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Ideology and Science

To reiterate the content of my last post, in 1984 I was expecting to field-test some theories about drug/ human interaction. My theories (hypotheses) grew firstly from the records of prehistoric drug use I had collated in the previous years. The advances of neurosciences in the decades of the 1960, 1970s and 1980s also educated and inspired my curiosity; particularly in the question of whether drug seeking is biologically derived or whether individual or societal pathologies drive it.

 

However, when I began shaping my hypotheses, I could find no references in popular culture of the 1980’s to the neuroscience concept that drug addiction is a ‘relapsing’ brain disease like schizophrenia or diabetes; that without formal medical treatment compulsive drug craving, seeking, and consuming take over individual lives and leads to their wreckage. No information seemed to exist either about the growing certainty that genetic factors play a part in the variability in susceptibility of each individual to becoming addicted.

 

I was not surprised by this omission. Through time and across regions, religions, politics, professional ethics and/or other socio-economic conditions have frequently controlled what individuals can consume, grow, learn, and manipulate with psychoactive substances, even those their society endorses. See for example, in the history of the Australia Aboriginal drug pituri (Duboisia Hopwoodii) the number of existing controls that ensured only respected elders chewed the drug.

 

To ensure my readers belief in the authenticity and reliability of my hypotheses, I jump ahead here to the period between 1990s -2014. Would this time span contain an explanation as to why no public knowledge or discussion appeared to exist in the early 1980s of drug use as a brain disease? Fortunately the period does oblige, at least partially.

 

Below, I quote from a journal article by Dr Al. Leshner, a neuroscientist fin the USA. Leshner holds a significant role in drug research, policy and administration. At least two of his papers discuss the question of why ‘drug use is a brain disease’ has been slow to enter the public discourse. Here is Al. Lashner’s profile. It comes from The American Association for the Advancement of Science.

leshner-alan[1]

Alan I. Leshner has been Chief Executive Officer of the American Association for the Advancement of Science and Executive Publisher of the journal Science since December 2001. Before coming to AAAS, Leshner was Director of the National Institute on Drug Abuse. He also has served asDeputy Director and Acting Director of the National Institute of Mental Health, held a variety of senior positions at the National Science Foundation, and served as a professor of Psychology at Bucknell University. Leshner received an undergraduate degree in psychology from Franklin and Marshall College, and M.S. and Ph.D. degrees in physiological psychology from Rutgers University.

These are extracts from his paper, Addiction is a Brain Disease and it Matters, in Science:

Dramatic advances over the past two decades in both the neurosciences and the behavioral sciences have revolutionized our understanding of drug abuse and addiction. Scientists have identified neural circuits that subsume the actions of every known drug of abuse, and they have specified common pathways that are affected by almost all such drugs. Researchers have also identified and cloned the major receptors for virtually every abusable drug, as well as the natural ligands for most of those receptors.

In addition, they have elaborated many of the biochemical cascades within the cell that follow receptor activation by drugs. Research has also begun to reveal major differences between the brains of addicted and nonaddicted individuals and to indicate some common elements of addiction, regardless of the substance.

That is the good news. The bad news is the dramatic lag between these advances in science and their appreciation by the general public or their application in either practice or public policy settings. There is a wide gap between the scientific facts and public perceptions about drug abuse and addiction. For example, many, perhaps most, people see drug abuse and addiction as social problems, to be handled only with social solutions, particularly through the criminal justice system. On the other hand, science has taught that drug abuse and addiction are as much health problems as they are social problems. The consequence of this gap is a significant delay in gaining control over the drug abuse problem.

Part of the lag and resultant disconnection comes from the normal delay in transferring any scientific knowledge into practice and policy. However, there are other factors unique to the drug abuse arena that compound the problem. One major barrier is the tremendous stigma attached to being a drug user or, worse, an addict. The most beneficent public view of drug addicts is as victims of their societal situation.

However, the more common view is that drug addicts are weak or bad people, unwilling to lead moral lives and to control their behavior and gratifications. To the contrary, addiction is actually a chronic, relapsing illness, characterized by compulsive drug seeking and use. The gulf in implications between the “bad person” view and the “chronic illness sufferer” view is tremendous. As just one example, there are many people who believe that addicted individuals do not even deserve treatment. This stigma, and the underlying moralistic tone, is a significant overlay on all decisions that relate to drug use and drug users.

