by Carl V Phillips
I was asked to write something about the “research result” that was the germ of this Daily Mail article. I realized that I could turn the whole article into a science lesson about not only the particular result, but about the general flaws in this field. So here it is, in the form of a “fixed it for you” rewrite of all of it.
To save you a bunch of jumping back and forth, I will quote each bit of the original before rewriting it. Is that pushing the boundaries of “fair use” for criticism purposes? Perhaps. But it is the f—ing Daily Mail, so I am not going to think too hard about it.
Vaping could put you at the same risk of getting heart disease as smoking cigarettes, research suggests.
Public Health England claims e-cigarettes are ’95 per cent safer than traditional tobacco’ and encourages smokers to make the switch.
But researchers have found the devices may trigger changes in cholesterol linked to killer heart disease, similar to cigarettes.
Vaping also stifled the heart’s ability to pump blood around the body just as much, if not more, than traditional forms of tobacco.
A new paper claims that for one particular effect of smoking — one of the many ways in which smoking causes heart disease, and not even close to one of the biggest ones — vaping may cause similar levels of effect.
Public Health England has tricked people into believing the best-case-scenario for vaping is that it causes 5% of the harm from smoking. This is an absurd claim, a made-up number that is based on nothing, and which is far higher than any reasonable estimate of the risk. But because even defenders of vaping are tricked into endorsing it, it makes a great starting point for those who want to print alarmist claims that “vaping is really much worse than that!”
Research has shown smoking cigarettes increases heart rate, tightens major arteries and can cause an irregular heart rhythm – all of which make your heart work harder.
The killer habit also raises blood pressure, which increases the risk of a stroke and a heart attack.
Smoking causes acute changes in the circulatory system, which can trigger cardiovascular events. Smoking also does enormous tissue damage to the heart and blood vessels and replaces oxygen in the blood with carbon monoxide, which are the reasons it causes a lot of cardiovascular disease.
Stimulant chemicals (e.g., caffeine, nicotine, antihistamines) cause acute changes similar to the minor effects of smoking, as does physical activity (e.g., going to the gym, having sex). Even many everyday activities have this effect (e.g., taking a hot shower, walking up the stairs). All of these exposures increase the very-short-run rate of having a stroke or heart attack. But since this is a very minor pathway from smoking to these outcomes, the risk is trivial compared to the total risk from smoking.
In addition, these acute outcomes are generally believed to be “harvesting effects” — that is, they trigger what were already imminent events. Someone who has a heart attack from walking up a flight of stairs probably would have had that heart attack later the same week if he had avoided stairs. Someone who is struck down by a trip to the gym or having sex probably would have suffered that outcome within a month or a year.
Scientists are unsure why e-cigarettes cause similar changes in heart health, even though they contain fewer harmful chemicals than standard cigarettes.
Scientists — at least those who understand these simple facts — would expect a nicotine dose from vaping or other smoke-free products to have these same very-short-term effects. They would be detectable using biomarkers (clinical tests) and would cause the occasional harvesting event, though at a rate so low it would be almost impossible to detect. These are a result of the mild stimulant itself, not the toxicant damage from breathing smoke.
E-cigarettes allow users to inhale nicotine in vapour form, rather than breathing in smoke from cigarettes which burn tobacco and produce tar.
But scientists are now advising users wean off e-cigarettes because of the ‘lack of information on long-term safety’ and a ‘growing body of data on their negative effects’.
Vaping is much better for you than smoking. It is not even clear it is bad for you at all, though there is reason to worry a little about anything that involves the lungs. Nevertheless, anti-tobacco activists — some of whom pose as scientists — have been as aggressive about discouraging vaping as they are about discouraging smoking. Indeed, they have become even more aggressive lately, after they belatedly decided that vaping poses a greater threat to their real mission, anti-tobacco extremism.
Our best estimates of the (minimal) health risks have not changed importantly since about 2007, so this trend is purely political and does not reflect any change in what we know. The trend has, however, produced a huge uptick in attempts to concoct “scientific” rationalizations for the political goals.
Researchers from Boston University analysed 476 participants aged between 21 and 45 with no previous heart issues. Of them, 94 were non-smokers, 45 e-cigarette users, 52 people who used both e-cigarettes and traditional tobacco and 285 cigarette smokers.
