Guilt Free Smoking Room

[Frankdee20]

@Elephanto: No fear mongering! I'm pretty sure these people smoked no additive tobacco:

Big Shocker: Most "Supercentenarians" were/are smokers

Jeanne Louise Calment

© The Birkshire Edge
Jeanne Louise Calment
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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 years.57Her 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

© Rediff
Jose lighting up
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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 birthday.58 Interestingly, Jose has smoked a pack of cigarettes every single day for the past 50 years.

Winnie Langley

© The Daily Mail
Winnie's 100th birthday
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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 life.59 Sadly, two years later Winnie's life was cut short at the young age of 102.

Emiliano Mercado Del Toro

© z3.invisionfree.com
Emiliano Mercado Del Toro
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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 causes.60

Sek Yi

© Reuters
Sek Yi puffin' away
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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


© Magazin
Bathulli having a smoke
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Batuli was born in Nepal in March 1903, which now makes her 112 years old. She is still alive, and has been smoking 30 cigarettes 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

© Getty Images
Christian tokin' on a cigar
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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
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Now concerning e-cigs and other substitutes to actually dragging on a real cigarette or pipe:

Nicotine is clearly very beneficial for cognitive function, but when compared to actually smoking tobacco, we can see that isolated nicotine simply isn't as effective. A study15 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 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.

I’m a smoker of 2 years, 38 years old. I believe Tobacco has other alkaloids eliciting an MAO I effect.

 

[Frankdee20]

The period when I used to smoke is probably the only time in my adult life where I've felt relatively euthyroid, there's no doubt smoking has a strong stimulatory impact on thyroid functioning probably through its anti-inflammatory effects, and its well established that quitting smoking can massively impair thyroid function for several years afterwards.

But personally I also started to feel the effects of chronically elevated cortisol after a few years of smoking and having weird stress symptoms that I've never had before, not sure how you can get around that really. Smoking seems to work like a crutch and will weaken you in the long run even if it does have positive effects initially, unlike coffee.

Its interesting though that smoking is associated both with elevated cortisol levels and elevated thyroid function, wonder how one would make sense of that from a Peat perspective.

What if you can keep it to like 5 cigarettes a day ?

 

[zewe]

I’m a smoker of 2 years, 38 years old. I believe Tobacco has other alkaloids eliciting an MAO I effect.

Interestingly, an unknown property of tobacco smoke has been shown to contain naturally occurring MAOIs. This is reflected in numerous studies18 demonstrating that smokers have significantly lower levels of both types of MAOs (A and B), which basically means that smoking acts as a natural antidepressant without any of the horrible side effects common to many synthetic pharmaceutical drugs.

 

[Collden]

What if you can keep it to like 5 cigarettes a day ?

Yeah most studies define light smoking as no more than 20 per day so there's not really much data about what harm less than that would cause, even though 5-10 cigs a day is probably a more standard consumption for smokers in Europe at least. I saw a study where increased CHD risk was not seen with less than 20 cigs per day.

I smoked on average 5 rollies per day though and did feel some negatives from that in the long run. My diet was pretty bad at the time as well though and I didnt drink coffee, so maybe you can do well with cigarettes if you take care to have a clean diet and do other healthy stuff like sun exposure and coffee. There was one study where smokers who spent a lot of time outdoors had the same mortality as non-smokers who spent less time outdoors.

 

[Frankdee20]

Interestingly, an unknown property of tobacco smoke has been shown to contain naturally occurring MAOIs. This is reflected in numerous studies18 demonstrating that smokers have significantly lower levels of both types of MAOs (A and B), which basically means that smoking acts as a natural antidepressant without any of the horrible side effects common to many synthetic pharmaceutical drugs.

I don’t think the concentration of Harmaline alkaloids in Tobacco is high enough to attribute the MAO inhibition to it. Must be something else too

 

[zewe]

I've read posts here at the forum where people are perplexed by urges to smoke. There is thought that smokers are genetically predisposed to smoking tobacco:

Tobacco provides protection?

