-
Journal of Circadian Rhythms Mar 2020The reproductive function of humans is regulated by several sex hormones which are secreted in synergy with the circadian timing of the body. Sleep patterns produce... (Review)
Review
The reproductive function of humans is regulated by several sex hormones which are secreted in synergy with the circadian timing of the body. Sleep patterns produce generic signatures that physiologically drive the synthesis, secretion, and metabolism of hormones necessary for reproduction. Sleep deprivation among men and women is increasingly reported as one of the causes of infertility. In animal models, sleep disturbances impair the secretion of sexual hormones thereby leading to a decrease in testosterone level, reduced sperm motility and apoptosis of the Leydig cells in male rats. Sleep deprivation generates stressful stimuli intrinsically, due to circadian desynchrony and thereby increases the activation of the Hypothalamus-Pituitary Adrenal (HPA) axis, which, consequently, increases the production of corticosterone. The elevated level of corticosteroids results in a reduction in testosterone production. Sleep deprivation produces a commensurate effect on women by reducing the chances of fertility. Sleeplessness among female shift workers suppresses melatonin production as well as excessive HPA activation which results in early pregnancy loss, failed embryo implantation, anovulation and amenorrhea. Sleep deprivation in women has also be found to be associated with altered gonadotropin and sex steroid secretion which all together lead to female infertility. Poor quality of sleep is observed in middle-aged and older men and this also contributes to reduced testosterone concentrations. The influence of sleep disturbances post-menopausal is associated with irregular synthesis and secretion of female sex steroid hormones.
PubMed: 32256630
DOI: 10.5334/jcr.190 -
Clinica Chimica Acta; International... Jun 2022A polycystic ovarian syndrome (PCOS) is the most common endocrine disorder affecting females. Furthermore, it is a heterogeneous disease with a variety of etiologies and... (Review)
Review
A polycystic ovarian syndrome (PCOS) is the most common endocrine disorder affecting females. Furthermore, it is a heterogeneous disease with a variety of etiologies and outcomes. Patients frequently complain about infertility, irregular menstruation, acne, seborrheic dermatitis, hirsutism, and obesity. PCOS can be caused by hypothalamic-pituitary-ovarian axis dysfunction, heredity, or metabolic abnormalities. PCOS is characterized by chronic low-level inflammation, which includes an imbalance in pro-inflammatory factor secretion, endothelial cell dysfunction, and leukocytosis. PCOS is also distinguished by hormonal and immune dysregulation. During PCOS, immune cells and immune regulatory molecules play critical roles in maintaining metabolic homeostasis and regulating immune responses. Because of oligo/anovulation, patients with PCOS have low progesterone levels. Therefore, low progesterone levels in PCOS overstimulate the immune system, causing it to produce more estrogen, which leads to a variety of autoantibodies. This review aims to summarize the immune regulation involved in the pathogenesis of PCOS and pave the way for the development of better PCOS treatment options in the near future.
Topics: Anovulation; Female; Hirsutism; Humans; Hyperandrogenism; Polycystic Ovary Syndrome; Progesterone
PubMed: 35447143
DOI: 10.1016/j.cca.2022.04.234 -
Journal of Clinical Pathology Sep 2019Subfertility affects one in seven couples and is defined as the inability to conceive after 1 year of regular unprotected intercourse. This article describes the... (Review)
Review
Subfertility affects one in seven couples and is defined as the inability to conceive after 1 year of regular unprotected intercourse. This article describes the initial clinical evaluation and investigation to guide diagnosis and management. The primary assessment of subfertility is to establish the presence of ovulation, normal uterine cavity and patent fallopian tubes in women, and normal semen parameters in men. Ovulation is supported by a history of regular menstrual cycles (21-35 days) and confirmed by a serum progesterone >30 nmol/L during the luteal phase of the menstrual cycle. Common causes of anovulation include polycystic ovary syndrome (PCOS), hypothalamic amenorrhoea (HA) and premature ovarian insufficiency (POI). Tubal patency is assessed by hysterosalpingography, hystero-contrast sonography, or more invasively by laparoscopy and dye test. The presence of clinical or biochemical hyperandrogenism, serum gonadotrophins (luteinising hormone/follicle stimulating hormone) / oestradiol, pelvic ultrasound to assess ovarian morphology / antral follicle count, can help establish the cause of anovulation. Ovulation can be restored in women with PCOS using letrozole (an aromatase inhibitor), clomifene citrate (an oestrogen antagonist) or exogenous gonadotrophin administration. If available, pulsatile gonadotrophin releasing hormone therapy is the preferred option for restoring ovulation in HA. Spermatogenesis can be induced in men with hypogonadotrophic hypogonadism with exogenous gonadotrophins. Unexplained subfertility can be treated with in vitro fertilisation after 2 years of trying to conceive. Involuntary childlessness is associated with significant psychological morbidity; hence, expert assessment and prompt treatment are necessary to support such couples.
