Comment
kinase,8 for example, have not shown analgesic efficacy in randomised clinical trials. Hence, direct translational research still awaits its breakthrough. One potential reason for the scarcity of translational success is that preclinical efficacy is mainly assessed on the basis of spinal reflex behaviour in animals, which does not capture the multidimensional chronic pain experience in human beings.9 Despite this, the preclinical studies of AT2R inhibitors published so far have shown efficacy on standard paw withdrawal thresholds and latencies to mechanical and thermal stimuli, while no cerebral-dependent behaviour has been investigated.4,5 However, problems with the use of reflex responses might be different in studies of peripherally and centrally acting drugs. Another potential reason for the apparent lack of success in translational pain research is the failure of clinical trials to show efficacy of analgesics. The study by Rice and colleagues1 has optimised the assay sensitivity in several ways, such as by including patients with postherpetic neuralgia—a patient group that have low placebo responses10—and by using an algorithm, masked to the patients and study staff, that excludes patients with highly variable or extreme baseline pain scores.11 Rice and colleagues’ study is well designed and executed, and while the results need to be reproduced, they are promising. Although the average effect size was small, roughly a third of the patients randomly allocated to EMA401 responded with more than 50% pain reduction, and the side-effect profile suggests that higher doses might be tolerated. Further studies that assess the optimum dose, possible predictors of response, and efficacy in combination with other neuropathic pain analgesics are warranted, as are studies of long-term efficacy and safety. On the basis of the proposed mechanism of action and positive results from preclinical models, it is reasonable to postulate
that AT2R antagonists could also be effective in other neuropathic pain disorders, such as peripheral nerve injury and chronic inflammatory pain.4,5 *Nanna Brix Finnerup, Cathrine Baastrup Danish Pain Research Center, Aarhus University, 8000 Aarhus C, Denmark fi[email protected] NBF has received honoraria for consulting or speaking from Astellas, Pfizer, Norpharma, and Grünenthal, and research support from Grünenthal. NBF and CB are members of the EUROPAIN project funded by the Investigational Medicines Initiative, a public–private partnership between the European Union and the European Federation of Pharmaceutical Industries and Associations (EFPIA); EFPIA’s partners are AstraZeneca, Boehringer Ingelheim, Pfizer, Eli Lilly, Esteve, UCB Pharma, Sanofi-Aventis, Grünenthal, Neuroscience Technologies, Astellas, and Abbott. 1
2 3 4
5
6
7
8
9 10
11
Rice ASC, Dworkin RH, McCarthy TD, et al, for the EMA401-003 study group. EMA401, an orally administered highly selective angiotensin II type 2 receptor antagonist, as a novel treatment for postherpetic neuralgia: a randomised, double-blind, placebo-controlled phase 2 clinical trial. Lancet 2014; published online Feb 5. http://dx.doi.org/10.1016/ S0140-6736(13)62337-5. Finnerup NB, Sindrup SH, Jensen TS. The evidence for pharmacological treatment of neuropathic pain. Pain 2010; 150: 573–81. Steckelings UM, Kaschina E, Unger T. The AT2 receptor—a matter of love and hate. Peptides 2005; 26: 1401–09. Smith MT, Woodruff TM, Wyse BD, et al. A small molecule angiotensin II type 2 receptor (AT2R) antagonist produces analgesia in a rat model of neuropathic pain by inhibition of p38 mitogen-activated protein kinase (MAPK) and p44/p42 MAPK activation in the dorsal root ganglia. Pain Med 2013; published online June 6. DOI:10.1111/pme.12157. Chakrabarty A, Liao Z, Smith PG. Angiotensin II receptor type 2 activation is required for cutaneous sensory hyperinnervation and hypersensitivity in a rat hind paw model of inflammatory pain. J Pain 2013; 14: 1053–65. Kalliomaki J, Jonzon B, Huizar K, et al. Evaluation of a novel chemokine receptor 2 (CCR2)-antagonist in painful diabetic polyneuropathy. Scand J Pain 2013; 4: 77–83. Goldstein DJ, Wang O, Gitter BD, Iyengar S. Dose-response study of the analgesic effect of lanepitant in patients with painful diabetic neuropathy. Clin Neuropharmacol 2001; 24: 16–22. Ostenfeld T, Krishen A, Lai RY, et al. Analgesic efficacy and safety of the novel p38 MAP kinase inhibitor, losmapimod, in patients with neuropathic pain following peripheral nerve injury: a double-blind, placebo-controlled study. Eur J Pain 2013; 17: 844–57. Vierck CJ, Hansson PT, Yezierski RP. Clinical and pre-clinical pain assessment: are we measuring the same thing? Pain 2008; 135: 7–10. Cepeda MS, Berlin JA, Gao CY, et al. Placebo response changes depending on the neuropathic pain syndrome: results of a systematic review and meta-analysis. Pain Med 2012; 13: 575–95. Dworkin RH, Turk DC, Peirce-Sandner S, et al. Considerations for improving assay sensitivity in chronic pain clinical trials: IMMPACT recommendations. Pain 2012; 153: 1148–58.
