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To make a claim that it's less dangerous over-all we need to wait for the curent generation of life-long-vapers to die so we can compare their life expectancy to their life-long-smoker and non-smoker-non-vaper counterparts.

Moving the goalposts. There is no such requirement in scientific research.

It's highly probable that vaping is less dangerous than smoking (that isn't a high bar to clear),

It's not only probable, but it is confirmed by strong evidence.

Until those studies are done,

Which studies? We've studied propylene glycol before. There are multiple studies that have been peer reviewed and used in government safety programs for decades now. More data and more research is always a good idea, but to claim that you are waiting for the results of a new study while also ignoring old studies is a bit absurd. Why not ignore the new studies too? You make no damn sense.

Paracetamol is metabolized whether there is alcohol involved or not; Paracetamol is unhealthy for the liver regardless.

Acetaminophen (*ahem*) is metabolized through two pathways. One uses reducing equivalents (-SH groups) and the other not. The first produces a non-toxic metabolite, the other does not. (check out this diagram) As long as you have reducing equivalents, you're fairly safe. Metabolizing alcohol uses up those reducing equivalents, so it makes acetaminophen toxicity a lot worse.

Sorry to reply to my own post but the PKC in question is protein kinase C delta, which is involved in a buttload of important pathways, and shutting it off would be problematic even if you could just kill it without messing with any other of the PKC family. PKC's are used throughout the body, since they add a phosphate group onto other enzymes, which is a sort of tagging system to mark the modified enzymes or activate them and allow them to do other things, but the specific effects/results vary depending on the cell. Metabolic and transcriptional control systems are *truly* complicated. So, in *my* (definitely not professional) opinion, I'm going to reiterate: it's very useful to have evidence that PKC-delta is responsible for killing dopamine-producing cells, but finding out why they're being killed seems a lot more useful theraputically than trying to reduce PKC-delta's activity/concentration. Maybe it's as simple as a defective cell-surface receptor that's getting modified by PKC-delta and we can target that, specifically.

Not that I recommend anyone do this, but there's evidence that replacing the reducing equivalents available to your liver with a supplement like SAMe can reduce hepatoxicity of acetaminophen(APAP).

Try knowing what you are talking about before you comment. First result for "taste in the gut" gives you this:

Taste receptors, the taste G-protein gustducin, and downstream signaling elements known to underlie the detection and transduction of bitter, sweet, and umami (monosodium glutamateâ"containing) compounds in taste buds of the tongue are present also in specific endocrine cells of the gut: the enteroendocrine K and L cells. Glucose in the gut activates sweet taste receptors and gustducin present in the intestineâ(TM)s enteroendocrine L cells, leading to secretion of glucagon-like peptide-1 (GLP-1) from these cells. GLP-1 and glucose-dependent insulinotropic peptide (GIP) are incretin hormones, which augment insulin release from the beta cells of the pancreas. GLP-1, GIP, and other gut hormones released from the K and L cells affect insulin secretion, glucose homeostasis, nutrient absorption and other gut functions. Glucose transport into enterocytes via Na+,glucose cotransporter 1 (SGLT1) and GLUT2 appears to be regulated by the gustducin- and sweet receptor-expressing enteroendocrine cells. In response to sugar ingestion, knockout mice lacking gustducin show deficits in the release of GLP-1 and insulin, in glucose homeostasis, and in upregulation of SGLT1. Apparently, the gut "tastes" sugars and sweeteners in much the same way as does the tongue and by using many of the same signaling elements. Taste receptors and other taste signaling elements in gut may be contributors to obesity, diabetes, metabolic syndrome and other diet-related disorders. Gut-expressed taste elements are attractive targets for therapeutic intervention.

The same sweetners that fool your sweet receptors on your tongue fool the sweet receptors in you gut messing with you insulin release amongst other things. We had a professor from OSU give a talk about it a few months ago.

Heres another link from the Royal Society of Chemistry:

A sugar-sensing receptor in the intestine could explain why drinking diet cola may hinder obese people who hope to lose weight1,2 and lead to new ways of treating obesity and diabetes.

This explains why humans and animals fail to lose weight with low-calorie artificial sweeteners: they stimulate increased glucose absorption from carbohydrate breakdown in the gut,' said Soraya Shirazi-Beechey, who led the Liverpool team.

I'm sorry, but heroin is not on the same level as oral opium or even smoking opium

Why do you say that? Heroin is a bit more potent than opium, but their effects are pretty much the same. See this paper:

A COMPARATIVE STUDY OF PHYSIOLOGICAL AND SUBJECTIVE EFFECTS OF HEROIN AND MORPHINE ADMINISTERED INTRAVENOUSLY IN POSTADDICTS

Perhaps you should do some research before spouting off caustic remarks like that. There are quite a few studies that show THC and other marijuana components could have anti-cancer & tumor properties. I've linked a few, you can do the rest of the legwork.

http://jpet.aspetjournals.org/cgi/content/abstract /jpet.103.061002v1
http://www.jci.org/cgi/content/full/111/1/43
http://www.fasebj.org/cgi/content/full/17/3/529
http://www.bizjournals.com/sanfrancisco/stories/20 05/08/29/newscolumn6.html

IANAR(researcher), but for journal references how about:

From M.A. Bozarth (1994). Pleasure systems in the brain. In D.M. Warburton (ed.), Pleasure: The politics and the reality (pp. 5-14 + refs). New York: John Wiley & Sons.

Based on research from the origanal study: