Overweight and obesity in children and adolescents are on the increase worldwide. Overweight and obesity increase the risk for the development of non-communicable diseases during childhood and adolescence, and predispose the individual to the development of overweight, obesity, cardiovascular disease, and metabolic and other disorders in adulthood. In Africa the number of overweight or obese children has doubled since 1990. In South Africa, overweight and obesity in children and adolescents are on the increase, but the prevalence varies with age, gender and population group. These differences are important when intervention programmes and policies are considered. South Africa faces a double burden of disease where undernutrition and overweight or obesity are found in the same populations, in the same households and even in the same children. Malnutrition is a major contributor to the double burden of disease in South African children and adolescents.

Ferritin is the intracellular protein responsible for the sequestration, storage and release of iron. Ferritin can accumulate up to 4500 iron atoms as a ferrihydrite mineral in a protein shell and releases these iron atoms when there is an increase in the cell's need for bioavailable iron. The ferritin protein shell consists of 24 protein subunits of two types, the H-subunit and the L-subunit. These ferritin subunits perform different functions in the mineralization process of iron. The ferritin protein shell can exist as various combinations of these two subunit types, giving rise to heteropolymers or isoferritins. Isoferritins are functionally distinct and characteristic populations of isoferritins are found depending on the type of cell, the proliferation status of the cell and the presence of disease. The synthesis of ferritin is regulated both transcriptionally and translationally. Translation of ferritin subunit mRNA is increased or decreased, depending on the labile iron pool and is controlled by an ironresponsive element present in the 5'-untranslated region of the ferritin subunit mRNA. The transcription of the genes for the ferritin subunits is controlled by hormones and cytokines, which can result in a change in the pool of translatable mRNA. The levels of intracellular ferritin are determined by the balance between synthesis and degradation. Degradation of ferritin in the cytosol results in complete release of iron, while degradation in secondary lysosomes results in the formation of haemosiderin and protection against iron toxicity. The majority of ferritin is found in the cytosol. However, ferritin with slightly different properties can also be found in organelles such as nuclei and mitochondria. Most of the ferritin produced intracellularly is harnessed for the regulation of iron bioavailability; however, some of the ferritin is secreted and internalized by other cells. In addition to the regulation of iron bioavailability ferritin may contribute to the control of myelopoiesis and immunological responses.

Background: Despite strong reservations regarding the validity of a number of heart rate variability (HRV) measures, these are still being used in recent studies. Aims: We aimed to compare the reactivity of ostensible sympathetic HRV markers (low and very low frequency [LF and VLF]) to that of electrodermal activity (EDA), an exclusively sympathetic marker, in response to cognitive and orthostatic stress, investigate the possibility of LF as a vagal-mediated marker of baroreflex modulation, and compare the ability of HRV markers of parasympathetic function (root mean square of successive differences [RMSSD] and high frequency [HF]) to quantify vagal reactivity to cognitive and orthostatic stress. Results: None of the purported sympathetic HRV markers displayed a reactivity that correlated with electrodermal reactivity. LF (ms²) reactivity correlated with the reactivity of both RMSSD and HF during baroreflex modulation. RMSSD and HF indexed the reactivity of the parasympathetic nervous system under conditions of normal breathing; however, RMSSD performed better as a marker of vagal activity when the task required breathing changes. Conclusions: Neither LF (in ms² or normalized units [nu]) nor VLF represent cardiac sympathetic modulation of the heart. LF (ms²) may reflect vagally mediated baroreflex cardiac effects. HRV linear analysis therefore appears to be restricted to the determination of vagal influences on heart rate. With regard to HRV parasympathetic markers, this study supports the suggestion that HRV frequency domain analyses, such as HF, should not be used as an index of vagal activity in study tasks where verbal responses are required, as these responses may induce respiratory changes great enough to distort HF power.

The validity of melatonin as an oncostatic agent Panzer A, Viljoen M. The validity of melatonin as an oncostatic agent. J. Pineal Res. 1997; 22: 184-202. 0 Munksgaard, Copenhagen Abstract: The validity of melatonin as a prominent, naturally occurring oncostatic agent is examined in terms of its putative oncostatic mechanism of action, the correlation between melatonin levels and neoplastic activity, and the outcome of therapeutically administered melatonin in clinical trials. Melatonin's mechanism of action is summarized in a brief analysis of its actions at the cellular level, its antioxidative functions, and its indirect immunostimulatory effects. The difficulties of interpreting melatonin levels as a diagnostic or prognostic aid in cancer is illustrated by referral to breast cancer, the most frequently studied neoplasm in trials regarding melatonin. Trials in which melatonin was used therapeutically are reviewed, i.e., early studies using melatonin alone, trials of melatonin in combination with interleukin-2, and controlled studies comparing routine therapy to therapy in combination with melatonin. A table compiling the studies in which melatonin was used in the treatment of cancer in humans is presented according to the type of neoplasm. Melatonin's suitability in combination chemotherapy, where it augments the anticancer effect of other chemotherapeutic drugs while decreasing some of the toxic side effects, is described. Based on the evidence derived from melatonin's antiproliferative, antioxidative, and immunostimulatory mechanisms of action, from its abnormal levels in cancer patients and from clinical trials in which melatonin was administered, it is concluded that melatonin could indeed be considered a physiological anticancer substance. Further well-controlled trials should, however, be performed in order to find the link between its observed effects and the underlying mechanisms of action and to define its significance as a therapeutic oncostatic agent.

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