetric
dimethyl arginine (ADMA) and l-arginine were also evaluated. RESULTS:
At baseline, patients showed a significantly lower FMD as compared with
age-matched healthy subjects (3.2 +/- 1.8 vs 6.3 +/- 1.9, respectively;
P < 0.001), while response to nitroglycerine was similar. After soy
diet, actual protein intake was not changed, cholesterol and lipid
peroxides were significantly reduced, and isoflavones were detectable
in plasma. Soy diet was associated with a significant improvement in
FMD (4.4 +/- 2.0; P = 0.003 vs baseline), while response to
nitroglycerine was unchanged. Improvement in FMD was related to
l-arginine/ADMA ratio changes, but no significant relation was found to
changes in cholesterol, lipid peroxides or genistein and daidzein
plasma concentrations. After 5 weeks of soy diet discontinuation, FMD
(3.3 +/- 1.7%) returned to baseline values and isoflavones were no
longer detectable in plasma. CONCLUSIONS: A soy protein diet for 5
weeks improves endothelial function in renal transplant patients. This
effect seems to be strictly dependent on soy intake as it disappears
after soy withdrawal and is mediated by an increase in the
l-arginine/ADMA ratio, independently of change in lipid profile,
oxidative stress or isoflavones.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://www.***.com/

Man Is A Herbivore!
http://www.***.com/

DEAD PEOPLE WALKING
http://www.***.com/

And animal studies suggest that _fish_ protein may prevent insulin
resistance and thus type 2 diabetes. And a Swedish study with humans
suggests that fish protein may protect type 1 diabetes patients from
microalbuminuria und thus perhaps from kidney damage.

Here some evidence: The study

Lavigne C, Tremblay F, Asselin G, Jacques H, Marette A.        
Prevention of skeletal muscle insulin resistance by dietary cod
protein in high fat-fed rats.
Am J Physiol Endocrinol Metab. 2001 Jul;281(1):E62-71.
PMID: 11404223 [PubMed - indexed for MEDLINE]
<http://ajpendo.physiology.org/cgi/content/full/281/1/E62>

suggests that fish protein may prevent high fat diet induced insulin
resistance and hence type 2 diabetes in rats. Selected excerpts:

    "In the present study, we tested the hypothesis that fish
    protein may represent a key constituent of fish with
    glucoregulatory activity. Three groups of rats were fed a high-
    fat diet in which the protein source was casein, fish (cod)
    protein, or soy protein; these groups were compared with a
    group of chow-fed controls. High-fat feeding led to severe
    whole body and skeletal muscle insulin resistance in casein- or
    soy protein-fed rats, as assessed by the euglycemic clamp
    technique coupled with measurements of 2-deoxy-D-[(3)H]glucose
    uptake rates by individual tissues. However, feeding cod
    protein fully prevented the development of insulin resistance
    in high fat-fed rats. These animals exhibited higher rates of
    insulin-mediated muscle glucose disposal that were comparable
    to those of chow-fed rats. The beneficial effects of cod
    protein occurred without any reductions in body weight gain,
    adipose tissue accretion, or expression of tumor necrosis
    factor-alpha in fat and muscle. Moreover, L6 myocytes exposed
    to cod protein-derived amino acids showed greater rates of
    insulin-stimulated glucose uptake compared with cells incubated
    with casein- or soy protein-derived amino acids. These data
    demonstrate that feeding cod protein prevents obesity-induced
    muscle insulin resistance in high fat-fed obese rats at least
    in part through a direct action of amino acids on insulin-
    stimulated glucose uptake in skeletal muscle cells.

    [...]

    In summary, the present study shows that dietary cod protein
    prevents the development of skeletal muscle insulin resistance
    in high fat-fed obese rats. The beneficial action of cod
    protein on insulin sensitivity occurred without reductions in
    body weight or adiposity, strongly suggesting that cod protein
    protects from obesity-induced insulin resistance. The effect of
    dietary cod protein appears to involve, at least in part, a
    direct action of cod protein-derived amino acids on insulin-
    stimulated glucose transport in skeletal muscle cells. Interest
    in the present data also arises from the fact that increased
    cod protein consumption is easily implementable in humans
    within guidelines of daily recommended allowances of essential
    nutrients (12, 18) and thus could represent a novel
    nutraceutical approach in preventing the development of insulin
    resistance in obesity. Because insulin resistance is a central
    factor in visceral obesity-associated complications such as
    hypertension, diabetes, and cardiovascular diseases (2, 6, 8),
    dietary cod protein may contribute to prevent the many
    metabolic aberrations that accompany the obese state."

