A Root-Cause Approach to Menopausal Insomnia and Brain Dysfunction: A Case Study

Discover how a 48-year-old woman overcame chronic insomnia, fatigue, and cognitive decline during menopause through a personalized, brain-first, hormone-balancing approach.

Stephanie Yang, ND

Abstract

Menopause is not only a hormonal milestone but also a neurological transition that can significantly affect sleep, cognition, and emotional regulation. This case study follows a 48-year-old woman experiencing chronic insomnia, cognitive decline, mood instability, and fatigue after the onset of menopause—despite an otherwise healthy lifestyle. Standard lab work failed to reveal a clear cause, but functional testing uncovered low sex hormones, elevated evening cortisol, and key nutrient deficiencies. Treatment began with nervous system and HPA axis support to stabilize circadian rhythms, followed by carefully introduced bioidentical hormone therapy. The patient experienced profound improvements in sleep quality, cognitive clarity, mood, and overall vitality. This case illustrates the importance of a brain-first, root-cause approach to menopausal care—addressing neuroendocrine function and resilience before introducing hormone replacement to ensure optimal outcomes.

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Introduction

Menopause is a major hormonal milestone that impacts not only the body but also the brain. It is preceded by perimenopause—the transitional phase that typically begins in a woman’s 40s—when levels of estrogen, progesterone, and testosterone start to fluctuate. Menopause is defined as 12 consecutive months without a menstrual period, with the average onset occurring around age 51 (range: 45–55). During this period, many women experience symptoms such as insomnia, brain fog, mood swings, and fatigue—often mistaken for stress, anxiety, or normal aging.

This case follows a 48-year-old woman who had not experienced a period for over a year, confirming the onset of menopause. She struggled with persistent insomnia, forgetfulness, emotional reactivity, and chronic fatigue, despite maintaining a healthy lifestyle. Although routine lab tests appeared normal, she felt unlike her usual self. Functional testing revealed low levels of progesterone, estrogen, and testosterone, elevated evening cortisol, and several key nutrient deficiencies—all contributing to her symptoms.

Treatment commenced with support for the nervous system, stress regulation, and correction of nutritional imbalances. Once her foundation was more stable, we introduced gentle bio-identical hormone therapy tailored to her needs. She experienced consistent improvements: deeper sleep, enhanced focus, a more stable mood, and a renewed sense of vitality.

This case highlights how both perimenopause and menopause are not merely hormonal events, but brain-based transitions. A brain-first, root-cause approach—supporting the HPA axis and neuroendocrine balance before introducing bio-identical hormones—can lead to more effective, lasting results in helping women feel like themselves again.

Case Presentation 

Patient Profile

• Name: Sophia (pseudonym)
• Age: 48
• Gender: Female
• Occupation: Project manager, tech firm
• Primary Concerns: Insomnia, brain fog, mood swings, fatigue

S: Subjective Findings

Sophia has reported persistent sleep difficulties for more than 18 months, including trouble falling asleep, frequent awakenings, and unrefreshing rest. She felt constantly fatigued. Cognitive symptoms included forgetfulness, finding words, difficulty concentrating, and impaired executive function. These changes impacted her work performance and strained her relationships at home.

She also described an increase in emotional sensitivity—crying easily, feeling overwhelmed by daily tasks, and experiencing anxiety and irritability without a clear cause. Her menstrual cycles had become irregular and shorter before stopping entirely over a year ago, marking the transition into menopause. She recalled occasional spotting, breast tenderness, and mood swings during that period.

Despite maintaining a healthy lifestyle—daily walks, a whole-food diet, and regular stress management—Sophia felt “wired but tired,” disconnected from herself, and on the brink of burnout.

