<p>meh, I'll just take post #100 here and now my post count is 700.</p>
<p>then why do our brains have THC receptors?</p>
<p><strong>to atomic</strong> dude. you so just described exactly how i feel when im high. lol.</p>
<p>Sure - these articles are from ProQuest and ScienceDirect.</p>
<p>Search terms: amphetamines methylphenidate addiction</p>
<p>Here's one from Cochrane Library - - search term methylphenidate:</p>
<p>Rush et al., (2005) that found that kids with ADHD are at increased risk of smoking, and methylphenidate doses are directly related to the numbers of cigarettes that are smoked, carbon monoxide levels, and puff counts. The same correlation is found with d-amphetamine (Dexedrine) use.</p>
<p>Rush, Higgins, Vansickel, Stoops, Lile, & Glaser. (2005). Methylphenidate increases cigarette smoking. Psychopharmacology, 181. Cochrane Library database.</p>
<p>Methylphenidate (Ritalin) abuse does seem to be a problem. McCabe et al.(as cited by Wu, Pilowsky, Schlenger, & Galvin, 2007) found that "close to one fourth (23%) of the students who received prescription stimulants reported being approached to divert (i.e., to sell, give, or trade) their stimulant medications."</p>
<p>Babcock and Byrne (as cited by Wu et al.) found that more than 16% of students attending a public college had misused methylphenidate.”Wu et al. examined a survey of 67,784 Americans aged 12 and older. They found that: “greater stimulant misuse was found among young adults, whites, American Indians/Alaska Natives, and those reporting more than one race. A very high prevalence of any stimulant misuse was also observed among those who had been arrested twice or more in the past year (28% among males and 40% among females) or who met the criteria for an alcohol or drug use disorder in the past year (ranging from 24% to 54%). There were few gender differences in the correlates of any stimulant misuse.”</p>
<p>Wu et al. continued: “Researchers have noted that early aggression or defiance often precedes illicit drug use (Dawes et al., 2000 and Neumark and Anthony, 1997). Assault weapon charges and delinquent acts have been reported among meth misusers in the United States (Zweben et al., 2004) and elsewhere (Yen et al., 2006). The high lifetime prevalence of stimulant misuse reported here is disturbing because of its negative medical consequences, associations with other drug use, and reported association with HIV-related risky sexual behaviors.”</p>
<p>“Methylphenidate, amphetamines or diet pills, and Dexedrine® were the prescription stimulants most likely to be misused, and there were gender differences in the stimulants of choice. Compared with female misusers of meth and prescription stimulants, male misusers of such stimulants were more likely to misuse methylphenidate (82% versus 65%), but were less likely to misuse diet pills or amphetamines (37% versus 49%).”</p>
<p>“almost all stimulant misusers had used alcohol, and the vast majority also had used multiple illicit drugs, such as marijuana, hallucinogens, cocaine/crack, inhalants, pain relievers, and tranquilizers, with the prevalences ranging from 34% to 99%. Meth misuers generally were more likely than misusers of prescription stimulants only to have ever used three or more illicit drug classes.”</p>
<p>Wu, Pilowsky, Schlenger, & Galvin. (2007). Misuse of methamphetamine and prescription stimulants among youths and young adults in the community. Drug and Alcohol Dependence, 89, 195-205. ScienceDirect database.</p>
<p>Collegeguy - are you suggesting that since our brains have THC receptors, we should use cannabis for recreational purposes? Do you also think that since our brains have opioid receptors, we should use heroin?</p>
<p>Are you implying that they exist for medical purposes only?</p>
<p>Hmm. Ok - so do you think that the presence of opioid receptors and THC receptors indicate that recreational drug use is somehow biologically ordained?</p>
<p>Where would you draw the line? Do you think pregnant women should use marijuana and heroin since they have these receptors?</p>
<p>"A smokeless cannabis-vaporizing device delivers the same level of active therapeutic chemical and produces the same biological effect as smoking cannabis, but without the harmful toxins, according to University of California San Francisco researchers.</p>
<p>Results of a UCSF study, which focuses on delivery of the active ingredient delta-9-tertrahydrocannibinol, or THC, are reported in the online issue of the journal "Clinical Pharmacology and Therapeutics."</p>
<p>"We showed in a recent paper in the journal 'Neurology' that smoked cannabis can alleviate the chronic pain caused by HIV-related neuropathy, but a concern was expressed that smoking cannabis was not safe. This study demonstrates an alternative method that gives patients the same effects and allows controlled dosing but without inhalation of the toxic products in smoke," said study lead author Donald I. Abrams, MD, UCSF professor of clinical medicine."</p>
<p>"Don't children born to pot-smoking mothers suffer from ``Fetal Marijuana Syndrome?''
