Understanding Stress-Induced Scalp Sensitivity: The HPA Axis, Substance P, and TRPV1 Connection

Why stress makes your scalp burn, itch, or shed—and what calming science-backed care can help

Disclaimer: This article is for informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your dermatologist or healthcare provider with any questions you may have regarding a medical condition.

1. What is the HPA axis and how does it relate to your scalp?

The hypothalamic pituitary adrenal (HPA) axis is the body’s primary stress response system: the brain’s hypothalamus triggers the pituitary, which in turn triggers the adrenal glands to release cortisol (a stress hormone).¹
When you are under emotional, psychological or physical stress, this system ramps up. For skin and scalp health this matters because research shows that not only the central HPA axis but also a cutaneous (skin) based HPA like system exists.²
In other words: your scalp does not just react to external triggers (like heat, chemicals or friction); it is wired to respond to stress via neuro endocrine signals. That means persistent stress can undermine scalp barrier integrity, alter hair follicle behavior and amplify sensitivity.³

Key takeaway: If your scalp feels on edge, tight, irritated or more reactive than usual, stress may be playing a hidden role, not just your shampoo or weather.

2. How can the HPA axis disturb scalp and hair follicle health?

Activated HPA signaling raises cortisol and related hormones, which in turn affect skin or scalp barrier function, hair cycle phases and local immune responses.⁴ For example:

• A study found that psychological stress impaired the skin barrier (more water loss, less hydration) via activation of 11β HSD1 (an enzyme that converts inactive cortisone to active cortisol in skin).⁵

• In hair follicle cells researchers found that corticotropin releasing factor (CRF), a key HPA axis hormone, inhibited hair growth and pushed follicles toward the resting (telogen) phase.⁶

For the scalp this means: If you are under chronic stress, you may notice increased itching, burning, sensitivity or diffuse hair shedding not just due to product misuse but due to internal stress wiring.
Tip: Tracking your stress levels alongside your scalp symptoms may uncover patterns you would not see otherwise.

3. What is Substance P and why should sensitive scalp folks care?

Substance P is a neuropeptide (a small signaling protein released by nerve endings) that plays a role in neurogenic inflammation, inflammation stimulated via nerves rather than classic immune triggers.⁷ It is released in response to stress and can:

• Trigger mast cell degranulation and local inflammation around hair follicles.⁸

• Down regulate hair growth related factors in the outer root sheath of hair follicles.⁹
  In scalp conditions (including sensitive scalp, hair shedding, scalp burning) Substance P is emerging as a key mediator of the link between nerve or brain signals and scalp inflammation.¹⁰

Practical lens: If your scalp reacts strongly to minor triggers (fragrance, heat, stress, brushing), Substance P may be one of the biochemical amplifiers making your nerves oversensitive.

4. What is TRPV1 and how does it amplify scalp sensitivity?

TRPV1 (transient receptor potential vanilloid 1) is an ion channel protein present on sensory nerve endings which acts as a heat or irritant detector.¹¹ When activated (by heat, capsaicin, acid, stress signals) it allows cations (like calcium) into the cell, triggering nerve firing, release of neuropeptides (like Substance P) and neurogenic inflammation.¹²
On the scalp this means TRPV1 rich nerves may over react to triggers like hot water, friction, scalp products, UV exposure or even stress mediated signals, leading to burning, stinging, itch, or hair follicle irritation.

Tip: Choosing gentler scalp care (cooler water, fewer fragrances, minimal mechanical friction) can reduce TRPV1 activation and give your scalp a break.

5. How do all three systems (HPA axis, Substance P, TRPV1) connect in a sensitive scalp?

Here is a simplified chain:

1. Stressor (emotional, physical, environmental) activates the HPA axis which raises cortisol in scalp or skin.

2. The stress signal also triggers neuro sensory nerves to release Substance P.

3. TRPV1 channels on those nerves respond to irritants or stress signals, triggering nerve firing and release of Substance P.

4. Substance P stimulates local inflammation (mast cells, cytokines) and may impair hair follicle growth or barrier function.

5. The result: a scalp that is more reactive, prone to barrier breakdown, itching, burning, redness or hair shedding.

When any of these pathways is chronically activated, your scalp becomes a stress sensor rather than just a passive organ. Mounting evidence indicates this mechanism underpins conditions such as scalp dysesthesia (burning scalp), sensitive scalp syndrome, diffuse hair shedding following stress, and exacerbations of inflammatory scalp disorders.¹³

6. What practical steps can you take both at home and with your dermatologist?

At home strategies for calmer scalp

• Use cool to lukewarm water when washing your scalp to reduce thermal activation of TRPV1.

• Choose fragrance free, minimal ingredient cleansers to minimize neuro irritant triggers.

• Wash and rinse gently to avoid vigorous scrubbing or mechanical friction which may activate sensory nerves.

• Incorporate stress management practices (breathing, meditation, good sleep) because lowering systemic HPA activation helps your scalp too.

• Try a scalp soothing mask (for example, containing panthenol, oat kernel extract, ceramides) once a week to reinforce barrier.

• Keep a symptom trigger diary: log stress levels, sleep, scalp symptoms, hair shedding. Over time you may spot patterns.

  
  

When to seek professional help

• If your scalp symptoms are persistent (weeks) and interfering with daily life (itching, burning, shedding) consult a dermatologist.

• Bring your trigger diary and mention your stress levels: ask about testing or therapies targeting neurogenic inflammation.

• Your dermatologist might consider treatments that specifically address Substance P or TRPV1 related pathways (medications, topical agents) or refer you to a trichologist (hair and scalp specialist).