Worldwide prevalence of non-partner sexual violence Published Online February 12, 2014 http://dx.doi.org/10.1016/ S0140-6736(13)62333-8 See Articles page 1648
1614
Non-partner sexual violence denotes that a person has been forced to have sex or to perform a sexual act when he or she did not want to, by anyone other than an intimate partner (eg, acquaintances, colleagues, friends, family members, military personnel, police, teachers, or strangers).1,2 Multicountry studies and
reviews have shown that 0·3–11·5% of women report having experienced non-partner sexual violence at some point during their lifetime.1,3 In The Lancet, Naeemah Abrahams and colleagues4 report a systematic review, controlled for confounding, of 7231 studies that yielded 412 estimates of the prevalence of non-partner www.thelancet.com Vol 383 May 10, 2014
sexual violence in 56 countries. The study is a landmark in its scale and rigour and offers a unique evidence base that confirms the need to address this public health challenge and violation of human rights worldwide. The authors estimate that during 1998–2011, 7·2% (95% CI 5·2–9·1) of women aged 15 years or older had ever experienced non-partner sexual violence. This estimate has substantial political and scientific importance and, for both reasons, warrants comment. Abrahams and colleagues also give some attention to comparisons of regional estimates for non-partner sexual violence. The highest estimates were in central (21%, 95% CI 4·5–37·5) and southern (17·4%, 11·4–23·3) sub-Saharan Africa. The lowest prevalence was seen in south Asia (3·3%, 0–8·3). Like other researchers,2 however, Abrahams and colleagues note that regional variation in levels of non-partner sexual violence should be interpreted with caution because of uncontrolled and potentially meaningful differences between the samples (purposively selected vs probability based), research tools (single vs multiple questions), periods of exposure (lifetime vs previous year), and survey designs (multipurpose vs violence specific). Moreover, four regions each had fewer than six estimates; only one estimate was available for central sub-Saharan Africa from one country in conflict (Democratic Republic of the Congo), and the meta-analysis controlled for few confounders. The authors identified the regions with the highest and lowest estimated prevalence of non-partner sexual violence even when the respective CIs overlapped with those for all or most other regions. Thus, because most adjusted regional estimates do not differ significantly, and higher estimated prevalence emerges from regions that have more datapoints, ranking regions on estimates of nonpartner sexual violence might not be warranted. Abrahams and colleagues note that their systematic review had conceptual and methodological challenges owing to differences between the included studies, which could affect the quality of the derived estimates. For instance, one challenge is the use of variable definitions for non-partner sexual violence.5 The term includes a range of victim-perpetrator relationships, sexual acts, and forms of coercion and contexts of vulnerability,1 but 91·5% of studies included relied on single general questions that related to forced sex or forced sexual acts against a woman’s wishes. The non-specificity about the range of potential perpetrators and acts might www.thelancet.com Vol 383 May 10, 2014
Simon Maina/AFP/Getty Images
Comment
substantially underestimate the scale of non-partner sexual violence against women. Despite these elements of caution, the major contribution of this study is its comprehensive inclusion of data to derive best estimates for the worldwide prevalence of non-partner sexual violence against women. An estimated prevalence of 5·2–9·1% is unacceptably high on public health and human rights grounds and, hopefully, will spur timely and systematic discussions about the use of standard definitions and improved research tools and data collection methods to improve disclosure of a highly stigmatised violation. Non-partner sexual violence has far reaching but underdocumented consequences for the social, economic, and health-related wellbeing of women and societies,4 and observed effects in conflict settings have unclear generalisability.6,7 Overall, these new estimates for non-partner sexual violence reflect responsible reporting of findings on an often sensationalised and oversimplified topic,8 which permits evidence-based responses. The data confirm that nonpartner sexual violence is neither rare nor geographically isolated9 and, thus, that existing laws and systems of accountability remain inadequate.10,11 Effective responses will require widespread legal and institutional change. Kathryn M Yount Hubert Department of Global Health, Emory University, Atlanta, GA 30322, USA [email protected] I declare that I have no competing interests.
