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1.
JAMA Psychiatry ; 81(5): 521-526, 2024 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-38381408

RESUMO

Importance: The rate of maternal mortality in the United States is 2-fold to 3-fold greater than that in other high-income countries. While many national initiatives have been developed to combat maternal mortality, these efforts often fail to include mental illness. Objective: To highlight the underrecognized contribution of mental illness to maternal mortality, which is nearly double that of postpartum hemorrhage. Evidence Review: A topic outline was developed to include challenges in measuring perinatal mental conditions and mortality rates; contributions of social determinants of health to mental conditions and mortality; perinatal psychiatric disorder characterization; mechanisms by which maternal mental illness increases mortality, specifically, suicide and addictive disorders; access limitations and care "deserts"; prenatal stress and its impact on reproductive outcomes; increasing clinician expertise through cross-disciplinary education; intervention sites and models; and asserting that mental health is fundamental to maternal health. Publications in the last 3 years were prioritized, particularly those relating to policy. References were selected through consensus. Sources were PubMed, Ovid, direct data published on government websites, and health policy sources such as the Policy Center for Maternal Mental Health. Findings: Priority was given to recent sources. Citations from 2022-2023 numbered 26; within the last 5 years, 14; and historical references, 15. Recommendations to address each topic area serve as concluding statements for each section. To mitigate the contributions of mental illness to the maternal mortality risk, a coordinated effort is required across professional and governmental organizations. Conclusions and Relevance: Concrete programmatic and policy changes are needed to reduce perinatal stress and address trauma, standardize the collection of social determinant of health data among perinatal patients, increase access to reproductive psychiatry curricula among prescribers, reduce perinatal mental health and obstetrical deserts, institute paid parental leave, and support seamless integration of perinatal and behavioral health care. Moreover, instead of focusing on a relatively minor portion of the contributors to health that current medical practice targets, fortifying the social foundation strengthens the prospects for the health of families for our current and future generations.


Assuntos
Mortalidade Materna , Transtornos Mentais , Complicações na Gravidez , Humanos , Feminino , Mortalidade Materna/tendências , Gravidez , Estados Unidos/epidemiologia , Complicações na Gravidez/mortalidade , Saúde Materna , Saúde Mental , Prioridades em Saúde , Determinantes Sociais da Saúde
2.
Reprod Sci ; 26(7): 972-978, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-30304995

RESUMO

Placental fatty acid oxidation (FAO) is impaired and lipid storage is increased in pregnancy states associated with chronic oxidative stress. The effect of acute oxidative stress, as seen in pregnancies complicated with asthma, on placental lipid metabolism is unknown. We hypothesized that induction of acute oxidative stress would decrease FAO and increase esterification. We assessed [3H]-palmitate oxidation and esterification in term placental explants from lean women after exposure to hydrogen peroxide (H2O2) for 4 hours. Fatty acid oxidation decreased 16% and 24% in placental explants exposed to 200 (P = .02) and 400 µM H2O2 (P = .01), respectively. Esterification was not altered with H2O2 exposure. Neither messenger RNA nor protein expression of key genes involved in FAO (eg, peroxisome proliferator-activated receptor α, carnitine palmitoyl transferase 1b) were altered. Adenosine triphosphate (ATP) levels decreased with induction of oxidative stress, without increasing cytotoxicity. Acute oxidative stress decreased FAO and ATP production in the term placenta without altering fatty acid esterification. As decreases in placental FAO and ATP production are associated with impaired fetal growth, pregnancies exposed to acute oxidative stress may be at risk for fetal growth restriction.


Assuntos
Metabolismo Energético , Mitocôndrias/metabolismo , Estresse Oxidativo , Ácido Palmítico/metabolismo , Placenta/metabolismo , Trifosfato de Adenosina/metabolismo , Adulto , Carnitina O-Palmitoiltransferase/genética , Carnitina O-Palmitoiltransferase/metabolismo , Células Cultivadas , Esterificação , Feminino , Humanos , Peróxido de Hidrogênio/administração & dosagem , Mitocôndrias/efeitos dos fármacos , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , PPAR alfa/genética , PPAR alfa/metabolismo , Placenta/efeitos dos fármacos , Gravidez , Adulto Jovem
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