Saturday, April 26, 2008

Bill to Legalize Marijuana Offered in U.S. House


Rep. Frank seeks to end Fed war on pot.

Nobody expects it to pass except its most ardent enthusiasts, but H.R. 5843, a bill "To Eliminate Most Federal Penalties for Possession of Marijuana for Personal Use, and for Other Purposes," sponsored by Rep. Barney Frank (D-MA) and Rep Ron Paul (R-TX), was introduced in the U.S. House of Representatives on April 17. It is not the first such attempt, nor is it likely to be the last.

The bill would remove federal penalties for personal possession of up to 100 grams of marijuana, or roughly 3 1/2 ounces. Not-for-profit transfers of up to an ounce of pot would also be legal under the statutes. A civil penalty of $100 would be levied for public use of marijuana.

The bill would not affect federal laws prohibiting major drug dealing, nor would it interfere with or hinder federal agencies prosecuting the cultivation and export of cannabis. In addition, the bill does not seek to alter the legal status of marijuana as a Schedule 1 drug under the Controlled Substances Act.

The bill is an a rational attempt to break through the confusion surrounding the various laws passed in at least twelve states that allow people to use marijuana for certain medical purposes. The confusion reached a peak last year when several medical marijuana dispensaries--operating legally under California statutes--were raided and their owners arrested by Federal drug enforcement authorities. The message from the hard-line Feds was: Even if it's legal in your state, it's not legal to us.

Rep. Frank has taken on this issue before. In 1970, he filed a bill to decriminalize marijuana in Massachusetts. He has also argued before NORML--the National Organization for the Reform of Marijuana Laws--that such issues rightly belong to the states.

In a letter to the Providence Journal, Frank also vowed to introduce a new version of his "State's Right to Medical Marijuana Act," which he has offered as legislation "every year since 1997."

"If the laws I am proposing pass," Frank explains at Daily Kos, "states will still be free to treat marijuana as they wish. But I do not believe that the federal government should treat adults who choose to smoke marijuana as criminals. Federal law enforcement is a serious business, and we should be concentrating our efforts in this regard on measures that truly protect the public."

Rep. Frank said on "Real Time with Bill Maher" that the new bill could be called the "Make Room for the Serious Criminals" act.

In a prepared statement, Rep. Frank said: "I think it is poor law enforcement to keep on the books legislation that establishes as a crime something which in fact society does not seriously wish to prosecute." The Massachusetts congressman added that "having federal law enforcement agents engaged in the prosecution of people who are personally using marijuana is a waste of scarce resources better used for serious crimes."

Sarah Rubenstein of The Wall Street Journal reports that groups such as the Massachusetts branch of D.A.R.E. and the Drug Enforcement Administration continue to oppose the legalization of marijuana because it would signal to children that the drug is benign.

Frank also noted in his letter to the Providence Journal that "bipartisan amendments have been introduced by my colleagues, Representatives Maurice D. Hinchey (D-NY) and Dana Rohrbacher (R-CA) every year since 2003 to preclude the use of federal funding to prosecute medical-marijuana patients by the Department of Justice. Each time the amendment has been voted on, it has failed in the House."

Photo Credit: Medical Marijuana Blog

Tuesday, April 22, 2008

Female Smokers and Menstruation


Better to quit after ovulation, study finds.

Women stand a better chance of successfully quitting smoking if they stop during the later phase of their monthly menstrual cycle, according to new research conducted at the University of Minnesota and published in the May 2008 edition of the journal Addiction.

Sharon Allen and co-workers discovered that women who quit smoking right before they start to ovulate--the so-called follicular stage--relapsed more often than women who quit during the "luteal" stage, defined as the two weeks between ovulation and the start of a new cycle. In the study, 86 percent of women who gave up smoking during the follicular phase relapsed during the first 30 days, compared to 66 per cent of women who quit during the later luteal phase.

"Our findings support an important role for ovarian hormones in nicotine addiction and smoking cessation," the authors wrote.

