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1.  Global, regional, and national levels and causes of maternal mortality during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013 
Kassebaum, Nicholas J | Bertozzi-Villa, Amelia | Coggeshall, Megan S | Shackelford, Katya A | Steiner, Caitlyn | Heuton, Kyle R | Gonzalez-Medina, Diego | Barber, Ryan | Huynh, Chantal | Dicker, Daniel | Templin, Tara | Wolock, Timothy M | Ozgoren, Ayse Abbasoglu | Abd-Allah, Foad | Abera, Semaw Ferede | Abubakar, Ibrahim | Achoki, Tom | Adelekan, Ademola | Ademi, Zanfina | Adou, Arsène Kouablan | Adsuar, José C | Agardh, Emilie E | Akena, Dickens | Alasfoor, Deena | Alemu, Zewdie Aderaw | Alfonso-Cristancho, Rafael | Alhabib, Samia | Ali, Raghib | Al Kahbouri, Mazin J | Alla, François | Allen, Peter J | AlMazroa, Mohammad A | Alsharif, Ubai | Alvarez, Elena | Alvis-Guzmán, Nelson | Amankwaa, Adansi A | Amare, Azmeraw T | Amini, Hassan | Ammar, Walid | Antonio, Carl A T | Anwari, Palwasha | Ärnlöv, Johan | Arsenijevic, Valentina S Arsic | Artaman, Ali | Asad, Majed Masoud | Asghar, Rana J | Assadi, Reza | Atkins, Lydia S | Badawi, Alaa | Balakrishnan, Kalpana | Basu, Arindam | Basu, Sanjay | Beardsley, Justin | Bedi, Neeraj | Bekele, Tolesa | Bell, Michelle L | Bernabe, Eduardo | Beyene, Tariku J | Bhutta, Zulfiqar | Abdulhak, Aref Bin | Blore, Jed D | Basara, Berrak Bora | Bose, Dipan | Breitborde, Nicholas | Cárdenas, Rosario | Castañeda-Orjuela, Carlos A | Castro, Ruben Estanislao | Catalá-López, Ferrán | Cavlin, Alanur | Chang, Jung-Chen | Che, Xuan | Christophi, Costas A | Chugh, Sumeet S | Cirillo, Massimo | Colquhoun, Samantha M | Cooper, Leslie Trumbull | Cooper, Cyrus | da Costa Leite, Iuri | Dandona, Lalit | Dandona, Rakhi | Davis, Adrian | Dayama, Anand | Degenhardt, Louisa | De Leo, Diego | del Pozo-Cruz, Borja | Deribe, Kebede | Dessalegn, Muluken | deVeber, Gabrielle A | Dharmaratne, Samath D | Dilmen, Uğur | Ding, Eric L | Dorrington, Rob E | Driscoll, Tim R | Ermakov, Sergei Petrovich | Esteghamati, Alireza | Faraon, Emerito Jose A | Farzadfar, Farshad | Felicio, Manuela Mendonca | Fereshtehnejad, Seyed-Mohammad | de Lima, Graça Maria Ferreira | Forouzanfar, Mohammad H | França, Elisabeth B | Gaffikin, Lynne | Gambashidze, Ketevan | Gankpé, Fortuné Gbètoho | Garcia, Ana C | Geleijnse, Johanna M | Gibney, Katherine B | Giroud, Maurice | Glaser, Elizabeth L | Goginashvili, Ketevan | Gona, Philimon | González-Castell, Dinorah | Goto, Atsushi | Gouda, Hebe N | Gugnani, Harish Chander | Gupta, Rahul | Gupta, Rajeev | Hafezi-Nejad, Nima | Hamadeh, Randah Ribhi | Hammami, Mouhanad | Hankey, Graeme J | Harb, Hilda L | Havmoeller, Rasmus | Hay, Simon I | Heredia Pi, Ileana B | Hoek, Hans W | Hosgood, H Dean | Hoy, Damian G | Husseini, Abdullatif | Idrisov, Bulat T | Innos, Kaire | Inoue, Manami | Jacobsen, Kathryn H | Jahangir, Eiman | Jee, Sun Ha | Jensen, Paul N | Jha, Vivekanand | Jiang, Guohong | Jonas, Jost B | Juel, Knud | Kabagambe, Edmond Kato | Kan, Haidong | Karam, Nadim E | Karch, André | Karema, Corine Kakizi | Kaul, Anil | Kawakami, Norito | Kazanjan, Konstantin | Kazi, Dhruv S | Kemp, Andrew H | Kengne, Andre Pascal | Kereselidze, Maia | Khader, Yousef Saleh | Khalifa, Shams Eldin Ali Hassan | Khan, Ejaz Ahmed | Khang, Young-Ho | Knibbs, Luke | Kokubo, Yoshihiro | Kosen, Soewarta | Defo, Barthelemy Kuate | Kulkarni, Chanda | Kulkarni, Veena S | Kumar, G Anil | Kumar, Kaushalendra | Kumar, Ravi B | Kwan, Gene | Lai, Taavi | Lalloo, Ratilal | Lam, Hilton | Lansingh, Van C | Larsson, Anders | Lee, Jong-Tae | Leigh, James | Leinsalu, Mall | Leung, Ricky | Li, Xiaohong | Li, Yichong | Li, Yongmei | Liang, Juan | Liang, Xiaofeng | Lim, Stephen S | Lin, Hsien-Ho | Lipshultz, Steven E | Liu, Shiwei | Liu, Yang | Lloyd, Belinda K | London, Stephanie J | Lotufo, Paulo A | Ma, Jixiang | Ma, Stefan | Machado, Vasco Manuel Pedro | Mainoo, Nana Kwaku | Majdan, Marek | Mapoma, Christopher Chabila | Marcenes, Wagner | Marzan, Melvin Barrientos | Mason-Jones, Amanda J | Mehndiratta, Man Mohan | Mejia-Rodriguez, Fabiola | Memish, Ziad A | Mendoza, Walter | Miller, Ted R | Mills, Edward J | Mokdad, Ali H | Mola, Glen Liddell | Monasta, Lorenzo | de la Cruz Monis, Jonathan | Hernandez, Julio Cesar Montañez | Moore, Ami R | Moradi-Lakeh, Maziar | Mori, Rintaro | Mueller, Ulrich O | Mukaigawara, Mitsuru | Naheed, Aliya | Naidoo, Kovin S | Nand, Devina | Nangia, Vinay | Nash, Denis | Nejjari, Chakib | Nelson, Robert G | Neupane, Sudan Prasad | Newton, Charles R | Ng, Marie | Nieuwenhuijsen, Mark J | Nisar, Muhammad Imran | Nolte, Sandra | Norheim, Ole F | Nyakarahuka, Luke | Oh, In-Hwan | Ohkubo, Takayoshi | Olusanya, Bolajoko O | Omer, Saad B | Opio, John Nelson | Orisakwe, Orish Ebere | Pandian, Jeyaraj D | Papachristou, Christina | Park, Jae-Hyun | Caicedo, Angel J Paternina | Patten, Scott B | Paul, Vinod K | Pavlin, Boris Igor | Pearce, Neil | Pereira, David M | Pesudovs, Konrad | Petzold, Max | Poenaru, Dan | Polanczyk, Guilherme V | Polinder, Suzanne | Pope, Dan | Pourmalek, Farshad | Qato, Dima | Quistberg, D Alex | Rafay, Anwar | Rahimi, Kazem | Rahimi-Movaghar, Vafa | Rahman, Sajjad ur | Raju, Murugesan | Rana, Saleem M | Refaat, Amany | Ronfani, Luca | Roy, Nobhojit | Sánchez Pimienta, Tania Georgina | Sahraian, Mohammad Ali | Salomon, Joshua A | Sampson, Uchechukwu | Santos, Itamar S | Sawhney, Monika | Sayinzoga, Felix | Schneider, Ione J C | Schumacher, Austin | Schwebel, David C | Seedat, Soraya | Sepanlou, Sadaf G | Servan-Mori, Edson E | Shakh-Nazarova, Marina | Sheikhbahaei, Sara | Shibuya, Kenji | Shin, Hwashin Hyun | Shiue, Ivy | Sigfusdottir, Inga Dora | Silberberg, Donald H | Silva, Andrea P | Singh, Jasvinder A | Skirbekk, Vegard | Sliwa, Karen | Soshnikov, Sergey S | Sposato, Luciano A | Sreeramareddy, Chandrashekhar T | Stroumpoulis, Konstantinos | Sturua, Lela | Sykes, Bryan L | Tabb, Karen M | Talongwa, Roberto Tchio | Tan, Feng | Teixeira, Carolina Maria | Tenkorang, Eric Yeboah | Terkawi, Abdullah Sulieman | Thorne-Lyman, Andrew L | Tirschwell, David L | Towbin, Jeffrey A | Tran, Bach X | Tsilimbaris, Miltiadis | Uchendu, Uche S | Ukwaja, Kingsley N | Undurraga, Eduardo A | Uzun, Selen Begüm | Vallely, Andrew J | van Gool, Coen H | Vasankari, Tommi J | Vavilala, Monica S | Venketasubramanian, N | Villalpando, Salvador | Violante, Francesco S | Vlassov, Vasiliy Victorovich | Vos, Theo | Waller, Stephen | Wang, Haidong | Wang, Linhong | Wang, XiaoRong | Wang, Yanping | Weichenthal, Scott | Weiderpass, Elisabete | Weintraub, Robert G | Westerman, Ronny | Wilkinson, James D | Woldeyohannes, Solomon Meseret | Wong, John Q | Wordofa, Muluemebet Abera | Xu, Gelin | Yang, Yang C | Yano, Yuichiro | Yentur, Gokalp Kadri | Yip, Paul | Yonemoto, Naohiro | Yoon, Seok-Jun | Younis, Mustafa Z | Yu, Chuanhua | Jin, Kim Yun | El SayedZaki, Maysaa | Zhao, Yong | Zheng, Yingfeng | Zhou, Maigeng | Zhu, Jun | Zou, Xiao Nong | Lopez, Alan D | Naghavi, Mohsen | Murray, Christopher J L | Lozano, Rafael
Lancet  2014;384(9947):980-1004.
