Smoking “causes hundreds of DNA changes”
bbc.com
bbc.com
Polonium-210 in tobacco contributes to many of the cases of lung cancer worldwide. Most of this polonium is derived from lead-210 deposited on tobacco leaves from the atmosphere; the lead-210 is a product of radon-222 gas, much of which appears to originate from the decay of radium-226 from fertilizers applied to the tobacco soils.
But u/searine mentioned that mined phosphate can be used on organic crops so maybe organic tobacco won't avoid the problem.
That tobacco contains lead and polonium had been known for decades, but I used to think that it originated from the decay of natural atmospheric radon and these plants just had some unusual tendency to accumulate heavy metals.
Maybe I should put my tinfoil hat on and run away from non-organic food too?
edit:
From the first source:
Tobacco farmers in developed countries primarily use manufactured fertilizer high in phosphates produced from apatite rock that contains radium-226 and descendant radioisotopes such as lead-210 and PO-210. Tobacco is a unique agricultural crop in that its flavor depends on nitrogen reduction, which occurs through the repeated application of high-phosphate fertilizers. The higher the phosphate level of the fertilizer, the higher the concentration of PO-210 in the tobacco plant. Tobacco grown in certain developing countries has approximately one third less radioactivity than tobacco grown in developed countries, and the radioactivity of tobacco grown in the United States has increased over time.
So maybe you are right.
The small yields will limit you to smoking only a few time a month.
You will want to taste that homegrown tobacco so you will most likely invest in a good old wooden pipe. This will make it so that you don't inhale the smoke into your lungs.
You will however still be at risk of mouth and throat cancer.
I have never used one (but I was always curious when I smoked) so maybe it's a silly question.
Take a look at this (formatting mine):
"The Breath Smoking Technique
It requires a relaxed setting, preferably sedentary and a very slow and calm breathing pattern.
The pipe bit is held to the lips continuously and all breathing is through the nose.
Every 2nd or 3rd slow breath through the nose, a tiny puff is taken through the stem, held in the mouth and slowly, very slowly, discharged back through the stem, raising but the faintest wisp of smoke from the top of the tobacco bowl, and then re-drawn back through the stem.
One does NOT inhale the smoke, but if one gets very good at it, one does not even have to puff: the slight vacuum created in the mouth by nose breathing will draw the finest of puffs through the stem.
The blowing back through the stem is alternated with regular, but very slight puffs so that the whole process of smoking seems as natural, regular and effortless as breathing.
I'm sure many smokers have discovered this technique, or variations of it, on their own.
The advantages are that mastering it will produce the coolest and most flavorful smoke possible, and the slow regular breathing will invoke the calmness and clarity of mind to perceive the results at their fullest."
- http://www.glpease.com/Articles/BreathSmoking.html
That being said, it's all a matter of preference. You can smoke a pipe like a cigarette if it makes you happy. There is no pipe police.
The best comparaison would be downing a shot of jager bomb vs. a nice glass of single malt whiskey that you will sip for an hour.
There's a good table of this about halfway down the page.
Looks like cancer is the single largest cause, accounting for about 2/5ths of the deaths.
Mining and it's by products are perfectly "organic".
https://www.ncbi.nlm.nih.gov/pubmed/25254600
The next link is the first source for the Wikipedia paragraph I originally quoted. They say that somebody found about half of the polonium contained in tobacco to be inside of the leaves.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2509609/
But then, it doesn't say much about marijuana buds because accumulation varies between plant species and parts of the same plant.
The plant might put a higher percentage of potassium in the fruit than exists in the soil, or it might not. So it isn't clear if it concentrates it (it certainly makes it more appealing to consume it).
I'm not sure if that matches your meaning or not.
I think even Fisher would be convinced [1].
[1] https://priceonomics.com/why-the-father-of-modern-statistics...
From your source:
> With more cancer genome sequences and the additional statistical power this will bring, new signatures may be found, the profiles of current signatures may be further refined, signatures may split into component signatures and signatures may be found in cancer types in which they are currently not detected.
Other avenues could be:
- Smoking is also associated with other cancers, such as esophageal cancer and bladder cancer. Generally the warnings don't mention this however. By examining the mutation patterns in an esophageal cancer, you could relate it more conclusively to smoking, and could therefore claim you were not warned about that specific risk.
- Tissue samples from lung cancers diagnosed 20 or 30 years ago are sitting in archival storage. You could sequence the whole genome or exome of these tumours for about $1000 - $2000. Statute of limitations aside, sequencing these tumours could reveal the tobacco signature as a basis for a claim from a time when it was less clear or less public what the risks were.
- Passive smokers could have a case if their cancer shows a tobacco signature.
