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by Maddy » Sun Aug 09, 2009 11:16 pm
by rrapt » Mon Aug 10, 2009 3:36 pm
by freemason9 » Wed Aug 12, 2009 10:11 pm
Maddy wrote:So how's it going, freemason9? Curious minds want to know and are still rooting for you!
by Maddy » Wed Aug 12, 2009 10:39 pm
Seventeen days since your first post! Very good!
by Penguin » Thu Aug 13, 2009 8:06 am
rrapt wrote:I've decided that most of the bad effects of smoking come from the secret additives. I smoke plain hand-rolled tobacco and it is MUCH better than the store-bought kind. No cancer yet.
So there's my denial, all illogical and self-serving for all to see.
--puffer
Summary
Introduction. In the European Union over 600 additives may be used in the manufacture of tobacco products under an extremely loose and de-centralised regulatory framework. Although tobacco additives are generally screened for their direct toxicity, there is virtually no assessment of the impact additives have on smoking behaviour or other undesirable external consequences. If a small quantity of a relatively benign substance added to a tobacco product can make the product more addictive, make it easier to start smoking or facilitate continued smoking then it may be causing great harm by 'leveraging' additional smoking. The additional smoking brings increased exposure to over 4,000 chemicals, including many that are highly toxic and carcinogenic. Given that over 500,000 people die prematurely in the European Union each year as a result of smoking-related disease, even a one per cent change in smoking attributable to the use of additives would have large absolute health consequences - tens of thousands of lives annually. For this reason, tobacco additives should be seen as major public health issue in their own right.
Evidence. This report draws on evidence from tobacco industry internal documents released during recent litigation in the United States and held on the Internet or in British American Tobacco's document depository in Guildford, UK. The views of the UK Government's scientific advisory committees since 1971 are also discussed - showing that the issue has been recognised and debated for more than twenty years.
Which brands use which additives? Though 600 additives are authorised for use in tobacco products, only the tobacco manufacturers can say which additives are used and in which brands. Not even the Government or the European Commission, which are responsible for the regulation of tobacco products have this information or the power to demand it.
Findings. Most additives are not necessary and few were used before 1970. The purpose of this report is to raise concerns about the impact of additives on smoking behaviour. The findings suggest that there is a case to answer and that there is need for increased regulatory scrutiny. There is cause for concern in the following areas.
* Additives are used to make cigarettes that provide high levels of 'free' nicotine which increases the addictive 'kick' of the nicotine. Ammonium compounds can fulfil this role by raising the alkalinity of smoke
* Additives are used to enhance the taste of tobacco smoke, to make the product more desirable to consumers. Although seemingly innocuous the addition of flavourings making the cigarette 'attractive' and 'palatable' is in itself cause for concern.
* Sweeteners and chocolate may help to make cigarettes more palatable to children and first time users; eugenol and menthol numb the throat so the smoker cannot feel the smoke's aggravating effects.
* Additives such as cocoa may be used to dilate the airways allowing the smoke an easier and deeper passage into the lungs exposing the body to more nicotine and higher levels of tar.
* Some additives are toxic or addictive in their own right or in combination. When additives are burned, new products of combustion are formed and these may be toxic or pharmacologically active.
* Additives are used to mask the smell and visibility of side-stream smoke, making it harder for people to protect themselves and undermining claims that smoking is anti-social without at the same time reducing the health risks of passive smoking.
Some of the world's biggest tobacco firms researched the lethal radioactive substance polonium – present in cigarettes – over a 40-year period but never published the results, according to a new scientific article.
Experts have examined more than 1,500 internal documents from tobacco companies.
Polonium 210 is known to cause lung cancers in animals and studies suggest it is responsible for 1 per cent of all lung cancers – equivalent to 11,700 deaths globally – each year in the US.
It is also the substance that poisoned the Russian dissident Alexander Litvinenko in London in 2006.
Yet tobacco companies, while attempting but failing to remove the substance from their products, have kept quiet about their research, experts say.
One of the documents – all of which were made public through legal actions – said publication would be "waking a sleeping giant". The authors of the article, published in the September edition of American Journal of Public Health, also say tobacco companies feared possible litigation.
The quoted studies show polonium is present on the tobacco leaf and inside it as part of its chemical make-up. Tobacco company scientists spent years trying to remove the substance by washing the leaf, achieving only partial success. Attempts at genetic modification and creating filters to remove it also failed.
7. Dr. Smith's Health Newsletter
Here may be an explanation: Dr. Jerome Marmorstein found radioactive polonium in the lungs of smokers and in tobacco grown since 1950. Polonium levels tripled in American tobacco between 1938 and 1960.
This radioactive polonium, plus some lead and radium found in cigarettes and the lungs is directly related to the fertilizer used in tobacco farm soil. The Tennessee Valley authority helped fund apatite rock grinding factories for the tobacco farmers. That's where the polonium came from.
Polonium emits the most carcinogenic form of radioactivity known, but has a short half-life (four months). However, it binds with radioactive lead which has a 22 year half-life, and then breaks down into radioactive polonium.
