High Protein and Coronary Blood Flow

[Paleowoman]

Could someone please comment on the article below -- it's worrying me...:confused:

Angiology. (javascript:AL_get(this, 'jour', 'Angiology.');) 2000 Oct;51(10):817-26.Related Articles, (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=11108325&tool=ExternalSearch) Links (javascript:PopUpMenu2_Set(Menu11108325);)

The effect of high-protein diets on coronary blood flow.

Fleming RM (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&itool=PubMed_Abstract&term=%22Fleming+RM%22%5BAuthor%5D).

The Fleming Heart and Health Institute and the Camelot Foundation, Omaha, Nebraska 68114, USA. rfmd1@uswest.net

Recent research has demonstrated that successful simultaneous treatment of multiple risk factors including cholesterol, triglycerides, homocysteine, lipoprotein (a) [Lp(a)], fibrinogen, antioxidants, endothelial dysfunction, inflammation, infection, and dietary factors can lead to the regression of coronary artery disease and the recovery of viable myocardium. However, preliminary work revealed that a number of individuals enrolled in the original study went on popular high-protein diets in an effort to lose weight. Despite increasing numbers of individuals following high-protein diets, little or no information is currently available regarding the effect of these diets on coronary artery disease and coronary blood flow. Twenty-six people were studied for 1 year by using myocardial perfusion imaging (MPI), echocardiography (ECHO), and serial blood work to evaluate the extent of changes in regional coronary blood flow, regional wall motion abnormalities, and several independent variables known to be important in the development and progression of coronary artery disease. Treatment was based on homocysteine, Lp (a), C-reactive protein (C-RP), triglycerides, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and fibrinogen levels. Each variable was independently treated as previously reported. MPI and ECHO were performed at the beginning and end of the study for each individual. The 16 people (treatment group/TG) studied modified their dietary intake as instructed. Ten additional individuals elected a different dietary regimen consisting of a "high-protein" (high protein group/HPG) diet, which they believed would "improve" their overall health. Patients in the TG demonstrated a reduction in each of the independent variables studied with regression in both the extent and severity of coronary artery disease (CAD) as quantitatively measured by MPI. Recovery of viable myocardium was seen in 43.75% of myocardial segments in these patients, documented with both MPI and ECHO evaluations. Individuals in the HPG showed worsening of their independent variables. Most notably, fibrinogen, Lp (a), and C-RP increased by an average of 14%, 106%, and 61% respectively. Progression of the extent and severity of CAD was documented in each of the vascular territories with an overall cumulative progression of 39.7%. The differences between progression and extension of disease in the HPG and the regression of disease in the TG were statistically (p<0.001) significant. Patients following recommended treatment for each of the independent variables were able to regress both the extent and severity of their coronary artery disease (CAD), as well as improve their myocardial wall motion (function) while following the prescribed medical and dietary guidelines. However, individuals receiving the same medical treatment but following a high-protein diet showed a worsening of independent risk factors, in addition to progression of CAD. These results would suggest that high-protein diets may precipitate progression of CAI) through increases in lipid deposition and inflammatory and coagulation pathways.

Publication Types:
Clinical Trial (javascript:AL_get(this, 'ptyp', 'Clinical Trial');)

[Gaelen]

Welcome in! The comment I'll make on the fly is that this is an old study (in study reporting terms) and sentence three is already out of date. You can see more current (and more relevant) studies at www.nutritionandmetabolism.com And if this study concerns you, I'd hunt up more current information to refute it. It's out there, but you can't stop doing your homework with the first abstract you find, especially when that abstract is six years old in a constantly evolving field. Happy hunting!

