Thursday, September 13, 2007
New Drug For Obesity
Wednesday, September 12, 2007
Drug addiction is a complex illness.
The path to drug addiction begins with the act of taking drugs. Over time, a person's ability to choose not to take drugs can become compromised. Drug seeking becomes compulsive, in large part as a result of the effects of prolonged drug use on brain functioning and, thus, on behavior.
The compulsion to use drugs can take over the individual's life. Addiction often involves not only compulsive drug taking but also a wide range of dysfunctional behaviors that can interfere with normal functioning in the family, the workplace, and the broader community. Addiction also can place people at increased risk for a wide variety of other illnesses. These illnesses can be brought on by behaviors, such as poor living and health habits, that often accompany life as an addict, or because of toxic effects of the drugs themselves.
Because addiction has so many dimensions and disrupts so many aspects of an individual's life, treatment for this illness is never simple. Drug rehabs must help the individual stop using drugs and maintain a drug-free lifestyle, while achieving productive functioning in the family, at work, and in society. Effective drug abuse and drug rehab treatment programs typically incorporate many components, each directed to a particular aspect of the illness and its consequences.
Three decades of scientific research and clinical practice have yielded a variety of effective approaches to drug addiction treatment. Extensive data document that drug addiction treatment is as effective as are treatments for most other similarly chronic medical conditions. In spite of scientific evidence that establishes the effectiveness of drug abuse treatment, many people believe that treatment is ineffective. In part, this is because of unrealistic expectations. Many people equate addiction with simply using drugs and therefore expect that addiction should be cured quickly, and if it is not, rehab is a failure. In reality, because addiction is a chronic disorder, the ultimate goal of long-term abstinence often requires sustained and repeated treatment episodes.
Drugs, Police & the Law
The Drug Policy Alliance has been involved in a number of legal challenges to the war on drugs, primarily through its Office of Legal Affairs. The organization has represented the leading medical and public health organizations, including the American Public Health Association, the American Society of Addiction Medicine, the National Association of Alcoholism and Drug Abuse Counselors, and the American College of Obstetricians and Gynecologists, in cases concerning the rights of patients to private and safe access to medical care and drug treatment, as well as the right to be free from pain and suffering. Drug Policy Alliance has also assembled and presented to various courts a wealth of scientific, medical and social science evidence regarding medicinal marijuana, cocaine and pregnancy, HIV/AIDS, access to sterile syringes, and the importance of diversity of treatment, among other issues.
The Drug Policy Alliance also continues to develop public health alternatives to the criminal-justice-based policies that characterize the War on Drugs. In particular, the Alliance has helped craft treatment-instead-of-incarceration ballot initiatives and legislation for various states and continues to assist state and local law makers and agencies develop laws, policies and practices that seek to reduce drug use and drug overdose, as well as the harms associated with drugs, drug prohibition and punitive drug law enforcement.Tuesday, September 11, 2007
Drug
Many details have recently been worked out describing events in any brain exposed to the most common addictive drugs: heroin, morphine, barbiturates, tranquilizers, and alcohol (all depressants that slow down processes in the brain and central nervous system); and cocaine, amphetamines, nicotine, and marijuana (all stimulants that generally excite them).
As the target organ of addiction, brain cells react to stimuli, including substances introduced from outside and hormones and chemicals we make ourselves. Those reactions lead to other chemical reactions and to changes in movement, thought, feelings, and memory. Drugs of abuse abet, or interfere with the chemical messengers, or neurotransmitters. The neurotransmitters that facilitate addiction are released by the 10 billion neurons that deal with information transfer.
Neurotransmitters circulate, collect, and act at specific sites on nearby cell surfaces called receptor proteins, each of which is shaped to fit and receive a particular neurotransmitter and bind it the way a lock "recognizes" a key. Only after a neurotransmitter binds can the signal it carries travel to the next cell. If the cell is flooded with too much neurotransmitter, an elegant "control" system is normally activated so that the cell reabsorbs the excess for later use. This process, called "reuptake," prevents too many chemical signals from circulating and filling too many receptors, which can lead to over-activity and serious mental and physical problems.
Neuroscientists now know that some abused substances block reabsorption, leaving too much neurotransmitter around. Others block the release of neurotransmitters. Although many neurotransmitters and chemicals that act like them have been identified, those most notably linked to addiction are norepinephrine, dopamine, serotonin, substance P, and gamma-aminobutyric add (GABA).
In 1973, Solomon Snyder, M.D., director of neuroscience at Johns Hopkins, and his then-graduate student Candace Pert, put a solid foundation under the new theory of addiction by finding receptors for opium in the brain. They accomplished this by tracking molecules of the drug with radioactive tags to their binding sites. Derivatives of heroin and morphine bind to those same sites. Methadone, a weak synthetic opiate, binds less tightly; one reason it satisfies an addict's craving is that it is addictive but does not produce a "high."
But Snyder and Pert also understood that their discovery had far greater implications. For if the brain had opiate receptors, it surely wasn't because nature intended man to fall victim to heroin addiction, but because the body itself must produce opiates. The discovery in 1975 of the brain's own opiates, called endorphins or enkephalins, demonstrated neurochemical sites of pleasure in the brain activated naturally by human activity.
Soon, scientists would learn that opiates keep opiate receptors constantly full, producing the physical tolerance so characteristic of heroin addiction. They discovered that the opiate-addicted brain also appears to close off some receptors so that desensitization occurs, encouraging larger and larger doses.
They found that cocaine affects nerve cells in the limbic system, the most ancient part of the brain and one closely tied to emotions. But rather than bind to a receptor, it interrupts the process of reuptake that terminates the action of dopamine. Cocaine is not only a blocker of dopamine uptake but of the reuptake of serotonin and norepinephrine as well.
All of this leads to vast overstimulation of nerve cells and creates intense feelings of excitement and joy. With cocaine, dopamine spills forth and floods our pleasure receptors. On the downside, cocaine eventually wipes out the brain's existing supply of these neurotransmitters temporarily, leading to a hellish withdrawal marked by severe depression, paranoia, intense irritability, and craving.
According to Steven Childers, psychedelic drugs of abuse such as LSD and "mushrooms" don't activate the ancient reward system regulated by dopamine, serotonin, and norepinephrine. Moreover, they appear to influence different parts of the brain involved in higher functions than emotions and pleasure. "For people who use these drugs, they are less an addiction than an intellectual drive to alter mood and produce higher levels of consciousness," he says. "And when we look at how they act in the brain, we can begin to understand why."
The two most common types of tranquilizers, barbiturates and benzodiazepines (Valium and its cousins), also act differently in the brain. They don't have their own receptors, but act on a "foster" receptor, GABA, which is predominantly an inhibitory, or slow-down, neurotransmitter. These drugs "deinhibit" and, in sort of a double-negative effect, increase inhibition, sedating the user. "What these drugs do is hyperactivate inhibition," notes Childers. "Increase GABA enough and you shut down the brain. That's what sedatives do." Alcohol also appears to act on GABA receptors, amphetamines interrupt dopamine balance, and nicotine stimulates the release of endorphins, at least at high doses.