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Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning
- Ethan S. Young, Jenalee R. Doom, Allison K. Farrell, Elizabeth A. Carlson, Michelle M. Englund, Gregory E. Miller, Megan R. Gunnar, Glenn I. Roisman, Jeffry A. Simpson
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- Journal:
- Development and Psychopathology / Volume 33 / Issue 1 / February 2021
- Published online by Cambridge University Press:
- 03 March 2020, pp. 301-312
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Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.
Intergenerational transmission of family meal patterns from adolescence to parenthood: longitudinal associations with parents’ dietary intake, weight-related behaviours and psychosocial well-being
- Jerica M Berge, Jonathan Miller, Allison Watts, Nicole Larson, Katie A Loth, Dianne Neumark-Sztainer
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- Journal:
- Public Health Nutrition / Volume 21 / Issue 2 / February 2018
- Published online by Cambridge University Press:
- 17 October 2017, pp. 299-308
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Objective
The present study examined longitudinal associations between four family meal patterns (i.e. never had regular family meals, started having regular family meals, stopped having regular family meals, maintained having regular family meals) and young adult parents’ dietary intake, weight-related behaviours and psychosocial well-being. In addition, family meal patterns of parents were compared with those of non-parents.
DesignAnalysis of data from the longitudinal Project EAT (Eating and Activity in Adolescents and Young Adults) study. Linear and logistic regressions were used to examine the associations between family meal patterns and parents’ dietary intake, weight-related behaviours and psychosocial well-being.
SettingSchool and in-home settings.
SubjectsAt baseline (1998; EAT-I), adolescents (n 4746) from socio-economically and racially/ethnically diverse households completed a survey and anthropometric measurements at school. At follow-up (2015; EAT-IV), participants who were parents (n 726) and who were non-parents with significant others (n 618) completed an online survey.
ResultsYoung adult parents who reported having regular family meals as an adolescent and as a parent (‘maintainers’), or who started having regular family meals with their own families (‘starters’), reported more healthful dietary, weight-related and psychosocial outcomes compared with young adults who never reported having regular family meals (‘nevers’; P<0·05). In addition, parents were more likely to be family meal starters than non-parents.
ConclusionsResults suggest that mental and physical health benefits of having regular family meals may be realized as a parent whether the routine of regular family meals is carried forward from adolescence into parenthood, or if the routine is started in parenthood.
Does growth restriction increase the vulnerability to acute ventilation-induced brain injury in newborn lambs? Implications for future health and disease
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- B. J. Allison, S. B. Hooper, E. Coia, G. Jenkin, A. Malhotra, V. Zahra, A. Sehgal, M. Kluckow, A. W. Gill, T. Yawno, G. R. Polglase, M. Castillo-Melendez, S. L. Miller
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- Journal:
- Journal of Developmental Origins of Health and Disease / Volume 8 / Issue 5 / October 2017
- Published online by Cambridge University Press:
- 09 August 2017, pp. 556-565
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Fetal growth restriction (FGR) and preterm birth are frequent co-morbidities, both are independent risks for brain injury. However, few studies have examined the mechanisms by which preterm FGR increases the risk of adverse neurological outcomes. We aimed to determine the effects of prematurity and mechanical ventilation (VENT) on the brain of FGR and appropriately grown (AG, control) lambs. We hypothesized that FGR preterm lambs are more vulnerable to ventilation-induced acute brain injury. FGR was surgically induced in fetal sheep (0.7 gestation) by ligation of a single umbilical artery. After 4 weeks, preterm lambs were euthanized at delivery or delivered and ventilated for 2 h before euthanasia. Brains and cerebrospinal fluid (CSF) were collected for analysis of molecular and structural indices of early brain injury. FGRVENT lambs had increased oxidative cell damage and brain injury marker S100B levels compared with all other groups. Mechanical ventilation increased inflammatory marker IL-8 within the brain of FGRVENT and AGVENT lambs. Abnormalities in the neurovascular unit and increased blood–brain barrier permeability were observed in FGRVENT lambs, as well as an altered density of vascular tight junctions markers. FGR and AG preterm lambs have different responses to acute injurious mechanical ventilation, changes which appear to have been developmentally programmed in utero.
