is a field attracting a great deal of attention in part because it is hoped that it will throw light on the so-called obesity epidemic currently affecting many countries, whether affluent or not. The same team that carried out the research reported above argues that growing evidence exists of ‘developmentally plastic processes’ that, in addition to lifestyle and individual genotypes, contribute significantly to obesity (Forrester et al. 2012). No claim is being made that such developmental pathways in which methylation processes are involved cause obesity directly, but that the risk of individuals genetically predisposed for developing obesity in later life is increased.
Based on a hypothesis known as the ‘mismatch pathway’, it is posited that ‘evolved adaptive responses of a developing organism to anticipate future adverse environments’ can have maladaptive consequences if the environment is not what has been ‘biologically anticipated’. In other words, if fetuses and young infants are exposed to nutritionally deprived diets, their bodies may be epigenetically prepared to deal with deprivation as they mature, as the marasmus study suggests, a situation that can cause havoc in energy-rich environments. In addition, maternal diabetes, maternal obesity and infant overfeeding are associated with increased risk of obesity in adult life (Gluckman and Hanson 2006). Clearly this account resembles the thrifty gene hypothesis put forward in 1962 by James Neel, an argument now outmoded in the post-genomic era; discussion about thrifty phenotypes has superseded it (Watve and Yajnik 2007).
Hannah Landecker argues that researchers presently understand food as an ‘epigenetic’ factor that functions in the regulation of gene expression, in turn, linked to several medical conditions including cancer, metabolic syndrome, obesity and diabetes. In other words, food is a form of ‘environmental exposure’ (Landecker 2011, 167) in which the environment is molecularised as food chemistry so that ‘the body’s molecules [are] hung in the same network of interactions as environmental molecules, a network anchored and organised through the temporarily sensitive interface of metabolism’ (Landecker 2011, 176). Landecker argues that this is a model ‘for how social things (food, in particular) enter the body, are digested, and in shaping metabolism, become part of the body-in-time, not by building bones and tissues, but by leaving an imprint on a dynamic bodily process’, namely, the expression of genes (Landecker 2011, 177).
Eliminating stunting
The President of the World Bank, Jim Yong Kim, a physician/anthropologist, has announced that he will ‘name and shame’ countries that fail to tackle the malnourishment and poor growth of their children (Boseley 2016, 1). Kim is clear that ‘stunting’, that is, children with height considerably below the average for their age, is not only a humanitarian disaster but also an economic one. His position is that fetal malnutrition during pregnancy and early childhood leads to serious neurological deficits, particularly in toxic environments, where recurrent infections are common, and when infants are given little or no stimulation. Kim stresses that stunted women frequently give birth to children who become stunted, with the result that ‘Inequality is baked into the brains of 25 per cent of all children before the age of five’ (Boseley 2016, 1). Crude estimates suggest that stunted children in India approach 40 per cent, in Pakistan 45 per cent, and in DR Congo 43 per cent; hence, Kim insists, ‘the most important infrastructure we can invest in is grey matter’. He seeks to rid the world of stunted children by 2030 by donating conditional cash transfers to mothers of stunted children, thus enabling them to feed and stimulate their children through play. It is reported that a trial run in Peru worked well (Boseley 2016, 2).
Jim Yong Kim plans to repeatedly bring up ‘this stain in our collective conscience’ at World Economic Forums in the coming years. Clearly interventions to eliminate stunting are of enormous importance, but key socio/economic variables noted by Kim have been set to one side in his Peruvian project, including unremitting poverty, unequal distribution of land and other resources, and increasingly toxic environments. In addition to which is the violence and counterinsurgency so evident in that country, ably documented by the anthropologist Kimberley Theidon (2013). The horrendous effects of climate change must now be added to this list.
Toxic living
For a decade or more, researchers have been working to elucidate the effects on neurodevelopment of exposure to neurotoxins in utero and during early life. Recent work has highlighted epigenetic effects and an apparent intergenerational aftermath of such exposures. A 2006 review of an array of 201 neurotoxins, ranging from arsenic to benzene and PCBs, concluded that exposure to hundreds of industrial chemicals is potentially damaging to the developing brains of children worldwide, although it is noted that both timing and the amount of exposure are significant (Grandjean and Landrigan 2006). Evidence links environmental pollutants to epigenetic marks associated with a range of disease endpoints, although it is emphasised that many of these changes have been shown to be reversible and hence preventive measures are feasible (Senut et al. 2012). Lead is the most closely researched toxin to date; it has been shown repeatedly that there is no safe level of exposure during the early years of development and that it causes many epigenetic effects. Decreased brain volume is recognised as lead-related brain atrophy, and is most pronounced in males (Cecil et al. 2008). Research has also shown negative effects of lead exposure on language function (Yuan et al. 2009).
Markowitz and Rosner graphically describe the ongoing lead paint scandal in the US that has steadily unfolded for more than a half-century (Markowitz and Rosner 2013). Over the years, millions of children have been exposed in their homes to potential lead poisoning, although reliable numbers are not available. It is estimated that today over 500,000 children between 1 and 5 years old have lead levels above that which policymakers currently regard as a safe level. Reminiscent of the infamous Tuskegee experiments conducted on African-Americans, 100 children, mostly African-American, some less than a year old, living in poor family dwellings where lead paint had been used, have been systematically studied for the effects of lead exposure on their development. A judge who presided over a lawsuit described these young research subjects as ‘canaries in the coalmine’ (Fowler 2013).
It has been shown that lead released from a woman’s bones during pregnancy can increase risk for preterm deliveries and low birth weight and, further, affect gene expression in infants involving changes to DNA methylation that may well have lifelong effects. One researcher is quoted as stating: ‘lead exposure, rather than a poor social environment, is a key contributor to […] subsequent cognitive and behaviour problems’ (Radiological Society of North America 2009). Such a claim prioritises one variable over another, causing a distortion. It is highly likely that lead exposure does irreparable harm to all humans, but those individuals who are at the greatest risk of being exposed are almost exclusively economically deprived. In 2014, in the impoverished town of Flint, Michigan, with a population of 100,000, nearly 60 per cent of whom are African-American, a water crisis exploded. It became clear that between 6,000 and 12,000 children had been extensively exposed to lead contamination when, in order to save money, the Flint water source was changed from a safe source, to one involving use of ageing pipes linked to the Flint river that leached lead into the water supply. As one commentator stated, ‘some of the darkest chapters in American industrialisation are written in lead’ (El Akkad 2016) and we learnt recently that ‘Dozens of California communities have seen recent rates of childhood lead poisoning that exceeds those of Flint, Michigan’ (Schneyer and Pell 2017).
Thanks to the intrepid battle fought by Rachel Carson, dichlorodiphenyltrichloroethane (DDT) was banned in the early 1970s, first in the US and then worldwide, although it continues to be used in certain malarial regions. Furthermore, the use of polychlorinated biphenyls (PCBs) is banned or severely restricted in most countries today, but about 10 per cent of the PCBs produced since the late 1920s remain in the environment today. They are released into the environment primarily from incinerators and build up in the fatty tissues of animals living in water or on land and are passed along the food chain to humans. Dioxins are found throughout the world and accumulate in the food chain, mainly in the fatty tissue of animals. They are highly toxic and cause reproductive