A follow-up study from the same research team:

Tremblay F, Lavigne C, Jacques H, Marette A.
Dietary cod protein restores insulin-induced activation of
phosphatidylinositol 3-kinase/Akt and GLUT4 translocation to the
T-tubules in skeletal muscle of high-fat-fed obese rats.
Diabetes. 2003 Jan;52(1):29-37.
PMID: 12502490 [PubMed - indexed for MEDLINE]
<http://diabetes.diabetesjournals.org/cgi/content/full/52/1/29>

    "Diet-induced obesity is known to cause peripheral insulin
    resistance in rodents. We have recently found that feeding cod
    protein to high-fat-fed rats prevents the development of
    insulin resistance in skeletal muscle. In the present study, we
    have further explored the cellular mechanisms behind this
    beneficial effect of cod protein on skeletal muscle insulin
    sensitivity. Rats were fed a standard chow diet or a high-fat
    diet in which the protein source was either casein, soy, or cod
    proteins for 4 weeks. Whole-body and muscle glucose disposal
    were reduced by approximately 50% in rats fed high-fat diets
    with casein or soy proteins, but these impairments were not
    observed in animals fed cod protein. Insulin-induced tyrosine
    phosphorylation of the insulin receptor and insulin receptor
    substrate (IRS) proteins were similar in muscle of chow- and
    high-fat-fed rats regardless of the dietary protein source.
    However, IRS-1-associated phosphatidylinositol (PI) 3-kinase
    activity was severely impaired (-60%) in muscle of high-fat-fed
    rats consuming casein or soy protein. In marked contrast,
    feeding rats with cod protein completely prevented the
    deleterious effect of fat feeding on insulin-stimulated PI 3-
    kinase activity. The activation of the downstream kinase
    Akt/PKB by insulin, assessed by in vitro kinase assay and
    phosphorylation of GSK-3beta, were also impaired in muscle of
    high-fat-fed rats consuming casein or soy protein, but these
    defects were also fully prevented by dietary cod protein.
    However, no effect of cod protein was observed on atypical
    protein kinase C activity. Normalization of PI 3-kinase/Akt
    activation by insulin in rats fed high-fat diets with cod
    protein was associated with improved translocation of GLUT4 to
    the T-tubules but not to the plasma membrane. Taken together,
    these results show that dietary cod protein is a natural
    insulin-sensitizing agent that appears to prevent obesity-
    linked muscle insulin resistance by normalizing insulin
    activation of the PI 3-kinase/Akt pathway and by selectively
    improving GLUT4 translocation to the T-tubules.

    [...]

    In summary, this study provides convincing evidence that
    dietary proteins are important modulators of insulin signaling
    and action in rat skeletal muscle. Furthermore, we showed that
    dietary cod protein is a potent and natural insulin-sensitizing
    agent that normalizes the activation status of the PI 3-
    kinase/Akt pathway coupled to an increased translocation of
    GLUT4 to the T-tubules in obese high-fat-fed rats.
    Identification of the precise molecular mechanism by which
    dietary cod protein improves insulin signaling to PI 3-
    kinase/Akt will help defining novel therapeutic tools for the
    prevention and treatment of insulin resistance."

Another potential benefit from fish protein: A Swedish study

Mollsten AV, Dahlquist GG, Stattin EL, Rudberg S.
Higher intakes of fish protein are related to a lower risk of
microalbuminuria in young Swedish type 1 diabetic patients.
Diabetes Care. 2001 May;24(5):805-10.
PMID: 11347734 [PubMed - indexed for MEDLINE]
<http://care.diabetesjournals.org/cgi/content/full/24/5/805>

found that fish protein may protect from microalbuminuria in type 1
diabetes. Brief excerpts:

    "... CONCLUSIONS: Total protein and fat intake were not associated
     with the presence of microalbuminuria, but a diet including a
     high amount of fish protein seemed to lessen the risk.

