Potential health benefits of smoking tobacco - Part Two

Original article here

How tobacco may have health benefits - the science:

Nicotine is one of the main components of tobacco and displays a wide variety of healing properties, hence why it is currently the subject of some fascinating new scientific research. To truly appreciate the benefits of nicotine however, we must first examine it’s primary mechanisms of action. Nicotine is the protoypic agonist of the nicotinic subtype of acetylcholine rectopors. What this basically means is that nicotine is compatible with acetylcholine receptors in the body and has the ability to bind to them. This action is responsible for triggering a cascade of chemical reactions, although it’s main effect is to stimulate the release of a wide variety of neurotransmitters including dopamine, serotonin, noradrenaline and primarily acetylcholine. According to Dr Gabriela Segura(12) “Acetylcholine is a neurotransmitter responsible for learning and memory. It is also calming, relaxing and is also a major factor regulating the immune system. Acetylcholine also acts as a major brake on inflammation in the body and inflammation is linked to every known disease.” When nicotine binds to α7 nAChR (acetylcholine receptors tied to immunity), it activates a system known as the ‘cholinergic anti-inflammatory pathway’ which is responsible for decreasing inflammation in the body. Therefore, nicotine is actually an anti-inflammatory molecule.

The paper(13) titled “Nicotine, an anti-inflammation molecule” deals with this topic extensively. According to the paper: Nicotine stimulation plays a key role in suppressing cytokine production, can significantly down-regulate and delay inflammatory and autoimmune responses in the central nervous system, and could further attenuate neuro-inflammation. Nicotine treated mice injected with lethal doses of influenza A virus infection also displayed longer survival rates when compared to control groups. The author finally states:

“These in vitro and in vivo results further confirmed the anti-inflammatory effect of nicotine. Our study offered the first evidence that the anti-inflammatory effect of nicotine in cigarette smoke might be the key contributor for the alleviation of the disease severity of both pdmH1N1 and H9N2 influenza A virus infection, and such anti-inflammatory effect was through the α7 nAChR signaling pathway.”

Considering the beneficial influence of acetylcholine on the brain and nervous system, lets take a look at how smoking affects brain function.

A commonly known fact amongst cognitive psychologists and neuroscientists is that nicotine significantly increases cognitive functioning. The U.S, government published a meta-analysis study(14) in 2010 which reviewed all of the literature on nicotine’s effect on the brain which was conducted by the National Institute on Drug Abuse. Out of a total of 256, 48 of the highest quality standardised computer test studies were chosen for review. On these tests, half of the participants received nicotine and the other half were given a placebo. The results showed that people who received nicotine performed better on almost every test despite whether they were smokers or not, and this was especially in areas of memory, speed, precision, focus and attention. The study also showed that nicotine users performed significantly better in other areas such as long-term memory, semantic memory, arithmetic & complex calculations, and gross motor skills.

Nicotine is clearly very beneficial for cognitive function, but when compared to smoking we can see that nicotine simply isn’t as effective. A study(15) conducted by Warburton et al found:

“[Smoke-free] nicotine produces improvements in mental efficiency, which are qualitatively similar to the improvements produced by smoking, although our findings on vigilance and rapid information processing indicate that the improvements are quantitatively smaller than those produced by smoking”

Another study(16) published in 2014 showed that an increase in nicotine receptors (induced by smoking) was associated with lower levels of social withdrawal and better cognitive function. There is actually a wealth of information on nicotine’s favourable physiological effects which can be retrieved from scientific data alone, yet none of this information manages to filter through to the public eye. However, this should not be surprising for those who understand how often mainstream media and Big Pharma effectively distort or suppress information which is not conducive to the official narrative they are attempting to convey.

Finally, to quote researcher David. M. Warburton from the Department of Psychology at the University of Reading(17):

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.

4.While some of the memory effects of nicotine may be due to enhanced attention, others seem to be the result of improved consolidation as shown by post-trial dosing.

