Addiction Treatment

Smokers often say they need a cigarette to calm their nerves, but a new study suggests that after a person kicks the habit, chronic stress levels may go down.

The findings, say researchers, should give smokers reassurance that quitting will not deprive them of a valuable stress reliever.

In a study of 469 smokers who tried to quit after being hospitalized for heart disease, the researchers found that those who remained abstinent for a year showed a reduction in their perceived stress levels. In contrast, stress levels were essentially unchanged among heart patients who went back to smoking.

The study, reported in the journal Addiction, supports the theory that, at least for some people, smoking actually contributes to chronic stress.

“Smokers often see cigarettes as a tool to manage stress, and ex-smokers sometimes return to smoking in the belief that this will help them cope with a stressful life event,” lead researcher Peter Hajek.

The reason for that difference has been unclear, but it could mean that people vulnerable to stress are more likely to take up smoking – and that taking away that habit could worsen their stress.

On the other hand, smoking itself may generate long-term stress, even if people feel it offers them temporary relief from trying situations.

The findings, according to the researchers, support the idea that dependency on cigarettes is itself a chronic source of stress.

“Many smokers worry that if they stop smoking, they will lose a valuable tool for coping with difficult situations and stresses in their lives,” Hajek noted.

These findings, he said, instead suggest that quitting may not only benefit smokers’ physical health, but possibly their mental well-being as well.

Smoking cigarettes is a significant risk factor for developing rheumatoid arthritis (RA) and may have a negative impact on the effectiveness of the so called anti-TNF inhibitors used to treat RA patients.

For both men and women, smoking at the time of the study initiation was shown to be a predictor for future diagnosis with RA.

Socio-economic status also had an impact on the risk of developing RA with “blue-collar workers” (those who do manual labour and earn an hourly wage) having an increased risk compared with “white-collar workers” (salaried professionals or educated workers)

“The results of our study have confirmed that whether or not an individual smokes cigarettes , and the type of job that they do are surprisingly robust predictors of developing RA,” according to the research team.

They continue: “Investigating the impact of different factors on the development of RA could help us to understand disease mechanisms and identify preventative strategies in the future.”

While compulsive gambling is only beginning to be addressed by mental health professionals, they must now increasingly face another affliction as well: Internet addiction.

“The problem isn’t widespread but we know of serious cases in which teenagers don’t leave the house, don’t have interpersonal relationships, and have been isolated in front of their computer screen for the past two or three years, and only speak in the language of the characters they play with in network video games,” says principal investigator Louise Nadeau.

“In a few years we’ll have couples in therapy because the Internet will have become their main occupation.”

There is no lack of data on compulsive gambling and alcoholism. But there is a vacuum when it comes to Internet addiction. “There is no reliable study or clinical data on the issue,” says Nadeau. “We are starting from scratch.”

A recent survey concluded that hundreds of patients have consulted a professional about this issue. Researchers hope to further develop this data and determine the clinical threshold of addiction, establish how the disease evolves and elaborate intervention techniques.

Nicotine exposure at a young age may alter the “hard-wiring” of the brain that occurs during adolescence and young-adulthood, contributing to future susceptibility for addiction, according to a University of Pittsburghstudy.

The research team, led by Jay W. Pettegrew, M.D., measured the effects of acute nicotine administration on nerve cell membranes – the functional communication centers of the brain.

According to their findings, nicotine induced molecular and metabolic changes in the brain, which resulted in the breakdown of the nerve cell membranes. These changes were especially observed in males.

Such findings could explain what has been noted in previous studies – that individuals who smoke as adolescents have a higher probability of being life-long smokers than those who start smoking later in life and are less likely to succeed with smoking cessation .

Morphine, as little as a single dose, blocks the brain’s ability to strengthen connections at inhibitory synapses, according to new Brown University research published in Nature.

The findings, uncovered in the laboratory of Brown scientist Julie Kauer, may help explain the origins of addiction in the brain. The research also supports a provocative new theory of addiction as a disease of learning and memory.

“We’ve added a new piece to the puzzle of how addictive drugs affect the brain ,” Kauer said. “We’ve shown here that morphine makes lasting changes in the brain by blocking a mechanism that’s believed to be the key to memory making. So these findings reinforce the notion that addiction is a form of pathological learning.”

Kauer is interested in how the brain stores information. Long-term potentiation, or LTP, is critical to this process.

In LTP, connections between neurons – called synapses, the major site of information exchange in the brain – become stronger after repeated stimulation.

In her experiments, Kauer found that LTP is blocked in the brains of rats given as little as a single dose of morphine.

“The persistence of the effect was stunning,” Kauer said. “This is your brain on drugs.”

The net effect of morphine and other opioids, Kauer found, is that they boost the brain’s reward response. “It’s as if a brake were removed and dopamine cells start firing,” she explained. “That activity, combined with other brain changes caused by the drugs, could increase vulnerability to addiction. The brain may, in fact, be learning to crave drugs.”

