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Luteal phase
Luteal phase
Luteal phase
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Menstrual cycle

The menstrual cycle is on average 28 days in length. It begins with menses (day 1–7) during the follicular phase (day 1–14), followed by ovulation (day 14) and ending with the luteal phase (day 14–28).[1] While historically, medical experts believed the luteal phase to be relatively fixed at approximately 14 days (i.e. days 14–28),[1] recent research suggests that there can be wide variability in luteal phase lengths not just from person to person, but from cycle to cycle within one person.[2] The luteal phase is characterized by changes to hormone levels, such as an increase in progesterone and estrogen levels, decrease in gonadotropins such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), changes to the endometrial lining to promote implantation of the fertilized egg, and development of the corpus luteum. In the absence of fertilization by sperm, the corpus luteum degenerates leading to a decrease in progesterone and estrogen, an increase in FSH and LH, and shedding of the endometrial lining (menses) to begin the menstrual cycle again.[1]

Hormonal events

[edit]

After ovulation and release of the oocyte, the anterior pituitary hormones–follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are released and cause the remaining parts of the dominant follicle to transform into the corpus luteum. It continues to grow during the luteal phase after ovulation and produces significant amounts of hormones, particularly progesterone, and, to a lesser extent, estrogen and inhibin. Progesterone plays a vital role in making the endometrium receptive to implantation of the embryo and supportive of early pregnancy. High levels of progesterone inhibit the follicular growth. The increase in estrogen and progesterone also lead to increased basal body temperature during the luteal phase.[3]

The LH surge that occurs during ovulation triggers the release of the oocyte and its cumulus oophorus from the ovary and into the fallopian tube and triggers the oocyte to divide and enter metaphase of meiosis II (46 or 2n chromosome) and extrude its first polar body. The oocyte will only continue through meiosis and extrude its second polar body once it is fertilized. Ovulation occurs ~35 hours after the beginning of the LH surge or ~10 hours following the LH surge. Several days after ovulation, the increasing amount of estrogen produced by the corpus luteum may cause one or two days of fertile cervical mucus, lower basal body temperatures, or both. This is known as a "secondary estrogen surge".[4]

The hormones released by the corpus luteum suppress production of the FSH and LH from the anterior pituitary gland. The corpus luteum relies on LH activation on its receptors in order to survive. The loss of the corpus luteum can be prevented by implantation of an embryo: after implantation, human embryos produce human chorionic gonadotropin (hCG),[5] which is structurally similar to LH and can preserve the corpus luteum. If implantation occurs, the corpus luteum will continue to produce progesterone for eight to twelve weeks, after which the placenta takes over this function.[6] In the absence of fertilization, hCG is not produced and the corpus luteum will atrophy in 10–12 days (Luteolysis or luteal regression). The death of the corpus luteum results in falling levels of progesterone and estrogen. The drop in ovarian hormones releases negative feedback on LH and FSH, thereby increasing LH and FSH concentrations and leading to shedding of the endometrium and another round of ovarian follicle selection.[7]

Uterine events

[edit]

During the follicular phase in the menstrual cycle, the uterine endometrium is in the proliferative phase which is characterized by an increase in circulating estrogen produced by the developing follicle. Increased estradiol alters the endometrial lining and promotes proliferation of epithelial cells, thickening of the tissue, and elongation of the spiral arteries that provide nutrients to the growing tissue. Estrogen also makes the endometrium more sensitive to progesterone in preparation for the luteal phase.[citation needed]

After ovulation and during the luteal phase, the uterine endometrium is in the secretory phase which is characterized by the production of progesterone from the growing corpus luteum. Progesterone inhibits endometrial proliferation, and preserves uterine tissue in preparation for fertilized egg implantation. At the end of the luteal phase, progesterone levels fall and the corpus luteum atrophies. The drop in progesterone leads to endometrial ischemia which will subsequently shed in the beginning of the next cycle at the start of menses.[1] This last stage in the luteal or secretory phase may be called the ischemic phase and lasts just for one or two days.[8]

Symptoms

[edit]

