Symptoms of High Cortisol Levels in Females: What to Look Out For

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Medically reviewed

Written by

Dr Paul Watson

Medically reviewed by

Dr Han Simpson

Published

April 7, 2026

Medical review date

September 8, 2026

Evidence searched through

September 8, 2026

Next review due

September 8, 2027

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General Readers & Patients

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Worldwide

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A woman in her 30s comes to clinic with a familiar set of complaints. She is exhausted, gaining weight around her middle, sleeping poorly, and feels emotionally unlike herself. Her periods have become unpredictable. Someone has already told her it is probably stress, probably age, probably lifestyle. That is where clinicians can miss the signal. The symptoms of high cortisol levels in females are often common in isolation and much more specific in combination.

Fatigue alone is nonspecific. Weight gain alone is nonspecific. Mood change alone is nonspecific. But central weight gain plus menstrual disruption plus new facial hair plus easy bruising should change the conversation.

Hypercortisolism is a classic mimicker. It can resemble PCOS, depression, hypothyroidism, metabolic syndrome, or the cumulative wear of a difficult year. In women, it also has a distinctly reproductive and dermatologic footprint that is easy to dismiss if each symptom gets managed separately by a different clinician.

That matters because untreated cortisol excess does not stay cosmetic. It affects blood pressure, glucose handling, bone, muscle, sleep, and psychiatric health. The practical challenge is not memorizing a long symptom list. It is learning to recognize the pattern early enough to investigate it properly.

Introduction When Common Symptoms Mask a Deeper Issue

A woman arrives in clinic after seeing three different specialists in one year. Gynecology has addressed irregular periods. Dermatology has treated acne and new facial hair. Primary care has documented weight gain, higher blood pressure, and poor sleep. Psychiatry has considered anxiety or depression. Each conclusion is plausible on its own. The missed question is whether all of these changes began as one endocrine problem with several disguises.

That pattern matters in women because cortisol excess often presents through reproductive and dermatologic clues before anyone names the metabolic disorder underneath. Hypercortisolism is uncommon, with endogenous Cushing syndrome affecting about 10 to 15 people per million annually according to the National Institute of Diabetes and Digestive and Kidney Diseases overview of Cushing syndrome. Its rarity does not make it optional in the differential. It makes pattern recognition more important.

Female patients are often missed for a practical reason. Their symptoms overlap with diagnoses clinicians see every day. Hirsutism can be filed under PCOS. Amenorrhea can be attributed to energy imbalance or hypothalamic dysfunction. Pelvic pain and cycle disruption may already be anchored to endometriosis. Mood change can be labeled primary psychiatric disease. Weight gain may trigger generic lifestyle advice before anyone asks whether the distribution, timing, and accompanying signs fit cortisol excess.

The endocrine logic is similar to hearing the same alarm from different rooms in the house. Each room suggests a local problem. One source can explain all of them.

A useful clinical habit is to group symptoms by system, then ask whether they evolved together. In women, the combination of central weight gain, menstrual change, easy bruising, proximal muscle weakness, new androgenic features, sleep disruption, or worsening glycemic control should prompt a more organized review. That is especially true when a patient already carries a diagnosis such as PCOS, because cortisol excess can imitate it, intensify it, or hide behind it.

When metabolic, reproductive, skin, and mood symptoms shift at the same time, look for one hormonal driver before treating each complaint as a separate problem.

Three bedside questions can sharpen suspicion early:

• Where has the weight changed most: face, abdomen, supraclavicular area, upper back, or diffusely?
• How has reproductive function changed: longer cycles, skipped periods, infertility, lower libido, or worsening premenstrual symptoms?
• Which associated signs appeared in parallel: bruising, muscle weakness, insomnia, hypertension, hyperglycemia, acne, or increased terminal hair growth?

These questions do more than build a symptom list. They help distinguish ordinary stress from a pathologic cortisol pattern and highlight the female-specific presentations that are easiest to dismiss when PCOS, endometriosis, depression, or simple “burnout” already seem to explain the case.

Understanding Cortisol and the HPA Axis

A clinician evaluating possible hypercortisolism needs a clear mental model of how cortisol is regulated. Without that model, it is easy to misread a mixed picture of fatigue, menstrual disturbance, weight redistribution, acne, insomnia, and mood change as several unrelated problems instead of one endocrine process with effects across multiple organs.