Topics: Female; Fertility; Humans; Infertility, Female; Infertility, Male; Male; Ovulation; Predictive Value of Tests; Pregnancy; Reproductive Techniques, Assisted; Risk Factors; Spermatogenesis; Time-to-Pregnancy; Treatment Outcome
PubMed: 31296604
DOI: 10.1136/jclinpath-2018-205579 -
Reproductive Biomedicine Online Dec 2016Studies over the last decade have demonstrated that some polycystic ovary syndrome (PCOS) patients have abnormal insulin sensitivity (insulin resistance), independently... (Review)
Review
Studies over the last decade have demonstrated that some polycystic ovary syndrome (PCOS) patients have abnormal insulin sensitivity (insulin resistance), independently from being overweight or obese. This induces the risk of developing type 2 diabetes in such PCOS patients. The use of insulin sensitizers (i.e. metformin), reduces such metabolic, and most hormonal, impairments. As metformin often induces side effects, new integrative strategies have been proposed to treat insulin resistance, such as the use of inositols. Such compounds are mainly represented in humans by two inositol stereoisomers: myo-inositol (MYO) and d-chiro-inositol (DCI). MYO is the precursor of inositol triphosphate, a second messenger that regulates thyroid-stimulating hormone (TSH) and FSH as well as insulin. DCI derives from the conversion of myo-inositol via an insulin-dependent pathway. Several preliminary studies have indicated possible benefits of inositol therapy in PCOS patients, but to date no meta-analysis has been performed. This review aims to give clinical insights for the clinical use of inositol in PCOS.
Topics: Female; Humans; Hyperandrogenism; Hyperinsulinism; Inositol; Inositol Phosphates; Insulin; Insulin Resistance; Obesity; Overweight; Polycystic Ovary Syndrome; Signal Transduction; Thyrotropin
PubMed: 27717596
DOI: 10.1016/j.rbmo.2016.08.024 -
International Journal of Molecular... Nov 2021Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among reproductive-aged women. It is characterized by chronic anovulation, hyperandrogenism, and... (Review)
Review
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among reproductive-aged women. It is characterized by chronic anovulation, hyperandrogenism, and the presence of polycystic ovary in ultrasound examination. PCOS is specified by an increased number of follicles at all growing stages, mainly seen in the preantral and small antral follicles and an increased serum level of Anti-Müllerian Hormone (AMH). Because of the strong correlation between circulating AMH levels and antral follicle count on ultrasound, Anti-Müllerian Hormone has been proposed as an alternative marker of ovulatory dysfunction in PCOS. However, the results from the current literature are not homogeneous, and the specific threshold of AMH in PCOS and PCOM is, therefore, very challenging. This review aims to update the current knowledge about AMH, the pathophysiology of AMH in the pathogenesis of PCOS, and the role of Anti-Müllerian Hormone in the treatment of this syndrome.
Topics: Anovulation; Anti-Mullerian Hormone; Female; Humans; Hyperandrogenism; Ovarian Follicle; Polycystic Ovary Syndrome; Ultrasonography
PubMed: 34830389
DOI: 10.3390/ijms222212507 -
European Review For Medical and... Jan 2021D-chiro-Inositol has been widely used in clinical practice to induce ovulation in women with polycystic ovary syndrome. Only recent evidence established that this... (Review)
Review
OBJECTIVE
D-chiro-Inositol has been widely used in clinical practice to induce ovulation in women with polycystic ovary syndrome. Only recent evidence established that this molecule acts through two different mechanisms, with potentially different outcomes. On the one hand, under a metabolic perspective, D-chiro-Inositol improves insulin signaling, thus restoring physiological insulin levels in resistant subjects. On the other hand, at a cellular level, it downregulates the expression of steroidogenic enzyme aromatase, which is responsible for the conversion of androgens to estrogens.
MATERIALS AND METHODS
We reviewed current literature in different databases, searching for D-chiro-Inositol in relation with one of the following keywords: myo-inositol, PCOS, infertility, insulin resistance, aromatase, androgen and inositol, testosterone, estrogen and inositol, estradiol, hypogonadotropic hypogonadism, fat tissue, estrogens and cancer, anovulation, uterine myoma, endometriosis, endometrial hyperplasia.
RESULTS
D-Chiro-Inositol treatment may be helpful in restoring physiological hormonal levels in various clinical disorders. However, D-Chiro-Inositol intervention should be carefully designed to avoid possible undesired side effects stemming from its multiple mechanisms of action.
CONCLUSIONS
We evaluated the optimal D Chiro-Inositol administration for different pathologies, defining dosages and timing. Even though further studies are required to validate our preliminary results, this paper is primarily intended to guide researchers through some of the pathways of D-Chiro-Inositol.
Topics: Aromatase; Down-Regulation; Female; Humans; Inositol; Insulin; Insulin Resistance; Male; Polycystic Ovary Syndrome
PubMed: 33506934
DOI: 10.26355/eurrev_202101_24412 -
The Medical Journal of Malaysia May 2022Abnormal uterine bleeding (AUB) is one of the commonest complaints of women in reproductive age and non-gravid state that brings them to the attention of the primary...