Changes in the level of progesterone during this phase may cause typical symptoms of pre-menstrual syndrome (PMS), such as:

  • Anxiety
  • Headaches
  • Mood swings
  • Irritability
  • Tender breasts
  • Weight gain
  • Trouble sleeping
  • Changes in sexual desire
  • Bloating
  • Emotional stresses

References

[edit]
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Luteal phase

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The luteal phase is the latter stage of the menstrual cycle in females, commencing immediately after ovulation and typically lasting around 10–16 days until the initiation of menstruation in the absence of pregnancy. During this phase, the ruptured ovarian follicle transforms into the corpus luteum, a temporary endocrine structure that primarily secretes progesterone under the influence of luteinizing hormone (LH), while also producing some estradiol. This hormonal surge, particularly the rise in progesterone, induces key physiological changes, including the maturation and secretory transformation of the uterine endometrium—developing complex glands, increased glycogen stores, and expanded spiral arteries—to create a receptive environment for potential embryo implantation. Additionally, progesterone thickens cervical mucus to form a barrier against pathogens and sperm, and it slightly elevates basal body temperature. If fertilization and implantation occur, the developing secretes human chorionic gonadotropin (hCG), which sustains the and its progesterone production, preventing endometrial breakdown and the onset of . In the event of no pregnancy, the regresses around day 14 of the luteal phase, leading to a sharp decline in progesterone and levels; this hormonal withdrawal triggers the shedding of the as menstrual bleeding. The luteal phase's relative consistency in length—contrasting with the more variable —contributes to the overall predictability of timing in many individuals, though disruptions such as luteal phase defects can impact fertility by impairing progesterone adequacy or endometrial receptivity. Symptoms commonly associated with this phase include (PMS) manifestations like mood changes, , and breast tenderness, attributable to the fluctuating hormones.

Definition and Overview

Definition

The luteal phase represents the second half of the , initiating immediately after and concluding with the onset of should not ensue. This phase is essential for reproductive readiness, primarily functioning to prepare the for the potential implantation of a fertilized under the dominant influence of progesterone produced by the . The name "luteal phase" derives from the corpus luteum, a transient that forms from the remnants of the ruptured following ; "" translates from Latin as "yellow body," reflecting the structure's characteristic yellowish coloration due to lipid content. For contextual understanding, the is commonly divided into four phases: the , , the luteal phase, and , with serving as the trigger that marks the transition into the luteal phase.

Duration and Timing

The luteal phase typically lasts around 10–16 days in most cycles (from ovulation to the next period), with an average of about 14 days in a standard 28-day , commencing immediately after , which usually occurs around day 14, and concluding with the onset of on day 28. This phase represents the latter half of the cycle, during which the forms from the ruptured and prepares the for potential implantation. Progesterone plays a key role in maintaining the luteal phase's length by supporting endometrial development. While the luteal phase is relatively consistent across cycles compared to the , its duration can vary from 10 to 16 days in healthy women, with a mean length of approximately 14 days; lengths of 9 days or fewer are often considered indicative of irregularities such as luteal phase defect. If fertilization and implantation occur, the phase extends beyond the typical endpoint into early pregnancy, preventing the decline in progesterone that would otherwise trigger . Several factors can influence the consistency and length of the luteal phase. Age-related changes, particularly during perimenopause, may lead to increased variability and shorter durations due to declining ovarian function. Stress has been linked to reduced progesterone levels during this phase, potentially contributing to shortened or inadequate luteal function. Additionally, health conditions such as dysfunction can disrupt luteal phase adequacy, resulting in irregularities that affect cycle timing. The duration of the luteal phase is primarily governed by hormonal regulation, specifically the lifespan of the corpus luteum and sustained progesterone production. There is no strong scientific evidence that intense sexual activity, orgasm, or associated uterine contractions shorten the luteal phase or cause menstruation to begin sooner after ovulation. Anecdotal reports occasionally suggest that uterine contractions might slightly accelerate the onset of bleeding if menstruation is already imminent, but such effects are inconsistent, minor, and not supported by robust clinical studies. In contrast, some observational research has associated the presence of sexual intercourse during the cycle with slightly longer luteal phase durations (e.g., mean 11.4 days versus 10.8 days in cycles without intercourse) and a lower likelihood of luteal phase deficiency, potentially indicating improved luteal function and fecundability.

