About 7.4 million people will be saved from premature death by 2050 due to the tobacco control measures, which have been put in place in 41 countries between 2007 and 2010, a new study has revealed.

The study demonstrates the success of the World Health Organization Framework Convention on Tobacco Control (WHO FCTC) in reducing tobacco use and, thus, saving lives.

Lead author David Levy, PhD, professor of oncology at Georgetown Lombardi Comprehensive Cancer Center in Washington, said that it is a spectacular finding that by implementing these simple tobacco control policies, governments can save so many lives.


Known as "MPOWER," the measures correspond to one or more of the demand reduction provisions included in the WHO FCTC: Monitoring tobacco use and prevention policies, Protecting people from tobacco smoke, Offering help to quit tobacco use, Warning people about the dangers of tobacco, Enforcing bans on tobacco advertising, Promotion and sponsorship, and Raising taxes on tobacco.

The authors did a modeling exercise and projected the number of premature deaths that would be averted by 2050 through the implementation of one or more of these measures.

Levy said that in addition to some 7.4 million lives saved, the tobacco control policies that they examined could lead to other health benefits like lesser adverse birth outcomes related to maternal smoking, including low birth weight, and reduced health-care costs and less loss of productivity due to less smoking-related disease.

If these high-impact tobacco control measures were implemented even more widely, millions more smoking-related deaths would be averted, Douglas Bettcher, MD, director of the department of non-communicable diseases at WHO, said.

Bettcher said that the tobacco use is the single most preventable cause of death in the world, with six million smoking-attributable deaths per year today, and these deaths are projected to rise to eight million a year by 2030, if current trends continue.
The study has been published in the Bulletin of the World Health Organization.

A single dose of a stimulant drug prescribed to treat Attention Deficit Hyperactivity Disorder (ADHD) could improve brain function and modify connectivity in parts of the brain that are involved with self-control and craving when given to cocaine addicts, according to a new study.

Methylphenidate (brand name Ritalin) normalizes certain brain circuits that underlie self-control and craving among cocaine-addicted individuals, researchers from the Icahn School of Medicine at Mount Sinai found.

Previous research has shown that oral methylphenidate improved brain function in cocaine users performing specific cognitive tasks such as ignoring emotionally distracting words and resolving a cognitive conflict. Similar to cocaine, methylphenidate increases dopamine (and norepinephrine) activity in the brain, but, administered orally, takes longer to reach peak effect, consistent with a lower potential for abuse. By extending dopamine`s action, the drug enhances signaling to improve several cognitive functions, including information processing and attention.

"Orally administered methylphenidate increases dopamine in the brain, similar to cocaine, but without the strong addictive properties," said Rita Goldstein, PhD, Professor of Psychiatry at Mount Sinai, who led the research while at Brookhaven National Laboratory (BNL) in New York. "We wanted to determine whether such substitutive properties, which are helpful in other replacement therapies such as using nicotine gum instead of smoking cigarettes or methadone instead of heroin, would play a role in enhancing brain connectivity between regions of potential importance for intervention in cocaine addiction."

Anna Konova , a doctoral candidate at Stony Brook University, who was first author on this manuscript, added, "Using fMRI, we found that methylphenidate did indeed have a beneficial impact on the connectivity between several brain centers associated with addiction."

Dr. Goldstein and her team recruited 18 cocaine addicted individuals, who were randomized to receive an oral dose of methylphenidate or placebo. The researchers used functional magnetic resonance imaging (fMRI) to measure the strength of connectivity in particular brain circuits known to play a role in addiction before and during peak drug effects. They also assessed each subject`s severity of addiction to see if this had any bearing on the results.

Methylphenidate decreased connectivity between areas of the brain that have been strongly implicated in the formation of habits, including compulsive drug seeking and craving. The scans also showed that methylphenidate strengthened connectivity between several brain regions involved in regulating emotions and exerting control over behaviors-connections previously reported to be disrupted in cocaine addiction.

"The benefits of methylphenidate were present after only one dose, indicating that this drug has significant potential as a treatment add-on for addiction to cocaine and possibly other stimulants," said Dr. Goldstein. "This is a preliminary study, but the findings are exciting and warrant further exploration, particularly in conjunction with cognitive behavioral therapy or cognitive remediation."

The study has been published in JAMA Psychiatry, a JAMA network publication.

Researchers have found just thinking about being stressed can make individuals fall seriously ill and even increase the chance of suffering a heart attack.