Cortisol production is governed by the hypothalamic-pituitary-adrenal axis, or HPA axis. The hypothalamus releases corticotropin-releasing hormone. That stimulates the pituitary to secrete adrenocorticotropic hormone. ACTH then drives the adrenal cortex to produce cortisol.

This sequence matters because each level can become abnormal for a different reason. The hypothalamus and pituitary may overdrive the system. The adrenal gland may produce cortisol autonomously. Exogenous glucocorticoids can also create the same downstream state. In practice, symptoms reflect the final biologic exposure to cortisol, while the evaluation must still identify where the signal originates.

Normal cortisol secretion is pulsatile and strongly circadian. Levels are highest in the early morning, then decline through the day and should be low late in the evening. That timing helps coordinate alertness, glucose availability, vascular tone, and immune activity.

Amount and timing both matter.

In pathologic hypercortisolism, the body may produce too much cortisol, fail to suppress cortisol at the appropriate time, or both. Late-night cortisol is especially informative because nighttime should be a physiologic quiet period. When that signal remains inappropriately active, patients may report a pattern that seems contradictory at first glance. They feel tired, but wired. They are fatigued in the daytime, yet struggle to sleep. That is not vague stress language. It reflects disruption of the normal hormonal clock.

Cortisol also has tissue-specific effects that help explain why female presentations are often missed. It raises hepatic glucose output, opposes insulin action, promotes protein breakdown in muscle, alters fat distribution, affects skin and connective tissue, suppresses gonadotropin signaling, and can increase androgenic features through adrenal pathways. In a woman who already carries a diagnosis such as PCOS, that overlap can blur the picture. Cycle irregularity, acne, hirsutism, weight gain, and subfertility may be attributed to the pre-existing diagnosis, even when cortisol excess is amplifying or imitating it.

The reproductive consequences are easy to underestimate. Chronic cortisol excess can dampen hypothalamic GnRH pulsatility, which then alters LH and FSH signaling downstream. Ovulation becomes less reliable. Cycles may lengthen or disappear. Libido may fall. In patients with endometriosis, the result can be even more confusing clinically, because pain, sleep disruption, inflammation, and hormonal treatment effects may already complicate the history.

This distinction provides the foundation for understanding the symptoms of high cortisol levels in females. The findings are not random. They represent the predictable output of a regulatory system that is overstimulated, mistimed, or no longer responding normally to feedback.

Key Symptom Clusters of High Cortisol in Females

A common clinic scenario is a woman referred for “weight gain and irregular periods” who already carries a diagnosis of PCOS. At first glance, the story seems familiar. Then the details sharpen the picture. Her rings no longer fit, her face looks fuller in photographs, bruises appear after minor bumps, blood pressure has crept up, and climbing stairs now feels strangely difficult. That pattern should shift your thinking from a single symptom to a multi-system endocrine syndrome.

The most reliable way to recognize hypercortisolism in women is to group findings into symptom clusters. Cortisol acts on metabolism, skin, muscle, mood, sleep, and reproductive signaling at the same time. Patients rarely present by saying, “I may have cortisol excess.” They present through whatever doorway is bothering them most, often gynecology, dermatology, primary care, psychiatry, or fertility care. Female-specific presentations are missed when each complaint is handled in isolation.

Metabolic clues

Cortisol-related weight change usually has a distribution pattern. Fat accumulates more in the face, trunk, and upper back, while the arms and legs may remain relatively less enlarged. Patients often describe this accurately before any formal examination. They say they are gaining weight “in a different way” than before.

This observation is clinically significant. Diffuse weight gain has a broad differential. Central redistribution paired with other endocrine features narrows it.

Glucose and blood pressure often change alongside body composition. Cortisol increases hepatic glucose output and opposes insulin action, so a patient may show worsening fasting glucose, a rising A1c, or new difficulty controlling previously stable diabetes. Hypertension may emerge during the same period. In women with presumed PCOS, this can be misleading because insulin resistance already sits in the background. The clue is not the existence of metabolic dysfunction alone, but the new combination of metabolic dysfunction with skin, muscle, and reproductive changes.