I don't see how this research changes anything from a legal perspective. We already knew smoking causes genetic mutations, but we also know people who've never been exposed to tobacco can develop lung cancer.
Inhaling the smoke of burning tobacco leaves can cause cancer. I am fairly certain nobody has as strong of an incentive to create cancer-free tobacco as tobacco companies do. That does not mean it is possible, right?
What's the safe, reasonable, recommended smoking amount?
My point is that reality limits how much safer you could make a product. Would it be nice for cigarette or alcoholic beverages to be safer? Yes. Is it possible? Apparently not.
Either tobacco becomes a controlled substance (I am deeply opposed to this given the catastrophic social consequences of prohibition in general), or adults behave like adults, understand the risks, decide for themselves and accept the consequences. Maybe it's because I'm European, but anything else sounds like insanity to me.
By the way, I am not being judgemental in any way. I am an ex-smoker and I drink socially. If people want to smoke (without polluting the environment of others who don't) it's their right, and I completely understand. I used to love it too.
What on earth are you talking about? Tobacco is already a controlled substance in more ways than nearly anything that you can buy at a store (including guns).
Where I live it is almost impossible to buy a gun. On the other hand, I can go downstairs and buy a pack of cigarettes with the same ease that I could buy bubble gum. No questions asked, no ID needed, no records.
"Some products are inherently unsafe, and that is precisely what the costumers want."
Swedish snus is made to minimize tobacco-specific nitrosamines (TSNAs), but seems to not address Polonium-210 on account of the radioactive stuff being "comparable to that from the natural background radiation sources or dental x-rays": https://harmreductionjournal.biomedcentral.com/articles/10.1...
That excuse doesn't seem to hold up to scrutiny. Who really wants to have 10-20 chest x-rays done per day? Are "dental" x-rays really as weak as "background" radiation?
Alcohol seems to be in a similar position - see the popularity of nice wine and beer over e.g. guzzling cheap spirits.
I think people want health AND pleasure, and are willing to do their own hedonic calculus.
Possible to improve? Yes, perhaps significantly. Economically and politically feasible? Maybe not so much.
Seems pretty standard to me, and I would have to guess that this is the kind of lawsuit that you would probably support if the product in question was, say, red meat instead of tobacco.
Anal point - why the apostrophe? Should it be "Smoking becauses hundreds..."?
> "Had I known as a teenager that smoking caused mutations which would stay with me for life then I would never had started"
It agree with you that it's a little silly, especially for young people, but it wasn't that long ago they started forcing cancer warnings on tobacco.
But really, I know it wouldn't have made a difference. From an early age I was taught at school that smoking would kill me and I started anyway. The idea that detailed knowledge of one particular cause of death would have made a difference is laughable. It's just a way of deflecting blame from one's own responsibility.
It's fair to say that everyone know smoking is bad by now, but does everyone possess a correct and complete enough understanding of how and why to meaningfully consent to the risks? If you understand that smoking can cause cancer, but not that it can cause cancer even years after you stop smoking, is that good enough? If you think you can go on a cleanse and purge the toxins from your body, are you really competent to consent to the long-term risks? We don't let minors do nearly anything, from sex to signing contracts to receiving medical treatment, because we do not believe they are mature enough to properly weigh the consequences. If a minor decides to begin smoking, are they able to meaningfully consent to the risks, even if they have been adequately explained?
All medical interventions are weighing hopefully large benefits against hopefully small side effects, but even terrible side effects can be acceptable if the benefits are large enough and people receiving the treatments have been adequately informed and can meaningfully consent.
In most parts you can legally have sex before you can legally smoke.
How can a company be held liable for people who choose to use their product illegally? This doesn't make sense.
(It's different of course if they are directly encouraging children to smoke. In that case, they should have the book thrown at them.)
> Smoking 'causes hundreds of DNA changes'
I'm guessing HN trimmed the closing quote to change it to:
> Smoking 'causes hundreds of DNA changes
It's now been changed to:
> Smoking “causes hundreds of DNA changes”
Those are weird quotes too, not the normal ". There are lots of different quote characters. :)
Pedants will probably like this magazine: http://media-cache-ak0.pinimg.com/736x/df/b7/74/dfb7741e5e84...
Nobody is getting tricked, here. People are selling a product that other people want.
I doubt it, he would probably say no progress has been made at all:
"Many would still fell, as I did about five years ago, that a good prima facie case had been made for further investigation. None think that the matter is already settled. The further investigation seems, however, to have degenerated into the making of more confident exclamations, with the studied avoidance of the discussion of those alternative explanations of the facts which still await exclusion.
