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Smoking lowers Parkinson's disease risk


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#1 doug123

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Posted 21 March 2007 - 08:09 AM


Reuters: News Source

Posted Image

Smoking lowers Parkinson's disease risk

Tue Mar 20, 2007 2:03PM EDT

By Megan Rauscher

NEW YORK (Reuters Health) - A new study adds to the previously reported evidence that cigarette smoking protects against Parkinson's disease. Specifically, the new research shows a temporal relationship between smoking and reduced risk of Parkinson's disease. That is, the protective effect wanes after smokers quit.

"It is not our intent to promote smoking as a protective measure against Parkinson's disease," Evan L. Thacker from Harvard School of Public Health emphasized in comments to Reuters Health. "Obviously smoking has a multitude of negative consequences. Rather, we did this study to try to encourage other scientists...to consider the possibility that neuroprotective chemicals may be present in tobacco leaves."

As reported in the March 6th issue of Neurology, Thacker and colleagues analyzed data, including detailed lifetime smoking histories, from 79,977 women and 63,348 men participating in the Cancer Prevention Study II Nutrition Cohort. During about 9 years of follow-up, 413 subjects developed definite or probable Parkinson's disease.


Compared to people who had never smoked and were considered to have "normal" Parkinson's disease risk, former smokers had a 22-percent lower risk of Parkinson's disease and current smokers had a 73-percent lower risk.

"The results were similar for men and women, and were also similar to the results of studies by many other researchers looking at the same topic," Thacker noted.

In former smokers, more years of smoking, fewer years since quitting, more cigarettes per day, and a higher total amount of lifetime smoking were all related to a lower Parkinson's disease risk. The researchers also found that the duration of smoking and the time since quitting influenced risk more than the average daily amount of smoking.

"A 30 percent to 60 percent decreased risk of Parkinson's disease was apparent for smoking as early as 15 to 24 years before symptom onset, but not for smoking 25 or more years before onset," the investigators report.

"The results of our study," Thacker said, "can probably be explained by something in cigarettes -- most likely in the tobacco itself -- actually protecting people against getting Parkinson's disease. That would be the simplest explanation that makes the most sense."

Studies to determine if, in fact, there are neuroprotective compounds in tobacco are warranted, the researchers say. "The observation that smokeless tobacco users also have a lower risk of Parkinson's disease suggests that the most likely candidates are not compounds generated by combustion, but rather constituents of the tobacco leaves."

SOURCE: Neurology, March 6,, 2007.

© Reuters 2006. All rights reserved. Republication or redistribution of Reuters content, including by caching, framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.

Reuters journalists are subject to the Reuters Editorial Handbook which requires fair presentation and disclosure of relevant interests.

#2 maestro949

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Posted 21 March 2007 - 10:05 AM

Smoke enough and you'll reduce the risk of to zero!

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#3 stretch

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Posted 08 April 2007 - 07:42 AM

Could the neuroprotection arise from MAOI effects of tobacco?

#4 nightlight

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Posted 08 April 2007 - 04:14 PM

Could the neuroprotection arise from MAOI effects of tobacco?


That is certainly one pathway, since long term tobacco smoking nearly halves MAO B levels (MAO B is 40% lower in smokers; dopamine release is also upregulated independently of MAO B inhibition). Tobacco smoke also nearly doubles glutathione and other internal antioxidants, which could play a role in neuroprotective effects of smoking against various environmental toxins which are associated with Parkinson's (such as pesticides, mercury...). Smoking also upregulates acetylcholine levels & number of nicotinic ACh receptors, as well as pregnenolone, DHEA and testosterone, while downregulating insuline growth factor IGF1 (the lowering of IGF1 is associated with increased longevity in animal experiments), all of which may stimulate independent neuroprotective and neuro-rejuvenating biochemical pathways. Although many of these MAO B and endocrine effects are not due to nicotine, nicotine does increase the levels of vascular growth factor (e.g. enhancing capillary vascularization).

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Neurology. 1999 Sep 22;53(5):1158.
Smoking and Parkinson's disease: a dose-response relationship
Gorell JM, Rybicki BA, Johnson CC, Peterson EL

Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA.

OBJECTIVE: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers.

METHODS: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based case-control study of men and women > or =50 years old in the Henry Ford Health System.

RESULTS: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to 1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD.

CONCLUSIONS: 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.


The most striking fact above is twelvefold reduction in Parkinson's rates in long term smokers (30+ pack-years). There is a related protective effect of smoking against Alzheimer's of similar magnitude (tenfold reduction), cited in an earlier thread. More discussion and further citations on MAOI B effects of tobacco smoking, along with comparisons to similar long term Deprenyl effects in animal studies, were given in an earlier thread (here, here, here).

Edited by nightlight, 08 April 2007 - 05:17 PM.


#5 edward

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Posted 08 April 2007 - 06:15 PM

The MAOI connection seems to be the most logical and has always been my conclusion as to any benefits derived from smoking. There are so many chemicals in cigarette smoke and the delivery system via the lungs puts them right into the bloodstream. I am not surprised that there are some positive effects. In my opinion though studies like this are interesting but have no practical value as smoking is so terrible for one's health. (I smoked for about 10 years from age 16 to 26 and it was hell trying to quit and once I did I felt a lot better).

Edited by edward, 08 April 2007 - 08:30 PM.


#6 stretch

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Posted 09 April 2007 - 07:21 AM

Excellent post nightlight!

On speakeasyforum's pictures that you linked, Deng Xiaoping had a pretty nice hair for a 90 year old. Barak's and Deng's choice of smoked cosmetics looks pretty powerful if it can preserve their skin like that.

Some of the members here already use Selegiline or Rasagiline but has any nonsmoker added nicotine to his stack?-)

#7 nightlight

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Posted 09 April 2007 - 07:29 PM

I am not surprised that there are some positive effects. In my opinion though studies like this are interesting but have no practical value as smoking is so terrible for one's health.


It may surprise some, but the pharmaceutical industry, which is on one hand the chief sponsor of antismoking "science" (along with the rest of the antismoking social engineering), is on the other hand seriously researching, albeit much more quietly, how to replicate some of the therapeutic magic of tobacco smoke (nicotine is only a small part of it). Here is a brief review of the neuroprotective aspects only (mostly of nicotine), published by the pharma sponsored organization SRNT (hence it includes the customary ritualistic denounciation of smoking at the top, while genuinely marveling at this ancient medicine throughout the rest of the article):

Potential Therapeutic Applications of Nicotine and Nicotine Analogues
SRNT Vol 1, No 4, 1995
John Baron (Dartmouth Medical School), Edward Levin (Duke University Medical Center), Alexandra Potter and Paul Newhouse (University of Vermont)

Cigarette smoking has a well-deserved bad reputation; it is among the leading causes of mortality and morbidity throughout the world, largely because of its strong effects on the risk of cancer, cardiovascular disease, and chronic lung disease. Nevertheless, nicotine is one of the most widely used drugs in the world, most commonly by chewing the leaves or inhaling the smoke from the leaves of a plant that synthesizes nicotine, tobacco. In spite of health warnings, hundreds of millions of people continue to use tobacco.

Why is tobacco so widely used? Addiction to nicotine is a common explanation for the persistence of nicotine use, once established. Because nicotine has multiple neural and functional effects, however, the simple addiction model may be too narrow to account for nicotine use.

A multifactorial model including a variety of nicotine effects, such as

* improved attentiveness and
* memory,
* quickened reaction time,
* reduced appetite, and
* lessening of anxiety and
* stress,

may be needed to explain why the drug is so widely sought after. These effects also suggest possible therapeutic uses of nicotine when delivered without hazardous compounds present in tobacco tar, as well as of novel nicotinic ligands.

For example, there is evidence to suggest that these agents may be useful in preventing or treating a wide variety of central nervous system (CNS) disorders, including

* Parkinson’s disease,
* Alzheimer’s disease,
* attention deficit/hyperactivity disorder, and possibly
* Tourette’s syndrome;

other conditions for which nicotinic agents could theoretically be helpful include

* obesity,
* depression, and
* anxiety.

In addition to its effects on CNS disorders and functioning, cigarette smoke seems to exert a protective or beneficial influence on some

* immunological and
* inflammatory disorders and on certain

* hormone-related and
* reproductive problems.

Although the moiety in cigarette smoking that underlies the effect of smoking on immunological or inflammatory disturbances is not clear, there are indications that it may be at least in part related to nicotine. If so, a role for nicotine therapy for those disorders could usefully be investigated. For the hormone-related disorders, the effects of smoking may well not be due to nicotine.

This article will highlight recent work examining the epidemiological and clinical evidence for the inverse association between cigarette smoking and a variety of disorders and review what is known about the mechanisms underlying these relationships. For a number of these diseases, the potential therapeutic value of nicotinic agents represents a particularly promising area of research. Even for conditions for which the smoke components responsible for the beneficial effects are unknown and/or unlikely to be nicotine, a better understanding of the relationship with smoking may help to clarify the etiology and suggest treatments and preventive measures that will likely be far safer than cigarettes.

Central nervous system functioning

Mental functioning in nonimpaired individuals. Smoking may affect CNS performance in non-diseased individuals. Smoking or nicotine clearly ameliorates the impairments associated with nicotine withdrawal; among smokers, cigarettes seem to provide modest improvements in vigilance and information processing, facilitation of some motor responses, and perhaps enhancement of memory. The use of smokers in much of the cognitive research has necessarily involved individuals with chronic nicotine exposure; this may well have played a role in the effects observed through withdrawal, tolerance or changes in receptors. Nonetheless, there are data suggesting that non-smokers may experience nicotine-related benefits in performance and information processing. Consistent with these findings, studies in animals have indicated that nicotine may improve learning and memory, although some investigations have also shown evidence of nicotine-associated impairments.