O: Objective Findings

Vitals: BP 100/71 mmHg, HR 73 bpm, BMI 24.1
Physical Exam: Oriented, fatigued appearance, emotionally subdued
Mental Health Screens:

• GAD-7: 13 (moderate anxiety)
• PHQ-9: 11 (moderate depression)

Laboratory Evaluation

Collected post-menopause (≥12 months without menses):

Hormonal Imbalances

Marker	Result	Clinical Interpretation
Progesterone	Low (<5 ng/mL)	Reflects loss of ovulation; contributes to reduced GABA activity, impacting sleep and mood
Estradiol	Low	Consistent with postmenopausal status; contributes to hot flashes, mood swings, and cognitive changes
Testosterone	Low	May contribute to decreased motivation, cognitive clarity, and libido
FSH (Follicle Stimulating Hormone)	Elevated (>25 IU/L)	Persistent elevation confirms menopause; reflects loss of ovarian follicular feedback

Stress and HPA Axis Function

Marker	Result	Clinical Interpretation
DHEA-S	High-normal	Reflects compensatory HPA activity
AM Cortisol	High-normal	Blunted morning output, suggesting impaired stress response
PM Cortisol	Elevated	Disrupted diurnal cortisol rhythm

Nutrient Deficiencies

Marker	Result	Clinical Interpretation
Vitamin B12	Low-normal	Suboptimal for neurological and cognitive support
Vitamin D	Low-normal	May contribute to fatigue, mood swings, and immune dysfunction
Ferritin	Normal	Adequate iron stores, not contributing to fatigue
TSH, CBC, CMP	WNL	No evidence of anemia or thyroid/metabolic dysfunction

Interpretation:

Sophia’s lab results confirmed menopause, indicated by low estradiol, low progesterone, and persistently elevated FSH, signifying the loss of ovarian follicular activity. Low testosterone also contributed to her cognitive and motivational symptoms. Elevated evening cortisol showed circadian rhythm disruption, correlating with her insomnia, mood instability, and fatigue. Micronutrient deficiencies exacerbated neurotransmitter imbalance and hindered energy metabolism, adding to her overall sense of burnout.

Assessment

Menopausal Insomnia and Cognitive Dysfunction (G47.00, R41.3)
Hormonal decline reduced GABAergic tone and disrupted REM sleep, triggering anxiety and insomnia. 

Cyclical Emotional Dysregulation (F41.8)
Estrogen fluctuations altered serotonin and dopamine signaling, leading to low mood and reduced motivation.

HPA Axis Dysregulation (R53.83)
A flattened cortisol rhythm with elevated evening levels impaired sleep initiation and reduced stress resilience.

Micronutrient Deficiencies (Z13.21)
Suboptimal B12 and Vitamin D reduced neurotransmitter synthesis and mitochondrial function.

Differential Diagnosis

Hypothyroidism, anemia, and generalized anxiety disorder were ruled out based on labs and clinical presentation.

P: Plan

Weeks 0–2: Calm the Nervous System, Regulate the HPA Axis
Goals: Stabilize circadian rhythm, reduce cortisol levels, enhance GABA activity, and restore foundational nutrients.
Outcomes: She is sleeping longer, waking with less anxiety, and experiencing a calmer mood with more consistent energy throughout the day.

Lifestyle Interventions:

• Morning light exposure or light therapy (10,000 lux) + screen curfew (at least two hours before bedtime)
• A high-protein breakfast stabilizes blood sugar and supports cortisol rhythm.

Targeted Supplementation:

• Magnesium glycinate (400 mg at bedtime): Enhances GABA receptor function and promotes deeper, more restful sleep.
• Vitamin D3 (5,000 IU/day): Enhances serotonin synthesis, supports neuroplasticity, and regulates mood.
• Activated B Complex (methylcobalamin and methylfolate) supports methylation pathways due to a confirmed MTHFR gene variant, enhancing mood, neurotransmitter synthesis, and cognition. 
• Adaptogen blend (Rhodiola rosea, Panax ginseng, and others): Enhances resilience, boosts energy levels, and balances neurotransmitters.
• Cortisol-regulating blend (Ashwagandha, Phosphatidylserine, and others): Reduces evening cortisol levels and promotes cognitive recovery.