[...]
the B.B.C. gave me the opportunity of putting forward examples of the two classes of alternative theories which any statistical association, observed without the predictions of a definite experiment, allows—namely, (1) that the supposed effect is really the cause, or in this case that incipient cancer, or a pre-cancerous condition with chronic inflammation, is a factor in inducing the smoking of cigarettes, or (2) that cigarette smoking and lung cancer, though not mutually causative, are both influenced by a common cause, in this case the individual genotype." https://www.york.ac.uk/depts/maths/histstat/fisher269.pdf
The current paper: "Although we cannot exclude roles for covariate behaviors of smokers or differences in the biology of cancers arising in smokers compared with nonsmokers, smoking itself is most plausibly the cause of these differences." http://dx.doi.org/10.1126/science.aag0299
Wow, just wow. This is standard Armitage & Doll model that has been taught since the 1950s.
Every time a cell divides there is some chance of a genetic error occurring. The more generations away from the zygote a cell is, the more genetic errors it will have accumulated.
Activities that damage tissue, etc and necessitate cell division to replenish the cells will contain cells with more errors.
Now that is a vague sketch, but many people have implemented mathematical/computational models based on that idea, beginning with Armitage and Doll in 1954. Unless he is going to reject the model that has been driving cancer research for half a century (which should be noted in the interview), there really is no mystery at all.
What I cannot explain briefly to a general audience is how quantum field theory and the standard model of particle physics works and how we can compute the probabilities from that.
Just because you know that something is happening, doesn't mean you understand anything about the underlying processes involved.
I don't think that is a fair comparison. My description had much more content than this, it was a high level overview of the proposed process. In contrast, your example does not explain anything.
> Activities that damage tissue, etc and necessitate cell division to replenish the cells will contain cells with more errors.
I don't see how your explanation could enable anything but a statistical model.
The underlying processes I'm talking about would be molecular interactions modeled through the domain of theoretical chemistry or even mechanical processes, probably involving the quantum mechanics of many particle systems. This is probably the mysterious and complex part that is not well understood. Your example does nothing to explain how that works.
Damage happens, yes, this much is clear, but how do the molecules of smoke interact with the cells in the lungs and other places in order to cause the mutations? Can we compute what happens when a nicotine molecule hits a lung cell? Probably not... because it is too complex and mysterious.
First, I wouldn't call Armitage and Doll a "statistical model", it is more a "rational model" derived from first principle considerations. "Statistical models" are stuff like linear regressions, at least to me.
Second, my explanation is useful in that if it is correct, we would need a certain combination of division and error rates to explain age-specific incidence curves. So, within the context of the model (which is commonly accepted), we can put upper lower bounds on these values from epidemiological data.
See for example my earlier discussion on this site[1]. Even if you disagree with my conclusions (somatic mutation can't do it... something is up and hundreds of billions to trillions of $ have been wasted barking up the somatic mutation tree), or find a mistake, that is still what it can be used for:
Second, the paper itself [2] talks about cancer rates and uses experimental data for it (I just glossed over it, so I can't give a decent summary). This is a statistical model.
I think we disagree since you misunderstand what the term statistical model means. Furthermore, you are misusing the term "first principles." First principles really means that you start from a well established theory that describes how something works. From there you predict mathematically, or with a computer simulation, what the reality is. Using experimental data is strictly forbidden.
From Wikipedia [3]: "In physics and other sciences, theoretical work is said to be from first principles, or ab initio, if it starts directly at the level of established science and does not make assumptions such as empirical model and fitting parameters."
I generally have no idea about cancer research, so I have to trust you and cannot comment on the usefulness of the approach.
[1] https://en.wikipedia.org/wiki/Armitage%E2%80%93Doll_multista...
[2] http://www.nature.com/bjc/journal/v91/n12/pdf/6602297a.pdf
2) Every model is originally based on some kind of observation. The Armitage-Doll model is basically "cancer is caused by the accumulation of errors in a single cell", then they go on and do the math from there. Sure, it would be great to know exactly what those errors are, how many it takes, which cells, etc so that we can constrain all the parameters. You are saying that "from first principles" precludes having any parameters, either free or determined by data?
3) As I said, I think the above is quite different from a statistical model like y = a +b*x + eps. Note: In some cases you can deduce an equation like that from an idea like Armitage-Doll, which is fine. Armitage-Doll definitely has more content to it.
Quoting myself rather than editing...Actually, I forgot they come right out and say it:
"This result will be valid for large values of t (of the order of a human lifetime) provided that p1t, p2t, y, prt are all sufficiently small (as could be assumed in an application of this theory to human cancer)." http://www.nature.com/bjc/journal/v91/n12/pdf/6602297a.pdf
But with low probability of mutation at a given site p, how can you get their model to turnover (as is seen in the age specific incidence data)? I don't think you can, however the turnovers easily appear if you allow high mutation rates along with high clearance rates. But those high mutation rates are inconsistent with the estimated mutation rates in human cells.
