Addiction neuroscience has been the topic of several discussion groups. Here are comments from one of those groups and my responses. Thanks to Adam Safron for permission to use his comments here.
Adam Safron: I conducted an unpublished review of the literature about 3 years ago and found that the neural correlates were highly similar for sex and other heterogeneous rewards, suggesting that there is an important sense in which reinforcement is reinforcement is reinforcement. Similar conclusions were arrived at in a recent review [The human sexual response cycle: Brain imaging evidence linking sex to other pleasures] by Georgiadis and Kringelbach
James Kohl: I published a review article last year that details the common molecular mechanisms and epigenetic effects of food odors and pheromones, which links effects on hormones and their affect on behavior to another work by Kringelbach (with others) “The functional human neuroanatomy of food pleasure cycles”
In my published review: “Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors,” I wrote: “The Public Policy Statement: Definition of Addiction (ASAM, 2011) represents a paradigm shift…. It dictates the adoption and integration of neuroscientific principles that are required in order to understand differences between genetically predisposed brain disease, naturally occurring variations of behavioral development, and choice. These neuroscientific principles include focus on how sensory input influences behavior. The statement specifically mentions food and sex along with drugs and alcohol; each seems to chemically condition changes in hormones and in behavioral responses.”
Adam Safron: What are the conditions under which addiction arises for drug rewards?
James Kohl: The conditions seem to invariably involve epigenetically-effected changes in hypothalamic gonadotropin releasing hormone (GnRH) pulse frequency and amplitude with their downstream effects on feedback loops important to behavioral development (serotoninergic, dopaminergic et al.)
Adam Safron: Is there a supra-linear dose-dependent relationship between drug administration and the probability of developing addiction?
James Kohl: That seems unlikely due to the fact that susceptibilities appear to be genetically predisposed and influenced by in utero chemical exchanges in placental mammals. These in utero chemical exchanges are probably responsible for some aspects of transgenerational epigenetic inheritance and “conditioning” of post-natal responses to sensory input from the social environment paired with nutrient availability (e.g., nutrient stress and social stress). For example, suckling at a mother’s breast or nipples links nutrition associated with food odors and also links pheromones in the context of social odors to either the presence or absence of nutrient-stress and social stress.
Adam Safron: What are the effects of age?
James Kohl: They are being detailed in the context of Hypothalamic programming of systemic ageing involving IKK-b,NF-kB and GnRH. Note: in 1995 I presented “Olfactory-genetic-neuronal-hormonal reciprocity in learning, memory, behavior and in immune function” at an Anti-Aging Medicine Conference. It is now clearer how similarities in olfaction and immune system functions link them to neuroendocrine and neuroimmune system cause and effect via epigenetic effects on hormones that affect behavior.
Adam Safron: Are young people more vulnerable to addiction and more likely to experience relapse?
James Kohl: Theoretically, yes. Maturation of the brain associated with GnRH, luteinizing hormone (LH) and with glucose and pheromone-dependent myelination may help to better establish cause and effect via what is known about the molecular mechanisms that link the epigenetic “landscape” to the physical “landscape” of DNA.
Adam Safron: Thought experiment: What if we replaced the word “addicted” with “oriented”?
James Kohl: Doing that would link both addiction and orientation to food odors and pheromones in species from microbes to man via the same molecular mechanisms, as we indicated in our 1996 review: From Fertilization to Adult Sexual Behavior. Our review helped lead to the inclusion of invertebrates in the connection from yeasts to mammals via: Organizational and activational effects of hormones on insect behavior. I used the honeybee model organism to exemplify the fact that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.”
Whether discussing the neuroscience of food addiction or other addictions, or discussing sexual or other orientations to rewards, the molecular mechanisms are the same. Species specificity is derived from the epigenetic effects of species-specific pheromones that selectively signal adaptively evolved nutrient-dependent pheromone-controlled reproductive fitness. I don’t know any other model with remotely similar explanatory power that can also be used to neuroscientifically explain both food addiction and sexual addiction. But I haven’t seen anyone mention my model in any discussions.
However, in Kohl (2012) I predicted the recent announcement by NIMH that they were abandoning the DSM-5. I wrote (and repeat with additional emphasis): “The Public Policy Statement: Definition of Addiction (ASAM, 2011) represents a paradigm shift that may move the current practice of clinical psychology forward. It dictates the adoption and integration of neuroscientific principles that are required in order to understand differences between genetically predisposed brain disease, naturally occurring variations of behavioral development, and choice. These neuroscientific principles include focus on how sensory input influences behavior. The statement specifically mentions food and sex along with drugs and alcohol; each seems to chemically condition changes in hormones and in behavioral responses.”
Only by ignoring what I’ve already written in the context of addiction neuroscience can discussion of cause and effect among psychologists continue to ignore neuroscientific principles and details about how food, sex, drugs, and alcohol chemically condition changes in hormones and behavior.
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.