Now lets take a look at some of the other potentially therapeutic and beneficial aspects of the tobacco plant:

Monoamine Oxidase Inhibition

Monoamine oxidases (MAO’s) are enzymes in the body that are responsible for degrading biogenic amine neurotransmitters such as Noradrenaline (Norepinephrine), Serotonin and Dopamine. Mono amine oxidase inhibitors (MAOI’s) are chemicals that inhibit the action of these enzymes to increase the availability and quantity of the biogenic amines. For this reason, MAOI containing drugs were developed by pharmaceutical companies in the late 1950’s and were sold as anti-depressants. Interestingly enough however, an unknown property of tobacco smoke has been shown to contain naturally occurring MAOI’s. This is reflected in numerous studies(18) demonstrating that smokers have significantly lower levels of both types of MAO’s (A and B), which basically means that smoking can act as a natural antidepressant without some of the horrible side effects common to many synthetic pharmaceutical drugs. Another interesting fact is that the drug “Deprenyl”, an MAOI, has also been shown(19,20) to markedly increase the lifespan of a variety of mammallian species in lab settings on several occasions. This fact is something to keep in mind, because we will be returning to it later on.

Glutathione: The “Master Antioxidant”

As an antioxidant, Glutathione’s function is to protect virtually every cell in the body by neutralizing damage caused by reactive oxygen-species, heavy metals, and peroxides/lipid-peroxides etc. It is a chief component of the body’s natural defence systems and is required for the accomplishment of a host of cellular processes which include cellular differentiation and proliferation. What makes glutathione so special is that, unlike other antioxidants, it is intracellular and has the ability to maintain other antioxidants in their reduced (active) form to maximise antioxidant activity. It plays a critical role in detoxification processes, hence why the majority of the body’s stores can be found in the liver. It also influences immune function significantly, and glutathione depletion has been associated with cancer, diseases of aging, cystic fibrosis, cardiovascular, inflammatory, immune, metabolic, and neurodegenerative diseases(21). The alternative health community acknowledges this molecule as the “mother of all antioxidants”, and rightly so. Interestingly, smokers lungs have been found to contain 80% more glutathione than the lungs of non-smokers(22). The author of the study states:

Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF [epithelial lining fluid] total glutathione, 98% of which was in the reduced form. [/quote]

What these findings suggest is that smoking tobacco may actually have a protective effect on lung tissue by up-regulating glutathione levels, however the mechanism behind this up-regulation was not covered in this particular study. Another experiment(23), however, sought to directly measure glutathione’s response to tobacco smoke and here’s what they found:

CS [cigarette smoke] exposure initially decreased ELF GSH [glutathione] levels by 50% but within 2 h GSH levels rebound to about 3 times basal levels and peaked at 16 h with a 6-fold increase and over repeat exposures were maintained at a 3-fold elevation for up to 2 months.

“CS exposures evoke a powerful GSH adaptive response in the lung and systemically. […] Factors that disrupt GSH adaptive responses may contribute to the pathophysiology of COPD.”

So first of all, they theorize that a smoking-induced “glutathione adaptive response” is the mechanism which drastically up-regulates glutathione systems in this case. This also implies that tobacco has a protective effect on the lungs. Secondly, they state that factors disrupting this mechanism may contribute to Chronic Obstructive Pulmonary Disorder (COPD). This statement contradicts mainstream health sources, because according to these sources, smoking is the main cause of COPD. Yet if smoking clearly upregulates the “glutathione adaptive response”, and COPD is caused by an under active “glutathione adaptive response”, then how can smoking alone be the main cause of COPD? Hmmmm...

Catalase and Superoxide Dismutase

Catalase is an antioxidant enzyme that functions to protect cells from the damaging effects of hydrogen peroxide by catalysing it’s conversion into oxygen and water. It is therefore an important component of the body’s immune and detoxification pathways. Superoxide dismutase (SOD) is also an important antioxidant enzyme that neutralizes superoxide, a by-product of oxygen metabolism. Together, these are two of the body’s most remarkable antioxidants which play critical roles in protecting against oxidative/peroxidative cellular damage and are closely tied to longevity. Much like glutathione, catalase and SOD also appear to be controlled by some kind of antioxidant “adaptive response”. A recent study(24) found that “Superoxide dismutase enzyme levels in the blood and saliva were significantly higher in smokers than in nonsmokers and the controls”. Furthermore, it was also discovered in a separate experiment(25) that tobacco smoke-exposed hamsters were shown to have roughly double the amount of both Catalase and Superoxide Dismutase than hamsters who were not exposed to smoke.

