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Increased sensitivity to pain

Serotonin

Serotonin is crucial in how we perceive pain, and when serotonin levels drop, sensitivity to pain can heighten. This explains why individuals suffering from depression, anxiety, or ongoing stress often report increased physical discomfort, including headaches, muscle soreness, and joint pain.

How Serotonin Influences Pain Sensitivity

  • Pain Regulation – Serotonin plays a vital role in managing pain signals within the brain and spinal cord. A deficiency in serotonin leads to an amplified perception of pain.
  • Chronic Pain Disorders – Low levels of serotonin are associated with conditions such as fibromyalgia, migraines, irritable bowel syndrome (IBS), and neuropathic pain.
  • Inflammation & Stress Reaction – Serotonin also has an impact on inflammation. Prolonged stress can deplete serotonin levels, exacerbating inflammatory pain.
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Dopamine

Dopamine is essential for how we perceive and manage pain. It influences the brain's reward system and helps control our experience of discomfort. When dopamine levels are low, often as a result of chronic stress, burnout, or neurological disorders, pain sensitivity can increase, causing even slight aches to feel more severe. This phenomenon is frequently observed in conditions such as fibromyalgia and chronic pain syndromes, where issues with dopamine lead to ongoing discomfort.

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Noradrenaline

In regions affected by injury or inflammation, noradrenaline can heighten the sensitivity of nerve endings, making them more reactive to pain signals. This occurs through the activation of specific adrenergic receptors on pain-sensing neurons, which lowers the pain threshold and amplifies the intensity of perceived pain—particularly in situations involving chronic stress, inflammation, or nerve injury.

Central Modulation – Alleviates Pain

Conversely, in the brain and spinal cord, noradrenaline typically exerts an inhibitory effect on pain. It operates through descending pain pathways (notably from the brainstem), assisting in the suppression of incoming pain signals before they reach full awareness. This function is part of the body's inherent pain-control mechanism. Certain antidepressants (such as SNRIs) boost noradrenaline levels in the CNS to alleviate chronic pain.

 

Stress-Pain Cycle

During acute stress, a brief surge of noradrenaline may actually numb pain temporarily to facilitate survival (the “fight or flight” benefit). However, under chronic stress, persistently high levels of noradrenaline can intensify pain and contribute to conditions like fibromyalgia, neuropathic pain, and tension-type headaches.

Pain that persists?

Tension that continues to escalate?

A body that aches without a clear cause?

You’re not imagining things. And it’s not solely physical. The reality is that your pain could be hormonal.

Adrenaline (Epinephrine)

Adrenaline is your body’s “fight or flight” hormone. In acute circumstances, it enhances energy and alertness while temporarily blocking pain. It’s your body’s way of signaling, “We’ll handle the pain later.” In cases of chronic stress or burnout, your body produces excessive adrenaline and subsequently crashes. This results in heightened pain sensitivity. You may begin to feel sore, tight, or even inflamed with the slightest provocation. Your muscles might ache, your neck and back may become stiff, and tension headaches could occur frequently.

Pain effects:

Heightened nerve sensitivity

Muscle tightness and jaw clenching

Headaches, migraines, and heart palpitations

A fatigued yet restless body with aches

A pervasive feeling of "what's the point?"

GABA (Gamma-Aminobutyric Acid)

GABA serves as your main calming neurotransmitter. It helps to slow the nervous system, curtail racing thoughts, and lessen the brain's pain signals. When GABA levels are low, your brain can become overly active, reacting strongly to minor discomforts. This can result in an emotional intensification of pain, reduced tolerance, and a tense, irritable body. An imbalance in GABA is often found alongside anxiety, insomnia, and symptoms similar to fibromyalgia.

Pain effects:

  • Restless body and diminished pain tolerance
  • Muscle tightness, jaw strain
  • Back and neck pain related to stress
  • Pain that intensifies with mental or emotional stress

DHEA (Dehydroepiandrosterone)

DHEA is a protective hormone that fights inflammation. It aids in tissue repair, balances the immune response, and protects the body from the effects of chronic stress.

DHEA levels can decline due to prolonged stress, overtraining, or hormonal issues like PCOS. This can leave your body in a state of low-grade inflammation, making you feel sore, sluggish, and slow to recover. You may experience unexplained joint pain, and even light activity can result in a lengthy recovery period.

Pain effects:

  • Ongoing joint and muscle discomfort
  • Ineffective tissue repair
  • Inflammation occurring without injury
  • Pain that exacerbates during menstrual cycles or hormonal changes

Cortisol

Cortisol plays a crucial role in managing inflammation, regulating pain, and aiding tissue recovery. It operates on a circadian rhythm—peaking in the morning and dipping at night—to maintain bodily balance. Elevated cortisol levels result in persistent inflammation and an overactive response from the body. Conversely, low cortisol levels hinder the body’s ability to manage inflammation effectively. Both scenarios can lead to chronic inflammation, slow healing, and heightened pain sensitivity. This is often seen in conditions like adrenal fatigue, PTSD, or prolonged burnout.

Pain impact:

  • Widespread aches, swelling in joints
  • Pain in trigger points, particularly in the shoulders and hips
  • Low energy in the morning accompanied by body stiffness.

Glutamate

What Role Does Glutamate Play in Pain?

Glutamate serves as the main excitatory neurotransmitter within the central nervous system, playing a significant role in:

  • Transmitting pain signals from the body to the brain
  • Enhancing pain perception within the spinal cord and brain
  • Perpetuating chronic pain through sensitization

Acute Pain:

When tissues are damaged or inflamed, glutamate is released at nerve endings and synapses in the spinal cord.

It activates NMDA and AMPA receptors, which heighten both the intensity and speed of pain signals relayed to the brain.

This mechanism allows the body to react swiftly to threats, but it also results in pain that feels sharp and severe.

Chronic Pain & Glutamate:

In cases of chronic pain, the nervous system becomes sensitized, which means:

  • The same stimulus can provoke more pain than expected (hyperalgesia)
  • Even non-threatening stimuli can trigger pain (allodynia)

This phenomenon is primarily due to ongoing glutamate activity that keeps the pain pathways active, even in the absence of new injuries.

Over time, glial cells become inflamed and struggle to eliminate excess glutamate, which exacerbates pain and emotional suffering.