• If hair shedding is significant, ask for detailed hair cycle evaluation (blood work, scalp microscopy) to rule out other causes plus stress related shedding.

Tip: Bring the phrase neuro endocrine scalp sensitivity to your appointment; it signals you are aware of the underlying mechanism, not just surface symptoms.

7. How can you measure progress and know your scalp is improving?

Here are useful metrics you and your clinician can track:

• Symptom severity score: rate scalp sensations (itch, burn, sting) from 0 to 10 weekly. Look for declining scores.

• Scalp barrier functioning: though not often measured in home care, dermatologists can check transepidermal water loss (TEWL) or hydration. A lower TEWL indicates improved barrier function; stress induced HPA activation was shown to increase TEWL.⁵

• Hair shedding count: count hairs lost daily when washing or brushing. A drop back toward normal range is a good sign.

• Trigger response frequency: if fewer stressors lead to scalp flares, that shows your sensitivity threshold is improving.

  
  

8. Common myths and clarifications

Myth: It is just my shampoo or hard water causing scalp discomfort.
Clarification: While those can contribute, if your scalp also flares with emotional stress, heat, sleep disruption or friction, then neuro endocrine pathways (HPA, Substance P, TRPV1) may be active.
Myth: If I relax, my scalp will automatically heal.
Clarification: Relaxation helps lower HPA activation but your scalp barrier and hair follicle environment may take weeks to recover. Consistent care and trigger management is needed.
Myth: Sensitive scalp is only cosmetic and not serious.
Clarification: While often non serious, chronic neuro genic scalp sensitivity can impact quality of life, sleep, mental health and may herald or worsen inflammatory scalp or hair conditions. Early intervention helps.

9. Final thoughts: take control of your scalp’s stress wiring

Your scalp is not simply acting up because of an irritating product or seasonal change. It is wired into your body’s stress response systems. By understanding how the HPA axis, Substance P and TRPV1 create a loop of sensitivity, you can bring targeted care, not just guesswork.
Start with gentle scalp protocols, track your stress and scalp reactions, and engage your dermatologist with this framework. With time your scalp can regain calm, your hair shedding can ease and your confidence in managing sensitive scalp conditions can grow. Early attention means fewer downstream surprises. You have got this.

Glossary

• HPA axis (hypothalamic pituitary adrenal axis): the body’s major stress response system, involving the hypothalamus, pituitary gland and adrenal glands.

• Cortisol: a steroid hormone released via the HPA axis; high levels or dysregulation can impair skin and scalp barrier function.

• Cutaneous HPA axis: a local version of HPA signaling present in skin and scalp cells (keratinocytes, hair follicle cells).

• Substance P: a neuropeptide released by sensory nerves in response to stress or irritant stimuli; triggers local inflammation and hair follicle effects.

• TRPV1 (transient receptor potential vanilloid 1): an ion channel on sensory nerves that detects heat, acid and irritants; activation leads to nerve firing and release of Substance P.

• Neurogenic inflammation: inflammation mediated via nerve signals (rather than purely immune cell triggers) in which sensory nerves release substances like Substance P.

• Barrier function (scalp or skin): the ability of the skin or scalp surface to retain moisture and keep out irritants, allergens and microbes.

• Telogen effluvium: a form of hair shedding in which hair prematurely shifts into the resting (telogen) phase, often stress triggered.

  
  

Claims Registry

#	Claim(s) supported	Source title + authors + year + venue	Accessed date	Anchor extract (<25 words)	Notes
1	Stress activates HPA axis and cortisol rises	Lin TK et al. 2017. Association between Stress and the HPA Axis in the Atopic Skin. PMC.	2025 11 02	“The central HPA axis both regulate skin barrier homeostasis and the inflammatory response in the skin.”	Clearly links HPA axis to skin function.
2	Skin barrier dysfunction under psychological stress via HPA activation	Choe SJ et al. 2018. Psychological Stress Deteriorates Skin Barrier Function. Sci Rep.	2025 11 02	“Psychological stress (PS) increases endogenous glucocorticoids (GC) by activating the HPA axis eventually impairs barrier function.”	Direct experimental evidence.
3	Hair follicle cells express HPA components; stress can cause hair loss	Lee EY et al. 2020. The local HPA axis in cultured human dermal papilla cells. BMC Mol Cell Biol.	2025 11 02	“The human skin expresses all elements of the HPA axis hair follicles a fully functional HPA axis exists in human DPCs.”	Connects HPA axis to hair follicle biology.
4	TRPV1 is a key sensory receptor for stress or irritant signals	Zhang M et al. 2023. TRP channel family review. Nature.	2025 11 02	“TRP channels are responsible for various sensory responses including stress.”	Places TRPV1 in sensory pathway context.
5	Substance P released under stress and contributes to skin inflammation or hair follicle damage	Kim C et al. 2022. Role of Substance P in Regulating Micro Milieu. Ann Dermatol.	2025 11 02	“A recent study showed that substance P (SP) damaged hair follicles activated perifollicular mast cells inhibited hair growth.”	Demonstrates Substance P relevance to hair or scalp.
6	Stress amplifies TRPV1 mediated neurogenic inflammation in skin	Grigore O et al. 2019. Role of stress in modulation of skin neurogenic inflammation. Exp Ther Med.	2025 11 02	“Studies highlighted stress modulating the density and activity of nociceptive nerve fibres increasing SP release from unmyelinated nerve endings of the skin.”	Connects stress to nerve activation to Substance P release.