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Hormonal Havoc: When Menopause or Andropause Supercharges Your Neurodivergent Superpowers (or Sabotages Them)

  • Jan 6
  • 13 min read

Dopamine Drought: How Midlife Hormonal Shifts Hijack Neurodivergent Brains


Estrogen quietly ghosts dopamine and exits stage left.

Progesterone stirs the pot.

Testosterone quietly fades.

Dopamine drops the script.


Suddenly, the neurodivergent brain is no longer running a tight operation — it’s directing a circus.


abstract blurry picture, visual  theme "distortion"
Credit to Egor Komarov via Unsplash

Welcome to the neurodivergent hormonal meltdown: a phase where executive function falters, sensory thresholds drop, and masking becomes metabolically unsustainable. What worked for decades begins to collapse. Traits once managed quietly surface — often for the first time, in full view.


This is not just a women’s issue. Similar dynamics emerge in andropause, driven by different hormones but governed by the same nervous system principles.


So no — this does not create chaos.

It reveals it.


Especially in neurodivergent brains that have long been running complex systems on borrowed neurochemical fuel.

What follows is not failure, but exposure. And with the right understanding of hormones, nervous system regulation, food, and fasting, it is also modifiable — and often reversible in impact.

The Big Reframe: Menopause, Midlife & the Neurochemical Shift

Menopause is often framed as a reproductive milestone.

Midlife crisis is often framed as a psychological or existential one.


For neurodivergent people, both are better understood as neurochemical events.

When estrogen and progesterone fluctuate and decline in women — and when testosterone gradually wanes in men — the effects are not confined to mood or energy. They directly alter the neurotransmitter systems that neurodivergent brains rely on most.


Hormonal shifts in midlife directly affect:

  • Dopamine availability and receptor sensitivity (motivation, focus, executive function)

  • Serotonin stability (mood regulation, social buffering)

  • GABA regulation (sensory gating, sleep quality)

  • Cortisol recovery curves (stress tolerance and recovery speed)


For many neurodivergent adults — especially those diagnosed later in life (40+) — this transition is often experienced as:

“I didn’t suddenly get worse — I just can’t compensate anymore.”
visual:TRAIT VISIBILITY & DIAGNOSIS
*Not new - now visible
MASKING & COMPENSATION
*Becomes metabolically unsustainable
HORMONAL BUFFERING
*Declines during midlife
NEURODIVERGENT TRAITS
*Stable across the lifespan
Midlife doesn't create neurodivergence.
It removes the hormonal buffering that kept it compensaated.

What collapses here is not ability, but masking capacity under hormonal load.

This Is Not Just ADHD

Although ADHD is often the most visible during midlife transitions, the underlying mechanism affects multiple neurodivergent profiles, across genders.


Autism & AuDHD

Hormonal shifts frequently lead to:

  • Lower sensory thresholds

  • Weakened social buffering

  • Prolonged recovery time after stress or interaction

  • Masking becoming neurologically and energetically unsustainable


HSP (Highly Sensitive Nervous Systems)

Midlife neurochemical changes can result in:

  • Intensified emotional absorption

  • Faster onset of overstimulation

  • Rising ethical strain, empathy fatigue, and nervous system exhaustion


Dyslexia & Dyspraxia

As hormonal buffering drops:

  • Cognitive load tolerance decreases

  • Sequencing, planning, and motor coordination require more effort

  • “I used to manage this” moments become more frequent and destabilizing


Mixed Neurodivergent Profiles

Midlife transitions often unmask previously compensated combinations of traits. This can lead to confusion, misdiagnosis, or self-blame — unless the hormonal and neurochemical context is recognized.


Core Insight

Menopause and midlife do not create neurodivergence.

They remove the hormonal scaffolding that made long-term compensation possible.


What emerges is not dysfunction — but information.


And that is precisely why late diagnosis so often follows.

Hormones & the Neurotransmitter Chain Reaction in Female Bodies


Neurodivergent nervous systems tend to rely more heavily on finely tuned neurochemical support than neurotypical ones. For decades, estrogen and progesterone quietly stabilized these systems, masking strain and compensating for higher cognitive and sensory demands.