It was found, while following more than 7,000 civil servants over a period of up to 18 years, how the increased perception of stress almost doubled the risk of suffering a heart attack.
The is the first time a link has been discovered between heart disease and people`s own view on how stress is affecting their health, Daily Mail reported.

It suggests the doctors should take a patients` perspective into account when managing stress-related complaints.

It could also mean that helping patients to unwind can reduce the risk of cardiovascular disease.

Participants, who had an average age of 49.5, were asked to what extent they felt day-to-day stress had affected their health. Besides taking their medical background into account, they were also asked about personal lifestyle factors such as smoking, alcohol consumption, diet, and exercise.

Lead author Hermann Nabi, from the Inserm medical research institute in Villejuif, France, said: "We found that the association we observed between an individual`s perception of the impact of stress on their health and their risk of a heart attack was independent of biological factors, unhealthy behaviours and other psychological factors.

"One of the important messages from our findings is that people`s perceptions about the impact of stress on their health are likely to be correct."

The Health Ministry has banned three medicines in a move to avert the health risks associated with them.

According to report in a leading daily, the manufacture and sale of all three drugs - painkiller Analgin, anti-diabetes drug Pioglitazone and its combinations, and anti-depressant Deanxit- have been banned under Section 26A of the Drugs and Cosmetics Act, 1940 with immediate effect, through a notification issued on June 18.

While Pioglitazone is banned in France as it is believed to cause urinary bladder cancer and heart failure, it is sold in the US and Europe with a boxed warning.
Analgin is sold under various trade names, including Metamizole, Algozone, Algocalmin, Analgin, Dipirona, Novalgin, Neo-Melubrina and Optalgin. It was withdrawn from the market in various countries after it was found that it can cause a potentially fatal condition called agranulocytosis.

Earlier in January 2013, manufacturers were given six months by the Drugs Controller General of India to establish safety and effectiveness of Deanxit for sale in the country as it has been banned in Denmark, its country of origin. Under the Drugs and Cosmetic Rule 30-B, a drug cannot be marketed in India unless it is approved in its country of origin. The drug is banned in other countries as well as its user experienced cardiovascular effects, dizziness, fatigue, insomnia and vomiting.

Researchers have been able to identify and deactivate a brain pathway, in rats, which is associated to memories that cause cravings for alcohol.

Lead author Segev Barak, PhD, UC San Francisco, said that one of the main causes of relapse is craving, triggered by the memory by certain cues - like going into a bar, or the smell or taste of alcohol.

He said that they learned that when rats were exposed to the smell or taste of alcohol there was a small window of opportunity to target the area of the brain that reconsolidates the memory of the craving for alcohol and to weaken or even erase the memory, and thus the craving.

In the first phase of the study, rats had the choice to freely drink water or alcohol over the course of seven weeks, and during this time developed a high preference for alcohol.

In the next phase, they had the opportunity to access alcohol for one hour a day, which they learned to do by pressing a lever. They were then put through a 10-day period of abstinence from alcohol.

Following this period, the animals were exposed for 5 minutes to just the smell and taste of alcohol, which cued them to remember how much they liked drinking it.

The researchers then scanned the animals` brains, and identified the neural mechanism responsible for the reactivation of the memory of the alcohol - a molecular pathway mediated by an enzyme known as mammalian target of rapamycin complex 1 (mTORC1).

They found that just a small drop of alcohol presented to the rats turned on the mTORC1 pathway specifically in a select region of the amygdala, a structure linked to emotional reactions and withdrawal from alcohol, and cortical regions involved in memory processing.

They further showed that once mTORC1 was activated, the alcohol-memory stabilized (reconsolidated) and the rats relapsed on the following days, meaning in this case, that they started again to push the lever to dispense more alcohol.

Barak said that the smell and taste of alcohol were such strong cues that we could target the memory specifically without impacting other memories, such as a craving for sugar.

In the next part of the study, the researchers set out to see if they could prevent the reconsolidation of the memory of alcohol by inhibiting mTORC1, thus preventing relapse. When mTORC1 was inactivated using a drug called rapamycin, administered immediately after the exposure to the cue (smell, taste), there was no relapse to alcohol-seeking the next day. Strikingly, drinking remained suppressed for up to 14 days, the end point of the study. These results suggest that rapamycin erased the memory of alcohol for a long period, said Ron.
The authors also said it would be interesting to test if rapamycin, an FDA-approved drug currently used to prevent organ rejection after transplantation, or other mTORC1 inhibitors that are currently being developed in pharmaceutical companies, would prevent relapse in human alcoholics.

The study has been published online in Nature Neuroscience.