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

First of all, one study27conducted 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." Given what we've already seen, these results are unsurprising. 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)28and 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 has beneficial effects on bone maintenance, growth and repair. Furthermore, according to L. Gullahorn, M.D, "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."31

Secondly, it is commonly known in the scientific community that neurological diseases such as Alzheimer's and Parkinson's present amuch lower risk in smokers; so much so that methods of treatment using nicotine (and its byproducts) are now being actively developed by pharmaceutical companies for new neurological treatments.

Thacker et al32 analyzed data from 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 their chances of contracting this disease. The authors 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 shown,35and 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 unsure 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 syndrome. 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 and 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 among schizophrenics are typically much higher than in the average population, with some studies36 showing that approximately 90% of them are smokers. Yet, curiously enough, schizophrenics have been shown37to 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, which may help schizophrenics filter out irrelevant external sensory information. A study38at 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 shown39 that the more cigarettes men smoked at an earlier age, the lower chance they had of developing schizophrenia later on in life.Their 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 lacks sufficient support for people with mental-health problems; what is even more appalling is that many institutions actually deprive in-patients of the right to smoke, despite it being one of their most effective means of self-medication.

Aside from neurological diseases, smoking has been found to consistently reduce the risk of developing Ulcerative Colitis, an inflammatory bowel disease. 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 again seems to indicate that smoking may be protective, and that people who quit smoking actually place themselves at higher risk. Additionally, smokers with Ulcerative Colitis have also been found to present more benign symptoms than those who did not smoke.41

Interestingly, smoking does notseem to benefit many who are diagnosed with Crohn's disease, which is another inflammatory bowel disease. Statistically, both men and women are at much higher risk of developing Crohn's if they are smokers, and one study42even suggests a threefold increased risk in women who smoked. This apparent anomaly makes no sense when we consider these data in isolation. However, a growing body of evidence is shining light on the possible genetic origins of this disease. Likewise, there is evidence to suggest that genetic factors may play a role in tobacco smoking/nicotine consumption - people may literally be genetically predisposed to smoke, or not.Similar genetic patterns in blood have been found among smokers when compared with non-smokers. Some genes have also been found43 to be more active in smokers, whilst others were less active compared to those of non-smokers. Researchers44theorize 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 a biological difference between smokers and non-smokers. Perhaps this could help explain why some people are naturally drawn to smoking when they are in their teenage years, while others go a whole lifetime without having the slightest 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 whatsoever from its protective properties. 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.

 

[zewe]

I was hoping to see some speculation on why all the anti-smoking propaganda when studies counter so many of the opposition's claims.

Here's some food for thought:

The Health & Wellness Show: The Truth About Tobacco with Richard White

Sott Editors
Sott.net
Fri, 19 Jun 2015 14:00 UTC



Smoking: it's healthier than Fascism!
Smoking is hazardous to your health and causes lung cancer... but is that really true? Are tobacco and cigarette smoking really the scourge that Big Pharma, the media and millions of people around the world believe it to be? Today we'll be talking with Richard White, author of Smoke Screens: The Truth About Tobacco. We'll examine studies on smoking, what researchers have to say, the scientists involved in the anti-smoking movement, previous attacks on smoking, the origins of the anti-smoking movement, the diseases said to be caused by smoking... and more!

Keeping your pets safe during the summer months is the topic of this week's Pet Health Segment.

Running Time: 01:59:00

Audio and transcript:
The Health & Wellness Show: The Truth About Tobacco with Richard White -- Sott.net

 

[Frankdee20]

Nice piece

 

[michael94]

I am with BenjaminBullock and the OP, Nicotine and even smokeless tobacco was just OK. Not that regular cigarettes did anything magical or esrth shattering for me, but they "felt" more enjoyable and useful. Edward Edmonds posted something how about the smoke itself specifically the carbon monoxide could have protective effects. I cannot speak for the other combustibles

 

[Such_Saturation]

9 chemicals identified so far in e-cig vapor that are on the California Prop 65 list

I think progesterone is also on that list lol

 

[zewe]

FYI

For anyone who is looking for a good tobacco source. You can order organic whole leaf tobacco and grind it yourself from this place, online. It’s excellent, pure and organic.
https://www.leafonly.com

If you know of another source, please advise.