Weeks 4–6: Begin Bioidentical Hormone Replacement

Goals: Replenish progesterone to support GABA pathways while introducing low-dose estrogen and testosterone to enhance cognitive and emotional function.
Outcomes: By Week 6, she is experiencing deeper, uninterrupted sleep, greater emotional resilience, and noticeable improvements in memory, focus, and motivation.

Hormone Therapy:

• Oral micronized progesterone (100 mg QHS): Supports GABA activity to promote deep sleep and reduce anxiety
• Transdermal estradiol (custom-compounded, titrated dose): Enhances serotonin, acetylcholine, and dopamine pathways for mood and cognitive support
• Topical testosterone cream (personalized dosing): Restores motivation, sharpens focus, and strengthens executive function

Weeks 7–12: Deep Recovery

Outcomes: The patient reports steady energy throughout the day, a stronger presence and clarity at work, and a renewed connection with herself and her family life.
Patient Reflection: “I experienced healing sleep for the first time in years. I finally feel like myself again.”

Discussion and Conclusion

Menopause is not merely a hormonal transition; it is also a neurological one. As levels of estrogen, progesterone, and testosterone begin to decline, brain function is directly affected. These hormones play a vital role in regulating mood, sleep, memory, and stress responses. When their levels decrease, it can lead to symptoms such as insomnia, anxiety, emotional reactivity, and brain fog—even before the more commonly recognized symptoms like hot flashes emerge.

Sophia’s case serves as a clear example. While her standard lab tests appeared normal, functional testing revealed a different narrative. She exhibited low progesterone, low-normal estrogen and testosterone, elevated evening cortisol, and nutrient deficiencies. Each of these findings corresponded directly to her symptoms. Low progesterone diminishes GABA activity in the brain, making it harder to relax and sleep. Low estrogen affects serotonin and dopamine levels, resulting in mood swings and memory problems. Low testosterone may lead to reduced motivation and poor focus. Nutritional deficiencies, such as low B12 and vitamin D, further contributed to her fatigue and cognitive issues.

Research supports this clinical picture:

• Progesterone aids in calming the brain and promoting sleep by enhancing GABA activity.¹
• Estrogen influences serotonin and dopamine, which support mood and memory.²
• Testosterone enhances energy, confidence, and executive function.⁵

We began Sophia’s treatment by calming her nervous system, supporting her stress response (HPA axis), and correcting nutrient deficiencies. Only after her system became more stable did we start bioidentical hormone therapy. This stepwise, brain-first approach made the hormones more effective and better tolerated.

Sophia’s progress highlights the effectiveness of addressing menopause at its root. By prioritizing support for the nervous system, we enabled her to sleep more soundly, think more clearly, and feel emotionally stable. Her story reminds us that bio-identical hormone replacement alone is insufficient; we must first prepare the brain and body to receive this support.

When we consider both hormones and the nervous system, women can genuinely reclaim their energy, clarity, and sense of self.

References

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2. Soares CN. Mood disorders in midlife women: understanding the critical window and its clinical implications. Menopause. 2014;21(2):198-206. doi:10.1097/GME.0000000000000080
3. Bromberger JT, et al. Major depression during and after the menopausal transition: Study of Women’s Health Across the Nation (SWAN). Psychol Med. 2010;40(9):1509–1518. doi:10.1017/S0033291709991804
4. Greendale GA, et al. Cognitive performance and estradiol levels in midlife women. Neurology. 2009;72(21):1850–1857. doi:10.1212/WNL.0b013e3181a7119e
5. Davis SR, Wahlin-Jacobsen S. Testosterone in women—the clinical significance. Lancet Diabetes Endocrinol. 2015;3(12):980–992. doi:10.1016/S2213-8587(15)00286-7