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S.2006]Differential regulation of metabolic, neuroendocrine, and immune function by leptin in humans8481-63Proceedings of the National Academy of Sciences USA10322Adaptation, Physiological/drug effects/immunology Adipose Tissue Adult Body Fat Distribution Body Weight/drug effects Cells, Cultured Fasting Female Hormones/blood Humans Immunity/*drug effects Immunity, Natural/drug effects Insulin-Like Growth Factor I/metabolism Leptin/analogs & derivatives/blood/*pharmacology Leukocyte Count Neurosecretory Systems/*drug effects/immunology/*metabolism T-Lymphocytes/cytology/drug effects/immunology Time FactorsMay 30fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16714386 0027-8424 (Print)OProceedings of the National Academy of Sciences of the United States of America16714386Division of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.eng7=7XCutolo, M. Capellino, S. Sulli, A. Serioli, B. Secchi, M. E. Villaggio, B. Straub, R. H.2006!Estrogens and autoimmune diseases538-47*Annals of the New York Academy of Sciences1089Novfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17261796 0077-8923 (Print)*Annals of the New York Academy of Sciences17261796Research Laboratory and Division of Rheumatology, Department of Internal Medicine, University of Genova, Viale Benedetto XV, 6, 16132 Genova, Italy. mcutolo@unige.iteng?Dabbs, James M., Jr.1996)Testosterone, aggression, and delinquency179-190=Pharmacology, Biology, and Clinical Applications of Androgens Kelly, ChuckNew YorkWiley-Liss, Inc.?J=de la Rochebrochard, E. de Mouzon, J. Thepot, F. Thonneau, P.2006bFathers over 40 and increased failure to conceive: the lessons of in vitro fertilization in France1420-4Fertility and Sterility855Adult Age Distribution Aged Aged, 80 and over Fathers/*statistics & numerical data Female Fertilization in Vitro/*statistics & numerical data France/epidemiology Humans Incidence Infertility, Female/*epidemiology/*therapy Male Maternal Age Middle Aged Paternal Age Pregnancy Pregnancy Outcome/*epidemiology Pregnancy Rate *Registries Research Support, Non-U.S. Gov't Risk Assessment/*methods Risk Factors Treatment Failure Treatment OutcomeMayehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16616749166167498INED, Le Kremlin-Bicetre, F-94276, France. roche@ined.fr?ODewey, K. G. Lovelady, C. A. Nommsen-Rivers, L. A. McCrory, M. A. Lonnerdal, B.1994oA randomized study of the effects of aerobic exercise by lactating women on breast-milk volume and composition.449-453New England Journal of Medicine330?Ellison, P. T.1990?Human ovarian function and reproductive ecology: New hypotheses933-952American Anthropologist92American AnthropologiistD?Ellison, P. T.19950Breastfeeding, fertility, and maternal condition'Breastfeeding: Biocultural Perspectives#Dettwyler, K. A. Stuart-Macadam, P. Hawthorne, NYAldinne de Gruyter?Ellison, P. T.19962Developmental influences on adult ovarian function725-734!American Journal of Human Biology8?Ellison, P. T.1999-Reproductive ecology and reproductive cancers184-209KHormones, Health, and Behavior: a Socio-Ecological and Lifespan PerspectivePanter-Brick, C. Worthman, C. CambridgeCambridge University Press^?Ellison, P. T.2001On Fertile Ground Cambridge, MAHarvard UniversityQ?JEllison, P. T.2003"Energetics and reproductive effort342-51!American Journal of Human Biology153Amenorrhea *Energy Metabolism Female Fertilization Humans Male Parenting Postpartum Period Pregnancy/*metabolism/physiology Probability Sexual Behavior/physiology Time FactorsMay-Junehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1270471012704710TDepartment of Anthropology, Harvard University, Cambridge, Massachusetts 02138, USA.6?JgEllison, P. T. Bribiescas, R. G. Bentley, G. R. Campbell, B. C. Lipson, S. F. Panter-Brick, C. Hill, K.2002IPopulation variation in age-related decline in male salivary testosterone 3251-3253Human Reproduction1712DecShttp://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1245663212456632Department of Anthropology, Harvard University, Cambridge, MA, Department of Anthropology, Yale University, New Haven, CT, USA, Department of Anthropology, University College London, London, UK, Department of Anthropology, Boston University, Boston, MA, USA, Department of Anthropology, Durham University, Durham, UK and Department of Anthropology, University of New Mexico, Albuquerque, NM, USA.?)Ellison, P. T. Valeggia, C. Sherry, D. S.2005Human birth seasonality.379-400SSeasonality in Primates: Studies of Living and Extinct Human and Non-Human Primates!Brockman, D. K. van Schaik, C. P. CambridgeCambridge University Press?JEllison, P. T. Valeggia, C. R.2003;C-peptide levels and the duration of lactational amenorrhea1279-80Fertility and Sterility805Amenorrhea/*etiology C-Peptide/*urine Female Humans Lactation/*urine Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Time FactorsNovehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1460759014607590?Emery Thompson, M.2005Reproductive endocrinology of wild female chimpanzees (Pan troglodytes schweinfurthii): Methodological considerations and the role of hormones in sex and conception.137-158American Journal of Primatology67q=7JPGomez, L. Carrascosa, A. Yeste, D. Potau, N. Rique, S. Ruiz-Cuevas, P. Almar, J.1999vLeptin values in placental cord blood of human newborns with normal intrauterine growth after 30-42 weeks of gestation10-4Hormone Research511Birth Weight *Embryonic and Fetal Development Female Fetal Blood/*chemistry Gestational Age Humans Infant, Newborn/*blood Leptin Male Placenta Pregnancy Proteins/analysis/*metabolism Reference Values Regression Analysis Sex Characteristicsfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10095163 0301-0163 (Print)Hormone research10095163Department of Pediatrics, Endocrine and Hormone Laboratory Units, Autonomous University, Children's Hospital Vall d'Hebron, Barcelona, Spain.eng=7J(Gray, P. B. Yang, C. F. Pope, H. G., Jr.2006lFathers have lower salivary testosterone levels than unmarried men and married non-fathers in Beijing, China333-9"Proceedings of the Royal Society B2731584Adult Child, Preschool China *Fathers Female Humans Male Paternal Behavior Questionnaires Research Support, Non-U.S. Gov't Salivary Glands/*metabolism Testosterone/*metabolismFeb 7fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16543176 0962-8452 (Print) Proceedings16543176WDepartment of Biochemistry, Harvard University, Cambridge, MA, USA. peter.gray@univ.edueng ?J5Habicht, J. P. Yarbrough, C. Lechtig, A. Klein, R. E.1973DRelationship of birthweight, maternal nutrition and infant mortality533-46Nutrition Reports International75Americas Biology *Birth Weight *Body Weight Central America Demography Developing Countries Growth Guatemala Health *Infant Mortality Latin America Morbidity *Mortality North America *Nutrition Physiology Population Population Dynamics *Pregnancy *Reproduction Rural Population physical growth and mental development in rural Guatemala was started in 1969. A program was launched involving supplementation of pregnant mothers with a protein and calorie supplement ("atole") in 2 villages and another calorie supplement ("fresco") in 2 other villages. This paper presents an integrated quantitative approach to the analysis of data collected in the maternal supplementation program using 2 examples. The first example compares the effects of maternal height and weight at conception, and maternal caloric supplementation during pregnancy on birthweight. It was found that maternal childhood nutrition is as important a determinant of birthweight as is caloric supplementation during pregnancy. Similarly, the nutritional status of the mother during conception is as powerful a determinant of birthweight as is caloric supplementation during pregnancy. Past obstetrical history and maternal age do not affect these interrelationships among birthweight and maternal height, weight at conception, and maternal supplementation. The second example involves a consideration of postnatal function of the child, as well as several prenatal factors which affect infant mortality. Infant mortality in the study villages was found to be 4 times greater for babies with birthweight of 2.5 kg or less at term ("small for dates" babies infant mortality rate, 121/1,000) than for heavier babies (infant mortality rate, 30/1000) (p0.05). By increasing maternal calorie supplementation during pregnancy, the number of babies weighing 2.5 kg or less was reduced from 20% among babies born to mothers ingesting less than 5000 calories during pregnancy to 5% among babies born to mothers who consume more than 20,000 calories during pregnancy. The findings suggest that village infant mortality can be lowered, and the birth of "small for dates" babies prevented by ensuring adequate levels of maternal nutrition during pregnancy. Efforts to improve maternal nutrition should start in childhood for optimum infant survival.Mayfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12306500 12306500=7JHamilton, J. B. Mestler, G. E.1969iMortality and survival: comparison of eunuchs with intact men and women in a mentally retarded population395-411Journal of Gerontology244$Adolescent Adult Age Factors Aged Animals Castration Cats Child Continental Population Groups Eunuchism/complications/*mortality Female Humans Intelligence Kansas Male Mental Retardation/*complications/mortality Middle Aged Ovary/surgery Sex Factors Testis/physiology/surgery Vital StatisticsOctehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=5362349 0022-1422 (Print)Journal of gerontology5362349eng?JDHarman, S. M. Metter, E. J. Tobin, J. D. Pearson, J. Blackman, M. R.2001Longitudinal effects of aging on serum total and free testosterone levels in healthy men. Baltimore Longitudinal Study of Aging724-31.0Journal of Clinical Endocrinology and Metabolism862Adult Aging/*blood Baltimore Caucasoid Race Human Hypogonadism/blood/epidemiology Longitudinal Studies Male Middle Age Radioimmunoassay Regression Analysis Reproducibility of Results Sex Hormone-Binding Globulin/*analysis Social Class Testosterone/*bloodhttp://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11158037 http://jcem.endojournals.org/cgi/content/full/86/2/724 http://jcem.endojournals.org/cgi/content/abstract/86/2/72411158037The Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. harman@kronofoundation.org*? Hawkes, K.2004'Human longevity: the grandmother effect128-9Nature4286979CAdult Aged Animals Child *Child Rearing *Evolution Female Fertility/physiology Humans *Intergenerational Relations Life Expectancy Longevity/*physiology Male Maternal Behavior Middle Aged Models, Biological Mothers Parenting *Postmenopause Primates/physiology Reproduction/*physiology Selection (Genetics) Survival AnalysisMar 11fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15014476 15014476?Hill, K. Hurtado, A. M.1991HThe evolution of reproductive senescence and menopause in human females.315-350 Human Nature2?J-Homko, C. J. Sivan, E. Reece, E. A. Boden, G.1999 Fuel metabolism during pregnancy119-25&Seminars in Reproductive Endocrinology172*Carbohydrate Metabolism Diabetes, Gestational/*metabolism Female Humans Insulin/pharmacology Insulin Resistance/physiology *Lipid Metabolism Pregnancy/*metabolism Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10528363 10528363Department of Obstetrics and Gynecology and Reproductive Sciences, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.=7J(Huxsoll, C. C. Price, E. O. Adams, T. E.1998Testis function, carcass traits, and aggressive behavior of beef bulls actively immunized against gonadotropin-releasing hormone1760-6Journal of Animal Science767*Aggression Animals Antibodies/blood *Behavior, Animal Cattle/immunology/*physiology/psychology Drug Combinations Drug Implants Estradiol/administration & dosage/analogs & derivatives Gonadorelin/*immunology Immunization, Secondary/veterinary Male Meat/*standards Progesterone/administration & dosage Research Support, Non-U.S. Gov't Testis/growth & development/*physiology Testosterone/blood Vaccination/*veterinary Weight GainJulehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9690630 0021-8812 (Print)Journal of animal science9690630IDepartment of Animal Science, University of California, Davis 95616, USA.engG?JIngemarsson, I.2003Gender aspects of preterm birth34-38=BJOG : An International Journal of Obstetrics and Gynaecology 110 Suppl 20Abortion, Spontaneous Acidosis/congenital Adolescent Adult Blood Glucose/analysis Chromosomes, Human, Y Delivery, Obstetric Female Fetal Blood/chemistry Gestational Age Human Infant, Newborn Infant, Premature/*physiology Lung Diseases/congenital Male Neurodegenerative Diseases/etiology Placenta Praevia/etiology Pregnancy Respiratory Distress Syndrome/etiology Sex Differentiation/*physiology Sex RatioAprehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1276310912763109KDepartment of Obstetrics and Gynecology, University Hospital, Lund, Sweden.N}7J%Jasienska, G. Nenko, I. Jasienski, M.2006cDaughters increase longevity of fathers, but daughters and sons equally reduce longevity of mothers422-5!American Journal of Human Biology183Adolescent Adult Aged Aged, 80 and over Child Child, Preschool Comparative Study *Family Characteristics Female Humans Longevity/*physiology Male Middle Aged *Nuclear Family *Parents Poland/epidemiology Research Support, Non-U.S. Gov't Rural Population/trends Survival RateMay-Junfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16634019 1042-0533 (Print)16634019}Department of Epidemiology and Population Studies, Jagiellonian University, 31-531 Krakow, Poland. jasienska@post.harvard.edueng=7JJasienska, G. Thune, I.2001.Lifestyle, hormones, and risk of breast cancer586-7British Medical Journal3227286Adult Breast Neoplasms/epidemiology/*etiology/metabolism Comparative Study Developing Countries Energy Intake/physiology Female Humans Incidence *Life Style Nutritional Status Progesterone/*metabolism Risk Factors Saliva/metabolism United StatesMar 10fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11238153 0959-8138 (Print)BMJ (Clinical research ed11238153wInstitute of Public Health, Jagiellonian University, Grzegorzecka 20, 31-531 Krakow, Poland. jasienska@post.harvard.edueng?:Johnson, J. Canning, J. Kaneko, T. Pru, J. K. Tilly, J. L.2004KGermline stem cells and follicular renewal in the postnatal mammalian ovary145-50Nature4286979jAging/physiology Animals Biological Markers Busulfan/pharmacology Cell Count *Cell Differentiation/drug effects Cell Division/drug effects Female Gene Expression Regulation, Developmental Male Meiosis/drug effects/genetics Mice Mice, Inbred C57BL Mice, Transgenic Oocytes/*cytology/drug effects/transplantation Oogenesis/drug effects/physiology Ovarian Follicle/*cytology/drug effects/*growth & development/transplantation Pregnancy Regeneration/drug effects/*physiology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Sexual Maturation Stem Cell Transplantation Stem Cells/*cytology/drug effectsMar 11fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15014492 15014492Vincent Center for Reproductive Biology, Vincent Obstetrics and Gynecology Service, Massachusetts General Hospital, and Department of Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School, Boston, Massachusetts 02114, USA.?