Making a Cognitive Sense of Censorship and Repression

Abstract

For some philosophers and thinkers (e.g., Jean-Paul Sartre), the repression theory of Sigmund Freud that posits a conscious ego and an unconscious id is an exercise in bad faith, a self-contradiction, and a metapsychological self-deception. The purpose of this paper is to demonstrate that Freud’s account of censorship and repression is cognitively sound, coherent, and within the realm of practical possibility. Informed by the epistemological insight of Thomas Aquinas and Bernard Lonergan on the vis cogitava, as well as recent findings of non-conscious cognition in neuropsychological studies, I will express how unconscious-conscious processing via repression is possible. 

Introduction

In the psychoanalysis of Sigmund Freud (1915d), repression involves turning or blocking away mental contents of unacceptable drives (e.g., sexual drives, aggressive thoughts, painful memories, and objectionable wishes) to the conscious personality and preventing them from emerging into consciousness. For him, drives produce affects-laden ideas, such as shame, guilt, and sadness. In his early psychoanalytic theory, Freud described repression as a dissociation of affects (emotive energies) from ideas. Following this dissociation, memories representing affective drives would disappear into unconsciousness, while affects, through associations, would further transform, disguise, or distort into useful and acceptable conscious ideas. In his later psychoanalytic theory, Freud (1915d, 1915e) saw repression simply as the prevention of unpleasurable affects loaded with ideas from reaching consciousness. In both descriptions, repression serves as a defense mechanism of the ego, blocking affect-loaded memories in the unconscious or dissociating affects from their memories and transforming the affects into other useful ideas (Freud, 1915d). In this way, unacceptable impulses escape or avoid the retaliation of the superego and the experience of other anxieties, the intensity of unpleasant drives decreases, and the energy investment for repression reduces. Further, Freud maintained that repressed materials are unconscious, but the process of repression may be unconscious or unconscious.  

 However, a fundamental question regarding the repression of unwanted affect-laden ideas into the unconscious is: how can the secondary process of psychic function, which is reflective and intentional (Breuer & Freud, 1895d) operate within the region of the unconscious in its function of repression, without the unconscious becoming conscious? In other words, if the unconscious must remain unconscious during the process of repression, how can the ego keep them unconscious while simultaneously remaining conscious of this function?  Another fundamental question regarding Freud’s theory of repression and censorship is: how can the unconscious ego make judgments and affirmations of the reality of what is pleasurable or unpleasurable, which is at the level of knowledge and still remains unconscious?  On this note, Sartre (1956) critiqued that the very idea of repression is problematic because it requires that the censor knows and does not know at the same time.  

A third question is: how can the affect-idea dissociation account of Freudian repression explain the persistent, powerful effect of the unconscious ideas toward the conscious thinking in the symptom-formation (e.g., in hysteria, anxiety, and depression, compulsion), since the affect-idea dissociation means that the repressed unconscious ideas are too weak to act on the conscious awareness?  In this paper, therefore, I will look at these epistemological difficulties of Freudian repression and censorship and show possible cognitive compatibilities of unconsciousness and consciousness. Examined in this light, I will show that repression plays an important role in non-conscious cognition.  

Repression in Freud’s Psychoanalysis

Repression is a motivated psychological activity toward rejecting unpleasurable and distressing mental contents resulting from the recognition of their incompatibility with the ego.  Repression deals with internal stimuli (i.e., undesirable mental contents). Hence, Freud (1915d, p. 146) noted that “if what was in question was the operation of an external stimulus, the appropriate method to adopt would obviously be flight; with an instinct, a flight is of no avail, for the ego cannot escape from itself.”  The primary purpose of repression is, therefore, to suppress unpleasurable contents arising from internal stimuli (1915d).  

Earlier and Later Accounts of Repression

In his early description of the process of repression in its psychoanalytic sense, as contained in his conflict theory of hysteria, Freud used the terms repression, suppression, inhibition, and dissociation interchangeably (Breuer & Freud, 1895d). In his words, repression involves “a question which the patient wished to forget, and therefore intentionally repressed from his conscious thought and inhibited and suppressed” (Breuer & Freud, 1895d, p. 10).  As already mentioned, in his early description of repression, Freud saw repression as an affect-idea dissociation.  In other words, he considered the process of repression a robbing off an affect its idea so that the idea becomes consigned to the unconsciousness while the affect becomes associated with other useful ideas or energies.  However, this idea of repression was not able to provide a comprehensive account of the basic mechanism of symptom formation and resistance. For him, ideas dissociated from their affects would lack sufficient energy and intensity to come back and disturb the conscious processes. As a rule, an unconscious material enters consciousness only when its intensity increases (Breuer & Freud, 1895d). However, Breuer, a collaborator of Freud, did not believe that ideas separated from affects were intense enough to disturb the conscious. He argued that it would be difficult for an idea to be sufficiently intense to provoke a lively motor act, for instance, without having enough intensity to become conscious (Breuer & Freud, 1895d). 

Consequently, in his later works, Freud bought the idea of Breuer’s earlier claims of the intensity of unconscious ideas and gave an upward drive account of repression (Boag, 2012; Freud, 1915d). In this later view of repression, Freud, therefore, argued that the mark of something repressed is the ability to become unconscious while maintaining its intensity, such that it remains causally active, pressing toward conscious thinking and generating symptoms as substitute satisfactions.  In other words, repressed materials remain explicitly intense.  Thus, Freud (1915d) noted: 

We have learnt from psycho-analysis that the essence of the process of repression lies, not in putting an end to, annihilating, the idea which represents an instinct, but in preventing it from becoming conscious. When this happens, we say of the idea that it is in a state of being “unconscious,” and we produce good evidence to show that even when it is unconscious it can produce effects, even including some which finally reach consciousness. (p. 166)

  In addition, Freud (1915d) maintained that repression would be made complete by assuming that, before the mental organization reaches this stage, the task of fending off instinctual impulses is dealt with by other vicissitudes (e.g., a reversal into the opposite or turning round upon the subject’s own self) which instincts may undergo. This substitution or distortion of the repressed is necessary to enable it to pass through the censors. Hence, this account of repression explained the idea of repression as resistance, as well as the mechanism of symptom and substitute formations (both of which signify a return of the repressed). This is quite different from the earlier affect-idea dissociation account of repression, by which the dissociated ideas lose their intensity while affects robbed off these ideas are associated with other useful ideas.  In any case, Freud generally underscored three possible vicissitudes of repressed drives: the affect may remain wholly or in part as it is; it may transform into a qualitatively different affect, above all into anxiety; or it is completely suppressed and inhibited from being turned into a manifestation of affect (Freud, 1915e).

Censorship and Repression Vis-a-Vis the Unconscious and the Conscious, and the Id, the Ego, and the Superego

The idea of censorship of foreign materials on the frontier between two agencies and that of press censorship informed Freud’s use of the metaphor of censorship in his psychoanalytic illustration of the repressive and filtering work of the mind. For him, the censor has a repressive function of blocking unacceptable, affect-laden memories or images from the unconscious and preventing them from emerging into consciousness.  In his views of the human mind, namely, topographical and structural models, the censor plays a vital role in its repressive function. The first view of the human mind is a topographical model in which Freud divided the psyche into systems, namely, the unconscious, preconscious, and conscious. However, he noted that the distinction between preconsciousness and unconsciousness as two kinds of unconsciousness is only in the descriptive sense (Freud, 1915e).  So, in the dynamic sense, only conscious and unconscious mind regions exist.

In this model of the psyche, the censor is seen as a “watchman” at the border between the two regions of the mind, performing the crucial role of repressing unacceptable wishes in the unconscious so that they do not have access to the preconscious and eventually to the conscious (Freud, 1915e). The censor, thus, plays a pivotal role in both the interrelation and differentiation of these psychic systems as an agent of repression lying on the border of the preconscious and the unconscious. This role of the censor as a watchman placed at the border between the unconscious and the conscious is also seen in Freud’s analysis of dreams. During dreams, the censor is somewhat relaxed (but not completely removed), such that certain repressed contents in the unconscious are allowed in disguised or distorted form into consciousness in dream representations (Freud,1900a, 1916-1917). However, during the period of wakefulness, the censor regains its strength and represses back any trace of partially revealed mental content. Thus, he argued that our inability to remember certain dream elements is due to censorship manifestation in dreams (Freud, 1916-1917). 

Using the analogy of the iceberg, he likened the conscious to the smaller part of an iceberg above the water surface that we are aware of, the preconscious to the part of the iceberg that is sometimes visible and sometimes submerged (i.e., those phenomena which we are not presently aware of but which can be easily brought into consciousness because their resistant is weak), and the unconscious mind, that we are not aware of, to the much larger mass hidden below the water level. The unconscious part of the mind is timeless, and it is the reservoir of instinctual drives, the id, in addition to the mental contents of sexual drives, forbidden desires, painful experiences, selfish needs, irrational wishes, aggressive thoughts, and other unacceptable experiences that have been repressed. For him, the unconscious phenomena exert a great power of control over our conscious thoughts and deeds, and they can be reflected in many ways through slips of the tongue, symptom formation, dreams, works of art, and jokes.  In psychotherapies, the unconscious materials creating abnormal behaviors are brought to awareness by lowering or eliminating the resistance of the censor and are integrated into the conscious part of the mind. 

The second view of the mind, which came as a later development of Freud’s psychoanalysis, is a structural model in which he developed the tripartite personality structures of the ego, the id, and the superego.  This, therefore, focuses on the roles of individuals rather than on systems or regions.  In this model, the unconscious system became the id.  It contains the drives, governed by the primary process, and is unconscious. The preconscious-conscious system became the ego, and it contains the materials available to awareness.  In this personality structure model, Freud perceived an “individual as a psychical id, unknown and unconscious, upon whose surface rests the ego, developed from its nucleus the pcpt system” (Freud, 1923b, p. 24). He, thus, maintained that the ego is not sharply separated from the id; rather, its lower portion merges into it (Freud, 1923b).

 On this note, Freud made a distinction between the unconscious ego and the conscious ego.  Whereas the unconscious ego behaves like the repressed, which is part of the id, and is governed by the primary mental process (e.g., spontaneous actions) of the psyche, the conscious ego represents reason and common sense and is governed by the secondary mental process (e.g., thinking, reflection, decision). Defenses of the ego, therefore, possess some characteristics of the primary mental process in that they function in part to reduce tension and, so, follow the pleasure principle.  They, however, also exhibit some characteristics of the secondary mental process, for they have a relation in time and reality.  Furthermore, the defense mechanisms of the ego that deal with the unconscious impulses are at the border of the id and the ego, much as the censor is at the border of the unconscious and preconscious-conscious systems. Additionally, Freud saw moral thinking as also having a strong unconscious component.  Therefore, he termed the moral aspect of the mind, which generates guilt when we act contrary to its roles, the superego (Freud, 1923b). 

Epistemological Difficulties of Freudian Theory of Repression and Censorship

As already indicated, Freud’s account of repression appears logically and epistemologically self-contradictory.  For instance, how can the secondary mental process of the ego that is thoughtful and reflective extend into the id and the unconscious without the unconscious becoming conscious?  In other words, how can a mental activity go into the unconscious-conscious processing such that the unconscious mental act is not affected by consciousness?  How can there be unconscious consciousness of what is forbidden and what is disguised, which must be tested before passing through the censor or becoming compatible with the ego?  How can the ego know and not know the same thing at the same time?  Freud himself described this seeming contradiction in his analogy of repression with being afflicted by the blindness of seeing-eye during his early account of repression (Breuer & Freud, 1895).  Hence, he expressed:

 I have never managed to give a better description than this of the strange state of mind in which one knows and does not know a thing at the same time. It is clearly impossible to understand it unless one has been in such a state oneself…I was afflicted by that blindness of the seeing eye which is so astonishing in the attitude of mothers to their daughters, husbands to their wives and rulers to their favourites. (p.117)

According to Boag (2012), this analogy of repression with being afflicted by the blindness of seeing-eye simply indicates that repression entails knowing in order not to know, which is a contradiction in terms.  In his work, Being and Nothingness, Sartre (1956) argued that for the censor to effectively do the work of repression and testing, it must know what it is inspecting and what it is repressing. Hence, it is a practical impossibility and theoretical absurdity for the censor to discern the impulses needing to be repressed without being conscious of discerning them. Therefore, Sartre concluded that Freud’s psychoanalytic theory, which posits a conscious ego and unconscious id, is an exercise in bad faith and a metapsychological self-deception.  Similarly, Maze and Henry (1996) observed that a careful examination of Freud’s theory reveals that repression involves knowing in order not to know.  In other words, the ego must know what it is not meant to know.  

Recognizing this epistemic difficulty, Freud himself came up with the idea of the unconscious ego and the conscious ego in his later work, The Ego and the Id.  On the one hand, the unconscious ego behaves exactly like the repressed (i.e., producing powerful effects without itself being conscious) and makes only a predictive judgment of what is pleasurable or unpleasurable, good or bad, harmful or beneficial. On the other hand, the conscious ego makes a judgment of what is real or hallucinatory. Nevertheless, this additional modification could not provide Freud with an escape from the sledgehammer of many critics, as the same problem of self-contradiction lingers. The fundamental question remains: since knowledge resides in judgment, how can the unconscious ego make judgments and affirmations of what is pleasurable or unpleasurable and remain unconscious? 

Cognition, Consciousness, and Knowledge

It will be highly important, at this juncture, to shed light on the meaning of cognition, consciousness, and knowledge so that we can clearly understand how they relate to repression and draw insight to unravel this “mystery” of Freudian repression and censorship. According to Lonergan (1957), whose epistemological theories are greatly aligned with those of traditional philosophers like Aristotle and Aquinas, cognition is a process that culminates in knowing.  It has three levels: the empirical level (e.g., sensing, perceiving, and imagining); the level of intelligence (inquiry, understanding, and formulation); and the level of reflection and judgment, where knowledge is gained.  In their acts, the senses can only experience data but cannot describe, formulate, distinguish, compare, relate, or define, for such activities are the work of intelligence or understanding. However, descriptions, definitions, formulations, comparisons, objects of thought, suppositions, considerations, etc., are still hypotheses, so they may be accurate or inaccurate, correct or mistaken. Pronouncing their correctness, truthfulness, and accuracy is the work of reflection and judgment, where knowledge is had (Lonergan, 1957). Therefore, like Aristotle and Aquinas, Lonergan affirmed that, although every element in the cognitional process is at least a partial increment, making some contribution to knowing, judgment is the total increment in the process. 

Therefore, in line with the traditional philosophy, knowledge is found in the act of judgment because it is the realm of truth and falsity, existence and non-existence, assenting and dissenting, affirmation and denial, agreeing or disagreeing, certitude and probability (Lonergan, 1957). Hence, cognition is a process that culminates in knowledge through acts of reflection and judgment. In other words, cognitive acts, such as mere perception, attention, cogitative/estimative sense (the primitive sense of the harmful and the beneficial), memory, understanding, and thought, are not knowledge until they involve the reflective judgment of the truthfulness of the existence of what is cognized. Consequently, knowing necessarily involves consciousness (an awareness immanent in our cognitional act, either awareness of some content/object or awareness of the acts), but consciousness is not necessarily knowing because experiences and understanding, while being acts of consciousness, are not yet judgment where knowledge essentially resides (Lonergan, 1957).

However, at the empirical level of human cognition, there is a special type of non-conscious estimation of what is harmful or beneficial, a kind of “judgment” that occurs in an internal sense that is known as the cogitative sense (vis cogitativa).  I will discuss this cogitative sense in detail later. Moreover, recent findings have shown that cognition, especially sense perception, can either occur consciously or unconsciously. This differentiation of knowledge from cognition and consciousness is very important in solving the puzzle of repression, which involves “being afflicted by the blindness of seeing-eye,” or knowing not to know (Breuer & Freud, 1895).

Resolving the Epistemic Paradox of Freudian Repression and Censorship

 To explain this seeming self-contradiction of Freud’s theory of censorship and repression, the epistemological insight of Aquinas and Lonergan on vis cogitativa and evidence from neuropsychological studies will be of great importance.

Censorship/Repression and the Vis Cogitativa

According to Avicenna, influenced by Aristotle’s notion of accidental sensible, lower animals have an estimative sense or intention (vis aestimativa), a receptive faculty of intention (i.e., per accident sensible) by which they instinctually react to harmful objects around them (Tellkamp, 2012).  Building on this idea, Aquinas held that the vis cogitativa incorporates the animal vis aestimativa, and, at the same time, plays the peculiar role of grasping intentions as standing under a common form.  So, the vis cogitativa, for Aquinas, is a special and primitive sense of the harmful and the beneficial, as well as a sense that grasps particular forms of objects in preparation for their intellectual abstractions.  Thus, he wrote:

 the power which is called “cogitativa” by the philosopher, is on the boundary of sensitive and intellective parts, whereby the sensitive part touches the intellective for it has something from the sensitive part, namely, that it considers particular forms; and it has something from the intellective, namely that it compares; and so it is men alone. (Sent. III, d, 23, q. 2, a. 2)

Therefore, for Aquinas, the vis cogitativa also does the work of passive intellect, by which, in Aristotle’s epistemology, phantasms (sensible images or representations of material contents, including particularity, size, and shape) are received before becoming dematerialized through the process of abstraction by the agency of active intellect to become universals. He thus called this faculty ratio particularis (particular reasoning), for it recognizes the same in many instances without requiring any intelligence (Aquinas, Sent. III, d, 23, q. 2, a. 2; Tellkamp, 2012).  Without the vis cogitativa, Aquinas argued, the soul cannot understand this life. Thus, no understanding or judgment can occur without this faculty, which must provide the phantasm needed for abstraction and universalization in the acts of conceptualization and judgment.

Now, Aquinas’s treatment of the vis cogitativa shows that it is both an estimative intention of instinctual and emotional reactions and an intentional cognitive grasping of material forms in preparation for intellectual acts, such as understanding and judgment. This is very insightful regarding the intentionality of the act of repression, as Freud indicated in his early account of repression, as well as his claim of unconscious-conscious interaction of the ego with the id via repression. Suffice it to mention that in the traditional philosophy, there are four distinct internal senses: the common sense, which unifies the perception of the various external senses and perceives the operation of each sensation; imagination or phantasm, which retains the material form perceived by external senses; the cogitative sense (vis cogitativa), which apprehends the particular forms, as well as makes an estimation of particular objects; and memory, which retains the intentions perceived by the vis cogitativa and the intellectual acts of understanding and judgment (Aquinas, Summa Theologica, I, q.78, a. 4). Hence, no confusion should exist between the act of judgment (which is based on reflective insight and knowing) and the vis cogitativa (which is a special type of spontaneous non-conscious or deliberate conscious evaluation at the level of sense perception).

