Health Nicotine acts at the neuro-muscular junction to stimulate muscles. Paradoxically, smokers report that it relaxes them. Explain.

One of the paradoxes about nicotine addiction is that smokers report feeling relaxed after using, in spite of the fact that nicotine is a biological stimulant. The phenomenon is known in the literature as Nesbitt's Paradox or simply the nicotine paradox. Early research into Nesbitt's Paradox revealed that there are a number of potential variables influencing the perception of a relaxed emotional response. Behavioral activity levels, the level of central nervous system arousal, the type of emotion being reported, time elapsed since the nicotine fix, and both rate and dose of administration are linked to perceived emotional responses to smoking cigarettes containing nicotine (Gilbert, 1979). Of these variables, the degree of nicotine deprivation has been most closely linked to the paradoxical sensation that a stimulant creates a relaxation response. The solution to the paradox, then, is that addiction to nicotine creates sensations of anxiety, irritability and distress, and these symptoms are alleviated by a "fix." As Parrott (2002) puts it, there is no paradox at all. Addiction creates withdrawal symptoms, which include heightened states of arousal. Smoking alleviates the withdrawal symptoms and therefore makes the smoker feel more relaxed.

One of the functions of smoking is "mood normalization," according to Parrott (2002, p. 27). In other words, smokers start to need nicotine in order to "feel" or "function" normally (Parrott, 2002, p. 27). This would account for the fact that smokers report feeling more relaxed after smoking. The central nervous system is measurably aroused, and yet psychologically the person is relieved after satisfying the craving to feed the addiction. It should also be noted that not all smokers report feeling reduced anxiety; many report feeling increased anxiety, agitation, and restlessness (Gilani, n.d.). How a person feels after smoking is related to how long the person has been addicted to cigarettes, how long the withdrawal period has lasted, and how anxiety-prone that person was regardless of smoking.

Therefore, the nicotine paradox is slightly more complex than being related only to nicotine withdrawal. Evatt & Kassel (2010) found that there are differences between smokers who are sensitive or prone to anxiety vs. those who are not as easily aroused. High anxiety smokers tend to report feeling more relaxed after smoking when in a stressful condition but did not report reduced anxiety after a low stress condition. In other words, persons prone to feeling a baseline level of anxiety react differently to nicotine than their lower anxiety counterparts. Persons not as prone to experiencing anxiety actually report that smoking calms them at all times (Evatt & Kassel, 2010). These findings would, however, substantiate the basic notion that Nesbitt's paradox is related more to nicotine withdrawal than to actual reductions in biological features of anxiety in smokers.

There are other variables that must be taken into consideration when evaluating the nicotine paradox. For example, persons who have pre-existing anxiety tendencies might be more prone to becoming addicted to cigarettes. That would mean that smokers set themselves up for a feedback loop in which their addiction creates an illusory means of self-medicating for anxiety disorder.

Immediate effects of smoking tobacco include an increase in blood pressure, and increase in heart rate, a thickening of the blood, narrowing of arteries, decrease in skin temperature, increase in respiration, stimulation of the central nervous system, and occasionally vomiting and diarrhea ("Nicotine Immediate Effects," n.d.). According to Gilani (n.d.), nicotine also stimulates the production of adrenaline and suppresses the appetite. Each of these symptoms is inversely related to relaxation biological responses, such as reduction in heart rate, respiration rate, and blood pressure. It is certainly ironic that nicotine can cause a biological response opposite to a psychological one. Yet as Gilani (n.d.) points out, studies have shown that nicotine has overall "positive effects on cognitive functions, such as learning, attention and memory," which could be why some smokers report feeling more relaxed after smoking (p. 1). Moreover, nicotine is linked to reductions in aggression even in animal studies, and releases neurotransmitters that can reduce pain and increase pleasure (Gilani, n.d., p. 1).

References

Evatt, D.P. & Kassel, J.D. (2010). Smoking, arousal, and affect: The role of anxiety sensitivity. Journal of Anxiety Disorders 24(1): 114-123.

Gilani, M. (n.d.). What are the immediate effects of nicotine? Retrieved online: http://www.ehow.com/list_6521349_immediate-effects-nicotine_.html

Gilbert, D.G. (1979). Paradoxical tranquilizing and emotion-reducing effects of nicotine. Psychological Bulletin 86(4): 643-661.