If a fetal cannabis syndrome exists, cases are so rare that it cannot be demonstrated. Many mothers use marijuana during pregnancy -- it controls the nausea called `morning sickness' and many say it actually increases the appetite and reduces stress. This is especially important in less developed countries, where modern medical care is not as easily available, but even so, the benefits of responsible marijuana use may outweigh the risks even under modern medicine.</p>
<p>Studies conducted in Jamiaca have shown that mothers who smoke marijuana have healthier children, but this may be due to the extra income generated by marijuana dealing and other factors. It has been a common ploy in the War on Drugs to claim that marijuana, and especially cocaine, causes birth defects or behavior problems like alcohol does. This scares caring mothers into thinking drugs are `evil.' The claims are not based on valid scientific research -- many of them do not even consider the life-style or living conditions of the mothers before pointing at drugs with the blame.</p>
<p>Obviously, pregnant mothers should not smoke as much pot as they possibly can. If marijuana is abused, it may hurt the health of both mother and child. Delta-9-THC does cross the placenta and enter the fetus. Oddly, though, the marijuana metabolite, 11-nor-9-carboxy-delta-9-THC does not, and the fetus does not break delta-9-THC down into 11-nor like the mother's body does, so unborn children are not exposed to 11-nor. The third trimester is the time when the child is most vulnerable. Parents should bear these facts in mind when they make decisions about using cannabis."</p>
<p><a href="http://www.bigeye.com/marijuana.htm%5B/url%5D">http://www.bigeye.com/marijuana.htm</a></p>
<p>Why do we have THC receptors?</p>
<p>The body does not have receptors that exclusively handle plant-derived cannabinoids. The THC receptors are part of the bodys endogenous cannabinoid system. Since 1992, several natural cannabinoids have been found in the human body, such as anandamide and 2-arachidonoylglycerol (2-AG). These ligands have been found to be important for our natural food intake regulation and energy homeostasis. Additionally, the endocannabinoid system includes an antagonist, virodhamine. </p>
<p>Dysfunction of the endocannabinoid is now suspected as a contributing factor for the development of diabetes and human abdominal obesity (Bluher, Engeli, Kloting, Berndt, et al., 2006).</p>
<p>Interestingly enough, researchers (Mechoulam, Berry, Avraham, Di Marzo, & Fride, 2006) analyzed human, bovine and goat milk, the food of newborns. Anandamide levels were low, but 2-AG (another endogenous cannabinoid) was present, and they found significant amounds of oleamide, 2-palmitoyl glycerol, and 2-linoleoyl glycerol. Oleamide is suspected to prevent anandamide hydrolysis and might cause increased endogenous cannabinoid levels.</p>
<p>Mechoulam et al. then studied the effects that endocannabinoids have on suckling in mouse pups. They believe that endocannabinoids, in particular, 2-AG from the pups brain which peaks on the 1st day of life, are required to initiate the suckling response/milk ingestion. We further postulate that from day 2, when the levels of 2-AG are lower again, endocannabinoids from maternal milk, maintain the suckling process.</p>
<p>Another interesting finding based on 12-day food restriction tests in mice is that diet restrictions over 12 days lowered the levels of 2-AG both in the hippocampus and the hypothalamus. . . The amounts of 2-AG in the hypothalamus depended on the severity of the diet restriction, while in the hippocampus the amount of 2-AG fell to a common level, irrespective of the diet restriction protocol. Although not conclusive, this suggests that this is part of the bodys protective system to allay hunger when food is restricted. It may also contribute to why people who start down a path to anorexia nervosa are not overcome with greater hunger as time goes on. It also helps to explain why hospice patients are said to not be hungry even though they are not eating anymore.</p>
