Epidemiological and nutrition transition in developing countries: impact on human health and development

Whereas common infectious and parasitic diseases such as malaria and the HIV/AIDS pandemic remain major unresolved health problems in many developing countries, emerging non-communicable diseases relating to diet and lifestyle have been increasing over the last two decades, thus creating a double burden of disease and impacting negatively on already over-stretched health services in these countries. Prevalence rates for type 2 diabetes mellitus and CVD in sub-Saharan Africa have seen a 10-fold increase in the last 20 years. In the Arab Gulf current prevalence rates are between 25 and 35% for the adult population, whilst evidence of the metabolic syndrome is emerging in children and adolescents. The present review focuses on the concept of the epidemiological and nutritional transition. It looks at historical trends in socio-economic status and lifestyle and trends in nutrition-related non-communicable diseases over the last two decades, particularly in developing countries with rising income levels, as well as the other extreme of poverty, chronic hunger and coping strategies and metabolic adaptations in fetal life that predispose to non-communicable disease risk in later life. The role of preventable environmental risk factors for obesity and the metabolic syndrome in developing countries is emphasized and also these challenges are related to meeting the millennium development goals. The possible implications of these changing trends for human and economic development in poorly-resourced healthcare settings and the implications for nutrition training are also discussed.

Polyunsaturated fatty acids in the pathogenesis and treatment of multiple sclerosis

Epidemiological, biochemical, animal model and clinical trial data described in this overview strongly suggest that polyunsaturated fatty acids, particularly n-6 fatty acids, have a role in the pathogenesis and treatment of multiple sclerosis (MS). Data presented provides further evidence for a disturbance in n-6 fatty acid metabolism in MS. Disturbance of n-6 fatty acid metabolism and dysregulation of cytokines are shown to be linked and a "proof of concept clinical trial" further supports such a hypothesis. In a randomised double-blind, placebo controlled trial of a high dose and low dose selected GLA (18:3n-6)-rich oil and placebo control, the high dose had a marked clinical effect in relapsing-remitting MS, significantly decreasing the relapse rate and the progression of disease. Laboratory findings paralleled clinical changes in the placebo group in that production of mononuclear cell pro-inflammatory cytokines (TNF-alpha, IL-1 beta) was increased and anti-inflammatory TGF-beta markedly decreased with loss of membrane n-6 fatty acids linoleic (18:2n-6) and arachidonic acids (20:4n-6). In contrast there were no such changes in the high dose group. The improvement in disability (Expanded Disability Status Scale) in the high dose suggests there maybe a beneficial effect on neuronal lipids and neural function in MS. Thus disturbed n-6 fatty acid metabolism in MS gives rise to loss of membrane long chain n-6 fatty acids and loss of the anti-inflammatory regulatory cytokine TGF-beta, particularly during the relapse phase, as well as loss of these important neural fatty acids for CNS structure and function and consequent long term neurological deficit in MS.