Why people (on the left and right) love conspiracies

“It was because he wanted there to be conspirators. It was much better to imagine men in some smoky room somewhere, made mad and cynical by privilege and power, plotting over the brandy. You had to cling to this sort of image, because if you didn’t then you might have to face the fact that bad things happened because ordinary people, the kind who brushed the dog and told their children bedtime stories, were capable of then going out and doing horrible things to other ordinary people. It was so much easier to blame it on Them. It was bleakly depressing to think that They were Us. If it was Them, then nothing was anyone’s fault. If it was Us, what did that make Me? After all, I’m one of Us. I must be. I’ve certainly never thought of myself as one of Them. No one ever thinks of themselves as one of Them. We’re always one of Us. It’s Them that do the bad things.”

Excerpt From

Terry Pratchett

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Zealotry, closed-mindedness

An extreme case is when someone says “no fact, no information could make me change my mind”.

A less extreme, and vastly more common, position is along the lines of “I would rather not listen to information that might lead me to reconsider” or “I will avoid, certainly not not seek out such information/views”. Or “I’ll ignore… deliberately not give this thinking time”.

And then there is “I’ll think ill of you if you say things that unsettle my beliefs. I’ll be offended by you.”

Or, even worse, “I’ll try to very hard to discredit you if you say things that unsettle my beliefs”.

Scientists, of all people, should be the most immune to this sort of thinking, but of course we are human, so not completely immune. Zealotry, closed mindedness, is something everyone needs work consciously to avoid.

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Does alcohol cause cancer ?

by Professor Byron Sharp

short answer: The scientific evidence is that alcohol helps cause (only) two cancers: aerodigestive and liver.  These are rare causes of death, so the increased chance that drinkers will die from these cancers is tiny.  A very large body of evidence continues to support a causal association between moderate drinking and longer life, due largely from less risk of diabetes and less risk of dying from heart disease.

sub-title: Can Good Intentions Corrupt Science?

Recently an article by a Kiwi Professor gained global press coverage with sensational headlines along the lines of “proof that alcohol causes cancer”.  This is a very significant claim which therefore deserves significant scrutiny.  Unfortunately in this case I’m afraid that there has been an abuse of science.  I’m very interested in the corruption of science, and science communication.  This doesn’t always arise from corrupt individuals – more common causes of  bias are good intentions, moral vanity, and a desire to please a dominant funding body.  That’s what it looks like here: perhaps a case of seeing what you want to see in the evidence, or perhaps even deliberately misusing the evidence to achieve a social/political objective (‘the ends justifies the means’)?

The scientific evidence suggests alcohol helps cause (only) two cancers, areodigestive and liver, though these are rare and the elevated risk of death is tiny.  It’s wrong and unethical to scare the public, and to misrepresent the medical evidence.

I’m going to document how Professor Jennie Connor’s article missed out important studies and misrepresented others (she even missed evidence that helps a part of her argument).

Connor’s Assertion

Connor’s conclusions are not based on new data, nor data analysis.  Her article was published in the journal Addiction‘s “for debate” section.  The article’s purpose was to examine whether it might be reasonable to consider the (weak) correlations seen in population studies as causal evidence that drinking alcohol increases your risk of cancer.

Connor says alcohol causes some cancers.  This conclusion is based almost entirely on epidemiological studies that show that in surveys of populations drinkers have slightly higher rates of some specific cancers (and slightly lower rates of a few others).  In doing so she places great faith in epidemiology, far more than many of her colleagues.  A more sober analysis would adopt the epidemiologists’ rule of not considering risk estimates of less than a factor of 3 as indicating any causality (see Taubes 1995 ‘Epidemiology faces its limits’, Science, 269:5221, 164-69), e.g. smokers  have more than 20 times the risk of lung cancer.   Unlike smoking, alcohol-cancer studies seldom report risk estimates anywhere near a factor of 3.