Summary
Background
The fifth Millennium Development Goal (MDG 5) established the goal of a 75% reduction in the maternal mortality ratio (MMR; number of maternal deaths per 100 000 livebirths) between 1990 and 2015. We aimed to measure levels and track trends in maternal mortality, the key causes contributing to maternal death, and timing of maternal death with respect to delivery.
Methods
We used robust statistical methods including the Cause of Death Ensemble model (CODEm) to analyse a database of data for 7065 site-years and estimate the number of maternal deaths from all causes in 188 countries between 1990 and 2013. We estimated the number of pregnancy-related deaths caused by HIV on the basis of a systematic review of the relative risk of dying during pregnancy for HIV-positive women compared with HIV-negative women. We also estimated the fraction of these deaths aggravated by pregnancy on the basis of a systematic review. To estimate the numbers of maternal deaths due to nine different causes, we identified 61 sources from a systematic review and 943 site-years of vital registration data. We also did a systematic review of reports about the timing of maternal death, identifying 142 sources to use in our analysis. We developed estimates for each country for 1990–2013 using Bayesian meta-regression. We estimated 95% uncertainty intervals (UIs) for all values.
Findings
292 982 (95% UI 261 017–327 792) maternal deaths occurred in 2013, compared with 376 034 (343 483–407 574) in 1990. The global annual rate of change in the MMR was −0·3% (−1·1 to 0·6) from 1990 to 2003, and −2·7% (−3·9 to −1·5) from 2003 to 2013, with evidence of continued acceleration. MMRs reduced consistently in south, east, and southeast Asia between 1990 and 2013, but maternal deaths increased in much of sub-Saharan Africa during the 1990s. 2070 (1290–2866) maternal deaths were related to HIV in 2013, 0·4% (0·2–0·6) of the global total. MMR was highest in the oldest age groups in both 1990 and 2013. In 2013, most deaths occurred intrapartum or postpartum. Causes varied by region and between 1990 and 2013. We recorded substantial variation in the MMR by country in 2013, from 956·8 (685·1–1262·8) in South Sudan to 2·4 (1·6–3·6) in Iceland.
Interpretation
Global rates of change suggest that only 16 countries will achieve the MDG 5 target by 2015. Accelerated reductions since the Millennium Declaration in 2000 coincide with increased development assistance for maternal, newborn, and child health. Setting of targets and associated interventions for after 2015 will need careful consideration of regions that are making slow progress, such as west and central Africa.
Funding
Bill & Melinda Gates Foundation.
doi:10.1016/S0140-6736(14)60696-6
PMCID: PMC4255481  PMID: 24797575
2.  Global, regional, and national incidence and mortality for HIV, tuberculosis, and malaria during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013 
Murray, Christopher J L | Ortblad, Katrina F | Guinovart, Caterina | Lim, Stephen S | Wolock, Timothy M | Roberts, D Allen | Dansereau, Emily A | Graetz, Nicholas | Barber, Ryan M | Brown, Jonathan C | Wang, Haidong | Duber, Herbert C | Naghavi, Mohsen | Dicker, Daniel | Dandona, Lalit | Salomon, Joshua A | Heuton, Kyle R | Foreman, Kyle | Phillips, David E | Fleming, Thomas D | Flaxman, Abraham D | Phillips, Bryan K | Johnson, Elizabeth K | Coggeshall, Megan S | Abd-Allah, Foad | Ferede, Semaw | Abraham, Jerry P | Abubakar, Ibrahim | Abu-Raddad, Laith J | Abu-Rmeileh, Niveen Me | Achoki, Tom | Adeyemo, Austine Olufemi | Adou, Arsène Kouablan | Adsuar, José C | Agardh, Emilie Elisabet | Akena, Dickens | Al Kahbouri, Mazin J | Alasfoor, Deena | Albittar, Mohammed I | Alcalá-Cerra, Gabriel | Alegretti, Miguel Angel | Alemu, Zewdie Aderaw | Alfonso-Cristancho, Rafael | Alhabib, Samia | Ali, Raghib | Alla, Francois | Allen, Peter J | Alsharif, Ubai | Alvarez, Elena | Alvis-Guzman, Nelson | Amankwaa, Adansi A | Amare, Azmeraw T | Amini, Hassan | Ammar, Walid | Anderson, Benjamin O | Antonio, Carl Abelardo T | Anwari, Palwasha | Ärnlöv, Johan | Arsenijevic, Valentina S Arsic | Artaman, Ali | Asghar, Rana J | Assadi, Reza | Atkins, Lydia S | Badawi, Alaa | Balakrishnan, Kalpana | Banerjee, Amitava | Basu, Sanjay | Beardsley, Justin | Bekele, Tolesa | Bell, Michelle L | Bernabe, Eduardo | Beyene, Tariku Jibat | Bhala, Neeraj | Bhalla, Ashish | Bhutta, Zulfiqar A | Abdulhak, Aref Bin | Binagwaho, Agnes | Blore, Jed D | Basara, Berrak Bora | Bose, Dipan | Brainin, Michael | Breitborde, Nicholas | Castañeda-Orjuela, Carlos A | Catalá-López, Ferrán | Chadha, Vineet K | Chang, Jung-Chen | Chiang, Peggy Pei-Chia | Chuang, Ting-Wu | Colomar, Mercedes | Cooper, Leslie Trumbull | Cooper, Cyrus | Courville, Karen J | Cowie, Benjamin C | Criqui, Michael H | Dandona, Rakhi | Dayama, Anand | De Leo, Diego | Degenhardt, Louisa | Del Pozo-Cruz, Borja | Deribe, Kebede | Jarlais, Don C Des | Dessalegn, Muluken | Dharmaratne, Samath D | Dilmen, Uğur | Ding, Eric L | Driscoll, Tim R | Durrani, Adnan M | Ellenbogen, Richard G | Ermakov, Sergey Petrovich | Esteghamati, Alireza | Faraon, Emerito Jose A | Farzadfar, Farshad | Fereshtehnejad, Seyed-Mohammad | Fijabi, Daniel Obadare | Forouzanfar, Mohammad H | Paleo, Urbano Fra. | Gaffikin, Lynne | Gamkrelidze, Amiran | Gankpé, Fortuné Gbètoho | Geleijnse, Johanna M | Gessner, Bradford D | Gibney, Katherine B | Ginawi, Ibrahim Abdelmageem Mohamed | Glaser, Elizabeth L | Gona, Philimon | Goto, Atsushi | Gouda, Hebe N | Gugnani, Harish Chander | Gupta, Rajeev | Gupta, Rahul | Hafezi-Nejad, Nima | Hamadeh, Randah Ribhi | Hammami, Mouhanad | Hankey, Graeme J | Harb, Hilda L | Haro, Josep Maria | Havmoeller, Rasmus | Hay, Simon I | Hedayati, Mohammad T | Pi, Ileana B Heredia | Hoek, Hans W | Hornberger, John C | Hosgood, H Dean | Hotez, Peter J | Hoy, Damian G | Huang, John J | Iburg, Kim M | Idrisov, Bulat T | Innos, Kaire | Jacobsen, Kathryn H | Jeemon, Panniyammakal | Jensen, Paul N | Jha, Vivekanand | Jiang, Guohong | Jonas, Jost B | Juel, Knud | Kan, Haidong | Kankindi, Ida | Karam, Nadim E | Karch, André | Karema, Corine Kakizi | Kaul, Anil | Kawakami, Norito | Kazi, Dhruv S | Kemp, Andrew H | Kengne, Andre Pascal | Keren, Andre | Kereselidze, Maia | Khader, Yousef Saleh | Khalifa, Shams Eldin Ali Hassan | Khan, Ejaz Ahmed | Khang, Young-Ho | Khonelidze, Irma | Kinfu, Yohannes | Kinge, Jonas M | Knibbs, Luke | Kokubo, Yoshihiro | Kosen, S | Defo, Barthelemy Kuate | Kulkarni, Veena S | Kulkarni, Chanda | Kumar, Kaushalendra | Kumar, Ravi B | Kumar, G Anil | Kwan, Gene F | Lai, Taavi | Balaji, Arjun Lakshmana | Lam, Hilton | Lan, Qing | Lansingh, Van C | Larson, Heidi J | Larsson, Anders | Lee, Jong-Tae | Leigh, James | Leinsalu, Mall | Leung, Ricky | Li, Yichong | Li, Yongmei | De Lima, Graça Maria Ferreira | Lin, Hsien-Ho | Lipshultz, Steven E | Liu, Shiwei | Liu, Yang | Lloyd, Belinda K | Lotufo, Paulo A | Machado, Vasco Manuel Pedro | Maclachlan, Jennifer H | Magis-Rodriguez, Carlos | Majdan, Marek | Mapoma, Christopher Chabila | Marcenes, Wagner | Marzan, Melvin Barrientos | Masci, Joseph R | Mashal, Mohammad Taufiq | Mason-Jones, Amanda J | Mayosi, Bongani M | Mazorodze, Tasara T | Mckay, Abigail Cecilia | Meaney, Peter A | Mehndiratta, Man Mohan | Mejia-Rodriguez, Fabiola | Melaku, Yohannes Adama | Memish, Ziad A | Mendoza, Walter | Miller, Ted R | Mills, Edward J | Mohammad, Karzan Abdulmuhsin | Mokdad, Ali H | Mola, Glen Liddell | Monasta, Lorenzo | Montico, Marcella | Moore, Ami R | Mori, Rintaro | Moturi, Wilkister Nyaora | Mukaigawara, Mitsuru | Murthy, Kinnari S | Naheed, Aliya | Naidoo, Kovin S | Naldi, Luigi | Nangia, Vinay | Narayan, K M Venkat | Nash, Denis | Nejjari, Chakib | Nelson, Robert G | Neupane, Sudan Prasad | Newton, Charles R | Ng, Marie | Nisar, Muhammad Imran | Nolte, Sandra | Norheim, Ole F | Nowaseb, Vincent | Nyakarahuka, Luke | Oh, In-Hwan | Ohkubo, Takayoshi | Olusanya, Bolajoko O | Omer, Saad B | Opio, John Nelson | Orisakwe, Orish Ebere | Pandian, Jeyaraj D | Papachristou, Christina | Caicedo, Angel J Paternina | Patten, Scott B | Paul, Vinod K | Pavlin, Boris Igor | Pearce, Neil | Pereira, David M | Pervaiz, Aslam | Pesudovs, Konrad | Petzold, Max | Pourmalek, Farshad | Qato, Dima | Quezada, Amado D | Quistberg, D Alex | Rafay, Anwar | Rahimi, Kazem | Rahimi-Movaghar, Vafa | Rahman, Sajjad Ur | Raju, Murugesan | Rana, Saleem M | Razavi, Homie | Reilly, Robert Quentin | Remuzzi, Giuseppe | Richardus, Jan Hendrik | Ronfani, Luca | Roy, Nobhojit | Sabin, Nsanzimana | Saeedi, Mohammad Yahya | Sahraian, Mohammad Ali | Samonte, Genesis May J | Sawhney, Monika | Schneider, Ione J C | Schwebel, David C | Seedat, Soraya | Sepanlou, Sadaf G | Servan-Mori, Edson E | Sheikhbahaei, Sara | Shibuya, Kenji | Shin, Hwashin Hyun | Shiue, Ivy | Shivakoti, Rupak | Sigfusdottir, Inga Dora | Silberberg, Donald H | Silva, Andrea P | Simard, Edgar P | Singh, Jasvinder A | Skirbekk, Vegard | Sliwa, Karen | Soneji, Samir | Soshnikov, Sergey S | Sreeramareddy, Chandrashekhar T | Stathopoulou, Vasiliki Kalliopi | Stroumpoulis, Konstantinos | Swaminathan, Soumya | Sykes, Bryan L | Tabb, Karen M | Talongwa, Roberto Tchio | Tenkorang, Eric Yeboah | Terkawi, Abdullah Sulieman | Thomson, Alan J | Thorne-Lyman, Andrew L | Towbin, Jeffrey A | Traebert, Jefferson | Tran, Bach X | Dimbuene, Zacharie Tsala | Tsilimbaris, Miltiadis | Uchendu, Uche S | Ukwaja, Kingsley N | Uzun, Selen Begüm | Vallely, Andrew J | Vasankari, Tommi J | Venketasubramanian, N | Violante, Francesco S | Vlassov, Vasiliy Victorovich | Vollset, Stein Emil | Waller, Stephen | Wallin, Mitchell T | Wang, Linhong | Wang, XiaoRong | Wang, Yanping | Weichenthal, Scott | Weiderpass, Elisabete | Weintraub, Robert G | Westerman, Ronny | White, Richard A | Wilkinson, James D | Williams, Thomas Neil | Woldeyohannes, Solomon Meseret | Wong, John Q | Xu, Gelin | Yang, Yang C | Yano, Yuichiro | Yentur, Gokalp Kadri | Yip, Paul | Yonemoto, Naohiro | Yoon, Seok-Jun | Younis, Mustafa | Yu, Chuanhua | Jin, Kim Yun | El Sayed Zaki, Maysaa | Zhao, Yong | Zheng, Yingfeng | Zhou, Maigeng | Zhu, Jun | Zou, Xiao Nong | Lopez, Alan D | Vos, Theo
Lancet  2014;384(9947):1005-1070.
Summary
Background
The Millennium Declaration in 2000 brought special global attention to HIV, tuberculosis, and malaria through the formulation of Millennium Development Goal (MDG) 6. The Global Burden of Disease 2013 study provides a consistent and comprehensive approach to disease estimation for between 1990 and 2013, and an opportunity to assess whether accelerated progress has occurred since the Millennium Declaration.
Methods
To estimate incidence and mortality for HIV, we used the UNAIDS Spectrum model appropriately modified based on a systematic review of available studies of mortality with and without antiretroviral therapy (ART). For concentrated epidemics, we calibrated Spectrum models to fit vital registration data corrected for misclassification of HIV deaths. In generalised epidemics, we minimised a loss function to select epidemic curves most consistent with prevalence data and demographic data for all-cause mortality. We analysed counterfactual scenarios for HIV to assess years of life saved through prevention of mother-to-child transmission (PMTCT) and ART. For tuberculosis, we analysed vital registration and verbal autopsy data to estimate mortality using cause of death ensemble modelling. We analysed data for corrected case-notifications, expert opinions on the case-detection rate, prevalence surveys, and estimated cause-specific mortality using Bayesian meta-regression to generate consistent trends in all parameters. We analysed malaria mortality and incidence using an updated cause of death database, a systematic analysis of verbal autopsy validation studies for malaria, and recent studies (2010–13) of incidence, drug resistance, and coverage of insecticide-treated bednets.
Findings
Globally in 2013, there were 1·8 million new HIV infections (95% uncertainty interval 1·7 million to 2·1 million), 29·2 million prevalent HIV cases (28·1 to 31·7), and 1·3 million HIV deaths (1·3 to 1·5). At the peak of the epidemic in 2005, HIV caused 1·7 million deaths (1·6 million to 1·9 million). Concentrated epidemics in Latin America and eastern Europe are substantially smaller than previously estimated. Through interventions including PMTCT and ART, 19·1 million life-years (16·6 million to 21·5 million) have been saved, 70·3% (65·4 to 76·1) in developing countries. From 2000 to 2011, the ratio of development assistance for health for HIV to years of life saved through intervention was US$4498 in developing countries. Including in HIV-positive individuals, all-form tuberculosis incidence was 7·5 million (7·4 million to 7·7 million), prevalence was 11·9 million (11·6 million to 12·2 million), and number of deaths was 1·4 million (1·3 million to 1·5 million) in 2013. In the same year and in only individuals who were HIV-negative, all-form tuberculosis incidence was 7·1 million (6·9 million to 7·3 million), prevalence was 11·2 million (10·8 million to 11·6 million), and number of deaths was 1·3 million (1·2 million to 1·4 million). Annualised rates of change (ARC) for incidence, prevalence, and death became negative after 2000. Tuberculosis in HIV-negative individuals disproportionately occurs in men and boys (versus women and girls); 64·0% of cases (63·6 to 64·3) and 64·7% of deaths (60·8 to 70·3). Globally, malaria cases and deaths grew rapidly from 1990 reaching a peak of 232 million cases (143 million to 387 million) in 2003 and 1·2 million deaths (1·1 million to 1·4 million) in 2004. Since 2004, child deaths from malaria in sub-Saharan Africa have decreased by 31·5% (15·7 to 44·1). Outside of Africa, malaria mortality has been steadily decreasing since 1990.
Interpretation
Our estimates of the number of people living with HIV are 18·7% smaller than UNAIDS’s estimates in 2012. The number of people living with malaria is larger than estimated by WHO. The number of people living with HIV, tuberculosis, or malaria have all decreased since 2000. At the global level, upward trends for malaria and HIV deaths have been reversed and declines in tuberculosis deaths have accelerated. 101 countries (74 of which are developing) still have increasing HIV incidence. Substantial progress since the Millennium Declaration is an encouraging sign of the effect of global action.