Parkinson’s disease

An inverse association between smoking and Parkinson’s disease (PD) is well established; ever smokers have about half the risk of never smokers. The association is not explained by defects in study design or analysis, although the possibility that individuals destined to be at high risk for Parkinson’s disease have an aversion to smoking has not been completely excluded.

Nicotine is thought to activate the nigrostriatal dopaminergic pathway and increase the release of dopamine in the striatum. Smoking or nicotine can reduce drug-induced parkinsonism, ameliorate Tourette’s syndrome, and neuroleptic tardive dyskinesia, effects that all point to a substantial impact of nicotine on the dopaminergic motor systems. Chronic nicotine dosing has also been shown to protect against degeneration of central dopamine neurons induced by mechanical lesions. Thus, the positive effects of nicotine on the movement disorders of PD are not surprising.

Other human and animal evidence also support a protective effect: Cigarette smoke or nicotine can ameliorate experimental parkinsonism in rodents.9,10 Two case studies by Fagerstrom and colleagues using nicotine gum and nicotine patch demonstrated diminished bradykinesia and increased energy in one patient, and diminished tremor and disorganized thinking in the other.11 Case studies by Ishikawa and Miyatake show reduced tremor, rigidity, bradykinesia, and gait disturbances which lasted 10-30 minutes after cigarette smoking in 6 patients with early onset PD.12

Alzheimer’s disease

The epidemiological data regarding a possible inverse association between cigarette smoking and Alzheimer’s dementia (AD) is certainly suggestive, although less compelling than that for PD.13 Deficits in short- and long-term memory, impaired attention, liberal response bias, and slowing of reaction times are hallmarks of the dementing picture seen in AD.

Nicotine has also been found in various studies to nicotine improve attentiveness, memory or learning in patients with Alzheimer’s disease.14-17 These effects may be related to direct nicotinic stimulation, which may be useful because Alzheimer’s patients have been consistently found to have decreased numbers of nicotinic receptors compared with age-matched controls.18-23

The potential effects of the loss of these receptors was examined by administering the nicotinic antagonist mecamylamine to young and elderly normals, AD and PD patients. Mecamylamine produced a dose-related impairment in acquisition of both verbal and non-verbal information, slowing of reaction times, and liberalizing of response bias.24 PD patients did not show the sensitivity that AD patients did, despite a prior finding that PD patients also show loss of nicotinic receptors. Studies with intravenous nicotine in AD patients have shown that nicotine can improve cognitive function in many of these same cognitive domains with a dose-related decline in errors on verbal learning tasks and increase in long-term recall.25,26 These results suggest that nicotinic modulation may alleviate cognitive impairments in various dementing disorders which show loss of nicotinic receptors.

Attention Deficit Hyperactivity Disorder (ADHD)

Individuals diagnosed as having ADHD also have higher rates of cigarette smoking than the general population.27 Nicotine administration has been shown to improve attentiveness, and nicotine also promotes the release of dopamine as does current pharmacologic treatments of ADHD. A study by Levin and colleagues showed significant reduction in reaction time, reaction time variability, and increased accuracy on several cognitive tasks with nicotine administration in 11 adults diagnosed with ADHD.28 Additionally, these subjects rated themselves as having significantly more vigor than when they were administered placebo. Further studies are continuing with chronic administration. Currently used treatments, methylphenidate, amphetamine and pemoline have this mechanism of action.

Tourette’s syndrome

Tourette’s (TS) is a disorder characterized by multiple motor and vocal tics. Some patients with TS do not fully respond to standard treatments and/or experience significant side effects with high doses of neuroleptics. Animal studies have found that nicotine dramatically potentiated the cataleptic effects of neuroleptics, while not producing these effects when administered alone.29 These studies have lead to open trials in adults and children to examine the possible benefit of augment nicotine treatment. Administration of nicotine gum or patch to patients showing incomplete responses to haloperidol produced dramatic relief of symptoms as soon as 20 minutes after administration. Improvement was seen in both the frequency and severity of motor and vocal tics as well as improved concentration and attention.

Preliminary studies by Sanberg and co-workers have found transdermal nicotine patches to be effective in reducing tic frequency in Tourette’s syndrome.30,31 Nicotine significantly facilitates the effectiveness of haloperidol and other dopamine receptor blockers which are the usual treatment for this disorder. This effect of nicotine is paradoxical since it causes dopamine release. Sanberg and coworkers have hypothesized that nicotine-induced GABA release in the striatum may be important for its effectiveness in Tourette’s syndrome. Unexpectedly, some patients showed sustained improvement in symptoms after a single exposure to nicotine, with suppression of symptoms lasting up to several weeks.32

Schizophrenia

Nearly 90% of schizophrenics smoke [NOTE: most of them chain smoke, yet they have 30-50 percent lower lung & other cancer rates, compared to general population of the same age]. One possible explanation for this phenomenon is that schizophrenics may smoke in part because nicotine may improve their ability to filter out and ignore irrelevant sensory information, which may be related to an impairment of inhibitory mechanisms which act to decrease attention to repeated stimuli (sensory gating).34

One of the neuronal mechanisms responsible for such gating involves the activation of nicotinic receptors in the hippocampus, which appear diminished in schizophrenics. Investigations have shown that schizophrenic patients and 50% of their first degree relatives show deficient sensory gating to repeated auditory stimuli (P50) and that nicotine transiently restores normal suppression (gating) of P50.34

Pretreatment with the ganglionic-type (C6) nicotinic antagonist mecamylamine did not block the restoration of gating, suggesting that this effect may be mediated through bungarotoxin-type nicotinic receptors. Drug strategies to improve sensory gating in schizophrenic patients using nicotinic agents may be an attractive therapeutic target Levin and colleagues recently found in a study of schizophrenics in a haloperidol dose effect study that the spatial working memory and spatial information processing speed deficits induced by haloperidol were attenuated by nicotine skin patches.35 In a related study, they found that higher haloperidol doses resulted in higher levels of ad lib smoking.36 Thus, schizophrenics may also smoke to counteract the adverse side effects of antipsychotic dopamine blockers. Interestingly, clozapine an atypical antipsychotic with less dopamine D2 receptor blockade actually caused a dose related decrease in ad libitum smoking.37

Body weight

An inverse association between cigarette smoking and body weight is well known.38 The weight difference between smokers and non-smokers appears to be larger at older ages, and is most marked for moderate smokers. Cessation of smoking is associated with weight gain, a factor which impedes smoking control efforts. The effect of smoking is not completely explained by differences in energy intake or physical activity; cigarette smokers seem to have a higher metabolic rate than non-smokers.39 The weight-reducing effects of smoking may well be due to nicotine, although there are also suggestions of a behavioral component.

Immunological and inflammatory disorders

Cigarette smoking seems to impair [affect] several aspects of immune functioning, including T-cell functioning and antibody response;40 consequently, a benefit for immunologically-mediated disorders is conceivable.

Inflammatory bowel disease

Illustrative of the diversity of sites of nicotine’s action in the body is preliminary evidence of a potential role in inflammatory bowel disease. Silverstein reported several cases which linked cessation of cigarette smoking to the onset of inflammatory bowel disease, and/or symptom improvement with nicotine administration via nicotine gum.41 These studies show that current smokers have a reduced risk and former smokers had a slightly increased risk of being diagnosed with ulcerative colitis (UC) and that the risk of onset of UC appears to be substantially increased shortly after quitting smoking. Initial clinical trials of the addition of nicotine gum to standard treatment in UC have shown improvement in about 50% of patients. A study of 6-week treatment with nicotine patches has also shown significant improvements in global clinical and histological appearance, severity of symptoms, and remissions.41

An inverse association between cigarette smoking and ulcerative colitis has been repeatedly documented. Current smokers have a relative risk of 0.5 or lower in comparison to never smokers, but former smokers have, if anything, an increased risk.42 These findings, and reports of the amelioration of ulcerative colitis symptoms by smoking or nicotine led to formal trials of transdermal nicotine. The pattern of response resembles that of corticosteroid therapy: a benefit for patients in relapse, but no effect in prolonging remission.43 The mechanisms for the effect remain unexplained, although several have been proposed, including changes in bowel mucus or prostaglandins, immune suppression, and other effects in the bowel.44

Aphthous ulcers

A protective effect of cigarette smoking or smokeless tobacco use and the risk of recurrent aphthous ulceration of the mouth has emerged in several studies, though not in all.43 Some investigators have published case reports noting a worsening of the ulcers after smoking cessation, with relief after resumption. These effects may be due to the increased oral keratinization associated with tobacco use; the possible efficacy of nicotine chewing gum suggests that nicotine is an active moiety.43

Extrinsic Allergic Alveolitis

Smoking is clearly inversely related to extrinsic allergic alveolitis (farmers’ lung, pigeon breeders’ lung), a chronic immunologically-mediated lung disorder. In addition to a lower risk of the clinical syndrome itself, smokers have lower levels of the serum antibodies associated with the disorder.45

Sarcoidosis

Several case-control studies have reported an inverse association between smoking and the risk of sarcoidosis.45 It is possible, however, that artifacts in the studies may have distorted the findings, and some negative reports have been published. The association thus remains uncertain, although the effects of smoking on lymphocyte populations make it plausible.