=7JKakarla, N. Bradshaw, K. D.20035Disorders of pubertal development: precocious puberty339-51!Seminars in Reproductive Medicine214Adolescent Animals Child Female Feminization/diagnosis/etiology Gonadotropins/physiology Humans Hypothalamus/physiology Male Ovary/physiology Pituitary Gland/physiology Puberty/physiology *Puberty, Precocious/diagnosis/drug therapy/etiology Testis/physiology Virilism/diagnosis/etiologyNovfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14724767 1526-8004 (Print)!Seminars in reproductive medicine14724767xDepartment of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9032, USA.eng?BKlibanski, A. Beitins, I. Z. Badger, T. Little, R. McArthur, J. W.1981+Reproductive function during fasting in men258-630Journal of Clinical Endocrinology and Metabolism532Adult *Fasting Food FSH/*blood/urine Gonadorelin/diagnostic use Human Kinetics LH/*blood/urine Male Middle Age Obesity/*metabolism Support, U.S. Gov't, P.H.S. Testosterone/*blood?Kline, J. Stein, Z. Susser, M.19899Conception to Birth: Epidemiology of Prenatal DevelopmentOxfordOxford University Press? Knott, C. D.2001(Female reproductive ecology of the apes.429-464(Reproductive Ecology and Human EvolutionEllison, P. T. HawthorneAldine de Gruyter?Kruger, D. J. Nesse, R. M.20044Sexual selection and the male:female mortality ratio66-85Evolutionary Psychology2=7JLa Cava, A. Matarese, G.2004 The weight of leptin in immunity371-9Nature Reviews Immunology45Cytokines/immunology Female Humans Immunity, Natural/*immunology Leptin/*immunology Male Models, Molecular Receptors, Cell Surface/*immunology Research Support, Non-U.S. Gov't Signal Transduction/immunologyMayfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15122202 1474-1733 (Print)Nature reviews15122202Autoimmunity and Tolerance Laboratory, Department of Medicine, University of California Los Angeles, 1000 Veteran Avenue 32-59, Los Angeles, California 90095-1670, USA. alacava@mednet.ucla.edueng? Lipson, S. F.2001,Metabolism, maturation, and ovarian function235-248(Reproductive Ecology and Human EvolutionEllison, P. T.New YorkAldine de Gruyter'?JLipson, S. F. Ellison, P. T.1996cComparison of salivary steroid profiles in naturally occurring conception and non-conception cycles2090-6Human Reproduction1110TAdult Body Weight Estradiol/*metabolism Female Fertilization/*physiology Humans Longitudinal Studies Menstrual Cycle/*physiology Osmolar Concentration Predictive Value of Tests Pregnancy Probability Progesterone/*metabolism Prospective Studies Radioimmunoassay Regression Analysis Research Support, U.S. Gov't, Non-P.H.S. Saliva/*metabolismOctehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8943508 8943508IDepartment of Anthropology, Harvard University, Cambridge, MA 02138, USA.s?J7Lunn, P. G. Austin, S. Prentice, A. M. Whitehead, R. G.1984yThe effect of improved nutrition on plasma prolactin concentrations and postpartum infertility in lactating Gambian women227-35&American Journal of Clinical Nutrition392Amenorrhea Anovulation Developing Countries Estradiol/blood Female Gambia Humans Infertility, Female/*blood *Lactation *Nutrition Postpartum Period Pregnancy Progesterone/blood Prolactin/*blood has been shown to be associated with a reduction in their plasma prolactin concentration. Women receiving food supplements during pregnancy as well as in lactation exhibited an even greater lowering of the postpartum plasma levels of this hormone. Consequently prolactin values of supplemented women returned more quickly to levels which allowed the resumption of menstrual and ovulatory activity. Concurrent measurements of the plasma concentrations of estradiol and progesterone in addition to prolactin allowed the calculation of prolactin values at which 1/2 the lactating women could be expected to have resumed menstruation and ovulation. These values were 1007 and 759 U/ml, respectively. Dietary improvement during lactation alone resulted in these critical prolactin concentrations being reached 21 weeks earlier than in nonsupplemented counterparts, while those receiving the extra food in both pregnancy and lactation showed a 35-week shortening of postpartum amenorrhea and infertility.Febehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6695825 6695825?JeLuukkaa, V. Pesonen, U. Huhtaniemi, I. Lehtonen, A. Tilvis, R. Tuomilehto, J. Koulu, M. Huupponen, R.1998@Inverse correlation between serum testosterone and leptin in men3243-60Journal of Clinical Endocrinology and Metabolism839Adult Aged Aging/blood Body Mass Index Cohort Studies Contraceptive Agents, Male Cross-Sectional Studies Humans Insulin/blood Kinetics Leptin Male Proteins/*metabolism Research Support, Non-U.S. Gov't Testosterone/analogs & derivatives/*blood/pharmacologySepdhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=97454369745436NDepartment of Pharmacology, University of Turku, Finland. virve.luukkaa@utu.fi?JMcNeilly, A. S.2001#Lactational control of reproduction583-90(Reproduction, Fertility, and Development137-8Amenorrhea Animals Breast Feeding Contraception Dopamine/physiology Female Fertility Gonadorelin/secretion Humans Lactation/*physiology Luteinizing Hormone/secretion Periodicity Prolactin/physiology Reproduction/*physiologyfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11999309 11999309MRC Human Reproductive Sciences Unit, University of Edinburgh Centre for Reproductive Biology, Scotland, UK. a.mcneilly@hrsu.mrc.au.ukz?/McNeilly, Alan S. Tay, Clem C. K. Glasier, Anna1994:Physiological mechanisms underlying lactational amenorrhea145-155QHuman Reproductive Ecology: Interactions of Environment, Fertility, and Behavior709Wood, James W.New York The New York Academy of SciencesQdemography endocrinology reproductive ecology steroid female reproductive ecology?Montagu, M. F. A.1946}Adolescent sterility: A study in the comparative physiology of the infecundity of the adolescent organism in mammals and man. Springfield C. C. Thomas=7@Muehlenbein, M. P. Alger, J. Cogswell, F. James, M. Krogstad, D.2005NThe reproductive endocrine response to Plasmodium vivax infection in Hondurans178-871American Journal of Tropical Medicine and Hygiene731Adult Androgens/blood Animals Hematocrit Honduras Humans Hydrocortisone/blood Malaria, Vivax/blood/*physiopathology/transmission Male Plasmodium vivax Reproduction/*physiology Testosterone/bloodJulfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16014855 0002-9637 (Print)5The American journal of tropical medicine and hygiene16014855lDepartment of Anthropology, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53201, USA. mpm1@uwm.edueng?J$Muehlenbein, M. P. Bribiescas, R. G.2005>Testosterone-mediated immune functions and male life histories527-58!American Journal of Human Biology175Animals Ecology Humans *Immunocompetence Immunosuppression Male Primates/*immunology/physiology *Reproduction Selection (Genetics) Testosterone/*immunologySep-Octehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1613653216136532Laboratory for Evolutionary Physiology and Parasitology, Department of Anthropology, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53211, USA. mpm1@uwm.edu=7JJMuehlenbein, M. P. Cogswell, F. B. James, M. A. Koterski, J. Ludwig, G. V.2006WTestosterone correlates with Venezuelan equine encephalitis virus infection in macaques19Virology Journal3Animals Encephalitis Virus, Venezuelan Equine/*physiology Encephalomyelitis, Venezuelan Equine/blood/immunology/*veterinary/virology Macaca fascicularis/*blood/*virology Male Testosterone/*blood Viremia/bloodfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16571136 1743-422X (Electronic)Virology journal16571136PDepartment of Anthropology, University of Wisconsin-Milwaukee, USA. mpm1@uwm.edueng?Muller, M. Wrangham, R. W.2004aDominance, aggression, and testosterone in wild chimpanzees: a test of the 'challenge hypothesis'113-123Animal Behavior67=7(Nieschlag, E. Nieschlag, S. Behre, H. M.1993Lifespan and testosterone215Nature3666452|Arteriosclerosis/etiology Coronary Disease/etiology Female Humans *Life Expectancy Male Orchiectomy Testosterone/*physiologyNov 18ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8232579 0028-0836 (Print)Nature8232579eng&?J+Odedina, F. T. Ogunbiyi, J. O. Ukoli, F. A.20060Roots of prostate cancer in African-American men539-43+Journal of the National Medical Association984Aprehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1662306616623066The Economic, Social & Administrative Pharmacy Division, Florida A&M University College of Pharmacy & Pharmaceutical Sciences, Tallahassee, USA. folakemi.odedina@famu.eduW? Owens, I. P.20028Ecology and evolution. Sex differences in mortality rate2008-9Science2975589Animal Autoantibodies/biosynthesis Body Constitution Carotenoids/metabolism Competitive Behavior Disease Susceptibility Female Free Radicals/metabolism Human Immune Tolerance Immunocompetence Male *Mammals/growth & development/parasitology/physiology *Mortality Parasitic Diseases/epidemiology/*etiology Parasitic Diseases, Animal/epidemiology/*etiology/immunology Risk-Taking Sex Behavior, Animal *Sex Characteristics Testosterone/physiologySep 20ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1224243012242430Department of Biological Sciences and NERC Centre for Population Biology, Imperial College London, Silwood Park, Ascot, Berkshire SL5 7PY, UK. i.owens@ic.ac.ukP}7JPParsons, J. K. Carter, H. B. Platz, E. A. Wright, E. J. Landis, P. Metter, E. J.2005cSerum testosterone and the risk of prostate cancer: potential implications for testosterone therapy2257-60,Cancer Epidemiology, Biomarkers & Prevention149Case-Control Studies Humans Male Middle Aged Prospective Studies Prostatic Neoplasms/drug therapy/*etiology/physiopathology Research Support, N.I.H., Extramural Research Support, U.S. Gov't, P.H.S. Risk Factors Testosterone/*bloodSepfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16172240 1055-9965 (Print)16172240vThe James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore, MD 21287, USA. parsonsk@jhmi.edueng?'Perrett, D. I. May, K. A. Yoshikawa, S.19944Facial shape and judgements of female attractiveness239-242Nature368March 17!psychology, mate choice,phenotypeNature ??Poppitt, S. D. Prentice, A. M. Goldberg, G. R. Whitehead, R. G.19947Energy-sparing strategies to protect human fetal growth118-25-American Journal of Obstetrics and Gynecology1711Adipose Tissue/physiology Adult Basal Metabolism Body Constitution Comparative Study Cross-Cultural Comparison Embryonic and Fetal Development *Energy Metabolism Female Humans Nutritional Status Pregnancy/*metabolism/physiology/statistics & numerical data Research Support, Non-U.S. Gov't Retrospective Studies Weight Gain/physiology that typically required to maintain normal function in the nonpregnant human female. Many women, however, especially in comparatively poor countries, are undernourished and can not freely secure and consume the additional nutrients which their bodies request. These women still manage to bear children successfully despite the nutritional constraints. The authors previously conducted parallel studies of the energy costs of pregnancy in poor women from a group of rural Gambian villages and in affluent women from Cambridge, United Kingdom. They identified important energy-sparing metabolic strategies which, in response to the energy stresses of pregnancy, help achieve a successful outcome under marginal nutritional conditions. This more recent study was conducted to test whether energy-sensitive adjustments in gestational metabolism observed in the former studies of Gambian and British women are a general phenomenon and to define the nutritional factors which direct them. Data are analyzed from all published studies in which the energy costs of pregnancy have been measured. This covers 360 pregnancies from the Netherlands, Sweden, Scotland, England, the Philippines, Thailand, and the Gambia. It is concluded that the energy needs of pregnancy are modulated over a wide range in response to maternal energy status. Energy costs of pregnancy varied widely between different communities, total costs were correlated with prepregnancy fatness and pregnancy weight gain, and marginally nourished women conserved energy by suppressing metabolic rate and by gaining little fat.Julehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8030686 8030686:Dunn Clinical Nutrition Centre, Cambridge, United Kingdom.?JgPrentice, A. M. Roberts, S. B. Prentice, A. Paul, A. A. Watkinson, M. Watkinson, A. A. Whitehead, R. G.1983_Dietary supplementation of lactating Gambian women. I. Effect on breast-milk volume and quality53-64$Human Nutrition - Clinical Nutrition371!Adult Bread Calcium, Dietary/administration & dosage Diet/*standards Dietary Proteins/administration & dosage Female Food, Fortified/*standards Gambia Humans *Lactation Milk Proteins/metabolism Milk, Human/*metabolism Nutritional Requirements Pregnancy Tea Vitamins/administration & dosageJanehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6341320 6341320ۿ?JvReed, W. L. Clark, M. E. Parker, P. G. Raouf, S. A. Arguedas, N. Monk, D. S. Snajdr, E. Nolan Jr., V. Ketterson, E. D.2006hPhysiological effects on demography: a long-term experimental study of testosterone's effects on fitness665-681The American Naturalist1675 May 1, 20068http://www.journals.uchicago.edu/cgi-bin/resolve?AN41049Am Nat,=7J:Roney, J. R. Hanson, K. N. Durante, K. M. Maestripieri, D.2006kReading men's faces: women's mate attractiveness judgments track men's testosterone and interest in infants2169-75"Proceedings of the Royal Society B2731598*Attitude Choice Behavior/*physiology *Cues *Face Female Humans Illinois Linear Models Male Paternal Behavior Photic Stimulation Sexual Behavior/*physiology Testosterone/*analysis Visual Perception/*physiologySep 7fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16901836 0962-8452 (Print) Proceedings16901836kDepartment of Psychology, University of California, Santa Barbara, CA 93106-9660, USA. roney@psych.ucsb.edueng?Rosenbaum, M. Leibel, R. L.1999pRole of gonadal steroids in the sexual dimorphisms in body composition and circulating concentrations of leptin. 