Raised plasma nerve growth factor levels associated with early-stage romantic love.
Psychoneuroendocrinology. 2006 Apr;31(3):288-94. Epub 2005 Nov 10. PMID: 16289361
Enzo Emanuele, Pierluigi Politi, Marika Bianchi, Piercarlo Minoretti, Marco Bertona, Diego Geroldi
Our current knowledge of the neurobiology of romantic love remains scanty. In view of the complexity of a sentiment like love, it would not be surprising that a diversity of biochemical mechanisms could be involved in the mood changes of the initial stage of a romance. In the present study, we have examined whether the early romantic phase of a loving relationship could be associated with alterations in circulating levels of neurotrophins (NTs). Plasma levels of NGF, BDNF, NT-3 and NT-4 were measured in a total of 58 subjects who had recently fallen in love and compared with those of two control groups, consisting of subjects who were either single or were already engaged in a long-lasting relationship. NGF level was significantly higher (p<0.001) in the subjects in love [mean (SEM): 227 (14) pg/ml] than in either the subjects with a long-lasting relationship [123 (10) pg/ml] or the subjects with no relationship [149 (12) pg/ml]. Notably, there was also a significant positive correlation between levels of NGF and the intensity of romantic love as assessed with the passionate love scale (r = 0.34; p = 0.007). No differences in the concentrations of other NTs were detected. In 39 subjects in love who-after 12-24 months-maintained the same relationship but were no longer in the same mental state to which they had referred during the initial evaluation, plasma NGF levels decreased and became indistinguishable from those of the control groups. Taken together, these findings suggest that some behavioural and/or psychological features associated with falling in love could be related to raised NGF levels in the bloodstream.
Article Published Date : Apr 01, 2006
Religion and spirituality: Pathways to positive body image.
Body Image. 2019 Jan 18;28:135-141
Authors: Tiggemann M, Hage K
Positive body image is a multidimensional construct referring to love, respect, and acceptance of one's body, including aspects inconsistent with sociocultural ideals. The aim of the present study was to investigate potential pathways leading from religion and spirituality to positive body image. Participants were 345 women who completed questionnaire measures of engagement with formal religion, spirituality, gratitude, self-objectification, and positive body image. Both engagement with formal religion and spirituality were found to be positively associated with positive body image. Further, mediation analyses showed that the relationship between spirituality and positive body image was mediated by gratitude and reduced self-objectification. It was concluded that a broader spiritual consciousness may assist women to develop a loving, appreciative, and respectful relationship with their bodies. In addition, gratitude and a de-emphasis on external appearance provide useful goals and potential intervention points for promoting positive body image.
PMID: 30665031 [PubMed - as supplied by publisher]
The dawn of algometry: Paolo Mantegazza's research on pain.
Funct Neurol. 2018 Oct/Dec;33(4):254-258
Authors: Cani V
By the 1860s, Paolo Mantegazza was a professor of general pathology at the University of Pavia, where he had graduated in medicine in 1854. There, he founded Italy's first laboratory of experimental pathology and did his first research on pain, the subject of various communications presented to the Istituto Lombardo in Milan. In 1880, Mantegazza published Physiology of Pain, one of the several "physiologies" (of pleasure, of love, of hatred, of woman) that he wrote during his career. In this book, a testament to his scientific versatility, experimental observations supplemented his insights into hygienism and anthropology. This research on pain also led to a dispute between Mantegazza and Cesare Lombroso, which was the start of the two scientists' estrangement.
PMID: 30663972 [PubMed - in process]
The Age-Well observational study on expert meditators in the Medit-Ageing European project.
Alzheimers Dement (N Y). 2018;4:756-764
Authors: Lutz A, Klimecki OM, Collette F, Poisnel G, Arenaza-Urquijo E, Marchant NL, De La Sayette V, Rauchs G, Salmon E, Vuilleumier P, Frison E, Vivien D, Chételat G, Medit-Ageing Research Group
Introduction: The Age-Well observational, cross-sectional study investigates the affective and cognitive mechanisms of meditation expertise with behavioral, neuroimaging, sleep, and biological measures sensitive to aging and Alzheimer's disease (AD).
Methods: Thirty cognitively unimpaired individuals aged 65 years or older with at least 10,000 hours of practice in mindfulness meditation (MM) and loving-kindness and compassion meditation (LKCM) are selected. The outcomes are the neuroimaging brain correlates of MM and LKCM and the assessments of long-term meditation practices on behavioral, neural, and biological measures as compared to nonmeditator older controls from the Age-Well randomized controlled trial.
Results: Recruitment and data collection began in late 2016 and will be completed by late 2019.
Discussion: Results are expected to foster the understanding of the effects of meditation expertise on aging and of the mechanisms of action underlying the meditation intervention in the Age-Well randomized controlled trial. These finding will contribute to the design of meditation-based prevention randomized controlled trials for the aged population and to the exploration of the possible long-time developmental trajectory of meditation training.
