Lecture proposes a philosophical synthesis of the key concepts of the alcohol addiction neuroscience (the anhedonia hypothesis, the want-like system, the incentive salience hypothesis) and psychology (the rational choice model). As a core component the experience is reconstructed to become habitual during subsequent alcohol misuse. The existential phenomenology (Ludwig Binswanger) interpretation is provided.
KEY HYPOTHESIS
The addictive intake of alcohol and other narcotic drugs forms a simple snippet of code that circumvents the physiological paths of the tricky' reward system into discerning behavioral patterns to achieve some useful aims.
A core component of this presentation is alcohol experience. We tried to consider it as a whole, to describe its fluidity as some totality and uniqueness at the same time. We have found that this alcohol experience should not be fully integrated into existing or airy future theories corrected by rigid methods or firm recommendations. The disclosure of air alcohol experience has accomplished the special philosophical mission. This approach has derived much of its inspiration by the spirit of classical psychoanalysis, which was first in the field of expertise corresponding pathological experience.
The peripeteia of addictive behavior offers such an example of aspiration to a momentary pleasure that leads to new troubles proceeding through a sequence of stages beginning with a deeper dividing of the Self, social stigmatization, social death and, finally, biological death. Thus, we face philosophical challenges. Internally, alcohol may be ideating as a rapid elevator to the Wonderland of dream, happiness, pleasure or calmness. But the best we can say here is that these wishes, wanting and liking act as certain hacked codes for both the mind and the neurobiology of the brain.
This presentation has shown that, although the brain impulses either trigger or support alcohol addiction, we can never confine mental activities to certain physical and chemical processes in a human brain, nor can we reduce our life to mere physiological reactions, behavior models and psychological affects.
2. KEY HYPOTHESIS
• The addictive intake of alcohol and
other narcotic drugs forms a simple
snippet of code that circumvents
the physiological paths of the tricky'
reward system into discerning
behavioral patterns to achieve
some useful aims
4. Medical definition
• Drug addiction manifests as a compulsive drive to take a drug
despite serious adverse consequences.
• This aberrant behavior has traditionally been viewed as a bad
"choice"
• This is because drugs of abuse impact many neuronal
circuits, including those involved in the processing of
response to rewarding and aversive stimuli, interoception,
emotions, decision making, and cognitive control, turning drug
use into an automatic compulsive behavior
.The ASAM principles of addiction medicine. Philadelphia: Wolters Kluwer Health/Lippincott Williams &
Wilkins.
9. DSM-5 Addiction Definition
‘All drugs that are taken in excess have in
common direct activation of the brain reward
system, which is involved in the reinforcement
of behaviors and the production of memories.
They produce such an intense activation of the
reward system that normal activities may be
neglected. Instead of achieving reward system
activation through adaptive behaviors, drugs of
abuse directly activate the reward pathways. The
pharmacological mechanisms by which each class
of drugs produces reward are different, but the
drugs typically activate the system and produce
feelings of pleasure, often referred to as a ‘high’’
Diagnostic and statistical manual of mental disorders: DSM-5. 5th ed. Washington D.C.: American Psychiatric
Association. 2013:481
11. How The Story Began
JAMES OLDS
May 30, 1922–August 21, 1976
• Considered as
discoverer of the
"reward" system in the
brain
• Jacobsen and Torkildsen
replicated work in human
Olds, James, and Peter Milner. 1954. “Positive reinforcement produced by electrical stimulation of septal
area and other regions of rat brain.” Journal of Comparative and Physiological Psychology 47(6):419–27
12. Electrode Stimulation
• Mild electrical stimulation of
subcortical structures
associated with the medial
forebrain bundle
• Animals would avidly perform
tasks in order to receive such
brain stimulation
• In the aftermath of this
discovery of the phenomenon
of brain stimulation reward
Gardner, Eliot L. 2011. “Addiction and Brain Reward and
Antireward Pathways.” Advances in psychosomatic
medicine 30:22
13. Animal vs Human
Reactions to Sweetness ‘Disgust’ Reactions to
Bitterness
Olney, Jeffrey J., Shelley M. Warlow, Erin E. Naffziger, and Kent C. Berridge. 2018. “Current perspectives on
incentive salience and applications to clinical disorders.” Current Opinion in Behavioral Sciences 22:59–69
14. RAT REWARD SYSTEMS
Olney, Jeffrey J., Shelley M. Warlow, Erin E. Naffziger, and Kent C. Berridge. 2018. “Current perspectives on
incentive salience and applications to clinical disorders.” Current Opinion in Behavioral Sciences 22:59–69
17. Addictive Substances
stimulants sedatives
pleasurable reinforcing
antinociceptive hallucinogens
rewarding
30,000,000 chemical substances are known
Yet, only approximately 100 (including
nicotine, ethanol, psychostimulants, opiates,
barbiturates, benzodiazepines and
cannabinoids) are addictive
18. Addictive Substances
Perhaps, all addictive drugs
(with the exception of the
LSD-like and mescaline-like
hallucinogens) activate the
reward circuitry of the brain
thereby producing the
subjective ‘high’ that the
drug abuser seeks.