<p>In any event, there are a variety of reasons that the body has THC receptors. </p>
<p>Medically, marijuana, hashish, ganja, and bhang (cannabis preparations) are still Category I with the DEA, a controlled substance that may not be prescribed. However, a state law in California permits patients to use small amounts of marijuana on a physicians order. </p>
<p>Other uses of these products can land you in jail.</p>
<p>References:
Bluher, Engeli, Kloting, Berndt, et al. (2006). Dysregulation of the peripheral and adipose tissue endocannabinoid system in human abdominal obesity. Diabetes, 55, 3053-3061. Retrieved from ProQuest database.</p>
<p>Mechoulam, Berry, Avraham, Di Marzo, & Fride. (2006). Endocannabinoids, feeding, and suckling from our perspective. International Journal of Obesity, 30, S24-S28. Retrieved from ProQuest database.</p>
<p>Sharkey (2006). Endocannabinoids: Biology, mechanism of action and functions. International Journal of Obesity, 30, S4-S6. Retrieved from ProQuest database.</p>
<p>Smoking pot to cope with morning sickness would be a short-sighted action.</p>
<p>“The results, controlled for potential confounding variables, show that exposure to marijuana during pregnancy was associated with subtle behavioral changes, especially in terms of arousal, regulation, and excitability, which can potentially interfere with the ability of these neonates to bond with their teenage mothers” From Barros, Guinsburg, Perez, Mitsuhiro, Chalem, Ramos, et al. (2006). Exposure to marijuana during pregnancy alters neurobehavior in the early neonatal period. The Journal of Pediatrics, 149, 781-787. Retrieved from ScienceDirect database.</p>
<p>“However, some findings are consistent. Lead and PCB's have a general effect on brain development, whilst marijuana and alcohol appear to have long-term effects specifically on attentional skills. The effects of alcohol increase with maternal age and binge drinking is more important than average intake.” Williams & Ross. (2007). Consequencs of prenatal toxin exposure for mental health in children and adolescents: A systematic review. European Child and Adolescent Psychiatry, 16, 243-254. Abstract retrieved from ProQuest database.</p>
<p>“Toddlers who were exposed to marijuana in utero appear less socially engaged and more fearful than non-exposed toddlers (Faden & Graubard, 2000). Studies also suggest that these children have greater inattention and impulsivity at 6 years of age (Leech et al., 1999) as well as diminished attention span and poor impulse control as adolescents (Fried & Watkinson, 2001).” Weiss, Jonn-Seed, & Harris-Muchell. (2007). The contribution of fetal drug exposure to temperament: Potential teratogenic effects on neuropsychiatric risk. Journal of Child Psychology and Psychiatry. Retrieved from Blackwell Synergy database.</p>
<p>“Overall, our results suggest that fetal drug exposure had a very circumscribed effect on a child's temperament at 6 months of age. Drug exposure was associated only with a child's distractibility, but accounted for a notable, moderate effect size as defined by Cohen (1987). This dimension of temperament has received strong support from previous studies in which increased distractibility and deficits in the ability to sustain attention have been found for infants, preschool and young school aged children exposed to cocaine prenatally (Bandstra et al., 2001; Coles et al., 1999; Garavan et al., 2000; Heffelfinger et al., 2002; Karmel & Gardner, 1996; Leech et al., 1999; Mayes, Grillon, Granger, & Schottenfeld, 1998; Noland et al., 2005; Nulman et al., 2001; Richardson et al., 1996; Savage et al., 2005; Singer et al., 2004). Similar difficulties with distractibility and attention have been noted for children exposed to marijuana (Fried & Smith, 2001; Fried & Watkinson, 2001; Goldschmidt et al., 2000; Leech et al., 1999; Noland et al, 2005), to opiates (Suess, Newlin & Porges, 1997), to alcohol (Burden, Jacobson, Sokol, & Jacobson, 2005; Kable & Coles, 2004; Lee, Mattson, & Riley, 2004), and to polydrug use (Butz, Pulsifer, Leppert, Rimrodt, & Belcher, 2003). Animal research provides additional evidence of attention deficits, increased reactivity, and a persistent hyperattentive response to novel stimuli in offspring who have prenatal exposure to cocaine and alcohol (Foltz et al., 2004; He, Bai, Champoux, Suomi, & Lidow, 2004; Schneider et al., 2002), with enduring effects into adulthood (Gendle et al., 2003, 2004; Hausknecht et al., 2005; Mactutus, 1999; Morgan et al., 2002). Results of these various studies suggest that distractibility and problems sustaining attention may occur from exposure to cocaine, opiates, alcohol or marijuana rather than being unique effects of any one type of substance.” Weiss, Jonn-Seed, & Harris-Muchell. (2007). The contribution of fetal drug exposure to temperament: Potential teratogenic effects on neuropsychiatric risk. Journal of Child Psychology and Psychiatry. Retrieved from Blackwell Synergy database.</p>
<p>“Prenatal exposure to marijuana, in addition to other factors, is a significant predictor of marijuana use at age 14.“ Day, Goldschmidt, & Thomas. (2006). Research report: Prenatal marijuana exposure contributes to the prediction of marijuana use at age 14. Addiction, 101, 1313. Abstract retrieved from ProQuest database.</p>
<p>“The present data provides evidence for impairments of the endogenous opioid ststem in association with in utero cannabis exposure in the human fetal brain. Maternal cannabis use was significantly associated with reduced mRNA expression levels for PENK in the putamen, increased mu expression in the amygdale, and decreased kappa expression in the mediodorsal thalamic nucleus. . . . [the results] are of significant relevance since the opioid system plays a critical role in the regulation of emotions, reinforcement, cognition, motor function and nociception.” Wang, Dow-Edwards, Anderson, Minkoff, & hurd. Discrete opioid gene expression impairment in the human fetal brain associated with maternal marijuana use. The Pharmacogenomics Journal, 6, 255. Retrieved from ProQuest database.</p>
<p>“Maternal use of any illicit or recreational drug around pregnancy was associated with an increased risk of neuroblastoma in offspring (OR = 1.82, 95% CI: 1.13, 3.00), particularly use of marijuana in the first trimester of pregnancy” Bluhm, Daniels, Pollock, & Olshan. (2006). Maternal use of recreational drugs and neuroblastoma in offspring: A report from the Children’s Oncology Group (United States). Cancer Causes and Control, 17, 663. Retrieved from ProQuest database.</p>
<p>“Maternal pregnancy use of cocaine and use of cigarettes were both associated with increased commission errors, indicative of inferior selective attention. Severity of maternal use of marijuana during pregnancy was positively correlated with omission errors, suggesting impaired sustained attention.” Noland et al. (2005). Prenatal drug exposure and selective attention in preschoolers. Neurotoxicology and Teratology, 27, 429-438. Retrieved from ScienceDirect database.</p>
<p>“Marijuana (n=44)- and nonmarijuana (n=95)-exposed fetuses had similar rates of growth with increased age. However, there was a 0.08-cm (95% CI −0.15 to −0.01) and 14.53-g (95% CI −28.21 to 0.86) significant reduction of foot length and body weight, respectively, for marijuana -exposed fetuses. Moreover, fetal foot length development was negatively correlated with the amount and frequency of marijuana use reported by the mothers. These findings provide evidence of a negative impact of prenatal marijuana exposure on the mid-gestational fetal growth even when adjusting for maternal use of other substances well known to impair fetal development” Hurd, Wang, Anderson, Beck, Minkoff, & Dow-Edwards. (2005). Marijuana impairs growth in mid-gestation fetuses. Neurotoxicology and Teratology, 27, 221-229. Retrieved from ScienceDirect database.</p>
