Native Americans appeared in 1820, Chinese in 1870, Japanese in 1890, Filipino, Hindu and Korean in 1920, Mexican in 1930, Hawaiian and Eskimo in 1960. In 1977, the Office of Management and Budget , which sets the standards for racial/ethnic classification in federal data collections including the US Census data, established a minimum set of categories for race/ethnicity data that included 4 race categories and two ethnicity categories . In 1997, OMB announced revisions allowing individuals to select one or more races, but not allowing a multiracial category. Since October 1997, the OMB has recognized 5 categories of race and 2 categories of ethnicity . In considering these classifications, the extent to which dominant race/ethnic characterizations are influenced both by bureaucratic procedures as well as by political decisions is striking. For example, the adoption of the term Asian-American grew out of attempts to replace the exoticizing and marginalizing connotations of the externally imposed pan-ethnic label it replaced, i.e. “Oriental”. Asian American pan-ethnic mobilization developed in part as a response to common discrimination faced by people of many different Asian ethnic groups and to externally imposed racialization of these groups. This pan-ethnic identity has its roots in many ways in a racist homogenizing that constructs Asians as a unitary group , and which delimits the parameters of “Asian American” cultural identity as an imposed racialized ethnic category . Today, the racial formation of Asian American is the result of a complex interplay between the federal state, diverse social movements, and lived experience. Such developments and characterizations then determine how statistical data is collected. In fact, the OMB itself admits to the arbitrary nature of the census classifications and concedes that its own race and ethnic categories are neither anthropologically nor scientifically based . Issues of ethnic classification continue to play an important role in health research. However, some researchers working in public health have become increasingly concerned about the usefulness or applicability of racial and ethnic classifications. For example, as early as 1992, a commentary piece in the Journal of the American Medical Association, challenged the journal editors to “do no harm” in publishing studies of racial differences .

Quoting the Hippocratic Oath, they urged authors to write about race in a way that did not perpetuate racism. However, while some researchers have argued against classifying people by race and ethnicity on the grounds that it reinforces racial and ethnic divisions; Kaplan & Bennett 2003; Fullilove, 1998; Bhopal, 2004, others have strongly argued for the importance of using these classifications for documenting health disparities . Because we know that substantial differences in physiological and health status between racial and ethnic groups do exist, relying on racial and ethnic classifications allows us to identify, monitor, and target health disparities . On the other hand, estimated disparities in health are entirely dependent upon who ends up in each racial/ethnic category, a process with arguably little objective basis beyond the slippery rule of social convention . If the categorization into racial groups is to be defended, we, as researchers, are obligated to employ a classification scheme that is practical, unambiguous, consistent, and reliable but also responds flexibly to evolving social conceptions . Hence, the dilemma at the core of this debate is that while researchers need to monitor the health of ethnic minority populations in order to eliminate racial/ethnic health disparities, they must also “avoid the reification of underlying racist assumptions that accompanies the use of ‘race’, ethnicity and/or culture as a descriptor of these groups. We cannot live with ‘race’, but we have not yet discovered how to live without it” .Reinarman and Levine have argued that investigations of ethnicity in alcohol and drugs research have typically taken the form, whether intentionally or not, of linking “a scapegoated substance to a troubling subordinate group – working-class immigrants, racial or ethnic minorities, or rebellious youth” . Different minority ethnic groups have often been framed at one time or another by their perceived use of alcohol and illicit drugs, regardless of their actual substance using behaviors and regardless of their relative use in comparison with drug and alcohol use among whites .In mainstream drug and alcohol research, traditional ethnic group categories continue to be assessed in ways which suggest little critical reflection in terms of the validity of the measurement itself.