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- By Mitchell Aboulafia, Frederick Adams, Marilyn McCord Adams, Robert M. Adams, Laird Addis, James W. Allard, David Allison, William P. Alston, Karl Ameriks, C. Anthony Anderson, David Leech Anderson, Lanier Anderson, Roger Ariew, David Armstrong, Denis G. Arnold, E. J. Ashworth, Margaret Atherton, Robin Attfield, Bruce Aune, Edward Wilson Averill, Jody Azzouni, Kent Bach, Andrew Bailey, Lynne Rudder Baker, Thomas R. Baldwin, Jon Barwise, George Bealer, William Bechtel, Lawrence C. Becker, Mark A. Bedau, Ernst Behler, José A. Benardete, Ermanno Bencivenga, Jan Berg, Michael Bergmann, Robert L. Bernasconi, Sven Bernecker, Bernard Berofsky, Rod Bertolet, Charles J. Beyer, Christian Beyer, Joseph Bien, Joseph Bien, Peg Birmingham, Ivan Boh, James Bohman, Daniel Bonevac, Laurence BonJour, William J. Bouwsma, Raymond D. Bradley, Myles Brand, Richard B. Brandt, Michael E. Bratman, Stephen E. Braude, Daniel Breazeale, Angela Breitenbach, Jason Bridges, David O. Brink, Gordon G. Brittan, Justin Broackes, Dan W. Brock, Aaron Bronfman, Jeffrey E. Brower, Bartosz Brozek, Anthony Brueckner, Jeffrey Bub, Lara Buchak, Otavio Bueno, Ann E. Bumpus, Robert W. Burch, John Burgess, Arthur W. Burks, Panayot Butchvarov, Robert E. Butts, Marina Bykova, Patrick Byrne, David Carr, Noël Carroll, Edward S. Casey, Victor Caston, Victor Caston, Albert Casullo, Robert L. Causey, Alan K. L. Chan, Ruth Chang, Deen K. Chatterjee, Andrew Chignell, Roderick M. Chisholm, Kelly J. Clark, E. J. Coffman, Robin Collins, Brian P. Copenhaver, John Corcoran, John Cottingham, Roger Crisp, Frederick J. Crosson, Antonio S. Cua, Phillip D. Cummins, Martin Curd, Adam Cureton, Andrew Cutrofello, Stephen Darwall, Paul Sheldon Davies, Wayne A. Davis, Timothy Joseph Day, Claudio de Almeida, Mario De Caro, Mario De Caro, John Deigh, C. F. Delaney, Daniel C. Dennett, Michael R. DePaul, Michael Detlefsen, Daniel Trent Devereux, Philip E. Devine, John M. Dillon, Martin C. Dillon, Robert DiSalle, Mary Domski, Alan Donagan, Paul Draper, Fred Dretske, Mircea Dumitru, Wilhelm Dupré, Gerald Dworkin, John Earman, Ellery Eells, Catherine Z. Elgin, Berent Enç, Ronald P. Endicott, Edward Erwin, John Etchemendy, C. Stephen Evans, Susan L. Feagin, Solomon Feferman, Richard Feldman, Arthur Fine, Maurice A. Finocchiaro, William FitzPatrick, Richard E. Flathman, Gvozden Flego, Richard Foley, Graeme Forbes, Rainer Forst, Malcolm R. Forster, Daniel Fouke, Patrick Francken, Samuel Freeman, Elizabeth Fricker, Miranda Fricker, Michael Friedman, Michael Fuerstein, Richard A. Fumerton, Alan Gabbey, Pieranna Garavaso, Daniel Garber, Jorge L. A. Garcia, Robert K. Garcia, Don Garrett, Philip Gasper, Gerald Gaus, Berys Gaut, Bernard Gert, Roger F. Gibson, Cody Gilmore, Carl Ginet, Alan H. Goldman, Alvin I. Goldman, Alfonso Gömez-Lobo, Lenn E. Goodman, Robert M. Gordon, Stefan Gosepath, Jorge J. E. Gracia, Daniel W. Graham, George A. Graham, Peter J. Graham, Richard E. Grandy, I. Grattan-Guinness, John Greco, Philip T. Grier, Nicholas Griffin, Nicholas Griffin, David A. Griffiths, Paul J. Griffiths, Stephen R. Grimm, Charles L. Griswold, Charles B. Guignon, Pete A. Y. Gunter, Dimitri Gutas, Gary Gutting, Paul Guyer, Kwame Gyekye, Oscar A. Haac, Raul Hakli, Raul Hakli, Michael Hallett, Edward C. Halper, Jean