Anyway, I hope someone checks into it because something is wrong with the mainstream model of carcinogenesis.
Edit:
It is also possible the data used to give the age-specific incidence (ie SEER) is fatally flawed and those turnovers are artefacts.
It's clearly a mathematical/statistical model of a phenomenon and not an explanation of the underlying processes.
http://www.nature.com/bjc/journal/v91/n12/pdf/6602297a.pdf
That is clearly a process, not like the example of Muons and Kaons proposed to be similar (ie "A is correlated with B").
Of course, the next step is to figure out htf this process works.
http://www.nature.com/nature/journal/v500/n7463/full/nature1...
In addition, nonbel's snarkiness and assumptions of ignorance end up misinforming HN readers more.
Scientists do not write these articles for the BBC. The reporters pick and choose what to take from the scientist, and report that. Most of the times they probably get most of the quote correct, or the scientist said something that had many of the words in the quote. But generally these types of articles are barely intelligible to the scientists that were interviewed for them.
>"The prevalence of somatic mutations was highly variable between and within cancer classes, ranging from about 0.001 per megabase (Mb) to more than 400 per Mb (Fig. 1). Certain childhood cancers carried fewest mutations whereas cancers related to chronic mutagenic exposures such as lung (tobacco smoking) and malignant melanoma (exposure to ultraviolet light) exhibited the highest prevalence. This variation in mutation prevalence is attributable to differences between cancers in the duration of the cellular lineage between the fertilized egg and the sequenced cancer cell and/or to differences in somatic mutation rates during the whole or parts of that cellular lineage1."
And that they believe these mutations are accumulating at a relatively constant rate over time:
>"The mutations in a cancer genome may be acquired at any stage in the cellular lineage from the fertilized egg to the sequenced cancer cell. The correlation with age of diagnosis is consistent with the hypothesis that a substantial proportion of signature 1A/B mutations in cancer genomes have been acquired over the lifetime of the cancer patient, at a relatively constant rate that is similar in different people, probably in normal somatic tissue"
So now let's implement their model with the required assumptions:
Define the probability a mutation occurs during a given cell division as p.
Define the probability does not occur during a given cell division as q = 1-p.
Define the number of accumulated mutations required for carcinogenesis as n.
Define the number of cell divisions that have passed since the zygote as d.
Define the number of cell lineages in the tissue as Ncell.
Define the proportion of cancer cells that go on to form detectable tumors as C.
Assume the mutations can only occur once per cell.
Assume the mutations are occurring at the same rate (ie p1 = p2 = ... = pn).
The probability the mutation did occur at some point up to time d must then be given by 1-q^d. And for the n required mutations we would get
(1-q^d)^n.
To get the probability of a cell lineage turning cancerous at a given age (ie the pdf of this distribution) we calculate the first derivative of that function (warning: this is a continuous approximation of a discrete process):
-n*q^d*log(q)*(1 - q^d)^(n-1)
C*Ncell*-n*q^d*log(q)*(1 - q^d)^(n-1)
In that paper, they report seeing a range of roughly 10^-9 to 10^-4 cancer-specific mutations per bp in already detected tumors. If those arose after 10 divisions, the mutation rate would be 10^-10 to 10^-5 mutations/bp/division, etc. So we can see those values are empirically determined upper bounds on the mutation rates. So lets use the higher of the two as our value of p. Let us also assume only n = 2 mutations are need accumulate to result in a detectable tumor. Using R to make the upper plot:
p = 10^-4; q = 1-p; n = 2; d = 1:20000
plot(d, -n*q^d*log(q)*(1 - q^d)^(n-1), type = "l",
xlab = "Divisions since Zygote", ylab = "Pr(a Cell Lineage Will Turn Cancerous)")
abline(v = log(1/n, base = q))
Actually, by setting the second derivative of that CDF to zero, we can see that the Armitage-Doll model predicts a peak in age-specific incidence at log(1/n, base = q) divisions (vertical line on the upper plot). That 10^-4 value comes from Melanoma, so let us also look at the age-specific incidence for that cancer (lower plot). There we see the peak incidence occurs at age ~age 90. So according to their model, the skin cells that are causing melanoma must be ~7k divisions separated from the zygote, corresponding to an average of ~78 divisions each year, or every ~5 days. Is that what happens?
Remember, we used a real upper, upper bound here on the mutation rate from their data, and only 2 required accumulated mutations. Even then we are getting into cells that are 78 generations separated from the zygote before being cancerous. What you will find is that the division rates required to fit what people really suggest (eg p=10^-7 and n=3) are insane according to the accepted model. If they have a different model than that, why do they not write it down and compare to epidemiological data?