Useful screening questions include:

• Has weight increased mainly in the abdomen, face, or upper back
• Has blood pressure risen over the same time frame
• Have glucose markers worsened as other physical changes appeared

Physical and skin findings

The examination often provides the clearest signal. Cortisol weakens collagen and connective tissue, so the skin loses some of its structural support. Broad violaceous striae on the abdomen, thighs, hips, or breasts carry more diagnostic weight than the thin pale stretch marks seen with ordinary weight fluctuation. Easy bruising should also raise suspicion, especially when the bruising seems disproportionate to the degree of trauma.

A rounded face and fullness over the dorsocervical area can appear gradually enough that family members normalize the change. Muscle catabolism is similarly underrecognized. Many women say they are exhausted, but a more precise question helps: “Is it harder to rise from a chair, climb stairs, or lift objects overhead?” That wording separates generalized fatigue from proximal muscle weakness.

Women may also develop:

• Hirsutism on the face, chest, or abdomen
• Acne or more oily skin
• Thin, fragile skin
• Proximal muscle weakness

That overlap with hyperandrogenic disorders matters. If hirsutism and acne worsen while striae, bruising, or proximal weakness appear, the problem may no longer fit neatly inside a prior PCOS label.

Reproductive symptoms

Reproductive symptoms are often the most underappreciated part of the presentation. Menstrual cycles may become infrequent, irregular, or absent. Libido may fall. Fertility may decline because ovulation becomes less reliable. These patients are frequently assessed first in gynecology or fertility settings, where the leading considerations may be PCOS, hypothalamic dysfunction, thyroid disease, or treatment side effects.

The challenge is overlap. Cortisol excess can imitate PCOS, intensify pre-existing PCOS, or sit beside it. A woman with longstanding irregular cycles may still develop hypercortisolism. The clinician’s task is to notice when the clinical picture becomes wider than the original diagnosis can comfortably explain.

Endometriosis adds another layer of complexity. Pelvic pain, poor sleep, chronic stress physiology, and hormonal therapies can cloud the timeline. If the history shifts to include central adiposity, bruising, weakness, hypertension, or marked mood change, it is worth reconsidering whether cortisol excess is contributing rather than attributing every new symptom to endometriosis alone.

A practical clue is tempo. Stable chronic symptoms that suddenly broaden into a multi-system pattern deserve a new differential diagnosis.

A brief clinical refresher may help:

Neuropsychiatric and sleep symptoms

Mood and cognition belong in every endocrine history. Hypercortisolism may present with anxiety, irritability, depression, poor concentration, and the subjective sense that thinking has become slower or less reliable. These symptoms can be misassigned to chronic stress, postpartum changes, perimenopause, or the psychological burden of infertility and pain disorders.

Sleep complaints also follow a pattern. Many patients report feeling tired through the day while becoming more alert at night. That history fits with circadian disruption rather than ordinary poor sleep hygiene. If this occurs beside central weight gain, menstrual change, bruising, or weakness, the combination becomes much more informative than the sleep complaint alone.

A quick pattern-recognition summary

Cluster	Typical findings in women
Metabolic	Central weight gain, rising blood pressure, insulin resistance, worsening glycemic control
Physical	Facial rounding, upper back fullness, violaceous striae, easy bruising, proximal weakness
Reproductive	Irregular periods, absent periods, reduced libido, impaired fertility
Neuropsychiatric	Anxiety, depression, irritability, poor concentration, nonrestorative sleep

The teaching point for practice is straightforward. Hypercortisolism in women is usually recognized by pattern recognition, not by any single complaint. The diagnosis becomes easier to consider once you stop asking whether one symptom fits and start asking whether several organ systems are changing in the same direction at the same time.

The Pathophysiology Behind Female Cortisol Symptoms

A common clinic scenario is the woman labeled as having “stress,” worsening PCOS, or difficult perimenopause because she has irregular cycles, weight gain, acne, poor sleep, and low mood. The pathophysiology matters because cortisol excess can produce all of those features through one coordinated disturbance, while also reshaping how existing gynecologic or metabolic conditions present.

Cortisol disrupts reproductive signaling

Female symptoms often begin at the interface between the HPA axis and the reproductive axis. Elevated cortisol suppresses hypothalamic GnRH pulsatility, alters pituitary gonadotropin output, and can blunt normal ovarian steroid signaling. Sakra World Hospital’s overview of high cortisol symptoms in females connects that biology with irregular menstrual cycles, reduced libido, and impaired fertility.