 Furthermore, Lonergan (1957), influenced by Aquinas’s epistemological insight, compared the Freudian censor with the vis cogitativa and showed how the repression is both conscious and unconscious, intentional and spontaneous. This similarity contributes immensely to resolving the difficulty of how the same ego both knows and does not know.  For Lonergan (1957), the vis cogitativa, in its role of estimation of what is harmful or beneficial and in preparation of particular forms of objects for their abstractions and insights, provides the connection between the unconscious and the conscious. Although Lonergan’s understanding of the unconscious is that it is an underlying neural system rather than a region of the human mind, he maintained that repressed materials that have passed the inspection of the censor (i.e., the vis cogitativa in this case) and so are compatible with the self (the ego) are presented by the vis cogitativa to judgment for insight. Thus, following Aquinas, he asserts that without the vis cogitativa there is no insight (understanding and judgment). For Lonergan, the censor primarily has a constructive role in selecting and arranging materials that emerge in consciousness in such a way that insight could occur. Also, it aberrantly has a repressive function to block or thwart the emergence of unwanted images that could give rise to insight (Lonergan, 1957). The avoidance of unwanted insight can be unconscious or conscious, spontaneous or deliberate.  

Censorship/Repression and Neurological Structures

 Empirical evidence has shown that, in addition to conscious cognitive processing, certain cognitions occur non-consciously, nondeclaratively, or implicitly. They include priming, procedural learning, classical conditioning, spatial memory, habituation, and sensitization (Breedlove & Watson, 2018).  For instance, Weiskrantz and Warrington (1970) conducted a neuropsychological dissociation of nondeclarative memory from explicit memory and found that amnesics, after reading a list of words, could not recall the list when tested explicitly but performed very well when presented with the starting alphabet of each word and asked to complete the words. Similarly, Butcher, Mineka, and Hooley (2014) also noted that an amnesic patient, when asked to dial numbers on the phone, randomly dialed his mother’s number without realizing what he was doing.

 In his explanation of brain mechanisms that contribute to unconscious repressions, Kissi (1986 ) underscored that mental processing in subcortical structures, which are located in the Thalamic-basal ganglia complex, prevents information about the repression of negative stimuli from reaching higher cortical structures for conscious processing. In other words, whenever negative stimuli are perceived at the subcortical level, the emotional component of the stimuli is recognized before the conscious component (Kissi, 1986). On this note, recent findings have shown that the thalamus relays information from fear-inducing stimuli to the amygdala either indirectly via the cortex and hippocampus, allowing for the conscious processing of threats, or directly, which bypasses the conscious processing, allowing for an unconscious fear appraisal and conditioning (Breedlove & Watson, 2018). In addition to the unconscious process of the amygdala in making a simple appraisal of a stimulus regarding its safety or dangerousness, Pally (1998) remarked that the orbitofrontal cortex’s reaction to complex information about a stimulus involves unconscious processing.

Conclusion

From both neurological and epistemological accounts of unconscious dynamic processes, it is clear that the human mind is capable of processing information unconsciously and consciously and that both unconscious and conscious repressions do occur. Using Thomistic-Lonerganian terminology, one can thus say that the censor and its repressive function are neither self-contradictory nor self-deceptive, but a cogitative primitive sense of processing threats and unpleasurable internal stimuli, which can occur both unconsciously or consciously, spontaneously or deliberately. When repression is unconscious, then there is a non-conscious (unconscious or preconscious) cognition of the spontaneous processing of the vis cogitativa toward the repressed unpleasure material.  Similarly, when repression is conscious, then there is a conscious cognition of the spontaneous or deliberate reaction of the vis cogitativa toward the repressed harmful materials, which may involve the role of thought, understanding, and even knowledge. Therefore, Freud’s psychoanalysis, which proposes a communication of the id with the ego, is supported and justified.

References

Aquinas, T. (1965).  Sententiae. (W. Barden, Ed. & Trans.). (Vol. 58). London: Eyre and Spottiswoode.

Aquinas, T. (1981). Summa theologica. (Fathers of English Dominican Province, Trans.). Westminister, MD: Christian Classics.

Boag, S. (2012). Freudian repression, the unconscious, and the dynamics of inhibition. London, United Kingdom: Karnac Books.

Breedlove, S. M., & Watson, N. V. (2018). Behavioral neuroscience (8th ed.) New York, NY: Oxford University Press.

Breuer, J., & Freud, S. (1895d). Studies on hysteria (1893-1895)S.E, II. London: Hogarth. 

Butcher, J., Mineka, S., & Hooley, J. (2014). Abnormal psychology (16th ed.). Upper Saddle River: Pearson.

Freud, S. (1900a). The Interpretation of DreamsS. E., 4-5.  London: Hogarth Press

Freud, S. (1915a). RepressionS. E., 14:141-148. London: Hogarth Press.

Freud, S. (1915b). The unconsciousS. E, 14:159-215. London: Hogarth Press.

Freud, S. (1916-1917). Introductory lectures on psycho-analysisS.E., 15-16. London: Hogarth Press.

Freud, S. (1923b). The Ego and the Id. S. E., 19:1-66. London: Hogarth Press.

Kissi, B. (1986 ). Conscious and unconscious program in the brain. New York, NY: Plenum Publishing Corporation.

Lonergan, B. (1957). Collected works of Bernard Lonergan: Insight (5th ed.).  (F. E. Crowe and R. M. Doram, Eds.). (Vol. 3). Toronto: University of Toronto Press 

Maze, J., & Henry, R. (1996). The problems of the concept of repression and proposals for their resolution. International Journal of Psychoanalysis, 77,1085-1110.

Pally, R. (1998).  Emotional processing: The mind-body connection. International Journal of Psychoanalysis,79, 349–362.

 Sartre, P. (1956). Being and Nothingness, (H. E. Barnes, Trans.). New York: Philosophical Library.

Tellkamp, J. A. (2012). Vis Aestimativa and vis cogitativa in Thomas Aquinas’s  commentary on the sentences. The Thomist: A Speculative Quarterly Review,76(4), 611-640. doi:10.1353/tho.2012.0003

Weiskrantz, L., & Warrington, E (1970). Verbal learning and retention by amnesic patients using partial information. Psychonomic Science20(4), 210-211. Retrieved from https://link.springer.com/content/pdf/10.3758/BF03329023.pdf

Dialectical Behavioral Therapy and Adolescents with Suicidal Behavior

Dialectical behavior therapy (DBT) is one of the acceptance-based therapies, which characterize the third generation of behavior therapy. Other acceptance-based therapies are acceptance and commitment therapy (ACT) and mindfulness. Dialectical behavioral therapy is an evidence-based therapy. Originally, Linehan (1993a, 1993b) developed DBT for adults with suicidal-related behavior, extreme emotional and behavioral dysregulation, and borderline personality disorder (BPD). Further research has also shown that DBT can be applied effectively to adolescents with suicide ideation and behavior (Fleischhaker et al., 2011; James et al., 2008; Miller et al., 2000; Woodberry & Popenoe, 2008). The purpose of this study is to examine the effectiveness of DBT application to adolescents with suicide ideation and behavior.

The Theoretical Foundation of Dialectical Behavioral Therapy

Primarily, DBT assumes that emotions precede the development of thoughts, and so are the primary causes of psychopathology (Seligman & Reichenberg, 2014). Thus, helping clients regulate their emotions will resolve several psychological. Secondly, DBT is founded on behavioral therapy and its principles. Historically, the first generation of behavior therapy involves classical (S-R) behaviorism and neobehaviorism, whereas the second generation (e. g., cognitive behavioral therapy) involves the rise of the cognitive revolution while retaining some behavioral principles (Guercio, 2020). The third wave behavioral therapy involves incorporating acceptance-based therapies into cognitive behavioral therapy (e. g., DBT). Hence, DBT clinicians incorporate behavioral techniques and principles (e. g., problem-solving, exposure, and cognitive reconstruction) to assess clients’ needs, help them define their goals, and acquire the essential skills for effective behavior (Budak et al., 2020).

Thirdly, DBT is founded on dialectical philosophy, which involves looking at reality and integrating the opposites. There is an alternative story or a dialectical pole in every person’s story. Similarly, DBT holds the assumption that clients are experiencing a dialectical conflict between themselves and their environment. Thus, DBT clinicians work to understand clients’ worlds and help them consider alternative possibilities (dialectic poles). Fourthly, as an acceptance-based therapy, DBT is founded on mindfulness meditation, acceptance, and other Zen practices. In mindfulness, thoughts are observed without judgment. Through acceptance, DBT clients learn to remain available to the present experience without attempting to end the painful experience or prolong the pleasant experience (Budak et al., 2020; Kramer et al., 2013). Based on acceptance and mindfulness principles, DBT assumes that trying to deny, avoid, and escape strong emotions paradoxically makes those emotions more intense.

Major Dialectical Behavioral Therapy Techniques

The major DBT strategies include: (a) dialectical techniques, (b) validation techniques, (c) problem-solving strategies, (d) stylistic communication strategies, and (d) case management techniques.

Dialectical Techniques

Dialectical strategies define DBT. In addition to functioning as a specific set of procedures, they organize therapy sessions and integrate other treatment strategies. In this way, dialectics attends to the entire therapy context and the oppositions naturally ensuing in the therapeutic relationship. Dialectical techniques include entering the paradox, playing the devil’s advocate, extending, using metaphor, making lemonade out of lemons. Entering the paradox requires the therapists to highlight the conflicting nature of the client’s behaviors, the therapeutic relationship, and reality in general. The therapist might enter the paradox with a client who refuses to admit her problems thus: no one comes to therapy to change good behavior. Other examples of paradoxes include unwillingness to experience anxiety perpetuate anxiety, one must accept people’s inability to accept, and treatment for insomnia is staying awake.

Metaphors, storytelling, analogies, or anecdotes help to teach the paradoxical nature of clients’ behavior and open up the possibilities for new behavior. For instance, using the metaphor of the sun, the therapists can tell the client who has agoraphobia, “it’s like living a life where you’re trying to hide from the sun because you might get burned.” Playing the devil’s advocate, another dialectical technique, is a form of reversal role in which the clinician holds the client’s distorted belief so that the client argues against the belief. For instance, the therapist holds a client’s belief that disagreement means hatred, while the client argues against it. Extending is another dialectical strategy, and it involves the therapist taking clients more seriously than they expect. For instance, a therapist might offer to give a client threatening to leave therapy referrals. Making lemonade out of lemons involves seeing something positive in the negative event. For instance, accepting suffering enhances sympathy.

Validation Techniques

Validating the client’s subjective experience requires accepting the client’s emotional, cognitive, or behavioral response to a situation. According to Linehan (1993a), validation occurs when the therapist communicates to clients that their responses make sense and are understandable within their current life context or situation. Heard and Linehan (1994) noted various levels in which validation can occur: active listening, reflecting the client’s experience back to the client, and noting the client’s unstated experience. Other levels are validating the response or experience in terms of past learning experience or present circumstances.

Problem Solving Techniques

These strategies focus on change. The first part of problem-solving involves behavioral analysis of the client’s dysfunctional behavior. To complete behavioral analysis, the client must accept that the problem occurred, describe the detailed behavior without judgment, and explain the effect of the behavior analysis (Heard and Linehan, 1994). The second part of problem-solving involves solution analysis. Behavioral skills used for solution analysis include cognitive modification/reconstruction, contingency management, exposure, and desensitization. Another important behavioral skill for solution analysis is skills training modules. The skills modules include mindfulness skills, distress tolerance skills, emotion regulation, and interpersonal effectiveness. The skills modules target confusion about oneself, impulsivity, emotional dysregulation, and interpersonal problem. These four behavior problems are the common features of suicide ideation and behavior (Miller et al., 2000).

Specifically, mindfulness skills include wise mind, observing, describing, participating, nonjudging, staying focused, doing what works. These skills treat confusion about oneself. Distress tolerance skills target impulsivity, and they include ACCEPTS (i. e., Activities, Contributing, Comparison, Emotions, Pushing away, Thoughts, Sensation), distract, self-soothe, pros and cons, radical acceptance. Emotion regulation skills target treating emotional dysregulation, and they include PLEASE (i. e., treat Physical iLlness, balance Eating, Avoid mood-altering drugs, balance Sleep, Exercise) building mastery, building positive experience, and acting opposite. The fourth skills module, interpersonal effectiveness skills, targets interpersonal problems. The modules include GIVE (i. e., be Gentle, act Interested, Validate, use an Easy manner), DEARMAN (i. e., Describe, Express, Assert, Reinforce, take hold of your Mind, Appear confident, Negotiate), and FAST (i. e., be Fair, no Apologies, Stick to values, be Truthful).

Stylistic communication Techniques

These strategies involve how the therapist interacts with the client. In DBT, stylistic strategies are grouped into reciprocal and irrelevant communication. According to Linehan (1993a), reciprocal communication styles include responsiveness, compassion, caring, self-disclosure, warmth, genuineness, attending to the clients mindfully without any prejudgment or noticing subtle responses. In contrast, irrelevant communication styles include confronting the client’s crazy behavior and unorthodox, unhallowed, impertinent, and incongruous responses to clients. However, therapists must apply irrelevant communication styles upon a foundation of relevant communication styles.

Case Management Techniques

These strategies involve helping clients manage their physical and social environment to facilitate their overall life functioning and wellness. In other words, the strategies help therapists respond to clients’ environment beyond the therapeutic relationship. Case management strategies comprise environmental intervention (therapists interacting with the client’s environment), consultation to the clients (helping clients interact with their environment), and supervision/consultation (According to Heard and Linehan, 1994).

Dialectical Behavioral Therapy Stages of Intervention

Dialectical behavioral therapy is a four-stage based intervention that incorporates many behavioral principles. The first stage is the pretreatment stage. Here the primary target is to familiarize clients with the treatment process, secure commitment to treatment, and facilitate attainment and basic competencies, such as keeping themselves safe, reducing self-harm (e. g., drug use, self-injury, unwise and sexual activity). Activities in this stage include: discussing DBT concepts; discussing clients’ responsibility, expectations, assessment, planning; overview of treatment stages; and teaching client relevant skills, such as self-care, emotional regulations, and interpersonal effectiveness. There four targets in this stage. The first and highest priority is to decrease life threatening behaviors, such as suicidal or parasuicidal behavior. It is possible that such behavioral problems do not occur. The second priority is to decrease therapy-interfering behavior (e. g., tardiness, not showing up for session, or not completing home assignments). The third priority is decreasing quality-of-life interfering behaviors, such as school problems, depression, anxiety, relationship problems, impulsivity, acting out problems, and substance abuse. The fourth priority is to increase behavioral skills.

The second stage is the decrease of traumatic experiences and associative symptoms of distress and anxiety. Desensitization and other strategies can be helpful here. However, many clients do not experience this type of response. In this case, they can move on to the third stage, which involves enhancing self-respect, resolving problems of living, and accomplishing individual goals. In stage four, the focus is to address deeper existential issues, including cultivating greater sense of freedom, creating joy, and finding happiness in life. To achieve these gains, there is the need to synthesize and generalize gains, integrate the past, present and future, develop spirituality, acceptance of self and reality, increase self-respect and achievement of individual goals, increase coping skills.

Applying Dialectical Behavior Therapy on Adolescents with Suicide-Related Behavior

Miller et al. (1997) proposed adaptations of DBT for adolescents (DBT-A) in their work Dialectical Behavior Therapy Adapted for Suicidal Adolescents. In this work, Miller et al. (1997) noted that the modifications of DBT for adolescents targeted adolescents with suicide ideation, suicide behavior, and non-suicidal self-harm. The adaptations include shortening the length of the treatment from I year to 12 weeks, reducing the total number of skills modules, and incorporating family members into treatments. Other modifications include simplifying the language used in handouts and skills training lectures and adding an optional 12-week follow-up patient consultation group.

Later, Miller et al. expanded on their research on DBT modifications for adolescents with emotional and behavioral dysregulation, including suicide ideation and behavior. They provided seven main adaptations of standard DBT. The first adaptation is to incorporate family members, usually parents, into treatment to serve as models and coaches for their adolescents in utilizing implementation skills, facilitate skill generalization for their adolescents, and provide skill reinforcement, support, and validation for them (Miller et al., 2007b). Incorporating family members provides the opportunity for role-playing skills, fosters interfamily support, reduces adolescents’ disruptive behaviors in the group, and enhances treatment compliance.

The second adaptation is conducting 3 to 4 family therapy sessions when the contingencies at home reinforce the dysfunctional behavior. Under these circumstances, the therapist initiates family therapy to enhance treatment by educating the family members about particular skills or aspects of treatment. In addition to modifying contingencies in the home, family therapy sessions improve family communication, and address parents’ emotional dysregulation, and help family members understand the adolescent’s emotional vulnerability (MacPherson et al., 2012). The third adaptation is developing and teaching the three adolescent-family dialectical dilemmas (MacPherson et al., 2012; Rathus & Miller, 2000). These dialectical dilemmas are excessive leniency versus authoritarian control, viewing the normal adolescent behavior as deviant versus the inability to perceive or address the adolescent deviant behavior, and forcing autonomy (e. g., through severing ties with the adolescent) versus fostering dependence (e. g., through excessive caretaking and overreliance on parents. The fourth adaptation is the reduction of treatment length from I year to 16 weeks. The therapy content (e. g., skills training modules) is increased to compensate for this reduction (Miller et al., 2007b).

The fifth adaptation is the second phase of the therapy, which involves a 16-week optional graduate group for clients who continue to show difficulties after completing the first phase of the treatment. The purpose of this graduate group is to reinforce and generalize skills taught in the first phase. Adolescents may repeat the graduate group as often as possible to attain their identified goals. The sixth adaptation involves slightly reducing the number of skills taught within each of the four skills modules (i. e., mindfulness, interpersonal effectiveness, emotional regulation, and distress tolerance) and adding a fifth adolescent-specific skills module, namely, walking the middle path for the adolescents and their family. This additional skills module teaches validation for self and others, behavioral principles (e. g., reinforcement, punishment, extinction, and shaping), and three adolescent-family dialectical dilemmas (MacPherson et al., 2012). The seventh and last adaptation involves modifying skills hands to improve their appeal and applicability to adolescents. Modifications include streamlined language, simplifying terminology and visual layouts, adapting examples of each skill, utilizing experiential and in vivo than didactic methods (MacPherson et al., 2012).

Research Supporting the Efficacy of Dialectical Behavioral Therapy on Adolescents with Suicide Behavior

Several empirical studies have evaluated DBT for adolescents with suicide ideation and suicidal behavior. For instance, Miller et al. (2000) treated adolescents (n = 33) with BPD using the four DBT skill modules: mindfulness, distress tolerance, emotion regulation skills, and interpersonal effectiveness skills. They found a statistically significant reduction in confusion about oneself, impulsivity, emotional instability, interpersonal problems and overall BPD symptom reduction. Similarly, James et al. (2008) examined the use of DBT in treating a community sample of female adolescents (n = 16) with persistent suicide ideation or severe, deliberate self-harm using DBT. Pre- and posttreatment assessments revealed a significant reduction of depression, hopelessness, episodes of deliberate self-harm, as well as increased general functioning. The authors also reported that the intervention was well accepted in a notoriously difficult group whenever it comes to psychotherapy.

Fleischhaker et al. (2011) used Rathus and Miller’s modified version of DBT for Adolescents to treat adolescents (n = 12) with suicidal behavior, non-suicidal self-injurious behavior, and BPD. Using pre/post comparison and a one-year follow-up, the authors measured the treatment efficacy. The study results indicated that suicidal behavior and non-suicidal injurious behavior reduced significantly over the year. Also, nine completed the therapy regularly out of ten patients diagnosed with BPD at the beginning of the therapy. Among these nine patients, BPD features persisted only in one participant one year after therapy. Thus, the intervention was well accepted by the patients and their family members, who also played a role in the treatment.