The ebb and flow of estrogen and progesterone during the menstrual cycle can have a direct effect on mood, as evidenced by the well-documented premenstrual syndrome, or PMS. In addition to mood factors, the researchers suggested that female hormones might play a role in the speed with which nicotine is metabolized.

The study of 200 female smokers was conducted by the Tobacco Use Research Center at the University of Minnesota. Earlier work by the group, published in Nicotine & Tobacco Research, had established a strong suspicion that "withdrawal symptomatology in short-term smoking cessation in women is increased in the late luteal phase when pre-menstrual symptomatology is the highest." The group concluded that "it seems prudent to recommend that women quit during the follicular phase of their cycle."

In short, the work suggests that female smokers would be well advised not to inaugurate a quit attempt in the ten days preceding ovulation.

Photo Credit: MedGadget

Tuesday, April 15, 2008

Food Addiction and Dopamine


Why your brain likes sweets.

The brain's ability to sniff out calories in the form of sugar depends upon sugar's drug-like effect on the dopamine-rich reward center known as the nucleus accumbens, according to a study published in the March 27 issue of Neuron. This tiny structure in the mid-brain is also the locus of reward activity for all addictive drugs.

In the study, Ivan de Araujo and colleagues at Duke University and the Universidade do Porto in Portugal demonstrated that lab mice lacking the ability to taste sweet foods still preferred sugary water to regular water. The genetically altered mice, lacking functional taste receptor cells for bitter and sweet, consistently chose to consume sugar water--even though they could not sense the sugar. (The lab animals were also prevented from smelling or sensing textural differences in the offerings.)

"Our findings suggest that calorie-rich nutrients can directly influence brain reward circuits that control food intake independently of palatability or functional taste transduction," the researchers wrote.

The findings offer new clues to obesity, and also bolster the contention that simple carbohydrate foods--because of their effect on reward pathways in the brain--can be addictive for certain people. As Tamas Horvath of Yale University's School of Medicine told Science News (sub. required): "This is a very exciting new element in how you get addicted to food. It doesn't even matter how it tastes."

In the same article, written by Amy Maxmen, study author de Araujo said: "The animal's reward processing systems were sensitive to changes in metabolism, not just flavor. This is a new system."

The "sweet-blind" animals did not go for the low-cal alternative, when they were offered water mixed with sucralose, otherwise known as Splenda. Low-cal sweeteners did not result in a similar dopamine boost along the reward pathways of the brain.

The brain's ability to "sense" calories may help explain why diet foods are often ignored in favor of sweets. As Ewan Callaway of New Scientist put it, "Anyone who has devoured a tub of ice cream in one sitting knows that delicious foods can override our body's pleas of 'enough.'" We have increased levels of dopamine in the nucleus accumbens to thank for that.

As De Araujo explained to New Scientist, "even when you do not stimulate the sensory pathways in the mouth you still have this reward signal in the brain."

In a preview of the article in the same issue of Neuron, Zane Andrews and Tamas Horvath speculate that "high-fructose corn syrup is an ubiquitous sweetener in American society.... It may be that fructose produces stronger activation of the reward system and that removing high-fructose corn syrup as a sweetener will curb some desire for these products."

Photo Credit: Biz/Ed

Thursday, April 10, 2008

Marijuana Withdrawal? What Marijuana Withdrawal?


AlterNet article calls pot addiction "laughable."

Wondering why you're feeling anxious, sleepless, irritable, sweaty, and scared when you stop daily pot smoking? Don't worry, Paul Armentano has the answer: You're full of bullshit.

Armentano, in an article for AlterNet entitled "B.S. on the idea of 'marijuana addiction'," asserts that "there's little consensus that such a syndrome is clinically relevant -- if it even exists at all."

The proof? "According to state and national statistics, up to 70 percent of all individuals in drug treatment for marijuana are placed there by the criminal justice system. Of those in treatment, some 36 percent had not even used marijuana in the 30 days prior to their admission. These are the 'addicts'?"