The increase in glutathione, catalase and superoxide dismutase may be partly be able to explain how tobacco smoke manages to prevent lung cancer in those inhalling radiation, exhaust fumes and asbestos. Such an increase in antioxidant activity could be the key factor which protects lung tissue against external damage.

Hormesis?

One common criticism made by anti-smokers is that tobacco smoke contains Carbon Monoxide, which is supposedly poisonous, so therefore smoking is bad. However, this view is based on the faulty assumption that any dose of carbon monoxide is harmful. No doubt, a high dose of carbon monoxide can be fatal. Interestingly low dose carbon monoxide appears to actually be hormetic. The process of Hormesis is characterised by the introduction of a low-dose toxin into the body which triggers the body to respond in a beneficial way. On the other hand, at high doses the same toxin has a detrimental effect. Hormesis is one of the body’s most effective means of making adaptive changes on the cellular level in response to external stressors by up-regulating detoxification pathways etc. Other popular hormetic agents include curcumin and polyphenol compounds in green tea. Heck, even exercise is said to be hormetic!

There is now a growing body of evidence demonstrating carbon monoxide’s potent hormetic effects and potential therapeutic benefits. Researchers at the Molecular Gastroenterology and Hepatology department of research at the University of Kyoto, Japan, say(26):

Recent accumulating evidence has suggested that carbon monoxide (CO) may act as an endogenous defensive gaseous molecule to reduce inflammation and tissue injury in various organ injury models, including intestinal inflammation.

…Potent therapeutic efficacies of CO have been demonstrated in experimental models of several conditions, including lung injuries, heart, hepatic and renal I-R injuries, as well as inflammation, including arthritis, supporting the new paradigm that CO at low concentrations functions as a signaling molecule that exerts significant cytoprotection and anti-inflammatory actions.

Now consider the fact that the human body continuously goes through a constant state of producing and recycling CO, and CO poisoning can only occur when the body becomes overburdened by an extremely large amount. Cigarette smoke contains such low quantities of CO that it would be pretty much impossible to smoke enough to induce poisoning. With this in mind, it is safe to assume that as long as someone doesn’t stick their head in front of a car exhaust pipe, the chances of them experiencing carbon monoxide poisoning from smoking tobacco are pretty low. To the contrary, the amount of carbon monoxide inhaled from cigarettes may actually have a hormetic effect.

Tobacco provides PROTECTION?

According to conventional medical dogma, tobacco is mankind’s worst enemy. As the evidence suggests, tobacco smoke possesses a wide variety of medicinal properties that are clearly beneficial to human health and longevity. To add to this, there have been several studies that demonstrate tobacco’s protective effects against numerous disease-causing agents and chronic health conditions.

First of all, one study(27) conducted on the respiratory health of aluminium potroom workers showed that “smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers”. Considering the above information, these results are not surprising. Furthermore, smoking also appears to protect against several other seemingly unrelated health issues.

For example, it has been well documented that smoking vastly decreases someone’s risk of developing osteoarthritis (OA)(28) and provides some level of protection against it. Smokers demonstrate significant protection at four sites commonly seen in OA patients (knee, spine, hand and foot)(29). Smoking also presents a negative correlation with large joint OA and has been shown to decrease the risk of OA in obese individuals(30). Experts have theorized that this may be because nicotine may has beneficial effect on bone maintenance, growth and repair, and according to L. Gullahorn, M.D(31) “of the more than 400 agents found in cigarette smoke, nicotine is one of the most physiologically active components. An in vitro study recently published demonstrates that nicotine is a potent stimulator of bone cell synthetic activity“.

Secondly, it is commonly known amongst the scientific community that neurological diseases such as Alzheimer’s and Parkinson’s present a much lower risk in smokers… so much so that methods of treatments using nicotine (and it’s byproducts) are now being developed by pharmaceutical companies as neurological treatments.

Thacker et al(32) analysed data including the smoking histories of 79,977 women and 63,348 men and found that, when compared with non smokers, former smokers had a 22% lower risk of developing Parkinson’s disease, while current smokers had a staggering 73% lower risk. Gorel et al(33) also reported an inverse association between smokers and Parkinson’s. But the interesting thing about this study was that the inverse association strongly increased with people who were heavy smokers. These results suggest that the more a person smokes, the lower the chances are of contracting this disease. The authors even concluded:

“The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.”

