INSTITUTE OF HEALTH SCIENCE,
SCHOOL OF MEDICINE
MICROBIOLOGY OF ENDOCRINE SYSTEM
GROUP ASSIGNMENT: MICROBIOTA AND REPRODUCTIVE HEALTH
NAME OF THE GROUP(3)
NO. FULL NAME ID. NO
1 Amanuel Tarekegn Abdisa 1404441
2 Gutu solomon Amente 1405467
3 Lidetu Kiphe Tekebo 1405877
4 Ebise Amanuel Gindaba 1412199
5 Asana Endalu 1303528
6 Saron Kejela Merdasa 1500047
SUBMITTED TO: MR. GIRMAYE
JULY, 2025
Contents
Aknowledgement……………………………………………………………………1
1. Introduction to gut microbiota and reproductive health……………………...2
2. How gut microbiota affect female reproductive health focusing on it’s;
2.1 Role in regulating hormone levels……………………………………..2
2.2 Relating to menstrual cycle…………………………………………….3
2.3 Relating to pregnancy out comes………………………………………6
2.4 Relating to conditions like polycystic ovary syndrome(PCOS)……..10
References…….……………………………………………………………………14
ACKNOWLEGMENT
We would like to express our sincere thanks to Mr Girmaye, for giving us the chance to explore
and reach out to the gut microbiota and reproductive health. As the science of it’s relations are
broad but, we discussed on some of it’s benefits and defect that can be caused to reproductive
health in relation to gut microbiota. The given assignment allowed us to gain something, and again
we would like to thank Mr Girmaye!
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1. INTRODUCTION TO GUT MICROBIOTA AND REPRODUCTIVE HEALTH
Numerous studies have established the importance of gut bacteria in sustaining general metabolic
and reproductive health by influencing physiological systems. The significance of
the reproductive microbiome in illnesses of the reproductive system has been substantially
studied in recent years.
Reproductive issues are becoming an increasing global problem. There is increasing interest in the
relationship between microbiota and reproductive health. Stable microbiota communities exist in
the gut, reproductive tract, uterus, testes, and semen. Various effects (e.g., epigenetic
modifications, nervous system, metabolism) of dysbiosis in the microbiota can impair gamete
quality; interfere with zygote formation, embryo implantation, and embryo development; and
increase disease susceptibility, thus adversely impacting reproductive capacity and pregnancy .
Recent advances suggest that gut microbial homeostasis is essential for reproductive health and
that perturbations in the gut microbiota can lead to reproductive pathologies.
2. HOW GUT MICROBIOTA AFFECT FEMALE REPRODUCTIVE HEALTH
FOCUSING ON IT’S;
2.1 ROLE IN REGULATING HORMONE LEVELS
The gut microbiome is known to influence the hormone levels in the host including estrogen levels
in females. This functional link between gut microbiota and estrogen was first noted three decades
ago. found that antibiotic supplementation decreased estrogen levels in women. The gut
microbiota principally regulates the estrogen level by secretion of β-glucuronidase (gmGUS), an
enzyme that converts conjugated estrogen into deconjugated estrogen in the GI tract facilitating it
to bind to estrogen receptors, resulting in subsequent signaling and physiological downstream
effects. A decreased β-glucuronidase activity as a result of gut microbial dysbiosis can result in
reduced deconjugation of estrogen and a decrease in the level of circulating estrogens. This further
alters the activation of estrogen receptors leading to pathologies such as obesity and
cardiovascular diseases. On the other hand, increased β-glucuronidase activity can result in
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elevated estrogens levels leading to pathologies, such as endometriosis and cancer. Thus, optimal
gmGUS activity is essential for maintaining estrogen levels in females.