This is surprising given that social scientists since the early 1990s have critiqued the propensity of researchers to essentialize identity as something ’fixed’ or ’discrete’ and to neglect to consider how social structure shapes identity formation. Recent social science literature on identity suggests that people are moving away from root edidentities based on place and towards a more fluid, strategic, positional, and context-reliant nature of identity . This does not mean, however,growing racks that there is an unfettered ability to freely choose labels or identities, as if off of a menu . An individual’s ability to choose an identity is constrained by social structure, context, and power relations. Structural constraints on identity formation cannot be ignored, as people do not exist as free floating entities but instead are influenced and constrained in various ways by their socioeconomic and geographical environment . As such, an identity is not just claimed by an individual but is also recognized and validated by an audience, resulting in a dialectical relationship between an individual and the surrounding social structures . Similarly, a ‘new’ perspective on ethnic identity specifically has emphasized the fluidity and contextually-dependent nature of ethnicity, minimizing notions about ethnicity as a cultural possession or birthright and instead emphasizing ethnicity as a socially, historically, and politically located struggle over meaning and identity . Ethnicity or ethnic identity is not some immutable sense of one’s identity but rather something produced through the performance of socially and culturally determined boundaries . Hence, individuals are not passive recipients of acquired cultures but instead active agents who constantly construct and negotiate their ethnic identities within given social structural conditions .In spite of these sociological contributions, which have enriched our understanding of identity generally and ethnicity specifically, the alcohol and drugs fields have not adequately integrated these perspectives, thwarting our ability to understand the relationships between ethnicity and substance use. As such, the field is ripe with correlations between ethnic group categories and substance use problems, resulting in solutions to problems that focus on reifying questionable social group categorizations and revealing little about how drugs are connected to identities and shaped by broader social and cultural structures. It is important to note that we do not intend to argue that existing categories of ethnicity be disregarded in the alcohol and drugs fields. As Krieger and colleagues have noted in another context , surveillance data documenting health disparities, in our case in substance use, are exceedingly important in terms of identifying potential inequities in health. However, without understanding the complexity of ethnic identity and its relationship to substance use, these surveillance data may perpetuate stereotypes and the victimization of specific socially-delineated ethnic groupings, obfuscate the root causes of substance use and elated problems, and reify politicized categories of ethnicity which may have little meaning for the people populating those categories. While acknowledging that socially-deliented ethnic categories are important for documenting social injustices, we must also be vigilant about questioning the appropriateness of those categories .

Conceptually this type of critical approach is important for considering how substance use is related to negotiations of ethnicity over time and place and bounded by structure. Maintaining a static and homogenous approach towards ethnic categorizations in the alcohol and drugs fields presents at least two problems. First, it risks overlooking how drugs and alcohol play into a person’s negotiation of identity, particularly ethnic identity, thus revealing little about the pathways that lead to substance use. Cultural researchers have long emphasized the importance of commodity consumption in the construction of identities and lifestyles , particularly within youth cultures , and how it can be an important factor in demarcating and constituting social group boundaries . A limited body of research in the alcohol and drugs field has emphasized the role of substance use in constructing and performing identities , particularly ethnic identities , uncovering how subgroups within traditionally-defined ethnic minority categories use drugs and alcohol to distinguish themselves from ethnically similar others. For example, in a qualitative study of Asian American youth in the San Francisco Bay area in the US, narratives illustrated how youths’ drug use and drug using practices were a way of constructing an identity which differentiated them from “other Asian” youth groups, specifically allowing them to construct an alternative ethnic identity that set them apart from the “model minority” stereotype . Thus taste cultures and consumption-oriented distinctions highlight the continuing salience of and interconnections not just between substance use and changing notions of ethnicity but also between substance use, class and ethnicity. Ethnic identity gets translated into social captial which in turn has ramifications for one’s economic and social standing . Second, failing to critically appraise our use of fixed and homogenous ethnicity categories in the alcohol and drugs fields jeopardizes our ability to identify the broader social and structural determinants of alcohol and drug use and related problems—like poverty, social exclusion, and discrimination—which are crucial issues for addressing social injustices. So often studies revealing correlations between ethnic categories and substance use related problems result in discussions about the importance of developing culturally-appropriate prevention and treatment interventions, overlooking the structural conditions that adversely affect socially-defined ethnic groupings and may result in some form of engagement with alcohol and/or drugs. For example, research on street cultures, where ethnic identifications and drugs play a central part, illustrates how some ethnic minority youth use and/or sell drugs to actively construct counter-images or ethnically-infused street cultures of resistance within their neighborhoods, which some researchers have called “neighborhood nationalism” , as a way of resisting or transcending “inferior images” ascribed to them by the wider society . These street cultures provide alternative definitions of self-identity, especially for young men, who live in communities marked by poverty and marginalization and who have little access to masculine status in the formal economy .