 

[Herbie]

FYI

For anyone who is looking for a good tobacco source. You can order organic whole leaf tobacco and grind it yourself from this place, online. It’s excellent, pure and organic.
https://www.leafonly.com

If you know of another source, please advise.

Pipe Tobacco and Pipe Tobacco Blends

@Travis, perhaps these do not have ammonia.

When I was in the Amazon of Peru, I smoked filterless mupachos which are nicotina rustica tobacco made in the jungle, maybe these don’t have added ammonia too and might be able to be shipped to the states.

 

[Travis]

Pipe Tobacco and Pipe Tobacco Blends

@Travis, perhaps these do not have ammonia.

When I was in the Amazon of Peru, I smoked filterless mupachos which are nicotina rustica tobacco made in the jungle, maybe these don’t have added ammonia too and might be able to be shipped to the states.

Judging by its taste and its effects, I am convinced that they ammonia isn't normally added to whole-leaves. If you were to try smoking some whole tobacco leaves for a few months and then have an American Spirit, I think you'd find that the latter will hit you much harder. American Spirit—like all others—adds ammonia to increase the pH of the tobacco, having the ultimate intent of deprotonating more nicotine towards the neutral form. Acidic nicotine is ionized, and for this reason it has an ionic attraction towards other charged particles and molecules: Basic nicotine, however, has no formal charge and hence has a higher mobility in gas phase. Acidic nicotine will volatilize at a lower temperature, allowing more to be inhaled and less pyrolyzed by the advancing flame front. Yet unfortunately: this enhanced mobility of nicotine is accompanied by ammonia gas, which has nitric oxide as a pyrolysis product. [NH₃ + O₂ = ṄO + H₃O⁺] I am convinced that inhaled reactive nitrogen gasses are responsible for the epidemiological links between cancer and 'cigarette smoking,' an not 'pipe smoking,' and also the lack of difference observed between smokers of 'light' cigarettes to 'regular' ones: Tobacco companies add more ammonia to light cigarettes to compensate for their inherently lower nicotine, allowing even a light cigarette to have as much vaporized nicotine as a unfiltered cigarette sans ammonia. Yet in a somewhat humorous fashion, this is often explained as 'smokers of light cigarettes inhaling deeper to compensate.' What are they compensating for when they both have comparable nicotine levels?

Should a person buy ammonia-free whole leaf tobacco they would also need to buy a shredder, unless of course they're committed to rolling cigars. Should a person buy a shredder, I'd avoid the cheap $30 aluminum one simply because the smallest misalignment—e.g. a bent rake—would lead to attrition and the resultant aluminum nanoparticles. I have unintentionally created these,.and no doubt have smoked vaporized aluminum before acquiring an all-stainless steel shredder. I feel buying the aluminum shredder would be tantamount to trading the reduced carcinogenicity of ammonia-free tobacco for enhanced Parkinson's potential. Aluminum welders and heavy users of cocaine—when 'cut' with double-acting baking powder [?]—are two high-risk Parkinson's groups that inhale aluminum. The substantia nigra is almost directly behind the olfactory bulb, and there are not many things besides Al³⁺ that will cause permanent nerve damage. The classic drug for inducing Parkinson's in animals in MPTP, yet the effects of this drug are reversible within weeks. A far better model for Parkinson's is injecting or inhaling aluminum, which has sequelae indistinguishable from Alzheimer's and Parkinson's in every way. Daniel Perl had been convinced in the 1980s that the only difference between the ALS, Parkinson's, and Alzheimer's was where the aluminum had tended to distribute.

 

[zewe]

@Travis Hi. What do you think of the shredders here.....quality and price?

All Tobacco Leaf - Tobacco Leaf Shredders

 

[Peater]

I'm a sucker for cigars. Partagas serie D if I want to get my socks blown off, Behike for special occasions, Montecristo or Aging Room for normal smokes.

Nice way to spend an hour or so. A cigar is an occasion.

