Malaria and Rome: A History of Malaria in Ancient Italy, Robert Sallares [reading a book TXT] 📗

human malaria parasites do appear to have some capacity to produce it themselves. Iron deficiency is inimical to the parasites, although its effects on the chances of the host’s developing malaria are unclear; different studies have yielded conflicting results in both humans and animals. Nevertheless iron supplements to the diet do appear to increase the risk and severity of attacks of malaria.

Studies in India have shown that a deficiency of riboflavin (vitamin B2) in vivo results in a reduced parasite reproduction rate. The best sources of riboflavin are milk, eggs, and liver. It is relatively scarce in cereals, especially if they are highly processed.⁸⁵

These are all deficiencies in the diet of the human hosts. Natural selection for resistance to malaria can also favour human genetic mutations that produce an inherited reduction in the uptake of essential nutrients, even if the nutrients are abundant in the diet. Some recent research in biochemistry at the hospital in Grosseto has produced very interesting results. It has been shown that there is a high frequency of familial flavin-deficient erythrocytes in Grosseto and in Ferrara in the Po delta (which had endemic malaria in the late medieval and early modern periods), but not in Florence, a city with no history of P. falciparum malaria. This inherited genetic condition causes a reduced uptake of riboflavin by red blood cells even if it is abundant in the diet. It is a product of natural selection for resistance to malaria under conditions of extreme pressure and illustrates the importance of malaria in the past as an agent of natural selection.⁸⁶

⁸⁵ Das et al. (1988), with Davidson et al. (1979: 140–2); Gilles and Warrell (1993: 64); Har-El and Chevion (1997); Dobson (1997: 336–8).

⁸⁶ Anderson, et al. (1994), cf. Anderson et al. (1995).

Demography of malaria

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Nevertheless, even with the help of this trait conferring a degree of resistance to malaria, life expectancy at birth in Grosseto in the nineteenth century was still only twenty (see Ch. 5. 4 below). In other parts of Italy, especially in the Mezzogiorno, Sicily, and Sardinia, where there was also intense pressure from malaria, other genetic traits conferring degrees of resistance to it attained high frequencies, notably glucose-6-phosphate dehydrogenase (G6PD) deficiency and thalassaemia. Research in Sardinia by Siniscalco and colleagues first provided strong support for Haldane’s hypothesis, proposed in 1949, that heterozygotes for thalassaemia have increased resistance to P. falciparum malaria. Although that research was later criticized because of problems concerning the geographical origin of some of the populations of the villages which were studied, the new techniques of molecular biology have not only confirmed Haldane’s idea over the last few years, but have also shown that the statistical correlation between high frequencies of thalassaemia mutations and the presence (past or present) of endemic malaria is valid not just in the Mediterranean, but all over the world wherever P. falciparum malaria occurs. Grmek has comprehensively studied the evidence for the history of thalassaemia, G6PD deficiency, and favism (which is associated with G6PD

deficiency) in antiquity.⁸⁷ G6PD deficiency reduces the activity of a gene that plays a critical role in a biochemical cycle that eliminates oxidizing agents from erythrocytes. It is thought, in general terms, that this results in the premature lysis of red blood cells before malaria parasites inside have completed their development, although the precise mechanism remains unclear. Thalassaemia (predominantly b-thalassaemia in Mediterranean populations) is caused by mutations in the globin genes which lead to an imbalance in the correct synthesis of the a-and b-globin chains of the haemoglobin molecule. Malarial parasites digest haemoglobin to obtain amino acids for protein synthesis.

Thalassaemia and G6PD deficiency are very common in the modern populations of areas in the Mediterranean which were colonized by Greeks and Phoenicians in antiquity. They also occur ⁸⁷ Siniscalco et al. (1961); Weatherall (1997), Grmek (1983: 355–407), Ruwende and Hill (1998), Astolfi et al. (1999), and Vezzoso (1946) on thalassaemia; Greene and Danubio (1997) and Battin (1998) on G6PD deficiency. Lieber (1973) suggested that the Pythagorean communities in the cities of Magna Graecia arose from ‘a society of favism sufferers’. This hypothesis is not impossible, but cannot be proved or disproved given the lack of contemporary evidence for the origin of these communities.

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but are not so frequent in Latium and Tuscany. The problem arises of whether thalassaemia was introduced into Italy by Greek colonists in the eighth century  or alternatively had been present in human populations in Italy since the Neolithic period.⁸⁸ These two possibilities are not necessarily mutually exclusive, since it is now known that numerous independent mutations for thalassaemia (and G6PD deficiency) in response to malaria have occurred in many different parts of the world.⁸⁹ Nevertheless, since high frequencies of thalassaemia in mainland Italy are mainly concentrated in regions that were colonized by Greeks, it is likely that Greek colonization did indeed play a critical role in the spread of thalassaemia in Italy. In view of Ampolo’s convincing arguments about the free movement of individuals (e.g. Demaratus of Corinth) and groups from state to state in archaic central Italy, there is little doubt that there were plenty of opportunities for gene flow between populations in the archaic period.⁹⁰ Nevertheless the fact that different genotypes conferring degrees of resistance to malaria attained high frequencies in different regions demonstrates that Latium and Tuscany had a different population history in antiquity from the other areas in question, never having been colonized by Greeks or Phoenicians. Presumably the original Greek colonists of Magna Graecia brought common mutations for thalassaemia and G6PD deficiency with them from Greece. It has been suggested that the two commonest mutations for b-thalassaemia in Mediterranean populations were both spread by colonization.

According to this hypothesis the b+IVS nt 110 mutation occurred in Greece and was then spread to southern Italy by Greek colonists, while the b°39 mutation originated in the Levant and was carried westwards by Phoenician colonists to North Africa, Sardinia, and the