Population and Poverty in Ireland on the Eve of the Great Famine.

We revisit the link between demographic pressure and economic conditions in pre-Famine Ireland and harness highly disaggregated parish-level data from the 1841 census in our analysis. The results indicate that on the eve of the Great Irish Famine of the 1840s, population pressure was positively associated with two measures of poverty-illiteracy and the prevalence of poor-quality housing. Malthus mattered in the sense that our results indicate that a "no population growth" scenario between 1800 and 1841 would have led to a 6% improvement in poor-quality housing and a 4% reduction in illiteracy. However, the strength of this relationship is reduced when additional explanatory factors are considered, and factors relating to location and economic geography offer greater explanatory power. Incorporation of data from the 1821 census reveals that in the two decades before 1841, population growth was fastest in areas under less population pressure, supporting the notion that preventive check forces were at play. These findings are consistent with some elements of Malthusian theory, although ultimately they refute the notion that overpopulation was the principal cause of pre-Famine Irish poverty.

Famine mortality and contributions to later-life type 2 diabetes at the population level: a synthesis of findings from Ukrainian, Dutch and Chinese famines.

Since the 1970s, influential literature has been using famines as natural experiments to examine the long-term health impact of prenatal famine exposure at the individual level. Although studies based on various famines have consistently shown that prenatal famine exposure is associated with an increased risk of type 2 diabetes (T2D), no studies have yet quantified the contribution of famines to later-life T2D at the population level. We, therefore, synthesised findings from the famines in Ukraine 1932-1933, the Western Netherlands 1944-1945 and China 1959-1961 to make preliminary estimates of T2D cases attributable to prenatal famine exposure. These famines were selected because they provide the most extensive and reliable data from an epidemiological perspective. We observed a consistent increase in T2D risk among prenatally exposed individuals in these famines, which translated into about 21 000, 400 and 0.9 million additional T2D cases due to prenatal famine exposure in Ukraine, Western Netherlands and China, respectively. The T2D increase related to famine exposure represented only around 1% of prevalent T2D cases in these countries. Our observations highlight the significant increase in later-life T2D risk among individuals with prenatal famine exposure but also the limited contribution of prenatal famine exposure to T2D epidemics at the population level.

How much schizophrenia do famines cause?

Since the 1970s, famines have been widely invoked as natural experiments in research into the long-term impact of foetal exposure to nutritional shocks. That research has produced compelling evidence for a robust link between foetal exposure and the odds of developing schizophrenia. However, the implications of that research for the human cost of famines in the longer run have not been investigated. We address the connection between foetal origins and schizophrenia with that question in mind. The impact turns out to be very modest-much less than one per cent of the associated famine death tolls-across a selection of case studies.