492 replies to this topic

[Lester]

dfowler, on Mar 5 2010, 09:16 PM, said:

http://www.cbsnews.c...in5433931.shtml

Oct. 28, 2009
Damage from Smoking is Swift, Irreversible
Study Says Even One Cigarette Can Stiffen Arteries in Young Smokers

Admit it. You're a mouthpiece of the Nanny State who is facilitating the evil attack on those good folks at big tobacco who merely want to improve the health of people all over the world through the wonder of cigarettes. And you're using these funds stolen from tobacco to push the Global Climate Change lie, so you can take control over ever more of peoples' daily lives.

This is truly insidious behavior and you should be ashamed.

Now forgive me, but I must go have a live-giving cigarette.

[shifter]

nightlight, on Feb 25 2010, 05:46 PM, said:

Tobacco is a potent medicinal plant and youth elixir used for over 8000 years. Antismoking "science" is a money making scam, resting entirely on the worst kind of junk science, created and financed chiefly by the pharmaceutical industry. The big pharma reflexively seeks to suppress other natural medicines and folk remedies as well, especially those that work. Tobacco being the most beneifical natural medicine humans have ever known (tell me which other substance, matural or synthetic, extends the lifespan by 20% in animal experiments, while keeping the brain sharp into the old age, doubles our main internal detox and antioxidant enzymes glutathione, catalase and SOD,...), is the main target of the pharma's attacks on natural medicines.

MAO-B Inhibitors like Selegiline have been know to increase the maximum lifespan in rats by up to 20%

Much cheaper, healither, keeps the brain very youthful, not look like a lower class bum and if you could replicate that 20% increase to a human thats a fair few decades.

And at least you wont have to stink and cough for over a century and smell and taste things the way they were meant to be.


With stupid views like pro smoking, you make it hard for anybody to take you serious on anything.

Edited by shifter, 06 March 2010 - 02:08 AM.

[nightlight]

atp, on Mar 5 2010, 05:20 PM, said:

nightlight, on Mar 5 2010, 08:57 AM, said:

That is result of:
a) correlation on non-randomized  samples
b) it ignores any confounding from therapeutic/protective effects of tobacco smoke (e.g. via self-medication mechanism)

a) why do you mean that the samples are non-randomized?

Evaluating (health) effects of some substance (device...) X on randomized sample means that scientist  randomly selects (e.g. by tossing a coin) which subjects in the study will receive the X (test group). The remaining subjects will not receive X and are used as controls  (in drug trials they would receive placebo). At the completion time of the study, all subjects are examined and health differences tallied. If the test group shows statistically significant excess in some health effect E, one can justifiably conclude that "X causes E" (within given statistical uncertainty interval based on sample size), since there is no plausible mechanism by which the scientist's coin toss would itself be the cause of health effect in E in subjects of the test group.

In contrast, when studying the same X on a non-randomized sample, a scientist examines comparable numbers of existent users of X and non-users of X and (statistically) compares the incidence of the health effect E between the two groups. But in this case, the same statistically significant excess of E among users of X does not imply "X causes E" since it may well be that there was some other factor F which caused E (directly or via some chain of intermediate causes and effects) and also caused the use of X (directly or otherwise). There is an unfortunate phenomenon in recent decades, especially in public health research (and other areas with high financial rewards), to publicly misrepresent such findings on non-randomized samples as scientific finding of "X causes E" (where X is usually whatever the sponsors of such "research" would like to suppress or tax), aptly named "junk science."

In other words, the positive correlation of X and E on non-randomized sample merely implies that X and E belong to some common web W of causes and effects, but doesn't tell us how are the two nodes X and E connected with each other, what kind of links connect the two. The most scientist can conclude is that the observed correlation is at best a hint that X may be causing E. Of course, once there are enough hints to justify the expense and efforts for further research, the much sharper tools of hard science (e.g. randomized trials, animal experiments, lab analysis of X and its relation to the etiology of E) need to be used to clarify the mechanism behind the hints from soft science (statistical correlations on non-randomized samples).

If E is some serious disease, such as cancers or heart disease, the hints about possible causal role of X in the onset of E, the high resolution tools of the hard science are urgently brought in to resolve the inherent ambiguities of the hints from soft science. The peculiar aspect of the antismoking "science" is that although the statistical hints about possible causal role of tobacco smoke in lung cancer go back at least to 1950 (it was actually German researchers who came with these hints in 1930s, since a German chancellor of that era intensely disliked smoking habit), it is still stuck in the hint phase, for more than six decades. Considering the seriousness of the lung cancer, the matter should have been completely resolved decades ago. This was so unusual that already in 1958, the father of modern statistical methods, famous British mathematician R. A. Fisher noticed it and wrote (pdf; this article also contains a very readable exposition of  the sample randomization topic you asked about):

Most of us thought at the time, on hearing the nature of evidence, which I hope to make clear a little later, that a good prima facie case had been made for further investigation. 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 to 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 confirming Dr. Hill's findings. I think they had concurred, but I think they were mere repetitions of evidence of the same kind...

Yet, the antismoking "science" still rests its case squarely on the same kind of soft science that Fisher objected to over half a century ago. There was plenty of hard science, since then, of course, yet the public narrative of the antismoking "science" is of the kind -- smokers have more of this or that disease, smokers spouses and children suffer more of this or that, people around smokers suffer more lung cancers,...  Why not publicize the results of hard science? They would of course, had it supported their narrative. Unfortunately, it all went the "wrong" way -- the smoking mice, rats, hamsters, dogs, monkeys... ended up better off than their non-smoking cohorts, living longer, staying thinner and sharper into the old age. So, what can poor scientists do, but publicize what works, the hints, and more hints. How could they possibly show graph after graph like this (described earlier):

Quote

b) why should this be taken into account, if you  see that more smokers have died than non-smokers, the essential hard fact which was measured

Suppose you wish to study the health effects of Prozac via soft science. Suppose also that researchers are constrained by taboo (b), from taking into account in their study any known medicinal effects of Prozac, and are not even allowed to mention any such effect in their paper. So, they pick 1000 subjects who use Prozac and 1000 that don't use it, and after thorough physical and psychological evaluation they 'discover' that there are significantly more subjects suffering from depression among Prozac users than among non-users, and among the latter, there is more depression among the ex-users of Prozac than among the never-users (the same kind of correlations you observe about smoking and 'smoking related diseases'). Would it be justified to conclude that this study shows that Prozac increases the risk of depression among its users? Of course not, since Prozac is used to treat depression, and that effect of Prozac explains why there is more depression among its users.

Under the analogous taboo for any substance X about the (known) medicinal effects of X, you could observe the same kind of misleading statistical associations (for users, ex-users and never-users of X), making it appear as if the substance X may be causing the very diseases for which it is actually protective or therapeutic. This apparent "paradox" is merely an artifact of the taboo on certain facts about X. Without the taboo, the observed correlations can be simply explained by the medicinal effects of X and not as the indicator that X may be causing diseases that it is actually protecting against or treating.

As you are already well aware, having participated in this thread, the antismoking "science" has a very strict taboo on quantifying and taking into account, and even against the mere mentioning, of any among myriad therapeutic and protective effects of tobacco smoke. That entire category of known facts simply does not exist in the antismoking Matrix. As result, they end up with precisely the kind of meaningless tautological "studies" about tobacco smoke as the contrived illustrations about Prozac or X above. Consider for example the well known potent anti-inflammatory effects of tobacco smoke and the inflammatory disease rheumatoid arthritis. You can find thousands of epidemiological "studies" finding positive correlations between smoking and RA, some were even cited by antismoking advocates in the present thread. None of such studies, under the taboo (b), will consider or even mention, let alone quantify the confounding, of anti-inflammatory effects of tobacco smoke. As result, you get precisely the type of correlations between smoking and RA as illustrated above for Prozac and depressions. Physicians, arthritis support groups, Wiki,... are all advising AR sufferers to stop smoking. But if one were to submit the same kind of paper on their "study" observing correlations between RA and any other  substance with anti-inflammatory properties, while never mentioning or accounting for confounding effects of these anti-inflammatory properties in their paper, they would have been laughed out of the journal. Hard science, of course confirms what should have been self-evident and taken into account in any of those thousands RA-smoking "studies" -- in animal experiments, tobacco smoke (and to a lesser degree, nicotine alone) is strongly protective against inflammatory damage of cartilage, delaying the onset of clinical RA and slowing down its progression after the onset (TS has also analgesic effects which help sufferers as well). This is precisely the "paradox" illustrated above with Prozac, and just like in that illustration, the "paradox" is the consequence of the taboo (b) -- therapeutic and protective effects of tobacco smoke simply do not exist in the antismoking "science", they cannot be mentioned or accounted for.

More amazingly, for over six decades since the birth of antismoking "science", that kind of "studies", all fully compliant with taboo (b), remain their strongest trump card, the master "proof" against smoking,  and that's practically all they have been trumpeting relentlessly throughout. That fact alone tells you more about the strength of their antismoking case than the oceans of words in all those "studies".

Edited by nightlight, 06 March 2010 - 04:30 AM.

[TheFountain]

shifter, on Mar 5 2010, 09:03 PM, said:

nightlight, on Feb 25 2010, 05:46 PM, said:

Tobacco is a potent medicinal plant and youth elixir used for over 8000 years. Antismoking "science" is a money making scam, resting entirely on the worst kind of junk science, created and financed chiefly by the pharmaceutical industry. The big pharma reflexively seeks to suppress other natural medicines and folk remedies as well, especially those that work. Tobacco being the most beneifical natural medicine humans have ever known (tell me which other substance, matural or synthetic, extends the lifespan by 20% in animal experiments, while keeping the brain sharp into the old age, doubles our main internal detox and antioxidant enzymes glutathione, catalase and SOD,...), is the main target of the pharma's attacks on natural medicines.

