In cocaine-dependent subjects, lower FA was reported in inferiorfrontal white matter at the anterior-posterior commissure plane, in frontal white matter at the anterior commissure-posterior commissure plane, and in the genu and rostral body of the anterior corpus callosum. Similarly, lower FA in the right frontal white matter is also frequently reported in methamphet amine users and alcohol drinkers, and recently reported in chronic ketamine users. Convergent evidence suggests that chronic drug use is associated with decreased FA in white matter of the multiple brain regions, especially in the frontal lobe. Results of this study, along with previous findings, suggest increased FA, such that the effects of chronic cigarette smoking on brain white matter are different from effects of other addictive drugs. Increased FA may reflect increased maturation in cell packing density, fiber diameter, and directional coherence. A possible explanation for increased FA could be the variety of neurogenic properties of nicotine. In addition to maintaining and reinforcing smoking behavior, nicotine is reported to have other properties, such as anxiolytic properties and learning and memory-enhancing properties. Despite the proposal that chronic nicotine exposure may ultimately bring no benefits on mood and cognition, nicotine per se is known to be a neuroprotective agent, and prevents arachidonic acid induced injury to neurons and apoptotic cell death. Also, previous studies have revealed that nicotine upregulates calcium binding proteins, increases the levels of intracellular calcium measured and stimulates nerve growth factor,indoor grow rack which could also be neuroprotective. These previous reported neuropro tective effects could be consistent with increased FA from chronic cigarette smoking.

However, increased FA in white matter of brain in chronic cigarette smokers may not be beneficial. For example, Hoeft et al reported that increased FA of right superior longitudinal fasciculus in Williams syndrome individuals was associated with deficits in visuospatial construction. Similarly, a study of attention deficit hyperactivity disorder also found a correlation between increased FA with deficits in cognitive function. Increased FA is also reported in euthymic bipolar patients. Furthermore, evidence from previous studies reveals that increased FA could be a marker of acute inflammatory processes affecting neural tissue, indicating greater inflammation or less myelination. Thus, our result of increased FA in white matter might be associated with inflammatory changes and axonal damage in fronto-parietal cortex in chronic cigarette smokers. An alternate interpretation for increased FA in chronic cigarette smoking and some psychiatric disorders could be that they reflect the compensatory mechanisms and could be the result of increases in local white matter density. The higher FA found here is consistent with another study using DTI in 10 chronic cigarette smokers. However, we did not replicate their finding of increased FA in the body and whole corpus callosum in chronic cigarette smokers. Also, a recent study found that both prenatal exposure and adolescent exposure to tobacco smoke were associated with increased FA in anterior cortical white matter. Gazdzinski et al, examined the impact of smoking on alcohol-dependent individuals and found that the combination of cigarette smoking and alcohol dependence results in significantly larger volumes of temporal and frontal white matter; recently, they further confirmed the increased FA result in a abstinent smoking and non-smoking alcoholics study. However, Gons RA et al studied 503 small-vessel disease subjects aged between 50–85 years and found that cigarette smoking is associated with the reduction of FA in cerebral white matter.

Age, use of medical drugs and co-morbid medical conditions may the leading cause of the inconsistent results. In our study, increased FA was found in parietal-frontal white matter in the chronic cigarette smokers relative to healthy non-smokers. This discrepancy might arise from sample differences, such as differences in ethnicity, levels of cigarette smoking , age and psychiatric comorbidity . Results of our study indicate that the maintenance of cigarette smoking might involve fronto-parietal circuitry. Scientific evidence indicaties that the fronto-parietal cortex is one of the crucial units that functionally connects interrelated brain regions. Dosenbach et al indicated that this fronto-parietal circuitry initiates and adjusts control. There is also evidence that there is a network of frontal and parietal areas, which shows significant interactions between changes to a particular stimulus dimension and the current focus of attention. Findings from a previous study suggest that during nicotine withdrawal, functional integration of fronto-parietal networks is abnormal in cannabis users. Previous studies and our results may indicate altered connectivity within a cognitive network that is mediated by abnormal neurogenic functional activation in chronic nicotine exposure. In order to fully understand the mechanism of structural alteration in fronto-parietal cortex of chronic smoking, further studies using techniques such as adaptation or multi-voxel pattern analysis will be needed. A number of limitations to our study should be addressed. First of all, possible sex differences in the response to nicotine may exist. We did not evaluate sex differences because of the relatively small number of female participants, which is a limitation of the study, although we matched for the gender proportion between smokers and healthy non-smokers. Second, education level was significant ly higher in the nonsmoker group compared to the smoker group.

