This review attempts to delineate the underlying mechanisms leading to the development of hypertension as well as the function of vitamins and minerals in the regulation of blood pressure. Physiological processes that regulate cardiac output and systemic vascular resistance impact on the control of blood pressure. Metabolic abnormalities associated with the tetrad of hypertension, dyslipidaemia, glucose intolerance and obesity share insulin resistance, which might be organ or cell specific, as an underlying feature representing different tissue manifestation of a common cellular ionic defect. As Ca is at the centre of ionic regulation of cellular functions, vitamins involved in Ca regulation have a significant role in the control of blood pressure. The endothelium-dependent vasodilator, NO, is susceptible to oxidative damage. Hence, antioxidant vitamins and related factors regulate blood pressure through protection of NO. Robust evidence for the involvement of vitamin B6 (pyridoxine), vitamin C, vitamin D and vitamin E in the regulation of blood pressure have been reported. The well-known roles of Na, K, Ca, Mg and Cl have been explored further. The action of various vitamins on blood pressure regulation cannot always be explained on the basis of their conventionally recognised “vitamin function”. The non-traditional functions of vitamins and their derivatives can be exploited as an adjunct to available pharmacological modalities in the treatment of hypertension.

Peripheral blood mononuclear cells (PBMC) accumulate biotin by a Na-dependent energy-requiring transporter. This transporter might be the so-called Na-dependent multivitamin transporter, but kinetic observations suggest the existence of a second, more specific, biotin transporter. PBMC respond to proliferation by increased uptake of biotin; the increase is probably mediated by an increased number of transporters on the cell surface. The inferred increase in the biotin transporter synthesis is relatively specific. The increased uptake of biotin into proliferating PBMC is consistent with the hypothesis that these cells have an increased demand for biotin. Indeed, proliferating PBMC increase expression of genes encoding β-methylcrotonyl-CoA carboxylase and propionyl-CoA carboxylase, generating a quantitatively significant increased demand for biotin as a coenzyme in newly-synthesized carboxylases. Moreover, expression of the holocarboxylase synthetase gene increases, consistent with the synthesis of new holocarboxylases. In addition, proliferating PBMC increase both the density of biotinylation of histones and the mass of biotinylated histones per cell, suggesting a potential role for biotin in transcription and replication of DNA.

Since pre-history, Cannabis sativa has been exploited for its potent and manifold pharmacological actions. Amongst the most renowned of these actions is a tendency to provoke ravenous eating. The characterization of the psychoactive principals in cannabis (exogenous cannabinoids) and, more recently, the discovery of specific brain cannabinoid receptors and their endogenous ligands (endocannabinoids) has stimulated research into the physiological roles of endocannabinoid systems. In this review, we critically discuss evidence from the literature that describe studies on animals and human subjects to support endocannabinoid involvement in the control of appetite. We describe the hyperphagic actions of the exogenous cannabinoid, Δ9-tetrahydrocannabinol, and the endogenous CB1 ligands, anandamide and 2-arachidonylglycerol, and present evidence to support a specific role of endocannabinoid systems in appetitive processes related to the incentive and reward properties of food. A case is made for more comprehensive and systematic analyses of cannabinoid actions on eating, in the anticipation of improved therapies for disorders of appetite and body weight, and a better understanding of the biopsychological processes underlying hunger.

Space flight is a new experience for man. Tension on the weight-bearing components of the musculo–skeletal system is greatly reduced, as is the work required for movement. The body responds by a reductive remodelling of the musculo–skeletal system. Protein is lost from muscles with anti-gravity functions. The rate of Ca loss from the weight-bearing bones is about 1 % per month. Voluntary dietary intake is reduced during space flight by about 20 %. These adaptations to weightlessness leave astronauts ill-equipped for life with gravity when they return to earth. Rates of energy expenditure are similar to that expected on the ground for comparable activities. Protein intake is adequate in flight but may be limiting after space flight due to substrate competition between repleting muscle and other anabolic processes. The most serious nutritional problem is the inability to maintain energy balance on missions with high exercise requirements. The poor dietary intake is probably a consequence of engineering-imposed environmental constraints. The low levels of lighting in the space vehicle may not be enough to promote vitamin D synthesis. Nevertheless, the evidence suggests that a normal well-balanced diet with plenty of fluids will be as healthy in space as on earth. The long-term goal of the manned space programme is to develop the means of sustaining human life beyond earth. This will involve the development of technologies to grow food, maintain a breathable atmosphere and recycle waste products with the only external input being energy.