     [...]

     In conclusion, our results do not give evidence for the
     suggestion that a high-protein diet increases the risk for
     incipient diabetic nephropathy. Rather, a diet rich in fish
     protein seems to provide protection from this complication."

No, Jesus was a fish eater.
No, before the invention of agriculture some 10000-15000 years ago our
hunter-gatherer ancestors evolved on and adapted to a high protein,
low carbohydrate diet, where carbohydrates provided 22-40% of
calories, and where animal meat was an important part of diet.

--
Matti Narkia

 > >

But our hunter-gatherer ancestors didn't live to see the ripe old age
of 30, in most cases.  It can be argued that we were gathers long
before we were hunters.  But only in recent history have people begun
dying from eating TOO MUCH food, regardless of whether it's meat or
not.   We've evolved enough to see what's killing us but haven't
evolved enough to stop doing it.

Even if that were true, it's irrelevant. The issue was what kind of
diet we have adapted to and at least for the last two million years
excluding the last 10000-15000 years of agriculture era that has been
a high protein, low carb diet containg large amount of meat.

As for the life expectation of our ancestora: not only were they
missing all medical care of modern times, but besides being hunters,
they were also hunted, and when they became too old to catch prey,
they probably died of hunger or became hunted down.

Some of our ancestor were vegetarian gatherers, but during the last
two million years of evolution, humans were primarily carnivorous,
i.e., flesh-eating hunters consuming a low-carbohydrate, high-protein
diet.

References:

Perspectives on Nutrition in Related Species
Man's Ancestry and Diet
Nutrition by Ron Kennedy, M.D., Santa Rosa, California
<http://www.medical-library.net/sites/_nutrition.html>:

Meat-eating was essential for human evolution, says UC Berkeley
anthropologist specializing in diet
<http://www.berkeley.edu/news/media/releases/99legacy/6-14-1999a.html>:

Hominid  Species Timeline
<http://www.wsu.edu/gened/learn-modules/top_longfor/timeline/timeline....>

Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA,
O'Keefe JH, Brand-Miller J.
Origins and evolution of the Western diet: health implications for the
21st century.
Am J Clin Nutr. 2005 Feb;81(2):341-54. Review.
PMID: 15699220 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/81/2/341>

Mann NJ.
Paleolithic nutrition: what can we learn from the past?
Asia Pac J Clin Nutr. 2004;13(Suppl):S17.
PMID: 15294479 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&...>

Cordain L, Eaton SB, Miller JB, Mann N, Hill K.
The paradoxical nature of hunter-gatherer diets: meat-based, yet
non-atherogenic.
Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S42-52. Review.
PMID: 11965522 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&...>

Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD.
Plant-animal subsistence ratios and macronutrient energy estimations
in worldwide hunter-gatherer diets.
Am J Clin Nutr. 2000 Mar;71(3):682-92.
PMID: 10702160 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/71/3/682>

Miller JC, Colagiuri S.
The carnivore connection: dietary carbohydrate in the evolution of
NIDDM.
Diabetologia. 1994 Dec;37(12):1280-6.
PMID: 7895958 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&...>

Colagiuri S, Brand Miller JC.
The metabolic syndrome: from inherited survival trait to a health care
problem.
Exp Clin Endocrinol Diabetes. 1997;105 Suppl 2:54-60. Review.
PMID: 9288547 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&...>

Colagiuri S, Brand Miller J.
The 'carnivore connection'--evolutionary aspects of insulin
resistance.
Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S30-5. Review.
PMID: 11965520 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&...>

On that I agree with you. As for meat, current meat of domesticated
farm raised grain-fed animals is very different from the meat of wild
stone age animals. Todays's meat is probably not healthy, at least not
in large amounts. I don't eat meat, but I eat plenty of fish.

--
Matti Narkia

Age is always stated as "average"
Some lived to a very old age, possibly 100.
Disease was not understood and most died from the environment or were
killed.  Some were eaten.
Wars and tribal genocides were the norm.

It is pretty difficult to be a gatherer and not a hunter.  That is a fairy
tale made by people who have probably never walked in the woods or forest,
much less tried to survive.
Fish has been key in human survival.