"Nicotine: Immediate Effects," (n.d.). Retrieved online: http://library.thinkquest.org/19796/data/e015.html

Parrott, A.C. (2002). Nesbitt's paradox resolved? Addiction 93(1): 27-39.

2. Research has shown that, on average, males develop schizophrenia...

What biological factors might account for this gender difference? Provide a summary of the evidence
Gender differences in schizophrenia etiology, onset, prevalence, and outcome are well recorded, but the biological reasons for the gender differences are not completely understood. Usall, Ochoa, Araya & Marquez (2003) conducted a study suggesting that women have better outcomes than men, but the research is riddled with internal flaws. For example, the study included 126 men and 74 women: hardly an even sample. This would seem to substantiate findings by Longenecker et al. (2010), in a meta-analysis that found that women are significantly under-represented in non-epidemiological research on schizophrenia. Furthermore, Usall et al. (2003) study fails to account for social and other variables that might cause the increased rate of male hospitalizations and increased length of male hospital stays. For example, it is possible that males exhibit more socially undesirable symptoms and thus find themselves hospitalized against their will more often. It is also possible that their behaviors in hospitals present more concerns than behaviors exhibited by female patients. Likewise, parents might be alert to symptoms in boys earlier than in girls because of gender differences in self-expression or socialization. Males with schizophrenia might exhibit "socially adverse illness behaviors," too, which would cause a perceived poorer outcome score in research (Hafner, 2003).

The robustness of research results would also be improved if "outcomes" were operationalized in terms of specific features of positive outcomes. Some research suggests that there are no gender differences between female and male schizophrenics in terms of social functioning, for example, (Mueser, et al., 2010). Other studies do show that males with schizophrenia exhibit poorer social functioning vs. females with schizophrenia (Hafner, 2003). The difference could be linked to poorer social development at illness onset (Hafner, 2003). Hafner (2003) also reports no gender differences in symptomology, lifetime risk, and symptom-related course of the illness even when age is a controlled variable. Because symptomology is measured in qualitative rather than quantitative terms generally, it may be difficult to know for sure whether outcomes are actually better for males vs. females. Social functioning remains a core dependent variable in outcome-based research.

Ochoa, et al. (2012) offers a unique hypothesis related to gender differences in schizophrenia outcomes. Males with schizophrenia are more likely to develop substance abuse problems. This may account for their longer periods of hospitalization, and worse exhibition of symptoms that can be considered social, cognitive, or affective. Still women do seem to have lower rates of relapse of symptoms and better remission outcomes vs. their male counterparts (Ochoa, et al., 2012).

Regardless of the confounding variables, the trend continues that males develop schizophrenia at an earlier age than females; and that men have poorer overall outcomes compared with females. Biological reasons for the gender differences might include both genetics and sex hormones (Roy, Maziade, Labbe & Merette, 2001). In particular, oestradiol is believed to have a "protective" effect for females with schizophrenia (Riecher-Rossler & Hafner, 2002, p. 58). However, this would not explain the situation entirely unless researchers can show that women who exhibit symptoms earlier and remain in hospitals longer have elevated levels of male hormones or decreased levels of female hormones. Research has shown a trend in hormone-related causes for gender differences in males vs. females. Hafner (2003), for example, found differences in pre- and post-menopausal women in terms of symptom severity. It is postulated that estrogen is linked to gene expression of schizophrenia and also on transmitter functioning (Hafner, 2003). As a result, estrogen therapies are being developed for their antipsychotic effects (Hafner, 2003).

Hormones have long been the subject of study in schizophrenia-related research. Some hormones have a gender-neutral response on the development of schizophrenia in the brain. Koenig, Kirkpatrick & Lee (2002) found that mothers experiencing traumatic stress during pregnancy were more likely to give birth to babies that developed schizophrenia, regardless of the child's gender.

Genetic differences have also been postulated as being related to the gender differential: with a possible difference in schizophrenia-related chromosomal abnormalities between males and females (Hafner, 2003). Maturation and morphology of the brain, including neurobiological structure, might also be different between male and female schizophrenia patients (Hafner, 2003).

References

Hafner, H. (2003). Gender differences in schizophrenia. Psychneuroendocrinology 28(2): 17-54.

Koenig, J.I., Kirkpatrick, B. & Lee, P. (2002). Glucocorticoid hormones and early brain development in schizophrenia. Neuropsychopharmacology 27.

Longenecker, J., Genderson, J., Dickinson, D., Malley, J., Elvevag, B., Weinberger, D.R. & Gold, J. (2010). Where…