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Abstract PURPOSE OF REVIEW: Persistent recommendations for universal restriction of dietary sodium intake are based on associations of sodium intake with blood pressure. No clinical trial data support an association of sodium intake with mortality and morbidity outcomes, however, while results of observational studies appear heterogeneous. Can these contradictory data be reconciled to inform health policy regarding sodium intake recommendations?
RECENT FINDINGS: We reported (2006) a statistically significant (P = 0.03) association of sodium intake less than 2.3 g/day with increased cardiovascular disease mortality (hazard ratio 1.37) in a representative sample of the US adult population with an observed baseline mean sodium intake of 2.7 g/day. Others reported (2004) a significant (P < 0.01) higher stroke death among males and borderline significant (P = 0.07) for females, for highest compared with lowest sodium tertile in a community in Japan with mean intake of 5.4 g/day.
SUMMARY: These results are consistent with earlier studies suggesting that the association of sodium with morbidity and mortality in industrial societies follows a 'J shape' with a direct association at high levels of average intake (over 4 g), an inverse association at lower levels (less than 2 g) and no measurable effect for the widely prevalent intakes in between.
PMID: 17556882 [PubMed - indexed for MEDLINE>View Thread
I hope you are well. I noticed that the mcdougall.com vegans, especially one well known culprit, are spreading misinformation about you.
He is suggesting without pointing your name directly, that you may have suffered a heart attack because you were only 75% compliant.
If all your "diversion" was eating a few oz of salmon or clams once a week then it is very easy to calculate that you must have been still ~95% compliant vegan!
You might perhaps want to rectify this distortion because it is an attempt at obfuscating the real issue (IMHO - hyperinsulinemia that has nothing to do with eating fish) and may give other vegans a false sense of security.
Best regards and best wishes for good health,
Stan (Heretic)View Thread
AbstractUrinary calcium excretion is strongly related to net renal acid excretion. The catabolism of dietary protein generates ammonium ion and sulfates from sulfur-containing amino acids. Bone citrate and carbonate are mobilized to neutralize these acids, so urinary calcium increases when dietary protein increases. Common plant proteins such as soy, corn, wheat and rice have similar total S per g of protein as eggs, milk and muscle from meat, poultry and fish. Therefore increasing intake of purified proteins from either animal or plant sources similarly increases urinary calcium. The effects of a protein on urinary calcium and bone metabolism are modified by other nutrients found in that protein food source. For example, the high amount of calcium in milk compensates for urinary calcium losses generated by milk protein. Similarly, the high potassium levels of plant protein foods, such as legumes and grains, will decrease urinary calcium. The hypocalciuric effect of the high phosphate associated with the amino acids of meat at least partially offsets the hypercalciuric effect of the protein. Other food and dietary constituents such as vitamin D, isoflavones in soy, caffeine and added salt also have effects on bone health. Many of these other components are considered in the potential renal acid load of a food or diet, which predicts its effect on urinary acid and thus calcium. "Excess" dietary protein from either animal or plant proteins may be detrimental to bone health, but its effect will be modified by other nutrients in the food and total diet.View Thread
http://nigeepoo.blogspot.ca/2012/03/warning-signs-to-look-out-for-when.htmlView Thread
H. Jay Dinshah was the founder and president of American Vegan Society. In his obituary , vegsource failed to mention the cause of death.
View Thread
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303886/View Thread
AbstractA role for the amount and type of dietary protein in the etiology of cancer has not been studied extensively. Nevertheless, there is no compelling evidence from epidemiological studies to indicate that protein, at levels usually consumed, is a risk factor for cancer. On the other hand, animal studies suggest that certain peptides and amino acids derived from dietary proteins may influence carcinogenesis. The predominant protein in milk, casein, its peptides, but not liberated amino acids, have antimutagenic properties. Animal models, usually for colon and mammary tumorigenesis, nearly always show that whey protein is superior to other dietary proteins for suppression of tumour development. This benefit is attributed to its high content of cystine/cysteine and gamma-glutamylcyst(e)ine dipeptides, which are efficient substrates for the synthesis of glutathione. Glutathione is an ubiquitous cellular antioxidant that directly or through its associated enzymes destroys reactive oxygen species, detoxifies carcinogens, maintains proteins in a reduced state and ensures a competent immune system. Various experiments showed that tumour prevention by dietary whey protein was accompanied by increased glutathione levels in serum and tissues as well as enhanced splenic lymphocyte proliferation, phagocytosis and natural killer, T helper and cytotoxic T cell activity. Whey protein components, beta-lactoglobulin, alpha-lactalbumin and serum albumin were studied infrequently, but results suggest they have anticancer potential. The minor component lactoferrin has received the most attention; it inhibits intestinal tumours and perhaps tumours at other sites. Lactoferrin acts by induction of apoptosis, inhibition of angiogenesis, modulation of carcinogen metabolising enzymes and perhaps acting as an iron scavenger. Supplementing cows with selenium increases the content of selenoproteins in milk, which on isolation inhibited colon tumorigenesis in rats.