The team found that bad cholesterol, known as LDL, was higher in sole e-cigarette users compared to non-smokers.
When you have more LDL than your body needs, it can cause plaque to build up in your arteries. This thick, hard plaque can clog your arteries like a blocked pipe.
Reduced blood flow can lead to a stroke or heart attack. If a clot completely blocks an artery feeding your heart, you can have a heart attack.
For example, a recent study out of Boston University found that vapers had a higher level of low-density lipoprotein cholesterol (LDL, the bad kind of serum cholesterol). The authors could have just noted that this was a curious finding that was probably caused by random error or study bias, given that there is no good reason to expect it is causal. This is especially true given that their study was underpowered and used sketchy methodology. The correct next step would have been for the authors to check what had been observed previously, in other studies, and perhaps to suggest it was worth investigating this possible curious relationship using better methodology.
But the incentive system for all public health researchers — and especially those researching exposures that are currently considered evil and are attracting a lot of funding — is to claim that they discovered something important. There is no penalty in public health science (such as it is) for making wild unsupported claims or for later being proven wrong. But there are ample rewards for saying what funders want to hear and for getting featured is clickbait news articles, no matter how unscientific their message is.
Lead author Sana Majid said: ‘Although primary care providers and patients may think that the use of e-cigarettes by cigarette smokers makes heart health sense, our study shows e-cigarette use is also related to differences in cholesterol levels.
It is especially easy to take advantage of the widespread confusion (which has been actively cultivated by both public health professionals and clickbait newspaper writers) of not recognizing the difference between a measurable change in a biomarker and a substantial risk, and even more so the confusion about overall risk versus a single causal pathway. This observation requires some unpacking:
A small change in one particular biomarker of risk, say LDL, sometimes represents an increase in someone’s risk. (This sets aside whether the associated exposure really caused it, or if it was just study error.) However, that “sometimes” reflects the fact that a biomarker can be increased via a pathway that does not increase risk. Having the higher level of that biomarker is a predictor of risk, on average, but raising the level in a particular way does not increase risk. For example, having a high body mass index (BMI) is a predictor of various bad outcomes. But the increased risk reflects the pathway to high BMI via a lack of exercise, and to some extent massive overeating. The body mass itself is a small part of the risk. If someone has a high BMI but exercises a lot, the extra risk is minimal. If someone acquires a high BMI by exercising a lot (bulking up at the gym), the increasing BMI is tracking a reduction in health risk. Thus, a particular exposure causing a particular biomarker change (again, assuming it even is causal) does not necessarily mean it has the same average effect as someone having that different biomarker level.
In addition, even if the increase in the LDL biomarker is causal and it represents the average additional risk from that higher level of LDL, it is still a trivial risk. Typically something like this would be something like a 0.5% increase in heart attack risk. That hypothetical effect is not nothing, of course. But it would merely mean in this case — pretending that 0.5% is a valid estimate — that vaping causes about 0.25% of the risk from smoking (so still small compared to Public Health England’s clever ruse).
Readers exposed to a biomarker statistic in isolation are very rarely told just how small an absolute risk it might represent. This is another trick related to causal pathways that is used to confuse readers. As already noted, smoking causes cardiovascular disease via damaging tissue and pumping in carbon monoxide, as well as via changing blood chemistry, blood pressure, and cardiac rhythm. The latter entries on that list are minor contributors to disease, as far as we can tell. So a discovery (pretend it is really a discovery) that “vaping is just as bad as smoking in terms of this one isolated measure of heart disease risk” is of little consequence in terms of overall risk. It is just one very minor pathway out of the many pathways via which smoking causes cardiovascular disease. But the average reader only understands the “just as bad as smoking” and “heart disease risk” bits of that. The activist “researchers” and clickbait publishers count on that and cultivate it.
‘The best option is to use FDA-approved methods to aid in smoking cessation, along with behavioural counselling.’
They then, with no apparent sense of irony, feel the need to recommend pharmaceutical nicotine products which have approximately the same effects as the nicotine from vaping.
However, the team’s research did not look at whether vape users had previously smoked cigarettes.
The high cholesterol levels therefore may have been caused by damage done by previous traditional tobacco use.