 

[Wolf]

Judging by its taste and its effects, I am convinced that they ammonia isn't normally added to whole-leaves. If you were to try smoking some whole tobacco leaves for a few months and then have an American Spirit, I think you'd find that the latter will hit you much harder. American Spirit—like all others—adds ammonia to increase the pH of the tobacco, having the ultimate intent of deprotonating more nicotine towards the neutral form. Acidic nicotine is ionized, and for this reason it has an ionic attraction towards other charged particles and molecules: Basic nicotine, however, has no formal charge and hence has a higher mobility in gas phase. Acidic nicotine will volatilize at a lower temperature, allowing more to be inhaled and less pyrolyzed by the advancing flame front. Yet unfortunately: this enhanced mobility of nicotine is accompanied by ammonia gas, which has nitric oxide as a pyrolysis product. [NH₃ + O₂ = ṄO + H₃O⁺] I am convinced that inhaled reactive nitrogen gasses are responsible for the epidemiological links between cancer and 'cigarette smoking,' an not 'pipe smoking,' and also the lack of difference observed between smokers of 'light' cigarettes to 'regular' ones: Tobacco companies add more ammonia to light cigarettes to compensate for their inherently lower nicotine, allowing even a light cigarette to have as much vaporized nicotine as a unfiltered cigarette sans ammonia. Yet in a somewhat humorous fashion, this is often explained as 'smokers of light cigarettes inhaling deeper to compensate.' What are they compensating for when they both have comparable nicotine levels?

Should a person buy ammonia-free whole leaf tobacco they would also need to buy a shredder, unless of course they're committed to rolling cigars. Should a person buy a shredder, I'd avoid the cheap $30 aluminum one simply because the smallest misalignment—e.g. a bent rake—would lead to attrition and the resultant aluminum nanoparticles. I have unintentionally created these,.and no doubt have smoked vaporized aluminum before acquiring an all-stainless steel shredder. I feel buying the aluminum shredder would be tantamount to trading the reduced carcinogenicity of ammonia-free tobacco for enhanced Parkinson's potential. Aluminum welders and heavy users of cocaine—when 'cut' with double-acting baking powder [?]—are two high-risk Parkinson's groups that inhale aluminum. The substantia nigra is almost directly behind the olfactory bulb, and there are not many things besides Al³⁺ that will cause permanent nerve damage. The classic drug for inducing Parkinson's in animals in MPTP, yet the effects of this drug are reversible within weeks. A far better model for Parkinson's is injecting or inhaling aluminum, which has sequelae indistinguishable from Alzheimer's and Parkinson's in every way. Daniel Perl had been convinced in the 1980s that the only difference between the ALS, Parkinson's, and Alzheimer's was where the aluminum had tended to distribute.

Agreed on American Spirits unless they're the Black variety. But then you're basically smoking fermented peppery tobacco.
As an anecdote, all the older people I've ever met doing tradework smoked a lot and retained their strength while the middle aged people that had reservations about smoking tended to be the fat lazy ones.

 

[Travis]

I'm a sucker for cigars. Partagas serie D if I want to get my socks blown off, Behike for special occasions, Montecristo or Aging Room for normal smokes.

Nice way to spend an hour or so. A cigar is an occasion.

I think is fun to roll cigars. Hand rolling them is perfectly acceptable if you are good at it, and even for somebody practicing or just having fun. My first cigar wasn't very nice at all, but that's to be expected on nearly all first attempts. It takes a bit of effort to get the proper humidity and shape, but this is certainly attainable at home with ammonia-free leaves. Yet I just stick to hand-rolled and tube-injected cigarettes mainly as I've always liked cigarettes more. My favorite cigar had always been Cohiba™, and my two favorite cigarettes are: Dunhill International, Nat Sherman MCD, Dji Sam Soe, and the ones I make from the Turkish Samsun Leaf.

Agreed on American Spirits unless they're the Black variety. But then you're basically smoking fermented peppery tobacco.
As an anecdote, all the older people I've ever met doing tradework smoked a lot and retained their strength while the middle aged people that had reservations about smoking tended to be the fat lazy ones.

