480 EDITORIAL COMMENTS

tional intakes, frequency and prevention of complications, psychological aspects, cost-effectiveness, role of care givers, etc.) is very different from what it had been for long-term HPN patients. All these items are open questions for short- term HPN populations, and prospective clinical trials in these subgroups of patients are now mandatory. Since performance of such trials could be limited by cultural, emotional, and economic forces, the role of national and supranational scien- tific societies and authorities is to initiate and support these works.

A. VAN GOSSUM, MD Medico-Surgical Department of Gastroenterology

HBpital Erasme UniversitC Libre de Bruxelles

Brussels, Belgium

B. MESSING, MD Medical Department of Gastroenterology

and Nutritional Support Services H6pital St. Lazare and Lariboisibre

Paris, France

REFERENCES

Shils ME, Wright WL, Tumbull A, et al. Long-term parenteral nutrition through external arteriovenous shunt. N Engl J Med 1970;283:341 Jeejeebhoy KN, Zohrab W, Langer B, et al. Total parenteral nutri- tion at home for 23 months, without complication and with good rehabilitation. Gastroenterology 1973;65:811 Fleming CR, McGill DB, Berkner S. Home parenteral nutrition as

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

primary therapy in patients with extensive Crohn’s disease of the bowel and malnutrition. Gastroenterology 1977;73: 1077 Van Gossum A, Espen-Han Group. Home parenteral nutrition (HPN) in adults: a multicentre survey in Europe in 1993. Clin Nutr 1996; 15:60 Messing B, Landais P, Goldfarb B, et al. Home parenteral nutrition in adults: a multicentre survey in Europe. Clin Nutr 1989;8:3 Howard L, Ament M, Fleming CR, et al. Current use and clinical outcome of home parenteral and enteral nutrition therapies in the United States. Gastroenterology 1995; 109:355 Takagi Y, Okada A. Candidates for small bowel transplantation: our experience and survey of home parenteral nutrition in Japan. Transplant Proc 1994; 26: 1446 Freund H, Rimon B. Home parenteral nutrition in Europe 1993 (letter). Clin Nutr 1996; 15:339 Dudrick SJ, Englert DM, Van Buren CT, et al. New concepts of ambulatory home hyperalimentation. JPEN 1979;3:72 Detsky AS, McLaughlin JR, Abrams HB, et al. A cost-utility analy- sis of the HPN urogramme at Toronto General Hosnital: 1970- 1982. JPEN 1986; l&49

Messing B, Lemann M, Landais P, et al. Prognosis of patients with non-malignant chronic intestinal failure receiving long-term home parenteral nutrition. Gastroenterology 1995; 108: 1005 Smith C. Quality of life in long-term total parenteral nutrition pa- tients and their family care givers. JPEN 1993; 17:501 Detsky A, McLaughlin JR, Abrams H, et al. A cost-utility analysis of the HPN programme at Toronto General Hospital: 1970- 1982. JPEN 1986; 15:384 Howard L. Home parenteral and enteral nutrition in cancer patients. Cancer 1993; 72:353 1 Elia M. An international perspective on artificial nutritional support in the community. Lancet 1995;345: 1345 Messing B. Nutrition parent&ale de longue dur&e chez l’adulte. Nutr Clin Metabol 1996; 10: 167

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Nutrition Vol. 13, No. 5, 1997

Healthy Body Weight Standards Let’s stop using height-weight tables as “health standards”

appropriate for all. They are not. Weights recommended as healthy for adults usually range from 19-25 kg/m* of height, known as body mass index (BMI). This range represents BMIs statistically associated with lowest morbidity or mortality rates in large epidemiologic studies. Although important for popula- tion comparisons and evaluations, “statistically best weights” have limited predictive value of health for genetically diverse individuals. Low correlations and coefficient of determination between BMI and risk factors indicate that body weight ex- plains little of the total variance and that healthy weights for many may be outside of the statistically “healthy” range.