When hormonal levels fluctuate and decline during perimenopause and menopause, these support structures weaken — and previously manageable traits intensify.


Neurodivergent brains often depend more strongly on:

  • Dopamine precision (ADHD, AuDHD)

  • Sensory filtering (autism, HSP)

  • Executive scaffolding (dyslexia, dyspraxia)

  • Emotional regulation bandwidth (mixed profiles)


When hormonal buffering drops, these domains are affected simultaneously rather than in isolation.

Why Dopamine Dysregulation Devastates

Estrogen plays a central role in dopamine regulation within the prefrontal cortex, the brain region responsible for focus, planning, emotional modulation, and executive control.


During menopause (typically ages 40–55):

  • Estrogen decline reduces dopamine availability by an estimated 30–50%

  • Brain fog, impulsivity, and rejection sensitivity increase

  • Executive functioning becomes significantly more energy-intensive


At the same time, progesterone fluctuations further destabilize neurotransmitter balance:

  • Rising and crashing progesterone dampens serotonin

  • Indirect dopamine effects via GABA disrupt emotional regulation

  • Sleep quality deteriorates, compounding cognitive strain


As a result, 70–80% of neurodivergent women report increased meltdowns, masking fatigue, and emotional volatility during this phase.

Why this matters

  • Symptoms are often misattributed to “aging,” stress, or new mental health conditions

  • Careers may suffer, with reported dropout or role reduction risks of up to 50%

  • Relationships strain under increased reactivity and reduced recovery capacity


Awareness changes the trajectory:

  • Hormonal testing becomes possible

  • Nutrition and nervous-system-aware strategies can reduce symptom intensity by up to 40%

  • Regulation replaces self-blame


Core pitfall: denial and pushing through

Core benefit: reclaimed clarity, agency, and capacity

The Estrogen–Progesterone–Dopamine Dance

Estrogen’s “Glow-Up” Phase


When estrogen levels are stable or high, it:

  • Boosts dopamine production

  • Blocks dopamine reuptake and degradation

  • Enhances dopamine receptor sensitivity

  • Strengthens prefrontal cortex efficiency


Functional outcome:

  • ADHD flow states feel accessible

  • Sensory input is easier to filter

  • Mood and cognitive stamina stabilize


Menopause shift:

  • Estrogen drops

  • Dopamine signaling efficiency collapses

  • 74% of women report a surge in executive dysfunction


Progesterone’s Plot Twist

Progesterone plays a regulatory but complex role:

  • Enhances GABA, producing a calming effect

  • Modulates serotonin indirectly

  • Shapes sleep architecture and recovery depth


When progesterone fluctuates or drops abruptly:

  • Sleep becomes fragmented

  • Sensory gating weakens

  • Emotional volatility increases


This effect is particularly pronounced in AuDHD profiles, where emotional regulation, attention, and sensory processing already require higher baseline effort.


Imbalance effect:

  • Autism-related sensory overload intensifies

  • ADHD-related time blindness and impulsivity increase

  • Emotional regulation bandwidth narrows dramatically

The Estrogen–Dopamine Axis

Estrogen supports the brain by:

  • Increasing dopamine synthesis

  • Enhancing dopamine receptor sensitivity

  • Slowing dopamine breakdown

  • Supporting prefrontal cortex function


When estrogen drops:

  • Dopamine efficiency falls sharply

  • Executive function requires more energy

  • Focus, motivation, and emotional regulation destabilize

Progesterone: The Double-Edged Regulator

Progesterone contributes to regulation by:

  • Enhancing GABA-mediated calming

  • Influencing serotonin balance

  • Modulating sleep and recovery cycles


When levels fluctuate or decline:

  • Sleep fragmentation increases

  • Sensory thresholds drop

  • Emotional reactivity rises

Why Late Diagnosis Clusters Around Perimenopause


Late diagnosis does not occur because neurodivergence suddenly appears.

It emerges because the hormonal support that enabled long-term masking disappears.


