Tag Archives: Alcohol

Cognitive Bias Modification for Addictive Behaviours

It can be difficult to change health behaviours. Good intentions to quit smoking or drink less alcohol, for example, do not always translate into action – or, if they do, the change doesn’t last very long. A meta-analysis of meta-analyses suggests that intentions explain, at best, a third of the variation in actual behaviour change.[1] [2] What else can be done?

One approach is to move from intentions to inattention. Quite automatically, people who regularly engage in a behaviour like smoking or drinking alcohol pay more attention to smoking and alcohol-related stimuli. To interrupt this process ‘cognitive bias modification’ (CBM) can be used.

Amongst academics, the results of CBM have been called “striking” (p. 464),[3] prompted questions about how such a light-touch intervention can have such strong effects (p. 495),[4] and led to the development of online CBM platforms.[5]

An example of a CBM task for heavy alcohol drinkers is using a joystick to ‘push away’ pictures of beer and wine and ‘pull in’ pictures of non-alcoholic soft drinks. Alcoholic in-patients who received just an hour of this type of CBM showed a 13% lower rate of relapse a year later than those who did not – 50/108 patients in the experimental group and 63/106 patients in the control group.[4]

Debate about the efficacy of CBM is ongoing. It appears that CBM is more effective when administered in clinical settings rather than in a lab experiment or online.[6]

— Laura Kudrna, Research Fellow

References:

  1. Sheeran P. Intention-behaviour relations: A conceptual and empirical review. In: Stroebe W, Hewstone M (Eds.). European review of social psychology, (Vol. 12, pp. 1–36). London: Wiley; 2002.
  2. Webb TL Sheeran P. Does changing behavioral intentions engender behavior change? A meta-analysis of the experimental evidence. Psychol Bull. 2006; 132(2): 249.
  3. Sheeran P, Gollwitzer PM, Bargh JA. Nonconscious processes and health. Health Psychol. 2013; 32(5): 460.
  4. Wiers RW, Eberl C, Rinck M, Becker ES, Lindenmeyer J. Retraining automatic action tendencies changes alcoholic patients’ approach bias for alcohol and improves treatment outcome. Psychol Sci. 2011; 22(4): 490-7.
  5. London School of Economics and Political Science. New brain-training tool to help people cut drinking. 18 May 2016.
  6. Wiers RW, Boffo M, Field M. What’s in a trial? On the importance of distinguishing between experimental lab studies and randomized controlled trials: The case of cognitive bias modification and alcohol use disorders. J Stud Alcohol Drugs. 2018; 79(3): 333-43.
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So Where Are We up to with Alcohol and Health?

First, let me come clean – I am a moderate drinker. No doubt about it. Five nights a week on a mean of two glasses, and two nights on a mean of three glasses. These are average sized glasses, so let’s say 24 units (1.5 x 16) per week. I love wine and seek good news…

The story so far:

  1. There is a ‘J-shaped’ curve of the association between alcohol and many diseases.[1]
    093 - Alcohol j curve
    * Cancer does not follow this pattern. Cancers of mouth, throat and gullet are almost certainly increased, and probably breast too.[2]
  2. But Mendelian randomisation (inheriting genes predisposing to alcohol consumption) does not show a J-shaped curve – risk rises incrementally.[3]
  3. Longitudinal studies show that, on one dimension of cognition, decline is faster in linear relationship to alcohol dose, and this finding ‘triangulates’ with a drop in right-sided hippocampal volume (detected by MRI) in relation to alcohol intake.[4]

Conclusion: the J-shaped curve is an artefact of selection bias.

