There is now compelling evidence for a link between enteric microbiota and brain function. The ingestion of probiotics modulates the processing of information that is strongly linked to anxiety and depression, and influences the neuroendocrine stress response.
This study found that taking a prebiotic called galactooligosaccharides for three weeks significantly reduced the amount of cortisol, a primary stress hormone in the body.
Chronic insomnia disorder is one of the most common problems in postmenopausal women, exacerbated by underdiagnosis and improper treatment.
This double-blinded, randomized, placebo-controlled trial was conducted to evaluate the potential of vitamin E to treat chronic insomnia as an alternative to sedative drugs and hormonal therapy.
The study enrolled 160 postmenopausal women with chronic insomnia disorder, divided randomly into two groups. The vitamin E group received 400 units of mixed tocopherol daily, while the placebo group received an identical oral capsule.
The primary outcome of this study was sleep quality assessed by the Pittsburgh Sleep Quality Index (PSQI), a self-evaluated and standardized questionnaire. The secondary outcome was the percentage of participants using sedative drugs. There were no significant differences in baseline characteristics between the study groups.
However, the median PSQI score at baseline was slightly higher in the vitamin E group compared with the placebo. After one month of intervention, the PSQI score was significantly lower (indicating better sleep quality) in the vitamin E group compared with the placebo.
Moreover, the improvement score was significantly higher in the vitamin E group compared with the placebo. In addition, there was a significant reduction in the percentage of patients using sedative drugs in the vitamin E group (15%), while this reduction was not statistically significant in the placebo group (7.5%).
This study demonstrates vitamin E’s potential as an excellent alternative treatment for chronic insomnia disorder that improves sleep quality and reduces sedative drug use.
Folate
Deficiency reduces circulating testosterone; Evidence suggests testosterone may regulate folate metabolism.1,2,3
Vitamin B6
Regulates sex hormones; Vitamin B6 reduces prolactin which stimulates hypothalamus to increase testosterone; B6 also a cofactor for dopamine synthesis which influences testosterone levels.4,5,6,7
Vitamin D
Actually a hormone, vitamin D regulates the synthesis of testosterone; Supplementation can significantly increase total, free and bioactive testosterone levels. 8,9,10,11,12
Vitamin K
Deficiency reduces testosterone production because the rate-limiting enzyme for testosterone synthesis (Cyp11a) is vitamin K dependent. 13,14,15
Vitamin E
Long term administration of some forms of vitamin E may reduce testosterone levels.16,17
Vitamin C
Studies suggest it protects prostate from testosterone induced tumors.18,19,20
Carnitine
Boosts dopamine, which is directly related to testosterone levels; May prevent testosterone decline after intense physical stress.21,22,23,24
Magnesium
Makes testosterone more biologically active in the body; Raises free and total testosterone levels in men.25,26,27
Zinc
Deficiency lowers testosterone levels; Inhibits prolactin secretion (testosterone
inhibiting hormone); Supplementation increases testosterone depending on baseline levels.28,29,30,31
Choline – Estrogen stimulates the breakdown of phosphatidylcholine (cell membrane) so those with low estrogen (postmenopausal women) require more choline; Detoxifies excess estrogen via methylation pathway.1,32,33
Folate – Deficiency reduces estrogen levels; Excess folate is linked to some types of estrogen-related breast cancer; Detoxifies excess estrogen via methylation pathway; Regulates estrogen’s effect on genes.1,2,3
Vitamin B6 – Protects genes from estrogen-induced damage thus lowering risk of hormone related cancers; Detoxifies excess estrogen via methylation pathway; Estrogen-based oral contraceptives cause B6 deficiency.4,5,6,7
Vitamin D – Regulates synthesis of estradiol and estrone; Enhances estrogen’s protective effect on bones.8,9,10
Vitamin C – Increases the most potent estrogen (estradiol) in women on hormone therapy; Lowers aromatase (enzyme that converts testosterone to estrogen) in ovaries.11.12.13
Vitamin K – Inhibits estrogen activity by binding to estrogen receptors; Lowers the ratio of estradiol (strong estrogen) to estrone (weaker estrogen).14,15
Vitamin E – Deficiency impairs estrogen detoxification pathway; Some forms of vitamin E inhibit estrogen action, especially in breast tissue; Low levels linked to higher estrogen.1,16,17
Vitamin A – Helps metabolize the biologically active estrogen (estradiol) to an inactive form (estrone).18,19
Calcium – Calcium-D-glucarate lowers estradiol levels; Helps breakdown estrogen in the liver and convert it to a less toxic form.1,20,21
Selenium – Estrogen levels affect how selenium is distributed to various tissues in the body.22,23
Magnesium – Cofactor for the enzyme that removes toxic forms of estrogen (catechol-O-methyltransferase); Estrogen alters magnesium levels throughout menstrual cycle.1,24,25,26
Zinc – Estrogen lowers risk of zinc deficiency; Zinc dependent proteins metabolize estrogen.26,27,28
Cysteine – Prevents oxidation of estrogen into a dangerous form that causes breast cancer.29,30,31
Social stress may release hormones that affect bone loss, a finding that might be linked to the higher incidence of bone fractures after the menopause.
In a study of more than 8000 women aged 50 to 79, researchers found that those who reported higher levels of social stress – defined as strained relationships or stress related to social ties – were also at higher risk of bone fractures.
Women who reported high social strain and poorer quality relationships – and therefore, higher levels of stress – were found to have a larger decline in their bone density measurements over these years.