The well known problem with epidemiology studies is that they show correlations that are often not causal – they can be completely spurious due to confounding factors.  For example, population data might show that elderly people who exercise regularly tend to live longer.  But elderly people who are afflicted with debilitating health issues are very likely to exercise less (many will be simply unable to undertake exercise), so really it is health that is determining both the exercise as well as the longevity.  Exercise might well be doing good but the risk estimate (for not exercising) is going to be inflated.

The problem with comparing alcohol drinkers, of various levels, to lifetime non-drinkers is that alcohol drinkers tend to smoke more, and they also tend to be less likely to live in rural areas and more likely to be wealthier.  Moderate drinkers might be people who tend to be adopt other healthy behaviours, while heavy drinkers may be self-medicating because of mental or physical ill-health.  The ability for statistics to control for such confounding correlations is rather poor.  So there are plenty of reasons for caution in treating a correlation seen in population data as causal.  Here are some funny examples of real but non causal correlations.

Connor understands that confounds produce spurious correlations yet refrains from discussing any likely confounds in her assessment of whether alcohol causes cancer.  Instead she goes off on a tangent discussing possible confounds for the well established link between drinking and a (substantially) lower risk of heart disease.  Here she suddenly loses her faith in epidemiology, i.e. when she doesn’t like the results.  For Connor to even discuss heart disease is rather odd, given that her article is about cancer.  And to discuss confounds for heart protection but then to dismiss potential confounds for her claimed causal link with cancer is at best an abrogation of scientific scepticism.

Inferring Causality

In the absence of controlled experiments (which for cancer research are pretty much impossible for ethical and practical reasons) we need other evidence to support treating a correlation in population studies as causal.  Connor’s article makes 3 such points:

1. First, Connor says, there is a dose-response relationship between alcohol consumption and some cancers, that is, any increase in drinking is associated with increased cancer risk.  However, she then (rightly so) contradicts herself in pointing out that for most of these cancers meta-analysis shows no risk for light drinking.  Connor should have noted that some meta-analyses show heightened risk only for the heaviest level of persistent drinking (which is problematic, as this group may contain alcoholics and people drinking as self-medication for health problems, a confound completely ignored by Connor (and many others)).

2. Second, Connor notes “evidence that, for some cancers, the risk associated with alcohol attenuates when drinking ceases”.  Now this is what we would expect if there were a causal relationship, yet it is odd that in such population studies the correlation between drinking and cancer risk drops so slowly, taking decades before drinking cessation results in the small elevated risk subsiding to that of a non-drinker.  This suggests the apparent alcohol risks have more to do with confounding factors than a direct causal relationship (i.e. lifestyle factors that slowly regress to the mean).  Regardless, this evidence is of poor quality, to quote from one of the meta-analyses that Connor references “Too few studies have addressed this question, and of the studies that have, all have significant limitations” and further “the only statistically significant relationship that we observe is that drinkers who recently quit drinking have a higher risk of liver cancer than current drinkers”.  It would  be wrong to make much of this evidence, because the models have huge error margins, and anyway they are hardly supportive of a causal link between alcohol and cancer.

3. Third, Connor briefly discusses potential biological mechanisms for how alcohol might cause cancer.  Alcohol in itself is not carcinogenic to human cells, and the epidemiology shows associations with only some cancers and not others (indeed, drinking appears to be protective against some cancers).  As Connor writes: “The mechanisms by which alcohol causes cancer are not well understood, but are thought to depend upon the target organ. Pure ethanol does not act as a carcinogen in animal studies, and evidence that it causes mutations directly in humans is weak”.  A possible mechanism is that bacteria in the mouth and digestive tract convert alcohol to acetaldehyde, which is a carcinogen.  As Connor notes “Stronger associations and more susceptibility at low doses is seen for the cancers where alcohol and [hence] acetaldehyde come into direct contact with the tissues”.  She doesn’t mention that this potential bio-mechanism is supported by the evidence that people whose genes mean they are slow to break down acetaldehyde (somewhat common in Asia, very rare for West Europeans), have substantially higher rates of oral/throat (aerodigestive) cancers.  Other potential biological mechanisms, such as alcohol increasing estrogen levels, remain very speculative and face a number of difficulties, such as explaining why women who drink alcohol have lower, not higher, rates of endometrial cancer (Je et al 2014, Sun et al 2010).

