Biology Investigatory Project: Effect of Cannabis on Human (PDF)
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This document is a biology investigatory project. It looks at the effect of cannabis on the human body, covering topics such as cannabinoids, mechanisms in the brain, and toxicity. The document appears to be a research report.
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Biology Investigatory Project E ect of Cannabis on Human Table of Contents: S. No Title Page No. 1 Introduction 3 2 Cannabinoids and Cannabinoid Receptors 3 3 Bi...
Biology Investigatory Project E ect of Cannabis on Human Table of Contents: S. No Title Page No. 1 Introduction 3 2 Cannabinoids and Cannabinoid Receptors 3 3 Biochemical Mechanisms in the Brain 3 4 Toxicity 4 5 E ect of Cannabis 5 6 Long-Term E ects of Cannabis 7 7 Conclusion 10 8 Bibliography 11 2 Introduction: Cannabis, also known as Marijuana, and by numerous other names. Cannabinoids are a group of substances found in the Cannabis plant. Cannabinoids produce their e ects by interacting with specific receptors, located within di erent parts of the central nervous system. Pharmacologically, the principal psychoactive constituent of Cannabis is tetrahydrocannabinol (THC). It is one of 483 known compounds in the plant, including at least 84 other cannabinoids, such as cannabidiol (CBD), cannabinol (CBN), tetrahydrocannabivarin (THCV), and cannabigerol (CBG). The e ects of cannabis are caused by chemical compounds in cannabis, including cannabinoids such as tetrahydrocannabinol (THC). Cannabis has both psychological and physiological e ects on the human body. Five European Countries, Canada, and twenty US states have legalized medical cannabis if prescribed for nausea, pain or the alleviation of symptoms surrounding chronic illness. Cannabis use is associated with social and behavioral problems and carries a risk to physical and mental health. These e ects caused by cannabis on di erent parts of the human body are investigated in this project. Cannabinoids and Cannabinoid Receptors: The most notably prevalent psychoactive substances in cannabis are cannabinoids, most notably THC. The cannabinoid receptor is a typical member of the largest known family of receptors called a G protein-coupled receptor. A signature of this type of receptor is the distinct pattern of how the receptor molecules span the cell membrane seven times. Biochemical Mechanisms in the Brain: Cannabinoids usually contain a 1,1'-di-methyl-pyran ring, constituting a family of about 60 bi-cyclic and tri-cyclic compounds. 3 Like most other neurological processes, the e ects of cannabis on the brain follow the standard protocol of signal transduction, the electrochemical system of sending signals through neurons for a biological response. The binding of cannabinoids to cannabinoid receptors decreases adenylyl cyclase activity, inhibit calcium N channels, and disinhibit K+A channels. There are at least two types of cannabinoid receptors (CB1 and CB2). The CB1 receptor is found primarily in the brain and mediates the psychological e ects of THC. The CB2 receptor is most abundantly found on cells of the immune system. Cannabinoids act as immunomodulators at CB2 receptors, meaning they increase some immune responses and decrease others. For example, non-psychotropic cannabinoids can be used as a very e ective anti-inflammatory. The a inity of cannabinoids to bind to either receptor is about the same, with only a slight increase observed with the plant-derived compound CBD binding to CB2 receptors more frequently. Cannabinoids likely have a role in the brain’s control of movement and memory, as well as natural pain modulation. Cannabinoids can a ect pain transmission and specifically, that cannabinoids interact with the brain's endogenous opioid system and may a ect dopamine transmission. This is an important physiological pathway for the medical treatment of pain. Toxicity: No fatal overdoses with cannabis use have been reported as of 2010.THC, the principal psychoactive constituent of the cannabis plant, has an extremely low toxicity and the amount that can enter the body through the consumption of cannabis plants poses no threat of death. The ratio of cannabis material required to produce a fatal overdose to the amount required to saturate cannabinoid receptors and cause intoxication is 4 approximately 40,000:1. It was found in 2007 that while tobacco and cannabis smoke are quite similar, cannabis smoke contained higher amounts of ammonia, hydrogen cyanide, and nitrogen oxides, but lower levels of carcinogenic polycyclic aromatic hydrocarbons (PAHs). Cannabis smoke contains thousands of organic and inorganic chemical compounds. Over fifty known carcinogens have been identified in cannabis smoke. These include nitrosamines, reactive aldehydes, and polycyclic hydrocarbons, including benz[a]pyrene. Marijuana smoke was listed as a cancer agent in California in 2009. E ect of Cannabis: General E ect: The location of the cannabinoid receptor exists on the cell membrane are both outside (extracellularly) and inside (intracellularly) the cell membrane. CB1 receptors, the bigger of the two, are extraordinarily abundant in the brain. CB2 receptors are structurally di erent, found only on cells of the immune system and seem to function similarly to its CB1 counterpart. CB2 receptors are most commonly prevalent on B-cells, natural killer cells, and monocytes, but can also be found on polymorphonuclear neutrophil cells, T8 cells and T4 cells. In the tonsils, the CB2 receptors appear to be restricted to B- lymphocyte-enriched areas. THC and endogenous anandamide additionally interact with glycine receptors. Psychoactive E ects: When THC enters the blood stream and reaches the brain, it binds to cannabinoid receptors. The endogenous ligand of these receptors is anandamide, the e ects of which THC emulates. This characteristic of the cannabinoid receptors results in changes in the levels of various neurotransmitters, especially dopamine and norepinephrine. Neurotransmitters which are closely associated with the acute e ects of cannabis ingestion, such as euphoria and anxiety. Some e ects may include a general 5 perception, euphoria, feelings of well- being, relaxation or stress reduction, increased appreciation of humor, music (especially discerning its various components/instruments) or the arts, joviality, metacognition and introspection, enhanced recollection (episodic memory), increased sensuality, increased awareness of sensation, increased libido and creativity. Abstract or philosophical thinking, disruption of linear memory and paranoia or anxiety are also typical. Anxiety is the most reported side e ect of smoking marijuana. Between 20 % to 30 % of recreational users experience intense anxiety and panic attacks after smoking cannabis, however, some report anxiety only after not smoking cannabis for a prolonged period. Cannabis also produces many subjective and highly tangible e ects, such as greater enjoyment of food taste and aroma, an enhanced enjoyment of music and comedy, and marked distortions in the perception of time and space. At higher doses, e ects can include altered body image, auditory and visual illusions, pseudo-hallucinatory, and ataxia from selective impairment of polysynaptic reflexes. In some cases, cannabis can lead to dissociative states such as depersonalization and derealization. Somatic E ects: Some of the short-term physical e ects of cannabis use include increased heart rate, dry mouth, reddening of the eyes (congestion of the conjunctival blood vessels), a reduction in intra-ocular pressure, muscle relaxation and a sensation of cold or hot hands and feet. Neurological E ects: The areas of the brain where cannabinoid receptors are most prevalently located are consistent with the behavioral e ects produced by cannabinoids. Brain regions in which cannabinoid receptors are very abundant are the basal ganglia, associated with movement control. 6 The cerebellum, associated with body movement coordination, the hippocampus, associated with learning, memory, and stress control, the cerebral cortex, associated with higher cognitive functions and the nucleus acumens, regarded as the reward center of the brain. Other regions where cannabinoid receptors are moderately concentrated are the hypothalamus, which regulates homeostatic functions, the amygdala, associated with emotional responses and fears, the spinal cord, associated with peripheral sensations like pain,the brain stem, associated with sleep, arousal, and motor control; and the nucleus of the solitary tract, associated with visceral sensations like nausea and vomiting. Experiments on animal and human tissue have demonstrated a disruption of short-term memory formation, which is consistent with the abundance of CB1 receptors on the hippocampus, the region of the brain most closely associated with memory. Cannabinoids inhibit the release of several neurotransmitters in the hippocampus such as acetylcholine, norepinephrine, and glutamate, resulting in a major decrease in neuronal activity in that region. This decrease in activity resembles a "temporary hippocampal lesion." In in-vitro experiments THC at extremely high concentrations, which could not be reached with commonly consumed doses, caused competitive inhibition of the AChE enzyme and inhibition of β-amyloid peptide aggregation, implicated in the development of Alzheimer's disease. