This paper presents comparative results on poverty in seven countries and regions of the European Community: Belgium, The Netherlands, Luxembourg, Lorraine, Ireland, Catalonia and Greece. The data are obtained from comparable socio-economic surveys in each country. Subjective as well as relative poverty lines are used. The results indicate that the subjective poverty lines are plausible in a comparative context, although the levels of the subjective standards are rather generous. The estimated equivalence scales are much flatter than the one recommended by the OECD. The extent of poverty is much greater in the "peripheral" EC-countries than in the "central" ones. Though similar factors are found to be associated with poverty in all countries, there are also important differences in the characteristics of the poor across countries. The impact of social security transfers on poverty appears to be much smaller in the southern countries Greece and Catalonia, than in the Benelux and Lorraine.

The mitochondrial malate aspartate shuttle system (MAS) maintains the cytosolic NAD+/NADH redox balance, thereby sustaining cytosolic redox-dependent pathways, such as glycolysis and serine biosynthesis. Human disease has been associated with defects in four MAS-proteins (encoded by MDH1, MDH2, GOT2, SLC25A12) sharing a neurological/epileptic phenotype, as well as citrin deficiency (SLC25A13) with a complex hepatopathic-neuropsychiatric phenotype. Ketogenic diets (KD) are high-fat/low-carbohydrate diets, which decrease glycolysis thus bypassing the mentioned defects. The same holds for mitochondrial pyruvate carrier (MPC) 1 deficiency, which also presents neurological deficits. We here describe 40 (18 previously unreported) subjects with MAS-/MPC1-defects (32 neurological phenotypes, eight citrin deficiency), describe and discuss their phenotypes and genotypes (presenting 12 novel variants), and the efficacy of KD. Of 13 MAS/MPC1-individuals with a neurological phenotype treated with KD, 11 experienced benefits—mainly a striking effect against seizures. Two individuals with citrin deficiency deceased before the correct diagnosis was established, presumably due to high-carbohydrate treatment. Six citrin-deficient individuals received a carbohydrate-restricted/fat-enriched diet and showed normalisation of laboratory values/hepatopathy as well as age-adequate thriving. We conclude that patients with MAS-/MPC1-defects are amenable to dietary intervention and that early (genetic) diagnosis is key for initiation of proper treatment and can even be lifesaving.

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