Reproductive and hormone-related disorders

Endometrial cancer

Endometrial cancer is the only malignancy that has repeatedly been found to be inversely related to cigarette smoking. Smokers have about half the endometrial cancer risk of non-smokers, an association that is most marked among post-menopausal women and weaker in former smokers.46 The lower body weight and earlier age at menopause in smokers does not explain the association. The endometrium is probably the only anatomic site where such an effect is conceivable: Here carcinogenesis from direct smoke contact is not an issue, and the "anti-estrogenic effect" of smoking might play a protective role.2

Other apparently beneficial effects have also been ascribed to the hormonal effects of smoking, including a

* reduced risk of uterine fibroids and
* endometriosis.2

Current epidemiological data are far from conclusive, however. Other effects on the female reproductive system, similarly not established, include a lower risks of vomiting of pregnancy and hypertensive disorders of pregnancy. For these, it is not clear what the mechanism of effect might be.43

Nicotine and nicotinic compounds as therapeutic agents

Nicotinic treatment holds considerable promise for preventing or treating a variety of conditions. Experimental studies with humans and animal models will help to identify critical mechanisms for the beneficial and adverse effects of nicotine. Much of the health risk associated with smoking, especially cancer and pulmonary disease, is attributable to some of the 4,000 compounds other than nicotine present in cigarette smoke. Nicotine apart from tobacco can be much safer, although like any drug it is not without adverse effects. When developing nicotine for therapeutic use, it is critical to determine the mechanisms of its actions so that its beneficial effects can be maximized and its adverse effects can be minimized. Alternate routes of nicotine administration may reduce adverse effects. For example, the nicotine skin patch seems to have much lower dependence liability than smoking because it is administered only once per day and produces a slow release of nicotine.47,48 Novel ligands may help determine which subtypes of nicotinic receptors are important for which effects of nicotine. Subtype selective ligands might have some of the beneficial effects of nicotine with fewer adverse side effects.

It is important to consider the mechanisms of action of nicotine to understand both its potential risks and benefits. Nicotine has complex primary actions at nicotinic receptors as well as primary effects at other receptor sites. Nicotine also has a cascade of secondary effects which involve a wide variety of neurotransmitter systems. All of these mechanisms may differentially contribute to the variety of functional effects of nicotine.

Nicotine is the prototypic agonist of the nicotinic subtype of acetylcholine receptor. This straightforward mechanism of action, however, is complicated in several respects. Nicotine potently stimulates the nicotinic receptor, but also can rapidly desensitize it. It is currently unclear precisely which of nicotine’s effects derive from its agonist actions and which from its desensitizing actions. A variety of nicotinic receptor subtypes have been identified. It is not clear which subtypes are important for which nicotine effects. In addition, nicotine has primary effects at other sites, such as N-methyl-D-aspartate (NMDA) receptors.49,50 Likewise NMDA ligands appear to have cross-reactivity with nicotinic receptors.51 This makes it difficult to sort out which receptor is responsible for the effects of nicotinic and NMDA ligands. Finally, an important component of nicotine effects is its ability to stimulate the release of a variety of neurotransmitters including acetylcholine, dopamine, norepinephrine and serotonin.52 This cascade of neurotransmitter release can have effects on a wide variety of neurobehavioral functions.

With increased understanding of the molecular biology of the nicotinic acetylcholine receptor (NAR), new molecules are being developed which have enhanced selectivity for nicotinic receptor subtypes, or which may be allosteric modulators of nicotinic receptor functioning. ABT-418 is a potent and selective NAR ligand which appears to be relatively selective for the alpha-4-beta-2 NAR subtype.53 Studies of the cognitive effects of ABT-418 in animal models showed positive effects on inhibitory avoidance, restored performance in septal-lesioned rats and enhanced primate performance on delayed matching-to-sample tasks.54 Other nicotinic agonists under development include GTS-21, an anabasine derivative which may have activity at alpha-7 NARs and may be neuroprotective. S-1663 appears to be selective for alpha-3-beta-4/2 NARs and may selectively enhance dopamine release and reduce neuroleptic-induced catalepsy. Novel selective nicotinic agonists may offer significant therapeutic advantages over nicotine itself.

Research is continuing in a number of directions to promote a better understanding of the role of nicotinic mechanisms in both CNS and peripheral disease states and to develop selective nicotinic agonists for clinical trials. Such efforts may open up a new era in nicotine pharmacology.


Edited by nightlight, 09 April 2007 - 08:11 PM.


#8 edward

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Posted 09 April 2007 - 08:51 PM

I have no problem with entertaining the idea of taking nicotine, using patches, gum or even smokeless tobacco as well as taking deprenyl. However actually taking up smoking again (for nootropic purposes) seems a little crazy as I personally witnessed how much better I was able to exercise and well breathe after I quit smoking.

#9 niner

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Posted 10 April 2007 - 04:31 AM

Nightlight, thanks for a fascinating example of hormesis, among other things. Still, I'm going to be a Butthead and come out and say it: I think your personal relationship with tobacco is causing you to oversell its benefits. For example, you say:

Tobacco smoke also nearly doubles glutathione and other internal antioxidants

but looking at the paper, that's only in alveolar epithelial cells, where glutathione levels are 140 times higher than plasma levels. And yet, among the papers citing this work are the following:

Cigarette Smoke Inhibits Alveolar Repair: A Mechanism for the Development of Emphysema
S. I. Rennard, S. Togo, and O. Holz, Proc. of the ATS, Nov 1, 2006; 3(8): 703 - 708.

Long term smoking with age builds up excessive oxidative stress in bronchoalveolar lavage fluid
K Nagai, T Betsuyaku, T Kondo, Y Nasuhara, and M Nishimura, Thorax, June 1, 2006; 61(6): 496 - 502.

Oxidative stress and redox regulation of lung inflammation in COPD.
I. Rahman and I. M. Adcock, Eur. Respir. J., July 1, 2006; 28(1): 219 - 242.

#10 nightlight

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Posted 10 April 2007 - 07:45 AM

Nightlight, thanks for a fascinating example of hormesis, among other things.  Still, I'm going to be a Butthead and come out and say it:  I think your personal relationship with tobacco is causing you to oversell its benefits. 


It isn't as if I am declaring here something particularly novel. People have cultivated tobacco for seven millennia and had smoked it for several more before that, as a potent medicinal plant. It was experienced as therapeutic and beneficial around the world, anywhere and shortly after its first appearance at any given place, without being brought in or sold as a medicinal plant.

It wasn't until 1950s, when US and UK governments needed a scapegoat to "explain" explosive rise in lung cancers and melanomas

Posted Image
Figure 4. Lung cancer death rates in Sweden

Posted Image
Figure 3. Skin melanoma mortality in Sweden since 1912

which correlated in space in time with the rise in radioactive fallouts from the atmospheric nuclear tests, that smoking and lung cancer theory was concocted by Richard Doll (on behalf of the UK government) and in the face of gross anomalies outright contradicting such explanation (and favoring protective role of tobacco smoke, instead, see also on anomalies in randomized intervention trials in humans) who subsequently made a career out of his unquestionable talent for that kind of shifting the blame onto the victim's lifestyle from those paying for his "reasearch" at the moment.

Posted Image
Figure 7. Asthma rates in Sweden in Finland

It took then a decade or so, before the pharmaceutical industry noticed how enormously beneficial the attack on this ancient medicinal plant was to its own profits, not just from selling pharmaceutical nicotine and smoking cessation "therapies" but far more from treating the resulting additional millions of asthma, allergies, Alzheimer's, Parkinson's, schizophrenia, depression, anxiety, ADHD, obese, diabetic,... patients. Intoxicated by these obscene windfalls the antismoking industry only then kicked into the higher gears, whipping up eventually the mass hysteria we have today. It is as if the biochemical effects of tobacco smoke were amplified by propagating upwards and outwards, from the biochemical networks at the molecular level into the larger economic and social networks above and around, from human organism into the social organism.

but looking at the paper, that's only in alveolar epithelial cells, where glutathione levels are 140 times higher than plasma levels.


Hence, you can measure it hundred times more accurately than in plasma. The glutathione upregulation (also of other internal antioxidants, as welll as of neutrophiles) is systemic and at a fundamental level, result of longer term smoking rather than a spike induced by few cigarettes at a particular location. This is at least in part due to the 'exercise effect', where a periodic, gentle oxidative load from tobacco smoke strengthens over time the very systems being exerted by it, no different in principle than the effects of aerobics on cardiovascular system or weight lifting on muscles.

And yet, among the papers citing this work are the following:

Cigarette Smoke Inhibits Alveolar Repair: A Mechanism for the Development of Emphysema
S. I. Rennard, S. Togo, and O. Holz, Proc. of the ATS, Nov 1, 2006; 3(8): 703 - 708.

Long term smoking with age builds up excessive oxidative stress in bronchoalveolar lavage fluid
K Nagai, T Betsuyaku, T Kondo, Y Nasuhara, and M Nishimura, Thorax, June 1, 2006; 61(6): 496 - 502.

Oxidative stress and redox regulation of lung inflammation in COPD.
I. Rahman and I. M. Adcock, Eur. Respir. J., July 1, 2006; 28(1): 219 - 242.


You will find plenty of "studies", those citing the one I mentioned and many others, deceptively labeling the observed upregulation of endogenous antioxidants in smokers as increase in 'oxidative stress markers', which is analogous to labeling larger muscles in weight lifters as increase of 'mechanical stress markers' or better heart and tissues oxygenation in joggers as higher 'oxygen depletion markers'.

In addition to that kind of verbal gimmickry (people will twist truth for much less money than what antismoking cartel is pouring into its "research"), another common sleight of hand is to pick a suitable phase and measurement location in the mentioned 'exercise cycle' which strengthens glutathione over time, such as the few percent drop in alveolar liquid after a cigarette (which is offset by a far greater systemic rise), and exclaiming, 'see smoking depletes glutathione'. Again, that's analogous to picking a phase and a measurement location in the weight lifter's exercise cycle, such as the point of maximum load on particular muscles from the weights, measuring the remaining lifting capacity of these muscles then proudly declaring to their sponsors, 'see the residual muscle capacity was reduced' by the evil weight lifting (that's exactly what they did for the transient vascular effects of tobacco smoke, which are actually beneficial over time, just as similar effects of aerobics exercise are, in order to proclaim that 30 seconds of SHS could cause heart attacks).

