Abstract:

Umanoff D¹ Substance, behavioral and belief addictions as a consequence of genetic diversity within the evolution-derived instinct decision-making apparatus.

I hypothesize and synthesize from current human and animal studies an evolution-derived neurological mechanism for instinct decision-making and discuss the addiction ramifications of genetic diversity within this system.  In a subgroup of organisms (people and other animals) with genetically determined critically low activity of the evaluator (the Feel O.K. System) of this mechanism, addictions of all kinds are inexorable as a result of unconscious attempts to raise the activity of this system. These addictions are derived from the instincts that intrinsically raise the activity of this system via reinforcing neurotransmitters and extrinsic chemical analogues of these same neurotransmitters (drugs) that similarly raise the activity of this system. Thus, addictions are "unintended" consequences of genetic variation of the decision-making apparatus and are all either instinct (behavioral addictions) or neurotransmitter substitute (drug) derived. The adaptive advantages of genetic diversity within this system during the era of evolutionary adaptation is discussed. Also discussed is the utility of this hypothesis for addiction related research, recovery, and public policy changes.

1. Hypoic's Handbook - The Evolutionary Origin, Genetic Blueprint, and Neurophysiological Foundation of Addictions, Dan F. Umanoff, M.D., 1996, 163 Hendrickson Ave., Rockville Centre, NY 11570

PAPER:

The fields of Evolutionary Psychology (EP) and Behavioral Genetics provide the most sensible and practical conceptual basis for understanding human behavior because of their dynamic principles and timeless perspective coincident with concrete biological premises. Intraspecies genetic variation within the framework of previous evolutionary mechanistic successes has always allowed for various degrees of useful adaptation to changing environments. However, this process can be a two edged sword in that previously successful adaptations may become liabilities in some future environment. Addiction is clearly the result of this evolutionary contingency.

The Homo Sapien species inherited from its predecessors many instincts along with a mechanism to regulate their use. I call this system, "The Decision-Making Apparatus." (DMA) Although the specific instincts and their control mechanism are currently only in the embryonic stages of being defined, there exists enough information to envision how this system might be arranged to explain various degrees of diverse human behavioral differences, including a wide array of addictions. The basic principle is that all humans have more or less the same basic genetic instincts and control mechanism while individual differences originate in alleles of modulating genes having differing biological activities. This principle runs through all life forms and all biological systems. In other words, we don't need to invoke completely unique mechanisms for each individual variation of behavior. Allelic variation within the control system will suffice to explain the gamut of behavioral variations within a species for a group of related behaviors. One example of this phenomenon is the genetic basis of biological temperament and the shuffling of temperament alleles at conception to yield various human functional personalities.

Besides explaining why humans become addicted, three ancillary questions must also be answered by any realistic addiction model. 1) Addiction is not universal. While most people can safely use addictors (defined below), why do some people become addicted to them and others not? 2) Specific addictions are not chance phenomena. Why do some addicts get addicted to some drugs and/or behaviors while other addicts are addicted to other drugs and/or behaviors? And 3) Addictions have a strong though nonspecific and variable inheritance. What trait(s) is/are inherited, how inherited, and how does this inherited trait produce the particular addiction(s) in the offspring? None of the current addiction models appreciates these questions or is able to answer them.

While instincts and their control alleles have been evolving for hundreds of millions of years, the completion of human instincts and allelic control genes took place some fifty to several hundred thousands of years ago. There hasn't been much time for evolutionary processes to reevaluate these latest behavioral adaptations so we are currently stuck with them. The adaptive environment (EEA - Era of Environmental Adaptation) then was quite different from today. Food and other commodities essential for survival were scarce and hard to come by. Life threatening danger was ever-present. Life itself was continuously on the verge of extinction. Instincts and their control alleles developed in this sparse environment. Mood-altering drugs did not yet exist and couldn't be anticipated by this evolving mechanism. Homo Sapiens survived and multiplied, and over time managed to turn shortages into surpluses and dangers into relative security. However, the genes that were successful in the adaptive environment are exactly the same ones that exist in humans who today live in an environment of drastically different circumstances. In the current environment of easy availability of those commodities the instinct controlling alleles evolved to successfully seek out, excessive seeking and lack of control over the use of these commodities and their neurophysiological simulators (drugs) in certain individuals became inexorable. The genetic alleles that were invaluable for survival in times of shortage, hardship, and danger are the same ones that when present in the right combination in certain people produce addictions in today's environment of excess commodities, commodity substitutes, and prevalent mood-altering drugs. These alleles in the FOKS of the DMA define Hypoism. Hypo-ism is the behavioral syndrome (or disease) caused by certain alleles exhibiting particularly low activity within the evaluative and reward mechanism of the DMA that incessantly and uncontrollably urge their bearers to blindly obey their excessive neuromodulatory demands; to passionately seek out addictors that results in the three cardinal manifestations of Hypoism: 1) Addictions, 2) Dangerous Decisions, and 3) Faulty Evaluations. Thus, alleles that were once (and still are in appropriate situations) indispensable to survival, are today also a liability in those individuals (hypoics) who have inherited a particular combination of them.