1784-1789'Journal of Endocrinology and Metabolism75'Journal of Endocrinology and Metabolism=7JwSantner, S. J. Albertson, B. Zhang, G. Y. Zhang, G. H. Santulli, M. Wang, C. Demers, L. M. Shackleton, C. Santen, R. J.1998YComparative rates of androgen production and metabolism in Caucasian and Chinese subjects2104-90Journal of Clinical Endocrinology and Metabolism836Adrenal Glands/metabolism Androgens/*biosynthesis/metabolism Androstenedione/metabolism *Asian Continental Ancestry Group China/ethnology Comparative Study *European Continental Ancestry Group Female Glucocorticoids/urine Humans Ketosteroids/urine Male Metabolic Clearance Rate Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Sex Hormone-Binding Globulin/metabolism Testosterone/metabolism Testosterone 5-alpha-Reductase/metabolism United StatesJunehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9626146 0021-972X (Print)4The Journal of clinical endocrinology and metabolism9626146lDepartment of Medicine, Pennsylvania State University, Milton S. Hershey Medical Center, Hershey 17033, USA.eng=7 J_Schubring, C. Prohaska, F. Prohaska, A. Englaro, P. Blum, W. Siebler, T. Kratzsch, J. Kiess, W.1999Leptin concentrations in maternal serum and amniotic fluid during the second trimenon: differential relation to fetal gender and maternal morphometry151-7DEuropean Journal of Obstetrics, Gynecology, and reproductive Biology862 Adult Amniotic Fluid/*metabolism *Body Mass Index Chorionic Gonadotropin/blood Estriol/blood Female *Fetus Humans Leptin/blood/*metabolism Male Middle Aged Pregnancy Pregnancy Trimester, Second Sex Factors *Skinfold Thickness Time Factors alpha-Fetoproteins/metabolismOctfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10509783 0301-2115 (Print)DEuropean journal of obstetrics, gynecology, and reproductive biology10509783,Evangelisches Krankenhaus, Giessen, Germany.eng? J!Smith, R. Mesiano, S. McGrath, S.2002+Hormone trajectories leading to human birth159-64Regulatory Peptides1082-3Female Hormones/*physiology Humans Infant, Newborn Labor, Obstetric/*physiology Models, Biological Myometrium/physiology Parturition/*physiology Placenta/physiology PregnancyOct 15fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12220740 12220740Mothers and Babies Research Center, John Hunter Hospital, The University of Newcastle, NSW 2308, Newcastle, Australia. mdrsm@mail. newcstle. edu.au? J4Spratt, D. I. Cox, P. Orav, J. Moloney, J. Bigos, T.1993MReproductive axis suppression in acute illness is related to disease severity1548-540Journal of Clinical Endocrinology and Metabolism766Acute Disease Adult Aged Aged, 80 and over *Critical Illness Female Gonadotropins/blood Human Hydrocortisone/blood Male Middle Aged Osmolar Concentration Prolactin/blood *Reproduction Severity of Illness Index Support, Non-U.S. Gov't Testosterone/bloodJundhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=85011638501163=Department of Medicine, Maine Medical Center, Portland 04102.u? Stearns, Stephen C.1992The Evolution of Life Histories249OxfordOxford University Press? PTamimi, R. M. Lagiou, P. Mucci, L. A. Hsieh, C. C. Adami, H. O. Trichopoulos, D.2003NAverage energy intake among pregnant women carrying a boy compared with a girl1245-6British Medical Journal3267401Adult Energy Intake/*physiology Female Fetus/*metabolism Humans Male Pregnancy/*metabolism Pregnancy Trimester, Second Prospective Studies Regression Analysis Research Support, U.S. Gov't, P.H.S. *Sex CharacteristicsJun 7ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1279174012791740SDepartment of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. ?J)Tay, C. C. Glasier, A. F. McNeilly, A. S.1996Twenty-four hour patterns of prolactin secretion during lactation and the relationship to suckling and the resumption of fertility in breast-feeding women950-5Human Reproduction115Adolescent Adult *Breast Feeding *Circadian Rhythm Female *Fertility Humans Lactation/*physiology Postpartum Period Prolactin/*secretion Research Support, Non-U.S. Gov't Time Factors WeaningMayehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8671369 8671369MRC Reproductive Biology Unit, University of Edinburgh Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9EW, UK.)?Tsai, L. W. Sapolsky, R. M.1996Rapid stimulatory effects of testosterone upon myotubule metabolism and sugar transport, as assessed by silicon microphysiometry357-64Aggressive Behavior225Kandrogens testosterone muscle metabolism microphysiometry glucose transport?JValeggia, C. Ellison, P. T.2004JLactational amenorrhoea in well-nourished Toba women of Formosa, Argentina573-95Journal of Biosocial Science365 Adolescent Adult Amenorrhea/ethnology/*physiopathology Argentina/epidemiology Breast Feeding/ethnology Child Female Fertility/*physiology Humans Lactation/ethnology/*physiology Middle Aged Pregnancy Prospective Studies Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.Sepfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15446353 15446353CDepartment of Anthropology, Harvard University, Cambridge, MA, USA.?JVihko, R. Apter, D.1984REndocrine characteristics of adolescent menstrual cycles: impact of early menarche231-6Journal of Steroid Biochemistry201.Adolescent Age Factors Body Composition Child Dehydroepiandrosterone/blood Estradiol/blood Female Follicle Stimulating Hormone/blood Humans Luteinizing Hormone/blood *Menarche Menstruation Progesterone/blood Prolactin/blood Puberty, Precocious/*blood Research Support, Non-U.S. Gov't Testosterone/bloodJanehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6231419 6231419?JJVillar, J. Cogswell, M. Kestler, E. Castillo, P. Menendez, R. Repke, J. T.1992KEffect of fat and fat-free mass deposition during pregnancy on birth weight1344-52-American Journal of Obstetrics and Gynecology1675Adipose Tissue/*metabolism Adult *Birth Weight Body Composition Female Follow-Up Studies Humans Pregnancy/*metabolism Prospective Studies Research Support, Non-U.S. Gov't Skinfold Thickness Weight GainNovehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1442988 1442988Division of Prevention Research, National Institute of Child Health and Human Development, National Institutes of Health, Baltimore, Maryland.?J,Vitzthum, V. J. Spielvogel, H. Thornburg, J.2004aInterpopulational differences in progesterone levels during conception and implantation in humans1443-83Proceedings of the National Academy of Sciences USA1016*Embryo Implantation Female *Fertilization Humans Longitudinal Studies Ovulation Pregnancy Progesterone/*blood Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.Feb 10fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14757831 14757831`Department of Anthropology, Indiana University, Bloomington, IN 47405, USA. vitzthum@indiana.edu?`Wang, C. Catlin, D. H. Starcevic, B. Leung, A. DiStefano, E. Lucas, G. Hull, L. Swerdloff, R. S.2004Testosterone metabolic clearance and production rates determined by stable isotope dilution/tandem mass spectrometry in normal men: influence of ethnicity and age2936-410Journal of Clinical Endocrinology and Metabolism896HAdult *Asian Continental Ancestry Group Comparative Study Deuterium/diagnostic use *European Continental Ancestry Group Humans Male Middle Aged Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Spectrum Analysis, Mass Testis/*metabolism Testosterone/*pharmacokineticsJunehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1518108015181080Department of Medicine, Harbor-University of California Los Angeles Medical Center and Research and Education Institute, Torrance, California 90509, USA. wang@gcrc.rei.edu=7J}Wang, C. Cunningham, G. Dobs, A. Iranmanesh, A. Matsumoto, A. M. Snyder, P. J. Weber, T. Berman, N. Hull, L. Swerdloff, R. S.2004Long-term testosterone gel (AndroGel) treatment maintains beneficial effects on sexual function and mood, lean and fat mass, and bone mineral density in hypogonadal men2085-980Journal of Clinical Endocrinology and Metabolism895Adolescent Adult Affect/*drug effects Aged Androgens/*administration & dosage/adverse effects/blood Biological Markers/blood Body Composition/*drug effects Bone Density/*drug effects Bone Remodeling/drug effects Dose-Response Relationship, Drug Drug Administration Schedule Estradiol/blood Follicle Stimulating Hormone/blood Gels Hematocrit Hemoglobins/metabolism Humans Hypogonadism/*drug therapy/metabolism/psychology Luteinizing Hormone/blood Male Prostate-Specific Antigen/blood Prostatic Hyperplasia/ultrasonography Research Support, U.S. Gov't, P.H.S. Sex Hormone-Binding Globulin/metabolism Sexual Behavior/*drug effects Testosterone/*administration & dosage/adverse effects/bloodMayfhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15126525 0021-972X (Print)4The Journal of clinical endocrinology and metabolism15126525Departments of Medicine/Pediatrics, Harbor-University of California, Los Angeles Medical Center and Research and Education Institute, Torrance, California 90509, USA. wang@gcrc.rei.edueng#?1Welle, S. Jozefowicz, R. Forbes, G. Griggs, R. C.1992kEffect of testosterone on metabolic rate and body composition in normal men and men with muscular dystrophy332-50Journal of Clinical Endocrinology and Metabolism742(Adult Basal Metabolism/*drug effects Body Composition/*drug effects Body Weight/drug effects Calorimetry Follow-Up Studies Human Male Muscular Dystrophy/*drug therapy/*physiopathology Reference Values Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Testosterone/*pharmacology/*therapeutic use"?7Willis, D. S. Mason, H. D. Gilling-Smith, C. Franks, S.1996Modulation by insulin of follicle-stimulating hormone and luteinizing hormone actions in human granulosa cells of normal and polycycstic ovaries.302-3090Journal of Clinical Endocrinology and Metabolism81?,Winkvist, A. Rasmussen, K. M. Habicht, J. P.19920A new definition of maternal depletion syndrome.691-694!American Journal of Public Health82?LWinters, S. J. Brufsky, A. Weissfeld, J. Trump, D. L. Dyky, M. A. Hadeed, V.2001rTestosterone, sex hormone-binding globulin, and body composition in young adult African American and Caucasian men1242-7 Metabolism5010;Adolescence Adult *Anthropometry *Caucasoid Race Circadian Rhythm Comparative Study Estradiol/blood Fasting Follicle Stimulating Hormone/blood Human Insulin/blood LH/blood Linear Models Male *Negroid Race Sex Hormone-Binding Globulin/*analysis Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Testosterone/*bloodOctShttp://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1158650111586501UDepartment of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA. |?J7Worthman, C. M. Jenkins, C. L. Stallings, J. F. Lai, D.1993Attenuation of nursing-related ovarian suppression and high fertility in well-nourished, intensively breast-feeding Amele women of lowland Papua New Guinea425-43Journal of Biosocial Science254` *Birth Intervals *Breast Feeding Child, Preschool *Developing Countries *Ethnic Groups Female Fertility/*physiology Follow-Up Studies Humans Infant Medicine, Traditional Menstrual Cycle/physiology *Nutritional Status Ovary/*physiology Papua New Guinea Prolactin/blood Research Support, Non-U.S. Gov't an infant under 5 years of age from 12 Amele villages in lowland Papua New Guinea, that women with good nutritional status experienced less variation in ovarian suppression than reported elsewhere among less well-nourished populations. Direct observations of nursing behavior were recorded during 660 hours. The average number of observations per child, which were conducted at different developmental stages, was 1.9. 1549 nursing events were recorded. 38 women had serum samples drawn to determine prolactin levels. Saliva samples were collected from 51 women for measurement of gonadal steroids. Women reported menstrual patterns in the preceding month. Measures were also taken of weight, skinfolds of the triceps and subscapular area, and mid-upper-arm circumference. Birth interval, completed fertility, and age at introduction of solid foods and denial of breast were obtained from ongoing demographic surveillance on nutrition in 1982-84 and 1982-83. Laboratory methods were described for serum prolactin and progesterone analysis. The results showed skewed results for the hormonal and some nursing variables, which were transformed by logarithmic functions. All Amele mothers practice indulgent demand feeding schedules. Supplementary foods are introduced at the median age of 7.4 methods. Early supplementation is liquids or semiliquids, followed by mashed starchy staples, and finally a standard diet. Cessation of breast feeding occurs at a subsequent pregnancy of the advanced age of the child (5 years). The median age of cessation was 36.3 months. The breast feeding pattern during the first 18 months was 1.5-3 times per hour for 1-3 minutes. Infant age was not linearly related to nursing frequency declines or feeding intervals. Nursing frequency was unrelated to morbidity. Prolactin declined strongly when bout frequency and interval were stable. Multiple regression findings were that duration of postpartum amenorrhea was explained by mother's parity and age, feeding interval, and time postpartum. Time of supplementary feeding was unrelated to duration of amenorrhea, nursing frequency, or feeding duration. 16% of interval variance was explained by length of postpartum amenorrhea, which was correlated with length of subsequent birth interval. 45% of the variance in prolactin was explained by triceps skinfolds and bout length.Octehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8227092 82270926Department of Anthropology, Emory University, Atlanta.?jEAeschlimann, P.B. Haberli, M.A. Reusch, T.B.H. Boehm, T. Milinski, M.2003qFemale sticklebacks Gasterosteus aculeatus use self-reference to optimize MHC allele number during mate selection119-126#Behavioral Ecology and Sociobiology54Lmate choice, MHC, fish, natural population, olfaction, odor, allele counting^?Alberts, S.C. 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Zufall, F.20063MHC peptides and the sensory evaluation of genotype100-107Trends in Neurosciences292Major histocompatibility complex mate choice olfactory recognition vomeronasal organ mammalian pheromones mating preferences mice sticklebacks signals mouseFeb://000236044300007 ISI:000236044300007?#>Bonneaud, C. Chastel, O. Federici, P. Westerdahl, H. Sorci, G.20061Complex Mhc-based mate choice in a wild passerine 1111-1116"Proceedings of the Royal Society B2731590Mhc mate choice outbreeding avoidance inbreeding avoidance heterozygote advantage Major histocompatibility complex house sparrow mating preferences atlantic salmon no evidence class-i alleles population domesticus selectionMay 7://000236852700012 ISI:000236852700012?$(Boulanger, L. M. Huh, G. S. Shatz, C. J.2001FNeuronal plasticity and cellular immunity: shared molecular mechanisms568-578Current Opinion In Neurobiology115Long-term potentiation nf-kappa-b receptor signal-transduction central-nervous-system mammalian visual-system retinal ganglion-cells class-i mhc synaptic plasticity neurite outgrowth gene-expressionOct://000171712000007 ISI:000171712000007?%Boulanger, L. M. Shatz, C. J.2004HImmune signalling in neural development, synaptic plasticity and disease521-531Nature Reviews Neuroscience57Mhc class-i major histocompatibility complex central-nervous-system hemochromatosis gene-product cell-surface expression primary sensory neurons hepatitis-virus type-4 neonatal fc receptor dyslexic-children interferon-gammaJul://000222435000011 ISI:000222435000011?&UCarosella, E.D. Moreau, P. Le Maoult, J. Le Discorde, M. Daussset, J. Rouas-Freis, N.2003CHLA-G molecules: from maternal-fetal tolerance to tissue acceptance199-252Advances in Immunology81?'Choudhury, S.R. Knapp, L.A.2001DHuman reproductive failure II: Immunogenetic and interacting factors135-160Human Reproduction Update 7?(+Colegrave, N. Kotiaho, J. S. Tomkins, J. L.2002[Mate choice or polyandry: reconciling genetic compatibility and good genes sexual selection911-917Evolutionary Ecology Research46female choice female control incompatibility indicator mechanism Cricket gryllus-bimaculatus female choice handicap principle field cricket evolution benefits incompatibility preferencesOct://000177917500008 ISI:000177917500008?)ADorak, M.T. Lawson, T. Machulla, H.K.G. Mills, K.I. Burnett, A.K.2002CIncreased heterozygosity for MHC class II lineages in newborn males263-269Genes And Immunity 3?