These difficulties notwithstanding, I believe that we can and must bridge this informational disconnection if we are going to make any real progress in controlling  drug abuse and addiction. It is time to replace ideology with science.

 

This is a shocking indictment. Blaming drug abuse on pathological social or personal conditions goes back at least to the 1950s over 62 years ago. It was not evidence based then. As a theory it did not help addicts then nor does it help now. It interferes with our legal and justice system, it sabotages our relationships with other countries, and costs immense sums of money.

Thinking solely as an anthropologist at the moment I ask myself what does the AngloSphere gain by maintaining this belief? It creates a group of scapegoats; without the weak and perverse drug users, we could not acknowledge a better class of people. At the same time, it manifests and reiterates the beliefs of revealed religions like Christianity, Islam and Judaism that mankind is full of sin.

 

Reference

Leshner, A.I. (1997). Addiction is a brain disease, Science, 278, pp.45–47.

It was the 1980’s, and  I had reached the point where my credibility as an anthropologist demanded I do field work. It would be something on drugs of course. But what exactly?

I decided to formulate some test hypotheses that would cover both social and biological aspects of drug consumption. My research into prehistoric drug use together with findings from ‘current’ neuropsychopharmacology (i.e. from the 1970’s -1980’s period)  would suggest these hypotheses. The  fact that I possessed the rare combination of both pharmacy and anthropology qualifications meant I had the chance to make a worthwhile contribution to an important issue of my time.

I ran into a problem straight away. I could find no references in popular culture of the 1980’s  to the neuroscience concept that drug addiction is a ‘relapsing’ brain disease like schizophrenia or diabetes; that even the though the initial act of consumption is entirely voluntary   brain disease develops over time and that without formal medical treatment, compulsive drug craving, seeking, and consuming take over (Leshner, 1990).

This  neuroscience discovery is, and remains, a gloomy finding. Al Gore might well think of it as another ‘Inconvenient Truth’  like ‘Climate Change’. Could I have been wrong in evaluating so highly the neuroscience research on psychoactive substances ? After all, I am a pharmacist not a pharmacologist. So it was possible the neuroscience findings held flaws I had missed.

Nevertheless, great synergy exists between patterns of prehistoric drug consumption and the neuroscience model of drug effects on individuals. A few examples make the point:   All else being equal, if human biology is capable of producing compulsive drug seeking and consumption, then you would expect to find drug plants among the earliest plants prehistoric people cultivated. Similarly, drugs should be  among the earliest items traded between different environments and populations. Finally, prehistoric populations with regional monopolies on drugs should demonstrate political and social changes forced upon them by the compulsive drug seeking from their addicted non-drug producing neighbours. See my earlier blogs for examples:

A. I. Leshner, “Science-Based Views of Drug Addiction and Its Treatment,” Journal of the American Medical Association 282 (1999): 1314­1316 (http://jama.ama-assn.org/issues/v282n14/rfull/jct90020.html

Knowledge is often slow to permeate throughout the public domain; sometimes it never does. What would be the result with the neuroscience research? The ideas that drug use and drug-seeking are biologically normal and that they result from initial contact between consumption of a psychoactive substance, and a seductive evolutionary process in consumers’ brains, may be too novel and too consequential for easy digestion. However if the neuroscience model were to be fully accepted and promoted, there would be significant losers. These would be the powerful professional groups and government departments currently supporting the belief that it is the weak, the socially disadvantaged, and the psychopath who turn to drug use/abuse for relief. This would not be the greatest concern however.

In his valedictory to C.R Schuster, the latter’s lab colleague and fellow scientist William Woolverton PhD., (July 2011) claimed that animal drug choice issues became his (Woolverton’s) continuing intellectual challenge and pleasure. However, he and others have been ‘bedeviled’ ever since by the question raised by animal drug choice research: does free will exist or not? I mention this story because I think this will be a common reaction to the neuroscience model of drug use/abuse.