Note also that various biochemical upregulations in smokers do require higher levels of nutrients and supplements (e.g. more vit C, E and selenium, needed in glutathione recycling). Unfortunately, those who still smoke under the present heavy handed social and economic pressures against smoking, are largely those the least likely to care about details such as nutrition and supplements. Hence these social engineering measures and the statistical correlations of smoking with diseases (along with variety of other misfortunes) form a self-reinforcing, positive feedback loop. The result of this dynamics is a much greater degree of statistical skewing and confounding than before, making thus the epidemiological "studies" gloating over the strengthening correlations between smoking and various diseases they keep "discovering", increasingly less indicative of any causative role of smoking in the ethiology of these diseases.

Edited by nightlight, 10 April 2007 - 09:47 AM.

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#11 ikaros

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Posted 10 April 2007 - 02:54 PM

NOTE: most of them chain smoke, yet they have 30-50 percent lower lung & other cancer rates, compared to general population of the same age


This is totally mindboggling. Do schizos have some super anticancer protection genes built into them??

#12 edward

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Posted 10 April 2007 - 02:55 PM

Nightlight,

How do you explain that 85-90% of the cases of lung cancer in this country occur in smokers. Only 10-15% of cases occur in non smokers. Lung cancer =s death or severe disability. If there was some protective effect then this simply would not be. Any positive effects on the nervous system are far outweighed by this simple statistic.

#13 luv2increase

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Posted 10 April 2007 - 06:24 PM

If one absolutely has to smoke cigs, smoke organic, non-cured tobacco cigs. Also, keep a good aerobic exercise regimen along with this and stray from beta-carotine.

Your best bet is to quit though ;)

I've done away with all tobacco for awhile now and have no regrets. I do regret it took be about 30 times of quitting to finally quit though.

#14 ikaros

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Posted 11 April 2007 - 04:22 PM

and stray from beta-carotine


Actually beta-carotene is beneficial to smokers, although if taken alone without complementary antioxidants it turns into pro-oxidant and increases odds to get cancer.

#15 nightlight

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Posted 13 April 2007 - 11:21 PM

Nightlight,
How do you explain that 85-90% of the cases of lung cancer in this country occur in smokers. Only 10-15% of cases occur in non smokers. Lung cancer =s death or severe disability. If there was some protective effect then this simply would not be. Any positive effects on the nervous system are far outweighed by this simple statistic.


Statistical correlation between some phenomena A (e.g. smoking) and B (disease) is not synonymous with A causes B. For example, use of breathing ventilators is correlated with respiratory problems, strokes, heart attacks... yet use of ventilators reduces breathing problems, risk of stroke, heart attack... Similarly, if your grades increased last semester, that doesn't mean they are now better than those of another student whose grades remained the same or decreased in that semester. The increase/decrease (in grades or in disease rates) is a derivative of a function, which is a very different quantity, the mass media obfuscation notwithstanding, than a function value (your grades or disease rate).

Some habit A can be protective or therapeutic against disease B and yet show positive correlation (of any strength) with B in the samples in which the real causes of B are not properly controlled (as it is the case with most cancers, where the fundamental etiology is not known).

In the example of ventilators use, if that is the only parameter under control (in addition to age) you will find that users of ventilators will have much shorter life expectancy than non-users, while the former users (self-selected) will fall somewhere in between. This is no different statistical phenomenon than what is found regarding smoking and the so-called 'smoking related' diseases.

Generally, a statistical correlation between phenomena A and B implies only that one or more of the following causal relations is the explanation:

1) A causes B
2) B causes A
3) Some other phenomenon C causes A and B

In case of B occurring later than A and without being anticipated (since the anticipation or fear of B could cause A), then possibility (2) is eliminated, leaving a choice (1) and/or (3). Normal science, takes therefore such statistical correlation of A and B as a hint for a followup research using the methods of hard science which can distinguish between the possible causal models (1) or (3).

Note also that (3) includes not just some gene C making carriers simultaneously more likely to smoke and more likely to develop lung cancer (both phenomena do have a strong genetic component), but also the situations where C is some well established carcinogenic substance which also has other irritating effects when inhaled, such as asbestos or many dusts in metal ores mines. Since the doubling of glutathione (and other antioxidants and detox enzymes) in smokers will help remove such toxins at twice the rate than in nonsmokers, smoking provides immediate relief against the acute irritating effects of C. Hence the exposure to C would make it more likely (compared to less exposed general population) that those exposed will smoke. C is thus a common cause, via unrelated pathways, of A and B, yielding an increased statistical correlation of A and B.

Unlike the normal science, the antismoking "science" (euphemism for the massive extortion racket) is still, half a century later, stuck in the hint phase. They are merely replicating the same statistical correlation of A and B which they had in 1950s, as if thousand virtual xerox copies of the finding that 'A correlates with B' alone will distinguish between the models (1) and (3). It was already by 1958, that Ronald A. Fisher pointed this very problem of the antismoking "science" of that time:

But the time has passed, and although further investigation, in a sense, has taken place, it has consisted largely of the repetition of observations of the same kind as those which Hill and his colleagues called attention several years ago. I read a recent article to the effect that nineteen different investigations in different parts of the world had all concurred in in confirming Dr. Hill's findings. I think they had concurred, but I think they were mere repetitions of evidence of the same kind...


What would Fisher say about it half a century later, with antismoking "science" still stuck in that same loop (well, what can poor folks do but stick with that which works, since going beyond, at the causal relations, always backfired). The reason Fisher was puzzled by the same situation already at that time is because when normal science encounters some correlation between the exposure to some substance A and cancer B, the immediate next step is to use hard science to test whether A causes B. For example, it is trivial to establish that radiation or inhalation of radioactive particles causes lung cancers -- you expose some mice to such radiation in dose of interest and they develop lung cancers like clockworks. The same goes for various chemical carcinogens for which OSHA and EPA set exposure limits based on easily reproducible animal tests (cancer is a primitive disease, not specific to humans).

So why then, fifty years later, are we still only handwaving statistical association of smoking and lung cancer, such as "85-90% of the cases..."? Can't we just make some animals breathe enough tobacco smoke and develop cancers at higher rates, so we can establish it once and for all? We could do that, and it was done, of course, except that the data went the "wrong way" -- the smoking mice gets fewer lung cancers than non-smoking mice, with dose-response relation showing that tobacco smoke is protective against lung cancers:

Inhalation Bioassy of Cigarette Smoke in Rats
A.P. Wehrner, et al. Battelle Pacific Northwest Labs, Richland WA
Journal of Toxiology & Applied Pharmacology, Vol. 61: pp 1-17 (1981)

The results show that the highest number of tumors occurred in the untreated control [non-smoking] rats. The next highest number of tumors occurred in rats subject to sham smoking, i.e. rats which were placed in the smoking machine without smoke exposure, and the lowest number of tumors occurred in the smoke-exposed rats. Among the latter, the largest number of tumors occurred in rats exposed to smoke from cigarettes having the lowest level of nicotine.


No matter how much tobacco smoke they made poor animals inhale, even in equivalents of a carton or more per day (through surgically implanted breathing tubes), the more they smoke the fewer lung cancers they get. It just doesn't work and it even contradicts their "theory" so they just gave it up.

With humans, we can't force them to smoke, or even not to smoke, hence the next best thing, closest to hard science, are randomized intervention trials -- you take a group of smokers, assign half of them randomly into a 'quit group' (strongly advised not to smoke), and a 'control group' (left alone, to smoke as they wish), then follow them up for some years or decades, observe the smoking rates (which are normally lower in 'quit group') and check for lung cancers or other diseases. That was done, of course, but only a handful of times in the early years of antismoking "science". As with animal experiments, the results of these few randomized intervention trials, whenever they showed anything at all, also went the "wrong way" -- the 'quit group' ends up with more lung cancers than the 'control group' (and generally higher death rates). You can read about these studies (which most people have never heard of) here: [1], [2], [3], [4], [5],[6].

It should be noted that even the bare statistical correlations often parroted, the "90 percent..." stuff and such, which could mean anything anyway, aren't even on their own nearly as firm as mass media and 'pedagogues' would like you to believe. The diagnostic bias over-diagnoses lung cancers in smokers and under-diagnoses them in non-smokers by about 30 percent each. Further, the 'smokers' variable yielding those large risk ratios, counts also ex-smokers (usually anyone who smoked for few months or longer in their life), who often have higher rates (depending on sampling criteria, especially age), of lung cancers than current smokers and who are now more numerous than smokers.

Another interesting bit of statistical trivia is that the absolute numbers of smokers and total number of cigarettes smoked today are in USA lower than in 1950 (also, back then people smoked mostly non-filtered cigarettes which had 2-3 times more "tar" and nicotine per cigarette, plus many more were exposed to SHS since no one knew it is so deadly), yet the absolute number of lung cancer deaths per year is more than 8 times larger today (from 20k in 1950 to over 160k in 2006).