I utilized neurobiological mechanisms and dynamic evolutionary psychology concepts to develop the Hypoism model of human behavior, and ultimately addictions. It is realistic, mechanistic, pathophysiological, consistent with clinical addictions, and should be particularly useful for stimulating future experimentation and thought into addiction etiology, recovery, and ultimately policy decisions. These concepts, some known, some hypothesized, include the following genetically determined mechanisms involved in behavior origination: They are omnipresent in mammals for maximizing instinctive decisions, but in hypoics produce addictions and other evaluative errors through the inexorable effects of hypoic alleles of their modulating genes. Graphics are referred to in blue (link to graphic on site).

• Instincts - Evolved in-born behavior prototypical repertoires available to respond to both internal and external stimuli. These have evolved to deal with survival needs. Instincts are reinforced by neurotransmitter release in the reward centers of the brain. [known]
• Neurotransmitter substitutes (mood altering drugs) - Exogenous chemical substances that stimulate brain reward centers similar to endogenous reward neurotransmitters. [known] Reward Cascade
• The Decision-Making Apparatus (DMA) - The cognitive mechanism that evolved to make decisions on the assigning and modulating of specific in-born instincts in response to stimuli. [hypothesized] The resultant behavior is, in general, most suited to deal successfully with the stimulus. For the most part, this mechanism functions unconsciously. "Normal" Decision-Making Apparatus
• The Feel O.K. System (FOKS) - The (emotional) evaluator within the DMA. Includes the mesolimbic reward cascade ending in the nucleus accumbens and possibly other reward and neurotransmitter feedback centers, memory of results of previous decisions, and possibly other evaluative mechanisms: an instinct evaluative feedback mechanism. Unconsciously evaluates various decision alternatives. [known and hypothesized]
• Autonomous Thinking Belief (ATB) - The final decision approval check point prior to the expression of the resultant action - behavior. [hypothesized]
• Addiction - The use of an addictor [instinct, commodity substitute and/or neurotransmitter substitute(s)] to change how one feels against one’s will.
• Addictor - FOKS activity raisers: All instincts, commodity substitutes (sugar, pornography, etc.) and neurotransmitter substitutes (mood-altering drugs).

1. The Decision-Making Apparatus is the result of hundreds of millions of years of evolutionary manipulation to maximize instinctive decisions.
2. The entire system is genetically determined. Cognitive Mechanisms are inherited, not specific behaviors.
3. The DMA/FOKS mechanism functions below consciousness but its results may be made more or less available to the conscious mind.
4. Many genes are involved in its architecture and functionality.
5. Alleles of these genes with differing activities exist in the human and animal gene pool. These alleles result in wide variation in functionality of this mechanism.
6. These alleles have survived evolutionary time because of their various adaptive benefits to the individual, group, and species.

   Thus, there is variability among animals and people in activity and strength of both the various instincts (Instinct Diversity) and the determinants of the decisions to use these instincts (DMA/FOKS Diversity).
   