Hampton, R. James Hankinson, K. R. Hanley, Russell Hardin, Robert M. Harnish, William Harper, David Harrah, Kevin Hart, Ali Hasan, William Hasker, John Haugeland, Roger Hausheer, William Heald, Peter Heath, Richard Heck, John F. Heil, Vincent F. Hendricks, Stephen Hetherington, Francis Heylighen, Kathleen Marie Higgins, Risto Hilpinen, Harold T. Hodes, Joshua Hoffman, Alan Holland, Robert L. Holmes, Richard Holton, Brad W. Hooker, Terence E. Horgan, Tamara Horowitz, Paul Horwich, Vittorio Hösle, Paul Hoβfeld, Daniel Howard-Snyder, Frances Howard-Snyder, Anne Hudson, Deal W. Hudson, Carl A. Huffman, David L. Hull, Patricia Huntington, Thomas Hurka, Paul Hurley, Rosalind Hursthouse, Guillermo Hurtado, Ronald E. Hustwit, Sarah Hutton, Jonathan Jenkins Ichikawa, Harry A. Ide, David Ingram, Philip J. Ivanhoe, Alfred L. Ivry, Frank Jackson, Dale Jacquette, Joseph Jedwab, Richard Jeffrey, David Alan Johnson, Edward Johnson, Mark D. Jordan, Richard Joyce, Hwa Yol Jung, Robert Hillary Kane, Tomis Kapitan, Jacquelyn Ann K. Kegley, James A. Keller, Ralph Kennedy, Sergei Khoruzhii, Jaegwon Kim, Yersu Kim, Nathan L. King, Patricia Kitcher, Peter D. Klein, E. D. Klemke, Virginia Klenk, George L. Kline, Christian Klotz, Simo Knuuttila, Joseph J. Kockelmans, Konstantin Kolenda, Sebastian Tomasz Kołodziejczyk, Isaac Kramnick, Richard Kraut, Fred Kroon, Manfred Kuehn, Steven T. Kuhn, Henry E. Kyburg, John Lachs, Jennifer Lackey, Stephen E. Lahey, Andrea Lavazza, Thomas H. Leahey, Joo Heung Lee, Keith Lehrer, Dorothy Leland, Noah M. Lemos, Ernest LePore, Sarah-Jane Leslie, Isaac Levi, Andrew Levine, Alan E. Lewis, Daniel E. Little, Shu-hsien Liu, Shu-hsien Liu, Alan K. L. Chan, Brian Loar, Lawrence B. Lombard, John Longeway, Dominic McIver Lopes, Michael J. Loux, E. J. Lowe, Steven Luper, Eugene C. Luschei, William G. Lycan, David Lyons, David Macarthur, Danielle Macbeth, Scott MacDonald, Jacob L. Mackey, Louis H. Mackey, Penelope Mackie, Edward H. Madden, Penelope Maddy, G. B. Madison, Bernd Magnus, Pekka Mäkelä, Rudolf A. Makkreel, David Manley, William E. Mann (W.E.M.), Vladimir Marchenkov, Peter Markie, Jean-Pierre Marquis, Ausonio Marras, Mike W. Martin, A. P. Martinich, William L. McBride, David McCabe, Storrs McCall, Hugh J. McCann, Robert N. McCauley, John J. McDermott, Sarah McGrath, Ralph McInerny, Daniel J. McKaughan, Thomas McKay, Michael McKinsey, Brian P. McLaughlin, Ernan McMullin, Anthonie Meijers, Jack W. Meiland, William Jason Melanson, Alfred R. Mele, Joseph R. Mendola, Christopher Menzel, Michael J. Meyer, Christian B. Miller, David W. Miller, Peter Millican, Robert N. Minor, Phillip Mitsis, James A. Montmarquet, Michael S. Moore, Tim Moore, Benjamin Morison, Donald R. Morrison, Stephen J. Morse, Paul K. Moser, Alexander P. D. Mourelatos, Ian Mueller, James Bernard Murphy, Mark C. Murphy, Steven Nadler, Jan Narveson, Alan Nelson, Jerome Neu, Samuel Newlands, Kai Nielsen, Ilkka Niiniluoto, Carlos G. Noreña, Calvin G. Normore, David Fate Norton, Nikolaj Nottelmann, Donald Nute, David S. Oderberg, Steve Odin, Michael O’Rourke, Willard G. Oxtoby, Heinz Paetzold, George S. Pappas, Anthony J. Parel, Lydia Patton, R. P. Peerenboom, Francis Jeffry Pelletier, Adriaan T. Peperzak, Derk Pereboom, Jaroslav Peregrin, Glen Pettigrove, Philip Pettit, Edmund L. Pincoffs, Andrew Pinsent, Robert