<p>“Offspring of mothers who reported using marijuana during pregnancy were at increased risk for both subsequent initiation of cigarette smoking (OR=2.58) and marijuana use (OR=2.76), as well as daily cigarette smoking (OR=2.36), as compared to offspring of whose mothers did not report using marijuana while pregnant. There was also evidence indicating that dose–response relationships existed between prenatal exposure to marijuana and offspring's use of cigarettes and marijuana. ” Porath & Fried. (2004). Effects of prenatal cigarette and marijuana exposure on drug use among offspring. Neurotoxicology and Teratology, 27, 267-277. Retrieved from ScienceDirect database.</p>
<p>“The active ingredient in marijuana, THC, freely crosses the placental barrier and directly affects the fetus. Because most marijuana-addicted parturients also abuse other substances such as tobacco, cocaine, and alcohol, it is difficult to identify the specific effects of cannabis on the fetus.[106 and 107] It appears that chronic use of marijuana results in decreased uteroplacental perfusion and IUGR. [106 and 107] Chronic use of marijuana may alter pituitary-adrenal axis and hormone production with adverse effects on fertility and pregnancy. [107 and 108] Suppression of ovulation has been reported in association with chronic cannabis smoking. [103] Placental production of both estrogen and progesterone may also be altered. There is some evidence that chronic cannabis use may be associated with functional brain changes and subtle impairment in cognitive function. [109]” Kuczkowski (2003). Anesthetic implications of drug abuse in pregnancy. Journal of Clinical Anesthesia, 15, 382-394. Retrieved from ScienceDirect database.</p>
<p>“There was a detectable decrement in birthweight for the offspring of women who used cannabis at least once per week before and throughout pregnancy. These infants were in the region of 90g lighter than offspring of other women even when due allowance was made for maternal social background, maternal characteristics and other substance use behaviours during pregnancy” Fergusson, Horwood, & Northstone. (2002). Maternal use of cannabis and pregnancy outcome. BJOG: An International Journal of Obstetrics and Gynecology, 109, 21-27. Retrieved from Blackwell Synergy database.</p>
<p>InquilineKea wrote: "Considering that the main side effect of quitting amphetamines is the major crash - the person's probably going to be sleeping through most of the withdrawal phase anyways."</p>
<p>Please don't forget that in addition to physical symptoms, drug dependence and abuse includes psychological consequences and tolerance. The psychological addiction to amphetamines happens quickly. Detoxing the drug is one thing, but once the drug is detoxed, users want it again. Because of the rapid build up of tolerance, larger and larger doses are required. </p>
<p>Make no mistake: withdrawal is unpleasant. Users crave drugs to avoid withdrawal symptoms.</p>
<p>
[quote]
Please don't forget that in addition to physical symptoms, drug dependence and abuse includes psychological consequences and tolerance. The psychological addiction to amphetamines happens quickly. Detoxing the drug is one thing, but once the drug is detoxed, users want it again. Because of the rapid build up of tolerance, larger and larger doses are required.</p>
<p>Make no mistake: withdrawal is unpleasant. Users crave drugs to avoid withdrawal symptoms.
[/quote]
</p>
<p>I was merely comparing amphetamine withdrawal with nicotine withdrawal. Nicotine's withdrawal symptoms are far more variegated than mere extreme fatigue. Of course, it's impossible to fully quantify withdrawal symptoms with mere numbers. But amphetamine withdrawal is not painful - it just sucks out motivation (and cocaine withdrawal is notorious for causing anhedonia in individuals for a number of months afterwards). Nicotine withdrawal is painful.</p>
<p>Tolerance is related to withdrawal, but it is not the same thing. One can become tolerant to a drug and still have relatively benign withdrawal symptoms after initiation of withdrawal</p>
<p>
[quote]
Withdrawal from long-term amphetamine use causes depression. Withdrawal is usually not life threatening and does not cause physically painful symptoms.