MAO-B Inhibitors like Selegiline have been know to increase the maximum lifespan in rats by up to 20%

Much cheaper, healither, keeps the brain very youthful, not look like a lower class bum and if you could replicate that 20% increase to a human thats a fair few decades.

And at least you wont have to stink and cough for over a century and smell and taste things the way they were meant to be.


With stupid views like pro smoking, you make it hard for anybody to take you serious on anything.

Well part of it is your fault too. He is saying things to purposefully bait you and you (as well as many other's) are falling for it. I voted we all stop responding to this thread about 10 pages ago. But If it's not doing anyone any harm, proceed with the time wasting.

[crauley]

Skotkonung, on Mar 6 2010, 12:50 AM, said:

As to my original comment on glycation:

Tobacco smoke is a source of toxic reactive glycation products
Increased levels of advanced glycation endproducts in the lenses and blood vessels of cigarette smokers.
Proteomic alteration in lung tissue of rats exposed to cigarette smoke.
Possible involvement of tobacco-derived advanced glycation end products (AGEs) in an increased risk for developing cancers and cardiovascular disease in former smokers.
Advanced glycation endproducts and cigarette smoking.

Yes, inhaling glycotoxins seems intelligent if one wants to avoid accelerated aging.

How about eating them?  (I guess you have another crusade on your hands )

See also Nightlight's 2007 discussion of this AGEs boogeyman.  That discussion begins here.

Edited by crauley, 06 March 2010 - 06:34 AM.

[nightlight]

dfowler, on Mar 5 2010, 08:16 PM, said:

(WebMD)  Cigarette smoking starts inflicting "very significant" damage on the arteries with the very first puffs taken by otherwise healthy young smokers, new research shows.

That seems to be an unpublished presentation and a press release for "news" media, not a study published in some journal. On the other hand, this 'arterial stiffness' (inverse of flow-mediated dilation, FMD) effect has blossomed lately into a whole thriving industry of antismoking 'scare stories' and you can find thousands of variations on the exactly same theme. The particular attraction of this (normal and entirely benign transient vascular) effect is that one can observe it in non-smokers after only few minutes of exposure to SHS, which is a priceless propaganda tool for further inflaming the antismoking hysteria among the non-smoking public. The effect has proven itself enormously helpful in stiffening the ongoing 'denormalization' campaign against smokers (the same label & practice were started in 1930s Germany against another minority, by coincidentally a passionately tobacco-phobic chancellor of the era, who also pioneered the techniques of  modern antismoking "science" and the related mass hysteria).  

A bit of important context coveniently missing in the article above is that a bowl of cornflakes along with myriad other daily activities or states (eating, getting in or out of shower, walking in colder/warmer room, common daily emotions, your friend saying Boo...),  natural circadian rhythms...  yield about the same or greater fluctuation of the scary "arterial stiffening", which are all as normal, benign and transient as the one after a cigarette. The SHS effects are an order of magnitude smaller.

The mere fact that these kinds of scientific "discoveries" are being foisted upon the public in 2009, crowning the six decades of vast research efforts seeking to scientifically demonstrate any harm, anything at all, from inhalation of tobacco smoke, tells you more on how deeply wholesome and beneficial this ancient medicinal miracle plant is, than all the survival graphs and links I have been posting around here.

Boo. Got heart attack yet?

Edited by nightlight, 06 March 2010 - 08:00 AM.

[nightlight]

shifter, on Mar 5 2010, 09:03 PM, said:

MAO-B Inhibitors like Selegiline have been know to increase the maximum lifespan in rats by up to 20% Much cheaper, healthier, keeps the brain very youthful, not look like a lower class bum and if you could replicate that 20% increase to a human thats a fair few decades.

Ok 20%, just like those hamsters in the large National Cancer Institute sponsored smoking experiments which went all "wrong" (they were meant to kick off a campaign for workplace smoking bans in 1970s, instead, it set them back by decade). Except that those smoking experiments were optimized to produce maximum harm from inhalation of tobacco smoke. I only wonder how good life-extender Selegiline would have turn out to be, had the researchers been paid to do their best to make it look bad. It doesn't take much overdosing on Selegiline to turn its effects into harmful. That's the difference between the isolated compound vs the highly optimized for 'you may not injure...' synergistic natural complex that has some amazing built in safeguards against just about any conceivable misuse, as this ancient medicine appears to have, recalling that it has been defying armies of antismoking researchers doing their best to make the inhalation of tobacco smoke cause harm for over six decades. And the experiments kept going the wrong way. Try that with any pharma substance and see how long it would take to make it do harm. Even the plain water is easier to coerce to do harm.

Further, by the time you buy pharma substitutes, if they exist at all and you can find a doc to prescribe them for you, for all other beneficial effects of this medicinal miracle plant (multiple cholinergic effects without adaptive downregulation, +dopaminergic, multiple anti-inflammatory effects, appetite & weight reduction, upregulation of glutathione, catalase, SOD, by 80-100%, neutrophiles, upregulation of telomerase, leptin, adiponectin, insuline sensitivity, pregnenolone, DHEA, BDNF (brain-derived neurotrophic factor). NGF (nerve growth factor), cAMP, NR2A by 60%, NR2B by 80%, MMPs (matrix metalloproteinases), downregulation of TNFa, NF-Kb, IGF-1 (in men), suppresses apoptosis, amyloidosis including beta-amyloidosis, ...), you're talking a wheelbarrow of pharmaceuticals (covering only the benefits known so far, likely a tip of the iceberg), costing a fortune to buy. But that's just the first step. Now you got to optimize the exact proportions and dosing of all the safe substitutes, and to match this ancient medicine, you need about 8000 years of testing on about two billion life-long test subjects, and you've replicated something you can have for under $8 a carton (for natural, additive free rolling tobacco+tubes; stuffing machines are one time cost of $20-40).

It should be pretty clear by now why has pharmaceutical industry invested billions into the antismoking enterprise, from churning antismoking junk science (while in their real labs, doing real science, quietly researching the seemingly endless list of beneficial medicinal effects of tobacco smoke), creating and financing nearly all "grass roots" antismoking groups, buying politicians a bureaucrats, antismoking laws and regulations, smoker denormalization campaign,...

[Blue]

Version 8.0

Changelog:
* Added to point 1 regarding exposure amount in the animal cancer studies
* Added 2 reviews to point 2
* Moved animal studies links to point 1
* Added to poin 2 that only a modest weight gain is seen in quitters
* Added to point 4 hamful effects described by Skotkonung
* Added to point 10 regarding Indian correspondence letter and lung cancer diagnosis after stopping smoking

1. Animal studies of TS (tobacco smoke) exposure and lung cancer. Yes, until recently they did not find much conclusive evidence. But now we have animal models where TS clearly causes lung cancer (the lifespan of TS models due to other diseases is discussed in the next post.) Smoking as shown can clearly cause lung cancer in certain species/models and humans happens to be another.

Studies (the result of which cannot be explained as due to exposure amounts causing "particle overloading" never seen in human smokers): 1 2 There are also several other models were having a "recovery" period without TS after the TS exposure causes lung cancer to appear. (More in  the next point.)

Reviews: 1 2 3 The last is Coggins latest review. Conclusions in his earlier reviews, when the latest research clearly showing TS causing lung caner were not available, are outdated.)

2. Animal studies of TS and lifespan. Yes, there is the hamster study showing lifespan increase from TS. Was in hamsters prone to amyloidosis which is a rare cause of death in humans, even if we count Alzheimers as due to amyloidosis (which is not proven).

TS is also well known for capacity to reduce weight. The hamsters, as well as the animals in several other TS animal studies, showed a large weight reduction. CR is the factor with best evidence for lifespan extension. The last study link above shows that TS causes a dose dependent CR in rats. Weight reduction also caused a clear decrease in tumors for both TS and non-TS mice. So this CR effect very likely offset the harmful effect of the smoke itself in animal studies. Further evidence for this is that after a TS period having a "recovery" period without TS (and thus CR and its protection ceasing) in some animal models have caused cancer, likely due to the earlier TS damage, to appear. Note that similar strong CR effect is not seen in human where quitting only causes an average weight gain of 5 kg.

Also, there are studies where TS causes a lifespan reduction. May be criticized for not representing the human situation but neither does amyloidosis prone hamsters on CR. Furthermore, the bad effects of TS may well come after say 5 or 10 years of exposure which would not be detected in these short-lived animal studies while a good CR effect would.

3. Regarding animal studies in general. The value of animal studies is very limited since humans are not short-lived animals with different metabolism and diseases. We cannot take some average of all animal models created to have certain diseases/properties and conclude that humans should have these characteristics. For example, we do not do this for characteristics like intelligence or amount of body hair. Herbivores do poorly on high fat diets. This is not evidence that high fat is bad for humans. We do not do animal studies to prove an effect of a substance in humans. Rather, we do animal studies as a rough guide for what should be further studied in human studies.

4. TS causes an upregulation of certain defence systems such as antioxidants and detoxication. That is what you expect from toxic substances. Upregulation cannot compensate for a heavy toxic insults. If you want to do upregulate with a mild toxic insult, then there are safer methods such as moderate exercise and ALA.

Furthermore, telomeres are shorter in humans smokers, smoking induces glycation and is a source of reactive glycation products. Additionally, nicotine appears to depress the immune response to malignant growths in exposed tissue. The toxic agents present in tobacco smoke include free radicals, redox cycling agents, and iron.  Smoking increases plasma malondialdehyde levels. 1 2 3

5. Nicotine may have certain beneficial effects when given alone. Like modulation of the immune system which may be beneficial under certain conditions. It not evidence for what TS with its enourmous amount of substances will do. The effect may well be the opposite due to the effects of other substances. If you want nicotine, despite it being extremely addicting, then it is better to only take nicotine. The same applies to other possible good substances in TS.

6. Certain nations like Japan and Spain have a long average life expectancy despite high prevalence of smoking. These nations do a lot of other healthy things. In particular good average diets. Smoking is important but not the only factor determining life expectancy.