So what’s new? First, a meta-analysis of longitudinal studies [5] shows a substantial protective effect against dementia for low to moderate alcohol intake (RR 0.63, 0.53-0.75) and also in Alzheimer’s disease (RR 0.57, 0.44-0.74). Second, there some evidence from these studies that chronic drinking is protective of cognitive decline, while episodic drinking is harmful at the same total intake. Third, a new longitudinal study suggests that chronic (i.e. non-binge) drinking is indeed protective against cognitive impairment in older people.[6]

This new study (the Rancho Bernardo study) is based on a cohort of 6,339 middle-class residents of a suburb in San Diego. Of the surviving residents, 2,479 attended a research clinic in 1985 where detailed alcohol histories were elicited. The participants were followed up every four years with cognitive tests. Co-variates were collected and added sequentially to a logistic regression model, starting with those (e.g. sex and age) least likely to be on the causal pathway linking alcohol to outcome. The APOE genotype was examined as an interaction term. Potential confounding effects of diet were also examined. Various sensitivity analyses were conducted. Drinking up to 3 units per day after age 65, and 4 units per day at a younger age significantly increased the chance of healthy survival, with an odds ratio exceeding 2. The J curve is there in the data, with the probability of healthy longevity increasing through no, low, moderate and even heavy drinking, only to decline again when drinking was ‘excessive’ (meaning over 4 drinks per day aged under 65 and over 3 per day for men over 65, and 3 or 2 drinks per day in younger or older women. And, yes, more frequent drinking is better than episodic drinking at a given intake – ORs of Cognitively Health Longevity increased three-fold with daily drinking vs. not drinking at all, but only two-fold if drinking was ‘infrequent’. Conclusions were robust to various sensitivity analyses.

What is the truth? No person knoweth it! But the idea that regular, moderate drinking offers some protective effects to trade-off against cancer risk has empirical support. I wonder if there are different genes predisposing to binge vs. steady drinking? I hypothesise that the genes are associated with poor impulse control leading to binge drinking. I hope that this hypothesis will now be put to an empirical test. Another question, of course, concerns the type of drink. The middle-class people in the Rancho Bernardo study may have favoured wine over other drinks – I hope so!

— Richard Lilford, CLAHRC WM Director

References:

  1. Di Castelnuovo A, Costanzo  S, Bagnardi  V, Donati  MB, Iacoviello  L, de Gaetano    Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies.  Arch Intern Med. 2006; 166(22): 2437-45.
  2. Lilford RJ. Oh Dear – Evidence Against Alcohol Accumulates. NIHR CLAHRC West Midlands News Blog. 7 December, 2017.
  3. Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. BMJ. 2014; 349: g4164.
  4. Lilford RJ. Alcohol and its Effects. NIHR CLAHRC West Midlands News Blog. 18 August, 2017.
  5. Peters R, Peters J, Warner J, Beckett N, Bulpitt C. Alcohol, dementia and cognitive decline in the elderly: a systematic review. Age Ageing. 2008; 37(5): 505-12.
  6. Richard EL, Kritz-Silverstein D, Laughlin GA, Fung TT, Barrett-Connor E, McEvoy LK. Alcohol Intake and Cognitively Healthy Longevity in Community-Dwelling Adults: The Rancho Bernardo Study. J Alzheimer’s Dis. 2017; 59: 803-14.

Oh Dear – Evidence Against Alcohol Accumulates

Yes, more research [1] [2] on alcohol – increases in cancers of mouth, throat and oesophagus. Not good places to have cancer. Direct contact of C2-H5-OH with the membrane is the likely causal mechanism. So here is an hypothesis – the more dilute a given amount of alcohol, the better. So I think beer > wine > spirits, ceteris paribus. I guess this has been tested? But next week I may have some more reassuring news for us oenophiles.

— Richard Lilford, CLAHRC WM Director

References:

  1. LoConte NK, Brewster AM, Kaur JS, Merrill JK, Alberg AJ. Alcohol and Cancer: A Statement of the American Society of Clinical Oncology. J Clin Oncol. 2017; 35: 1-11.
  2. The Lancet. Alcohol and cancer. Lancet. 2017. 390: 2215.

Alcohol and its Effects

News blog readers may be familiar with the famous ‘J curve’ relating alcohol consumption to health outcomes, including brain health.[1] The J curve shows a negative correlation between alcohol consumption and cognitive functioning at a low level of alcohol consumption (< 7 units/week), turning to a positive association in quantities exceeding about 28 units/week. One large glass of wine per day should be safe according to this finding. However, the data from which these findings are derived is cross-sectional. The BMJ has recently published a longitudinal study of alcohol and its effect on both cognition and brain structure (as measured by functional MRI).[2] The news is bad I am afraid. In the words of the editor, Fiona Godlee, ‘better’ research flattens the J curve.[3] The study seems to show a linear increase in risk with increasing intake of alcohol. The result was statistically significant for people drinking more than about two small glasses of wine per day. Why was a harmful effect at low dose detected in this longitudinal study but not the cross-sectional studies? So here is the thing – people with higher cognitive functioning tend to have higher alcohol consumption at baseline. In fact, the ‘cleverer’ the person, the more they tend to drink. The result is a difference in the findings of cross-sectional and longitudinal studies. While cross-sectional studies show no difference in cognition with moderate alcohol intake, the longitudinal studies show that cognition and brain structure decline at relatively low levels of alcohol consumption. To put this another way, moderate alcohol intake abolishes the cognitive advantage that moderate alcohol consumers have at baseline. Interestingly, not all parts of the brain are equally affected on MRI. Likewise the effect on cognition is not global; it affects lexical more than semantic fluency, for example. This is an extremely well-written, detailed and interesting study. The cohort of people who participated in the study were civil servants followed up for 30 years. The results are of immense public health importance. Human happiness, wealth and prosperity all relate to brain function. A person’s intellectual endowment is a precious gift and should not be lightly squandered.  I will take these findings too heart, both in my personal life and as a public health practitioner. It is really a question of long-term loss vs. short-term gain – alcohol is a pleasant social lubricant, much beloved of myself, and a small glass of wine has even been shown to improve creative problem-solving![4]

— Richard Lilford, CLAHRC WM Director

References:

  1. Di Castelnuovo A, Costanzo  S, Bagnardi  V, Donati  MB, Iacoviello  L, de Gaetano    Alcohol dosing and total mortality in men and womenArch Intern Med. 2006; 166(22): 2437-45.
  2. Topiwala A, Allan C, Valkanova V, et al. Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study. BMJ. 2017; 357:j2353.
  3. Godlee F. Better research flattens the J shaped curve. 2017; 357: j2755.
  4. Benedek M, Panzierer L, Jauk E, Neubauer AC. Creativity on tap? Effects of alcohol intoxication on creative cognition. Consciousness Cognition. 2017. [ePub].

Legalisation of Marijuana

Having borne down heavily on tobacco, it seems like everyone is now campaigning to make marijuana legal – are they mad?

A libertarian would say that there is no case to ban tobacco (or effectively ban it by draconian taxes on consumption). All tobacco can do is kill you, and as long as you know this you may use it. Marijuana is a different case altogether. It appears that it does not just kill you, it maims you – and not just your body, but you – your personality, your memory, your intelligence, i.e. your essence. And it is particularly attractive to teenagers – those with the most precious and vulnerable brains. Use is increasing in the US and has increased in association with decriminalisation, even if cause and effect is hard to prove.[1] Meanwhile a recent longitudinal cohort study found that persistent cannabis dependence was linked to downward socioeconomic mobility, financial difficulties, workplace problems, and relationship conflict.[2] It gets worse, the concentration of psycogenic compounds is increasing in the plant due to selective breeding. The attitude and fashion among liberal metropolitans “tobacco is vulgar, but marijuana is cool.” Have we gone mad? If we could confine the need to people over 18, and campaign against it, then over time we could reduce use. But a chemical that actually alters the structure of the adolescent brain and is more ubiquitous than boxing? We urgently need more information on the effects legalising cannabis has on usage. Also, more research on its effects on the brain using functional MRI. I wonder if Mendelian randomisation could shed light on causality?

— Richard Lilford, CLAHRC WM Director

References:

  1. Azofeifa A, Mattson ME, Grant A. Monitoring Marijuana Use In the United States: Challenges in an Evolving Environment. JAMA. 2016; 316:1765-6.
  2. Cerdá M, Moffitt TE, Meier MH, et al. Persistent Cannabis Dependence and Alcohol Dependence Represent Risks for Midlife Economic and Social Problems: A Longitudinal Cohort Study. Clin Psychol Sci. 2016; 4(6): 1028-46.