features of the CSI already discussed, there is the inference that hypercholesterolemia inevitably leads to atherogenesis, which has its own multiple etiology. Furthermore, the postulates of Connor et at1 encourage people to think in terms of individual foods as being good or bad for health promotion, a fallacy that should not be encouraged in the practice of clinical nutrition.

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SJ Connor, JR Gustafson, SM Artaud-Wild, DP Flavell, CJ Classick-Kohn, LF Hatcher, and WE Connor, Lancet i: 1229-1232, 1986 DH Blankenhorn, N Engl J Med 312:

ES Fetcher, N Foster, JT Anderson, F Grande, and A Keys, Am J Clin Nutr 20:

A Keys, JT Anderson, and F Grande, Lancet i: 943-966, 1957 DM Hegsted, RB McGandy, ML Myers, and FJ Stare, Am J Clin Nutr 17: 281-295, 1965 RB Shekelle, AM Shryock, 0 Paul, M Lep- per, J Starnler, S Liu, and WJ Raynor Jr, N Engl J Med 304: 65-70, 1981 DB Zilversrnit, J Am Diet Assoc 74: 562-565, 1979 G Schonfeld, W Patsch, LL Rudel, C Nel- son, M Epstein, and RE Olson, J Clin Invest

American Heart Association, Circulation

851 -853, 1985

475-492, 1967

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69: 1065A-l090A, 1984

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Report of the National Cholesterol Educa- tion Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, Arch Intern Med 148:

EH Ahrens Jr, W lnsull Jr, R Blornstrand, J Hirsch, TT Tsaltas, and ML Peterson, Lan- cet i: 943-953, 1957 H Tunstall-Pedoe, WCS Smith, IK Crornbie, and M Thornson, Lancet ii: 344-345(Ltr), 1986 AH Kitchin and RWD Turner, Lancet ii: 344(Ltr), 1986 K Liu, J Starnler, D Moss, D Garside, V Persky, and I Soltero, Lancet ii: 782-785, 1979 SH Goodnight Jr, WS Harris, WE Connor, and DR Illingworth, Arteriosclerosis 2:

RN Wolf and SM Grundy, Arteriosclerosis

Animal and Vegetable Proteins in Lipid Me- tabolism and Atherosclerosis. MJ Gibney and D Kritchevsky, Editors. AR Liss, New York, NY, 1983 SM Grundy, N Engl J Med 314: 745-748, 1986 EH Ahrens Jr, W lnsull Jr, R Blornstrand, J Hirsch, TT Tsaltas, and ML Peterson, Lan- cet i: 943-953, 1957 A Keys, JT Anderson, and F Grande, Metab- olism 14: 759-765, 1965 AN Howard and J Marks, Lancet ii: 255-256(Ltr), 1977

36-61, 1988

87-1 13, 1982

3: 160-169, 1983

HOSPITAL MALNUTRITION STILL ABOUNDS

Failure to identify and treat malnourished patients in our hospitals can be attributed to a correctable lack of physician awareness.

Key Words: hospital, malnutrition, education, physicians

It has now been 20 years since the publica- tion of Dudrick’s landmark article announc- ing the success of total parenteral nutrition (TPN)’ in supporting growth and develop- ment in animals. Almost 15 years have passed since reports appeared document-

ing a substantial prevalence (approxi- mately 50 percent) of malnutrition among hospitalized surgical2 and medical pa- t i e n t ~ . ~ Butterworth4 characterized this sit- uation by saying, “Malnutrition is the skele- ton in the hospital’s closet.” Despite extensive current use of TPN in selected hospital patients (15 percent of hospital ad- missions, or about 5.5 million patients in

NUTRITION REVIEWSIVOL 46, N O SISEPTEMBER 1988 31 5

19845 at a cost of $200/day for TPN and $2l/day for enteral nutrition6), there are disturbing indications that awareness of malnutrition by physicians with training in internal medicine may have advanced very little over the past two decades.

Roubenoff et a17 studied the problem of why malnutrition among hospitalized medi- cal patients remains largely undetected and untreated. Physician awareness may be the key. This lack of awareness seems to be due to inadequate training, since the Roubenoff study demonstrated a willing- ness by internists to rapidly correct their educational deficit, with consequent im- provement in patient care. Furthermore, extensive training was not necessary. Some lectures and a simple nutritional screening tool were sufficient to correct this deficiency.

The study was conducted among all pa- tients admitted to a general medical ward of the Osler Medical Service at the Johns Hopkins Hospital, Baltimore, Maryland, where care is provided by a house staff team of chief resident, residents, interns, and medical students.

Three periods were studied: Period I of 14 days during which observations were made and data collected, Period II of 2 days in which two 2-hour educational sessions were conducted, and a second 14-day term (Period Ill) during which the nutritional screening tool taught in Period II was em- ployed. The screening tool was based on weight as a percent of ideal and usual body weight, serum albumin, total lymphocyte count, and 11 historic parameters sugges- tive of nutritional risk (eg, anorexia, diar- rhea, vomiting, dysphagia).

A pretest at the beginning of Period II and a posttest at the end of Period Ill for nutritional knowledge relevant to hospital practice and the educational material pre- sented were conducted. Whereas the house staff correctly identified two of 16 patients as being malnourished in Period I, in Period I1 14 of 14 were correctly identi- fied. Nutritional care of patients improved in Period I l l , as did nutritional knowledge among the house staff.