We believe that use of these tables as authoritative indicators of health cause more harm than good.‘,’ The greatest harm comes when they are applied to very overweight people who have little chance of attaining a statistically desirable weight. Changes in diet and exercise habits to produce improved fitness and modest weight loss will greatly ameliorate health parame- ters in most severely overweight individuals far before they reach a BMI of 25. It is wrong and harmful to incorrectly suggest that health can only be attained by a weight that falls

within some standard “healthy” range. It is equally wrong to suggest that all persons who have weights that fall within the prescribed range have “healthy weights.” High rates of an- orexia and bulimia nervosa may be caused, in part, by repeated emphasis on thinness undergirded by these tables. The “be thin at any cost attitude,” so prevalent in young females, contributes to unhealthy ways to regulate weight, such as smoking and pathogenic eating and exercise habits. Standard height-weight tables are frequently used to justify social or job discrimination against those whose weight exceeds the desirable weight stan- dards. For these reasons and those outlined below, scientists should not focus on “aesthetically” or “statistically desirable weights” for individuals, but should focus on ways to improve health status through prudent fitness and dietary habits.

The highly variable nadirs of statistically best BMI for health from various studies vary from 20 or less to 2.5 or more de- pending on age, sex, diet (vegetarians versus nonvegetarians), smoking status, length of the study, economic status, and the dependent variable measured (mortality or morbidity). For ex- ample, the lowest mortality rate occurred in the lowest BMI group ( 52 1) of Seventh Day Adventist adult men.3 This group

EDITORIAL COMMENTS

also ate the most fruits and vegetables, and smoked the least. Similar results were found for nonsmoking, stable-weight nurses for whom early deaths were excluded in a 16-y cohort study.” BMIs of 20 or below are almost always associated with the lowest prevalence and incidence rates of type II diabetes mellitus. At the other end of the spectrum, a recent meta-analy- sis’ of 17 cohort studies with adult men using mortality rates as the endpoint yielded best BMIs of 23-28, which are 527% above midpoint values in the “ 1959 Desirable Weight Tables.” In adults who are relatively old, or have existing diseases such as diabetes mellitus or hypertension, higher BMIs are usually associated with increased survival rates. For example, Chaturvedi et al.,h based on a cohort study of men and women with type 1 diabetes mellitus from nine centers worldwide, concluded that except in very lean persons who have high mortality rates, body weight is not significantly associated with mortality.

Despite the diversity in results and low coefficients of deter- mination, many health scientists use a narrow BMI range as an indicator of health and specific BMI cutoff for loss of health for all. An increasing number of scientists are objecting to the misuse of these standards. Ernsberger,’ for example, stated, “Instead of the current focus on maintaining weight within set limits, physicians should emphasize appropriate diet composi- tion (low-fat, high-fiber) and exercise for all their patients.” Sims.’ with similar views on the appropriate use of height- weight tables. noted:

I heartily agree that to emphasize maintenance of body weight within the narrow limits prescribed by the life in- surance people or the NIH Consensus statement is inappro- priate, and would add that the Metropolitan Life Insurance Tables, 1959 and 1983, with their attempt at using height and weight to define “Desirable” weights applicable to all comers. should be placed in a medical museum.

Keys,” a long-time opponent of misuse of height-weight tables, also noted, ‘.. . the risk of premature death is not a simple direct function of relative body weight. Apparently this fact, well established from various prospective studies, is not yet common knowledge in the medical profession, let alone the general public.” Fitzgerald and Jarrett”’ have concluded that “until we have a better understanding of the confounding vari- ables. the relation between body weight and mortality will re- main enigmatic.”

Proponents of ‘-healthy-weight tables” acknowledge the low correlations between mortality and morbidity rates and BMI in nonsmoking populations, but argue that the correlations are suppressed because BMI is not a direct measure of body- fat percentage (%BF) A high %BF is viewed as the cause of health risks associated with high BMIs, whereas a high percent- age of muscle is seen as protective. This perspective is exempli- fied in the fourth edition of Dietary Guidelinesfor Americans" : “Weight ranges are shown in the chart because people of the same height may have equal amounts of body fat but different amount of muscle and bone. . . The higher weights in the healthy weight range apply to people with more muscle and bone.” The weakness of the association between BMI, as a surrogate for %BF, and mortality rate, however, is not directly related to the fact that BMI is an inconsistent indicator of %BF. Several epidemiologic studies have found that BMI is statistically equivalent or superior to %BF as an indicator of health risk.“.” Animal studies, likewise, have shown that nei- ther body size nor %BF is an acceptable indicator of health. Bertrand et al.‘” observed that %BF did not affect longevity in inbred, ad libitum-fed animals. But, when feed intake was restricted to increase longevity, animals with the highest %BF lived longest. Harrison et al.” found that genetically fat ob/ob