For millennia, peoples, societies and religious sects have debated whether individuals make free choices about their lives without the interference of Gods, or Fate, or other external influences. Today, this issue seems dormant. Nevertheless, many of our significant cultural constructions, like religion, moral authority and the legal system, stand upon the concept that individuals have free will.  It is difficult to see how these could continue to be compatible with accepting the biological basis of drug addiction.

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To date, my posts about prehistoric drugs have roughly followed the time sequence in which these interests absorbed my attention. My next step was planning my fieldwork. Traditionally in anthropology, novices best prove their abilities by living unsupported in the toughest community they can stomach. Naturally it must also be relevant to your hypotheses. Mine was based on inferences from pituri and the neurological model of drug abuse. So I needed   an isolated drug using community that might serve as an ethnographic model as close as possible to a prehistoric community.

I do intend to include an account of this field work in this blog because it is very relevant. However I (or rather my shell) is becoming very aged and I feel I might not be able to finish it.  So, my next post will leave you with a 2013 account of what I see as the current situation with the neurological model of drug use.

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Bibliography

Woolverton, W. (2011). A Tribute to Charles Schuster, PhD. Psychopharmacology and Substance Abuse e Newsletter, July.

http://www.apadivisions.org/division-28/publications/newsletters/psychopharmacology/2011/07/charles-schuster-tribute.aspx

An example of how excessive [drug] behavior occurs might be provided by the socioeconomically deprived ghetto youngster who becomes involved with heroin use through peer pressure and finds such use an acceptable means of alleviating negative personal feelings (anxiety, insecurity, hostility, and frustration) allowing him to ‘feel good’ about himself and his environment.  On the other hand, a middle‑class, Irish Catholic, white male may resort to excessive alcohol use as the preferred vehicle for alleviating his hypophoric state and thus capture the same ‘feel good’ aura (Mule 1984:53).

Keup (1982:10) listed thirty‑seven named, separate, socio-cultural factors involved in “the aetiology  of maladaption [with drugs] the vicious circle of  causative factors involving the family, the youth and  industrial society”. He presents profiles of young drug  abusers, classifying them as either conformists, searchers,  experimenters, gluttons, or dionysians.

I have not written earlier about traditional explanations of drug use and drug abuse because the topic lacked relevance in a prehistoric context. Now I do so. You need to understand the old traditional model to understand the contribution  the neurosciences makes to understanding drug use/abuse. Apart from other issues the latter model is central to my question of whether drug use is result of socio-cultural conditioning or whether it is something rooted deep in mammal brain structures.

Examples of  ’the traditional explanation’ of drug misuse or abuse appear in the introductory quotes. As you can see, social causality and psychological dynamics rate as the villains. These explanations go back at least to the 1940s, possibly much earlier. Not only did individuals adopt these perspectives but so did institutions  ostensibly friendly to drug abusers. The Odyssey House movement refers to clients as ‘sociopaths’ who have never learnt either to trust or to cope.  Even  Alcoholics Anonymous, which is founded upon the concept that  alcohol abuse is a disease, also paradoxically argues that  the blame for contracting the disease rests with the  victim, referring to the “serious character flaws which made  problem drinkers of us” in the first place (Alcoholics  Anonymous quoted in Milam and Ketcham 1985:140). Some scientists imply a criticism of this model  claiming  that,  since 1984  virtually all forms of psychopathology have  been given causal roles in the use/abuse of drugs of psychoactive drugs. The implication here, I believe, is that if the one action is attributed multiple causes, then none of the causes may be correct (Schuster, Renault and Blaine 1979).

 This echoed my own feelings that the traditional explanation of drug misuse or abuse was unhelpful.  And like many people I had one or two heavy drug (alcohol)  users in my social group, and I was saddened by the social stigma they attracted. So I began  following the neuroscience research in the early 1980s through my pharmacy background. I found it exciting. It satisfactorily linked drug chemistry to brain chemistry in arguing that the drugs we consume to alter our moods, soothe our anxieties, explore our creativity, revitalize our courage etcetera, all contain neurotransmitter chemicals identical to neurotransmitters in our brains. The addition of  drug plant neurotransmitter to the neurotransmitters natural to our brain, caused the brain to react by changing the synthesis of the ‘home-grown’ neurotransmitters, or by altering their storage or  release. This was the means by which drug consumption allows individuals to alter their emotions, mood, memory, powers and perceptions of self and others.

