No abstract

We hypothesized that in patients with chronic obstructive pulmonary disease, loss of fat-free mass (FFM) and loss of bone mineral density (BMD) were related to (1) each other and may be clinically inapparent, (2) urinary markers of cellular and bone collagen protein breakdown, and (3) severity of lung disease. Eight-one patients and 38 healthy subjects underwent dual-energy X-ray absorptiometry to determine body composition and BMD. Urinary protein breakdown markers, inflammatory mediators, and their soluble receptors were determined. Thirty-three patients had a low fat-free mass index (kg/m(2)), 17 of whom had a normal body mass index. Thirty-two percent of patients (13% of healthy subjects) had osteoporosis at the hip or lumbar spine. The marker of cellular protein breakdown was elevated in patients and related to lung disease severity and body composition. The marker of bone collagen breakdown was greater in patients with osteoporosis. Inflammatory mediators were elevated in patients. Loss of FFM and loss of BMD were related, occurred commonly, and could be subclinical in patients with chronic obstructive pulmonary disease. Loss of both was greatest with severe lung disease. Increased excretion of cellular and bone collagen protein breakdown products in those with low FFM and BMD indicates a protein catabolic state in these patients.

The effect of dietary advice on nutrient intakes was examined in a random subsample of 459 men who were taking part in a randomized controlled trial of secondary prevention of myocardial infarction. The trial is of factorial design, to examine the effect of three dieteary aims, alone and in combination: A reduction in total fat to 30% of energy, together with an increase in polyunsaturated/saturated fat ratio (P/S) to 1.0. An increase in fatty fish consumption to at least 300 g/week (3 g eicosapentaenoic acid (EPA)). An increase in cereal fibre intake to 18 g/day (total fibre 30 g/day). Men were randomly allocated to one of the eight regimens (fat, fish, fibre, fat plus fish, fat plus fibre, fish plus fibre, fat plus fish plus fibre, or none of these) and are being followed up for at least two years. Six months after the advice was given, nutrient intakes were assessed from 7‐d weighed intake records. Of those advised to reduce fat intake and increase P/S ratio, mean intakes were 31% of energy and 0.85, respectively. This compared with 35% of energy and 0.45 for those not given this advice. Mean EPA intake was 2.5 g/week for the fish advice group and 0.79 g/week for the no fish advice group. Mean cereal fibre intake of the fibre advice group was 15 g/d (26 g/d total fibre) compared with 9 g/d (20 g/d total fibre) for the no fibre advice group. Thus for each of the dietary aims, the advice had a substantial effect on intakes.

Factors influencing compliance with dietary advice were investigated in the Diet and Reinfarcation Trial [DART). In terms of achieved intakes, smokers had a lower mean P/S ratio and fibre intake than non-smokers; manual workers had a lower mean fibre intake than non-manual workers; and obese men had a higher percentage of energy from fat and lower P/S ratio than nonobese men. However the effect of the advice (difference in intakes of those advised and thosen not advised) was similar in smokers and non-smokers and was similar in all social classes. The effect of fat advice was less among obese men than among non-obese men, probably as a result of weight-reducing advice given to all overweight men. Fat advice tended to have a greater effect among those who gave up smoking after their heart attack than among nonsmokers and those who continued to smoke but the difference was not statistically significant. This suggests that advice on diet and smoking can be given simultaneously and still be effective.