*Downing, J. E. G. Miyan, J. A.2000TNeural immunoregulation: emerging roles for nerves in immune homeostasis and disease281-289Immunology Today216Sympathetic nervous-system stress-induced modulation gene-related peptide difficile toxin-a mast-cells neurogenic inflammation brain rat innervation stimulationJun://000087357600007 ISI:000087357600007?+kEEkblom, R. Saether, S.A. Grahn, M. Fiske, P. Kalass, J.A. Hoglund, J.2004oMajor histocompatibility complex variation and mate choice in a lekking bird, the great snipe (Gallinago media) 3821-3828Molecular Ecology13iMHC, bird, mate choice, heterozygote advantage, lek, disassortative mating, class IIB, natural population?,Garrigan, D Hedrick, P. W.2003LPerspective: detecting adaptive molecular polymorphism: lessons from the MHC 1707-1722 Evolution578xAdaptive polymorphism, balancing selection, major histocompatibility complex, neutral theory, nonsynonymous substitution?-+Genin, E. Ober, C. Weitkamp, L. Thomson, G.2000$A robust test for assortative mating119-124"European Journal of Human Genetics82assortative mating HLA Hutterites power robustness inbreeding admixture Major histocompatibility complex mate selection hla humans mhc preferences choice genes locusFeb://000086709400006 ISI:000086709400006?.#Graham, A.L. Allen, J.E. Read, A.F.20057Evolutionary causes and consequences of immunopathology373-3973Annual Review of Ecology Evolution and Systematics 36?/Hedrick, P. W.20025Pathogen resistance and genetic variation at MHC loci 1902-1908 Evolution5610frequency-dependent selection, heterozygote advantage, HLA, MHC, overdominance, polymorphism, balancing selection, model, temporal variation, pathogens?0Hedrick, P.W. Black, F.L.19978HLA and mate selection: no evidence in South Amerindians505-511"American Journal of Human Genetics61F?1Hedrick, P. W. Thomson, G.1988CMaternal-fetal interactions and the maintenance of HLA polymorphismGenetics119205-212"?2"Hughes, Austin L. Yeager, Meredith1998INatural selection at major histocompatibility complex loci of vertebrates415-435Annual Review Of Genetics32qreview, MHC, overdominance hypothesis, patterns of substitution, trans-species polymorphism, hitchhiking, introns?30Hunt, J.S. Petroff, M.G. McIntire, R.H. Ober, C.2005'HLA-G and immune tolerance in pregnancy681-693 FASEB Journal19?4 Hviid, T.V.F.2006VHLA-G in human reproduction: aspects of genetics, function and pregnancy complications209-232Human Reproduction Update12?5:Hviid, T.V.F. Hylenius, S. Lindhard, A. Christiansen, O.B.2004rAssociation between human leukocyte antigen-G genotype and success of in vitro fertilization and pregnancy outcome66-69Tissue Antigens64-?6XIshitani, A. Sageshima, N. Lee, N. Dorofeeva, N. Hatake, K. Marquardt, H. Geraghty, D.E.2003Protein expression and peptide binding suggest unique and interacting functional roles for HLA-E, F, and G in maternal-placental immune recognition 1376-1384Journal of Immunology171?7;Suma Jacob Martha K. McClintock Bethanne Zelano Carole Ober2002PPaternally inherited HLA alleles are associated with women's choice of male odor175-179Nature Genetics306MHC, HLA, odor, olfactory preferences, kin recognition?8Klein, J. Sato, Akie2000<Advances in immunology: the HLA system (second of two parts)782-786New England Journal of Medicine34311]review, deficiencies, abnormalities, infectious disease associations, cancer, transplantation?9aLe Maoult, J. Le Discorde, M. Rouas-Freis, N. Moreau, P. Menier, C. McCluskey, J. Carosella, E.D.2003IBiology and functions of human leukocyte antigen-G in health and sickness273-284Tissue Antigens62mO?: Lechler, R. Warrens, A.2000HLA in health and disease San DiegoAcademic Press2nd?;Leinders-Zufall, T. Brennan, P. Widmayer, P. Chandaramani, P. Maul-Pavicic, A. Jager, M. Li, X.H. Breer, H. Zufall, F. Boehm, T.2004EMHC class I peptides as chemosensory signals in the vomeronasal organ 1033-1037Science306?<$Marrack, P. Kappler, J. Kotzin, B.L.2001+Autoimmune disease: why and where it occurs899-905Nature Medicine7?=Mays, H. L. Hill, G. E.2004;Choosing mates: good genes versus genes that are a good fit554-559Trends in Ecology and Evolution1910Major-histocompatibility-complex extra-pair paternity sexual selection self-incompatibility poecilia-reticulata female choice lek paradox heterozygosity compatibility birdsOct://000224474700008 ISI:000224474700008?>*McClelland, E. E. Penn, D. J. Potts, W. 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L.2003^Conditional tradeoffs between aging and organismal performance of Indy long-lived mutant flies 3369-33733Proceedings of the National Academy of Sciences USA1006drosophila melanogaster mortality life span fecundity fertility drosophila-melanogaster life-span caloric restriction metabolic-rate longevity evolution age transporter selection elegansMAR 18://000181675200071 0027-8424ISI:000181675200071Marden, Jh Penn State Univ, Dept Biol, Mueller Lab 208, University Pk, PA 16802 USA Penn State Univ, Dept Biol, Mueller Lab 208, University Pk, PA 16802 USA Univ Connecticut, Ctr Hlth, Dept Genet & Dev Biol, Farmington, CT 06030 USAEnglish,? Martin, G. M.2002RKeynote: mechanisms of senescence – complificationists versus simplificationists65-73$Mechanisms of Ageing and Development1232-3eAging: *genetics: metabolism Animal Energy Intake Evolution Human Life Expectancy Mice Point MutationMech Ageing Devb? Masoro, E. J.2000(Caloric restriction and aging: an update299-305Experimental Gerontology353Aging: *physiology Animal Blood Glucose: metabolism DNA Damage Energy Intake Food Deprivation: *physiology Insulin: blood Longevity: physiology Mice Models, Biological Oxidative Stress Rats Stress: physiopathology Exp Gerontol[? Medawar, P.B.1952An Unsolved Problem of BiologyLondon H.K. Lewis}7 fMurphy, C. T. McCarroll, S. A. Bargmann, C. I. Fraser, A. Kamath, R. S. Ahringer, J. Li, H. Kenyon, C.2003WGenes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans277-284Nature4246946JUL 17://000184183900032 0028-0836ISI:000184183900032Kenyon, C Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Cambridge, Wellcome CRC Inst, Cambridge CB2 1QR, England Univ Cambridge, Dept Genet, Cambridge CB2 1QR, EnglandEnglishJ}7 JPartridge, L. Barton, N. H.1996On measuring the rate of ageing 1365-1371"Proceedings of the Royal Society B2631375zdrosophila-melanogaster natural-populations mortality-rates senescence evolution life reproduction mutation mammals modelsOCT 22://A1996VQ62200015 0962-8452ISI:A1996VQ62200015Partridge, L Univ Coll London,Dept Biol,Wolfson House,4 Stephenson Way,London Nw1 2he,England Univ Edinburgh,Icapb,Edinburgh Eh9 3jt,Midlothian,ScotlandEnglish}7 JPartridge, L. Gems, D.2006NBeyond the evolutionary theory of ageing, from functional genomics to evo-gero334-340Trends in Ecology and Evolution216life-span extension insulin-like signals caenorhabditis-elegans natural-selection c-elegans dietary restriction longevity assurance daf-2 mutants extended life honey-beeJUN://000238697200009 0169-5347ISI:000238697200009Partridge, L Univ Coll London, Dept Biol, Ctr Res Aging, Darwin Bldg,Gower St, London WC1E 6BT, England Univ Coll London, Dept Biol, Ctr Res Aging, London WC1E 6BT, EnglandEnglishA}7 +Pletcher, S. D. Houle, D. Curtsinger, J. W.1998_Age-specific properties of spontaneous mutations affecting mortality in Drosophila melanogaster287-303Genetics1481life-history characters polygenic mutation quantitative traits genetic-variation adult drosophila environmental variation deleterious mutations selection lines inbred strains expressionJAN://000071494000027 0016-6731ISI:000071494000027Pletcher, SD Univ Minnesota, Dept Ecol Evolut & Behav, 1987 Upper Buford Circle, St Paul, MN 55108 USA Univ Minnesota, Dept Ecol Evolut & Behav, St Paul, MN 55108 USA Univ Toronto, Dept Zool, Toronto, ON M5S 3G5, CanadaEnglish&}7 +Pletcher, S. D. Houle, D. Curtsinger, J. W.1999sThe evolution of age-specific mortality rates in Drosophila melanogaster: genetic divergence among unselected lines813-823Genetics1532polygenic mutation quantitative genetics deleterious mutations inbred strains life-span populations senescence selection traits maintenanceOCT://000083051400025 0016-6731ISI:000083051400025Pletcher, SD Max Planck Inst Demog Res, Doberaner Str 119, D-18057 Rostock, Germany Univ Minnesota, Dept Ecol Evolut & Behav, St Paul, MN 55108 USA Univ Toronto, Dept Zool, Toronto, ON M5S 3G5, CanadaEnglish7}71Pletcher, S. D. Khazaeli, A. A. Curtsinger, J. W.2000oWhy do life spans differ? Partitioning mean longevity differences in terms of age-specific mortality parameters B381-B389IJournals of Gerontology Series a-Biological Sciences and Medical Sciences5583drosophila-melanogaster selection senescence beetleAUG://000165312000003 1079-5006ISI:000165312000003Pletcher, SD Max Planck Inst Demog Res, Doberaner Str 114, D-18057 Rostock, Germany Univ Minnesota, Dept Ecol Evolut & Behav, St Paul, MN 55108 USAEnglish5=7JPromislow, D. E.2004<Protein networks, pleiotropy and the evolution of senescence1225-34"Proceedings of the Royal Society B2711545*Aging *Evolution Gene Expression Genes, Fungal/physiology *Models, Biological *Phenotype Proteins/*metabolism/*physiology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Yeasts/*genetics/metabolismJun 22fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15306346 0962-8452 (Print)GProceedings of the Royal Society of London Series B-Biological Sciences15306346\Department of Genetics, University of Georgia, Athens, GA 30602-7223, USA. promislow@uga.edueng? Promislow, D. E. Pletcher, S. D.2002Advice to an aging scientist841-50$Mechanisms of Ageing and Development1238Mech Ageing Dev)?JRogina, B. Helfand, S. L.2004SSir2 mediates longevity in the fly through a pathway related to calorie restriction 15998-60033Proceedings of the National Academy of Sciences USA10145Nov 9ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1552038415520384Department of Genetics and Developmental Biology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA.?X5Rogina, B. Reenan, R. A. Nilsen, S. P. Helfand, S. L.2000JExtended life-span conferred by cotransporter gene mutations in Drosophila 2137-2140Science290Science}7 Rose, M. R.1984GLaboratory evolution of postponed senescence in Drosophila melanogaster 1004-1010 Evolution385://A1984TR39600007 0014-3820ISI:A1984TR39600007;Rose, Mr Dalhousie Univ,Dept Biol,Halifax B3h 4j1,Ns,CanadaEnglish}7"Spencer, C. C. Promislow, D. E. L.2005VAge-specific changes in epistatic effects on mortality rate in Drosophila melanogaster513-521Journal of Heredity965quantitative trait loci life-span antagonistic pleiotropy expression patterns natural-selection genetic-variation senescence evolution longevity ultrabithoraxSEP://000232103800005 0022-1503ISI:000232103800005Spencer, Cc Univ British Columbia, Dept Zool, 6270 Univ Blvd, Vancouver, BC V6T 1Z4, Canada Univ Georgia, Dept Genet, Athens, GA 30602 USAEnglish}7J3Stearns, S. C. Ackermann, M. Doebeli, M. Kaiser, M.2000GExperimental evolution of aging, growth, and reproduction in fruitflies 3309-33133Proceedings of the National Academy of Sciences USA977life-history evolution lifespan age at maturity body size drosophila life-history traits drosophila-melanogaster correlated responses artificial selection laboratory evolution mortality plateaus temperature senescence rates ageMAR 28://000086195200064 0027-8424ISI:000086195200064~Stearns, Sc Univ Basel, Inst Zool, Rheinsprung 9, CH-4051 Basel, Switzerland Univ Basel, Inst Zool, CH-4051 Basel, SwitzerlandEnglish}7Stearns, S. C. Kaiser, M.1996eEffects on fitness components of P-element inserts in Drosophila melanogaster: Analysis of trade-offs795-806 Evolution502aging drosophila genetic engineering life-history evolution lifespan trade-offs correlated responses artificial selection reproduction senescence cost evolutionAPR://A1996UJ15600029 0014-3820ISI:A1996UJ15600029HStearns, Sc Univ Basel,Inst Zool,Rheinsprung 9,Ch-4051 Basel,SwitzerlandEnglishm}7J-Stewart, E. J. Madden, R. Paul, G. Taddei, F.2005TAging and death in an organism that reproduces by morphologically symmetric division295-300 PLoS Biology32qyeast saccharomyces-cerevisiae escherichia-coli daughter cells bacteria longevity evolution mutation polarity oldFEB://000227404100014 1544-9173ISI:000227404100014Stewart, Ej Inserm, U571, Paris, France INSERM, U571, Paris, France Univ Paris, F-75252 Paris, France Inst Hautes Etud Sci, F-91440 Bures Sur Yvette, FranceEnglishx}7Tatar, M. Bartke, A. Antebi, A.20039The endocrine regulation of aging by insulin-like signals 1346-1351Science2995611life-span c-elegans caenorhabditis-elegans growth-hormone thyroid-hormones oxidative damage nervous-system drosophila receptor longevityFEB 28://000181192300039 0036-8075ISI:000181192300039Tatar, M Brown Univ, Dept Ecol & Evolutionary Biol, Box G-W, Providence, RI 02912 USA Brown Univ, Dept Ecol & Evolutionary Biol, Providence, RI 02912 USA So Illinois Univ, Dept Med, Springfield, IL 62794 USA Max Planck Inst Mol Genet, D-14195 Berlin, GermanyEnglish]?iGTatar, M. Kopelman, A. Epstein, D. Tu, M. P. Yin, C. M. Garofalo, R. S.2001gA mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function107-110Science2925514ScienceD?Tuljapurkar, S.1980,Population Dynamics in Variable EnvironmentsLecture Notes in Biomathematics Levin, S.New YorkSpringer-Verlag}7(Van Voorhies, W. A. Fuchs, J. Thomas, S.2005/The longevity of Caenorhabditis elegans in soil247-249Biology Letters12kageing senescence caenorhabditis elegans population-growth c-elegans nematode reproduction evolution systemJUN 22://000232167100037 1744-9561ISI:000232167100037Van Voorhies, WA New Mexico State Univ, Program Mol Biol, MSC 3MLS, Las Cruces, NM 88003 USA New Mexico State Univ, Program Mol Biol, MSC 3MLS, Las Cruces, NM 88003 USA New Mexico State Univ, Dept Entomol Plant Pathol & Weed Sci, MSC 3BE, Las Cruces, NM 88003 USAEnglish}7IVellai, T. Takacs-Vellai, K. Zhang, Y. Kovacs, A. L. Orosz, L. Muller, F.2003<Genetics - Influence of TOR kinase on lifespan in C. elegans620-620Nature4266967caenorhabditis-elegansDEC 11://000187132800027 0028-0836ISI:000187132800027Vellai, T Univ Fribourg, Dept Biol, CH-1700 Fribourg, Switzerland Univ Fribourg, Dept Biol, CH-1700 Fribourg, Switzerland Lorand Eotvos Univ, Dept Gen Zool, H-1117 Budapest, Hungary Lorand Eotvos Univ, Dept Genet, H-1117 Budapest, Hungary Agr Biotechnol Ctr, H-2100 Godollo, HungaryEnglish}7J(Watve, M. Parab, S. Jogdand, P. Keni, S.2006VAging may be a conditional strategic choice and not an inevitable outcome for bacteria 14831-148353Proceedings of the National Academy of Sciences USA10340<leslie matrix prokaryotic cell division evolution senescenceOCT 3://000241069300035 0027-8424ISI:000241069300035Watve, M Anujeeva Biosci Pvt Ltd, Pune 411030, Maharashtra, India Anujeeva Biosci Pvt Ltd, Pune 411030, Maharashtra, India Abasaheb Garware Coll, Dept Microbiol, Pune 411004, Maharashtra, IndiaEnglish?Williams, G. C.1999JThe 1999 Crawford Prize lectures. The Tithonus error in modern gerontology405-415Quarterly Review of Biology74=7 PWood, J. G. Rogina, B. Lavu, S. Howitz, K. Helfand, S. L. Tatar, M. Sinclair, D.2004JSirtuin activators mimic caloric restriction and delay ageing in metazoans686-9Nature4307000:Aging/drug effects/*physiology Alleles Animal