Obesity & Aggregate Fertility: An Extension of the Low Fertility Trap Hypothesis* Layton M. Field, PhD – Mount St. Mary’s University Lindsey B. Field, M.S., RDN, LD – Mount St. Mary’s University * Please contact the corresponding author (Layton Field; lfield@msmary.edu) for the most recent version of this paper.
Background Virtually every corner of the globe is experiencing some degree of fertility decline. According to the Central Intelligence Agency’s World Factbook 118 countries currently have an estimated total fertility rate below 2.1 (U.S. Central Intelligence Agency 2016). Popular discourse often views these declines as successful completions of the demographic transition in which lagging fertility rates finally decline to replacement levels. Undoubtedly, the early work of Notestein (1945, Notestein 1953) and Davis (1945, Davis 1963) in crafting this eloquent theory helps make sense of fertility decline at various points in modern history. Yes, demographic transition theory works well for some regions of the world. However, we also know that fertility decline in some countries does not quite fit with the demographic transition paradigm (Connelly 2008, Hodgson 1988, Szreter 1993). More importantly, several countries have witnessed continued fertility decline once the country’s respective fertility reached replacement levels. This has become known as the second demographic transition (Sobotka 2008). The second demographic transition is often characterized by decreases in desired family size, the postponement of union formation, and the delay in childbearing, all of which negatively influences overall fertility levels. Ultimately, these sustained fertility declines in much of Western Europe and Southeast Asia have necessitated a new approach to understanding fertility decline as fertility decline has given rise to substantial population aging in those regions. Some have suggested ways in which the graying of populations will impact future social, economic, and international arrangements (Last 2013, Wattenberg 2005). As such, population aging may require more countries to invest in pronatalist policies to positively impact fertility, though current pronatalist policies appear to have a very limited effect on fertility levels (Boling 2008, Lutz and Skirbekk 2005, McDonald 2006).
Thus, assisting the efficacy of pronatalist policies may require authorities to rethink many of the current constraints that negatively impact fertility. Recently, the Low Fertility Trap Hypothesis (LFTH) provides an excellent theoretical framework for understanding the conditions which suppress fertility. Essentially, LFTH posits that countries that fall below a total fertility rate of 1.5 are likely to become trapped “if a trap is defined as an unpleasant situation (governments would rather see higher fertility) into which one enters unintentionally and which it is very difficult to get out of” (Lutz, Skirbekk and Testa 2006:173). Furthermore, LFTH states there are three concurrent mechanisms operating to suppress fertility levels including demographic, social, and economic factors. Demographically, as fertility declines and populations age future mothers decline as a share in the total population. For example, we know that the share of women in childbearing ages is similar between the United States and Europe, 40 percent to 38 percent respectively (Johnson, Field and Poston 2015). However, the stock of future mothers is quite different with Europe’s future mothers repr esenting only 15 percent of the population compared to the United States at 20 percent. In other words, a smaller number of future mothers in Europe will have to have more children in order to offset the effect of population aging in Europe. Socially, LFTH suggests that norms and expectations surrounding family formation and ideal family size will continue to negatively influence fertility (Lutz, Skirbekk and Testa 2006). For instance, as couples opt to have fewer children, the next generation will internalize that norm and continue to have fewer children. This is also apparent in the demographic literature as some evidence suggests continual declines in desired fertility levels (Goldstein, Lutz and Testa 2003). Finally, from an economic standpoint couples balance the cost of childbearing against their desired standard of living and future earning potential (Lutz, Skirbekk and Testa 2006). Not
surprisingly, as couples become accustomed to a more expensive lifestyle, many will likely opt to have fewer children based on the rationale that their earning potential is incapable of providing for multiple children while maintaining their standard of living. As noted previously, LFTH provides a relatively simple explanation for why fertility continues to decline and may in fact become trapped in low fertility countries. Of course, a single theory will not likely accurately explain every scenario. In fact, we suggest that a fourth mechanism may also pressure fertility in a downward direction, namely, biology. Clearly, there are heritable characteristics that span the range of genetic variance which impact both fecundity and fertility (Kohler et al. 2006). However, we suggest there is growing evidence that increases in excess body fat, leading to obesity, also contribute to declines in fertility. Prior demographic research has substantiated a connection between obesity and declines in fertility although the direct biological connection was less clear and much of the relationship was attributed to union formation patterns that vary by obesity status (Jokela, Elovainio and Kivimäki 2008). Today, however, the maternal nutrition literature suggests a more direct connection between obesity and fecundity. Carrying around excess body fat has been directly linked to decreased fecundity and fertility among women (Stang and Huffman 2016). Women who are overweight or obese have increasing amounts of central adiposity, fat that accumulates around the abdominal area. Adipose tissue has been shown to reduce fertility among women through it role in the metabolism of sex hormones and associated enzymes and can delay fecundability compared to normal weight women (BMI of 18.5-24.9 kg/m 2 ) (Diamanti ‐ Kandarakis and Bergiele 2001, Law, Maclehose and Longnecker 2007, Stang and Huffman 2016, Wise et al. 2009). For example, Robker and colleagues (2009) studied the pre-ovulatory follicular environment among women from different
BMI groups: moderate (BMI = 18-24.9 kg/m 2 ); overweight (BMI= 25.0-29.9); and obese n=32 (BMI= ≥30 kg/m 2 ). The women were patients at an infertility clinic undergoing in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI). Women in the obese group had significantly fewer oocyte (immature egg cell) extraction from the ovary compared to the overweight group (P=0.016) and obese women produced a lower number of embryos per female compared to the other two groups (P=0.44). The researchers found a positive correlation between increases in BMI and elevated levels of insulin (P=0.0008), glucose (P=0.00), lactate (P=0.01), and triglycerides (P=0.0003), and C-reactive protein (P<0.0003), metabolites collected from the follicular fluid. C-reactive protein is an inflammatory marker that is usually elevated in obese individuals. These significant alterations in the follicular microenvironment can influence the functionality of the ovary and therefore the quality of the oocycte. Subsequently, egg fertilization and implantation into the uterine wall may be compromised. Certainly, the link between fecundity and obesity will become more pressing as the number of individuals categorized as obese in the United States, and abroad, continues to increase. Currently, 38.3% of U.S. women in their peak fertility years are considered obese and another third are overweight decreasing their fecundability ratio (Wise et al. 2009). Another 17.1% of adolescent girls/women 12-19 years of age, many of whom are at or nearing reproductive age, are also obese (Ogden CL et al. 2015). Similarly, other countries including Australia (28.4%), Mexico (26.8%), the United Kingdom (26%), Germany (23.3%) and New Zealand (32.0%) report a high prevalence of obesity that could be associated with low levels of fertility (Australian Bureau of Statistics 2012, Health and Social Care Information Centre 2016, New Zealand Government 2016).
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