Another mechanism by which the gut microbiome might influence sex-steroid hormone levels in
females is by producing short-chain fatty acids (SCFAs). SCFAs are the primary by-products of
bacterial anaerobic fermentation of dietary fibers in the intestine. Acetate (C2), propionate (C3),
and butyrate (C4) are the most abundant SCFAs that are produced by gut microbes. Importantly,
butyrate has been shown to regulate the synthesis of P4 (progesterone) and E2 (estradiol) in
porcine granulosa cells (PGCs) via the cAMP signaling pathway. In this interesting in vitro study,
the PGCs were treated with lower concentrations of butyric acid stimulate the progesterone
secretion; however, higher butyrate concentrations significantly inhibited the progesterone
secretion. Gut-derived butyrate contributes to nonalcoholic fatty liver disease in pre-menopause
women due to estrogen deficiency. These studies highlight the plausible mechanism by which the
dietary constituents and microbiota-derived metabolites may contribute to the regulation of
estrogen and progesterone level in females; however, the underlying molecular mechanism is not
clear yet. Nonetheless, the significance of gut microbiota in female reproductive pathologies is
now well established, including PCOS, endometriosis, and other reproductive tract conditions.
2.2 RELATING TO MENSTRUAL CYCLE
How Gut Health Impacts Menstrual Cycle Symptoms
To understand better the connection between irregular periods and gut health, let’s look at how your gut
health may impact your menstrual cycle symptoms.
A Two-Way Relationship
As we discussed earlier, not all bacteria are the same. Some bacteria in your gut are beneficial for your
health, others are not so much. Gut dysbiosis means that there is an imbalance in your gut microbiome and
there are too many bad bacteria present. Your diet, lifestyle, environmental factors, your health, medication
use, stress, and other factors can influence your gut microbiome and your menstrual cycle.
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If your estrogen levels are too high, food moves slower through your gut. This may result in bloating and
constipation during your period. This means your hormonal levels affect not only your period but your gut
too.
However, your gut microbiome plays a critical role in your hormonal levels, including your estrogen levels.
A healthy gut supports healthy hormone levels, but an unhealthy gut can increase estrogen levels and is
linked to obesity, chronic inflammation, endometriosis, PCOS, and all kinds of other estrogen-related
diseases.
Gut Health and PMS
Your gut health may have a major influence on your premenstrual symptoms, including bloating, cramps,
and mood changes . A healthy gut microbiome can support normal digestion, which may help to decrease
the buildup of gas, bloating, and water weight before menstruation.
Your gut microbiome also plays a role in the production and release of serotonin and other
neurotransmitters. If you have poor gut health, your body may not be releasing enough or a steady supply of
these ‘happy chemicals’, which may impact your mood during PMS.
Moreover, chronic inflammation related to poor gut health may further amplify your PMS and period
symptoms. Leaky gut syndrome and other gut health issues may interfere with hormonal balance and the
gut’s ability to metabolize and recycle estrogen and progesterone. This can lead to or increase symptoms,
including bloating, fatigue, irregular periods, acne, and PMS.
Gut Microbiome Before Menstruation
Researchers noted lower levels of Bacteroidetes phylum in those with PMDs, as well as a decrease
in, Butyricicoccus, Extibacter, Megasphaera, and Parabacteroides, and and an increase in Anaerotaenia in
the PMDs group.
They found that the reduction of Parabacteroides and Megasphaera may be associated with increased
premenstrual symptoms. However, we need more research on the topic to further understand these
differences, their causes, and the implications of the gut flora before menstruation in those with PMDs.
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Gut microbiota, a collection of bacteria, archaea, fungi, and viruses, is vital in maintaining our
health. Gut microbiota is fully established after birth, although some limited microbial
communities may be detected prenatally. Changes in gut microbiota occur over the life span and
are specifically modified during life stages such as infancy, childhood, and puberty, when
microbiota acquires sexually dimorphic characteristics, and aging.
The gut microbiota is also modified during pregnancy and nursing and is critical during fetal and
infant development. Several recent studies have shown that the maternal gut microbiota during the
early postnatal period affects the infant’s nervous system’s activity. However, more information is
needed regarding the role of maternal gut microbiota during fetal development. Animal studies
have demonstrated that maternal microbiota during pregnancy impacts fetal brain development
and postnatal behavior. Depletion of the maternal microbiota with antibiotics during pregnancy
was shown to result in a deficiency of thalamocortical axons, impaired thalamic axon outgrowth in
the fetus, and altered tactile sensitivity in adult offspring. In contrast, selective reconstitution of
the maternal gut microbiome prevented abnormalities in fetal thalamocortical exogenesis. A recent
human study involving 1064 pregnant mothers and their 1074 children reported an association
between the composition of maternal fecal microbiota during pregnancy and internalizing
behavior associated with anxiety in children at the age of two years. Furthermore, fecal samples
from pregnant mothers of children with normative behavior showed higher microbial alpha
diversity and higher levels of butyrate-producing bacteria. Thus, both animal and human studies
point to an essential role of maternal microbiota during pregnancy in promoting fetal
neurodevelopment.
