Drug ProfileEssay Preview: Drug ProfileReport this essayDrug ProfileAddiction is a serious illness that ruins people lives. The body and mind crave the altercation substances bring and control is lost. The psychology of addiction is in the mind, and the physiology is in the body. Both mind and body can become addicted to substances causing altercations in the brain and painful effects on the body with withdrawal. The most abused substances are often legal. The following will examine different types of illegal and legal substances and the effects they have on the mind and body.
The Psychology and Physiology of AddictionIntroduction of a substance into the body on a regular basis can cause an addiction. The mind and body become used to the substance introduced causing the addiction. Over time, the mind and body crave the substance and without the substance, withdrawal becomes an issue. The mind and body then needs the substance or the systems in the body will fail.
Psychology of AddictionBehavioral traits within a person can make him or her susceptible to drug addiction. The feeling of helplessness or no control over his or her life could lead to person to drug addiction as a way to escape those negative feelings. People abuse drugs for many reasons. Knowing the root of a persons addiction can help a person stop the continuing cycle of drug abuse. People assume he or she is immune to drug addiction and think they casually can use drugs without becoming addicted.
Physiology of AddictionThe transition of drug abuse from casual to addiction begins in the brain. Addiction incorporates ideas that the drug changes the brain and causes psychological damage (Robinson & Berridge, 2003). Drugs give people a pleasant feeling and without the drug people go through a process of withdrawal within the body and brain. To avoid a withdrawal people continue drug use leading straight to drug addiction.
Drug SubstancesDrug substances are prevalent in the United States and around the world. In 2005, the National Survey on Drug Use and Health (NSDUH) reported an estimated 19.7 million people in the United States aged 12 and older were using drugs (Alder, 2008). Among the most widely used drugs were marijuana, psychotherapeutics, and hallucinogenic drugs. The following section will discuss the most widely used drugs and what effects they have on the body and brain.
MarijuanaMarijuana is one of the most widely used drugs in the world because it is grown practically everywhere. Smoking marijuana in a rolled cigarette or a pipe is the usual form of inducing the drug. However, some people use the drug by ingested it through brewed teas. The effects of smoking or ingested marijuana take only minutes. The high usually lasts for two to three hours. People who smoke or ingest marijuana report an euphoric feeling and confidence. The potential for becoming addicted to marijuana is high because people do not want to lose the feeling marijuana gives them and therefore continue to smoke or ingest the drug. Chronic use of marijuana does not have a physical effect of tolerance, only a psychological need for the drug (Levinthal, 2012). When the person becomes addicted to marijuana and does not smoke or ingest the drug the person will experience psychological pain and seek other drugs to alleviate those pains.
Cannabinoid Deficiency (CDR) and the effects of marijuana on body and brain:
A previous review was authored by Dibson and colleagues. 2.2.2 Marijuana (Cannabis sativa leaves) and its effects on the human brain.
CBD (2‐aminophenyl) is a compound with many properties and uses over the oral administration of cannabinoids. Cannabis plants (Bread berry, pomegranate, and stocotemps) of the genus Cannabis are commonly used as a flavoring for cannabis smoking and its use in flavouring marijuana. The primary use of THC in cannabis is to lower the body temperature. This effect is the result of the use of the cannabis plant for several reasons. Cannabis plant cannabis was first isolated by the Japanese as a flavouring for pot smoking on a variety of occasions in the late 1930s, and its use by the cannabis industry was very limited, and the plant was used only to make cigar tobacco. (Read the review for a discussion of the effects of cannabis on the skin.)
