Usefulness of mindfulness for the management of anxiety, stress, and quality of life in infertile women. A clinical exploratory study.

BACKGROUND: Infertility increases stress and affects life quality. Mindfulness reduces stress and improves life quality, but its role in infertility remains unclear. OBJECTIVE: To evaluate the effect of mindfulness on stress and quality of life of women with infertility. MATERIAL AND METHODS: An exploratory clinical study was conducted in women under infertility treatment, together with an 8-week mindfulness intervention (MND) or only infertility treatment (CTRL). Anxiety and quality of life were assessed at baseline and at the end of intervention with IDARE and FertiQoL questionnaires respectively, as well as salivary alpha-amylase and cortisol concentrations. Non-parametric statistics was used for analysis using an alpha value of 0.10. RESULTS: 14 MND and 15 CTRL completed follow-up. At baseline, CTRL patients exhibited better quality of life than MND; anxiety scores correlated negatively with quality of life. At the end of intervention, cortisol concentrations (p = 0.097), and the increments of amylase (p = 0.039), were higher in CTRL than in MND. Increases in quality of life were associated with basal anxiety score (p = 0.002), improvements in tolerability (p < 0.001), and mindfulness intervention (p = 0.014). CONCLUSION: Our results suggest that mindfulness reduces stress and improves quality of life in women under infertility treatment.

ANTECEDENTES: La infertilidad incrementa el estrés y afecta la calidad de vida. OBJETIVO: Evaluar el efecto de mindfulness (atención plena) sobre la ansiedad, estrés y calidad de vida de mujeres infértiles. MATERIAL Y MÉTODOS: Estudio exploratorio en pacientes tratadas por infertilidad más una intervención de ocho semanas con mindfulness (grupo MND) o solo tratamiento de la infertilidad (grupo de control). Al inicio y después de ocho semanas se evaluaron la ansiedad (Inventario de Ansiedad Rasgo-Estado), la calidad de vida (FertiQoL), y las concentraciones salivales de α-amilasa y cortisol. Se utilizó estadística no paramétrica, con α = 0.10. RESULTADOS: 14 mujeres del grupo MND y 15 del grupo de control completaron el seguimiento. Al inicio, las pacientes del grupo de control mostraron mejor calidad de vida; las puntuaciones de ansiedad correlacionaron negativamente con la calidad de vida. Al final, el incremento de cortisol (p = 0.097) y amilasa (p = 0.039) fueron mayores en el grupo de control. Los incrementos en la calidad de vida se asociaron a ansiedad basal (p = 0.002), incremento en la subescala tolerabilidad (p < 0.001) y mindfulness (p = 0.014). CONCLUSIÓN: Los resultados sugieren que mindfulness disminuye el estrés y mejora la calidad de vida de pacientes bajo tratamiento de la infertilidad.

Changes in receptivity epithelial cell markers of endometrium after ovarian stimulation treatments: its role during implantation window.

BACKGROUND: To compare the expression of receptivity markers in epithelial and stromal cells in the endometrium of ovulatory women and infertile with hypothalamic pituitary dysfunction (HPD), untreated or treated with clomiphene citrate (CC), or with recombinant follicle stimulating hormone (rFSH). METHODS: Twelve control ovulatory and 32 anovulatory women, 22 of whom received ovulation induction with CC (n = 12) or rFSH (n = 10). Endometrial biopsies were obtained during the mid-secretory phase. Hormonal secretion was measured by chemiluminescence immunoassay, endometrial dating and cellular expression and distribution of receptivity proteins were evaluated by quantitative immunohistochemistry. RESULTS: CC or rFSH treatments, modified the expression of epithelial receptivity markers, such as Glycodelin A, beta-catenin, CD166/ALCAM and IGF-1R, but not in stromal markers. Also, a change in their cell distribution was observed. CONCLUSIONS: Treatment of infertile women with HPD modified the expression and distribution of receptivity markers in the mid-secretory phase of the endometrium in epithelial but not stromal cells, which can help to explain changes in the receptivity of the endometrium during treatments and suggest an important role of these cells in the receptivity window.

Which side of the coin are you on regarding possible postnatal oogenesis?

It is well known that oocytes are produced during fetal development and that the total number of primary follicles is determined at birth. In humans, there is a constant loss of follicles after birth until about two years of age. The number of follicles is preserved until the resumption of meiosis at puberty and there is no renewal of the oocytes; this dogma was maintained in the last century because there were no suitable techniques to detect and obtain stem cells. However, following stem cell markers, several scientists have detected them in developing and adult human ovarian tissues, especially in the ovarian surface epithelial cells. Furthermore, many authors using different methodological strategies have indicated this possibility. This evidence has led many scientists to explore this hypothesis; there is no definitive consensus to accept this idea. Interestingly, oocyte retrieval from mature ovaries and other tissue sources of stem cells has contributed to the development of strategies for the retrieval of mature oocytes, useful for assisted reproductive technology. Here, we review the evidence and controversies on oocyte neooogenesis in adult women; in addition, we agree with the idea that this process may occur in adulthood and that its alteration may be related to various pathologies in women, such as polycystic ovary syndrome, premature ovarian insufficiency, diminished ovarian reserve and several infertility and genetic disorders.