Gardner, Eliot L. 2011. “Addiction and Brain Reward and Antireward Pathways.” Advances in psychosomatic
medicine 30:22–60
19. Animal Models
Laboratory animals volitionally self-administer ethanol , just as humans do. Furthermore, the rank
order of appetitiveness in animals parallels the rank order of appetitiveness in humans.
20. Animal Models
• Mice and rats can also voluntarily
drink large quantities of alcohol,
which leads to strong intoxication
• Some of the behavioral
characteristics of addictions
events, can be satisfactorily
modelled in laboratory animals.
• However, face validity is often a
result of anthropomorphic
interpretations of an animal’s
behavior.
Sanchis-Segura, Carles, and Rainer Spanagel. 2006.
“Behavioural Assessment of Drug Reinforcement and
Addictive Features in Rodents: An Overview.” Addiction
biology 11(1):2–38
21. Animal vs Human
Reactions to Sweetness ‘Disgust’ Reactions to
Bitterness
Olney, Jeffrey J., Shelley M. Warlow, Erin E. Naffziger, and Kent C. Berridge. 2018. “Current perspectives on
incentive salience and applications to clinical disorders.” Current Opinion in Behavioral Sciences 22:59–69
23. Addictive Drugs Act To Enhance Brain
Reward Mechanisms
Gardner, Eliot L. 2011. “Addiction and Brain Reward and Antireward Pathways.” Advances in psychosomatic
medicine 30:22–60
24. “Orchestrate” The Reward Profile Of Ethanol
Serotonin
Dopamine
GABA
Opioids
Alcohol Reward
Koob, George F. 2000. “Neurobiology of addiction: toward
the development of new therapies.” Annals of the New
York Academy of Sciences 909(1):170–85
26. Reward Pathways Are Very Old
• Surprisingly the brain structure that responsible
for reward lays in the old areas of the brain and so
is not strongly human
• The areas of brain govern our biological reward
system that appeared long before we (as species)
had begun to exist. We can metaphorically
describe the reward system as a trace of God in
the human mind
• These brain structures are referred to as reward
pathways, which are very old from an evolutionary
point of view and which presumably evolved to
mediate an individual’s responses to natural
rewards, such as food, sex, and social interaction
Arias-Carrión, Oscar, Maria Stamelou, Eric Murillo-Rodríguez, Manuel Menéndez-González, and Ernst Pöppel.
2010. “Dopaminergic Reward System: A Short Integrative Review.” International archives of medicine 3:24.
27. Addiction Is A Brain Disease
Alan I. Leshner
Director of (NIDA) from 1994-2001.