The brain’s reward system becomes involved also. As a result, every drug-consuming mammal, whether human or non-human, immediately experiences the urge to continue using psychoactive substances.  Even before any adjustment to the physical body occurs, this form of biological addiction affects all mammals who sample psychoactive substances, whether housewives or CEOs, parrots or bears. With  their first taste of a drug, innocent consumers fall victim to an evolutionary ‘tweak’. The addict is innocent.

Nevertheless not every human individual slips into chronic drug seeking as a result of this exposure. Dr C.R.  Schuster, who in1980 headed the lab for psychopharmacology at  the University of Chicago, noted that a range of cultural and environmental factors may and does limit initial drug use. My accounts of prehistoric drug use reveals some of these environmental factors: for example  continuing supply shortages of pituri and exact knowledge of where it grew, certainly limited use. Socio-cultural restraints shaped consumption too. Aboriginal societies were mostly gerontologies at the time. Powerful older men ensured that life’s goodies went only to powerful older men; and only revered older men knew the secrets of curing Duboisia hopwoodii plants to produce ‘real’ pituri.

I saw  this new research—animal models of drug abuse together with the existence of a reward structure in the brain—as an entirely novel paradigm, full of promise in a world where the old model was visibly failing.

Below I have summarized the two models as I understand them to be. This  will be followed by discussion of what I regard as significant aspects of the neuroscience model.

 

The diagram below shows the differences between the two models as I understand them.

PSYCHO-ACTIVE DRUG ISSUES

 

ISSUE TRADITIONAL MODEL  NEUROSCIENCE  MODEL
EXPLANATION OF  WHY PSYCHO-ACTIVE DRUG PLANTS IMMEDIATELY  REWARD  USERS No explanation Drug plants contain chemical analogues of brain neurotransmitters; drugs can replace the latter, and  act on reward strata in human (+ animal)  brains.
INHERENT PATTERN OF DRUG USE  Moderate drug use until and unless addiction develops  Being biological in origin, initial drug use is reinforced, leading to  unrestrained drug use, in absence of existing or imposed restraints 
ROLE OF SOCIO-CULTURAL FACTORS INCL. LEGAL, ECONOMIC + PERSONAL  Adverse socio-cultural factors incl. individual psycho- pathologies lead to 

Excessive Drug  Use/Abuse

 

Positive socio-cultural factors +  accurate drug information alter   unrestrained drug use toModerate Drug Use 

Such observations suggest that pre-existing psychopathology is not a requisite for initial or even continued drug taking’and that drugs themselves are powerful reinforcers, even in the absence of physical dependence (Gilman et al. 1985:534).

Please note: the above quote was in my previous post. It is repeated here because it should have been followed by the following paragraph:

The ‘reinforcing capacity of a drug’ became the term referring to a particular drug’s inherent capacity to induce animals to repeat actions which result in drug administration. The reinforcing factor appeared to differ for each drug. For example, under a that particular laboratory set-up, rats would press a bar 250 times to obtain caffeine, 4,000 times for heroin, but 10,000 consecutive times to obtain cocaine (Spotts and Shontz 1980:15).

Although wild animals do not have comparable access to drugs, there are numerous examples of them ingesting psychoactive substances. There is a close association between reindeer and the psychoactive fly agric mushroom in Siberia (Furst 1976:101). It is commonly accepted that grazing animals prefer fermented fallen fruit and that birds sometimes select nectars which intoxicate. Altogether, by the 1980s, increasing evidence demonstrated that animals seek out psychoactive experiences. Researchers from the University of California claim knowledge of more than 2,000 cases of animals consuming psychoactive substances, of which 310 were investigated and their use found to be ‘intentional and addictive’ (Greenberg 1983:300). And see next post.

About the same time as queries began about excessive drug seeking, a rush of interest grew in the unfolding science of neurobiology. Instead of electricity firing the brain as formerly thought, scientists discovered that central nervous system activity depended upon at least fifty chemical compounds academics named ‘neurotransmitters’. The latter controlled and coordinated flows of information between the neurons within the brain, including data about emotions, memories and pleasures.

