1. Skinfold thicknesses at four sites – biceps, triceps, subscapular and supra-iliac – and total body density (by underwater weighing) were measured on 209 males and 272 females aged from 16 to 72 years. The fat content varied from 5 to 50% of body-weight in the men and from 10 to 61% in the women.

2. When the results were plotted it was found necessary to use the logarithm of skinfold measurements in order to achieve a linear relationship with body density.

3. Linear regression equations were calculated for the estimation of body density, and hence body fat, using single skinfolds and all possible sums of two or more skinfolds. Separate equations for the different age-groupings are given. A table is derived where percentage body fat can be read off corresponding to differing values for the total of the four standard skinfolds. This table is subdivided for sex and for age.

4. The possible reasons for the altered position of the regression lines with sex and age, and the validation of the use of body density measurements, are discussed.

1. Skinfold thickness, body circumferences and body density were measured in samples of 308 and ninety-five adult men ranging in age from 18 to 61 years.

2. Using the sample of 308 men, multiple regression equations were calculated to estimate body density using either the quadratic or log form of the sum of skinfolds, in combination with age, waist and forearm circumference.

3. The multiple correlations for the equations exceeded 0.90 with standard errors of approximately ±0.0073 g/ml.

4. The regression equations were cross validated on the second sample of ninety-five men. The correlations between predicted and laboratory-determined body density exceeded 0.90 with standard errors of approximately 0.0077 g/ml.

5. The regression equations were shown to be valid for adult men varying in age and fatness.

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. The adipokinome (which together with lipid moieties released, such as fatty acids and prostaglandins, constitute the secretome of 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.

The different compartments of the gastrointestinal tract are inhabited by populations of micro-organisms. By far the most important predominant populations are in the colon where a true symbiosis with the host exists that is a key for well-being and health. For such a microbiota, ‘normobiosis’ characterises a composition of the gut ‘ecosystem’ in which micro-organisms with potential health benefits predominate in number over potentially harmful ones, in contrast to ‘dysbiosis’, in which one or a few potentially harmful micro-organisms are dominant, thus creating a disease-prone situation. The present document has been written by a group of both academic and industry experts (in the ILSI Europe Prebiotic Expert Group and Prebiotic Task Force, respectively). It does not aim to propose a new definition of a prebiotic nor to identify which food products are classified as prebiotic but rather to validate and expand the original idea of the prebiotic concept (that can be translated in ‘prebiotic effects’), defined as: ‘The selective stimulation of growth and/or activity(ies) of one or a limited number of microbial genus(era)/species in the gut microbiota that confer(s) health benefits to the host.’ Thanks to the methodological and fundamental research of microbiologists, immense progress has very recently been made in our understanding of the gut microbiota. A large number of human intervention studies have been performed that have demonstrated that dietary consumption of certain food products can result in statistically significant changes in the composition of the gut microbiota in line with the prebiotic concept. Thus the prebiotic effect is now a well-established scientific fact. The more data are accumulating, the more it will be recognised that such changes in the microbiota's composition, especially increase in bifidobacteria, can be regarded as a marker of intestinal health. The review is divided in chapters that cover the major areas of nutrition research where a prebiotic effect has tentatively been investigated for potential health benefits. The prebiotic effect has been shown to associate with modulation of biomarkers and activity(ies) of the immune system. Confirming the studies in adults, it has been demonstrated that, in infant nutrition, the prebiotic effect includes a significant change of gut microbiota composition, especially an increase of faecal concentrations of bifidobacteria. This concomitantly improves stool quality (pH, SCFA, frequency and consistency), reduces the risk of gastroenteritis and infections, improves general well-being and reduces the incidence of allergic symptoms such as atopic eczema. Changes in the gut microbiota composition are classically considered as one of the many factors involved in the pathogenesis of either inflammatory bowel disease or irritable bowel syndrome. The use of particular food products with a prebiotic effect has thus been tested in clinical trials with the objective to improve the clinical activity and well-being of patients with such disorders. Promising beneficial effects have been demonstrated in some preliminary studies, including changes in gut microbiota composition (especially increase in bifidobacteria concentration). Often associated with toxic load and/or miscellaneous risk factors, colon cancer is another pathology for which a possible role of gut microbiota composition has been hypothesised. Numerous experimental studies have reported reduction in incidence of tumours and cancers after feeding specific food products with a prebiotic effect. Some of these studies (including one human trial) have also reported that, in such conditions, gut microbiota composition was modified (especially due to increased concentration of bifidobacteria). Dietary intake of particular food products with a prebiotic effect has been shown, especially in adolescents, but also tentatively in postmenopausal women, to increase Ca absorption as well as bone Ca accretion and bone mineral density. Recent data, both from experimental models and from human studies, support the beneficial effects of particular food products with prebiotic properties on energy homaeostasis, satiety regulation and body weight gain. Together, with data in obese animals and patients, these studies support the hypothesis that gut microbiota composition (especially the number of bifidobacteria) may contribute to modulate metabolic processes associated with syndrome X, especially obesity and diabetes type 2. It is plausible, even though not exclusive, that these effects are linked to the microbiota-induced changes and it is feasible to conclude that their mechanisms fit into the prebiotic effect. However, the role of such changes in these health benefits remains to be definitively proven. As a result of the research activity that followed the publication of the prebiotic concept 15 years ago, it has become clear that products that cause a selective modification in the gut microbiota's composition and/or activity(ies) and thus strengthens normobiosis could either induce beneficial physiological effects in the colon and also in extra-intestinal compartments or contribute towards reducing the risk of dysbiosis and associated intestinal and systemic pathologies.

