1 Vudojinn

Paramethoxyamphetamine Classification Essay

Drugs, Alcohol and Other Means to Induce Hallucinations, Ecstasies or Euphoria

To seek help in overcoming an addiction, click here.
To reorder your life or find support groups, click here.

Education is the key to reducing drug abuse among young and old alike. Only education in our schools, churches, the media and the Web can bring to potential users and parents concerned for their young concrete information on consequences, detection, traffic, treatment and other aspects of the drug problem. Absolute honesty is necessary. Our kids are smart and recognize when they are being manipulated; information presented to influence behavior is readily discernible and just as readily dismissed.

Begun in October 2000 by Ken Wear. Completeness and accuracy will require extended time, research, and cooperation of others possessing information. I solicit your help. To reach me, click here for e-mail form.

For indications a person may be addicted, click here.
For help with addiction and treatmentclick here
To help reorder your life or locate a support group click here
The Web has grown tremendously since I undertook this page; it is invaluable, but start here.
For notes on the politics of drug abuse, click here; on drugs and life's game, click here; on delivery of educational information click here.

How to use: Search for the topic or name of the substance of interest and then use the link (if any). To return to the point of linking, use the BACK button on your monitor screen.
USE OF COLOR: Red for the greatest harm or more dangerous, blue for definitions, green for street names of drugs and violet for proper names of drugs and for headers.

A high may be characterized as a brief euphoric relaxing of inhibitions, as well as reduction of mental awareness and physical control; in moderation said to encourage social intercourse; often reduces libido. For a discussion, click here.

Absinthe: a strong alcoholic liqueur, green in color and very bitter is taste. Diluted with cold water poured over a spoonful of sugar into a shot of absinthe; solution turns opaque white as the essential oils precipitate out. Some ascribe aphrodisiac and narcotic properties. Illegal in the U.S. because most brands contain artemisia absinthium.
Acid: LSD
Actiq: an opioid, (registered) trade name for fentanyl
Addiction: the condition of having given oneself over to some strong habit. For a discussion, including signs to look for and dealing with addicts, click here. (Also defined as an uncontrollable craving, seeking or continued use)
Alcohol: Potable alcohol is ethyl alcohol; methyl alcohol is poisonous. �Moonshine� (private distillation, illegal when unregulated, untaxed and sold for profit) often has ingredients added to provide �kick� and that may be medically dangerous.
Ethyl alcohol and beverages containing it are regulated, sold and taxed as recreational drugs; regulations differ in various states and communities.
Some individuals have a genetic predisposition to alcohol abuse -- it runs in families; for them it is wise to avoid alcohol altogether.
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Alcoholic beverages: For a partial list (no recipes) click here.
Alcoholism: Addiction to alcohol. For a discussion, click here.
Amphetamine: (C10H15N). Colorless, volatile liquid (C9H13N in sulfate or phosphate form). Stimulates central nervous system; used to enhance performance. Induces feeling of high energy and loss of appetite. Became popular in U.S. in 1930s when Cocaine was illegal and amphetamines plentiful, legal and inexpensive. See methamphetamine.
Angel dust: PCP
Ativan: Trade name for benzodiazepine
Barbiturates: Class of drugs (salt or ester of barbituric acid C4H4


3.1. Caffeine

Caffeine is a natural alkaloid found in plants, exactly 1,3,7-trimethylxanthine. Coffee and tea, the most widely consumed psychostimulants in the world, contain several chemical components that can be responsible for beneficial and adverse health effects, including caffeine and antioxidants (e.g. polyphenols, catechins and flavonoids) and other unidentified substances that activate the sympathetic system [11]. In Europe, the typical dose for a cup a coffee is 60-70 mg of caffeine, and about 35 mg for a cup of tea, while a glass of coca cola contains about 46 mg and an energy drink about 80 mg [12].

In the United States, the average consumption of caffeine is 280 mg per day, which is the equivalent of 2 cups per day. People taking four or more cups are considered as heavy coffee users. Coffee is preferred to tea in most developed countries (except in England and Ireland) where 71.5% of the worldwide coffee consumption [13] is used. Tea is preferred to coffee in the developing countries, particularly in Argentina, Chile, Paraguay and Uruguay, and in Asia. These countries count for 76.6% of the tea consumption in the world. The total quantity of tea consumed is much higher than coffee, and tea is thus the second beverage consumed after water.

Caffeinated soft drinks are also emerging source of caffeine intake, especially for teenagers. The caffeine content in these drinks can vary between 50 to 500 mg per can or bottle [14]. We will not discuss here substances that can be added to caffeinated beverages and potentially change their health properties, such as cream, milk or sugar.

Caffeine is rapidly absorbed and undergoes demethylation in the liver via the enzyme cytochrome P450 1A2. Defect of this enzyme is associated with prolonged caffeine half-life [15]. The genetic polymorphism in this pathway may explain differences in outcomes of studies about caffeine and its health consequences. Once in the blood, caffeine exerts its action as a potent antagonist of central and peripheral nervous system adenosine receptors. As these act as inhibitory neurotransmitters, caffeine stimulates excitatory neurotransmitters [16].