481

mice with 67% BF lived only 68% as long as their thin siblings with 22% BF when both groups were fed ad libitum. However, when feed was restricted to extend longevity, the genetically obese animals lived 14% longer than the thin ad libitum-fed controls even though the %BF remained more than two times as high in the genetically obese animals (48 versus 22% BF) Boissonneault et a1.16 showed that an increase in %BF from 16 to 24% in rats produced by feeding a high-fat diet was associ- ated with a dramatically higher rate of carcinogen-induced mammary cancers when the diet was fed ad libitum, but with a dramatically lower rate when the diet was fed at 80% ad libitum. Obesity is associated with many health risks, but nei- ther a high body weight nor a high %BF per se, is directly the cause of these problems. As fat cells enlarge in response to a chronic positive energy balance and can no longer adequately remove excesses of glucose and lipids from the blood, insulin resistance develops. The enlarged fat cells secrete more leptin ” and tumor necrosis factor-alpha ( TNF-cu ) .” Increased levels of TNF-Q have been suggested as an important factor in the development of insulin resistance, which is believed to underlie hyperglycemia, hypertension, and dyslipidemias, the primary risks associated with obesity. These problems. called syndrome X, can be alleviated only by reducing the level of glucose and lipids to which fat cells are exposed, or by reducing fat-cell size, thereby restoring their ability to store any excesses of these substances circulating in the blood. Methods that accom- plish these changes are reduced caloric intake, increased energy expenditure, or reduced absorption through gastric surgery. It is unnecessary to reduce %BF or body size to “normal” to eliminate most or all of the risk associated with obesity. This fact has been demonstrated repeatedly. Insulin levels and other indicators of fat-cell function change more per BMI unit with weight loss than with weight gain.‘” Blair’” has shown, for example, that obesity-related risks are low in “fit” individuals whether they are obese or not. The goal to maintain or restore fat-cell function through improved exercise and dietary habits and modest weight loss is a more promising strategy than the more difficult and medically unnecessary goal of attaining a “healthy weight” for everyone. We believe Sims’ call to place desirable height-weight tables in a medical museum should be implemented now. The change in emphasis between the 1990” and 1995” “ Dietary Guidelines for Americans” from “main- tain a healthy weight” to “balance the food you eat with physi- cal activity to maintain or improve your weight“ is an important step in the right direction.

R. PAUL ABERNATHY, PHD Department of Foods and Nutrition

DAVID R. BLACK, PHD Department of Health, Kinesiology, and Leisure Studies

Purdue University West Lafayette, Indiana, USA

REFERENCES

I.

2.

3.

4.

5.

Abernathy RP, Black DR. Is adipose tissue oversold as a health risk? .I Am Diet Assoc 1994;94:641 Abernathy RP, Black DR. Healthy body weights: an alternative perspective. Am .I Clin Nutr 1996;63( supp1.)448S Linsted K, Tonstad S, Kuzma JK. Body mass index and patterns of mortality among Seventh-day Adventist men. Int J Obes 1991; 15:397 Manson JE, Willett WC, Stampfer MJ, et al. Body weight and mortality among women. N Engl J Med 1995;333:677 Troiano RP, Frongillo EA, Jr, Sobal J, Levitsky DA. The relation- ship between body weight and mortality: a quantitative analysis of

482 EDITORIAL COMMENTS

6.

7.

8.

9.

10.

11.

12.

13.

14.

combined information from existing studies. Int J Obesity 1996; 20:63 Chaturvedi N, Stevens LK, Fuller JH. Mortality and morbidity associated with body weight in people with IDDM. The WHO Multinational Study of Vascular Disease in Diabetes. Diabetes Care 1995; 18761 Emsberger P. Obesity is hazardous to your health: negative. De- bates in Med 1989;2:103 Sims EAH. Obesity is hazardous to your health: affirmative. De- bates in Med 1989;2: 103 Keys A. Is there an ideal body weight (letter). Br Med J 1986;293:1023 Fitzgerald AP, Jarrett RJ. Body weight and coronary heart disease mortality: an analysis in relation to age and smoking habit. 15 years follow-up data from Whitehall Study. Int J Obesity 1992; 16:119 Dietary Guidelines for Americans, 4th ed. Washington DC: USDA, USHHS. Home and Garden Bulletin No. 232, 1995; 17:21 Spiegelman D, Israel RG, Bouchard C, Willett WC. Absolute fat mass, percent body fat, and body-fat distribution: which is the real determinant of blood pressure and serum glucose? Am J Clin Nutr 1992;55:1033 Weinsier RL, Norris DJ, Birch R, et al. The relative contribution of body fat and fat pattern to blood pressure level. Hypertension 1985;7:578

15.

