The listed mechanistic elements certainly do not exhaust all potential sources of SUD liability variance even at the neurobiological level. Depending on the focus and the biological level of research, addiction has been characterized as a disorder of the brain, learning, memory, neuromaturation and neuroplasticity, homeostatic regulation, compulsion, etc. The notion of addiction is also applied to other human dependency-like characteristics and behaviors unrelated to drugs, such as attachment, gambling, sex and food consumption and other consummatory behaviors, possibly having overlapping neurophysiologic substrates. For instance, the central ghrelin signaling system, known as a regulator of eating behavior, is likely also involved in reward and associated dopaminergic activity related to various psychoactive substances (alcohol, cocaine, amphetamine) (Jerlhag et al., 2010). Impaired psychological self-regulation contributing to SUD risk may manifest in early-onset overeating, which in turn increases the rate of reproductive maturation (Must et al., 2005; Wang, 2002), resulting in a greater likelihood of affiliation with deviant/older peers and substance use. Leptin is involved in both fat metabolism and pubertal development in girls (Li et al., 2005), while its contribution to eating