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is considerably superior inhibitor of A aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may impact the progression of this debilitating disease. Long-Term E ects of Cannabis: Acute psychosis: Although there has been an association noted between cases of acute psychosis and long- term cannabis use, the precise nature of the relationship is controversial; evidence 7 suggests that cannabis use may worsen psychotic symptoms and increase the risk of relapse. Chronic psychosis: According to research, Long term cannabis use increases the risk of psychosis in people with certain genetic or environmental vulnerabilities but does not cause psychosis. Important predisposing factors include genetic liability, childhood trauma and urban upbringing. Cannabis use may cause permanent psychological disorders in some users such as cognitive impairment, anxiety, paranoia, and increased risks of psychosis. Key predisposing variables include age of first exposure, frequency of use, the potency of the cannabis used, and individual susceptibility. Schizophrenia: Among people with schizophrenia there is insu icient evidence to determine whether cannabis use leads to improvement or deterioration of the condition, but patients who use cannabis have been found to display increased cognitive performance compared to non-users. Use of cannabis in adolescence or earlier increases the risk of developing schizoa ective disorders in adult life, although the proportion of these cases is small. Susceptibility is most often found in users with at least one copy of the polymorphic COMT gene. Cannabis with a high THC to CBD ratio produces a higher incidence of psychological e ects. CBD may show antipsychotic and neuroprotective properties, acting as an antagonist to some of the e ects of THC. Studies examining this e ect have used high ratios of CBD to THC, and it is unclear to what extent these laboratory studies translate to the types of cannabis used by real life users. Research has shown that CBD can safely prevent psychosis in general. 8 Depressive disorder: Less attention has been given to the association between cannabis use and depression, though according to the Australian National Drug & Alcohol Research Centre, it is possible since cannabis users who have depression are less likely to access treatment than those with psychosis. Teenage cannabis users show no di erence from the general population in incidence of major depressive disorder (MDD), but an association exists between early exposure coupled with continued use into adult life and increased incidence of MDD in adulthood. Among cannabis users of all ages, there may be an increased risk of developing depression, with heavy users seemingly having a higher risk. Cancer: According to a 2013 literature review, marijuana could be carcinogenic, but there are methodological limitations in studies making it di icult to establish a link between marijuana use and cancer risk. The authors say that bladder cancer does seem to be linked to habitual marijuana use, and that there may be a risk for cancers of the head and neck among long-term (more than 20 years) users. Gordon and colleagues said, "there does appear to be an increased risk of cancer (particularly head and neck, lung, and bladder cancer) for those who use marijuana over a period of time, although what length of time that this risk increases is uncertain." Respiratory e ects: A 2013 literature review by Gordon and colleagues concluded that inhaled marijuana is associated with lung disease. Based on various methods of cannabis consumption, smoking is considered the most harmful, the inhalation of smoke from organic materials can cause various health problems (e.g., coughing and sputum).Isoprene helps to modulate and slow down reaction rates, contributing to the significantly di ering qualities of partial combustion products from various sources. 9 Reproductive and endocrine e ects: Cannabis consumption in pregnancy is associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits in o spring. Although most of the research has concentrated on the adverse e ects of alcohol, there is now evidence that prenatal exposure to cannabis has serious e ects on the developing brain and is associated with deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence. A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as it may interact with the endocannabinoid system, medical cannabis has several potential beneficial e ects. Evidence is moderate that it helps in chronic pain and muscles spasms. Lesser evidence supports its use to help with nausea during chemotherapy, improve appetite in those with HIV/AIDS and help with sleep. The National Institute on Drug Abuse (NIDA) states that cannabis is unlikely to be useful as medicine as it is an unpurified plant containing numerous chemicals with unknown health e ects. it is typically consumed by smoking further contributing to potential adverse e ects and its cognitive impairing e ects may limit its utility. Conclusion: Cannabinoids have served numerous roles in medicine, culture, and recreation for almost as long as recorded human history. With pharmaceutical and illicit forms available to patients, healthcare providers and other interprofessional healthcare team members must be equipped with the knowledge to identify symptoms of cannabinoid abuse and toxicity and take steps to mitigate adverse outcomes. However, medical professionals must also understand medical conditions that may respond to treatment with appropriately dosed and administered cannabinoids. 10 Bibliography: https://www.ncbi.nlm.nih.gov/ https://www.nccih.nih.gov/ https://adf.org.au/drug-facts/cannabinoids/ https://en.wikipedia.org/wiki/Cannabinoid https://www.sciencedirect.com/topics/medicine-and-dentistry/cannabinoid 11