The maternal organism during pregnancy undergoes significant anatomical and physiological
changes designed to support fetal nutritional and energy demands, regulate fetal growth and
differentiation, and assure immunological tolerance. These changes affect every organ system in
the body and metabolic, endocrine, immune, and neuronal functions. In humans, the changes begin
early in the first trimester, peaking at the time of labor and reverting to prepregnancy levels by a
few weeks into the postpartum. Metabolic changes during pregnancy involve higher accumulation
of fat and cholesterol due to increased leptin, insulin, and insulin resistance, resulting in pregnant
women gaining more fat and cholesterol. During pregnancy, there is an increase in
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proinflammatory gut bacteria associated with increased levels of proinflammatory cytokines.
These changes further improve energy storage in fat, providing for fetal growth.
2.3 RELATING TO PREGNANCY OUTCOMES
Maternal Gut Microbiota–Fetal Interaction during Pregnancy: Role of the Placenta
The interaction between the maternal gut microbiota and the fetus remains a subject of intense
debate centered around the dogma of a “sterile womb”, postulating no contact between maternal
gut bacteria and the fetus and, instead, fetus dependence on the metabolites derived from the
maternal gut microbiota. More recent evidence suggests a maternal gut microbiota translocation to
the uteroplacental unit.
Irrespective of the microbiota present in the uterus, maternal gut microbiota metabolites supply
energy, nutrients, and vitamins such as B complex, folate, choline, betaine, and short-chain fatty
acids (SCFAs) derived from the dietary fiber fermentation, polyphenols that provide nutritional
programming of fetal growth and development via epigenetic mechanisms, and neurotransmitters.
Maternal metabolites pass from the gut lumen to the circulation, access the fetus through the
placenta, reach fetal circulation, and provide the nutrients required for fetal growth and
development. These nutrients also impact gene expression and brain development. Some
metabolites also cross the fetal blood–brain barrier (BBB) and are involved in fetal CNS and
immune system development by regulating dendritic T-cell functions and cytokine production.
The placenta is a critical structure for normal fetal development. The placenta forms a primary
barrier between the maternal environment and the fetus, regulating gas exchange, hormone
production, and secretion of nutrients. In healthy pregnancies, the placenta also harbors
microbiota. It has been speculated that the placental microbiota may contribute to fetal immune
system development during the second trimester of pregnancy. The placental microbiota is unique,
resembles maternal oral microbiota and can adversely affect pregnancy outcomes. Interestingly,
placental membranes defend the fetal environment and have bactericidal properties as they contain
cells, extravillous trophoblasts, natural killer cells, leukocytes, and macrophages. Although the
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bacteria can pass the barrier due to bacterial ligands, they are most likely not viable and
fragmented. It is also possible that specific microorganisms may hide inside placental trophoblasts.
In mice, fetal placental vascularization occurs between gestation days 8–11 when the placenta
gains contact with maternal circulation and transport from the maternal circulation to the fetus is
initiated. Metabolites of maternal gut microbiota, such as SCFAs, are transferred to the liver, enter
the bloodstream, pass across the placental barrier, enter the fetal circulation, and contribute to the
formation of BBB and innate immune development. Maternal stress during the first week of
pregnancy in mice induces rapid and lasting alterations in maternal gut microbiota resulting in
alterations of placental transfer of nutrients in a sex-specific manner where male but not female
offspring demonstrate significant neurodevelopmental changes in the hypothalamic and limbic
circuit and the regulation of stress responsivity. These findings indicate that the composition of
maternal gut microbiota during pregnancy is a crucial contributor to the metabolic programming
of offspring.