If each molecule of tobacco smoke has some probability p of causing the final cancerous mutation of a lung cell upon interaction with it, and the total number of such molecule-cell contacts per second has declined by a factor 2-3 over half a century in between (while there was a similar number of cigarettes smoked, they had 2-3 times higher "tar" per cigarette), how would one simulate via a computer model the eightfold rise in the number of such mutations? Plain old random number generator striking with probability p some population of cells surely can't do anything remotely what our current "theory" of lung cancer is proclaiming. To make the simulation work as imagined by our smoking-causes-lung-cancer "theory", one would need some kind of smart molecules, which learned over these decades how to aim better into the right section of the lung cell's DNA, maybe something like bacteria evolving antibiotic resistance. Except that molecules don't do that. And what's in it for them even if they knew how? If they're so smart, wouldn't they also be able to figure out that this particular DNA aim will hurt their future numbers? Well, that's how absurd it is. It is interesting that even back in 1950s, when Richard Doll concocted our modern lung cancer from tobacco smoke "theory" , the famous British mathematician Ronald A. Fisher (the father of modern statistics) noted a similar anomaly (some kind of "smart molecules" would be needed explain it within their "theory") in Doll's data, as recounted here:

These strong opinions for and against smoking were not supported by much evidence either way until 1950 when Richard Doll and Bradford Hill showed that smokers seemed more likely to develop lung cancer. A campaign was begun to limit smoking. But Sir Ronald Fisher, arguably the greatest statistician of the 20th century, had noticed a bizarre anomaly in their results. Doll and Hill had asked their subjects if they inhaled. Fisher showed that men who inhaled were significantly less likely to develop lung cancer than non-inhalers. As Fisher said, "even equality would be a fair knock-out for the theory that smoke in the lung causes cancer."

Doll and Hill decided to follow their preliminary work with a much larger and protracted study. British doctors were asked to take part as subjects. 40.000 volunteered and 20,000 refused. The relative health of smokers, nonsmokers and particularly ex-smokers would be compared over the course of future years. In this trial smokers would no longer be asked whether they inhaled, in spite of the earlier result.

Fisher commented: "I suppose the subject of inhaling had become distasteful to the research workers, and they just wanted to hear as little about inhaling as possible". And: "Should not these workers have let the world know not only that they had discovered the cause of lung cancer (cigarettes) but also that they had discovered the means of its prevention (inhaling cigarette smoke)? How had the MRC [Medical Research Council] the heart to withhold this information from the thousands who would otherwise die of lung cancer?"

Five year's later, in 1964, Doll and Hill responded to this damning criticism. They did not explain why they had withdrawn the question about inhaling. Instead they complained that Fisher had not examined their more recent results but they agreed their results were mystifying. Fisher had died 2 years earlier and could not reply.

This refusal to consider conflicting evidence is the negation of the scientific method. It has been the hallmark of fifty years of antismoking propaganda and what with good reason may well be described as one of the greatest scandals in 500 years of modern science.


These correlations are also sensitive to the intensity of the antismoking propaganda -- in countries or populations with high intensity of antismoking propaganda, the correlations are stronger, with lung cancer "risk factors" 8-15, while in countries with lower propaganda they go as low as 1.3-1.6 (see ref [3]). For example, Japanese men smoke more than twice as often as American men, yet they have 2-3 times fewer lung cancers, while living longer, than Americans (Greece vs USA has similar relation; see also [4]). A more drastic example are Semai people of Malaysia, who start smoking at age two, as a way of weaning themselves from nursing, and then happily continue smoking, completely worry free, into the ripe old age. They were studied in 1970s for 'smoking related' diseases, which included chest X-rays for all 12000 Semai adults, and not a single lung cancer was found (cf. Dr. G. Y. Caldwell, British Medical Journal, Feb. 26 1977, V. 1 (6060) p. 580).

Even within the same country, there are populations who are outside of the "matrix", as it were, such as schizophrenics (who live in their own "matrix" distinct from ours). As noted in the article quoted above, they smoke at huge rates (over 90%, mostly chain smokers), yet they get 30-50 percent fewer lung cancers than general population.

One of the mechanisms behind such damaging effects of antismoking propaganda (in addition to the detection and recall biases discussed in references given above, which are boosted by the propaganda and which in turn skew the statistical sampling) is the "witch doctor effect" (negative placebo):

J. Hatton, R. Harris Murder a Cigarette: the Smoking Debate

There was a study in Heidelberg, described by Professor Eysenck in Psychological Reports (1989) in which 528 men were asked whether they, as smokers, were convinced that they would be very likely to develop lung cancer, heart disease, or other 'smoking related diseases'.

The 72 who answered 'yes', while admitting that their views were taken from information in the media, had an almost three times higher death rate at the end of 13 years than those who were not so influenced.

Fear can kill. This has been known since disease was first studied. We are entitled to wonder how many people have been killed more by the fear of 'smoking related diseases' than by any actual disease itself.


Leslie Kenton Modern-day Death Curses

Almost everybody has heard of death curses: psychological literature is laced with accounts of how Aboriginal witch doctors have quite literally brought about the death of the young and healthy by cursing them. No sooner do these people learn of the fate which has been cast for them than they begin inexplicably to sicken and eventually to die. It appears that through complex biological processes, their simple belief in the curse brings about destruction of their organism.

In civilized society we tend to look upon such phenomena as anthropological curiosities - products of primitive superstition which simply don't touch us in our more enlightened age. What we are not aware of however is that many of us in the civilized world are also under our own brand of `death curses'. They may be subtler than those issued by witch doctors but they can be every bit as potent in bringing about the physical and mental decline which we have come to associate with aging.

Common (and usually unconscious) notions such as `retirement', `middle-age', `It's all down hill after forty', and `At your age you must start taking things more easily', are widely held. They can exert a powerful effect on the process of aging by creating destructive self-fulfilling expectations about age decline. Instead of facing the future full of confidence and excitement about what lies ahead, optimism is replaced by anxiety as we are warned to `Be careful', or `Don't take chances on a new career at your age.'


Another mechanism is that such antismoking social engineering by itself reshapes the statistical distribution of various parameters, so that in our present antismoking "matrix" a random sample of 'smokers' is quite different from a random sample of 'non-smokers' in many other ways (mostly negatively affecting the 'smokers' sample), not just smoking.

For an example on how social engineering can do that, consider that since tobacco is an ancient medicinal plant with numerous therapeutic and protective effects, as illustrated in earlier posts here, people who still smoke despite the obscene financial shakedown and vicious social abuse of smokers, are largely those who truly need it. For example, a blue collar worker, exposed to toxic vapors and dusts at work, will find that smoking provides easily noticeable, immediate relief, due to near doubling of glutathione from smoking (which in turn will double, among others, the excretion rates of toxic metals, hence halve the effective exposure). Similarly, the upregulation of neutrophiles (the frontline defense against microbes and other organic antigens) by tobacco smoke strengthens the resistance against infections and neutralizes quickly most allergens (smoking was traditionally used to treat such problems and has spread through Europe based on similar observations; even the medical textbooks until 1950s advised smoking as a relief for asthma).

While there was always some fraction of people smoking as a form of spontaneous self-medication, their proportion has become much greater since anyone who doesn't really need to smoke for therapeutic reasons will have all other reasons to quit or not start. Smoking is thus increasingly becoming a marker of hardship (i.e. of some unfavorable combination of genetic and environmental factors which causes people to smoke as a self-medication).

Therefore, pointing these days at the statistical correlations of smoking with various diseases, or any other kind of misery, is as meaningless as 'discovering' that people using respirators have lower life expectancy or that aspirin users have more headaches than general population.

In the light of that observation, the present antismoking hysteria (which is merely a facade for the plain old extortion racket by the pharmaceutical industry), with its shakedown, social discrimination and "denormalization" of smokers, is about as noble an undertaking as ripping the breathing and IV tubes out of hospital patients. Antismoking con has indeed become increasingly evil in recent years, almost comparable to any genocide in human history since that is what it comes down to -- you either 'convert' (quit smoking) and get damaged or killed from the resulting biochemical meltdown (as you can note in the MAO B graphs earlier, biochemistry of smokers is dramatically different from that of nonsmokers; nicotine is only a minor signaling mechanism within the larger symbiotic intertwining of the two complex biochemical networks) and pharmaceutical snake oils elbowing in, trying to replace numerous therapeutic effects of this ancient medicine, or you keep smoking and die from the "death curse" or get sick and die from exposure in the rain, snow, car fumes... after being "denormalized" and shoved out into the street by the hysterical mobs.

Edited by nightlight, 16 April 2007 - 12:33 PM.

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#16 roidjoe

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Posted 14 April 2007 - 03:37 AM

Is it not fairly obvious that tobacco smoke would both a) increase the risk of cancer and b) "strengthen" lung tissues in smokers. This is just simply due to the carcinogens mutating and damaging DNA within the cells - if the areas damaged do not cause cancer, and immortal reproduction of the cell, and in doing so it raises the bodies defenses to future damage - it would be a beneficial event. But, considering this, there is always the possibility of the carcinogen damaging multiple points on chromosomes that affect anti-cancerous systems, such as p53, thus promoting the growth of cancer. It does take multiple mutations to different parts of DNA to cause most cancers, not just one. So now we can see that while smoke can clearly increase the bodies defense it caries an increased risk of lung cancer.

How can it not be obtusely obvious that cigarettes, laden with toxic chemicals, are damaging lung tissues and promoting the growth of cancers? Only masked in the form of self deception.


Another interesting bit of statistical trivia is that the absolute numbers of smokers and total number of cigarettes smoked today are in USA lower than in 1950 (also, back then people smoked mostly non-filtered cigarettes which had 2-3 times more "tar" and nicotine per cigarette, plus many more were exposed to SHS since no one knew it is so deadly), yet the absolute number of lung cancer deaths per year is more than 8 times larger today (from 20k in 1950 to over 160k in 2006).

You do realize that mutations accumulate over time and that most cancers are caused by multiple mutations - and somone smoking for 10 years in 1950 (assuming he started in 1940) would be smoking for 66 years in 2006 (assuming he was still alive) and thus the chance of getting cancer is increased.

It isn't as if I am declaring here something particularly novel. People have cultivated tobacco for seven millennia and had smoked it for several more before that, as a potent medicinal plant. It was experienced as therapeutic and beneficial around the world, anywhere and shortly after its first appearance at any given place, without being brought in or sold as a medicinal plant.

There is a difference between present day cigarettes and cultivated tobacco. Another ridiculous inference.