No, these are not necessarily the addicts. These are people undergoing mandatory treatment dictated by the criminal justice system. As Armentano points out, they may or may not have been using drugs before their court-mandated treatment sessions.

In contrast, marijuana addicts are people with a propensity for addiction who suffer a clearly delineated, verifiable, and vivid set of withdrawal symptoms when they try to quit. Armentano doesn't seem to have much interest in this cohort.

Armentano cites a study by the nonpartisan National Academy of Sciences Institute of Medicine--and then completely misses the point. According to the report, "[A]lthough [some] marijuana users develop dependence, they appear to be less likely to do so than users of other drugs (including alcohol and nicotine), and marijuana dependence appears to be less severe than dependence on other drugs."

What part of "some marijuana users develop dependence" does Armentano not understand?

The author appears to be making the common mistake of assuming that if pot causes withdrawal in some people, then it must cause withdrawal in everybody. And if it doesn't, it's not very addictive. This kind of thinking has been overtaken by the growing understanding that a minority of people suffer a chemical propensity for addiction that puts them at high risk, compared to casual, recreational drug users. The fact that most people don't get addicted to pot and don't suffer from withdrawal is no more revealing than the fact that a majority of drinkers do not become alcoholics.

The author further suggests that, since the Institute of Medicine report characterizes symptoms of weed withdrawal as "mild and subtle," there is nothing to this subject but hot air. Another way to think of "mild and subtle" is: not potentially life threatening, as in the case of abrupt withdrawal from alcohol. Pot doesn't kill. But we knew that already.

In addition, the author highlights the Institute of Medicine's estimate that "fewer than 10 percent of those who try cannabis ever meet the clinical criteria for a diagnosis of "drug dependence" (based on DSM-III-R criteria)." But this common estimate falls right in line with overall estimates placing the total addictive population for all drugs at between 10 and 15 per cent of the population.

Perhaps the most egregious error in the piece is the assertion that "pot's mild after-effects do not appear to be either severe or long-lasting enough to perpetuate marijuana use in individuals who have decided to quit." This statement is simply not true, as an overwhelming number of heavy pot smokers can attest. (For dozens of case histories that refute this contention, see the comments section of my post, Marijuana Withdrawal.)

The author also asserts that "the concept of pot addiction is big business," but it is unclear what he means by this, beyond his dismissive vote-of-no-confidence on anti-craving medications as an adjunct to addiction treatment.

I do, however, agree completely with Armentano on one point: None of this justifies "the continued arrest of more than 800,000 Americans annually" for pot violations.

Photo Credit: Javno

Saturday, April 5, 2008

Salvia: The Mystery Drug


Tripping with the kappa opiate receptor.

Over the past few years, a little known and highly unusual psychedelic drug has claimed the interest of drug users and drug scientists alike. Salvia divinorum, a green, leafy plant native to the Mazateca region of Mexico, provides its users with a short but intense hallucinogenic experience. A member of the mint family, it is not among the ornamental garden plants sold under the name Salvia at local nurseries.

The high is unlike that from LSD or psychedelic mushrooms, users say, nor is it anything like the experience of smoking marijuana. Salvia is not currently controlled by federal law, but dozens of states have moved to outlaw cultivation and sale of the plant, which is currently freely available for purchase on the Internet.

As an herb with psychedelic properties, Salvia divinorum is of pharmaceutical interest because of its uncommon affinity for opium/endorphin receptors—specifically the kappa opioid receptor. Most drugs with classical “psychotomimetic” properties, like LSD and MDMA, are highly selective for the 5-HT(2A) serotonin receptor.

Salvia is not one of these. Like ibogaine, another hallucinogenic shrub with a weak affinity for kappa opiate receptors, Salvia’s active ingredient--Salvinorin A--causes psychoactive effects not usually associated with stimulation of the brain’s internal opioid system. Previous research had identified a few such compounds, such as enadoline, which produced similar hallucinogenic effects.