7. Jeanne Calment, the person with longest confirmed lifespan, smoked a very low amount. She was an exception (who also had a diet with great amounts of several healthy foods). Very long-lived people in general do not smoke and those who do are sicker. Also, low exposure is not good or neutral. There have been lots research finding harmful effects from low dose secondhand smoking exposure in humans. 1 2 3

8. Several human randomized controlled studies studying the effect of giving advise to stop smoking have not found improved health. Note that getting people to quit permanently is very difficult with even intensive counseling only achieving success in a small minority, Often people do not change their lifestyle before they get seriously sick. So most likely the permanent quitters in these studies were sicker than the non-quitters. The permanent quitters were certainly not randomized and controlled. They were not what the study were studying primarily. Furthermore, there are studies were giving advise improve health. (In lung disease patients. A highly motivated group): 1

In contrast, there are numerous studies of successful quitting that shows that this greatly improves health. That the quitters may have different health initially than the non-quitters is an obvous confounding factor that a good study can control for. Some examples: 1 2 3

9. There may be some confounding factors missed by epidemiologists in the thousands of studies showing harmful effect of TS. Of course theoretically possible, just very, very unlikely. Epidemiologists have certainly not ignored obvious ones like smoking being more prevalent among those with lower SES in every study.

Self-medication while having symptomatic disease is excluded by prospective studies. Also difficult to explain why the health of quitters improve if TS is actually helping against the disease. Regarding a possible factor before symptomatic disease  that is improved by TS, such as tiredness improved by nicotine, there is no evidence that, for example, one get tired decades before getting a lung cancer diagnosis. Again, not theoretically impossible that something like this exists, but since we have no evidence it is very unlikely. Similarly, UFOs using advanced technology may be falsifying our studies for unknown reasons. Not theoretically impossible. By using similar arguments one can argue that junk food and obesity is not with 100% certainty shown to be harmful and actually may be healthy and people may use them for self-medication.

If ignoring evidence for not being 100% certain, then there is no evidence for any prescription drugs either, also placebo-controlled, randomized studies rely on probability, there is always a very small chance that the result showing an effect is a false positive due chance or a confounding factor missed even by controlled experiments.

10. TS may protect against certain diseases like Parkinson or Alzheimer among those with Apo E4. A double standard. Epidemiologic evidence is only accepted when the result happens to favor TS. Does not change the situation for most diseases and the overall morbidity/mortality. Also, smoking is a risk factor for rheumatoid arthritis and cognitive decline despite what has been implied using point 4 and 5 and a mouse study. 1 2

There is also a claim that stopping smoking can increase the risk of soon receiving a lung cancer diagnosis in humans but this is only based on a correspondence letter from India not examining possible confounding factors such that smoking was stopped due general and lung illness.

For some general descriptions of health effects see: 1 2

Edited by Blue, 06 March 2010 - 11:16 AM.

[maxwatt]

crauley, on Mar 6 2010, 01:23 AM, said:

Skotkonung, on Mar 6 2010, 12:50 AM, said:

As to my original comment on glycation:

Tobacco smoke is a source of toxic reactive glycation products
Increased levels of advanced glycation endproducts in the lenses and blood vessels of cigarette smokers.
Proteomic alteration in lung tissue of rats exposed to cigarette smoke.
Possible involvement of tobacco-derived advanced glycation end products (AGEs) in an increased risk for developing cancers and cardiovascular disease in former smokers.
Advanced glycation endproducts and cigarette smoking.

Yes, inhaling glycotoxins seems intelligent if one wants to avoid accelerated aging.

How about eating them?  (I guess you have another crusade on your hands )

See also Nightlight's 2007 discussion of this AGEs boogeyman.  That discussion begins here.

Actually, eating AGEs does not seem to be particularly bad for humans.  We have evolved enzymes to neutralize them over millenia of eating cooked food.  If you feed a rat the amount of dietary ages a human typically consumes, it dies quickly.  Dogs, the only other animal that has eaten cooked food for the last 50,000 years, has a similar ability to neutralize orally ingested ages.

However, the enzymes do not appear to be present in the lungs.

Edited by maxwatt, 06 March 2010 - 10:55 AM.

[donjoe]

Skotkonung, on Mar 6 2010, 01:50 AM, said:

These types of comments are up there with holocaust denialism, AIDS denialism, etc. To those of us who have seen the true cost of smoking by the loss of loved ones to smoking induced lung cancer and other smoking related illnesses, this is a subject not to be taken lightly.

Yes, exactly, they are opinions some people hold and for which they should never be punished by law, since the practice of punishing "crimes of opinion" is starkly against Human Rights (specifically against the right to Freedom of Speech). The only limits to Freedom of Speech that I find to be acceptable are those banning hate speech and death threats, which your statements were much closer to than his. Not to mention you just admitted your statements were motivated by irrational/emotional reasons. Imagine what would happen if we let all our laws be dictated by unreason. Maybe you'd like to live in a world like that, but I sure wouldn't.

Edited by donjoe, 06 March 2010 - 11:04 AM.

[bacopa]

http://www.medicalne...icles/81087.php

Smoking Causes Irreversible Gene Damage
Main Category: Smoking / Quit Smoking
Also Included In: Cancer / Oncology;  Lung Cancer
Article Date: 31 Aug 2007 - 2:00 PDT

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BC Cancer Agency researchers, led by Drs. Stephen Lam and Wan Lam, have discovered new evidence that explains why former smokers are still susceptible to lung cancer after they have stopped smoking for many years.

Published today in the online journal BMC Genomics, the study shows that in former smokers, some genes associated with tobacco smoking return to levels similar to people who never smoked, while other genes appear to be permanently damaged.

"The study is important because it helps to explain why heavy smokers who have stopped smoking are still at risk of lung cancer," says Dr. Stephen Lam, one of the principal investigators and chair of the BC Cancer Agency's lung tumour group. "Fifty percent of patients with newly diagnosed lung cancer are now former smokers."

Using samples from the lungs of 24 current, former, and non-smokers, researchers created libraries using a technique called serial analysis of gene expression (SAGE), which helps to identify patterns of gene activity. They identified close to 600 genes that were differentially expressed between current and non-smokers. This is the largest human SAGE study reported to date.

Only about a fifth of the genes in a cell are switched on at any given time, but environmental factors such as smoking lead to changes in gene activity. Of the 600 genes identified, changes in almost one third of them are irreversible in former smokers. Specifically, some DNA repair genes are irreversibly damaged by smoking, and smoking also switched off genes that help combat lung cancer development. Nearly another third of the genes displayed changes that are reversible by stopping smoking.

"Further investigation into the genes and functions that do not revert to normal levels upon smoking cessation may provide us with new insight into the development of lung cancer," says Raj Chari, lead author of the study and graduate student at the BC Cancer Agency.

The researchers also identified a number of genes not previously associated with smoking, which are switched on in active smokers. One example is CABYR, which is involved in helping sperm to swim, and is also associated with brain tumours. The researchers also further investigated changes in genes involved in airway repair and regeneration, and within this group identified genes that fell into three categories following cessation of smoking: reversible (TFF3, CABYR), partially reversible (MUC5AC) and irreversible (GSK3B). These findings were tested against a second cohort of current, former and non-smokers.

It is estimated that more men and women will die from lung cancer than from prostate breast and colorectal cancer combined. In 2007, approximately 2,723 British Columbians will be diagnosed with lung cancer and 2,298 will die of it.

The BC Cancer Agency is currently enrolling people in a project called the Lung Health Study, which focuses on the early detection of lung and bronchial cancer, and the identification of new agents that may halt or slow the growth of abnormal cells in these organs. Former smokers between the ages of 45 and 74 who have smoked at least one package of cigarettes per day for 30 years are the primary target of the study.

Core support for research at the BC Cancer Agency is provided by the BC Cancer Foundation. This study was also funded by Genome Canada/ Genome BC and the National Cancer Institute (USA).

The BC Cancer Agency, an agency of the Provincial Health Services Authority, is committed to reducing the incidence of cancer, reducing the mortality from cancer, and improving the quality of life of those living with cancer. It provides a comprehensive cancer control program for the people of British Columbia by working with community partners to deliver a range of oncology services, including prevention, early detection, diagnosis and treatment, research, education, supportive care, rehabilitation and palliative care. The BC Cancer Foundation raises funds to support research and enhancements to patient care at the BC Cancer Agency.

http://www.bccancer.bc.ca

[nightlight]

Blue, on Mar 5 2010, 08:09 AM, said:

That is at best a very misleading statement regarding the F344 study which does not apply to B63CF study as noted below.

In the subsequent B63CF paper they comment on the exposure level in this F344 rat experiments as follows (p. 286):

This exposure level was selected because previous studies in F344 rats showed that it was sufficient to induce lung tumors without a significant increase in mortality (9).

Combine with their explicit statements in this F344 paper:

p. 280: "A slight reduction of survival suggested that the HS level was at the maximum tolerated dose as commonly defined."
p. 290: "Although the HS exposure might have exceeded the MTD (...), it is unlikely that the LS level reached the MTD.

As explicitly acknowledged by the authors, they drove up the exposure as far as they could until whatever the edge of "significant increase in mortality" was reached. They chose not to say what that "significant increase" threshold was or to provide actual figures for the number of asphyxiated animals (HS females were hit the hardest), even though they knew perfectly well what all those numbers were. Then they equivocate on MTD status even for the LS (lower smoke) group, as if someone hid those numbers from them, so poor little contractors, for no fault of their own, just can't be sure whether even LS group had reached the MTD.  Yaeh, sure, dog ate their homework.

Quote

From the FS344 study (HS = high smoke, LS = low smoke)
"It seems likely that the carcinogenicity in the present study was a response to chemical carcinogens rather than a nonspecific response to "particle overloading," such as that caused by exposures to diesel emissions and some non-mutagenic solid particles administered  above the "maximum tolerated dose" (MTD) (Mauderly, 1996Go).