Additionally, Woodberry and Popenoe (2008) examined the DBT program for adolescents (n=28) with suicidal and self-injuring behavior in a community outpatient treatment settings. The study involved an uncontrolled pre- to posttreatment design. The authors also reported including parents (n = 19) who collected reports for adolescents and parental change. The study results showed a large and significant reduction of suicide behavior among the adolescents (n = 27, d= .73, p = .001). Similarly, there was a significant decrease in the frequency of self-harming behavior (n = 27, d= .62, p = .004). The percentage of adolescents wanting to kill themselves reduced from 32% to 5 %, and those not wanting to kill themselves increased from 32% to 63%. However, the authors reported that confounding variables (e. g., medication, maturation, placebo, selection bias, and clinical instability) might have contributed to the reported changes in the absence of a control group.

Conclusion

Dialectical behavior therapy, one of the acceptance-based therapies, can be applied effectively to adolescents with suicidal-related behavior. Family therapy sessions are an important requirement for DBT with adolescents to address contingencies at home reinforcing dysfunctional behavior. Major DBT techniques for effective treatment include dialectical techniques, validation techniques, problem-solving strategies, skill training modules, and stylistic communication strategies. However, the skills training modules (mindfulness, distress tolerance, emotion regulation, and interpersonal effectiveness) are highly effective in treating confusion about oneself, impulsivity, emotional dysregulation, and interpersonal problem, which are common features of suicidal behavior.

References

Budak, A. M., Kocabas, E. O., & Goksu, H. (2020). Dialectical behavioral therapy from the lifespan perspective. Psikiyatride Güncel Yaklaşımlar-Current Approaches in Psychiatry, 12(2), 287-298 doi: 10.18863/pgy.59854

Kramer, G. P., Bernstein, D. A., & Phares, V. (2014). Introduction to clinical psychology (8th ed.). New York: Pearson.

Fleischhaker, C., Bohme, R., Sixt, B., Bruck, C., Schneider, C., & Schulz, E. (2011). Dialectical behavioral therapy for adolescents (DBT-A): A clinical trial for patients with suicidal and self-injurious behavior and borderline symptoms with a one-year follow-up. Child and Adolescent Psychiatry and Mental Health, 5, 3-10.

Guercio, J. M. (2020). The importance of a deeper knowledge of the history and theoretical foundations of behaviorism and behavior therapy: Part 2-1960–1985. American Psychological Association 20 (3), 174-195.

Heard, H. L. & Linehan, M. (1994). Dialectical Behavior Therapy: An Integrative Approach to the Treatment of Borderline Personality Disorder. Journal of Psychotherapy Integration, 4 (1), 55-82.

James, A. C., Taylor, A., Winmill, L., & Alfoadari, K. (2008). A preliminary community study of dialectical behaviour therapy (DBT) with adolescent females demonstrating persistent, deliberate self-harm (DSH). Child and Adolescent Mental Health, 13, 148-152.

Linehan, M. M. (1993a). Cognitive-behavioral treatment of borderline personality disorder. Guilford Press.

Linehan, M. M. (1993b). Skills training manual for treating borderline personality disorder. Guilford Press.

MacPherson, H. A., Cheavens, J. S., & Fristad, M. A. (2012). Dialectical Behavior Therapy for Adolescents: Theory, Treatment Adaptations, and Empirical Outcomes. Clinical Child and Family Psychology Review, 16(1).

Miller, A. L., Rathus, J. H., & Linehan, M. M. (2007b). Dialectical behavior therapy with suicidal adolescents. Guilford Press.

Miller, A. L., Rathus, J. H., Linehan, M. M., Wetzler, S., & Leigh, E. (1997). Dialectical behavior therapy adapted for suicidal adolescents. Journal of Practical Psychiatry and Behavioral Health, 3, 78–86.

Miller, A. L., Wyman, S. E., Huppert, J. D., Glassman, S. L., & Rathus, J. H. (2000). Analysis of behavioral skills utilized by suicidal adolescents receiving dialectical behavior therapy. Cognitive and Behavioral Practice, 7, 183-187.

Rathus, J. H., & Miller, A. L. (2000). DBT for adolescents: Dialectical dilemmas and secondary treatment targets. Cognitive and Behavioral Practice, 7, 425-434.

Seligman, L., & Reichenberg, L. W. (2014). Theories of counseling and Psychotherapy: Systems, strategies, and skills (4th ed.). Boston: Pearson.

Woodberry, K. A., & Popenoe, E. J. (2008). Implementing dialectical behavior therapy with adolescents and their families in a community outpatient clinic. Cognitive and Behavioral Practice, 15, 277-286.

The Odds of Developing Heart Disease for Tobacco Smokers Compared to Non Smokers

Abstract

Background: Cardiovascular diseases (CVDs) or diseases of the heart and blood vessels are one of the largest causes of death. More than 16 million Americans have a CVD. Approximately smoking causes one of every four deaths from CVD.

Objective: To predict the odds of developing heart disease in a lifetime among tobacco smokers compared to non-smokers using a simple binary logistic regression.

Methodology: Respondents (n = 55271), aged 12 and above, for the 2014 National Survey on Drug Use and Health (NSDUH) in the Inter-university Consortium for Political and Social Research (ICPSR) datasets were use. The NSDUH is a quarterly and annual nationwide survey that primarily measures the prevalence and correlates of drug use in the United States both on the national and state level. Respondents were selected from the civilian, non-institutionalized population residing in the United States. The 2014 NSDUH was transferred into the SPSS and a simple binary logistic regression analysis was performed to predict the odds of developing a CVD in a lifetime among cigarette smokers compared to non-smokers. The number of respondents is enough to provide the confidence that the false null hypothesis for the study analysis will be correctly rejected at least 80% of the time.

Results: The result of the regression indicates that a full model chi test for the variable eversmokecigrarette as the predictor variable was statistically significant χ²(1) = 192.494, p < .001. Wald’s statistical value for respondents who reported having smoked cigarettes was statistically significant, Wald χ² =176.136, p < .001. Thus, the odds of developing heart disease in a lifetime among respondents who reported ever smoking cigarettes and those who never reported smoking cigarettes differ significantly from 1.00. Further analysis indicates that the odds of developing heart disease for cigarette smokers were approximately 2.232 times higher than those of non-cigarette smokers with a 95% CI [1.983, 2.513].

Conclusion: Cigarette smoking significantly increases the odds of developing CVD in a lifetime. Therefore, cigarette smoking is harmful to hearth health. Cigarette smokers are more likely to develop heart disease in a lifetime compared to non-cigarette smokers.

Key words: Cardiovascular disease, Smoking, Cigarette, Heart disease, Coronary heart disease, Cerebrovascular disease, Stroke, Heart failure, Atherosclerosis, Cardiovascular mortality

Introduction

Studies have shown that cardiovascular diseases (CVD) or diseases of the heart and the blood vessels are one of the largest causes of death in the United States of America, and that more than 16 million Americans have a CVD. The annual mortality rate of Americans from coronary heart disease is about 993000 (CDC, n.d.). About 25500 die of cerebrovascular diseases (stroke) annually, and about 15500 die of other vascular diseases annually. Approximately, smoking causes one of every four deaths from CVDs (CDC, n.d.). Additionally, almost all deaths from abdominal aortic aneurysms are caused by smoking. Therefore, tobacco smoking is a primary cause of CVD (DʼAlessandro et al., 2012; Papathanasiou et al., 2014). Cardiovascular diseases include coronary artery constriction, heart attack, cerebrovascular diseases or strokes, peripheral vascular disease (PVD), peripheral artery disease (PAD), and abdominal aortic aneurysm. The risk of developing a CVD, including aortic aneurysms, due to tobacco smoking increases with the number of cigarettes smoked per day and when smoking continues for years (Burns, 2003; Pyrgakis, 2009).

Studies have also shown that tobacco smoke contains about 4000 chemical substances, including nicotine and carbon monoxide (CO), associated with CVDs, other serious health problems, and a high mortality rate (APA, 2013; Papathnasiou et al., 2014; West, 2017). For instance, tobacco smoking lowers high-density lipoproteins (HDL or good cholesterol), increases low-density lipoproteins (LDL or bad cholesterol), and causes a build-up of bad cholesterol, fats, and other substances (or plaque) in the aorta and coronary arteries (DʼAlessandro et al., 2012; Papathanasiou et al., 2014). This build-up of plaque leads to atherosclerosis, the hardening and thickening of the artery walls, leading to the arteries becoming narrower and slowing down the blood flow. Ultimately, several CVDs ensue, including arteriosclerosis (also known as coronary artery disease or coronary heart disease), a condition affecting the arteries that supply the heart with blood, and cerebrovascular diseases (stroke), loss of brain function when blood flow to the brain is interrupted. Atherosclerosis due to cigarette smoking is also associated with a myocardial hypercoagulable state, stable angina, heart attack, cardiac arrest, peripheral arterial disease, and peripheral vascular disease (Tonstad & Johnston, 2006). Peripheral arterial disease and peripheral vascular disease occur when the thickened and narrowed arteries reduce blood flow to the pelvis, arms, hands, legs, hands, and feet. Smoking also causes abdominal Aortic Aneurysm, damage to the abdominal aorta. A ruptured abdominal aortic aneurysm is life-threatening.

However, limited research has been conducted to gain insight into the odds of developing CVD by cigarette smokers compared to non-smokers. Therefore, the problem to be addressed in this study is the odds of developing CDVs by cigarette smokers compared to non-cigarette smokers. Specifically, I will address this problem by performing a simple logistic regression analysis, in which smoking a cigarette predicts developing a heart problem in a lifetime compared to non-smoking a cigarette. Since CDV is a significant health problem, underscoring the likelihood of smokers developing a heart problem compared to non-smokers would impact some motivational behavior in reducing these odds. This study will help health providers provide well-informed information on the odds of developing heart diseases to their clients who smoke cigarettes.

Study Purpose

The purpose of this descriptive quantitative study is to predict the odds of developing heart disease in a lifetime among cigarette smokers compared to non-cigarette smokers using respondents (n = 55271) for the 2014 National Survey on Drug Use and Health (NSDUH) in the Inter-university Consortium for Political and Social Research (ICPSR) datasets (U. S. Department of Health and Human Services, 2016). The independent (predictor) variable is the categorical variable eversmokecigrarette (CiGARETTEEVER) with two grouping levels: 0 (no) and 1 (yes). The dependent (outcome) variable for this study is the categorical variable, had heart disease in lifetime (HARTDLIF) with two grouping levels: 0 (no) and 1 (yes).

Research Question and Hypotheses

Question. How much higher are the odds of developing heart disease in a lifetime for cigarette smokers compared to non-cigarette smokers?
Null Hypothesis. The odds of developing heart disease in a lifetime for cigarette smokers and non-cigarette smokers are equal to 1.00, or the probability of developing heart disease in a lifetime for cigarette smokers and non-cigarette smokers is equal to .50 (or 50%).

Alternative hypothesis. The odds of developing heart disease in a lifetime among tobacco smokers and non-cigarette smokers differ significantly from 1.00, or the probability of developing heart disease for cigarette smokers and non-cigarette smokers varies significantly from .50 (or 50%).

Methodology

The NSDUH is a survey series in the Inter-university Consortium for Political and Social Research (ICPSR) datasets. The NSDUH is a quarterly and annual nationwide survey that primarily measures the prevalence and correlates of drug use in the United States, both at the national and state levels. Respondents were aged 12 and above and were selected from the civilian, non-institutionalized population residing in the United States. They provided information on the use of illicit drugs (e.g., heroin, cocaine, hallucinogens, marijuana), alcohol, tobacco, and non-medical use of prescription drugs (e.g., pain relievers, sedatives, and tranquilizers). Respondents also provided information about their physical and mental health, age when a substance was first used, lifetime substance use, usage for the past month and past year, illegal activities, arrest records, problems resulting from drugs and needle-sharing. The survey also included questions concerning health care access and coverage, treatment history for substance abuse and mental health-related disorders, perceived needs for treatment, and questions (e.g., dependence and abuse) based on the criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM).

For the 2014 NSDUH, nationwide 91, 640 respondents were selected. Only 56271 participants made the final sample. This final sample represented the United States’ general population. However, the valid number of respondents for this current study was 54163 (98%), while 1108 (2%) were missing. In addition to representing the general U. S. population, the number of respondents for this study is enough to provide the confidence that the false null hypothesis for the binary logistic regression will be correctly rejected at least 80% of the time. In other words, the binary logistic regression analysis for the current study has enough statistical power to reject the false null hypothesis correctly. For this 2014 survey, questions introduced in previous administrations were retained. Most survey questions were sensitive. Consequently, interviewers used audio computer-assisted self-interviewing (ACAS) to provide participants with a private and confidential mode to collect questions about illicit drugs and other sensitive behaviors. However, interviewers used personal computer-assisted personal interviewing (CAPI) to collect information from respondents on less sensitive items (U. S. Department of Health and Human Services, 2016).

Furthermore, I transferred the 2014 NSDUH from the ICPSR dataset into SPSS and performed a simple binary logistic regression analysis to predict the odds of developing CVD in a lifetime among cigarette smokers compared to non-smokers. In this logistic regression, the independent (predictor) variable was the dummy coded variable eversmokecigrarette (CiGARETTEEVER), which I created from the categorical variable ever smoked cigarettes (CIGEVER) with two grouping levels 1 (yes) and 2 (no) and recoded as 0 (no) and 1 (yes). The never-smoked cigarette group was the reference group to which the ever-smoked cigarette group was compared. Also, 46.8.% of respondents reported that they had never smoked cigarettes, while 53.2% reported that they had smoked cigarettes (see Table 5). The dependent (outcome) variable was the categorical variable, had heart disease in a lifetime (LIFHARTD) with two grouping levels: 0 (no) and 1 (yes). Additionally, based on the cross-tabulation from SPSS (see Table 5), I displayed the binary logistic regression raw score summary in Table 4.

Results

The results of the regression revealed that a full model chi test for the variable eversmokecigrarette (CiGARETTEEVER) as the predictor variable was statistically significant χ²(1) = 192.494, p < .001 (see Table 6). Similarly, Wald’s statistical value (-3.354 = -4.157 + .803) for the B1 coefficient or the logit L1 for the eversmokedcigaretter group (X = 1) was statistically significant, Wald χ² =176.136, p < .001 (see Tables 4 and 8). Like the coefficient B1, the Wald’s statistical value (-4.157) for coefficient B0 or the logit L0 for the never-smoked cigarette group (reference group; X = 0) was also statistically significant; Wald χ² =6651.27, p < .001 (see Tables 4 and 8). These results mean that the odds of developing heart disease in a lifetime among respondents who reported ever smoking cigarettes and those who never reported smoking cigarettes differed significantly from 1.00 (Warner, 2013). In other words, the risk of developing heart disease was different from 50% (Warner, 2013). Thus, developing heart disease in a lifetime does not have an equal chance of occurring among cigarette smokers and non-cigarette smokers. Therefore, the null hypothesis is rejected.

Further analyses indicated that the Exp(B) for an ever-smoked cigarette group was 2.232 with 95% CI [1.983, 2.513] (see tables 8). Put in another way, the odds ratio (conditional odds of cigarette smokers developing CVD divided by the conditional odds of non-cigarette smokers developing CVD) was approximately 2.232 (see table 4). This finding means that the odds ratio of developing heart disease for cigarette smokers were approximately 2.232 times higher than the non-cigarette smokers. In other words, cigarette smokers are 2.232 times more likely to develop heart disease in a lifetime compared to non-cigarette smokers. There was a 95% confidence that the odds of developing heart disease in a lifetime for cigarette smokers were between 1.983 and 2.513 higher times than non-cigarette smokers. We can conclude that cigarette smoking significantly increases the odds of developing CVD in a lifetime. However, the result indicates Cox and Snell’s R2 as .004 and Negelkerche’s R2 as .017 (see Table 7). The Cox and Snell’s R2 value means that the predictor variable, cigarette smoking, accounted for .4% of the variance in the odds of developing heart disease. This is a small effect (Warner, 2013). This means that several other factors (e.g., differences in age, high blood pressure, other substance use, etc. might account for the rest of the variance of the odds of developing heart disease.

Additionally, I displayed the binary logistic regression raw score based on the cross-tabulation from SPSS (see Tables 4 and 5) to examine how other functions, including the conditional probability and risk ratio, are related to the odds ratio of developing CVD for cigarette smokers. The logistic regression raw scores indicate that the conditional probability of cigarette smokers developing CVD was approximately .0338 (i.e., 973/2783), while the risk ratio of developing CVD for cigarette smokers compared to non-cigarette smokers was approximately 2.191(i. e., the conditional probability of cigarette smokers divided by the conditional probability of non-cigarette smokers = .0337788/.0154192). This result means that the risk of developing heart disease was approximately 2.191 times higher for respondents who smoked cigarettes than for non-smokers. This figure is closer to the odds ratio (2.232) of developing heart disease for respondents who smoked cigarettes compared to those who never smoked cigarettes.

Table 1

Case Processing Summary

Cases
ValidMissingTotal
NPercentNPercentNPercent
EversmokedCigarette * HAD HEART DISEASE IN LIFETIME5416398.0%11082.0%55271100.0%

Table 2

Dependent Variable Encoding
Original ValueInternal Value
No (LIFHARTD=6,99)0
Yes (LIFHARTD=1)1

Table 3

Categorical Variables Codings

FrequencyParameter coding
(1)
EversmokedCigarette.0025358.000
1.00288051.000

Table 4

Ever smoked CigaretteNo LIFHARTDYes LIFHARTDTotalConditional ProbabilityConditional OddsLogitOdd RatioRisk RatioConstant
0 (no)2496739125358.0154192.0156606-4.15660.4479615.456475-.4.154
1 (yes)2783297328805.0337788.0349597-3.353552.2323342.190697.803

Table 5


EversmokedCigarette * HAD HEART DISEASE IN LIFETIME Crosstabulation

HAD HEART DISEASE IN LIFETIMETotal
No (LIFHARTD=6,99)Yes (LIFHARTD=1)
EversmokedCigarette.00Count2496739125358
% within HAD HEART DISEASE IN LIFETIME47.3%28.7%46.8%
1.00Count2783297328805
% within HAD HEART DISEASE IN LIFETIME52.7%71.3%53.2%
TotalCount52799136454163
% within HAD HEART DISEASE IN LIFETIME100.0%100.0%100.0%

Table 6

Omnibus Tests of Model Coefficients

Chi-squaredfSig.
Step 1Step192.4941.000
Block192.4941.000
Model192.4941.000

Table 7

Model Summary
Step-2 Log likelihoodCox & Snell R SquareNagelkerke R Square
112544.204a.004.017
a. Estimation terminated at iteration number 7 because parameter estimates changed by less than .001.

Table 8

Variables in the Equation

BS.E.WalddfSig.Exp(B)95% C.I.for EXP(B)
LowerUpper
Step 1aEversmokedCigarette(1).803.061176.1361.0002.2321.9832.513
Constant-4.157.0516651.2791.000.016

a. Variable(s) entered on step 1: EversmokedCigarette.

