mugacoffee
Jedi Master
Thanks guys. I'm on the ol' iodine and have been since nov. tomorrow I start the salt drinks. Will check iodine thread..
A new article was posted on SOTT today about high GI foods being a risk for lung cancer. In the study they found that non-smokers were more at risk as well, but still said people shouldn't smoke. Thought it was pretty funny. 
http://www.sott.net/article/314032-White-bread-bagels-increase-risk-of-lung-cancer-by-49-percent-with-non-smokers-more-at-risk-study-finds
http://www.sott.net/article/314032-White-bread-bagels-increase-risk-of-lung-cancer-by-49-percent-with-non-smokers-more-at-risk-study-finds
N
Nico
Guest
Is there any chance the "genetic smoker's profil" might change in the course of life, due for exemple to epigenetics ? The C's told to Ark that to begin using "spiritual" smoking he had to begin the "work". So in conjonction with the transformation of DNA which is a benefit of Working I suppose that one could become a holy smoker ?
I start smoking because of the "exteriors" benefits describe by the researches here on the forum, such as protecting the lungs and increasing psychic capabilities but at some point I asked myself if I was really right for that, because of symptomes of mine like a burning in the left lung, some headache and white tongue. Then this morning, after reducing smoking during two days, I tried to smoke more mindfully, and in following my sensations, several new smells and tastes came up, and also a thought of what Gurdjieff said about tobacco which have the symbolic three forces in it. So as my perceptions evolved I maybe have became a more smoker... or not.
Good to all.
I start smoking because of the "exteriors" benefits describe by the researches here on the forum, such as protecting the lungs and increasing psychic capabilities but at some point I asked myself if I was really right for that, because of symptomes of mine like a burning in the left lung, some headache and white tongue. Then this morning, after reducing smoking during two days, I tried to smoke more mindfully, and in following my sensations, several new smells and tastes came up, and also a thought of what Gurdjieff said about tobacco which have the symbolic three forces in it. So as my perceptions evolved I maybe have became a more smoker... or not.
Good to all.
Ok guys. I have been researching tobacco a lot recently and have been wanting to understand the physiology behind why smoking is actually beneficial for one's health. This information is slightly lacking on the forum and SOTT, and to be honest - it has not been fully explicated anywhere online. So I decided to compose an article which included everything that I have come to understand about tobacco and which is all backed up by hard scientific evidence that I have derived mainly from online journals. I had originally submitted it to SOTT yesterday, and I am also going to post some of it here. As I said, there is a LOT of information that has not been made available. Redfox suggested on another thread that I respost this information on this thread, and I fingured it would probably be best to present the rest of the info aswell.
I will cut out some sections of the article and try to include mainly the research:
[...]
But in spite of this, the relatively few pieces of unbiased and objective scientific research on smoking have provided us with some fascinating data which I will attempt to briefly summarise below.
First of all, a recent study suggested that people with a diet high in GI (Glycemic index) foods (such as breads, pastas and rice) were almost 50% more likely to develop lung cancer. Within these results, non-smokers were found to be twice as likely to develop the cancer when compared with smokers. This finding alone could be explained as simply being anomalous, but as we move one through the evidence base, you will begin to understand how it fits into the bigger picture.
There was another study3 that measured the carcinogenic effects of radon after radioactive uranium ore dust was inhaled by dogs. Paradoxically, unlike the usual fatalities witnessed in other dogs during similar experiments, none of the dogs exposed to tobacco contracted cancer. The author stated “exposure to cigarette smoke was found to have a mitigating effect on radon daughter-induced tumors”. Similarly an experiment4 on irradiated rats showed that those who smoked and were irradiated showed significantly less inflammation in the lungs than those who did not smoke. In many ways, the smoking group resembled the non-irradiated controls. According to the author “this experimental study further supported the suppressive effect of smoking on radiation-induced pneumo-nitis.”
In human research, one analysis5 showed that the risk of developing lung cancer from asbestos exposure was “significantly increased in non-smokers in six of the studies [reviewed]”. Another study6 suggested that the risk of developing lung cancer from asbestos exposure is approximately three times higher in non-smokers than it is in smokers. After breast cancer radiotherapy treatment, smokers have also been observed7 to display a “significantly decreased inflammatory reaction i.e., reduced levels of mast cells and lymphocytes, compared to both non-smoking controls and patients”. In these instances, some effect of smoking clearly erected a protective barrier against radiation damage and asbestos.