While the fetus is initially protected from harmful substances in maternal blood by the placenta,
subsequent maturation of the BBB provides a second specific safeguard against pathogens and
potentially toxic substances critical for healthy brain development during pregnancy. In rodents,
BBB is formed at gestational day 13.5–15.5, but the early BBB differs from adults with a higher
concentration of the tight junctions (TJ proteins) and extracellular matrix components. In germ-
free mice, the BBB is leaky at gestational day 16.5, suggesting that the maternal microbiota is
critical for developing a functional BBB. In humans, some efflux transporters that can exclude
toxins are already present at eight weeks of gestation, and BBB components are present at 12
weeks of gestation. It is widely believed that during gestation and in newborns, this barrier is
immature or “leaky”, rendering the developing brain more vulnerable to drugs or toxins entering
the fetal circulation from the mother.
It has been suggested that increased intestinal permeability in early pregnancy is associated with
increased maternal levels of LPS, and cytokines at the endometrial level, facilitating the
translocation of bacterial metabolites and bacteria from the intestinal lumen into maternal
circulation. Some bacteria may travel to the placenta via the bloodstream after gut epithelium
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translocation by dendritic cells as they migrate to lymphoid organs. In addition, maternal oral
bacteria entering the bloodstream have also been suggested as a source of fetal microbiota. This
early prenatal microbiota may imprint immune systems in preparation for postnatal microbiota
seeding. Following birth, the human intestine is rapidly colonized by microbiota, mostly strict
anaerobes. By the end of the first year, infants possess an individually distinct microbiota; by 2–5
years, the microbiota fully resembles adults in terms of composition and diversity.
The initial diffusion of maternal metabolites across the placenta facilitates the fetal nervous system
and HPA axis development. It is followed by the infiltration of gut bacteria via the placenta and
translocation into the fetal circulation. Thus, gut microbiota colonization may begin during fetal
life. Some bacteria may infiltrate the fetal intestine, but they are insufficient and very distinct to
trigger the activation of the intestinal epithelium tolerance that occurs during the first contact with
microbiota after birth.
EFFECT OF MATERNAL GUT MICROBIOTA DURING PREGNANCY ON FETAL GBA
DEVELOPMENT
While there is much research on the role of gut microbiota and GBA during the postnatal period,
little is known about gut microbiota and GBA during the prenatal period. Because of the fetal
developmental trajectory, there is no functional GBA during fetal life. In humans, the rudimentary
GBA development during the fetal period is regulated by maternal gut microbiota.
At birth, massive amounts of maternal vaginal, fecal, and skin microbiota colonize the emerging
rudimentary gut of the newborn delivered by the vagina; newborns delivered by C-section are
exposed to the skin microbiota. Additional maternal microbiota is transferred during nursing; the
composition of microbiota transferred via milk is affected by maternal health and gestational age.
Gut closure around six months marks the formation of functional GBA. Functional GBA consists
of a bidirectional network involving the CNS, ANS, ENS, VN, neuroendocrine and neuroimmune
systems, the HPA, and the gut/gut microbiota. The microbiota is a powerhouse of the GBA,
providing bioconversion of nutrients, detoxification, regulation of immunity, and protection
against pathogenic microbes.
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Accumulating preclinical and clinical data suggest the critical role of maternal gut microbiota in
regulating fetal development by transferring maternal metabolites and other factors to the fetus via
the placenta. So, while fully functional bidirectional offspring GBA develops postnatally, the
rudimentary GBA is assembled under the maternal-gut microbiota regulation during the fetal
period.
Impact of Maternal Microbiota during Pregnancy on Fetal CNS
Maternal gut microbiota during pregnancy is crucial for fetal CNS development. Additionally,
other factors such as maternal genetics, diet, health status, stress, and medication contribute to the
outcome.
The link between maternal gut microbiota and fetal neurodevelopment is based on animal and
human studies. Rodent studies have shown gender-dependent abnormal fetal brain development in
germ-free mice. The microbiota-deficient mice showed altered gene expression involved in
neurotransmission, neuroplasticity, metabolism, and morphology in the hippocampus and
thalamocortical neurodevelopment linked to sensorimotor behavior and pain perception
postnatally.