1615
Comment
1 2 3
4
5 6
Dartnall E, Jewkes R. Sexual violence against women: the scope of the problem. Best Pract Res Clin Obstet Gynaecol 2013; 27: 3–13. Vanwesenbeeck I. Sexual violence and the MDGs. Int J Sex Health 2008; 20: 25–49. García-Moreno C, Jansen HA, Ellsberg M, Heise L, Watts C. WHO multi-country study on women’s health and domestic violence against women: initial results on prevalence, health outcomes and women’s responses. Geneva: WHO, 2005. Abrahams N, Devries K, Watts C, et al. Worldwide prevalence of nonpartner sexual violence: a systematic review. Lancet 2014; published online Feb 12. http://dx.doi.org/10.1016/S0140-6736(13)62243-6. Lawry L, Reis C, Kisielewski M, Asher J. Problems in reporting sexual violence prevalence. Am J Public Health 2011; 101: 2004–05. Johnson K, Scott J, Rughita B, et al. Association of sexual violence and human rights violations with physical and mental health in territories of the Eastern Democratic Republic of the Congo. JAMA 2010; 304: 553–62.
7
8 9 10
11
Watts CH, Foss AM, Hossain M, Zimmerman C, von Simson R, Klot J. Sexual violence and conflict in Africa: prevalence and potential impact on HIV incidence. Sex Transm Infect 2010; 86 (suppl 3): iii93–99. Peterman A, Palermo T, Bredenkamp PC. Peterman et al respond. Am J Public Health 2011; 101: 2005. The Lancet. Sexual violence: a global awakening, from India. Lancet 2013; 318: 2. García-Moreno C, Stöckl H. Protection of sexual and reproductive health rights: addressing violence against women. Int J Gynaecol Obstet 2009; 106: 144–47. Yount KM, VanderEnde K, Zureick-Brown S, Minh TH, Schuler SR, Hoang TA. Measuring attitudes about women’s recourse after exposure to intimate partner violence: The ATT-RECOURSE scale. J Interpers Violence 2013; published online Dec 24. DOI:10.1177/0886260513511536.