Abnormal uterine bleeding (AUB) is one of the commonest complaints of women in reproductive age and non-gravid state that brings them to the attention of the primary care doctor or the gynaecologist. Anovulation without any medical illness or pelvic pathology seems to be the common cause. Bleeding due to a wide variation in pathology both inside and outside the reproductive tract can be termed as anovulatory bleeding. Therefore, it is mandatory to elicit a focused menstrual history and appropriate evaluation followed by a pelvic examination. This includes a vaginal speculum examination to differentiate anovulatory bleeding from other causes of bleeding. In contrast, Heavy menstrual bleeding (HMB) is referred to as an ovulatory bleeding exceeding 8 days duration and is often caused by uterine fibroids or adenomyosis, a copper IUD or coagulation disorders. PALM-COEIN classification is a system designed by the Federation Internationale de Gynaecologie et d'Obstetrique to define the precise underlying causes of AUB. Aetiology of AUB can be classified as the following acronym "PALM-COEIN": Polyp, Adenomyosis, Leiomyoma, Malignancy and hyperplasia, Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic and Not yet classified. AUB describes a range of symptoms, such as HMB, intermenstrual bleeding (IMB) and a combination of both heavy and prolonged menstrual bleeding (MB). Dysfunctional uterine bleeding (DUB) and menorrhagia are now better described as AUB. Newborn girls sometimes spot for a few days after birth, due to placental oestrogenic stimulation of the endometrium in utero.
Topics: Adenomyosis; Female; Humans; Infant, Newborn; Leiomyoma; Menorrhagia; Placenta; Pregnancy; Uterine Hemorrhage
PubMed: 35638495
DOI: No ID Found -
Clinical Medicine Insights.... 2019Polycystic ovary syndrome (PCOS) and hyperprolactinemia (HPRL) are the two most common etiologies of anovulation in women. Since the 1950s, some authors think that there... (Review)
Review
Polycystic ovary syndrome (PCOS) and hyperprolactinemia (HPRL) are the two most common etiologies of anovulation in women. Since the 1950s, some authors think that there is a pathophysiological link between PCOS and HPRL. Since then, many authors have speculated about the link between these two endocrine entities, but no hypothesis proposed so far could ever be confirmed. Furthermore, PCOS and HPRL are frequent endocrine diseases and a fortuitous association cannot be excluded. The evolution of knowledge about PCOS and HPRL shows that studies conducted before the 2000s are obsolete given current knowledge. Indeed, most of the studies were conducted before consensual diagnosis criteria of PCOS and included small numbers of patients. In addition, the investigation of HPRL in these studies relied on obsolete methods and did not look for the presence of macroprolactinemia. It is therefore possible that HPRL that has been attributed to PCOS corresponded in fact to macroprolactinemia or to pituitary microadenomas of small sizes that could not be detected with the imaging methods of the time. Recent studies that have conducted a rigorous etiological investigation show that HPRL found in PCOS correspond either to non-permanent increase of prolactin levels, to macroprolactinemia or to other etiologies. None of this recent study found HPRL related to PCOS in these patients. Thus, the link between PCOS and HPRL seems to be more of a myth than a well-established medical reality and we believe that the discovery of an HPRL in a PCOS patient needs a standard etiological investigation of HPRL.
PubMed: 31523136
DOI: 10.1177/1179558119871921 -
The Journal of Endocrinology Jun 2017Endocrine disrupting chemicals are ubiquitous chemicals that exhibit endocrine disrupting properties in both humans and animals. Female reproduction is an important... (Review)
Review
Endocrine disrupting chemicals are ubiquitous chemicals that exhibit endocrine disrupting properties in both humans and animals. Female reproduction is an important process, which is regulated by hormones and is susceptible to the effects of exposure to endocrine disrupting chemicals. Disruptions in female reproductive functions by endocrine disrupting chemicals may result in subfertility, infertility, improper hormone production, estrous and menstrual cycle abnormalities, anovulation, and early reproductive senescence. This review summarizes the effects of a variety of synthetic endocrine disrupting chemicals on fertility during adult life. The chemicals covered in this review are pesticides (organochlorines, organophosphates, carbamates, pyrethroids, and triazines), heavy metals (arsenic, lead, and mercury), diethylstilbesterol, plasticizer alternatives (di-(2-ethylhexyl) phthalate and bisphenol A alternatives), 2,3,7,8-tetrachlorodibenzo-p-dioxin, nonylphenol, polychlorinated biphenyls, triclosan, and parabens. This review focuses on the hypothalamus, pituitary, ovary, and uterus because together they regulate normal female fertility and the onset of reproductive senescence. The literature shows that several endocrine disrupting chemicals have endocrine disrupting abilities in females during adult life, causing fertility abnormalities in both humans and animals.
Topics: Animals; Endocrine Disruptors; Environmental Pollutants; Female; Fertility; Humans
PubMed: 28356401
DOI: 10.1530/JOE-17-0023