Discussion

The odds of developing heart disease in a lifetime among respondents who reported having ever smoked cigarettes and those who never reported smoking cigarettes differed significantly. Cigarette smoking was associated with a higher tendency to develop heart disease in a lifetime compared to non-cigarette smoking. Thus, developing heart disease in a lifetime does not have an equal chance of occurring among cigarette smokers and non-cigarette smokers. Precisely, the results showed that the odds of developing heart disease for cigarette smokers were approximately 2.232 times higher than those of non-cigarette smokers. In other words, cigarette smokers were 2.232 times more likely to develop heart disease in a lifetime compared to non-cigarette smokers. There was a 95% confidence that the odds of developing heart disease in a lifetime for cigarette smokers were between 1.983 and 2.513 times higher than those of non-cigarette smokers. The odds ratio figure (2.232) was closer to the risk ratio figure (2.191) in the developing heart disease for respondents who smoked cigarettes compared to those who never smoked cigarettes. Therefore, we conclude that cigarette smoking significantly increases the odds of developing CVD in a lifetime. However, cigarette smoking accounted for .4% of the variance in the odds of developing heart disease, which is a small effect (Warner, 2013). In other words, several other factors (e.g., differences in age, high blood pressure, other substance use, etc. might account for the rest of the variance of the odds of developing a CVD.

Although several studies have associated cigarette smoking with several health problems, including CVD, limited studies have evaluated the odds of developing CVD for cigarette smokers compared to non-cigarette smokers in a general form. The few related studies indicating the tendency to develop some forms of CVD for cigarette smokers compared to non-cigarette smokers are consistent with the current study. For instance, Banks et al. (2019) conducted a study on the risk of developing 36 subtypes of CVD with 188,167 CVD- and cancer-free participants, aged 45 years and older, from the general Australian population who joined the 45 and Up Study from 2006 to 2009. These participants completed a poster questionnaire by the end of 2015 and were followed up through repeated data collection and data linkage. The study results indicate that of the 36 common specific CVD subtypes, there was a significant increase in event rates for 29 subtypes in current smokers. Adjusted risk ratios in current smokers compared to never smokers indicated the following: 1.63 with 95% CI [1.56, 1.71] for any major CVD; 2.45 with 95 CI [2.22, 2.70] for acute myocardial infarction; 2.16 with 95% CI [1.93, 2.42] for stroke; and 2.23 with 95% CI [1.96, 2.53) for heart failure. Others included 5.06 with 95% CI [4.47, 5.74] for PAD; 1.50 with 95% CI [1.24, 1.80] for paroxysmal tachycardia; 1.31 with 95% CI [1.20, 1.44] for atrial fibrillation/flutter; 1.41 with 95% CI [1.17, 1.70] for pulmonary embolism.

Shinton and Beevers (1989) conducted a meta-analysis of 32 studies on the relation between cigarette smoking and stroke. They found that the overall risk of stroke associated with cigarette smoking was 1.5 with 95% CI (1. 4, 1. 6). The result of their study also revealed that the relative risk of developing cerebral aneurysms and subarachnoid hemorrhage for cigarette smokers was 2.93 with 95% CI [2.48, 3.46], and the relative risk of developing cerebral infarction associated with cigarette smoking was 1.92 with 95% CI [1.71, 2.16]. Hacksaw et al. (2018) also conducted a meta-analysis of 55 publications containing 141 cohort studies on the risk of coronary heart disease and stroke based on low cigarette consumption. They found that the pooled relative risk for coronary heart disease among men was 1.48 for smoking one cigarette per day and 2.04 for 20 cigarettes per day (or 1.74 and 2.27, respectively, using relative risks adjusted for multiple factors). The study results also show that the pooled relative risks for coronary heart disease among women were 1.57 for smoking one cigarette per day and 2.84 for 20 cigarettes per day (or 2.19 and 3.95 using relative risks adjusted for multiple factors). For stroke, the pooled relative risks for men were 1.25 for smoking one cigarette per day and 1.64 for smoking 20 cigarettes per day (or 1.30 and 1.56, respectively, using relative risks adjusted for multiple factors). In women, the pooled relative risks were 1.31 and 2.16 for smoking one cigarette per day and 20 cigarettes per day (1.46 and 2.42, respectively, using relative risks adjusted for multiple factors).

Implications for Social Change and Limitation

In addition to supporting and increasing the number of few studies on the odds of developing CVD associated with cigarette smoking compared to non-cigarette smokers, this study has important consequences for cigarette smokers who believe that smoking does not harm the heart. This study will improve healthy living among Americans and the wide world population. Additionally, it will help health providers, educators, and policymakers to provide well-informed information on the odds of developing heart diseases regarding cigarette smoking. This evidence-based information will enhance behavioral motivation towards tobacco smoking cessation and promote positive social change at the individual, community, and social levels. Moreover, it will open the door to more specific research on the odds of developing heart diseases based on a specific number of cigarettes smoked per day, week, or month and the odds of developing each specific subtype of CVD for cigarette smokers.

Finally, this study has a few limitations. The primary limitation of this study is that I used a secondary data source. Using individuals currently engaging in tobacco smoking would yield more accurate findings than secondary data sources. Additionally, the study does not evaluate the odds of developing heart diseases based on a specific number of cigarettes smoked per day, week, or month or the odds of developing each specific subtype of CVD for cigarette smokers. The study only broadly evaluated the odds of developing heart diseases for cigarette smokers compared to non-cigarette smokers. Several other variables could also be considered in evaluating the odds of developing heart diseases. For instance, adding variables, such as age differences, high blood pressure, any other substance use, would increase the statistical significance of the full model chi test for the logistic regression, the Wald statistical significance for smoking cigarettes, and the odds of developing a CVD for cigarette smokers in comparison to non-cigarette smokers.

Acknowledgments

I thank God almighty for the health and wisdom to produce this work. I also thank the thousands of people who participated in the 2014 National Survey on Drug Use and Health (NSDUH). My profound gratitude goes to Dr. Monny Sklov, whose feedback on this work provided great insight fine tuning this work. Many thanks also go to all those who provided me with a conducive environment while producing this work

Data Availability and Ethical Terms

This study uses data from the Inter-university Consortium for Political and Social Research (ICPSR) datasets. The identity of individuals and establishments were not disclosed. All direct identifiers and any other characteristic that might lead to identification are omitted from the dataset. The data in this dataset were used for statistical reporting and analysis only. There was no attempt to learn the identity of any person or establishment included in these data. There was also no attempt to link this dataset with individually identifiable data from other datasets. Additionally, there was no attempt to engage in any efforts to assess disclosure methodologies applied to protect individuals and establishments or any research on methods of re-identification of individuals and establishments.

Contributors and Conflicts of Interest Statement

Enyinna Akanaefu is the only author who contributed to writing this article. This article does not involve any funding, and the author has no conflicts of interest at this time.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

Banks, E., Joshy, G., Korda, R. J., Stavreski, B., Soga, K., Egger, S., Day, C., Naomi E. Clarke, N .E., Lewington, S., & Lopez, A. D.(2019). Tobacco smoking and risk of 36 cardiovascular disease subtypes: Fatal and non-fatal outcomes in a large prospective Australian study. British Medical Journal, 17, 128. (2019) doi:10.1186/s12916-019-1351-4

Burns, D. (2003). Epidemiology of smoking-induced cardiovascular disease. Progress in Cardiovascular Diseases, 46(1), 11-29. doi: 10.1016/S0033-0620(03)00079-3

Centers for Disease Control and Prevention. (n. d). Smoking and cardiovascular diseases. Retrieved from https://www.cdc.gov/tobacco/data_statistics/sgr/50th-anniversary/pdfs/fs_smoking_CVD_508.pdf

DʼAlessandro, A., Boeckelmann, I., Hammwhöner, M., & Goette, A. (2012). Nicotine, cigarette smoking and cardiac arrhythmia: An overview. European Journal of Preventive Cardiology, 19(3), 297-305. doi: 10.1177/1741826711411738

Hacksaw, A., Morris, J., Boniface, S., Tang, J-L., Milenković, D. (2018). Low cigarette consumption and risk of coronary heart disease and stroke: Meta-analysis of 141 cohort studies in 55 study reports. British Medical Journal, 360, j5855.

Papathanasiou, G.,Mamali, A., Papafloratos, S., & Zerva, E. (2014). Effects of smoking on cardiovascular function: The role of nicotine and carbon monoxide. Health Science Journal, 8(2), 274-290.

Pyrgakis, V. (2009). Smoking and cardiovascular disease. Hellenic Journal of Cardiology, 50, 231-234.

Shinton R, & Beevers G. (1989). Meta-analysis of relation between cigarette smoking and stroke. British Medical Journal, 298, 789-794. doi:10.1136/bmj.298.6676.789

Tonstad, S., & Johnston, J. (2006). Cardiovascular risks associated with smoking: a review for clinicians. European Journal of Cardiovascular Prevention & Rehabilitation,13(4), 507-514.

United States Department of Health and Human Services. Substance Abuse and Mental Health Services Administration. Center for Behavioral Health Statistics and Quality. 2014 National Survey on Drug Use and Health. Ann Arbor, MI: Inter-university Consortium for Political and Social Research, 2016. doi: 10.3886/ICPSR36361.v1

Warner, R. M. (2013). Applied statistics from bivariate through multivariate techniques (2nd ed.). Thousand Oaks, CA: Sage Publications.

West, R. (2017). Tobacco smoking: Health impact, prevalence, correlates and interventions. Psychology & Health, 32(8), 1018–1036. doi: 10.1080/08870446.2017.1325890

Using Behaviour Modification Therapy to Treat Attention Deficit/Hyperactivity Disorder

Attention deficit/hyperactivity disorder (ADHD) is a behaviour problem by which young people, especially children, find it difficult to focus their attention, either by way of being under active, or being hyper active/impulsive. Three main subgroup of ADHD are: hyperactive-impulsive ADHD, inattentive ADHD, and combined ADHD (Albeyatti, 2007). People with hyperactive-impulsive ADHD are hyperactive, impulsive or both (e.g., they are extremely noisy, self-talking, interrupt and intrude upon others, constantly moving, have difficulty waiting in queue, and normally have violent and angry behavior). On the other hand, people with inattentive ADHD are underactive and find it extremely difficult to give close attention to details (e.g., they make careless mistakes, they are forgetful and disorganized, perform very poorly in academic studies, etc.), and the combined ADHD has characterises of both hyper-impulsive and inattentive ADHD (Albeyatti, 2007). Attention deficit/hyperactivity disorder is one of the behavior problem that could be treated using behavior modification. Also, this technique is helpful in the treatment of other behavior problems, such as obsessive-compulsive disorder (OCD), self injurious behavior (SIB), autism, phobias, and generalized anxiety disorder(Martin & Pear,1988).

Behavior Modification

Behavior modification is a therapeutic approach that systematically applies learning principles of operant conditioning to change a problem behavior (Martin & Pear, 1988). These operant learning principles include positive reinforcement, negative reinforcement, positive punishment, negative punishment, extinction, continuous reinforcement schedule (CFR), and partial reinforcement schedules (e.g., fixed interval, variable interval, fixed ratio, and variable ratio). These principles can be applied with such behaviour modification procedures as prompting, shaping, differential reinforcement of other behavior (DRO), chaining, fading, token economies, etc. to change a problem behaviour. In this writing, I will discuss the treatment of ADHD with DRO, a behavior modification procedure

Treatment of Attention Deficit/Hyperactivity Disorder Using the Behaviour Modification Procedure of Differential Reinforcement of Other Behavior

As a behavior modification procedure, DRO involves reinforcing a behavior other than the problem behaviour, when the problem behaviour does not occur for a specific period of time. This reinforcement is contingent on the absence or omission of target problem behaviour and sometimes called differential reinforcement to zero responding (Cooper, Heron, & Heward, 2007). The DRO intervention is implemented in two ways: interval DRO and momentary DRO. The Interval procedure involves providing reinforcement if problem behavior does not occur throughout the entire interval, whereas the momentary DRO procedures involves delivering the reinforcement/reward if the other behavior is exhibited at the time of prompts (Daddario, Anhalt, & Barton, 2007). Once behaviour control has been established, the interval required for delivery of the reinforcement progressively increases (Daddario et al., 2007).

After diagnosing a child with hyperactive-impulsive ADHD and obtaining the baseline data that determine the average duration between behaviors or the inter-response interval (through which the schedule of reinforcement that is to be delivered if the target behaviour does not occur is ascertained, for instance, reinforcement will be delivered at the end of 5 minutes if the target behavior has not been exhibited), the hyperactive-impulsive ADHD can be corrected. At this stage, correcting hyperactive-impulsive ADHD will involve reinforcing immediately and consistently after each period of time intended for the child to be calm and focused has elapsed without symptoms of hyperactive-impulsive ADHD occurring, but withholding reward if the symptom occurs.

When the treatment is effective, there is will be a progressive increase in the period of the child’s calmness or non occurrence of hyperactive-impulsive ADHD that will elapse before reinforcement is given, until the child gets to be normally calm and focused. However, we must also note that certain medicines such as methylphenidate when coupled with behavior modification techniques can be of tremendous help in the treatment of ADHD.

Furthermore, to treat a problem behavior, the therapist conscientiously and ethically follows these stages: obtaining the consent of the client and respecting the client’s right to terminate service at any time; assessing the problem behavior to identify the cause through the analysis of the client’s current environment; collecting baseline data, describing to the client or client’s surrogate the conditions necessary for the program to be effective and those that will hamper its effectiveness; applying the treatment program, ongoing data collection; and following up the treatment after completion to determine whether or not the initial improvements reached during the treatment are maintained after the program has ended (Bailey & Burch, 2011; Martin & Pear, 1988). Finally, behaviour modification would be an effective technique because it involves rigorous and effective methods that are ethically guided and applied by therapists.

Conclusion

There is no gainsaying that behavior modification has been successfully used in correcting problem behaviors. Nevertheless, many critics have argued that the operant learning principle of reinforcement is manipulative, violates people’s autonomy, and removes internal freedom. All these objections, notwithstanding, behavior modification has been a wonderful way of replacing problem behaviors with desirable ones in many settings of life.

References

Albeyatti, A. (2007). Attention deficit hyperactivity disorder. In A. A. Hosin (Ed.), Autism ADHD, Anorexia Nervosa: Essays on Three Childhood Disorders (pp.17-52). New York: The Edwin Mellan Press.

Bailey, J. S., & Burch, M. R. (2011). Ethics for behavior analysts: 2nd Expanded. New York: Routledge.

Cooper, J. O., Heron, T. E., & Heward, W. L. (2007). Applied behavior analysis (2nd ed.). Upper Saddle River, New Jersey: Pearson Education.

Daddario, R., Anhalt, K., & Barton, L. (2007). Differential reinforcement of other behavior applied classwide in a child care setting. International Journal of Behavioral Consultation and Therapy, 3, 342-348.

Martin, G., & Pear, J. (1988). Behaviour modification: What it is and how to do it(3rd ed.).Englewood Cliff, NJ: Prentice-Hall.

Effects of Smoking Addiction and Cessation on Stress, Health, and Hunger

Abstract

Tobacco smoking is associated with high morbidity and mortality rates. It harms virtually every organ of the body, causes several health problems (e.g., cancer, abdominal obesity, cardiovascular diseases, and pulmonary diseases), and exposes the body to a high risk of death. Tobacco smoking also has effects on stress and hunger. On the other hand, tobacco smoking cessation has several health benefits, although short-term withdrawal symptoms may accompany the effort to quit. Several factors militate against efforts to quit tobacco smoking. In this review, I examined the evidence on the effects of tobacco smoking and its cessation on stress, hunger, and health and provided insight and motivation to overcome several essential factors interfering with quitting smoking. The study also highlighted evidence of many beneficial effects of tobacco smoking cessation. Additionally, the study underscored numerous treatment programs that have been developed to help tobacco smokers quit smoking and handle cravings and nicotine withdrawal symptoms. The study concludes that the benefits of tobacco smoking cessation outweigh its negative impacts. These benefits cannot be compared to the elusive benefits of tobacco smoking, which eventually become harmful to health.

Keywords: Tobacco; Smoking; Cigarette; Addiction; Cessation; Health; Hunger; Stress

Introduction

Tobacco smoking is a behavior that easily ends in addiction. This is because smoking is embedded in the social context; tobacco smoke contains nicotine, which has addictive properties, and people find it extremely difficult to deal with withdrawal symptoms when trying to break their smoking habit (Butcher et al., 2014). Smoking addiction involves continuously engaging in smoking behavior despite adverse outcomes, unsuccessful attempts at quitting, significant interference with personal work, tolerance, and withdrawal (Lewis, 2014). Unfortunately, studies have shown that, in addition to nicotine, tobacco smoke also contains more than 4000 chemical substances, such as carbon monoxide. Like nicotine, a poisonous alkaloid, most of these chemicals have various harmful effects on the body, including reduction of appetite, higher levels of stress and anxiety, poor health, and a high mortality rate (Papathanasiou et al., 2014).

Statistically, tobacco smoking is the most common cause of preventable deaths and diseases in the developed world. One in seven deaths is associated with tobacco consumption (Naqvi et al., 2007; Papathanasiou et al., 2014). These findings are worrisome because many people are chronic smokers and struggle to quit smoking even when it has caused them serious illnesses, such as lung cancer. Studies have also shown that most smokers who attempt to quit do not use recommended cessation methods, and most of them relapse within the first eight days after quitting (CDC, 2008). Only 4% – 7% of adults who do not use recommended cessation methods are likely to be successful in quitting smoking (CDC, 2008). The purpose of this study is to provide a comprehensive explanation of the potential effects of smoking addiction and cessation on stress, health, and appetite using several literature reviews. This explanation will provide essential insight regarding helping clients quit smoking tobacco. I will also briefly highlight numerous treatment programs that have been developed to help smokers quit smoking and handle nicotine withdrawal symptoms.

Effects of Smoking Addiction and Cessation on Stress

In response to stress, the body activates the sympathetic-adrenomedullary (SAM) system and the hypothalamus-pituitary-adrenal (HPA) system (Butcher et al., 2014). Activating both systems leads to the production of stress hormones (e.g., cortisol, adrenaline, and noradrenaline), the release of the body’s store of energy, and subsequent readiness of the body for fight or flight. Along the SAM axis, the hypothalamus activates the sympathetic nervous system (SNS), which stimulates the core adrenal gland known as the adrenal medulla. Consequently, the adrenal medulla releases the hormones adrenaline (epinephrine) and noradrenaline (norepinephrine), which increase the heart rate, breathing, muscle tension, concentration of attention on the stressors, etc. Along the HPA axis, the hypothalamus stimulates the anterior pituitary gland by secreting corticotropin-releasing hormone (CRH). The anterior pituitary gland, in turn, releases the adrenocorticotrophic hormone (ACTH), which stimulates the outer adrenal gland known as the adrenal cortex. The adrenal cortex secretes hormones, such as glucocorticoid (known as cortisol in humans), which also prepares the body for action by, among other things, increasing the blood sugar level and metabolism (Breedlove & Watson, 2018; Butcher et al., 2014). However, long-term activation of SAM and HPA systems in response to prolonged stress is dangerous to health because it keeps a high level of stress hormones in circulation, causing a reduced body immune system.