Funding
Bill & Melinda Gates Foundation.
doi:10.1016/S0140-6736(14)60844-8
PMCID: PMC4202387  PMID: 25059949
3.  Global, regional, and national levels of neonatal, infant, and under-5 mortality during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013 
Wang, Haidong | Liddell, Chelsea A | Coates, Matthew M | Mooney, Meghan D | Levitz, Carly E | Schumacher, Austin E | Apfel, Henry | Iannarone, Marissa | Phillips, Bryan | Lofgren, Katherine T | Sandar, Logan | Dorrington, Rob E | Rakovac, Ivo | Jacobs, Troy A | Liang, Xiaofeng | Zhou, Maigeng | Zhu, Jun | Yang, Gonghuan | Wang, Yanping | Liu, Shiwei | Li, Yichong | Ozgoren, Ayse Abbasoglu | Abera, Semaw Ferede | Abubakar, Ibrahim | Achoki, Tom | Adelekan, Ademola | Ademi, Zanfina | Alemu, Zewdie Aderaw | Allen, Peter J | AlMazroa, Mohammad AbdulAziz | Alvarez, Elena | Amankwaa, Adansi A | Amare, Azmeraw T | Ammar, Walid | Anwari, Palwasha | Cunningham, Solveig Argeseanu | Asad, Majed Masoud | Assadi, Reza | Banerjee, Amitava | Basu, Sanjay | Bedi, Neeraj | Bekele, Tolesa | Bell, Michelle L | Bhutta, Zulfiqar | Blore, Jed | Basara, Berrak Bora | Boufous, Soufiane | Breitborde, Nicholas | Bruce, Nigel G | Bui, Linh Ngoc | Carapetis, Jonathan R | Cárdenas, Rosario | Carpenter, David O | Caso, Valeria | Castro, Ruben Estanislao | Catalá-Lopéz, Ferrán | Cavlin, Alanur | Che, Xuan | Chiang, Peggy Pei-Chia | Chowdhury, Rajiv | Christophi, Costas A | Chuang, Ting-Wu | Cirillo, Massimo | Leite, Iuri da Costa | Courville, Karen J | Dandona, Lalit | Dandona, Rakhi | Davis, Adrian | Dayama, Anand | Deribe, Kebede | Dharmaratne, Samath D | Dherani, Mukesh K | Dilmen, Uğur | Ding, Eric L | Edmond, Karen M | Ermakov, Sergei Petrovich | Farzadfar, Farshad | Fereshtehnejad, Seyed-Mohammad | Fijabi, Daniel Obadare | Foigt, Nataliya | Forouzanfar, Mohammad H | Garcia, Ana C | Geleijnse, Johanna M | Gessner, Bradford D | Goginashvili, Ketevan | Gona, Philimon | Goto, Atsushi | Gouda, Hebe N | Green, Mark A | Greenwell, Karen Fern | Gugnani, Harish Chander | Gupta, Rahul | Hamadeh, Randah Ribhi | Hammami, Mouhanad | Harb, Hilda L | Hay, Simon | Hedayati, Mohammad T | Hosgood, H Dean | Hoy, Damian G | Idrisov, Bulat T | Islami, Farhad | Ismayilova, Samaya | Jha, Vivekanand | Jiang, Guohong | Jonas, Jost B | Juel, Knud | Kabagambe, Edmond Kato | Kazi, Dhruv S | Kengne, Andre Pascal | Kereselidze, Maia | Khader, Yousef Saleh | Khalifa, Shams Eldin Ali Hassan | Khang, Young-Ho | Kim, Daniel | Kinfu, Yohannes | Kinge, Jonas M | Kokubo, Yoshihiro | Kosen, Soewarta | Defo, Barthelemy Kuate | Kumar, G Anil | Kumar, Kaushalendra | Kumar, Ravi B | Lai, Taavi | Lan, Qing | Larsson, Anders | Lee, Jong-Tae | Leinsalu, Mall | Lim, Stephen S | Lipshultz, Steven E | Logroscino, Giancarlo | Lotufo, Paulo A | Lunevicius, Raimundas | Lyons, Ronan Anthony | Ma, Stefan | Mahdi, Abbas Ali | Marzan, Melvin Barrientos | Mashal, Mohammad Taufiq | Mazorodze, Tasara T | McGrath, John J | Memish, Ziad A | Mendoza, Walter | Mensah, George A | Meretoja, Atte | Miller, Ted R | Mills, Edward J | Mohammad, Karzan Abdulmuhsin | Mokdad, Ali H | Monasta, Lorenzo | Montico, Marcella | Moore, Ami R | Moschandreas, Joanna | Msemburi, William T | Mueller, Ulrich O | Muszynska, Magdalena M | Naghavi, Mohsen | Naidoo, Kovin S | Narayan, KM Venkat | Nejjari, Chakib | Ng, Marie | Ngirabega, Jean de Dieu | Nieuwenhuijsen, Mark J | Nyakarahuka, Luke | Ohkubo, Takayoshi | Omer, Saad B | Caicedo, Angel J Paternina | Wyk, Victoria Pillay-van | Pope, Dan | Prabhakaran, Dorairaj | Rahman, Sajjad UR | Rana, Saleem M | Reilly, Robert Quentin | Rojas-Rueda, David | Ronfani, Luca | Rushton, Lesley | Saeedi, Mohammad Yahya | Salomon, Joshua | Sampson, Uchechukwu | Santos, Itamar S | Sawhney, Monika | Schmidt, Jürgen C | Nazarova, Marina Shakh | She, Jun | Sheikhbahaei, Sara | Shibuya, Kenji | Shin, Hwashin Hyun | Shishani, Kawkab | Shiue, Ivy | Sigfusdottir, Inga Dora | Singh, Jasvinder A | Skirbekk, Vegard | Sliwa, Karen | Soshnikov, Sergey S | Sposato, Luciano A | Stathopoulou, Vasiliki Kalliopi | Stroumpoulis, Konstantinos | Tabb, Karen M | Talongwa, Roberto Tchio | Teixeira, Carolina Maria | Terkawi, Abdullah Sulieman | Thomson, Alan J | Lyman, Andrew L Thorne | Toyoshima, Hideaki | Dimbuene, Zacharie Tsala | Uwaliraye, Parfait | Uzun, Selen Begüm | Vasankari, Tommi J | Vasconcelos, Ana Maria Nogales | Vlassov, Vasiliy Victorovich | Vollset, Stein Emil | Vos, Theo | Waller, Stephen | Wan, Xia | Weichenthal, Scott | Weiderpass, Elisabete | Weintraub, Robert G | Westerman, Ronny | Wilkinson, James D | Williams, Hywel C | Yang, Yang C | Yentur, Gokalp Kadri | Yip, Paul | Yonemoto, Naohiro | Younis, Mustafa | Yu, Chuanhua | Jin, Kim Yun | Zaki, Maysaa El Sayed | Zhu, Shankuan | Lopez, Alan D | Murray, Christopher J L
Lancet  2014;384(9947):957-979.
Summary
Background
Remarkable financial and political efforts have been focused on the reduction of child mortality during the past few decades. Timely measurements of levels and trends in under-5 mortality are important to assess progress towards the Millennium Development Goal 4 (MDG 4) target of reduction of child mortality by two thirds from 1990 to 2015, and to identify models of success.
Methods
We generated updated estimates of child mortality in early neonatal (age 0–6 days), late neonatal (7–28 days), postneonatal (29–364 days), childhood (1–4 years), and under-5 (0–4 years) age groups for 188 countries from 1970 to 2013, with more than 29 000 survey, census, vital registration, and sample registration datapoints. We used Gaussian process regression with adjustments for bias and non-sampling error to synthesise the data for under-5 mortality for each country, and a separate model to estimate mortality for more detailed age groups. We used explanatory mixed effects regression models to assess the association between under-5 mortality and income per person, maternal education, HIV child death rates, secular shifts, and other factors. To quantify the contribution of these different factors and birth numbers to the change in numbers of deaths in under-5 age groups from 1990 to 2013, we used Shapley decomposition. We used estimated rates of change between 2000 and 2013 to construct under-5 mortality rate scenarios out to 2030.
Findings
We estimated that 6·3 million (95% UI 6·0–6·6) children under-5 died in 2013, a 64% reduction from 17·6 million (17·1–18·1) in 1970. In 2013, child mortality rates ranged from 152·5 per 1000 livebirths (130·6–177·4) in Guinea-Bissau to 2·3 (1·8–2·9) per 1000 in Singapore. The annualised rates of change from 1990 to 2013 ranged from −6·8% to 0·1%. 99 of 188 countries, including 43 of 48 countries in sub-Saharan Africa, had faster decreases in child mortality during 2000–13 than during 1990–2000. In 2013, neonatal deaths accounted for 41·6% of under-5 deaths compared with 37·4% in 1990. Compared with 1990, in 2013, rising numbers of births, especially in sub-Saharan Africa, led to 1·4 million more child deaths, and rising income per person and maternal education led to 0·9 million and 2·2 million fewer deaths, respectively. Changes in secular trends led to 4·2 million fewer deaths. Unexplained factors accounted for only −1% of the change in child deaths. In 30 developing countries, decreases since 2000 have been faster than predicted attributable to income, education, and secular shift alone.
Interpretation
Only 27 developing countries are expected to achieve MDG 4. Decreases since 2000 in under-5 mortality rates are accelerating in many developing countries, especially in sub-Saharan Africa. The Millennium Declaration and increased development assistance for health might have been a factor in faster decreases in some developing countries. Without further accelerated progress, many countries in west and central Africa will still have high levels of under-5 mortality in 2030.
Funding
Bill & Melinda Gates Foundation, US Agency for International Development.
doi:10.1016/S0140-6736(14)60497-9
PMCID: PMC4165626  PMID: 24797572
4.  Association of dietary pattern and body weight with blood pressure in Jiangsu Province, China 
BMC Public Health  2014;14(1):948.
Background
To identify risk factors, associations between dietary patterns, body mass index (BMI), and hypertension in a Chinese population.
Methods
Dietary intake was assessed in 2518 adults by a 3-day 24 h recall and a food frequency questionnaire. Salt and oil intake was assessed by weighing records. Four dietary patterns were identified using principal component analysis. Overweight and obesity was determined according to the Chinese cut-offs for BMI. High blood pressure was defined as systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg. Prevalence ratios (PR) were calculated using Poisson regression.