Feed Animals Caenorhabditis elegans/drug effects/*physiology *Caloric Restriction Drosophila melanogaster/drug effects/genetics/*physiology Feeding Behavior/drug effects/physiology Female Fertility/drug effects/physiology Flavonoids/pharmacology Genotype Longevity/drug effects/*physiology Male Mutation/genetics Phenols/pharmacology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Sirtuins/*agonists/metabolism Stilbenes/pharmacology Survival Rate Time FactorsAug 5fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15254550 1476-4687 (Electronic)Nature15254550iDepartment of Pathology, Harvard Medical School, 77 Ave. Louis Pasteur, Boston, Massachusetts 02115, USA.eng<7! Adair, L. S.2001&Size at birth predicts age at menarcheE59 Pediatrics1074Adolescent Adult Age Factors Anthropometry/methods Birth Weight/*physiology Body Mass Index Child Child, Preschool Cohort Studies Embryonic and Fetal Development/*physiology Female Health Surveys Humans Infant Infant, Newborn/*growth & development Menarche/*physiology Mothers/statistics & numerical data Pregnancy Proportional Hazards Models Seasons Sexual Maturation/physiology Skinfold ThicknessAprq OBJECTIVE: This study examines the relationship of intrauterine growth, measured by size and maturity at birth, to age at menarche, while also considering a wide range of other factors that may affect maturation. The research is motivated by the current debate about the importance of the prenatal environment as a determinant of later disease risk. METHODS: Data were collected during the Cebu Longitudinal Health and Nutrition Survey. This community-based study has followed a cohort of several thousand Filipino infants since their birth in 1983 to 1984. Participants live in urban and rural communities of Metro Cebu, the second largest metropolitan area of the Philippines. The analysis sample includes 997 girls 14 to 15 years of age. The main outcome measure is age at menarche, determined from girls' self-report of the month and year of first menses. Factors that influenced age at menarche were identified using Weibull parametric survival time models. The main exposure variables of interest included weight and length (measured by trained field staff) and gestational age (assessed from mother's reported date of last menstrual period, augmented by clinical assessments at birth). The analysis also takes into account a wide range of other factors that are likely to affect age at menarche. These include the girls' early postnatal growth rates, premenarcheal body composition (body mass index and skinfold thicknesses measured at 8 years), current diet (measured by two 24-hour dietary recalls), and socioeconomic conditions of the household in which they live. We also assessed the contribution of maternal characteristics, including age at menarche, height, and nutritional status while pregnant with the study child. RESULTS: The median age at menarche calculated from the hazard model is 13.1 years, with 50% of girls attaining menarche between 12.4 and 13.9 years. Earlier menarche is characteristic of girls who live in urban, higher socioeconomic status households, as indicated by higher maternal education, better housing quality, and possession of assets, such as a TV or refrigerator. Age at menarche is significantly associated with birth characteristics. Although birth weight alone was not significantly related to age at menarche, girls who were relatively long and thin at birth (>49 cm, <3 kg) attained menarche ~6 months earlier than did girls who were short and light (<49 cm, <3 kg). This effect of thinness at birth is most pronounced among girls with greater than average growth increments in 6 months of life. The effects of birth size are not modified when body mass index and skinfold thicknesses at 8 years are taken into account. Effects of birth size on age at menarche also remain significant when maternal nutritional status during pregnancy and the girl's current diet and socioeconomic indicators are taken into account. CONCLUSIONS: The study provides additional evidence of fetal programming of later health outcomes by showing that future growth and maturation trajectories are established in utero. Furthermore, rapid postnatal growth potentiates the effects of size at birth and is related independently to earlier pubertal maturation.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11335780 gJournal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. United States1098-4275 (Electronic) Pediatrics11335780Department of Nutrition, University of North Carolina, Schools of Medicine and Public Health, Chapel Hill, North Carolina 27516-3997, USA. linda_adair@unc.eduengh?" DJP Barker1994*Mothers, Babies, and Disease in Later LifeLondonBMJ PublishingG?# DJ Barker1999QThe fetal origins of coronary heart disease and stroke: evolutionary implications246-250Evolution in Health and Disease SC StearnsOxfordOxford University PressFirst?$=Barker, D. J. Osmond, C. Golding, J. Kuh, D. Wadsworth, M. E.1989fGrowth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease564-7British Medical Journal29866732Adult Aging *Birth Weight *Blood Pressure Body Height Cardiovascular Diseases/ep [Epidemiology] *Cardiovascular Diseases/mo [Mortality] Cardiovascular Diseases/pp [Physiopathology] Child Female Fetal Development Gestational Age Great Britain Human Infant, Newborn Male Mothers Pulse Support, Non-U.S. Gov'tIn national samples of 9921 10 year olds and 3259 adults in Britain systolic blood pressure was inversely related to birth weight. The association was independent of gestational age and may therefore be attributed to reduced fetal growth. This suggests that the intrauterine environment influences blood pressure during adult life. It is further evidence that the geographical differences in average blood pressure and mortality from cardiovascular disease in Britain partly reflect past differences in the intrauterine environment. Within England and Wales 10 year olds living in areas with high cardiovascular mortality were shorter and had higher resting pulse rates than those living in other areas. Their mothers were also shorter and had higher diastolic blood pressures. This suggests that there are persisting geographical differences in the childhood environment that predispose to differences in cardiovascular mortality.EnglishBMJ ~?%Bateson, P. Barker, D. Clutton-Brock, T. Deb, D. D'Udine, B. Foley, R. A. Gluckman, P. Godfrey, K. Kirkwood, T. Lahr, M. M. McNamara, J. Metcalfe, N. B. Monaghan, P. Spencer, H. G. Sultan, S. E.2004)Developmental plasticity and human health419-21Nature4306998Adaptation, Physiological/*physiology Animals Body Constitution Cues Disease Susceptibility Embryonic and Fetal Development/*physiology Energy Metabolism Female *Health Humans Infant, Newborn Male Nutrition/*physiology Pregnancy Public HealthJul 22Many plants and animals are capable of developing in a variety of ways, forming characteristics that are well adapted to the environments in which they are likely to live. In adverse circumstances, for example, small size and slow metabolism can facilitate survival, whereas larger size and more rapid metabolism have advantages for reproductive success when resources are more abundant. Often these characteristics are induced in early life or are even set by cues to which their parents or grandparents were exposed. Individuals developmentally adapted to one environment may, however, be at risk when exposed to another when they are older. The biological evidence may be relevant to the understanding of human development and susceptibility to disease. As the nutritional state of many human mothers has improved around the world, the characteristics of their offspring--such as body size and metabolism--have also changed. Responsiveness to their mothers' condition before birth may generally prepare individuals so that they are best suited to the environment forecast by cues available in early life. Paradoxically, however, rapid improvements in nutrition and other environmental conditions may have damaging effects on the health of those people whose parents and grandparents lived in impoverished conditions. A fuller understanding of patterns of human plasticity in response to early nutrition and other environmental factors will have implications for the administration of public health.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15269759&1476-4687 (Electronic) Journal Article15269759zSub-Department of Animal Behaviour, University of Cambridge, High Street, Madingley, Cambridge CB3 8AA, UK. ppgb@cam.ac.uk~?&-Benyshek, D. C. Johnston, C. S. Martin, J. F.2006Glucose metabolism is altered in the adequately-nourished grand-offspring (F(3) generation) of rats malnourished during gestation and perinatal life1117-9 Diabetologia495Mayehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16557373!0012-186X (Print) Journal Article16557373kDepartment of Anthropology, University of Nevada, Las Vegas, NV, 89154-5003, USA, daniel.benyshek@unlv.edu.0?';Bertram,C. Trowern,A.R. Copin,N. Jackson,A.A. Whorwood,C.B.2001The maternal diet during pregnancy programs altered expression of the glucocorticoid receptor and type 2 11beta-hydroxysteroid dehydrogenase: potential molecular mechanisms underlying the programming of hypertension in utero. 2841-2853 Endocrinology142t2' Diet expression glucocorticoid hypertension in utero maternal mechanism mechanisms molecular N Pregnancy receptor2001///31095)TY - JOUR RP - NOT IN FILE U1 - export"Endocrinology J1 - Endocrinology. <7(KBoiko, J. Jaquet, D. Chevenne, D. Rigal, O. Czernichow, P. Levy-Marchal, C.2005GIn situ lipolytic regulation in subjects born small for gestational age565-70)International Journal of Obesity (London)296\Abdomen Adipose Tissue/*metabolism Adrenergic beta-Agonists/diagnostic use Adult Case-Control Studies Chi-Square Distribution Fatty Acids, Nonesterified/blood Female Glycerol/metabolism Humans Infant, Newborn Infant, Small for Gestational Age/*metabolism Insulin/diagnostic use Insulin Resistance Isoproterenol/diagnostic use *Lipid Metabolism MaleJunFOBJECTIVE: Subjects born small for gestational age (SGA) who are prone to develop insulin resistance in adulthood display an abnormal development pattern of the adipose tissue during fetal and postnatal life. Since the lipolytic activity of the adipose tissue is critical in the development of insulin resistance, the purpose of this study was to investigate whether SGA itself might affect lipolysis regulation. STUDY DESIGN: We studied the effect of catecholamines, by local injection of isoproterenol, and the effect of insulin, using two-step infusion at 8 and 40 mU/m2/min, on the in situ lipolysis of the subcutaneous abdominal adipose tissue of 23 subjects born SGA and 23 born appropriate for gestational age (AGA), using the microdialysis technique. RESULTS: Under isoproterenol infusion, the increase in dialysate glycerol concentration was significantly 1.5-fold higher in the SGA than in the AGA group (P=0.02) and induced a 20% increase in the plasma FFA concentration (P=0.04), whereas no significant increase was observed in the AGA group. The antilipolytic action of insulin on dialysate glycerol concentration was similar in both groups throughout the insulin infusion. CONCLUSION: Subjects born SGA demonstrated a hyperlipolytic reactivity to catecholamines, which might be regarded as an additional deleterious component of the insulin resistance associated with SGA. In contrast, being born SGA does not directly affect the antilipolytic action of insulin, showing that it does not play a major role in causing the long-term metabolic complications associated with reduced fetal growth.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15889114 aClinical Trial Controlled Clinical Trial Journal Article Research Support, Non-U.S. Gov't England0307-0565 (Print)'International journal of obesity (2005)15889114HINSERM Unit 457 Hopital R Debre, Paris, France. jacquet@rdebre.inserm.freng v<7)Cettour-Rose, P. Samec, S. Russell, A. P. Summermatter, S. Mainieri, D. Carrillo-Theander, C. Montani, J. P. Seydoux, J. Rohner-Jeanrenaud, F. Dulloo, A. G.2005Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat: a link between catch-up growth and later metabolic syndrome751-6Diabetes543BAdipose Tissue/*growth & development/*metabolism Animals Blood Glucose/physiology Body Composition Body Weight Energy Metabolism Fatty Acid Synthetase Complex/metabolism Food Deprivation/physiology Glucose/*metabolism Growth Insulin/pharmacology Lipid Metabolism Male Muscle, Skeletal/*metabolism Rats Rats, Sprague-DawleyMarCatch-up growth, a risk factor for later obesity, type 2 diabetes, and cardiovascular diseases, is characterized by hyperinsulinemia and an accelerated rate for recovering fat mass, i.e., catch-up fat. To identify potential mechanisms in the link between hyperinsulinemia and catch-up fat during catch-up growth, we studied the in vivo action of insulin on glucose utilization in skeletal muscle and adipose tissue in a previously described rat model of weight recovery exhibiting catch-up fat caused by suppressed thermogenesis per se. To do this, we used euglycemic-hyperinsulinemic clamps associated with the labeled 2-deoxy-glucose technique. After 1 week of isocaloric refeeding, when body fat, circulating free fatty acids, or intramyocellular lipids in refed animals had not yet exceeded those of controls, insulin-stimulated glucose utilization in refed animals was lower in skeletal muscles (by 20-43%) but higher in white adipose tissues (by two- to threefold). Furthermore, fatty acid synthase activity was higher in adipose tissues from refed animals than from fed controls. These results suggest that suppressed thermogenesis for the purpose of sparing glucose for catch-up fat, via the coordinated induction of skeletal muscle insulin resistance and adipose tissue insulin hyperresponsiveness, might be a central event in the link between catch-up growth, hyperinsulinemia and risks for later metabolic syndrome.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15734852 >Journal Article Research Support, Non-U.S. Gov't United States0012-1797 (Print)Diabetes15734852XDepartment of Internal Medicine, Faculty of Medicine, University of Geneva, Switzerland.eng?