Short preamble: I was expecting to find a damning litany of studies admonishing everyone to run, not walk, from smoking. What I found instead was quite surprising. It would seem quite possible that there are certain high-risk groups (for particular diseases) for whom, in the right amount (and concomitant “harm-reduction” strategies designed to mitigate some of the purely harmful constituents of cigarette smoke), cigarette smoking may actually be a net health benefit.
Again, don’t shoot the messenger. To be sure, smoking kills an absurd amount of people every year and if it were up to me every tobacco executive who knew the dangers of smoking (but hid it or otherwise intentionally deceived the public) would be spending life in prison.
Given how well educated the public are on the dangers of cigarette smoking I chose instead to make the focus of this post the undeniable benefits associated with smoking.
Have a look at the data and decide for yourself:
I know, shocking. But this irony wouldn't be complete without her male counterpart:
The longest living man (Shigechiyo Izumi) in history, himself living to be a staggering 120 and 237 days old was...well, you get the idea; the dude was a lifelong smoker as well.
Now they both look fairly busted to be sure, but how do you think you’ll look at 122 years old? Perhaps smoking is the only way you’ll find out. Eheh.
So in the 70’s the government funded extensive research into the dangers of smoking. Their findings continue to confound. Have a look at the research, the daily smoking hamsters lived 22% longer than their buzzkill non-smoking peers:
There also appear to be a number of “harm reduction” techniques that work to offset the clear toxicity of cigarette smoking, these range from IV glutathione to resveratrol (as discussed in the following study):
Resveratrol Protects against Cigarette Smoke–Induced Oxidative Damage and Pulmonary Inflammation
Biodynamics of smoking cigarettes
Interestingly smoking is both a stimulant and depressant and Arousal is increased by the increase of norepinephrine.
Research suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine. This stimulates nerve transmission. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, nicotine potently enhances the actions of norepinephrine and dopamine in the brain, causing a drug effect typical of those of psychostimulants. At higher doses, nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain-killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use.
Pain is also reduced by the increases of acetylcholine and beta-endorphin. Anxiety is reduced by the increase of beta-endorphin. Nicotine also extends the duration of positive effects of dopamine and increases sensitivity in brain reward systems. Most cigarettes (in the smoke inhaled) contain 1 to 3 milligrams of nicotine.
Smoking appears to lowers risks from these and other diseases, cancers, and ailments:
An association between smoking and a lower incidence of Parkinson's disease has been observed in a number of studies. An analysis of longitudinal studies found a protective effect against Parkinson's disease for current and former smokers compared with those who had never smoked; the risk of Parkinson's disease was reduced by about half among everyday smokers (RR 0.51; 95% CI, 0.43–0.61) and this protective effect was more pronounced among current smokers, where the risk was about one-third that of never smokers (RR 0.35; 95% CI, 0.26–0.47). Similar findings of a protective effect for Parkinson's disease were also reported from a case–control study conducted in Japan.
Nicotine is thought to be the chemical in tobacco smoke mostly likely to be implicated in this finding, but there may be other chemicals or compounds involved. Based on data from 2004–05 we can derive theoretical estimates that about 97 deaths from Parkinson's disease are prevented by smoking in Australia annually. Finally, recent research also suggests that nicotine can improve compromised semantic processing in Parkinson's disease, and also influence semantic processing in healthy older individuals.
A study has shown a protective effect of nicotine itself on neurons due to nicotine activation of α7-nAChR and the PI3K/Akt pathway which inhibits apoptosis-inducing factor release and mitochondrial translocation, cytochrome c release and caspase 3 activation.
Pre-eclampsia (hypertension in pregnancy)
This part below is probably of most interest to women considering pregnancy and worth considering:
Pre-eclampsia is a potentially serious condition in pregnancy in which the mother develops high blood pressure, fluid retention and abnormal kidney function. Smokers are less likely to develop pre-eclampsia than non-smokers; recent research points to the impact of smoking on the ratio of soluble fms-like tyrosine kinase-1 (sFlt-1) to placental growth factor (PlGF) as one possible pathway20, however the mechanism by which the observed protective effects occur remains poorly understood.
Nicotine reduces the chance of preeclampsia, and atopic disorders such as allergic asthma. A plausible mechanism of action in these cases may be nicotine acting as an anti-inflammatory agent, and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects.
The teratogenic properties of nicotine has been investigated. According to a study of ca. 77,000 pregnant women in Denmark, women who used nicotine gum and patches during the early stages of pregnancy were found to face an increased risk of having babies with birth defects. The study showed that women who used nicotine-replacement therapy in the first 12 weeks of pregnancy had a 60% greater risk of having babies with birth defects compared to women who were non-smokers.
While 60% is a terrifying number, we should first think about what percent of 77,000 women had babies and weren't exposed to nicotine had babies w/ birth defects…that would be a very low number…it’s that number that you’d increase by 60%…still scary, but not terrifying.
Tobacco use among pregnant women has also been correlated to increased frequency of ADHD. Children born to mothers who used tobacco were two and a half times more likely to be diagnosed with ADHD. Froelich estimated that "exposure to higher levels of lead and prenatal tobacco each accounted for 500,000 additional cases of ADHD in U.S. children".