Hormonal Regulation

Key Hormones

The luteal phase is characterized by the production of key hormones primarily from the , which forms from the ruptured following . Progesterone is the dominant secreted by the during this phase, serving as the primary regulator essential for reproductive processes. The also produces , particularly , in secondary amounts, which complements progesterone's actions in maintaining the hormonal milieu post-ovulation. Luteinizing hormone (LH), secreted by the gland, plays a crucial role in supporting the 's function throughout the luteal phase. LH acts as the primary luteotropic factor, stimulating the development and ongoing steroidogenesis within the . In the event of fertilization and implantation, (hCG), produced by the developing embryo and early placenta, takes over to sustain activity. hCG mimics LH's effects, binding to the same receptors to prolong progesterone secretion and prevent luteal regression.

Dynamics of Hormone Production

Following ovulation, progesterone production by the begins to rise sharply, reaching peak levels of approximately 25 mg per day around 8-9 days post- (mid-luteal phase, typically days 20-22 in a 28-day cycle). This elevation is driven by (LH) stimulation and supports endometrial preparation for potential implantation. If does not occur, progesterone levels start to decline after this peak, falling to baseline by the end of the luteal phase, which triggers the onset of . Estrogen levels, primarily , exhibit a distinct pattern during the luteal phase. Post-ovulation, initially decreases from pre-ovulatory highs but experiences a secondary rise in the mid-luteal phase, peaking alongside progesterone before dropping sharply toward the phase's end. This fluctuation alters the estrogen-to-progesterone ratio, facilitating progression through the cycle by modulating endometrial receptivity and inhibiting further follicular development. Hormonal regulation involves intricate feedback loops. Progesterone and exert on the hypothalamic-pituitary axis, suppressing (GnRH) pulse frequency and thereby inhibiting (FSH) and LH secretion to prevent new follicle maturation. In the event of pregnancy, (hCG) from the implanting embryo provides positive feedback, rescuing the and sustaining progesterone production to maintain the . The decline phase is marked by luteolysis, the regression of the , which typically initiates around 9-11 days post-ovulation (approximately day 25 in a 28-day cycle). This process is primarily mediated by prostaglandin F2α (PGF2α) secreted from the , with the precise triggers in humans involving additional factors such as oxytocin pulses; the declining hormonal milieu contributes to the rapid drop in both progesterone and , removing negative feedback inhibition and allowing FSH to rise, thereby initiating the .

Physiological Changes

Ovarian Changes

Following ovulation, the ruptured ovarian follicle undergoes rapid transformation known as luteinization, where granulosa and theca interna cells differentiate into large and small luteal cells, respectively, forming the within 6-12 hours. This process is triggered by the preovulatory (LH) surge, which induces cellular , proliferation, and the expression of steroidogenic enzymes in these cells. The is a highly vascularized endocrine structure, characterized by extensive that supplies nutrients and oxygen to support its secretory role; this vascular network develops rapidly post-formation, peaking around day 7 after . Luteal cells accumulate droplets rich in esters, which impart the structure's distinctive yellow (luteal) appearance and serve as precursors for synthesis. The gland consists of a central cavity remnant of the follicle, surrounded by layers of luteinized cells embedded in , enabling efficient secretion of progesterone as its primary function. Maintenance of the relies on pulsatile LH stimulation from the pituitary, which sustains luteal cell viability and progesterone production for approximately 10-12 days in the absence of . If fertilization occurs, (hCG) from the developing embryo rescues the by mimicking LH action, prolonging its lifespan and progesterone output for 6-8 weeks until the assumes hormonal support. In the non-pregnant cycle, regression—or luteolysis—begins around day 10-12 post-ovulation, initiated by intraovarian production of , which binds to receptors on luteal cells, triggering , reduced , and cessation of steroidogenesis. This leads to structural degeneration, with luteal cells undergoing , , and hyalinization, ultimately forming a white scar-like remnant known as the .