Now why is this? Is it: (1) the high nicotine leading to increased glucose flux? the (2) high nicotine increasing and cholinergic activity? or (2) is it the other way around? I feel that when I'm high in plasma nitric oxide I have a disinclination to smoke, which naturally would just make things worse. Even ammonia-free tobacco has more nitric oxide gas than the ambient air, in most cases, yet there appears to be no studies that discriminate between the two types. Yet, perhaps there is one out there somewhere?

I don't want to give the impression that all nonsmokers have high blood nitrogen levels—most do seem motivated more by social considerations—yet there could be a few physiological states that could be inherently incompatible with smoking. Yet nicotine reliably increases glucose flux and cholinergic activity, the former enhancing the metabolic rate and the latter nervous activity.

Duelli, R. "Brain glucose transporters: relationship to local energy demand." Physiology (2001)

'To stimulate various brain regions chronically, rats obtained a continuous infusion of a nicotine solution for 1 wk. Under these conditions, local glucose utilization is chronically increased in specific brain structures. Moreover, glucose transporter densities of Glut1 and Glut3 showed a distinct increase only in brain structures with an elevated local cerebral glucose utilization. Thus the density of glucose transporters can be chronically raised in specific brain regions as a response to an enhanced metabolic rate for glucose. The increase in the local densities of glucose transporters (mean +19%) is paralleled by an increase in local cerebral glucose utilization (mean +15%). The close correlation between Glut1 or Glut3 densities and local cerebral glucose utilization shown for control conditions was maintained during nicotine infusion.' ―Duelli​

Hahn, B. "Nicotine-induced enhancement of attention in the five-choice serial reaction time task: the influence of task demands." Psychopharmacology 162.2 (2002): 129-137.

'Nicotine (0.05–0.2 mg/kg, s.c.) repeatedly improved accuracy and reduced omission errors and reaction times, leading to increases in numbers of reinforcers earned. Anticipatory responding was increased. Parametric modifications intended to increase demands on sustained attention did not affect performance in a manner suggesting that this subtype of attention was being taxed, and the effects of nicotine were not more marked under such conditions.' ―Hahn​

Semenova, S. "Chronic nicotine administration improves attention while nicotine withdrawal induces performance deficits in the 5-choice serial reaction time task in rats." Pharmacology, biochemistry, and behavior (2007)

'Nicotine appears to enhance attention, while nicotine withdrawal leads to attentional deficits in humans that are ameliorated with nicotine administration. However, there has been much debate as to whether nicotine improves performance under baseline conditions, or only ameliorates attentional deficits. Thus, we studied the effects of acute and chronic nicotine administration and nicotine withdrawal on attentional performance in the 5-choice serial reaction time task (5-CSRTT) in Wistar and Sprague Dawley (SD) rats under baseline conditions. Wistar rats performed with higher accuracy compared to SD rats. Acute nicotine administration induced small increases in accuracy and correct responses, impulsivity and speed of responding and decreases in omission errors. These effects were more pronounced in less accurate rats or after task modifications were implemented to disrupt the rats' performance. Chronic nicotine administration via minipumps consistently increased accuracy during days 4-6 of nicotine infusion after the effect of nicotine on impulsivity during days 1-3 dissipated. By contrast, nicotine withdrawal induced decreases in correct responses, and increases in omissions and latencies to respond, but had no effect on accuracy. These results provide evidence that chronic, but not acute, nicotine administration induced accuracy improvement under baseline conditions, while nicotine withdrawal produced some limited performance deficits.' ―Duelli​

Hoffmann, D. "Changes in cigarette design and composition over time and how they influence the yields of smoke constituents." NCI smoking and tobacco control monograph (1995)

'The list of additives also contains inorganic salts, such as ammonium and potassium carbonates, and bicarbonates. These additives possibly increase the pH of cigarette smoke. Beyond pH 6.0, cigarette smoke contains increasing amounts of unprotonated nicotine; with smoke pH at 6.9, about 10percent of the nicotine is present in the smoke in free form; at pH 7.85 this rises to 50 percent (Brunnemann and Hoffmann, 1974). The free nicotine is present predominantly in the vapor phase of the smoke and is more quickly absorbed through the oral mucosa than nicotine in salt form (Armitage and Turner, 1970). Data are urgently needed for examining the change in pH of the smoke of cigarettes with additives.' ―Hoffmann
​

