Nutritional intervention as an essential part of multiple sclerosis treatment?

Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system. In addition to the genetic, epigenetic and immunological components, various other factors, e.g. unhealthy dietary habits, play a role in the MS pathogenesis. Dietary intervention is a highly appealing approach, as it presents a simple and relatively low risk method to potentially improve outcomes in patients with brain disorders in order to achieve remission and improvement of clinical status, well-being and life expectancy of patients with MS. The importance of saturated fat intake restriction for the clinical status improvement of MS patients was pointed for the first time in 1950s. Recently, decreased risk of first clinical diagnosis of CNS demyelination associated with higher intake of omega-3 polyunsaturated fatty acids particularly originating from fish was reported. Only few clinical trials have been performed to address the question of the role of dietary intervention, such is e.g. low saturated fat diet in MS treatment. This review summarizes current knowledge about the effect of different dietary approaches (diets low in saturated fat and dietary supplements such as fish oil, lipoic acid, omega-3 polyunsaturated fatty acids, seeds oils, high fiber diet, vitamin D, etc.) on neurological signs, patient's well-being, physical and inflammatory status. So far the results are not conclusive, therefore much more research is needed to confirm and to understand the effectiveness of these dietary interventions in the long term and well defined studies.

Growth hormone response to different consecutive stress stimuli in healthy men: is there any difference?

The contribution of growth hormone (GH), released during acute and repeated stressful situations, to the development of stress-related disorders is often neglected. We have hypothesized that the modulation of the GH response to sequential stress exposure in humans depends mainly on the nature of the stressor. To test this hypothesis, we compared GH responses to different stressful situations, namely aerobic exercise, hypoglycemia and hyperthermia, which were applied in two sequential sessions separated by 80-150 min. In addition, administration of the dopaminergic drug apomorphine was used as a pharmacological stimulus. GH responses to submaximal exercise (bicycle ergometer, increasing work loads of 1.5, 2.0 and 2.5 W/kg, total duration 20 min) and hyperthermia in a sauna (80 degrees C, 30 min) were prevented when preceded by the same stress stimulus. Hypoglycemia induced by insulin (0.1 IU/kg intravenously) resulted in a significant GH response also during the second of the two consecutive insulin tests, though the response was reduced. Administration of apomorphine (0.75 mg subcutaneously) or insulin prevented the increase in GH release in response to a sequential bolus of apomorphine, while hypoglycemia induced a significant elevation in GH levels even if applied after a previous treatment with apomorphine. In conclusion, the feedback inhibition of the GH response to a sequential stress stimulus depends on the stimulus used. Unlike in the case of exercise and hyperthermia, mechanisms involved in the stress response to hypoglycemia appear to overcome the usual feedback mechanisms and to re-induce the GH response when applied after another stimulus.