After adjusting for age, race, education, and other life style effects such as smoking and hormone therapy use, the team found that for each point of higher social strain as measured by the questionnaires, there was an associated increase of about 0.08 per cent loss of bone mineral density at the femoral neck – a portion of the hip. They also saw about 0.1 per cent greater loss across the whole hip, and about 0.7 per cent greater loss at the lower spine.
Previous research found that higher levels of stress hormones such as cortisol were associated with lower bone mineral density in the spine, and the team suggests that social stress may increase fracture risk by altering bone-regulating hormones.
Postmenopausal women may be more likely to experience social stress than their male peers. “There is research showing that social stress is higher in aging women than in men and this may be attributed to women being more likely to be caregivers in older age,” says Follis.
The team found that women with low social strain tended to be more educated and more physically active than those with high social strain. Black, Latina, and Native American women were more likely to report high social strain than White and Asian women.
To date, the involvement of α-Lactalbumin (α-LA) in the management of polycystic ovary syndrome (PCOS) refers to its ability to improve intestinal absorption of natural molecules like inositols, overcoming the inositol resistance. However, due to its own aminoacidic building blocks, α-LA is involved in various biological processes that can open new additional applications.
A great portion of women with PCOS exhibit gastrointestinal dysbiosis, which is in turn one of the triggering mechanisms of the syndrome. Due to its prebiotic effect, α-LA can recover dysbiosis, also improving the insulin resistance, obesity and intestinal inflammation frequently associated with PCOS. Further observations suggest that altered gut microbiota negatively influence mental wellbeing.
Depressive mood and low serotonin levels are indeed common features of women with PCOS. Thanks to its content of tryptophan, which is the precursor of serotonin, and considering the strict link between gut and brain, using α-LA contributes to preserving mental well-being by maintaining high levels of serotonin.
In addition, considering women with PCOS seeking pregnancy, both altered microbiota and serotonin levels can induce later consequences in the offspring. Therefore, a deeper knowledge of potential applications of α-LA is required to transition to preclinical and clinical studies extending its therapeutic advantages in PCOS.
NOTE: α-LA is high in whey protein
Polycystic ovary syndrome (PCOS) is an endocrine and metabolic syndrome (MS) with a complex etiology, and its pathogenesis is not yet clear. In recent years, the correlation between gut microbiota (GM) and metabolic disease has become a hot topic in research, leading to a number of new ideas about the etiology and pathological mechanisms of PCOS.
The literature shows that GM can cause insulin resistance, hyperandrogenism, chronic inflammation and metabolic syndrome (obesity, diabetes) and may contribute to the development of PCOS by influencing energy absorption, the pathways of short chain fatty acids (SCFA), lipopolysaccharides, choline and bile acids, intestinal permeability and the brain–gut axis.
As part of the treatment of PCOS, fecal microbiota transplantation, supplementation with prebiotics and traditional Chinese medicine can be used to regulate GM and treat disorders.
This article reviews possible mechanisms and treatment options for PCOS, based on methods which target the GM, and offers new ideas for the treatment of PCOS.
Low estrogen levels can make women more vulnerable to trauma at some points in their menstrual cycles, while high levels of the female sex hormone can partially protect them from emotional disturbance, according to new research.
…Low estrogen levels can make women more vulnerable to trauma at some points in their menstrual cycles, while high levels of the female sex hormone can partially protect them from emotional disturbance, the research suggests.
Depression and anxiety disorders are twice as common in women as in men, but the reason for this gender difference is unclear. The new work, reviewed by Harvard’s Mohammed Milad and colleagues in a commentary, suggests that women are most at risk for symptoms of post-traumatic stress disorder (PTSD) when their estrogen is low during the menstrual cycle.
…Estrogen calms the fear response in healthy women and female rats, according to the Harvard researchers, who were led by Kelimer Lebron-Milad, an HMS instructor of psychiatry. The Emory researchers, led by postdoctoral researcher Ebony Glover, showed that the same is true for women suffering from PTSD. The higher the estrogen was in their blood when they trained on a fear-extinction task, the less likely women were to startle.
…PTSD is common in women after a trauma such as rape or sexual assault, which studies say are experienced by 25 to 30 percent of women in their lifetimes, and the symptoms last on average four times as long in women as in men after trauma. This new research suggests the reason for this susceptibility may be the monthly menstrual change in estrogen.
Menopause is associated with increased risks for cardiovascular disease, osteoporosis, and cancer. Many women experience declining energy, mood, cognitive function and memory during
menopause.
Rhodiola rosea extracts have been shown to enhance mood, cognitive function, and memory. Moreover, these extracts possess anti-stress, neuroprotective, cardiovascular-protective, and anticarcinogenic properties, which are particularly valuable to counteract some of the common health risks seen in women as they age. R. rosea is low in side effects compared to synthetic selective estrogen receptor modulators (SERMS).
Preclinical and clinical studies suggest that R. rosea extracts provide a combination of effects that could counteract the adverse consequences of estrogen decline by improving neurological, endothelial, and cardiovascular functions.
As a natural SERM, R. rosea could alleviate menopause-related symptoms while conferring additional neuro-protective, cardio-protective, anti-stress, anti-fatigue, osteoprotective, and other health benefits.
