Resurrecting New Zealand's public healthcare system or a charity hospital in every town?

Radical market-oriented health reforms in New Zealand in the early 1990s failed to deliver key financial targets, resulted in unnecessary patient deaths, adversely affected public healthcare services, induced serious tensions between clinicians and managers and encouraged a predisposition to private healthcare. A more co-operative health system was implemented in the late 1990s but remaining problems of inadequate patient access led to establishment of a charity hospital in Christchurch which, by November 2018, had registered over 18 000 patient visits. This is one indication of the need to resurrect our public healthcare system. In this paper, we discuss briefly the health reforms of the 1990s then, for discussion and debate, provide seven suggestions for how this resurrection might be achieved thereby avoiding the need for charity hospitals throughout the country.

Genetic benefits of consanguinity through selection of genotypes protective against malaria.

Consanguineous marriages are usually socially driven and can be genetically harmful. The detrimental effects of inbreeding are the consequence of homozygosity of harmful genes. On the other hand, beneficial effects of inbreeding, theoretically, could be expected in those who are homozygous for protective recessive and codominant genes. Here, we argue that the most common monogenetic conditions in humans, namely, alpha-thalassemia, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hemoglobin C, and Duffy antigen negative red blood cells, which have evolved under pressure from malaria, had their survival and selection enhanced by consanguineous marriages in malaria-infested regions of the world. This hypothesis is supported by several observations. First, the presence of two mutations in homozygotes involving the listed conditions (except G6PD deficiency) imparts better protection against malaria than the presence of one or no mutation (heterozygous or normal genotypes, respectively); consanguinity increases the number of homozygotes, especially at low allele frequency. For G6PD deficiency, inbreeding could increase the allele frequency of the G6PD-deficient allele. Second, there is overlap between, on the one hand, the geographic distributions of malaria, thalassemias, and other red blood cell conditions that protect against malaria and, on the other hand, consanguineous marriages. Third, the distribution of different intensities of malaria infestation is matched with the frequency of human inbreeding. These observations, taken together, offer strong support to the hypothesis that the culture of consanguineous marriages and the genetics of protection against malaria have co-evolved by fostering survival against malaria through better retention of protective genes in the extended family.