Estimated associations were imprecise because of the small number of units that were included in the analysis,but are meaningful for the study jurisdictions. Cities and unincorporated county areas that had 8 or more cannabis control policies generally had greater population density, more renters, fewer family households, more crowded households, and higher densities of social organizations compared with jurisdictions with fewer policies. More restrictive jurisdictions were also older, with more Asian and Black residents, and fewer Latinx and White residents. Again, cannabis control policies followed socioeconomic status: populations in areas that permitted retail cannabis business but were covered by more cannabis control policies were more educated with less poverty and higher median income. Results of sensitivity analyses breaking the policy score into quarters instead of halves showed patterns consistent with the main results, with the most pronounced differences for jurisdictions with the fewest cannabis control policies .We examined local variation in the adoption of cannabis control policies in relation to social advantage for 241 of California’s 539 cities and unincorporated county areas. Following statewide recreational cannabis legalization, a majority of these jurisdictions banned all cannabis businesses. The 25% of jurisdictions that allowed retail cannabis businesses varied widely in their adoption of 19 policies . This study is among the first to investigate patterns in local cannabis control policies relative to socioeconomic and demographic characteristics.
We found that all-out bans on cannabis businesses were more common in localities with higher income and education levels, grow rack and communities with disproportionately more Asian residents and fewer Black and Latinx residents. Among jurisdictions permitting retail cannabis businesses, recommended cannabis control policies were more frequently adopted in jurisdictions with less poverty and more Black residents, although there was variation by policy. This uneven application of cannabis control policies has the potential to exacerbate cannabis related health disparities in communities already at higher risk of poor health outcomes. Recreational cannabis legalization has been framed as a way to repair racial injustices stemming from discriminatory drug policies, but just implementation of cannabis legalization is also a concern. Commercial cannabis may offer business opportunities, which has motivated some jurisdictions to offer priority licensing for people negatively impacted by historical cannabis criminalization. Communities with more Black and Hispanic residents have more illegal cannabis outlets that may not comply with requirements such as product safety standards; legalizing cannabis outlets allows localities to regulate them and thereby potentially promote public health. Yet our findings also suggest potential for legalization to exacerbate longstanding racial/ethnic and socioeconomic inequities. Cannabis is not harmless. Cannabis use disorder occurs in 20% of lifetime cannabis users, with 11% of these cases severe enough to prevent individuals from participating in major life activities .
While valid medicinal uses exist, cannabis use has been linked to potential harms including motor vehicle crashes, psychotic disorders, respiratory disease, and low birth weight. Thus, communities that increase access to cannabis by permitting cannabis businesses—particularly commercial retail—may experience increases in cannabis use and associated negative health consequences. Communities with less social advantage may haveless power to resist policies that enable legal or illicit cannabis sales, consistent with research showing that cannabis outlets are disproportionately located in neighborhoods with more low-income and racial/ethnic minority residents. Economically disadvantaged communities were more likely to allow commercial cannabis businesses, and on average less likely to deploy recommended policies that curb the availability of commercial cannabis and exposure to some of its harms. This finding is consistent with previous research showing that higher socioeconomic-status communities were more likely to have comprehensive tobacco smoke-free air laws. Jurisdictions with greater proportions of Black residents adopted significantly more cannabis control policies regulating retail cannabis businesses, if allowed. This finding may have positive implications for health disparities and may reflect that some cities with previous experience of social activism to promote local alcohol control are translating these lessons to cannabis. Cannabis control policies were also more common in places with higher population density. Urban areas in California are more politically liberal and, thus, more likely to adopt a variety of public health policies, including those pertaining to cannabis. Larger cities may also have more capacity to consider public health concerns and develop more extensive regulatory approaches.
The optimal policy strategy for local cannabis is unknown, as most local cannabis policies have not yet been evaluated. However, if lessons learned from alcohol and tobacco apply to cannabis, then cities covered by more cannabis control policies may benefit while rural areas may face more exposure to health harms. We found notable patterns in the types of cannabis control policies adopted by more and less socially advantaged jurisdictions. More advantaged jurisdictions generally adopted more restrictions on physical cannabis access . Less advantaged jurisdictions generally had more restrictions related to retail cannabis’s presence in the neighborhood environment . These distinct policy combinations may be motivated by different underlying interests . Local policy patterning may also reflect the “not-in-my-backyard” phenomenon. Wealthy, White, and socially advantaged groups within local jurisdictions often have a disproportionate voice in local politics, allowing them to influence decision-making in the interests of keeping commercial cannabis out of their own neighborhoods. If NIMBYism is at play, it would be consistent with other areas of health—NIMBYism has been shown to thwart public health equity in local policy making on issues ranging from homelessness to AIDS, alcohol control, and air pollution, and is a manifestation of structural racism. Public health researchers and health equity advocates should therefore monitor this concern in local cannabis policy making going forward. As with other areas, ensuring equitable local policies may involve combatting NIMBYism through public policy or engagement strategies. Cancer and AIDS patients experience weight loss and Thissue wasting due to increased metabolic demand and decreased nutritional intake . These complications are important indicators of patient prognosis and may directly result in death . To prevent adverse outcomes related to malnutrition, various treatments have been utilized including corticosteroids, metoclopramide, and progestational agents . Another appetite stimulant, medicinal marijuana, greenhouse grow tables has been at the center of controversy regarding its therapeutic effect, route, dose, and side effects . Not only has medicinal marijuana been shown to relieve pain, anxiety, and depression, but also, studies among HIV patients reported appetite stimulation and weight gain as the primary reason for medicinal marijuana use . Marijuana or Cannabis Sativa contains the active component delta-9- tetrahydrocannabinol . The Food and Drug Administration approved the use of dronabinol, the oral form of THC, for the treatment of anorexia in AIDS patient, but since THC is not water soluble, smoking marijuana remains the most efficient delivery method for THC . Seconds after the first puff of a cannabis cigarette, THC is detectable in the plasma whereas oral administration of THC results in detectable plasma levels within one to two hours . THC may be taken orally in fat containing food or dissolved in suitable pharmaceutical oil, but the absorption remains delayed and variable because of gastric acid degradation and the first pass liver effect. . Due to the potential benefits for cancer and AIDS patients and the recent discovery of the endocannabinoid system, medicinal marijuana’s role in appetite stimulation has been an active area of research. In 1997, researchers initially found that THC did not produce acute appetite stimulation in the rat , but further studies disproved this previous hypothesis. Today, THC is known to bind to cannabinoid receptors located in the brain and may play a critical role in the leptin pathway, a critical system for appetite stimulation. This paper will explore the current knowledge of medicinal marijuana and its role in appetite stimulation.For many years, the effects of THC on the brain remained a mystery.