Unlike HRT, preliminary evidence indicates that orally ingested R. rosea extracts are unlikely to cause estrogenic effects or increased the risk of cancer in hormone sensitive tissues. R. rosea extracts and salidroside do not significantly stimulate, but rather inhibit growth of human breast cancer in vitro and in vivo in some studies. Human studies are needed to verify the safety of R. rosea in postmenopausal women who are at increased risk or who are being treated for breast cancer.
Further research on the use of R. rosea alone and in combination with other adaptogens during menopause would enable development of this promising alternative SERM.
The key gut microbial biomarkers for polycystic ovarian syndrome (PCOS) and how dysbiosis causes insulin resistance and PCOS remain unclear.
Objective: To assess the characteristics of intestinal flora in PCOS and explore whether abnormal intestinal flora can affect insulin resistance and promote PCOS and whether chenodeoxycholic acid (CDCA) can activate intestinal farnesoid X receptor (FXR), improving glucose metabolism in PCOS.
Results: Bacteroides was significantly enriched in treatment-naïve PCOS patients. The enrichment in Bacteroides was reproduced in the PCOS mouse model. Gut microbiota removal ameliorated the PCOS phenotype and insulin resistance and increased relative FXR mRNA levels in the ileum and serum fibroblast growth factor 15 levels. PCOS stool-transplanted mice exhibited insulin resistance at 10 weeks but not PCOS. Treating the PCOS mouse model with CDCA improved glucose metabolism.
Conclusions: Bacteroides is a key microbial biomarker in PCOS and shows diagnostic value. Gut dysbiosis can cause insulin resistance. FXR activation might play a beneficial rather than detrimental role in glucose metabolism in PCOS.
Endometriosis is a chronic gynecologic disease process with multifactorial etiology. Increased oxidative stress, a result of increased production of free radicals or depletion of the body’s endogenous antioxidant defense, has been implicated in its pathogenesis. Oxidative stress is thought to promote angiogenesis and the growth and proliferation of endometriotic implants. Oxidative stress in the reproductive tract microenvironment is known to negatively affect sperm count and quality and may also arrest fertilized egg division leading to embryo death. Increased DNA damage in sperm, oocytes, and resultant embryos may account for the increase in miscarriages and fertilization and implantation failures seen in patients with endometriosis.
The evidence linking endometriosis and infertility to endogenous pro-oxidant imbalance provides a rationale for the empiric use of antioxidant therapy. Vitamin C and E deficiency has been demonstrated in women with endometriosis. Observational and randomized controlled studies have shown vitamin C and E combination therapy to decrease markers of oxidative stress.
SOURCE: Studies on Women’s Health
Endometriosis is a chronic gynecologic disease process with multifactorial etiology. Increased oxidative stress, a result of increased production of free radicals or depletion of the body’s endogenous antioxidant defense, has been implicated in its pathogenesis. Oxidative stress is thought to promote angiogenesis and the growth and proliferation of endometriotic implants. Oxidative stress in the reproductive tract microenvironment is known to negatively affect sperm count and quality and may also arrest fertilized egg division leading to embryo death. Increased DNA damage in sperm, oocytes, and resultant embryos may account for the increase in miscarriages and fertilization and implantation failures seen in patients with endometriosis.
The evidence linking endometriosis and infertility to endogenous pro-oxidant imbalance provides a rationale for the empiric use of antioxidant therapy. Vitamin C and E deficiency has been demonstrated in women with endometriosis. Observational and randomized controlled studies have shown vitamin C and E combination therapy to decrease markers of oxidative stress.
Endometriosis is a painful condition of the female reproductive organs that can result in heavy bleeding, scarring, fatigue, infertility, and more.
A study published in April 2018 using data collected from 70,835 premenopausal women has examined if there is a connection between fruit and vegetable consumption and endometriosis. While there didn’t appear to be an association between total vegetable intake and risk of endometriosis, citrus fruits were associated with a lower risk of the disease. Based on data from food frequency questionnaires every four years between 1991 to 2013, women consuming ≥1 servings of citrus fruits per day had a 22% lower endometriosis risk compared to those consuming <1 serving per week.
The researchers concluded, “Our findings suggest that a higher intake of fruits, particularly citrus fruits, is associated with a lower risk of endometriosis, and beta-cryptoxanthin in these foods may partially explain this association.”
2018
As search for optimal therapy continues for endometriosis, aid of dietary supplements is gaining attention. Supplements can be used for their anti-inflammatory, anti-oxidant, anti-proliferative and immune modulatory characteristics. We reviewed the literature, evaluated and synthesized effects of vitamin D, zinc, magnesium, omega 3, propolis, quercetin, curcumin, N-acetylcysteine, probiotics, resveratrol, alpha lipoic acid, vitamin C, vitamin E, selenium and epigallocatechin-3-gallate. Based on results of in vitro, animal and human studies, it might be safe to say that dietary supplements can be used as a complementary treatment for endometriosis.
2021
To prove the efficacy of oral vitamin B1 administration for the treatment of primary dysmenorrhoea, a randomised, double-blind, placebo-controlled study was carried out on 556 girls aged 12-21 yr, having moderate to very severe spasmodic dysmenorrhoea.
Thiamine hydrochloride (vitamin B1) was given in a dose of 100 mg orally, daily for 90 days.
The combined final results of both the ‘active treatment first’ group and the ‘placebo first’ group, after 90 days of vitamin B1 administration, were
The results remained the same two months later as well when no drug was administered. Unlike all the current treatments which are suppression-oriented, this curative treatment directly treats the cause, is free from side effects, is inexpensive and easy to administer.
