If you haven't seen it yet, pop over to Puddlecote's place to see how Martin McKee has been lying to the Chief Medical Officer.
Wednesday, 20 January 2016
Tuesday, 19 January 2016
A crucial point about alcohol research
There are still so many things to say about the junk science that has been created to support the new alcohol guidelines, but a crucial point that is often overlooked was made in the Guardian's letters page last week.
The answer is that the guidelines and the epidemiology are both ultimately rooted in research that takes people's self-reported consumption at face value. We know that people only report a half to two-thirds of what they actually drink. If the epidemiology shows that 14 units offers peak protection, the real figure is probably more like 21 or 28 units. If the epidemiology shows that 30 units is safe, we can assume it's more like 45 units.
You only ever hear about under-reporting when campaigners are saying 'OMG! We're drinking more than we thought'. This is not really true since we know how much is sold from tax receipts, but under-reporting has a profound impact on what we believe about safe and harmful drinking because epidemiologists do not have their subjects' tax receipts. As the letter above suggests, under-reporting can only lead to an exaggerated perception of risk.
What is not clear about the new guidelines for alcohol consumption is whether the risks are calculated on what people actually drink or what they report that they drink. In 2013, the Institute of Alcohol Studies used market research data and assessed the average consumption of all those above 15 in the UK at 11.7 litres a year or 1,170 units. That’s 22.5 units per week on average. The same publication gives reported rates of consumption that seem to be about half this level. If the damage from alcohol is mapped against reported consumption – and rules are drawn up on this basis – these rules will be overly strict for those who assess their alcohol consumption honestly.
Robert East
Professor emeritus, Kingston University
The answer is that the guidelines and the epidemiology are both ultimately rooted in research that takes people's self-reported consumption at face value. We know that people only report a half to two-thirds of what they actually drink. If the epidemiology shows that 14 units offers peak protection, the real figure is probably more like 21 or 28 units. If the epidemiology shows that 30 units is safe, we can assume it's more like 45 units.
You only ever hear about under-reporting when campaigners are saying 'OMG! We're drinking more than we thought'. This is not really true since we know how much is sold from tax receipts, but under-reporting has a profound impact on what we believe about safe and harmful drinking because epidemiologists do not have their subjects' tax receipts. As the letter above suggests, under-reporting can only lead to an exaggerated perception of risk.
Monday, 18 January 2016
Exploiting the workers, NHS style
You may have heard that the boss of NHS England wants to bring in a pretend tax on soft drinks (really just a price hike) on hospital property.
It's been amusing to watch the bien pensants slap him on the back for price gouging in a virtual monopoly when the main effect will be to take more money from the supposedly hard-pressed doctors, nurses, porters and cleaners of the health service.
I've written about for Spectator Health. Do have a read.
It's been amusing to watch the bien pensants slap him on the back for price gouging in a virtual monopoly when the main effect will be to take more money from the supposedly hard-pressed doctors, nurses, porters and cleaners of the health service.
I've written about for Spectator Health. Do have a read.
Well said
Simon Cooke on the public health industry...
Too right. Do read the rest.
It is hard to think of a section of government that so completely (and for its practitioners unconsciously) embraces the warnings about soft totalitarianism set out by Orwell and Huxley - and especially the latter with his observation that totalitarianism would be a matter of acceptance not something violently imposed by a powerful, all-seeing state. Restrictions on our lives - repeat the mantra of don't smoke, don't drink, eat the right food - are accepted because the experts with their evidence tell us that embracing these restrictions is the right thing. Just as as self-appointed stasi helped enforce the smoking ban, we will see similar as new fussbuckets arise to challenge those who drink openly, who eat sugary or salted foods.
The truth about public health spending is that nearly all of it is wasted, is money spent on promoting an ideology of control. No lives are saved by public health's actions. No money is saved for the wider health system by the interventions of public health. No-one's wellbeing is improved by public health. Indeed for many thousands the actions of these ideologues result in a worse life. Yet in my city of Bradford over £30 million is spend on public health programmes, money that could fix the roads, could provide care for the elderly, could smarten up parks. Instead we'll spend it on nannying the hell out of the population, on promoting an unpleasant controlling ideology founded on a myth of wellbeing that has no basis in fact or substantive value to the poor masses it is being imposed upon.
Too right. Do read the rest.
Friday, 15 January 2016
The research behind those alcohol guidelines
This is a guest post by Chris Oakley...
This statement is taken from the executive summary of the recently issued Alcohol Guidelines Review. The review is the work of “expert” groups and the implication of this carefully worded text is that experts have reviewed a new body of evidence that shows the well-established and well researched health benefits of alcohol to be very much less important than previously thought and to be dependent on age and sex.
This seems to be how the press has interpreted the report and if they are to be believed so has the DH. According to the Daily Mail:
This devastating news for moderate drinkers was reported very widely indeed, usually with some reference to protective effects only applying to post-menopausal women and always with the implication that the findings reflected the latest published research.