>The absence of consistent correlation of all other signatures with age suggests that mutations associated with these have been generated at different rates in different people, possibly as a consequence of differing carcinogen exposures or after neoplastic change has been initiated.
This is a classic crackpot technique: selectively quote just the parts that you want them to say, twist it a bit further to your needs, then proceed with an overly simplistic, but supposedly impressive analysis. I don't know or really think that you are a crackpot, but the quoting behavior is quite telling.
Getting back to your original comment, you accuse the authors of this paper:
http://science.sciencemag.org/content/354/6312/618.full
of not knowing what they're talking about. But in reality, you have already mistaken the type of process that's being talked about. Stratton is talking about a biological and chemical process. You're talking about a "random" process from statistics. An old theory, that uses simplifying assumptions that do not apply with this data.
And finally, the most obvious reason that the Armitage Doll process is not the best explanation is that AD were looking at the process of carcinogenesis. This paper is looking at the various processes of mutations that happen because of a carcinogen. These are different things, especially since mutational processes accelerate after carcinogenesis. I believe the paragraphs that you would find most interesting from the paper are here:
>Signature 5 is found in all cancer types, including those unrelated to tobacco smoking, and in most cancer samples. It is “clocklike” in that the number of mutations attributable to this signature correlates with age at the time of diagnosis in many cancer types (17). Signature 5, together with signature 1, is thought to contribute to mutation accumulation in most normal somatic cells and in the germline (17, 23). The mechanisms underlying signature 5 are not well understood, although an enrichment of signature 5 mutations was found in bladder cancers harboring inactivating mutations in ERCC2, which encodes a component of NER (24).
>Signature 5 (or a similar signature that is difficult to differentiate from signature 5 because of the relatively flat profiles of these signatures) was increased by a factor of 1.3 to 5.1 (q < 0.05; table S2) in smokers versus nonsmokers in all cancer types together and in lung squamous, lung adenocarcinoma, larynx, pharynx, oral cavity, esophageal squamous, bladder, liver, and kidney cancers. The association of smoking with signature 5 mutations across these nine cancer types therefore includes some for which the risks conferred by smoking are modest and for which normal progenitor cells are not directly exposed to cigarette smoke (Table 1). Given the clocklike nature of signature 5 (17), its presence in the human germline (23), its ubiquity in cancer types unrelated to tobacco smoking (18), and its widespread occurrence in nonsmokers, it seems unlikely that signature 5 mutations associated with tobacco smoking are direct consequences of misreplication of DNA damaged by tobacco carcinogens. It is more plausible that smoking affects the machinery generating signature 5 mutations (24). Presumably as a consequence of the effects of smoking, signature 5 mutations correlated with age at the time of diagnosis in nonsmokers (P = 0.001) but not in smokers (P = 0.59).
Armitage Doll relates at most tangentially to what is being reported by these scientists.
>"An old theory, that uses simplifying assumptions that do not apply with this data."
Yes, get rid of one simplifying assumption that was originally introduced for computational reasons and is totally unnecessary today (low mutation rate), and you can see it is impossible for that theory fit the age-specific incidence data using accepted mutation rates + division rates.
Something is wrong, yet in the supplement of the Alexandrov et al (2016) paper, which has the same first and last authors as Alexandrov et al (2013) paper you cited, they use this model without comment on that issue.
Also, in the 2013 paper, Armitage-Doll is not mentioned but it is clear to anyone familiar with that model that it is guiding their interpretation of the results.
Why is that cell allowed to exist then? Isn't there a quality control mechanism or something, that can detect an error occurred and delete the cell?
However, as with anything digital, there is some error rate still. The most common type of cancer mutation will deactivate, p53, a protein that is one of the checkpoint genes.
Having an error rate is essential for evolution and variety, so its not entirely a bad thing.
Wikipedia's entry is a pretty good entry point:
Acute myeloid leukaemia (AML) Bladder
202 399
Cervix Colorectal cancer
168 559
Esophageal Adenocarcinoma Esophageal Squamous
242 292
Gastric cancer Kidney
472 257
Larynx Liver
123 392
Lung Adeno Lung Squamous
678 175
Oral cavity Ovarian cancer
363 458
Pancreas Pharynx
239 76
Small Cell Lung Cancer
148
"Comparison of overall methylation between smokers and non-smokers was performed for all tobacco-associated cancer types for which there were available data from Illumina Infinium HumanMethylation450 BeadChip array, where each array contains 473,864 autosomal CpG probes. The examined data were downloaded from the original data source (Table S1)
[...]
distributions were subsequently compared between smokers and non-smokers using a two-sample Student’s t-test. Results were considered significant for Bonferroni threshold of 10-7."