The authors7 felt that results from this study support the thesis that educating physicians in clinical nutrition changes their behavior regarding nutritional assess- ment and therapy. The authors recom- mended that a simple nutritional risk screen be made part of the admitting pro- cedure of acutely ill patients and that a di- etitian or other nutrition educator become an integral part of the ward team.

This study raises other concerns also touched on by the authors. Roubenoff et a17 commented that the house staff would have recently graduated and that their knowledge, or lack of knowledge, reflected their medical education. Why is nutrition education in medical schools so poor or in- adequate? Is it attributable to lack of stu- dent interest and motivation? Is it the in- flexible curriculum, or is it that too few physicians are trained in both medicine and nutrition science? There are many fac- ulty members involved in clinical investiga- tion who are knowledgeable in nutrition. So what is the problem?

The root causes are multiple, but include 1) a rigid curriculum, 2) lack of training pro- grams that are federally funded (given the limited remuneration possible from sub- specialty training in clinical nutrition), and 3) lack of a defined role for the clinical nu- tritionist in the hospital setting, due in part to limited reimbursement for nutrition pro- cedures and practice.

One long-term solution would be to pro- vide improved nutrition training in two medical subspecialties, gastroenterology and critical care medicine, whose practi- tioners now often see many of the mal- nourished medical patients. It would be like “waiting for Godot” to expect new funding that would support a specialty of clinical nutrition in the present era of cost contain- ment. Another positive step would be to in- clude clinical nutrition as a required course in the medical school curriculum.

Meanwhile, as Roubenoff et a17 suggest, a physician education program involving nutrition risk screening and greater use of dietitians for education and monitoring is the most viable interim solution.

316 NUTRITION REVIEWSIVOL 46, NO SISEPTEMBER 1988

1. SJ Dudrick, DW Wilmore, HM Vars, and JE Rhoads: Long-Term Parenteral Nutrition and Growth, Development, and Positive Ni- trogen Balance. Surgery 64: 134-142, 1968

2. BR Bistrian, GL Blackburn, E Hallowell, and R Heddle: Protein Status of General Surgi- cal Patients. JAMA 230: 858-860, 1974

3. BR Bistrian, GL Blackburn, J Vitale, and M Cochran: Prevalence of Malnutrition in Gen- eral Medical Patients. JAMA 235: 1567- 1570, 1976

4. CE Butterworth: The Skeleton in the Hospi-

tal Closet. Nutr Today 9: 4-8, 1974 5. EP Steinberg and GF Anderson: Implication

of Medicare’s Prospective Payment System for Specialized Nutrition Services. Nutr Clin Pract 1: 12-28, 1986

6. D Roberts, D Thelen, and S Weinstein: Par- enteral and Enteral Nutrition-A Cost Bene- fit Audit. Minn Med 65: 707-910, 1982

7. R Roubenoff, RA Roubenoff, J Preto, and CW Balke: Malnutrition among Hospitalized Patients. A Problem of Physician Aware- ness. Arch Intern Med 147: 1462- 1465,1987

DENTAL CARIES AND DENTAL FLUOROSIS

Minimal fluorosis has increased in children from areas with water fluoridated above optimal levels, but caries prevention is unaffected and no

change in water fluoride levels is recommended at this time.

Key Words: water fluoride, fluoride from non- water sources, dental fluorosis, dental caries

Surveys on dental caries and dental fluoro- sis were conducted in 1980 and 1985 on schoolchildren in seven communities in Illi- nois where the water supplies naturally contained fluoride varying from optimal amounts (defined for the Northern Temper- ate Zone as 1 .O ppm) to four times ( 4 x ) op- timal.’ As expected, results for the 807 children in the 1980 survey indicated that the mean dental caries scores expressed as decayed, missing, and filled surfaces (DMFS) were lower in areas where the water naturally contained 2, 3, and 4 x op- timal fluoride than in areas with optimal water fluoride. Substantial increases in dental fluorosis were observed where the fluoride levels were above optimal, with this condition most frequent and severe where the fluoride in the water was 4 x op- timal. Again this was consistent with obser- vations from past decades. At the optimal fluoride level, a high percentage of chil- dren had no evidence of fluorosis and none

of the remainder had fluorosis beyond the whitish discolorations of the “question- able” level and only cosmetic significance.

Evaluation of fluorosis severity first was made with the classification system devel- oped by Dean,* in which the scores as- signed ranged from 0 (normal) to 4 (se- vere). Horowitz et a13 were dissatisfied with this system for three reasons: 1) only one score was assigned per tooth instead of a separate score for each tooth surface; 2) the questionable fluorosis category is diffi- cult to define or interpret precisely, and 3) lack of sensitivity where fluorosis is severe. To correct these problems the investiga- tors3 developed criteria for values from 0 (normal) to 7 (most severe) and assigned a value for each tooth surface. This Tooth Surface Index of Fluorosis (TSIF) system was then used for the same 807 children. An especially interesting observation was that the children in the 8- to 10-year age group had a slightly higher frequency of fluorosis and a small increase in severity in comparison with the children in the 13- to 15-year-old group. Yet all children had

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