[/quote]
</p>
<p>You are right that amphetamine withdrawal does not seem to be linked with painful symptoms. Withdrawal may feature paranoia. This would certainly not be a lot of fun even if it is not painful.</p>
<p>My main point is that ampehtamine use is linked with psychological dependency more than physical dependency. The withdrawal is not painful, but the cravings for more based on psychological dependency further the addiction.</p>
<p><a href="http://www.emedicine.com/med/topic3114.htm%5B/url%5D">http://www.emedicine.com/med/topic3114.htm</a></p>
<p>I havent found a lot of research describing what to expect during amphetamine withdrawal. McGregor et al. (2005) confirmed that The natural history of amphetamine withdrawal is still poorly understood, despite a small number of studies which have provided limited information on withdrawal symptoms over time. One of the hardest aspects of drug cessation is that many addicts relapse during the days and weeks after trying to quit (Brecht, von Mayrhauser, & Anglin, as cited in McGregor et al.).</p>
<p>McGregor et al. (2005) studied only 21 patients at a treatment hospital in Thailand, but they give us some insights. First, there appear to be two phases to methamphetamine withdrawal: acute (7-10 days) with a linear decrease in symptomology, followed by the subacute (2 weeks) phase. Methamphetamine withdrawals main features were found to be sleeping and appetite increases. The first weeks course was characterized by inactivity, anhedonia, dysphoria, and fatigue. Vivid dreams, cravings, poor concentration, tension, anxiety, and irritability were also noted. The most persistent symptoms proved to be the increases in sleeping and appetite, lasting through week 3. Bradycardia was noted in weeks 2 and 3, thought to be a rebound cardiac function phenomenon. Suicidal ideation and paranoia were measured at low levels throughout all three weeks. Those patients with greater dependence or more advanced age were found to have a harder time.</p>
<p>McGregor, Srisurapanont, Jittiwutikarn, Laobhripatr, Wongtan, & White. (2005). The nature, time course, and severity of methamphetamine withdrawal. Society for the Study of Addiction, 100, 1320-1329. Academic Search Premiere database.</p>
<p>
[quote]
Responsible people do not use illicit drugs. However, some people who should be treated for other problems, like depression, sometimes resort to self-medicating themselves (Volkow & Li, 2005).
[/quote]
</p>
<p>I find the implied absolutism of this passage interesting. A lot of researchers have funding from the NIH and other agencies - and are interested in promoting research that will ultimately result in more revenue for health-care services. We see this all the time with certain mental illnesses, for example. If you have the symptoms of depression - you're told to seek medical assistance. Of course the research shows that medical assistance for depression is more effective than not seeking medical assistance for it. But no agency has any motives to encourage people to initially seek non-dangerous solutions to their problems - changing one's thinking strategies WITHOUT therapy, for example. As we all know - therapy for mental illnesses is extremely slow, costly, and non-optimal for the individual.</p>
<p>Interesting research kcollegekid. One of the problems with such clinical trials is that they only last for several weeks. It is entirely possible that tolerance may take several months to finally subside - as the body may have scaled-back dopamine receptors for months to come.</p>
<p>Bias is always a problem to consider in research, books, websites, . . .</p>
<p>There are a lot of clinical trials that last for prolonged periods of time. The length of a study is often dictated by what seems to be the time frame of the phenomenon. It might indeed be cost prohibitive and counter-productive to carry on some studies for months or years. In the case of McGregor et al., their research purpose was to provide a snapshot of the withdrawal phenomenon. Their underlying motive was likely that they want to learn how practitioners can intervene to improve the experiences for these types of patients. </p>
<p>There isn't much that can be said if there is an inherent distrust of the establishment's research systems and peer-review processes. </p>
<p>I would disagree with the generalization that "therapy for mental illnesses is extremely slow, costly, and non-optimal for the individual"</p>
<p>Some therapies are indeed slow, some are costly, and some are non-optimal.</p>
<p>Other therapies are quick or intermediate term, some are inexpensive or covered by third parties, and some are definitely optimal. Some are optimal but expensive, others are intermediate term but expensive, . . .</p>
<p>Case in point: acute time-limited anxiety. Easily treated with a short course of Xanax. Inexpensive, optimal results.</p>
<p>Another example: many, but not all, people are helped by SSRIs for depression and other mental disorders. They act on a more intermediate term. Some SSRIs are expensive, others less so. Perfect, no. Better than treatments 50 years ago? Definitely.</p>
<p>One suggestion from my abnormal psych teacher was to combine, for example, a benzodiazepine with an SSRI for generalized anxiety disorder. The benzodiazepine provides immediate relief from the anxiety, but it is unsuitable for long term use. After three weeks, the benzo can be tapered. By then, the SSRI will be taking effect. </p>
<p>For our age group, the only SSRI that the FDA allows is Prozac. All of the SSRIs carry a suicide risk. That's a definite negative.</p>
<p>
[quote]
There are a lot of clinical trials that last for prolonged periods of time. The length of a study is often dictated by what seems to be the time frame of the phenomenon. It might indeed be cost prohibitive and counter-productive to carry on some studies for months or years. In the case of McGregor et al., their research purpose was to provide a snapshot of the withdrawal phenomenon. Their underlying motive was likely that they want to learn how practitioners can intervene to improve the experiences for these types of patients.