So it is not like figure one from that Lew paper, because their effect size is not normalized to the inter-individual variance. This is a point in their favor.
However, the sample sizes do match up to those found in table S1 (which I posted above). From the data provided, we cannot tell whether that difference in p-values is solely due to sample size or not. They need to tell us the variance for each CpG/tissue combo as well.
Edit: Corrected autocorrect
Source: an email from my undergrad genetics professor
Alcohol can cause inflammation, triggering various parts of the immune system to kick in. This could result in the release of free radicals from these immune cells, which promotes DNA mutations.
1. http://www.cancer.org/cancer/cancercauses/othercarcinogens/g...
[0] http://www.cancerresearchuk.org/about-cancer/causes-of-cance...
And while the first world doesn't benefit directly anymore, typical brewing and fermenting processes ensured a drink was sanitary due to lengthy boiling times or yeast out-competing other microbes. Alcohol and hops/flavorings provide antimicrobial effects, acetobacter competed and inhibited against other water-born bacterial and mold growth. Alcoholic beverages are an easy way to store and preserve calories in times of scarcity, etc. It's quite likely that those who chose low-alcohol beverages were saved from other water-born diseases and lived longer thanks to it.
I agree vegans probably still get cell damage from the food they eat, but that's not proof positive because they would still die from cancer even if they didn't.
A wonderfully aromatic plant …
It'd be interesting if tobacco could be safer, but isn't, because the manufacturers don't want to incur the expense and anti-tobacco folks want to keep people from smoking at all, not make it safer (c.f. vaping, which is — I think — basically harmless and yet is banned as much as smoking is).
> The most harmful cancer-causing substances in smokeless tobacco are tobacco-specific nitrosamines.
> Cancers linked to the use of smokeless tobacco include:
* Mouth, tongue, cheek, and gum cancer
* Cancer in the esophagus
* Pancreatic cancer
If there were a way to make tobacco healthy, I think the manufacturers would have spared no expense to do so, because the death of a customer prevents them from spending more money on what is sold.
(No idea about anti-vaping people, though.)
https://scholar.google.com/scholar?q=swedish%20snus
The Lancet article is good, but there's a universal consensus.
I can't imagine that cigarettes would work with steamed leaves.
edit: And you'd have to vape the steamed leaf cigarettes, of course.
So no, it does not work exactly like that. Some chemical compounds trigger mutations at a higher rate than others.
>"These considerations of mechanism suggest that at chronic doses close to the toxic dose, any chemical, whether synthetic or natural, and whether genotoxic or nongenotoxic, is a likely rodent and human carcinogen. Not all chemicals would be expected to be carcinogens at high doses; the MTD may not be reached (101) or the chemical may be toxic without causing cell killing or mitogenesis."
This isn't correct and is a common misconception about evolution. The process which does this is natural selection, and it only occurs through the organism being unable to reproduce as well as an organism with beneficial evolutionary changes.
With humans in the modern world, there is no natural selection because of state benefits that keep people alive and able to reproduce who would usually be unable to do so in a world without safety nets.
So in the modern world, any evolution in humanity - either positive or negative - will perdure. In effect we've ended the traditional form of evolution ages ago when we became civilized.
Also, why do you say 'some'? It would stop all negative mutations, as all people are given the ability to reproduce. Your argument seems to be that people with negative mutations would not be attractive, but often they are attractive to others with negative mutations themselves. Or just people who no longer breed purely based on biological fitness - again because of modern civilization.
There is definitely no contradiction there. Genes will still evolve, but it will no longer be through a process of natural finding the most positive genes. Or I'd guess you could say that we will now evolve towards genes that enable the largest families. And the largest families are predominantly in poor suburbs. The actual environment is artificial though, as those families would not be able to survive on their own without support. Taken to an extreme, it would technically be 'evolution to destruction' by selecting for negative traits that make it impossible to survive outside of the safety net. Luckily we're nowhere near that kind of extreme.
What's "positive"?
> The actual environment is artificial though, as those families would not be able to survive on their own without support.
I apologise to those who are offended by my stereotyping - If anything, I'd expect it's some of these people who are most able to survive on their own in the scenario of nuclear apocalypse and all major cities destroyed.
In such a scenario people like software engineers on HN, may even have lack the traits for survival (inherited or learned) - many of us do not know how to fix our own cars or grow our own crops.
Also, the entire world does not have modern safety nets, not even close.
Anyway, by all means, continue smoking if you think it's going to give you some sort of superpowers or immunity that you can pass on to your progeny. Most likely it'll just give you a disease.