The problem is that this interpretation is not backed by published research and what the Daily Mail is reporting the DH as saying is not true. The claim that a protective effect is only seen in women over 55 is in fact based entirely on an unpublished speculative report produced for Public Health England by a team from Sheffield University led by Dr John Holmes.
Holmes and his team are the same people who came up with a magic bullet in the form of a minimum unit price (MUP) model that they claimed would target problem drinkers without impacting everyone else. Many people were intrigued by the model including me so I went to the trouble of wading through the extensive analysis that was supposed to be the basis for MUP and was shocked to find that it was not only not supported by the literature but was at odds with many of the most relevant publications. The Sheffield team ploughed ahead regardless and were paid by two governments and the BBC for a model that is economically counterintuitive and contradicts much of the published evidence. Fortunately, I was not alone and many people came to understand that MUP would not target the people Holmes said it would and would be a regressive unpopular tax. Some persist in an irrational belief in MUP including Nicola Sturgeon and some of the members of the “expert” alcohol guideline groups who are still lobbying for it when they are not being impartial experts.
It is hard to imagine, based on the academic quality of the MUP modelling, how anyone might consider the Sheffield team suitable candidates for remodelling UK alcohol guidelines and utterly incredible that its findings should be given precedence over knowledge gleaned from decades of oft tested published research, but that appears to be what has happened.
The Sheffield report repeatedly challenges the widely held belief that moderate alcohol consumption has significant benefits. Both it and the DH guidelines claim or imply that there is widespread scientific controversy on this issue but an in depth analysis using the most relevant references included and omitted from the Sheffield report demonstrates that the controversy is largely confined to John Holmes et al and Tim Stockwell, a man who is still trying to claim that MUP reduced deaths in parts of Canada based on evidence that nobody else seems able to see and which is at odds with official figures.
The Sheffield report claims that protective effects are disputed, may be overestimated and are probably limited to particular groups within society. We might assume that those groups would be the post-menopausal women and perhaps older men mentioned in the guidelines and that there is a body of evidence proving it but in fact the report provides only one reference, a Canadian paper written by Michael Roerecke and Jürgen Rehm, who conclude that their findings...
This is at odds with the Sheffield report, the proposed UK guidelines (which now give men and women the same 'limits') and the attendant publicity.
Elsewhere in the Sheffield report we are told that the same Roerecke and Rehm paper is used as a basis for risk functions that suggest that “drinking up to 8 units a day for males and 4 units a day for females is associated with a reduced risk of IHD (Ischaemic heart disease) relative to abstainers. This is true but in a separate analysis Roerecke and Rehm fail to find a statistically significant dose response relationship between people consuming at the lower and upper ends of the moderate spectrum, prompting speculation that protective effects peak at just one drink per day - speculation that the Sheffield report and the expert group seize upon as fact.*
Confused? That’s hardly surprising. The evidence is less than clear and to their credit Roerecke and Rehm explain this in terms of the limitations of the epidemiological data that they are working with.
Interestingly they go on to say:
This translates as “there is biological evidence to support a protective effect and it is more robust than the epidemiological evidence.”
But the Sheffield report in a statement thought so important that it appears in a special box claims that:
In a considered response to Tim Stockwell in the journal Addiction Roerecke and Rehm observe that...
It is hard to disagree that these statements also apply to key elements of the evidence that underpins the proposed new UK guidelines. The Alcohol Guidelines Review is careful to talk about net benefits that take into account detrimental effects but some serious questions need to be asked about the manner in which the net effects were arrived at.
There is one recent UK study that claims alcohol benefits are only relevant in older women. It isn’t referred to in either the DH Guidelines Review or the Sheffield report.*** The reason for its omission is perhaps that it was discredited as statistically illiterate by the UK’s most famous statistician. That same statistician, David Spiegelhalter was apparently consulted on the proposed alcohol guidelines. I would love to reads his analysis of the Sheffield report with which his name is likely to be inextricably linked.****
In my view, the guidelines and supporting data need to be assessed by competent statisticians and presented by a much more objective group of “experts” before anyone can take them seriously. Someone in Westminster should perhaps mull on the value of exercises such as this review and consider what they tell us about standards at the Department of Health.
“The benefits for heart health of drinking alcohol are less, and apply to a smaller group of the population, than previously thought. The Sheffield report commissioned for the expert group included a UK analysis which has found that the net protective effect from mortality that may be attributable to drinking regularly at low levels appears now to be significant only for women aged 55+ (with men aged over 55+ showing such a net protective effect only of negligible size).”
This statement is taken from the executive summary of the recently issued Alcohol Guidelines Review. The review is the work of “expert” groups and the implication of this carefully worded text is that experts have reviewed a new body of evidence that shows the well-established and well researched health benefits of alcohol to be very much less important than previously thought and to be dependent on age and sex.
This seems to be how the press has interpreted the report and if they are to be believed so has the DH. According to the Daily Mail:
“The Department of Health said researchers at Sheffield University analysed a number of studies showing alcohol only protected the hearts of women over 55. Even so, this was only for small amounts – less than one unit a day …”
This devastating news for moderate drinkers was reported very widely indeed, usually with some reference to protective effects only applying to post-menopausal women and always with the implication that the findings reflected the latest published research.