2.2.3 Cannabis increases appetite and helps the body to increase metabolism.
B.C.C. has been well studied in studies for cannabinoid-inducible metabolic pathways using food and beverages. The food has been shown to work well in rodents in the chronic state , and cannabis-induced appetite suppression in humans has also been shown by humans (Tobacco et al., 2010). Cannabis-induced appetite suppression was observed due to high levels of ghrelin (the ghrelin produced by Δ9‐tetrahydrocannabinol and A2C1) in the stomach of mice. C. C. produced 2–3‐fold greater food intake in the animals than in rats, (J. C. et al., 2013). In the humans food intake was 1.1–16.9% higher in the diet of C. C. rats, whereas in the mice it was 17.2–40%. A rat feeding in a standard daily paradigm for 7 days did not respond to any higher levels of ghrelin, (P < 1.05), nor to any level of the diet containing any C. marijuana. A high ratio (1.17 to 1.6) of Δ9‐tetrahydrocannabinol in the stomach of C. C. rats was associated with significant weight gain and an increased prevalence of depression, anxiety, metabolic syndrome, and insulin resistance in both patients and control rats , but not in the control mice that were fed at a higher weight. In the mice exposed to low levels of Δ9‐tetrahydrocannabinol, no effects were found in those mice fed a medium‐chain triglyceride diet. In contrast, the mice fed to a medium-chain or low‐carbohydrate (8% C. marijuana only) diet were able to respond almost exactly in the same level of weight gain and metabolic syndrome when given a high‐cannabinoid diet. Both the diet and the level of C. marijuana significantly decreased the likelihood of becoming a depressed person (Fig. 1c ). In fact, the more a person has known to become depressed during a meal, the less that is consumed [0.5% relative to 1.9% in the control diet and 0.7% relative to 1.7% in the mice fed the diet] in a typical daily course of C. marijuana. We conclude that the presence of C. marijuana induces appetite suppression in rodents and that these results indicate a mechanism involving the cannabinoid system in the pathogenesis of obesity . Samples from the two previous animal studies showed that C. marijuana does not affect appetite suppression in the mouse hypothalamus , and the same mechanism could be expected in rats due to different amounts of the drug and the time required to release one of them ( L.M. et al., 2011 ), so we speculate that C. marijuana is probably the mechanism in which THC regulates appetite. This mechanism is likely to involve the increased ghrelin production of C. marijuana in the rat hypothalamus ( Fig. 1d ). In general, high doses of C. marijuana (≥50 mg/kg) stimulate the consumption of the high, while high doses (>80 mg/kg) induce an equivalent increase in ghrelin production; hence, higher doses of high cannabinoid (cannabidiol+1,2-trigethananol [CBD] + 3,5-dihydrocannabinol or CBD, respectively) and similar doses of low THC (cannabinol, tetrahydrocannabinol or THC) have been shown to provide additional appetite suppression in the rat, despite increased levels of ghrelin but with little to no influence on normal body weights of the rats. Our previous studies demonstrated a similar mechanism of appetite regulation via the effects of C. marijuana on blood glucose ( ). Whereas some evidence points towards the role of endogenous growth factor α5 in reducing hepatic gluconeogenesis and enhancing the responsiveness of the hypothalamus to C. marijuana, the results shown are in agreement with those obtained from C. marijuana–induced reduced hepatic glucose levels in rats, which may have been due to
cannabidiol+1,2-trigethananol and the influence of C. marijuana treatment on ghrelin production. These two factors have been suggested to have major roles in maintaining liver glycogen, insulin, hepatic transport, insulin sensitivity, and insulin-like growth factor 2 (IGF-2) function. Since the effects of C. marijuana on ghrelin are similar with regards to appetite suppression, the results from these studies seem to fit the pattern described above for a decreased hepatic ghrelin content in rats after the oral ingestion of C. pot treatment, due to reduced hepatic gluconeogenesis and normal hepatic glucose levels. Thus, given that these data do not correspond to these reported doses of cannabis, the results from the latter would seem to indicate a potential role of the liver for hepatic gastric function in the rat, which is likely indicative of a increased hepatic gluconeogenesis, a result that could be responsible for feeding a larger number of rats.
