Fundamental to the understanding of any biological process, including mental illnesses, involves understanding their evolutionary context. There are few readily apparent evolutionary advantages for the development of a high prevalence of major depressive illnesses among Homo sapiens. Major depression frequently destroys peoples lives and has a chronic recurring course. Major depression is defined by DSM-IV diagnostic criteria (American Psychiatric Association, 1994) by the loss of the ability to function in family or job life for at least 2 wk, as a a result of disturbances in mood, sleep, concentration, self-esteem, appetite, physical energy, and sexual energy or function. This disease not only directly reduces the likelihood of procreation but also causes significant disruption in social and family interactions. Prior to 1910, the prevalence of major depression may have been nearly 100-fold less than current rates (Klerman et al., 1985). The increased rates of prevalence of affective disorders that have been identified among birth cohorts during the last century in the United States has been well documented (Klerman et al., 1985; Wickramaratne, 1989; Burke et al., 1991; Robins et al., 1994). These increased prevalence rates of depressive disorders during the last century have also been described in several other industrialized nations, including Germany, Taiwan, Canada, and others (Klerman &Weissman, 1989; Cross National Collaborative Group, 1992). The argument that this cohort effect arose from changes in gene frequency over these few decades has been questioned and other potential explanations that have been offered, including nutritional, environmental, and social causes (Bebbington, 1994). Several investigators (Eaton et al., 1998; Broadhurst et al., 1998) have postulated that our genetic patterns evolved in the context of a nutritional milieu that allowed for optimal brain development and psychiatric functioning. Unfortunately, with regard to essential fatty acid intake, the modern diets of postindustrialized societies appear to be discordant with our genetic pattern and may contribute to the increased prevalence rates of major depression (Hibbeln and Salem, 1995). Homo sapiens are thought to have evolved consuming diets rich in directly available long-chain omega-3 fatty acids, which may have been permissive for the development of proportionally larger brains (Eaton et al., 1998; Broadhurst et al., 1998; Walter et al., 2000). However, during the last century, diets of industrialized societies have significantly diverged from these traditional diets, reducing the absolute amounts of EPA and DHA intake while increasing the relative intake of omega-6 fatty acids, which compete with omega-3 functions (Eaton et al., 1998). The ratios of omega-6 to omega-3 fatty acids are estimated to be between 0.4 and 2.8 in Paleolithic and evolutionary diets, including models in which either plants and hyper animal butchering were considered as sole sources of food. These models did not include seafood consumption, which would bring the ratios even lower. In contrast, current average ratios are estimated to be approximately 17 in typical Western industrialized societies (Eaton et al., 1998) and we have observed schizophrenics with AA/EPA ratios in red blood cells of more than 70 (unpublished data). These changes in the dietary intake are based not only on decreased seafood consumption but also on the increased production of seed oils (in particular, soybean and corn oils). These seed oils have much higher ratios of linoleic to a-linolenic acids compared to leafy plants, wild game, and seafood (Sinclair et al., 1987; Naughton et al., 1986). Clearly, there have been numerous dramatic changes in human civilization in the last century that may have contributed to the increased prevalence of major depression. However, because changes in the dietary intake of essential fatty acids appear to be able to directly influence central nervous system function, these nutritional factors should be carefully considered (Hibbeln and Salem, 1995). Quantitative assessment of this hypothesis is, unfortunately, difficult because of the uneven quality and paucity of historical dietary data.
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