So, the mutations discussed in the article have nothing to do with evolution, because they are somatic, and not passed on to offsprig. But even if smoking caused germ cell line mutations, it's also important to note that "highly evolved" is a mostly nonsensical phrase that has no real meaning, and there is absolutely no guarantee that any individual germ line mutations would confer a selective advantage to the off-spring- in fact, the majority of the time, specific mutations are neutral or harmful. Thus, even if smoking did increase the mutation rate in the germ line of a smoker, any given smoker kid would probably just have more problems than benefits. And because mutation rate is (maybe this is somewhat controversial) a phenotype that can and has evolved into itself, changing it artificially through smoking would likely result in a net reduction in "evolvability" as it has been called. Anyways these are all long term (and I mean LONG) population level effects and have nothing to do with individuals being "more evolved".
Just trying to make the point that the original assumption was three times removed from a sound understanding of evolution and showed some pretty big misconceptions.
So, my thinking is, in the same way that you lose quality as you make a copy of a copy in a copy machine the same happens to the cell's DNA. The more a cell has to divide the less the DNA can remain without errors. DNA can tolerate a number of errors but it can eventually lead to cancer. My guess is that not one issues causes the DNA changes but and array of them given the number of substances a cigarette has.
https://www.yahoo.com/beauty/are-former-smokers-safe-after-1...
I feel with industrialized cigarettes, most users feel obligated to consume it completely.
My father-in-law would smoke a portion of the cigarette, put it out, and resume later.
The main reason tobacco is so dangerous is because you are inhaling smoke and carcinogens that are created in the burning. Burning organic or non-organic makes no difference. You are like firefighter in a burning house without a mask when you inhale.
http://www.livescience.com/7914-warning-homegrown-tobacco-de...
Go live in North Korea or Venezuela if you desire having a dear leader who tells you what you should do with your life and leave us alone.
If you want to live here you either accept that you are in a society of free people who actually have a free will or you move somewhere else where you'll find like minded drones serving their dear leader who in turn takes care of them like a father figure.
We are not going to give up our freedom and turn into weak minded persons just to accommodate you.
On top of that you probably do not even realise that you are arguing here for limiting freedom of speech.
> Where you see people shouting "freedom" the loudest, I see fear, distrust, and anger.
Am I supposed to feel bad now? I don't, I still want to keep freedom of speech.
> I'm just pointing out that no one is as free as you think you are because you always have influences.
Ominous and sometimes invisible influencers everywhere. Best way to deal with it: Censorship.
Yes, absolutely. If people want to ruin their lives it's not my responsibility to keep them from doing it. It's their own decision and all consequences are their own problem.
Government regulation isn't necessarily always bad. There is no absolutist one-size-fits-all solution for all problems. Would I like the government to tell me what I can and cannot do, absolutely not. I would protest with you if I think government is overreaching. But, would I concede that there are certain issues (which might not affect me, but might affect lot of others) where the government has to intervene, of course, yes.
No offense, but unless you post some really reputable source, I'm gonna trust my cardiologist over some guy on the internet.
Here's a bunch of references: http://www.sciencedirect.com/science/article/pii/S0309174014...
This idea isn't, and never was grounded in evidence. It's based on very poor science done in the 20th century. The old guard of doctors and health officials will be looked at in the same way we look at geocentrists now. They hold a lot of the blame for the current obesity crisis we have.
2005 study on marijuana smoke > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1277837/
Any yearly tests to perform?
I was a 10cigs a day smoker for 15 years(quit some years ago) and it really weights heavy on my mind that there is nothing I can do about my past mistakes.
However withdrawal from benzodiazepines and alcohol are both very dangerous and can lead to death.
http://americanaddictioncenters.org/withdrawal-timelines-tre...
I believe that while both nicotine and opiates can be addictive from first use, it takes a much longer prolonged use of nicotine to form a strong physical dependence (from personal experience, on the order of a few years of regular use), unlike opiates which can form a strong physical dependence after just a short time (as little as just a few weeks of regular use).
I smoke a pipe on weekends. I have no physical craving for tobacco during the week and sometimes I just don't want to even on the weekends. The most amount of cigarettes I had throughout my life was probably equal to one pack and I never inhaled it because I don't feel like choking on smoke.
The worst effect I get with nicotine is dizziness but never any physical dependency or withdrawal from its absence in my body.
I just wish they did more studies on the effects of occasional use of tobacco, via pipes and cigars to see the effect of what occasional smoking does to someone.
http://media.economist.com/sites/default/files/imagecache/or...
Edit: here another chart showing the 'dependence' of tobacco is very high:
http://medicalmarijuana.procon.org/files/1-medical-marijuana...
Of course the vast majority said they'd smoke a cigarette.
I've never been a heroin addict, but I've been a tobacco smoker for many years and I can confirm that smoking a cig was definitely the most important thing I had to do in the morning.