1. Skinfold thickness and body density were measured on 105 young adult men and women and 86 adolescent boys and girls.

2. The correlation coefficients between the skinfold thicknesses, either single or multiple, and density were in the region of −0.80.

3. Regression equations were calculated to predict body fat from skinfolds with an error of about ±3.5%.

4. A table gives the percentage of the body-weight as fat from the measurement of skin-fold thickness.

1. The effect of ammonia concentration on microbial protein production was determined in continuous-culture fermentors charged with ruminal contents obtained from steers fed on either a protein-free purified diet, a maize-based all-concentrate diet, or a forage–concentrate (23:77) diet. Urea was infused into the fermentors to maintain various concentrations of ammonia in the incubating mixtures.

2. Under nitrogen-limiting conditions, microbial protein yield measured as tungstic acid-precipitable N (TAPN) increased linearly with supplementary urea until ammonia started to accumulate in the incubating ingesta. Increasing the ammonia concentration beyond 50 mg NH3-N/l had no effect on microbial protein production.

3. The molar proportions of volatile acids produced were not affected by the level of urea supplementation. Total acid production was decreased slightly under N-limiting conditions, but not to the same extent as microbial protein production.

4. Estimated yield of microbial dry matter/mol ATP produced averaged 15·6 when non-limiting N as urea was provided with the purified diet.

5. These results suggest that addition of non-protein N supplements to ruminant rations are warranted only if the prevailing concentration of ruminal ammonia is less than 50 mg NH3-N/l ruminal fluid.

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.

The gut is an obvious target for the development of functional foods, acting as it does as the interface between diet and the metabolic events which sustain life. The key processes in digestive physiology which can be regulated by modifying diet are satiety, the rate and extent of macronutrient breakdown and absorption from the small bowel, sterol metabolism, the colonic microflora, fermentation, mucosal function and bowel habit, and the gut immune system. The intestinal microflora is the main focus of many current functional foods. Probiotics are foods which contain live bacteria which are beneficial to health whilst prebiotics, such as certain non-digestible oligosaccharides which selectively stimulate the growth of bifidobacteria in the colon, are already on the market. Their claimed benefits are to alleviate lactose maldigestion, increase resistance to invasion by pathogenic species of bacteria in the gut, stimulate the immune system and possibly protect against cancer. There are very few reports of well-designed human intervention studies with prebiotics as yet. Certain probiotic species have been shown to shorten the duration of rotavirus diarrhoea in children but much more work is needed on the mechanism of immunomodulation and of competitive exclusion and microflora modification. The develop-ment of functional foods for the gut is in its infancy and will be successful only if more fundamental research is done on digestive physiology, the gut microflora, immune system and mucosal function.