Guess what, Humans, bears, pigs are more alike than any other digestive and
nutrient system.

What is killing us and making us obese is the grain-based diet. It
isn't that we are eating too much, it is that we are eating too much
grain, refined grain products, and sugars. Not to mention vegetable
oils that are new to our diet. Especially the hydrogenated vegetable
oils. Just like refined white flour and refined white sugar, overly
processed refined hydrogenated vegetable oils are slow poisons.

TC

That's a fallacy brought to us by the latest in a long string of fade
diets -- "low-carb".  While refined carbs via soda pop, sugary juices,
and products made from gummy white flour are certainly a significant
part of the problem, to make no mention of, or worse completely
exonerate, deep-fried [Long John Silver's] fish, greasy [Big Mac/Burger
King/Wendy's] double-bacon cheeseburgers, slimey [Kentucky Fried]
chicken, and artery-stopping [Pizza Hut] "Meat Lovers" pizza is a huge
disservice to this NG.  And your continuous attempt to link and confuse
refined grain with nutrious whole grain and hydrogenated oils with
healthy unrefined vegetable oils, at best, could be described as
mischievous.  So why don't you just stop the nonsense?  

Patrick

He can't. He's crazy.

One the one hand it is a "fallacy" and on the other hand it is a
"significant part of the problem" ????? Which one is it? Is it a
"fallacy" or is it a "significant part of the problem"? Make up your
mind.

with a large order of chips and a large soda

with a super sized fry and a 3/4 gallon jug of sugar water

and a fries and drink

and a fries and drink

on a one-inch thick white flour crust and with a large soda

"nutritious" whole grain is only refined white grain flour with the
left overs mixed back in. It is still over processed stale grain with
all kinds of added chemicals to preserve it and stop it from clumping.
You've been had by the grain industry.

And there is nothing magical in grains that cannot be gotten in greater
amounts and in better forms from real fresh whole produce. Grains are
entirely superfluous to the human diet.

Name me one vegetable oil that is not refined. Except for extra {*filter*}
olive oil. Name me one that isn't heated, treated, filtered and
processed to death. Do you know what they do to corn oil, canola oil,
soy oil and other vegetable oils before it is poured in a bottle and
shipped to your grocer? You would be surprised how heavily processed it
actually is. It is rendered as dead a cooking.net">food as refined white flour and
ultra high temp pasteurized milk. These foods are processed to death
and it does not matter how fancy, glossy and green the label is, it is
still a dead food.

There is nothing mischievous about the {*filter*}that is foisted upon us as
supposedly healthy foods.

TC

Some info on vegetable oil processing:

http://en.wikipedia.org/wiki/Vegetable_oil

http://waltonfeed.com/omega/wht-oil.html

http://www.cip.ukcentre.com/marg1.htm

TC

He can't. He's possessed by a single idea.

As are you, doncha know.

TC

1. Keep calories from carbohydrates under 40% of the diet no matter whether
so called simple or complex.
2. Avoid hydrogenated or partially hydrogenated oils of any kind

Meat NEVER hurt any normal person.

Protein, oils, and fiber are a requirement.
It takes a lot of vegetables and fruits to get sufficient fiber.  They also
contain carbohydrates.  That doesn't leave much room for too much meat and
very little room for much grains and practically NO room for soda pop or
candy.

BTW a Big Mac with onions, lettuce, tomatoes, cheese (no fries), (no pop of
ANY kind) is one of the healthier dinners around.  It's all relative.

I tend to agree with you, except it seems that you are using the terms
"simple carbs" and "complex carbs" in the wrong context.

Simple carbs are sugars which have simple singular molecular
structures. Complex carbs are starches which have complex chains of
molecules connected together. They are both refined high-GI carbs and
they both have similar effects to the human body, ie. obesity,
diabetes, etc.

I think you meant to suggest that carbs be kept to less than 40%
whether they are refined high-GI carbs or real fresh whole-food carbs.

I agree with the less than 40% carb consumption overall, but refined
carbs (sugars and starches) are slow poisons that provide no useful
nutrition and cause short-term nutrient depletion, immediate nutrient
displacement, chronic inflammation on a molecular level, and long term
chronic disease. The less the better.

TC

What about the bun? What's that good for?