The pharmaceutical industry has already taken a look at the kappa-opioid agonists in the ongoing search for new painkillers, and has so far discovered the usual psychedelic trap of too many unpredictable side effects for a commercial medication.

Classified as an “atypical” psychedelic, the salvia high is intense, dream-like, and short-lived, tapering off after about 30 minutes. An ounce of salvia in leaf form sells for as little as $40, but more concentrated liquid extracts sell for as much as $60 per gram.

Salvia’s addictive potential is low to nonexistent. No hallucinogen such as LSD or peyote has ever been found to be addictive in the classical sense.

Nonetheless, fearing that the inexpensive plant might become “the next marijuana,” as an Associated Press report put it last month, 24 states have passed, or are considering, legislation to restrict access to salvia. Elsewhere, sale of the drug has been restricted in Spain, Italy, Sweden, Belgium, Australia, and other countries. In the AP article, a Florida state legislator alleged—with unintended irony: “As soon as we make one drug illegal, kids start looking around for other drugs they can buy legally. This is just the next one.”

There are many reasons why Salvia divinorum is not likely to be “the next one.” According to drug expert Rick Doblin of the Multidisciplinary Association for Psychedelic Studies (MAPS), salvia “tastes terrible” and is “not going to be extremely popular.” The popular drug information site EROWID describes salvia as “more scary than fun” for many users, concluding that, whether smoked or swallowed, the plant is “aversive for many who try it.” Like ibogaine, salvia is no party drug. It can result in confusion, dizziness, depersonalization, and all the other hallmarks of a “bad trip.”

A related question is the extent to which kappa opioid receptor boosters might reduce the craving for addictive drugs. Ibogaine has been touted for having precisely this effect on heroin addicts and others. However, an early study of kappa opioid receptor-active compounds did not find any reduction in self-administration of cocaine.

The National Institute of Drug Abuse (NIDA) is studying salvia. The Drug Enforcement Administration (DEA), citing salvia as a “drug of concern,” is evaluating it.

Photo Credit: http://www.salvia-divinorum-extract-now.com/

Thursday, April 3, 2008

The Genetics of Cigarettes


Mutations on chromosome 15 linked to lung cancer.


A variation among the genes that code for nicotine receptors in the brain has been linked with increased cigarette smoking and a heightened risk for lung cancer, according to three new studies released this week.

Two studies in Nature, and one in Nature Genetics, demonstrated that people who inherited the genetic variation, or allele, from one parent—roughly 50 percent of the population--had a 30 percent higher risk of developing lung cancer. “What’s more,” according to Michael Hopkin at Nature News, “another 10 percent of the population is likely to carry two copies of this set of mutations, raising cancer risk by as much as 80 percent relative to people with equivalent lifestyles without the cancer-linked gene variant.”

More than 35,000 Caucasian smokers in Europe and North America took part in the government-funded research. It was the strongest evidence to date of a firm link between genetics and lung cancer. It was also added evidence for the existence of biological proclivities in addicted cigarette smokers.

Earlier studies had demonstrated that having a parent or sibling with lung cancer could triple the odds of developing the disease. But teasing out the precise genes responsible has been, as always, a frustrating hunt.

Christopher Amos of the University of Texas, author of one of the studies, characterized the variant as “kind of a double whammy gene” in an Associated Press article by Seth Borenstein. Amos said of the nicotinic acetylcholine receptor gene alleles on chromosome 15: “It also makes you more likely to be dependent on smoking and less likely to quit smoking.” In the same article, psychiatry professor Dr. Laura Bierut of Washington University in St. Louis said that the three studies are “really telling us that the vulnerability to smoking and how much you smoke is clearly biologically based.”

Study author Kari Stefansson of Iceland’s deCode Genetics believes strongly that the genetic variation in question makes people more susceptible to nicotine addiction, and increases the difficulties of quitting: “In our study, we found if you have one allele you smoke about one more cigarette per day; if you have 2 alleles you average two more cigarettes per day.”