Well, "It seems likely" doesn't sound like an establishing of an experimental fact but rather like a self-serving conjecture i.e. they are merely wishfully hypothesizing that their experiment may have demonstrated lung carcinogenicity of TS (or it may have been something else). The few little monkey wrenches in their wishful theorizing are:

a) There is an  anomaly in their data (Table 4, p. 285), listing the results and showing that smoking males in LS group had over 4 times fewer lung malignancies than the non-smoking males. That doesn't fit too well with their  'lung carcinogenicity' theory of tobacco smoke, since more of 'carcinogenic smoke' in LS group compared to non-smoking controls, somehow caused fewer lung malignancies in LS group. Surely, some strange causality and carcinogenicity.

b) The stuff that matters: Smoking animals outlived nonsmoking animals.

c) The authors chose not to quantify (or even to mention it) the well known effects of nicotine and NO from TS as promoters of angiogenesis (especially in combination),  on the vascularization in the lungs of smoking rats (note that lungs were larger in smoking rats, cf. Table 3), and of course they didn't take into account the effect of improved lung vascularization on the rate of growth of tumors (another well known phenomenon; common cancer treatments rely on it, by suppressing angiogenesis). So far, you have kept pretending to be unaware of such well known facts, hence your "logic" seems to be: since such facts don't exist, the authors were perfectly justified in choosing not to measure this effect and quantify its contribution to the observed increase in growth of lung tumors, therefore they are justified in declaring that all such growth was "likely" due to lung 'carcinogenicity' of tobacco smoke.

The little problem with that "logic" is that these well known facts do exist e.g. here is quote from an abstract of one such 2001 paper in Nature which also clarifies the general mechanism (you can find hundreds more):

We provide anatomic and functional evidence that nicotine induces angiogenesis. We also show that nicotine accelerates the growth of tumor and atheroma in association with increased neovascularization. Nicotine increased endothelial-cell growth and tube formation in vitro, and accelerated fibrovascular growth in vivo. In a mouse model of hind-limb ischemia, nicotine increased capillary and collateral growth, and enhanced tissue perfusion. In mouse models of lung cancer and atherosclerosis, we found that nicotine enhanced lesion growth in association with an increase in lesion vascularity. These effects of nicotine were mediated through nicotinic acetylcholine receptors at nicotine concentrations that are pathophysiologically relevant. The endothelial production of nitric oxide, prostacyclin and vascular endothelial growth factor might have a role in these effects.

Can you explain on what basis were the authors of the F344 rats and B63CF mice experiments justified in attributing ("likely") the growth of respiratory tumors to the "carcinogenicity" of TS while choosing to disregard and fail to quantify the role of the well known vascular effects of TS (described in the quote), which were perfectly consistent with their observed redistribution of tumors (more tumors in respiratory system, fewer elsewhere, exactly as the redistributed vascularization due to inhalation of TS would predict it),  with increased lung weight in smoking animals and with extended lifespan of smoking animals.

The authors blatantly turned blind eye to the well known facts on vascularization and its relation of tumor growth, and simply declared (figuring, why bother measuring and quantifying the role of vascular effects, after all we are in antismoking "science", who's going to ask questions, anyway) -- the observed redistribution of tumors "likely" due to "carcinogenicity" of TS.

Yet somehow, this "TS harmed" smoking animals outlived the "TS unharmed" non-smoking animals. I got it now -- "TS harming" means "extending life" while "not harming by TS" means "shortening life". I can live with that, although in the olden days they used to say that same thing as "Smoking is good for you."

Quote

Another example of the TS dose dependent weight reduction:
http://toxsci.oxford...l/81/2/280/FIG1

That's a common knowledge, even high schools girls smoke to keep appetite and weight down, but for some reason you keep repeating it in every post. How exactly does that bit of trivia falsify the empirical fact that smoking animals outlive non-smoking animals? Since you stepped into this thread of your own volition, you will just have to live the rest of your life knowing that smoking animals outlive non-smoking animals. Deal with it.

[kismet]

nightlight, on Mar 6 2010, 11:04 AM, said:

c) The authors chose not to quantify (or even to mention it) the well known effects of nicotine and NO from TS as promoters of angiogenesis (especially in combination), on the vascularization in the lungs of smoking rats (note that lungs were larger in smoking rats, cf. Table 3), and of course they didn't take into account the effect of improved lung vascularization on the rate of growth of tumors (another well known phenomenon; common cancer treatments rely on it, by suppressing angiogenesis). So far, you have kept pretending to be unaware of such well known facts, hence your "logic" seems to be: since such facts don't exist, the authors were perfectly justified in choosing not to measure this effect and quantify its contribution to the observed increase in growth of lung tumors, therefore they are justified in declaring that all such growth was "likely" due to lung 'carcinogenicity' of tobacco smoke.
....
The authors blatantly turned blind eye to the well known facts on vascularization and its relation of tumor growth, and simply declared (figuring, why bother measuring and quantifying the role of vascular effects, after all we are in antismoking "science", who's going to ask questions, anyway) -- the observed redistribution of tumors "likely" due to "carcinogenicity" of TS.

  "carcinogenicity /car·ci·no·ge·nic·i·ty/ (kahr″sĭ-no-jĕ-nis´ĭ-te) the ability or tendency to produce cancer" TS increased cancer, by whatever means, therefore it is a carcinogen or cancer-promoter (and that is using your own logic!)

Quote

That's a common knowledge, even high schools girls smoke to keep appetite and weight down, but for some reason you keep repeating it in every post. How exactly does that bit of trivia falsify the empirical fact that smoking animals outlive non-smoking animals? Since you stepped into this thread of your own volition, you will just have to live the rest of your life knowing that smoking animals outlive non-smoking animals. Deal with it.

You really need to read up on your biogerontology and the importance of dietary restriction.
Smoking -> reduces calorie intake -> reduced calorie intake extends life. So, why not bypass the redundant smoking step and just eat less? I mean you just wrote yourself that tobacco smoke is a carcinogen. Whether directly or indirectly via nicotine, doesn't matter when using the correct and straight-forward definition of 'carcinogen'. Just eating less is considerably cheaper and safer, isn't it?

And the same does not apply to the toxin nicotine. By and large you cannot smoke w/o getting nicotine and/or if you could, you'd still gain nothing: the life span increase is explained by simple dietary restriction which can be done voluntarily, bypassing the redundant and dangerous step of smoking.

No one ever denied that smoking animals outlived controlled and it does not make anyone cry at night. That's what the data shows. The point is that it's irrelevant.

Edited by kismet, 06 March 2010 - 04:00 PM.

[nightlight]

maxwatt, on Mar 6 2010, 05:55 AM, said:

Actually, eating AGEs does not seem to be particularly bad for humans.  We have evolved enzymes to neutralize them over millenia of eating cooked food.  If you feed a rat the amount of dietary ages a human typically consumes, it dies quickly....

The 100 mg total tobacco smoke matter per pack absorbed by lungs, only the tiny fraction of which are glycotoxins (that's blend dependent, lower for additive free tobacco, the way it was optimized for human smoking). In that kind of very low dose, the glycotoxins are in fact highly beneficial, as recent paper demonstrated (I conjectured this phenomenon a year before this paper came out within the AGE discussion, in my first smoking debare here, see hypothesis H2; of course that was easy to anticipate since with biochemical networks of tobacco, the finely tuned synergy with human biochemical networks implies you won't ever go wrong if you always assume it is going to do the best that can be done for its synergistic partner):

Dicarbonyls Stimulate Cellular Protection Systems in Primary Rat Hepatocytes and Show Anti-inflammatory Properties
T. M.  Buetler  et al.  (Annals N Y Acad Sci. 2008 Apr;1126:113-7)

Advanced glycation endproducts (AGEs) and their precursor dicarbonyls are generally perceived as having adverse health effects. They are also considered to be initiators and promoters of disease and aging. However, proof for a causal relationship is lacking. On the other hand, it is known that AGEs and melanoidins possess beneficial properties, such as antioxidant and metal-chelating activities. Furthermore, some AGEs may stimulate the cellular detoxification system, generally known as the phase II drug metabolizing system. We show here that several reactive dicarbonyl intermediates have the capability to stimulate the cellular phase II detoxification systems in both a reporter cell line and primary rat hepatocytes. In addition, we demonstrate that dicarbonyls can attenuate the inflammatory signaling induced by tumor necrosis factor-α in a reporter cell system.

Quote

However, the enzymes do not appear to be present in the lungs.

Considering the above hormetic effects, just what the doctor orderd. Would you expect any less from the 'most precious gift of gods'? (It's actually never too late start benefiting from this ancient synergy, it doesn't hold grudges -- the oldest man on record started smoking at age 70, then lived for another 50 years, sharp as atack.)

[Matt]

I also think we should STOP responding to such rubbish!  this is a life extension forum o.O !!! Why is this even up for debate whether smoking is harmful or not. It can contibute absolutely NOTHING to our goals, the most useful topic ever.
kismet is right about the DR effect.

Edited by Matt, 06 March 2010 - 05:28 PM.

[donjoe]

Matt, on Mar 6 2010, 07:24 PM, said:

Why is this even up for debate whether smoking is harmful or not

Let's see... because we're not dogmatic religious fanatics and we make the rational choice of debating things when someone shows up claiming to have new (previously not considered) evidence?

As much as you may hate to admit this, any complex substance will have some good effects and some bad effects on health, and the trick with those is to determine which effects are more numerous/intense/important in order to decide whether usage of that substance is likely to be mostly beneficial or mostly harmful.

[Lester]

nightlight, on Mar 6 2010, 12:10 PM, said:

Considering the above hormetic effects, just what the doctor orderd. Would you expect any less from the 'most precious gift of gods'? (It's actually never too late start benefiting from this ancient synergy, it doesn't hold grudges -- the oldest man on record started smoking at age 70, then lived for another 50 years, sharp as atack.)

Honestly, this is a tour de force comedy routine. I'm enjoying every moment of the insanity.

