British Journal of Nutrition

White adipose tissue is now recognised to be a multifunctional organ; in addition to the central role of lipid storage, it has a major endocrine function secreting several hormones, notably leptin and adiponectin, and a diverse range of other protein factors. These various protein signals have been given the collective name ‘adipocytokines’ or ‘adipokines’. However, since most are neither ‘cytokines’ nor ‘cytokine-like’, it is recommended that the term ‘adipokine’ be universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It is suggested that the term is restricted to proteins secreted from adipocytes, excluding signals released only by the other cell types (such as macrophages) in adipose tissue. Theadipokinome(which together with lipid moieties released, such as fatty acids and prostaglandins, constitute thesecretomeof fat cells) includes proteins involved in lipid metabolism, insulin sensitivity, the alternative complement system, vascular haemostasis, blood pressure regulation and angiogenesis, as well as the regulation of energy balance. In addition, there is a growing list of adipokines involved in inflammation (TNFα, IL-1β, IL-6, IL-8, IL-10, transforming growth factor-β, nerve growth factor) and the acute-phase response (plasminogen activator inhibitor-1, haptoglobin, serum amyloid A). Production of these proteins by adipose tissue is increased in obesity, and raised circulating levels of several acute-phase proteins and inflammatory cytokines has led to the view that the obese are characterised by a state of chronic low-grade inflammation, and that this links causally to insulin resistance and the metabolic syndrome. It is, however, unclear as to the extent to which adipose tissue contributes quantitatively to the elevated circulating levels of these factors in obesity and whether there is a generalised or local state of inflammation. The parsimonious view is that the increased production of inflammatory cytokines and acute-phase proteins by adipose tissue in obesity relates primarily to localised events within the expanding fat depots. It is suggested that these events reflect hypoxia in parts of the growing adipose tissue mass in advance of angiogenesis, and involve the key controller of the cellular response to hypoxia, the transcription factor hypoxia inducible factor-1.

A deficiency of dietary protein or amino acids has long been known to impair immune function and increase the susceptibility of animals and humans to infectious disease. However, only in the past 15 years have the underlying cellular and molecular mechanisms begun to unfold. Protein malnutrition reduces concentrations of most amino acids in plasma. Findings from recent studies indicate an important role for amino acids in immune responses by regulating: (1) the activation of T lymphocytes, B lymphocytes, natural killer cells and macrophages; (2) cellular redox state, gene expression and lymphocyte proliferation; and (3) the production of antibodies, cytokines and other cytotoxic substances. Increasing evidence shows that dietary supplementation of specific amino acids to animals and humans with malnutrition and infectious disease enhances the immune status, thereby reducing morbidity and mortality. Arginine, glutamine and cysteine precursors are the best prototypes. Because of a negative impact of imbalance and antagonism among amino acids on nutrient intake and utilisation, care should be exercised in developing effective strategies of enteral or parenteral provision for maximum health benefits. Such measures should be based on knowledge about the biochemistry and physiology of amino acids, their roles in immune responses, nutritional and pathological states of individuals and expected treatment outcomes. New knowledge about the metabolism of amino acids in leucocytes is critical for the development of effective means to prevent and treat immunodeficient diseases. These nutrients hold great promise in improving health and preventing infectious diseases in animals and humans.

In 1229 subjects, 521 males and 708 females, with a wide range in body mass index (BMI; 13.9–40.9 kg/m²), and an age range of 7–83 years, body composition was determined by densitometry and anthropometry. The relationship between densitometrically-determined body fat percentage (BF%) and BMI, taking age and sex (males =1, females = 0) into account, was analysed. For children aged 15 years and younger, the relationship differed from that in adults, due to the height-related increase in BMI in children. In children the BF% could be predicted by the formula BF% = 1.51xBMI–0.70xage–3.6xsex+1.4 (R² 0.38, SE of estimate (see) 4.4% BF%). In adults the prediction formula was: BF% = 1.20xBMI+0.23xage−10.8xsex–5.4 (R² 0.79, see = 4.1% BF%). Internal and external cross-validation of the prediction formulas showed that they gave valid estimates of body fat in males and females at all ages. In obese subjects however, the prediction formulas slightly overestimated the BF%. The prediction error is comparable to the prediction error obtained with other methods of estimating BF%, such as skinfold thickness measurements or bioelectrical impedance.

Food systems need to produce enough of the essential trace element Se to provide regular adult intakes of at least 40 μg/d to support the maximal expression of the Se enzymes, and perhaps as much as 300 μg/d to reduce risks of cancer. Deprivation of Se is associated with impairments in antioxidant protection, redox regulation and energy production as consequences of suboptimal expression of one or more of the Se-containing enzymes. These impairments may not cause deficiency signs in the classical sense, but instead contribute to health problems caused by physiological and environmental oxidative stresses and infections. At the same time, supranutritional intakes of Se, i.e. intakes greater than those required for selenocysteine enzyme expression, appear to reduce cancer risk. The lower, nutritional, level is greater than the typical intakes of many people in several parts of the world, and few populations have intakes approaching the latter, supranutritional, level. Accordingly, low Se status is likely to contribute to morbidity and mortality due to infectious as well as chronic diseases, and increasing Se intakes in all parts of the world can be expected to reduce cancer rates.