Saponins are steroid or triterpenoid glycosides, common in a large number of plants and plant products that are important in human and animal nutrition. Several biological effects have been ascribed to saponins. Extensive research has been carried out into the membrane-permeabilising, immunostimulant, hypocholesterolaemic and anticarcinogenic properties of saponins and they have also been found to significantly affect growth, feed intake and reproduction in animals. These structurally diverse compounds have also been observed to kill protozoans and molluscs, to be antioxidants, to impair the digestion of protein and the uptake of vitamins and minerals in the gut, to cause hypoglycaemia, and to act as antifungal and antiviral agents. These compounds can thus affect animals in a host of different ways both positive and negative.

In a previous clinical study, a probiotic formulation (PF) consisting of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 (PF) decreased stress-induced gastrointestinal discomfort. Emerging evidence of a role for gut microbiota on central nervous system functions therefore suggests that oral intake of probiotics may have beneficial consequences on mood and psychological distress. The aim of the present study was to investigate the anxiolytic-like activity of PF in rats, and its possible effects on anxiety, depression, stress and coping strategies in healthy human volunteers. In the preclinical study, rats were daily administered PF for 2 weeks and subsequently tested in the conditioned defensive burying test, a screening model for anti-anxiety agents. In the clinical trial, volunteers participated in a double-blind, placebo-controlled, randomised parallel group study with PF administered for 30 d and assessed with the Hopkins Symptom Checklist (HSCL-90), the Hospital Anxiety and Depression Scale (HADS), the Perceived Stress Scale, the Coping Checklist (CCL) and 24 h urinary free cortisol (UFC). Daily subchronic administration of PF significantly reduced anxiety-like behaviour in rats (P < 0·05) and alleviated psychological distress in volunteers, as measured particularly by the HSCL-90 scale (global severity index, P < 0·05; somatisation, P < 0·05; depression, P < 0·05; and anger–hostility, P < 0·05), the HADS (HADS global score, P < 0·05; and HADS-anxiety, P < 0·06), and by the CCL (problem solving, P < 0·05) and the UFC level (P < 0·05). L. helveticus R0052 and B. longum R0175 taken in combination display anxiolytic-like activity in rats and beneficial psychological effects in healthy human volunteers.

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.

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.

The ‘malnutrition universal screening tool’ (‘MUST’) for adults has been developed for all health care settings and patient groups, but ease of use and agreement with other published tools when screening to identify malnutrition requires investigation. The present study assessed the agreement and the prevalence of malnutrition risk between ‘MUST’ and a variety of other tools in the same patients and compared the ease of using these tools. Groups of patients were consecutively screened using ‘MUST’ and: (1) MEREC Bulletin (MEREC) and Hickson and Hill (HH) tools (fifty gastroenterology outpatients); (2) nutrition risk score (NRS) and malnutrition screening tool (MST; seventy-five medical inpatients); (3) short-form mini nutritional assessment (MNA-tool; eighty-six elderly and eighty-five surgical inpatients); (4) subjective global assessment (SGA; fifty medical inpatients); (5) Doyle undernutrition risk score (URS; fifty-two surgical inpatients). Using ‘MUST’, the prevalence of malnutrition risk ranged from 19–60% in inpatients and 30% in outpatients. ‘MUST’ had ‘excellent’ agreement (κ 0.775–0.893) with MEREC, NRS and SGA tools, ‘fair–good’ agreement (κ 0.551–0.711) with HH, MST and MNA-tool tools and ‘poor’ agreement with the URS tool (κ 0.255). When categorisation of malnutrition risk differed between tools, it did not do so systematically, except between ‘MUST’ and MNA-tool (P=0.0005) and URS (P=0.039). ‘MUST’ and MST were the easiest, quickest tools to complete (3–5 min). The present investigation suggested a high prevalence of malnutrition in hospital inpatients and outpatients (19–60% with ‘MUST’) and ‘fair–good’ to ‘excellent’ agreement beyond chance between ‘MUST’ and most other tools studied. ‘MUST’ was quick and easy to use in these patient groups.