Smoking may also protect against different kinds of environmental pollution, such as exhaust fumes. A recent study8 on miners has shown a strong link between diesel engine exhaust fume exposure and lung cancer. The results show that miners who were heavily exposed have three times the higher risk of dying from lung cancer compared with miners with low exposure. Whereas for non-smokers, the risk was seven times higher.
According to the World Health Organisation9 “Tobacco use is the single most important risk factor for cancer causing... around 70% of global lung cancer deaths.” Examining the statistics paints a slightly different picture however, and it becomes clear that this statement is simply not true.
Above are statistics provided by the World Economic Forum with data collected showing the countries that smoke the most cigarettes per capita. If smoking is the cause of 70% of all lung cancer cases globally, then it would make sense that the lung cancer statistics match up with the results on this table. For example China, Russia, USA, Indonesia and Japan should theoretically have the highest rates of lung cancer because they have the highest rate of smoking. Except they don't.
Interestingly, the above lung cancer statistics taken from the World Cancer Research Fund International only feature one of the countries said to have the highest smoking rate, and that's the USA. This data completely disproves what the WHO and other health authorities have said for years about smoking causing lung cancer. Smoking clearly does NOT cause lung cancer.
The Black Lung Lie
Another common misconception surrounding smoking cigarettes is that they are capable of turning the lungs black. What most are unaware of though is that this is physically impossible. The lung tissue can only turn black when it is either cancerous, or when significant amounts of elemental carbon is inhaled for prolonged periods of time. Where can you find elemental carbon? In coal mines, not in cigarettes. Here are some first hand accounts from professionals working from within the field of medicine10:
Finally, here is a quote from Richard White's Smoke Screens11:
I will cut out some sections of the article and try to include mainly the research:
[...]
But in spite of this, the relatively few pieces of unbiased and objective scientific research on smoking have provided us with some fascinating data which I will attempt to briefly summarise below.
First of all, a recent study suggested that people with a diet high in GI (Glycemic index) foods (such as breads, pastas and rice) were almost 50% more likely to develop lung cancer. Within these results, non-smokers were found to be twice as likely to develop the cancer when compared with smokers. This finding alone could be explained as simply being anomalous, but as we move one through the evidence base, you will begin to understand how it fits into the bigger picture.
There was another study3 that measured the carcinogenic effects of radon after radioactive uranium ore dust was inhaled by dogs. Paradoxically, unlike the usual fatalities witnessed in other dogs during similar experiments, none of the dogs exposed to tobacco contracted cancer. The author stated “exposure to cigarette smoke was found to have a mitigating effect on radon daughter-induced tumors”. Similarly an experiment4 on irradiated rats showed that those who smoked and were irradiated showed significantly less inflammation in the lungs than those who did not smoke. In many ways, the smoking group resembled the non-irradiated controls. According to the author “this experimental study further supported the suppressive effect of smoking on radiation-induced pneumo-nitis.”
In human research, one analysis5 showed that the risk of developing lung cancer from asbestos exposure was “significantly increased in non-smokers in six of the studies [reviewed]”. Another study6 suggested that the risk of developing lung cancer from asbestos exposure is approximately three times higher in non-smokers than it is in smokers. After breast cancer radiotherapy treatment, smokers have also been observed7 to display a “significantly decreased inflammatory reaction i.e., reduced levels of mast cells and lymphocytes, compared to both non-smoking controls and patients”. In these instances, some effect of smoking clearly erected a protective barrier against radiation damage and asbestos.
Smoking may also protect against different kinds of environmental pollution, such as exhaust fumes. A recent study8 on miners has shown a strong link between diesel engine exhaust fume exposure and lung cancer. The results show that miners who were heavily exposed have three times the higher risk of dying from lung cancer compared with miners with low exposure. Whereas for non-smokers, the risk was seven times higher.
According to the World Health Organisation9 “Tobacco use is the single most important risk factor for cancer causing... around 70% of global lung cancer deaths.” Examining the statistics paints a slightly different picture however, and it becomes clear that this statement is simply not true.
Above are statistics provided by the World Economic Forum with data collected showing the countries that smoke the most cigarettes per capita. If smoking is the cause of 70% of all lung cancer cases globally, then it would make sense that the lung cancer statistics match up with the results on this table. For example China, Russia, USA, Indonesia and Japan should theoretically have the highest rates of lung cancer because they have the highest rate of smoking. Except they don't.
