"biomedical research, just another job…"I'm particularly offended by the use of "cute" monkey cartoons by people working in labs that hurt these animals. This one is on the front page of the Taffe Lab site (aka: Primate Neurobehavioral Laboratory -- Committee on the Neurobiology of Addictive Disorders
T H E S C R I P P S R E S E A R C H I N S T I T U T E.) What pukes.
The National Library of Medicine has indexed approximately 38,000 scientific papers related to experimental alchohol exposure in animals (and 30,000 dealing with alcohol use in humans); one might think that taxpayers wouldn't be forced to pay for demonstrations that alcohol consumption affects learning in adolescent monkeys. But you'd be wrong.
And, if you think that the people being "paid" by you and me to run these silly and cruel demonstrations are greatful that the government is taking money from us and giving it to them, you'd be wrong again. And, if you think government shouldn't be spending taxpayer money on stupid demonstrations like this, well then, you must either hate children or know nothing about modern science. If you think these people do what they do because of some altristic drive to help humanity, read DrugMonkey's post "Scientific Meeting 101: The Schmoozery" (June 19th, 2007):
This brings us to issues of career and what you want to work on scientifically. “I don’t DO AIDS work”, is the usual response. Well do you want a grant or not? Find a collaborator that knows lentiviral models but doesn’t know drugs. Two Aims for me, one Aim for “Congressionally mandated area of interest” and there you go!Taffe says, "We are ... investigating whether chronic alcohol drinking in adolescent animals leads to slowed acquisition of a number of behavioral tasks."
Taffe's demonstrations are particularly stupid and odious in light of the unambiguous uncontested fact that alcohol interfers with cognitive and neurophysiological development in humans.
The American Medical Association says that, "based on two decades of comprehensive research on how alcohol affects the brains of youth:"(my emphasis)
Frontal lobe development and the refinement of pathways and connections continue until age 16, and a high rate of energy is used as the brain matures until age 20. Damage from alcohol at this time can be long-term and irreversible. In addition, short-term or moderate drinking impairs learning and memory far more in youth than adults. Adolescents need only drink half as much to suffer the same negative effects.For some reason, they failed to include more demonstrations that young monkeys have trouble learning when they are forced into alcoholism.
Drinkers vs. non-drinkers: research findings
Adolescent drinkers scored worse than non-users on vocabulary, general information, memory, memory retrieval and at least three other tests
Verbal and nonverbal information recall was most heavily affected, with a 10 percent performance decrease in alcohol users
Significant neuropsychological deficits exist in early to middle adolescents (ages 15 and 16) with histories of extensive alcohol use
Adolescent drinkers perform worse in school, are more likely to fall behind and have an increased risk of social problems, depression, suicidal thoughts and violence
Alcohol affects the sleep cycle, resulting in impaired learning and memory as well as disrupted release of hormones necessary for growth and maturation
Alcohol use increases risk of stroke among young drinkers
Adverse effects of alcohol on the brain: research findings
Youth who drink can have a significant reduction in learning and memory, and teen alcohol users are most susceptible to damaging two key brain areas that are undergoing dramatic changes in adolescence:
The hippocampus handles many types of memory and learning and suffers from the worst alcohol-related brain damage in teens. Those who had been drinking more and for longer had significantly smaller hippocampi (10 percent).
The prefrontal area (behind the forehead) undergoes the most change during adolescence. Researchers found that adolescent drinking could cause severe changes in this area and others, which play an important role in forming adult personality and behavior and is often called the CEO of the brain.
Compared to students who drink moderately or not at all, frequent drinkers may never be able to catch up in adulthood, since alcohol inhibits systems crucial for storing new information as long-term memories and makes it difficult to immediately remember what was just learned.
Additionally, those who binge once a week or increase their drinking from age 18 to 24 may have problems attaining the goals of young adulthood—marriage, educational attainment, employment, and financial independence. And rather than "outgrowing" alcohol use, young abusers are significantly more likely to have drinking problems as adults.