Results
Of the subjects, 26.7% had high blood pressure. Subjects with overweight and obesity were more likely to have high blood pressure than those with normal weight (PR, 95% CI: 1.60, 1.40-1.87; 2.45, 2.11-2.85, respectively). Subjects with a ‘traditional’ dietary pattern were more likely to have high blood pressure (P for trend = 0.001), whereas those with a ‘macho’ or ‘sweet tooth’ dietary pattern were less likely to have high blood pressure (P for trend = 0.004 and <0.001, respectively). More than half of the population had salt intakes > 9 g/d, and blood pressure increased with salt intake (P for trend <0.001). Subjects with a ‘traditional’ dietary pattern had the highest salt intake (12.3 g/d).
Conclusion
A traditional dietary pattern is associated with high blood pressure among the population of Jiangsu Province, which may be mainly due to high salt intake. Moreover, high BMI is an important determinant of high blood pressure. Both issues need to be addressed by lifestyle interventions.
doi:10.1186/1471-2458-14-948
PMCID: PMC4176575  PMID: 25216777
Dietary pattern; Body weight; Salt; Blood pressure; China
5.  Higher dietary salt intake is associated with microalbuminuria, but not with retinopathy in individuals with type 1 diabetes: the EURODIAB Prospective Complications Study 
Diabetologia  2014;57(11):2315-2323.
Aims/hypothesis
High dietary salt intake has been associated with elevated BP and may also have a deleterious effect on microvascular complications. We studied the cross-sectional associations between dietary salt intake (estimated from 24 h urinary sodium excretion) and urinary potassium excretion on the one hand, and the prevalence of microvascular complications on the other, in individuals with type 1 diabetes.
Methods
We measured sodium and potassium concentrations in two 24 h urine samples in 1,212 individuals with type 1 diabetes (40 ± 10 years old, 51% men) who participated in the EURODIAB Prospective Complications Study. We used multiple logistic regression analyses to investigate associations between dietary salt intake and microvascular complications adjusted for age and sex, and additionally for BMI, smoking, urinary potassium excretion, antihypertensive medication and physical activity, and total energy, protein, alcohol, saturated fat and fibre intake.
Results
After full adjustment, 1 g/day higher dietary salt intake was positively associated with the presence of microalbuminuria (OR 1.06 [95% CI 1.01, 1.10]), but not macroalbuminuria (OR 0.99 [95% CI 0.94, 1.05]), non-proliferative retinopathy (OR 1.00 (95% CI 0.96, 1.04]) or proliferative retinopathy (OR 1.02 (95% CI 0.95, 1.08]). After excluding individuals with cardiovascular disease and/or antihypertensive medication (n = 418), we found a non-significant association with microalbuminuria (OR 1.04 [95% CI 0.99, 1.10]) and macroalbuminuria (OR 1.05 [95% CI 0.96, 1.16]). The association between dietary salt intake and microalbuminuria was stronger in individuals with a BMI above 25 kg/m2 (OR 1.11 [95% CI 1.04, 1.18]) than in those with BMI below 25 kg/m2 (OR 1.03 [95% CI 0.97, 1.09]). No significant associations were found between urinary potassium excretion and microvascular complications.
Conclusions/interpretation
In individuals with type 1 diabetes, higher dietary salt intake, as determined by 24 h urinary sodium excretion, may be positively associated with microalbuminuria, particularly in overweight individuals.
Electronic supplementary material
The online version of this article (doi:10.1007/s00125-014-3367-9) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
doi:10.1007/s00125-014-3367-9
PMCID: PMC4181505  PMID: 25172228
Albuminuria; Dietary salt intake; Microvascular complications; Potassium excretion; Retinopathy; Sodium excretion; Type 1 diabetes
6.  Habitual coffee consumption and blood pressure: An epidemiological perspective 
This paper summarizes the current epidemiological evidence on coffee consumption in relation to blood pressure (BP) and risk of hypertension. Data from cross-sectional studies suggest an inverse linear or U-shaped association of habitual coffee use with BP in different populations. Prospective studies suggest a protective effect of high coffee intake (4 or more cups per day) against hypertension, mainly in women. Furthermore, the risk of hypertension may be lower in coffee abstainers. Randomized controlled trials, which are mostly of short duration (1–12 weeks), have shown that coffee intake around 5 cups per day causes a small elevation in BP (∼2/1 mmHg) when compared to abstinence or use of decaffeinated coffee. With regard to underlying biological mechanisms, most research has been devoted to BP-raising effects of caffeine. However, there are many other substances in coffee, such as polyphenols, soluble fibre and potassium, which could exert a beneficial effect in the cardiovascular system. Although the precise nature of the relation between coffee and BP is still unclear, most evidence suggests that regular intake of caffeinated coffee does not increase the risk of hypertension.
PMCID: PMC2605331  PMID: 19183744
epidemiology; coffee; blood pressure; hypertension
7.  DHA Serum Levels Were Significantly Higher in Celiac Disease Patients Compared to Healthy Controls and Were Unrelated to Depression 
PLoS ONE  2014;9(5):e97778.
Objectives
Celiac disease (CD), a genetically predisposed intolerance for gluten, is associated with an increased risk of major depressive disorder (MDD). We investigated whether dietary intake and serum levels of the essential n-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic acid (EPA) and docosahexanoic acid (DHA) found in fatty fish play a role in this association.
Methods
Cross-sectional study in 71 adult CD patients and 31 healthy volunteers, matched on age, gender and level of education, who were not using n-3 PUFA supplements. Dietary intake, as assessed using a 203-item food frequency questionnaire, and serum levels of EPA and DHA were compared in analyses of covariance, adjusting for potential confounders. Serum PUFA were determined using gas chromatography.
Results
Mean serum DHA was significantly higher in CD patients (1.72 mass%) than controls (1.28 mass%) after multivariable adjustment (mean diff. 0.45 mass%; 95% CI: 0.22–0.68; p = 0.001). The mean intake of EPA plus DHA did not differ between CD patients and controls after multivariable adjustment (0.15 and 0.22 g/d, respectively; p = 0.10). There were no significant differences in intake or serum levels of EPA and DHA between any of the CD patient groups (never depressed, current MDD, minor/partially remitted MDD, remitted MDD) and controls.
Conclusions
Patients on a long term gluten-free diet had similar intakes of EPA plus DHA compared to controls. Contrary to expectations, DHA serum levels were significantly higher in CD patients compared to healthy controls and were unrelated to MDD status.
doi:10.1371/journal.pone.0097778
PMCID: PMC4026409  PMID: 24841484
8.  Effect of Alpha Linolenic Acid Supplementation on Serum Prostate Specific Antigen (PSA): Results from the Alpha Omega Trial 
PLoS ONE  2013;8(12):e81519.
Background
Alpha linolenic acid (ALA) is the major omega-3 fatty acid in the diet. Evidence on health effects of ALA is not conclusive, but some observational studies found an increased risk of prostate cancer with higher intake of ALA. We examined the effect of ALA supplementation on serum concentrations of prostate-specific antigen (PSA), a biomarker for prostate cancer.
Methods
The Alpha Omega Trial (ClinicalTrials.gov Identifier: NCT00127452) was a double-blind, placebo-controlled trial of ALA and the fish fatty acids eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) on the recurrence of cardiovascular disease, using a 2×2 factorial design. Blood was collected at the start and the end of the intervention period. The present analysis included 1622 patients with a history of a myocardial infarction, aged 60–80 years with an initial PSA concentration <4 ng/mL. They received either 2 g per day of ALA or placebo in margarine spreads for 40 months. T-tests and logistic regression were used to assess the effects of ALA supplementation on changes in serum PSA (both continuously and as a dichotomous outcome, cut-off point: >4 ng/mL).
Findings
Mean serum PSA increased by 0.42 ng/mL on placebo (n = 815) and by 0.52 ng/mL on ALA (n = 807), a difference of 0.10 (95% confidence interval: −0.02 to 0.22) ng/mL (P = 0·12). The odds ratio for PSA rising above 4 ng/mL on ALA versus placebo was 1.15 (95% CI: 0.84–1.58).
Interpretation
An additional amount of 2 g of ALA per day increased PSA by 0.10 ng/mL, but the confidence interval ranged from −0.02 to 0.22 ng/mL and included no effect. Therefore, more studies are needed to establish whether or not ALA intake has a clinically significant effect on PSA or prostate cancer.