The main chemical transmitters include dopamine, acetylcholine, nor epinephrine, serotonin, gamma amino butyric acid, and the recently discovered opioid peptides. Each possesses a specific molecular and spatial arrangement which enables it to ‘plug’ into a receptor in a target neuron, rather like a key into a lock. The neuron is thus activated: information passes from one neuron to the next, and the neurotransmitter, its function accomplished, decays.

This may seem far distant from packing a cone or sipping gin and tonic. Here is the connection. Human and non- human mammals are not the only natural phenomena containing neurotransmitters. Some plants contain (almost) identical chemicals. A unique situation results. The nicotine in tobacco, for example, fits receptors designed for the acetylcholine receptor and, once plugged into the receptor, nicotine activates the same processes that acetylcholine can activate. Similarly, morphine from opium poppies fits receptors for the body’s endogenous opiates… and so on for each of those plants which contain chemical compounds which are analogous to brain neurotransmitters.

Olds, acknowledged now as one of the fathers of neuroscience, raised the suggestion that mammal brains (that is, those of human plus non-human mammals) might possess a ‘reward’ strata; Olds had in mind some sort of pay-off which would automatically follow mating, eating, and drinking, and thus encourage repetition of these acts. The concept of a reward structure gradually found acceptance, and in 1976 Olds suggested that drug use may also involve the neural substrate concerned with the brain reward system. Olds based this on the structural resemblances between psychoactive drugs and neurotransmitters, and the fact that drug use clearly reinforced further drug use.

Subsequent studies justify Old’s hypothesis and revealed that people consuming drugs are strengthening or inhibiting neurotransmitters in their brains, or changing their synthesis, storage or release. Through this, drug consumers alter emotions, mood, memory, reasoning powers and perceptions of self and others (Levine 1978:344; Nahas 1981).

However, some differences exist between the two situations: ie in the behaviour of brain transmitters versus drugs analogous to natural brain transmitters. Appetite, satiation, sexual depletion and other biological restraints govern mammal capacity to eat drink, and mate. Consequently the latter activities are not constantly reinforced to the extent that drug use is. See below. Additionally, the plant chemicals drug users select are much more resistant to decay than are the mammal neurotransmitters of which the plant chemical are analogues. Consequently plant chemicals remain longer at the site than the genuine neurotransmitters, and often become potent neurotoxic agents (Kosterlitz and Hughes 1978:412).

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The results of animal research has received extensive critical scrutiny. It has to do with money. New synthetic drugs are more likely to receive approval from the United States Food and Drug Administration if they have little or no reinforcing capacity. To evaluate this, three research methods are utilized: drug substitution procedures; continuous self administration with naive animals; and use of escape/avoidance behavioral baselines (Thompson and Young 1978:119 129). Tests use a variety of species (e.g. rat, dog, cat, and non human primates); and investigators use different devices (e.g. lever press, panel press), and different routes of drug administration (e.g. intravenous, oral, intragastric, and inhalation) (Kalant et al.1978:466). Research indicates a number of factors exist which can modify individual animal response. However test results for particular drugs are consistent from laboratory to laboratory even with different experimental parameters and test situations.

Neither is the applicability of the findings to human beings in doubt. The Committee on Problems of Drug Dependence of the National Research Council National Academy of Sciences has addressed this matter as have Thompson and Young (1978), and Johanson and Balster (1978). These sources conclude that the model is valid in respect to humans since the results with a particular drug are consistent from laboratory to laboratory. And these results accord with empirical observation: laboratory animals largely self administer the same drugs which are abused by humans, but do not self administer drugs which are not abused by humans. Hallucinogens seem to be an exception; laboratory animals do not self administer these, even though humans do. However, as noted earlier, there are records of wild animals seeking out hallucinogenic plants so the problem here may be one of failure to deliver the drug to the appropriate tissue.

The conclusion therefore, is that drug users everywhere experience changes in the functioning of reward processes in the limbic system of the brain. As a result, in a situation free of effective controls, users in any society with open access to drugs will consume them in an open ended, unscheduled fashion, and without reference to controls which operate with foods, that is, appetite and satiation.