Yet another study(34) also concluded “we report here that nicotine afforded neuroprotection to dopamine neurons”.

Similar results have also been found in studies on Alzheimer’s disease. A strong inverse association between smokers and individuals with Alzheimer’s has been shown(35), and according to the author:

“the risk of Alzheimer’s disease decreased with increasing daily number of cigarettes smoked before onset of disease”.

With these results in mind, smoking tobacco seems to be an effective preventative measure. Researchers are still speculative as to how this protection and treatment occurs, although most seem to be confident that it is related to nicotine. Nicotine has also been used to effectively treat individuals with Attention Deficit Hyperactivity Disorder and Tourette’s sydrome. In addition to this, cotinine is a substance that is now being studied for its potential therapeutic benefits. It is one of nicotine’s metabolites and has been shown to improve learning, memory and which also has the ability to protect brain cells from the damage caused by both of these diseases

Another well documented fact is that the rates of smoking amongst schizophrenic’s are typically much higher than in the average population, with some studies(36) showing that approximately 90% are smokers. Yet, curiously enough, schizophrenics have been shown(37) to be between 30-60% less likely to develop lung and other cancers. So what do these figures suggest about smoking as the main cause for cancer? I will let you decide.

It has been theorized that these high smoking rates could be due to the stimulating cognitive effects of nicotine may help schizophrenics filter out irrelevant external sensory information. A study(38) at Yale university found:

“when study subjects with schizophrenia stopped smoking, attention and short-term memory were more impaired, but, when they started smoking again, their cognitive function improved.”

Evidence from Sweden has also shown(39) that the more cigarettes men smoked at an earlier age, the lower chance they had of developing schizophrenia later on in life. The conclusion was that smoking can act as a neuro-protective preventative measure against developing schizophrenia.

Western medicine is renowned for pumping patients full of dangerous and ineffective medications for the profit of Big Pharma corporations. The system not only provides a lack of genuine support to people with mental-health problems, but what is even more appalling is that many institutions actually deprive in-patients of the right to smoke, despite it being one of the most effective means of self-medication.

Aside from neurological diseases, smoking has been found to consistently reduce the risk of developing Ulcerative Colitis. According to Lashner et al(40) “Non-smokers are approximately three times more likely to develop Ulcerative colitis”. One review(41) suggests that current smokers are associated with an approximately 42% reduced risk, however former smokers are associated with increased risk when compared to non-smokers. This evidence seems to indicate that smoking may be protective, and people who quit smoking actually place themselves at a higher risk. To add to this, smokers with Ulcerative colitis have also been found to present more benign symptoms than those who did not smoke(41).

Interestingly, smoking does not seem to benefit many of the people who are diagnosed with Crohn’s disease though. Both men and women are at a much higher risk of developing Crohn’s if they are smokers, and one study(42) even suggests a threefold increased risk in women who smoked. This unusual fact seemingly doesn’t make any sense if we consider these data alone. However, a growing body of evidence is shining light on possible the genetic origins of this disease. Likewise, an increasing amount of evidence is coming to light regarding the possible genetic component that may play a role in tobacco smoking and nicotine consumption. Similar genetic patterns in blood have been found among smokers when compared to non-smokers. Some genes have also been found(43) to be more active in smokers, whilst others were less active when compared to non smokers. Researchers(44) theorise that genes responsible for neurotransmitter production and metabolism, cell receptor regulation and nicotine metabolism may play an important role in determining whether someone is likely to smoke or not.

What strikes me as most compelling here is that the evidence points to there being an undeniable biological difference between smokers and non-smokers. Perhaps this can help to explain why some people are naturally drawn to smoking when they are in their teenage years, while others go a whole lifetime without having any urge to smoke. It may also account for why some smokers can live a very long life without developing lung cancer, whereas someone else may smoke for a couple of years and not benefit from the protective properties whatsoever. With genetics in mind, the Crohns/Ulcerative Colitis paradox doesn’t seem so odd. Perhaps someone’s smoking-compatible genetics may also act as a protective factor against other pathological conditions? Science is yet to answer these questions.

End of part two.....