GLP-1 Antagonist Uncovered for Neuro-Immune Mechanism

Understand the significance of GLP-1 antagonists for neuroimmune mechanisms in the latest healthcare advancements.

Abstract

As a clinician deeply immersed in functional and integrative medicine, I, Dr. Alex Jimenez, have observed a growing number of patients experiencing a perplexing and distressing side effect of GLP-1 receptor agonists like retatrutide: severe skin sensitivity. This condition, often described as feeling like a constant sunburn or as if sandpaper has been rubbed on the skin, is medically termed drug-induced cutaneous allodynia and hyperesthesia. Traditional medical approaches often focus on symptom management with antihistamines, which can provide limited relief while introducing side effects like sedation. This post aims to move beyond surface-level treatment by exploring the deep physiological mechanisms driving this reaction. We will delve into how these powerful metabolic drugs interact with GLP-1, GIP, and glucagon receptors distributed throughout the peripheral nerves, immune cells, and skin. By understanding how these interactions lead to nerve hyperexcitability, mast cell degranulation, and a pro-inflammatory state, we can develop a more effective, targeted treatment strategy. This comprehensive guide will illuminate the intricate neuro-immuno-endocrine processes at play and introduce an integrative protocol combining nutritional support, targeted supplementation, and chiropractic care to restore balance and alleviate this painful condition.

At Injury Medical Clinic PA, our unique, multidisciplinary approach is central to how we manage complex conditions like this. I work closely with Dr. Maria Guadalupe Cardenas, MD, our esteemed Medical Director. Dr. Cardenas is Board Certified in Internal Medicine and brings over four decades of invaluable experience to our practice. As my collaborative physician (NPI #1164426749, Texas MD License #J2933), she ensures our patients receive comprehensive, medically supervised care that seamlessly integrates my expertise in chiropractic, functional medicine, and advanced practice nursing. This partnership bridges the gap between conventional medicine and evidence-based complementary therapies, offering a holistic framework that addresses the root cause of dysfunction, not just the symptoms. Together, we guide our patients through their healing journey, leveraging the combined strengths of chiropractic adjustments, rehabilitation, functional nutrition, and medical oversight to achieve optimal health outcomes.

A New Challenge in Metabolic Health: When Your Skin Is On Fire

In my practice, I’ve dedicated my career to unraveling complex health puzzles. As a Doctor of Chiropractic, an Advanced Practice Registered Nurse, and a board-certified Family Nurse Practitioner and Functional Medicine Practitioner, I am constantly seeking to understand the “why” behind my patients’ symptoms. Recently, a particularly distressing issue has been appearing with increasing frequency in my clinical observations: patients on newer weight-loss medications, specifically GLP-1 receptor agonists like retatrutide, are reporting a bizarre and painful skin sensitivity.

They describe it in vivid, unsettling terms. “Dr. Jimenez, it feels like my skin is sunburnt from the inside out.” “The seams on my shirt feel like razor blades.” “Even a gentle breeze or the touch of my bedsheets is excruciating.” This isn’t a simple rash or an allergic reaction with hives. This is a profound, nerve-based pain known as cutaneous allodynia (pain from a stimulus that doesn’t normally cause pain) and hyperesthesia (abnormally increased sensitivity of the skin).

The conventional response has often been to prescribe antihistamines, treating the issue as a simple allergic or histamine-mediated reaction. While this might offer a sliver of relief, it often comes with the unwelcome side effect of sedation and, more importantly, fails to address the root cause. The pain persists because the underlying neurological and immunological dysregulation remains untouched. To truly help my patients, I knew I had to dig deeper, to connect the dots between this powerful class of drugs and the body’s intricate signaling networks.

The Neuro-Immuno-Endocrine Cascade: More Than Just Weight Loss

To understand this phenomenon, we must first appreciate that medications like retatrutide are not just simple appetite suppressants. They are potent modulators of our neuro-immuno-endocrine axis. These drugs are designed to target three key receptors involved in metabolism and appetite regulation:

1. Glucagon-Like Peptide-1 (GLP-1) Receptors
2. Glucose-Dependent Insulinotropic Polypeptide (GIP) Receptors
3. Glucagon (GCG) Receptors

While these receptors are famous for their roles in the pancreas and brain in controlling blood sugar and hunger, groundbreaking research has revealed their presence in a vast array of other tissues, including the skin, peripheral nerves, immune cells (like mast cells and keratinocytes), and throughout the central and peripheral nervous system.

When a patient takes a triple-agonist drug like retatrutide, they are essentially activating these receptors system-wide. It’s like throwing a grenade into the middle of a complex, interconnected communication network. The drug doesn’t care that its primary purpose is weight loss; it sends a powerful signal to every receptor it can find, triggering a cascade of downstream effects that can lead to this profound state of skin sensitivity. Let’s break down exactly how this happens, piece by piece.

