The recent recognition of the problem of adult malnutrition requires methods for specifying the severity of undernutrition. The measurement of mid upper arm circumference (MUAC) can now be used as a screening method for underweight (normally assessed from the BMI) or as an additional criterion with the BMI to identify the preferential loss of peripheral tissue stores of fat and protein. By analysing and extrapolating anthropometric data from nine detailed adult surveys from Asia, Africa and the Pacific a series of MUAC cut-off points have now been identified to allow the screening of individual adults under extreme conditions, e.g. during famine. Grade 4 malnutrition is now specified for those with a MUAC <200 mm for men and <190 mm for women since these MUAC values correspond to the loss of fat stores at BMI of <13. Food supplementation is clearly needed in these individuals. Extreme wasting (grade 5 malnutrition) corresponds to MUAC values of <170 and <160 mm for men and women respectively. These adults have extremely low BMI, i.e. about 10, have lost mast, if not all, of their protein stores and are at a high risk of imminent death. These individuals will need immediate special feeding regimens to ensure their sumval. The sex-specific MUAC values corresponding to BMI of 16, 13 and 10 can now therefore be used for rapid screening and the choice of remedial action.

To investigate possible differences in the relationship between multi-frequency impedance and bodywater compartments (total body water (TBW) and extracellular water (ECW)) measured by dilution techniques in two European populations, we studied forty Italian (twenty male and twenty female) and forty-three Dutch (twenty-three male and twenty female) healthy subjects aged 19–41 years. The main differences in body build between the two groups were height, trunk length and the two ratios TBW/height and ECW/height. Population-specific prediction formulas for ECW (at 1 kHz) and TBW (at 100 kHz) were developed. The prediction errors for ECW and TBW were about 0·6 and 1·5 kg respectively, (CV 4%) in both groups. Cross-validation analysis showed no significant error in the prediction of TBW but a slight error (range – 4·9 to + 2·8 %) in the ECW prediction. The biases in both TBW and ECW were correlated with ECW/TBW (r – 0·44, P < 0·0005 and r + 0·52, P <0·0005 respectively) in the two groups; the biases in ECW were also related to ECWIheight (r 0·51, P < 0·001), TBW/height (r 0·25, P < 0·05), trunk length (r 0·36, P < 0·001) and Z1/Z100 (r 0·32, P < 0·01). In conclusion, the water distribution between the extra- and intracellular compartments emerged in the present study as the major cause of error in the prediction of body water, and in particular of ECW from impedance measurements with a population-specific equation. Moreover, body build, expressed as TBW/height and ECW/height, had an impact on the bias.

Minke whales (Balaenopteva acutorostruta) have developed a compartmentalized stomach system, which includes a non-glandular forestomach containing high concentrations of indigenous bacteria. The forestomach contents serve as microbial substrate, and samples were collected from fiveadult minke whales eating capelin (Mallotus villosus) and crustaceans (Thysanoessa sp.). Chemical analysis of the forestomach contents revealed that they consisted of crude protein (650 (SD 58) g/kg DM), lipid (330 (SD77) g/kg DM) and water-soluble carbohydrates (53.3 (SD 7·3) g/kg DM). The contribution of energy from volatile fatty acids (VFA), produced by forestomach bacterial fermentation, to the total energy budget was estimated. The forestomach concentration ofVFA ranged from 13·2 to 68·5 mmol/l, and the pH was 5·83 (SD 0·41). VFA pool size ranged from 72·8 to 638·1 mmol and represented from 0·169 to 2·107 kJ/kg live weight (W)0·75 Maximal recorded forestomach VFA production rate was 1694 mmol/h in one capelin-eating minke whalewith 42·6 litres of forestomach fluid. Energy from VFA produced by forestomach fermentation represented 6–107 kJ/kg w0·75 per d, which accounts for only 0·9–16·9% of the average daily energy expenditure of minke whales. This study suggests that the bacterial fermentation in the minke whale forestomach varies, depending on the volume and the quality of substrate available, inlinencing fermentation rates and concentration of VFA. Due to the small relative size of the forestomach, the contribution of VFA to the daily energy requirement in minke whales would be of less importance than in ruminants even when assuming the same production rate of VFA as in a ruminant.