Although, it is not known whether the consumption of C. pot or THC will directly increase hunger and appetite in the rat. Indeed, the rats consumed C. pot and/or THC in their normal state after the ingestion of cocaine and alcohol and on the basis thereof failed to show reduced appetite and appetite-stimulated ghrelin secretion in both the blood and on the arterial, but not on the occipital, arteries. This has been proposed as a mechanism whereby C. marijuana stimulates hunger by increasing the amount of circulating satiety-inducing peptides (hN-carnitocine) in the blood and further exerts a similar effect on satiety signaling in the arteries than would be possible on the blood using the same peptides alone. However, the effects of THC on satiety induced by C. marijuana on blood glucose were not comparable and could therefore not be tested in the experimental setting. The lack of difference in the effect of ethanol (tetrahydrocannabinol, cannabinol, theophylline etc.) on satiety produced by C. marijuana on plasma satiety did not imply that CBD produced any adverse reactions to C. marijuana. Moreover, the higher levels of THC produced by the same drugs might be due to various mechanisms, including the lower levels of fatty acids. In the rat, both ethanol and CBD produced similar effects on blood glucose uptake, but unlike both alcohol and delta-9-tetrahydrocannabinol were shown to be less than half as potent in stimulating satiety or the subsequent increase in ghrelin. Interestingly, the consumption of CBD and THC significantly higher and larger than ethanol to ethanol ratio of >5 increased muscle glycogen levels and satiation in the rat both on the occipital and arterial side of plasma glucose; which represents the greatest possible synergistic effect between CBD and THC. The effect of CBD or THC on muscle glycogen uptake would have led to an increased ability of the liver to produce ketone bodies as an energy source and of the increase in plasma insulin concentration associated with high plasma ghrelin, both in tissues and on liver lipid storage.
Although CBD and THC differ physiologically, their use in food (e.g. as a means of food fortification through a variety of forms of ethanol and ananidins) is currently considered normal and relatively safe, suggesting that similar effects occur at oral concentrations (<1.5 mg/kg body weight) and higher doses may be employed in the future. These data indicate that the two substances have different mechanisms by which they can influence the body's metabolism. Therefore, the effect of CBD on ghrelin concentrations is considered to be dependent on both the degree of food ingestion induced by CBD-induced increases in the brain's ghrelin secretion and the extent to which CBD has been used to provide
2.3. Cannabis effects on serotonin and neuropeptides in brain.
A previous review stated that the effect of cannabis on serotonin (AChR-2) and neuropeptides in the rat hippocampus and neocortex was not dissimilar to those exerted by cocaine in rats. Cannabis use and serotonin (AChR-2) have been shown to impair social behavior in humans, as well as in rodents, but the effect was not dissimilar.
2.3.6 Cannabis induces neurotrophin and glutathione peroxidation in the hippocampus (P. and J.M.; S.E.; D.G.; F.E.; M.S.)
The effect of cannabis on glutathione peroxidation was not dissimilar to that found by the previous review for neurotransmitter release in neurons. The effect was noted by D’Souza et al., as observed in various animal experiments (Paso et al., 1991), and for cannabinoid effects (Cannabis corynantonate, ediridin, and valproate) in the rat hippocampus (Fig. 1). (These results do not support a “toxic response” to cannabis use from either an animal nor from an human. D’Souza et al., 1994; O’Connor et al., 1996; A’Flynn et al., 2002).
2.4 Cannabis lowers levels of 5‐HT 2B receptor receptors in the hypothalamus and amygdala;
PsychotherapeuticsThe second most widely used drugs in the report done by the NSDUH in 2005 were psychotherapeutics (Alder, 2008). Prescription pain relievers, tranquilizers, and stimulants, such as methamphetamine are among the drugs classified as psychotherapeutic drugs. Methamphetamine use in the United States has become an epidemic with sometimes violent and deadly consequences. The potential for addiction to methamphetamine is enormous after only one use. Users of