When Ornish talks, I listen

[Guest guest]

Hi All,

When Ornish talks, I listen.

I have heard the criticisms of the Ornish diet. Lifestyle factors

being altered does affect the outcome, I would agree. Motivation

is important.

Still, there is:

" 10%-fat, whole-foods diet

low in saturated fat and refined carbohydrates and high in complex

carbohydrates decreased LDL cholesterol levels by an average of 40%

after 1 year in patients not taking lipid-lowering drugs (5). Also,

patients lost 24 pounds during the first year and had kept off more

than half of that weight 5 years later while controls following an

AHA/NCEP diet did not lose weight. Exercise levels between the

groups were not significantly different. "

and

" Myocardial perfusion improved on a

very low-fat whole foods diet but worsened on the Atkins diet (9).

Advocates of a low-carbohydrate diet must prove its efficacy in ran-

domized,

controlled trials using direct measures of cardiovascular

disease, not just risk factors or epidemiologic studies, especially

since

diets high in saturated fat and red meat are linked to heart disease,

cancer, osteoporosis, and renal disease. "

and

" We need to move beyond the simplistic notion that whatever

raises high-density lipoprotein (HDL) cholesterol levels is beneficial

and anything that lowers them is harmful. High-density lipoprotein

cholesterol levels may decrease in patients who reduce dietary fat and

cholesterol intake because their need for HDL cholesterol is not as

great—in simple terms, when you have less garbage, you need fewer

garbagemen. "

Please see the below.

COMMENTS AND RESPONSES

2 Nov 2004 Ann Intern Med. 141, (9) 738-739.

Dean Ornish

Low-Carbohydrate Diets

TO THE EDITOR:

Although purporting to show that a low-carbohy-drate

" Atkins " diet is more beneficial than a conventional " low-fat "

American Heart Association/National Cholesterol Education Pro-gram

(AHA/NCEP) diet, the studies by Yancy and Stern and co-workers

(1, 2) showed that neither diet effectively decreases weight or

levels of low-density lipoprotein (LDL) cholesterol. In both studies,

LDL cholesterol levels did not change significantly and there were no

significant differences in weight after 1 year (only about 3% weight

loss). Similar findings were also seen in an earlier study (3).

The conventional AHA/NCEP " low-fat " diet is not very low in

fat or cholesterol and reduces LDL cholesterol levels by only 5% in

most patients, if at all (4). Since this diet is often high in refined

carbohydrates (which increase triglyceride levels), low-carbohydrate

diets often show greater reductions in triglyceride levels, especially

when patients take fish oil. In contrast, a 10%-fat, whole-foods diet

low in saturated fat and refined carbohydrates and high in complex

carbohydrates decreased LDL cholesterol levels by an average of 40%

after 1 year in patients not taking lipid-lowering drugs (5). Also,

patients lost 24 pounds during the first year and had kept off more

than half of that weight 5 years later while controls following an

AHA/NCEP diet did not lose weight. Exercise levels between the

groups were not significantly different.

Risk factors such as lipids and lipoproteins must be distin-guished

from direct measures of disease. Studies using serial coronary

arteriography to assess patients consuming an AHA/NCEP diet

showed that coronary atherosclerosis worsened in most (4). In con-

trast,

patients who followed an unrefined foods diet with only 10%

fat (mostly fruits, vegetables, whole grains, and legumes) had signif-

icant

regression of coronary atherosclerosis after 1 year on quantita-tive

coronary arteriography and even more regression after 5 years

(5). In addition, they had 2.5 times fewer cardiac events than con-

trols

following an AHA/NCEP diet, who showed more progression

of atherosclerosis after 5 years than after 1 year. There was a direct

correlation between intake of dietary cholesterol and total fat and

changes in coronary atherosclerosis. Others have found similar results

(7). Also, 99% of experimental group patients stopped or reversed

the progression of coronary heart disease, as measured by cardiac

positron emission tomography scans (8).

Only 1 peer-reviewed study examined the effects of the Atkins

diet on cardiovascular disease. Myocardial perfusion improved on a

very low-fat whole foods diet but worsened on the Atkins diet (9).

Advocates of a low-carbohydrate diet must prove its efficacy in ran-

domized,

controlled trials using direct measures of cardiovascular

disease, not just risk factors or epidemiologic studies, especially

since

diets high in saturated fat and red meat are linked to heart disease,

cancer, osteoporosis, and renal disease.

The harmful effects of a high-fat diet may be mediated through

other mechanisms besides traditional risk factors. For example, di-

etary

fat intake increases plasma levels of factor VII coagulant activity

(4). Indeed, 1 man in the low-carbohydrate group in Yancy and

colleagues' study (1) developed angina and coronary artery disease

near the end of the study even though his risk factors had improved,

and a patient in Stern and colleagues' study died of ischemic cardio-

myopathy

(2).

We need to move beyond the simplistic notion that whatever

raises high-density lipoprotein (HDL) cholesterol levels is beneficial

and anything that lowers them is harmful. High-density lipoprotein

cholesterol levels may decrease in patients who reduce dietary fat and

cholesterol intake because their need for HDL cholesterol is not as

great—in simple terms, when you have less garbage, you need fewer

garbagemen. No data prove that physiologic reduction of HDL cho-

lesterol

levels with a low-fat diet is detrimental (10).

The debate should not focus only on low carbohydrate versus

low fat. Patients have a spectrum of dietary choices. To the degree

that they reduce their intake of refined carbohydrates and excessive

fats and increase their intake of unrefined carbohydrates (fruits,

veg-etables,

whole grains, legumes) and sufficient -3 fatty acids, they

may feel better, lose weight, and gain health.