B. Pippin, Alvin Plantinga, Louis P. Pojman, Richard H. Popkin, John F. Post, Carl J. Posy, William J. Prior, Richard Purtill, Michael Quante, Philip L. Quinn, Philip L. Quinn, Elizabeth S. Radcliffe, Diana Raffman, Gerard Raulet, Stephen L. Read, Andrews Reath, Andrew Reisner, Nicholas Rescher, Henry S. Richardson, Robert C. Richardson, Thomas Ricketts, Wayne D. Riggs, Mark Roberts, Robert C. Roberts, Luke Robinson, Alexander Rosenberg, Gary Rosenkranz, Bernice Glatzer Rosenthal, Adina L. Roskies, William L. Rowe, T. M. Rudavsky, Michael Ruse, Bruce Russell, Lilly-Marlene Russow, Dan Ryder, R. M. Sainsbury, Joseph Salerno, Nathan Salmon, Wesley C. Salmon, Constantine Sandis, David H. Sanford, Marco Santambrogio, David Sapire, Ruth A. Saunders, Geoffrey Sayre-McCord, Charles Sayward, James P. Scanlan, Richard Schacht, Tamar Schapiro, Frederick F. Schmitt, Jerome B. Schneewind, Calvin O. Schrag, Alan D. Schrift, George F. Schumm, Jean-Loup Seban, David N. Sedley, Kenneth Seeskin, Krister Segerberg, Charlene Haddock Seigfried, Dennis M. Senchuk, James F. Sennett, William Lad Sessions, Stewart Shapiro, Tommie Shelby, Donald W. Sherburne, Christopher Shields, Roger A. Shiner, Sydney Shoemaker, Robert K. Shope, Kwong-loi Shun, Wilfried Sieg, A. John Simmons, Robert L. Simon, Marcus G. Singer, Georgette Sinkler, Walter Sinnott-Armstrong, Matti T. Sintonen, Lawrence Sklar, Brian Skyrms, Robert C. Sleigh, Michael Anthony Slote, Hans Sluga, Barry Smith, Michael Smith, Robin Smith, Robert Sokolowski, Robert C. Solomon, Marta Soniewicka, Philip Soper, Ernest Sosa, Nicholas Southwood, Paul Vincent Spade, T. L. S. Sprigge, Eric O. Springsted, George J. Stack, Rebecca Stangl, Jason Stanley, Florian Steinberger, Sören Stenlund, Christopher Stephens, James P. Sterba, Josef Stern, Matthias Steup, M. A. Stewart, Leopold Stubenberg, Edith Dudley Sulla, Frederick Suppe, Jere Paul Surber, David George Sussman, Sigrún Svavarsdóttir, Zeno G. Swijtink, Richard Swinburne, Charles C. Taliaferro, Robert B. Talisse, John Tasioulas, Paul Teller, Larry S. Temkin, Mark Textor, H. S. Thayer, Peter Thielke, Alan Thomas, Amie L. Thomasson, Katherine Thomson-Jones, Joshua C. Thurow, Vzalerie Tiberius, Terrence N. Tice, Paul Tidman, Mark C. Timmons, William Tolhurst, James E. Tomberlin, Rosemarie Tong, Lawrence Torcello, Kelly Trogdon, J. D. Trout, Robert E. Tully, Raimo Tuomela, John Turri, Martin M. Tweedale, Thomas Uebel, Jennifer Uleman, James Van Cleve, Harry van der Linden, Peter van Inwagen, Bryan W. Van Norden, René van Woudenberg, Donald Phillip Verene, Samantha Vice, Thomas Vinci, Donald Wayne Viney, Barbara Von Eckardt, Peter B. M. Vranas, Steven J. Wagner, William J. Wainwright, Paul E. Walker, Robert E. Wall, Craig Walton, Douglas Walton, Eric Watkins, Richard A. Watson, Michael V. Wedin, Rudolph H. Weingartner, Paul Weirich, Paul J. Weithman, Carl Wellman, Howard Wettstein, Samuel C. Wheeler, Stephen A. White, Jennifer Whiting, Edward R. Wierenga, Michael Williams, Fred Wilson, W. Kent Wilson, Kenneth P. Winkler, John F. Wippel, Jan Woleński, Allan B. Wolter, Nicholas P. Wolterstorff, Rega Wood, W. Jay Wood, Paul Woodruff, Alison Wylie, Gideon Yaffe, Takashi Yagisawa, Yutaka Yamamoto, Keith E. Yandell, Xiaomei Yang, Dean Zimmerman, Günter Zoller, Catherine Zuckert, Michael Zuckert, Jack A. Zupko (J.A.Z.)