Adhesion molecules changes at 20 gestation weeks in pregnancies complicated by preeclampsia.

OBJECTIVES: To examine soluble E-selectin, L-selectin, P-selectin, ICAM-1, and VCAM-1 levels in normotensive and preeclamptic pregnancies. To determine cut-offs useful for preeclampsia early detection. STUDY DESIGN: A cohort of nulliparous women was recruited at family medicine clinics in Mexico City. Preeclampsia developed in 75 patients; 125 normotensive controls were matched. Adhesion molecules were assessed in serum obtained at 20 gestation weeks and in third trimester pregnancies. Predictive values and odds ratios for preeclampsia development were calculated with the 20 gestation week results. Threshold values were selected based on ROC curves values. RESULTS: In women with subsequent preeclampsia, sL-selectin and sVCAM-1 concentrations were significantly lower, whereas sE-selectin, sP-selectin and sICAM-1 levels were significantly higher, compared with controls at mid-pregnancy (p<0.05). The odds ratio for low sL-selectin was 25.6 (95% CI, 8.9-73.5; cut-off, 1414 ng/ml). The sensitivity, specificity, and positive and negative predictive values of low sL-selectin for preeclampsia development were 84, 90, 39, and 98%, respectively, whereas its sensitivity, specificity, and positive and negative predictive values for severe preeclampsia development (cut-off, 1210 ng/ml) were 100, 98, 60, and 100%, respectively. CONCLUSIONS: Early enhanced activation of endothelial cells, platelets and leukocytes seem to be present in preeclamptic patients, especially in those that develop severe preeclampsia. Low sL-selectin levels at 20 gestation weeks may be an indicator of preeclampsia development.

The FTO gene is associated with adulthood obesity in the Mexican population.

Common polymorphisms in the fat mass and obesity-associated gene (FTO) have shown strong association with obesity in several populations. In the present study, we explored the association of FTO gene polymorphisms with obesity and other biochemical parameters in the Mexican population. We also assessed FTO gene expression levels in adipose tissue of obese and nonobese individuals. The study comprised 788 unrelated Mexican-Mestizo individuals and 31 subcutaneous fat tissue biopsies from lean and obese women. FTO single-nucleotide polymorphisms (SNPs) rs9939609, rs1421085, and rs17817449 were associated with obesity, particularly with class III obesity, under both additive and dominant models (P = 0.0000004 and 0.000008, respectively). These associations remained significant after adjusting for admixture (P = 0.000003 and 0.00009, respectively). Moreover, risk alleles showed a nominal association with lower insulin levels and homeostasis model assessment of B-cell function (HOMA-B), and with higher homeostasis model assessment of insulin sensitivity (HOMA-S) only in nonobese individuals (P (dom) = 0.031, 0.023, and 0.049, respectively). FTO mRNA levels were significantly higher in subcutaneous fat tissue of class III obese individuals than in lean individuals (P = 0.043). Risk alleles were significantly associated with higher FTO expression in the class III obesity group (P = 0.047). In conclusion, FTO is a major risk factor for obesity (particularly class III) in the Mexican-Mestizo population, and is upregulated in subcutaneous fat tissue of obese individuals.

Methionine inhibits cellular growth dependent on the p53 status of cells.

BACKGROUND: Methionine, an essential amino acid, is important for normal growth and development, as it is required for both protein and polyamine synthesis as well as in methylation reactions. It has been reported that high concentrations of methionine inhibit cellular growth and gene expression in the human breast tumor-derived MCF-7 cells. These effects are thought to be mediated by the modulation of p53. However, the generalizability of this observation and the precise role of p53 in methionine-induced growth suppression needs to be determined. METHODS: To determine if the inhibition of cell growth by methionine applies to other cell lines and to characterize further the role of p53 in methionine-induced growth suppression, we have assessed the effects of methionine on cellular growth and proliferation and p53 expression in cells expressing native p53, eg, breast cancer MCF-7 cells and prostate cancer LNCaP cells, and also in cells expressing a mutated (point) form of p53, eg, prostate cancer DU-145 cells. These cell lines were treated with varying concentrations of L-methionine. The effects of L-methionine on cell growth were assayed by using cell viability assays and immunostaining for Ki-67, a cell proliferation marker. The effects of methionine on p53 expression were assessed by using reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot analysis. The role of p53 in L-methionine-mediated growth suppression was evaluated using short-interference RNA for p53 (siRNA-p53), immunoprecipitation, and direct DNA sequencing. RESULTS: We demonstrated that methionine at a concentration of 1 to 5 mg/mL inhibited the growth of both MCF-7 and LNCaP cells. In association with the inhibition of growth, methionine also inhibited native p53 expression at the mRNA and protein levels, respectively. Furthermore, transfection with siRNA-p53, to knock down p53 expression, increased cell growth and proliferation of the LNCaP cells even when they were exposed to methionine. In contrast, the same treatment did not diminish growth or proliferation of the DU-145 cells. Also, the expression of mutated p53 at the mRNA or protein levels was not altered. CONCLUSION: Our results extend a prior observation to other cell lines and demonstrate that high concentrations of methionine suppress the expression of native but not mutated p53. These inhibitory effects on cellular growth are, in part, due to inhibition of cellular proliferation probably via a p53-dependent pathway.