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The role of dietary protein in low dose chronic alfatoxin B1 (AFB1) liver injury in Rhesus monkeys has been studied using 0.16 and 0.5 ppm of AFB1 in diet. The high and low protein diet contained 20% and 5% casein, respectively. Following 32 weeks of intoxication with 0.16 ppm of AFB1, histological examination revealed mild alterations in low protein group only. However, distinct histochemical and ultra-structural alterations indicative of toxic liver injury are present in both the groups fed AFB1, though more prominent in animals fed a low protein diet. Monkeys on low protein diet surviving for 90 weeks or more show foci of preneoplastic lesions, whereas those on high protein diet reveal no such alterations at the corresponding time interval. With 0.5 ppm of AFB1 in diet, the pattern of toxic liver injury is similar to that of 0.16 ppm of AFB1 in diet. However, the liver damage is more prominent with this dose. The hepatic injury again is more accentuated in the low protein group as compared with the high protein group. No preneoplastic lesions are observed, possibly due to a poor survival (less than 70 weeks) in the low protein animals with this dose. The animals in the high protein group surviving even beyond 90 weeks do not show any preneoplastic/neoplastic lesions. It appears that in the simian model used by us, the liver injury caused by AFB1 is accentuated by simultaneous restriction of dietary protein and in animals on such combined regimen preneoplastic lesions appear around 90 weeks of experiment. These observations suggest a synergism between protein calorie malnutrition and aflatoxin induced hepatocarcinogenesis and may explain the higher incidence of hepatocellular carcinoma in certain areas of the world where contamination of foods with aflatoxin and malnutrition are prevalent.
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"Furthermore, there is a linear relationship between the risk of CV death and the 2-hour oral glucose tolerance test (OGTT). Increased mortality is evident at OGTT levels of approximately 90 mg/dL (5 mmol/L), which is well below current definitions of type 2 diabetes. Biphasic insul"View Thread
You may find that interesting (see FIG.1). This is a very thought provoking though speculative article:
http://high-fat-nutrition.blogspot.ca/2012/05/on-glut5.html
Regards,
H.View Thread
http://pi-bill-articles.blogspot.com/2011/03/track-your-plaque-program-by-william.html
If you read it you will see that typically, one's plaque increases by 30 to 35% per year and this program is considered successful if the increase is only 5 to 10% per year!! This is success? I thought the program promised reversal. And it takes several years because he recommends the calcium scan involving the equivalent of several months worth of radiation in one shot be done every twelve months. Plus a diet that requires lots of protein and fats.
So when he documents success he is talking about less progress. And popping lots of supplements. I am not impressed.
DoloresView Thread
AbstractDiabetes mellitus is characterized by hyperglycemia and associated with aberrations in the metabolism of carbohydrate, protein, and lipid that result in development of secondary complications. Extensive studies have indicated that nutritional therapy plays a pivotal role in the controlling or postponing of development of these secondary complications. Several functional foods have been shown to possess hypoglycemic and hypolipidemic properties. Flax seed (FS) is a functional food that is rich in omega 3 fatty acids and antioxidants and is low in carbohydrates. In exploratory studies, FS was incorporated in recipes, which resulted in a reduction in the glycemic index of the food items. These observations prompted us to investigate the efficacy of FS supplementation in type 2 diabetics (n = 29). Subjects were assigned to the experimental (n = 18) or the control group (n = 11) on the basis of their desire to participate in the study. The experimental group's diet was supplemented daily with 10 g of FS powder for a period of 1 month. The control group received no supplementation or placebo. During the study, diet and drug intake of the subjects remained unaltered. The efficacy of supplementation with FS was evaluated through a battery of clinico-biochemical parameters. Supplementation with FS reduced fasting blood glucose by 19.7% and glycated hemoglobin by 15.6%. A favorable reduction in total cholesterol (14.3%), triglycerides (17.5%), low-density lipoprotein cholesterol (21.8%), and apolipoprotein B and an increase in high-density lipoprotein cholesterol (11.9%) were also noticed. These observations suggest the therapeutic potential of FS in the management of diabetes mellitus.