• Addiction is a chronic,
relapsing brain disease
with a social context
• A genetic component
• This model of addiction,
which we would describe
as a natural science
Olds, James, and Peter Milner. 1954. “Positive reinforcement produced by electrical stimulation of septal
area and other regions of rat brain.” Journal of Comparative and Physiological Psychology 47(6):419–27
29. Worlds of Animals and Humans
Jakob von Uexküll
1864–1944
Nobody is a product of their
environment but everybody is
the master of one's Umwelt.
Uexküll, J. B., 1934. Streifzüge durch die Umwelten von Tieren und Menschen Ein Bilderbuch unsichtbarer
Welten.
30. Uexküll’s Umwelt
• The first principle of Umwelt is that “all
animal subjects, fare inserted into their
environments to the same degree of
perfection.
• Umwelt, within which the animal
establishes its “specific set of
relationships to its sources of
nourishment, its prey, its enemies, its
sexual mates, and so on
• Vital processes, and which can include
the subject, the living self; or life itself
32. Basic Worlds of Human
Mitwelt
Umwelt
Eigenwelt
Brain
• the Eigenwelt, the sphere of
man in relation to himself
• Umwelt -- the world of man
in his biological environment
• Mitwelt, man in personal
relations with fellowmen
35. The Dichotomy Of The First And Third Person
• Northoff speaks of the structures he called
neuronal states-, second, he considers the
mental states
• Neuronal states, which are related to
biology and belong to sciences. We can
speak of them in the third person or as
inanimate objects
• We can speak of our brain in third-person
perspective and speak of ourselves in first-
person perspective.
Northoff, Georg. 2004. Philosophy of the brain: The brain problem. Vol. 52. Netherlands: John Benjamins Pub..
36. Phänomenologie des Geistes
Hegel, Georg W. F. Phenomenology of spirit (1807)
Die Befriedigung -- Satisfaction2
Die Begierde -- Desire1
37. Discipline, Obedience, Self-Cultivation
• Desire and the Self certainty obtained in its gratification, are
conditioned by the object, for self a certainty comes from
superseding this other…
• Self consciousness is thus certain of itself only by superseding this
other that presents itself to self consciousness as an independent
life; self-consciousness is Desire.[…]it destroys the independent
object and thereby gives itself the certainty of itself as a true
certainty.
• Without the discipline of service and obedience, fear remains at the
formal stage, and does not extend to the known real world of
existence. Without the formative activity, fear remains inward and
mute, and consciousness does not become explicitly for itself …
38. Dienstes, Gehorsams und Bilden
• Die Begierde und die in ihrer Befriedigung erreichte Gewißheit
seiner selbst ist bedingt durch ihn, denn sie ist durch
Aufheben dieses Anderen
• Selbstbewußtsein [ist] hiermit seiner selbst nur gewiß durch
das Aufheben dieses Anderen, das sich ihm als selbständiges
Leben darstellt; es ist Begierde
• Ohne die Zucht des Dienstes und Gehorsams bleibt die
Furcht beim Formellen stehen und verbreitet sich nicht über
die bewußte Wirklichkeit des Daseins. Ohne das Bilden bleibt
die Furcht innerlich und stumm, und das Bewußtsein wird
nicht für es selbst.
40. Yevarouski, Valery. 2017. “Hijacking Sorrow, Joy,
Pleasure and Reward: A Philosophical Interpretive
Framework for the Theory of Alcohol Addiction.”
Sociologija. Mintis ir veiksmas 41(2):99–135.
42. Alcoholic experience
Valery Yevarouski
E-mail: walewr@gmail.com
The Centre for History of
Philosophy and
Comparative Studies
The Institute of Philosophy
of the National Academy of
Sciences of Belarus
Vilnius 2018
Editor's Notes
Drug addiction
Drug addiction manifests as a compulsive drive to take a drug despite serious adverse consequences. This aberrant behavior has traditionally been viewed as a bad "choice" that is made voluntarily by the addicted person, a view that engendered the lingering stigma of addiction as a moral failure. However, addiction researchers have collected converging evidence showing that chronic drug abuse changes the brain in ways that can lead to the profound behavioral disruptions seen in addicted individuals. This is because drugs of abuse impact many neuronal circuits, including those involved in the processing of response to rewarding and aversive stimuli, interoception, emotions, decision making, and cognitive control, turning drug use into an automatic compulsive behavior.
