Starvation Mortality Research Articles

Demographic Responses to Food Shortages in the Sahel

To MALTHUS AND HIS CONTEMPORARIES, it seemed self-evident that crop failures and food shortages would inevitably produce starvation, sickness, and excess mortality among the poor in the stricken populations. Certainly, the African historical record is full of periods of crisis mortality, many of them linked to famine and some of them occurring well into the twentieth century (see Watts, 1983 for a chronology from northern Nigeria, and Carreira, 1982 for a welldocumented account of famine-induced mortality in the Cape Verde Islands). Although the data on famine mortality for most of sub-Saharan Africa are very poor, close examination of some of the better documented crises suggests that war and epidemics may be much more important killers than rank starvation. As Figure 1 shows, there is some geographical coincidence between wars and famine in contemporary Africa (Griffiths, 1988). Even the highest estimates of mortality in the Sahelian droughts of the 1970s and 1980s pale into insignificance in comparison with the numbers of excess deaths associated with the great 1918-19 African influenza epidemic, with the Biafran war of secession of 196769, or with the wars in Uganda.I There may well be some circumstances in contemporary Africa where a direct relationship between food production and mortality can be observed, but generally, the world has changed in several important ways that make it less and less likely that mass starvation will be the inevitable result of either natural calamity or excessive population growth. We cannot of course exclude the possibility of future high mortality levels resulting from civil or international war. In this essay, my main interest is in demographic changes associated with food shortages arising not from war but from other dislocations or breakdowns of the economy-some provoked by natural calamities but most if not all having roots in the structure and organization of production and its social and cultural context.

Effect of prolonged starvation on reticuloendothelial function and survival following trauma.

The effects of prolonged starvation on reticuloendothelial system (RE) function and on the survival of animals following trauma were studied. Rats were fasted for 51/2 days (water ad lib) after which a two-cm midline incision was made and the cecum ligated (CL). Food and water were allowed 36 h after CL and survival was measured over 5 days. The mortality rate in these animals was 60% (15/25) compared to 0% (0/15) in CL rats fasted for 24 h. Starvation alone for 7 days did not produce any deaths but after 11 days of starvation mortality was 100%. Another group of animals were fasted for 51/2 days and were used to study RE function 10 h following CL. There was no significant difference in the intravascular clearance rates in injected lipid emulsion in various groups of animals, indicating that total phagocytic function was not changed by prolonged starvation plus CL (SCL). However, emulsion retention in the spleen, expressed as per cent injected dose per gm tissue, decreased by 53% and the lung retention increased by 988% following SLC. Serum GOT levels were not affected by prolonged starvation alone; however, SCL resulted in its elevation (37 vs. 82 IU/ml). Hepatic ATP levels (micromoles/g) decreased from 2.47 to 1.95 following 51/2 days starvation and following SCL, it decreased to 1.75. These results indicate that the increased metabolic demand following trauma (i.e., CL), coupled with prolonged starvation, altered RE function with splenic lipid emulsion uptake decreasing and pulmonary uptake increasing. The relationship of these findings to immune function remains to be determined. Although the precise cause of increased mortality is not known, altered metabolic and RE function may play a role.

Brood reduction in birds: Selection for fratricide, infanticide and suicide?

Kin selection and inclusive fitness concepts are used to formulate a general theory accounting for the phenomenon of brood reduction in birds. The theory shows that as starvation mortality increases, selection favours at first fratricide, then fratricide plus infanticide, and finally fratricide, infanticide and suicide (by the nestling with the shortest life expectancy). A theoretical treatment of the alternative option, food sharing accompanied by concomitant reduction in growth rate, shows the latter to be ineffective when nest predation is high. Brood reduction is not limited in this manner. The theory allows several testable predictions about the incidence of starvation, starvation mortality, and sibling aggression, as well as their brood-size dependence and timing. These predictions are largely supported by the available evidence.

Biological notes of Amoebidium parasiticum found in Puerto Rico

Several aspects of the biology of Amoebidium parasiticum were studied with Aedes aegypti as a major host. In the life cycle of the fungus, presence of two reproductive phases, sporangiospore phase and amoeboid-cyst phase, were confirmed. However, fusion of amoeboids, which was reported earlier, was not observed. Variations in vegetative growth of the thalli and fungal association with other microorganisms in natural conditions were observed. The fungus grew well on all parts of the external surface of the insect, but a particular preference was noted for antennae and anal gills. The fungus has a broad host spectrum, attaching on the species of Cladocera, Copepoda, Culex, and Aedes. However, growth was poor on Anopheles. The fungus never attached on the local species of Ostracoda. The fungus does not cause mortality among Aedes aegypti larvae under optimal rearing conditions for the host, but under starvation mortality of fungus-associated larvae increased significantly over that of controls. A heat-stable, dialyzable fraction of the homogenate of Aedes aegypti increased the percentage of amoebogenesis. Three hormones, eedysterone, juvenile hormone, and diosgenin, were also tested for their amoebogenicity, but the results were negative.