Vaporizing tobacco might be of interest in the future.

Edited by roidjoe, 14 April 2007 - 07:28 AM.


#17 roidjoe

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Posted 14 April 2007 - 03:51 AM

http://toxsci.oxford...t/full/81/2/280

Chronic Inhalation Exposure to Mainstream Cigarette Smoke Increases Lung and Nasal Tumor Incidence in Rats

An animal model of lung carcinogenicity induced by chronic inhalation of mainstream cigarette smoke would be useful for research on carcinogenic mechanisms, smoke composition-response relationships, co-carcinogenicity, and chemoprevention. A study was conducted to determine if chronic whole-body exposures of rats would significantly increase lung tumor incidence. Male and female F344 rats (n = 81 to 178/gender) were exposed whole-body 6 h/day, 5 days/week for up to 30 months to smoke from 1R3 research cigarettes diluted to 100 (LS) or 250 (HS) mg total particulate matter/m3, or sham-exposed to clean air ©. Gross respiratory tract lesions and standard lung and nasal sections were evaluated by light microscopy. A slight reduction of survival suggested that the HS level was at the maximum tolerated dose as commonly defined. Cigarette smoke exposure significantly increased the incidences of non-neoplastic and neoplastic proliferative lung lesions in females, while nonsignificant increases were observed in males. The combined incidence of bronchioloalveolar adenomas and carcinomas in females were: HS = 14%; LS = 6%; and C = 0%. These incidences represented minima because only standard lung sections and gross lesions were evaluated. Mutations in codon 12 of the K-ras gene occurred in 4 of 23 (17%) tumors. Three mutations were G to A transitions and one was a G to T transversion. The incidence of neoplasia of the nasal cavity was significantly increased at the HS, but not the LS level in both males and females (HS = 6%, LS = 0.3%, C = 0.4% for combined genders). These results demonstrate that chronic whole-body exposure of rats to cigarette smoke can induce lung cancer.



#18 nightlight

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Posted 14 April 2007 - 05:57 PM

... Male and female F344 rats (n = 81 to 178/gender) were exposed whole-body 6 h/day, 5 days/week for up to 30 months to smoke from 1R3 research cigarettes diluted to 100 (LS) or 250 (HS) mg total particulate matter/m3, or sham-exposed to clean air ©. Gross respiratory tract lesions and standard lung and nasal sections were evaluated by light microscopy. A slight reduction of survival suggested that the HS level was at the maximum tolerated dose as commonly defined. Cigarette smoke exposure significantly increased the incidences of non-neoplastic and neoplastic proliferative lung lesions in females, while nonsignificant increases were observed in males....


Thanks for posting the link to this 2004 "study" from Pfizer staffers and a private lab contractors, since it illustrates quite nicely my point, that antismoking "science" is a pure, unadulterated pharmaceutical grade fraud. Here are some observations after a quick scan of the "study":

a) Their test animals were F344 rats, the little cancer machines, genetically optimized over past three decades to die at average age of 24 months riddled with multiple cancers from head to toe, of all kinds imaginable and then some (e.g. a quarter of the males gets breast cancers, while 65-90 percent of them gets testicular cancers...).

b) This "approach" of using little genetic cancer machines followed by subjective eyeballing of tumors in cherry picked tissue samples was "invented" in the early years of antismoking "science", then finely tuned into an art over the four decades since. Namely, it was already obvious early on that regular lab animals evaluated using objective, unambiguous criteria, such as a death from lung cancer, go invariable the "wrong way" (showing that smoking is protective against lung cancers), and that sponsors won't fund that kind of results. They wanted to see harm done by tobacco smoke no matter what, and if no real harm can be produced, well, the ingenous "scientists" defined their own kind of "harm" which they can produce and manipulate at will.

c) In addition to the subjectivity in outcome evaluation criteria, another advantage of the cancer rats for antismoking "science" is that their cancers grow very rapidly and everywhere, competing fiercely with each other for scarce blood and nutrient supplies. Hence they grow bigger and more numerous wherever one raises blood & nutrient supplies.

The Pfizer hacks knew, of course, that nicotine upregulates vascular growth factor. Better vascularization (e.g. better branching of capillaries) and stronger, quicker self-repairing blood vessels are normally a good thing for an organism. Tobacco smoke, being a finely optimized medicinal miracle, has other components working synergistically with nicotine to further enhance these vascular benefits (for a healthy animal) e.g. nitric oxide in low concentration of tobacco smoke acts as a neurotransmitter, signaling a request for increase in blood supplies (vasodilating Viagra effect), which works well with the improved vascularization. The carbon monoxide (also in low concentration of tobacco smoke) has similar biochemical signaling role in circulation, especially in improving tissue oxygenation. Simultaneously, the transient vasoconstricting effects of stimulated sympathetic nervous system (due to nicotine induced acetylcholine boost), reduce blood supplies to the limbs (where there are the fewest cancers in these cancer rats).

But, with cancer rats all these circulatory benefits also mean more blood and nutrients for cancer cells at the places where tobacco smoke is the most concentrated. Hence the cancers, initiated and growing already on their own by the genetic design of the rats, will have a competitive advantage in the locations where tobacco smoke is absorbed such as mouth, nose, bronchi, lungs. Smoking cancer rats will therefore have more of and bigger tumors there, fewer and smaller elsewhere (there are only so much blood and nutrients to go). This F344 effect, "discovered" in the study above, has in fact been known for decades (cf. review [1] p. 97):

Chronic Inhalation of Cigarette Smoke by F344 rats
W.E. Dalbey at al., Oak Ridge Nat. Lab., Inst. Environ. Health...
'J. National Cancer Inst., 64 (2): 383-390 (Feb 1980)

"Smoke exposure did not change the total number of tumor-bearing animals relative to controls; however exposed rats had significantly fewer tumors in the hypophyses, hematopletic-lymphoid  system, uteri and ovaries, but an increased number of tumors in the respiratory tracts and dermes."

These animal data fit in with the concepts of Prof. Oeser in Berlin and Dr. Lock in Hamburg, that, if properly assessed, the epidemiological data on cancers in general and for specific organs, indicate that total cancer rates have not changed, and that the only thing which has changed is that the increase in one type of cancer is compensated for by a decrease in other organ cancers.


In short, these cancer rat experiments demonstrate absolutely nothing about the mythical cancer causing powers of tobacco smoke. Instead, they merely confirm the well known vascular and circulatory benefits of tobacco smoke. In fact, this is a very common sleight of hand in antismoking "science" -- they take some health benefit of tobacco smoke, such as circulatory & vascular, endocrine, glutathione,... then apply it to cancer rats, where, as in any cancer, there is a reversal of values so that good, invigorating effects (in healthy animals) become harmful effects in cancer rats (since cancer can use them for itself).

d) Exposure levels in the experiment were astronomical -- their "low" exposure LS group had 100 mg of smoke particles per m^3, while high exposure HS group had 250 mg/m^3. Compare with a 10mg of smoke particles in today's full flavor cigarette -- the poor rats were chain smoking equivalents of 10-25 full flavor cigarettes/5 minutes being pumped into a tiny 1 m^3 box, for 6 hours per day, 5 days/week, for 30 months (oddly, their avg. life-span is 24 months). The same authors have done similar experiments to test carcinogenic properties of diesel exhaust (which they did find), where their low exposure group had 286 times less particle matter per 1m^3 than here. They were clearly very eager to please Pfizer management with their evils-of-tobacco "science".

e) "Smoking" pattern was also optimized to do harm. Normal smoking, with a 5 minutes per cigarette (broken further into 20-30 puffs), about 20 times per day, is a wholesome healthy exercise for the main biochemical networks in human body (neurotransmitters, immune, endocrine, nervous, cardiovascular systems), with harmoneously nesting and alternating active and resting phases, all optimally controled and paced by the built in biological feedback of the networks themselves, just as you do with any unforced, spontaneous exercise. Thus for these systems, smoking is analogous to taking 20 few minute breaks from your desk to lift 30 pound weights 20-30 times per session, pacing yourself for the most pleasing effect. It's a very healthy, invigorating kind of load and rhythm.

In contrast, the above "study" would have you take 10 times heaver weights and hold them up steady, fixed at an angle of maximum effort, for 6 hours in the air. Would that "setup" qualify as a "proof" that the normal weight lifting exercises, with spontaneous load and pacing described above, is bad for you? This is in fact why nicotine patches or even gums are not nearly as good for you, and are possibly harmful, as the nicotine from regular smoking, even ignoring the myriad of synergistic effects of other components in the real tobacco smoke (e.g. nicotine lacks MAOI B magic, vasodilating effects of NO and CO, as well as IGF1 glutathione, neutrophiles, testosterone, DHEA... rejuvenation).

That's the level of absurdity and transparent desperation (read their intro section to get a gist of it) reached by the antismoking "science" in 2003, after fifty years of the most intense and expensive search to find, using hard science, at least something harmful about this ancient miracle medicine. And it plainly doesn't work. In fact, they showed quite the opposite:

f) Despite their obvious care not to accidentally step into the "wrong" kind of results, which are quite common in this antismoking business unless one is very careful (after all it's not easy to "prove" that the most potent and wholesome medicinal plant humans have ever known is bad for you), they still managed to trip themselves -- their LS smoking rats lived significantly longer than nonsmoking rats, even though they smoked order of magnitude more, and much more unnaturally at that, than humans would. The HS group has, by authors' own acknowledgment, exceeded the MTD (maximum tolerated dose) for these rats i.e. the smoke was so heavy and oppressing, it physically asphyxiated some of them and consequently the HS females died slightly sooner than nonsmoking females (the HS males somehow made it to the nonsmoking lifespans within statistical error).