Alcohol addiction is a transdisciplinary problem
On the one hand, the psychiatry with the help of biochemistry and neurobiology suggests that the work of neurotransmitters in the human brain is disrupted (Courtwright 2010; Koob and Volkow 2010; Panksepp, Knutson and Burgdorf 2002). On the other hand, the psychology represents addiction as disorder of choice (Heyman 2010) or thoughtless actions (cognitive behavioral therapy (CBT) (Beck and Dozois 2014; Kaden 2001; Kadden 2007; Riper et al. 2014)). ‘CBT attempts to disrupt the learned association between drug-related cues or stimuli and drug craving or use by understanding and changing these behavior patterns’ (Ruiz, Strain and Lowinson 2011:593). Finally, we can consider the depth psychology including psychoanalysis, psychodynamic psychotherapy (Cassidy and Shaver 2008; Schneider, Pierson, and Bugental 2015). These branches of clinical psychology intend to remove the disharmony between different areas of the human mind. They also try to minimize many mental sufferings such an alcohol addiction by working with the unconscious (Flores 2001; Khantzian 2015; Wurmser 1987). Similarly, with this three-element scheme a philosopher (Shelby 2016; Shelby and Fiala 2013) can model other variants of inner and outer structures in the architecture of the soul that responsible for addiction and search for their balance. Alas, we will not do it without the verb ‘to try’. The borders between neurobiology, psychology and psychoanalysis are not clear (we mean their impact on human behavior and not the difference between disciplinary approaches). Therefore, any efforts to understand, to change or to correct an addictive behavior will have a probability of success and not the success.
According to neuroscience, the addiction is merely a disease of the brain; for psychology, it acts as an inability to make the right choices or as an expression of a disturbing thought; according to sociology, it becomes a sort of deviant behavior (Roman, Trice 1968; Blum 1984; Blum, Roman and Bennett 1989; Roman 2015). Quite contrary, we are seeking for a combination of these tactics and methods. Moreover, we do not ignore the cultural factors and we express regarding the independence of addictive behavior from any disastrous impact of one's social environment. We are going to discuss a domain of applicability of such philosophical concepts as the freedom of choice, self-perception of freedom, the free-will to the addiction studies. Second, we will explore the dissonance of addictive (and, in this sense, extremely egoistic) aspirations to the immediate pleasure with such morally recognized priorities as an intrinsic value of human life
Drugs, both legal (e.g., alcohol, nicotine) and illegal (e.g., cocaine, methamphetamine, heroin, marijuana) as well as abused psychotherapeutics (opioid analgesics, stimulant medications, benzodiazepines) can be abused for various reasons, including the experiencing of pleasure, altered mental states, improved performance, or, in certain instances, as an attempt to self-medicate a mental disorder. The repeated use of a psychoactive drug, in vulnerable individuals, can result in addiction, which is characterized by an intense desire for the drug combined with an impaired ability to control that urge, even in the face of well known adverse, eve|n catastrophic consequences (e.g. incarceration, loss of child custody, loss of medical license). (Ries et al. 2014:67)
The brain’s reward circuitry was first discovered by Olds and Milner [6] at McGill University in the early 1950s. They found that animals would repeatedly return to an area of the laboratory in which they had received mild electrical stimulation of subcortical structures anatomically associated with the medial forebrain bundle. Subsequently, they found that animals would avidly perform tasks (e.g. depressing wall- mounted levers in their test chambers) in order to receive such brain stimulation.
