Re: Arteries as a function of present diet. Long reply HTML



Pritikin!!! that was the other name I could not recall....

thanks Jeff



"JEFF" <ROHDD@xxxxxxxxxxx> wrote in message
news:NDXze.7974$Eo.2315@xxxxxxxxxxxxx
> "Juhana Harju" <shantigiri@xxxxxxxxxxxxx> wrote in message
>
> "..........but it is not easy and it requires commitment."
>
> Pritikin program which is much less strict than Ornish will acomplish the
> same thing.
> J
> "On June 19, 1987, just two years after Nathan Pritikin's death, the
> Journal of the American Medical Association announced a study that showed
> regression of atherosclerosis in the coronary arteries of humans. The
> two-year study was done by David Blankenhorn and his associates at the
> University of Southern California in Los Angeles. Blankenhorn got his
> results by reducing the blood cholesterol of his patients by 26 percent, a
> drop similar to the one achieved at the Pritikin Longevity Centers. The
> scientists lowered blood cholesterol by using diet and drugs. However, the
> study made clear that a low-fat, low-cholesterol diet alone could achieve
> the same results.
>
> Blankenhorn's study provided the long-awaited "final proof" that
> atherosclerosis could, in fact, be reduced and even eliminated from the
> coronary arteries of people simply by lowering blood cholesterol.
>
> The study made front page headlines around the country because, for the
> first time, it showed that the underlying cause of most heart disease
> could be eliminated. "
>
> --------------
>
> Annals of internal medicine
>
> http://www.annals.org/
>
> Lipid Reduction by Diet Alone
>
> In the Leiden Intervention Trial [10], plasma lipid levels were modified
> by diet alone. A modest reduction (10.1%) in the total cholesterol value
> was achieved in 39 patients over the 2-year study period. Although overall
> progression was noted in 307 lesions (percent diameter stenosis by
> computer-assisted angiographic quantitation, 44.1% +/-31.6% at baseline
> and 48.6% +/-30.9% at follow-up), 18 patients had no worsening of lesion
> percent diameter stenosis. Notably, the total cholesterol level and the
> total cholesterol/high-density lipoprotein (HDL) cholesterol ratio were
> lower in patients without lesion progression than in patients with lesion
> progression (absolute change in mean vessel diameter, 0.002 +/-0.23 mm in
> patients with a total cholesterol/HDL cholesterol ratio <6.9 compared with
> 0.237 +/-0.32 mm in patients with a total cholesterol/HDL cholesterol
> ratio >6.9; P = 0.001).
>
> Lipid Reduction by Combined Diet and Lifestyle Changes
>
> In the Lifestyle Heart Trial [8], 41 patients were randomly assigned to
> either a change in both diet and lifestyle or no intervention and followed
> for 1 year. In the treatment group, total cholesterol was reduced by 24%,
> and low-density lipoprotein (LDL) cholesterol was reduced by 37%. Using
> computer-assisted quantitative angiographic methods, the investigators
> found 105 lesions at baseline angiography in the 22 patients receiving
> intervention and 95 lesions in the 19 controls. During the study period,
> the intervention group showed an overall decrease in percent diameter
> stenosis (40.4% +/-16.9% to 37.8% +/-16.5%), whereas controls showed an
> overall increase in percent diameter stenosis (42.7% +/-15.5% to 46.1%
> +/-18.5%; P = 0.001). In the intervention group, progression was noted in
> 4 (18%) patients, and regression was noted in 18 (82%); conversely, in the
> control group, no change or progression was noted in 11 patients (58%),
> and regression was found in 8 (42%).
>
> In a similar study of 113 patients randomly assigned to usual care or diet
> and exercise (but no drug therapy), body weight decreased by 5%, total
> cholesterol decreased by 10%, triglycerides decreased by 24%, and HDL
> cholesterol increased by 3% in the treatment group [12]. Paired coronary
> arteriograms obtained 12 months apart were analyzed using
> computer-assisted methods, and a change in lesions of more than 10% in
> diameter stenosis or of 0.18 mm in minimal luminal diameter was scored as
> lesion progression (+1), lesion regression (-1), or no change [0]. Segment
> scores were added to show an overall net change. In the treatment group,
> 30% of patients showed regression, 50% of patients had no change, and 20%
> of patients had progression. In the control group, 42% of patients showed
> progression, 54% had no change, and 4% showed regression (P = 0.03). The
> average change in minimal luminal diameter for the 122 lesions was 0.0
> +/-0.38 mm in the treatment group and -0.13 +/-0.45 mm in the control
> group (P = 0.01).