This does not imply that the effects of drugs on reward centres always ‘induce a compulsive drug oriented behaviour’ (Nahas 1981:1). It is the chemical interaction between drugs and neurotransmitters which is similar in both human and non human animals, not the subsequent behaviour.

Human behaviour depends upon values: social, economic, legal and religious. In fact, the late Schuster, one of the seminal figures in research into drug seeking behaviour among animals, clearly appreciated the sociological implications of his work, particularly the increased importance it gives to social controls.

We are depending on a variety of countervailing influences to prevent the organism [Homo sapiens] from engaging in behavior which evolutionary mechanisms have made extremely seductive…. Why is it that members of this symposia audience, most of whom have access to the major drugs of abuse do not use them in an unregulated manner? We know far too little about the social and psychological factors which produce this resistance to the abuse of drugs. It is our position that this is a major area which must be researched if we are to develop effective prevention to unregulated drug use. In conclusion, our major message is that drug taking is biologically normal and society must learn to live with that fact and to develop the necessary constraints to prevent unregulated drug use (Schuster, Renault and Blaine 1979:17) (italics added).

Bibliography

The Committee on Problems of Drug Dependence of the National Research Council National Academy of Sciences
Furst, P. (1972). Flesh of the gods:the ritual use of hallucinogens. London:George Allen & Unwin.

(1979). Hallucinogens and culture.San Francisco: Chandler & Sharp.

Gilman, A.G., L.S. Goodman, T.W. Rall, and F. Murad (eds.) (1985). Goodman and Gilman’s pharmacological basis of therapuetics. 7th ed. New York: Macmillan.

Greenberg, J. (1983). Natural habits in natural habitats. Science News 124: 300-301.
Johanson, C., and R. Balster. (1978). A summary of the results of a drug self-administered study using substitution procedures in rhesus monkeys. Bulletin on Narcotics 30: 627-628.

Kalant, H. et al. (1978). Behavioral aspects of addition: group report. In J. Fleishman (ed.) The bases of addiction: Report of the Dahlem Workshop on the Bases of Addiction. Abakon: Verlagsgesellscgaft.
Kosterlitz, H.W. & J. Hughes. (1978). Endogenous opoid peptides. In J. Fleishman (ed.) The bases of addiction: Report of the Dahlem Workshop on the Bases of Addiction. Abakon: Verlagsgesellscgaft.

Levine, R.R. (1978). Pharmacology: Drug actions and reactions. Boston: Little Brown and Company.

Nahas, G.G. (1981). A pharmacological classification of drugs  of abuse. Bulletin on Narcotics 33: 1-19.

Schuster, C.R., P.F. Renault, and J. Blaine. (1979). An analysis of the relationship of psychopathology to non-medical drug use. In R. Pickens and L. Heston (eds.) Psychiatric factors in drug abuse. New York: Grune & Stratton.

Spotts, J. & F. Shontz. (1980). Cocaine users : a representative approach. New York: Macmillan Publishing Company.

As the prehistoric period begins to close up everywhere—even in the isolated crannies and corners of the world—millennia of prehistoric drug use have left us with no understanding at all of why people use psychoactive dugs. Human beings eat and drink only those substances which nourish their bodies, drugs excepted. They don’t eat soil or grasses  except under bizarre conditions. A half answer might be that we use drugs because drugs satisfy us just as food does. But this begs the question, why should feelings of reward attach to drugs when those same feelings do not attach to any substance accept those that our bodies need ?

In a reversal of natural sequencing, the answer to ‘why do individuals use drugs?’ became clear  following research into ‘why do some individuals overuse drugs?’

 This research began in the USA in the 1960s, following the influx of what seemed excessive student drug use and multiple drug use on US campuses. At the time, the current explanatory paradigm emphasized the causal relationship between drug seeking behaviour and physical dependence, a physiological state which could be empirically verified. Accordingly, early experiments used as subjects already drug dependent animals; it being both unethical and difficult to use people in this type of investigation.

Laboratory animals quickly learn to self administer most of the drugs commonly used by individuals for non‑ medical, recreational purposes. These included  opoids, barbiturates, alcohol, anesthetic gases, local anesthetics, volatile solvents, and central nervous system stimulants like  phencyclidine, nicotine and caffeine. However, animals avoided using substances ignored by humans. This indicated, at first thought, a causal relationship between physical  dependence and drug‑seeking behaviour.