Another favorite trick of public health “scientists” is the Study Limitations paragraph. Sometimes this throw-away paragraph, buried in the Discussion section, notes one of the legitimate weaknesses of the study, such as the failure to control for the confounding effect of previous smoking in the Boston University study. But mostly that paragraph is the equivalent of a stage magician’s misdirection tactics: Several aspects of the study that are less-than-ideal but not really serious problems are listed, while real fatal flaws are never mentioned.
What is worse, when a serious problem is acknowledged (e.g., apparent uncontrolled confounding that seems like it has a huge effect on the reported estimate), that is all is done: it is acknowledged. But legitimate scientific analysis does not offer some ritualized confessional process, wherein someone can sin and then just have its implications washed away by admitting to it. If the authors know such problems exist, they have no business reporting the estimate they derived as if it were a best estimate of causation (or even of association in many cases). They should figure out how to incorporate the resulting uncertainty into their results reporting, or not report those results at all. Yet in the results section, abstract, title, and press releases the authors declare they have found a particular precise relationship. Then in one of the last few paragraphs of the paper, they openly admit that their methods cannot actually support that conclusion even roughly, let alone at the precision they claimed. That is not ok.
A separate study, by the Cedars-Sinai Medical Center in Los Angeles, found vaping was worse for heart blood flow than cigarettes.
Researchers analysed 19 young adult smokers – aged between 24 and 32 – immediately before and after vaping or smoking a cigarette.
They examined the heart’s function using an ultrasound while participants were at rest and after performing a handgrip exercise to simulate physiologic stress.
In smokers who use traditional cigarettes, blood flow increased modestly after inhalation and then decreased with subsequent stress.
However, in smokers who used e-cigarettes, blood flow decreased after both inhalation at rest and after handgrip stress.
Given the random errors and biases in highly-specific studies, it is easy to produce alarmist reports based on biomarkers when that is the goal. The studies are cheap and easy to crank out. For example, “researchers” out of Cedars-Sinai Medical Center used ultrasound to look at the effects of vaping and smoking on a 19 young smokers. They got different blood flow results for smoking and vaping, and declared that this suggests something is worse about vaping as compared to smoking, in terms of health risk, even though there is no reason to conclude this.
Lead author Florian Rader, medical director of the Human Physiology Laboratory at the Cedars-Sinai Medical Center, said: ‘These results indicate that e-cig use is associated with persistent coronary vascular dysfunction at rest, even in the absence of physiologic stress.’
Co-author Susan Cheng, director of public health research, also at Cedars-Sinai Medical Center, added: ‘We were surprised by our observation of the heart’s blood flow being reduced at rest, even in the absence of stress, following inhalation from the e-cigarette.
The authors even admitted that this result was not in keeping with any hypothesis they had. But instead of admitting that with such a small sample size, it was thus probably meaningless random error, nor even offering the obvious alternative hypotheses (e.g., smokers who are not used to vaping might have a one-time response to the novel exposure that does not persist with continued use), they simply declared that this represents a health risk.
Unlike with the LDL example, in this case they do not even have a reason to believe that this biomarker difference is, on average, associated with greater disease risk. Does their reported result of a transitory decrease in blood flow after puffing a vape (in contrast with their reported increase in blood flow after puffing a cigarette) represent an increase in risk? They have no legitimate way to even guess. They could not have even given this context like “if real, this represents 0.25% of the cardiovascular risk caused by smoking”, even if they wanted to (which, of course, they did not). What they have is the merely the functional equivalent of when you smell some foul odor or see some problem with a food and quip “that can’t be good for you.”
‘Providers counseling patients on the use of nicotine products will want to consider the possibility that e-cigs may confer as much and potentially even more harm to users and especially patients at risk for vascular disease.’
Both studies are being presented at the American Heart Association (AHA) Scientific Session conference in Philadelphia this week.
In any case, even if every last one of these results (which get churned out so that people can use them as an excuse to go to conferences) were real, which is undoubtedly not the case, the best estimate of the total resulting risk would probably still fall short of Public Health England’s fictitious 5%. Any suggestion that all of these results taken together, let alone just a few of them, means that vaping is as harmful as smoking is just utterly absurd. Anyone who claims that is probably both incompetent to judge and dishonest.