- Edited by Robert Audi, University of Notre Dame, Indiana
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- The Cambridge Dictionary of Philosophy
- Published online:
- 05 August 2015
- Print publication:
- 27 April 2015, pp ix-xxx
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A roadmap for Antarctic and Southern Ocean science for the next two decades and beyond
- M.C. Kennicutt II, S.L. Chown, J.J. Cassano, D. Liggett, L.S. Peck, R. Massom, S.R. Rintoul, J. Storey, D.G. Vaughan, T.J. Wilson, I. Allison, J. Ayton, R. Badhe, J. Baeseman, P.J. Barrett, R.E. Bell, N. Bertler, S. Bo, A. Brandt, D. Bromwich, S.C. Cary, M.S. Clark, P. Convey, E.S. Costa, D. Cowan, R. Deconto, R. Dunbar, C. Elfring, C. Escutia, J. Francis, H.A. Fricker, M. Fukuchi, N. Gilbert, J. Gutt, C. Havermans, D. Hik, G. Hosie, C. Jones, Y.D. Kim, Y. Le Maho, S.H. Lee, M. Leppe, G. Leitchenkov, X. Li, V. Lipenkov, K. Lochte, J. López-Martínez, C. Lüdecke, W. Lyons, S. Marenssi, H. Miller, P. Morozova, T. Naish, S. Nayak, R. Ravindra, J. Retamales, C.A. Ricci, M. Rogan-Finnemore, Y. Ropert-Coudert, A.A. Samah, L. Sanson, T. Scambos, I.R. Schloss, K. Shiraishi, M.J. Siegert, J.C. Simões, B. Storey, M.D. Sparrow, D.H. Wall, J.C. Walsh, G. Wilson, J.G. Winther, J.C. Xavier, H. Yang, W.J. Sutherland
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- Journal:
- Antarctic Science / Volume 27 / Issue 1 / February 2015
- Published online by Cambridge University Press:
- 18 September 2014, pp. 3-18
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Antarctic and Southern Ocean science is vital to understanding natural variability, the processes that govern global change and the role of humans in the Earth and climate system. The potential for new knowledge to be gained from future Antarctic science is substantial. Therefore, the international Antarctic community came together to ‘scan the horizon’ to identify the highest priority scientific questions that researchers should aspire to answer in the next two decades and beyond. Wide consultation was a fundamental principle for the development of a collective, international view of the most important future directions in Antarctic science. From the many possibilities, the horizon scan identified 80 key scientific questions through structured debate, discussion, revision and voting. Questions were clustered into seven topics: i) Antarctic atmosphere and global connections, ii) Southern Ocean and sea ice in a warming world, iii) ice sheet and sea level, iv) the dynamic Earth, v) life on the precipice, vi) near-Earth space and beyond, and vii) human presence in Antarctica. Answering the questions identified by the horizon scan will require innovative experimental designs, novel applications of technology, invention of next-generation field and laboratory approaches, and expanded observing systems and networks. Unbiased, non-contaminating procedures will be required to retrieve the requisite air, biota, sediment, rock, ice and water samples. Sustained year-round access to Antarctica and the Southern Ocean will be essential to increase winter-time measurements. Improved models are needed that represent Antarctica and the Southern Ocean in the Earth System, and provide predictions at spatial and temporal resolutions useful for decision making. A co-ordinated portfolio of cross-disciplinary science, based on new models of international collaboration, will be essential as no scientist, programme or nation can realize these aspirations alone.
Initial Results of an Intercomparison of AMS-Based Atmospheric 14CO2 Measurements
- John Miller, Scott Lehman, Chad Wolak, Jocelyn Turnbull, Gregory Dunn, Heather Graven, Ralph Keeling, Harro A J Meijer, Anita Th Aerts-Bijma, Sanne W L Palstra, Andrew M Smith, Colin Allison, John Southon, Xiaomei Xu, Takakiyo Nakazawa, Shuji Aoki, Toshio Nakamura, Thomas Guilderson, Brian LaFranchi, Hitoshi Mukai, Yukio Terao, Masao Uchida, Miyuki Kondo
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- Journal:
- Radiocarbon / Volume 55 / Issue 3 / 2013
- Published online by Cambridge University Press:
- 09 February 2016, pp. 1475-1483
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- 2013
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This article presents results from the first 3 rounds of an international intercomparison of measurements of Δ14CO2 in liter-scale samples of whole air by groups using accelerator mass spectrometry (AMS). The ultimate goal of the intercomparison is to allow the merging of Δ14CO2 data from different groups, with the confidence that differences in the data are geophysical gradients and not artifacts of calibration. Eight groups have participated in at least 1 round of the intercomparison, which has so far included 3 rounds of air distribution between 2007 and 2010. The comparison is intended to be ongoing, so that: a) the community obtains a regular assessment of differences between laboratories; and b) individual laboratories can begin to assess the long-term repeatability of their measurements of the same source air. Air used in the intercomparison was compressed into 2 high-pressure cylinders in 2005 and 2006 at Niwot Ridge, Colorado (USA), with one of the tanks “spiked” with fossil CO2, so that the 2 tanks span the range of Δ14CO2 typically encountered when measuring air from both remote background locations and polluted urban ones. Three groups show interlaboratory comparability within l% for ambient level Δ14CO2. For high CO2/low Δ14CO2 air, 4 laboratories showed comparability within 2%. This approaches the goals set out by the World Meteorological Organization (WMO) CO2 Measurements Experts Group in 2005. One important observation is that single-sample precisions typically reported by the AMS community cannot always explain the observed differences within and between laboratories. This emphasizes the need to use long-term repeatability as a metric for measurement precision, especially in the context of long-term atmospheric monitoring.
