The present review attempts to provide an update of the scientific knowledge on the renal toxicity which occurs in human subjects as a result of chronic ingestion of low-level dietary Cd. It highlights important features of Cd toxicology and sources of uncertainty in the assessment of health risk due to dietary Cd. It also discusses potential mechanisms for increased susceptibility to Cd toxicity in individuals with diabetes. Exposure assessment on the basis of Cd levels in foodstuffs reveals that vegetables and cereals are the main sources of dietary Cd, although Cd is also found in meat, albeit to a lesser extent. Cd accumulates particularly in the kidney and liver, and hence offal contains relatively high amounts. Fish contains only small quantities of Cd, while crustaceans and molluscs may accumulate larger amounts from the aquatic environment. Data on Cd accumulation in human kidney and liver obtained from autopsy studies are presented, along with results of epidemiological studies showing the relationship between renal tubular dysfunction and kidney Cd burden. These findings suggest that a kidney Cd level of 50 μg/g wet weight is a maximum tolerable level in order to avoid abnormal kidney function. This renal Cd burden corresponds to a urinary Cd excretion of 2 μg/d. Accordingly, safe daily levels of Cd intake should be kept below 30 μg per person. Individual variations in Cd absorption and sensitivity to toxicity predicts that a dietary Cd intake of 30 μg/d may result in a slight renal dysfunction in about 1 % of the adult population. The previous guideline for a maximum recommended Cd intake of 1 μg/kg body weight per d is thus shown to be too high to ensure that renal dysfunction does not occur as a result of dietary Cd intake.

The term essential fatty acid no longer clearly identifies the fatty acids it was originally used to describe. It would be more informative if the concept of essentiality shifted away from the symptoms arising from the lack of de novo synthesis of linoleate or α-linolenate and towards the adequacy of the capacity for synthesis and conservation of both the parent and the derived long-chain polyunsaturates. For instance, despite the existence of the pathway for synthesis of docosahexaenoate from α-linolenate, the former would be more correctly classified as ‘conditionally indispensable’ because the capacity of the pathway appears insufficient during early development, although it may be sufficient later in life in healthy individuals. Similarly, despite the inability to synthesize linoleate de novo, abundant linoleate stores and its relatively slow turnover in healthy adults probably makes linoleate ‘conditionally dispensable’ for long periods. There are two other anomalies with the terms essential and non-essential fatty acids: (1) under several different experimental circumstances, the C-skeleton of essential fatty acids is avidly used in the synthesis of non-essential fatty acids; (2) to function normally, the brain is required to endogenously synthesize several non-essential fatty acids. As with essential amino acids, which have been reclassified as indispensable or conditionally indispensable, such a change in terminology should lead to an improved understanding of the function and metabolism of polyunsaturates in particular, and long-chain fatty acids in general.

Milk contains various components with physiological functionality. Peptides derived from caseins and whey proteins including opioid peptides, antihypertensive peptides, casein phosphopeptides, α- and β-lactorphins and albutensin have been shown to possess various bioactive properties. This review considers an overview of the bioactive components in milk proteins and whey and their physiological function.

Rheumatoid arthritis (RA) is characterized by inflammation of the synovial tissues in the joints. A number of papers related to dietary components that are associated with this inflammation are reviewed. In addition, the ecological approach is used to study the links between diet and RA. Multi-country data for prevalence of RA for females from eight and fifteen countries were compared statistically with components of national dietary supply. Fat from meat and offal for the period 2 years before the prevalence data was found to have the highest statistical association with the prevalence of RA (r2 0·877, P<0·001 for eight countries). The statistical correlations for meat and offal were almost as high as those for their fat. Similar correlations were found for temporal changes in indices of effects of RA in several European countries between 1968 and 1978 as more meat was added to the national diets, although the correlations were higher for meat than for fat. It is hypothesized that meat and offal may be a major factor contributing to the inflammation in RA. In the present short review, the author examines some of the data that associate meat consumption with RA and the possible factors, e.g. fat, Fe and nitrite, which may contribute to the inflammation.