Britt Chudleigh/Mint Images/Corbis
Alcohol minimum unit pricing and socioeconomic status
Published Online February 10, 2014 http://dx.doi.org/10.1016/ S0140-6736(14)60154-9 See Articles page 1655
1616
Floor prices for alcohol, beneath which alcohol cannot be sold, are in place in Moldova, Russia, Ukraine, Uzbekistan, some US states (eg, Connecticut), and eight of the ten Canadian provinces. In 2012, Scotland legislated alcohol minimum unit pricing—a lowest price per unit of alcohol—the introduction of which is pending legal challenge. In the UK, minimum unit pricing is the subject of substantial political and policy debate. UK alcohol prices in the off-trade, particularly supermarkets, have risen more slowly than have taxes on alcohol.1 Harmful drinkers favour cheap off-trade alcohol,2 which is targeted by minimum unit pricing. Drinkers on low income also favour cheap alcohol.3 The UK Government reneged on its plans to introduce a minimum unit price of £0·45, citing concerns that responsible drinkers on a low income might be disadvantaged.4 However, the burden of minimum unit pricing on people from lowincome groups would be small, at worst.5,6 People from low socioeconomic status backgrounds have fewer resources to protect themselves from the ill effects of drinking, and have high levels of alcohol-related mortality and hospital admission at all levels of drinking compared with people from higher socioeconomic status backgrounds.7 In The Lancet, John Holmes and colleagues8 report their assessment of the effect of the proposed £0·45 minimum unit price in England as a function of income and socioeconomic status, based on their Sheffield Alcohol Policy Model. This model combines an econometric model, which relates changes in the price of alcohol to changes in alcohol consumption, and an epidemiological model, which translates alcohol
consumption to mortality and morbidity. In response to the minimum unit price, the study predicts that harmful drinkers in the lowest income quintile would reduce their annual alcohol consumption by 7·6% (about 4 weeks’ worth of alcohol) and spend less on alcohol overall, whereas harmful drinkers in the highest quintile would only reduce their consumption by 1%. Responsible drinkers in the lowest quintile would reduce consumption by 1·6% and also spend less on alcohol. Public health outcomes were predicted by occupation or socioeconomic status. In Holmes and colleagues’ study8 the lowest socioeconomic groups made up about 41% of the population, but were estimated to account for 59% of the alcoholassociated health costs. 10 years after introduction of minimum unit pricing, annual alcohol-related health costs for this group were reduced by 4·7%; this reduction accounting for 88% of population-wide savings. The study assumed that retailers would only increase prices to the minimum threshold, providing a conservative estimate of the effect of minimum unit pricing. Canada’s experience is that retailers also increase the price of more expensive forms of alcohol to maintain relative price structures.9 The Sheffield Alcohol Policy Model would ideally be built on a dataset including people’s alcohol purchases, consumption, location of purchase, and price. No such dataset exists, so the model links the 2009 General Lifestyle Survey (containing information on mean weekly and highest daily alcohol consumption by beverage types) and the UK Living Costs and Food Survey (containing information on alcoholic beverages www.thelancet.com Vol 383 May 10, 2014
kinase,8 for example, have not shown analgesic efficacy in randomised clinical trials. Hence, direct translational research still awaits its breakthrough. One potential reason for the scarcity of translational success is that preclinical efficacy is mainly assessed on the basis of spinal reflex behaviour in animals, which does not capture the multidimensional chronic pain experience in human beings.9 Despite this, the preclinical studies of AT2R inhibitors published so far have shown efficacy on standard paw withdrawal thresholds and latencies to mechanical and thermal stimuli, while no cerebral-dependent behaviour has been investigated.4,5 However, problems with the use of reflex responses might be different in studies of peripherally and centrally acting