Nicotine may promote lung cancer yet nicotine receptor antagonists may offer treatment options for patients with lung cancer. A lung cancer treatment that inhibits nicotine receptors was shown to double survival time in mice.
© AFP/File Frederick Florin
June 08, 2009, (Sawf News) - Nicotine may promote lung cancer yet nicotine receptor antagonists may offer treatment options for patients with lung cancer. A lung cancer treatment that inhibits nicotine receptors was shown to double survival time in mice.
Changes in genes encoding nicotine receptors are strongly associated not only with the tendency to smoke, but with susceptibility to lung cancer. Nicotine exposure also heightens the expression of the nicotine receptors, which leads to increased cell proliferation and inhibition of apoptosis, further setting the stage for cancer.
Patrizia Russo, Ph.D. and Laura Paleari, Ph.D. of the Lung Cancer Unit of the National Cancer Research Institute in Genoa, Italy and colleagues from San Raffaele Pisana Scientific Institute for Research, Hospitalization and Health Care (IRCCS), Catholic University, Campus Biomedico University in Rome, Mario Negri Institute in Milan and CEA Gyf sur Yvette in France showed in past research that an antagonist of nicotine acetylcholine receptors (nAChRs), may serve as an anticancer agent. The antagonist, called d-tubocurarine/a-Cobratoxin (a-CbT), specifically targeted the a7 subunit of nAChRs, the area primarily associated with increased cell proliferation.
In this study, the authors took the research a step further and showed that a-CbT could inhibit non-small cell lung carcinoma (NSCLC) growth and prolong life in non-obese/severe combined immunodeficient (NOD/SCID) mice that had human NSCLC grafted to their lungs.
In addition to control mice that were untreated, the researchers randomized one third of the mice to receive standard chemotherapy.
They found that NOD/SCID mice treated with the standard chemotherapy agent, cisplatin, had a 16 percent longer median survival time than untreated mice (p= 0.05). Mice treated with a-CbT, however, had an increased median survival time of 1.7-fold over the cisplatin-treated mice and 2.1-fold over the no-treatment controls (p=0.0005).
"The results of this study show that a-CbT, a powerful, high-affinity a-7-nAChR inhibitor, induces antitumor activity against NSCLC by triggering apoptosis," wrote Dr. Russo. "The prolonged survival of a-CbT-treated animals in our mouse model of NSCLC is most likely the result of several mechanisms, including various antiproliferative and antiangiogenic effects."
The research also found that unaffected (i.e., noncancerous) cells showed no inhibition of proliferation when treated with a-CbT. This may be due to the reduced number of receptor binding sites on normal cells as opposed to cancerous cells. Conversely, they reported that cancer cells with the greatest number of receptor binding sites seemed to respond with the greatest sensitivity to the treatment.
An editorial in the same issue of the journal asked if nicotine may be to lung cancer what estrogen is to breast cancer. Eliot R. Spindel, M.D., Ph.D., of Oregon Health & Science University, stated that estrogen can stimulate the development of breast cancer and estrogen-receptor antagonists, such as tamoxifen, provide therapeutic benefit. In support of a carcinogenic role for estrogen, the incidence of breast cancer appears to be decreasing as estrogen hormone replacement therapy is being used less often. Likewise, nicotine may promote lung cancer yet nicotine receptor antagonists may offer treatment options for patients with lung cancer.
John Heffner, M.D., past president of the ATS stated that "this research clearly has profound clinical implications regarding the role of nicotine in stimulating lung cancer and nicotine receptor antagonists in treating the disease. The highly addictive nature of nicotine, however, complicates patients' ability to quit smoking and avoid ongoing nicotine exposure."
"This [addictive nature of nicotine] underscores the importance of potential FDA regulation of nicotine in tobacco products to limit exposure to this drug that promotes tumor growth," wrote Dr. Spindel
Cannabis use and risk of lung cancer: a case–control study
S. Aldington1, M. Harwood1, B. Cox2, M. Weatherall3, L. Beckert1, A. Hansell4, A. Pritchard1, G. Robinson1, R. Beasley1,5 on behalf of the Cannabis and Respiratory Disease Research Group
1 Medical Research Institute of New Zealand, 3 Wellington School of Medicine & Health Sciences, Wellington, 2 Hugh Adam Cancer Epidemiology Unit, University of Otago, Dunedin, New Zealand, 4 Imperial College London, London, and 5 University of Southampton, Southampton, UK.
A case–control study of lung cancer in adults ≤55 yrs of age was conducted in eight district health boards in New Zealand. Cases were identified from the New Zealand Cancer Registry and hospital databases. Controls were randomly selected from the electoral roll, with frequency matching to cases in 5-yr age groups and district health boards. Interviewer-administered questionnaires were used to assess possible risk factors, including cannabis use. The relative risk of lung cancer associated with cannabis smoking was estimated by logistic regression.
In total, 79 cases of lung cancer and 324 controls were included in the study. The risk of lung cancer increased 8% (95% confidence interval (CI) 2–15) for each joint-yr of cannabis smoking, after adjustment for confounding variables including cigarette smoking, and 7% (95% CI 5–9) for each pack-yr of cigarette smoking, after adjustment for confounding variables including cannabis smoking. The highest tertile of cannabis use was associated with an increased risk of lung cancer (relative risk 5.7 (95% CI 1.5–21.6)), after adjustment for confounding variables including cigarette smoking.