Anthropometry involves the external measurement of morphological traits of human beings. It has a widespread and important place in nutritional assessment, and while the literature on anthropometric measurement and its interpretation is enormous, the extent to which measurement error can influence both measurement and interpretation of nutritional status is little considered. In this article, different types of anthropometric measurement error are reviewed, ways of estimating measurement error are critically evaluated, guidelines for acceptable error presented, and ways in which measures of error can be used to improve the interpretation of anthropometric nutritional status discussed. Possible errors are of two sorts; those that are associated with: (1) repeated measures giving the same value (unreliability, imprecision, undependability); and (2) measurements departing from true values (inaccuracy, bias). Imprecision is due largely to observer error, and is the most commonly used measure of anthropometric measurement error. This can be estimated by carrying out repeated anthropometric measures on the same subjects and calculating one or more of the following: technical error of measurement (TEM); percentage TEM, coefficient of reliability (R), and intraclass correlation coefficient. The first three of these measures are mathematically interrelated. Targets for training in anthropometry are at present far from perfect, and further work is needed in developing appropriate protocols for nutritional anthropometry training. Acceptable levels of measurement error are difficult to ascertain because TEM is age dependent, and the value is also related to the anthropometric characteristics of the group or population under investigation. R > 0·95 should be sought where possible, and reference values of maximum acceptable TEM at set levels of R using published data from the combined National Health and Nutrition Examination Surveys I and II (Frisancho, 1990) are given. There is a clear hierarchy in the precision of different nutritional anthropometric measures, with weight and height being most precise. Waist and hip circumference show strong between-observer differences, and should, where possible, be carried out by one observer. Skinfolds can be associated with such large measurement error that interpretation is problematic. Ways are described in which measurement error can be used to assess the probability that differences in anthropometric measures across time within individuals are due to factors other than imprecision. Anthropometry is an important tool for nutritional assessment, and the techniques reported here should allow increased precision of measurement, and improved interpretation of anthropometric data.

Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.

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 (n 1768, aged 3–18 years). The interviews were repeated after 6 and 21 years (n 1200 and n 1037, 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.

Studies of food habits and dietary intakes face a number of unique respondent and observer considerations at different stages from early childhood to late adolescence. Despite this, intakes have often been reported as if valid, and the interpretation of links between intake and health has been based, often erroneously, on the assumption of validity. However, validation studies of energy intake data have led to the widespread recognition that much of the dietary data on children and adolescents is prone to reporting error, mostly through under-reporting. Reporting error is influenced by body weight status and does not occur systematically across different age groups or different dietary survey techniques. It appears that the available methods for assessing the dietary intakes of children are, at best, able to provide unbiased estimates of energy intake only at the group level, while the food intake data of most adolescents are particularly prone to reporting error at both the group and the individual level. Moreover, evidence for the existence of subject-specific responding in dietary assessments challenges the assumption that repeated measurements of dietary intake will eventually obtain valid data. Only limited progress has been made in understanding the variables associated with misreporting in these age groups, the associated biases in estimating nutrient intakes and the most appropriate way to interpret unrepresentative dietary data. Until these issues are better understood, researchers should exercise considerable caution when evaluating all such data.

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 (n 34) and overweight (n 16) 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 of Bifidobacterium and Bacteroides and increased numbers of Staphylococcus, Enterobacteriaceae and Escherichia coli were detected in overweight compared with normal-weight pregnant women. E. coli numbers were higher in women with excessive weight gain than in women with normal weight gain during pregnancy, while Bifidobacterium and Akkermansia muciniphila showed an opposite trend. In the whole population, increased total bacteria and Staphylococcus numbers were related to increased plasma cholesterol levels. Increased Bacteroides numbers were related to increased HDL-cholesterol and folic acid levels, and reduced TAG levels. Increased Bifidobacterium numbers were related to increased folic acid levels. Increased Enterobacteriaceae and E. coli numbers were related to increased ferritin and reduced transferrin, while Bifidobacterium levels 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.

Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1α-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1α-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5–15 μg/d.