Min menu


Discover a way to quit smoking by stimulating the brain

brain chemistry changes after quitting smoking when do dopamine levels return to normal after quitting smoking quitting smoking brain fog reddit how long does it take for brain chemistry to return to normal after quitting smoking nicotine withdrawal too much oxygen after quitting smoking blood circulation after quitting smoking nicotine brain fog reddit

A team of scientists from the Dijon Burgundy University Medical Center in France have discovered a way to get the smoker to quit by non-invasive stimulation of the brain.

According to the journal Addiction, the non-surgical brain stimulation method NIBS, is currently used in the treatment of alcohol and drug addiction disorders and other psychoactive substances. But researchers in the new study decided to determine its effectiveness in treating nicotine addicts.

To this end, they conducted a systematic review and comprehensive analysis of NIBS 'effectiveness in smoking cessation over a prolonged period. In addition, seven other studies involved about 700 patients.

The researchers found that smoking addicts who underwent NIBS in 3-6 months had a chance to quit for a prolonged period, 2.39 times higher than smokers who were exposed to fictitious NIBS.

Solve the mystery of why many "lifelong smokers" don't have lung cancer!

  • Smoking cigarettes is the first risk factor for lung cancer, with tobacco products causing up to 90% of lung cancer deaths in the United States.
  • The safest way to protect yourself from lung cancer is undoubtedly to avoid smoking cigarettes
  • but at the same time, it is also true that not all lifelong smokers are sentenced to cancer.

In fact, the vast majority do not. Scientists have long questioned why, and a new study, "Beta Hair", adds to the idea that genes have a role to play.

Researchers found an inherent advantage among people who smoke but never develop lung cancer. Cells lining their lungs appear to be less likely to mutate over time.

Results suggest that DNA repair genes are more active among some individuals, which can protect against the onset of cancers, even when cigarettes are smoked regularly.

The study benefited from the genetic features taken from the trachea of 14 never-smokers, and 19 light, medium and heavy smokers.

Surface cells collected from participants' lungs were individually arranged to measure mutations in their genomes.

  1. Epidemiologist and pulmonologist Simon Spivak
  2. of the Albert Einstein College of Medicine, explains
  3. "These lung cells live for years, even decades
  4. and therefore mutations can accumulate with age and smoking. 
  5. Of all types of lung cells, these are among the most vulnerable to cancer. "

The results show "unequivocally" that human lung mutations increase with normal age, and among smokers, DNA damage is more important.

Tobacco smoke has long been associated with DNA damage in the lung, but the new study found that not all smokers in the same boat.

While someone's smoking amount was associated with an increase in cell mutation rates, after about 23 years of smoking one can a day, this is a risk.

"Heavier smokers did not have the brunt of mutations" says Spivak. Our data indicate that these individuals may have survived for a long time despite their excessive smoking because they were able to suppress further accumulation of mutations ".

The results can help explain why 80 to 90% of lifelong smokers do not have lung cancer. It can also help explain why some people who do not smoke at all have tumours.

  • While toxic tobacco smoke appears to cause additional cell mutations in the lung
  • the evolution of these mutations into tumours depends on the body's ability to repair DNA or reduce DNA damage.
  • Genes involved in DNA repair can be inherited or acquired
  • and silencing repair genes has been associated with tumor development in previous research.

Nor are genes the only factors affecting a person's risk of cancer. Environmental factors such as diet can also affect nutrients in the body that affect tumor development.