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      Mental Health, Mitochondria, and the Battle of the Sexes

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          Abstract

          This paper presents a broad perspective on how mental disease relates to the different evolutionary strategies of men and women and to growth, metabolism, and mitochondria—the enslaved bacteria in our cells that enable it all. Several mental disorders strike one sex more than the other; yet what truly matters, regardless of one’s sex, is how much one’s brain is “female” and how much it is “male”. This appears to be the result of an arms race between the parents over how many resources their child ought to extract from the mother, hence whether it should grow a lot or stay small and undemanding. An uneven battle alters the child’s risk of developing not only insulin resistance, diabetes, or cancer, but a mental disease as well. Maternal supremacy increases the odds of a psychosis-spectrum disorder; paternal supremacy, those of an autism-spectrum one. And a particularly lopsided struggle may invite one or the other of a series of syndromes that come in pairs, with diametrically opposite, excessively “male” or “female” characteristics. By providing the means for this tug of war, mitochondria take center stage in steadying or upsetting the precarious balance on which our mental health is built.

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          Global causes of maternal death: a WHO systematic analysis.

          Data for the causes of maternal deaths are needed to inform policies to improve maternal health. We developed and analysed global, regional, and subregional estimates of the causes of maternal death during 2003-09, with a novel method, updating the previous WHO systematic review. We searched specialised and general bibliographic databases for articles published between between Jan 1, 2003, and Dec 31, 2012, for research data, with no language restrictions, and the WHO mortality database for vital registration data. On the basis of prespecified inclusion criteria, we analysed causes of maternal death from datasets. We aggregated country level estimates to report estimates of causes of death by Millennium Development Goal regions and worldwide, for main and subcauses of death categories with a Bayesian hierarchical model. We identified 23 eligible studies (published 2003-12). We included 417 datasets from 115 countries comprising 60 799 deaths in the analysis. About 73% (1 771 000 of 2 443 000) of all maternal deaths between 2003 and 2009 were due to direct obstetric causes and deaths due to indirect causes accounted for 27·5% (672 000, 95% UI 19·7-37·5) of all deaths. Haemorrhage accounted for 27·1% (661 000, 19·9-36·2), hypertensive disorders 14·0% (343 000, 11·1-17·4), and sepsis 10·7% (261 000, 5·9-18·6) of maternal deaths. The rest of deaths were due to abortion (7·9% [193 000], 4·7-13·2), embolism (3·2% [78 000], 1·8-5·5), and all other direct causes of death (9·6% [235 000], 6·5-14·3). Regional estimates varied substantially. Between 2003 and 2009, haemorrhage, hypertensive disorders, and sepsis were responsible for more than half of maternal deaths worldwide. More than a quarter of deaths were attributable to indirect causes. These analyses should inform the prioritisation of health policies, programmes, and funding to reduce maternal deaths at regional and global levels. Further efforts are needed to improve the availability and quality of data related to maternal mortality. © 2014 World Health Organization; licensee Elsevier. This is an Open Access article published without any waiver of WHO's privileges and immunities under international law, convention, or agreement. This article should not be reproduced for use in association with the promotion of commercial products, services, or any legal entity. There should be no suggestion that WHO endorses any specific organisation or products. The use of the WHO logo is not permitted. This notice should be preserved along with the article's original URL.
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            What Is the Male-to-Female Ratio in Autism Spectrum Disorder? A Systematic Review and Meta-Analysis

            To derive the first systematically calculated estimate of the relative proportion of boys and girls with autism spectrum disorder (ASD) through a meta-analysis of prevalence studies conducted since the introduction of the DSM-IV and the International Classification of Diseases, Tenth Revision.
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              Persistent epigenetic differences associated with prenatal exposure to famine in humans.

              Extensive epidemiologic studies have suggested that adult disease risk is associated with adverse environmental conditions early in development. Although the mechanisms behind these relationships are unclear, an involvement of epigenetic dysregulation has been hypothesized. Here we show that individuals who were prenatally exposed to famine during the Dutch Hunger Winter in 1944-45 had, 6 decades later, less DNA methylation of the imprinted IGF2 gene compared with their unexposed, same-sex siblings. The association was specific for periconceptional exposure, reinforcing that very early mammalian development is a crucial period for establishing and maintaining epigenetic marks. These data are the first to contribute empirical support for the hypothesis that early-life environmental conditions can cause epigenetic changes in humans that persist throughout life.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Biomedicines
                Biomedicines
                biomedicines
                Biomedicines
                MDPI
                2227-9059
                26 January 2021
                February 2021
                : 9
                : 2
                : 116
                Affiliations
                Dipartimento di Psicologia Generale, University of Padova, Via Venezia 8, 35131 Padova, Italy
                Author notes
                Author information
                https://orcid.org/0000-0003-2763-0902
                https://orcid.org/0000-0003-4807-7077
                Article
                biomedicines-09-00116
                10.3390/biomedicines9020116
                7911591
                33530498
                17e2ef8c-bf6b-4ad0-a8ae-3153347a09f2
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 04 January 2021
                : 22 January 2021
                Categories
                Review

                mitochondria,sex differences,sex chromosomes,imprinted genes,diametric theory,kinship theory,parent–offspring conflict

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