The effect of alcohol on overnight energy expenditure and substrate disposal was studied in eleven subjects (five men, six women) using whole-body indirect calorimetry for 15·5 h after test meals. Three test meals were studied in random order with at least 48 h between treatments: control, 50% of maintenance energy needs provided as 14, 40 and 46% energy from protein, fat and carbohydrate respectively; alcohol addition, control plus 23% energy as alcohol; alcohol substitution, control with alcohol replacing 23% of carbohydrate energy. ANOVA revealed no significant sex effects. Alcoholinduced thermogenesis dissipated only 15 (SD 14)% of the alcohol energy. Alcohol addition had no significant effect on protein or carbohydrate oxidation but fat oxidation was suppressed (P < 0·0005) to an extent equivalent to storing 74 (SD 51)% of the alcohol energy as fat. Alcohol substitution reduced carbohydrate oxidation (P < 0·009) to an equivalent of 42 (SD 41)% and also spared fat (P < 0·005) to an equivalent of 59 (SD 37)% of the alcohol energy. It is concluded that alcohol has no special thermogenic capacity, and that its energy can be accounted for in a similar way to carbohydrate.

The influence of administering the methylated products choline and creatine on methionine irreversible loss rate (ILR) and recycling from homocysteine has been investigated in sheep fed close to energy and N equilibrium. Two methods to estimate methionine recycling were compared. The first involved & [U-13C& ]methionine infused as part of a labelled amino acid mixture obtained from hydrolysed algal protein. In this approach the isotope dilution of methionine with all five C atoms labelled (m+5) will represent the ILR which does not recycle through homocysteine, while that which includes molecules with C-l–C-4 labelled will allow for loss of the labelled methyl (5)-C atom and replacement by an unlabelled moiety in the remethylation of homocysteine. The second method involved a combined infusion of [l-13C]- & [S-methyl-2H3& rsqb;methionine. These two approaches gave similar data for methionine ILR which does not include label recycled to the amino acid from homocysteine but differed for recycled methionine fluxes. Consequently the two procedures differed in the calculated extent of homocysteine methylation under control conditions (6 v. 28). These extents of remethylation are within the range observed for the fed human subject, despite the fact that fewer dietary methyl groups are available for the ruminant. Using combined data from the infwions, significant depression of methionine recycling occurred in blood (P <0·05), with a similar trendfor plasma (P = 0·077), when choline plus creatine were infused. Wool growth, assessed by intradermal injection of [35S]cysteine, was not altered by supplementation with the methylated products. From changes in the label pattern of free methionine in aortal, hepatic portal and hepatic venous blood during U-13C-labelled algal hydrolysate infusion, the major sites of homocysteine remethylation appear to be the portal-drained viscera and the liver. This was confirmed by analysis of free methionine enrichments in various tissues following dual infusion of & [1J3C& ]- and & [S-methyl-2H3methionine, with the greatest activities occurring in rumen, jejunum and liver. Of the non-splanchnic tissues examined, only kidney exhibited substantial methionine cycling; none was detected in muscle, heart, lung and skin. The implications of methyl group provision under net prduction conditions are discussed.

Nitrogen retention and lysine oxidation were measured in growing pigs given diets which supplied 0, 0·2 or 0·8 of the lysine requirement, with other amino acids in relative excess. Eight groups of three female littermate pigs were used: one of each group was given each of the three diets. In half the pigs (four groups) N retention was measured at body weights (W) of approximately 25,35 and 45 kg. The other four littermate groups of three pigs were given the same three diets; when they reached 35 kg W they were given a continuous (6h) primed infusion of L-[6-3H]lysine. Lysine oxidation was estimated from the production of tritiated water. Rates of both N retention and lysine oxidation increased significantly with lysine intake; mean values (g/kg W0·75 per d) for the three diets respectively were for N retention, 0·00, 0·32 and 1·22, and for lysine oxidation 0·051, 0·058 and 0·078. From the N balance results (assuming a constant lysine concentration in body protein) the efficiency of utilization of absorbed lysine was estimated to be 0·85; from the oxidation results (assuming lysine absorbed but not retained is oxidized) the estimate was 0·95.