Despite convincing in vitro evidence, a vitamin C–E interaction has not been confirmed in vivo. This study was designed to examine the effects of supplementation with either vitamin C or E on their respective plasma concentrations, other antioxidants, lipids and some haemostatic variables. Fasting blood was collected before and after intervention from thirty healthy adults in a double-blinded crossover study. Baselines for measured variables were established after 2 weeks of placebo supplementation, followed by daily supplementation with 73·5 mg RRR-α-tocopherol acetate or 500 mg ascorbic acid, and placebo, for 6 weeks. A 2 month washout preceded supplement crossover. Mean values showed that plasma lipid standardised α-tocopherol increased with ascorbic acid supplementation: from 4·09 (SEM 0·51) TO 4·53 (sem 0·66) μmol/mmol total cholesterol plus triacylglycerol (P < 0·05), and plasma ascorbic acid increased from 62·8 (sem 14·9) to 101·3 (sem 22·2) μmol/l (P < 0·005). Supplementation with (RRR)-α-tocopherol acetate increased plasma α-tocopherol from 26·8 (sem 3·9) to 32·2 (sem 3·8) μmol/l (P < 0·05), and lipid-standardised α-tocopherol from 4·12 (sem 0·48) to 5·38 (sem 0·52) μmol/mmol (P < 0·001). Mean plasma ascorbic acid also increased with vitamin E supplementation, from 64·4 (sem 13·3) to 76·4 (sem 18·4) μmol/l (P < 0·05). Plasma ferric reducing (antioxidant) power and glutathione peroxidase (U/g haemoglobin) increased in both groups, while urate, total cholesterol and triacylglycerol levels decreased (P < 0·05 throughout). Results are supportive of an in vivo interaction between vitamins C and E.

In areas where iodized salt is not available, oral iodized oil is often used to correct I deficiency despite a lack of consensus on the optimal dose or duration of effect, particularly in children, a main target group. Annual doses ranging from 400 to 1000 mg have been advocated for school-age children. Because lower doses of iodized oil have been shown to be effective in treating I deficiency in adults, the aim of this study was to evaluate the efficacy and safety of a low dose of oral iodized oil in goitrous I-deficient children. Goitrous children (n 104, mean age 8·4 years, range 6–12 years, 47 % female) received 0·4 ml oral iodized poppyseed-oil containing 200 mg I. Baseline measurements included I in spot urines (UI), serum thyroxine (T4), whole blood thyroid-stimulating hormone (TSH), and thyroid-gland volume using ultrasound. At 1, 5, 10, 15, 30 and 50 weeks post-intervention, UI, TSH and T4 were measured. At 10, 15, 30 and 50 weeks, thyroid-gland volume was remeasured. At 30 and 50 weeks the mean percentage change in thyroid volume from baseline was -35 % and -41 % respectively. The goitre rate fell to 38 % at 30 weeks and 17 % at 50 weeks. No child showed signs of I-induced hypo- or hyperthyroidism. UI remained significantly increased above baseline for the entire year (P < 0·001); the median UI at 50 weeks was 97 μg/l, at the World Health Organization cut-off value (100 μg/l) for I-deficiency disorders risk. In this group of goitrous children, an oral dose of 200 mg I as Lipiodol (Guerbert, Roissy CdG Cedex, France) was safe and effective for treating goitre and maintaining normal I status for at least 1 year.

This present paper reviews the reliability and validity of visual analogue scales (VAS) in terms of (1) their ability to predict feeding behaviour, (2) their sensitivity to experimental manipulations, and (3) their reproducibility. VAS correlate with, but do not reliably predict, energy intake to the extent that they could be used as a proxy of energy intake. They do predict meal initiation in subjects eating their normal diets in their normal environment. Under laboratory conditions, subjectively rated motivation to eat using VAS is sensitive to experimental manipulations and has been found to be reproducible in relation to those experimental regimens. Other work has found them not to be reproducible in relation to repeated protocols. On balance, it would appear, in as much as it is possible to quantify, that VAS exhibit a good degree of within-subject reliability and validity in that they predict with reasonable certainty, meal initiation and amount eaten, and are sensitive to experimental manipulations. This reliability and validity appears more pronounced under the controlled (but more artificial) conditions of the laboratory where the signal: noise ratio in experiments appears to be elevated relative to real life. It appears that VAS are best used in within-subject, repeated-measures designs where the effect of different treatments can be compared under similar circumstances. They are best used in conjunction with other measures (e.g. feeding behaviour, changes in plasma metabolites) rather than as proxies for these variables. New hand-held electronic appetite rating systems (EARS) have been developed to increase reliability of data capture and decrease investigator workload. Recent studies have compared these with traditional pen and paper (P&P) VAS. The EARS have been found to be sensitive to experimental manipulations and reproducible relative to P&P. However, subjects appear to exhibit a significantly more constrained use of the scale when using the EARS relative to the P&P. For this reason it is recommended that the two techniques are not used interchangeably.