References

1. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-

carbohydrate,

ketogenic diet versus a low-fat diet to treat obesity and

hyperlipidemia: a randomized,

controlled trial. Ann Intern Med. 2004;140:769-77. [PMID: 15148063]

2. Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, et

al. The effects

of low-carbohydrate versus conventional weight loss diets in severely

obese adults:

one-year follow-up of a randomized trial. Ann Intern Med.

2004;140:778-85. [PMID:

15148064]

3. GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS,

et al. A

randomized trial of a low-carbohydrate diet for obesity. N Engl J

Med. 2003;348:

2082-90. [PMID: 12761365]

4. Ornish D. Intensive lifestyle changes in the management of

coronary heart disease.

In: Braunwald E, ed. on's Advances in Cardiology. New York:

McGraw-Hill;

2002.

5. Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt

TA, et al.

Intensive lifestyle changes for reversal of coronary heart disease.

JAMA. 1998;280:

2001-7. [PMID: 9863851]

6. Ornish D. Was Dr Atkins right? J Am Diet Assoc. 2004;104:537-42.

[PMID:

15054336]

7. Esselstyn CB Jr. Updating a 12-year experience with arrest and

reversal therapy for

coronary heart disease (an overdue requiem for palliative

cardiology). Am J Cardiol.

1999;84:339-41, A8. [PMID: 10496449]

8. Gould KL, Ornish D, Scherwitz L, Brown S, Edens RP, Hess MJ, et

al. Changes in

myocardial perfusion abnormalities by positron emission tomography

after long-term,

intense risk factor modification. JAMA. 1995;274:894-901. [PMID:

7674504]

9. Fleming RM. The effect of high-protein diets on coronary blood

flow. Angiology.

2000;51:817-26. [PMID: 11108325]

10. Connor WE, Connor SL. Should a low-fat, high-carbohydrate diet be

recom-mended

for everyone? The case for a low-fat, high-carbohydrate diet. N Engl

J Med.

1997;337:562-3. [PMID: 9262503]

Frederick F. Samaha, MD

Stern, MD

2 Nov 2004 Ann Intern Med. 141, (9) 739

IN RESPONSE: We share Dr. Ornish's concerns that neither the

conventional low-fat diet nor the low-carbohydrate diet in our study

reduced total or LDL cholesterol levels. The scientific evidence that

aggressive LDL cholesterol lowering reduces atherosclerosis and isch-

emic

coronary events is strong, although complicated by concomi-tant

beneficial effects on inflammatory markers such as C-reactive

protein. The evolving data regarding the long-term benefits of in-

Letters

creasing HDL cholesterol levels and lowering triglyceride levels, at

least by pharmacologic means, are also promising with regard to

impact on coronary heart disease (1). Moreover, abnormal levels of

HDL cholesterol and triglycerides are core features of the metabolic

syndrome, which has been strongly associated with atherosclerosis

(2). Nevertheless, we agree that extrapolation of these findings to

dietary effects on HDL cholesterol may be complicated by unknown

effects on reverse cholesterol transport.

The referenced study of patients following an extremely low-fat

diet (3) provided important preliminary findings regarding favorable

effects of this diet on LDL cholesterol levels and coronary artery

disease. However, this study was also limited by its small size (40

patients) and by uncontrolled confounding variables, such as limiting

counseling on exercise, smoking cessation, and stress management to

the experimental group. The experimental group also lost more

weight. In contrast, a much larger study of 423 patients following a

Mediterranean diet that did not severely restrict fat decreased long-

term

cardiovascular event rates (4). In truth, we still do not know the

ideal dietary composition to prevent cardiovascular disease and in-

crease

weight loss. A focus on fat restriction that results in excessive

refined carbohydrate intake would be expected to exacerbate features

of the metabolic syndrome and thus may increase cardiovascular risk.

We hope the available studies show that the ideal goals of dietary

modification should be to reduce LDL cholesterol levels and improve

features of the metabolic syndrome. A diet that helps attain either of

these goals merits further investigation to determine its impact on

long-term cardiovascular outcomes.

We also want to clarify that the patient in our study with an

ischemic cardiomyopathy already had this condition before enroll-ment,

as stated in the manuscript.

Frederick F. Samaha, MD

Stern, MD

References

1. Rubins HB, Robins SJ, D, Fye CL, JW, Elam MB, et

al. Gem-fibrozil

for the secondary prevention of coronary heart disease in men with

low levels of

high-density lipoprotein cholesterol. Veterans Affairs High-Density

Lipoprotein Cho-lesterol

Intervention Trial Study Group. N Engl J Med. 1999;341:410-8. [PMID:

10438259]

2. Solymoss BC, Bourassa MG, Campeau L, Sniderman A, Marcil M,

Lesperance J, et

al. Effect of increasing metabolic syndrome score on atherosclerotic

risk profile and

coronary artery disease angiographic severity. Am J Cardiol.

2004;93:159-64. [PMID:

14715340]

3. Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt

TA, et al.

Intensive lifestyle changes for reversal of coronary heart disease.

JAMA. 1998;280:

2001-7. [PMID: 9863851]

4. de Lorgeril M, Salen P, JL, Monjaud I, Delaye J, Mamelle N.

Mediterranean

diet, traditional risk factors, and the rate of cardiovascular

complications after myocar-dial

infarction: final report of the Lyon Diet Heart Study. Circulation.

1999;99:779-

85. [PMID: 9989963]

Cheers, Alan Pater