Pryor, W. "Electron-spin resonance study of mainstream and sidestream cigarette smoke: nature of the free radicals in gas-phase smoke and in cigarette tar." Environmental health perspectives (1983)

'Oxides of nitrogen occur in cigarette smoke at levels as high as 1400 micrograms per cigarette (22); the NOx in fresh smoke is mainly nitric oxide. Nitric oxide is relatively unreactive toward organic materials (23); however, it is known to be oxidized to NO₂ in the smoke stream, and nitrogen dioxide is quite reactive toward a number of types of organic substances (25).' ―Hoffmann
​

Miller, J. "Kinetic modeling of the oxidation of ammonia in flames." Combustion Science and Technology (1983)

'We have investigated theoretically a variety of burner-stabilized and freely propagating NH₃/O₂ and NH₃/H₂/O₂ flames. The agreement between theory and experiment is generally good except, perhaps, for very rich names, where it appears that the kinetic model may be missing important pyrolysis steps. Nevertheless, the important NO and Nz formation reactions can be identified. In lean flames, nitric oxide is produced primarily through the nitroxyl (HNO) intermediate, formed either by the reaction of NH2 with oxygen atoms or NH with hydroxyl and oxygen molecules. Similarly, in lcan flames conversion of NO to N₂ is by reaction with NH₂ or NH, forming NNH or N₂0 as intermediates. Under richer conditions NHz and NH are rapidly converted to nitrogen atoms, and the extended Zcl'dovich mechanism becomes responsible for NO formation and the conversion of ṄO to ṄO₂.' ―Miller
​

Cooney, R. "Gamma-tocopherol detoxification of nitrogen dioxide: superiority to alpha-tocopherol." Proceedings of the National Academy of Sciences (1993)

'In the vitamin E group, α-tocopherol is generally considered to be the most potent antioxidant with the highest vitamin bioactivity, yet γ-tocopherol is produced in greater amounts by many plants and is the principal tocopherol in the United States diet. This report describes a fundamental difference in the chemical reactivities of α-tocopherol and γ-tocopherol with nitrogen dioxide (ṄO₂), which leads to the formation of a nitrosating agent from α-tocopherol, but not from γ-tocopherol. Nitric oxide (ṄO) is a major product of the reaction of γ-tocopherol with ṄO₂, while α-tocopherol reacts with ṄO₂ to form an intermediate tocopheroxide analogue. The biological significance of γ-tocopherol is supported by epidemiological data as well as the observation that it is a more potent inhibitor than α-tocopherol of neoplastic transformation during the post-initiation phase in 3-methylcholanthrene-treated murine fibroblasts. This latter property suggests the superiority of γ-tocopherol in a mammalian biological assay and a role for endogenous ṄO production in promotion of neoplasic transformation.' ―Cooney​

Jiang, Q. "γ-Tocopherol and its major metabolite, in contrast to α-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells." Proceedings of the National Academy of Sciences (2000)

'Cyclooxygenase-2 (COX-2)-catalyzed synthesis of prostaglandin E₂ (PGE₂) plays a key role in inflammation and its associated diseases, such as cancer and vascular heart disease. Here we report that γ-tocopherol (γT) reduced PGE₂ synthesis in both lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and IL-1btreated A549 human epithelial cells with an apparent IC₅₀ of 7.5 and 4 μM, respectively. The major metabolite of dietary γ-tocopherol, 2,7,8-trimethyl-2-(carboxyethyl)-6-hydroxychroman (γ-CEHC), also exhibited an inhibitory effect, with an IC₅₀ of 30 μM in these cells. In contrast, α-tocopherol at 50 μM slightly reduced (25%) PGE₂ formation in macrophages, but had no effect in epithelial cells. The inhibitory effects of γ-tocopherol and γ-CEHC stemmed from their inhibition of COX-2 activity, rather than affecting protein expression or substrate availability, and appeared to be independent of antioxidant activity' ―Jiang
​