The problem is that this interpretation is not backed by published research and what the Daily Mail is reporting the DH as saying is not true. The claim that a protective effect is only seen in women over 55 is in fact based entirely on an unpublished speculative report produced for Public Health England by a team from Sheffield University led by Dr John Holmes.
Holmes and his team are the same people who came up with a magic bullet in the form of a minimum unit price (MUP) model that they claimed would target problem drinkers without impacting everyone else. Many people were intrigued by the model including me so I went to the trouble of wading through the extensive analysis that was supposed to be the basis for MUP and was shocked to find that it was not only not supported by the literature but was at odds with many of the most relevant publications. The Sheffield team ploughed ahead regardless and were paid by two governments and the BBC for a model that is economically counterintuitive and contradicts much of the published evidence. Fortunately, I was not alone and many people came to understand that MUP would not target the people Holmes said it would and would be a regressive unpopular tax. Some persist in an irrational belief in MUP including Nicola Sturgeon and some of the members of the “expert” alcohol guideline groups who are still lobbying for it when they are not being impartial experts.
It is hard to imagine, based on the academic quality of the MUP modelling, how anyone might consider the Sheffield team suitable candidates for remodelling UK alcohol guidelines and utterly incredible that its findings should be given precedence over knowledge gleaned from decades of oft tested published research, but that appears to be what has happened.
The Sheffield report repeatedly challenges the widely held belief that moderate alcohol consumption has significant benefits. Both it and the DH guidelines claim or imply that there is widespread scientific controversy on this issue but an in depth analysis using the most relevant references included and omitted from the Sheffield report demonstrates that the controversy is largely confined to John Holmes et al and Tim Stockwell, a man who is still trying to claim that MUP reduced deaths in parts of Canada based on evidence that nobody else seems able to see and which is at odds with official figures.
The Sheffield report claims that protective effects are disputed, may be overestimated and are probably limited to particular groups within society. We might assume that those groups would be the post-menopausal women and perhaps older men mentioned in the guidelines and that there is a body of evidence proving it but in fact the report provides only one reference, a Canadian paper written by Michael Roerecke and Jürgen Rehm, who conclude that their findings...
“...support current low-risk drinking guidelines, if these recognize lower drinking limits for women”.
This is at odds with the Sheffield report, the proposed UK guidelines (which now give men and women the same 'limits') and the attendant publicity.
Elsewhere in the Sheffield report we are told that the same Roerecke and Rehm paper is used as a basis for risk functions that suggest that “drinking up to 8 units a day for males and 4 units a day for females is associated with a reduced risk of IHD (Ischaemic heart disease) relative to abstainers. This is true but in a separate analysis Roerecke and Rehm fail to find a statistically significant dose response relationship between people consuming at the lower and upper ends of the moderate spectrum, prompting speculation that protective effects peak at just one drink per day - speculation that the Sheffield report and the expert group seize upon as fact.*
Confused? That’s hardly surprising. The evidence is less than clear and to their credit Roerecke and Rehm explain this in terms of the limitations of the epidemiological data that they are working with.
Interestingly they go on to say:
“Regarding causality of effects, a potential cardioprotective association is supported by short-term experimental evidence on surrogate biomarkers, such as increasing HDL cholesterol, reducing fibrinogen levels, and inhibition of platelet activation. Indeed, this might be the strongest argument for causality given that observational findings are always prone to residual confounding and bias due to study design.”
This translates as “there is biological evidence to support a protective effect and it is more robust than the epidemiological evidence.”
But the Sheffield report in a statement thought so important that it appears in a special box claims that:
“many researchers…point to a lack of well evidenced biological processes that could explain the effect”.
Clearly those many researchers don’t include Roerecke and Rehm who are just about the only people other than the Sheffield team and Tim Stockwell who might be claimed to be contributors to scepticism over the protective effects of alcohol.**
In a considered response to Tim Stockwell in the journal Addiction Roerecke and Rehm observe that...
“...some researchers in the field may be using different standards in assessing the cardioprotective effect of alcohol vs. its detrimental effect.”
They go on to point out that they...
“...sense a desire by some in the field to apply tough standards on protective effects and more lenient standards on other effects”.
It is hard to disagree that these statements also apply to key elements of the evidence that underpins the proposed new UK guidelines. The Alcohol Guidelines Review is careful to talk about net benefits that take into account detrimental effects but some serious questions need to be asked about the manner in which the net effects were arrived at.
There is one recent UK study that claims alcohol benefits are only relevant in older women. It isn’t referred to in either the DH Guidelines Review or the Sheffield report.*** The reason for its omission is perhaps that it was discredited as statistically illiterate by the UK’s most famous statistician. That same statistician, David Spiegelhalter was apparently consulted on the proposed alcohol guidelines. I would love to reads his analysis of the Sheffield report with which his name is likely to be inextricably linked.****
In my view, the guidelines and supporting data need to be assessed by competent statisticians and presented by a much more objective group of “experts” before anyone can take them seriously. Someone in Westminster should perhaps mull on the value of exercises such as this review and consider what they tell us about standards at the Department of Health.