So for aerodigestive cancers, we see the highest correlations in epidemiology data (though nowhere like the magnitude for smoking), and we have a plausible mechanism (the culprit being acetaldehyde).  Plus we can add the evidence that Connor missed – there are much higher rates of aerodigestive cancer among people who do not have the genes to quickly metabolise acetaldehyde (Seitz and Becker 2007).  This is by far the best case for making a causal connection between drinking alcohol and a cancer.  Though it must be noted that aerodigestive cancers are rare (eg a tiny 0.3% of US deaths are from oral cancers, and most of these are caused by smoking, age and genes) – even though most of the population drinks alcohol.

For the other cancers Connor mentions, the evidence of causality is extremely poor.  In contrast, the evidence is vastly more convincing that drinking alcohol moderately reduces heart disease, diabetes, dementia, and overall mortality.  In addition to meta-analyses of  many population studies, we have plausible biological mechanisms, supported by lab studies, animal experiments, and hospital trials.  Meta-analysis of dozens of experiments shows administering alcohol to subjects leads to rapid positive changes in biomarkers for heart health (Brien et al 2011).  We also see changes in drinking linked to changes in rates of heart disease, diabetes and overall mortality, e.g. people who increase their drinking lower their risk of heart disease.  In sum, this is what a plausible case for causality looks like.

So apart from aerodigestive and perhaps liver cancer, Connor is wrong, the evidence does not support the hypothesis that drinking alcohol causes cancer.  And even for oral/throat cancer, the risk may be confined to smokers and people with particular ALDH enzyme mutations.

Alcohol does not increase risk of dying from breast cancer

But that’s if we stop with Connor’s superficial analysis.  There is more evidence to consider if we are to form a proper judgement about causality.  Read on…

Connor concluded that drinking probably was causal for 7 cancers.  This has a nice ring about it…. like the 7 Deadly Sins.  Now, Connor used the old medical convention of labeling cancer according to where the tumour occurs.  It’s possible to talk of hundreds if not thousands of different cancers, but more reasonably it’s not seven.  It’s actually (1) oral/throat/oesophagus (aerodigestive cancers) which we have already discussed, (2) liver, (3) colorectal, and (4) breast cancer.  It’s this last one that drives most public health forecasts that reductions in drinking will reduce cancer deaths.  This is because breast cancer is the most common potentially deadly cancer for women.  That said, less than 3% of female deaths in the USA are from breast cancer.  90% of breast cancer diagnoses turn out not to be fatal, due to curative treatment but also because many breast cancer diagnoses are for non-fatal cancer – ‘over-diagnosis’ is a very real problem.

Breast cancer is a prime example of why Connor should have discussed evidence on confounding factors, and should have distinguished between diagnosis and mortality statistics.  Meta-analysis shows no link between drinking and breast cancer mortality, nor with recurrence (Gou et al 2013).  A new study from the Women’s Health Initiative (Lowry 2016) again shows no link between mortality and drinking before or after breast cancer diagnosis.  A smaller US study published in the same year showed the same thing, women who drank (at all levels from 1-36 standard drinks per week) before their breast cancer diagnosis had no higher risk of dying from the cancer than the non-drinkers (Din et al 2016).  Similarly a large study with long follow-up of women with breast cancer (Newcomb et al 2013) showed breast cancer patients had better chances of survival if they were regular drinkers before diagnosis.  If they altered their drinking after diagnosis this did not alter their chance of dying from breast cancer.  But an increase in drinking was associated with an overall increase in life expectancy (largely due to substantially fewer heart disease deaths among those who increased their alcohol consumption).  This is strong causal evidence that alcohol prevents heart disease, and it seriously conflicts with the idea that alcohol causes breast cancer.

Similarly while animal experiments show that alcohol consumption results in less heart disease, and longer life overall, they do not show a link between alcohol consumption and breast cancer (see Hackney et al 1992, Singletary 1997).  Alcohol actually reduced the risk of breast cancer metastasis in mice (Vorderstrasse et al 2012).