Osteoporosis as a worldwide problem is discussed in the present review and the question of improving peak bone mass to reduce the risk of osteoporosis and osteoporotic fracture is addressed. The available evidence points to pre-puberty and puberty as the most opportune periods for intervention, but the potential for achievable increments in bone mass is shown to be small compared with the overwhelming influence of heredity, body composition and hormonal factors on bone. Lean body mass appears to be positively correlated with bone mass, while black–white racial differences in bone mass appear to be related to greater lean mass and lower bone turnover rate in blacks. Within races, twin and parent–offspring models have suggested that 46–80 % of the variance in bone mineral density can be explained by inherited factors; however, the mechanism of the genetic influence on bone density remains poorly understood. Moderate regular exercise seems to maintain bone mass while more vigorous regular exercise increases it in children and young adults. Ca intake has been found to be positively associated with bone mass in many but not all studies, possibly because of a ceiling at about 1300–1500 mg/d for young people. Other nutritional variables, including vitamin D, have been little investigated in relation to childhood and adolescent bone mass. The influence of milk as a source of highly bioavailable Ca and other nutrients has also been less frequently investigated, which is of concern given the cessation of school milk programmes in Western countries over the last three decades. Intervention studies to improve bone health in young people have mainly been based on Ca milk or exercise. The evidence points to the benefits to bone of such interventions, particularly when commenced pre-puberty, and it seems that daily consumption of 200–300 ml milk/d by children and adolescents has no adverse side effects. The benefits to bone are almost universally shown to be lost fairly rapidly after Ca or exercise intervention ceases; there is therefore no justification in terms of bone health for short-term interventions of this nature. The question of withdrawal of milk supplementation has undergone very little examination. Further, very little evidence is available on the effects of long-term interventions of any sort on bone health. Nevertheless, the data obtained so far permit the suggestion that promotion of Ca intake (e.g. at the higher level of current recommendations) and exercise commencing in the pre-pubertal period should be adopted as policy now.

Health benefits for man have been associated with conjugated linoleic acid (CLA) and dairy products are highlighted as offering the best opportunity to increase CLA consumption. CLA is synthesised in the rumen as an intermediate in the biohydrogenation of linoleic acid to stearic acid. The supplies of both intermediates and endproducts of biohydrogenation are affected by the substrate supply and extent of biohydrogenation, thus influencing the CLA content of milk from ruminants. The majority of CLA is present in the rumen in the form of the cis-9,trans-11 isomer. The transfer efficiency of CLA to milk fat is affected by the presence of different isomers of CLA. Ruminant mammary and adipose cells are able to synthesise cis-9,trans-11-CLA from trans-11-18:1 (vaccenic acid) by the action of the Δ9-desaturase enzyme. Plant oils are high in both linoleic and linolenic acids, which results in increased CLA production in the rumen and in the mammary gland. The CLA content of milk increases when cows are offered grazed grass. Many published studies examining the CLA concentration of processed milk were confounded by variations in the concentration of CLA in the raw milk.

Conjugated linoleic acid (CLA) refers to a group of fatty acid isomers of linoleic acid. Recent research shows that CLA affects body composition, lipoprotein metabolism, inflammationand carcinogenesis. Therefore, CLA may have potential as a therapeutic nutrient with respect to many common diseases, including obesity, atherosclerosis, chronic inflammatory diseases and cancer. Animal studies show that CLA is a potent anti-adipogenic nutrient, reducing adipose tissue mass and increasing lean mass. However, the effect of CLA on body composition in human subjects has been less spectacular. Several studies have demonstrated that CLA significantly improves plasma cholesterol and triacylglycerol metabolism in a number of animal models. These studies also showed that CLA inhibits the progression and pathogenesis of atherosclerosis. Whilst CLA has also been shown toimprove triacylglycerol metabolism in human subjects, it has not been determined whether CLA affects atherogenesis. Animal models show that CLA-rich diets modulate the inflammatory response and preliminary trials with human subjects show that CLA affects the cell-mediated immune response. The molecular basis of the health effects of CLA has not been elucidated, but it is probable that CLA mediates its effect in a number of ways including altered eicosanoid or cytokine metabolism and/orby a direct effect of dietary fats on gene transcription. Most of our knowledge is based on in vitro and animal studies; the challenge is to define the nature and molecular basis of any health effects of CLA in human subjects.