Endometriosis is a common chronic inflammation causing major problems including infertility. The role of omega-3 and omega-6 fatty acids as their potential anti-inflammatory effects in endometriosis needs to be further explored. The objective of this study was to compare serum phospholipid fatty acid profile in endometriosis patients with controls, and to explore the correlation of this profile with the severity of the disease.
Methods:
Sixty-four endometriosis patients and 74 control women, in reproductive age, participated in this study. Among the endometriosis patients, 19 cases were in stage I, 27 cases in stage II, 8 cases in stage III, and 10 cases in stage IV. Each patient underwent laparoscopy. Before surgery, 5 ml of blood was obtained. After extraction of the total lipids, serum total phospholipid fraction was isolated by thin layer chromatography. Fatty acid composition of the phospholipid fraction was determined by gas chromatography and the resulted profile was compared in endometriosis patients and controls. The profile was also compared in the endometriosis group based on the severity of disease.
Results:
Stearic acid was significantly lower in the endometriosis group as compared to controls (P= 0.030). No other fatty acid compositions were significantly different between patients and controls. Serum ratio of eicosapentaenoic acid (EPA) to arachidonic acid (AA) was in reasonable correlation with the severity of endometriosis (r = 0.34, P = 0.006).
Conclusion:
According to these findings, levels of fatty acids in serum total phospholipids seem not to be a marker for endometriosis, but the EPA to AA ratio was a relevant factor indicating severity of illness.
——
EPA is hypothesized to reduce disease severity through their anti-inflammatory and immunomodulatory effects [25]. EPA is the most important component of omega-3 and AA, an omega-6 fatty acid and plays an important role in biological systems. AA has a substrate role for production of certain mediators such as PGE2 and leukotriene (LTB4). PGE2 and LTB4 are initiators for endometriosis and pain [24]. On the other hand, EPA plays a role in biosynthesis of LTB5 and PGE3 which have less inflammatory effect compared with PGE2 and LTB4 [24]. EPA is a competitive inhibitor in conversion of AA to LTB4 and PGE2 [26]. Irrespective of study design, our results were in agreement, in part, with the in vitro experiments by Gazvani et al. [20] that showed a high ratio of omega-3 to omega-6 in endometrial cell culture from endometriosis patients induce higher concentrations of IL-8 productions in cell supernatant. IL-8 as a pro-inflammatory and angiogenic cytokine has a significant role in endometriosis [27].
Infertility affects as many as 12.3% of women ages 15-44 (or 7.5 million women) in the United States.
Consequently, it is imperative to find methods to help women overcome infertility so that they may conceive a healthy child.
Many of the current treatments for infertility are costly, have low success rates, and have the potential to negatively affect long-term health. The common medical interventions used for infertility include fertility medications, in-vitro fertilization (IVF), and intrauterine insemination (IUI). Fertility medications, such as clomiphene and gonadotropins, stimulate growth of the ovarian follicle, followed by follicular rupture induced by a human chorionic gonadotropin (hCG) trigger shot.
These medications are often used in conjunction with IVF and IUI. IVF is an assisted reproductive technology that includes combining an egg and a sperm in a laboratory and then transferring the fertilized embryo into the uterus. IUI involves placing the sperm inside of the uterus to help with fertilization. Although less invasive and expensive than IVF, in IUI the sperm has to fertilize the egg on its own within the woman’s reproductive tract.
Research suggests a link between a variety of health conditions and subsequent infertility, including polycystic ovarian syndrome (PCOS), endometriosis, advanced maternal age (AMA), high body mass index (BMI), the MTHFR genetic mutation, hypothyroidism (both clinical and subclinical), and poor ovarian reserve.
In this article, we provide case evidence for alternative methods for managing infertility that are effective at improving the underlying condition leading to infertility – methods that are less expensive than medical intervention and are supportive of long-term health.
NAC (N-acetylcysteine) treatment or no treatment was offered to 92 consecutive Italian women referred to our university hospital with ultrasound confirmed diagnosis of ovarian endometriosis and scheduled to undergo laparoscopy 3 months later.
According to patients acceptance or refusal, NAC-treated and untreated groups finally comprised 73 and 72 endometriomas, respectively.
After 3 months, within NAC-treated patients cyst mean diameter was slightly reduced (−1.5 mm) versus a significant increase (+6.6 mm) in untreated patients (P = 0.001).
Particularly, during NAC treatment, more cysts reduced and fewer cysts increased their size.
Our results are better than those reported after hormonal treatments.
Twenty-four NAC-treated patients—versus 1 within controls—cancelled scheduled laparoscopy due to cysts decrease/disappearance and/or relevant pain reduction (21 cases) or pregnancy (1 case).
Eight pregnancies occurred in NAC-treated patients and 6 in untreated patients.
We can conclude that NAC actually represents a simple effective treatment for endometriosis, without side effects, and a suitable approach for women desiring a pregnancy
A specialised microbial community in humans is the vaginal microbiome. Successful human reproduction depends heavily on the correct balance of these microbes.
An optimal vaginal microbiome results in the production of lactic acid and hydrogen peroxide, maintaining a level of acidity that keeps pathogenic bacteria at bay.
When the vaginal community becomes disturbed, on the other hand, acidity decreases. Pathogenic or other opportunistic bacteria may then invade, which can cause bacterial vaginosis. This is best described as a state of dysbiosis rather than infection.
Research suggests that probiotic supplementation may be of benefit in maintaining homeostasis of the vaginal microbiome thereby reducing the risk of infection, dysbiosis and subsequent inflammation and immune dysfunction.