Interestingly, the above lung cancer statistics taken from the World Cancer Research Fund International only feature one of the countries said to have the highest smoking rate, and that's the USA. This data completely disproves what the WHO and other health authorities have said for years about smoking causing lung cancer. Smoking clearly does NOT cause lung cancer.
The Black Lung Lie
Another common misconception surrounding smoking cigarettes is that they are capable of turning the lungs black. What most are unaware of though is that this is physically impossible. The lung tissue can only turn black when it is either cancerous, or when significant amounts of elemental carbon is inhaled for prolonged periods of time. Where can you find elemental carbon? In coal mines, not in cigarettes. Here are some first hand accounts from professionals working from within the field of medicine10:
Finally, here is a quote from Richard White's Smoke Screens11:
The Health benefits of Tobacco
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 Segura12 “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 paper13 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 study14 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 study15 conducted by Warburton et al found that “[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 study16 published in 2014 showed that an increase in nicotine receptors (induced by smoking) was associated with lower levels of social withdrawal, better cognitive function, and blunted emotional and motivational responses. 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 effectively distorts or dismisses inconvenient truths 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 Reading17:
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 Segura12 “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 paper13 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 study14 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 study15 conducted by Warburton et al found that “[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 study16 published in 2014 showed that an increase in nicotine receptors (induced by smoking) was associated with lower levels of social withdrawal, better cognitive function, and blunted emotional and motivational responses. 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 effectively distorts or dismisses inconvenient truths 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 Reading17:
Now lets take a look at some of the other potentially therapeutic and beneficial aspects of the tobacco plant...
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:
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:
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:
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.
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:
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:
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:
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.
Tobacco: Natures Defence?
According to conventional medical dogma, tobacco is mankind's worst enemy. As the evidence suggests however, 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 study27 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 what we now know about tobacco, these results are not surpising. Furthermore, smoking also appears to protect against several other seemingly unrelated issues that are separate from the lungs.
For example, it has been well documented that smoking can strongly decrease someone's risk of developing osteoarthritis28 and provide some level of protection. 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 individuals30. 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.D31 “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 as neurological treatments.
Thacker et al32 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 al33 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 study34 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 shown35, 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 one of the best preventative measures that someone could possibly take. 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, and 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 studies36 showing that approximately 90% are smokers. Yet curiously enough, schizophrenics have been shown37 to be between 30-60% less likely to develop lung and other cancers. So what do these figures suggest about smoking as the cause for cancer? I will let you decide.
It has been theorized that such high smoking rates could be because the stimulating cognitive effects of nicotine may help schizophrenics filter out irrelevant external sensory information. A study38 at Yale university found that “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 shown39 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. Pharmaceutical-based western medicine is renowned for pumping patients full with dangerous and innefective medications for the profit of large Pharma corperations. The system not only provides a lack of genuine support to people with mental-health issues, but what is even more appalling is that many instituitions actually deprive in-patients of the right to smoke. Tobacco is the most effective form of medicine for many these people, but when deprived of this they are condemned to a life of unneccesary suffering and confusion.
Aside from certain neurological diseases, smoking has been has been found to consistently reduce the risk of developing Ulcerative Colitis. According to Lashner et al40, “Non-smokers are approximately three times more likely to develop Ulcerative colitis”. One review41 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 clearly indicates that smoking is protective, and people who quit smoking actually place themselves at a higher risk of developing the condition! To add to this, smokers with Ulcerative colitis have also been found to present more benign symptoms than those who did not smoke41.
Interestingly however, smoking does not seem to benefit many of the people who are diagnosed with Crohn's disease. Surprisingly, both men and women are at a much higher risk of developing Crohns if they are smokers, and one study42 even suggests a threefold increased risk in women who smoke. 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 smokers and nicotine consumption. Similar genetic patterns in blood have been found among smokers when compared to non-smokers. Some genes have also been found43 to be more active in smokers, whilst others were less active when compared to non smokers. Researchers44 theorize that genes responsible for neurotransmitter production and metabolism, cell receptor regulation and nicotine metabolism may play an important role in determining whether someone smokes 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.
Nonetheless, if you are one of those people who smokes, or are an ex-smoker who found it difficult to give up the habit in the past, then there is a chance that you are one of those that are genetically compatible. Next, lets move onto energy functioning.