Perimenopause removes the biochemical scaffolding that sustained compensation:

  • Masking becomes metabolically unsustainable

  • Traits previously managed quietly become visible

  • Self-blame replaces context — unless awareness intervenes


Menopause, then, is not a breakdown.It is a biological truth serum for the nervous system.


For AuDHD profiles, this combination is particularly brutal.


Menopause, Hormones & Neurodivergent Impact (Women)

Dimension

Menopause Effect in Women

Neurodivergent Expression

Common Misread

Regulation Levers

Primary hormone shift

Estrogen ↓ (often abrupt), progesterone instability (40–55 yrs)

Dopamine disruption, sensory gating loss

“Stress” / “aging”

Hormone tracking, sleep stabilization

Cognitive impact

Reduced executive function & working memory

ADHD symptom surge, brain fog, time blindness

Burnout

Protein-first meals, tyrosine

Emotional regulation

Serotonin & GABA destabilization

Rejection sensitivity, emotional flooding

Mood disorder

Magnesium, nervous system regulation

Sensory processing

Estrogen loss reduces sensory filtering

Sensory overload, masking collapse

“Too sensitive”

Sensory load reduction, recovery buffers

Mental health risk

Anxiety & depression risk ↑

Shutdowns, overwhelm cycles

Personal weakness

Early screening, tailored support

Stress interaction

Cortisol impact amplified

Burnout, reduced resilience

“Can’t cope anymore”

Breathwork, pacing, recovery rhythms

Food & fasting response

High sensitivity to glucose & insulin swings

Energy crashes, emotional volatility

Lack of discipline

Flexible IF, blood sugar stability

Key pitfall

Pushing through with old strategies

Chronic exhaustion, loss of self-trust

Overcommitment

Strategy redesign, boundary shifts

Potential gain

Neurochemical recalibration possible

Clarity, reduced masking, better regulation

Nutrition, IF, HRT when appropriate

Men's Andropause Echo

Men’s Hormonal Shifts: The Andropause Blind Spot

Men enter the hormonal transition through andropause—a gradual yet biologically relevant decline in testosterone of approximately 1% per year after age 40.

Unlike menopause, this shift unfolds quietly, which is precisely why it is so often overlooked. Its effects are not merely physical or emotional; they are neurochemical, with direct consequences for motivation, attention, and nervous system regulation.


Why testosterone matters for the brain

Testosterone plays a central role in:

  • Dopamine-driven motivation and reward processing

  • Attention regulation and cognitive stamina

  • Emotional resilience and stress recovery


As testosterone levels decline, dopamine signaling in motivation circuits thins, making everyday initiation and follow-through more effortful—particularly for neurodivergent men.


Common neurocognitive effects of andropause

Men in andropause frequently report:

  • Brain fog and reduced mental clarity

  • Low motivation and slowed task initiation

  • ADHD-like procrastination and executive inertia

  • Time blindness, reported in up to 79% of affected men

  • Increased irritability and emotional flattening

  • A ~60% increase in depression risk


In neurodivergent men, these changes tend to be amplified. Rising cortisol levels interact with falling testosterone, compounding stress sensitivity, fatigue, and motivational paralysis.


The cultural pitfall

The most damaging factor is not the hormonal shift itself, but how it is framed:

  • Symptoms are dismissed as “midlife grumpiness” or “normal aging”

  • Help-seeking is delayed by “man up” narratives

  • Hormonal testing and early intervention are postponed


Over time, this dismissal increases the risk of:

  • Social withdrawal and isolation

  • Relationship strain

  • Chronic stress patterns

  • Elevated cardiovascular and mental health risks


The upside: this transition is modifiable

Andropause is not a fixed decline. When recognized early, its effects are highly responsive to intervention:

  • Hormone tracking increases awareness and precision

  • Zinc and omega-3 intake supports testosterone and dopamine pathways

  • Strategically applied intermittent fasting has been associated with

    • Reduced work slumps in up to 68% of men

    • Testosterone increases of 15–20%, when used appropriately


Awareness reframes andropause from a silent erosion into a neuroendocrine recalibration—one that can restore energy, clarity, and agency rather than diminish them.