Concerning, CB1 receptor agonists, Gardner and colleagues found that THC facilitates brain stimulation reward ,vertical grow rack system whereas other investigators found no effects of the syntheticagonists CP55,940 or AMG-3 and some investigators have found a reduction of brain stimulation reward with CB1 receptor agonists . These discrepancies, which are likely due to procedural differences, remain to be resolved. A caveat of all experiments with directly acting CB1 receptor agonists is that, for several reasons, these drugs do not provide a realistic picture of the physiological role of the endocannabinoids. First, anandamide is a partial agonist , whereas synthetic CB1 receptor agonists are often full agonists and have higher affinities for CB1 receptors . Second, anandamide and 2-AG have very short half-lives , whereas THC and synthetic CB1 receptor agonists have relatively long half-lives. Finally, systemic injections of these compounds result in the activation of all brain areas containing CB1 receptors, whereas physiological activation of endocannabinoid synthesis and release is likely to be region, neuron or even synapse specific . The availability of mice genetically deprived of CB1 receptors in a tissue-specific manner may help address this possibilityAssessment of the roles the endocannabinoid system plays in brain reward processes was greatly facilitated by the discovery of selective CB1 receptor antagonists/inverse agonists such as rimonabant and AM251 . CB1 receptor antagonists decrease the rewarding effects of a wide variety of abused drugs under certain conditions. For example, the rewarding effects of opioids are generally decreased in both intravenous self-administration and conditioned place preference procedures . There have also been reports that rimonabant and AM251 reduce the rewarding effects of methamphetamine , alcohol and nicotine .

CB1 receptor antagonists do not generally alter self-administration of cocaine under low fixed-ratio schedules or conditioned place preference procedures , but AM251 has been found to significantly reduce self-administration of cocaine under progressive-ratio schedules and rimonabant prevents relapse to cocaine-induced and cue-induced cocaine-seeking behaviour . This suggests that the appetitive and conditioned effects of cocaine, but not its direct reinforcing effects, depend on CB1 receptor activation. The effects of rimonabant on opioid reward may be mediated primarily in the NAcc, as blockade of CB1 receptors in this area reduces heroin self-administration . On the other hand, the modulation of ethanol reward by the CB system appears to take place both in the NAcc and in the prefrontal cortex . The brain sites where CBs act to alter the rewarding effects of nicotine and psychostimulants are not known at present. Drugs of abuse share the ability to elevate extracellular levels of dopamine in the shell of the NAcc, as measured by in vivo microdialysis, and this effect is believed to play an important role in their reinforcing effects . CB1 receptor antagonists have been shown to block the elevations of accumbal dopamine levels induced by administration of nicotine or ethanol , but not by administration of heroin , morphine or cocaine . Transient surges of dopamine in the NAcc, as measured by cyclic voltammetry, are also produced by drugs of abuse and are believed to be involved in drug seeking . Interestingly, the transient increases in dopamine produced by administration of nicotine, ethanol and cocaine in the shell of the NAcc of freely moving rats are all blocked by CB1 receptor antagonists . Consistent with a role for endocannabinoids in the rewarding effects of food and in the regulation of appetite and food intake , blocking endocannabinoid tone with CB1 receptor antagonists reduces intake of food and sweet solutions . Also, injection of rimonabant within 24 h of birth completely prevents milk intake and causes almost 100% mortality in mouse pups . The motivational effects of food measured by a progressive-ratio schedule of food reinforcement and the appetitive aspects of food reward are significantly reduced by rimonabant in rats, indicating that some aspects of food intake regulation involve reward and motivational processes.