>
> Lipid Reduction by Drug Therapy
>
> The National Heart, Lung, and Blood Institute study tested the effect of
> cholestyramine on coronary atherosclerosis in 116 hyperlipidemic patients;
> cholesterol levels in treated patients were reduced by 26% [11]. Paired
> baseline and 5-year cineangiograms were analyzed subjectively by a
> majority consensus of three observers. Patients were classified as showing
> definite lesion progression (at least one lesion with definite
> progression, no lesion with regression), probable lesion progression (at
> least one lesion with probable progression, no lesion with either definite
> regression or definite progression), probable lesion regression (at least
> one lesion with probable regression, no lesion with either definite
> regression or definite progression), definite lesion regression (at least
> one lesion with definite regression, no lesion with progression), mixed
> lesion response (both progression and regression in the same patient), and
> no lesion change. Using these criteria, the study found probable lesion
> progression in 32% of treated patients and 49% of control patients and
> definite progression in 25% and 35% of treated and control patients,
> respectively. Because many patients showed a mixed lesion response,
> statistically significant differences in the primary analysis were not
> observed. In the Cholesterol Lowering Atherosclerosis Study [13], 162 men
> receiving coronary bypass grafting were randomly assigned to treatment
> with colestipol and nicotinic acid or to placebo. Reductions of 26% in
> total cholesterol and 43% in LDL cholesterol and an increase of 37% in HDL
> cholesterol were observed in treated patients after 2 years of follow-up.
> In addition, new lesions developed in 10% of treated patients and in 22%
> of placebo recipients during the 2-year period. By 4 years [18], the
> frequency of new lesion development was 14% in treated patients and 38% in
> placebo recipients (P = 0.001). Furthermore, 18% of lesions in the treated
> group had regressed compared with 6% of lesions in the placebo group (P =
> 0.04); similarly, 52% of lesions in the treated group had not progressed
> compared with 15% of lesions in the placebo group (P < 0.001).
>
> In the Familial Atherosclerosis Treatment Study [7], 146 patients with
> angiographic evidence of coronary artery atherosclerosis and at least one
> segment of significant stenosis, a familial history of coronary artery
> disease, and elevated lipid concentrations were randomly assigned to
> conservative therapy, treatment with a combination of lovastatin and
> colestipol, or treatment with niacin and colestipol. In the two treatment
> groups, LDL concentrations decreased (46% in the lovastatin-colestipol
> group and 32% in the niacin-colestipol group) and HDL concentrations
> increased (15% and 43%, respectively) significantly. Paired angiograms
> were analyzed using the worst stenosis in each of nine standard proximal
> segments of the three major epicardial coronary arteries. The average
> percent diameter stenosis of the worst lesion in all segments was
> calculated, and regression or progression was expressed as the change in
> this value between the baseline and follow-up angiograms. In the placebo
> group, the mean percent diameter stenosis progressed by +2.1% +/-3.9%; in
> the niacin-colestipol group, the mean percent diameter stenosis
> regressed -0.9% +/-3.0%; in the lovastatin-colestipol group, the mean
> percent diameter stenosis regressed -0.7% +/-5.3% (P = 0.003). Similarly,
> the mean change in minimal lesion diameter was -0.05 +/-0.14 mm in the
> placebo group, +0.035 +/-0.13 mm in the niacin-colestipol group, and
> +0.012 +/-0.16 mm in the lovastatin-colestipol group (P = 0.01). In the
> placebo group, lesion progression was noted in 46% of lesions, lesion
> regression in 11% of lesions, and no change in 43% of lesions. In the
> niacin-colestipol group, lesion progression was noted in 25% of lesions,
> regression in 39% of lesions, and no change in 36% of lesions. In the
> lovastatin-colestipol group, lesion progression was noted in 21% of
> lesions, lesion regression in 32% of lesions, and no change in 47% of
> lesions. Only 5 of the 120 patients had a mixture of segment progression
> and regression.
>
> Lipid Reduction by Diet plus Medication
>
> In a trial of 72 patients with heterozygous familial hypercholesterolemia
> [15], patients were randomly assigned either to diet and low-dose
> colestipol or to diet, high-dose colestipol, and niacin (switching to
> lovastatin when it became available). Paired angiograms obtained 26 months
> apart were analyzed using criteria similar to those used in the Familial
> Atherosclerosis Treatment Study [7]. Notably, only three patients had
> objective evidence of coronary artery disease before the initial
> angiogram. In the low-dose colestipol group, LDL cholesterol levels
> decreased 38.1%, serum triglycerides decreased 18.9%, and HDL cholesterol
> levels increased 28%. In the 457 lesions analyzed, mean change in percent
> area stenosis was +0.80% +/-5.07% in the low-dose colestipol group
> and -1.53% +/-4.34% in the high-dose colestipol group (P = 0.039).