[Blue]

Lets quote the FS344 study again including the parts you do not mention (HS = high smoke, LS = low smoke):

"The similarity of smoke doses achieved in the present study to doses incurred by human smokers is uncertain. Finch et al. (1998)Go proposed on the basis of estimated weekly particle doses per unit of lung weight that the LS and HS exposure rates might simulate humans smoking between one and two, and between three and four packs/day, respectively. Finch et al. (1998)Go also measured carboxyhemoglobin levels in four males and four females in each group immediately after a daily exposure during week 32. The mean ± SD carboxyhemoglobin levels (there was no gender difference) were: C = 1.6 ± 0.5%; LS = 9.6 ± 1.0%; and HS = 19.1 ± 2.6%, suggesting that the HS level simulated human exposures to more than three packs/day. Therefore, despite the uncertainties in the correspondence between lung doses of cigarette smoke components in rats and humans, we estimate that the LS and HS exposures in the present study roughly simulated the doses achieved by humans smoking at moderate and very high rates."

"It seems likely that the carcinogenicity in the present study was a response to chemical carcinogens rather than a nonspecific response to "particle overloading," such as that caused by exposures to diesel emissions and some non-mutagenic solid particles administered above the "maximum tolerated dose" (MTD) (Mauderly, 1996Go). MTD is generally defined as the highest dose (exposure) that does not cause life span shortening for causes other than carcinogenicity (Haseman and Lockhart, 1994Go). The HS level met this definition because it significantly, although only slightly, shortened survival among HS females, but not males, and the tumors were not considered to have caused death. "

"Although the HS exposure might have exceeded the MTD (which may also be true for exposures of human heavy smokers), it is unlikely that the LS level reached the MTD. The increased neoplasia at the LS level suggests that the tumors were not solely a response to overwhelming exposures. In addition, only three keratinizing squamous cysts were observed among the 163 HS rats, a lesion found at much higher incidence in "overloading" exposures of rats to diesel emissions or carbon black (Nikula et al., 1995Go). Finally, the finding of mutations in the K-ras gene in tumors in the present study, a lesion not induced in tumors in rats exposed heavily to diesel emissions or carbon black (Belinsky et al., 1995Go), is further evidence that the lung carcinogenicity in the present study was not a nonspecific response to "particle overloading."

"In summary, this study demonstrated that chronic, whole-body inhalation exposure of rats to cigarette smoke at and below the MTD produces exposure-related increases in the incidences of lung and nasal tumors and other proliferative and nonproliferative lesions."

Regarding your "anamoly" in table 4. That lung malignant neoplasia occurred in "4 times" fewer LS males than control males. Well, in actual numbers this was 3 vs. 1 malignant neoplasias. When the number is so small this may well be a random artifact. Regarding LS femals vs. control females the numbers were 0. vs. 4. You must look at some larger groupings, such as also including as yet benign neoplasia, to see more significant results. "Although statistically significant, lung neoplasia occurred at low incidence in the rats (HS {approx} 14%, LS {approx} 6% for females, and HS {approx} 9% for males)." The authors discuss several possible explanation for the differences between males and females (see the article if interested) http://toxsci.oxford...t/full/81/2/280

Regarding your vascularization hypothesis, you have not provided any evidence for that, even if it is the main cancer causing mechanism mechanism and not just one of many, it reduces tumor growth outside the lungs as you would like to think. In fact, you previously cited a study showing that tumor growth outside the lungs was increased by TS, weakening your case. In contrast, we know that TS causes dose dependent weight reduction and that weight reduction in both TS and non-TS animals very strongly reduces tumor growth. So the case for TS causing CR causing reduced tumor growths is much, much stronger than a your vascularization theory. Furthermore, it is logically strange. How can very a small growth such as a benign neoplasia or  a hyperplasia in one small area in the lungs take away enough nutrition to affect the rest of the body?

Regarding the effect of nicotine alone and upregulation of various systems by TS see points 4 and 5 here http://www.imminst.o...o...st&p=389481

Regarding the lifespan of the animals and CR in humans and animals, see points 2 and 3 here http://www.imminst.o...o...st&p=389481

Edited by Blue, 06 March 2010 - 10:40 PM.

[shifter]

I have to laugh when I see the animal experiments and how the rats did better.

Rats do not live as long as long as us! So lets select a really fat model rat that dies from cardiovascular disease early on from being overweight and give them cigarette smoke which should keep their weight down. They will die of old age before any ill or detrimental effects from 'smoking'.

I also actually work in a laboratory that uses mice for experiments and control groups are always very carefully selected to give the researchers the results they want to see!! Want different results? Use another model. Or make up your own model with careful selective breeding and KO genes etc.

Its like the mice fed resveratrol. It was said that the model of mice they used were naturally overweight and they did nicely on the compound. So that experiment does nothing for me. I'm not overweight. Maybe a selective diet could have achieved the same result in those mice.

Maybe we can expose some mice or rats to asbestos. When they die from old age in 2-3 years and NOT from asbestos related cancers etc, we can say 'SEE!! ASBESTOS IS SAFE FOR HUMANS!' Lets ignore the fact that some diseases or cancers can emerge decades after exposure.


The argument that the tobacco was used 8000 years ago in medicine so must be healthy is also flawed. People back then had no idea of all the processes happening to them inside the body or long term implications of the things they used. If somebody back then died from lung cancer or other smoking related diseases, it would never have been recorded or blamed on the tobacco. They had no idea what they were dealing with and I doubt they lived long enough for a many of the detrimental effects to kick in. They would probably smoke it, and it would relieve stress and make them feel great/non depressed etc so in their minds it was a great thing! And when they didn't smoke, they would feel terrible so they kept doing it. Doesn't mean it was healthy.

Also if I were a smoker and went to hospital and I knew my lungs have had it and cancer etc. I'd probably tell the doc and my family I quit too. They would not care/be as sympathetic as much to treat somebody who brought it upon themselves and will keep on doing it after treatment anyway.

Are there any studies that show how cigarette smoke effects the logic/reasoning centres of the brain? Because for somebody to use 'epic beard guy' as a reason why smoking is great and dismisses EVERY study that shows that smoking is harmful, and shows us pathetic well set up experiments using RATS as the model, and honestly believes within themselves that smoking does NOT DO ANY HARM and actually PROMOTES BETTER HEALTH AND LONGEVITY, I would think that persons ability to reason and comprehend logic is compromised.

And if there aren't any studies showing this, then I guess this thread is a good starting point for a future one!!!

[nightlight]

kismet, on Mar 6 2010, 10:56 AM, said:

"carcinogenicity /car·ci·no·ge·nic·i·ty/ (kahr″sĭ-no-jĕ-nis'ĭ-te) the ability or tendency to produce cancer" TS increased cancer, by whatever means, therefore it is a carcinogen or cancer-promoter (and that is using your own logic!)

As argued above in #372, the effect observed in those mice & rat experiments is fully consistent with pure angiogenic effect of TS (nicotine, especially when amplified with low dose NO from tobacco smoke, is a potent angiogenic agent (no pharmaceutical comes even close) acting through upregulation of VEGF and bFGF angiogenic factors, possibly few more).

Carcinogenic effect requires causal role in the production/etiology of cancer. They have not demonstrated any such effect since they disregarded and failed to quantify (or to even merely mention in order to dismiss it under some pretext) the strong vascular redistribution process, which in turn induced corresponding redistribution of the tumor growth rates, which has the same pattern as the observed tumor distribution (more respiratory tumors, fewer other tumors). Since their explanation had to discard some known facts (angiogenic effects & failure to account for it), i.e. they had to drop the known data points, in order to weave  their self-serving  TS-is-carcinogenic narrative, their model is inferior to angiogenic model, which uses all data points, i.e which does not have to discard any established facts or observations.  Any angiogenic agent taken via inhaler will produce similar redistribution of tumor growth rates. Note also that in F344 rat case, the LS group had fewer malignancies in the lungs i.e. despite better angiogenesis in the lungs, the TS had revealed a separate global tumor suppressing effect. This same protective/anticarcinogenic effect of TS was observed in experiments that didn't impose so-called "recovery period" (abrupt quitting; see post #277 for discussion and experiments for this effect).

Angiogenic agents are not carcinogens. If you were to now stretch semantics of 'carcinogen' to include any angiogenic agent, using a rationale that improved angiogenesis helps cancer grow after the onset of the expansion phase, then you could include by the same rationale nearly everything you ingest since that provides building materials and energy that helps cancer grow, too. In such semantics, an apple is carcinogenic, too, since it provides sugar, minerals, and anything else cancer cells need to grow and multiply (after all, the cells of apple have everything another cell, cancer cell included, may need to do all their 'cell stuff'). The nutrition provided by apple and enhanced angiogenesis provided by tobacco smoke are both beneficial effects. Yet, after the onset of cancer, these benefits become coopted by the cancer cells and they end up helping it grow. Similarly, what was extremely harmful to body prior to cancer, such as chemo drugs, radiation, limb amputations, ectomies of various organs,...  becomes life saving.

In other words the value system of 'harmful' and 'beneficial'/therapeutic, is flipped upside down in a body with cancer. Antismoking propaganda thrives on playing transparent little semantic games around this value flip, e.g. by pointing at the angiogenic effects of TS as some horribly harmful effect, by describing it chiefly in the context of growing cancer. Another favorite target of these silly games is another beneficial, life-extending effect of TS -- the upregulation of telomerase by TS, normally a holy grail of life-extension and rejuvenation,  but which is only brought up in the context of cancers and the obvious harm the effect produces (if it were all by itself the sole effect in isolation)... etc.