drugs. Another potential reason for the apparent lack of success in translational pain research is the failure of clinical trials to show efficacy of analgesics. The study by Rice and colleagues1 has optimised the assay sensitivity in several ways, such as by including patients with postherpetic neuralgia—a patient group that have low placebo responses10—and by using an algorithm, masked to the patients and study staff, that excludes patients with highly variable or extreme baseline pain scores.11 Rice and colleagues’ study is well designed and executed, and while the results need to be reproduced, they are promising. Although the average effect size was small, roughly a third of the patients randomly allocated to EMA401 responded with more than 50% pain reduction, and the side-effect profile suggests that higher doses might be tolerated. Further studies that assess the optimum dose, possible predictors of response, and efficacy in combination with other neuropathic pain analgesics are warranted, as are studies of long-term efficacy and safety. On the basis of the proposed mechanism of action and positive results from preclinical models, it is reasonable to postulate
that AT2R antagonists could also be effective in other neuropathic pain disorders, such as peripheral nerve injury and chronic inflammatory pain.4,5 *Nanna Brix Finnerup, Cathrine Baastrup Danish Pain Research Center, Aarhus University, 8000 Aarhus C, Denmark fi[email protected] NBF has received honoraria for consulting or speaking from Astellas, Pfizer, Norpharma, and Grünenthal, and research support from Grünenthal. NBF and CB are members of the EUROPAIN project funded by the Investigational Medicines Initiative, a public–private partnership between the European Union and the European Federation of Pharmaceutical Industries and Associations (EFPIA); EFPIA’s partners are AstraZeneca, Boehringer Ingelheim, Pfizer, Eli Lilly, Esteve, UCB Pharma, Sanofi-Aventis, Grünenthal, Neuroscience Technologies, Astellas, and Abbott. 1
2 3 4
5
6
7
8
9 10
11
Rice ASC, Dworkin RH, McCarthy TD, et al, for the EMA401-003 study group. EMA401, an orally administered highly selective angiotensin II type 2 receptor antagonist, as a novel treatment for postherpetic neuralgia: a randomised, double-blind, placebo-controlled phase 2 clinical trial. Lancet 2014; published online Feb 5. http://dx.doi.org/10.1016/ S0140-6736(13)62337-5. Finnerup NB, Sindrup SH, Jensen TS. The evidence for pharmacological treatment of neuropathic pain. Pain 2010; 150: 573–81. Steckelings UM, Kaschina E, Unger T. The AT2 receptor—a matter of love and hate. Peptides 2005; 26: 1401–09. Smith MT, Woodruff TM, Wyse BD, et al. A small molecule angiotensin II type 2 receptor (AT2R) antagonist produces analgesia in a rat model of neuropathic pain by inhibition of p38 mitogen-activated protein kinase (MAPK) and p44/p42 MAPK activation in the dorsal root ganglia. Pain Med 2013; published online June 6. DOI:10.1111/pme.12157. Chakrabarty A, Liao Z, Smith PG. Angiotensin II receptor type 2 activation is required for cutaneous sensory hyperinnervation and hypersensitivity in a rat hind paw model of inflammatory pain. J Pain 2013; 14: 1053–65. Kalliomaki J, Jonzon B, Huizar K, et al. Evaluation of a novel chemokine receptor 2 (CCR2)-antagonist in painful diabetic polyneuropathy. Scand J Pain 2013; 4: 77–83. Goldstein DJ, Wang O, Gitter BD, Iyengar S. Dose-response study of the analgesic effect of lanepitant in patients with painful diabetic neuropathy. Clin Neuropharmacol 2001; 24: 16–22. Ostenfeld T, Krishen A, Lai RY, et al. Analgesic efficacy and safety of the novel p38 MAP kinase inhibitor, losmapimod, in patients with neuropathic pain following peripheral nerve injury: a double-blind, placebo-controlled study. Eur J Pain 2013; 17: 844–57. Vierck CJ, Hansson PT, Yezierski RP. Clinical and pre-clinical pain assessment: are we measuring the same thing? Pain 2008; 135: 7–10. Cepeda MS, Berlin JA, Gao CY, et al. Placebo response changes depending on the neuropathic pain syndrome: results of a systematic review and meta-analysis. Pain Med 2012; 13: 575–95. Dworkin RH, Turk DC, Peirce-Sandner S, et al. Considerations for improving assay sensitivity in chronic pain clinical trials: IMMPACT recommendations. Pain 2012; 153: 1148–58.