Scientists at the University of Cambridge have discovered why some individuals may be predisposed to drug addiction and believe it may lead to better treatments for this brain disorder.

The new findings, published in today’s edition of Science, may lead to more targeted treatments for addiction and other compulsive behaviour disorders with fewer side effects than current alternatives.

Certain changes in brain chemistry have been linked with drug addiction in humans. However, previous studies were unable to conclude whether individuals were predisposed to drug addiction because of these chemical changes or if chronic drug use itself caused the chemical changes in the brain.

Now a group of researchers at the Cambridge Behavioural and Clinical Neuroscience Institute, may have resolved this debate by demonstrating that changes in a neurotransmitter receptor in a particular part of the brain actually pre-dates drug abuse .

The findings may have important ramifications for a range of addictive substances, including nicotine and opiates, where high consumption rates have also been linked to a similar reduction in this particular brain receptor.

The next step is identifying the gene or genes that cause this diminished supply of brain receptors. This may provide important new leads in the search for improved therapies for attention deficit/hyperactivity disorder (ADHD) and compulsive brain disorders such as drug addiction and pathological gambling.”

Researchers have identified, for the first time, long-term changes in the brain circuitry of methamphetamine-addicted mice that can explain why the craving of addiction is so stubborn and long-lived. The research could lead to more effective treatments for addiction to methamphetamine and related drugs.

In their experiments, the researchers treated mice with methamphetamine and studied how long exposure to the drug affected levels of the brain chemical dopamine. Researchers have long known that methamphetamine and amphetamine enhance release of dopamine at the connections between neurons, called synapses.

Dopamine is one of the brain’s major neurotransmitters, the chemical messengers by which one neuron triggers its neighbor to fire a nerve impulse.

The researchers concentrated on the dopamine machinery in certain parts of the brain, believed to harbor the “habit” circuitry central to the compulsive drug-seeking of addiction to methamphetamine and amphetamine.

Their studies revealed that giving the animals the drug long enough to cause chronic effects caused a depression of the synaptic dopamine machinery in the corticostriatal region that lasted for months after the drug was withdrawn. However, giving the animals a dose of methamphetamine reversed the depressive effects on the synaptic machinery.

They concluded that the mechanism they discovered “might provide a synaptic basis that underlies addiction and habit learning and their long-term maintenance.”

Permanent drug seeking and relapse after renewed drug administration are typical behavioral patterns of addiction. Molecular changes at the connection points in the brain’s reward center are directly responsible for this. The results provide researchers with new approaches in the medical treatment of drug addiction.

Addiction leaves detectable traces in the brain: In particular regions of the brain, which produce the messenger substance dopamine, the drug cocaine causes changes at the synapses, the points of connection between two neurons. As a result, the modified synapse becomes able to transmit nervous signals with enhanced strength, and drug addiction develops.

Using genetic engineering have now been able to selectively switch off those substances under the influence of cocaine.

The scientists performed standardized tests to measure addictive behavior in the animals. At first sight, both the genetically modified and the control animals displayed the usual behavior under the influence of cocaine.

Says lead investigator Günther Schütz: “Our results open up whole new prospects for treating addiction.”

A research team has found that test mice with cocaine cravings had increased amounts of melanin-concentrating hormone (MCH) and dopamine in their brain. When experimental compounds blocking MCH proteins were administered, those cravings disappeared.

Their findings could mean a new approach to overcoming addiction.

The study identified how dopamine works in the brain’s “pleasure center” to create an addictive response to cocaine use.

Dopamine is a neurotransmitter essential to the normal functioning of the central nervous system. It also is associated with feelings of pleasure and is released in the brain during eating, sex and drug use. Heightened levels of the neurotransmitter have been detected in drug addicts.

The study is the first to detail the effects of MCH and dopamine in cocaine addiction and show that it occurs in a portion of the brain believed to play an important role in addiction and feelings of pleasure and fear.

In humans, MCH is also involved with the regulation of feeding behavior and energy balance. High levels of the hormone can intensify feelings of hunger, and researchers worldwide have been seeking compounds to lower MCH for potential use in the treatment of obesity.

Although ecstasy and cocaine are psychoactive substances frequently used by teenagers, very few studies have been done to analyse the short and long-term consequences of joint exposure to these drugs.

Exposure to ecstasy or cocaine during adolescence increases the so called “reinforcing effects” that make people vulnerable to developing a drug addiction. This is the main conclusion of a recent study, which has shown for the first time how these changes persist into adulthood.

The study, published in the journal Addiction Biology , shows for the first time that exposure to these drugs during adolescence leads to long-lasting changes that increase the likelihood of addiction in the long term.

The research team studied the joint consumption of different drugs in mice in order to carry out an in-depth examination into the effects of this interaction.

The results highlight that the so-called “reinforcing effects” are greater in adult mice treated with ecstasy or cocaine during adolescence than in adolescent mice not exposed to these drugs.

“Adolescence is a critical stage in development, during which time drug consumption affects certain brain processes in ways that cause changes that persist right through to adulthood”, adds the scientist.