This system originates in the anterior bed nuclei of the medial forebrain bundle (an array of deep subcortical limbic loci anterior to the hypothalamus and preoptic area), descends to the ventral tegmental area of the midbrain via the medial forebrain bundle, and then ascends via the medial forebrain bundle to a select group of forebrain limbic loci including the nucleus accumbens, olfactory tubercle and frontal cortex. Wise and Bozarth [13] were the first to realize that this assortment of brain loci and tracts constituted a neural circuit containing three synaptically connected, in- series neuronal elements: a descending link running from the anterior bed nuclei of the medial forebrain bundle to the ventral tegmental area, an ascending link running from the ventral tegmental area to the nucleus accumbens, and a further ascending link running from the nucleus accumbens to the ventral pallidum. The first link is the descending myelinated fiber tract first identified by Gallistel et al. [12], of unknown neurotransmitter type, although very recent evidence raises, by inference, the possibility that glutamate in the ventral tegmental area might play a role [14
Electrical brain stimulation reward is remarkable for the intensity of the reward and reinforcement produced [1]. When the stimulating electrode is properly on target within the ventral tegmental area, medial forebrain bundle or nucleus accumbens, laboratory animals will volitionally self- stimulate those areas at maximal rates. They will, tellingly, ignore readily available food, water, toys and sexually receptive animals of the opposite sex in order to self- deliver the brain stimulation reward. They will also volitionally accept aversive and painful consequences in order to self- deliver the brain stimulation reward.
Addiction is defined as a syndrome in which drug use pervades all facets of the user’s life, even precipitating in the loss of social compatibility (e.g. loss of partner and friends, loss of job, crime...) [1]. It is obvious that addiction is a genuinely human phenomenon; and one that is therefore no reproducible within the unavoidable constraints imposed by the laboratory setting. However, some of the behavioural characteristics of this syndrome, such as resumption of drug seeking/drug consumption after a protracted abstinence (relapse), can be satisfactorily modelled in laboratory animals. For example, experimental procedures can be designed to be as simple as possible, thereby maximizing internal validity and thus reproducibility. Conversely, procedures can aim to be as holistic as possible, thereby favouring the possible relevance to human situations. Neither one of these two approaches is perfect; each has its respective drawbacks. Indeed, methods designed attending only to internal validity may finally exclude variables of relevance to understanding, explaining or predicting the phenomenon of interest. On the other hand, very complex procedures enhance the difficulty of arriving at conclusions and reduce the capability of both inferring causal relationships between variables and of establishing predictions.
This animal model has produced an impressive amount of information on brain mechanisms involved in addiction and on vulnerability factors in addiction. Recently, this model has been turned to the elucidation of incentive motivational factors in addiction, mechanisms underlying relapse to addiction and possible pharmacotherapeutic treatments for addiction.
I argue that animal models of voluntary drug intake—under nonoperant and operant conditions—and addiction models based on the Diagnostic and Statistical Manual of Mental Disorders are crucial and informative tools for the identification of pathological mechanisms, target identification, and drug development. These models provide excellent face validity, and it is assumed that the neurochemical and neuroanatomical substrates involved in drug-intake behavior are similar in laboratory rodents and humans. Consequently, animal models of drug consumption and addiction provide predictive validity.
Humans and laboratory animals, such as monkeys, rats, and mice, voluntarily take drugs by different routes of administration, be it orally or intravenously. If unlimited voluntary intravenous access to heroin or cocaine is provided, laboratory animals can easily overdose to death. Lethal overdosing also frequently happens in drug users. Mice and rats can also voluntarily drink large quantities of alcohol, which leads to strong intoxication. These characteristic features seen in drug-taking behavior in laboratory animals resemble drug-taking behavior in humans and suggests a high degree of face validity. How'ever, face validity is often a result of anthropomorphic interpretations of an animal’s behavior. If, however, behavioral features are evolutionarily de- veloped, real face validity is inferred. For example, behavioral fear responses are critical to most species for survival and developed over millions of years.
Incentive Salience [ɪn'sentɪv] ['seɪlɪən(t)s]
The reward system is described neurobiologically with the help of chemical and physiological processes in the brain (Koob, Arends and Le Moal 2014; Koob and Kreek 2007). Dopamine (Berridge and Robinson 2003), serotonin (Higgins and Fletcher 2003) and other neurotransmitters which are referred to the biochemical analysis of the reward system do not associate with fanfares, prizes, and other means of human reward. Everybody feel pleasure often, but our knowledge of this feeling (as all others) is extremely limited.