What can be done to stop this epidemic?
The AMA advocates numerous ways to combat this growing epidemic, including:
Reducing access to alcohol for children and youth
Reducing sales and provision of alcohol to children and youth
Increasing enforcement of underage drinking laws
Providing more education about the harmful effects of alcohol abuse
Reducing the demand for alcohol and the normalization of alcohol use by children and youth
Nevertheless, look what Taffe did, his reasons for doing so, and the money he got to do it:
SCRIPPS RESEARCH INSTITUTEConsider this: If Taffe is so unable to distinquish between important and trivial uses of taxpayer dollars (to say nothing of his apparent inability to make meaningful career choices), it is unlikely that his ability to discriminate between meaningful and trivial research data will be much better. Not only is his choice of research question questionable, but his inabilty to distinguish between meaningful and meaningless makes any of his research conclusions more than just a little suspect.
Michael A. (DrugMonkey) Taffe
COGNITIVE EFFECTS OF ALCOHOL IN PERI-ADOLESCENT MONKEYS
2007: (not listed)
Semi-total: $523,772 (of our money)
Abstract: DESCRIPTION (provided by applicant): Recreational overuse of alcohol among adolescent populations remains a significant and growing public health concern. Surveys report that 10% of eighth graders and up to a third of high school seniors consume binge quantities of alcohol on at least a biweekly basis. Heavy drinking during this critical period of formal education and significant brain development may pose serious risk for later intellectual and cognitive function. The proposed studies will develop a novel nonhuman primate model to evaluate the consequences of heavy drinking during adolescence task acquisition and performance in a range of cognitive domains. The Aims under investigation are 1) To determine if chronic oral alcohol intake slows acquisition of a battery of cognitive and behavioral tests in peri-adolescent monkeys; 2) To determine the cognitive and behavioral effects of withdrawal from chronic alcohol exposure; and 3) To determine if a history of chronic oral alcohol intake alters monkeys' cognitive and behavioral sensitivity to challenge with specific psychoactive compounds.
Peri-adolescent monkeys will be trained on a battery of tests which probe learning, memory, attention and motor functions. A flavorant-fade procedure will be used to generate consistent, high levels of alcohol drinking in the experimental group which will be allowed to orally self-administer alcohol (M-F) throughout the 18 month test acquisition period. Radiotelemetric measurement of circadian patterns of body temperature and locomotor activity, and cerebrospinal fluid monoamine / metabolite concentrations will be used as correlates for the behavioral measures. Access to alcohol will be discontinued following acquisition of all behavioral tests to evaluate possible effects of withdrawal on the behavioral and physiological measures. Acute doses of psychoactive compounds will be employed to probe possible persisting behavioral sensitivities to serotonergic, dopaminergic, GABAergic or glutamatergic challenge. This exploratory study will provide evidence regarding the risks posed to cognition by heavy alcohol drinking in the peri-adolescent period.
As his on-line moniker suggests, DrugMonkey's current main income stream comes from his obsession with Ecstasy, or MDMA (3,4 methylenedioxymethamphetamine). From 2005 through 2007, we've awarded him a total of $1,223,322 to demonstrate that monkeys are affected by MDMA and related compounds. In a 2006 paper, he wrote:
Six male rhesus monkeys (Macaca mulatta; Chinese origin) participated[!] in this study. Animals were 6–10 years of age... Animals on this study had previously been immobilized with ketamine (5–20 mg/kg) no less than semiannually for purposes of routine care and some experimental procedures. Animals also had various acute exposure to scopolamine, raclopride, methylphenidate, SCH23390, Δ9-THC, nicotine and mecamylamine in behavioral pharmacological studies and 4 had been exposed to an oral ethanol induction procedure. No experimental drug treatments had been administered for a minimum of one year prior to the start of telemetry studies and thus were not anticipated to have any bearing on the results of the current study....Radio telemetric transmitters (TA10TA-D70; Transoma / Data Sciences International) were implanted subcutaneously in the flank....Now we know.