Overworked? Exhausted? Powering between career, family and friends and frazzled and libido-less as a result? No wonder you’re moody! But as New York psychiatrist Julie Holland explains in her radical and eye-opening new book, the first step to overcoming the lows is to accept that being testy is in our nature – we were made to be Moody Bitches.
Being a successful modern woman is hard, and for so many of us the constant flux in our hormones and the dip and dives our mood swings take makes it that much harder. For over 17 years, women have visited celebrated psychopharmacologist Dr Julie Holland looking for the miracle cure to eradicate these feelings. Now, in her illuminating and honest Moody Bitches, she details the invaluable advice she shares with her patients, revealing how suppressing our natural emotions is actually damaging. Instead she offers tried and tested alternatives to help keep the moods under control, making exhaustion and low sex-drive a thing of the past.
From the meds you can trust to those you can’t; from the foods you should be eating, the healthy behaviours you should be practising and the herbal remedies that actually work, Dr Julie imparts wisdom from years of not only professional but personal experience too. Simple yet revolutionary, Moody Bitches is the life-changing self-help book for women and those who love them.
Supplementation with myo-inositol may be considered a reliable option in the treatment of metabolic syndrome in postmenopausal women.
The aim of this study was to evaluate whether myo-inositol, an insulin-sensitizing substance, may improve some features of metabolic syndrome in postmenopausal women.
Eighty postmenopausal women affected by the metabolic syndrome were enrolled prospectively in the study and treated with diet plus supplementation of myo-inositol (2 g BID plus diet: intervention group) or with diet plus placebo (control group) for 6 months. They were evaluated at baseline and after 6 months for insulin resistance (homeostasis model assessment ratio [HOMA] insulin resistance), lipid profile, and blood pressure.
Myo-inositol plus diet improved systolic and diastolic blood pressure, HOMA index, cholesterol, and triglyceride serum levels with highly significant differences, compared with the groups treated only with diet and placebo. In the group treated with myo-inositol, a decrease in diastolic blood pressure (−11%), HOMA index (−75%), and serum triglycerides (−20%) and an improvement in high-density lipoprotein cholesterol (22%) were shown.
Supplementation with myo-inositol may be considered a reliable option in the treatment of metabolic syndrome in postmenopausal women.
Polycystic ovary syndrome (PCOS) is a complex and common endocrine disorder characterized by hyperandrogenism, which is accompanied by follicle growth arrest at the small antral stage, minimal granulosa cell proliferation, and chronic anovulation.
Polyunsaturated fatty acids (PUFAs) are necessary for the body’s metabolism, growth and development. Although PUFAs play an important role in the regulation of female reproduction, their role in ovarian development in PCOS is still unclear.
The present study was conducted to investigate the effects of different ratios of n-3/n-6 PUFAs (omega-3/omega-6) on ovary development in PCOS rats. Serum levels of reproductive hormones and enzymes related to steroidogenesis were assessed.
The results indicated that PUFAs (n-3/n-6: 1/15) significantly increased ovarian weight and improved the ovarian structure although they had no significant effect on body weight in PCOS rats.
Meanwhile, apoptosis was attenuated accompanied by increased cell proliferation by PUFAs (n-3/n-6: 1/15). Moreover, serum levels of hormones (FSH and E2) were also significantly increased by PUFAs (n-3/n-6: 1/15) accompanied by decreased T levels.
To investigate whether PUFAs regulate the expression of enzymes related to hormone synthesis, western blotting was used to determine the protein levels of CYP51, CYP19, StAR and 3β-HSD.
The results showed that PUFAs significantly increased the protein levels of all of these enzymes. These results indicate that PUFAs enhance the reproductive performance of PCOS by increasing the expression of steroidogenesis enzymes, which are related to hormone secretion and ovarian functions.
These findings provide evidence that a balanced n-3/n-6 PUFA ratio is beneficial for PCOS reproduction.
Polycystic ovarian syndrome (PCOS) is a common endocrine disease across the world. Because gut microbiota play a key role in the pathogenesis of PCOS, probiotics may alleviate PCOS symptoms through the regulation of intestinal flora. The effects of 8 lactic acid bacterial strains on PCOS were investigated. Letrozole was used to produce a PCOS rat model and a 4-week-strain-intervention was performed. Diane-35, as a clinical PCOS treatment medicine, was effective in attenuating rats’ reproductive disorders.
Lactobacillus plantarum HL2 was protective against ovary pathological changes and restored luteinizing hormone, follicle stimulating hormone and testosterone levels.
Bifidobacterium longum HB3 also alleviated ovary abnormalities and decreased testosterone levels.
Administration of lactic acid bacteria up-regulated short-chain fatty acid levels.
Based on 16S rRNA sequencing, lactic acid bacteria improved letrozole induced gut microbiota dysbiosis with different degrees.
Akkermansia, Roseburia, Prevotella, Staphylococcus and Lactobacillus genera were correlated with sex hormone levels. Some of the sex hormone-related gut microbiota were restored by treatment with the strains.
These results demonstrated that lactic acid bacteria alleviated PCOS in a rat model by regulating sex hormone related gut microbiota. Modifying gut microbiota by probiotic interventions may thus be a promising therapeutic option for PCOS.
Gastrointestinal and central function are intrinsically connected by the gut microbiota, an ecosystem that has co-evolved with the host to expand its biotransformational capabilities and interact with host physiological processes by means of its metabolic products.