Worldwide prevalence of non-partner sexual violence Published Online February 12, 2014 http://dx.doi.org/10.1016/ S0140-6736(13)62333-8 See Articles page 1648
1614
Non-partner sexual violence denotes that a person has been forced to have sex or to perform a sexual act when he or she did not want to, by anyone other than an intimate partner (eg, acquaintances, colleagues, friends, family members, military personnel, police, teachers, or strangers).1,2 Multicountry studies and
reviews have shown that 0·3–11·5% of women report having experienced non-partner sexual violence at some point during their lifetime.1,3 In The Lancet, Naeemah Abrahams and colleagues4 report a systematic review, controlled for confounding, of 7231 studies that yielded 412 estimates of the prevalence of non-partner www.thelancet.com Vol 383 May 10, 2014
sexual violence in 56 countries. The study is a landmark in its scale and rigour and offers a unique evidence base that confirms the need to address this public health challenge and violation of human rights worldwide. The authors estimate that during 1998–2011, 7·2% (95% CI 5·2–9·1) of women aged 15 years or older had ever experienced non-partner sexual violence. This estimate has substantial political and scientific importance and, for both reasons, warrants comment. Abrahams and colleagues also give some attention to comparisons of regional estimates for non-partner sexual violence. The highest estimates were in central (21%, 95% CI 4·5–37·5) and southern (17·4%, 11·4–23·3) sub-Saharan Africa. The lowest prevalence was seen in south Asia (3·3%, 0–8·3). Like other researchers,2 however, Abrahams and colleagues note that regional variation in levels of non-partner sexual violence should be interpreted with caution because of uncontrolled and potentially meaningful differences between the samples (purposively selected vs probability based), research tools (single vs multiple questions), periods of exposure (lifetime vs previous year), and survey designs (multipurpose vs violence specific). Moreover, four regions each had fewer than six estimates; only one estimate was available for central sub-Saharan Africa from one country in conflict (Democratic Republic of the Congo), and the meta-analysis controlled for few confounders. The authors identified the regions with the highest and lowest estimated prevalence of non-partner sexual violence even when the respective CIs overlapped with those for all or most other regions. Thus, because most adjusted regional estimates do not differ significantly, and higher estimated prevalence emerges from regions that have more datapoints, ranking regions on estimates of nonpartner sexual violence might not be warranted. Abrahams and colleagues note that their systematic review had conceptual and methodological challenges owing to differences between the included studies, which could affect the quality of the derived estimates. For instance, one challenge is the use of variable definitions for non-partner sexual violence.5 The term includes a range of victim-perpetrator relationships, sexual acts, and forms of coercion and contexts of vulnerability,1 but 91·5% of studies included relied on single general questions that related to forced sex or forced sexual acts against a woman’s wishes. The non-specificity about the range of potential perpetrators and acts might www.thelancet.com Vol 383 May 10, 2014
Simon Maina/AFP/Getty Images
Comment
substantially underestimate the scale of non-partner sexual violence against women. Despite these elements of caution, the major contribution of this study is its comprehensive inclusion of data to derive best estimates for the worldwide prevalence of non-partner sexual violence against women. An estimated prevalence of 5·2–9·1% is unacceptably high on public health and human rights grounds and, hopefully, will spur timely and systematic discussions about the use of standard definitions and improved research tools and data collection methods to improve disclosure of a highly stigmatised violation. Non-partner sexual violence has far reaching but underdocumented consequences for the social, economic, and health-related wellbeing of women and societies,4 and observed effects in conflict settings have unclear generalisability.6,7 Overall, these new estimates for non-partner sexual violence reflect responsible reporting of findings on an often sensationalised and oversimplified topic,8 which permits evidence-based responses. The data confirm that nonpartner sexual violence is neither rare nor geographically isolated9 and, thus, that existing laws and systems of accountability remain inadequate.10,11 Effective responses will require widespread legal and institutional change. Kathryn M Yount Hubert Department of Global Health, Emory University, Atlanta, GA 30322, USA [email protected] I declare that I have no competing interests.
1615
Comment
1 2 3
4
5 6
Dartnall E, Jewkes R. Sexual violence against women: the scope of the problem. Best Pract Res Clin Obstet Gynaecol 2013; 27: 3–13. Vanwesenbeeck I. Sexual violence and the MDGs. Int J Sex Health 2008; 20: 25–49. García-Moreno C, Jansen HA, Ellsberg M, Heise L, Watts C. WHO multi-country study on women’s health and domestic violence against women: initial results on prevalence, health outcomes and women’s responses. Geneva: WHO, 2005. Abrahams N, Devries K, Watts C, et al. Worldwide prevalence of nonpartner sexual violence: a systematic review. Lancet 2014; published online Feb 12. http://dx.doi.org/10.1016/S0140-6736(13)62243-6. Lawry L, Reis C, Kisielewski M, Asher J. Problems in reporting sexual violence prevalence. Am J Public Health 2011; 101: 2004–05. Johnson K, Scott J, Rughita B, et al. Association of sexual violence and human rights violations with physical and mental health in territories of the Eastern Democratic Republic of the Congo. JAMA 2010; 304: 553–62.