Moderating role of the MAOA genotype in antisocial behaviour
- David M. Fergusson, Joseph M. Boden, L. John Horwood, Allison Miller, Martin A. Kennedy
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- The British Journal of Psychiatry / Volume 200 / Issue 2 / February 2012
- Published online by Cambridge University Press:
- 02 January 2018, pp. 116-123
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- February 2012
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Background
Recent studies have examined gene×environment (G×E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between exposure to adversity and antisocial behaviour. The present study examined a novel method for assessing interactions between a single gene and multiple risk factors related to environmental and personal adversity.
AimsTo test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to a series of risk factors.
MethodParticipants were 399 males from the Christchurch Health and Development Study who had complete data on: (a) MAOA promoter region variable number tandem repeat genotype; (b) antisocial behaviour (criminal offending) to age 30 and convictions to age 21; and (c) maternal smoking during pregnancy, IQ, childhood maltreatment and school failure.
ResultsPoisson regression models were fitted to three antisocial behaviour outcomes (property/violent offending ages 15–30; and convictions ages 17–21), using measures of exposure to adverse childhood circumstances. The analyses revealed consistent evidence of G x E interactions, such that those with the low-activity MAOA variant who were exposed to adversity in childhood were significantly more likely to report offending in late adolescence and early adulthood.
ConclusionsThe present findings add to the evidence suggesting that there is a stable G x E interaction involving MAOA, a range of adverse environmental and personal factors, and antisocial behaviour across the life course. These analyses also demonstrate the utility of using multiple environmental/personal exposures to test G×E interactions.
MAOA, abuse exposure and antisocial behaviour: 30-year longitudinal study
- David M. Fergusson, Joseph M. Boden, L. John Horwood, Allison L. Miller, Martin A. Kennedy
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- Journal:
- The British Journal of Psychiatry / Volume 198 / Issue 6 / June 2011
- Published online by Cambridge University Press:
- 02 January 2018, pp. 457-463
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- June 2011
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Background
Recent studies have raised issues concerning the replicability of gene × environment (G × E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between abuse or maltreatment exposure and antisocial behaviour. This study attempted to replicate the findings in this area using a 30-year longitudinal study that has strong resemblance to the original research cohort.
AimsTo test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to abuse exposure.
MethodParticipants were 398 males from the Christchurch Health and Development Study who had complete data on: MAOA promoter region variable number tandem repeat genotype; antisocial behaviour to age 30; and exposure to childhood sexual and physical abuse.
ResultsRegression models were fitted to five antisocial behaviour outcomes (self-reported property offending; self-reported violent offending; convictions for property/violent offending; conduct problems; hostility) observed from age 16 to 30, using measures of childhood exposure to sexual and physical abuse. The analyses revealed consistent evidence of G × E interactions, with those having the low-activity MAOA variant and who were exposed to abuse in childhood being significantly more likely to report later offending, conduct problems and hostility. These interactions remained statistically significant after control for a range of potentially confounding factors. Findings for convictions data were somewhat weaker.
ConclusionsThe present findings add to the evidence suggesting that there is a stable G × E interaction involving MAOA, abuse exposure and antisocial behaviour across the life course.
Life stress, 5-HTTLPR and mental disorder: findings from a 30-year longitudinal study
- David M. Fergusson, L. John Horwood, Allison L. Miller, Martin A. Kennedy
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- Journal:
- The British Journal of Psychiatry / Volume 198 / Issue 2 / February 2011
- Published online by Cambridge University Press:
- 02 January 2018, pp. 129-135
- Print publication:
- February 2011
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Background
Recent meta-analyses have raised concerns about the replicability of gene × environment interactions involving the serotonin transporter gene (5-HTTLPR) in moderating the associations between adverse life events and mental disorders.
AimsTo use data gathered over the course of a 30-year longitudinal study of a New Zealand birth cohort to test the hypothesis that the presence of short (‘s’) alleles of 5-HTTLPR are associated with an increased response to life stress.
MethodParticipants were 893 individuals from the Christchurch Health and Development Study who had complete data on: the 5-HTTLPR genotype; psychiatric disorders up to the age of 30; and exposure to childhood and adult adverse life events.