In fact, this particular trap has been plaguing antismoking "science" from the beginning, as reluctantly acknowledged (buried inside a longer sentence) in a similar cancer rodent "study" from quarter century ago ([1] p. 98):

Inhalation Studies with Syrian Golden Hamsters
A.P. Wehrner, et al, Battelle Pacific Northwest Labs,
Prog. Exp. Tumor Res. 24: 177-198 (1979)

"The increased incidences in the smoke-exposed hamsters were not necessarily caused by the smoke exposures, but might be explained by the significantly longer life-span of the smoke-exposed hamsters."



== Reference

1. Scientific literature review -- "Critical Comments on Recent Data Omitted from the 1982 Surgeon General's Report on Cancer" at Tobacco Documents Repository

Edited by nightlight, 15 April 2007 - 12:43 AM.


#19 roidjoe

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Posted 14 April 2007 - 08:17 PM

You have to stop referring to smoking as tobacco smoke - no, while the majority of the smoke may be from tobacco, there are other additive chemicals that are also in the smoke, therefore it is cigarette smoke. Pure tobacco smoke is very different.

Cigarette smoke has mutagens and will cause mutations to DNA of tissues that come in contact with it. The accumulation of mutations will increase the risk of cancer.

#20 nightlight

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Posted 14 April 2007 - 11:33 PM

Is it not fairly obvious that tobacco smoke would both a) increase the risk of cancer and b) "strengthen" lung tissues in smokers.


That is as "obvious" as the analogous "conjecture" that weight lifting would both a) increase the risk of muscle cancers and b) "strengthen" muscle tissues in weight lifters.

This is just simply due to the carcinogens mutating and damaging DNA within the cells - if the areas damaged do not cause cancer, and immortal reproduction of the cell, and in doing so it raises the bodies defenses to future damage - it would be a beneficial event.
...
How can it not be obtusely obvious that cigarettes, laden with toxic chemicals, are damaging lung tissues and promoting the growth of cancers?  Only masked in the form of self deception.


That is the usual antismoking tale targeting the ignorant and left tailers of the Bell Curve. Your cellular metabolism of anything you ingest, food, beverages, supplements, smoke, ... in any way or form, ends up using internal enzyme and oxidative processes to break down the consumed cells, proteins, fats,... into simple molecules (such as amino acids, nucleotides, monosacharides,...). The oxidative process and enzymes which can do that, can also do the same with the large molecules (e.g. proteins, DNA) of your own cells, damaging them.

That's like using knife to cut raw ingredients while preparing a meal -- there is always a bit of hazard that you will cut yourself. Hence, our metabolic processes are inherently hazardous. And your cells do that hazardous job routinely all the time, every day with everything you ingest.

The job of cellular biochemical networks is to tidy and fix it all up, all the time as they do their daily metabolic chores. There is nothing specifically "damaging" (if you wish to call the normal metabolic work that) about metabolizing the organic molecules of tobacco smoke that is not similar to metabolizing of everything else you ingest.

Live cells have been ingesting and metabolizing oxidated organic molecules since the dawn of life on Earth, for hundreds millions years. In fact the very primordial soup where the life itself was spun into existence a billion or two years ago by the lightening strikes into the rich organic broth, consisted of the same kind of "scary" organic molecules that a burned bit of a dried tobacco leaf will generate today. If live cells have learned by now how to do anything safely at all, that would be it -- the metabolizing of the most basic stuff of life which they have been enjoying since the days they began feasting on the primordial soup.

Therefore, pointing at the "scary" tobacco smoke as something uniquely hazardous, in the knife and food cutting analogy, would be like trying to scare away your wife from dangers of broccoli (e.g. because you hate broccoli), by describing to her in great detail and in slow motion how a knife she uses to cut it might slip and chop off her finger, then you go on describing what happens with the chopped finger as she picks it up from the floor, puts it on the ice and drives with it in a hurry to the emergency room... And all that surely proves to her that broccoli is extremely dangerous and should never be prepared in any civilized home. There. That's the precise equivalent of the usual 'tobacco smoke causes mutations' scary story cooked up by the antismoking con artists, that you have been so kind to refresh for all of us here.

The only actual differences go in favor of tobacco smoke:

a) The quantity of tobacco particles inhaled from a cigarette is 20mg per cigarette (of which 20% is absorbed, the rest is exhaled), hence 4 mg of matter per cigarette taken into your system, or 100 mg per pack. The food and beverages you take into your system will have about 10,000 times larger quantity of matter that needs to be broken down in oxidative processes (with potential DNA damage along the way), just the same.

b) The quantities of harmful pesticides, additives and other contaminants (such as mercury or radioactive Po 210 from fertilizers, another favorite bogy man from antismoking "science"), scale the same way -- they are thousands of times larger in the food and beverages you consume every day than in a pack of cigarettes you might smoke (and further 2-3 orders of magnitude smaller in SHS if you are sitting in a room with a smoker).

c) Since the tobacco leaf matter is burned before inhalation, significant part of the oxidative breakdown of the ingested matter is done outside of your body. In contrast, much of the oxidative breakdown for the foods and beverages has to be done inside your digestive system (mouth, stomach, intestine, liver,...). Cooking food helps offload some of that hazardous metabolic work, of course, which is why humans have been doing it ever since discovering fire.


...the absolute numbers of smokers ... in USA lower than in 1950 ... yet the absolute number of lung cancer deaths per year is more than 8 times larger today (from 20k in 1950 to over 160k in 2006).

If each molecule of tobacco smoke has some probability p of causing the final cancerous mutation of a lung cell upon interaction with it, and the total number of such molecule-cell contacts per second has declined by a factor 2-3 over half a century in between... how would one simulate via a computer model the eightfold rise in the number of such mutations?


You do realize that mutations accumulate over time and that most cancers are caused by multiple mutations - and someone smoking for 10 years in 1950 (assuming he started in 1940) would be smoking for 66 years in 2006 (assuming he was still alive) and thus the chance of getting cancer is increased.


That's a nice story, but no one has been able to fit a plausible probabilistic model of mutations, delayed or otherwise, to fit the observed secular trends in total numbers of lung cancers and pounds of tobacco consumed. The two curves simply don't fit with each other, no matter how you shift and twist them around.

We also ought not to forget the context of the above -- we are talking here about mere statistical correlations. Even if one could somehow fit these two curves perfectly, down to the last odd blip on each of them, that would still only represent a finding of a statistical correlation of A and B. The question whether (1) A causes B or whether (3) some C causes A and B remains to be answered. Correlation of A and B, even when perfect, is still only a hint for hard science to disentangle the causal web underlying it.

But since there isn't even the proper correlation which holds coherently over longer time (such as 20th century trends in the total numbers of lung cancers and tobacco consumed), the question whether we are dealing with '(1) A causes B', or '(3) some C causes A and B' is moot altogether. The point I am making here is that even the correlations, meaningless as they are regarding the underlying causality, aren't there in a coherent fashion (see Birch cited earlier as [3], also Colby [4]). Before one can argue whether the correlation is explained best by the causal model (1) or (3) there has to be a proper, coherent correlation to start with. And there isn't one.

Stepping back now from statistics, just consider the plain fact that in 2004 you have that entirely bogus study with 'cancer rats' trying to prove, by hook or by crook, that smoking can cause cancers. Now, they have been trying to do this for over fifty years, with no money or resources spared. And that was "it", the climax of all that vast "science" as of 2004, The Proof. They're surely in a very bad shape if that was "it" in 2004.

When people realized that radiation might be causing cancers, it was a matter of year or two and a comparatively negligible expense before clean experiments could demonstrate causal relation as a hard scientific fact.

Here, we are over half a century and untold billions of research dollars later, after some shaky correlation was observed by Doll and Hill (with its odd inhaler vs non-inhaler anomaly they tried to conceal and which they "solved" later by not asking the 'inhaling' question any more). It obviously doesn't work, no matter how many decades and how much money you throw at it, simply because tobacco smoke doesn't cause lung or any other cancers (it is in fact partially protective against various carcinogenic exposures due in part to glutathione and neutrophil upregulation in smokers). In short, tobacco smoking is good for you.


People have cultivated tobacco for seven millennia and had smoked it for several more before that, as a potent medicinal plant.


There is a difference between present day cigarettes and cultivated tobacco. Another ridiculous inference.


As with any other consumable, it's up to you to set threshold of purity you are comfortable with. There are several naturally grown, additive and pesticide free whole leaf tobacco products in the market (e.g. American Spirit, cigarettes and hand rolling tobacco, see other brands here).

Granted, most supermarket junk cigarettes are made of additive laden 'tobacco' sheets (tobacco scraps mixed with wood pulp, colorings and flavorings). But that's not any different than the distinctions between organically grown whole foods and the additive laden junk "foods" and beverages filling up supermarket shelves.

The only real difference is that with junk foods and beverages you ingest thousands times larger quantities of junk than with junk cigarettes, no matter what you smoke.

My "wisdom" on the subject is that with food and tobacco, one should stick with the time proven traditional ways of preparing and consuming them. For cigarettes, that means a plain old fashioned, hand rolled, non-filtered cigarette (or a pipe or cigar) using additive free, organically grown whole leaf tobacco, the way they did it for millennia.

The only remaining thing that is harmful about it is the "death curse" (negative placebo) from the antismoking conmen. If you don't buy into their voodoo, though, their curse is as harmless as that of some half naked witch doctor pointing a bone at you.

Edited by nightlight, 16 April 2007 - 12:13 PM.

  • Good Point x 1

#21 EmbraceUnity

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Posted 15 April 2007 - 12:42 AM

I am wondering what the effects of smoking would be on exercise if one takes precautions such as using organic tobacco and a vaporizer. Most smokers cannot run without getting winded very quickly, and I doubt this could be prevented even under the best circumstances. This alone is a serious drawback.