---
I can't resist adding a few footnotes - CJS
* The peak in protection is almost certainly below 14 units per week but that has no bearing on what the 'safe' level should be. If it is considered safe to not drink, any mortality risk below that of a non-drinker must also be safe. In the Neverland of Sheffield's computer model that level is reached at 14 units. In the real world, as observational data show, it is at least twice that.
** The claim that there are no biological mechanisms to explain the protective effect is such a tired zombie argument - see p. 7 of the previous evidence review from 21 years ago.
*** There is an obvious point that I haven't heard anyone make regarding the protective effects of alcohol 'only' applying to people over the age of 55, namely that heart disease overwhelmingly affects people aged over 55. Sally Davies has strongly implied, if not explicitly stated, that there are no benefits to drinking under this age, but the beneficial impact on heart health is likely the result of long term moderate consumption. The benefits may only pay off in late middle and old age, but they accrue earlier.
**** It should be remembered that even that study - which went out of its way to downplay the benefits of drinking - found that men aged 50-64 years who consumed 15.1 to 20 units of alcohol per week halved their mortality risk compared with nondrinkers - and this finding was statistically significant. This makes the CMO’s decision to reduce the guidelines from 21 units to 14 units per week for men all the more baffling. Moreover, the study did not merely show a reduction in mortality for women over 55 consuming up to 5 units per week, as Sally Davies suggested on the Today programme. It showed a statistically significant reduction in female mortality at every level of drinking up to and over 20 units per week. The strongest effect was shown at the level of 15.1 to 20 units per week with mortality rates falling by around 40 per cent for women over 65 and by around 46 per cent for women aged 50-64 years. In other words, the optimal effect is seen only when people drink above the existing guidelines.
Wednesday, 13 January 2016
Doll parts
I've got an article up at Spectator Health contrasting the 'public health' reaction to two epidemiological findings associated with Richard Doll. The first involved smoking, the second involved drinking.
Do read the whole thing.
As before, a noisy minority continued to deny these findings. They insisted that the biological pathways were unproven, though plausible pathways had been identified. They made generic criticisms of epidemiology that could apply to any observational research, though they never made them of studies which showed negative effects from drinking. Above all, they treated the sick quitter hypothesis as an unanswered question, never acknowledging that it had been tested extensively.Decades after the evidence on moderate alcohol consumption had first been identified, those who refused to accept it were embroiled in a campaign of doubt and denial similar to what Doll had witnessed in the mid-20th century, but this time the naysayers were on the inside of the public health establishment, albeit in its neo-temperance wing. For years, they chipped away at the science, repeating the same old criticisms, cherry-picking studies and demanding an impossible burden of proof from researchers. They received a sympathetic hearing from their public health colleagues who had long struggled with the nuanced message that heavy drinking was bad while moderate drinking was good. Preferring a simple, clear, strong message that alcohol was dangerous, they were similarly inclined to dismiss or downplay the epidemiology.
Do read the whole thing.
Tuesday, 12 January 2016
Doubt is their product
The changes to the drinking guidelines last week represented the first review of the evidence since 1995. The Chief Medical Officer, Sally Davies, and the Sheffield alcohol researchers who advised her went out of their way to downplay and dismiss the evidence that moderate consumption reduces heart disease risk and overall mortality. Why?
First, let's familiarise ourselves with what the review found back in 1995:
Pretty clear, no? In addition to finding a clear relationship between moderate consumption and lower mortality risk - which could not be explained by confounding factors - the working group identified several plausible biological pathways which explained how the effect came about.
It is important to stress that the 'sick quitter' hypothesis - which says that unhealthy former drinkers could explain why teetotallers don't live as long - had already been tested extensively by 1995. In 2002, Richard Doll discussed it in an essay titled 'Proof of causality':
In the last fifteen years, research has continued to show that the J-curve is not the result of 'sick quitters' or other confounding (eg. here, here, here, here and here). A meta-analysis of 34 prospective studies in 2006 showed a clear J-curve that could not be explained by 'sick quitters'. This is how epidemiology is supposed to work. People suggest alternative explanations, new studies test the alternative hypothesis and if the association survives all tests the relationship is assumed to be causal.
In any other field, the debate would have been put to bed years ago. It has been kept alive because many people in 'public health' desperately want to believe that alcohol has no (health) benefits. Almost unbelievably, Sally Davies described the J-curve as an 'old wives' tale' last week. She drew on a report she had commissioned from Sheffield University (the same people who devised the minimum pricing computer model). You can read it here.
The Sheffield report starts the campaign of doubt early in the main text when it mentions the protective effect of moderate drinking and says...
It's worth looking at what all those references refer to:
(10) is an opinion piece in Addiction which discusses the same confounding variables which Doll said had been overcome in 2002.
(11) is a study that doesn't really 'dispute' the J-curve.
