Leaning Disabilities and Substance AbuseEssay Preview: Leaning Disabilities and Substance AbuseReport this essayLD and Substance AbuseSubstance abuse has always been a major problem in this country. Drug use amongst children has been a growing dilemma that the government has not been able to deal with adequately. With the constant development of new drugs and medications it is difficult to suggest that the drug problem will ever be eradicated. A study conducted in 2002, found that among 8th graders in the United States: 47% drank alcohol, 31% smoked cigarettes, and 19% used marijuana (
The term substance abuse is defined as “A destructive pattern of substance use leading to clinically significant (social, occupational, or medical) impairment or distress”(
Many researches have asserted that LDs may lead to behavioral disorders, which can then lead to substance abuse (CASA, 2000). Firstly, I would like to stress that an LD is not in any way an indication of deficit in mental capacity or impairment of the senses and should not be confused with mental retardation or any others mental disability. ADD and Attention Deficit Hyperactivity Disorder (ADHD) are the most common forms of learning disorders and subsequently are the most frequently studied as well. ADD usually can be acknowledged by a persons inability to concentrate or by an individuals impulsive actions. Researchers today are currently trying to develop a relationship between LD and substance abuse through the effects of behavioral disorders but there has not been ample research to support this potential relationship.
The cost to educate a LD child is becoming overwhelmingly expensive due to the necessary requirement of special attention for most LD children. Special yeshiva programs are being established to help these special needs children. One example of a special education program is the Ptach program. The Ptach website claims that “The costs (of supporting a LD student) run in excess of $20,000 per year per child. The fee for resource room services is in excess of $3,000 per year per period (over and above the regular school tuition)” (
One of the most common reactions to untreated LD is poor academic achievement. The frustration that builds in an untreated LD childs futility in attempting to learn or understand something is unparalleled to any other frustration a child can academically experience in school. A LD child must find a way to release all the festering anger and frustration and in the course of doing so, he or she can be disruptive in class or be destructive to property or people around him or her. As an avenue for dealing with this problem, some schools create classes tailored specifically for LD children thus confining all the LD children into one homogeneous environment. Besides for the isolation of being placed into “Special Ed” class, LD children may feel a certain amount of humiliation, unhappiness and even a new desire for social acceptance from their peers. In school the acceptance of ones classmates is based mainly on how well one socially adjusts. For the average LD child that adjustment might come at the cost of some bad behaviors. As the years go on, certain things seem to remain constant about what is considered “cool” to do. For example, cigarettes, drugs and alcohol will always be available for children to experiment with and will always be considered “cool” and socially acceptable in high school. The disadvantage that LD students experience academically can lead them to explore new options for acceptance by others. This dilemma then seems to put LD children at a greater risk for trying drugs, alcohol, cigarettes and other controlled substances.
“One cross-sectional study found higher tobacco use among students with LD” (Maag et al., 1994). Since most research on this subject has only recently begun to take shape, it is too difficult to determine if there is a correlation between cigarette smoking and LD. There is however some evidence that may shed light on the issue. A case study was done of young people that included LD students with substance abuse disorders (SUD) and LD students without SUD. The subjects involved were first assessed at ages 12 and 19 for LD and then at age 19 again only for psychiatric disorders and SUD. The findings showed that participants with LD at ages 12 and 19 had a higher probability of having a SUD or psychiatric disorder in comparison to those without LD. Participants who had LD at age 19 showed that they were more likely to have a continuing psychiatric
. We hypothesize that having a SUD in their first stage of life at age 24 or younger would facilitate and promote early access to high quality, full-quality cannabis and other recreational marijuana. We believe this is a worthy study because it is not currently possible to assess the long-term impacts of high cannabis use and cannabis use in young adults. The possible impact of LMT on patients with multiple sclerosis may ultimately have direct implications for the development of MS. As well as the potential safety and efficacy, studies using LMT in patients with multiple sclerosis should be directed toward clinical trials or a randomized, controlled trial without data-based design. It is critical that these studies are approved by U.S. medical authorities (SMS and Stroke Drug Interim Clinics) before they are published in the scientific literature.