In conclusion, the results of the present study indicate that long-term cannabis use increases the risk of lung cancer in young adults.
Heavy marijuana use not linked to lung cancer
24. May 2006 16:09
Despite popular belief, a new study shows that people who smoke marijuana do not appear to be at increased risk of developing lung cancer.
It seems even heavy, long-term marijuana users do not appear to increase the risk of head and neck cancers, such as cancer of the tongue, mouth, throat, or esophagus.
Senior researcher, Donald Tashkin, M.D., Professor of Medicine at the David Geffen School of Medicine at UCLA in Los Angeles says the findings were a surprise as they expected to find that a history of heavy marijuana use would increase the risk of cancer from several years to decades after exposure to marijuana.
The study looked at people in Los Angeles County - 611 who developed lung cancer, 601 who developed cancer of the head or neck regions, and 1,040 people without cancer who were matched on age, gender and neighborhood.
The researchers used the University of Southern California Tumor Registry, which is notified as soon as a patient in Los Angeles County receives a diagnosis of cancer.
The study was limited to people under age 60 as those born prior to 1940, were unlikely to be exposed to marijuana use during their teens and 20s - the time of peak marijuana use.
Dr. Tashkin says people who were exposed to marijuana use in their youth are only now getting to the age when cancer typically starts to develop.
The participants were questioned about lifetime use of marijuana, tobacco and alcohol, as well as other drugs, their diet, occupation, family history of cancer and socioeconomic status.
Dr. Tashkin says the subjects' reported use of marijuana was similar to that found in other surveys.
The heaviest smokers in the study had smoked more than 22,000 marijuana cigarettes, or joints, while moderately heavy smokers had smoked between 11,000 to 22,000 joints.
Even these smokers did not have an increased risk of developing cancer and people who smoked more marijuana were not at any increased risk compared with those who smoked less marijuana or none at all.
The study found that 80% of lung cancer patients and 70% of patients with head and neck cancer had smoked tobacco, while only about half of patients with both types of cancer smoked marijuana.
A clear association was seen between smoking tobacco and cancer.
The study found a 20-fold increased risk of lung cancer in people who smoked two or more packs of cigarettes a day and the more tobacco a person smoked, the greater the risk of developing both lung cancer and head and neck cancers.
by rrapt » Thu Aug 13, 2009 2:21 pm
by Sweejak » Sat Aug 15, 2009 2:07 pm
There is light at the end of the tunnel!
by freemason9 » Sat Aug 15, 2009 10:23 pm
Sweejak wrote:There is light at the end of the tunnel!
Oh that IS funny.
My quitting technique is to start smoking later. An hour later every day, or an hour later every time you think you can handle and hour later. I'm at 3PM right now and down to half a pack from a full pack. I don't think I can recommend this technique for those who have a free schedule (out of work) because it makes you stay up later and later so you can smoke sooner.
I hate addiction, but I love smoke. Probably the most missed thing about smoking is the extra nuance you can add to a conversation with hand motions, flicking an ash, and blowing smoke in all kinds of ways. It's a whole language.
I allow people to smoke anywhere in my vicinity if they want to, in my office, in my car, in the shop, in the studio.
by Sweejak » Sat Aug 15, 2009 11:01 pm
by freemason9 » Sat Aug 15, 2009 11:09 pm
Sweejak wrote:No I'm not, you don't know me, and if you think you've quit after a month or whatever you've got you're the one who is full of shit.
I've quit using this method and quit for years. Don't ask me why I started back up again, but I'm doing what worked for me. Your mileage may vary.
by Sweejak » Sat Aug 15, 2009 11:19 pm
by freemason9 » Sat Aug 15, 2009 11:23 pm
Sweejak wrote:Yeah, that's exactly right.
Why did I start back? Stress I think. My kid cell phoned me while he was being arrested and like an automaton I bought a pack and that was all she wrote. I don't think it had much if anything to do with a method I'd used years earlier. Do you?
What I've described is almost exactly what happens when people try to quit alcohol. With your logic this means that nobody should to go to AA because not everyone succeeds.
I haven't had a drink in 19 years. If I fall then it can only mean that AA's technique doesn't work.
Hey Mason, "keep coming back."
by Sweejak » Sat Aug 15, 2009 11:30 pm
by freemason9 » Sat Aug 15, 2009 11:37 pm
Sweejak wrote:I detect a certain amount of stress in your recent string of posts. Have a drink.
"Keep coming back" is an AA saying, one among many. I think it's a very effective program. I went for about 3 months but gradually faded away. I credit them and their fellowship with helping me to quit alcohol.
I think some addictions are permanent, hence you can never actually quit, you're always quitting, every hour, every day.
by Maddy » Sat Aug 15, 2009 11:50 pm
Sweejak wrote:I think some addictions are permanent, hence you can never actually quit, you're always quitting, every hour, every day.
No one's taking away all of my fun!Return to The Lounge & Member News
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