However, according to Denise Gellene of the Los Angeles Times: “The studies were divided on whether the genetic variant directly increased the risk of lung cancer or did so indirectly by predisposing people to smoking.” In a third study, Paul Brennan of the International Agency for Research on Cancer in Lyon, France noted no evidence of a link between the rogue gene and nicotine addiction itself.

It is not clear whether non-smokers with the mutation suffer an increased risk of lung cancer as well. (However, even smokers who lack the gene variant are still ten times as likely to develop lung cancer than nonsmokers).

About one million people die annually from lung cancer. According to the World Health Organization, smoking is the leading cause of preventable death worldwide.

Graphics Credit: Technology Review

Saturday, March 29, 2008

Amphetamine Blues


How meth addiction happens.


If alcohol’s impact on brain cells is wide-ranging and diffuse, and marijuana’s impact is selective and subtle, the impact of cocaine and amphetamine is much more straightforward. “There is certainly lots of evidence for common neurological mechanisms of reward across a wide variety of drugs,” said Dr. Robert Post, chief of the biological psychiatry branch at NIMH.

Animals will readily administer cocaine and amphetamine, Dr. Post once explained to me, but when researchers surgically block out areas of the brain that are dense with dopamine receptors, the picture changes dramatically. “The evidence definitely incriminates dopamine in particular,” said Dr. Post. “In animal models, if you make selective lesions in the dopamine-rich areas of the brain, particularly the nucleus accumbens in the limbic system, the animals won’t self-administer either amphetamine or cocaine.”

When you knock out large slices of the nucleus accumbens, animals no longer want the drugs. So, one cure for addiction has been discovered already—but surgically removing chunks of the midbrain won’t do, of course.

At the heart of the meth high is a chemical paradox. The entire range of stimulative effects hits the limbic system within seconds of being inhaled or inject, and the focused nature of the impact yields an astonishingly pleasurable high.

But the long-term result is exactly the opposite. The body’s natural stock of these neurotransmitters starts to fall as the brain, striving to compensate for the artificial flooding of the reward center, orders a general cutback in production. At the same time, the receptors for these neurotransmitters become excessively sensitive due to the frequent, often unremitting nature of the stimulation.

The release of dopamine and serotonin in the limbic structure called the nucleus accumbens lies at the root of active drug addiction. It is the chemical essence of what it means to be addicted. The pattern of neural firing that results from this surge of neurotransmitters is the “high.” Dopamine is more than a primary pleasure chemical—a “happy hormone,” as it has been called. Dopamine is also the key molecule involved in the memory of pleasurable acts. Dopamine is part of the reason why we remember how much we liked getting high yesterday.

One reason why amphetamine addicts will continue to use, even in the face of rapidly diminishing returns, is simply to avoid the crushing onset of withdrawal. Even though the drug may no longer be working as well as it once did, the alternative--the psychological and physical cost of withdrawal--is even worse. When addicts talk about “chasing a high,” the metaphor can be extended to the losing battle of neurotransmitter levels. In the jargon used by Alcoholics Anonymous, addicts generally have to get worse before they can get better.

Speed, then, is diabolically well suited to the task of artificially stimulating the limbic reward pathway. Molecules of amphetamine displace dopamine and norepinephrine in the storage vesicles, squeezing those two neurotransmitters into the synaptic gap, and keeping them there, where they repeatedly stimulate their receptors. By mechanisms less well identified, cocaine accomplishes the same feat. Speed also interferes with the return of dopamine, norepinephrine, and serotonin molecules to their storage sacs, a procedure known as reuptake blocking—the same mechanism by which the so-called selective serotonin reuptake inhibitors (SSRI) antidepressants increase the availability of serotonin in the brain.

Adapted from The Chemical Carousel: What Science Tells Us About Beating Addiction © Dirk Hanson 2008, 2009.

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