The first major step in understanding the mechanism of THC was brought about by Matsuda et al with the discovery of cannabinoid receptors. Further research identified two cannabinoid receptors, CB1 and CB2, which are coupled to G inhibitory proteins . Activation of these Gi proteins inhibits adenylate cyclase with subsequent inhibition of AMP’s conversion to cAMP. Due to their role as neuromodulators at axon terminals, cannabinoid receptors are hypothesized to be presynaptic rather than postsynaptic . CB1 receptors are located on neurons in the brain, spinal cord, peripheral nervous system, and some peripheral organs and Thissue whereas CB2 receptors are located primarily in immune cells . More specifically, CB1 receptors are located in axons and nerve terminals . The frontal regions of the cerebral cortex, basal ganglia, cerebellum, hippocampus, hypothalamus, and anterior cingulated cortex of the limbic forebrain contain a high density of CB1 receptors . After the identification of cannabinoid receptors, the endogenous ligands for these receptors known as endocannabinoids were discovered. . Of the three arachidonic acid derivatives known as endocannabinoids, N-archidonyl–ethanolamine or anandamide has been the most extensively studied thus far . These endocannabinoids are released locally on demand and are rapidly inactivated by an enzyme, fatty acid amide hydrolase, which provides a possible pharmaceutical target for the modification of cannabinoids and their effect on the brain . The endocannabinoid anandamide was proven to stimulate food intake in rats, and the CB1 antagonist rimonabant also known as SR141716 suppressed food intake, which resulted in decreased body weight in adult non-obese rats . In a related study, rimonabant was given to diet-induced obesity model mice, and the suppression of appetite and food intake was significant . Further research on mice demonstrated that CB1 knockout mice were significantly leaner than CB1 mice, which helped researchers conclude that endogenous cannabinoids are important in both feeding and peripheral metabolic controls . In an attempt to understand more precise mechanisms of CB1, one study discovered a relationship between ghrelin and CB1 antagonists. Ghrelin, a peptide hormone secreted by the fundus of the stomach, stimulates hunger. Rats that were treated with CB1 receptor antagonists, rimonabant and oleoylethanolamide, demonstrated a decreased level of ghrelin . Research has revealed that endocannabinoids may play an integral role in the leptin pathway, which may be the key to understanding their role in appetite stimulation. Leptin is the main signal in which the hypothalamus senses nutritional state and modulates food intake. In one study, a deffective leptin signaling pathway resulted in increased levels of hypothalamic endocannabinoids which points to a strong association between the leptin signaling pathway and the endocannabinoid system . One mechanism in which leptin decreases feeding is through the inhibition of neuropeptide Y production. Further, neuropeptide Y may be related to the endocannabinoid system. One study proved that the administration of SR141716, a CB1 antagonist, eliminated neuropeptide Y-induced overeating and reduced ethanol and sucrose intake in CB1 wild type mice . Although marijuana may prevent cachexia associated with AIDS and cancer, health care providers must consider the side effects associated with smoking marijuana. Similar to the toxicities associated with cigarettes, smoking marijuana leads to cellular dysplasia and subsequent increase risk for the development of pulmonary malignancy . A different inhalation pattern of marijuana smokers results in a 50% increase exposure to procarcinogen benz-alpha-pyrene and carboxyhemoglobin compared to cigarette smokers . In addition, researchers have identified alveolar macrophage damage as a result of marijuana use . Since a large proportion of CB1 receptors are located in the brain, marijuana users have been thought to experience neurologic side effects. Unfortunately, many studies have yielded conflicting results of both neuroprotective and neural damaging actions . One systematic review found that marijuana use was associated with lower education attainment and increased utilization of illicit drugs, but a relationship with psychological health problems could not be proven . Although staThistics did not prove or disprove this relationship, the evidence points in the direction of marijuana’s negative impact on psychosocial functioning and psychopathology . Marijuana may adversely affect learning, memory, and psychomotor and cognitive performance . In addition, marijuana may influence various forms of impulsivity , driving ability , and flying ability . One phenomenon associated with increased marijuana intake is “cannabis psychosis” which can present with delusions, grandiose identity, persecution, auditory hallucinations, and blunting of emotion . In addition, marijuana use may exacerbate existing psychotic illness . Smoking marijuana may be detrimental to AIDS and cancer patients. First, smoking marijuana may cause hypotension and tachycardia, a stressful response on the body . Inaddition, these immunocompromised patients may be exposed to life threatening microbes such as Klebsiella, Enterobacter, Group D Streptococcous, Salmonella, and Shigella, which have been cultured from marijuana .