Results: MDMA significantly increased body temperature within 10–15 mins of drug administration ... Effects of MDMA on temperature did not last beyond the first three hours after dosing.
MDA also significantly increased body temperature ...
METH also significantly increased body temperature in the first few hours after administration, however the timecourse differed notably ...
Grant Number: 1R01DA018418-01A1Now, DrugMonkey, as you might imagine, is particularly sensitive to laypeople and scientists who think that MDMA might not be a significant health risk; or, heaven forbid, could even be beneficial in some cases. You can imagine what that could do to his income.
Project Title: BEHAVIORAL TOXICITY OF MDMA IN RHESUS MONKEYS
Michael A. (DrugMonkey) Taffe firstname.lastname@example.org ASSISTANT PROFESSOR
Abstract: DESCRIPTION (provided by applicant): Recreational use of (+/-) 3,4 -methylenedioxymethamphetamine (MDMA, "Ecstasy") has become increasingly popular in recent decades. Major surveys in the US report steep increases in the rate of MDMA use while use of a number of other recreational drugs has been stable or in decline. College age adults have lifetime prevalence rates of 12-18% thus a substantial fraction of the population is exposed to MDMA. Numerous studies have shown that abstinent MDMA users exhibit deficits on a range of cognitive tasks. Work in nonhuman primate models over past decades has shown that high doses of MDMA (10 mg/kg); when administered at 12 hr intervals for 4 days, selectively reduce markers for serotonin (5-HT) axons and terminals in many brain regions. However, such MDMA-associated 5-HT neurotoxicity is not sufficient to produce cognitive or motor alterations in monkeys under unchallenged conditions. Prior monkey models have not employed repeated, intermittent dosing patterns similar to human users, however. To investigate the novel hypothesis that cognitive and motor disturbances in human users of MDMA result from repeated cycles of 5HT axon pruning/reinnervation, experiments will be conducted in rhesus macaques under the following Aims. Specific Aim I: To determine if repeated, intermittent exposure to a low dose of MDMA results in detectable neurochemical, behavioral or electrophysiological alterations. Specific Aim II: To determine if a short-interval, multi-dose exposure to low doses of MDMA ("MDMA stacking") results in a neurochemical, behavioral and electrophysiological profile similar to that produced by the repeated, high-dose, long interval regimen that produces serotonin neurotoxicity. Specific Aim III: To determine if repeated episodes of exposure to MDMA result in progressive electrophysiological, neurochemical or chronophysiological disturbance. Specific Aim IV: To determine if a history of MDMA exposure impairs acquisition and performance of a battery of neuropsychological tests.
Project Start: 01-APR-2005
Project End: 31-MAR-2010
ICD: NATIONAL INSTITUTE ON DRUG ABUSE
But, even if Ecstasy has some risks, it doesn't seem to be widely used. The National Institute on Drug Abuse (NIDA) reports:
Annual prevalence of ecstasy use in 10th and 12th grades in 1996 was 4.6%—actually considerably higher than among college students and young adults at that time—but it fell in both grades over the next two years.And, in any case, what does the temperature rise in monkeys injected with MDMA, MDA, or methamphetamine have to do with kids experimenting with drugs? Like the AMA's recommendations regarding alcohol use by kids, the answers don't lie with more experiments on monkeys.
Use then rose sharply in both grades in 1999 through 2001, bringing annual prevalence up to 6.2% among 10th graders and 9.2% among 12th graders.
In 2000 and 2001, use also began to rise among 8th graders, to 3.5%.
In 2002, use decreased sharply—by about one fifth—in all three grades, followed by an even sharper decline in all grades in 2003. Although the drops continued in all three grades in 2004, they decelerated considerably.
By 2005 the decline had halted among 8th and 10th graders but continued among 12th graders. In 2006, use among 8th and 10th graders stayed level but use among 12th graders increased.
Annual prevalence rates are down by between one half and nearly two thirds in all three grades compared with recent peaks in 2001.
Check out DrugMonkey's publishing history.