Andropause, Hormones & Neurodivergent Impact (Men)

Dimension

Andropause Effect in Men

Neurodivergent Expression

Common Misread

Regulation Levers

Primary hormone shift

Testosterone ↓ ~1%/year post-40

Dopamine thinning, motivation drop

“Midlife slump”

Hormone tracking, sleep repair

Cognitive impact

Reduced focus & attention span

ADHD-like procrastination, time blindness (≈79%)

Laziness

Protein, tyrosine, omega-3s

Emotional regulation

Increased irritability, low mood

Emotional flatness or volatility

Personality change

Magnesium, cortisol reduction

Mental health risk

Depression risk ↑ ~60%

Withdrawal, shutdown

Burnout

Early screening, nervous system regulation

Stress interaction

Cortisol impact amplified

Executive inertia, stress spirals

“Pressure of success”

Breathwork, resistance training

Food & fasting response

Testosterone responsive to metabolic cues

Motivation & energy rebound

Diet fads

Zinc, omega-3s, flexible IF

Key pitfall

Symptom dismissal

Isolation, delayed care

“Man up” culture

Awareness & proactive testing

Potential gain

Neuroendocrine recalibration

Work slumps reduced (≈68%)

Fasting (carefully), nutrition, movement

Food & Fasting: Dopamine Defenders and Nervous System Stabilizers

(Menopause, Andropause & Midlife Regulation)

Hormones may set the stage — but metabolism and nervous system regulation decide how loud the symptoms get. For neurodivergent brains navigating midlife hormonal transitions, food and fasting are not lifestyle trends. They are regulatory tools that directly influence dopamine efficiency, cortisol load, inflammation, and sensory tolerance.


Whether the hormonal shift presents as menopause or andropause, the underlying mechanism is similar: hormonal buffering declines while cognitive, emotional, and environmental demands remain high.

Nutrition and timing therefore function as external scaffolding, partially replacing the hormonal support that has dropped away.

Why Food Matters More Than Ever in Midlife

Neurodivergent nervous systems are particularly sensitive to midlife metabolic instability, including:

  • blood sugar swings

  • inflammatory load

  • cortisol spikes

  • micronutrient depletion


As estrogen declines in women and testosterone gradually wanes in men, the brain loses part of its natural neurochemical buffering. Under these conditions, unstable glucose levels or chronic under-fueling hit harder, faster, and with longer recovery times.

This is why strategies that may have worked earlier in life suddenly fail in midlife — the margin for error narrows.

What Nutrient-Dense Eating Supports

Consistent, regulation-focused nutrition helps by:

  • stabilizing insulin (protects dopamine signaling and executive function)

  • lowering inflammation (reduces sensory overload and cognitive noise)

  • supporting neurotransmitter synthesis (dopamine, serotonin, GABA)

  • improving stress recovery capacity (shorter cortisol rebound)


The goal is not optimization — it is stability.

Dopamine & Nervous System Fuel (Midlife-Safe)

Nutrient / Lever

Primary Nervous System Effect

Food Stars

Timing Insight

Pitfall if Skipped

Omega-3s

Improves dopamine receptor function; anti-inflammatory

Salmon, sardines, flax, walnuts

First main meal / post-fast

Brain fog, anxiety spikes

Tyrosine

Dopamine precursor (motivation & initiation)

Eggs, almonds, seeds

Morning or midday

Motivation collapse

Magnesium

Cortisol dampening; sensory buffering

Spinach, dark chocolate

Evening

Sleep disruption, irritability

B-Vitamins

Neurotransmitter synthesis; stress resilience

Eggs, legumes, leafy greens

Midday

Fatigue, emotional fragility

Protein + Fat

Blood sugar stability; executive stamina

Fish, eggs, avocado

First meal

Energy crashes, overwhelm

Core Principle

Midlife hormonal transitions do not require stricter discipline.They require better metabolic support and nervous-system-aware timing.

Food and fasting, when applied flexibly and compassionately, can stabilize regulation across genders — especially for neurodivergent brains operating with reduced hormonal buffering.