I might say something doubtful, but it seems so. In fact, both pleasure and disgust are not just reactions to signals from the world around us but also to the physiological and even chemical processes as such. The complex mechanism of dopamine release in the human brain is a natural process with physical, chemical and biological characteristics. However, no human approaches work in it. In other words, the sugar is not sweet. This characteristic cannot be applied to the reaction of our body to eating of sugar or to the combination of neurotransmitters making us find it sweet (Pecina, Berridge 2005). It is purely subjective estimation. However, we can go even further. The tastes can be divided into pleasant or geek. This division is a prompt to the body on what to do with food (Harington et al., 2016; Pandurangan, Hwang 2015). From this viewpoint, our actions can be estimated as beneficial, harmful and useless. Tire first ones should be kept, the
second ones should be avoided, and the third ones ought to be used to help the first ones with maximum efficiency. Thus, we get back to the reward system description. A person that believes in his or her unhappiness may simply think so. But we may say he or she lacks the internal potencies to stimulate the reward system properly (Volkow, Wise 2005).
One of the most striking features of drug addiction is how few chemicals are subject to abuse. If one takes all congeners of all known chemicals, approximately 30,000,000 chemical substances are known [1]. Yet, only approximately 100 (including nicotine, ethanol, psychostimulants, opiates, barbiturates, benzodiazepines and cannabinoids) are addictive. In truth, 100 is a stunningly small subset of 30,000,000. It poses the question: what makes those 100 chemicals addictive, while the remaining 30,000,000 chemicals lack this property
After all, upon cursory examination, there seem few pharmacological similarities among addictive drugs. Some - including barbiturates, ethanol, opiates and benzodiazepines - are sedatives, while others - including nicotine, cocaine and the amphetamines - are stimulants. Some - including opiates and cannabinoids - are antinociceptive, while others (in the proper laboratory or clinical situations) are pronociceptive.
However, a few commonalities are both apparent and instructive. All addictive drugs are subjectively rewarding, reinforcing and pleasurable [1].
And fourth, the reward structure we talk about is not entirely human. Remember its characteristics as an old structure of a humanoid brain that we got from animals and other biological ancestors. In this respect, its functioning is implicit for the whole humanoid mind structure and is in some contradiction with the nature of human activity at same time.
Let us imagine what the reward system can be as a function of animal behavior that is not burdened by social meanings and customs. It will not be too bold and suppose that animal ability to plan does exist but at a very rudimentary level (Bekoffet al. 2002; Lurz 2011). Thus, if we could talk to a bat (a kind of resorting to Thomas Nagel’s parallel (1974)), we would fail in persuading it to do something to get a reward in, say, a year. My research of intellectual history reveals that humanity, at its social level of evolution, not the biological one, had a long journey of the enlargement of our time intervals. The continued development taught us to plan for years to come and not just to live this day. Of course, only the bat can give the best answer to how harmonic its reward system function is in respect to its activities (for instance, predicting hunting targets or choosing the right mating partner). And, what is also important, how precisely probable behavior errors are corrected.
Incentive Salience [ɪn'sentɪv] ['seɪlɪən(t)s]
It should be ascertained that the reward center in the entire system of the human mind no longer seems to be simple. Moreover, it can be called an uncertainty raised to the fourth power. First, we are sure that the available knowledge about this part of the processes in the brain is very limited. Despite the improvement of tools and more sophisticated measurements, most conclusions in neurosciences are made because of indirect data, such as animal models (Lynch et al. 2010). Second, the reward system is not a rational structure and is therefore certainly uncontrollable by human logic. We tried to give it a digital character, and we can even describe the reward system as a set of algorithms. However, these algorithms are not a product of human consciousness and the rule of its construction is not known. Third, since we say that neuro- biological reward is the basis of the emotional system, then every situation of rein forcement is different - not to say unique. It is impossible to build up an ideal system where every step will bring only positive emotions.