The effect of mimosine on a perfused area of skin tissue was studied using an isolated perfusion technique. Four mature Angora wethers (body weight 35 (SE 2·3) kg) were cannulated bilaterally with indwelling silicone catheters in the superficial branches of the deep circumflex iliac artery and vein. Mimosine (40 mg/kg metabolic weight (W0·75) per d) was infused intra-arterially into one iliac artery of each goat for 3 d and saline was infused in the contralateral (control) iliac artery. Iliac venous blood samples were taken from both sides along with arterial samples from the carotid artery. Mimosine infusion elevated plasma mimosine in the carotid artery (52·6 (SEM 19·21)µmol/I) and iliac vein on the saline-treated side to 54·1 (SEM 16·31)µ/I and in the iliac vein on the mimosine-treated side to 191·3 (SEM19·14) µmol/I (P < 0·01). Mimosine decreased feed intake (2·3 v. 0·6 kg/d, SEM 0·29; P < 0·001) and water consumption (5·2 v. 1·3 litres/d, SEM 0·67; P < 0·001). Mimosine did not cause defleecing in the area of infusion and was cleared from the bloodstream within 12 h of cessation of infusion. The following effects were also observed during mimosine infusion: decrease in plasma amino acids to half pre-infusion values (methionine 22·7 v. 13·1 µmol/l, SEM 1·41; lysine 95·9 p. 37·4 µmol/l, SEM 4·28; P < 0·001); decreases in plasma triiodothyronine (1495 v. 695 ng/l, SEM 43·1; P < 0·001), thyroxine (61·5 v. 19·5 µg/l, SEM 1·8; P < 0·001) and insulin (28·7 v. 17·3 µIU/ml, SEM 1·89; P < 0·01) concentrations; increase in plasma cortisol (14 v. 62 µg/l, SEM 0·35; P < 0·001) concentration; decreases in levels of plasma Zn and Mg (0·97. v. 0·49 mg/l, SEM 0·063; P < 0·001 and 21·4 v. 14·6 mg/l, SEM 1·74; P < 0·001 respectively). All reported variables returned to their normal values 24 h after cessation of mimosine infusion except feed intake which was affected for a longer period. Mohair length and diameter were not affected by mimosine infusion. The toxicity of mimosine may be due to the drastic depletion of Zn and Mg in the blood as mimosine possesses very strong chelating properties and is excreted in the urine as a chelate.

The aims of the present study were to establish a suitable criterion for estimating the vitamin E requirement for young pigs, and to investigate the influence of dietary fats on the requirement of this nutrient. In Expt 1 weaned pigs were given a semi-purified diet supplemented with 0,20, or 100 mg DL- α-tocopheryl acetate/kg. Pigs in Expt 2 were fed on diets containing 10 g sunflower oil (SO) stripped of vitamin E/kg in diets 1 and 2, 100 g SO/kg in diets 3 and 4, and 100 g tallow/kg in diet 5. Diets 2, 4 and 5 were supplemented with DL-α-tocopheryl acetate at 20 mg/kg for 0·28 d and 50 mg/kg for 29–56 d of the experiment respectively. Results showed that vitamin E concentrations in plasma and tissues reflected dietary levels of vitamin E. No apparent clinical signs of vitamin 'E deficiency were observed, but pigs fed on diets without vitamin E supplementation showed a higher (P < 0·05) lipid peroxidation status as indicated by thiobarbituric acid-reactive substances in erythrocytes, and ethane and pentane levels in exhaled gases than those fed on supplemental diets. This indicated that the former was deficient in vitamin E. Data in Expt 1 suggested that supplementation with 20 mg DL-α-tocopheryl acetate/kg is adequate for young pigs when the diet contains 30 g lard/kg. However, results in Expt 2 showed that this level was inadequate when the diet contains 100 g SO/kg or its equivalent to 70 mg polyunsaturated fatty acids (PUFA)/g. Vitamin E and lipid peroxidation status of pigs were affected by both dietary vitamin E and dietary PUFA. This demonstrates that the requirement for vitamin E in young pigs increases as PUFA levels in the diet increase. The present study shows that lipid peroxidation response of pigs is a suitable index to evaluate vitamin E requirements.

Cu has long been known to influence immune responses. An in vitro model system was established in which human myeloid(HL-60), B-lymphoid (Raji) and T-lymphoid (Molt-3) cell lines could be grown in culture media of varying Cu levels. Initially Cu was removed from the medium by dialysisof fetal calf serum against a metal-ion chelator, minor depletion of other trace metals being obviated by repletion with appropriate metal salts. The growth rate of HL-60 was significantly (P<0·05) inhibited by 72 h Cu depletion. Molt-3 cells required a longer period, up to 144 h, in Cudepleted medium before growth was impaired. Raji-cell growth was not affected. These results confirmed clinical observations that T-cell functions were more sensitive to Cu deprivation than B cells. Analysis of intracellular metal levels in Molt-3 cells showed that Cu levels had been significantly lowered (P <0·05) although Ca2+ levels were raised. Intracellular activity of the antioxidant enzyme superoxide dismutase (EC 1. 15. 1. 1) was significantly impaired (P<0·05) in Molt-3 cells grown in Cudepleted medium. Activity of the mitochondria1 enzyme cytochrome c oxidase (EC 1. 9. 3. 1) was also significantly impaired (P <0·05) by Cu depletion. Each of these findings indicates an increase in the potential for cellular damage by reduced antioxidant activity, impairment of normal mitochondrial activity and excessive Ca2+influx. A major consequence of the type of damage occurring under these circumstances is membrane disruption. This was confirmed by scanning electron microscopy of Molt-3 cells grown under varying Cu levels.