Several benefits can be attributed to caffeine-containing beverages. Neuro-psychological effects of caffeine are increased alertness, energy and concentration, especially if consumers are tired or night workers [17,18]. It has been suggested in a randomized study that caffeine also improves mood and working memory [19], even if some authors have postulated that these effects would be attributable to the reversal of effects due to caffeine withdrawal [20].

Somatic consequences of caffeine include a proven analgesic effect for tension or migraine headache at a dose superior to 65 mg [21], even if caffeine is also a potential cause of chronic migraine and rebound headache if chronically consumed [22]. A dose-effect relationship for the protection towards Parkinson’s disease [23] has been suggested, as is an association with a reduction of risk for Alzheimer’s disease [24] (relative risk of 0.7). There might also be also a protective effect of caffeine for myocardial infarction, even if it can trigger arrhythmia [25] and coronary events [26] in very susceptible individuals, probably depending on the personal caffeine metabolism (slow metabolisers being at higher risk). Caffeine containing beverages can raise the blood pressure in non-tolerant individuals, but has no long term effect on blood pressure in daily consumers [27]. Concerning the glucose metabolism, several prospective long term studies have shown that consumption of coffee or tea is associated with an improved insulin sensitivity, also in the diabetic patient [28,29], with a clear preventive action against type 2 diabetes, in normal subjects or in those with impaired glucose tolerance [30,31]. A strong inverse dose-dependent relationship between coffee drinking and alcoholic cirrhosis has been shown in a large US cohort study (relative risk ranging from 0.6 95% CI 0.6-0.8 for 1-3 cups per day to 0.2, 0.1-0.4 for drinkers of more than 4 cups) [32]. Coffee consumption seems to reduce the incidence of gout in a dose dependent manner [33]. Physical capacities are also ameliorated by caffeine [34] with a maximal benefit at a dose of 2-3 mg/kg. High caffeine intake used to be considered as doping, with a limitation of 2 to 3 cups of coffee per day (or equivalent), but this has been abandoned (ref: www.wada-ama.org).

Considering all-cause mortality, it has been shown in large cohort studies [35] (more than 100,000 persons followed for 18 years at minimum) that all-cause mortality was reduced at a relative risk of 0.8 for men (95% CI 0.62-1.04) and 0.83 for women (95% CI 0.73-0.95). The borderline statistical insignificance for men warrants further study. Most of this mortality reduction was due to a diminished cardiovascular mortality. There would be reasons to postulate that caffeine decreases risk of cancer because of its antioxidant properties, but this never has been proven scientifically, and study results are conflicting [36].

Negative consequences of caffeine include an increased risk for osteoporosis, and possibly for bone fracture, in particular for women with low calcium intake and high caffeine intake [37,38]. A link with increased risk of anxiety symptoms has been suggested, but evidence of causality is lacking. Nevertheless, caffeine has been associated with anxiety, nervousness, irritability, insomnia and even panic attacks [39,40]. In people suffering from anxiety or stress disorders, caffeinated beverages should be discussed, and discouraged if symptoms are found to be worsened by caffeine.

The abuse or dependence potential of caffeine has not been convincingly demonstrated [41], and there is little evidence to say that tolerance develops [42]. For these reasons, no diagnosis of caffeine dependence exists in the Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) [43]. Still, it is clear that a caffeine withdrawal syndrome does exist. It is benign, with the principal symptoms being headache, tiredness, decreased attentiveness and contentedness [44]. This happens to 50% of people who stop drinking coffee; the most frequent symptom is the headache. It may happen from a dose as low as 100 mg/day and develop within 12 to 24 hours after the last dose. It lasts normally 1 or 2 days, but may persist as long as 9 days. A progressive reduction of caffeine intake is recommended if abstinence is planned, but no substitution is necessary if an unplanned abstinence occurs.

Summing up: caffeine has probably more advantages than risks for health, in the general population. Only patients suffering from important or unstable coronary heart disease or those at risk for or having osteoporosis should be advised to take no caffeine or in small amounts (1 to 2 cups a day). For persons with an anxiety disorder, a less clear recommendation can be made, because of a lack of arguments for a causal relationship.

3.2. Nicotine

As discussed in the Introduction, the prevalence of use of nicotine is basically that of tobacco, which makes nicotine the second most used psychostimulant. It is a natural alkaloid component found in tobacco leaves. Each puff of cigarette contains about 50 micrograms of nicotine. Nicotine can be absorbed through the lung and the gastro-intestinal system, but its absorption through the oral mucosa has been shown to be the principal route of absorption for smokers who do not inhale and for smokeless tobacco users [45].