First, each individual act of alcohol consumption causes an irregular set of reactions (not well understood or described). Second, the phenomenon of alcohol impact on the human body can be compared with a picture of a barrel of honey mixed with razor blades. In other words, a bunch of odd and even unpleasant sensations go with the relaxation or euphoric effect opposite to the expected ones (Koob, Le Moal 2008).
Ethanol hypnotics have been hypothesized to produce their reinforcing actions through a number of neurochemical systems, where multiple neurotransmitters combine to “orchestrate” the reward profile of ethanol. Acting neuropharmacologically on what have been termed ethanol-receptive elements, one of the major sites proposed for ethanol reinforcement has been the modulation of GABA receptors. GABAergic antagonists reverse many of the behavioral effects
Ethanol reinforcement also appears to involve activation of brain dopamine systems
Also, modulation of various aspects of brain serotonin systems including increases in the synaptic availability of serotonin with precursor loading, blockade of serotonin reuptake, or blockade of certain serotonin receptor subtypes can decrease ethanol
Koob, George F. 2000. “Neurobiology of addiction: toward the development of new therapies.” Annals of the New York Academy of Sciences 909(1):170–85
Alcohol activates y-aminobutyric acid-A (GABAa) receptors in the ventral tegmental area, nucleus accumbens, and amygdala via either direct actions at the GABAa receptor or through the indirect release of GABA. Alcohol is hypothesized to facilitate the release of opioid peptides in the ventral tegmental area, nucleus accumbens, and central nucleus of the amygdala. Alcohol facilitates the release of dopamine in the nucleus accumbens via an action either in the ventral tegmental area or the nucleus accumbens.
It should be ascertained that the reward center in the entire system of the human mind no longer seems to be simple. Moreover, it can be called an uncertainty raised to the fourth power. First, we are sure that the available knowledge about this part of the processes in the brain is very limited. Despite the improvement of tools and more sophisticated measurements, most conclusions in neurosciences are made because of indirect data, such as animal models (Lynch et al. 2010). Second, the reward system is not a rational structure and is therefore certainly uncontrollable by human logic. We tried to give it a digital character, and we can even describe the reward system as a set of algorithms. However, these algorithms are not a product of human consciousness and the rule of its construction is not known. Third, since we say that neuro- biological reward is the basis of the emotional system, then every situation of rein forcement is different - not to say unique. It is impossible to build up an ideal system where every step will bring only positive emotions. And fourth, the reward structure we talk about is not entirely human. Remember its characteristics as an old structure of a humanoid brain that we got from animals and other biological ancestors. In this respect, its functioning is implicit for the whole humanoid mind structure and is in some contradiction with the nature of human activity at same time.
Let us imagine what the reward system can be as a function of animal behavior that is not burdened by social meanings and customs. It will not be too bold and suppose that animal ability to plan does exist but at a very rudimentary level (Bekoffet al. 2002; Lurz 2011). Thus, if we could talk to a bat (a kind of resorting to Thomas Nagel’s parallel (1974)), we would fail in persuading it to do something to get a reward in, say, a year. My research of intellectual history reveals that humanity, at its social level of evolution, not the biological one, had a long journey of the enlargement of our time intervals. The continued development taught us to plan for years to come and not just to live this day. Of course, only the bat can give the best answer to how harmonic its reward system function is in respect to its activities (for instance, predicting hunting targets or choosing the right mating partner). And, what is also important, how precisely probable behavior errors are corrected.