Edited by progressive, 15 April 2007 - 05:50 AM.


#22 nightlight

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Posted 15 April 2007 - 02:31 AM

I am wondering what the effects of smoking would be on exercise if one takes the proper precautions by using organic tobacco and a vaporizer. Most smokers cannot run without getting winded very quickly, and I doubt this could be prevented even under the best circumstances. This alone is a serious drawback.


Posted Image Posted Image

Tobacco was traditionally used by soldiers throughout the world, from ancient Native American warriors milennia ago, right up to the war in Iraq. In the British Empire era, smoking was compulsory for students in their elite boys schools (to improve health and get performance edge in sports). The Semai of Malaysia start smoking at age two. Medical textbooks, until 1950s advised smoking for congestive repiratory problems, and even today cold medicines use dopamine boosting for the same reason (which clean tobacco smoke does via multiple synergistic mechanisms much more effectively and more pleasantly).

Smoking is also much more prevalent among physical laborers, miners, firemen, blue collar workers,... If you take a look at a recent German study of aluminum workers, it becomes obvious why they smoke more -- smoking reduces respiratory problems (caused in this case by inhalation of aluminm dusts) sixfold compared to non-smokers. The same "smoker's paradox" was observed numerous times for all kinds of miners and other workers heavily exposed to noxious metallic dusts. They smoke because it tangibly and immediately helps their breathing. So, no, I don't think a clean tobacco smoke would cause any problem.

People nowdays do smoke different cigarettes than those our ancestors smoked. The principal difference is that we use filters, which shifts the delicately balanced biochemistry of the inhaled smoke, which was finely tuned over the millenia of cultivation, into some arbitrary artificial range of medicinal ingredients. Hence the biochemical signaling, which is vital for the proper feedback on the dosing and rhytms of the nested cycles (puffs, whole cigaretts, night breaks) is off. Filters also shed synthetic fibers (they even made Kent's filters from asbestos for several years) which, unlike the natural tobacco leaf particles, are non-biodegradable, hence the lung cells have to enclose these fibers into the mucous liquid to ease their excretion via cough.

Posted Image Posted Image

Our modern and "improved" cigarettes, similarly to our foods, also contain variety of additives with questionable benefits to smoker. As with foods, the market does offer plain old additive free whole tobacco leaf, for rolling the old style cigarettes, which is what I do. Some people grow and cure their own tobacco in the back yards, or even in the apartments.

Edited by nightlight, 17 April 2007 - 02:29 PM.

  • Agree x 1

#23 EmbraceUnity

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Posted 15 April 2007 - 05:37 AM

I would like to see a study to verify that pure tobacco smoking improves athletic performance, and until then I will remain highly skeptical.

#24 Shepard

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Posted 15 April 2007 - 05:50 AM

On a related note, we should all mourn the recent passing of America's greatest smoker of unfiltered cigarettes: Kurt Vonnegut.

#25 roidjoe

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Posted 15 April 2007 - 06:02 AM

I would like to see a study to verify that pure tobacco smoking improves athletic performance, and until then I will remain highly skeptical.

All stimulants will have an acute positive impact on performance.

#26 infinitethought

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Posted 15 April 2007 - 07:08 PM

I have no problem with entertaining the idea of taking nicotine, using patches, gum or even smokeless tobacco as well as taking deprenyl. However actually taking up smoking again (for nootropic purposes) seems a little crazy as I personally witnessed how much better I was able to exercise and well breathe after I quit smoking.


I am wondering what the effects of smoking would be on exercise if one takes precautions such as using organic tobacco and a vaporizer. Most smokers cannot run without getting winded very quickly, and I doubt this could be prevented even under the best circumstances. This alone is a serious drawback.


Both these responses bring up very poignant and interesting points.

But in my mind there is a very easy answer to this. Taking a brief view of our society we see one thing that stands out. Excess.
Obviously if one does anything in excess, it's unhealthy.

The same for tobacco. How many packs do these winded smokers smoke? 2 packs or more?

What would happen if they smoked tobacco as the American Indians smoked tobacco?
Pure tobacco and in moderation?

If you smoked 1-5 pure organic cigarettes made from rice, hemp or vegetable based rolling papers a day, would you have trouble breathing?
If you smoked 10-50 commercial carcinogen filled cigarettes, and the corresponding chlorine, slow-burning toxins added to the papers, a day, would you have trouble breathing?

Are you getting winded from an organic substance, tobacco. Or are you getting winded from all the synthetic toxins added to the commercial cigarette. Not to mention using a lighter and inhaling lighter fluid?

A lot of other factors are involved, due to our (forced) reliance on Petroleum (a lethal carcinogen) and the amount of toxins in the air from this product, and additionally the toxins from aerosol spraying from Military K-1 Tankers in the skies, under the false guise of Geo-Engineering.

http://www.americanc...articleID=21473
”It is believed that barium salt, polymer fibers and other chemicals, in the atmosphere are the physical irritants that are either directly or indirectly responsible, for the recent epidemic increase in cases of nose bleed, asthma, allergies, pneumonia, upper respiratory symptoms and a noticeable increase in arthritis symptoms, recently reported nationwide. Chemicals illegally sprayed into the atmosphere are producing atmospheric and ground conditions detrimental to human and animal health but favorable to the growth of harmful molds and fungus. These conditions are not conducive to good health. The soluble salts of barium, an earth metal, are toxic in mammalian systems. They are absorbed rapidly from the gastrointestinal tract and are deposited in the muscles, lungs, and bone. No case data is available from the medical community on the long term effects of barium in the human body.”

”The programs are secret because the Federal EPA and State Environmental Quality Agencies need to "not know" about what the by-products of the metabolites of biological, illegal and harmful agents are. It's for that reason the project has been declared secret from the citizens of the countries.”

So, now we know and it is as much as we suspected, so I guess the question becomes, what next? As I enjoyed the fine southern weather the last couple days and watched planes, sometimes five at a time, leave their trails across the sky, I heard we were expecting a terribly violent storm and I wondered, why doesn’t everyone see the pattern?"


Mankind is reaching the saturation point on the use of these dangerous chemicals. These synthetic substances DO NOT mix with the human organic body. More and more see this and know this.
It will NOT continue because of dispertion of knowledge to the masses.
Once everyone knows the dire risks involved with the use of toxic chemicals, public opinion takes over, and there is nothing the Corporations will be able to do against it.

The same will happen with the truth about the beneficial effects of tobacco.
Which by the way is right around the corner.
Second Hand Smoke and it's laughable "dangers" propogandered by the Highest Doctor, the Surgeon General, n this country? Most Everyone sees right through it.

Reminds of the stupid commercial where a chain smoking husband is crying because his wife died from his second hand smoke.
Geeeee.....brings up the obivious question that a even a frikkin two year old can see.

SHOULDN'T HE HAVE DIED FIRST !

(Their stupidity, always amazes me!)


Everyone will see all this knowledge. (Big Pharma is squirming and getting desperate.)
This has to do with the 100th monkey effect. IE: Once something is known it expands exponentially.

#27 djmmm

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Posted 15 April 2007 - 11:25 PM

second hand smoke:

"sidestream smoke was produced in larger quantities and contained, per cigarette, 2 times more nicotine and 12 times more ammonia..."

"...sidestream smoke contained, per unit cigarette, higher concentrations of carcinogenic polycyclic aromatic hydrocarbons, per unit mass, including four times more 3,4 benzopyrene..."

http://www.ncbi.nlm....0&dopt=Abstract

#28 edward

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Posted 16 April 2007 - 01:11 PM

Nightlife, do you work for the tobacco industry? Maybe part time a consultant or perhaps in PR?

#29 nightlight

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Posted 16 April 2007 - 07:23 PM

Nightlife, do you work for the tobacco industry? Maybe part time a consultant or perhaps in PR?


Nop. I am theoretical physicist (I also post on on sci.physics.research and PhysicsForum) working for a computer company as a chief scientist. No relation with tobacco industry except as a customer. (BTW my screen name is "nightlight".)

Edited by nightlight, 17 April 2007 - 04:30 PM.


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#30 infinitethought

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Posted 16 April 2007 - 08:43 PM

second hand smoke: 

"sidestream smoke was produced in larger quantities and contained, per cigarette, 2 times more nicotine and 12 times more ammonia..."

"...sidestream smoke contained, per unit cigarette, higher concentrations of carcinogenic polycyclic aromatic hydrocarbons, per unit mass, including four times more 3,4 benzopyrene..."

http://www.ncbi.nlm....0&dopt=Abstract


"....the results prove that secondhand smoke concentrations are 2.6 - 5,000
times SAFER than OSHA indoor air quality standards require for secondhand
smoke."
From British Medical Jounal.
http://tobaccocontro...bstract/14/1/60

I don't know about you, but I'd rather trust info I hear from a non-governmental agency. We all know how "honest" our government is.

Here's an interesting PDF on how the Surgeon General does their research.

The “science” behind the surgeon general’s latest report on
secondhand smoke does not support officials’ claims.

http://www.data-yard...lation_4-07.pdf

----

OSHA itself has stated regarding secondhand smoke:

"Field studies of environmental tobacco smoke indicate that under normal conditions, the components in tobacco smoke are diluted below existing Permissible Exposure Levels (PELS.) as referenced in the Air Contaminant Standard (29 CFR 1910.1000 )...It would be very rare to find a workplace with so much smoking that any individual PEL would be exceeded."

-Letter From Greg Watchman, Acting Ass't Sec'y, OSHA, To Leroy J Pletten, PHD, July 8, 1997

--

So djmm, you tell me, WHAT is the truth?

--
BTW: All the above knowledge I got from http://cleanairquality.blogspot.com/ who is a NON-SMOKER opposing draconian bans, BECAUSE he was put out of business by these same bans.




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