The half-life of nicotine is two hours. Approximately 80 to 90% of nicotine is metabolized by the lungs, liver and kidneys. Its principle metabolite cotinine, which has a half-life of 15 to 20 hours, is active with stimulant properties. Approximately 17% of nicotine is excreted unchanged in the urine and nicotine can be found in the milk of lactating women. The metabolism of nicotine explains a racial difference in tobacco related disease. Black people have higher nicotine intake and slower cotinine metabolism, accounting for more tobacco related diseases, even with the same daily intake of nicotine [46]. An important variability exists in nicotine metabolism through the cytochrome P450-2A6 pathway, resulting in important differences in plasma nicotine and cotinine concentration, for people taking a similar dose of nicotine. A few individuals have slow metabolism, but uncertainty exists about a possible link with susceptibility to nicotine addiction [47]. The nicotinic receptor genes polymorphism account for different nicotinic acetylcholine receptors and an important variability in addictive potential for nicotine and smoking [48]. Nicotine is a hepatic enzymatic inductor and when stopped, certain drugs can require a dosage reduction. These include acetaminophen, caffeine, imipramine, oxazepam, pentazocine, propranolol and theophylline [49]. A decrease in circulating catecholamines may warrant a decrease of dose of adrenergic antagonists such as prazosin and labetalol, or an increase in dose of adrenergic substances such as isoproterenol and phenylehrine [50]. An increase in insulin absorption also exists and may necessitate a dosage reduction to avoid hypoglycemia.

Nicotine is a potent ganglionic and central nervous stimulant. It binds to nicotinic cholinergic receptors that are located in the brain, autonomic ganglia, adrenal glands and at neuromuscular junctions [49]. Nicotine induces a complex pattern of mixed sympathetic and parasympathetic responses, but its resultant major effect is sympathetic neural stimulation. It can be central or peripheral, including a catecholamine release from the adrenal glands and a direct release from vascular nerve endings. It also enhances the release of the following neurotransmitters: epinephrine, norepinephrine, dopamine, acetylcholine, serotonin, vasopressin, glutamate, nitric oxide, calcitonin growth-related peptide and β-endorphin [51]. The highly addictive potential of nicotine has been linked to its dopaminergic properties [52], and its rapid and short action. Nicotine improves cognitive performances by improving learning, memory and attention.. These effects of nicotine have been exploited in the treatment of neurodegenerative diseases, as for example in the treatment of Alzheimer’s disease patients where nicotine has been shown to attenuate the decline of the attention deficits symptomatic of this disease [53].

When considering health effects of nicotine, most studies concern smokers, so the independent effects of nicotine and smoking cannot always be separated. In the following paragraphs we have tried to separate both effects when possible. Nicotine increases cardiovascular risks by itself, without the known negative effects of smoke. It transiently increases the blood pressure with approximately 5 to 10 mmHg [54] and the heart rate up with 10 to 15 beats per minute [55]. Despite the acute effect on the arterial pressure, habitual smokers do not have higher blood pressure than nonsmokers [56]. It may be related to the decreased body weight of nicotine users, and a vasodilator effect of cotinine [57]. The cardiovascular risk is also increased by the coronary vasoconstriction and reduced coronary blood flow [58]. From studies conducted with smokers, the effects of nicotine on the cerebral circulation are both vasoconstriction and vasodilatation [59]. The vasoconstriction is partially due to thromboxane A2 release, the vasodilatation by the local formation of nitric oxide. Another deleterious effect of nicotine is a hypercoagulable state, due to platelet activation and increased fibrinogen level [60,61]. All this has a clinical importance because thrombosis is a major factor in vascular events in smokers [62]. Cigarette smoking increases the risk of myocardial infarction and sudden death more than angina pectoris does. Nicotine seems to play a role in this pathophysiology [63]. After a coronary event, smokers who continue to smoke after thrombolysis have a very high risk of reinfarction or reocclusion [64]. The risk of continued smoking in a stented coronary lesion is less clear [65]. Another way the cardiovascular damage is increased is through the endothelial dysfunction induced by nicotine or smoke. Even without atherosclerosis smokers have a paradoxical response to acetylcholine, which appears to result from impaired release of nitric oxide (NO) by the endothelium [66]. The vascular protector roles of NO are vasodilatation, reduction in platelet aggregation, smooth muscle cell proliferation, and monocytes adhesion to the endothelium.

The lipid metabolism is influenced by nicotine in the way that is largely unknown [67], but the increased cardiovascular risk seems to be independent of this change [68]. Nicotine also contributes to the development of insulin resistance. This have been suggested in a study of 40 non-obese middle-age men, in whom long term use of nicotine-containing gums was associated with the onset of insulin resistance and hyperinsulinemia [69].

The cardiovascular safety of nicotine replacement for smokers willing to quit has been suggested through the Lung Health Study cohort [70]. In this study on 5,887 middle-aged smokers with chronic obstructive pulmonary disease, no difference in hospital admissions for cardiovascular events was found between smokers and those who quit smoking with nicotine replacement. Two other controlled trials of nicotine replacement also provided no evidence for an increase in coronary events in patient with coronary disease [71,72].

Although there is no definite evidence that nicotine itself could induce cancer, several studies suggest that nicotine might play a role as a carcinogen, independent of smoke. This has been supported by the fact that nicotine promotes in vivo the growth of cancer cells and the proliferation of endothelial cells [73]. Different studies reported that nicotine suppressed apoptosis induced by different stimuli such as chemotherapeutic agents in Non Small Cell Lung Cancer treatment [74]. This explains maybe why the efficacy of the treatment of a cancer can be diminished by nicotine.

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