Well, I couldn't find any of the data on sott or on the forum. So on my 4 days off work, I basically just trawled through online journals and found loadddds of information that simply hasnt been put out there yet. I will copy and past from the article with the references and studys.
Mono Amine 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 this enzyme to increase the levels of these neurotransmitters and thereby elevating the mood of the individual. 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 studies18
demonstrating that smokers have significantly lower levels of both types of MAO's (A and B), which basically means that smoking acts as a natural antidepressant – without any of the horrible side-effects common to many pharmaceuticals. Another interesting fact is that the drug “Deprenyl”, an MAOI, has also been shown19,20 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 (free radicals), heavy metals, and peroxides/lipid-peroxides. 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 diseases21. 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-smokers22. 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.
Higher concentrations of glutathione in the lungs offer increased protection against foreign material and pathogenic agents. 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 experiment23, 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.
The author said: “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 the “glutathione adaptive response” is the mechanism which drastically up-regulates glutathione systems, both in the lungs and throughout the rest of the body in response to tobacco smoke. 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 smoking OBVIOUSLY doesn't cause COPD. We may even go so far as to assume that smoking can actually
prevent COPD.
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 study24 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 sparate experiment25 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 the protects lung tissue and rids the body of any nasty toxins inhaled via the respiratory tract.
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. But what these anti-smokers probably don't realise is that Carbon Monoxide is actually
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, and is a sure way to protect against disease. Other popular hormetic agents include curcumin, a compound found in green tea, and exercise.
Fortunately for smokers, 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, says26:
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 your body is in a constant state of producing and recycling CO, and CO poisoning only can 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 any kind of poisoning. With this in mind, you can now feel safe in knowing that as long as you don't stick your head in front of a car exhaust pipe, the chances of you experiencing carbon monoxide poisoning is near enough
zero. To the contrary, the amount of carbon monoxide inhaled from cigarettes will likely have a hormetic affect on your body.
References:
18. Fowler J, Volkow N, Wang G, Pappas N, Logan J, Shea C et al. Brain monoamine oxidase A inhibition in cigarette smokers. Proceedings of the National Academy of Sciences [Internet] 1996 [cited 2016 Mar 10];93:14065-14069. Available from: http://www.pnas.org/content/93/24/14065.full
19. Milgram N, Racine R, Nellis P, Mendonca A, Ivy G. Maintenance on L-deprenyl prolongs life in aged male rats. [Internet]. PubMed, NCBI1990 [cited 2016 Mar 10];Available from: http://www.ncbi.nlm.nih.gov/pubmed/2118586
20. Yen T, Knoll J. Extension of lifespan in mice treated with Dinh lang (Policias fruticosum L.) and (-)deprenyl. [Internet]. PubMed, NCBI1992 [cited 2016 Mar 10];Available from: http://www.ncbi.nlm.nih.gov/pubmed/1304677
21. Ballatori N, Krance S, Notenboom S, Shi S, Tieu K, Hammond C. Glutathione dysregulation and the etiology and progression of human diseases. Biological Chemistry 2009;390.
22. Cantin A, North S, Hubbard R, Crystal R. Normal alveolar epithelial lining fluid contains high levels of glutathione. Journal of Applied Physiology [Internet] 1987 [cited 2016 Mar 10];63:152-157. Available from: http://jap.physiology.org/content/63/1/152
23. Gould N, Min E, Gauthier S, Martin R, Day B. Lung glutathione adaptive responses to cigarette smoke exposure. Respiratory Research 2011;12:133.
24. Jenifer H, Bhola S, Kalburgi V, Warad S, Kokatnur V. The influence of cigarette smoking on blood and salivary super oxide dismutase enzyme levels among smokers and nonsmokers—A cross sectional study. Journal of Traditional and Complementary
Medicine 2015;5:100-105.
25. Mccusker K, Hoidal J. Selective Increase of Antioxidant Enzyme Activity in the Alveolar Macrophages from Cigarette Smokers and Smoke-exposed Hamsters. Am Rev Respir Dis 1990;141:678-682.
26. Naito Y, Uchiyama K, Takagi T. Therapeutic Potential of Carbon Monoxide (CO) for Inflammatory Bowel Disease. Digestion 2015;91.