GnRH sets the rhythm for reproductive timing. When cortisol disrupts that rhythm, LH and FSH secretion becomes less coordinated, ovulation becomes less reliable, and the menstrual cycle may lengthen, shorten, or disappear. In practice, this is one reason hypercortisolism in women is easy to misread as functional hypothalamic dysfunction, PCOS, or a nonspecific response to chronic illness.

The effect is often more confusing in patients who already carry a diagnosis such as PCOS or endometriosis. Cortisol excess can layer cycle disruption on top of baseline ovulatory dysfunction, making the menstrual history look familiar while the underlying driver has changed.

Cortisol alters androgen balance

Cortisol excess may also increase adrenal androgen production. That helps explain why some women present with hirsutism, acne, or scalp hair thinning alongside metabolic and menstrual complaints.

For residents, the useful mental model is overlap with distortion. Hypercortisolism can imitate parts of PCOS, but it rarely stops there. The woman with new androgenic symptoms plus bruising, proximal muscle weakness, skin thinning, or broader catabolic features is not showing a simple isolated androgen disorder. She may be showing the combined effects of glucocorticoid excess on adrenal output, gonadal signaling, connective tissue, and muscle protein balance.

That distinction changes management. If cortisol is the upstream driver, treating only the cosmetic or reproductive manifestations will miss the endocrine disorder generating them.

Circadian disruption explains the tired but wired pattern

Cortisol symptoms in women also reflect mistimed secretion, not just excess quantity. Under normal conditions, cortisol peaks in the early morning and falls overnight. In hypercortisolism, that daily slope can flatten. A patient may feel exhausted during the day yet become alert at night because the signal that should quiet down has stayed active.

High nocturnal cortisol also helps explain fragmented sleep, early morning awakenings, and the sense of being physiologically activated despite fatigue. Clinically, that pattern becomes more informative when it appears beside menstrual change, central adiposity, or mood symptoms, because it points toward endocrine circadian disruption rather than isolated poor sleep habits.

Why body composition changes in a characteristic way

Cortisol acts on adipose tissue, liver, skeletal muscle, and pancreatic glucose regulation at the same time. The result is a shift toward visceral fat accumulation, increased hepatic glucose output, reduced insulin sensitivity, and progressive muscle breakdown.

That combination explains a pattern many women describe clearly. Their waist circumference rises, their limbs may not enlarge proportionally, and daily function worsens because proximal muscles are weaker even before formal testing shows it. The body is being pushed to store fuel centrally while dismantling peripheral protein stores. In endocrinology, that is a recognizable hormonal pattern, not a failure of effort.

Skin and connective tissue findings are part of the same biology

The skin findings are not cosmetic side notes. Cortisol impairs collagen synthesis and weakens connective tissue integrity. That is why women with cortisol excess may develop easy bruising, wide violaceous striae, slower healing, and skin that feels thinner or more fragile.

These clues matter because they often separate hypercortisolism from overlapping conditions. PCOS can explain hirsutism and irregular cycles. It does not explain classic skin fragility well. Endometriosis can explain pain and fatigue. It does not explain proximal myopathy or broad catabolic skin changes.

The clinical takeaway

Female cortisol symptoms are best understood as linked consequences of one hormonal disturbance affecting reproductive timing, androgen balance, circadian signaling, metabolism, muscle, and connective tissue. That framework helps clinicians avoid a common error in women. Assigning each symptom to a different familiar diagnosis instead of asking whether one endocrine process is driving all of them at once.

Distinguishing Hypercortisolism Differential Diagnosis and Investigations

The diagnostic work begins with restraint and pattern recognition. Not every woman with fatigue, weight gain, and irregular periods has Cushing syndrome. But not every such patient has uncomplicated PCOS or lifestyle-related stress either.

Start with the mimickers

Several conditions overlap with hypercortisolism:

• PCOS, because of hirsutism, cycle irregularity, and metabolic features
• Hypothyroidism, because of fatigue, weight change, and low mood
• Depression, because mood change, sleep disturbance, and reduced energy are prominent
• Metabolic syndrome, because central adiposity, hypertension, and glucose abnormalities are common

The discriminating step is to ask whether signs from different systems are occurring together in a way that points to cortisol excess.