The (weak) correlation seen in population studies between drinking and breast cancer diagnosis is then probably due to a confounding factor, as so often can happen in population studies.  In this case it is probably simply that drinkers are more likely to screen for breast cancer (shown in Mu and Mukamal 2016) – screening definitely increases diagnosis.  Women from lower socio-economic superbs are less likely to drink and less likely to be screened for cancers (see here).  Land et al 2014, which screened all their subjects (i.e. controlling for screening incidence), showed no link between drinking and breast cancer – indeed drinking was associated with slightly less risk of diagnosis (of both breast and colon cancer).

Colorectal cancer?

The modest degree of increased risk of colorectal cancer for alcohol drinkers may also be spurious or exaggerated for the same reason – drinkers screen more, which results in more diagnoses.  As far as a potential biological mechanism, some fecal bacteria have been shown (in lab studies) to convert alcohol to acetaldehyde (Jokelainen et al 1994).  But then other bacteria have been shown to break down acetaldehyde (Nosova et al 2000) – the flora of the human gut are complex and not well researched.  Acetaldehyde has been shown to exist in the colons of rats but the level was not affected by feeding the rats alcohol (Seitz et al 1990).  Research is needed to see if drinking really can increase acetaldehyde levels in the colon.  In humans alcohol is absorbed in the stomach and small intestine which makes it harder to explain how alcohol might reach the colon where it might be converted to acetaldehyde by bacteria.  Whereas the risk of oral cancer is much higher among people without the genes to produce some acetaldehyde processing enzymes, this does not appear to be the case for colorectal cancer (Tiemersma et al 2003) (though the link between drinking and colorectal cancer is highest in Asian studies while barely statistically significant in Europe/America/Australia (Fedirko et al 2011)).  So a causal link between drinking alcohol and colorectal cancer remains speculative, and if there is a link, it is not strong – drinkers still get colorectal cancer at much the same rate as non/rare drinkers.

Liver Cancer?

That leaves us only with liver cancer remaining to be discussed.  This is a rare but deadly cancer, causing 1% of deaths in the USA, though most cases are due to viral infection (hepatitis), then obesity, diabetes, other disease, and genetics.  We perhaps again have the plausible biological mechanism of acetaldehyde but only at high levels of drinking as the liver is very efficient and fast at breaking down acetaldehyde.   It’s more plausible that alcohol, through its effect on liver disease, leads to higher risk of liver cancer.  However very few drinkers develop liver disease, so the degree of absolute increase in risk in absolute terms is tiny and probably only for long-term alcoholics or those unlucky enough to have liver damage from hepatitis or other causes.

Alcohol is a surprisingly benign hepatotoxin (i.e. the liver is remarkably good at dealing with it).  In mice and rat laboratory studies it isn’t possible to induce cirrhosis from alcohol alone, and this may be the case for humans as well.


Drinkers live longer.  Do they die more from cancer?

So it’s plausible that alcohol contributes to two cancers, both rather rare, and its influence can’t be great.  If this conclusion is correct then we would not expect drinkers to die much more often from cancer, and this is exactly what is observed in longitudinal population studies.  Meta-analyses of mortality studies report cancer death is barely higher among drinkers than occasional/zero drinkers, and confined to the cohort who admit to consumption of more than 50g of alcohol per day (see Jin et al 2012, table 2) which is very probably an under-estimate of actual consumption.  In Thun et al 1997 (a study of death among middle class, middle aged and elderly Americans) the heaviest drinkers showed higher rates of death from alcoholism and injury, as expected; they were also more likely to die from aerodigestive and liver cancer, again as we now expect, though none of these deaths were common; as expected, they were less likely than non/light drinkers to die from heart disease, stroke and other circulatory disease (each of which were major causes of death); there was no consistent relationship between rates of drinking and rates of death from colorectal or breast cancer, as we now should expect.  So the evidence fits together – drinking alcohol might ever so slightly increase the risk of dying from aero-digestive or liver cancer, that’s all.