PMID: 30662933 [PubMed]
A Nationwide, Population-Based Prevalence Study of Genetic Muscle Disorders.
Neuroepidemiology. 2019 Jan 18;52(3-4):128-135
Authors: Theadom A, Rodrigues M, Poke G, O'Grady G, Love D, Hammond-Tooke G, Parmar P, Baker R, Feigin V, Jones K, Te Ao B, Ranta A, Roxburgh R, On Behalf of the MDPrev Research Group
BACKGROUND: Previous epidemiological studies of genetic muscle disorders have relied on medical records to identify cases and may be at risk of selection biases or have focused on selective population groups.
OBJECTIVES: This study aimed to determine age-standardised prevalence of genetic muscle disorders through a nationwide, epidemiological study across the lifespan using the capture-recapture method.
METHODS: Adults and children with a confirmed clinical or molecular diagnosis of a genetic muscle disorder, resident in New Zealand on April 1, 2015 were identified using multiple overlapping sources. Genetic muscle disorders included the muscular dystrophies, congenital myopathies, ion channel myopathies, GNE myopathy, and Pompe disease. Prevalence per 100,000 persons by age, sex, disorder, ethnicity and geographical region with 95% CIs was calculated using Poisson distribution. Direct standardisation was applied to age-standardise prevalence to the world population. Completeness of case ascertainment was determined using capture-recapture modelling.
RESULTS: Age standardised minimal point prevalence of all genetic muscle disorders was 22.3 per 100,000 (95% CI 19.5-25.6). Prevalence in Europeans of 24.4 per 100,000, (95% CI 21.1-28.3) was twice that observed in NZ's other 3 main ethnic groups; Māori (12.6 per 100,000, 95% CI 7.8-20.5), Pasifika (11.0 per 100,000, 95% CI 5.4-23.3), and Asian (9.13 per 100,000, 95% CI 5.0-17.8). Crude prevalence of myotonic dystrophy was 3 times higher in Europeans (10.5 per 100,000, 9.4-11.8) than Māori and Pasifika (2.5 per 100,000, 95% CI 1.5-4.2 and 0.7 per 100,000, 95% CI 0.1-2.7 respectively). There were considerable regional variations in prevalence, although there was no significant association with social deprivation. The final capture-recapture model, with the least deviance, estimated the study ascertained 99.2% of diagnosed cases.
CONCLUSIONS: Ethnic and regional differences in the prevalence of genetic muscle disorders need to be considered in service delivery planning, evaluation, and decision making.
PMID: 30661069 [PubMed - as supplied by publisher]
Associations of blood mercury and fatty acid concentrations with blood mitochondrial DNA copy number in the Seychelles Child Development Nutrition Study.
Environ Int. 2019 Jan 17;124:278-283
Authors: Xu Y, Wahlberg K, Love TM, Watson GE, Yeates AJ, Mulhern MS, McSorley EM, Strain JJ, Davidson PW, Shamlaye CF, Rand MD, Myers GJ, van Wijngaarden E, Broberg K
BACKGROUND: Fish contains methylmercury (MeHg) which can cause oxidative stress and neurodevelopmental toxicity at sufficiently high doses. Fish also contains polyunsaturated fatty acids (PUFA) which have both antioxidant (n-3) and oxidant (n-6) properties. Mitochondrial DNA (mtDNA) is sensitive to oxidative stress but has not been previously studied in relation to MeHg exposure or PUFA status.
OBJECTIVE: To investigate the associations between MeHg exposure and PUFA status during pregnancy with relative mitochondrial DNA copy number (RmtDNAcn) in mothers and their newborns.
METHODS: In total, 1488 mother-child pairs from the Seychelles Child Development Study Nutrition Cohort 2 were included in this study. Total Hg was measured in maternal blood collected at 28 weeks' gestation, maternal hair at delivery, and in fetal cord blood. PUFA (n-3 and n-6) were measured only in maternal blood. RmtDNAcn was measured by qPCR in both maternal and cord blood.
RESULTS: Increasing maternal blood Hg (β = 0.001, 95%CI: 0.000, 0.002) and n-3 PUFA concentrations (β = 0.183, 95%CI: 0.048, 0.317) were associated with higher maternal RmtDNAcn. Increasing maternal n-6 PUFA (β = -0.103, 95%CI: -0.145, -0.062) and n-6/n-3 ratio (β = -0.011, 95%CI: -0.017, -0.004) were associated with lower maternal RmtDNAcn. Increasing fetal cord blood Hg was associated with lower fetal RmtDNAcn (β = -0.002, 95%CI: -0.004, -0.000). Neither maternal blood Hg nor PUFA status was associated with fetal RmtDNAcn.
CONCLUSIONS: Our findings suggest that MeHg and PUFA may influence mitochondrial homeostasis although the magnitude of these associations are small. Future studies should confirm the findings and explore the underlying mechanisms.
PMID: 30660840 [PubMed - as supplied by publisher]