(12) is a letter from Tim Stockwell and friends responding to a meta-analysis in the British Medical Journal which found that the link between good cardiovascular health and moderate alcohol consumption was 'beyond question'. That meta-analysis is not cited in the Sheffield report at all, nor is the authors' reply which accuses Stockwell et al. of adopting 'an extreme methodological position, proposing to dismiss an entire body of literature on the basis of the presence of predictable limitations in individual studies. This dogmatic and dichotomous approach to the evaluation of epidemiological studies is counterproductive to scientific epistemology.' If you read Stockwell's letter, you will see that they have a point.
(13) is an opinion piece by Tim Stockwell and friends casting doubt on the alcohol-health link.
(14) is a study that clearly found lower heart disease risk among moderate drinkers.
(15) is a comment piece by Tim Stockwell and friends.
(16) is a revised meta-analysis by Tim Stockwell and friends which claimed that the protective effect of alcohol disappears when adjustments are made to the data and some studies are excluded.
(17) is a study which found that a gene associated with not drinking was also associated with better cardiovascular health.
(18) is a meta-analysis which concluded that 'some form of a cardioprotective association was confirmed in all strata' but that this 'cannot be assumed for all drinkers'. Its authors have since published a meta-analysis which found clear evidence of a J-curve, even when only lifetime abstainers were included (ie. no 'sick quitters').
(19) is a short opinion piece by (you guessed it!) Tim Stockwell.
There you have it - the case for the prosecution. Not quite a one man crusade by Tim Stockwell but not far off. Needless to say, you can find dissenting voices and contrary evidence in any field of research, but on the basis of these minority reports the Sheffield crew not only portray the science as highly contentious but also predict that the science will eventually agree with Tim Stockwell.
Towards the end of the report, the Sheffield boys and gals address the J-curve at more length. They start by acknowledging (but not referencing) the evidence...
There is a 'but' coming, of course...
Those references are some of the articles and studies mentioned above plus a comment piece in Alcohol from 2007 which said 'In view of the potential risks of alcohol, a more cautious view about the beneficial effects of alcoholic beverages is warranted.' It is notable that all the citations given to prove the existence of a 'debate' here are from people on one particular side of the debate. This is a bias that permeates the Sheffield report. For example, no fewer than twelve Tim Stockwell publications are cited in the report, along with eight publications by John Holmes of Sheffield University. By comparison, there are zero citations of studies by people like Richard Doll who produced several studies showing (and testing) the J-curve, nor is there any mention of people like Di Castelnuovo who conducted the 2006 meta-analysis.
The Sheffield crew then proceed to give four possible reasons why this 'extensive literature' is wrong...
This is a reference to this study which found that moderate drinkers had a 26-48 per cent lower risk of heart disease mortality. The study included graphs showing a clear J-curve for all-cause mortality (the one below is for men).
The protective effect for heart disease was only statistically significant for people who did not have a disease at the time of enrolment, but even among those who had a disease upon enrolment, heart disease risk was not higher.
That's what epidemiologists are supposed to do. Smokers are different to nonsmokers in ways that have nothing to do with tobacco. Promiscuous people are different to virgins. People who drink large quantities of sugary drinks are different to people who don't. This is why epidemiologists adjust for factors that might bias the results. Alcohol research is no different to any other type of observational research in that respect - and, as Doll pointed out, non-drinkers tend to lead healthier lifestyles than drinkers, therefore any bias likely leads in the opposite direction to what the Sheffield authors are implying.
Rather than explaining what it is about the characteristics of non-drinkers that invalidate alcohol research when the characteristics of smokers do not invalidate tobacco research, the Sheffield crew ignore all the studies that have tested for confounding variables and return the subject of sick quitters:
Reference 15 and 16 are two similar studies from the pen of Tim Stockwell and friends. One is a revised meta-analysis which controversially claimed that the protective effect of alcohol disappears when studies are excluded and adjustments are made to the data. Reference 18 is a meta-analysis which concluded that 'some form of a cardioprotective association was confirmed in all strata' but that this 'cannot be assumed for all drinkers'.
It is certainly true that including 'sick quitters' biases the results and makes the J-curve look steeper than it is. That is why most studies in the last 25 years have excluded former drinkers and still find strong evidence of a J-curve. The Sheffield authors choose not to mention this or cite those studies, preferring instead to imply that this is an unanswered question.
This was acknowledged in the government's 1995 report. It is why people are advised to drink moderately, not heavily. It does not mean that there is 'no safe level of drinking', nor does it mean that the protective effect is an 'old wives' tale'.
Reference 18 is the same study they have cited twice already. This point really just reiterates what was said earlier about there being differences between teetotallers and drinkers. In effect, they are saying that there might be some other factor that might make teetotallers die younger than drinkers but we don't know what it is. Well, there might be, just as there might be something about smokers which has nothing to do with smoking that makes them more likely to get lung cancer, but the temperance lobby has been hunting pretty hard for this mysterious explanation for a long time and come up empty-handed.
This is the sum total of their objections to the J-curve. Essentially, they are just saying 'confounding factors' over and over again without acknowledging that that question has been emphatically answered. It is difficult to see how any amount of evidence could satisfy them and it is notable that they do not raise the same objections to the epidemiological evidence linking moderate alcohol consumption to various cancers, most of which is weaker and all of which is susceptible to the same potential biases and confounding. This point was well made by two scientists when Tim Stockwell demanded an almost impossible burden of proof in 2013...