The possibility of achieving blood-lipid-lowering characteristics of pig fat by increasing the content of unsaturated fat in pig feed was evaluated. Three pig feeding regimens were applied: basal feed (no added fat or vitamin E), basal feed + rapeseed oil (60 g/kg feed), and basal feed + rapeseed oil (60 g/kg) + vitamin E (200 mg/kg). Meat and meat products from the three pig groups were incorporated into diets providing 86 g pig fat/10 MJ. The diets were served to twelve healthy human male subjects for 3 weeks each in a randomised crossover design. The diets prepared from pigs fed rapeseed oil had a lower content of saturated fatty acids (approximately 9 v. 11 % of energy) and a higher content of polyunsaturated fatty acids (approximately 6 v. 4 % of energy) than the diet prepared from pigs fed the basal feed. Diets based on fat from pigs fed the rapeseed oil resulted in significantly lower (approximately 4 %, P = 0·019) total serum cholesterol concentration compared with the diet from pigs fed the basal feed. No differences were observed in LDL-, HDL- or VLDL-cholesterol, or in triacylglycerol or VLDL-triacylglycerol concentrations. Addition of vitamin E to the pig feed resulted in only a minor increase in vitamin E content in the human subjects' diet and the vitamin E content was low in all three pig diets. Plasma vitamin E concentration in the human subjects at the end of the period with diets from pigs fed rapeseed oil without vitamin E was significantly lower (P = 0·04) than in the other two diet periods. In conclusion, an increased content of rapeseed oil in pig feed changes the fatty acid composition of the pig fat in a way that has a potential to reduce blood cholesterol concentrations in human subjects. However, intake of pig fat with a higher content of unsaturated fatty acids needs to be matched by a higher dietary intake of vitamin E.

Observational studies support the role of modifying lifestyle-related risk factors such as diet, physical activity and alcohol use in stroke prevention. For example, increased Na intake is associated with hypertension, and reduction in salt consumption may significantly lower blood pressure and may reduce stroke mortality. Moderately elevated homocysteine levels may be associated with stroke and are associated with deficiency of dietary intake of folate, vitamin B6 and vitamin B12. Consumption of a diet rich in fruits, vegetables, folate, K, Ca, Mg, dietary fibre, fish and milk may protect against stroke. Regular physical activity may also protect against stroke through its role in controlling various risk factors such as hypertension, diabetes mellitus and obesity. The role of fat intake as a risk factor for stroke remains uncertain, whereas the association between stroke and cholesterol has more convincingly been demonstrated by the recent intervention trials using statins. There is also evidence that a low serum albumin may be causally linked to stroke risk and outcome and that a significant number of stroke patients are undernourished on admission and their nutritional status deteriorates further whilst in hospital. Undernutrition is associated with increasing morbidity and mortality and nutritional supplements may have some beneficial effect on some outcome measures.

Colonic fermentation of organic matter to short-chain fatty acids has been implicated in the improvement in insulin sensitivity achieved by feeding diets rich in complex carbohydrates. The present study assessed the potential role of the colon in determining postprandial glucose kinetics. Metabolic responses to a complex-carbohydrate test meal were determined in conjunction with a primed continuous infusion of D-[6,6-2H]glucose in a group of ileostomists and sex-matched controls. Glucose disposal (GD) was computed using non-steady-state kinetics on a single compartment model. Insulin sensitivity was derived using cumulative GD as the dependent variable, and time and the integrated insulin concentration as independent variables. The ileostomist group had a significantly higher postprandial plasma insulin concentration (P=0·034) compared with the control group, but no difference in the plasma glucose concentration. Total GD was similar in each group, although the insulin-dependent GD was substantially lower in the ileostomists (0·46 v. 0·13 mg glucose/min per pmol, P=0·015). The ileostomist group also showed a 50 % lower rate of glucose oxidation in the postprandial period (P=0·005), although the rate of non-oxidative GD was not significantly affected. The present study indicates that loss of the colon is associated with several characteristics of the insulin resistance syndrome, and favours a view that the colon has a role in the control of postprandial glucose.