Dietary patterns are useful in nutritional epidemiology, providing a comprehensive alternative to the traditional approach based on single nutrients. The Cardiovascular Risk in Young Finns Study is a prospective cohort study with a 21-year follow-up. At baseline, detailed quantitative information on subjects' food consumption was obtained using a 48 h dietary recall method (n1768, aged 3–18 years). The interviews were repeated after 6 and 21 years (n1200 andn1037, respectively). We conducted a principal component analysis to identify major dietary patterns at each study point. A set of two similar patterns was recognised throughout the study. Pattern 1 was positively correlated with consumption of traditional Finnish foods, such as rye, potatoes, milk, butter, sausages and coffee, and negatively correlated with fruit, berries and dairy products other than milk. Pattern 1 type of diet was more common among male subjects, smokers and those living in rural areas. Pattern 2, predominant among female subjects, non-smokers and in urban areas, was characterised by more health-conscious food choices such as vegetables, legumes and nuts, tea, rye, cheese and other dairy products, and also by consumption of alcoholic beverages. Tracking of the pattern scores was observed, particularly among subjects who were adolescents at baseline. Of those originally belonging to the uppermost quintile of pattern 1 and 2 scores, 41 and 38 % respectively, persisted in the same quintile 21 years later. Our results suggest that food behaviour and concrete food choices are established already in childhood or adolescence and may significantly track into adulthood.

This paper assesses critically the science base that underpins the argument that oxidative damage is a significant causative factor in the development of human diseases and that antioxidants are capable of preventing or ameliorating these disease processes. The assessment has been carried out under a number of headings, and some recommendations for future research are made based on the present day knowledge base.

Obesity is associated with complications during pregnancy and increased health risks in the newborn. The objective of the present study was to establish possible relationships between gut microbiota, body weight, weight gain and biochemical parameters in pregnant women. Fifty pregnant women were classified according to their BMI in normal-weight (n34) and overweight (n16) groups. Gut microbiota composition was analysed by quantitative real-time PCR in faeces and biochemical parameters in plasma at 24 weeks of pregnancy. Reduced numbers ofBifidobacteriumandBacteroidesand increased numbers ofStaphylococcus,EnterobacteriaceaeandEscherichia coliwere detected in overweight compared with normal-weight pregnant women.E. colinumbers were higher in women with excessive weight gain than in women with normal weight gain during pregnancy, whileBifidobacteriumandAkkermansia muciniphilashowed an opposite trend. In the whole population, increased total bacteria andStaphylococcusnumbers were related to increased plasma cholesterol levels. IncreasedBacteroidesnumbers were related to increased HDL-cholesterol and folic acid levels, and reduced TAG levels. IncreasedBifidobacteriumnumbers were related to increased folic acid levels. IncreasedEnterobacteriaceaeandE. colinumbers were related to increased ferritin and reduced transferrin, whileBifidobacteriumlevels showed the opposite trend. Therefore, gut microbiota composition is related to body weight, weight gain and metabolic biomarkers during pregnancy, which might be of relevance to the management of the health of women and infants.

Following the publication of the landmark trial of Clarket al.in 1996 that appeared to show that Se could reduce the risk of cancer, awareness of the importance of Se to human health has markedly increased. As a result, there is now much more aggressive marketing of Se supplements and functional foods, even in situations where additional consumption of Se is inappropriate. The present review addresses how Se gets into the food chain, the wide variability in Se content of foods and the very different levels of intake between countries and regions. Though it is clear that there are adverse consequences for health of both deficient and excessive intake, health effects at intermediate levels of intake are less certain. Thus it is difficult to define optimal intake which depends on a large number of factors, such as which functions of Se are most relevant to a particular disease state, which species of Se is most prominent in the Se source, which health condition is being considered, the adequacy or otherwise of intake of other nutrients, the presence of additional stressors, and lastly whether the ability to make selenoproteins may be compromised. These complexities need to be understood, particularly by policy makers, in order to make informed judgments. Potential solutions for increasing Se intake, where required, include agronomic biofortification and genetic biofortification or, for individuals, increased intake of naturally Se-rich foods, functional foods or supplements. The difficulties of balancing the risks and benefits in relation to Se intake are highlighted.

Women (n 160) aged 50 to 65 years were asked to weigh their food for 4 d on four occasions over the period of 1 year, using the PETRA (Portable Electronic Tape Recorded Automatic) scales. Throughout the year, they were asked to complete seven other dietary assessment methods: a simple 24 h recall, a structured 24 h recall with portion size assessments using photographs, two food-frequency questionnaires, a 7 d estimated record or open-ended food diary, a structured food-frequency (menu) record, and a structured food-frequency (menu) record with portion sizes assessed using photographs. Comparisons between the average of the 16 d weighed records and the first presentation of each method indicated that food-frequency questionnaires were not appreciably better at placing individuals in the distribution of habitual diet than 24 h recalls, due partly to inaccuracies in the estimation of frequency of food consumption. With a 7 d estimated record or open-ended food diary, however, individual values of nutrients were most closely associated with those obtained from 16 d weighed records, and there were no significant differences in average food or nutrient intakes.