Nevertheless, the Sheffield authors believe that they have thrown enough mud to make some of it stick and conclude:
There is little consensus in the public health community about the presence of a cardioprotective effect, but the public health community should not be mistaken for the scientific community. There is little consensus in the anti-vaxxer community about the protective effect of vaccines and there will never be agreement from people like Tim Stockwell about the benefits of alcohol. Rather than waiting for a consensus amongst people who hate alcohol, let's trust the evidence.
First, let's familiarise ourselves with what the review found back in 1995:
'For a number of years studies have provided evidence that there is a relationship between moderate alcohol consumption and a reduced risk of death from all causes, and that this benefit was found in people who regularly consumed as little as 1 unit per day.'
'It is now established that the main specific pathology which benefits from alcohol consumption is coronary heart disease.'
'The epidemiological evidence alone linking alcohol and CHD now makes the existence of a protective effect appear very likely. The written and oral evidence received by the Group confirmed that most of the technical epidemiological criteria for a causal association are now fulfilled.'
'A key issue previously complicating the epidemiological data has been the so called “sick quitter” hypothesis outlined by Professor A G Shaper... However, a number of studies since 1987 have controlled for these factors so that we believe Professor Shaper’s reservations cannot be considered as a major explanation of the cardio-protective effect. Other confounding factors such as tobacco use, obesity, diet and age have now been controlled for in enough studies to allow us, on the basis of expert testimony, to be confident that the basic protective effect for CHD by alcohol is scientifically valid.'
'All the evidence we have received confirms that the relationship between all-cause mortality and alcohol consumption follows a J-shaped curve. Non drinkers have higher all-cause mortality than light and moderate drinkers, and heavy drinkers have even higher all cause mortality than either group.'
'All cause mortality is at its lowest at modest drinking levels (at about 1 unit a day for men and women) and does not exceed the mortality level of abstainers until consumption levels which are somewhat higher than the current recommended sensible drinking levels of 14 units per week for women and 21 units for men.'
Pretty clear, no? In addition to finding a clear relationship between moderate consumption and lower mortality risk - which could not be explained by confounding factors - the working group identified several plausible biological pathways which explained how the effect came about.
It is important to stress that the 'sick quitter' hypothesis - which says that unhealthy former drinkers could explain why teetotallers don't live as long - had already been tested extensively by 1995. In 2002, Richard Doll discussed it in an essay titled 'Proof of causality':
One possibility, that the non-drinkers included ex-drinkers who might have given up because of ill health, was excluded by cohort studies in which ex-drinkers and lifelong non-drinkers had been classed separately and by data like our own, which included information on past medical histories and showed the same proportional reduction in risk in drinkers irrespective of any previous history of vascular disease.
Another possibility was that drinkers might have differed from non-drinkers in other ways that would affect the risk of the disease, by, for example, including lower proportions of cigarette smokers, having a lower mean blood pressure and body mass index, a higher level of physical activity, or higher socioeconomic status (Shaper 1995). In fact, an association with smoking has the opposite effect to that postulated, as smoking is more prevalent in drinkers than in non-drinkers (Jarvis 1994), and allowance for it actually increases the evidence of benefit associated with drinking. In many studies it has been taken into account, as have all the other suspect factors in some of the more detailed studies, such as those by Stampfer, et al. (1988), and Thun, et al. (1997). When these factors were all allowed for, the observed differences were hardly altered.
Confounding, often a serious concern when risks vary by less than two-fold, has in this case been tested and found wanting... That the inverse relationship between ischemic heart disease and the consumption of small or moderate amounts of alcohol is, for the most part, causal should, I believe, now be regarded as proved (Doll et al. 1997).
In the last fifteen years, research has continued to show that the J-curve is not the result of 'sick quitters' or other confounding (eg. here, here, here, here and here). A meta-analysis of 34 prospective studies in 2006 showed a clear J-curve that could not be explained by 'sick quitters'. This is how epidemiology is supposed to work. People suggest alternative explanations, new studies test the alternative hypothesis and if the association survives all tests the relationship is assumed to be causal.
In any other field, the debate would have been put to bed years ago. It has been kept alive because many people in 'public health' desperately want to believe that alcohol has no (health) benefits. Almost unbelievably, Sally Davies described the J-curve as an 'old wives' tale' last week. She drew on a report she had commissioned from Sheffield University (the same people who devised the minimum pricing computer model). You can read it here.
The Sheffield report starts the campaign of doubt early in the main text when it mentions the protective effect of moderate drinking and says...
These effects are disputed,(10-13) may be overestimated (14-17) and are probably limited to particular groups within society (18) (see Section 5.4.1.2). If, as appears possible, scientific opinion develops to conclude cardioprotective effects are in fact overestimated and only occur up to very low levels of consumption (e.g. 5 units per week); one of the researchers responsible for the Canadian approach concluded that this would leave the Canadian guideline “in trouble”.(19)
It's worth looking at what all those references refer to:
(10) is an opinion piece in Addiction which discusses the same confounding variables which Doll said had been overcome in 2002.