Trial registration information
ClinicalTrials.gov; Identifier: NCT00127452. URL: http://www.clinicaltrials.gov/ct2/show/NCT00127452.
doi:10.1371/journal.pone.0081519
PMCID: PMC3859488  PMID: 24349086
9.  No effects of n-3 fatty acid supplementation on serum total testosterone levels in older men: the Alpha Omega Trial 
The intake of the n-3 fatty acids alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) has been related to testosterone levels in epidemiological analyses. The aim of this study was to assess whether the n-3 fatty acids affects testosterone levels in post-myocardial infarction (MI) patients, who are at risk of testosterone deficiency. In a double-blind, placebo-controlled trial of low-dose supplementation of n-3 fatty acids, we included 1850 male post-MI patients aged 60–80 y who participated in the Alpha Omega Trial. Patients were randomly allocated to margarines that provided 400 mg/d of EPA–DHA (n=453), 2 g/d of ALA (n=467), EPA–DHA plus ALA (n=458), or placebo (n=472). Serum testosterone levels were assessed at baseline and after 41 months using whole day blood samples obtained at the subjects' home or at the hospital. Subjects were on average age of 68.4 (SD 5.3) years old and had baseline mean serum total testosterone of 14.8 (SD 5.6) nmol/L. The four randomized groups did not differ for baseline characteristics. ALA, EPA–DHA, and EPA–DHA plus ALA supplementation did not affect serum total testosterone compared to placebo. Moreover, n-3 fatty acid supplementation did not affect the risk of incident testosterone deficiency (n=76 with total testosterone <8.0 nmol/L). We conclude that n-3 fatty acids supplementation did not affect serum total testosterone in men who had had a MI.
doi:10.1111/j.1365-2605.2012.01255.x
PMCID: PMC3387289  PMID: 22394170
n-3 polyunsaturated fatty acids; alpha-linolenic acid; eicosapentaenoic acid; docosahexaenoic acid; testosterone
10.  Effects of n-3 fatty acids on major cardiovascular events in statin users and non-users with a history of myocardial infarction 
European Heart Journal  2012;33(13):1582-1588.
Aims
Recent secondary prevention trials have failed to demonstrate a beneficial effect of n-3 fatty acids on cardiovascular outcomes, which may be due to the growing use of statins since the mid-1990s. The aim of the present study was to assess whether statins modify the effects of n-3 fatty acids on major adverse cardiovascular events in patients with a history of myocardial infarction (MI).
Methods and results
Patients who participated in the Alpha Omega Trial were divided into consistent statin users (n = 3740) and consistent statin non-users (n = 413). In these two groups of patients, the effects of an additional daily amount of 400 mg eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA), 2 g α-linolenic acid (ALA), or both on major cardiovascular events were evaluated. Multivariable Cox's proportional hazard models were used to calculate adjusted hazard rate ratios (HRadj). Among the statin users 495 (13%) and among the statin non-users 62 (15%) developed a major cardiovascular event. In statin users, an additional amount of n-3 fatty acids did not reduce cardiovascular events [HRadj 1.02; 95% confidence interval (CI): 0.80, 1.31; P = 0.88]. In statin non-users, however, only 9% of those who received EPA–DHA plus ALA experienced an event compared with 18% in the placebo group (HRadj 0.46; 95% CI: 0.21, 1.01; P= 0.051).
Conclusion
In patients with a history of MI who are not treated with statins, low-dose supplementation with n-3 fatty acids may reduce major cardiovascular events. This study suggests that statin treatment modifies the effects of n-3 fatty acids on the incidence of major cardiovascular events.
ClinicalTrials.gov number: NCT00127452.
doi:10.1093/eurheartj/ehr499
PMCID: PMC3388014  PMID: 22301766
n-3 fatty acids; Eicosapentaenoic acid; Docosahexaenoic acid; α-linolenic acid; Cardiovascular diseases; Statins; Lipids
11.  N-6 and N-3 Fatty Acid Cholesteryl Esters in Relation to Fatal CHD in a Dutch Adult Population: A Nested Case-Control Study and Meta-Analysis 
PLoS ONE  2013;8(5):e59408.
Background
Dietary polyunsaturated fatty acids (PUFA) are inversely related to coronary heart disease (CHD) in epidemiological studies. We examined the associations of plasma n-6 and n-3 PUFA in cholesteryl esters with fatal CHD in a nested case-control study. Additionally, we performed a dose-response meta-analysis of similar prospective studies on cholesteryl ester PUFA.
Methods
We used data from two population-based cohort studies in Dutch adults aged 20–65y. Blood and data collection took place from 1987–1997 and subjects were followed for 8–19y. We identified 279 incident cases of fatal CHD and randomly selected 279 controls, matched on age, gender, and enrollment date. Odds ratios (OR) were calculated per standard deviation (SD) increase of cholesteryl ester PUFA.
Results
After adjustment for confounders, the OR (95%CI) for fatal CHD per SD increase in plasma linoleic acid was 0.89 (0.74–1.06). Additional adjustment for plasma total cholesterol and systolic blood pressure attenuated this association (OR:0.95; 95%CI: 0.78–1.15). Arachidonic acid was not associated with fatal CHD (OR per SD:1.11; 95%CI: 0.92–1.35). The ORs (95%CI) for fatal CHD for an SD increase in n-3 PUFA were 0.92 (0.74–1.15) for alpha-linolenic acid and 1.06 (0.88–1.27) for EPA-DHA. In the meta-analysis, a 5% higher linoleic acid level was associated with a 9% lower risk (relative risk: 0.91; 95% CI: 0.84–0.98) of CHD. The other fatty acids were not associated with CHD.
Conclusion
In this Dutch population, n-6 and n-3 PUFA in cholesteryl esters were not significantly related to fatal CHD. Our data, together with findings from previous prospective studies, support that linoleic acid in plasma cholesteryl is inversely associated with CHD.
doi:10.1371/journal.pone.0059408
PMCID: PMC3669344  PMID: 23741290
12.  Fish oil and omega-3 fatty acids in cardiovascular disease: do they really work? 
European Heart Journal  2011;33(4):436-443.
Omega-3 fatty acids, which are found abundantly in fish oil, exert pleiotropic cardiometabolic effects with a diverse range of actions. The results of previous studies raised a lot of interest in the role of fish oil and omega-3 fatty acids in primary and secondary prevention of cardiovascular diseases. The present review will focus on the current clinical uses of omega-3 fatty acids and provide an update on their effects. Since recently published trials in patients with coronary artery diseases or post-myocardial infarction did not show an effect of omega-3 fatty acids on major cardiovascular endpoints, this review will examine the limitations of those data and suggest recommendations for the use of omega-3 fatty acids.
doi:10.1093/eurheartj/ehr362
PMCID: PMC3279313  PMID: 21933782
Fish oils; Cardiovascular disease
13.  n-3 Fatty Acids, Ventricular Arrhythmia–Related Events, and Fatal Myocardial Infarction in Postmyocardial Infarction Patients With Diabetes 
Diabetes Care  2011;34(12):2515-2520.
OBJECTIVE
We carried out a secondary analysis in high-risk patients with a previous myocardial infarction (MI) and diabetes in the Alpha Omega Trial. We tested the hypothesis that in these patients an increased intake of the n-3 fatty acids eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and α-linolenic acid (ALA) will reduce the incidence of ventricular arrhythmias and fatal MI.
RESEARCH DESIGN AND METHODS
A subgroup of 1,014 post-MI patients with diabetes aged 60–80 years was randomly allocated to receive one of four trial margarines, three with an additional amount of n-3 fatty acids and one placebo for 40 months. The end points were ventricular arrhythmia–related events and fatal MI. The data were analyzed according to the intention-to-treat principle, using multivariable Cox proportional hazards models.
RESULTS
The patients consumed on average 18.6 g of margarine per day, which resulted in an additional intake of 223 mg EPA plus 149 mg DHA and/or 1.9 g ALA in the active treatment groups. During follow-up, 29 patients developed a ventricular arrhythmia–related events and 27 had a fatal MI. Compared with placebo patients, the EPA-DHA plus ALA group experienced less ventricular arrhythmia–related events (hazard ratio 0.16; 95% CI 0.04–0.69). These n-3 fatty acids also reduced the combined end-point ventricular arrhythmia–related events and fatal MI (0.28; 0.11–0.71).
CONCLUSIONS
Our results suggest that low-dose supplementation of n-3 fatty acids exerts a protective effect against ventricular arrhythmia–related events in post-MI patients with diabetes.
doi:10.2337/dc11-0896
PMCID: PMC3220851  PMID: 22110169
14.  Vitamin K Intake and Plasma Desphospho-Uncarboxylated Matrix Gla-Protein Levels in Kidney Transplant Recipients 
PLoS ONE  2012;7(10):e47991.
Vitamin K is essential for activation of γ-carboxyglutamate (Gla)-proteins including the vascular calcification inhibitor matrix Gla-protein (MGP). Insufficient vitamin K intake leads to production of uncarboxylated, mostly inactive proteins and contributes to an increased cardiovascular risk. In kidney transplant recipients, cardiovascular risk is high but vitamin K intake and status have not been defined. We investigated dietary vitamin K intake, vascular vitamin K status and its determinants in kidney transplant recipients. We estimated vitamin K intake in a cohort of kidney transplant recipients (n = 60) with stable renal function (creatinine clearance 61 [42–77] (median [interquartile range]) ml/min), who were 75 [35–188] months after transplantation, using three-day food records and food frequency questionnaires. Vascular vitamin K status was assessed by measuring plasma desphospho-uncarboxylated MGP (dp-ucMGP). Total vitamin K intake was below the recommended level in 50% of patients. Lower vitamin K intake was associated with less consumption of green vegetables (33 vs 40 g/d, p = 0.06) and increased dp-ucMGP levels (621 vs 852 pmol/L, p<0.05). Accordingly, dp-ucMGP levels were elevated (>500 pmol/L) in 80% of patients. Multivariate regression identified creatinine clearance, coumarin use, body mass index, high sensitivity-CRP and sodium excretion as independent determinants of dp-ucMGP levels. In a considerable part of the kidney transplant population, vitamin K intake is too low for maximal carboxylation of vascular MGP. The high dp-ucMGP levels may result in an increased risk for arterial calcification. Whether increasing vitamin K intake may have health benefits for kidney transplant recipients should be addressed by future studies.
doi:10.1371/journal.pone.0047991
PMCID: PMC3485347  PMID: 23118917
15.  Cardiovascular risk factor management of myocardial infarction patients with and without diabetes in the Netherlands between 2002 and 2006: a cross-sectional analysis of baseline data 
BMJ Open  2012;2(6):e001360.