Nicotine is a strong activator of both SAM and HPA axes (Richards et al., 2011; Rohleder & Kirschbaum, 2006). Along the HPA axis, it binds to cholinergic receptors on the locus coeruleus and hypothalamus, inducing the release of CRH and subsequent production of cortisol. Along the SAM axis, smoking causes the release of adrenaline and noradrenaline, as well as an increase in systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate, and respiration (Richards et al. 2011). In other words, among smokers, there is a tendency for increased levels of stress hormones (e.g., cortisol and adrenaline) and physiological responses (e.g., increased heart rates and respiratory rates). On this note, researchers observed that similar to behavioral stressors, cigarette smoking stresses the body by eliciting physiological responses, including an increase in cortisol release, heart rate, breathing, arterial blood pressure, and forearm blood flow (Richards et al., 2011; Tsuda et al.,1996). Hence, smoking addiction has been associated with stress responsiveness. For instance, Kirschbaum et al. (1992) reported a constant increase in cortisol levels compared to nonsmokers. In this study, they collected saliva samples of ten female smokers and ten female nonsmokers at 20-minute intervals over a 12-hour period. They observed that smokers showed a significant elevation of cortisol levels compared to nonsmokers. Similarly, Steptoes and Ussher (2006) reported that cigarette smoking is associated with a sharp elevation of cortisol levels. In the first part of their study, they collected saliva samples of 196 middle-aged men and women on working and weekend days and found that cortisol levels were significantly higher in smokers. In the second part of the study, they monitored the cortisol levels of 112 smokers who ceased smoking for about six weeks. Conversely, they found that smoking cessation was associated with abrupt decreases in salivary cortisol.

Further research has also shown that chronic smoking causes a blunted responsiveness in the HPA axis. For instance, Richards et al. (2011) noted that tolerance to the action of the HPA system builds as smoking continues. In this situation, the stress hormones, such as cortisol, adrenaline, and noradrenaline, continue to be high but with an acute tolerance to the physiological effects (e.g., increased heart rates and breathing) due to the activation of these axes. Hence, the result is blunted HPA axis stress reactions, preventing the body from responding appropriately to other stressful stimuli. According to Richards et al. (2011), this physiological tolerance is associated with decreased reinforcing effects of smoking. Such blunted responsiveness to stress has been associated with the disinhibition of inflammatory pathways and consequent stimulation of cardiovascular morbidity and mortality among smokers (Rohleder & Kirschbaum, 2006).

Furthermore, tobacco smoking also causes increased oxidative stress, an imbalance between free radicals (oxygen-containing molecules) and antioxidants in the body. Tobacco smoke contains a large number of free radicals and weakens the antioxidant defensive mechanism that regulates these large number of smoking-mediated free radicals (Papathanasiou et al., 2014). Consequently, chronic smoking leads to increased oxidative stress, which causes damage to cells and changes cellular deoxyribonucleic acid (DNA), impairing the immune response, worsening existing diseases, and increasing inflammation (Hoey & Van, 2019). In addition, smoking addiction leads to chronic high blood sugar accumulation that stresses organ functions. As already seen, nicotine activates both SAM and HPA systems, causing the release of stress hormones, such as cortisol, adrenalin, and noradrenaline. This response strongly hampers insulin production, which reduces glucose catabolism (Papathanasiou et al., 2014). Hence, researchers have observed that smoking addiction leads to chronic accumulation of glucose in the body, which stresses organ functions and results in many health problems (Hoey & Van, 2019; Papathanasiou et al., 2014).

Additionally, tobacco smoking cessation leads to withdrawal symptoms, including anxiety, increased appetite, restlessness, anger, depressed mood, irritability, frustration, attention problems, and insomnia (APA, 2013). These symptoms are very stressful and can even cause clinically significant impairment in social, occupational, or other important areas of functioning (APA, 2013). In their study on the effects of recent smoking and temporary cessation, Tsuda et al. (1996) found that compared to recent smokers, the abstinent group had mood deterioration, a heightened perception of stress during the task, high ratings of restlessness, the urge to smoke, and impairment of behavioral performance. According to Hoey and Van (2019), physiological reactions to tobacco withdrawal are the major causes of stress and nicotine dependence. Because withdrawal symptoms due to smoking cessation (e.g., anxiety, increased appetite, restlessness, anger, depressed mood, irritability, frustration, attention problem, insomnia) are very stressful and can cause clinically significant impairment in social, occupational, or other important areas of functioning, smokers are discouraged from quitting smoking. This is because negative reinforcement occurs when resuming tobacco smoking eliminates or reduces unpleasant feelings. Such negative reinforcing effects often contribute to physical dependence (Carlson & Birkett, 2017). Although withdrawal symptoms and negative reinforcement cannot completely explain tobacco addiction and physical dependence, how knowledge of such phenomena is a source of power to quitting smoking

Effect of Smoking Addiction and Cessation on Health

As indicated earlier, tobacco smoking is a leading cause of preventable deaths and diseases worldwide. The World Health Organization listed tobacco as one of the greatest public health threats the world has ever faced (WHO, 2021). Although nicotine and CO are the leading culprits of the harmful effects of smoking, other chemical substances in tobacco smoke are also dangerous to health. For instance, empirical evidence has shown that 60 out of 4000 or more chemical substances in tobacco smoke are carcinogenic, leading to cancer of the lungs, mouth, throat (pharynx), voice-box (larynx), esophagus, pancreas, stomach, and bladder, kidney, cervix, and ureter (Papathanasiou et al., 2014). These chemical substances can also cause cellular genetic mutations that make the body very vulnerable to cancer.

Both nicotine and CO in tobacco smoke are implicated in diseases of the heart and the blood vessels or cardiovascular diseases), which include constriction of the coronary artery, heart attack, cerebrovascular disease or stroke, peripheral vascular disease, and aortic aneurysm (DʼAlessandro et al., 2012; Papathanasiou et al., 2014). For instance, tobacco smoking leads to cardiovascular diseases by causing atherosclerosis. Smoking lowers high-density lipoproteins (HDL or good cholesterol), increases low-density lipoproteins (LDL or bad cholesterol), and causes a build-up of bad cholesterol, fats, and other substances (or plaque) in the aorta and coronary arteries (DʼAlessandro et al., 2012; Papathanasiou et al., 2014). This plague build-up leads to atherosclerosis, the thickening of artery walls, leading the arteries to become narrower and slowing down the blood flow. Ultimately, several cardiovascular diseases ensue, including arteriosclerosis (also known as coronary artery disease or coronary heart disease), a condition affecting the arteries that supply the heart with blood; cerebrovascular diseases (stroke); and loss of brain function when blood flow to the brain is interrupted. Atherosclerosis due to smoking is also associated with myocardial infarction, hypercoagulable state, stable angina, peripheral arterial disease, and peripheral vascular disease (Tonstad & Johnston, 2006). Peripheral arterial disease and peripheral vascular disease occur when the thickened and narrowed arteries reduce blood flow to the pelvis, arms, hands, legs, hands, and feet. Similarly, smoking prevents insulin production, which leads to glucose accumulation in the body. In turn, excess fatty tissue glucose is converted to triglycerides, whose high concentration contributes to arteriosclerosis. Therefore, smoke-induced insulin resistance is a significant risk factor for the development of arteriosclerosis, which increases the risk of stroke, heart attack, cardiac arrest, and other cardiovascular diseases (Papathanasiou et al., 2014).

Furthermore, smoking causes respiratory diseases. On this note, Cummings (1982) emphasized that smokers frequently develop severe and prolonged upper respiratory tract infections, bronchitis, and emphysema. Buttressing this fact, Roleder and Kirschbaum (2006) remarked that smokers show signs of low-grade systematic inflammation and are vulnerable to chronic airway inflammation. Although this issue seems to contradict the anti-inflammatory effect of nicotine, they explained that the blunted HPA system responsiveness to acute psychological stress is associated with airway inflammation in smokers. Similarly, Papathanasiou et al. (2014) reported that tobacco smoking results in intravascular inflammation, promoting atherosclerosis and cardiovascular diseases. Other ways tobacco smoking is harmful to health include: CO-induced reduction of oxygen-carrying capacity of the blood, which leads to increased red cell mass; impotence (as a result of atherosclerotic changes in the hypogastric-cavernous arterial bed); endangering the health and life of fetuses among pregnant women who smoke endanger the health and life of their fetuses (e. g., low birth weight, placental abruption, spontaneous abortion, premature births, and low neonatal Apgar score); and peptic ulcer (Cummings, 1982; Mosharraf et al., 2019; Tonstad & Johnston, 2006). It is also worth noting that smoking is associated with health risk behaviors. In their study with 93 adolescents, Busen et al. (2001) found that it was easier for current smokers to use alcohol and marijuana than nonsmokers.

Effects of Smoking Addiction and Cessation on Appetite

According to Chao et al. (2017), tobacco smoking is highly associated with obesity-related behavior, including an unhealthy diet. It is a common belief that smoking suppresses appetite and increases satiety. This view is not far from the truth. According to Jo et al. (2005), nicotine inhibits melanin-concentrating hormone (MCH) neurons of the lateral hypothalamus (LH), thus suppressing appetite. MCH and orexin (or hypocretin) are two major peptides produced by neurons in the LH that have been implicated in stimulating hunger and reducing metabolic rate. Thus, they increase appetite and preserve the body’s energy storage (Carlson & Birkett, 2017; Jo et al., 2005). Both peptides are known as orexigens. Additionally, Miyata et al. (1999) found that nicotine administration into lateral hypothalamic (LH) circuits significantly decreases food intake by modulating the neurotransmitters serotonin and dopamine. 

However, several studies have shown that smokers have more frequent cravings for food high in fat than nonsmokers and so have a significant risk of abdominal obesity. For instance, Pepino et al. (2009) reported that current smokers have more high-fat food cravings and intakes than former smokers among women. In this study, 229 women completed the Food Craving Inventory designed to measure the frequency of overall food cravings and cravings for specific types of food, including high-fat foods, starches, sweets, and fast-food fats. Also, the height and weight of participants were measured, and their body mass index (BMI) was computed. The result of the study indicated that current smokers craved foods higher in fat and carbohydrates than never-smokers. Surprisingly, never-smokers craved high-fat and starchy foods more than former smokers. Thus, this means that craving for high-fat foods among smokers is related to the effects of smoking as such (Pepino et al., 2009). Using more diverse and larger participants (n = 712) who completed questionnaires on food cravings, dietary intake, smoking history, and weight and height, Chao et al. (2017) reported the same effect of smoking on appetite. After controlling for depression, stress, BMI, and demographic factors, they observed that compared to never and former smokers, current smokers more frequently crave and consume foods that are sweet, starchy, and high in fat. Hence, the authors concluded that smokers have a greater risk of abdominal fat accumulation than nonsmokers. In addition, Dare et al. (2015) reported that heavier smokers had the risk of abdominal obesity than light smokers.

On the other hand, smoking cessation causes increased appetite. One explanation of this phenomenon is that the body has reversed its ability to suppress appetite. On this note, Carlson and Birkett (2017) maintained that the absence of nicotine in the brain resumes the stimulation of MCH, increasing appetite and decreasing metabolic rate. Another explanation is the possibility of reinforcement substitution in which rewards of food replace rewards of smoking (Harris et al., 2016). Additionally, the view that taste buds and smell are reactivated after quitting smoking, causing increased food intake, is an impelling explanation for this phenomenon. Consequently, when people try to quit smoking, they are often discouraged by the high level of hunger, overeating, and weight gain that accompanies it (Harris et al., 2016; Jo et al., 2005). Therefore, awareness of this phenomenon will help both therapists and clients gain insight into clients’ struggles to quit tobacco smoking.

Beneficial Effects of Smoking Cessation

All hope is not lost regarding the harmful effects of tobacco smoking. Fortunately, scientific evidence has revealed many beneficial effects of smoking cessation at any age, but indicating that quitting at younger ages is associated with greater decreases in premature mortality (CDC, 2008). According to Tonstad and Johnston (2006), some of the mechanisms by which smoking causes its deleterious effects on the body are reversible. For instance, smoking cessation decreases inflammatory responses, rapid restoration of circulating endothelial progenitor cells, and prevents the progression of irreversible smoking-induced cardiovascular diseases, such as atherosclerosis and lipid deposits in the intima artery (Tonstad & Johnston, 2006). On this note, a large number of studies have shown that, compared to current smokers, former smokers have a reduced risk of death from coronary heart disease after about two years of quitting smoking (Fichtenberg & Glantz, 2000). This risk declines to the level of never smokers after about ten years (Tonstad & Johnston, 2006). Similarly, the risk of myocardial infarction decreases to the level of never smokers after about three years (Rosenberg et al., 1985; Rosenberg et al.,1990).

Furthermore, Tonstad and Johnston (2006) also remarked that smokers with peripheral vascular diseases who stopped smoking had a decreased risk of amputation following surgery and an increased chance of overall survival. Besides, they have increased exercise tolerance. Compared to current smokers, former smokers also have a lower risk of abdominal aortic aneurysms (Tonstad & Johnston, 2006). Moreover, Cummings (1982) reported that smoking cessation reduces cough and sputum production, improves forced respiratory volume, and serves as essential ulcer treatment as medication. In general, smoking cessation is associated with many health benefits, including reducing mortality from cardiovascular diseases, pulmonary diseases, and cancer. West (2017) reported that coronary heart disease, stroke, chronic obstructive pulmonary disease, and cancers of the lungs and upper airways are preventable if smoking cessation occurs in early adulthood. Existing coronary heart disease and stroke due to tobacco smoking are reversible if smoking cessation occurs in early adulthood. West (2017) also underscored that miscarriages and underdevelopment of the fetus are preventable if smoking cessation occurs early in pregnancy. Similarly, this risk is mitigated by quitting smoking at any time in pregnancy. Therefore, the benefits of tobacco smoking cessation outweigh its negative impacts. These benefits cannot be compared to the elusive benefits of tobacco addiction.

Treatment Programs for Quitting Smoking

As highlighted earlier, people find it very discouraging to quit smoking because of cravings for smoking and withdrawal symptoms, such as anxiety, increased appetite, restlessness, anger, depressed mood, irritability, frustration, and insomnia. Methods adopted to help smokers handle cravings and nicotine withdrawal effects while quitting smoking include physicians’ advice, contingency contracting, enhancing self-efficacy, relaxation training, deep breathing, aversive conditioning, remembering the reason for quitting, and stimulus control techniques (Cummings, 1982). For instance, physicians’ advice to quit is very beneficial, especially for those who have developed withdrawal symptoms. Cummings (1982) reported that 63% of smokers with myocardial infarctions who received antismoking advice from physicians ceased smoking and remained abstinent for at least one year. In contingency contracting, the smoker goes into a contract with nonsmokers to quit and remain abstinent by depositing something (e.g., money) that will be lost if the quitting fails.

Additionally, stimulus control techniques help smokers identify and record smoking-associated stimuli (e. g., social-environmental cues) that have acquired the ability to produce craving, drug effects, and withdrawal symptoms; avoid these situations or modify responses to them; and reduce cravings for smoking. One way to modify responses to social-environmental cues associated with smoking is by learning combine cue exposures to extinguish conditioned responses to these cues. According to Brandon et al. (2007), repeated exposures to drug-associated stimuli without reinforcement enhances the extinction of conditioned responses to these stimuli. Similarly, providing clients with a portable stimulus associated with extinction (e.g., token, cognitive cue) improves the efficacy of cue exposure and improves smoking addiction treatment. Empirical evidence has also shown that extinction cues significantly aid clients’ retrieval of the extinction memory and significantly reduce craving and salivation to substance-associated cues in a novel context following extinction (Brook, 2000; Collins & Brandon, 2002).

Furthermore, enhancing self-efficacy among clients struggling to quit smoking can also be effective. Several strategies exist to facilitate self-efficacy among clients. According to Kaddena and Litta (2011), an essential way to improve self-efficacy for positive treatment outcomes is by using motivational interviewing (MI). In this procedure, therapists will be supportive of clients and express their confidence in clients’ ability to change, elicit change talks in the client (e.g., How is tobacco smoking affecting your health?) and commitment language (e.g., How strong is your commitment to stop tobacco smoking? What steps have you already taken to smoking?). Therapists also enhance clients’ self-efficacy by using use the confidence ruler exercise (e.g., what would help your confidence to rise from a 2 to a 3), setting a small behavioral task for clients to accomplish (e.g., reducing smoking from one a day to one in four days), celebrating clients or use reinforcement means when they accomplish the task and reviewing clients’ past success and current strength. Other ways to enhance self-efficacy include assisting clients in clearing out negative thoughts, learning from others’ success, and using coping skills (e.g., problem-solving, communication skills, and social skills).

Conclusion

Addiction to smoking has dangerous effects on health, including oxidative stress, abdominal obesity, cardiovascular diseases, pulmonary diseases, and cancer. Smoking harms virtually every organ of the body, exposing the body to a high risk of death. On the other hand, smoking cessation has several health benefits, especially reducing the risk of death from these diseases, although short-term withdrawal symptoms may accompany the effort to quit. However, the benefits of tobacco smoking cessation outweigh its negative impacts. These benefits cannot be compared to the elusive benefits of tobacco smoking, which eventually become harmful to health. Therefore, it is advisable for smokers who are trying to quit to seek advice from physicians or other medical experts and employ several other techniques to handle their nicotine withdrawal effects. In addition to the physician’s advice, empirical evidence supports that other methods, including contingency contracting, enhancing clients’ self-efficacy, relaxation training, remembering the reason for quitting, and stimulus control techniques, are effective in helping clients quit smoking. However, more research is needed to understand specific situations and conditions in which each technique works best.

Acknowledgments

I thank God almighty for the health and wisdom to produce this work. Many thanks also go to all those who provided me with a conducive environment while producing this work

Data Availability Statement

Data sharing was not applicable to this study as no datasets were generated or analyzed during the current study. The data collection method was solely previous studies on the effects of tobacco smoking on stress, hunger, and health.

Statement Regarding Informed Consent

Informed consent from individual participants was not applicable for the current study as data sharing was not applicable, and no datasets were generated or analyzed in the current study.

Statement Regarding Ethical Approval

All the previous studies used for the current study were duly acknowledged. Additionally, the current study does not involve human participants or data sharing. Therefore, ethical approval regarding participants and data sharing was not applicable for the current study.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

Brandon, T. H., Virdrine, J. I., & Litvin, E. B. (2007). Relapse and relapse prevention. Annual Review of Clinical Psychology, 3, 257-284. doi: 10.1146/annurev.clinpsy.3.022806.091455

Breedlove, S. M., & Watson, N. V. (2018). Behavioral neuroscience (8th ed.) New York, NY: Oxford University Press.

Brooks, D. C. (2000). Recent and remote extinction cues reduce spontaneous recovery. The Qaurterly Journal of Experimental Psychology, 53(1), 25-58. doi: 10.1080/027249900392986

Busen, N. H., Modeland, V., & Kouzekanani, K. (2001). Adolescent cigarette smoking and health risk behavior. Journal of Pediatric Nursing,16(3), 187-193. doi: 10.1053/jpdn.2001.24182.

Butcher, J. N., Hooley, J. M., & Mineka, S. (2014). Abnormal psychology (16th ed.). Boston: Pearson.

Carson, N. R., & Birkett, M. A. (2017). Physiology of behavior (12th ed.). New York: Pearson.

Centers for Disease Control and Prevention. (2008). Cigarette smoking among adults. United States, 2006. MMWR. 57(45), 1221-1226.