Finally, it is worth noting that there is one clear way in which drinking alcohol (at least to non-alcoholic levels) increases your chance of getting cancer, and that is through its effect on living longer.  For most cancers, age is the dominant ’cause’ (e.g. half of all colorectal cancers occur in people aged over 70 years old, half of breast cancers are for women aged over 62).  Drinkers live longer, largely due to reduced levels of heart disease (also diabetes, and dementia).  Perhaps it’s also due to drinkers being more social or some other beneficial behaviours – but whatever the mechanisms, drinkers live longer and will therefore will survive long enough to get more cancer – because everyone has to die from something and the incidence of the vast majority of cancers increases substantially with age.  This fact alone is enough to produce an association, but not a direct causal one, between drinking and cancer.


Thanks to these people for helping improve my earlier drafts:

Dr Nick Danenberg, Ehrenberg-Bass Institute for Marketing Science, University of South Australia.

Ian Olver, Professor of Translational Cancer Research, Director Sansom Institute for Health Research, University of South Australia.

Philippa Martyr, Communications and Research Officer, North Metropolitan Health Service Mental Health; Adjunct Senior Research Fellow, Psychiatry and Clinical Neurosciences, University of Western Australia.

Wiemer Snijders, consultant, The Commercial Works, Netherlands.

Malcolm Wright, Professor of Marketing, Massey University, New Zealand.

Copies were emailed to Prof Jennie Connor at her Otago University email address on 8th and 24th of August, inviting her to correct any errors or omissions.  She has not yet replied.



Bagnardi et al (2015) “Alcohol consumption and site-specific cancer risk: a comprehensive dose–response meta-analysis” in British Journal of Cancer 112, 580–593 | doi: 10.1038/bjc.2014.579.

Brien, Susan et al (2011) “Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of international studies”, in British Medical Journal, BMJ 2011;342:bmj.d636

Connor, Jennie (2016) “Alcohol consumption as a cause of cancer”, in Addiction, “For Debate” section. doi:10.1111/add.13477

Din N; Allen IE; Satariano WA; Demb J; Braithwaite D. (2016) “Alcohol consumption and mortality after breast cancer diagnosis: the Health and Functioning in Women study”,   Breast Disease Vol 36, No 2-3, 2016, pp77-89.

Fedirko, Tramacere, Bagnardi, Rota, Scotti, Islami, Negri, Straif, Romieu, La Vecchia, Boffetta & Jenab (2011) “Alcohol drinking and colorectal cancer risk: an overall and dose–response meta-analysis of published studies” in Annals of Oncology 22: 1958–1972, doi:10.1093/annonc/mdq653

Gou, Xie, Yang, Liu, Zhang, Li, and He (2013) “Alcohol Consumption and Breast Cancer Survival: A Meta- analysis of Cohort Studies”, in Asian Pacific Journal of Cancer Prevention, Vol 14, No 8, pages 4785-4790. DOI:http://dx.doi.org/10.7314/APJCP.2013.14.8.4785

Je, DeVivo and Giovannucci (2015) “Long-term alcohol intake and risk of endometrial cancer in the Nurses’ Health Study, 1980–2010”, in British Journal of Cancer (2014) 111, 186–194 | doi: 10.1038/bjc.2014.257

Jin, Cai, Guo, Zhu, Li, Yu, Zhang and Chen (2012) “Alcohol drinking and all cancer mortality: a meta-analysis” in Annals of Oncology 24: 807–816, 2013 doi:10.1093/annonc/mds508


Jokelainen, Roine, Vaananen, Farkkila, Salaspuro (1994) “Invitro acetaldehyde formation by human colonic bacteria”, in Gut, 35: 1271-1274


Hackney, John F.  and Robert W. Engelman & Robert A. Good (1992) “Ethanol calories do not enhance breast cancer in isocalorically fed C3H/Ou mice”, in Nutrition and Cancer, 18:3, 245-253, DOI: 10.1080/01635589209514225