However, when we explicitly explored the impact of education level on bilateral fronto-parietal white matter in the smoker group, we found no significant correlation . This suggests that our findings cannot simply be explained in terms of this variable. In conclusion, our DTI data further support the hypothesis that smokers and non-smokers differed in bilateral fronto-parietal white matter integrity. These findings support the hypothesis that chronic cigarette smoking involves alteration of fronto-parietal connectivity.During the later part of the 1990s and into the first half of the current decade we have witnessed substantial reductions in the proportion of daily smokers among adolescents in the US. But according to a recent report by the Monitoring the Future survey, this trend is beginning to slow . Despite an overall decrease in tobacco use among adolescents in the United States, in 2005 over half of adolescents reported lifetime experimentation with smoking . Hispanic adolescents reported higher rates than non-Hispanic Whites and African Americans . Among adolescents, use of alcohol is more common than tobacco. This is true for all major ethnic groups. Hispanics have the highest rates of lifetime alcohol use ; rates among African Americans are lowest, and then non-Hispanic Whites . Racial/ethnic trends of marijuana use are similar to those for alcohol. Lifetime use of marijuana is highest for Hispanic adolescents . In California, the most populous state in the US, ethnic minorities surpassed whites as the majority population in 2000 . Increasing numbers of Latinos largely fueled this shift. Given the tremendous growth of this population there is a need for continued assessment of risk behaviors. Yet, research has been slow to adopt measurement and methodologies that are specific to the Latino population ,indoor farming equipment and still fewer have studied risk behaviors in Latino youth living in close proximity to an international border. Previous research has shown heightened rates of risk behaviors in border cities .Parenting, i.e., parenting practices, represents an area of significant influence in the area of adolescent risk behavior prevention . Parenting practices have been estimated to account for as much as 40% of the variance in children’s risk behaviors . In the early years of a child’s life, parents are the primary administrators of punishing and reinforcing stimuli in the child’s immediate environment, save the most basic biological contingencies . Administering contingent consequences can be a difficult job that requires surprising precision. Some of the common errors in parenting practices include inconsistent and poor timing of reinforcement and inappropriate timing and type of punishment . With the development of language, parents rely heavily on verbal stimuli to communicate contingencies to the child . This added component is an additional source of error in parenting practices. For example, the promise of a reward is very enticing, and the behavioral outcome is very desirable to parents. Such outcomes probably maintain the practice in parents. Nevertheless, after repeated errors the child quickly discriminates that the parent is “all talk”. Employing contingency management procedures imprecisely can lead to difficulties in child behavior and a developmental trend that potentially escalates problem behavior. When used appropriately, however, these strategies can establish pro-social skills and support children to, for example, avoid alcohol, tobacco and other drugs . Parents of children who are non-compliant often demonstrate poor contingency management, including inconsistent discipline and poor monitoring . Parent reactions to child behavior, often in the form of reactive parenting, can shape anti social or undesirable practices . Imprecise contingency management can lead to difficulties in behavior and a developmental trend that can escalate problem behavior . In cases of deteriorating parent-child relationship, adolescents who are further along the risk continuum may be more susceptible to peer influences to initiate risk practices .

This parallels the concept of motivating operations , one that is highlighted in the applied behavior analysis literature. One of the pioneering figures in the field, Jack Michael, defines the concept as an environmental event, operation, or stimulus condition that affects behavior by altering the magnitude or direction of effect for contingent consequences . Operationally in this context, in the teenage years adolescents are exposed to stimuli that enhance the reinforcing effect of peers. The contrary is also true: there is a tendency for parents’ reinforcing effect to diminish during these critical years. One possible antidote is for parents to increase positive involvement in their child’s life so they can differentially change the frequencies of certain behaviors as a function of the value of the contingent punishing or reinforcing stimuli they deliver. To the extent to which they can do this, they may be able to buffer environmental influences that increase risk for certain risk behaviors . In children as young as middle school, where reported alcohol rates exceed 50%, tobacco 20% and marijuana 12%, parental influence has at least been shown to reduce risks for alcohol use . Much of the research in parenting and parenting practices has involved an assessment of the parent’s behavior as reported by their children and is usually collected through interviews and questionnaires. Such practices and measures have high face validity, but they have inherent weaknesses, as they are generally limited to self-report. Interviews and questionnaires are not ideal measures, no matter whether it is the child or the parent that responds. Alternatives to self-report measures may include direct observation, either in person or with the use of video equipment. In light of the additional expense of direct observation, select few researchers have expanded their research to include responses from both the parent and the child. The justification for this approach derives from the notion that effects of parenting practices should be centered on the children’s own perspectives. Nevertheless, recent details have emerged about a learning or socialization process in which parents and children have reciprocal behavioral influences, i.e., parents influence kid’s behavior, and kids also influence parent’s behavior . From this perspective, an assessment of the parents’ practices from their own point of view and that of their children may be warranted . A more complete understanding of parental influence must be preceded by an increased understanding of the discrepancies between parents’ and children’s reports of parenting behaviors . Consistent with this perspective, recent studies have shown that discrepancies in perceptions between adolescents and their parents may be negatively related to adolescent adjustment , including increased levels of conflict and stress within the family resulting in a myriad of problem behaviors . The limited number of studies comparing parents’ and children’s reports of parenting behaviors reveal that parents frequently overestimate their involvement, especially in monitoring and discipline . Involvement in school can encompass several areas including regular attendance, academic achievement and academic clubs, sports, and other extracurricular activities.Engagement in any of these school activities is negatively associated with initiating alcohol use . In general, being more active in school has been associated with an attenuated probability for participation in risky behaviors . School performance has been shown to be negatively associated with smoking initiation among non-Hispanic whites and Hispanics . Around the onset of puberty, peer influence becomes more salient and powerful, both because of modeling effects and peer reinforcement . For example, having at least one smoking peer greatly increases risk for smoking initiation and progression to daily smoking .