Rose Marie Robertson, the AHA’s deputy chief science and medical officer, said: ‘There is no long-term safety data on e-cigarettes.
We have enough data from analytic chemistry plus toxicology, legitimate clinical studies that are based on reasonable hypotheses rather than being cheap fishing expeditions, and a lack of observed unexpected outcomes (e.g., there are no “popcorn lung” cases) to be confident that the risk from vaping is trivial. It would be good to have some longer-term observational epidemiology to confirm this. It would be better still to have the testimony of an omniscient god who just told us the answer. But lacking either of those, we should do what real scientists do: Make the best assessment we can based on the evidence we have. Real scientists — and normal people who naturally think like scientists more than most “public health scientists” do — never suggest that the lack of the Word of God, nor any other data they wish they had, means we should pretend utter ignorance.
‘However, there are decades of data for the safety of other nicotine replacement therapies.’
The AHA recommends people quit smoking using patches, inhalers and gum that ‘are FDA-approved and proven safe and effective’.
Much of what we know about the safety of vaping, and the lack of real health outcomes from the measurable acute biomarker effects of nicotine, come from what we know about other nicotine sources. Most importantly, any risks of real cardiovascular outcomes (or cancer, etc.) from Western-style smokeless tobacco use are clearly below the limits of what we can detect via the extensive epidemiology. We also have a tiny bit of evidence about the use of pharmaceutical nicotine, mostly the same exposure as vaping, which further supports this. (We have limited data about long-term use of pharmaceutical products because the industry tries to maintain the fiction that their products are used only short-term, even though they are mostly used long-term like any other tobacco product. Thus, funders discourage research on their long-term effects.)
It comes after 40 Americans have been killed by mysterious lung diseases linked to vaping across 24 US states.
In the interests of ending this article with a non-sequitur we would like to mention that people buy a lot of drugs on the street with unknown cocktails of active drugs and potentially harmful inactive ingredients, and are sometimes poisoned as a result. Since vaping is also drug use, it stands to reason that vaping must be bad. That’s just basic clickbait logic.
Pingback: Vaping Digest November 13th – vapers.org.uk
Is it fair to criticise PHE for using the results of an MCDA study as the basis for their decision to endorse vaping? It’s not as though PHE hid the source of their evidence. A multi-criteria decision analysis is a useful way to present complex sets of data in an accessible way and when David Nutt famously set out the relative harms of the popular drugs used in the UK that way, it was so obvious that official drug policy in the UK is not in any way based on Science that it got him fired from the Advisory Council on the Misuse of Drugs. He also was criticised for his use of an MCDA approach in an editorial in The Lancet because of the method lacking mathematical rigour. Nutt’s response is that it is an attempt to move the discussion into the realm of examining the Science rather than the historical approach of applying the prejudices of political parties to drug policy and that in the pursuit of the perfect we should not dismiss out of hand the good.
The basis of the 95% safer than smoking claim for vaping is also an MCDA. A group of experts rated smoking and vaping on several measures of harm. The 95% result is meaningful in the context of how it was arrived at but misleading otherwise. For instance, I have seen a claim that it proves that vaping is 5% as harmful as smoking cigarettes. No it does not. The study only reduces the estimates of a group of experts about the relative harms of cigarette smoking and vaping to a single figure, which, while it is useful in the right context, is by no means a mathematical absolute. A rigorous analysis of all the data might arrive at a 5 nines figure (99.999% safer) or perhaps lower than 95%, but more likely closer to the 100% mark.
Perhaps if we all emphasise the actual meaning, source and context of the “95% safer” claim it will become clearer to the average Joe and to the Scientific community too.
Yes. Most definitely yes. “Someone else said it first” is not a defense for “I amplified and endorsed something that is obviously false.”
Actually the PHE authors did try to hide it after initially admitting it. The authors knew very well that they were citing non-science (indeed, nonsense), so backpedalled after they were called out on it (but without much credibility and without withdrawing the claim — very Trump-like).
MCDA is a fancy term for “making shit up”. It is not a legitimate way to seek the truth. You say it yourself.
If you wish to understand more, read my takedown of the Nutt et al paper in the archives, published shortly after it came out.
Hey thanks for sharing this