7
8 9 10
11
Watts CH, Foss AM, Hossain M, Zimmerman C, von Simson R, Klot J. Sexual violence and conflict in Africa: prevalence and potential impact on HIV incidence. Sex Transm Infect 2010; 86 (suppl 3): iii93–99. Peterman A, Palermo T, Bredenkamp PC. Peterman et al respond. Am J Public Health 2011; 101: 2005. The Lancet. Sexual violence: a global awakening, from India. Lancet 2013; 318: 2. García-Moreno C, Stöckl H. Protection of sexual and reproductive health rights: addressing violence against women. Int J Gynaecol Obstet 2009; 106: 144–47. Yount KM, VanderEnde K, Zureick-Brown S, Minh TH, Schuler SR, Hoang TA. Measuring attitudes about women’s recourse after exposure to intimate partner violence: The ATT-RECOURSE scale. J Interpers Violence 2013; published online Dec 24. DOI:10.1177/0886260513511536.
Britt Chudleigh/Mint Images/Corbis
Alcohol minimum unit pricing and socioeconomic status
Published Online February 10, 2014 http://dx.doi.org/10.1016/ S0140-6736(14)60154-9 See Articles page 1655
1616
Floor prices for alcohol, beneath which alcohol cannot be sold, are in place in Moldova, Russia, Ukraine, Uzbekistan, some US states (eg, Connecticut), and eight of the ten Canadian provinces. In 2012, Scotland legislated alcohol minimum unit pricing—a lowest price per unit of alcohol—the introduction of which is pending legal challenge. In the UK, minimum unit pricing is the subject of substantial political and policy debate. UK alcohol prices in the off-trade, particularly supermarkets, have risen more slowly than have taxes on alcohol.1 Harmful drinkers favour cheap off-trade alcohol,2 which is targeted by minimum unit pricing. Drinkers on low income also favour cheap alcohol.3 The UK Government reneged on its plans to introduce a minimum unit price of £0·45, citing concerns that responsible drinkers on a low income might be disadvantaged.4 However, the burden of minimum unit pricing on people from lowincome groups would be small, at worst.5,6 People from low socioeconomic status backgrounds have fewer resources to protect themselves from the ill effects of drinking, and have high levels of alcohol-related mortality and hospital admission at all levels of drinking compared with people from higher socioeconomic status backgrounds.7 In The Lancet, John Holmes and colleagues8 report their assessment of the effect of the proposed £0·45 minimum unit price in England as a function of income and socioeconomic status, based on their Sheffield Alcohol Policy Model. This model combines an econometric model, which relates changes in the price of alcohol to changes in alcohol consumption, and an epidemiological model, which translates alcohol
consumption to mortality and morbidity. In response to the minimum unit price, the study predicts that harmful drinkers in the lowest income quintile would reduce their annual alcohol consumption by 7·6% (about 4 weeks’ worth of alcohol) and spend less on alcohol overall, whereas harmful drinkers in the highest quintile would only reduce their consumption by 1%. Responsible drinkers in the lowest quintile would reduce consumption by 1·6% and also spend less on alcohol. Public health outcomes were predicted by occupation or socioeconomic status. In Holmes and colleagues’ study8 the lowest socioeconomic groups made up about 41% of the population, but were estimated to account for 59% of the alcoholassociated health costs. 10 years after introduction of minimum unit pricing, annual alcohol-related health costs for this group were reduced by 4·7%; this reduction accounting for 88% of population-wide savings. The study assumed that retailers would only increase prices to the minimum threshold, providing a conservative estimate of the effect of minimum unit pricing. Canada’s experience is that retailers also increase the price of more expensive forms of alcohol to maintain relative price structures.9 The Sheffield Alcohol Policy Model would ideally be built on a dataset including people’s alcohol purchases, consumption, location of purchase, and price. No such dataset exists, so the model links the 2009 General Lifestyle Survey (containing information on mean weekly and highest daily alcohol consumption by beverage types) and the UK Living Costs and Food Survey (containing information on alcoholic beverages www.thelancet.com Vol 383 May 10, 2014
