Introduction A number of different theoretical approaches to understanding the etiology of ejaculatory dysfunction have been proposed, but no behavior genetic study has yet, to our knowledge, been conducted to explore the genetic and environmental influences on ejaculatory dysfunction. Aim The aim of the present study was to explore the genetic and environmental effects on premature (PE) and delayed (DE) ejaculation in a population-based sample. Methods The genetic and environmental influences on PE and DE were investigated in a population-based sample of 1,196 Finnish male twins, age 33–43 years, with 91 identical and 110 complete twin pairs. Several different aspects of ejaculatory function were measured by a self-report questionnaire (e.g., latency time, subjective experience of ejaculatory control). Factor analyses distinguished two subcomponents of ejaculatory function, and subsequently, composite variables measuring PE and DE were created. Structural equation modeling was performed on the composite variables. Main Outcome Measures Measurement of genetic and environmental effects on PE and DE. Results The results suggested moderate genetic influence (28%) on PE, but not on DE (0%). There was a moderate familial effect on DE with shared environmental effects accounting for 24% of the variance. However, omission of the shared environmental component did not directly result in a significantly decreased model fit for DE, and omission of the additive genetic component did not directly result in a significantly decreased fit for the PE model. Conclusions The findings from the present study provide useful information regarding the etiology and understanding of ejaculatory dysfunction.
The association between disordered eating and gender identity was examined in a sample of 20 (11 female-to-male, 9 male-to-female) transgender Finnish adults, aged 21-62 years. Using semi-structured interviews, participants' own understanding of the underlying causes of their disordered eating was analyzed, as well as the effect of gender reassignment on eating behaviors and cognitions. A majority of the participants reported current or past disordered eating. Participants most frequently described strive for thinness as an attempt to suppress features of one's biological gender, or accentuate features of one's desired gender. Gender reassignment was primarily perceived as alleviating symptoms of disordered eating.
The effects of electromagnetic fields (EMF) emitted by cellular phones on the event related desynchronization/synchronization (ERD/ERS) of the 4-6, 6-8, 8-10, and 10-12 Hz electroencephalogram (EEG) frequency bands were studied in 24 normal subjects performing an auditory memory task. This study was a systematic replication of our previous work. In the present double blind study, all subjects performed the memory task both with and without exposure to a digital 902 MHz field in a counterbalanced order. We were not able to replicate the findings from our earlier study. All eight of the significant changes in our earlier study were not significant in the present double blind replication. Also, the effect of EMF on the number of incorrect answers in the memory task was inconsistent. We previously reported no significant effect of EMF exposure on the number of incorrect answers in the memory task, but a significant increase in errors was observed in the present study. We conclude that EMF effects on the EEG and on the performance on memory tasks may be variable and not easily replicable for unknown reasons.
The existence of genetic effects on gender atypical behavior in childhood and sexual orientation in adulthood and the overlap between these effects were studied in a population-based sample of 3,261 Finnish twins aged 33-43 years. The participants completed items on recalled childhood behavior and on same-sex sexual interest and behavior, which were combined into a childhood gender atypical behavior and a sexual orientation variable, respectively. The phenotypic association between the two variables was stronger for men than for women. Quantitative genetic analyses showed that variation in both childhood gender atypical behavior and adult sexual orientation was partly due to genetics, with the rest being explained by nonshared environmental effects. Bivariate analyses suggested that substantial common genetic and modest common nonshared environmental correlations underlie the co-occurrence of the two variables. The results were discussed in light of previous research and possible implications for theories of gender role development and sexual orientation.
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