According to conventional medical dogma, tobacco is mankind's worst enemy. As the evidence suggests however, 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 study27 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 what we now know about tobacco, these results are not surpising. Furthermore, smoking also appears to protect against several other seemingly unrelated issues that are separate from the lungs.
For example, it has been well documented that smoking can strongly decrease someone's risk of developing osteoarthritis28 and provide some level of protection. 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 individuals30. 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.D31 “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 as neurological treatments.
Thacker et al32 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 al33 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 study34 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 shown35, 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 one of the best preventative measures that someone could possibly take. 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, and 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 studies36 showing that approximately 90% are smokers. Yet curiously enough, schizophrenics have been shown37 to be between 30-60% less likely to develop lung and other cancers. So what do these figures suggest about smoking as the cause for cancer? I will let you decide.
It has been theorized that such high smoking rates could be because the stimulating cognitive effects of nicotine may help schizophrenics filter out irrelevant external sensory information. A study38 at Yale university found that “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 shown39 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. Pharmaceutical-based western medicine is renowned for pumping patients full with dangerous and innefective medications for the profit of large Pharma corperations. The system not only provides a lack of genuine support to people with mental-health issues, but what is even more appalling is that many instituitions actually deprive in-patients of the right to smoke. Tobacco is the most effective form of medicine for many these people, but when deprived of this they are condemned to a life of unneccesary suffering and confusion.
Aside from certain neurological diseases, smoking has been has been found to consistently reduce the risk of developing Ulcerative Colitis. According to Lashner et al40, “Non-smokers are approximately three times more likely to develop Ulcerative colitis”. One review41 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 clearly indicates that smoking is protective, and people who quit smoking actually place themselves at a higher risk of developing the condition! To add to this, smokers with Ulcerative colitis have also been found to present more benign symptoms than those who did not smoke41.
Interestingly however, smoking does not seem to benefit many of the people who are diagnosed with Crohn's disease. Surprisingly, both men and women are at a much higher risk of developing Crohns if they are smokers, and one study42 even suggests a threefold increased risk in women who smoke. 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 smokers and nicotine consumption. Similar genetic patterns in blood have been found among smokers when compared to non-smokers. Some genes have also been found43 to be more active in smokers, whilst others were less active when compared to non smokers. Researchers44 theorize that genes responsible for neurotransmitter production and metabolism, cell receptor regulation and nicotine metabolism may play an important role in determining whether someone smokes 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.
Nonetheless, if you are one of those people who smokes, or are an ex-smoker who found it difficult to give up the habit in the past, then there is a chance that you are one of those that are genetically compatible. Next, lets move onto energy functioning.
Smoking and Mitochondrial function
In order to understand how tobacco may affect mitochondrial function, first it is imperative to have a basic understanding of how the mitochondria work and what their function is.
Structures called mitochondria are located within the cell and are known as the “powerhouse” responsible for generating energy to supply the body's metabolic requirements. The mitochondria's function is to take electrons from the environment and use them to synthesise what is known as Adenosine Triphosphate (ATP), the body's energy source. Through a process called cellular respiration, electrons taken from digested food are shuttled past the mitochondrial membrane with help from specific molecules (via electron chain transport) so that the mitochondria can create ATP. ATP is used to fuel almost every cellular process in the body and is absolutely essential for all bodily functions, therefore maintaining healthy mitochondrial function is of vital importance.
One of the key players involved in ATP production and mitochondrial health is the enzyme Nicotinamide adenine dinucleotide (NAD). NAD is present in all living cells and is available in two forms: NADH and NAD+. Both forms are essential for proper cellular energy transfer, and insufficient amounts can result in mitochondrial dysfunction. NADH's main function is to transfer electrons to the mitochondria to facilitate ATP synthesis. Once NADH has lost it's electrons, it converts to NAD+. NAD+ has been shown45 to increase the rate of DNA repair, stress resistance, and regulate cell apoptosis. Furthermore, NAD+ also restores tissue integrity, induces homoeostasis, and increases longevity of the cell46. The cell senses levels of NAD+ as a measure of mitochondrial energy production and rate of metabolism. For this reason, the amount of NAD+ converted actually plays a significant role in regulating the rate of ATP synthesis and cellular metabolism47. Low levels of NAD+ reduce mitochondrial energy production, decrease the number of mitochondria in the cell48 and contribute significantly to muscular ageing processes49. Interestingly, NAD+ also has the ability to alter gene expression by “switching off” genes associated with degenerative processes50.