Also if I had to spend my last money on food or a pack of cigarettes, obviously and without further consideration, I would choose the cigarettes.
So yeah, pretty addictive.
I've stopped smoking 18 months ago, but even after 1.5 years, I still get the urge to smoke almost every day.
I have anecdotally heard that if one had not smoked by adulthood, chances of addiction are fairly low.
Its hard to get rid of those sort of addictions.
Actually, that's incorrect. Nicotine acts as a stimulant and constricts blood vessels, which causes all kinds of serious circulatory problems in the long term - high blood pressure, heart attacks, strokes and so on.
Unfortunately there's no easy way around nicotine, you just have to stop ingesting it.
The gum/patch can alleviate the withdrawal symptoms, but you'll still have to quit the gum.
From http://whyquit.com/pr/082613.html
A 2013 Gallup Poll finds that 92% of successful ex-smokers did not use the nicotine patch, gum, Zyban, Chantix or Champix, that most quit smoking cold turkey.
http://circ.ahajournals.org/content/130/16/1418
"There are some studies of prolonged nicotine replacement therapies (NRT) in smokers who have quit smoking. In these studies, no adverse effects have been found when nicotine medication was administered for months to several years. Other studies indicate that patients with known cardiovascular disease tolerate NRT well for periods up to 12 weeks. "
By far, the danger is in the smoking, not the nicotine in your bloodstream.
The Gallup survey
http://www.gallup.com/poll/163763/smokers-quit-tried-multipl...
allowed an open-ended response, so someone "might have decided to quit" or quit because "it was time" but also used an NRT to help them through the cravings and not have mentioned that to the interviewer.
There are few short term advantages to quitting smoking - your sense of smell improves and you have more spare time on your hands - other than that, there's little to brag about.
By going through this short term suffering, you're improving your long term health.
If someone (God) came to you and said: "Hey, I'll add 10 healthy years to your life if you agree to go through a period of feeling shitty and some mental fog and restlessness and nervousness for a couple of months".
I guess we'd all agree to such a deal and it's pretty much the deal you have right now, so hang on.
Congratulations on your decision and good luck !
I'd choose the food.
Cigarettes, on the other hand, I've smoked a couple of times (1 or 2 cigarettes each time), and every time there's been this thought at the back of my head "I should get some cigarettes" for most of the following day. It's obviously not addiction and easy enough to ignore, but it's definitely a noticeable effect. Interestingly two lengthy (4 hour plus) shisha sessions didn't have the same effect (was a little light-headed and felt like I'd had about 50 cups of coffee, but no effects or cravings the following day).
Though if you count only DNA changes in smokers' lungs, probably none. Or we would have found some superhuman abilities in smokers by now.
Also, vaping fluids don't contain the many, many compounds which are present in tobacco smoke and known to be dangerous, so it seems quite likely it's significantly safer. The unanswered questions are over what long-term inhalation of vaping fluid might do.
Yes.
https://www.eurekalert.org/pub_releases/2016-11/raba-evd1104...
* it was published in 1999
* in a very sketchy journal
* did you even read what you linked ? it is arguing semantics:
>If they would say that smoking increases the incidence of
>lung cancer or that smoking is a risk factor in the
>development of lung cancer, then I would agree. The
>purpose of this article is to emphasize the need to use
>language appropriately in both the medical and scientific
>literature (the media, as a whole, may be a lost cause).You cannot remove these hydrocarbons from tobacco as they are only present during pyrolysis.
Further reading: https://www.amazon.com/Chemical-Components-Tobacco-Smoke-Sec...
That book is authored by Alan Rodgman (bio below).
After joining R.J. Reynolds Tobacco Co.’s research department in 1954, Rodgman initiated the company’s research on cigarette smoke composition. He personally conducted and actively directed environmental tobacco smoke research until 1987.
Rodgman became director of research in 1976. During his career, he served on the editorial board of Tobacco Science, the Council for Tobacco Research, the Coresta Scientific Commission and several U.S. government tobacco-related committees.
He was a member of the Chemical Institute of Canada and the American Chemical Society for 60 years and a member of the New York Academy of Sciences for 40 years.
Rodgman published numerous scientific papers on tobacco smoke composition and served as a reviewer for tobacco-related manuscripts. In 2003 he was awarded the inaugural Tobacco Science Research Conference Lifetime Achievement Award for his tobacco-related research and activities. In late 2008 Rodgman co-authored The chemical components of tobacco and tobacco smoke, for which the authors jointly received the 2010 Coresta Award.
Well, as a past smoker I too have special interest. But also, as a logical person, I'd expect all you'd find of cancer in "archaeological evidence" of human remains are those which afflict bones. So you're not really making a case. Also:
http://scienceblog.cancerresearchuk.org/2010/10/14/claims-th...