Differential Diagnosis High Cortisol Symptoms vs Mimickers

Feature	High Cortisol (Cushing’s)	PCOS	Hypothyroidism	Depression
Weight pattern	Central gain with face and upper back prominence	Variable, often central	Generalized gain or fluid retention feel	Variable
Menstrual pattern	Irregular or absent periods, often with broader systemic signs	Irregular periods common	Can be irregular	Can be altered indirectly
Hair changes	Hirsutism may occur with skin fragility clues	Hirsutism common	Hair thinning more typical than hirsutism	Not a defining feature
Skin findings	Purple striae, easy bruising, thin skin	Acne may occur, classic striae less typical	Dry skin more typical	No characteristic endocrine skin pattern
Muscle symptoms	Proximal weakness	Not typical as a core sign	Fatigue more than proximal weakness	Low energy more than true weakness
Sleep and mood	Tired but wired pattern, anxiety or depression	Variable	Sluggishness and somnolence more common	Primary mood symptoms dominate
Blood pressure and glucose	Often rise alongside other signs	Metabolic issues may occur	Less characteristic pattern	Secondary changes possible

Screening tests that make sense clinically

The Cleveland Clinic review of cortisol notes that up to 80% of women with Cushing syndrome experience hirsutism and menstrual irregularities, and that diagnostic delays average 2 to 3 years. The same source highlights multimodal testing, including late-night salivary cortisol, where more than 4 nmol/L offers 95% sensitivity, and the low-dose dexamethasone suppression test, where failure to suppress below 1.8 mcg/dL is indicative.

That delay is the practical reason to test when the pattern is persuasive.

First-line biochemical screening

1. Late-night salivary cortisol
   Useful because cortisol should be low at night. An elevated late-night value suggests loss of normal circadian suppression.

2. Low-dose dexamethasone suppression test
   This asks whether an external glucocorticoid signal can appropriately suppress cortisol production. Failure to suppress raises concern for autonomous or dysregulated cortisol production.

3. 24-hour urinary free cortisol
   Helpful when you need an integrated measure across a full day rather than a single time point.

Common pitfalls

False reassurance often comes from ordering one test in the wrong context and stopping there. Timing matters. Medication history matters. Shift work, estrogen exposure, and exogenous steroid use can complicate interpretation.

Residents should ask directly about:

• Prednisone, dexamethasone, methylprednisolone, inhaled steroids, topical steroids, or joint injections
• Sleep schedule, especially night-shift work
• Recent severe illness or acute stress
• Hormonal medications

If the pretest suspicion is high, use more than one screening approach and interpret the result in clinical context.

Determining the source

Once biochemical evidence supports hypercortisolism, the next question is cause.

Broadly, think in two buckets:

• Exogenous cortisol exposure, such as prolonged corticosteroid therapy
• Endogenous overproduction, often requiring ACTH-based evaluation and targeted imaging

The investigation sequence should be deliberate. Confirm excess first. Localize second. Imaging before biochemical confirmation creates noise and incidental findings that may mislead rather than help.

Management Principles for High Cortisol Levels

Treatment only works when it targets the driver. Symptom management alone rarely solves the problem.

Treat the cause, not just the consequences

When cortisol excess is exogenous, management usually means reviewing the steroid regimen carefully and tapering when clinically safe. That must be done thoughtfully. Abrupt withdrawal can create its own dangers.

When cortisol excess is endogenous, treatment depends on source. Pituitary disease, adrenal disease, and ectopic ACTH production require different strategies. Surgery is often central when a resectable lesion is identified. Some patients need medical therapy to reduce cortisol production or block its effects. Others need radiation as part of longitudinal care.

The common error is trying to “out-lifestyle” a hormonal disease.

According to Ubie Health’s discussion of high cortisol in women, high cortisol drives visceral fat accumulation by upregulating glucocorticoid receptors in adipose tissue and impairs insulin sensitivity through enhanced hepatic glucose production. That helps explain why some women gain weight despite unchanged caloric intake, and why conventional dieting may be ineffective if the hormonal source is not addressed.

Manage the complications in parallel

A patient with hypercortisolism does not have one problem. She usually has several interacting ones.

That means a real management plan should include:

• Blood pressure control
• Glucose management
• Bone protection and fracture risk assessment
• Psychiatric support
• Sleep evaluation
• Muscle rehabilitation and fall-risk awareness

Some of these improve after the cortisol source is treated. Some persist and need direct care.