(11) is a study that doesn't really 'dispute' the J-curve.
(12) is a letter from Tim Stockwell and friends responding to a meta-analysis in the British Medical Journal which found that the link between good cardiovascular health and moderate alcohol consumption was 'beyond question'. That meta-analysis is not cited in the Sheffield report at all, nor is the authors' reply which accuses Stockwell et al. of adopting 'an extreme methodological position, proposing to dismiss an entire body of literature on the basis of the presence of predictable limitations in individual studies. This dogmatic and dichotomous approach to the evaluation of epidemiological studies is counterproductive to scientific epistemology.' If you read Stockwell's letter, you will see that they have a point.
(13) is an opinion piece by Tim Stockwell and friends casting doubt on the alcohol-health link.
(14) is a study that clearly found lower heart disease risk among moderate drinkers.
(15) is a comment piece by Tim Stockwell and friends.
(16) is a revised meta-analysis by Tim Stockwell and friends which claimed that the protective effect of alcohol disappears when adjustments are made to the data and some studies are excluded.
(17) is a study which found that a gene associated with not drinking was also associated with better cardiovascular health.
(18) is a meta-analysis which concluded that 'some form of a cardioprotective association was confirmed in all strata' but that this 'cannot be assumed for all drinkers'. Its authors have since published a meta-analysis which found clear evidence of a J-curve, even when only lifetime abstainers were included (ie. no 'sick quitters').
(19) is a short opinion piece by (you guessed it!) Tim Stockwell.
There you have it - the case for the prosecution. Not quite a one man crusade by Tim Stockwell but not far off. Needless to say, you can find dissenting voices and contrary evidence in any field of research, but on the basis of these minority reports the Sheffield crew not only portray the science as highly contentious but also predict that the science will eventually agree with Tim Stockwell.
Towards the end of the report, the Sheffield boys and gals address the J-curve at more length. They start by acknowledging (but not referencing) the evidence...
An extensive literature including well-executed meta-analyses of high quality primary studies have found an association between moderate drinking and reduced risk of cardiovascular disease and particularly ischaemic heart disease.
There is a 'but' coming, of course...
This literature has attracted substantial debate regarding whether evidence is sufficient to conclude that low levels of alcohol consumption have a causal relationship with improved cardiovascular health. The debate includes detailed critique of both observational and meta-analytic studies, exploration of potential biological mechanisms explaining observed cardioprotective effects and arguments regarding the public health relevance of establishing the veracity of cardioprotective effects given alcohol’s undisputed risk for other diseases and the various alternative options for reducing cardiovascular risk.(10,12,13,17,94)
Those references are some of the articles and studies mentioned above plus a comment piece in Alcohol from 2007 which said 'In view of the potential risks of alcohol, a more cautious view about the beneficial effects of alcoholic beverages is warranted.' It is notable that all the citations given to prove the existence of a 'debate' here are from people on one particular side of the debate. This is a bias that permeates the Sheffield report. For example, no fewer than twelve Tim Stockwell publications are cited in the report, along with eight publications by John Holmes of Sheffield University. By comparison, there are zero citations of studies by people like Richard Doll who produced several studies showing (and testing) the J-curve, nor is there any mention of people like Di Castelnuovo who conducted the 2006 meta-analysis.
The Sheffield crew then proceed to give four possible reasons why this 'extensive literature' is wrong...
First, there is evidence that participants in epidemiological cohort studies may differ with regard to their underlying health status compared to the general population. One reason for this is such studies often recruit participants with no underlying health conditions at baseline. The resulting potential for bias was demonstrated in a major European prospective cohort study which included at baseline people with chronic disease. Risk estimates were calculated for both the whole cohort and for a subsample of the cohort who were free of chronic disease at enrolment. Relative risk of cardiovascular mortality was lowest in those with light to moderate alcohol use; however, this was only the case among the subsample free from chronic disease at enrolment. This suggests sample selection processes for typical cohort studies may disproportionately exclude those at cardiovascular risk from moderate drinking leading to overestimation of any cardioprotective effect.
This is a reference to this study which found that moderate drinkers had a 26-48 per cent lower risk of heart disease mortality. The study included graphs showing a clear J-curve for all-cause mortality (the one below is for men).
The protective effect for heart disease was only statistically significant for people who did not have a disease at the time of enrolment, but even among those who had a disease upon enrolment, heart disease risk was not higher.
Second, estimates of risk relationships between alcohol consumption and health conditions are commonly quantified by calculating the risk of a given level of consumption relative to the risk of zero consumption (i.e. abstention). In practice, this means assuming that, after controlling for a range of confounding factors such as age and gender, drinkers and abstainers only meaningfully differ in terms of their alcohol consumption and a narrow set of other factors.
