Wednesday, January 28, 2015

Smoking and Sadness


The chemistry of sorrow during nicotine withdrawal.

When you smoke a cigarette, nicotine pops into acetylcholine receptors in the brain, the adrenal glands, and the skeletal muscles, and you get a nicotine rush. Just like alcohol, a cigarette alters the transmission of several important chemical messengers in the brain. “These are not trivial responses,” said Professor Ovide Pomerleau of the University of Michigan Medical School. “It’s like lighting a match in a gasoline factory.”

Experiments at NIDA’s Addiction Research Center in Baltimore have confirmed that nicotine withdrawal not only makes people irritable, but also impairs intellectual performance. Logical reasoning and rapid decision-making both suffer during nicotine withdrawal. Acetylcholine appears to enhance memory, which may help explain a common lament voiced by many smokers during early withdrawal. As summarized by one ex-smoker, “I cannot think, cannot remember, cannot concentrate.”

But there is another, less widely discussed aspect of nicotine withdrawal: profound sadness. Profound enough, in many cases, to be diagnosed as clinical unipolar depression.

 Of course, people detoxing from addictive drugs like nicotine are rarely known to be happy campers. But quitting smoking, for all its other withdrawal effects, reliably evokes a sense of acute nostalgia, like saying goodbye to a lifelong friend. The very act of abstinence produces sadness, joylessness, dysphoria, melancholia—all emotional states associated with unipolar depression.

Work undertaken by Dr. Alexander Glassman and his associates at the New York State Psychiatric Institute has nailed down an unexpectedly strong relationship between prior depression and cigarette smoking, and the findings have been confirmed in other work. This sheds important light on the question of why some smokers repeatedly fail to stop smoking, regardless of the method or the motivation.  The problem, as Glassman sees it, is “an associated vulnerability between affective [mood] disorders and nicotine.”

A group of Canadian researchers, working out of the Centre of Addiction and Mental Health (CAMH), and the Department of Psychiatry at the University of Toronto, believe they have isolated the specific neuronal mechanisms responsible for the profound sadness of the abstinent smoker.

Writing in the Archives of General Psychiatry, the investigators, who had access to what the CAMH proudly calls the only PET scanner in the world dedicated to mental health and addiction research, gave PET scans to 24 healthy smokers and 24 healthy non-smokers. Non-smokers were scanned once, while heavy and moderate cigarette smokers were scanned after smoking a cigarette, and also after a period of acute withdrawal. Earlier research of this kind had focused on nicotine’s effect on dopamine release. But Ingrid Bacher and her coworkers in Toronto were measuring MAO-A levels in the prefrontal and anterior cingulate regions, two areas known to be involved in “affect,” or emotional responses. When patients suffering from major depressive disorders get scanned, they tend to show elevated levels of MAO-A. The so-called MAO-A inhibitors Marplan, Nardil, Emsam, and Parnate are still in use as antidepressant medications. In general, the higher the levels of MAO-A, the lower the levels of various neurotransmitters crucial to pleasure and reward. A high level of MAO-A would suggest that the enzyme was significantly altering the activity of serotonin, dopamine, and norepinephrine in brain regions involved in mood.

The researchers found that smokers in withdrawal had 25-35% more MAO-A binding activity than non-smoking controls. “This finding may explain why heavy smokers are at high risk for clinical depression," says Dr. Anthony Phillips, Scientific Director of the Canadian Institutes of Health Research's (CIHR's) Institute of Neurosciences, Mental Health and Addiction, which funded this study.

Although researchers involved in these kinds of drug studies almost always claim that the work is likely to lead to new pharmacological therapies, the plain truth is that such immediate spinouts are rare. But in this case, it does seem like the study provides a clear incentive to investigate the clinical standing of MAO-A inhibitors as an adjunct therapy in stop-smoking programs. “Understanding sadness during cigarette withdrawal is important because this sad mood makes it hard for people to quit, especially in the first few days,” said Dr. Jeffrey Meyer, one of the study authors.

As one addiction researcher noted, an associated vulnerability to depression “isn’t going to cover everybody’s problem, and it doesn’t mean that if you give up smoking, you’re automatically going to plunge into a suicidal depression. However, for people who have some problems along those lines, giving up smoking definitely complicates their lives.”


Bacher, I., Houle, S., Xu, X., Zawertailo, L., Soliman, A., Wilson, A., Selby, P., George, T., Sacher, J., Miler, L., Kish, S., Rusjan, P., & Meyer, J. (2011). Monoamine Oxidase A Binding in the Prefrontal and Anterior Cingulate Cortices During Acute Withdrawal From Heavy Cigarette Smoking Archives of General Psychiatry, 68 (8), 817-826 DOI: 10.1001/archgenpsychiatry.2011.82

(First published 8-4-11).