Landino, L. "Peroxynitrite, the coupling product of nitric oxide and superoxide, activates prostaglandin biosynthesis." Proceedings of the National Academy of Sciences (1996)

'Peroxynitrite activates the cyclooxygenase activities of constitutive and inducible prostaglandin endoperoxide synthases by serving as a substrate for the enzymes’ peroxidase activities. Activation of purified enzyme is induced by direct addition of peroxynitrite or by in situ generation of peroxynitrite from ṄO coupling to superoxide anion.' ―Jiang
​

Lu, G. "A γ-tocopherol-rich mixture of tocopherols inhibits chemically induced lung tumorigenesis in A/J mice and xenograft tumor growth." Carcinogenesis (2010)

'The NNK plus B[a]P treatment induced 21 tumors per lung on Week 19; dietary 0.3% γ-TmT treatment during the entire experimental period significantly lowered tumor multiplicity, tumor volume and tumor burden (by 30, 50 and 55%, respectively). [...] In the xenograft tumor model of human lung cancer H1299 cells in NCr-nu/nu mice, 0.3% dietary γ-TmT treatment significantly reduced tumor volume and tumor weight by 56 and 47%, respectively. In both the carcinogenesis and tumor growth models, the inhibitory action of γ-TmT was associated with enhanced apoptosis and lowered levels of 8-hydroxydeoxyguanine, γ-H2AX and nitrotyrosine in the tumors of the γ-TmT-treated mice.' ―Lu​

 

[Fractality]

Judging by its taste and its effects, I am convinced that they ammonia isn't normally added to whole-leaves. If you were to try smoking some whole tobacco leaves for a few months and then have an American Spirit, I think you'd find that the latter will hit you much harder. American Spirit—like all others—adds ammonia to increase the pH of the tobacco, having the ultimate intent of deprotonating more nicotine towards the neutral form. Acidic nicotine is ionized, and for this reason it has an ionic attraction towards other charged particles and molecules: Basic nicotine, however, has no formal charge and hence has a higher mobility in gas phase. Acidic nicotine will volatilize at a lower temperature, allowing more to be inhaled and less pyrolyzed by the advancing flame front. Yet unfortunately: this enhanced mobility of nicotine is accompanied by ammonia gas, which has nitric oxide as a pyrolysis product. [NH₃ + O₂ = ṄO + H₃O⁺] I am convinced that inhaled reactive nitrogen gasses are responsible for the epidemiological links between cancer and 'cigarette smoking,' an not 'pipe smoking,' and also the lack of difference observed between smokers of 'light' cigarettes to 'regular' ones: Tobacco companies add more ammonia to light cigarettes to compensate for their inherently lower nicotine, allowing even a light cigarette to have as much vaporized nicotine as a unfiltered cigarette sans ammonia. Yet in a somewhat humorous fashion, this is often explained as 'smokers of light cigarettes inhaling deeper to compensate.' What are they compensating for when they both have comparable nicotine levels?

Should a person buy ammonia-free whole leaf tobacco they would also need to buy a shredder, unless of course they're committed to rolling cigars. Should a person buy a shredder, I'd avoid the cheap $30 aluminum one simply because the smallest misalignment—e.g. a bent rake—would lead to attrition and the resultant aluminum nanoparticles. I have unintentionally created these,.and no doubt have smoked vaporized aluminum before acquiring an all-stainless steel shredder. I feel buying the aluminum shredder would be tantamount to trading the reduced carcinogenicity of ammonia-free tobacco for enhanced Parkinson's potential. Aluminum welders and heavy users of cocaine—when 'cut' with double-acting baking powder [?]—are two high-risk Parkinson's groups that inhale aluminum. The substantia nigra is almost directly behind the olfactory bulb, and there are not many things besides Al³⁺ that will cause permanent nerve damage. The classic drug for inducing Parkinson's in animals in MPTP, yet the effects of this drug are reversible within weeks. A far better model for Parkinson's is injecting or inhaling aluminum, which has sequelae indistinguishable from Alzheimer's and Parkinson's in every way. Daniel Perl had been convinced in the 1980s that the only difference between the ALS, Parkinson's, and Alzheimer's was where the aluminum had tended to distribute.

