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of external forces driving this acceleration of female maturation remains largely uniden-
tifi ed. If “puberty begins with a kiss [
6
],” is it conceivable that perturbation of kisspeptin
signaling by environmental hormone mimics might underlie this and other adverse
health trends? Disruption of the kisspeptin system is an appealing hypothesis because
aberrant organization or function of this system could manifest as a wide range of seem-
ingly disparate, but related, disorders including altered pubertal timing, fertility prob-
lems, and metabolic disorder. Although this area of kisspeptin research is relatively new
and limited in scope, it is evident that the ontogeny and function of kisspeptin (and
related RF-amide) pathways, particularly the sexually dimorphic aspects, are vulnerable
to endocrine disruption. Because kisspeptin signaling pathways likely evolved to help
coordinate reproductive status with salient environmental cues, this may be an unfortu-
nate liability of a system honed to optimize reproductive fi tness. Thus, understanding
how kisspeptin signaling pathways are perturbed by EDCs could have a profound
impact on the fi elds of evolutionary ecology and toxicology by demonstrating that dis-
ruption within one key neuroendocrine system could ultimately underlie a suite of
adverse human health trends including early female puberty, unexplained infertility [
7
-
9
],
obesity [
10
,
11
], and related neuroendocrine disorders.
The Endocrine Disruption Hypothesis
The term “endocrine disruptor” was coined at a small working group convened at
the Wingspread Conference Center in 1991 to discuss what common mechanism(s)
might underlie a suite of concerning effects observed in wildlife [
12
,
13
] and if
these phenomena were predictive of adverse human health outcomes. Effects
included thinning eggshells in birds, abnormal gonadal and genital morphology in
alligators, altered sex ratios in turtle clutches, and a rapidly increasing prevalence of
intersex in fi sh. Controversial since it was fi rst voiced, the endocrine disruption
hypothesis posits that environmental chemicals have the capacity to interfere with
the endocrine system and confer disease in wildlife and humans. Within less than a
decade, numerous international agencies assembled their own meetings to weigh in
on the issue and craft a common defi nition. The United States Environmental
Protection Agency (EPA) currently defi nes an EDC as, “an exogenous chemical
substance or mixture that alters the structure or function(s) of the endocrine system
and causes adverse effects at the level of the organism, its progeny, populations or
subpopulations of organisms based on scientifi c principles, data, weight-of-evidence,
and the precautionary principle” (EDSTAC Final Report; available at
http://www.
epa.gov/endo/pubs/edspoverview/fi nalrpt.htm
)
. Although it remains a highly con-
troversial topic, in 2009, the Endocrine Society issued a statement supporting the
hypothesis and concluding that experimental and epidemiological studies have suf-
fi ciently converged with human clinical observations “to implicate EDCs as a sig-
nifi cant concern to public health.” In June of 2012, The Endocrine Society followed
up on this document and published its own defi nition of an EDC, which is nearly
identical to the EPA's but eliminates the requirement that the effects be “adverse.”
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