7. Instincts are utilized by the DMA when particular internal or external stimuli lower FOKS activity.
8. Use of instincts and commodity substitutes are rewarded and reinforced by release of certain neurotransmitters in the brain reward centers raising the activity of the FOKS and ending the response to the stimulus.
9. Neurotransmitter substitutes raise FOKS activity directly.
10. A (hypoic) subpopulation of animals (documented by voluntary, spontaneous, and reproducible experimental drug addictions in in-bred lab animals with certain genetically transmitted low activity genetic alleles) and people have genetically-determined critically low activity of the FOKS and are subject to addiction to addictors. The critically low activity of the FOKS in these organisms defines their Hypoism, a necessary and sufficient prerequisite for addiction - the sine qua non. Bell Curve of FOKS Activity and DMA/FOKS Addiction Machine.
11. Addiction in all its diverse forms is, thus, a particular neurophysiologically-induced behavior that occurs only in hypoics and results from unconscious attempts to raise and maintain FOKS activity above this critical level. Addiction Table. Nonhypoics don't have the necessary pathophysiology to be hypoic-type addicts. Physiological addiction to certain chemicals such as opiates is thus differentiated from true hypoic-type addiction, a genetically based pathophysiological state that exists prior to and independent of physiological addiction.
12. Offspring receive a stochastic shuffling of the parental genes and their alleles that determine the functionality of the FOKS/DMA mechanism and place that organism somewhere on the FOKS activity bell curve. FOKS activity below a critical level determines the presence of Hypoism.
13. Specific addictions in specific hypoics are predilected but not predetermined by the specific genetically defined allelic deficiencies received by each individual hypoic. Hypoics are born, not made. Hypoism (the cognitive mechanism) is inherited, not the specific addiction such as alcohol addiction (so-called alcoholism).
14. This model predicts that addictions can only occur in hypoics and that all FOKS raisers are capable of being addictors.
15. Neurophysiological adaptation perpetuates this neurobiological state and leads to progression, the exaggerated negative consequences of the addiction that occurs as the particular addiction matures over time. Neurophysiological Adaptation
16. The hypothesis predicts the inexorable hereditary transmission of addictability (if the right combination of alleles is transmitted to the offspring) but not of specific addictions, although there is definite predilection for specific addictions within this model. Only addictability and its degree are inexorable in this model.
17. CONCLUSION: ADDICTION IS AN "UNINTENDED" CONSEQUENCE OF EVOLUTIONARY DIVERSITY OF THE DECISION-MAKING APPARATUS DESIGNED TO DEAL WITH INSTINCTIVE BEHAVIOR. Because most common addictors have only recently become available in forms able to be addicted to by hypoics (drugs - including alcohol and tobacco, abundant and concentrated food, pornography, gambling, money, shopping, etc.) addiction is misperceived as a recent and modern phenomenon. On the contrary, addiction has probably existed in unrecognized form as prototypical behavioral addictions as long as man has walked on earth.

Once we are able to envision the decision-making apparatus as an evolved genetic mechanism for instinct related decisions we can then enlist principles of biological evolution, genetic variation and diversity, natural selection, and other EP principles to hypothesize its etiologic role in addictions, and we can appreciate addiction as an inevitable manifestation of this process. Hypoism is just another example of an evolved mechanism meant to perform one particular survival function being transformed into quite another unexpected outcome in a new and drastically different environment. Thus, addiction, as we experience it today, is an "unintended" consequence of evolution. A recent monumental study (1) which looked at low activity ADHD-associated genetic alleles of the DRD2 and DRD4 dopamine receptors in a particular African clan confirmed and validated this entire Hypoism concept and its behavioral consequences. [ADHD is a subgroup of people with Hypoism] The implications of this hypothesis will be derived from the thorough scientific delineation of the DMA, its position within the nervous system, its various connections with other functional units of the brain, its coordination with these neurological units, and its relationship and accessibility to the conscious mind. At this point of time, these implications point to the Autonomous Thinking Belief as the safest and most effective avenue for healthy intervention of addictions. Intervention here safely preserves the integrity of the hypoic's FOKS, his individuality. Intervention here enhances the positive aspects of his genetic diversity while freeing him from the addictions, other deleterious Hypoism manifestations, and the need to use substitute addictions to quell the imperious FOKS/DMA urges to similarly detrimental effect. Intervention of the FOKS/DMA.

This scheme incorporates existing and accepted EP genetic mechanisms as well as some hypothesized neurological modules to provide a rational basis for the establishment of a testable neurobiological model for the behavior we currently call addictions and compulsions. The Hypoism hypothesis uses a pathophysiological model just as we use to delineate other medical entities without needing to invoke irrelevant or actually harmful psychobabble, superstitious, pseudospiritual or mythological etiology. Hopefully, the Hypoism hypothesis will stimulate research into a realistic way of conceptualizing addiction that will lead to addiction intervention and policy to the benefit of addicts and society, something that is clearly lacking under today’s addiction nonpathophysiological paradigm. I believe that only EP has the necessary conceptual tools to produce a full and functional understanding of the manifold positive and negative aspects of Hypoism's impact on individuals and society.

The hypothesis is summarized in the Hypoism Chart and the Hypoism Windmill. The windmill is the same as the back cover on the site menu list under - Learn more about the Book.

References:

(1) Dan T.A. Eisenberg, Benjamin Campbell, Peter B. Gray, Michael D. Sorenson, Dopamine receptor genetic polymorphisms and body composition in undernourished pastoralists: An exploration of nutrition indices among nomadic and recently settled Ariaal men of northern Kenya, BMC Evolutionary Biology 2008, 8:173