As a nerve protective agent, I wonder how effective nicotine is at counteracting aluminum's toxic effects on the nerves?

 

[Travis]

As a nerve protective agent, I wonder how effective nicotine is at counteracting aluminum's toxic effects on the nerves?

I don't think anything can stop aluminum, yet there are things that can chelate it before it reacts. Calcium actually seems to antagonize Al³⁺-toxicity likely by either direct displacement or competition, and also the silica ion binds it very well. The aluminum ion (Al³⁺) is unique in that it forms very stable products with phosphate, and the most characteristic inclusion body in Alzheimer's is the neurofibrillary tangle—essentially highly-phosphorylated τ-proteins crosslinked through aluminum ions. Yet the diagnostic criteria of Alzheimer's has been diluted over the years to mean basically 'high dementia,' so today there are many things that can be said to cause it. The evidence for Aluminum-induced dementia and Parkinson's is overwhelming, yet the political clout of ALCOA effectively has shifted this from the spotlight in the 1980s to the backburner. Aluminum compounds are still routinely-added to certain foods, and there is a significant risk of inhalation in many occupations and hobbies. I think we all intuitively know by know that too much aluminum is neurotoxic, yet amazingly some people will try to deny this; it appears to be the vaccine producers and their mouthpieces who do this the most, and ALCOA probably spends a considerable amount of effort in avoiding culpability by financially-influencing scientists. For decades Daniel Perl had been the most committed scientific activist for this link, yet they apparently had made him an offer he couldn't refuse and he now sidesteps the issue.

 

[Fractality]

I don't think anything can stop aluminum, yet there are things that can chelate it before it reacts. Calcium actually seems to antagonize Al³⁺-toxicity likely by either direct displacement or competition, and also the silica ion binds it very well. The aluminum ion (Al³⁺) is unique in that it forms very stable products with phosphate, and the most characteristic inclusion body in Alzheimer's is the neurofibrillary tangle—essentially highly-phosphorylated τ-proteins crosslinked through aluminum ions. Yet the diagnostic criteria of Alzheimer's has been diluted over the years to mean basically 'high dementia,' so today there are many things that can be said to cause it. The evidence for Aluminum-induced dementia and Parkinson's is overwhelming, yet the political clout of ALCOA effectively has shifted this from the spotlight in the 1980s to the backburner. Aluminum compounds are still routinely-added to certain foods, and there is a significant risk of inhalation in many occupations and hobbies. I think we all intuitively know by know that too much aluminum is neurotoxic, yet amazingly some people will try to deny this; it appears to be the vaccine producers and their mouthpieces who do this the most, and ALCOA probably spends a considerable amount of effort in avoiding culpability by financially-influencing scientists. For decades Daniel Perl had been the most committed scientific activist for this link, yet they apparently had made him an offer he couldn't refuse and he now sidesteps the issue.

Does calcium only protect against aluminum exposure starting in the stomach? There is also the issue of aluminum in the atmosphere from geoengineering. I should drink more Gerolsteiner and horsetail tea for silica. I wonder if fasting for 24-48 hours or longer would help remove it too?

From Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workersBritish Medical Journal, Occupational and Environmental Medicine (Vol. 56, 468-472, 1999):

Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers, with lower results for forced vital capacity (FVC) (98.8% predicted), forced expiratory volume in one second (FEV1) (96.1% predicted) and peak expiratory flow (PEF) (80.2% predicted) compared with controls (114.2, 109.9, and 105.9% predicted; each p < 0.001). Conversely, effects of smoking on lung function were only detectable in non-exposed controls (current smokers v non-smokers: FVC 98.8% v 114.2% predicted; p < 0.01; FEV1 95.5 v 109.9% predicted; p < 0.05)." (NOTE: The key result is that for the exposure controlled group (the potroom workers) the smoking reduced the risk of lung damage sixfold compared to never-smokers.)