ResultsA series of 104 regression models were fitted to four mental health outcomes (depressive symptoms, major depression, anxiety disorder and suicidal ideation) observed at ages 18, 21, 25 and 30 using 13 measures of life-course stress that spanned childhood and adult stressors. Both multiplicative and additive models were fitted to the data. No evidence was found that would support the hypothesis that ‘s' alleles of 5-HTTLPR are associated with increased responsivity to life stressors.
ConclusionsThe present findings add to the evidence suggesting that it is unlikely that there is a stable gene × environment interaction involving 5-HTTLPR, life stress and mental disorders.
Contributors
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- By Shamsuddin Akhtar, Greg Albert, Sidney Allison, Muhammad Anwar, Haruo Arita, Amanda Barker, Mary Hanna Bekhit, Jeanna Blitz, Tyson Bolinske, David Burbulys, Asokumar Buvanendran, Gregory Cain, Keith A. Candiotti, Daniel B. Carr, Derek Chalmers, John Charney, Rex Cheng, Roger Chou, Keun Sam Chung, Anna Clebone, Frederick Conlin, Susan Dabu-Bondoc, Tiffany Denepitiya-Balicki, Jeanette Derdemezi, Anahat Kaur Dhillon, Ho Dzung, Juan Jose Egas, Stephen M. Eskaros, Zhuang T. Fang, Claudia R. Fernandez Robles, Victor A. Filadora, Ellen Flanagan, Dan Froicu, Allison Gandey, Nehal Gatha, Boris Gelman, Christopher Gharibo, Muhammad K. Ghori, Brian Ginsberg, Michael E. Goldberg, Jeff Gudin, Thomas Halaszynski, Martin Hale, Dorothea Hall, Craig T. Hartrick, Justin Hata, Lars E. Helgeson, Joe C. Hong, Richard W. Hong, Balazs Horvath, Eric S. Hsu, Gabriel Jacobs, Jonathan S. Jahr, Rongjie Jaing, Inderjeet Singh Julka, Zeev N. Kain, Clinton Kakazu, Kianusch Kiai, Mary Keyes, Michael M. Kim, Peter G. Lacouture, Ryan Lanier, Vivian K. Lee, Mark J. Lema, Oscar A. de Leon-Casasola, Imanuel Lerman, Philip Levin, Steven Levin, JinLei Li, Eric C. Lin, Sharon Lin, David A. Lindley, Ana M. Lobo, Marisa Lomanto, Mirjana Lovrincevic, Brenda C. McClain, Tariq Malik, Jure Marijic, Joseph Marino, Laura Mechtler, Alan Miller, Carly Miller, Amit Mirchandani, Sukanya Mitra, Fleurise Montecillo, James M. Moore, Debra E. Morrison, Philip F. Morway, Carsten Nadjat-Haiem, Hamid Nourmand, Dana Oprea, Sunil J. Panchal, Edward J. Park, Kathleen Ji Park, Kellie Park, Parisa Partownavid, Akta Patel, Bijal Patel, Komal D. Patel, Neesa Patel, Swati Patel, Paul M. Peloso, Danielle Perret, Anthony DePlato, Marjorie Podraza Stiegler, Despina Psillides, Mamatha Punjala, Johan Raeder, Siamak Rahman, Aziz M. Razzuk, Maggy G. Riad, Kristin L. Richards, R. Todd Rinnier, Ian W. Rodger, Joseph Rosa, Abraham Rosenbaum, Alireza Sadoughi, Veena Salgar, Leslie Schechter, Michael Seneca, Yasser F. Shaheen, James H. Shull, Elizabeth Sinatra, Raymond S. Sinatra, Neil Singla, Neil Sinha, Denis V. Snegovskikh, Dmitri Souzdalnitski, Julie Sramcik, Zoreh Steffens, Alexander Timchenko, Vadim Tokhner, Marc C. Torjman, Co T. Truong, Nalini Vadivelu, Ashley Vaughn, Anjali Vira, Eugene R. Viscusi, Dajie Wang, Shu-ming Wang, J. Michael Watkins-Pitchford, Steven J. Weisman, Ira Whitten, Bryan S. Williams, Jeremy M. Wong, Thomas Wong, Christopher Wray, Yaw Wu, Anthony T. Yarussi, Laurie Yonemoto, Bita H. Zadeh, Jill Zafar, Martha Zegarra, Keren Ziv
- Edited by Raymond S. Sinatra, Jonathan S. Jahr, University of California, Los Angeles, School of Medicine, J. Michael Watkins-Pitchford
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- Book:
- The Essence of Analgesia and Analgesics
- Published online:
- 06 December 2010
- Print publication:
- 14 October 2010, pp xi-xviii
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8 - Conflict and Hurt in Close Relationships
- from PART III - HURTFUL ACTS
- Edited by Anita L. Vangelisti, University of Texas, Austin
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- Book:
- Feeling Hurt in Close Relationships
- Published online:
- 04 August 2010
- Print publication:
- 31 July 2009, pp 143-166
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Summary
According to Vangelisti (2007), “whenever two people communicate, they risk hurting each other” (p. 121). Such risk is elevated when the communication involves conflict. Interactions involving conflicts tend to be more arousing and to elicit more negative emotions than do other conversations (Levenson & Gottman, 1985). The heightened affective intensity associated with conflict provides abundant occasions for hurt feelings. Indeed, the apparent connection between conflict and hurt is strong enough that some scholars treat being hurt as synonomous with interpersonal conflict (e.g., Wainryb, Brehl, & Matwin, 2005). Other scholars simply assume that conflict is inherently hurtful; for instance, one study examining the “most frequently used strategies of relational conflict resolution” was titled “You always hurt the one you love…” (Fitzpatrick & Winke, 1979, p. 3).