Friday, January 23, 2015

The Losing Battle For Perpetual Reward


Or why you can't stay high forever.

The amphetamine high, like the cocaine high, is a marvel of biochemical efficiency. Stimulants work primarily by blocking the reuptake of dopamine molecules in the synaptic gap between nerve cells. Dopamine remains stalled in the gap, stimulating the receptors, resulting in higher dopamine concentrations and greater sensitivity to dopamine in general. Since dopamine is involved in moods and activities such as pleasure, alertness and movement, the primary results of using cocaine or speed—euphoria, a sense of well being, physical alertness, and increased energy—are easily understood. Even a layperson can tell when lab rats have been on a meth binge. The rapid movements, sniffing, and sudden rearing at minor stimuli are not that much different in principle from the outward signs of meth intoxication among higher primates.

Chemically, cocaine and amphetamine are very different compounds. Psychoactively, however, they are very much alike. Of all the addictive drugs, smoked cocaine and speed have the most direct and most devastatingly euphoric effect on the dopamine systems of the brain. Cocaine and amphetamine produce rapid classical conditioning in addicts, demonstrated by the intense cravings touched off by such stimuli as the sight of a building where the user used to buy or sell. Environmental impacts of this nature can produce marked blood flow increases to key limbic structures in abstinent addicts.

In clinical settings, cocaine users have a hard time distinguishing between equal doses of cocaine and Dexedrine, administered intravenously. As we know, it is the shape of the molecule that counts. The amphetamines are shaped like dopamine and norepinephrine, two of the three reward chemicals. Speed, then, is well suited to the task of artificially stimulating the limbic reward pathway. Molecules of amphetamine displace dopamine and norepinephrine in the storage vesicles, squeezing those two neurotransmitters into the synaptic gap and keeping them there. By mechanisms less well identified, cocaine accomplishes the same feat. Both drugs also interfere with the return of dopamine, norepinephrine, and serotonin molecules to their storage sacs, a procedure known as reuptake blocking. Cocaine works its effects primarily by blocking the reuptake of dopamine.

Amphetamine was once one of the most widely prescribed drugs in the pharmacological cornucopia. It exists in large part now as a recreational drug of choice, abuse, and addiction. The same is true of cocaine. It was replaced as a dental anesthetic long ago, in favor of non-addictive variants like Novocain. The same tragic list of statistical side effects that apply to abusers of alcohol, heroin and nicotine also apply to stimulant abusers: Increased risk of car accidents, homicides, heart attack, and strokes.

In the late 1990s, scientists at Johns Hopkins and NIDA showed that opiate receptors play a role in cocaine addiction as well. PET scans demonstrated that cocaine addicts showed increased binding activity at mu opiate receptors sites in the brain during active cocaine addiction. Take away the cocaine, and the brain must cope with too many empty dopamine and endorphin receptors. It is also easy to understand the typical symptoms of cocaine and amphetamine withdrawal: lethargy, depression, anger, and a heightened perception of pain. Both the cocaine high and the amphetamine high are easily augmented with cigarettes or heroin. These combinations result in “nucleus accumbens dopamine overflow,” a state of neurochemical super saturation similar to the results obtained with the notorious “speedball”—heroin plus cocaine.

With the arrival of smokable forms of cocaine and amphetamine, the race to pin down the biology of stimulation became even more urgent. Stimulants in smokable form—crack and ice—are even more rapidly addictive for addiction-prone users. “The reason has to do with the hydraulics of the blood supply,” a researcher at the University of Minnesota explained to me. “High concentrations are achieved with each inhalation, and sent right upstairs to the brain—but not all of the brain simultaneously. The target of the flow of blood is the limbic system, whereas the remainder of the brain is exposed to much milder concentrations.”

This extraordinarily concentrated jolt to the reward center is the reason why smokable cocaine and speed are able to pack such a wallop. The entire range of stimulative effects hits the ventral tegmental area and associated reward regions of the brain in seconds, and the focused nature of the impact yields an astonishingly pleasurable high.

But the long-term result is exactly the opposite. It may sound dour and religious, but the scientific fact of the matter is that continuous chemical pleasure extracts its fee in the end: The body’s natural stock of these neurotransmitters starts to fall as the brain, striving to compensate for the artificial flooding of the reward center, orders a general cutback in production. At the same time, the receptors for these neurotransmitters become excessively sensitive due to the frequent, often unremitting nature of the stimulation.

“It’s clear that cocaine causes depletion of dopamine, norepinephrine, serotonin—it is a general neurotransmitter depleter,” said my research source. “That may account for many of the effects we see after someone has stopped using cocaine. They’re tired, they’re lethargic, they sleep; they may be depressed, moody, and so on.” Continued abuse of stimulant drugs only makes the problem worse. One reason why cocaine and amphetamine addicts will continue to use, even in the face of rapidly diminishing returns, is simply to avoid the crushing onset of withdrawal. Even though the drugs may no longer be working as well as they once did, the alternative—the psychological cost of withdrawal—is even worse. In the jargon used by Alcoholics Anonymous, addicts generally have to get worse before they can get better.