PMID: 22432725 [PubMed - in process> LinkOut - more resourcesView Thread
see my post here .Regards,
H.View Thread
http://www.youtube.com/watch?v=-wKKVV8VQ9o&feature=relatedView Thread
My brother was on statins and blood pressure meds before he went on a plant based diet and his cholesterol went very low. It went up when he was on a plant based diet and the doctor took him off the statins. Not by very much, but over 150.
There was a study in the New England Journal of Medicine which used massive doses of statins which lowered the cholesterol but one fourth of the patients either had a coronary event or died within 2.5 years.
So it wonders me if I should change my almost 100% plant based diet at all as long as I have to take a satin anyway.
And then there are those like the 97 year old patient I recently heard of whose cholesterol is over 260 who has high LDL but has managed to make it to 97. How many of us are using one diet or another when all along there might be no need and we would be healthy no matter what we did?
DoloresView Thread
Ancient Egyptian mummies have been found riddled with "modern" degenerative diseases, including heart disease, rheumatoid arthritis, diabets and other. From eating fish and meat? I don't think so! The grains are the most likely culprit!
Mass consumption of grains (and starchy vegetables!) has only been possible since the advent of modern style agriculture, settled communities using fire and cooking, that is around 7500BC in the Middle East and somewhat later elsewhere.
DMW mentioned the plants' anti-oxidant.
I think that is a very complex subject. If you read the refs I posted in the other thread, they may indicate that consumption of plants is a double-edged sword. It adds antioxidants and vitamins but it also accelerates DNA damage.
On the positive side:
- yes it is better to eat plants than nothing, if nothing else is available. Regardless of what has been said a death by starvation is worse than eating some dodgy wild fruit or vegetables, for a short while, until a next successful hunt or fish catch.
- yes, plants do contain soma anti-oxidant and vitamins, but also ...
on the negative side:
- those same plants may contains some phytotoxins and large amount of compounds (notably fructose) that generate troublesome metabolic byproducts using up those anti-oxidants and vitamins (i.e. carbs metabolism requires vitamin C) and tying up a large portion of body's immune system for cleanup.
- most plants' macronutrients are not very compatible with human digestion and requirements. Most commonly available plants are very high (too high) in carbohydrates. Those that are not high in carbs are often (with some rare exceptions) high in the type of fats (polynsaturated) that are not as well tolerated as animal fats, in large meal staple quantities. Those plants that are not very high in carbs and fats, are high in a kind of proteins (aminoacids) that are also not well matched to human requirements.
Heretic
[br>View Thread
There are some studies, like The China Study, by Dr. T. Colin Campbell, which supports the concept that the less animal food and the more plant foods in one's diet the better. But interestingly, while some of these studies are often used to defend a vegan diet, none of the studies show that complete abstinence from animal food is best. Why? This is because in many of these studies, there were no groups in the studies that completely abstained from animal foods. Proving less is better doesn't automatically mean that none is optimal, unless, of course, there are studies to prove this assertion, alsoView Thread
Didi
Drs Sinatra and William Davis would point to the size of your cholestrol particles and Lpa.They have a number of suggestions about reducing the size of particles and greatly reducing risk.Look into it and then ignore it if you don't like what they say.Both treat heart disease on a daily basis....and claim geat success.View Thread
http://www.vegsource.com/news/2010/07/china-study-author-colin-campbell-slaps-down-critic-denise-minger.htmlView Thread
I begun one morning by frying myself a scrambled eggs on double slices of bacon. The first scrambled eggs and the first bacon perhaps since 1988 or so. Bacon tasted too salty, eggs tasted tasteless, I didn't enjoy it. I was used to eating a slice or 2 of sourdough brown bread with a nanometer thick monomolecular layer of flora margarine and a jam.