Abnormalities in this microbiota-gut-brain axis have emerged as a key component in the pathophysiology of depression, leading to more research attempting to understand the neuroactive potential of the products of gut microbial metabolism.
This review explores the potential for the gut microbiota to contribute to depression and focuses on the role that microbially-derived molecules – neurotransmitters, short-chain fatty acids, indoles, bile acids, choline metabolites, lactate and vitamins – play in the context of emotional behaviour.
The future of gut-brain axis research lies is moving away from association, towards the mechanisms underlying the relationship between the gut bacteria and depressive behaviour.
We propose that direct and indirect mechanisms exist through which gut microbial metabolites affect depressive behaviour: these include (i) direct stimulation of central receptors, (ii) peripheral stimulation of neural, endocrine, and immune mediators, and (iii) epigenetic regulation of histone acetylation and DNA methylation.
Elucidating these mechanisms is essential to expand our understanding of the aetiology of depression, and to develop new strategies to harness the beneficial psychotropic effects of these molecules.
Overall, the review highlights the potential for dietary interventions to represent such novel therapeutic strategies for major depressive disorder.
Polycystic ovary syndrome (PCOS) is characterized by androgen excess, ovulatory dysfunction and polycystic ovaries1, and is often accompanied by insulin resistance2.
The mechanism of ovulatory dysfunction and insulin resistance in PCOS remains elusive, thus limiting the development of therapeutics. Improved metabolic health is associated with a relatively high microbiota gene content and increased microbial diversity3,4.
This study aimed to investigate the impact of the gut microbiota and its metabolites on the regulation of PCOS-associated ovarian dysfunction and insulin resistance. Here, we report that Bacteroides vulgatus was markedly elevated in the gut microbiota of individuals with PCOS, accompanied by reduced glycodeoxycholic acid and tauroursodeoxycholic acid levels.
Transplantation of fecal microbiota from women with PCOS or B. vulgatus-colonized recipient mice resulted in increased disruption of ovarian functions, insulin resistance, altered bile acid metabolism, reduced interleukin-22 secretion and infertility.
Mechanistically, glycodeoxycholic acid induced intestinal group 3 innate lymphoid cell IL-22 secretion through GATA binding protein 3, and IL-22 in turn improved the PCOS phenotype.
This finding is consistent with the reduced levels of IL-22 in individuals with PCOS. This study suggests that modifying the gut microbiota, altering bile acid metabolism and/or increasing IL-22 levels may be of value for the treatment of PCOS.
Catechol-O-Methyltransferase (COMT) is one of the several enzymes that degrade dopamine, epinephrine, and norepinephrine. COMT breaks down dopamine mostly in the part of the brain responsible for higher cognitive or executive function (prefrontal cortex).
COMT helps break down estrogen byproducts that have the potential to cause DNA mutations and cause cancer.
If you have higher COMT levels:
If you have lower levels of COMT, the following may counteract some of the effects of the gene:
Catechol estrogens form from CYP enzymes breaking down Estradiol and Estrones. Catechol estrogens can break DNA and cause cancer and autoimmune conditions. COMT methylates (using SAM) and inactivates these catechol estrogens (2- and 4-hydroxycatechols). The products of COMT methylation are 2- and 4-o-methylethers, which are less harmful and excreted in the urine (they have anti-estrogen properties). However, if COMT is inhibited too much either because of genetics or dietary inhibition, it should result in higher levels of catechol estrogens, especially if glucuronidation and sulphation pathways are not working. 4-Hydroxyestrone/estradiol was found to be carcinogenic in the male Syrian golden hamster kidney tumour model, whereas 2-hydroxylated metabolites were without activity. 4-Hydroxyestrogen can be oxidized to quinone intermediates that react with purine base of DNA, resulting in depurination adduct that generates cancerous mutations. Quinones derived from 2-hydroxyestrogens are less toxic to our DNA. Estrone and estradiol are oxidized to a lesser amount to 2-hydroxycatechols by CYP3A4 in the liver and by CYP1A in extrahepatic tissues or to 4-hydroxycatechols by CYP1B1 in extrahepatic sites, with the 2-hydroxycatechol being formed to a larger extent .
It has been observed that tissue concentration of 4-hydroxyestradiol is highest in malignant cancer tissue, out of all the estrogens. The concentration of these Catechol Estrogens in the hypothalamus and pituitary are at least ten times higher than parent estrogens. Catechol Estrogens have potent endocrine effects and play an important role in hormonal regulation (those produced by hypothalamus and pituitary).
Increased availability of estrogen and estradiol for binding and hypothalamic sites would facilitate the formation of Catechol Estrogens. These estrogens affect Luteinizing Hormone (LH) and maybe follicle-stimulating hormone (FSH) and prolactin. Catecholestradiol competes with estradiol for estrogen binding sites in the anterior pituitary gland and hypothalamus and dopamine binding sites on anterior pituitary membranes.
Other possible mechanisms of inactivation of these catechol estrogens include conjugation by glucuronidation and sulphation. High concentration of 4-hydroxylated metabolites caused insufficient production of methyl, glucuronide or sulfate conjugate which in turn results in catechol estrogen toxicity in cells and oxidation to semiquinone and quinone, which may reduce glutathione (GSH). These oxidation products could lead to DNA mutations. The quinone/semiquinone redox system produces superoxide ions (O2¯ ) which can react with NO to form peroxynitrite, which could cause DNA damage. In summary, CEs lead to the production of potent ROS, capable of causing DNA damage, thus playing an important role not only in causing cancer but also in systemic lupus erythematosus (SLE) and Rheumatoid Arthritis. The abilities of the estrogens to induce DNA mutations were ranked as follows: 4-hydroxyestrone (most damaging) > 2-hydroxyestrone > 4-hydroxyestradiol >2-hydroxyestradiol > > Estradiol, Estrone.
