Oy vey. Statistician/statistical geneticist here. The second article is too harsh on the first. The point is subtle and hard to express: carcinogens set the odds, but importance of the part of the risk due to "biological luck," the part that comes from the mutation chain, means whether you individually are affected is random in a way that makes it hard to bother protecting yourself.
Let's say (arbitrary numbers) having poisonium in the food supply increases the lifetime population rate of cancer of the thingamajig from 0.11% to 0.12%. In the US, banning poisonium will save 300 million * (0.12%-0.11%) = 30,000 people, very predictable and important. However, if you personally go on a poisonium-free diet, you decrease your personal risk by 0.01%. You chances go from about 1 in 1000 to about 1 in 1000... so maybe if it involves any effort, you should spend your time doing something else to improve your health.
It's different if the carcinogens targeted specific vulnerable groups. If there was one gene that makes you instantly get cancer at the first whiff of poisonium, we would screen everyone for that gene. The difference between the 0.12 and 0.11 would be due that gene. Everyone with that gene would be put on poisonium-free diets. Everyone else can eat all the poisonium they want, and would still have 0.11 risk. (This is more or less the situation with the active ingredient in aspartame sweetener, though the disease is not cancer)
I don't like the use of the word "luck" in these descriptions, since both genetic and mutation chain randomness are a kind of luck. Also, the studies give quality numbers across many cancers, but the basic concept has been a mainstream model of cancer risk for a long time.
Absolutely nothing about the data collected related to different human populations just different types of tissue.
Further, I don't see anything that relates to % of biomass of the tissue just total cell divisions. Presumably the skin, lungs, a digestive track tissues are at high risks because they compromise a lot of tissue, it divides rapidly, and it's not protected from environmental factors ex: sunlight/smoking/spicy food. However, I suspect the paper digs into things a little further to account for such factors.
Yeah, I'm talking about the different populations thing to illustrate an extreme example about the 'luck' concept. It's not directly related to the study.
Not sure I understand the % biomass issue. The tissues you're referring to - epithelial - are the ones doing the bulk of the cell division in adults, and the ones where you'd typically get the (early stage) cancers. Something like smoking increases your risk in two ways. You get a higher mutation rate (chemicals enter your cells and mess with DNA replication). You also increase the number of 'lung cells' you need to clean out and replace, causing more cell division. Obesity (and size in general) has a direct theoretical effect: more cells = more opportunities to divide = more risk events. Caloric restriction presumably is the opposite of that: do nothing and eat nothing, don't have your cells get replaced, and you reduce the number of risk events.
I think the deeper question in cancer math, if you get the single-gene level biologists and population level statisticians to talk to each other, is how much of the cancer is due to mechanics (number of cells, division counts) that are out of our control, mechanics that we can affect, genetics that are out of our control, and how much is genetics that are fragile but susceptible to prevention and early treatment. That's the sweetspot; that's what we ultimately want to find - genetic markers of things that are going to break but can be patched or protected or fixed.
That's why we want accurate models of risk - in different kinds of tissues - in the first place.
It seems like more cells = more risks of mutation = more risk of cancer. So, I would presume it's something that needs to be accounted for in their model.
However, based on the wording that seems to be total cell divisions and I don't know enough about rates of cell division or cancer to tell from that chart. In the end a gall bladder weighs less than 1/4th of a pound where the small intestine is ~3.5 pounds so it hardly seems like they can just ignore it.
Though, if it's really just cell divisions and not organ weight that matters then that's a much stronger finding IMO.
PS: And no I am not paying 20$ to read the actual article. Though if it's free somewhere I would like to read it.
The fact that species with more cells don't get more cancer is known as Peto's paradox. Perhaps it is also true at the tissue level. See http://en.wikipedia.org/wiki/Peto%27s_paradox
Bit of a tangent, but can you elaborate on that aspartame comment? I've found it difficult to research aspartame risks online, since the vast majority of what comes up appears to be unsubstantiated FUD, and the official sources (FDA etc.) don't appear to recognize any risk whatsoever. There does seem to be a general public perception that aspartame is "bad for you" in some way though.
As to the other "generally bad for you" ideas, they're not solidly substantiated. The idea that artificial sweeteners somehow lead you to eat more by messing up feedback regulation is actively studied, but I wouldn't say established.
Phenylalanine is one of the amino acids that you always need and have around in some quantities. But if you get too high a concentration in the brain, it becomes too easy to make the neurotransmitter Phenethylamine. That's got a list of possible effects for different people - could be a stimulant, could be a migraine trigger - but, especially since it doesn't do the same thing for everybody, there is no consensus for what it does. Nor have I seen good numbers on how much is too much.
Let's say (arbitrary numbers) having poisonium in the food supply increases the lifetime population rate of cancer of the thingamajig from 0.11% to 0.12%. In the US, banning poisonium will save 300 million * (0.12%-0.11%) = 30,000 people, very predictable and important. However, if you personally go on a poisonium-free diet, you decrease your personal risk by 0.01%. You chances go from about 1 in 1000 to about 1 in 1000... so maybe if it involves any effort, you should spend your time doing something else to improve your health.
It's different if the carcinogens targeted specific vulnerable groups. If there was one gene that makes you instantly get cancer at the first whiff of poisonium, we would screen everyone for that gene. The difference between the 0.12 and 0.11 would be due that gene. Everyone with that gene would be put on poisonium-free diets. Everyone else can eat all the poisonium they want, and would still have 0.11 risk. (This is more or less the situation with the active ingredient in aspartame sweetener, though the disease is not cancer)
I don't like the use of the word "luck" in these descriptions, since both genetic and mutation chain randomness are a kind of luck. Also, the studies give quality numbers across many cancers, but the basic concept has been a mainstream model of cancer risk for a long time.