Land, Liu, Wickerham, Constantino, and Ganz (2014) “Cigarette smoking, physical activity, and alcohol consumption as predictors of cancer incidence among women at high risk of breast cancer in the NSABP P-1 Trial”, in Cancer Epidemiology Biomarkers and Prevention, 23(5): 823–832. doi:10.1158/1055-9965.EPI-13-1105-T

Lowry, Sarah J.  and Kris Kapphahn, Rowan Chlebowski, and Christopher I. Li (2016) “Alcohol Use and Breast Cancer Survival among Participants in the Women’s Health Initiative”, in Cancer Epidemiology, Biomarkers and Prevention, 25(8); 1268–73. doi: 10.1158/1055-9965.EPI-16-0151

Mu L, and KJ Mukamal (2016) “Alcohol consumption and rates of cancer screening: Is cancer risk overestimated?”, in Cancer Causes Control, Feb, 27(2):281-9. doi: 0.1007/s10552-015-0692-3.

Newcomb Polly A. and Ellen Kampman, Amy Trentham-Dietz, Kathleen M. Egan, Linda J. Titus, John A. Baron, John M. Hampton, Michael N. Passarelli, and Walter C. Willett (2013) “Alcohol Consumption Before and After Breast Cancer Diagnosis: Associations With Survival From Breast Cancer, Cardiovascular Disease, and Other Causes” in Journal of Clinical Oncology, DOI: 10.1200/JCO.2012.46.5765

Nosova, H. Jousimies-Somer, K. Jokelainen, R. Heine, M. Salaspuro (2000) “ACETALDEHYDE PRODUCTION AND METABOLISM BY HUMAN INDIGENOUS AND PROBIOTIC LACTOBACILLUS AND BIFIDOBACTERIUM STRAINS”, in Alcohol and Alcoholism, DOI: http://dx.doi.org/10.1093/alcalc/35.6.561 561-568

Seitz, HK, and Becker P. Alcohol Metabolism and Cancer Risk. Alcohol Research & Health. 2007;30(1):38-47

Singletary, Keith (1997) “Ethanol and Experimental Breast Cancer: A Review”, in Alcoholism: Clinical and Experimental Research, Vol. 21, No. 2. pp 334-339.

Sun Q, Xu L, Bo Zhou, Wang Y, Jing Y, Wang B (2011) “Alcohol consumption and the risk of endometrial cancer: a meta-analysis”, Asia Pacific Journal of Clinical Nutrition, 20(1): 125–133.

Taubes, Gary (1995) “Epidemiology faces its limits”, in Science, 269:5221, 164-69.

Thun, Petro, Lopez, Monaco, Henley, Heath and Doll (1997) “ALCOHOL CONSUMPTION AND MORTALITY AMONG MIDDLE-AGED AND ELDERLY U.S. ADULTS”, in The New England Journal of Medicine, Vol.337, No.27.

Vorderstrasse, B.A., Wang, T., Myers, A.K., Katherine L. Wyrick and Gary G. Meadows (2012) “Alcohol consumption suppresses mammary tumor metastasis in a syngeneic tumor transplantation model”, in Breast Cancer Research and Treatment 136: 729. doi:10.1007/s10549-012-2275-2

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Misleading alcohol cancer statistics

UK Cancer Research’s blog published a post saying that the public didn’t know much about the cancer risks of drinking alcohol.  They reached this conclusion by surveying people on the risks of individual cancers, for example, 80% of people said they thought alcohol increased the risk of liver cancer (UKCR gave them good marks for this but didn’t class this as important because almost no one gets alcohol induced liver cancer (a mere 400 cases a year in the UK)).  Whereas only 18% of people linked alcohol to breast cancer (when it’s supposed to cause 3,200 cases a year).

UKCR also said that people weren’t aware of the UK’s drinking guidelines and concluded that more needed to be done educating the public on the cancer risks of alcohol (a not so subtle call for more donations?).

I posted this comment in reply:

Telling people about estimated risks of drinking for individual cancers is likely to confuse people.  For them to then calculate their own risk they need to also know their risk of being afflicted with that individual cancer.