 But logic and  empirical observation led to further investigation.  It revealed that some drugs which do not produce physical  dependence nevertheless produce drug‑seeking behaviour in  experimental animals.  Moreover, it was realized that, even with drugs that produce physical  dependence, the initial drug‑seeking behaviour could not be  attributed to physical dependence since this takes time to  become established.  The general text book Goodman and  Gilman’s Pharmacological Basis of Therapeutics (1985) describes  this research thus:

 

Such observations suggest that pre‑existing psychopathology is not a requisite for initial or even continued drug taking, and that drugs themselves are powerful reinforcers, even in the absence of physical dependence (Gilman et al. 1985:534).

  Although  wild animals do not have comparable access to drugs, there  are numerous examples of them ingesting psychoactive  substances.  There is a close association between reindeer and the psychoactive fly‑agaric mushroom in Siberia (Furst  1972:101).  It is commonly accepted that grazing animals  prefer fermented fallen fruit and that birds sometimes select nectars which intoxicate.  Altogether, there is  increasing evidence that animals seek out psychoactive  experiences.  Researchers from the University of California  claim knowledge of more than 2,000 cases of animals  consuming psychoactive substances, of which 310 were  investigated and their use found to be ‘intentional and  addictive’ (Greenberg 1983:300).

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Simultaneous with the above research, a rush of interest began in the newly unfolding science of neurobiology. Instead of electricity firing the brain as formerly thought, scientists discovered that central nervous system activity depended upon least fifty chemical compounds named neurotransmitters. The latter controlled and coordinated flows of information between the  neurons within the brain, including data about  emotions, memories and pleasures.

 The main chemical transmitters  include dopamine, acetylcholine, nor epinephrine, serotonin,  gamma‑amino butyric acid, and the recently discovered opoid  peptides. Each possesses a specific molecular and spatial  arrangement which enables it to ‘plug’ into a receptor in a  target neuron, rather like a key into a lock.  The neuron is thus activated, information passes from one neuron to the  next, and the neurotransmitter, its function accomplished, decays.

 This may seem far distant from  packing a cone or sipping gin and tonic.  Here is the connection. Humans and non- human animals are not the only natural phenomena containing neurotransmitters. Some plants contain (almost) identical chemicals.  A unique situation results. The nicotine in  tobacco, for example, fits receptors designed for  the acetylcholine receptor and, once plugged into the receptor, nicotine  activates the same processes that acetylcholine can activate. Similarly, morphine from opium poppies fits receptors  for the body’s endogenous opiates… and so on. 

However, one difference exists  between plant chemicals and the mammal neurotransmitters of  which they are analogues. Plant neurotransmitters are  much more resistant to inactivation by biotransformation  processes. Therefore plant neurotransmitters often become potent neurotoxic  agents (Kosterlitz and Hughes 1978:412).  Thus, the effect of  psychoactive drugs is to potentiate or inhibit  neurotransmitters, or alter their synthesis, storage or  release.  By this means drug use modifies memory, learning,  emotions, mood, and perceptions of self and others (Levine  1978:344). 

That leaves unanswered the question, “why do drugs make us feel good?”

 Bibliography

Furst, P. (1972). Flesh of the gods: The ritual use of hallucinogens.London. George Allen & Unwin.

Greenberg, M. (1983). Natural highs in natural habitats. Science News, 124, 300-301.

Gilman, A.G., Goodman, L.S., Rall, T.W, & Murad, F. (1985). Goodman and Gilman’s pharmacological basis of therapeutics. New York. MacMillan.

Kosterlitz, H.W., and Hughes, J. (1978). Endogenous opoid peptides. In J. Fishman (Ed) The bases of addiction: Report of the Dahlem Workshop on the bases of addiction. Abakon. Verlagagesellschaft.

Levine, R.R. (1978). Drug actions and reactions. Boston. Little Brown and company.

Schuster, C. (197) Drugs as reinforcers in monkey and man. Pharmacological Reviews 27:511-251