Objective
We examined levels and trends in cardiovascular risk factors and drug treatment in myocardial infarction (MI) patients with and without diabetes.
Design
Cross-sectional analysis of baseline Alpha Omega Trial data, a randomised controlled trial.
Setting
32 hospitals in the Netherlands.
Participants
In total, we had 1014 MI patients with diabetes (74% men) and 3823 without diabetes (79% men) aged 60–80 years, analysed over the period 2002–2006.
Results
Between 2002 and 2006, a significantly decreasing trend in the prevalence of obesity (−5%, ptrend=0.02) and in systolic blood pressure (BP) levels (−5 mm Hg, ptrend<0.0001) was demonstrated in non-diabetic patients, but not in diabetic patients. In 2006, obesity, mean systolic BP and serum triglyceride levels were significantly higher, whereas high-density lipoprotein cholesterol levels were lower in diabetic patients compared to those without. Prescription of antihypertensive drug (diabetic vs non-diabetic patients respectively, 95% vs 93%, p=0.08) and statin treatment were high (86% and 90%, p=0.11).
Conclusions
A high proportion of MI patients with and without diabetes was similarly treated with cardiovascular drugs. In spite of high drug treatment levels, more adverse risk factors were found in patients with diabetes.
doi:10.1136/bmjopen-2012-001360
PMCID: PMC3532965  PMID: 23117562
Epidemiology; Preventive Medicine
16.  Dairy intake in relation to cardiovascular disease mortality and all-cause mortality: the Hoorn Study 
European Journal of Nutrition  2012;52(2):609-616.
Purpose
Existing data from prospective cohort studies on dairy consumption and cardiovascular diseases are inconsistent. Even though the association between total dairy and cardiovascular diseases has been studied before, little is known about the effect of different types of dairy products on cardiovascular diseases (CVD). The objective of this study was to examine the relationship between (type of) dairy intake and CVD mortality and all-cause mortality in a Dutch population.
Methods
We examined the relationship between dairy intake and CVD mortality and all-cause mortality in 1956 participants of the Hoorn Study (aged 50–75 years), free of CVD at baseline. Hazard ratios with 95 % CIs were obtained for CVD mortality and all-cause mortality per standard deviation (SD) of the mean increase in dairy intake, with adjustment for age, sex, BMI, smoking, education, total energy intake, alcohol consumption, physical activity, and dietary intakes.
Results
During 12.4 years of follow-up, 403 participants died, of whom 116 had a fatal CVD event. Overall dairy intake was not associated with CVD mortality or all-cause mortality. Each SD increase in high-fat dairy intake was associated with a 32 % higher risk of CVD mortality (95 % CI; 7–61 %).
Conclusion
In this prospective cohort study, the intake of high-fat dairy products was associated with an increased risk of CVD mortality.
doi:10.1007/s00394-012-0363-z
PMCID: PMC3573184  PMID: 22555618
Dairy; Cardiovascular diseases; Mortality; Prospective
17.  Gender-Specific Associations of Marine n-3 Fatty Acids and Fish Consumption with 10-Year Incidence of Stroke 
PLoS ONE  2012;7(4):e33866.
Background
There is some evidence that the association of fish and marine fatty acids with stroke risk differs between men and women. We investigated the gender-specific associations of habitual intake of the marine fatty acids eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) and fish on incident stroke in a population-based study in the Netherlands.
Methods
We prospectively followed 20,069 men and women, aged 20–65 years, without cardiovascular diseases at baseline. Habitual diet was assessed with a validated 178-item food frequency questionnaire. Incidence of stroke was assessed through linkage with mortality and morbidity registers. Cox proportional hazards models were used to estimate multivariable-adjusted hazard ratios (HR) and 95% confidence intervals (95%CI).
Results
During 8–13 years of follow-up, 221 strokes occurred. In women, an inverse dose-response relation (P-trend = 0.02) was observed between EPA-DHA intake and incident stroke, with an HR of 0.49 (95% CI: 0.27–0.91) in the top quartile of EPA-DHA (median 225 mg/d) as compared to the bottom quartile (median 36 mg/d). In men, the HR (95%CI) for the top quartile of EPA-DHA intake was 0.87 (0.51–1.48) (P-trend = 0.36). Similar results were observed for fish consumption and stroke incidence.
Conclusion
A higher EPA-DHA and fish intake is related to a lower stroke risk in women, while for men an inverse association could not be demonstrated.
doi:10.1371/journal.pone.0033866
PMCID: PMC3322144  PMID: 22496770
18.  Sources of Dietary Protein in Relation to Blood Pressure in a General Dutch Population 
PLoS ONE  2012;7(2):e30582.
Background
Little is known about the relation of different dietary protein types with blood pressure (BP). We examined whether intake of total, plant, animal, dairy, meat, and grain protein was related to BP in a cross sectional cohort of 20,820 Dutch adults, aged 20–65 y and not using antihypertensive medication.
Design
Mean BP levels were calculated in quintiles of energy-adjusted protein with adjustment for age, sex, BMI, education, smoking, and intake of energy, alcohol, and other nutrients including protein from other sources. In addition, mean BP difference after substitution of 3 en% carbohydrates or MUFA with protein was calculated.
Results
Total protein and animal protein were not associated with BP (ptrend = 0.62 and 0.71 respectively), both at the expense of carbohydrates and MUFA. Systolic BP was 1.8 mmHg lower (ptrend<0.01) in the highest (>36 g/d) than in the lowest (<27 g/d) quintile of plant protein. This inverse association was present both at the expense of carbohydrates and MUFA and more pronounced in individuals with untreated hypertension (−3.6 mmHg) than in those with normal (+0.1 mmHg) or prehypertensive BP (−0.3 mmHg; pinteraction<0.01). Meat and grain protein were not related to BP. Dairy protein was directly associated with systolic BP (+1.6 mmHg, ptrend<0.01), but not with diastolic BP (ptrend = 0.24).
Conclusions
Total protein and animal protein were not associated with BP in this general untreated Dutch population. Plant protein may be beneficial to BP, especially in people with elevated BP. However, because high intake of plant protein may be a marker of a healthy diet and lifestyle in general, confirmation from randomized controlled trials is warranted.
doi:10.1371/journal.pone.0030582
PMCID: PMC3274530  PMID: 22347387
19.  The effect of plant sterols on serum triglyceride concentrations is dependent on baseline concentrations: a pooled analysis of 12 randomised controlled trials 
European Journal of Nutrition  2012;52(1):153-160.
Purpose
Plant sterols (PS) are well known for their low-density lipoprotein cholesterol-lowering effect. Until recently, they were believed to have little or no impact on blood triglycerides (TG). However, studies taken individually were possibly lacking statistical power to detect modest TG decreases. This study was performed to quantify the TG-lowering effect of PS by pooling individual subject data from 12 randomised controlled trials that investigated the effects of PS on blood lipids.
Methods
The main outcome variable was the control-adjusted PS effect on relative (%) and absolute (mmol/L) changes in TG. The relative and absolute changes in high-density lipoprotein cholesterol (HDL-C) were also assessed. Differences in changes of serum lipid concentrations between PS and control treatments were estimated by an ANCOVA using a random effect model which included PS intake (active or control), study and predefined subject characteristics.
Results
The twelve randomised controlled trials included in total 935 hypercholesterolaemic subjects not preselected based on their baseline TG concentrations. In most studies, the PS dose ranged between 1.6 and 2.5 g/day. PS intake significantly lowered serum TG by 6.0% (95% CI: −10.7, −1.2) or 0.12 mmol/L (95% CI: −0.20, −0.04). No significant interaction was observed between PS intake and baseline TG concentrations on relative changes, but, on absolute changes, interaction was significant with larger TG decreases observed with higher TG concentrations at baseline. No effects were observed on HDL-C concentrations.
Conclusions
These results show that PS exert a modest TG-lowering effect which is dependent on baseline concentrations.
doi:10.1007/s00394-011-0297-x
PMCID: PMC3549411  PMID: 22252793
Plant sterols; Triglycerides; Cholesterol; Pooled analysis; Diet and lifestyle
20.  Paternal and Maternal History of Myocardial Infarction and Cardiovascular Diseases Incidence in a Dutch Cohort of Middle-Aged Persons 
PLoS ONE  2011;6(12):e28697.
Background
A positive parental history of myocardial infarction (MI) is an independent risk factor for cardiovascular diseases (CVD). However, different definitions of parental history have been used. We evaluated the impact of parental gender and age of onset of MI on CVD incidence.
Methods
Baseline data were collected between 1993 and 1997 in 10 524 respondents aged 40–65 years. CVD events were obtained from the National Hospital Discharge Register and Statistics Netherlands. We used proportional hazard models to calculate hazard ratios (HR) and 95% confidence intervals (CI) for CVD incidence and adjusted for lifestyle and biological risk factors.