That's what epidemiologists are supposed to do. Smokers are different to nonsmokers in ways that have nothing to do with tobacco. Promiscuous people are different to virgins. People who drink large quantities of sugary drinks are different to people who don't. This is why epidemiologists adjust for factors that might bias the results. Alcohol research is no different to any other type of observational research in that respect - and, as Doll pointed out, non-drinkers tend to lead healthier lifestyles than drinkers, therefore any bias likely leads in the opposite direction to what the Sheffield authors are implying.
Rather than explaining what it is about the characteristics of non-drinkers that invalidate alcohol research when the characteristics of smokers do not invalidate tobacco research, the Sheffield crew ignore all the studies that have tested for confounding variables and return the subject of sick quitters:
This assumption has been questioned and the characteristics of abstainers and their similarity to the general population have been closely scrutinised. Most significantly, the classification of former drinkers as abstainers has raised particular concerns, particularly where those former drinkers have stopped drinking due to health problems. Meta-analyses which disaggregate abstainers (e.g. never drinkers, former drinkers, occasional drinkers) have concluded that using a single abstainer category leads to overestimation of the cardioprotective effect of alcohol.(15,16,18)
Reference 15 and 16 are two similar studies from the pen of Tim Stockwell and friends. One is a revised meta-analysis which controversially claimed that the protective effect of alcohol disappears when studies are excluded and adjustments are made to the data. Reference 18 is a meta-analysis which concluded that 'some form of a cardioprotective association was confirmed in all strata' but that this 'cannot be assumed for all drinkers'.
It is certainly true that including 'sick quitters' biases the results and makes the J-curve look steeper than it is. That is why most studies in the last 25 years have excluded former drinkers and still find strong evidence of a J-curve. The Sheffield authors choose not to mention this or cite those studies, preferring instead to imply that this is an unanswered question.
Third, alcohol consumption is typically measured in epidemiological studies of long-term health risks as average daily consumption. However, recent evidence incorporating data on frequency of heavy drinking occasions (defined as more than 7.5 units on a single day) has shown an elevated ischaemic heart disease risk for moderate drinkers who have heavy drinking occasions at least once per month when compared to moderate drinkers with fewer heavy drinking occasions. Further analyses suggest any cardioprotective effect from moderate drinking may be attenuated or no longer present among those who have heavy drinking occasions at least monthly.
This was acknowledged in the government's 1995 report. It is why people are advised to drink moderately, not heavily. It does not mean that there is 'no safe level of drinking', nor does it mean that the protective effect is an 'old wives' tale'.
Fourth, alcohol consumption is only one of many variables which have a positive or negative association with an individual’s cardiovascular risk and it has been argued that “groups with different drinking habits differ in several other ways than their drinking, making it difficult to separate the effects of drinking habits from other factors”. For example, both increasing age and smoking status increase individual risk of ischaemic heart disease and estimated risk relationships for alcohol consumption can be adjusted to account for these confounding factors. However, a recent major meta-analysis noted substantial unexplained heterogeneity in risk estimates suggesting other important confounding factors were not controlled for.(18)
Reference 18 is the same study they have cited twice already. This point really just reiterates what was said earlier about there being differences between teetotallers and drinkers. In effect, they are saying that there might be some other factor that might make teetotallers die younger than drinkers but we don't know what it is. Well, there might be, just as there might be something about smokers which has nothing to do with smoking that makes them more likely to get lung cancer, but the temperance lobby has been hunting pretty hard for this mysterious explanation for a long time and come up empty-handed.
This is the sum total of their objections to the J-curve. Essentially, they are just saying 'confounding factors' over and over again without acknowledging that that question has been emphatically answered. It is difficult to see how any amount of evidence could satisfy them and it is notable that they do not raise the same objections to the epidemiological evidence linking moderate alcohol consumption to various cancers, most of which is weaker and all of which is susceptible to the same potential biases and confounding. This point was well made by two scientists when Tim Stockwell demanded an almost impossible burden of proof in 2013...
... it seems that some researchers in the field may be using different standards in assessing the cardioprotective effect of alcohol vs. its detrimental effect. Consider two examples. One is the effects of alcohol on colon cancer. Would the same arguments used to judge the relationship between alcohol and ischaemic heart disease not hold for this relation as well? The other example is the more than 200 other risk relations between alcohol and disease and injury outcomes. Of course, this is not a good argument against scrutinizing the cardioprotective effect of alcohol, but we sense a desire by some in the field to apply tough standards on protective effects and more lenient standards on other effects, where sometimes the responses to very simple survey questions such as ‘Did your partner’s alcohol consumption contribute to your marriage problems?’ are accepted as causal evidence.
Nevertheless, the Sheffield authors believe that they have thrown enough mud to make some of it stick and conclude:
Given these critiques, there is little consensus in the scientific community regarding the presence or size of any cardioprotective effect.
There is little consensus in the public health community about the presence of a cardioprotective effect, but the public health community should not be mistaken for the scientific community. There is little consensus in the anti-vaxxer community about the protective effect of vaccines and there will never be agreement from people like Tim Stockwell about the benefits of alcohol. Rather than waiting for a consensus amongst people who hate alcohol, let's trust the evidence.
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