In addition, AM251 decreases hedonic reactions to sucrose and increases aversive reactions to quinine . Consistent with these preclinical findings, rimonabant has been found to be effective in the clinical treatment of obesity , although the clinical efficacy of this agent appears to be primarily due to its ability to alter peripheral lipid metabolism, rather than to reduce food intake . As in the case of CB1 receptor agonists, the effects of CB1 receptor antagonists on brain stimulation reward are somewhat controversial. Rimonabant has been shown to increase the threshold for brain stimulation reward in some studies or to produce no change in brain stimulation reward thresholds in other studies .Mice genetically engineered to lack CB1 receptors do not show dramatic changes in body weight, food consumption or fertility , suggesting that CB1 receptors modulate rather than mediate basic reward functions or that other systems can compensate for their absence. By using CB1-null mice, the role of CB1 receptors in the rewarding effects of drugs of abuse has been confirmed. For example, in these mutant mice morphine is not self administered , does not induce conditioned place preferences and does not elevate dopamine levels in the NAcc . Also, the rewarding effects of alcohol are reduced in CB1-null mice, as demonstrated by data showing that CB1-null mice do not develop conditioned place preference with this drug and that they do not prefer it over water in a two-bottle free-choice paradigm . However, another study reported that CB1-null mice show slight and short-lasting decreases in preference for ethanol. Development of conditioned place preferences with cocaine is unaltered in CB1-null mice . On the other hand, development of cocaine self-administration behaviour under fixed-ratio schedules of reinforcement in CB1-null mice was reported to be unaltered when mice were restrained , but was reduced in freely moving mice . In addition, cocaine self-administration was significantly reduced under a progressive-ratio schedule of self-administration in CB1-null mice . These contrasting results highlight the fact that, when working with genetically modified mice such as CB1-null mice, not only methodological differences but also differences in the genetic background may result in very different and sometimes contrasting behavioural outputs . It is interesting to note that CB1-null mice show normal elevations in dopamine levels in the NAcc following administration of cocaine ,grow vertical but no elevations following administration of morphine or ethanol , compared with wild-type controls. Finally, CB1-null mice do not develop conditioned place preferences to nicotine , but they self-administer the drug like wild-type controls . It remains to be seen whether increasing the effort needed to obtain nicotine, as with cocaine , could reveal a role of CB1 receptors in some aspects of nicotine reinforcement as suggested by the results with CB1 receptor antagonists . CB1-null mice have also provided evidence for the involvement of the endocannabinoid system in food reward. For example, CB1-null mice eat less than their wild-type control litter mates after food restriction . Moreover, CB1-null mice respond less for sucrose in a two-lever paradigm, have lower break points under progressive-ratio schedules of sucrose delivery and show less preference for sucrose over water in a two-bottle free-choice procedure .

Genetic ablation of CB1 receptors results in small reduction in body weight, reduction in adiposity and resistance to diet-induced obesity . However, as in the case of CB1 receptor antagonists, these effects appeared to be related more to increased metabolic energy consumption than to differences in rewarding effects of food or hypophagia . Interestingly, in the study by Fride et al. , administration of rimonabant in mice pups lacking CB1 receptors still induced a decrease in milk intake and survival rate, suggesting that some of the effects of CBs on food intake may be mediated by still uncharacterized CB receptors. To date, no study has investigated the effects of CB1 receptor deletion on brain stimulation reward. On the other hand, it should be noted that CB1-null mice show increased anhedonia after chronic mild stress , a measure of reduced activity of the reward system and a model of depression , further supporting a role for the endocannabinoid system in brain reward functions.Although measurements of the effects of systemic or intracranial injections of anandamide provide useful information on the functions of the endocannabinoid system, to provide support for a role of neurally released anandamide in brain reward processes it is also important to measure anandamide released in the brain by different abused drugs, by food and by electrical brain stimulation. Release of neurotransmitters such as dopamine or glutamate can be readily measured by micro-dialysis techniques, but only a few studies have employed microdialysis techniques to measure extracellular brain levels of endocannabinoids . Thus, most information on the modification of endocannabinoid levels comes from measurements of tissue levels in different brain areas. Measuring tissue level of anandamide has the limitation that only one time point can be established at a time, limiting information on the pattern of endocannabinoid release. Using tissue levels, it has been demonstrated that chronic administration of several drugs of abuse leads to region specific increases in anandamide levels. For example, when administered chronically, THC decreases levels of anandamide in the striatum , ethanol decreases levels of anandamide in the midbrain but not in the striatum , nicotine decreases levels of anandamide in the striatum but not in the midbrain , and cocaine and morphine do not alter anandamide levels, either in the striatum or midbrain . However, it is difficult to determine from these studies whether measured levels of endocannabinoids reflected the consequences of chronically administered drug or withdrawal. Vigano et al. compared the effects of chronic versus acute administration of morphine on endocannabinoid levels in the brain. They found that acute administration of morphine increased anandamide levels in the striatum, whereas chronic treatment with the drug failed to do so. In addition, they found that chronic treatment with morphine did not alter the ability of a challenge dose of morphine to increase anandamide levels in the striatum; that is, repeated administration of morphine did not induce sensitization or tolerance to this effect . Thus, chronic administration of drug followed by withdrawal, chronic administration of drug followed by an acute drug challenge and acute administration of drug can lead to very different changes in brain anandamide levels. Such profiles of release may indicate that anandamide is released in response to relevant changes in homoeostasis but not when an adaptive response has already occurred.