In fact it was precisely through enjoying these 'scare stories' about how bad TS effects are in the context of lung & other cancers, and by flipping their value system upside down i.e. by considering the same effect in non-cancer/healthy state, that I found backing in literature for the most interesting and most beneficial effects of tobacco smoke. Cancer is a kind of a misguided attempt to recapture the lost youth and start all over, guided unfortunately by much too primitive back-to-nature vision (we have quite a few of such 'pre-cancerous lesions'  within our social organism). Consequently the TS effects discovered within the context of lung cancer, tend to be mostly those of rejuvenating and life-extending kind and they are of that general type in non-cancer/healthy state for which they were meant and optimized in the first place. Cancer is merely an attempt of cooption by the 'back-to-nature' insurgency of this miracle medicine which cannot be coopted. The cooption invariably fails (although cancer may prevail anyway, without the help of TS) because there are too many built in safeguards, preventing it from doing harm to smoker.

These safeguards become evident when you recall that in animal experiments even in cancer states, the smoking animals still outlive the non-smoking ones, 'scare stories' notwithstanding  Even a stronger safeguard has manifested in the F344 rats experiment for the LS group (similar to highest human dosing, although still highly oppressive compared to human smoking,  due to near-MTD concentrations, lack of self-dosing and pacing feedbacks, and without short cycles, like puffs, cigarettes). The LS group had even fewer respiratory malignancies than the controls (and of course, fewer of all others, too), despite the redistributive angiogenic effect of TS[/b] which is the strongest in the respiratory system. Having learned this lesson from the rats experiment, in their mice experiment that followed  researchers simply dropped HS & LS male and LS females groups, all the anomalous tables that were getting too embarrassing to show in public and that would have complicated immensely their antismoking narrative, keeping only the HS females mice, by far the worst off smoking group from the rats experiment (due to extreme, asphyxiating overdose). Yet despite all precautions with HS female mice, the overdosing above the MTD, yet they still somehow outlived the non-smoking females. That's how hard it is to outwit this medicinal magic and coerce it to do harm, when it is obeying the three "you may not injure..." class of laws encoded into its biochemical networks by the gods long forgotten. The experimenters above had ran afoul of the 2nd law, as did many before them.

To clarify some more the situation above, lets step one level up in the hierarchy of networks (see on general intelligent networks and application to our context here, posts #324), from the biochemical networks making our bodies to the social networks i.e. to society as a whole, which is a higher level intelligent organism,  a purposeful anticipatory system in pursuit of its own happiness just as you or I do (in the conventional language, this superorganism is labeled as god, its 'mind stuff'' as holy spirit, its gamete is the 'son' of the trinity,...; this works also down from you, as a social superorganism of the society of cells making up your body...).  

From perspective, where human individuals are cells of the social superorganism, vascular system is the ground transportation system (roads, bridges, railways, tunnels). Normally we consider good transportation system, its maintenance, upgrades beneficial to society. Yet, if there is a war or insurgency or rebellion, suddenly the old benefits becomes liabilities, since they allow enemy to transport their own forces and conquer us quicker. Indeed, had France at the start of WWII been less developed, such as Balkans (that didn't have many usable roads for panzers, or much of infrastructure of any kind), Germans would have had much harder time conquering them into submission. Now the antismoking argument against angiogenic effects of TS is like someone in a country arguing that we ought not to improve our roads, build new ones, maintain our infrastructure in order,... because if there is a war or insurgency, the hostile forces will use them against us, hence we are better off, in peace time (analogous to normal, pre-cancer life) letting them fall apart and stop expanding & improving them. So, by watching those kinds of semantic games at this level, where we as individuals are actually 'cells' of the superorganism, the sterile vapidity of such self-serving rationales becomes crystal clear.

Quote

You really need to read up on your biogerontology and the importance of dietary restriction.

I think CR is overrated. It barely gets life-extensions bit above these TS ones. Considering that TS experiments are highly optimized over decades of iterations (see that "recovery period" analysis) to desist that very life-extending effect and to cause the maximum harm to animals via inhalation of TS, the best these experienced researchers knew how. And that is in 2004-5 experiments, with half a century of tuning the scheme and still no luck. The edge of asphyxiation smoke concentrations, unnaturally oppressive smoke  for 6 hours with no letup to alternate air and smoke as humans smoke, no feedback driven self-dosing and self-pacing, no nested cycles...   I am amazed that those rodents did so well e.g. in 250 mg/m3 female mice (the worst case for TS from rat study), right at the edge of asphyxiation, at the end of experiment, there were 47.3% live smoking mice and 19.9% nonsmoking mice.

The same research group did also diesel fumes inhalation tests, labeled as having much higher concentrations than any normal human exposures. The particle density here in "low" group was 0.35 mg/m3, while tobacco "low" group was 100 mg/m3, i.e. "low" tobacco had  286 times greater concentration of particles.

So, this was maximally adversarial research for TS, optimized for maximum harm. Had it been optimized for maximum benefit (especially if tuned for decades), it wouldn't surprise me if instead of 20% longer the smoking mice ends up living 40% longer. Humans smokers obviously optimize for maximum benefit (guided by natural biological feedbacks).

The main practical objection to CR, though, is that it is low a energy, low intensity, semi-hybernated life, biologically suspended in waiting for better times.  I would guess also that it is a low mental throughput and performance, low dopamine, low ACh type of state.  At least that's how some TV interview that I accidentally ran into struck me.  I I just wouldn't care to be in such state even if it would formally gain clock-years, since it would surely lose life-years, in my accounting where the number of bits of information flowing in and out are the bonus points I seek to maximize.

The fundamental objection to general pursuit of that kind  is that I don't share view that either subjective 'self' or its physical implementation (as a given body), is what is to be kept, or can be kept, persisting as the same kind of entity. The pattern of activity making up self which is seeking immortality is meant to unfold in stages, into a larger pattern at a new level,  which doesn't look anything like the little pattern that spawned it, just as you don't look anything like the fertilized egg that unfolded into your present pattern. Each of us is a shot toward spawning an immortal being, and as with gametes that were to become you, the self needs to become 'fertilized' before the next phase can begin. For us talking here at this level of existence, the conventional name for this 'fertilization' is 'enlightenment' (or cosmic consciousness,... the names vary, but the essence is the same). In this state the 'self' is suddenly seen as a little activity pattern implemented on a little fragile, transient biochemical network, your current body (brain is one of its subnets), which is going to perish in just a flicker, one way or another, whether it is 1.0 flickers or 1.2 flickers or.8 flickers, it comes down to a flicker no matter what you do. The process of unfolding of 'self' into your next 'Self' is essentially a process of recoding the 'self' pattern from the little fragile network, which is about to be gone in a flicker, into a larger, live, intelligent pattern, unfolding within the superorganism, the new substratum for its next physical body and 'mind stuff'. Superorganism is an intelligent network, just like your own current implementation of self, except that this one is incomprehensibly more powerful natural computer and a far more durable hardware than your present one. As the process of recoding proceeds, it unfolds spontaneously by its own will and laws that are beyond the grasp of the little 'self''. The latter will continue dissolving as the 'Self' is becoming more alive and more aware. And then, the flicker has just gone by as if nothing of importance has happened, the little 'self' and its fragile vehicle are no more, and new 'Self' is now all on its own, a pulsating, ephemeral pattern, uncertain and quivery in a world unknown, but alive an awake.

Quote

Smoking -> reduces calorie intake -> reduced calorie intake extends life. So, why not bypass the redundant smoking step and just eat less? I mean you just wrote yourself that tobacco smoke is a carcinogen. Whether directly or indirectly via nicotine, doesn't matter when using the correct and straight-forward definition of 'carcinogen'. Just eating less is considerably cheaper and safer, isn't it?

While there is some overlap between the two approaches, they are different in too many ways to even remotely be reducible to the other. CR effect of smoking is a mere unimportant, mostly unnoticed side effect of simply being able to go on, too busy with life, to get hungry all that often or to bother with concerns about food. I haven't stepped on a scale in years, have no idea what I weigh. As long as I fit in the jeans and shirt that's good enough and it isn't worth further attention or time. I don't even know how many cigs I smoke per day or worry about it. I make (stuff tobacco into non-filtered tubes using a little stuffing machine; smoked through cigarette holder) 3-4 at a time, smoke when my biochemical networks signal -- next. When they're gone I make another few. In late evening, when phones are quiet for the day, I go to a closet with collection of all kinds of fancy tobaccos, with names like Gauloises, Black Death (with big skull and crossbones on the pouch), Manitou, Ryback, Samson,...  and make one to be enjoyed for its own sake, in a complete peace when time doesn't matter and nothing else is going on, but a bluish smoke leisurely swirling toward the ceiling, an impish flutter every now and then from the gods long forgotten.

[nightlight]

... snipped long self-serving narrative by the authors of mice/rat experiments...

Blue, on Mar 6 2010, 05:16 PM, said:

Regarding your "anamoly" in table 4. That lung malignant neoplasia occurred in "4 times" fewer LS males than control males. Well, in actual numbers this was 3 vs. 1 malignant neoplasias.

For absolute figures to be an "anomaly" I mentioned, the sample sizes would have to be equal. That 3 vs 1 is not a correct ratio for the "anomaly" I noted, or it is highly misleading if you didn't mean to indicate a ratio, since the sample sizes were unequal. The proper ratio for the "anomaly" is (3/118) vs (1/178) which is ~4.52... and I actually truncated it down to 4.

While the absolute numbers of lung malignancies above were small, thus they could easily be due to a chance, other experiments (including even larger animals, like dogs exposed to radon or radon+tobacco, where the smoking dogs get substantially fewer radon induced lung cancers) along with the fact these researchers in their next experiment dropped the LS groups from their experiment (since it doesn't "work"), and got rid of the males altogether, tell us more than clearly that the "anomaly" is not due to chance but it is quite typical result.

Note also that the total number of animals wasn't too small, and the failure to show alleged "carcinogenicity" of TS on these LS samples, doesn't help their hypothesis, in addition to all its other problems.

Quote

Regarding your vascularization hypothesis, you have not provided any evidence for that, even if it is the main cancer causing mechanism and not just one of many, it reduces tumor growth outside the lungs as you would like to think.