Uterine and Endometrial Changes

During the luteal phase, the undergoes a secretory transformation primarily driven by progesterone, shifting from proliferation to differentiation to support potential implantation. This involves the development of coiled glands that secrete nutrients, with increased stores in epithelial cells to provide reserves. Glandular changes include the formation of tortuous, saw-toothed glands filled with subnuclear vacuoles in the early secretory period, progressing to supranuclear vacuoles and secretory material by mid-phase, enhancing the endometrium's nutritive capacity. increases as spiral arteries elongate and coil more prominently, expanding their surface area to facilitate nutrient delivery to the functional endometrial layer. Stromal alterations feature progressive , starting superficially post-ovulation and becoming generalized, alongside early pre-decidualization where stromal cells enlarge and accumulate , preparing for potential decidual response. Concurrently, progesterone induces leukocytic infiltration into the stroma, with acidophilic cells decreasing as leukocytes increase, contributing to immune modulation. Cervical mucus thickens into a viscous, paste-like plug under progesterone influence, forming a barrier that impedes ascent and penetration while maintaining uterine protection. In the absence of implantation, declining progesterone levels trigger of spiral arteries, leading to ischemia and breakdown of the functional layer. This results in shedding of the superficial endometrium as , with the basal layer preserved for regeneration in the subsequent cycle.

Symptoms and Effects

Physical and Emotional Symptoms

During the luteal phase of the , a rise in progesterone levels contributes to various physical symptoms experienced by many menstruating individuals. Common manifestations include tenderness and swelling, abdominal due to fluid retention, abdominal cramps, increased , headaches, and cravings for specific foods, particularly those high in carbohydrates or sweets. These symptoms are generally mild and self-limiting, resolving with the onset of . Emotional symptoms during this phase often stem from fluctuations in both and progesterone levels, which can influence activity and mood regulation. Individuals may notice mood swings, heightened , increased anxiety, or transient feelings of depression, typically appearing as the phase progresses. These affective changes are linked to the relative decline in toward the end of the luteal period, exacerbating emotional sensitivity in some cases. The intensity and presence of these physical and emotional symptoms exhibit considerable variability among individuals, influenced by factors such as overall cycle regularity, age, and lifestyle elements like stress or diet. Symptoms vary widely, with many individuals experiencing no symptoms at all or only mild ones, such as bloating or mood changes, while others may have abdominal cramps or more pronounced effects. The absence of specific symptoms, including abdominal cramps, is a common normal variation attributable to individual differences in hormonal responses. Symptoms often intensify during the late luteal phase, closer to , but remain mild and within a normal range for most menstruating people, affecting daily functioning minimally without indicating underlying . The lack of such symptoms is typically not a cause for concern unless accompanied by other signs of reproductive or health issues.

Relation to Premenstrual Syndrome

Premenstrual syndrome (PMS) is defined as a recurrent disorder characterized by a cluster of somatic, cognitive, and affective symptoms that manifest during the late luteal phase of the menstrual cycle, causing significant distress or functional impairment, and resolve within a few days after the onset of menstruation. A severe variant, premenstrual dysphoric disorder (PMDD), affects approximately 3-8% of women and is recognized in the DSM-5 with stricter criteria. These symptoms, which can include mood swings, irritability, fatigue, bloating, and breast tenderness, are absent or minimal during the follicular phase. Globally, PMS affects up to 47.8% of women of reproductive age, with approximately 20-30% experiencing severe symptoms that substantially interfere with daily life and work. The luteal phase connection arises primarily from the hormonal milieu, where symptoms intensify in the late stage due to the precipitous drop in progesterone and levels as the regresses. This hormonal withdrawal is thought to trigger PMS through altered production, which influences function in the , and disrupted serotonin signaling, as estrogen decline correlates with reduced serotonin availability. General symptoms of the luteal phase, such as mild or mood changes, may represent a less intense precursor to the patterned exacerbation seen in PMS. Diagnosis requires prospective tracking to confirm that symptoms emerge 5 to 11 days prior to menses, peak in severity just before , and are not present in the week post-menses or during other cycle phases. strategies target luteal imbalances through interventions like exercise and dietary adjustments, intermittent use of selective serotonin reuptake inhibitors (SSRIs) to stabilize mood, and hormonal therapies such as combined oral contraceptives to suppress and stabilize levels.