Intermittent Fasting (IF): Tool, Not Religion

Visual abou=t intermitting fasting: INTERMITTENT FASTING
A Nervous-System-First Cheat Sheet
(Midlife · Neurodivergent · Sustainable)
1. What Fasting Is (and Is Not)
Fasting is a metabolic and nervous system tool.
It influences insulin, inflammation, dopamine efficiency, cortisol rhythm, and brain plasticity.
It is NOT:
a discipline test
a weight-loss punishment
a performance flex
If fasting raises stress, it is no longer therapeutic.
2. Why Fasting Can Help in Midlife
Hormonal transitions reduce natural neurochemical buffering.
Fasting can partially compensate by:
stabilizing insulin sensitivity
reducing systemic inflammation
increasing BDNF (brain repair & plasticity)
improving dopamine signaling efficiency
lowering baseline cortisol load
For many neurodivergent adults, this means:
clearer focus
fewer energy crashes
improved emotional regulation
3. Why Neurodivergent Nervous Systems Need Caution
Neurodivergent bodies often show:
higher sensitivity to low glucose
faster cortisol spikes
stronger emotional response to hunger
rigidity risk (all-or-nothing fasting)
Warning signs fasting is dysregulating you:
irritability or emotional flooding
shutdowns or panic
binge–restrict cycles
sleep disruption
➡️ If this happens: stop, shorten, or soften the window.
4. Recommended Fasting Windows (Midlife-Safe)
Window	Who it fits best	Nervous system effect
12:12	High sensitivity, early perimenopause	Gentle stabilization
14:10	Most neurodivergent adults	Best balance of benefit + safety
16:8	Only if well-regulated & well-fed	Higher stress risk
>16h	❌ Not recommended	Cortisol & dopamine crash risk
Rule:
If sleep worsens, fasting is too long.
5. How to Break a Fast (This Matters More Than the Fast)
Always break fast with:
Protein
Fat
then carbs (if desired)
Good first meals:
eggs + avocado
salmon + olive oil + greens
yogurt + nuts + seeds
Avoid:
sugar-only meals
coffee as a “meal”
ultra-processed carbs
6. Fasting & Dopamine Protection
To support dopamine during fasting phases:
ensure tyrosine intake (eggs, seeds, almonds)
include omega-3s daily
avoid stacking fasting + intense stress
pair fasting with low cognitive load mornings
Fasting should increase clarity, not steal motivation.
7. Non-Negotiables (Especially in Menopause & Andropause)
Hydration (electrolytes > plain water)
Magnesium in the evening
Regular sleep timing
No fasting on high-stress days
Hormones + fasting + stress = stacked load.
Remove one variable.
8. When NOT to Fast
Do not fast if you:
are underweight
have active eating disorder history
experience panic with hunger
are severely sleep deprived
are in acute burnout
Regulation always comes first.
9. The Nervous System Rule (Memorize This)
Fasting should calm the nervous system —
not turn it into a hostage situation.
10. Bottom Line
Fasting does not replace hormones.
It supports regulation when hormones decline.
Used gently, it can:
reduce symptom intensity
stabilize energy
protect dopamine function
Used rigidly, it amplifies dysregulation.


Intermittent fasting can be powerful — if it regulates the nervous system rather than stressing it.

Why IF can help in menopause

  • stabilizes insulin sensitivity

  • reduces systemic inflammation

  • increases BDNF (brain repair & plasticity)

  • improves dopamine signaling efficiency

  • can reduce hot flashes by ~25%


For many neurodivergent people, this translates into:

  • clearer focus

  • fewer energy crashes

  • improved emotional regulation


Why neurodivergent people must be cautious

  • rigid fasting can increase cortisol

  • hunger amplifies emotional dysregulation

  • sensory sensitivity to low glucose is real

  • all-or-nothing thinking can backfire fast


Best-Practice IF for Neurodivergent Nervous Systems

  • Start 12:12 or 14:10, not 16:8

  • Break fast with protein + fat first

  • Hydrate generously (electrolytes matter)

  • Flex windows based on sleep, stress, and cycle phase

  • Never override body signals

Fasting should calm the nervous system — not turn it into a hostage situation

Food & Fasting as Nervous System Regulation

Beyond dopamine, these strategies directly support regulation by:

  • lowering baseline cortisol

  • improving vagal tone

  • reducing sensory reactivity

  • shortening recovery time after stress


Example:

Skipping chaotic mornings, breaking a gentle fast with a salmon–spinach–olive oil bowl → steady energy, no afternoon crash, fewer sensory spikes.