These brain structures are referred to as reward pathways, which are very old from an evolutionary point of view and which presumably evolved to mediate an individual’s responses to natural rewards, such as food, sex, and social interaction. Drugs of abuse activate these reward pathways, in the absence of natural rewards, with a force and persistence not seen under normal conditions. Over time, repeated drug exposure causes adaptations in the brain’s reward pathways, which seem to have two major consequences. First, during periods of active drug use or shortly after ceasing drug intake, the ability of natural rewards to activate the reward pathways is diminished, and the individual experiences depressed motivation and mood. Taking more drug is the quickest, easiest way for a person with addiction to feel “normal” again. Second, drug use causes long-lasting memories related to the drug experience, such that even after prolonged periods of withdrawal (months, years), stressful events or exposure to the drug or to drug-associated cues can trigger intense craving, and in many cases relapse, in part by activating the brain’s reward pathways. Roughly half of the risk for addiction is genetic, although few specific genes that constitute this risk have to date been identified (6,7). A great deal of effort is aimed at identifying these specific genes and the mechanisms by which diverse nongenetic factors interact with the genes to influence the development of an addictive disorder.
It is accepted that human brain consists of two types of structures (Hofman 2014). There are new and old ones. The new structures are the direct consequence of the evolution of the homo sapience. The old segments of a human brain were inherited from progression of our biological predecessors like apes, reptiles or for example fishes. Surprisingly the brain structure that responsible for reward lays in the old areas of the brain and so is not strongly human. It is quite tricky: all human’s higher nervous activity, social achievements and losses can be ended with the processes in the depths of the brain. The areas of brain govern our biological reward system that appeared long before we (as species) had begun to exist. We can metaphorically describe the reward system as a trace of God in the human mind
Twenty years ago Alan Leshner, the former director of the National Institute on Drug Abuse, proclaimed that “addiction is a brain disease and it matters.”77 Although this statement gave an enormous boost to addiction research from a neuroscience perspective,
Current addiction scholarship traces the development of this paradigm from the official position of the National Institute on Drug Abuse (NIDA). Particularly, David Courtwright has noticed the following:
The key elements of the NIDA brain disease paradigm can be simply stated. They are that addiction is a chronic, relapsing brain disease with a social context, a genetic (or, more precisely, a gene-environment-stress-interactive) component, and significant comorbidity with other mental and physical disorders. Although drug use often begins voluntarily and develops overtime, users lose control with the onset of addiction. (Courtwright 2010: 137)
This model of addiction, which we would describe as a natural science approach, grows from earlier attempts to conceptualize alcoholic behavior implied in the medical frame. Elvin Morton Jellineks disease concept of alcoholism (Jellinek 1960) is considered as a key milestone of detecting alcoholism as a developed disease. However, the disease concept of addiction is harshly criticized by many psychologists and sociologists ‘as reductively inattentive to individual values and social context’.
The special objective of this article is to suggest the insights that we have found from the philosophical reflections on the experience of alcohol addiction. We describe its subjectiveness comprehensively with employing a certain conceptual design. At the same time, this experience offers intimacy and shows its ideographic structure. Within the framework of sociological theory, we can call such a technique an intra-case generalization (Salvatore 2014). As a philosophical discourse, our reflections on the essence of alcoholic experience fit into the tradition of Daseinsanalyse
Jakob v., A Foray into the Worlds of Animals and Humans [1934]: With a Theory of Meaning / Jakob Von Uexküll ; Translated by Joseph D. O'Neill ; Introduction by Dorion Sagan ; Afterword by Geoffrey Winthrop-Young. Vol. 12. 1st ed. Minneapolis, Minn.: University of Minnesota Press
Here we need to go further in our discussions on environment complex. Therefore, we are going to add another scheme originating from neurophilosophy: the dichotomy of the first and third person, suggested by Georg Northoff (2004). First, Northoff speaks of the structures he called neuronal states-, second, he considers the mental states. Neuronal states, which are related to biology, can be studied empirically and belong to sciences. It means we can speak of them (1) in the third person or (2) as inanimate objects. For instance, we can disturb the neurotransmitters in diverse ways to regulate sleep, mood and appetite by trying various medications. Mental states are the neurobiological resuIts of brain functioning. Brain death means the termination of every process of the human body, including mental and spiritual ones. It means that we can grasp the mental-brain relationship only ifwe turn oft certain brain structures or slow them down to such a degree that we can reach, for instance, a coma or stupor.