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Smoking changes brain chemistry
by Radiological Society of North America
Reposted from:
http://www.eurekalert.org/pub_releases/2006-11/rson-scb112206.php
CHICAGO -- Chronic smoking affects nerve cells and alters the chemical makeup of the brain, according to research presented today at the annual meeting of the Radiological Society of North America (RSNA).
"This is the first imaging study to focus on the relationship between brain metabolites and nicotine dependence," said Okan Gür, M.D., from the Department of Radiology at the University of Bonn in Germany.
Dr. Gür and colleagues used proton magnetic resonance spectroscopy (MRS) to study 21 men and 22 women, age 21 to 59, in a smoking cessation program two weeks after quitting and again six months later. Patients were encouraged to use nicotine patches during the initial six weeks of smoking cessation; however, only 36 of the patients complied.
Proton MRS is able to measure brain metabolism at the cellular level and can provide detailed chemical data about the brain's metabolites, which are involved in many physical and chemical processes within the body.
The researchers compared the data collected from the smokers to proton MRS data collected from 35 age- and gender-matched healthy controls.
The results showed that the nicotine-dependent patients had significantly decreased concentrations of the amino acid N-acetylaspartate (NAA) in the anterior cingulate cortex (ACC), the part of the brain that processes pleasure and pain. The decreased NAA levels were evident regardless of whether or not the patient used a nicotine patch and correlated directly with the patient's smoking history: the greater the number of pack years (one pack per day for one year equals one pack year), the lower the NAA level.
"The ACC is involved in mediating conditioned reinforcement, craving and relapsing behavior in addiction," said study co-author Christian G. Schütz, M.D., M.P.H., from the Department of Psychiatry at the University of Bonn. "Lower NAA levels have been implicated as indicators of neuronal or axonal dysfunction."
Reduced NAA levels have been reported for a number of psychiatric and mood disorders, including schizophrenia, dementia and bipolar disorder, as well as in cases of substance abuse, particularly alcohol dependence.
Choline concentrations in the ACC were slightly lower in the smokers compared with the nonsmokers, and lower still in the female smokers compared with the male smokers.
Choline is significantly involved in cell membrane metabolism, which is essential for cardiac and brain function. Reduced choline levels can be a precursor to the breakdown of cell membranes.
Concentration of total creatine (tCr) levels in the frontal lobes was typically higher in the smokers who did not use patches compared to those who did. The metabolite tCr plays an important role in supplying energy to the muscle cells. Higher tCr levels have been associated with stimulant use. Furthermore, the researchers found that high tCr levels predicted a higher likelihood of relapse.
Upon follow-up after six months, the researchers found that most metabolite concentrations, including that of NAA, had normalized in the 25 ex-smokers who did not relapse.
"These findings further emphasize the importance of quitting smoking," Dr. Gür said. "The degree of reduction of NAA in the ACC depends on the amount of tobacco consumed over time, but it appears to normalize after smoking cessation."
###
Co-authors are Hans H. Schild, M.D., Wolfgang Block, Ph.D., Frank Träber, Ph.D., and Wolfgang Maier, M.D.
http://www.eurekalert.org/pub_releases/2006-11/rson-scb112206.php
CHICAGO -- Chronic smoking affects nerve cells and alters the chemical makeup of the brain, according to research presented today at the annual meeting of the Radiological Society of North America (RSNA).
"This is the first imaging study to focus on the relationship between brain metabolites and nicotine dependence," said Okan Gür, M.D., from the Department of Radiology at the University of Bonn in Germany.
Dr. Gür and colleagues used proton magnetic resonance spectroscopy (MRS) to study 21 men and 22 women, age 21 to 59, in a smoking cessation program two weeks after quitting and again six months later. Patients were encouraged to use nicotine patches during the initial six weeks of smoking cessation; however, only 36 of the patients complied.
Proton MRS is able to measure brain metabolism at the cellular level and can provide detailed chemical data about the brain's metabolites, which are involved in many physical and chemical processes within the body.
The researchers compared the data collected from the smokers to proton MRS data collected from 35 age- and gender-matched healthy controls.
The results showed that the nicotine-dependent patients had significantly decreased concentrations of the amino acid N-acetylaspartate (NAA) in the anterior cingulate cortex (ACC), the part of the brain that processes pleasure and pain. The decreased NAA levels were evident regardless of whether or not the patient used a nicotine patch and correlated directly with the patient's smoking history: the greater the number of pack years (one pack per day for one year equals one pack year), the lower the NAA level.
"The ACC is involved in mediating conditioned reinforcement, craving and relapsing behavior in addiction," said study co-author Christian G. Schütz, M.D., M.P.H., from the Department of Psychiatry at the University of Bonn. "Lower NAA levels have been implicated as indicators of neuronal or axonal dysfunction."