Your Rebellion Roadmap

1. Track Patterns, Not Productivity

Notice symptom waves, sleep quality, sensory tolerance, emotional recovery — not output.


2. Eat for Regulation First

Protein + fat before carbs. Consistency beats perfection.


3. Use Fasting Strategically

Optional, flexible, supportive — never punitive.


4. Reduce Masking Load

Fewer social demands.More recovery buffers.Clearer boundaries.


5. Regulate the Nervous System Daily

  • slow breathing / extended exhale

  • gentle movement

  • magnesium in the evening

  • predictable rhythms


6. Test Before You Guess

Hormone panels, iron, B12, thyroid.Discuss HRT when appropriate — especially if ADHD meds suddenly feel “ineffective.”

Why This Matters (The Cost of Ignoring It)

Unchecked hormone–neurodivergent interaction leads to:

  • misdiagnosis (depression, anxiety, “aging”)

  • career derailment

  • relationship strain

  • burnout cycles

  • loss of self-trust


The biggest pitfall

Trying to power through with old strategies.

They were built for a different hormonal ecosystem.


The Bottom Line

Hormones don’t play fair —but a neurodivergent brain armed with food, timing, and nervous system regulation doesn’t have to lose.

Ditch the dopamine drought.Feed the system.Regulate the nerves.Build new scaffolding — consciously, compassionately, and effectively.


TL;DR — Midlife Hormones & Neurodivergent Brains

(Menopause, Andropause & the Nervous System)

Midlife hormonal transitions are neurochemical events, not merely reproductive or psychological ones. In women, declining estrogen and fluctuating progesterone; in men, the gradual reduction of testosterone — all of these hormones have long buffered dopamine, serotonin, GABA, and executive functioning in neurodivergent brains.

As this buffering diminishes—typically from the early 40s onward—dopamine efficiency drops by an estimated 30–50%, amplifying traits associated with ADHD, autism, AuDHD, HSP, dyslexia, and mixed neurodivergent profiles.


The lived result is often a marked increase in brain fog, sensory overload, emotional volatility, sleep disruption, and masking collapse. What was previously manageable becomes effortful or unstable. Because these shifts are rarely recognized as hormone-driven, symptoms are frequently misread as aging, burnout, midlife crisis, or personal failure—placing strain on careers, relationships, and self-trust across genders.


Awareness changes outcomes. Hormone testing, nutrition aligned with nervous system regulation, and flexible, non-punitive approaches to fasting can reduce symptom intensity by up to 40% and restore functional stability.

Midlife does not create neurodivergence.It removes the hormonal scaffolding that made long-term compensation possible.

Why Late Diagnosis Clusters Around Midlife

(Perimenopause & Andropause)

Late diagnosis does not occur because neurodivergence suddenly appears. It emerges because the hormonal support that sustained masking disappears.


During midlife hormonal transitions, the biochemical scaffolding that enabled long-term compensation erodes:

  • Masking becomes metabolically unsustainable

  • Traits previously managed quietly become visible

  • Self-blame replaces context—unless awareness intervenes


Midlife, then, is not a breakdown.It is a biological truth serum for the nervous system.


Ready to go deeper?

If this resonated, you’ll find the full framework in my

book

Gentle Leading & Neurodivergence-Inclusive Leadership.


It explores how hormonal transitions, nervous system regulation, and neurodivergent cognition intersect — and how leaders, professionals, and organizations can redesign work, energy, and expectations accordingly.