> Moreover, in the low-dose colestipol group, 13 patients had definite
> lesion progression and 4 had definite lesion regression; in the high-dose
> colestipol group, 8 had lesion progression and 13 had lesion regression (P
> = 0.06).
>
> In the St. Thomas' Atherosclerosis Regression Study [16], 90 men with
> coronary artery disease and mild hypercholesterolemia were randomly
> assigned to usual care, diet alone, or diet and cholestyramine. Patients
> assigned to diet alone showed a 14.2% decrease in total cholesterol and a
> 16.2% decrease in LDL. Those assigned to diet and cholestyramine showed a
> 25.3% decrease in total cholesterol and a 35.7% decrease in LDL. Paired
> angiograms obtained 39 months apart were analyzed using computer-assisted
> methods, and the mean lesion diameter of 13 arterial segments was
> obtained. Notably, the mean arterial diameter progressed in the usual care
> group by 0.201 +/-0.062 mm, regressed by 0.003 +/-0.087 mm in the diet
> alone group, and regressed by 0.103 +/-0.051 mm in the diet plus
> cholestyramine group (P = 0.012). Overall progression was less frequent in
> the diet group (15%) and the diet plus cholestyramine group (12%) than in
> the control group (46%, P = 0.01). Similarly, the proportion of patients
> who showed overall improvement in mean luminal diameter was greater in the
> diet group (38%) and in the diet plus cholestyramine group (33%) than in
> the control group (4%, P = 0.01).
>
> Cites:
>
> 7. Brown G, Albers JJ, Fisher LD, Schaefer SM, Lin JT, Kaplan C, et al.
> Regression of coronary artery disease as a result of intensive
> lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl
> J Med. 1990;323:1289-98.[Abstract]
>
> 8. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA,
> et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle
> Heart Trial. Lancet. 1990;336:129-33.[Medline]
>
> 10. Arntzenius AC, Kromhout D, Barth JD, Reiber JH, Bruschke AV, Buis B,
> et al. Diet, lipoproteins, and the progression of coronary
> atherosclerosis. The Leiden Intervention Trial. N Engl J Med.
> 1985;312:805-11.[Abstract]
>
> 11. Brensike JF, Levy RI, Kelsey SF, Passamani ER, Richardson JM, Loh IK,
> et al. Effects of therapy with cholestyramine on progression of coronary
> atherosclerosis: Results of the NHLBI Type II Coronary Intervention Study.
> Circulation. 1984;69:313-24.[Abstract]
>
> 12. Schuler G, Hambrecht R, Schlierf G, Niebauer J, Hauer K, Neumann J, et
> al. Regular physical exercise and low-fat diet. Effects on progression of
> coronary artery disease. Circulation. 1992;86:1-11.[Abstract]
>
> 13. Blankenhorn DH, Nessim SA, Johnson RL, Sanmarco ME, Azen SP,
> Cashin-Hemphill L. Beneficial effects of combined colestipol-niacin
> therapy on coronary atherosclerosis and coronary venous bypass grafts.
> JAMA. 1987;257:3233-40.[Abstract]
>
> 14. Brown BG, Lin JT, Kelsey S, Passamani ER, Levy RI, Dodge HT, et al.
> Progression of coronary atherosclerosis in patients with probable familial
> hypercholesterolemia. Quantitative arteriographic assessment of patients
> in NHLBI type II study. Arteriosclerosis. 1989;9(Suppl I):I81-90.
>
> 15. Kane JP, Malloy MJ, Ports TA, Phillips NR, Diehl JC, Havel RJ.
> Regression of coronary atherosclerosis during treatment of familial
> hypercholesterolemia with combined drug regimens. JAMA.
> 1990;264:3007-12.[Abstract]
>
> 16. Watts GF, Lewis B, Brunt JN, Lewis ES, Coltart DJ, Smith LD, et al.
> Effects on coronary artery disease of lipid-lowering diet, or diet plus
> cholestyramine, in the St Thomas' Atherosclerosis Regression Study
> (STARS). Lancet. 1992;339:563-9.[Medline]
>
>


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