Reduced NAA levels have been reported for a number of psychiatric and mood disorders, including schizophrenia, dementia and bipolar disorder, as well as in cases of substance abuse, particularly alcohol dependence.
Choline concentrations in the ACC were slightly lower in the smokers compared with the nonsmokers, and lower still in the female smokers compared with the male smokers.
Choline is significantly involved in cell membrane metabolism, which is essential for cardiac and brain function. Reduced choline levels can be a precursor to the breakdown of cell membranes.
Concentration of total creatine (tCr) levels in the frontal lobes was typically higher in the smokers who did not use patches compared to those who did. The metabolite tCr plays an important role in supplying energy to the muscle cells. Higher tCr levels have been associated with stimulant use. Furthermore, the researchers found that high tCr levels predicted a higher likelihood of relapse.
Upon follow-up after six months, the researchers found that most metabolite concentrations, including that of NAA, had normalized in the 25 ex-smokers who did not relapse.
"These findings further emphasize the importance of quitting smoking," Dr. Gür said. "The degree of reduction of NAA in the ACC depends on the amount of tobacco consumed over time, but it appears to normalize after smoking cessation."
###
Co-authors are Hans H. Schild, M.D., Wolfgang Block, Ph.D., Frank Träber, Ph.D., and Wolfgang Maier, M.D.
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Posted: Wednesday, November 29, 2006 | PermalinkComments 1 - 5 of 5 |
Reload Comments | Back to Top | Page Numbers2. Comment #20236 by Homo economicus on February 1, 2007 at 8:10 am
Well at least on July 1st onwards people where I work should become less depressed thanks to a smoke free environment. Other Comments by Homo economicus
3. Comment #108454 by DrMotley on January 7, 2008 at 12:05 am
NICOTINE BENEFITSBy Wanda Hamilton
Researchers have long been aware that fewer smokers get Alzheimer's and Parkinson's diseases than non-smokers. Up to April l992, of the 17 studies on Alzheimer's and smoking which had been published in peer-reviewed journals, 13 reported a reduced risk for smokers and only four found no difference between smokers and non-smokers. Similar findings have been published on the effect of smoking and Parkinson's disease.
In an article in The Times of London (9/7/93), Dr. James Le Fanu provided an examination of the research on smoking and its apparent protective effect for certain diseases. Dr. Le Fanu stated unequivocally: "Smokers have a 50 per cent reduced risk of developing Alzheimer's--and the more smoked the greater the protection." He also noted that emerging research points to a similar effect of smoking on Parkinson's disease.
So striking was the apparent protective effect of smoking on Alzheimer's and Parkinson's that increasingly biomedical researchers are experimenting with nicotine to treat the symptoms of these dread disease in-patients who have been diagnosed as having them. Results from these experiments have all showed promise in alleviating the symptoms of these diseases with the administration of nicotine.
The mechanism by which the nicotine in tobacco works to protect smokers is that it increases the number of so-called "nicotinic" receptors in the brain, which in turn influence the production and release of the neurotransmitter acetylcholine. Those who come down with Alzheimer's show a marked loss of "nicotinic" receptors in their brains and thus have reduced levels of acetylcholine, which is necessary for memory and other brain functions.
Research has shown that tobacco smoke (and the nicotine therein) inhibits the activity of monoamine oxidase B (MAOB). Experiments on mice which were genetically engineered to be without the gene for MAOB "were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease," (Dr. Jean C. Shih researcher at the University of Southern California, as reported in Reuters, 10/7/97, "Isoenzyme Inhibited by cigarette Smoke May Have Role in Aging and Neurodegeneration"). The findings of Dr. Shih and her colleagues point to a protective effect from smoking on the aging of the brain.
Other diseases for which smoking and nicotine appear to be protective are ulcerative colitis, Tourette's Syndrome, and possibly rheumatoid arthritis and colorectal cancer.
Below are excerpts from some recent articles and studies on nicotine, Alzheimer's, Parkinson's, cognitive abilities, Tourette's and ulcerative colitis.
"In human studies, reported performance improvements with post-trial administration of nicotine have all involved associated learning (Mangan and Golding l883; Colrain et al, l992; Warburton et al, l992).... Nicotine improves performance by increasing the attentional resources available for such strategic processing," [Rusted JM, et al, "Facilitation of memory by post-trial administration of nicotine: evidence for attentional explanation," Psychopharmacology, 108(4):452-5, l992].