I fully expected my mild transitional chest pain of "unknown" origin that I experienced since around 1996 (until 2001) to get worse, I expected my sporadic once-a-month episodes of tachycardia (had all my life, more frequent after 1996, gone by 2001) but to become less sporadic. I expected my daily afternoon symptoms of hypoglycemia tiredness, shakiness mental fuziness and stress-outedness (since mid 1990-ties until 1999) to get worse and I did not expect at all my painful dry eyes symptoms (had it from around 1991 until 2000) requiring daily eye drops, to change.
Well, I didn't die! Perhaps if I added some buttered lobster...

Best regards ,
Heretic
P.S.
I realize the tone of my story may seem a bit odd. I have to add this to explain why: ever since my out of body/near-death experience in 1979 I do not react on threats like others, and I do not treat most intellectual beliefs and theories very seriously. I also do not have a fear of death!View Thread
Here's an amazing reference
www.pubmed.com/18799354
Dr. Ornish collaborated with Nobel Prize winner Dr. Elizabeth Blackburn. She got the 2009 Nobel Prize in Medicine, for work with telomeres, and the discovery of telomerase, the enzyme that repairs telomeres.
Telomeres are like the plastic sleeve on the ends of shoelaces, except telomeres are on the ends of DNA twisted pairs, in our chromosomes. As we age, the telomeres shorten, and when the telomeres get too short, the DNA unravels, and then we unravel. It's a theory of aging.
The Ornish diet increased telomerase by 30%. That is amazing.
Best regards, EngineerGuyView Thread
One has to keep in mind that a high insulin level may also be maintained by the pancreas itself, in some cases if it is strong enough and if it is stimulated by food or other factors to secrete insulin..
Conversely, a poor glucose control (without excess insulin) would render a patient much more vulnerable to kidney failure, peripheral neuropaties and eye problems , but less so to heart attacks! In the days before insulin, the main diabetic risk was from kidney failure, not from heart disease.
The key to reduce the overall risk in diabetes (type 2 and 1 (see Dr. Richard Bernstein's "Normal Sugar" book)) is to do both:
1) minimize the overall requirement for insulin
AND
2) normalize blood glucose level at all time (80-140mg/dl)
H.View Thread
Another myth?
What do you think Heretic,EG?View Thread
Do more than just suggest....tell them this is the way its going to be.Period.View Thread
On Easter, I indulged in ham and I eat fish and clams a couple of times a week. I do not think that the 100% blockage they stented happened over night. Another artery was also 100% blocked but that one had built collaterals. Yet another artery was 50% blocked and another between 60 and 70 % blocked.
Diabetics frequently die of heart disease. But I was lulled into complacency because my blood sugars were pretty good after 20 years and on no meds--just diet and exercise. I had an HbA1c of 5.4. Of course now I am determined to get it lower. Cholesterol was 166, LDL 103 and triglycerides 88. Eating as much fruit and starches as I do I was surprised at the trigs. A couple of my doctors assumed I was only borderline diabetic. No.
OK guys. Now what? Strictly eliminate all animal food? I was already not eating dairy, fats or oils (do we count the occasions at my daughter's when I help myself to the snack foods she always has around?)
Esselstyn says moderation kills. It almost did with me. Or do I take a closer look at H's diet and give up rice, potatoes, a diet of mostly vegetables, fruits, beans and use a stick of butter on the few vegetables I would eat and eat the end of the roast beef with mostly fat? The doctors did not talk at all about diet and gave me a booklet with what looks to me like a version of the standard american diet. Neither H nor EG would follow such a diet. This is America. We take pills.
As you can see this is not merely an academic problem for me and I cannot afford to speculate. Because here I am--someone whose drug use amounted to maybe 10 tylenol in the last couple of years, stuck with taking plavix, aspirin, pravachol, lisinopril and metropolol. I am afraid to be non compliant which is my inclination. So I am now subject to all the stupid side effects of these drugs. So much for courteous debate. What do I do?
Dolores
P.S. The only pain I suffer now is from the chest compression. Evidently it is not done in real life the way you see it in the movies. They have to make sure the chest compresses 2 and a half inches down. I am going to get a medic alert bracelet that reads--start with the paddles.View Thread
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