The influence of high CaCO3, intake on the bioavailability of Fe from FeSO4, was assessed during Fe repletion of rats with Fe-deficiency-induced anaemia. Fe-deficient rats with a mean blood haemoglobin concentration of 4. 1 mmol/l were fed on purified Fe-adequate diets containing either 6.2 or 25.0g CaCO,/kg (ten rats per group). Haemoglobin repletion after 14 d was significantly depressed by high CaCO, intake (9.5 v. 9.8 mmol/l for high and low CaCO, intake respectively; P = 0·03), as was apparent Fe retention (367 v. 552 µg/d during days 5–7, P<0·001; 146 v. 196 µg/d during days 19–21, P < 0·001). The concentration of Fe in the liquid phase of the proximal half of the small intestine was significantly lower in the high-CaCO, group (3.71 v. 520 µg/g digesta; P = 0-02). Mucosal uptake and mucosal transfer of Fe were determined with orally administered 59Fe and Cr as a non-absorbable marker. Mucosal transfer was significantly diminished by CaCO, loading (90 v. 100% of mucosal uptake; P = 0·04), whereas mucosal uptake was not. 59Fe retention values at 14 d after administration were not significantly different (57.6 v. 51.9%; P = 0·14). Fe contents of liver and spleen were significantly decreased by high compared with low CaCO, intake (879 v. 590 pg Fe in liver, P < 0·001; 92 v. 63pg Fe in spleen, P <0·001). It is concluded that high intake of CaCO, depresses Fe bioavailability in rats. The CaCO,-induced decrease in Fe solubility in the digesta probably was associated with an increased efficiency of mucosal Fe uptake so that the amount of mucosal uptake remained unaltered. The CaCO,-induced decrease in Fe transfer through the mucosal cytoplasm and/or basolateral membrane may have been responsible for the concurrent decrease in Fe bioavailability.

We measured the vitamin K status in postmortem human tissues (brain, heart, kidney, liver, lung, pancreas) to see if there is a tissue-specific distribution pattern. Phylloquinone (K1,) was recovered in all tissues with relatively high levels in liver, heart and pancreas (medians, 10·6 (4·8), 9·3 (4·2), 28·4 (12·8) pmol(ng)/g wet weight tissue); low levels (< 2 pmol/g) were found in brain, kidney and lung. Menaquinone-4 (MK-4) was recovered from most of the tissues; its levels exceeded the K1 levels in brain and kidney (median, 2·8 ng/g) and equalled K1 in pancreas. Liver, heart and lung were low in MK–4. The higher menaquinones, MK-6–11, were recovered in the liver samples (n 6), traces of MK-6–9 were found in some of the heart and pancreas samples. The results show that in man there are tissue-specific, vitamin-K distribution patterns comparable to those in the rat. Furthermore, the accumulation of vitamin K in heart, brain and pancreas suggests a hitherto unrecognized physiological function of this vitamin.

The effect of the testosterone derivative oxymetholone alone or in combination with the H1receptor antagonist ketotifen, which has recently been shown to block tumour necrosis factor α (TNFα), on weight gain and performance status in human immunodeficiency virus (HIV) patients with chronic cachexia was evaluated in a 30 week prospective pilot study. Thirty patients were randomly assigned to either oxymetholone monotherapy (n 14) or oxymetholone plus ketotifen (n 16). Patients receiving treatment were compared with a group of thirty untreated matched controls, who met the same inclusion criteria. Body weight and the Karnofsky index, which assessesthe ability to perform activities of daily life, and several quality-of-life variables were measured to evaluate response to therapy. The average weight gain at peak was 8. 2 (SD 6. 2) kg ( + 14. 5 % of body weight at study entry) in the oxymetholone group (P<0·0.001), and 6.1 (SD 4.6) kg (+ 10.9 %) in the combination group (P<0·005), compared with an average weight loss of 1.8 (SD 0.7) kg in the untreated controls. The mean time to peak weight was 196 weeks in the monotherapy group and 20.8 weeks in the combination group. The Karnofsky index improved equally in both groups from 56% before to 67% after 20 weeks of treatment (P< 0·05). The quality of life variables (activities of daily life, and appetite/nutrition) improved in 68 % (P<0·05)and 91%(P< 0·01) of the treated patients respectively. Oxymetholone was safe and promoted weight gain in cachectic patients with advanced HIV-1 infection. The addition of ketotifendid not further support weight gain. These results suggest the need for a randomized, double-blind, placebo-controlled multicentre trial.