[/quote]
</p>
<p>That's true. It's just that we need to take caution when we're trying to gauge the long-term effects of various drugs - which have not been thoroughly reported (due to the lack of long-term studies). </p>
<p>==
[quote]
There isn't much that can be said if there is an inherent distrust of the establishment's research systems and peer-review processes.
[/quote]
</p>
<p>I wouldn't say that I distrust it that much - I trust it to the extent that I find the research literature helpful as long as I'm aware of the constraints of the study. What I do object to - is the fact that the medical establishment has prescribed drugs like Avandia - even though it was well known before FDA approval that Avandia had cardiovascular complications - and that there were many far safer alternatives to the drug.. Many doctors are also somewhat ignorant of the research literature - rather - they tend to rely on personal experience based on their previous patients (some of them are certainly aware of it - some of them are not). Of course, it's advised that the patient get a second opinion.</p>
<h1>As for the assertion that "therapy for mental illnesses is extremely slow, costly, and non-optimal for the individual" - that can be interpreted on multiple levels. First of all, it can be the best system possible and still yet "extremely slow, costly, and non-optimal for the individual." It's just a matter of perspective. Though my perspective was somewhat extreme - yes - therapies for some conditions (phobias among them) are extremely effective. It is just that therapies for other conditions (depression) are often not much more effective than placebo (they are more effective, but not significantly more so - and then I fail to cite, thereby making an overgeneralization - I'm sure that there is research that goes both directions).</h1>
<p>
[quote]
For our age group, the only SSRI that the FDA allows is Prozac. All of the SSRIs carry a suicide risk. That's a definite negative.
[/quote]
</p>
<p>Yes, that's true. One problem is that we don't know enough about our treatments - but at the same time - that we can only learn more by testing treatments on people - which carries inherent risks to the patient.</p>
<p>Oh and true - the medical establishment does distribute literature regarding self-help. The self-help literature on depression per se may not be pervasive enough yet (that therapy does work indicates that depression is not purely a chemical thing). Self-help manuals, admittedly, would work better in prevention than treatment for depression (since once people are "down there" - it's difficult to merely get out by self-help) - but self-help manuals can help one recognize the symptoms while they are still controllable.</p>
<p>...Which reminds me...maybe OCD is also somewhat preventable if caught early enough...</p>
<p>==
Sometimes, the patient can do better than the doctor, if the patient is well-informed of the research literature (and if the patient is not predisposed to hypochondria). Most of the time, patients don't have the initiative to read the literature (almost all the time). But the research does indicate that self-medication hurts the patient (most of the time) - as research on those with ADD show. So the cases where the patient does better than the doctor probably constitute a minority of cases.</p>
<p>What do you mean by a self-help manual for treatment of depression?</p>
<p>What would be the advice in this manual?</p>
<p>As far as people reading research and self-prescribing, it is far better to find some research that you think pertains to your case and take it to your physician to discuss. </p>
<p>Obviously, physicians can't read all of the journals that are published. Research does not talk about all of the pros and cons, so it would be a mistake for a lay person to decide on self-treatment based on personal readings. </p>
<p>If you can't talk about it with a physician, it is probably not a legitimate use of the drug. </p>
<p>Why risk getting a criminal record?</p>
<p>If someone is determined to try illicit drugs, that person will rationalize that experiment. </p>
<p>If it is legitimate, the physician will likely endorse the use and provide a script.</p>