Chao, A. M., White, M. A., Grilo, C. M., & Sinha, R. (2017). Examining the effects of cigarette smoking on food cravings and intake, depressive symptoms, and stress. Eating Behavior,24, 61-65. doi: 10.1016/j.eatbeh.2016.12.009

Collins, B. N, & Brandon, T. H. (2002). Effects of extinction context and retrieval cues on alcohol cue reactivity among nonalcoholic drinkers. Journal of Consulting and Clinical. Psychology,70(2), 390-397. doi: 10.1037//0022-006X.70.2.390

Cummings, S. R. (1982). Kicking the habit: Benefits and methods of quitting cigarette smoking. The Western Journal of Medicine, 137(5), 143-147.

DʼAlessandro, A., Boeckelmann, I., Hammwhöner, M., & Goette, A. (2012). Nicotine, cigarette smoking and cardiac arrhythmia: An overview. European Journal of Preventive Cardiology, 19(3), 297-305. doi: 10.1177/1741826711411738

Dare, S., Mackay, D. F., Pell, J. P. (2015). Relationship between smoking and obesity: A cross-sectional study of 499504 middle-aged adults in the UK general population. PLoS One,10(4),1-12. doi: 10.1371/journal.pone.0123579

Fichtenberg, C. M., & Glantz, S. A. (2000). Association of the California Tobacco control program with decline in cigarette consumption and mortality from heart diseases. The New England Journal of Medicine, 343(24), 1772- 1777. doi: 10.1056/NEJM200012143432406

Harris, K. K., Zopey, M., & Friedman, T. (2016). Metabolic effects of smoking cessation. Nat Rev Endocrinol, 12(5), 299–308. doi:10.1038/nrendo.2016.32.

Hoey, N. M., & Van, P. D. (2019). Stress and smoking. Salem Press Encyclopedia of Health. Retrieved from the Walden Library databases

Jo, Y. H., Wiedl, D., & Role, L. W. (2005). Cholinergic modulation of appetite-related synapse in mouse lateral hypothalamic slice. Journal of Neuroscience, 25(48), 11133-11144. Retrieved from https://www.jneurosci.org/content/jneuro/25/48/11133.full.pdf

Kaddena, R. M., & Litta, M. D. (2011). The role of self-Efficacy in the treatment of substance use disorders. Addictive Behavior, 36(12), 1120-1126. doi:10.1016/j.addbeh.2011.07.032.

Kirschbaum, C., Wust, S., & Strasburger, C. J., (1992). Normal cigarette smoking increases free cortisol in habitual smokers. Life Sci. 50(6), 435–442. doi: 10.1016/0024-3205(92)90378-3

Lewis, T. F. (2014). Substance abuse and addiction treatment: Practical application of counseling theory. Boston: Pearson.

Mendelson, J. H., Goletiani, N., Scholar, M. B., Siegel, A., & Mello, N. (2008). Effects of smoking successive low-and high-nicotine cigarette on hypothalamic-pituatary-adrenal axis hormones and mod in men. Neuropsychopharmacology, 33,749-760. doi: 101038/sj.npp.1300753

Miyata, G., Meguid, M.M., Fetissov, S., Torelli, G. F., & Kim, H. (1999). Nicotine’s effect on hypothalamic neurotransmitters and appetite regulation. Surgery, 126(2), 255-263. doi: 10.1016/S0039-6060(99)70163-7

Mosharraf, S., Allahdadian, M., & Reyhani, Mitra. (2019). Comparison of adverse pregnancy outcomes between hookah and non-smoking women. Journal of Midwifery & Reproductive Health, 7(1), 1499-1505. doi:1022038/jmrh.2018.27116.1292

Naqvi, N. H. Rudrauf, D., Damasio, H., & Bechara, A. (2007). Damage to the insula disrupts addiction to cigarette smoking. Science, 315, 531-534. doi: 10.1126/science.1135926

Papathanasiou, G.,Mamali, A., Papafloratos, S., & Zerva, E. (2014). Effects of smoking on cardiovascular function: The role of nicotine and carbon monoxide. Health Science Journal, 8(2), 274-290.

Pepino, M. Y., Finkbeiner, S., & Mennella, J. A. (2009). Similarities in food cravings and mood states between obese women and women who smoke tobacco. Obesity,17(6), 1158-1163. doi:10.1038/oby.2009.46

Richards, J. M., Stipelman, B. A., Bornovalova, M. A., Daughters, S. B., Sinha, R., & Lejuez, C.W. (2011). Biological mechanisms underlying the relationship between stress and smoking: State of the science and directions for future work. Biological Psychology,88 (1), 1-12. doi: 10.1016/j.biopsycho.2011.06.009

Rohleder, N., & Kirschbaum, C. (2006). The hypothalamic-pituitary-adrenal (HPA) axis in habitual smokers. International Journal of Psychophysiology, 59(3), 236-243. doi: 10.1016/j.ijpsycho.2005.10.01

Rosenborg, L., Kaufman, D. W., Helmrich, S. P., & Shapiro, S. (1985). The risk of myocardial infarction after quitting smoking in men under 55 years of age. The New England Journal of Medicine, 313 (24),1511-1514. doi: 10.1056/NEJM198512123132404

Rosenberg, L., Palmer, J. R., & Shapiro, S (1990). Decline in the risk of myocardial infarction among women who stop smoking. The New England Journal of Medicine,322 (4), 213-217. doi: 10.1056/NEJM19900125322040

Steptoe, A., Ussher, M. (2006). Smoking, cortisol, and nicotine. International Journal of Psychophysiology, 59(3),228-235. doi: 10.1016/j.ijpsycho.2005.10.01

Tonstad, S., & Johnston, J. (2006). Cardiovascular risks associated with smoking: a review for clinicians. European Journal of Cardiovascular Prevention & Rehabilitation,13(4), 507-514.

Tsuda, A., Steptoe, A, West, R., Fieldman, G., & Kirschbaum, C. (1996). Cigarette smoking and psychophysiological stress responsiveness: Effects of recent smoking and temporary abstinence. Psychopharmocology, 126, 226-233.

West, R. (2017). Tobacco smoking: Health impact, prevalence, correlates and interventions. Psychology & Health, 32(8), 1018-1036. doi: 10.1080/08870446.2017.1325890

World Health Organization. (2021, July, 26). Tobacco. Retrieved from https://www.who.int/news-room/fact-sheets/detail/tobacco

Behavioral Principles in Stimulant Abuse

Substance abuse is the continual use of a substance despite adverse outcomes. Substance addiction, a term that has fallen out of favor with many researchers and clinicians, is compulsive persistent substance use regardless of adverse effects. It usually involves engaging in specific behavior to get the drugs, unsuccessful attempts at quitting, significant interference with personal work, the inability to take responsibility, tolerance, and withdrawal (Lewis, 2014). Studies have shown that reinforcement, classical conditioning, and social cognitive learning principles lead to habitual and compulsive substance use behavior despite the negative consequences. Precisely, the reinforcing effects of substance use lead to drug-seeking behavior, whereas classical conditioning and social cognitive learning are associated with attentional bias, habitual, and compulsive behavior toward substance use. The purpose of this study is to explore how the behavioral principles of reinforcement, classical conditioning, and social cognitive learning contribute to stimulant abuse and how the three learning principles affect the psychological and pharmacological treatment of stimulant abuse. Understanding this topic will help therapists devise a treatment that will break clients’ stimulant dependence behavior.

Effects of Behavioral Principles in Stimulant Abuse

When people engage in stimulant abuse, they often lose control and the behavior becomes automatic and compulsive. Specific reinforcing brain mechanisms, as well as other psychological processes, have been implicated for this behavior. Understanding these processes will help psychopharmacotherapists work with clients with stimulant abuse problems effectively.

Reinforcement and Stimulant Abuse

Reinforcement, in addition to classical conditioning, leads to habitual, compulsive stimulant use behavior despite the negative consequence. Evidence has shown that taking drugs has positive and negative reinforcing effects leading to the future frequency of drug-taking. On this note, Everitt and Robbins (2005) reported that when people take a drug voluntarily, reinforcement occurs when a response produces a desirable stimulus (positive reinforcement) or removes an aversive stimulus (negative reinforcement), such that in both cases, the future frequency of the response increases. Similarly, Carlson and Birkett (2017) noted that drugs activate positive reinforcement brain mechanisms, strengthening the response that was just made and leading to abuse potential. Additionally, the reinforcing effects are stronger and lead to increased abuse potential when the drug is taken through fast-acting routes, such as injection and inhalation.

Like every substance of abuse, stimulants (amphetamines, methamphetamines, cocaine, ecstasy), including stimulant prescription medications (e.g., Ritalin, Cylert, Provigil, and Adderall), exert positive reinforcing effects by triggering the release of dopamine in the nucleus accumbens (NAC) of the mesolimbic system. On this note, Di Chiara (1995) and Volkow (2010) underscore that increased activities of dopaminergic neurons of the mesolimbic system (which begins in the ventral tegmental area (VTA) of the midbrain, projecting their axons to the limbic system of the forebrain that nucleus accumbens (NAC) have been implicated for the pleasurable sensation that comes from using drugs and their positive reinforcing effects. However, different drugs stimulate the dopaminergic system differently. For example, cocaine increases dopamine by blocking dopamine transporters, thus interfering with its removal from the synaptic space, whereas alcohol increases dopamine indirectly by affecting neurotransmitters that regulate dopamine cell-firing in the VTA (Volkow, 2010). In any case, the faster a drug produces its effects, the more it produces reinforcement and increases abuse potential and physical dependence. For instance, intravenous injection and inhalation are fast routes that produce effects within seconds. Thus, injecting or inhaling cocaine or other stimulant drugs produces high levels of reinforcing effects and abuse potential. Similarly, irrespective of the routes, stimulants drugs absorbed faster in the body produce higher reinforcing effects and physical dependency than those that take some time to absorb.

Furthermore, negative reinforcement also occurs when stimulant drugs eliminate or reduce unpleasant feelings (e. g., anxiety, depression, and sadness). Such negative reinforcing effects contribute to physical dependence. For instance, Carlson Birkett (2017) reported that the use of nicotine, cocaine, amphetamine eliminates or reduces sadness, depression, and several other unpleasant feelings, which negatively reinforce the future use of the drugs whenever unpleasant feelings occur or are anticipated. Additionally, negative reinforcement, which leads to physical dependence, occurs when individuals who are struggling to stop substance abuse go back to take the same drug because it reduces unpleasant withdrawal symptoms (the opposite of the effects of the drug). However, positive reinforcement, withdrawal symptoms, and negative reinforcement cannot completely explain stimulant abuse and physical dependence. Empirical evidence has shown that withdrawal symptoms can occur even after an individual has refrained from taking the drug for a long time. Classical conditioning has been implicated in withdrawal symptoms after individuals have quitted using drugs for a long time (Carlson & Birkett, 2017; Tim & Leukefeld, 1993; Wikler, 1973).

Classical Conditioning and Substance Abuse

Classical conditioning is associated with habitual and compulsive behavior toward stimulant use (Everitt & Robbins, 2005). Evidence has also shown that repetitive use of the same drug can produce condition responses (CRs). In other words, through the process of classical conditioning, a stimulus that has been associated with drugs in the past can acquire the ability to elicit expectancy of substance availability and cravings. On this note, Tim and Leukefeld (1993) stressed that after repeated pairing, environmental stimuli could acquire the ability to elicit craving and produce stimulant-like effects, including euphoria, pharmacological withdrawal effects, and placebo effects. Explaining how classical conditioning contributes to habitual and compulsive substance use behavior, Volkow et al. (2011) observed that changes in the dorsal striatum occur as drug-seeking behavior causes dopamine release in the NAC. According to Volkow et al., compared to nonusers, cocaine abusers showed a much smaller release of dopamine in the NAC when injected with methylphenidate (a stimulant prescription medication) but showed increased release of dopamine in the dorsal striatum when shown a video of people smoking cocaine. In other words, after repeatedly abusing cocaine, dopamine released will begin to occur in the dorsal striatum because of drug-associated cues than in the NAC because of the drug itself. Consequently, the compulsion to continue to take stimulant drugs is motivated more by drug-related cues than by the pleasurable effects.

According to Tim and Leukefeld (1993), there may be thousands of environmental stimuli pairings with withdrawal symptoms or euphoric effects during the patient’s lifetime before seeking treatment. External states serving as stimulant-associated stimuli that can acquire the ability to produce craving, drug effects, and withdrawal symptoms, include drug-procuring environment, drug-using environment, people, liquor bottle, needles, piles of white powder, discussions on drugs, smells signaling that drug is about to appear, signpost or posters showing needles and drug labels, etc. Internal states serving as stimulant-associated cues include sadness, loneliness, boredom, and depression. Thus, cues associated with drug effects or drug withdrawal symptoms might play an essential role in triggering relapse to drug use in abstinence. For instance, Wikler (1973) conducted a study with participants who had been completely opioid-free for several months in group therapy sessions. He noted that when the group started talking about drugs, many participants began to yawn, sniffle, and tear their eyes, which are signs of opioid withdrawal syndrome.

Furthermore, stimulant-related stimuli can elicit the expectancy of stimulant availability because, through classical conditioning, stimulant users orient their attention toward predictive conditional stimuli when they are encountered. Field and Cox (2008) called this orientation of one’s attention toward stimulants or any other drug attentional bias and observe that it leads to subjective cravings towards the drug. The authors further suggested that a reciprocal causal relationship exists between subjective craving and attentional bias. In other words, attentional bias causes cravings, which, in turn, lead to attentional bias. Thus, situations associated with cravings, including external and internal cue exposures, deprivation, priming, could lead to attentional bias. Additionally, Field and Cox (2008) observed that any goal related to drug use, whether it is the goal to use the drug (appetitive goal) or conscious attempts to suppress cravings, avoid the drug, and avoid attending to its cues (aversive goal), produces attentional bias toward the drug. This observation is consistent with the findings of Vadhan et al. (2007), in which they observed that compared to the nontreatment-seeking participants, treatment-seeking cocaine abusers color-named cocaine-related words more slowly than neutral words, although they had used cocaine less frequently than the nontreatment-seeking group. They also noted that impulsivity and impaired inhibitory control mediate attentional bias.

Social Learning and Stimulant Abuse

Social learning is a behavioral principle based on Bandura’s social cognitive theory (SCT), in which individual behavior is determined by the interacting influences of personal, behavioral, and environmental variables, known as reciprocal determinism (Lee et al., 2018). The environmental variables are the perceived or physical environmental factors promoting, permitting, or discouraging a particular behavior. These factors include: social role models (e. g., teachers, parents, opinion leader, friends, siblings) influencing the individual through observational learning; cultural beliefs about the standards, social acceptability, and the prevalence of a behavior; perception of social support or encouragement; facilitation to engage in health behavior (e.g., opportunities, instructions, feedback, rewards); and sociostructural barriers, which impede engagement in the health behavior (Glanz et al., 2015; Schunk & DiBenedetto, 2020). Personal cognitive factors involve the individual’s ability to self-regulate or self-determine behavior and reflect upon and analyze behavior (e. g., setting goals, choosing activities, self-evaluations of progress, and social comparisons). Personal factors revolve around three primary constructs: self-efficacy (confidence to engage in behavior), expected outcomes (ability to foresee the outcomes of a given behavior pattern, and knowledge or the level of understanding about enacting a behavior (Glanz et al., 2015). Behavioral factors include behavioral skills, efforts, and persistence to perform a behavior successfully, intentions, reward, and punishment (Glanz et al., 2015; Schunk & DiBenedetto, 2020). Behavor factors affect health directly. They are actions that are health-enhancing or health-compromising.

Empirical evidence has shown that two of these constructs, namely, self-efficacy and outcome expectations, have been implicated in drug abuse and addiction. Self-efficacy involves having confidence in the ability to execute a specific health behavior. It affects the motivation to execute the behavior change. Outcome expectations consist of the perceived benefits or disadvantages of engaging in a specific behavior, sociostructural variables encompass external barriers (e. g., physical, social, and environmental barriers) to achieving a behavior change, while the goals comprise the actions required to accomplish a behavior (Knowlden et al., 2018). For instance, Brandon et al. (2007) reported that perceived outcomes impact the expected effects of substance consumption. For instance, cocaine users’ expectation that cocaine produces stress relief, a profound feeling of well being, enhanced alertness, a decrease in anxiety, an increase in strength, and an increase in confidence, mastery, and power strongly motivates them to use cocaine whether or not cocaine produces these effects. Brandon et al. also reported that self-report questionnaires indicate that the magnitude of perceived benefits is predictive of every phase of substance use, including initiation, poorer treatment outcomes, and relapse. Additionally, self-efficacy about maintaining abstinence is a strong predictor of long-term treatment outcomes.

Applying Behavioral Principles in the Psychopharmacological Treatment for Stimulant Abuse

As already indicated, learning how behavioral principles could be applied in the psychological and pharmacological treatment of stimulant abuse will help therapists devise a treatment that will break clients’ stimulant dependence behavior.

Reinforcement Principles

Stimulant prescription medications and drugs to maintain abstinence from stimulant drugs and prevent relapse operate on reinforcement principles, including positive reinforcement, negative reinforcement, and punishment. Based on the reinforcement principles, Brandon et al. (2017) emphasized that they could be divided into two broad categories: stimulant medications and drugs that block reinforcing effects and those that stimulate reinforcing brain mechanisms. Stimulant medication drugs that block reinforcing effects include aversives (e.g., disulfiram) and antagonists (e.g., naltrexone and other opiate receptor blockers such as naloxone). For instance, disulfiram (Antabuse) produces unpleasant physical effects serving to extinguish an addictive behavior through punishment (teaching patients aversion to stimulant use) as it blocks the stimulant-induced reinstatement of stimulant-seeking behavior. Naltrexone (an antagonist) produces dysphoria and anhedonia as it blocks the dopamine receptors and their reinforcing effects. Many people do not tolerate the unpleasant feelings these drugs produce. These medications help treat stimulant abuse or addiction when patients can bear the unpleasant feelings associated with them.

Applying reinforcement principles can improve the effectiveness of aversive and antagonist stimulant medications. Firstly, the sequence of consequences (reinforcement or punishment) should be an essential consideration. When reinforcement is experienced first or punishment delayed, the power of punishment to shape behavior weakens (Woolverton et al., 2012). For instance, pear approval for stimulant abuse (reinforcement) could weaken the effect of aversive stimulant medication that teaches patients aversion to stimulant use. Secondly, when too much time passes between the behavior and the consequence (reinforcement or punishment), the reinforcement or punishment’s power to shape behavior weakens. For instance, when using aversive stimulant medications that produce unpleasant feelings, such as disulfiram, pharmacotherapists must ensure that there is no intermittent reinforcement between doses to avoid interference with the learned extinction process. Consistently taking the medication and experiencing unpleasant feelings associated with stimulant abuse improves treatment effectiveness. Thirdly, using doses of aversive stimulant medication that are low relative to the bodyweight might also decrease the effectiveness of stimulant abuse treatment (Haile et al., 2012). In other words, the use of weigh-base aversive stimulant medication doses increases stimulant medication treatment.