A study using Swedish birth registry data on more than 600,000 births examined the effects of snuff and cigarette smoking on pre-eclampsia risk and whether changes in tobacco habits during pregnancy affected the risk of developing term pre-eclampsia. Compared with non-tobacco users, light smokers experienced a one-third reduction in risk (OR 0.66; 95% CI, 0.61–0.71) and heavy smokers a halving of risk (OR 0.51; 95% CI, 0.44–0.58) with OR lower for term than preterm pre-eclampsia. The study found that tobacco combustion products rather than nicotine are the probable protective ingredients against pre-eclampsia in cigarette smoke and further concluded that it is smoking behavior in the middle or late rather than in the beginning of pregnancy that seems to have the greatest effect on the risk of pre-eclampsia. The US Surgeon General has concluded that 'the decreased risk of pre-eclampsia among smokers compared with non-smokers does not outweigh the adverse outcomes that can result from prenatal smoking. These conclusions are underscored by findings from a recent case–control study conducted in Canada where notwithstanding a (non-significant) reduction in the risk of pre-eclampsia, persistent smoking was also associated with a 10-fold increase in the risk of low birthweight (OR 10.2; 95% CI, 2.49–41.8) and a four-fold increase in the risk of preterm birth (OR 3.59; 95% CI, 1.06–12.1).
Those at risk for Primary Sclerosing Cholangitis “PSC” might want to drop their wheatgrass shots and pick up the closest cigarette. Kidding of course. In Norway, Denmark, and Sweden PSC is the main cause of liver transplants. A new study there involving 500 PSC patients found that smoking cigarettes exerted significant protection from the disease:
Here are some of the more pronounced dangers and benefits to human cognitive function associated with smoking:
Nicotine's mood-altering effects are different by report: in particular it is both a stimulant and a relaxant. First causing a release of glucose from the liver and epinephrine(adrenaline) from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, sharpness, calmness, and alertness. Like any stimulant, it may very rarely cause the often uncomfortable neuropsychiatric effect of akathisia. By reducing the appetite and raising the metabolism, some smokers may lose weight as a consequence.
When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates the release of many chemical messengers such as acetylcholine, norepinephrine, epinephrine, vasopressin [this is an interesting one that I was clueless to - vasopressin is a potent nootropic!] ,histamine, arginine, serotonin, dopamine, autocrine agents, and beta-endorphin. This release of neurotransmitters and hormones is responsible for most of nicotine's effects. Nicotine appears to enhance concentration and memory due to the increase of acetylcholine. It also appears to enhance alertness due to the increases of acetylcholine and norepinephrine.
Studies have indicated that nicotine can be used to help adults suffering from autosomal dominant nocturnal frontal lobe epilepsy. The same areas that cause seizures in that form of epilepsy are responsible for processing nicotine in the brain.
Studies suggest a correlation between smoking and schizophrenia, with estimates near 75% for the proportion of schizophrenic patients who smoke. Although the nature of this association remains unclear, it has been argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine. Other research found that mildly dependent users got some benefit from nicotine, but not those who were highly dependent.
Research at Duke University Medical Center found that nicotine may improve the symptoms of depression. Nicotine appears to improve ADHD symptoms. Some studies have focused on benefits of nicotine therapy in adults with ADHD.
While acute/initial nicotine intake causes activation of nicotine receptors, chronic low doses of nicotine use leads to desensitisation of nicotine receptors (due to the development of tolerance) and results in an antidepressant effect, with research showing low dose nicotine patches being an effective treatment of major depressive disorder in non-smokers.
Nicotine (in the form of chewing gum or a transdermal patch) has been explored as an experimental treatment for OCD. Small studies show some success, even in otherwise treatment-refractory cases.
A meta-analysis of research into the effects of nicotine and smoking on human performance found positive effects of nicotine or smoking on six domains: (i) fine motor, (ii) alerting attention-accuracy, (iii) response time (RT), (iv) orienting attention-RT, (v) short-term episodic memory-accuracy, and (vi) working memory-RT (effect size range = 0.16 to 0.44). There is evidence that nicotine may stimulate immediate and sustained improvements in working memory, that nicotine replacement in smokers avoids cognitive impairment through direct pharmacological effects on brain neuronal activity, and that nicotine may improve prospective memory (the retrieval and implementation of a previously encoded intention).
Interesting reference material:
Here is a link containing additional information that better explain the biomechanics of cigarettes, for good and ill as it were:
In smaller doses (an average cigarette yields about 1 mg of absorbed nicotine), the substance acts as a stimulant in mammals, while high amounts (500–1000 mg) can be harmful. This stimulant effect is likely a major contributing factor to the dependence-forming properties of tobacco smoking. According to the American Heart Association, nicotine addiction has historically been one of the hardest addictions to break, while the pharmacological and behavioral characteristics that determine tobacco addiction are similar to those determining addiction to heroin and cocaine. The nicotine content of popular American-brand cigarettes has slowly increased over the years, and one study found that there was an average increase of 1.78% per year between the years of 1998 and 2005. This was found for all major market categories of cigarettes.
Although population level effectiveness has not been demonstrated, the primary therapeutic use of nicotine is in treating nicotine dependence in order to eliminate smoking with the damage it does to health. Controlled levels of nicotine are given to patients through gums, dermal patches, lozenges, electronic/substitute cigarettes or nasal sprays in an effort to wean them off their dependence.
For instance, studies suggest that smokers require less frequent repeated revascularization after percutaneous coronary intervention(PCI). Risk of ulcerative colitis has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking. Smoking also appears to interfere with development of Kaposi's sarcoma in patients with HIV.
Tobacco smoke has been shown to contain compounds capable of inhibiting monoamine oxidase [this is mainly what Selegiline does], which is responsible for the degradation of dopamine in the human brain. When dopamine is broken down by MAO-B, neurotoxic by-products are formed, possibly contributing to Parkinson's and Alzheimers disease.
The relationship between smoking and inflammatory bowel disease has been firmly established, but remains a source of confusion among both patients and doctors. It is negatively associated with ulcerative colitis but positively associated with Crohn's disease. In addition, it has opposite influences on the clinical course of the two conditions with benefit in ulcerative colitis but a detrimental effect in Crohn's disease.