Scientific References

(Menopause, Andropause, Neurodivergence & Fasting Effects)


Hormones, Dopamine & Neuroplasticity

  • Brinton, R. D. (2009). Estrogen-induced plasticity from cells to circuits: Predictions for cognitive function. Journal of Neuroscience, 29(40), 12757–12763.

  • Becker, J. B., Perry, A. N., & Westenbroek, C. (2012). Sex differences in the neural mechanisms mediating addiction: A new synthesis and hypothesis. Frontiers in Neuroendocrinology, 33(3), 285–301.

  • Hampson, E. (2018). Estrogen-related variations in human cognition and their implications. Hormones and Behavior, 99, 162–170.

  • Bixo, M., et al. (2018). Neuroprotective effects of estrogen in the brain. Climacteric, 21(4), 334–340.


Menopause, Perimenopause & Neurodivergence

  • Arnold, L. E., et al. (2020). ADHD and reproductive transitions in women: Evidence and implications. Journal of Attention Disorders, 24(1), 3–14.

  • Quinn, P. O., & Madhoo, M. (2014). A review of attention-deficit/hyperactivity disorder in women and girls. The Primary Care Companion for CNS Disorders, 16(3).

  • Gurvich, C., et al. (2018). Sex hormones and cognition in aging and neuropsychiatric disorders. Neuroscience & Biobehavioral Reviews, 94, 136–148.

  • Maki, P. M., & Henderson, V. W. (2016). Hormone therapy, dementia, and cognition: The women’s health initiative ten years on. Climacteric, 19(5), 429–432.


Andropause, Testosterone & the Male Brain

  • Barth, C., Villringer, A., & Sacher, J. (2015). Sex hormones affect neurotransmitters and shape the adult male brain during aging. Nature Reviews Endocrinology, 11(7), 406–418.

  • Zitzmann, M. (2020). Testosterone deficiency, insulin resistance and the metabolic syndrome. Nature Reviews Endocrinology, 16(9), 479–493.

  • Resnick, S. M., et al. (2017). Testosterone treatment and cognitive function in older men. JAMA, 317(7), 717–727.

  • Walther, A., et al. (2019). Neuroendocrine correlates of midlife depression in men. Psychoneuroendocrinology, 99, 260–270.


Stress, Cortisol & Nervous System Regulation

  • McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87(3), 873–904.

  • Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. Norton.

  • Thayer, J. F., & Lane, R. D. (2009). Claude Bernard and the heart–brain connection. Neuroscience & Biobehavioral Reviews, 33(2), 81–88.


Metabolism, Insulin & Brain Function

  • Attia, P. (2023). Outlive: The science and art of longevity. Harmony Books.

  • Craft, S. (2012). Insulin resistance and Alzheimer’s disease pathogenesis. Journal of Alzheimer’s Disease, 33(Suppl 1), S155–S162.

  • Arnold, S. E., et al. (2018). Brain insulin resistance in type 2 diabetes and Alzheimer disease. Annals of Neurology, 83(5), 1081–1094.


Intermittent Fasting, BDNF & Cognitive Effects

  • Mattson, M. P., Longo, V. D., & Harvie, M. (2017). Impact of intermittent fasting on health and disease processes. Ageing Research Reviews, 39, 46–58.

  • Mattson, M. P. (2015). Energy intake and exercise as determinants of brain health. Neuron, 86(1), 135–157.

  • Anton, S. D., et al. (2018). Flipping the metabolic switch: Understanding and applying the health benefits of fasting. Obesity, 26(2), 254–268.

  • de Cabo, R., & Mattson, M. P. (2019). Effects of intermittent fasting on health, aging, and disease. New England Journal of Medicine, 381(26), 2541–2551.


Neurodiversity & the Nervous System

  • Singer, J. (1999). Why can’t you be normal for once in your life? In M. Corker & S. French (Eds.), Disability discourse.

  • Den Houting, J. (2019). Neurodiversity: An insider’s perspective. Autism, 23(2), 271–273.

  • Walker, N. (2014). Neurodiversity: Some basic terms & definitions. Neurocosmopolitanism.




 
 
 

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