Furthermore, the second category of medications for stimulant abuse, which stimulate reinforcement (e.g., ropinirole, aripiprazole, amantadine, L-dopa, methylphenidate, bromocriptine, and bupropion), may reduce stimulant dependence. However, these drugs have much abuse potential as the drugs they replace (Carlson & Birkett, 2017). Using reinforcement principles can minimize the reinforcing effects of such medications. Precisely, the lower the reinforcer, the lower the reinforcing effects. Therefore, patients should take low doses of these medications and avoid faster routes (e. g., injection). Similarly, using partial agonists (e. g., buprenorphine, dianicline, and cytisine), which enable low-level of dopamine release is very helpful. Additionally, patients should be helped reinstate other channels of reinforcement, such as friendship, marital relationship, good time with loved ones, and work, which substance abuse has destroyed. As in the case of other substance abuse, individuals with stimulant use disorder usually destroy or block other means of pleasure or reinforcement in their lives. In this way, the drug of abuse becomes the only means of reinforcement. Helping clients re-open these other channels of reinforcement reduces dependency on the stimulant medications that activate reinforcing brain mechanisms.

Classical Conditioning Principles

Applying classical conditioning principles in the pharmacological treatment for stimulant abuse also contributes to the treatment effectiveness. Fundamentally, psychopharmocotherapists need to know how classical conditioning impedes clients’ medications effectiveness and how to help them unlearn such behavior. For instance, helping clients to learn combine cue exposures to facilitate extinction of conditioned response to stimulant-associated stimuli that have acquired the ability to produce craving, drug effects, and withdrawal symptoms will greatly improve stimulant disorder treatment effectiveness. According to Brandon et al. (2007), repeated exposures to drug-associated stimuli without reinforcement enhances the extinction of conditioned response to these stimuli. Additionally, empirical evidence shows that extinction cues significantly aids patients’ retrieval of the extinction memory and significantly reduces craving and salivation to substance-associated cues in a novel context following extinction (Brook, 2000; Collins & Brandon, 2002). In other words, providing patients with a portable stimulus associated with extinction (e.g., token, cognitive cue) improves the efficacy of cue exposure and improves stimulant abuse treatment effectiveness.

Social Cognitive Learning

As already indicated, the social learning construct of self-efficacy about maintaining abstinence is a strong predictor of long-term stimulant treatment outcomes. Enhancing self-efficacy among clients undergoing stimulant treatment will improve the treatment effectiveness. Several strategies exist to facilitate self-efficacy among clients. According to Kadden and Litt (2011), an essential way to improve self-efficacy for positive stimulant treatment outcomes is using motivational interviewing (MI). In this procedure, psychopharmotherapists will be supportive to clients and express their confidence in clients’ ability to change, elicit change talks (e. g., How is cocaine use affecting your health and marriage?) and commitment language (e.g., How strong is your commitment to changing your cocaine abuse? What steps have you already taken to curb your cocaine use?), use the confidence ruler exercise (e.g., what would help your confidence to rise from a 3 to a 4), set a small behavioral task for clients to accomplish and celebrate clients or use reinforcement means when they accomplish the task and review clients’ past success and current strength. Other ways to enhance self-efficacy include assisting clients in clearing out negative thoughts, learning from others’ success, and using coping skills (e.g., problem-solving, communication skills, and social skills).

Furthermore, helping clients to highlight the negative outcome expectation of stimulant abuse and positive outcome expectations of abstaining from stimulant use improves stimulant treatment effectiveness. For instance, using the MI procedure, psychophamacotherapists might ask clients: How is your cocaine abuse affecting your health? How will your change positively affect your health and your relationship with your family members? How will your change affect the way your wife and children treat you? What might you want to do to change the way you treat them? How is your substance use affecting your occupational and social life?

Conclusion

It is clear that reinforcement, classical conditioning, and social cognitive learning principles contribute immensely to drug-seeking behavior, habitual or compulsive behavior, and relapse in relation to stimulant abuse. Additionally, to improve stimulant pharmacological treatment effectiveness, I encourage therapists to pay attention to how these behavioral principles interfere with the effectiveness of the pharmacological stimulant abuse treatment. For instance, when using aversive stimulant medications that produce unpleasant feelings, psychopharmacotherapists must ensure that there is no intermittent reinforcement between doses to avoid interference with the learned extinction process. Again, I encourage psychopharmacotherapists to help clients unlearn stimulant abuse behavior using behavioral principles. For instance, repeated exposures to stimulant-associated stimuli without reinforcement enhance the extinction of conditioned response to these stimuli. Further support of the extinction process by providing clients with a portable stimulus associated with the extinction (e.g., token, cognitive cue) improves the efficacy of cue exposure and improves stimulant abuse treatment effectiveness. However, It is imperative to underscore that many other variables (e.g., biological factor, sociological factor, cultural influence, peer, etc.) apart from behavioral principles might also play a role in clients’ stimulant abuse behavior. Therefore, Psychophartherapists should consider the entire context surrounding clients’ substance abuse during treatment.

References

Brandon, T. H., Virdrine, J. I., & Litvin, E. B. (2007). Relapse and relapse prevention. Annual Review of Clinical Psychology, 3, 257-284. doi: 10.1146/annurev.clinpsy.3.022806.091455

Brooks, D. C. (2000). Recent and remote extinction cues reduce spontaneous recovery. The Qaurterly Journal of Experimental Psychology, 53(1), 25-58. doi: 10.1080/027249900392986

Carlson, N. R., & Birkett, M. A. (2017). Physiology of behavior. (12th ed.). New York: Pearson.

Collins, B. N, & Brandon, T. H. (2002). Effects of extinction context and retrieval cues on alcohol cue reactivity among nonalcoholic drinkers. Journal of Consulting and Clinical. Psychology,70(2), 390-397. doi: 10.1037//0022-006X.70.2.390

Di Chiara G. (1995). The role of dopamine in drug abuse viewed from the perspective of its role in motivation. Drug and Alcohol Dependency, 38, 95-137. doi: 10.1016/0376-8716(95)01118-I

Everitt, B. J., & Robbins, T. W(2005). Neural system of reinforcement for drug addiction: From action to habit to compulsion. Nature Neuroscience, 8(11), 1481-1489. doi: 10.1038/nn1579

Field, M., & Cox, W. M. (2008). Attentional bias in addictive behaviors: A review of its development, causes, and consequences. Drug and Alcohol Dependence 97, 1–20. doi: doi:10.1016/j.drugalcdep.2008.03.030

Glanz, K., Rimer, B. K., & Viswanath, K. (Eds.). (2015). Health behavior: Theory, research, and practice (5th ed.). Jossey-Bass.

Haile, C. N., De La Garza II, R., Mahoney III, J. J., Nielsen, D. A, Kosten, T. R., & Newt, T. F. (2012). The impact of disulfiram treatment on the reinforcing effects of cocaine: A randomized clinical trial. PLOS ONE 7(2): e47702. https://doi.org/10.1371/journal.pone.0047702

Kaddena, R. M., & Litta, M. D. (2011). The role of self-Efficacy in the treatment of substance use disorders. Addictive Behavior, 36(12), 1120-1126. doi:10.1016/j.addbeh.2011.07.032.

Knowlden, A. P., Robbins, R., & Grandner, M. (2018). Social cognitive models of fruit and vegetable consumption, moderate physical activity, and sleep behavior in overweight and obese men. Health Behavior Research, 1(2), 5. doi: 10.4148/2572-1836.1011

Lee, C. G., Park, S., Lee, H. S., Kim, H., & Park, J. (2018). Social cognitive theory and physical activity among Korean male high-school students. American Journal of Men’s Health, 12(4) 973-980. doi: 10.1177/1557988318754572

Lewis, T. F. (2014). Substance abuse and addiction treatment: Practical application of counseling theory. Boston: Pearson.

Schunk, D. H., & Maria K. DiBenedetto, M. K. (2020). Motivation and social cognitive theory. Contemporary Educational Psychology, 60, 101832. doi:10.1016/j.cedpsych.2019.101832

Tim, F. M., & Leukefield, C. G. (1993). Cocaine treatment: Research and clinical perspectives. National Institute of Drug Abuse Research Monograph Series.

Vadhan, N. P., Carpenter, K. M., Copersino, M. L., Hart, C. L., Foltin, R. W., & Nunes, E. V., (2007). Attentional bias towards cocaine-related stimuli: Relationship to treatment-seeking for cocaine dependence. American Journal of Drug Alcohol Abuse 33 (5), 727-736. doi: 10.1080/00952990701523722

Volkow, N. D. (2010). Opioid-dopamine interactions: Implications for substance use disorders and their treatment. Biological Psychiatry, 68(8), 685-686. doi: 10.1016/j.biopsych.2010.08.002

Volkow, N. D. Wang, G. J., Fowler, J. S., Tomasi, D., & Telang, F. (2011). Addition: Beyond dopamine reward circuitry. Proceedings of the National Academy of Sciences,108(37), 15037-15042. doi: 10.1073/pnas.1010654108

Wikler, A. (1973). Dynamics of drug dependence: Implications of a conditioning theory for research and treatment. Arch Gen. Psychiatry, 28 (5), 611-616. doi: 10.1001/archpsyc.1973.01750350005001.

Woolverton, W. L., Freeman, K. B., Myerson, J., & Green, L. (2012). Suppression of cocaine self-administration in monkeys: Effects of delayed punishment. Psychopharmacology, 220(3), 509–517. doi:10.1007/s00213-011-2501-3

Ethnic Inequalities and the Impact of Violation of Biafran Rights on the Psyche of Biafrans in Nigeria

People should have equal opportunity to claim their rights because human rights principles apply to all persons equally. Therefore, ethnic inequality is a threat to human rights, which have adverse outcomes, including intergenerational trauma, degenerated cultural aggression, anger, and distrust, and a sense of powerlessness and helplessness (Johnston et al., 2009; Mushtaq & Fatima, 2016). In Nigeria, several ethnic inequalities exist across several dimensions, such as political offices at the federal executive branch of government, health care, education system, regional development, police roadblocks, airports, seaports, fair hearing in the law court, respect for human life, etc. In all these dimensions, South-eastern part of Nigeria (Biafra) has suffered the most injustice and violations of human rights due to ethnic inequalities in Nigeria (Ugorji, 2017)

Theretical Framework Shaping Actions Regarding Human Rights

Human rights are preserved and regulated in the domain of justice, which is a basic necessity for social coexistence, freedom, peace, and material and human development (Soderstrom et al., 2019).  For instance, natural rights to life, property, and liberty are preserved by attributive justice; civil, political, social, cultural, and economic rights are regulated by distributive and social justice; and contractual rights are preserved by commutative justice to the human person (Gopakumar, 2012; Pazhyampallil, 2004).  Consequently, the violation of human rights is a gross offense against justice, which results in the destruction of society’s physical, social, moral and spiritual being (Ul Haq & Dar, 2014).

Correspondingly theoretical frameworks on justice shape actions in relation to human rights.  Equity theory is one of the major frameworks guiding distributive justice, which preserves and regulates several human rights, including civil, political, social, cultural, and economic rights (Kazemi & Tornblom, 2008).  According to this theory paradigm, for fairness to prevail, outcomes must be proportional to contribution.  In other words, people perceive fairness when the ratio of their inputs and outcomes stand in an obverse relation to the inputs and outcomes of referent or similar others.  For instance, people will perceive inequity when their high outputs are rewarded with low payment while others whose outputs are low receive high payment (Kazemi & Tornblom, 2008)

Biafra and Ethnic Inequalities in Nigeria

In Nigeria, people from old South-east (Biafra) contribute most to the Nigerian economy but receive the least from the national purse (Ochinex, 2017). The entire crude oil sustaining the economy of Nigeria comes from the old South-eastern Nigeria. According to Ochinex (2017), Nigerians abroad remit billions of dollars to Nigeria annually, which contributes significantly to the national economy. Sixty percent of this remittance comes from 1gbos of South-eastern Nigeria. Similarly, those who do foreign business and import goods into the Nigerian market are mainly from South-east (Ochinex, 2017). There are several other ways South-easterners contribute to the economy of Nigeria far way beyond any other region in the country. Nollywood, through which Nigeria receives billions of dollars, is dominated by Igbos; a very high percentage of those who represent the country in sports is from the old South-east; four out of the six most industrialized cities in Nigeria are in the old South-east (Onitsha, Nnewi, Port Harcourt, and Aba); and 70% of the investments in Abuja and about 30-40% of those in Lagos are owned by Igbos (Ochinex, 2017). This is to mention a few.

Despite all these contributions to the Nigerian economy, the old South-eastern region (Biafra) receives the least from the national purse and suffers most injustice and human rights violations in terms of distributive, procedural, and social justice in Nigeria. For instance, in March 2020, the federal government of Nigeria allocated $0 to the present-day South-east zone in the distribution of a $22.7 billion loan to all regions of Nigeria (Iroanusi, 2020). Also, indigenes of the South-east region are the least employed in the federal political offices. Moreover, the Nigerian government has systematically underdeveloped the South-eastern part of Nigeria (Biafra land). Although more than 60% of Nigerians living outside the country come from South-east and more than 80% doing foreign businesses and importing goods into the country come from South-east too, the region has no working seaports, no embassy, and only two international airports in Enugu and Port Harcourt. Furthermore, the region has unimaginable bad roads but uncountable police checkpoints. The intention of Nigerian authorities for doing all this is to frustrate any economic growth in the region and to hold it down forever. To crown it all, Nigerian authorities, including security forces, have shown a total lack of respect for the life of people from Biafra. For instance, they kill unarmed people who identify themselves as pro-Biafrans without any provocation (Duggan & Busari, 2016; Ibekwe, 2016). In addition, they torture and give them degrading and inhuman treatments, imprison them unlawfully, and deny them a fair hearing in the law court.

The Impact of the Violation of the Fundament Human Rights of Biafrans on the Psyche of Biafrans

The extrajudicial killings that Nigerian security forces carried out on unarmed pro-Biafrans in 2016, the continual inhuman treatments on pro-Biafrans, current incessant killings of Biafrans by the same security forces and Fulani herders, and the criminal silence by Nigerian authorities (Duggan & Busari, 2016; Ibekwe, 2016) are all indications of ethnic inequalities concerning respect for human life in Nigeria. Some obvious psychological effects of these cruel and degrading treatments against Biafrans include ethnic distrust, aggression, anger, sadness, and hatred toward not only Nigerian authorities, but to everyone keeping quiet to such gross human rights violations. For instance, on August 17, 2019, at Nuremberg, Germany, Indigenous People of Biafra (IPOB) gave the Nigerian Deputy Senate President, Ike Ekweremadu, the beating of his life during the annual cultural festival of Ndigbo (Sunday, 2019). This action was a means of venting out their anger on authorities from Biafra land (old South-east region) that are keeping silent to the gross violation of human rights going on in south-eastern Nigeria.

Another effect of ethnic inequalities and human rights violations in Biafran land by the Nigerian government is unresolved intergenerational traumas (Ugorji, 2017; Otas, 2017). The traumas that go with the experience of human rights violations (e.g., extrajudicial killings, torture, and degrading treatments) can always create a deep wound in the psyche of the people, making it difficult to resolve in both individuals and communities. Although the violation of Biafran rights (e.g., extrajudicial killings and dehumanizing treatments) may cause individuals to suffer various forms of psychological disorders(e.g., post-traumatic stress disorder, panic disorder, depression, and anxiety), it inevitably leads to unresolved ethnic and intergenerational traumas. In other words, the community also carries the trauma. Consequently, the trauma will always resurface in the future through human rights movements against breaches of injustice by the community members (Otas, 2017). The only way to resolve this intergenerational trauma is to give Biafrans the justice they have been demanding.

Conclusion

It is time to give justice to Biafrans. The Nigerian state has committed enough atrocities against Biafrans. The world can no longer pretend to be uninterested in the gross violation of human rights going in Biafra land by the Nigerian government. The United Nations takes a greater share of the blame for allowing these human rights violations to continue without giving justice to Biafrans. One thing is certain, agitations for the independence of the Biafran state will never stop unless justice is given to Biafrans.

References

Duggan, B., & Busari, S. (2016). Nigerian officers killed 150 peaceful protesters, Amnesty report claims. Retrieved from https://www.cnn.com/2016/11/24/africa/nigeria-security-forces-biafra-protesters

Gopakumar, S. S. (2012). Human rights violations. International Research Journal of Commerce Arts and Science, 3(2), 882-887. Retrieved from https://www.academia.edu

Kazemi, A., Tornblom, K. (2008). Social psychology of justice: Origins, central issues, recent developments, and future directions. Nordic Psychology, 60(3), 209-234. Retrieved from the Walden Library databases 

Pazhayampallil, T. (2004). Pastoral guide: Fundamental theology and virtues (4th ed.). New Delhi: Rekha Printers Private Ltd.

Soderstrom, K., Hagenaars, P., Wainwright, T., & Wagner, U. (2019). Human rights matter to psychology: Psychological matters to human rights. European Psychologist, 24(2), 99-101. doi:10.1027/1016-9040/a000365

Ul Haq, I., & Dar, M A. (2014). Human rights violation in Kashmir. European Academic Research, 2(7), 9230-9242. Retrieved from https://www.academia.edu/12938405/Human_Rights_Violations_in_Kashmir

Ibekwe, N. (2016). How Nigerian security forces killed 150 pro-Biafran protesters. Retrieved from https://www.premiumtimesng.com/news/headlines/216166-nigerian-security-forces-killed-150-pro-biafra-protesters-amnesty-international.html

Iroanusi, Q. (2020). South-east senators protest ‘exclusion’ from $22.7bn loan, others. Retrieved from https://www.premiumtimesng.com/news/top-news/381611-south-east-senators-protest-exclusion-from-22-7bn-loan-others.html

Johnson, V., Allotey, P., Mulholland, K., & Markovic, M. (2009). Measuring the health impact of human rights violations related to Australian asylum policies and practices: A mixed methods study. BMC International Health and Human Rights,9 (1), 1-12. doi:10.1186/147-698X-9-1

Mushtag, S., & Fatima, Z. (2016). Psychological impact of human rights violations on Kashmiri people. Indian Journal of Applied Research, 6(10), 449-452. Retrieved from http://www.academia.edu

Ochinex, M. (2017). Igbo/Southeast contribution to Nigeria. Retrieved from ttps://www.nairaland.com/3852482/igbos-southeast-contributions-nigerias-econom

Otas, B. (2017). “Healing will come with justice, but Nigeria isn’t ready:” The Biafra war, 50 years on. Retrieved from https://www.equaltimes.org/healing-will-come-with-justice-but

Sunday, P. (2019). Nigerians React To IPOB’s Attack On Ike Ekweremadu. Retrieved from https://www.naijanews.com/2019/08/18/nigerians-reactto-ipobs-attack-on-ikeekweremadu

Ugorji, B. (2017). Indigenous People of Biafra (IPOB): A revitalized social movement in Nigeria. Retrieved from https://www.icermediation.org/publications/indigenouspeople-of-biafra-ipob-a…

Violations of Human Rights in South-Eastern Nigeria (Biafra)

The human person is a center of respect, sacredness, and dignity, regardless of race, color, religion, sex, and nationality. This inherent dignity of the human person implies necessarily inalienable, inviolable, and fundamental human rights. Entrusted with the care of its citizens, human rights protection is the responsibility incumbent upon the state and its public authorities, such as the president, governors, policy-makers, school teachers and professors, hospital managers, health professionals, non governmental organization, etc. (Patel, 2019). Therefore, it is gross human rights violations when the state and its public authorities abuse, ignore, or deny fundamental human rights.