You are missing the point of the argument completely. I provided the evidence that TS in variety of animals (including mice & other small rodents) has a strong angiogenic effect and separately that enhanced angiogenesis allows tumors to grow faster in the regions with enhanced angiogenesis. Therefore, the observed distribution of the spontaneously produced tumors (these were specially bred mice & rats,  to grow genetically produced tumors like mushrooms, through their whole body) is of the same general pattern as the one that the TS induced redistributed vascularization (enhanced angiogenesis, with most dramatic effect in the respiratory system) would have yielded. These researchers are perfectly aware of this well known effect covered by large quantities of research and literature and know exactly that the effect described could potentially account for their observation.

What any honest research (unlike the one discussed) would do is to measure the redistribution of vascularization and quantify the size of that well known effect (as some other examples I gave you did) along with its effect on the tumor distribution (which would also have the same pattern as the one they observed). Then, they would subtract the vascularization caused changes in tumor growth rates from the observed rates. What is left (if anything) represents the result of "carcinogenicity" of TS. Of curse, we know well why these researchers chose to drop the "wrong" data points (the well known facts ended effects described above) --since the number would come out negative.

We know that from other similar experiments (cited throughout the thread) the "carcinogenicity" of tobacco smoke is negative, meaning tobacco smoke protected the animals and suppressed their genetically caused tumors, in lungs and everywhere else. For example this is a citation and a quote provided earlier in the discussion of the "recovery period":

"Another experimental paper (G.M. Curtin et al, 2004) explains the "recovery period" somewhat more bluntly:"

[p. 26] Demonstration of increased tumor formation required that the standardized 20-week exposure period be followed by a 16-week recovery period, during which mice were provided filtered air. Bogen and Witschi (2002) provided justification for the recovery period; more specifically, it was suggested that tobacco smoke exposure suppresses the growth of premalignant foci, and that smoke induced lung tumor risk occurs predominantly via a genotoxic mechanism. Consequently, the recovery period allows tobacco smoke-induced genetic damage to progress to tumors.

Note also that in the quote above, term "suggested" (meaning 'hypothesized') refers to conjectured "genotoxic" effect, while the 'suppressive effect of TS on the growth of premalignant foci' (e.g. produced genetically or with real carcinogens) is an observed empirical fact. The authors are trying to explain (away) why do you need "recovery period" (quitting) so they offer a conjecture that TS has caused "genotoxic" effect, which will manifest itself only after you remove tobacco smoke via "recovery period", to eliminate the observed protective effect of TS and allow conjectured "genotoxic" effect of TS to cause lung cancers.

The most amazing aspect above is not so much the protective effects of tobacco smoke against cancers (that's old new, known for decades among researchers, but not by public and most doctors), but knowing exactly the effect of quitting ("recovery" period), which they are trying to explain away above, why are they forcing tens of millions of smokers in USA alone to quit. Even if conjectured "genotoxic" effect were true (it is a mere wishful conjecture so far), while the "suppressive" effect of TS is empirical fact, hence they are deliberately causing tens of thousands of deaths from lung cancer among the smokers who yielded to the pressures to quit. Unlike associations on non-randomized samples (such as 'smokers have more' of this that disease), the "causing" above is actually a scientifically established fact on variety of animals (from small rodents and up to dogs).

To summarize again the point you missed (quite a few times) -- the authors deliberately:

a) ignored the well known (and backed by refs in our discussion) angiogenic effects of TS (or nicotine alone)
b) ignored the well known effect of vascularization on growth of cancers
c) failed to notice that (a) and (b) would produce the same pattern of tumor growth as the observed one

When researchers leave out 'data points' (known facts & their own observations) that don't fit or which contradict their conclusion, even just one point let alone three, that's called scientific fraud. In the language of the antismoking "science" such things are, of course, called "proof" of the conclusion, as you repeatedly illustrated it in this thread on this very example.

Thanks also for keeping all of us here up date with the ever evolving language of antismoking "science" since it kind of looks similar to English, yet not quite, and without your heroic efforts we could have easily missed this latest development on what "proof" means in this fascinating language.

Quote

In fact, you previously cited a study showing that tumor growth outside the lungs was increased by TS, weakening your case.

You missed the point again. That was skin TS exposure showing the effect of TS on the vascularization (which at the time you incorrectly claimed isn't proven), and the resulting effect vascularization has on growth of tumors, which the researchers in that example interpreted correctly, since they measured all the relevant variables. The reason for giving you that reference was to show what a more "honest research" would do regarding these well known effects and phenomena.

Edited by nightlight, 07 March 2010 - 09:55 PM.

[Blue]

Since you largely ignored the points in my last post I will just link to it again:
http://www.imminst.o...o...st&p=389575

I will just point out that only around 5% of even the HS rats got malignant lesions in the lungs and only around 2.5% malignant lesions in the nasal cavity. These are the only ones that could possible have grown so large as to steal enough nutrition to affect the rest of body. The rest of the lesions were small non-spreading localized pre-cancer lesions. So in no way can large, parasitic lung/nasal cancers have affected the tumor rates for the rest of the body for the overwhelming majority of rats. Or are you arguing that TS increases vasculatization in healthy lung tissues and thus the lungs steal nutrients from the rest of the body? In that case the rest of body would have had harmful effects also just like you see for chemotherapy which is very harmful also for healthful cells. Note that a CR effect does not have this problem since it likely stops tumor growths at an early stage by reducing damage to cells, unlike vasculatization which is only a problem for large tumors that must have their own blood vessels.

Edited by Blue, 08 March 2010 - 05:13 AM.

[Blue]

Version 9.0

Changelog:
*Added a list of studies by maxwatt to point 4
*Added self-medication against schizophrenia as noted by maxwatt to point 9
*Moved Indian correspondence letter to point 8 from 10

1. Animal studies of TS (tobacco smoke) exposure and lung cancer. Yes, until recently they did not find much conclusive evidence. But now we have animal models where TS clearly causes lung cancer (the lifespan of TS models due to other diseases is discussed in the next post.) Smoking as shown can clearly cause lung cancer in certain species/models and humans happens to be another.

Studies (the result of which cannot be explained as due to exposure amounts causing "particle overloading" never seen in human smokers): 1 2 There are also several other models were having a "recovery" period without TS after the TS exposure causes lung cancer to appear. (More in  the next point.)

Reviews: 1 2 3 The last is Coggins latest review. Conclusions in his earlier reviews, when the latest research clearly showing TS causing lung caner were not available, are outdated.

2. Animal studies of TS and lifespan. Yes, there is the hamster study showing lifespan increase from TS. Was in hamsters prone to amyloidosis which is a rare cause of death in humans, even if we count Alzheimers as due to amyloidosis (which is not proven).

TS is also well known for capacity to reduce weight. The hamsters, as well as the animals in several other TS animal studies, showed a large weight reduction. CR is the factor with best evidence for lifespan extension. The last study link above shows that TS causes a dose dependent CR in rats. Weight reduction also caused a clear decrease in tumors for both TS and non-TS mice. So this CR effect very likely offset the harmful effect of the smoke itself in animal studies. Further evidence for this is that after a TS period having a "recovery" period without TS (and thus CR and its protection ceasing) in some animal models have caused cancer, likely due to the earlier TS damage, to appear. Note that similar strong CR effect is not seen in human where quitting only causes an average weight gain of 5 kg.

Also, there are studies where TS causes a lifespan reduction. May be criticized for not representing the human situation but neither does amyloidosis prone hamsters on CR. Furthermore, the bad effects of TS may well come after say 5 or 10 years of exposure which would not be detected in these short-lived animal studies while a good CR effect would.

3. Regarding animal studies in general. The value of animal studies is very limited since humans are not short-lived animals with different metabolism and diseases. We cannot take some average of all animal models created to have certain diseases/properties and conclude that humans should have these characteristics. For example, we do not do this for characteristics like intelligence or amount of body hair. Herbivores do poorly on high fat diets. This is not evidence that high fat is bad for humans. We do not do animal studies to prove an effect of a substance in humans. Rather, we do animal studies as a rough guide for what should be further studied in human studies.

4. TS causes an upregulation of certain defence systems such as antioxidants and detoxication. That is what you expect from toxic substances. Upregulation cannot compensate for a heavy toxic insults. If you want to do upregulate with a mild toxic insult, then there are safer methods such as moderate exercise and ALA.

Furthermore, telomeres are shorter in humans smokers, smoking induces glycation and is a source of reactive glycation?products. Additionally, nicotine appears to depress the immune response to malignant growths in exposed tissue. The toxic agents present in tobacco smoke include free radicals, redox cycling agents, and iron.  Smoking increases plasma malondialdehyde levels. 1 2 3 4

5. Nicotine may have certain beneficial effects when given alone. Like modulation of the immune system which may be beneficial under certain conditions. It not evidence for what TS with its enourmous amount of substances will do. The effect may well be the opposite due to the effects of other substances. If you want nicotine, despite it being extremely addicting, then it is better to only take nicotine. The same applies to other possible good substances in TS.

6. Certain nations like Japan and Spain have a long average life expectancy despite high prevalence of smoking. These nations do a lot of other healthy things. In particular good average diets. Smoking is important but not the only factor determining life expectancy.

7. Jeanne Calment, the person with longest confirmed lifespan, smoked a very low amount. She was an exception (who also had a diet with great amounts of several healthy foods). Very long-lived people in general do not smoke and those who do are sicker. Also, low exposure is not good or neutral. There have been lots research finding harmful effects from low dose secondhand smoking exposure in humans. 1 2 3

8. Several human randomized controlled studies studying the effect of giving advise to stop smoking have not found improved health. Note that getting people to quit permanently is very difficult with even intensive counseling only achieving success in a small minority, Often people do not change their lifestyle before they get seriously sick. So most likely the permanent quitters in these studies were sicker than the non-quitters. The permanent quitters were certainly not randomized and controlled. They were not what the study were studying primarily. Furthermore, there are studies were giving advise improve health. (In lung disease patients. A highly motivated group): 1

There is also a claim that stopping smoking can increase the risk of soon receiving a lung cancer diagnosis in humans but this is only based on a correspondence letter from India not examining possible confounding factors such that smoking was stopped due general and lung illness.