[mcsblues]

It might also help to understand who Dr Richard Fleming is ... ;)

"In the PBS interview, Ornish claimed that research has shown diets like Atkins to worsen blood flow to the heart. His source for this frightening allegation? None other than Nebraska's Dr. Richard Fleming, the same Dr. Richard Fleming who came under attack earlier this year after he obtained the late Dr. Atkins' confidential death report under dubious circumstances and then passed it onto to his publicity-hungry associates at the PCRM. Like Ornish, Fleming is an outspoken critic of high-protein diets. Fleming also appears to have a special knack for obtaining negative findings about these regimens that no other researcher has ever been able to duplicate. In 2002, for instance, he presented the only published study to have ever found greater weight loss in individuals randomized to follow a high-carbohydrate, low-fat diet than those following a low carbohydrate diet. I have written at length elsewhere (http://www.theomnivore.com/Did%20the%20Atkins%20Diet%20really%20kill%20Dr%20A tkins.html) why this study is unlikely to be worth the paper it is written on.
The validity of Fleming's research that allegedly shows high-protein diets to impede blood flow to the heart is also extremely doubtful.
In August 2000, the journal Angiology published the results of an eight-month study by Fleming in which nineteen people "without prior history of documented heart disease" were assigned to a multi-faceted drug and dietary intervention, the aim of which was to halt the progression of atherosclerosis. Fleming wrote that, "…despite our best efforts, patients within the study subgrouped themselves unintentionally with three individuals deciding to go on a high-protein diet for varying periods of time during these 8 months."(25)
According to Fleming, those following his 15% protein, 70% carbohydrate, and 15% fat diet experienced reductions in homocysteine, triglycerides, and C-reactive protein (CRP), while the disobedient on-again, off-again high-protein dieters allegedly experienced an increase in all these variables. Furthermore, while the low-fat dieters reportedly experienced a regression of coronary artery disease (determined by echocardiography and myocardial perfusion imaging), the intermittent high-protein dieters allegedly experienced continued progression of atherosclerosis.
In October 2000, Fleming presented another paper reporting the twelve-month results of the same study. In this new paper, the study group had suddenly expanded to twenty-six individuals, with seven additional patients surfacing in the high-protein group. Why these additional high-protein dieters were never mentioned in the earlier paper was not explained, despite the claim that all twenty-six were followed for one year. Again, the hapless high-protein dieters were reported to fare much worse than the low-fat group; the low-fat dieters were claimed to have reduced the extent and severity of their atherosclerosis, while the high-protein group allegedly experienced a worsening of these variables.(26)
According to Fleming, increased CRP levels in the high-protein group were indicative of increased inflammatory activity, while the increase in homocysteine levels "…no doubt reflects an increased dietary loading of protein (methionine) and possibly increased physiologic stress". Exactly what Fleming means by the term "physiologic stress", and why a high-protein diet would cause an increase in this vague and all-encompassing syndrome, is anyone's guess.
His assertion that increased dietary methionine increases blood homocysteine levels is pure bunk; researchers have shown that dietary methionine has no effect upon homocysteine in humans.(27) What does raise homocysteine levels is deficient levels of vitamins B6, B12, and folic acid.
The richest source of B6 and B12 is meat (and organ meats in the case of folic acid). Not surprisingly, researchers have repeatedly found that omnivores display lower homocysteine levels than vegetarians.(28-30)
As for his alleged finding of increased CRP levels among the high-protein dieters, other researchers comparing high-protein, low-carbohydrate diets with low-fat diets have found no difference in CRP levels at maintenance calorie intakes, and greater reductions on low-carbohydrate diets at restricted calorie intakes.(31,32)
It is interesting to note that Fleming claims the renegade subjects went on and off the high-protein diet during his study, which effectively means they were alternately following multiple dietary patterns. Despite this, Fleming ascribes the blame for the alleged harmful changes solely to high-protein dieting.
Until someone who is not a fervent critic of high-protein and low-carbohydrate diets can replicate Fleming's extremely questionable findings, the Omaha cardiologist's research should not be cited as 'proof' that these diets are harmful.
It is most revealing that Ornish cites Fleming's doubtful research every chance he gets, but remains silent on the multitude of studies that totally contradict the latter's unusual findings."


http://www.theomnivore.com/Ornish.html