To follow on, SIRT1 (sirtuin) is a NAD-dependent protein coded for by the SIRT1 gene that cannot function without NAD+. So when NAD+ levels decrease, SIRT1 levels also decrease, and vice versa. SIRT1 turns out to be one of the single most important enzymes in control of epigenetic expression, metabolism and longevity. Through a process called acetylation, acetyl groups are added to proteins in response to stress, oxidation or inflammation, which causes the proteins to eventually become defective. Sirtuins, however, remove the acetyl groups to allow for those proteins to stay functional for a longer period of time. This gives the body the opportunity to expend less energy recycling, and more energy on other processes. Studies have shown that SIRT1 inhibits MTOR pathway signalling, increases leptin sensitivity51, increases T3 hormone sensitivity52, and also increases the skin' sensitivity to Vitamin D53. SIRT1 also inhibits/ switches off genes associated with inflammation54, blood sugar regulation, and body fat accumulation/storage55.
So, how does this relate to smoking tobacco?
A study56 conducted by Cancer Research in 2012 showed:
Considering the fact that SIRT1 is anti-inflammatory and can only function in the presence of NAD+, these findings suggest that NAD+ may also be up-regulated in smokers. An elevated level of NAD+ indicates an increase in mitochondrial functioning and ATP synthesis which are both absolute markers for longevity and overall better quality health! This finding can provide us with valuable insight in to how so many smokers end up leading such long, disease-free lives. For those people who are genetically compatible, consuming tobacco smoking is not a burden on the body. These people do not live to such old-ages despite their smoking habits, they live so long because of smoking And below are some perfect examples of this:
Most of oldest people in the world... were ALL smokers
Jeanne Louise Calment
French supercentenarian Jeanne Louise Calment was born on February 21st 1875, and on the 4th of August 1997, she was confirmed to have died from natural causes. She lived for a total of 122 years57. Her secret? Calment smoked from the age of 21 up until the ripe old age of 117 when she finally decided to give up the habit.
Jose Aguinelo dos Santos
Jose Aguinelo dos Santos, a Brazilian man whose parents were African slaves, was born on July 7th 1888. In July 2014, Jose reached his 126th birthday58. Interestingly, Jose has smoked a pack of cigarettes every single day for the past 50 years.
Winnie Langley
Britain's 'oldest smoker', Winnie Langley was born in Croydon in 1907. At her 100th birthday party, Winnie said: “I have smoked ever since infant school and I have never thought about quitting”. It is thought that she smoked more that 170,000 cigarettes throughout her life59. Sadly, two years later Winnie's life was cut short at the young age of 102.
Emiliano Mercado Del Toro
Born on Auguest 21st 1891 in Puerto Rico, Emiliano smoked for a whole 76 years before giving up at the age of 90. In 2007, Emiliano passed away at age 115 from natural causes60. Another obvious example of how smoking clearly shortens the life-span
Sek Yi
Sek Yi, was a devout buddhist and a martial arts expert who was believed to have been born in 1881. In October 2003, Sek passed away at the age of 122 years old. Sek attibuted his longevity and that of his 108 year old wife to smoking and prayer. In an interview, Sek said: "When I was young I used to chew betel, but people made fun of me saying I was like a woman, so I took up smoking."61
Batuli Lamichhane
Batuli was born in Nepal in March 1903, which now makes her 112 years old. She is still alive, and has been smoking 30 cigarrettes a day for the past 95 years ever since she was 17. Apparently, Batuli “claims it’s her daily habit that has helped her outlive almost everyone else in her village – and her own children”62.
Christian Mortensen
Finally, danish-american supercentenarian Christian Mortensen was born on August 16th 1882. Christian passed away on April 25th 1998 at the age of 115 years old. When asked what his secret to a long life was, he said: “Friends, a good cigar, drinking lots of good water, no alcohol, staying positive and lots of singing will keep you alive for a long time.”63.
List of References can be found here
Keyhole, that is great work. You have done a fabulous job of collating that data. It will keep me busy for weeks. Tons of posts for Facebook in there. Many thanks
Yup, great job Keyhole. :)
N
Nico
Guest
Thank you for sharing, it made me realize some things :).
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