Clinical Significance

Associated Disorders

The luteal phase defect (LPD), also known as luteal phase deficiency, is characterized by a shortened luteal phase duration of less than 10 days or inadequate progesterone production by the , leading to insufficient endometrial development. Potential causes include disruptions in the hypothalamic-pituitary-ovarian axis, such as abnormal or inadequate stimulation, as well as external factors like or excessive exercise that impair function. Diagnosis typically involves assessing luteal phase length through tracking, measuring mid-luteal serum progesterone levels (with values below 10 ng/mL sometimes used as a threshold, though this is arbitrary and not validated), or performing an endometrial to evaluate secretory transformation, though the latter is less commonly used due to its invasiveness. However, the diagnosis and clinical significance of LPD remain controversial, with no validated tests or treatments shown to improve outcomes in natural cycles. Modern has refined earlier concepts of "inadequate luteal phase" by recognizing LPD as a multifactorial condition rather than a singular entity, emphasizing progesterone resistance in the alongside production deficits. Premenstrual dysphoric disorder (PMDD) represents a severe variant of premenstrual symptoms, primarily involving significant mood disturbances such as , depression, and anxiety that occur exclusively during the luteal phase and resolve post-menses. It affects approximately 3-8% of menstruating women, with symptoms meeting diagnostic criteria for at least five affective or somatic changes in most cycles. Genetic factors, including variations in the ESR1 gene encoding , contribute to susceptibility, while altered systems—particularly serotonin signaling—play a key role in the cyclic exacerbation of mood symptoms due to luteal phase hormone fluctuations. Luteal phase bleeding manifests as abnormal mid-cycle or intermenstrual spotting, often resulting from endometrial instability during progesterone withdrawal or exposure. This condition is frequently linked to , where unopposed leads to irregular endometrial proliferation and breakthrough bleeding, or structural issues like endometrial polyps that disrupt the vascular integrity of the luteal-phase . Hyperprolactinemia, an elevated serum level, adversely affects the luteal phase by interfering with function, often resulting in shortened phase duration and reduced progesterone output. This disruption occurs through prolactin-mediated suppression of and , impairing follicular development and luteal maintenance, and is commonly observed in conditions like prolactinomas.

Role in Fertility and Reproduction

The luteal phase is essential for , as it establishes a narrow of uterine receptivity for implantation. Progesterone produced by the induces endometrial proliferation and secretory transformation, thickening the lining to support attachment. This implantation typically spans cycle days 20 to 24 in a standard 28-day , aligning with the arrival of the fertilized egg in the approximately 6 to 10 days post-ovulation. Upon successful fertilization, the luteal phase sustains early through a critical rescue mechanism. The implanting secretes (hCG), which signals the to persist and continue progesterone secretion, preventing luteolysis and endometrial shedding. This hormonal support maintains the for about 8 to 10 weeks, after which the assumes primary progesterone production to nurture fetal development. Inadequate luteal phase function has been associated with impaired and implicated in approximately 3.7% to 20% of cases, potentially contributing to disrupted endometrial receptivity, implantation failure, or early , though not proven as an independent cause. Observational studies have associated sexual intercourse during the menstrual cycle with longer luteal phase durations and higher fecundability compared to cycles without intercourse, though these associations do not establish causality. In assisted reproduction techniques like fertilization (IVF), luteal phase support with exogenous progesterone is routinely administered starting shortly after retrieval to replicate natural conditions and time transfers for optimal implantation success. From an evolutionary perspective, the luteal phase enhances by synchronizing peak uterine receptivity with the limited viability of gametes and the preimplantation , an that originated by extending the ancestral ovarian cycle to support in eutherians.

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