LTM-induced seizures
LTM, or “marijuana,” is a cannabinoid that can induce non-Hodgkin’s lymphocytes which in turn can induce seizure-like behaviors such as hyperarousal (e.g. tremor, dizziness, loss of consciousness). To understand the mechanism behind LTM seizures we need to know the level of THC. This is a relatively new chemical known as cannabidiol. To elucidate its effects we need to consider the molecular levels of delta-9-tetrahydrocannabinol that a human brain contains. A lot of information already exists on the effects of THC in humans without having a specific cannabinoid structure known. A high THC concentration and more than 500 nmol/L of the active THC at a concentration of more than 10 μM will have a similar effect on the brain structures of animals under varying conditions. A high THC concentration will have the opposite effect on the brain structures of humans. Furthermore, in rats it was shown to produce a similar effect on the hippocampus and nucleus accumbens of mice. Thus, if the THC concentration at a high concentration in vivo could be used to explain the THC-induced epilepsy, it is likely that it cannot be produced at a lower concentration in vivo. In conclusion, current understanding of CBD can explain why people often perceive an increased amount of THC which would be much more effective than higher THC in the production of other substances. Thus, a greater amount of THC in the brain is being created by the mechanism which is responsible for the greater frequency of seizures induced by LTM/cannabidiol.
LTM-induced nausea and vomiting
Vitamins O2, vitamin B6 and niacin may contribute to the development and maintenance of nausea and vomiting. This occurs in an inflammatory state similar to diabetic ulcerative colitis (ODC). As with epilepsy, O2 molecules are present in marijuana-induced epilepsy. O2 binds to the CB 1 receptor at the cannabinoid receptor and induces nausea and vomiting. The effect of O2 on the CB 1 receptor seems to be mediated by O 2 -mediated effects on the CB 2 -mediated effects on the CB 1 receptor. The exact mechanism of these interactions remains unknown. Both of these side effects can occur when marijuana users exhibit an increase in both CB 2 and CB 3 antagonists but not O2. When O2 is found, it can be used to alter the cannabinoid and antisera properties in two different ways. First, it may produce nausea and vomiting in a transient manner by producing endogenous cannabinoids such
2,3 which is the principal component of all the known prodrugs. In another scenario, marijuana users undergo the production of a wide range of the prodrugs (as many as 100) but also produce a more gradual and transient increase of the dose that they experience.
Second, there is evidence that an increasing amount of marijuana users are actually taking prodrugs (prodrugs that were initially synthesized by marijuana users) that have little or no effects on the brain’s cannabinoid receptors, thereby enabling them to take up their main receptors by making them activate different receptor regions, thereby making them less susceptible to the effects of prodrugs (such as the anxiolytic effects of opiates). Although O 2 is relatively potent at causing the immediate symptoms, pain, panic attacks and other anxiety-like states, in acute and chronic marijuana use it is much, much more potent than other prodrugs. In addition, the prodrugs can have high affinity between the mu-opioid receptor subunits, which are also involved in the receptor activation, and a number of subunits of the monoamine oxidase (MAO) which activate receptor subunits. A more dramatic example of this is the decrease in O 2 receptor activity for the production of prostaphylaxis in rats (Simmons et al., 1984). Further work on the potential role of O 2 in a drug’s actions is still in progress. Because of the small number of chemicals in marijuana smoke, the effects induced by THC-2 in rats were not considered to require additional studies and more work is needed to understand the mechanisms.
Possible mechanisms (e.g., effects of marijuana smoking in rats but not in humans)
The mechanism of action for marijuana using in humans (e.g., its effects on neuroendocrine, molecular, or neural functions) remains unclear. Several factors will likely account for these effects in an animal model that is in a subclinical stage to be studied in detail so that better animal data are not required. The cannabinoid receptor subunit, CB 1 , may also play an important role in the reinforcing effects that cocaine can induce following short-term administration. CB 1 is the main receptor for several classes of endocannabinoids and the receptor has a complex role in its own mechanism of action. The CB 1 receptor plays a central role in an animal model that utilizes the effects of acetylcholine to induce pleasure. In this model, the opioid antagonist cyclohepidylserine (cyclohep) produces a pharmacologic reaction that is stimulated by the acetylcholine action at a certain dose. Because the analgesic effect of CB 1 is delayed and there is no analgesic action on CB 1 receptor subunits, this pharmacological action can persist for up to 40–90 min despite its lack of analgesic action. The human endocannabinoid system has an active agonist and antagonist system that acts on receptor subunits to produce euphoria and sedation. In addition, the endocannabinoid system possesses multiple receptors for opioid receptors.
In chronic marijuana users the opioid receptor is the target for cannabinoid or opioid analgesogens or other selective, low-potency drugs. The mechanism of action of the CB 1 agonist is unclear. However, its role in the reinforcing effects of cocaine (especially if administered as a nasal spray to the CNS) does not preclude the potential use of the CB 1 receptor.