Since the creation of Nigeria by Britain, gross violations of human rights have been occurring from time to time. However, since 2015, Nigerians have witnessed unprecedented violations of human rights by the state and its public authorities. Although every part of the country in one way or the other witnesses injustice, the south-eastern part of Nigeria (Biafra) has been witnessing unimaginable inhuman treatments and violations of human rights by the Nigerian authorities. Biafrans in the south-eastern part of Nigeria have been struggling for self-determination and creation of independent Biafran state for some decades. This struggle took a more refined and determined dimension since 2012.

Consequently, Nigerian authorities have been doing everything to suppress the struggle, committing all sorts of atrocities and inhuman treatment against pro-Biafrans. On this note, Amnesty International noted that since 2015 Nigerian army and police have been killing innocent unarmed pro-Biafrans at a number of peaceful demonstrations without Nigerian authorities investigating into such extrajudicial killings. For instance, Amnesty International has it on record that Nigerian security forces killed at least 150 pro-Biafrans in Aba, Abia State on February 9, 2016 during their prayer session and in Onitsha, Anambra State on May 30, 2016 during their rally (Duggan &amp; Busari, 2016). Amnesty International research also showed that after these incidents, Nigerian security forces would go ahead to make arbitrary arrests of pro-Biafrans, including wounded victims in the hospital and torture them ruthlessly, for instance, by pouring acid on them (Ibekwe, 2016).

There are several other documented extrajudicial killings that Nigerian security forces have carried out on pro-Biafrans. Similarly, there are numerous forms of human rights violations committed against South-easterners by Nigerian authorities, including burning of people’s houses, unlawful detention of innocent citizens, inequality before the law, blatant insecurity, suppression of freedom of speech, interference with people’s privacy, home, and correspondence, etc. Although, not a Biafran, the case of Omoyele Sowore, a prominent journalist, is a clear current suppression of freedom of speech and unlawful detention that has been going on in Nigeria (Adebayo, 2019). The abduction of Nnamdi Kanu, the leader of Indigenous People of Biafra from Kenya by the Nigerian political authority is another clear violation of human right. I will review most of these human rights violations in my subsequent posts. In any case, what is obvious is that these killings and several forms of degrading and inhuman treatment on pro-Biafrans have continued up until today.

Finally, several fundamental questions regarding human rights violations going on in South-Eastern Nigeria abound. What are the effects of human rights violation on the well-being of Biafrans? What could be done to reduce these abuses? What are the roles of organizations, such as the church, health professions, and teachers’ union in reducing these violations? Why is the United Nations, from which the modern human rights frameworks grew, keeping quiet and turning its face away from inhuman treatments against Biafrans in Nigeria? These fundamental questions will form the framework by which I will organize subsequent posts on human rights violations in south-eastern Nigeria.

Conclusion

Human rights are founded inviolable moral claims inherent in every human person. It is quite disheartening that often times many authorities violate them with impunity without the law catching up with them. It is also more unfortunate that most times the powers that be turn their faces away from such inhuman treatments. Therefore, it is essential to always frequently remind Nigerian leaders and her public authorities of their responsibilities to protect the rights of the citizens entrusted in their care. This reminder is more pressing not only to Nigeria leaders but also to all the leaders violating, denying or ignoring the human rights of their citizens.

References

Adebayo, B. (2019). Nigeria refuses to release prominent journalist. Retrieved from Retrieved from https://www.koamnewsnow.com/news/world-news/

Duggan, B., & Busari, S. (2016). Nigerian officers killed 150 peaceful protesters, Amnesty report claims. Retrieved from https://www.cnn.com/2016/11/24/africa/nigeria-security-forces-biafra-protesters

Ibekwe, N. (2016). How Nigerian security forces killed 150 pro-Biafran protesters. Retrieved from https://www.premiumtimesng.com/news/headlines/216166-nigerian-security-forces-killed-150-pro-biafra-protesters-amnesty-international.html

Patel, N. (2019). Human right-based approach to applied psychology. European Psychologist, 24(2), 113-124. doi: 10.1027/1016-9040/a000371

Euthanasia and the Ordinary and Extraordinary Means of Sustaining Life: The Church’s Position

Etymologically, the term euthanasia comes from two Greek words eu (well) and thanasia (dying). Therefore, euthanasia, from its root words, means dying well, easy death without severe suffering, mercy killing, and ending a human life for the purpose of putting an end to extreme suffering. In its medical application, euthanasia involves the intentional killing of a tormented incurable patient by the use of lethal means (e.g., sedatives, narcotics, poison) or through the omission or withdrawal/discontinuation of life-sustaining means (Peschke, 1999). Similarly, the Church understands euthanasia as an action or omission, which is of itself and by intention causes the death of another person to eliminate all suffering (John Paul II, 1995). All forms of euthanasia can be active or passive. In both definitions, euthanasia terms of reference are to be found in the intention of the will and the method used. Euthanasia is active when positive means (e.g., injecting poison into the sick person) result in the termination of human life. On the other hand, euthanasia is passive when there is an omission or a withdrawal/discontinuation of life-sustaining means (e.g., food, water, and medications). The purpose of this paper is to examine the position of the Church on withholding or withdrawing life-sustaining means in relation to euthanasia.

The General Position of the Church on Euthanasia

The Church teaches that the life of the human person, who is an image of God, is sacred and inviolable at all stages because, from its beginning, it involves the creative action of God and remains forever in a special relationship with the Creator, who is its sole end (John Paul II, 1995). Therefore, the Church asserts that it belongs only to God to take life. Precisely, the Church emphasizes that no one in any way is permitted to kill an innocent human being, including a fetus or embryo, an infant, an adult, an older adult, one suffering from an incurable disease, or a person who is dying (John Paul II, 1995). No one is permitted to ask for euthanasia either for oneself or for another person or consent to it either explicitly or implicitly. Also, no authority can legitimately recommend or permit euthanasia (John Paul II, 1995). Engaging in euthanasia is a violation of the divine law, an offense against the dignity of the human person, a crime against life, and an attack on humanity (John Paull II. 1995). So, euthanasia is murder and intrinsically evil.

However, the fundamental problem is that some acts that terminate human life can be clearly categorized as euthanasia (e.g., actively poising a sick person), whereas several other acts that terminate human life are not easily categorized as euthanasia. In other words, specific grey areas abound regarding actively or passively causing another person’s death to end the person’s suffering. For instance, a doctor can give a patient a pain relief medication, and it eventually results in the patient’s death. Can such treatment be categorized as euthanasia or not? Also, withdrawing life-sustaining means can lead to death. When is withholding or withdrawing life-sustaining euthanasia, and when is it not euthanasia? As indicated earlier, I will examine the teaching of the Church on withholding or withdrawing life-sustaining means in relation to euthanasia.

Debates Over Withholding or Discontinuing Life-Sustaining Means

Several means exist to sustain human life. Some of these means are easily obtainable (e.g., food, water, exercise, and sleep), and others are not easily obtainable and often carry a lot of burden on family members (e.g., life-sustaining machines). Often, circumstances exist when family members are overwhelmed by the burden of expensive life-sustaining means and tend to discontinue their support. Given the position of the Church on euthanasia, several ethical questions abound regarding life-sustaining means and medical treatments. Among these questions, two are paramount for our discussion. Are there conditions when withholding or withdrawing life-sustaining means is no longer euthanasia? Or must one always have recourse to all remedies in all circumstances to sustain human life? To answer these questions, moralists have distinguished between ordinary and extraordinary means.

Ordinary and Extraordinary Means

Ordinary means are all medical procedures that offer a reasonable hope of benefits for the patient and can be obtained and used without excessive expenses. Moralists hold that one is obliged to use ordinary means unless they are no longer useful, such as in the case of unconscious imminently dying patients (Pazayampallil, 2004). So, withholding or discontinuing ordinary means is without any doubt euthanasia, unless they are no more useful as in the case of unconscious, imminently dying patients. Additionally, a patient who refuses ordinary means and dies has committed suicide.

On the contrary, extraordinary means do not offer a reasonable hope of benefits and cannot be used or obtained without excessive expenses, pain, or other inconveniences. According to moral scholars, one is never obliged to use extraordinary means. However, medical techniques have undergone rapid progress, such that medical procedures considered extraordinary in the past (e.g., major surgeries) are seen as ordinary today. Similarly, several forms of treatment considered extraordinary in one country are considered ordinary in another country. Additionally, medical treatment considered ordinary by one family might be seen as extraordinary by another family. So, the distinction between ordinary and extraordinary means lacks precision and so carries ambiguities. Consequently, the question of obligation to use a means or not is imprecise. Therefore, for the sake of precision, moral theologians today prefer to use the distinction proportionate and disproportionate means.

Proportionate and Disproportionate Means

Determining whether a means is proportionate or disproportionate involves weighing the risk or burden the means will impose on the patient, its complexity, its costs, and the possibility of using it against the benefits of the means. The procedure is proportionate if the benefits outweigh the burden (Negri, 2018; Sacred Congregation for the Doctrine of the Father, 1980). However, some moralists have argued that the distinction between proportionate means and proportionate means is not without ambiguities. In other words, this distinction does seem to offer a more precise criterion for judging the morality of medical treatments than the old distinction between ordinary and extraordinary means. For instance, some means used on one person can be proportionate (e.g., yielding promising results) in one perspective but disproportionate (e.g., producing a high cost) from another perspective.

Church’s Clarifications

To facilitate a proper application of the general principles of proportionate and disproportionate means, Sacred Congregation for the Doctrine of the Faith (1980) made specific clarifications on the criteria for the moral permissibility regarding withholding or withdrawing life-sustaining means. First and foremost, it is permissible to manage the normal means of medical treatment. Therefore, no one is obliged to use medical procedures that are already in use but carry a risk or are burdensome to patients. Refusing such medical procedures should not be seen as suicide or euthanasia. On the contrary, such refusal means that one has accepted the condition of being human, wishes to avoid the application of a medical procedure that is disproportionate to the expected results or desires not to impose excessive expense on the family or community.

Furthermore, if there are no other remedies, using available advanced medical procedures is permissible, even if these means are still at the trial stage and may carry specific risks. However, having recourse to such advanced medical techniques must be done with the patient’s consent. When the result falls short of the expectation, it is permitted to interrupt these means. However, the reasonable wishes of the patient and the patient’s family must be put into consideration before the interruption. Also, the interruption must involve putting into account the advice of doctors who are competent to judge whether the means and personnel are disproportionate to the foreseen results (e.g., the techniques impose on the patient strain or suffering, which are far higher than its benefits).

Additionally, when inevitable death is imminent despite the means used, it is permissible in conscience to decide to refuse forms of treatment that would only secure a prolongation of death (i.e., a precarious and burdensome extension of life), so long as the regular care is not interrupted. In such a circumstance, no one has any reason to blame oneself for failing to help the person in danger. Elaborating on the imminence of death and withdrawal or omission of life-sustaining means, Pazhayampallil (2004) presented the specific criteria. For an unconscious, imminently dying person, providing nutrition, hydration, or any other form of treatment is useless. For a conscious, imminently dying patient, nutrition, hydration, and treatments are also useless and possibly constitute a burdensome prolongation of life. For an unconscious, non-dying patient, nutrition, hydration, and medications are neither useless nor a burden for the patient unless clear evidence indicates that they are burdensome. Finally, for a conscious, irreversible ill, but not imminently dying patient, nutrition, hydration, and medications are also neither useless nor burdensome to the patient unless clear evidence shows that they are burdensome.

Conclusion

From this discussion, it is clear that withdrawing or withholding life-sustaining means when death is imminent is not euthanasia. Also, death due to withholding or withdrawing burdensome or disproportionate treatments is not euthanasia. However, certifying when death is imminent and when procedures are burdensome or disproportionate is a responsibility incumbent upon competent physicians. Finally, although death is part of the human condition and is neither evil nor defeat, hastening death, suicide, and murder through euthanasia is intrinsically evil.

References

John Paull. (1995). Evangelium vitae [Encyclical letter] Retrieved from http://www.vatican.va/content/john-paul-ii/en/encyclicals/documents/hf_jp-ii_enc_25031995_evangelium-vitae.html `

Negri, S. (2018, May 3). The duty to preserve life. [Blog post]. Retrieved from https://www.catholic.com/magazine/online-edition/the-duty-to-preserve-life

Pazhayampallil, T. (2004). Pastoral guide: Fundamental theology and virtues (4th ed.). New Delhi: Rekha Printers Private Ltd.

Peschke, K. H. (1999). Christian ethics: Moral theology in the light of Vatican II. (Vol. 2). Bangalore: Theological Publications.

Sacred Congregation for the Doctrine of the Faith (1980) Declaration on euthanasia. Retrieved from http://www.vatican.va/roman_curia/congregations/cfaith/documents/rc_con_cfaith_doc_19800505_euthanasia_en.html

Parenting Styles and Empirical Outcomes

Parents have different styles of raising their children. Some may emphasize the importance of respect and obedience from their children; some others may show a great deal of warmth and emotion to their children; others still may be low both in parental control and affection. Thus, parenting style is the general way parents relate to and discipline their children (Lammana et al., 2015). There are two dimensions of parenting style: parental warmth (emotional nurturing and support) and parental monitoring (direction, guidance, control, or restriction) of their children. Based on these dimensions, three parenting styles can be possible: authoritarian, authoritative, and permissive parenting styles (Baumrind, 1991). In this study, I will examine how each parenting style is high or low in relation to the two dimensions of parenting style; that is, parental warmth and control. I will also examine the empirical evidence supporting the effectiveness of each parenting style.

Authoritarian Parenting Style

The authoritarian parenting style is one that involves low emotional warmth and nurturing but high (if not excessively high) parental direction and control. Authoritarian parents emphasize respect and obedience from their children. They always use harsh restrictions and rules to let their children know that they are in charge. They do not encourage verbal interaction. They are more likely to spank their children or use otherwise harsh punishment to control their children’s behavior (Baumrind, 1991; Dominguez & Carton, 1997; Lammna et al., 2015).

Studies have shown that the authoritarian parenting style is associated with children’s decreased sense of personal effectiveness and mastery over situation, low level of self-actualization, children’s and adolescents’ depression, and poor mental health (Dominguez & Carton, 1997; Hall, 2008; Moorman & Pomerantz, 2008). Also, this parenting style is associated with low school performance, behavior problems, high rates of teen sexuality and pregnancy, and juvenile delinquency (Dominguez & Carton, 1997; Hall, 2008; Moorman & Pomerantz, 2008; Waldfogel, 2006).

Authoritative Parenting Style

This parenting style has both parental warmth/nurturing and non excessively high monitoring/direction. It combines parental nurturing and support with conscientious parental direction, and thus, comprises warmth, firmness, and fairness simultaneously. Hence, parents using the authoritative parenting style would not make their decisions final with regard to their children’s wills and desires but would also consider their children’s wishes and opinions. They would equally value their children’s achievements and support their efforts. This parenting style, therefore, gives children the opportunity of exploring their potentials, and so encourages a child’s individuality, emerging independence and talents without, at the same time, letting down parental directions and controls (Baumrind, 1989; 1991; Lammana et al., 2015). Empirical evidence has shown that children of authoritative parents, regardless of family structure, were more likely than others to do better in school, developed emerging talents and maturity, had high levels of independence, became socially competent, had relatively high self-esteem and became self-actualized (Baumrind, 1989, 191; Crawford & Novak, 2008; Dominguez & Carton, 1997).

Permissive Parenting Style

Permissive parenting style, the third parenting style, is one that is low on parental control/monitoring but may or may not be high on parental warmth. It is seen as being a neglectful parenting style. Permissive parents tend not to take an active role in shaping and determining their children’s behavior, make a few demands, and use little punishment (Baumrind, 1991). Permissive parenting has two variants. The first form of permissive parenting style is characterized by a situation of permissive-indulgent, which gives children low parental restriction but high on emotional warmth/nurturing. The so-called “spoiled child” has been associated with this parenting style (Lammana et al., 2015). The second form of permissive parenting style involves emotional-neglect, being low on both parental monitoring and emotional warmth/nurturing. Like the authoritarian parenting style, research showed that the permissive parenting style was also associated with children’s and adolescents’ depression, poor mental health, low school performance, behavior problem, high rate of teen sexuality and pregnancy, and juvenile delinquency (Hall, 2008; Moorman & Pomerantz, 2008; Waldfogel, 2006).

Experts’ Views on the Three Parenting Styles

Among the three parenting styles that we have described above, the authoritative parenting style is recommended by most experts as the most effective parenting style. This is because it is a parenting style that combines parental warmth with conscientious (non excessively high) parental direction. In other words, the authoritative parenting style involves simultaneously emotional nurturing and support, firmness, and fairness. Put in a different explanation, it avails children the opportunity of exploring their potentials, while at the same time, consciously setting limits and clearly communicating and enforcing rules.

Furthermore, research has shown that children of authoritative parents do better in school, develop emerging talents and independence, have high esteem, and are socially competent and self-actualized. For instance, among the white, middle-class children, empirical evidence has shown that an authoritative parental style is the most effective of the three possible styles (Lammana et al., 2015). Additionally, college students who reported that their parents gave them warmth and emotional support without harsh control and monitoring (i.e., an authoritative parenting style) were more self-actualized than those whose parents were authoritarian (Dominguez & Carton, 1997). Consequently, the authoritative parenting style is sometimes known as positive parenting.

Conclusion

It is important to emphasize that the authoritarian/authoritative/permissive model has been accused of being bias and ethnocentric or Eurocentric by some scholars. For these scholars, the authoritative parenting style can only predict the behavior for children of European descent and does not seem to do so among children of other races/ethnicity. In other words, the European family background and the parenting style are used as a standard for other parenting styles. In any case, we must underscore the success of the authoritative parenting style in raising children. However, its non-punishing character seems to render it ineffective when used by parents of other races/ethnicities that have a long tradition of disciplining their children with punishment.

References

Baumrind, D. (1991). Parenting styles and adolescent development. In J. Brooks-Gunn, R. Lerner, & A. C. Petersen (Eds.). The Encyclopedia of Adolescence (pp.746-758). New York: Garland.

Crawford, E. A., & Novak, K. B. (2008). Parent-child relations and peer association as mediators of the family structure-substance use relationship. Journal of Family Issues, 29, 155-184. Retrieved from the Walden Library databases

Dominguez, M. M., & Carton, J. S. (1997). The relationship between self-actualization and parenting style. Journal of Social Behaviour and Personality, 12 (4), 10903-1100. Retrieved from the Walden Library databases

Hall, S, K. (2008). Raising kids in the 21st century. West Sussex, UK: Wiley-Blackwell.

Lammana, M. A., Riedmann, A., & Stewart, S. (2015). Marriage, families, and relationships: Making choices in a diverse society (12th ed.). USA: Cengage Learning.

Moorman, E., & Pomerantz, E. (2008). The role of mothers’ control in children mastery orientation: A time frame analysis. Journal of Family Psychology, 22 (5),1281-1304. doi: 10.1037/0893-3200.22.5.734

Waldfogel, J. 2006). What do children need? Public Policy Research, 13, 26-34. doi: 10.1111/j.1070-3535.2006.00417.x.