*Chong,S. Whitelaw,E.2004Epigenetic germline inheritance692-696)Current Opinion in Genetics & Development142004///33824ITY - JOUR filed in 'epigenetic' subject file RP - IN FILE U1 - export <7+\Cicognani, A. Alessandroni, R. Pasini, A. Pirazzoli, P. Cassio, A. Barbieri, E. Cacciari, E.2002ILow birth weight for gestational age and subsequent male gonadal function376-9Journal of Pediatrics14138Adolescent Adult Case-Control Studies Follicle Stimulating Hormone/blood Gonadal Disorders/*epidemiology Humans Infant, Newborn *Infant, Small for Gestational Age Inhibins/blood Luteinizing Hormone/blood Male Quebec/epidemiology Statistics, Nonparametric Testis/growth & development/metabolism Testosterone/bloodSepOBJECTIVE: To verify whether a reduced birth weight for gestational age was associated with a testicular dysfunction in postpubertal boys.Study design: Boys born small for gestational age (SGA) (n = 25) were compared to 24 born with an appropriate weight. All subjects were postpubertal (mean age 17.5 +/- 1.3 and 17.6 +/- 2.0 years, respectively). The following clinical and endocrinologic variables were evaluated: final height, target height, body mass index, testicular volume, follicle-stimulating hormone, luteinizing hormone, testosterone, and inhibin B. RESULTS: The SGA group had reduced testicular size (16.3 +/- 2.7 mL vs 22.8 +/- 3.2 mL; P <.0001) with a lower testosterone level (3.76 +/- 1.35 ng/mL vs 4.77 +/- 1.55 ng/mL; P <.05) and a higher LH value (4.41 +/- 1.61 IU/L vs 3.44 +/- 1.29 IU/L; P <.05). Among the SGA group, 54% had a mean testicular volume >2 SD below the control mean (ie, <16 mL) and in these subjects, the inhibin B level was low (143 +/- 46 pg/mL vs 229 +/- 76 pg/mL; P <.0001). SGA patients with smaller testes had lower final height relative to target height(P <.05 vs patients with larger testes) and for the SGA group, inhibin B correlated with testicular size (P <.0001). Positive correlations also were found between the reduction of final height relative to target height and testicular volume (P <.005) and inhibin B values (P <.05). CONCLUSIONS: SGA subjects have pituitary-gonadal axis function that tends toward hypogonadism. There is a disruption of the exocrine function in subjects with smaller testicular size who failed to show a complete height catch-up growth. This study supports a link between low birth weight and lower fertility in adult males.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12219058 Journal Article United States0022-3476 (Print)The Journal of pediatrics12219058HDepartments of Pediatrics and Neonatology, University of Bologna, Italy.eng ~?,J'Drake, A. J. Walker, B. R. Seckl, J. R.2005cIntergenerational consequences of fetal programming by in utero exposure to glucocorticoids in ratsR34-8SAmerican Journal of Physiology - Regulatory, Integrative and Comparative Physiology2881RAnimals Birth Weight/drug effects Body Weight/drug effects Dexamethasone/*pharmacology Female Glucocorticoids/*pharmacology Glucose Intolerance/physiopathology Liver/enzymology Male Phenotype Phosphoenolpyruvate Carboxykinase (GTP)/metabolism Pregnancy *Prenatal Exposure Delayed Effects Rats Rats, Wistar Research Support, Non-U.S. Gov'tJanEpidemiological studies linking low birth weight and subsequent cardiometabolic disease have given rise to the hypothesis that events in fetal life permanently program subsequent cardiovascular risk. The effects of fetal programming may not be limited to the first-generation offspring. We have explored intergenerational effects in the dexamethasone-programmed rat, a model in which fetal exposure to excess glucocorticoid results in low birth weight with subsequent adult hyperinsulinemia and hyperglycemia underpinned by increased activity of the key hepatic gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK). We found that the male offspring of female rats that had been exposed prenatally to dexamethasone, but were not manipulated in their own pregnancy, also had reduced birth weight (5.66 +/- 0.06 vs. 6.12 +/- 0.06 g, P < 0.001), glucose intolerance, and elevated hepatic PEPCK activity (5.7 +/- 0.6 vs. 3.3 +/- 0.2 nmol.min(-1).mg protein(-1), P < 0.001). These effects resolved in a third generation. Similar intergenerational programming was observed in offspring of male rats exposed prenatally to dexamethasone mated with control females. The persistence of such programming effects through several generations, transmitted by either maternal or paternal lines, indicates the potential importance of epigenetic factors in the intergenerational inheritance of the "programming phenotype" and provides a basis for the inherited association between low birth weight and cardiovascular risk factors.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15178540!0363-6119 (Print) Journal Article15178540Endocrinology Unit, School of Molecular and Clinical Medicine, University of Edinburgh, Molecular Medicine Center, Western General Hospital, United Kingdom. mandy.drake@ed.ac.uk?-CM Dwyer NC Strickland1994Supplementation of a restricted maternal diet with protein or carbohydrate alone prevents a reduction in fetal muscle fibre number in the guinea-pig173-180British Journal of Nutrition722~?.Eaton, S. B. Konner, M.1985MPaleolithic nutrition. A consideration of its nature and current implications283-9New England Journal of Medicine3125YAgriculture Animals Calcium, Dietary/analysis Cholesterol, Dietary/analysis Civilization Diet Dietary Fats/analysis Dietary Fiber/analysis Energy Intake Evolution Fatty Acids/analysis Food Analysis Food Supply History, Ancient Humans Life Style Meat *Nutrition Nutritional Requirements *Paleontology Potassium/analysis Sodium/analysis VegetablesJan 31dhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2981409;0028-4793 (Print) Historical Article Journal Article Review2981409I?02Eriksson,J.G. Forsen,T.J.. Osmond,C. Barker,D.J.P.2003EPathways of infant and childhood growth that lead to type 2 diabetes. 3006-3010 Diabetes Care26 11,2' childhood diabetes Growth infant pathways 2003///Nov31849LTY - JOUR Gluckman-insulin Gluckman-programming RP - IN FILE U1 - export?1NEriksson,J.G. Lindi,V. Uusitupa,M. Forsen,T.J. Laakso,M. Osmond,C. Barker,D.J.2002The effects of the Pro12Ala polymorphism of the peroxisome proliferator-activated preceptor-gamma2 gene on insulin sensitivity and insulin metabolism interact with size at birth. 2321-2324Diabetes51 7/gene Insulin Insulin metabolism metabolism size 2002///July31068bTY - JOUR Gluckman/Hanson Book Gluckman-programming Gluckman-insulin RP - IN FILE U1 - export<72$Fernandez-Twinn, D. S. Ozanne, S. E.2006bMechanisms by which poor early growth programs type-2 diabetes, obesity and the metabolic syndrome234-43Physiology and Behavior883~Adaptation, Physiological Animals Diabetes Mellitus, Type 2/embryology/*etiology Female Fetal Development/*physiology Fetal Growth Retardation/physiopathology Humans Metabolic Syndrome X/embryology/*etiology Models, Animal Obesity/embryology/*etiology Phenotype Pregnancy Pregnancy Complications *Prenatal Exposure Delayed Effects Prenatal Nutrition Physiology Stress/*complicationsJun 30"Fetal programming is gaining momentum as a highly documented phenomenon which links poor early growth to adult disease. It is backed up by large cohorts in epidemiological studies worldwide and has been tested in various animal models. The root causes of programming link closely with maternal condition during pregnancy, and therefore the fetal environment. Suboptimal fetal environments due to poor or inadequate nutrition, infection, anemia, hypertension, inflammation, gestational diabetes or hypoxia in the mother expose the fetus to hormonal, growth factor, cytokine or adipokine cues. These in turn act to alter metabolic, immune system, vascular, hemodynamics, renal, growth and mitochondrial parameters respectively and most evidently in the later stages of life where they impact on the individual as poor glucose homeostasis, insulin resistance, type 2 diabetes, hypertension, cardiovascular disease, obesity and heart disease. These events are compounded by over-nutrition or lifestyle choices which are in conflict with the programming of the fetus. We and others have utilised various species to test the early life programming hypothesis and to identify key molecular mechanisms. With parallel studies of human cohorts, these molecular markers can be validated as realistic targets for intervention.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16782139 $Journal Article Review United States0031-9384 (Print)Physiology & behavior16782139Department of Clinical Biochemistry, University of Cambridge, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QR, United Kingdom. df220@cam.ac.ukeng ~?3OFlorencio, T. T. Ferreira, H. S. Cavalcante, J. C. Luciano, S. M. Sawaya, A. L.2003Food consumed does not account for the higher prevalence of obesity among stunted adults in a very-low-income population in the Northeast of Brazil (Maceio, Alagoas)1437-46&European Journal of Clinical Nutrition5711Adult Body Composition Body Constitution Body Height/*physiology Body Mass Index Brazil *Eating Female Growth Disorders/*physiopathology Humans Male Mental Recall Obesity/*epidemiology/etiology *Poverty Prevalence Research Support, Non-U.S. Gov'tNov^OBJECTIVE: To study the food pattern of stunted and nonstunted, obese and nonobese individuals in a very-low-income population. DESIGN: A household survey. SETTING: Slum set up by the 'Homeless Movement', city of Maceio (Alagoas), Brazil. SUBJECTS AND METHODS: A total of 532 adults classified by sex, stature (Z -2s.d. of the NCHS curves), and body mass index (BMI) were compared using the following variables: waist circumference, waist-hip circumference ratio (W/H), percentage body fat (skinfold thickness and bioelectrical impedance), and food intake (24-h recall). RESULTS: The prevalence of stunting was 22.6%. In all, 30% of the stunted subjects were overweight or obese, compared with 23% for the nonstunted individuals (P<0.05). In women, logistic regression analysis showed a strong association among weight, abdominal fat, and stunting (r=0.81). No significant differences were observed in the values of W/H or in the qualitative menu of the different categories. Energy intake was below the RDA figures (about 63%). There was similarity among the groups regarding the proportion of macronutrients, except for the fact that stunted obese women ingested less fat and protein than nonstunted obese women. Stunted obese individuals consumed less energy (5962 kJ) than the population as a whole (6213 kJ), an amount far lower than their average needs, which were calculated on the basis of their shorter stature (8109 kJ). CONCLUSION: The observed energy consumption seems compatible with the panorama of undernutrition present in the population, but it does not explain the high prevalence of obesity detected.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14576757!0954-3007 (Print) Journal Article14576757Department of Physiology, Federal University of Sao Paulo, Rua Botucatu, Ciencias Biomedicas, Sao Paulo, SP, Brazil. telmatf_a@hotmail.com;?4 Forsdahl,A.1977tAre poor living conditions in childhood and adolescence an important risk factor for arteriosclerotic heart disease?91-951British Journal Preventative and Socical Medicine312gA Adolescence Aged As childhood correlation disease factor heart infant Infant Mortality mortality risk 1977/06//Norwegian counties show considerable variations in their rates of mortality from arteriosclerotic heart disease. These variations cannot be explained by present-day differences in standard of living. Such differences did exist in the past as was shown by large variations in infant mortality. A significant positive correlation has been found between the county age-adjusted mortality from arteriosclerotic heart disease in people aged between 40 and 69 years and county infant mortality relating to the early years in the same cohorts. The findings suggest that great poverty in childhood and adolescence followed by prosperity, is a risk factor for arteriosclerotic heart disease277822TY - JOUR 77222939 RP - NOT IN FILE U1 - export ~?5Garrett, J. L. Ruel, M. T.2005lStunted child-overweight mother pairs: prevalence and association with economic development and urbanization209-21Food and Nutrition Bulletin262Adult Africa Asia Body Height Body Mass Index Body Weight Child Child Nutrition Disorders/*epidemiology Demography Developing Countries Female Health Surveys Humans Latin America Male *Mothers Prevalence Public Policy Rural Health *Social Class Urban Health *UrbanizationJunThis paper explores the prevalence of the coexistence of a stunted child and an overweight mother in the same household (SCOWT), a somewhat paradoxical phenomenon when found in the developing world. It tests whether this phenomenon is associated with a country's level of economic development and urbanization and, by implication, the nutrition transition. It then highlights policy directions for public nutrition. Data from 42 Demographic and Health Surveys in Africa, Asia, and Latin America were used. Stunting was defined as height-for-age < -2 SD of the reference population, and maternal overweight as a body-mass index > 25 kg/m2. World Bank and United Nations figures were used for gross domestic product (GDP) per capita (an indicator of economic development) and for level of urbanization. Descriptive statistics were derived, and regression analysis was used to model the association between economic development, urbanization, and the prevalence of pairs of stunted children and overweight mothers. The prevalence of this phenomenon is generally below 10%, except in four countries, three of them in Latin America. The phenomenon is generally more prevalent in Latin America than in Africa, though not necessarily more prevalent in urban than in rural areas. The analysis finds that the phenomenon is associated with economic development, but not urbanization, and that it does differ between urban and rural areas and regions. The association with GDP per capita supports the hypothesis that SCOWT increases with economic development, up to a point. SCOWT appears to be most prevalent, as expected, in those countries in the midst of the nutrition transition. Recognizing this phenomenon is important for delineating strategies that respond to the differential needs of individuals within the household and do not just affect the household as a whole. This may become especially important with future economic development and, potentially, urbanization.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16060222!0379-5721 (Print) Journal Article16060222Food Consumption and Nutrition Division, International Food Policy Research Institute, Washington, DC 20006, USA. j.garrett@cgiar.orgI?6Gluckman, Peter D. Hanson, Mark20056The Fetal Matrix: Evolution, Development, and Disease xiv, 257 p.New YorkCambridge University PressbDevelopmental biology. Embryology, Human. Human evolution. Medicine, Preventive. Medical genetics.qhttp://www.loc.gov/catdir/toc/cam041/2004045815.html http://www.loc.gov/catdir/description/cam041/2004045815.html ill. ; 25 cm.0521834570 0521542359 (pb.)QH491 .G584 2005 612.6/4?7Gluckman,P.D. Hanson,M.A.2006+Developmental Origins of Health and Disease CambridgeCambridge University PressDevelopmental disease Health2006///33826)TY - BOOK RP - NOT IN FILE U1 - export'?8%Gluckman,P.D. Hanson,M.A. Beedle,A.S.2007gEarly life events and their consequences for later disease: a life history and evolutionary perspective1-99!American Journal of Human Biology191A disease history200634146)TY - JOUR RP - NOT IN FILE U1 - export?91Gluckman,P.D. Hanson,M.A. Spencer,H.G. Bateson,P.2005Environmental influences during development and their later consequences for health and disease: implications for the interpretation of empirical studies.671-677"Proceedings of the Royal Society B272 development disease2005///32359lTY - JOUR see PDF version in "Timing of Puberty" folder in LifeHistoEvo database RP - IN FILE U1 - export=?: Godfrey,K.20064The 'developmental origins' hypothesis: epidemiology6 -32+Developmental Origins of Health and DiseaseGluckman,P.D. Hanson,M.A. CambridgeCambridge University Press)Developmental disease epidemiology Health2006///34015)TY - CHAP RP - NOT IN FILE U1 - export?;]Hahn,T. Barth,S. Graf,R. Engelmann,M. Beslagic,D. Reul,J.M.H.M. Holsboer,F. Dohr,G. Desoye,G.1999IPlacental glucose transporter expression is regulated by glucocorticoids. 