It would be better to instead tell people of the modest risk of being diagnosed with any cancer if they drink heavily (eg Allen 2009), yet this would also be misleading because many cancer diagnoses (eg breast, prostate) are false or for benign/indolent cancers.  So it would be more correct to tell them how much drinking might increase their chance of dying from a cancer (eg Gou et al 2013 which shows no risk for breast cancer death), or better yet dying from any cancer (eg Jin et al 2013).  But this would still be misleading because cancer is only one cause of death (and not so such a risk for younger people).

So it would be more responsible to tell the public about the evidence on drinking and life expectancy, and on their chances of ‘ageing successfully’ (without the impairment of chronic diseases like diabetes and dementia).  Understandably, this is what most people want to know.  The evidence here is that regular drinking of alcohol has a positive, that’s not negative, association with life expectancy (eg Doll et al 2005, Di Castelnuovo 2006) and disease-free ageing (eg Sun et al 2011), up to levels of daily alcohol consumption far higher than the current UK guidelines.  And, as one important part of a small suite of healthy behaviours that, in combination, have a dramatic association with disease-free survival (Khaw et al 2008, Ford et al 2011).

To not tell the public this is misleading.  But to instead confuse them with far less important statistics about individual cancers, while well meaning, is not responsible.


PS Non-alcoholic alcohol drinkers live longer than non-drinkers, and are less likely to die from heart disease.  Logically then they should be more likely to die from cancer simply because everyone has to die from something.

For a comprehensive analysis of alcohol and health research see Tony Edwards’ excellent book.

This article was not funded, commissioned or paid for by anyone.


Allen et al 2009 in Journal of the National Cancer Institute – a prospective cohort study of 1.2 million UK women (“the Million Women Study”).  Results: Compared to very light drinkers (less than 2 drinks a week) women drinking up to 3 times as much had 2% increase of cancer diagnosis, women drinking up to 7 times as much had a 5% increase in relative risk, and the heaviest drinking 5% of women had a 15% increase in relative risk of cancer diagnosis.  Though this result is largely due to breast cancer diagnoses (and most of these cases are not deadly, many are benign).  Other interesting findings include no link to liver cancer for wine drinkers.  No link to oral/throat cancer for non-smokers who drink.  And reductions in risk for some cancers (such as Non-Hodgkin lymphoma among the heaviest two levels of drinking).

Gou et al 2013 in Asian Pacific Journal of Cancer Prevention, Vol 14 – meta analysis of 25 cohort studies across nine countries.  Results: no association between alcohol consumption (pre and post diagnosis) and breast cancer mortality, nor with breast cancer recurrence after treatment.

Jin et al (2012) in Annals of Oncology, 24: 807-816 – a meta-analysis of 18 cohort studies examining alcohol consumption and risk of dying from any cancer.  The data included 48,000 deaths from cancer in the studies.  Results: A j-shaped relationship between drinking and cancer mortality was found.  Light and moderate drinkers either had less risk, or no elevated risk compared with non/occasional drinkers.  Overall drinkers (at any level) had a very small (5%) increased risk of dying from cancer, compared to non drinkers.  There was a tiny (4%) elevation in risk at around (claimed) consumption of 30g per day, while heavy consumption (more than 50g a day) was associated with a modest 30% higher risk.

Khaw et al (2008) in PloS Med, 5(1):12 – a prospective study of 20,000 people aged 45-79 in the UK examining four healthy behaviours (non-smoking, exercise, drinking, eating fruit and veg) and mortality risk.  Conclusions: Four health behaviours combined predict a 4-fold difference in total mortality in men and women, with an estimated impact equivalent to 14 y in chronological age.  Several other studies of combinations of healthy behaviours show very similar results.

Klatsky et al (2015) in The Permanente Journal, Spring 2015, Vol.19 No.2 – cohort study of 125,000 people over almost 30 years.  Results: compared to lifelong abstainers daily drinkers were 10-20% more likely to be diagnosed with cancer, no results were reported for lighter, less frequent drinkers.