Berberine inhibits the proliferation of human uterine fibroid cells
Treatment of fibroid cells with berberine inhibited cell proliferation by approximately 60%.
COX-2 is a critical enzyme that converts arachidonic acid into prostaglandin E2 (PGE2) and is commonly overexpressed in many solid tumors, including colorectal, breast, prostate, and ovarian neoplasms.
Increased expression of COX-2 and the associated PGE2 production have been demonstrated to significantly enhance carcinogenesis. Ke et al. reported that COX-2 expression was significantly up-regulated in uterine fibroids and that the inhibition of COX-2 activity significantly reduced the proliferation of the uterine fibroids smooth muscle cells, which suggests that COX-2 is involved in the pathogenesis of uterine fibroids.
In turn, berberine has been reported to induce cancer cell apoptosis and suppress cancer cell migration in many neoplastic cell lines, including melanoma, non–small cell lung cancer (40), and oral cancer, an effect mediated through the reduced expression of COX-2.
Consistent with these observations, our data indicate that BBR significantly reduced COX-2 expression in uterine cells, which suggests that COX-2 may also play a role in mediating BBR-induced apoptosis in human uterine cells.
Berberine inhibits the proliferation of human uterine fibroid cells
‘I look at the clock… it’s 3am’: Why can’t women sleep?
…A new book from the US … appears at first glance to be more of a feminist manifesto for Generation Xers than a self-help manual for insomniacs. On closer inspection, though, a picture starts to form that’s recognisable to any woman who is knee-deep in the mothering, marriage and career years. Disregarding the generational focus of the book’s premise, it offers, not a cure, but insight and some unpalatable news about the lives of women today. Every right we’ve earned, every advance we’ve made, every career we are now free to embark on continues to co-exist with our near full-time engagement in the oldest job in the world: keeping hearth and home.
Despite a century of emancipation, women still do most of the backstage work that keeps the show on the road. Scratch the surface of this national insomnia pandemic and you discover that inequality is at the heart of the malaise. Aside from sexual politics and headline grabbers, such as #MeToo, most women’s lives aren’t improving quantifiably, they’re just different from 50 years ago.
“It’s great that men and women are equals in the workplace, but what this means in reality is that women are effectively taking on twice the load,” says Dr Elle Boag, associate professor in social psychology at Birmingham City University. “Only too often we do the work, the domestic labour and the childcare (to be fair, sometimes these chores are shared). We’ve adopted this multitasking role and it’s become normative.” So, it’s no surprise that when we go to bed we find we can’t switch off.
Metabolic syndrome is a cluster of conditions that occur together, including
Having just one of these conditions doesn’t mean you have metabolic syndrome but as you develop more of these conditions, your risk of complications such as type 2 diabetes and heart disease, rises higher and higher.
Research shows that the more carbohydrates you eat, the more likely you are to have metabolic syndrome:
Breathing is information. The more stressed you feel, the faster you breathe, and your brain will notice this and read it as a signal that things are not going well. That fast, shallow breathing which happens when you’re stressed is effectively telling your brain that you’re running from a lion. But the reverse of this rule is also true: if you breathe slowly, you’re giving your brain a signal that you’re in a place of calm. You will start to feel less stressed. Studies have even shown that the right kind of breathing can reduce our perception of pain. Both the pace at which you breathe and how deeply you breathe change your stress response. If all you do for one minute is slow your breathing down and aim for six breaths (one breath is in and out) in that minute, it will reduce the stress state and stimulate the thrive state.
A daily practice of breathing – Breathing practice is especially worth considering if you’re the kind of person who finds meditation difficult. You don’t have to stick to the same practice each time. Play around. Listen to your body. Experiment. I’m sure that, within a few days, you’ll find a technique that works for you. Aim to do at least one of these practices every day. Even one minute per day of focused, intentional breathing can make a big difference.
We tend to think that a loss of mental acuity is just part of getting older — but age is not the only contributing factor to cognitive decline. Our lifestyle also plays a key role. Failing to follow a nutritious diet, a lack of sleep and exercise, ongoing stress, smoking, drinking alcohol excessively and environmental pollutants can all damage our brain cells.
Fortunately, mental deterioration is not irreversible. In fact, the brain is incredibly dynamic and has the potential and the ability to change at any point throughout our entire life – and you have the power to enhance your brain function, protect your brain from damage and counteract the effects of aging! That is, if you’re willing to fuel the brain and tweak your everyday decisions.
Here are 5 small changes you can make in your life that can mean big differences in your cognitive abilities.
As women start to produce less estrogen and enter perimenopause, they are likely to experience a mix of challenging symptoms. These include hot flashes, insomnia, night sweats, vaginal dryness, and mood swings.
Menstrual periods may get lighter or heavier and less regular, but once a woman has not had a period for 12 months, they are in menopause. Then, the symptoms experienced over the previous years begin to subside.
There is a range of vitamins and supplements available to help women manage the symptoms of perimenopause and menopause.