The human brain and nervous system begin to develop during the embryonic period starting at six
weeks and continue through the end of pregnancy, with development proceeding postnatally into
puberty and beyond. Structural and functional, time-specific neurodevelopmental changes occur
during gestation, including axonal growth, synapse formation, and dendritic and axonal
arborization, followed by synaptic connections. Maternal gut microbiota during pregnancy
regulates metabolites that reach the fetus via transplacental signaling and enter the fetal brain.
Maternal gut microbiota promotes healthy fetal brain development and affects structural and
functional brain connectivity, impacting the offspring’s cognitive and behavioral development.
Clinical studies suggest maternal gut microbiota dysbiosis during pregnancy impacts the fetal
CNS’s physiological and functional development. Specifically, microbial depletion due to
infection or antibiotic treatment during pregnancy alters fetal neurodevelopment, contributing to
abnormal brain structure and function underlying maladaptive, autism-like behaviors in offspring.
Depletion of maternal gut microbiota during pregnancy also affects gene expression in the
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developing fetal brain, including genes regulating new axons expression connecting the thalamus
with the cortex responsible for sensory functions.
In addition to metabolites, gut microbiota produces neurotransmitters and neuromodulators,
serotonin (or 5-hydroxytryptamine (5-HT)), gamma-aminobutyric acid (GABA), and SCFAs.
These bioactive factors are transported to the fetal brain via blood vessels after crossing the
placenta and BBB. The placenta is enriched with a complex vascularization for fetal blood supply
that requires extensive angiogenesis. During pregnancy, maternal gut microbiota produces SCFAs
involved in neuronal, intestinal, and pancreatic differentiation, facilitated by G protein-coupled
receptors. Maternal gut metabolites also promote fetal thalamocortical exogenesis. A region-
specific change in the neurotransmitter system was noted in the brains of germ-free mice that
showed increased serotonin (5-HT) concentration in the hippocampus.
Notably, the placenta synthesizes 5-HT that impacts fetal CNS development by regulating cell
proliferation, migration, and wiring during prenatal development. It has been shown that the 5-HT
precursor, tryptophan, is derived from maternal gut metabolites. Placental 5-HT reaches the fetal
forebrain during cortical neurogenesis and the initial axon growth period. In mice, serotonergic
neurons appear in the fetal mouse hindbrain on E10.5, and by E14.5, these neurons reach the
neocortex; 5-HT signaling is also vital for the thalamocortical axons. Chronic mild stress during
pregnancy in rats increases free tryptophan concentration in the maternal blood and the fetal brain,
increasing anxiety in the offspring. In humans, placental synthesis of 5-HT occurs during the first
and second trimesters of pregnancy. Disruption of placental 5-HT signaling results in long-term
behavioral abnormalities such as anxiety postnatally.
2.4 RELATING TO CONDITIONS LIKE POLYCYSTIC SYNDROME(PCOS)
PCOS is a heterogeneous endocrine, neuroendocrine, and metabolic disorder that leads to difficult
pregnancies or infertility in 6.5−8.0% of reproductive-age women. The main characteristics of
PCOS are hyperandrogenism, oligo/amenorrhoea, and polycystic ovarian morphology. Although
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genetic, lifestyle, and intrauterine factors have been suggested, the general etiology of PCOS is
unclear. However, the gut microbiome contributes to several additional characteristics of PCOS
such as obesity, insulin resistance, and low-grade inflammation
Gut microbiome in PCOS patients
Several investigators have compared the gut microbial compositions in stool samples from people
with and without PCOS. Lull et al. identified four genera that differed between 102 patients with
PCOS (n = 102) and 201 age- and BMI-matched healthy controls (n = 201). The abundance of two
genera from Clostridiales, Ruminococcaceae UCG-002, and Clostridiales Family XIII AD3011
were correlated with several PCOS-related markers such as cystic ovarian morphology and higher
testosterone levels. Moreover, patients with PCOS and pre-diabetes had significantly lower alpha
diversity (Shannon index) and higher abundance of the Dorea and Bacteroides (Ruminococcus
torques group and Lachnospiraceae UCG-004) genera than PCOS patients with normal glucose
tolerance. Liang et al. reported that gamma-aminobutyric acid-producing bacteria,
including Parabacteroides distasonis and Bacteroides fragilis, were increased in PCOS patients,
whereas Escherichia coli showed a positive relationship with serum luteinizing hormone (LH)