"1. Nicotine improves attention in a wide variety of tasks in healthy volunteers. 2. Nicotine improves immediate and longer-term memory in healthy volunteers. 3. Nicotine improves attention in patients with probable Alzheimer's Disease," [Warburton D M, "Nicotine as a cognitive enhancer," Progress in Neuro-Psychopharmacology and Biological Psychiatry, 16(2): 181-91, Mar l992]
"Researchers observed lessening of tic frequency and severity 3 minutes after subjects chewed [nicotine] gum, even more so at 10 minutes." [Rickards E H, "Nicotine gum in Tourette's disorder," American Journal of Psychiatry, 149(3):417, Mar l992. Note: the subjects were all children with Tourette's disorder].
"In humans, nicotine-induced improvement of rapid information processing is particularly well documented.... Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine." [Levin E D, "Nicotinic systems and cognitive function," Psychopharmacology, 108(4):417-31, l992]
"Improvement in attention, learning, reaction time, and problem solving have been reported.... Different processes, including attention, stimulus evaluation, and response selection, appear to be involved in the effect of nicotine on human information processing." [Le Houezec J, Benowitz N L, "Basic and clinical psychopharmacology of nicotine," Clinics in Chest Medicine, 12(4):681-99, Dec l991].
"Despite the absence of change in memory functioning, these results demonstrate that DAT [Alzheimer's disease] patients have significant perceptual and visual attentional deficits which are improved by nicotine administration." [Jones G M, Sahakian B J, et al, "Effects of acute subcutaneous nicotine on attention, information processing and short-term memory in Alzheimer's disease," Psychopharmacology, 108(4):485-94, l992].
"When you look at people who smoke, and people who don't smoke...you find those who smoke cigarettes are about half as likely to get Parkinson's disease." [Dr. David Morens of the University of Hawaii School of Public Health as quoted in "Stunned docs discover cigarettes stop Parkinson's," by Roger Field, New York Post, 6/15/95. Dr. Morens and colleagues examined 34 studies on smoking and Parkinson's. Their study was published in the June, l995 issue of Neurology].
According to a study conducted at Surrey University and published in the journal Psychopharmacology, smokers are more mentally alert at night than non-smokers. Rosemary Brook, spokeswoman for Surrey University's psychopharmacology unit, said, "The results showed that smokers were subsequently able to perform various tests of reaction, memory recall and other related tasks consistently better than the non-smokers," [Reported on the BBC News, 4/8/98, "Cigarettes 'keep you sharp after dark'."
In a presentation at the 151st annual meeting of the American Psychiatric Association (June 8, l998 in Toronto), Dr. Paul Newhouse of the University of Vermont reported on his research on treating Parkinson's disease with nicotine. "Preliminary analysis shows improvements after acute nicotine administration in several areas of cognitive performance." These areas included reaction time and central processing speed. The researchers also reported that after chronic use of nicotine on Parkinson's patients, motor function and the ability to move also improved. [Reported by Reuters, 6/8/98, "Nicotine patch promising for Parkinson's"].
"The influence of smoking on the risk of developing ulcerative colitis is well documented. Compared with lifetime nonsmokers, the risk is reduced in smokers...." [Tysk C, Jarnerot G, "Has smoking changed the epidemiology of ulcerative colitis?" Scandinavian Journal of Gastroenterology, 27(6):508-12, Jun l992].
"When association between cigarette smoking and UC [ulcerative colitis] are examined, never-smokers are approximately three times more likely to develop UC than smokers. A consistent finding from study to study is that quitters have a mildly increased risk of developing UC which suggests that cigarette smoking may have a protective effect," [Lashner B A, "Inflammatory bowel disease: family patterns and risk factors," Comprehensive Therapy, 18(8):2-4, Aug l992].
"It is beyond doubt that smokers are protected against ulcerative colitis, and the more that is smoked the greater the protection--so those on 25 cigarettes a day or more have a risk as little as one-tenth that of non-smokers," (Dr. Martin Osbourne, surgeon at the Royal Free Hospital in London, as quoted in the Daily Telegraph, 9/7/93)
Other Comments by DrMotley
4. Comment #108455 by DrMotley on January 7, 2008 at 12:06 am
THERAPEUTIC EFFECTS OF SMOKING AND NICOTINE,lost of solid articles on forces.org
Other Comments by DrMotley
5. Comment #108456 by Roland_F on January 7, 2008 at 12:38 am
3. Comment #108454 by DrMotleyI am no medical expert to judge which of the articles are right : from 2007 => stop smoking, from 1992 smoke as much as you can.
I just know that Philipp Morris was financing massive pseudeo scientific studies to proof that everyone should smoke as it's so very healthy.
Of course what's a few million US$ to buy positive study outcomes compared with Multibillion $ class action lawsuits,
Other Comments by Roland_F
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1. Comment #10808 by Jim on November 29, 2006 at 9:17 am
Wow. So as I understand it, people who smoke when they are anxious and/or depressed may feel better in the short term, but they're doing greater harm to their psychological state. That's interesting.