If you feel as though you can’t do as much physically as you’ve gotten older, there may be a reason. Both aging and menopause are known to affect sarcopenia, which is a loss of muscle mass and strength, which in turn affects balance, gait, and overall ability to perform tasks of daily living. A new study is one of the first to link alcohol consumption with a higher prevalence of sarcopenia in postmenopausal women. The study outcomes are being published online today in Menopause, the journal of The North American Menopause Society (NAMS).
Previous studies of postmenopausal women have suggested the beneficial effect of estrogen therapy on muscle mass and function. Because of this, it is believed that postmenopausal women are more vulnerable to sarcopenia. Although alcohol is known to inhibit skeletal muscle protein synthesis, few studies have examined the relationship between sarcopenia and alcohol-drinking patterns.
…Study results published in the article “Associations between high-risk alcohol consumption and sarcopenia among postmenopausal women” show that the prevalence of sarcopenia was found to be nearly four times greater for the high-risk, alcohol-drinking group than the low-risk group.
…With this study suggesting that more muscle loss leads to sarcopenia and other studies suggesting that even one drink of alcohol may increase the risk of breast cancer, postmenopausal women should limit their alcohol intake.”
The therapeutic benefits of omega-3 fatty acids – which are abundant in certain fish oils – have long been known. In the 1950s, upon the discovery that omega-3 improves brain development, cod liver oil was given for free to young children, pregnant women, and nursing mothers. In the 80s, scientists reported that eskimos enjoy better coronary health than their mainland counterparts as a result of their fish rich diets. And in 2009, a study published in the Menopause journal suggested that omega-3 helps reduce the frequency of hot flushes in menopausal women.
As you can see, the hype that surround omega-3 is warranted, and not something to be shied away from.
The Truth About Fats
Many women are concerned about fat, and wrongly believe that consuming fat will make them overweight. The truth is, however, that an extremely low-fat diet won’t regulate your weight – and it certainly won’t enhance your health. Fat can be hugely beneficial in the right form, and by consuming fatty acids such as omega-3, you will surely be more healthy.
Research has confirmed that omega-3 fatty acids may have an excellent effect on impacting degenerative diseases, such as heart disease, rheumatoid arthritis, hypertension, Alzheimer’s disease, diabetes, and many more. As for menopause, omega-3 fatty acids contain anti-inflammatory properties shown to have a positive effect on many of the symptoms associated with “the change”.
What can omega-3 help with?
Because of its wonderful properties, omega-3 can greatly help women during menopause. It helps treat a range of menopausal symptoms, such as:
Postmenopausal women with a more diverse population of gut bacteria may be more efficient at breaking down estrogen, a new study suggests. Because estrogen plays a role in causing breast cancer, researchers speculate a healthy bacterial population may lower the risk for cancer.
“The composition and diversity of the intestinal microbiota were associated with patterns of estrogen metabolism that are predictive of the risk of breast cancer in postmenopausal women,”
Estrogen is metabolized in the liver and in other tissues such as the breast, yielding fragments that are excreted in urine or, through bile, into the gut. Gut microbes can degrade these metabolites, allowing them to be reabsorbed into the bloodstream and further recycled in the liver. Dr. Fuhrman and colleagues suggest that women whose gut bacteria more efficiently process estrogen may have a lowered risk for breast cancer.
Postmenopausal vulvovaginal atrophy is associated with age-related changes in the vaginal microbiome, with a shift from Lactobacillus-dominated strains in premenopause to a predominance of anaerobic organisms, new research shows.
“We have not yet identified specific interventions, but we are interested in pursuing personalized selections of probiotics and prebiotics for a given woman,” said lead investigator Rebecca Brotman, PhD.
“We have been advocating probiotics or prebiotics to improve vaginal health for almost 30 years,” said Gregor Reid, PhD.
“I 100% support the conclusions of this work. It is nice to see confirmation of work we published in 2011, with an aberrant microbiota associated with some cases of vulvovaginal atrophy,” Dr. Reid told Medscape Medical News (PLoS One, 2011;6:e26602).
Brain imaging and gene analyses in twins reveal that white matter integrity is linked to an iron homeostasis gene.
Iron deficiency is a well-known cause of impaired cognitive, language, and motor development, but a report out today (January 9) in Proceedings of the National Academy of Sciences reveals that even in apparently healthy young adults, variations in iron levels correlate with variations in brain structure integrity.
“[The researchers] make a very interesting connection between the issue of iron metabolism and the integrity of white matter, more specifically myelin”—the cellular sheath that enwraps and insulates neuronal axons—said George Bartzokis of the University of California, Los Angeles, who was not involved in the study. “This would have been predicted by what is known about myelin, because it actually contains a lot of iron, so it is important that [they have] directly demonstrated this in humans with imaging.
More forgetful? Not thinking as clearly? Simple arithmetic coming more slowly? Worried that mental functions are worsening? Are the processes of ageing catching up? There is much that can be done to prevent worsening mental functioning and memory loss. For some, memory loss heralds the onset of dementia. Regardless of a person’s occupation or social environment, loss of memory is the most feared consequence of ageing…
…Specific nutritional interventions and nutritional supplements can help to detox and protect individual cells of the brain and nervous system.
Connecting women, science and spirit, the Gynelogic Sunday Supplement delivers a bi-monthly dose of news, views and reviews, as seen through my lady lens.
Connecting women, science and spirit, the Gynelogic Sunday Supplement delivers a bi-monthly dose of news, views and reviews, as seen through my lady lens.