1445-14520Journal of Clinical Endocrinology and Metabolism84Oexpression glucocorticoid glucocorticoids Glucose Glucose transporter placental1999///28412)TY - JOUR RP - NOT IN FILE U1 - exportLJ Clin Endocrinol Metab J1 - Journal of Clinical Endocrinology & MetabolismS?<Hales,C.N. Barker,D.J.1992RType 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis595-601 Diabetologia357'2' diabetes Diabetes Mellitus Phenotype 1992/07//24933pTY - JOUR 92354829 Gluckman-programming FILE IN THRIFTY PHENOTYPE/GENOTYPE FOLDER RP - IN FILE U1 - export}?=Hattersley,A.T. Tooke,J.E.1999The fetal insulin hypothesis: an alternative explanation of the association of low birthweight with diabetes and vascular disease. 1789-1792 The Lancet353 9166'diabetes disease fetal Insulin vascular1999///32004LTY - JOUR Gluckman-programming Gluckman-insulin RP - IN FILE U1 - exportLancet J1 - Lancet.:?>+Ibáñez,L. Ong,K. Dunger,D.B. de Zegher,F.2006zEarly development of adiposity and insulin resistance following catch-up weight gain in small-for-gestational-age children 2153-21580Journal of Clinical Endocrinology and Metabolism916ychildren development Evolution Insulin Insulin Resistance Puberty resistance Small for Gestational Age weight Weight Gain2006///33866UTY - JOUR filed in 'Evolution of Puberty' subject folder RP - IN FILE U1 - exportLJ Clin Endocrinol Metab J1 - Journal of Clinical Endocrinology & Metabolism <7?J&Jasienska, G. Thune, I. Ellison, P. T.2006Fatness at birth predicts adult susceptibility to ovarian suppression: an empirical test of the Predictive Adaptive Response hypothesis12759-623Proceedings of the National Academy of Sciences USA10334*Adaptation, Physiological Adult Birth Weight/*physiology *Disease Susceptibility Empirical Research Estradiol/metabolism Exercise Female Humans *Models, Biological Nutritional Status/*physiology Ovarian Diseases/*physiopathology Overweight/*physiology Saliva/metabolismAug 22pPoor fetal environments are thought to produce adaptive changes in human developmental trajectories according to the Predictive Adaptive Response hypothesis. Although many studies have demonstrated correlations between indicators of fetal environment and negative adult health outcomes, the adaptive significance of these outcomes is unclear. Our study explicitly tests the adaptive nature of fetal programming in humans. We show that differences in nutritional status at birth are associated with adaptive differences in the sensitivity of adult ovarian function to energetic stress. Women who were born as relatively fat babies do not exhibit ovarian suppression in response to moderate levels of physical activity at adulthood, in contrast to women who were born as skinnier babies. The levels of estradiol in women born in the highest tertile of ponderal index (an indicator of neonatal nutritional status) were 37% and 46% higher, respectively, than levels of estradiol in women born in the low and middle ponderal index tertiles. These findings suggest that fetal programming of reproductive function results in developmentally plastic, but essentially adaptive, shifts in set points of ovarian response to energetic stress, such that women who were gestated under conditions of energetic constraint show greater sensitivity to energetic stress in adulthood. Our results have practical implications in terms of behavioral strategies for reducing the risk of breast cancer. We suggest that the amount of activity necessary to reduce levels of estrogen, which may in turn reduce cancer risk, can depend on a woman's nutritional status at birth.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16908839 >Journal Article Research Support, Non-U.S. Gov't United States0027-8424 (Print)OProceedings of the National Academy of Sciences of the United States of America16908839Department of Epidemiology and Population Studies, Collegium Medicum, Jagiellonian University, Grzegorzecka 20, 31-531 Krakow, Poland, and Ulleval University Hospital, Oslo, Norway. jasienska@post.harvard.edueng?@Jimenez-Chillaron,J.C. Hernandez-Valencia,M. Lightner,A. Faucette,R.R. Reamer,C. Przybyla,R. Ruest,S. Barry,K. Otis,J.P. Patti,M.E.2006Reductions in caloric intake and early postnatal growth prevent glucose intolerance and obesity associated with low birthweight 1974-1984 Diabetologia49 8Obirthweight Caloric Intake Glucose Glucose Intolerance Growth obesity postnatal2006///33982%TY - JOUR RP - IN FILE U1 - export?AKlose,R.J. Bird,A.P.20063Genomic DNA methylation: the mark and its mediators89-97Trends in Biochemical Sciences31DNA DNA Methylation2006///33781)TY - JOUR RP - NOT IN FILE U1 - export?BKrützfeldt,J. Stoffel,M.2006?MicroRNAs: a new class of regulatory genes affecting metabolism9-12Cell Metabolism4 A gene Genes metabolism2006///34190*TY - JOUR RP - NOT IN FILE U1 - export D?CC Kuzawa P Gluckman M Hanson20074Developmental perspectives on the origins of obesity3Adipose Tissue and Adipokines in Health and DiseaseG Fantuzzi T Mazzone Totowa, NJ Humana Press ~?E Kuzawa, C. W.2005qFetal origins of developmental plasticity: are fetal cues reliable predictors of future nutritional environments?5-21!American Journal of Human Biology171Adaptation, Physiological/*genetics Animals Birth Weight/physiology Energy Metabolism/genetics/physiology Environment Female Fetal Development/*physiology Humans Maternal-Fetal Exchange/physiology Neuronal Plasticity/genetics/*physiology Nutrition Disorders/*etiology/genetics Phenotype Phylogeny Pregnancy *Prenatal Exposure Delayed Effects Prenatal Nutrition/*physiology Research Selection (Genetics)Jan-FebhEvidence that fetal nutrition triggers permanent adjustments in a wide range of systems and health outcomes is stimulating interest in the evolutionary significance of these responses. This review evaluates the postnatal adaptive significance of fetal developmental plasticity from the perspective of life history theory and evolutionary models of energy partitioning. Birthweight is positively related to multiple metabolically costly postnatal functions, suggesting that the fetus has the capacity to distribute the burden of energy insufficiency when faced with a nutritionally challenging environment. Lowering total requirements may reduce the risk of negative energy balance, which disproportionately impacts functions that are not essential for survival but that are crucial for reproductive success. The long-term benefit of these metabolic adjustments is contingent upon the fetus having access to a cue that is predictive of its future nutritional environment, a problem complicated in a long-lived species by short-term ecologic fluctuations like seasonality. Evidence is reviewed suggesting that the flow of nutrients reaching the fetus provides an integrated signal of nutrition as experienced by recent matrilineal ancestors, which effectively limits the responsiveness to short-term ecologic fluctuations during any given pregnancy. This capacity for fetal nutrition to minimize the growth response to transient ecologic fluctuations is defined here as intergenerational "phenotypic inertia," and is hypothesized to allow the fetus to cut through the "noise" of seasonal or other stochastic influences to read the "signal" of longer-term ecologic trends. As a mode of adaptation, phenotypic inertia may help the organism cope with ecologic trends too gradual to be tracked by conventional developmental plasticity, but too rapid to be tracked by natural selection. From an applied perspective, if a trait like fetal growth is designed to minimize the effects of short-term fluctuations by integrating information across generations, public health interventions may be most effective if focused not on the individual but on the matriline.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15611967(1042-0533 (Print) Journal Article Review15611967kDepartment of Anthropology, Northwestern University, Evanston, Illinois 60208, USA. kuzawa@northwestern.edun?FKuzawa,C.W. Adair,L.S.2003mLipid profiles in adolescent Filipinos: relation to birth weight and maternal energy status during pregnancy.960-966&American Journal of Clinical Nutrition77 8Adolescent Birth weight energy maternal Pregnancy weight2003///325009TY - JOUR Gluckman-metabolism RP - IN FILE U1 - exportAm J Clin Nutr?GALillycrop,K.A. Phillips,E.S. Jackson,A.A. Hanson,M.A. Burdge,G.C.2005Dietary protein restriction of pregnant rats induces and folic acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring 1382-1386Journal of Nutrition135 Xexpression Folic Acid gene gene expression maternal protein protein restriction rat Rats2005///32682%TY - JOUR RP - IN FILE U1 - export?H\Mackay, Judith Mensah, George A. Mendis, Shanthi Greenlund, Kurt World Health Organization.,2004%The Atlas of Heart Disease and Stroke112 p.GenevaWorld Health OrganizationDHeart Diseases Atlases. Cerebrovascular disease Atlases. Cardiology Atlases. Heart Diseases epidemiology Atlases. Cerebrovascular Accident Atlases. Cerebrovascular Accident epidemiology Atlases. Risk Factors. World Health. Health Promotion. C¶ur Maladies Atlas. Accidents vasculaires câerâebraux Atlas. Cardiologie Atlas.@http://www.who.int/cardiovascular%5Fdiseases/resources/atlas/en/gJudith McKay and George A. Mensah with Shanthi Mendis and Kurt Greenlund. col. ill., col. maps ; 25 cm.RC683 .M23 2004 616.12j?I=McCarron,P. Davey Smith,G. Hattersley,A.T. ALSPAC Study Team,2004dType 2 diabetes in grandparents and birth weight in offspring and grandchildren in the ALSPAC study.517-522,Journal of Epidemiology and Community Health582' Birth weight diabetes weight2004///32538<TY - JOUR Gluckman-grandmothers RP - IN FILE U1 - export8?JMcMillen,I.C. Robinson,J.S.2005XDevelopmental origins of the metabolic syndrome: prediction, plasticity, and programming571-633Physiological Reviews85 6Developmental metabolic plasticity prediction Syndrome2005///33517)TY - JOUR RP - NOT IN FILE U1 - export Physiol Rev~?K"Miles,H. Hofman,P.L. Cutfield,W.S.2005mIVF children are taller with increased IGF-I, IGF-II and IGFBP-3 levels suggesting altered genetic imprinting1016Pediatric Research5857children Genetic IGF-I IGF-II IGFBP-3 IGFBP3 imprinting2005///335259TY - JOUR RP - NOT IN FILE U1 - export Y2 - -32676///'Pediatr Res J1 - Pediatr Res. J2 - PR~?LCMoore, S. E. Halsall, I. Howarth, D. Poskitt, E. M. Prentice, A. M.2001UGlucose, insulin and lipid metabolism in rural Gambians exposed to early malnutrition646-53Diabetes Medicine188GAdult Anthropometry Blood Glucose/*metabolism Blood Pressure Body Height Body Weight Female Gambia/epidemiology Humans Hunger Infant, Low Birth Weight Infant, Newborn Insulin/*blood Insulin Resistance/*physiology Lipids/*blood Male Nutrition Disorders/*blood/*epidemiology/physiopathology Risk Factors *Rural Population SeasonsAugAIMS: There is now substantial evidence to suggest that susceptibility to certain non-communicable diseases may be increased by early undernutrition. In rural Gambia, an annual hungry season reduces birth weight by 200-300 g and increases the prevalence of low birth weight (< 2500 g) from 11% to 24%. The aim of this study was to investigate whether fetal nutritional stress (using season of birth as a proxy measure for prenatal growth retardation) or early childhood malnutrition (using historical anthropometric records) had a residual influence on risk factors for cardiovascular disease in a cohort of rural Gambian adults. METHODS: Two hundred and nineteen adults (mean age = 35.8 years; mean body mass index = 21.3 kg/m2; women = 181) for whom month of birth and infant anthropometric records were available participated in this study. Risk factors for cardiovascular disease were measured. RESULTS: No differences were found between season of birth groups (hungry vs. harvest) and fasting measures of glucose, insulin, lipids, fibrinogen or cortisol, or against 30 and 120 min glucose and insulin levels following an oral glucose tolerance test, or blood pressure. Similarly, these risk factors for adult disease were not related to the subjects' weight-for-age as children. CONCLUSIONS: Moderate-to-severe fetal and childhood malnutrition in rural Gambia caused no detectable impairment of the glucose/insulin axis, or of other cardiovascular disease risk factors in adults remaining lean and fit on a low-fat diet.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11553202!0742-3071 (Print) Journal Article11553202=MRC Keneba, The Gambia, West Africa. Sophie.Moore@LSHTM.ac.uk"?MMorley,R. Lucas,A.1997$Nutrition and cognitive development.123-134British Medical Bulletin53 1development Nutrition 1997///Jan32197uTY - JOUR Gluckman-fetal Gluckman-nutrition Gluckman-programming FILED IN LUCAS FOLDER RP - IN FILE U1 - export?N Morton,S.M.B.20063Maternal nutrition and fetal growth and development98-129,Developmental Origins of Health and Disease Gluckman,P.D. Hanson,M.A. CambridgeCambridge University Presshdevelopment Developmental disease fetal Fetal Growth Growth Health maternal maternal nutrition Nutrition2006///33671)TY - CHAP RP - NOT IN FILE U1 - export?O Neel,J.V.1962KDiabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?353-362"American Journal of Human Genetics14 %A diabetes Diabetes Mellitus Genotype1962///31048)TY - JOUR RP - NOT IN FILE U1 - exportAm J Hum GenetE?P)Nightingale,K.P. O'Neill,L.P. Turner,B.M.2006aHistone modifications: signalling receptors and potential elements of a heritable epigenetic code125-136+Current Opinion in Genetics and Development16 2A receptor receptors signalling2006///34189*TY - JOUR RP - NOT IN FILE U1 - export  F~?QOken, E. Gillman, M. W.2003Fetal origins of obesity496-506Obesity Research1142Adipose Tissue Adolescent Adult Birth Weight Body Composition Body Constitution Body Mass Index Cardiovascular Diseases Female Humans Male Obesity/epidemiology/*etiology/genetics Pregnancy *Prenatal Exposure Delayed Effects Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Risk FactorsApr_The worldwide epidemic of obesity continues unabated. Obesity is notoriously difficult to treat, and, thus, prevention is critical. A new paradigm for prevention, which evolved from the notion that environmental factors in utero may influence lifelong health, has emerged in recent years. A large number of epidemiological studies have demonstrated a direct relationship between birth weight and BMI attained in later life. Although the data are limited by lack of information on potential confounders, these associations seem robust. Possible mechanisms include lasting changes in proportions of fat and lean body mass, central nervous system appetite control, and pancreatic structure and function. Additionally, lower birth weight seems to be associated with later risk for central obesity, which also confers increased cardiovascular risk. This association may be mediated through changes in the hypothalamic pituitary axis, insulin secretion and sensing, and vascular responsiveness. The combination of lower birth weight and higher attained BMI is most strongly associated with later disease risk. We are faced with the seeming paradox of increased adiposity at both ends of the birth weight spectrum-higher BMI with higher birth weight and increased central obesity with lower birth weight. Future research on molecular genetics, intrauterine growth, growth trajectories after birth, and relationships of fat and lean mass will elucidate relationships between early life experiences and later body proportions. Prevention of obesity starting in childhood is critical and can have lifelong, perhaps multigenerational, impact.