16.

17.

18.

19.

20.

21.

mass and cellularity in adult life of rats fed ad libitum or a life- promoting restricted diet. J Gerontol 1980;35:827 Harrison DE, Archer JR, Astole CM. Effect of food restriction on aging: separation of food intake and adiposity. Proc Nat1 Acad Sci USA 1984;81:1835 Boissonneault GA, Elson CE, Pa&a NM. Net energy effects on dietary on chemically induced mammary carcinogenesis in F344 rats. J Nat1 Cancer Inst 1986; 117: 1164 Houseknecht KL, Flier SN, Frevert EU, et al. Leptin secretion by the adipocyte: regulation with genetic and dietary obesity and search for an intracellular storage pool (abstract). Exp Clin Endo- crinol Diabetes 1996; 104(stmol 2):8 Hotamisligil GS, Peraldi Pi B;hav&i A, et al. IRS-mediated inhibi- tion of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. Science 1996; 27 1:665 Strain G, Zumoff B, Rosner W, Pi Sunyer X. The relationship between serum levels of insulin and sex hormone binding globulin in man: the effect of weight loss. J Clin Endocrinol Metab 1994;79:1173 Blair SN. Abstract, ILSI 1996 Annual Meeting, Cancun, Mexico; January 22-24, 1996 Dietary Guidelines for Americans, 3rd ed. Washington, DC: USDA, USHHS. Home and Garden Bulletin, 1990

Bertrand HA, Lynd FT, Masoro ET, Yu BP. Changes in adipose PI1 SO899-9007(97)00116-O

Nutrition Vol. 13, No. 5, 1997

Glucocorticoids and Energy Expenditure: Relevance to the Regulation of Energy

Balance in Man

From the observations of patients with abnormal secretion of glucocorticoids, it has long been known that these hormones alter the energy balance equation. Weight gain and obesity are observed in more than 90% of patients with Cushing’s syndrome, ’ and weight loss and anorexia are frequent features of Addison’s disease.’ All three terms of this equation, i.e., energy intake, energy expenditure, and energy stores, are af- fected by excessive or insufficient glucocorticoid secretion. In the past 10 y a renewed interest for this subject has been brought about by the results of two areas of research: first, the abnormal- ities in energy storage associated with excess glucocorticoids, i.e., increased body weight and abdominal fatness, have been recognized as major predicting factors for cardiovascular dis- eases.3 Secondly, research in rodents has shown not only that obesity could be prevented by adrenalectomy in most experi- mental models,4 but also that glucocorticoids, together with insulin, regulate food intake and fat deposition5 The recent findings that the messenger RNAs for leptin, a protein that is produced by adipose tissue and regulates food intake,6 and for neuropeptide Y,’ a peptide that stimulates food intake, are controlled by glucocorticoids emphasize the importance of these hormones in the regulation of energy balance.

The relevance of these discoveries for the understanding of energy balance regulation in humans and of its most common disorder in developed countries, obesity, is still far from being clear. Methodologic difficulties render this area of research difficult. Abnormalities in cortisol secretion or in the respon- siveness of the hypotbalamo-pituitary-adrenal axis (HPA) have been described in some obese individuals.’ These findings sug- gest that a relatively excessive secretion of cortisol may be in part responsible for obesity. Whether these disturbances in cortisol secretion are a cause or a consequence of obesity is not known however.

The ability to inhibit the glucocorticoid receptor in man with RU 486 offers a research tool and may help to understand the role of cortisol in energy balance regulation. RU 486 is a potent antagonist of glucocorticoid action because of its affinity for the GR receptor.’ Blockade of the GR receptor at the hypothalamo- pituitary level induces an increase in HPA activity and stimu- lates cortisol secretion. The administration of this drug, there- fore, has two consequences: the stimulation of the secretion of corticotropin-releasing factor (CRF) and corticotropin (ACTH), and stimulation of cortisol secretion. We believe that this in- creased secretion of cortisol does not override the inhibition of