When addicts talk about “chasing a high,” the metaphor can be extended to the losing battle of neurotransmitter levels.

[First published September 28, 2011]

Graphics Credit: http://www.keepcalm-o-matic.co.uk

Monday, January 12, 2015

Next acudetox counseling training by Dr. Michael O.Smith in Delhi on 25th Jan,2015





Nada India Foundation and Budha Acupuncture Centre are pleased to announce the next NADA Ear Acupuncture (Acudetox Counselling) workshop  as per NADA Protocol for addiction treatment and general well  being will be held at  Buddha Acupuncture Centre,3261,Ram Nagar Shahdara, Delhi-32 on 25 Jan 2015 (10 AM-5 PM).

The workshop will be conducted by Dr.Michael O.Smith psychiatrist & acupuncturist and Dr.Raj Kumar ,MBBS ,NADA,ADS.  NADA Protocol was developed by Dr.Michael O.Smith psychiatrist  and facilitated by Suneel Vatsyayan,Chairperson,Nada India.
The workshop aims to facilitate a shared understanding of importance of barrier free services and skill in use ear acupuncture for protection and recovery as an adjunct treatment at all stages of addiction treatment (pre-admission, detoxification and rehabilitation and after care).  This workshop also provides trainees with skills to use ear acupuncture as per NADA protocol .This also enables trainees in building greater confidence in producing effective approach in dealing with people who avoid treatment,  

The programme brief is discussed below. The course shall provide:

• Class room inputs

• Reading Material

• Rigorous hands on practice

• Complementary advisory and troubleshooting support services through electronic media or phone.
If you are interested in the programme, please send an email along with filled registration form nadaindia@gmail.com . The registration fee for the workshop is Rs.1200/- (One Thousand and two hundred only for physicians and acupuncturist for Acupuncture Detoxification Specialist  training ) Rs.1200/- for Acupuncture Detoxification Associates and Rs.600/- (Six hundred only as Acupuncture Detoxification  Assistants ) for counselors, social workers and addiction professionals which includes a lunch, tea, online course material and video on NADA protocol etc. and certificate. You can send the cheque in the name of “Nada India Foundation”.  Since the number of participants for the workshop will be limited, please confirm your participation at the earliest by calling Dr.Raj Kumar(Mob:- 09873498780) Ms.Pallavi 09810594544 and send an email nadaindia@gmail.com 
I shall be happy to answer any queries that you may have in this regard.

I look forward to your kind cooperation.

With best regards,
Yours Sincerely,
Dr.Ajay Vats,NADA,ADS 
www.acudetoxindia.com


The contribution for workshop does not include boarding and lodging of the trainees

Wednesday, January 7, 2015

Rotting from the Inside


Smoking and the decline of the body. 

We all know smoking is bad for your health. It causes lung cancer and emphysema and contributes to heart disease. But that’s not the end of the list. Recently, Public Health England, a government organization, collected and analyzed research on the contribution smoking makes to other forms of internal body damage. Authored by Dr. Rachael Murray of the UK Centre for Tobacco and Alcohol Studies and the University of Nottingham, the study looked at the correlation between smoking and the musculoskeletal system, the cognitive system, dental health, and vision.

And the results of various meta-analyses are exactly as grim as we might expect. (You can download the PDF HERE.)

Bones, Muscle, and Tissue

Smoking does steady harm to the musculoskeletal system of habitual smokers. Osteoporosis in mature smokers may result from a loss of bone mineral density, a condition for which smoking “is a long established contributing risk factor.” There are a number of ways smoking can affect bone mineral density, says the report, including “decreased calcium absorption, lower levels of vitamin D, changes in hormone levels, reduced body mass, increased free radicals and oxidative stress, higher likelihood of peripheral vascular disease and direct effects of toxic components of tobacco smoke on bone cells.”

Moreover, smoking and broken bones go together like apple pie and ice cream, or in this case, bangers and mash. Overall in the UK, “current smokers have been reported to be at a 25% increased risk of any fracture,” the report concludes. The author notes that the greatest risk for smokers are seen at the hip and the lumbar spine, and women smokers in particular “were at a 17% greater risk of hip fracture at age 60, 41% at 70, 71% at 80 and 108% at 90.” The risk of fracture and the increased bone repair time decreases slowly in former smokers, and it may take 5 to 10 years before abstinent smokers see any statistical benefits.

Researchers have also documented a causal relationship between cigarette smoking and the onset of rheumatoid arthritis. But it is not known whether smoking cessation benefits existing patients with this condition.