levels and LH: follicle-stimulating hormone (FSH) ratios. As the higher level of LH is associated
with PCOS condition. Lindheim et al. found that the stool microbiome of PCOS patients (n = 25)
showed lower diversity and different phylogenetic composition than that of healthy controls (n =
25). The authors did not observe any significant differences in any taxa with a relative abundance
>1%. However, when assessing rare taxa, the relative abundances of bacteria from the phylum
Tenericutes, specifically the order ML615J-28, and the family S24-7 (phylum Bacteroidetes) were
significantly lower and associated with reproductive parameters in PCOS patients. Additionally,
PCOS patients showed alterations in some, but not all, markers of gut barrier function and
endotoxemia. Finally, Qi et al. examined 43 healthy controls (n = 43) and 50 PCOS patients (n =
50) and found that Bacteroides vulgatus was elevated in the gut microbiota of individuals with
PCOS. B. vulgatus are gram-negative anaerobic bacteria inhabiting the distal human gut and are
typically non-pathogenic in healthy individuals. These bacteria deconjugate the bile acids
synthesized in the liver, such as glycodeoxycholic acid and tauroursodeoxycholic acid. A negative
correlation between the abundances of B. vulgatus and glycodeoxycholic acid and
tauroursodeoxycholic acid in PCOS patients. Collectively, these studies revealed that PCOS is
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associated with alterations in the gut microbiome, but no cause–effect relationships have been
determined.
While most investigators have examined the microbiota in stool, only a few have examined the
bacterial composition in saliva. For example, one study of the salivary microbiome revealed that
PCOS patients (n = 24) had fewer bacteria from the phylum Actinobacteria than healthy controls
(n = 20). PCOS patients also exhibited a borderline significant shift in bacterial community
composition in unweighted UniFrac analysis. UniFrac, one of the distance metrics used to measure
beta diversity, collects phylogenetic information to compare microbial communities in different
samples. It measures the evolutionary distance among sets of taxa in a phylogenetic tree as a
fraction of the branch length of the tree. An unweighted UniFrac analysis can be used to ascertain
the incidence of variation among the samples; however, weighted UniFrac can additionally
quantify the variation occurring in different lineages.
The alpha diversity and weighted UniFrac analysis were unchanged between PCOS patients and
controls. No differences were observed at any taxonomic level. The authors also noted altered gut
microbiota in stool samples, though the findings were not identical. One group used 16S rRNA
sequencing to examine fecal microbial diversity profiles of healthy women (n = 48), women with
polycystic ovarian morphology (PCOM) (n = 42), and women diagnosed with PCOS by the
Rotterdam criteria (n = 73). Patients with PCOS had lower microbial diversity than healthy
controls and those with PCOM had an alpha diversity that was intermediate between that of
healthy control and PCOS groups. Regression analysis showed that hyperandrogenism, total
testosterone, and hirsutism were negatively correlated with alpha diversity.
Several investigators have examined associations between fecal bacteria (gut microbiota) and
PCOS in patients with and without obesity. For example, Liu et al. examined the gut microbiome
in 33 patients with PCOS (12 non-obese and 21 obese) and 15 healthy controls (9 non-obese and 6
obese) and found that the co-abundance groups (CAGs) increased in the PCOS patients. CAGs are
the clustering of bacterial species based on the SparCC (Sparse Correlations for Compositional
data) correlation coefficients of their relative abundance. SparCC is a mathematical approach to
estimating correlation values from compositional data. Additionally, abundances of Bacteroides,
Escherichia/Shigella, and Streptococcus were negatively correlated with Ghrelin expression and
positively correlated with testosterone and BMI. Therefore, the downregulation of Ghrelin is
associated with PCOS. Liang et al. analyzed data from 20 patients with PCOS (10 lean and 10
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overweight) and 20 healthy controls (10 lean and 10 overweight) and reported that the intake of
dietary fiber and vitamin D was significantly decreased in the PCOS group. Dietary fiber plays a
crucial role in the composition of the gut microbiota where it acts as a prebiotic to support
beneficial gut bacteria (probiotics) and suppresses harmful bacteria. Future studies should further
investigate the link between diet, PCOS, and the gut microbiome.
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