Why integrated management is not optional

Residents sometimes think full management can wait until after definitive endocrine treatment. In practice, that is risky.

A woman with cortisol excess may arrive with hypertension, dysglycemia, weakness, low mood, and poor sleep all at once. If you address only the lesion and ignore the physiology already in motion, she remains vulnerable while waiting for endocrine recovery.

The root cause deserves priority, but the comorbidities deserve action on day one.

A practical treatment mindset

Three principles keep management grounded:

First, identify whether steroids from outside the body are contributing. This includes oral, injected, inhaled, and topical formulations.

Second, coordinate care across specialties. Endocrinology, primary care, gynecology, psychiatry, and sometimes surgery all have roles.

Third, set realistic expectations. Patients often want to know whether every symptom will disappear quickly. Recovery is usually uneven. Blood pressure, glucose, mood, body composition, sleep, and menstrual function may improve on different timelines.

That conversation matters because many women with symptoms of high cortisol levels in females have already been told the changes were their fault. A clear medical explanation can be therapeutic in itself.

The Overlooked Link Between Cortisol PCOS and Endometriosis

The usual teaching separates endocrine disorders into neat boxes. Real patients do not cooperate with that structure.

A woman with PCOS may also have stress-related cortisol dysregulation or true hypercortisolism. A woman with endometriosis may experience symptom amplification when stress physiology remains chronically activated. If the clinician insists on treating each label in isolation, important interactions get missed.

PCOS and cortisol can amplify each other

Benenden Hospital’s discussion of high cortisol in females describes emerging data suggesting chronic stress is linked to significantly higher cortisol in PCOS patients, amplifying insulin resistance and hirsutism. That emerging signal is still useful. It highlights a common blind spot. When a woman with PCOS reports worsening cycle irregularity, increasing facial hair, poorer sleep, and harder-to-control weight, clinicians often intensify standard PCOS management without reassessing the stress-hormone side of the picture.

Endometriosis deserves the same integrative thinking

The relationship with endometriosis is less quantified in the material provided, but the clinical logic is strong. Cortisol dysregulation can disturb sex hormone balance and worsen the lived burden of pelvic pain, sleep disruption, fatigue, and mood symptoms.

This does not mean cortisol is the sole cause of endometriosis symptoms. It means the hormonal environment can shape symptom intensity and resilience.

What to do in clinic

For residents, the practical lesson is to ask whether the patient’s “baseline diagnosis” still explains the full picture.

Consider deeper evaluation when you see:

• A known PCOS patient with new easy bruising, proximal weakness, or central fat redistribution
• A patient with endometriosis whose sleep and mood have deteriorated alongside metabolic changes
• A fertility patient whose cycle dysfunction is broader than expected for the known diagnosis

In women already discussing ovulation treatment or fertility pathways, it can help to place cortisol in the broader hormonal conversation. Related fertility discussions often intersect with choices such as letrozole vs clomid, but ovulation-focused decisions should not distract clinicians from identifying a cortisol-driven pattern when one is present.

A prior diagnosis should guide thinking, not trap it.

A better clinical frame

Instead of asking, “Does she have PCOS or cortisol excess?” it is often better to ask, “Is cortisol excess worsening an existing reproductive endocrine disorder?”

That shift changes management. It encourages clinicians to look beyond symptom suppression and consider sleep timing, psychiatric burden, steroid exposure, metabolic health, and formal cortisol testing when the pattern warrants it.

Conclusion Key Takeaways and Curated References

The symptoms of high cortisol levels in females become easier to recognize when you stop chasing single complaints and start looking for a coordinated endocrine pattern. In women, the pattern often spans weight distribution, skin, menstrual function, mood, sleep, and metabolic health.

Key clinical takeaways

• Think in clusters. Central weight gain, hirsutism, menstrual irregularity, easy bruising, proximal weakness, and sleep disruption are more meaningful together than apart.
• Respect the female-specific pattern. Reproductive changes and androgen-related symptoms may be the earliest clues.
• Confirm biochemically. Cortisol disorders should be tested, not guessed.
• Treat the source and the fallout. Blood pressure, glucose, bone health, mood, and sleep need active management while the cause is being addressed.
• Revisit old labels. PCOS or endometriosis may coexist with cortisol-related dysfunction rather than fully explain the presentation.