As for soft tissue damage, a meta-analysis of 40 studies showed that smoking was associated with “a 33% increased prevalence of low back pain within the previous 12 months, 79% increased prevalence of chronic back pain and 114% increased prevalence of disabling lower back pain” among British smokers. Another study of 13,000 subjects showed that current and ex-smokers experienced up to 60% more pain in the lower back, upper neck and lower limbs than people who had never smoked. Smokers were also “74% more likely than non-smokers to have a rotator cuff tear,” Dr. Murray writes.

The Brain in Your Head

Chronic cigarette smoking hastens the decline in cognitive function that occurs with age. And there is a disturbing link between tobacco smoking and dementia: “A meta-analysis of eight studies published in 2008 reported that current smokers were 59% more likely than never-smokers to suffer Alzheimer’s disease and 35% more likely to suffer vascular dementia.” Earlier studies showed even higher risk percentages. Here, there is the possibility that smoking succession could reduce dementia onset. Two meta-analyses included in the report showed no association between former smoking and risk of dementia.

General cognitive impairment in adults over 50 is “consistently associated” with smoking, according to the UK report. “Faster declines in verbal memory and lower visual search speeds have been reported in male and female smokers aged 43 and 53, with the effect largest in those who smoked more than 20 cigarettes per day, independent of other potentially confounding factors.”

Dental Damage

Smoking is the primary cause of oral cancer, and the risk of developing it is three times less for non-smokers. Smoked and smokeless tobacco are linked to various non-malignant maladies of the soft and hard tissues in the oral cavity. Alcohol is a risk factor for oral cancer as well, “and is almost tripled in alcohol drinkers who smoke.”

Peridontitis, the inflammatory condition marked by bleeding gums and degeneration leading to tooth loss (and an associated greater risk of coronary heart disease) is three to four times as common in adult smokers. And although there are other confounding socioeconomic influences, smoking is also a risk indicator for missing teeth in older smokers and previous smokers. The increased peridontitis risk lasts for several years after smoking cessation.

As for cavities and general tooth decay (caries), “Although the association between smoking and prevalence of dental caries can be attributed to poor dental care and oral hygiene, a cross-section study with a four-year follow-up found that daily smoking independently predicts caries development in smokers.” 

A Dim View

Neovascular and atrophic age-related macular degeneration, the eye conditions that cause a gradual loss of vision, are causally related to cigarette smoking. "A recent meta-analysis reported significant increases in macular degeneration of between 78% and 358%, depending on the study design." Smokers tend to develop the disease ten years earlier than non-smokers, and heavy smokers are at particular risk.

Finally, a number of cohort and case-control studies show a statistically significant link between smoking and cataracts, the cloudy patches over the eye that cause blurred vision. In current smokers, the increased risk is pegged at about 50%. "Smoking cessation reduces risks over time, however, the larger the exposure the longer it takes for the risk to reduce and this risk is unlikely to return to that of a never smoker."


Saturday, January 3, 2015

The Greeks and the Romans on Alcohol


Wine and Beer in Antiquity

"When men drink, then they are rich and successful and win lawsuits and are happy and help their friends. Quickly, bring me a beaker of wine, so that I may wet my mind and say something clever."
Aristophanes

"I like best the wine drunk at the cost of others."
Diogenes

"Persians are quite devoted to drinking wine….”                                                                   
Herodotus

“We should not drink like the Carmani… These people, namely, eager to prove their friendship in their drinking bouts, open the veins of the forehead, and mixing the blood which streams down in their wine, they imbibe it, in the belief that to taste each other’s blood is the highest proof of friendship.”
Poseidonius

“The wine urges me on, the bewitching wine, which sets even a wise man to singing and to laughing gently and rouses him up to dance and brings forth words which were better unspoken.”
Homer

“This is the great evil in wine, it first seizes the feet; it is a cunning wrestler.”
Plautus

 “Wine prepares the heart for love unless you take too much.”
Ovid

“Three bowls only do I mix for the temperate—one to health, which they empty first, the second to love and pleasure, the third to sleep. When this is drunk up wise guests go home. The fourth bowl is ours no longer, but belongs to violence; the fifth to uproar, the sixth to drunken reveal, the seventh to black eyes.”
Dionysus, by way of Eubulus

 “The peoples of the Mediterranean began to emerge from barbarism when they learnt to cultivate the olive and the vine.”                                             
Thucydides

 “…the Egyptians became fond of wine and bibulous; and so a way was found among them to help those who could not afford wine, namely, to drink that made from barley; they who took it were so elated that they sang, danced, and acted in every way like persons filled with wine.”
Athenaeus


Sources:

http://www.theworldwidewine.com/Wine_quotes/Greek_and_Roman_wine_quotes.php

http://www.academia.edu/1803087/

http://www.beekmanwine.com/factsquotes.htm


Graphics Credit: http://www.opwine.com/