In contrast, there are numerous studies of successful quitting that shows that this greatly improves health. That the quitters may have different health initially than the non-quitters is an obvous confounding factor that a good study can control for. Some examples: 1 2 3

9. There may be some confounding factors missed by epidemiologists in the thousands of studies showing harmful effect of TS. Of course theoretically possible, just very, very unlikely. Epidemiologists have certainly not ignored obvious ones like smoking being more prevalent among those with lower SES in every study.

Self-medication against symptoms is possible for certain diseases like schizophrenia where nicotine may be beneficial against certain symptoms. But more generally self-medication against symptomatic disease is avoided by prospective studies of not symptomatic persons. Also difficult to explain why the health of quitters improve if TS is actually helping against the disease. Regarding a possible factor before symptomatic disease that is improved by TS, such as tiredness improved by nicotine, there is no evidence that, for example, one get tired decades before getting a lung cancer diagnosis. Again, not theoretically impossible that something like this exists, but since we have no evidence it is very unlikely. Similarly, UFOs using advanced technology may be falsifying our studies for unknown reasons. Not theoretically impossible. By using similar arguments one can argue that junk food and obesity is not with 100% certainty shown to be harmful and actually may be healthy and people may use them for self-medication.

If ignoring evidence for not being 100% certain, then there is no evidence for any prescription drugs either, also placebo-controlled, randomized studies rely on probability, there is always a very small chance that the result showing an effect is a false positive due chance or a confounding factor missed even by controlled experiments.

10. TS may protect against certain diseases like Parkinson or Alzheimer among those with Apo E4. A double standard. Epidemiologic evidence is only accepted when the result happens to favor TS. Does not change the situation for most diseases and the overall morbidity/mortality. Also, smoking is a risk factor for rheumatoid arthritis and cognitive decline despite what has been implied using point 4 and 5 and a mouse study. 1 2

For some general descriptions of health effects see: 1 2

Edited by Blue, 08 March 2010 - 05:11 AM.

[Athanasios]

Something occurred to me about the CR of the hamsters. They would not be getting special chow so it would definitely not be CRON (CR with Optimum Nutrition) if they were eating less.

[Blue]

cnorwood, on Mar 8 2010, 01:15 AM, said:

Something occurred to me about the CR of the hamsters. They would not be getting special chow so it would definitely not be CRON (CR with Optimum Nutrition) if they were eating less.

The hamsters did not have an optimal lifestyle. They would likely live longer if they did not smoke and had optimal nutrition. The survivial curve for the B6CSF mice, where we have almost a complete proper one unlike the rather misleading percent difference curve for the hamsters, is not very impressive compared to the ones the CR society like to show. Then again these are all different animal models so hard to make any comparisons.

Edited by Blue, 08 March 2010 - 05:58 AM.

[N.T.M.]

lol What a joke.

Let me let you guys in on a little secret: While smoking is certainly healthful, the real health panacea here is cancer. I swear that shit's amazing. You get lucky enough to get that and you're set for a healthy long-lived future decades past your non-cancerous buddies.

[Skötkonung]

maxwatt, on Mar 6 2010, 02:55 AM, said:

crauley, on Mar 6 2010, 01:23 AM, said:

Skotkonung, on Mar 6 2010, 12:50 AM, said:

As to my original comment on glycation:

Tobacco smoke is a source of toxic reactive glycation products
Increased levels of advanced glycation endproducts in the lenses and blood vessels of cigarette smokers.
Proteomic alteration in lung tissue of rats exposed to cigarette smoke.
Possible involvement of tobacco-derived advanced glycation end products (AGEs) in an increased risk for developing cancers and cardiovascular disease in former smokers.
Advanced glycation endproducts and cigarette smoking.

Yes, inhaling glycotoxins seems intelligent if one wants to avoid accelerated aging.

How about eating them?  (I guess you have another crusade on your hands )

See also Nightlight's 2007 discussion of this AGEs boogeyman.  That discussion begins here.

Actually, eating AGEs does not seem to be particularly bad for humans.  We have evolved enzymes to neutralize them over millenia of eating cooked food.  If you feed a rat the amount of dietary ages a human typically consumes, it dies quickly.  Dogs, the only other animal that has eaten cooked food for the last 50,000 years, has a similar ability to neutralize orally ingested ages.

However, the enzymes do not appear to be present in the lungs.

I think we are also forgetting that ingesting a substance is an entirely different mechanism of delivery than breathing a substance. Both mechanisms can have significant variances in efficacy. For instance, marijuana must be eaten in higher quantities than smoked. Cocaine is rarely eaten (?), it is usually smoked or snorted, etc. Lots of compounds are much more potent when smoked as opposed to eaten. It stands to reason that advanced glycation end products are higher in smokers because there is a high rate of absorption through the lungs.\

Furthermore, I think you'll find (referring to the OP) that many people here try and avoid AGEs in food whenever possible.

Edited by Skotkonung, 08 March 2010 - 06:44 AM.

[Skötkonung]

donjoe, on Mar 6 2010, 03:04 AM, said:

Skotkonung, on Mar 6 2010, 01:50 AM, said:

These types of comments are up there with holocaust denialism, AIDS denialism, etc. To those of us who have seen the true cost of smoking by the loss of loved ones to smoking induced lung cancer and other smoking related illnesses, this is a subject not to be taken lightly.

Yes, exactly, they are opinions some people hold and for which they should never be punished by law, since the practice of punishing "crimes of opinion" is starkly against Human Rights (specifically against the right to Freedom of Speech). The only limits to Freedom of Speech that I find to be acceptable are those banning hate speech and death threats, which your statements were much closer to than his. Not to mention you just admitted your statements were motivated by irrational/emotional reasons. Imagine what would happen if we let all our laws be dictated by unreason. Maybe you'd like to live in a world like that, but I sure wouldn't.

I guess you missed all of the studies I posted, because my position is not entirely based in emotion although there is certainly an emotional component. I am after all a human and I have experienced loss due to the topic at hand. I never made any death threats either, nor hate speech. You can look at the definition of hate speech if you are confused.

I just hope when the OP is dying of lung cancer some years from now, that he remembers all of the comments he has made promoting tobacco usage.

[nightlight]

Blue, on Mar 8 2010, 12:08 AM, said:

Since you largely ignored the points in my last post I will just link to it again:...

I prefer not to waste time of the readers here by refuting the same flawed argument more than 2-3 times per thread. Since you seem to have different preferences, I am sure there will be someone else in the forum who will enjoy running with you around the same circle 5-6 times per thread, and who knows,  maybe even 10-15 times. You never know.

Quote

I will just point out that only around 5% of even the HS rats got malignant lesions in the lungs and only around 2.5% malignant lesions in the nasal cavity. These are the only ones that could possible have grown so large as to steal enough nutrition to affect the rest of body. The rest of the lesions were small non-spreading localized pre-cancer lesions. So in no way can large, parasitic lung/nasal cancers have affected the tumor rates for the rest of the body for the overwhelming majority of rats. Or are you arguing that TS increases vasculatization in healthy lung tissues and thus the lungs steal nutrients from the rest of the body? In that case the rest of body would have had harmful effects also just like you see for chemotherapy which is very harmful also for healthful cells. Note that a CR effect does not have this problem since it likely stops tumor growths at an early stage by reducing damage to cells, unlike vasculatization which is only a problem for large tumors that must have their own blood vessels.

You can keep rationalizing and conjecturing and elucidateng away as you wish, but at the bottom of it, the rock solid empirical fact remains that at the end of the crowning experiment of six decades of antismoking "science" there were more than twice smoking  mice alive than the wholesome non-smoking mice. And this despite the asphyxiating concentrations of smoke driven right to the edge of mice just dropping dead from the lack of air. Further, despite their obvious efforts at optimization, iterating experiments to maximize the harm to the smoking animals -- they simply dropped all the "wrong" groups used in the previous F344 rats experiment, keeping only the highest exposure female mice in the "improved" experiment, the group that fared the worst, by far, in the previous experiments (dying excessively from asphyxiation). Since even with odds stacked like that it still didn't work, they had to disregard three incovenient facts and observations, listed in the post above, contradicting the desired conclusion, and only then the pinnacle of the six decades of antismoking "science" was finally reached:



Congrat... Oops.

[nightlight]

Skotkonung, on Mar 8 2010, 01:51 AM, said:

I guess you missed all of the studies I posted, because my position is not entirely based in emotion although there is certainly an emotional component. I am after all a human and I have experienced loss due to the topic at hand. I never made any death threats either, nor hate speech. You can look at the definition of hate speech if you are confused.

You posted piles of usual junk science -- unwarranted wishful leaps to "conclusions" based on correlations observed on non-randomized samples, which also disregard the confounding from numerous medicinal effects of tobacco smoke (see the refs and discussion on self-medication with tobacco if you are not familiar with this phenomenon or with relevance of its confounding role).

Using such "scientific" method with any medicinal substance, hence disregarding its known medicinal properties, you will obtain exactly the same kind of stats and correlations as those you are trumpeting as "The Proof". For example if your look at 1000 people who use Prozac and 1000 who don't, and you disregard and fail to account for the confounding from the medicinal properties of Prozac, you will "discover" many more cases of depression among the users of Prozac than among the non-users. And among the latter, you will find more depression among the ex-users than among the never-users of Prozac, althought the ex-users will still fare better than current-users.

Amazing, exactly like what you find with tobacco smoking under the requirement to disregard, as it  is rule in antismoking "science", the known therapeutic and protective effects of tobacco smoke. Find a research that accounts for those confounding effects and quantifies their contribution to the observed correlations, then you've got something intersting to show. Otherwise it is as exciting "discovery" as the Prozac linked to depression "discovery" above.