Results
At baseline, 36% had a parental history of MI. During 10-year follow-up, 914 CVD events occurred. The age and gender adjusted HR was 1.3 (95% CI 1.1–1.5) for those with a paternal MI, 1.5 (1.2–1.8) for those with a maternal MI and 1.6 (1.2–2.2) for those with both parents with an MI. With decreasing parental age of MI, HR increased from 1.2 (1.0–1.6) for age ≥70 years to 1.5 (1.2–1.8) for age <60 years for a paternal MI and from 1.1 (0.9–1.5) to 2.2 (1.6–3.0) for a maternal MI. The impact of having a mother with MI before age 60 significantly differed in women [(2.9 (1.8–4.6)] and men [1.5 (0.9–2.6)]. Adjustment only slightly influenced HRs for maternal MI.
Conclusions
Respondents with a parental history of MI have an increased CVD incidence, in particular with parental onset of MI before age 70. A maternal history of MI before age 60 was the strongest predictor of CVD incidence.
doi:10.1371/journal.pone.0028697
PMCID: PMC3241680  PMID: 22194890
21.  C-reactive protein haplotypes and dispositional optimism in obese and nonobese elderly subjects 
Inflammation Research  2011;61(1):43-51.
Background
Chronic low-grade inflammation, characterized by elevated plasma levels of C-reactive protein (CRP), has been inversely associated with dispositional optimism. Using a Mendelian randomization design, this study explores whether CRP haplotypes that determine CRP plasma levels are also associated with dispositional optimism.
Methods
In a sample of 1,084 community-dwelling subjects (aged 60–85 years) from three cohort studies (Arnhem Elderly Study, n = 426; Leiden Longevity Study, n = 355; Zutphen Elderly Study, n = 303), six CRP polymorphisms (rs2808628, rs2808630, rs1205, rs1800947, rs1417938, and rs3091244) coding for five common haplotypes were genotyped. The association of CRP haplotypes with CRP plasma levels and dispositional optimism was analyzed using multivariable linear regression models. Subanalyses were stratified by body mass index (BMI ≥25 kg/m2).
Results
CRP haplotypes determined CRP plasma levels (adjusted β = 0.094, p < 0.001). In the whole group, no association was found between CRP haplotypes and dispositional optimism scores (adjusted β = −0.02, p = 0.45). In BMI strata, CRP haplotypes were associated with increasing levels of plasma CRP levels (adjusted β = 0.112; p = 0.002) and lower dispositional optimism levels (adjusted β = −0.068; p = 0.03) in the obese group only.
Conclusions
These results suggest that genetically increased CRP levels are involved in low dispositional optimism, but only in case of obesity.
doi:10.1007/s00011-011-0387-5
PMCID: PMC3249168  PMID: 21979869
Obesity; CRP; Dispositional optimism; Inflammation; Genotypes; Haplotypes
22.  Telomere Length and Mental Well-Being in Elderly Men from the Netherlands and Greece 
Behavior Genetics  2011;42(2):278-286.
Telomeres, repetitive DNA sequences that promote chromosomal stability, have been related to different measures of mental well-being and self-rated health, but mainly in women during adulthood. We aimed to investigate whether accelerated telomere shortening is associated with poor mental well-being and poor self-rated health in community-dwelling elderly men. Leukocyte telomere length was measured using quantitative PCR in two different samples of 203 elderly men (mean age 78 years) from the Netherlands in 1993, and 123 elderly men (mean age 84 years) from Greece in 2000. We also obtained follow-up data in 2000 from 144 Dutch subjects, of whom 75 had paired telomere length data in 1993 and 2000. Mental well-being was conceptualized as dispositional optimism, depressive symptoms, cognitive functioning, and loneliness. Linear regression analyses were used to study the association between telomere length, measures of mental well being, and self-rated health, while adjusting for potential confounders. In cross-sectional analyses, leukocyte telomere length was not associated with measures of mental well-being and self-rated health, neither in the Netherlands nor in Greece. Also, the rate of leukocyte telomere shortening (mean decrease: 0.28 kbp over 7 years) in the 75 Dutch participants with longitudinal data was not associated with changes in different measures of mental well-being and self-rated health. Thus, our results provide no support for a relationship between leukocyte telomere length and mental well-being in elderly community-dwelling men.
doi:10.1007/s10519-011-9498-6
PMCID: PMC3276762  PMID: 21870178
Telomere length; Mental well-being; Self-rated health; Cognitive function; Cohort study
23.  Parental longevity correlates with offspring’s optimism in two cohorts of community-dwelling older subjects 
Age  2011;34(2):461-468.
Dispositional optimism and other positive personality traits have been associated with longevity. Using a familial approach, we investigated the relationship between parental longevity and offspring’s dispositional optimism among community-dwelling older subjects. Parental age of death was assessed using structured questionnaires in two different population-based samples: the Leiden Longevity Study (n = 1,252, 52.2% female, mean age 66 years, SD = 4) and the Alpha Omega Trial (n = 769, 22.8% female, mean age 69 years, SD = 6). Adult offspring’s dispositional optimism was assessed with the Life Orientation Test—Revised (LOT-R). The association between parental age of death and levels of optimism in the offspring was analysed using linear regression analysis within each sample and a meta-analysis for the overall effect. In both samples, the parental mean age of death was positively associated with optimism scores of the offspring. The association remained significant after adjustment for age, gender, living arrangement, body mass index, smoking status, education and self-rated health of the offspring. The pooled B coefficient (increase in LOT-R score per 10-year increase in parental mean age of death) was 0.30 (SE = 0.08, p < 0.001). In conclusion, parental longevity was positively associated with optimism in adult offspring, suggesting a partial linked heritability of longevity and optimism.
doi:10.1007/s11357-011-9236-2
PMCID: PMC3312631  PMID: 21472382
Longevity; Dispositional optimism; Personality; Maternal inheritance
24.  Alpha-Linolenic Acid Intake and 10-Year Incidence of Coronary Heart Disease and Stroke in 20,000 Middle-Aged Men and Women in The Netherlands 
PLoS ONE  2011;6(3):e17967.
Background
Whether intake of alpha-linolenic acid (ALA), the plant-derived n-3 polyunsaturated fatty acid (PUFA), could prevent cardiovascular diseases is not yet clear. We examined the associations of ALA intake with 10-year incidence of coronary heart disease (CHD) and stroke in the Netherlands.
Methods
Data were collected from a general population of 20,069 generally healthy men and women, aged 20 to 65 years. Habitual diet was assessed at baseline (1993–1997) with a validated 178-item food frequency questionnaire. Incidences of CHD and stroke were assessed through linkage with mortality and morbidity registers. Hazard ratios (HR) were calculated with multivariable Cox proportional hazards models, adjusted for age, gender, lifestyle, and dietary factors.
Results
During 8–13 years of follow-up, we observed 280 incident CHD events (19% fatal) and 221 strokes (4% fatal). Intakes of energy-adjusted ALA in quintiles ranged from less than 1.0 g/d in the bottom quintile (Q1) to more than 1.9 g/d in the top quintile (Q5). ALA intake was not associated with incident CHD, with HRs varying between 0.89 and 1.01 (all p>0.05) in Q2–Q5 compared with the bottom quintile of ALA intake. For incident stroke, however, participants in Q2–Q5 had a 35–50% lower risk compared with the reference group. HRs were 0.65 (0.43–0.97), 0.49 (0.31–0.76), 0.53 (0.34–0.83), and 0.65 (0.41–1.04) for Q2–Q5 respectively.
Conclusion
In this general Dutch population, ALA intake was not associated with incident CHD. The data suggested that a low intake of ALA may be a risk factor for incident stroke. These results warrant confirmation in other population-based studies and in trials.
doi:10.1371/journal.pone.0017967
PMCID: PMC3064584  PMID: 21464993
25.  Plasma Protein Profiling Reveals Protein Clusters Related to BMI and Insulin Levels in Middle-Aged Overweight Subjects 
PLoS ONE  2010;5(12):e14422.
Background
Biomarkers that allow detection of the onset of disease are of high interest since early detection would allow intervening with lifestyle and nutritional changes before the disease is manifested and pharmacological therapy is required. Our study aimed to improve the phenotypic characterization of overweight but apparently healthy subjects and to identify new candidate profiles for early biomarkers of obesity-related diseases such as cardiovascular disease and type 2 diabetes.
Methodology/Principal Findings
In a population of 56 healthy, middle-aged overweight subjects Body Mass Index (BMI), fasting concentration of 124 plasma proteins and insulin were determined. The plasma proteins are implicated in chronic diseases, inflammation, endothelial function and metabolic signaling. Random Forest was applied to select proteins associated with BMI and plasma insulin. Subsequently, the selected proteins were analyzed by clustering methods to identify protein clusters associated with BMI and plasma insulin. Similar analyses were performed for a second population of 20 healthy, overweight older subjects to verify associations found in population I. In both populations similar clusters of proteins associated with BMI or insulin were identified. Leptin and a number of pro-inflammatory proteins, previously identified as possible biomarkers for obesity-related disease, e.g. Complement 3, C Reactive Protein, Serum Amyloid P, Vascular Endothelial Growth Factor clustered together and were positively associated with BMI and insulin. IL-3 and IL-13 clustered together with Apolipoprotein A1 and were inversely associated with BMI and might be potential new biomarkers.
Conclusion/ Significance
We identified clusters of plasma proteins associated with BMI and insulin in healthy populations. These clusters included previously reported biomarkers for obesity-related disease and potential new biomarkers such as IL-3 and IL-13. These plasma protein clusters could have potential applications for improved phenotypic characterization of volunteers in nutritional intervention studies or as biomarkers in the early detection of obesity-linked disease development and progression.
doi:10.1371/journal.pone.0014422
PMCID: PMC3009718  PMID: 21203453

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