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12690076(1071-7323 (Print) Journal Article Review12690076Department of Ambulatory Care and Prevention, Harvard Medical School/Harvard Pilgrim Health Care, Boston, Massachusetts, USA. emily_oken@harvardpilgrim.org?R&Painter,R.C. Roseboom,T.J. Bleker,O.P.2005MPrenatal exposure to the Dutch famine and disease in later life: an overview.345-352Reproductive Toxicology20 3disease Prenatal2005///33979)TY - JOUR RP - NOT IN FILE U1 - exportReprod Toxicol. U|7S\Pembrey, M. E. Bygren, L. O. Kaati, G. Edvinsson, S. Northstone, K. Sjostrom, M. Golding, J.2006=Sex-specific, male-line transgenerational responses in humans159-66"European Journal of Human Genetics142(Adult Body Mass Index Child England/epidemiology Family Characteristics *Fathers Female Humans Inheritance Patterns/*genetics Longevity/genetics Male Nutritional Status/genetics Risk Factors Sex Chromosomes/*genetics Sex Factors Smoking/*adverse effects/*epidemiology/genetics Sweden/epidemiologyFebTransgenerational effects of maternal nutrition or other environmental 'exposures' are well recognised, but the possibility of exposure in the male influencing development and health in the next generation(s) is rarely considered. However, historical associations of longevity with paternal ancestors' food supply in the slow growth period (SGP) in mid childhood have been reported. Using the Avon Longitudinal Study of Parents and Children (ALSPAC), we identified 166 fathers who reported starting smoking before age 11 years and compared the growth of their offspring with those with a later paternal onset of smoking, after correcting for confounders. We analysed food supply effects on offspring and grandchild mortality risk ratios (RR) using 303 probands and their 1818 parents and grandparents from the 1890, 1905 and 1920 Overkalix cohorts, northern Sweden. After appropriate adjustment, early paternal smoking is associated with greater body mass index (BMI) at 9 years in sons, but not daughters. Sex-specific effects were also shown in the Overkalix data; paternal grandfather's food supply was only linked to the mortality RR of grandsons, while paternal grandmother's food supply was only associated with the granddaughters' mortality RR. These transgenerational effects were observed with exposure during the SGP (both grandparents) or fetal/infant life (grandmothers) but not during either grandparent's puberty. We conclude that sex-specific, male-line transgenerational responses exist in humans and hypothesise that these transmissions are mediated by the sex chromosomes, X and Y. Such responses add an entirely new dimension to the study of gene-environment interactions in development and health.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16391557 pALSPAC Study Team Wellcome Trust Comparative Study Journal Article Research Support, Non-U.S. Gov't England Ejhg1018-4813 (Print)16391557Clinical and Molecular Genetics Unit, Institute of Child Health, University College London, England, UK. M.Pembrey@bristol.ac.ukengm<7T Popkin, B. M.2004AThe nutrition transition: an overview of world patterns of changeS140-3Nutrition Reviews627 Pt 2Body Composition/*physiology Chronic Disease/*epidemiology Developing Countries/economics/statistics & numerical data Diet/*trends Exercise/physiology Female *Health Transition Humans Life Style Male Obesity/epidemiology Poverty World HealthJulEThis paper examines the speed of change in diet, activity, and obesity in the developing world, and notes potential exacerbating biological relationships that contribute to differences in the rates of change. The focus is on lower- and middle-income countries of Asia, Africa, the Middle East, and Latin America. These dietary, physical activity, and body composition changes are occurring at great speed and at earlier stages of these countries' economic and social development. There are some unique issues that relate to body composition and potential genetic factors that are also explored, including potential differences in body mass index (BMI)--disease relationships and added risks posed by high levels of poor fetal and infant growth patterns. In addition there is an important dynamic occurring--the shift in the burden of poor diets, inactivity and obesity from the rich to the poor. The developing world needs to give far greater emphasis to addressing the prevention of the adverse health consequences of this shift to the nutrition transition stage of the degenerative diseases.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15387480 sR01-hd30880/hd/nichd R01-hd38700/hd/nichd Journal Article Research Support, U.S. Gov't, P.H.S. Review United States0029-6643 (Print)Nutrition reviews15387480Department of Nutrition, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27516-3997, USA.eng ~?U-Popkin, B. M. Richards, M. K. Montiero, C. A.1996oStunting is associated with overweight in children of four nations that are undergoing the nutrition transition3009-16Journal of Nutrition12612SBody Mass Index Brazil/epidemiology Child Child Nutrition Disorders/complications Child, Preschool China/epidemiology Comparative Study Growth Disorders/complications/*epidemiology/ethnology Humans Nutrition Surveys Obesity/complications/*epidemiology/ethnology Poverty Prevalence Russia/epidemiology South Africa/epidemiology World HealthDecA higher risk of obesity in stunted children has been described in Hispanic-American, Jamaican and Andean populations, but little systematic exploration has been done concerning this area in nutrition. This paper examines the relationship between stunting and overweight status for children aged 3-6 and 7-9 y in nationally representative surveys in Russia, Brazil, and the Republic of South Africa and a large nationwide survey in China. Using identical cut-offs for body mass index, the prevalence of child overweight in these countries ranges from 10.5 to 25.6% (based on the 85th percentile); recent NHANES III results indicate that this prevalence is around 22% in the U.S. Stunting is also common in the surveyed countries affecting 9.2-30.6% of all children. Our results showed a significant association between stunting and overweight status in children of all countries. The income-adjusted risk ratios of being overweight for a stunted child ranged from 1.7 to 7.8. Clearly, there is an important association between stunting and high weight-for-height in a variety of ethnic environmental and social backgrounds. Although the underlying mechanisms remain unexplored, this association has serious public health implications particularly for lower income countries. As these countries enter the nutrition transition experiencing large changes in dietary and activity patterns, they may face, among other problems, additional difficulties in their fight against obesity.dhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9001368!0022-3166 (Print) Journal Article9001368oDepartment of Nutrition, School of Public Health, University of North Carolina at Chapel Hill, 27516-3997, USA.~?VPrentice, A. M. Moore, S. E.2005>Early programming of adult diseases in resource poor countries429-32!Archives of Diseases in Childhood904Adult Child Child Nutrition Disorders/*complications/economics *Developing Countries Genotype *Health Status Humans Income Nutritional Status Phenotype *Poverty Areas Risk Factors Survival AnalysisAprConsiderable evidence now exists to suggest that early exposure to nutritional deprivation can have long term consequences to health, with low birth weight now considered a risk factor for later health outcomes such as coronary heart disease, stroke, type 2 diabetes, and the metabolic syndrome. Of importance, such effects are most exaggerated when faced with over-nutrition in later life, forming the basis for the "thrifty phenotype" hypothesis. The evidence in support of these associations comes largely from retrospective cohort studies in which adult outcomes were correlated with birth weight records. Relatively little data is available from developing countries, where long term record keeping of birth weight data has not been a high priority. Arguably however, such countries are at the greatest risk from the mismatch of early nutritional deprivation and later nutritional affluence. This paper explores the importance of the "developmental origins of health and disease" hypothesis in resource poor countries.ehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15781942&1468-2044 (Electronic) Journal Article15781942xMRC International Nutrition Group, London School of Hygiene & Tropical Medicine, London, UK. Andrew.Prentice@lshtm.ac.uk ?W5Ramakrishnan,U. Martorell,R. Schroeder,D.G. Flores,R.19993Role of intergenerational effects on linear growth. 544S-549SJournal of Nutrition129 Growth role1999///32537?TY - JOUR Gluckman-transgeneration RP - IN FILE U1 - export?XFRassoulzadegan,M. Grandjean,V. Gounon,P. Vincent,S. Gillot,I. Cuzin,F.2006KRNA-mediated non-Mendelian inheritance of an epigenetic change in the mouse469-474Nature441 mouse2006///33834)TY - JOUR RP - NOT IN FILE U1 - exportNature <7YrRobinson, S. M. Batelaan, S. F. Syddall, H. E. Sayer, A. A. Dennison, E. M. Martin, H. J. Barker, D. J. Cooper, C.2006tCombined effects of dietary fat and birth weight on serum cholesterol concentrations: the Hertfordshire Cohort Study237-44&American Journal of Clinical Nutrition8417Aged Anticholesteremic Agents/therapeutic use Birth Weight/*physiology Cholesterol/*blood Cholesterol, HDL/blood Cholesterol, LDL/blood Cohort Studies *Diet Dietary Fats/*administration & dosage/metabolism Fasting/blood Female Humans Linear Models Male Middle Aged Prospective Studies Questionnaires Sex FactorsJulkBACKGROUND: Blood cholesterol responses to the manipulation of dietary fat vary widely between persons. Although epidemiologic evidence suggests that prenatal growth and nutrition influence adult cholesterol homeostasis, whether prenatal growth modifies the association between dietary fat intake and serum cholesterol concentration in adults is unknown. OBJECTIVE: The aim was to examine the relation between fat intake and serum cholesterol concentrations in men and women whose birth weights were known. DESIGN: We studied a cohort of men and women aged 59-71 y. Diet was assessed with a food-frequency questionnaire. Total, HDL-, and LDL-cholesterol concentrations and the ratio of HDL to LDL cholesterol were measured in fasting blood samples from 574 men and 562 women who did not have coronary heart disease. RESULTS: Total and saturated fat intakes were not associated with serum cholesterol concentrations in men or women. However, subdivision by birth weight showed associations in men but not in women. High intakes of total and saturated fat were associated with reduced HDL-cholesterol concentrations in men with birth weights < or =3.2 kg (7 lb) but not in men with higher birth weights. Similar effects on the HDL-to-LDL cholesterol ratio were observed (P for interaction = 0.02 for total fat and 0.01 for saturated fat). When 32 men taking cholesterol-lowering medication were excluded, the interactions were strengthened (P = 0.008 and 0.006, respectively). CONCLUSION: The adverse effects of high intakes of total and saturated fat on serum cholesterol concentrations in men may be confined to those with lower birth weights.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16825701 YHertfordshire Cohort Study Journal Article Research Support, Non-U.S. Gov't United States0002-9165 (Print)*The American journal of clinical nutrition16825701Medical Research Council Epidemiology Resource Centre, University of Southampton, Southampton General Hospital, Southampton, United Kingdom. smr@mrc.soton.ac.ukeng <7[Stearns, S. C. Ebert, D.20011Evolution in health and disease: work in progress417-32Quarterly Review of Biology764Adaptation, Physiological/genetics Animals Drug Resistance/genetics *Evolution Follicular Atresia/genetics Genomics Humans Menstruation Nerve Regeneration *Research VirulenceDecrThis article surveys progress in Darwinian medicine since 1991. Evolutionary thinking has been providing an increasing flow of fresh ideas into medical science, ideas that would not be suggested by other perspectives. Recent contributions have shed new light on the evolution of virulence, of antibiotic resistance, of oocytic atresia, of menopause, of the timing of the expression of genetic disease, of links between mate choice and disease resistance, and of genomic conflict between mother and fetus over resource provisioning. An important consequence of changes from the environment of evolutionary adaptedness concerns reproductive cancers; the incidence of reproductive cancers may be linked to changes in the frequency of menstruation in postindustrial societies. Other intriguing developments include some unanticipated and undesirable consequences of good hygiene, hope from an unexpected quarter for progress on nerve and muscle regeneration, evolutionary interpretations of mental disease, and insights from functional genomics into the nature of tradeoffs. The application of evolutionary thinking to problems in medical research and practice has thus yielded an abundant and growing harvest of insights. Some are well founded, others remain speculative. The field is moving from an initial phase dominated by speculation and hypothesis formation into a more rigorous phase of experimental testing of explicit alternatives. Currently the most promising areas, those in which experimental rigor can be applied efficiently, include experimental evolution and functional genomics. The pioneers can be proud of what they have set in motion.fhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11783396 $Journal Article Review United States0033-5770 (Print)The Quarterly review of biology11783396Department of Ecology and Evolutionary Biology, Yale University New Haven, Connecticut 06520-8106, USA. stephen.stearns@yale.edueng <7\kStettler, N. Stallings, V. A. Troxel, A. B. Zhao, J. Schinnar, R. Nelson, S. E. Ziegler, E. E. Strom, B. L.2005Weight gain in the first week of life and overweight in adulthood: a cohort study of European American subjects fed infant formula1897-903 Circulation11115Adult Body Mass Index Body Weight Child Cohort Studies European Continental Ancestry Group Female Follow-Up Studies Humans *Infant Formula Infant, Newborn Logistic Models Male Obesity/epidemiology/*etiology United States *Weight GainApr 19BACKGROUND: Successful prevention of obesity and related cardiovascular risk factors requires a clear understanding of its determinants over the life course. Rapid infancy weight gain is associated with childhood obesity, whereas low infancy weight is associated