Despite the belief that conflict and hurt are closely related, there is surprisingly little research that systematically examines their association. This lack of focus on hurt and conflict is remarkable given that other emotions, like anger, are frequently linked to conflict (e.g., Notarius, Lashley, & Sullivan, 1997). Clearly, addressing this gap in the literature could be useful, potentially answering questions such as “How can individuals make their conflicts less hurtful?” and “Can (and should) people prevent hurt feelings from leading to interpersonal conflicts?” A single chapter can only begin to address such questions, but our goals are (a) to adumbrate the research that does exist on conflict and hurt and (b) to provide an initial framework for thinking about how the hurtful aspects of conflict can be reduced.
A dopamine transporter polymorphism is a risk factor for borderline personality disorder in depressed patients
- PETER R. JOYCE, PATRICK C. McHUGH, JANICE M. McKENZIE, PATRICK F. SULLIVAN, ROGER T. MULDER, SUZANNE E. LUTY, JANET D. CARTER, CHRISTOPHER M. A. FRAMPTON, C. ROBERT CLONINGER, ALLISON M. MILLER, MARTIN A. KENNEDY
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- Journal:
- Psychological Medicine / Volume 36 / Issue 6 / June 2006
- Published online by Cambridge University Press:
- 20 April 2006, pp. 807-813
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Background. Borderline personality disorder (BPD) is often co-morbid with major depression and may complicate its treatment. We were interested in differences in genetic and developmental risk factors between depressed patients with or without a co-morbid BPD.
Method. Out-patients with major depressive disorder were recruited for two treatment trials. Assessment of depressed patients included the assessment of personality disorders, developmental risk factors and DNA samples for genetic analyses.
Results. In each study there was a significant association between the 9-repeat allele of the dopamine transporter (DAT1) and BPD, with odds ratios (OR) >3 and p[les ]0·02. This association remained significant when developmental risk factors for BPD (childhood abuse and neglect and borderline temperament) were also included in the analyses. The OR was even larger in the depressed patients aged [ges ]35 years (OR 9·31, p=0·005).
Conclusion. This replicated association in depressed patients between the 9-repeat allele of DAT1 and BPD may provide clues to understanding the neurobiology of BPD. The finding that the association is larger in the older depressed patients, suggests that the 9-repeat allele may be associated with a poorer prognosis BPD, rather than a young adult limited variant of BPD.
Reversed diurnal variation in depression: associations with a differential antidepressant response, tryptophan:large neutral amino acid ratio and serotonin transporter polymorphisms
- PETER R. JOYCE, RICHARD J. PORTER, ROGER T. MULDER, SUZANNE E. LUTY, JANICE M. McKENZIE, ALLISON L. MILLER, MARTIN A. KENNEDY
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- Journal:
- Psychological Medicine / Volume 35 / Issue 4 / April 2005
- Published online by Cambridge University Press:
- 17 March 2005, pp. 511-517
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Background. Although diurnal variation of mood is a widely recognized symptom of depression, the clinical, neurobiological and psychopharmacological significance of this symptom has not previously been reported.
Method. A total of 195 depressed out-patients underwent a detailed clinical and neurobiological assessment, and were then randomized to treatment with either fluoxetine or nortriptyline.
Results. Of the 195 depressed patients, 62 had a pattern of reversed diurnal variation (i.e. worse in the evening). Those with reversed diurnal variation had a poorer response to a serotonergic antidepressant, were less likely to have bipolar II disorder, had a higher tryptophan:large neutral amino acid ratio and had different allele frequencies of the polymorphisms in the promoter region of the serotonin transporter.
Conclusions. These findings raise the possibility of serotonergic influence on diurnal variation, and that the symptom of reversed diurnal variation is of relevance to antidepressant prescribing.