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The Enlightenment can’t be stopped

Once upon a time the people who opposed freedom of speech, votes/rights for women, and the enlightenment in general were the rich and powerful. Particularly church leaders. In spite of their immense power and resources it was an argument that they would progressively lose.

Today, Islamist extremists like Boko Harem are the ones trying to wind the clock back on enlightened values. They will lose just like the Popes and Kings of the past.

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Ideology does make people do bad things

The Secular Party of Australia have called this week’s Martin Place hostage taking an act of Islamic terrorism. A number of their followers on Facebook, who presumably are normally happy for the Secular Party to point out the problems caused by religious belief, are this time uncomfortable with saying that religion was a motivation for this crime. They argue that he was a mentally ill person and that this was the cause.

Now, of course most Muslims are peaceful people. And disapprove strongly about this crime incident. However the same can be said for most people who suffer mental illness. Most people who suffer from even very serious mental illness do not approve of ISIS, nor hate the Australian govt for fighting against the attempt by ISIS to forcibly take over Iraq.

So even if mental illness played a role here it did so along with religious belief. They are undoubtedly a dangerous combination. And sadly probably have a tendency to occur together.

Furthermore, in defence of the Secular Party’s comment, the hostage taker himself said his actions were motivated by Islam. It seems presumptuous of people to ignore this, to ignore the consistency with his behaviours, but to assume mental illness.

If he had a Mohawk haircut and maintained a right-wing blog then no one would doubt that his ideology played a crucial role (even if he was mentally ill) in his chosen actions. What he instead did was make trembling hostages hold up a flag that said “Allah is the one true God and Mohammad is his messenger” and so on. To argue that this has nothing to do with religious ideology seems wrong or disingenuous.

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Why all the attention on Gaza?

I find it hard to understand the press fascination with Gaza.  And the anti-Israel feeling that gets whipped up.

 It’s not a large conflict.  More people have been killed in the Ukraine recently and this civil war has received less coverage (even with the jet airliner shooting).
On one side of the conflict in Gaza there are some religious nuts and local gang-leaders (among the many civilians who would rather get on with their lives in peace).  There are many young religious men.  Who are happy to build tunnels and shoot rockets even though this is purely terrorism, they can never win a war against the most advanced military power (a nuclear one at that) in the region.  But they hold out hope of all Muslims rising up and wiping the Jews off the earth (so they can move onto the next group of infidels?).
On the other side is a democratic state with elected leaders who have to do something when rockets are fired.  Their voters include moderates who say “just clean up after the suicide bomber, don’t give them publicity, just everyone keep calm and carry on”.  But also hawks (some religious nuts) who argue for extreme military response.  The average person on the street puts a lot of pressure on politicians when they fear that their children might be bombed tomorrow.
Of course, it is terrible that Israel’s action results in the killing of innocent civilians.  But there is plenty of evidence of considerable restraint.  They could wipe out Gaza in a week, but they don’t.
What would English government do if a well armed group of French Catholics (Guy Fawkes’ heirs) had an enclave in Tyburn and were shooting rockets at the rest of London to avenge their martyrs?
It’s like Northern Ireland, it will never be solved until the leaders of Gaza have the political power to sit down and negotiate a peace.  For a long time now they have been unable to.  Arafat was corrupt, but there was probably more hope than now under Hamas.  Any agreement they make will be instantly broken by a substantial number of people who are committed to war with Israel for ideological (religious) reasons and for practical reasons (their power over people in Gaza depends on this conflict).  It was like this in Northern Ireland for decades until the people got tired of all the death and finally the moderates gained political control over the IRA.
I suspect that American negotiations, and special envoys like Tony Blair only made the situation worse.  They give it oxygen.  They give the nutters an important stage to stand on.  Northern Ireland was resolved during Blairs tenure but I suspect that was just good timing. The result of decades of changes on the ground.  Of course Tony sees it differently and thinks he can work wonders in Gaza.
Again, I’m surprised how much press (and politician) attention given to each of these little conflicts.  When there are far larger religious wars raging in the Middle East and Africa.  Wars that have the potential to create terrorist states.
This article reflects my personal views. It was not commissioned or paid for by anyone.
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