The Peripheral Nerve Connection: Unraveling GLP-1 and Nerve Hyperexcitability

GLP-1 Receptors on Pain-Sensing Nerves

One of the most crucial breakthroughs in understanding this side effect came from a landmark 2023 study published in Nature Metabolism. Researchers demonstrated conclusively that peripheral nerves are studded with GLP-1 receptors. Specifically, these receptors are found on the very nerve fibers responsible for sensing our environment:

• Small C-fibers: These are unmyelinated nerve fibers that transmit signals for pain (especially slow, burning, or aching pain), temperature, and itch.
• A-delta fibers: These are thinly myelinated fibers that transmit sharp, well-localized pain and temperature sensations.

These are the exact neurons that tell your brain about touch, temperature, and potential harm. When you take a GLP-1 agonist, these receptors are directly stimulated. The neurons don’t interpret this signal in the context of your metabolic goals; they receive a powerful “go” signal. This chronic stimulation cranks them up and makes them hyperexcitable.

The Concept of Peripheral Sensitization

In neuroscience, this state is known as peripheral sensitization. Imagine the volume dial on a stereo. Normally, it’s set at a reasonable level. But with chronic GLP-1 stimulation, that dial is turned all the way up. The nerves enter a state of heightened alert, where their firing threshold drops significantly.

• Before the medication: A light touch from your shirt is just a light touch. The signal is too weak to trigger a pain response.
• After the medication: That same light touch is now enough to push the hyperexcitable nerve past its firing threshold. It sends a barrage of “pain” signals up the spinal cord to the brain.

This is the essence of allodynia. The stimulus hasn’t changed, but the nervous system’s interpretation of it has been dramatically altered. The slightest provocation—the brush of clothing, the warmth of shower water, the pressure from bedsheets—is now perceived as a painful, noxious event. This is why patients report feeling as though their skin has been sandpapered; their sensory nervous system is in a state of high alarm, misinterpreting innocuous sensations as threats. This isn’t damage or an allergy in the traditional sense; it’s a functional change in how your nerves are behaving, a real-time rewriting of your body’s sensory set points.

The Immune System’s “Border Patrol”: GIP Receptors and Mast Cell Degranulation

Mast Cells: The Body’s Biological Hand Grenades

The nervous system isn’t acting alone in this process. The immune system is a key player, and the link here is the GIP receptor. Research has shown that GIP receptors are densely expressed on the surface of mast cells.

Think of mast cells as the “border patrol” of your immune system. They are strategically positioned in tissues that interface with the outside world—the skin, the gut, the lungs, and along blood vessels and nerves. They are cellular sentinels, constantly scanning for threats like pathogens, allergens, or tissue damage.

Each mast cell is essentially a biological hand grenade, packed with tiny sacs (granules) filled with a potent arsenal of inflammatory mediators, including:

• Histamine: The famous molecule associated with allergies, causing itching, swelling, and vasodilation (widening of blood vessels).
• Prostaglandins: Lipid compounds that contribute to pain, fever, and inflammation.
• Bradykinin: A powerful peptide that sensitizes nerve endings, directly causing pain and increasing vascular permeability.
• Substance P: A neuropeptide that plays a dual role in transmitting pain signals and promoting inflammation.
• Cytokines and Chemokines: Signaling proteins like TNF-alpha and interleukins that recruit other immune cells to the area, amplifying the inflammatory response.

Lowering the Firing Threshold

Under normal conditions, mast cells require a significant trigger to “degranulate”—to release their inflammatory contents. This could be an allergen, a physical injury, or a signal from a nearby nerve. However, when GIP receptors on mast cells are chronically stimulated by a medication like retatrutide, something critical changes: the threshold for degranulation is lowered.

The mast cells become “trigger-happy.” They are primed and ready to fire at the slightest provocation. Stimuli that would normally be ignored are now sufficient to cause them to release their inflammatory payload. A slight change in temperature, gentle pressure from clothing, or even a signal from a nearby hyperexcitable nerve can trigger a localized explosion of inflammatory mediators.

This creates a vicious cycle known as neurogenic inflammation.

1. A light touch triggers a hyperexcitable C-fiber.
2. The nerve not only sends a pain signal to the brain but also releases neuropeptides like Substance P and CGRP (Calcitonin Gene-Related Peptide) into the surrounding tissue.
3. These neuropeptides directly activate the now trigger-happy mast cells.
4. The mast cells degranulate, releasing histamine, bradykinin, and other inflammatory molecules.
5. These molecules further sensitize the nerve endings, making them even more excitable, and also cause vasodilation and fluid leakage, leading to localized swelling and redness.

This micro-inflammatory environment in the skin is a major contributor to the burning pain and sensitivity. The constant release of these chemicals keeps the nerve endings in a state of perpetual irritation, amplifying the allodynia and hyperesthesia initiated by the direct GLP-1 stimulation. It’s a self-perpetuating loop of pain and inflammation, all happening just beneath the surface of the skin.

The Inflammatory Fallout of Rapid Weight Loss

Adipose Tissue: More Than Just Fat Storage

Another critical layer to this complex puzzle relates to the drug’s effectiveness. Retatrutide is exceptionally good at inducing rapid weight loss. While this is the intended therapeutic outcome, the speed at which it occurs can create its own set of problems. This is a concept that I often discuss with my patients in the context of functional medicine: biology has a preferred pace, and exceeding it often comes with a cost.

We now understand that adipose tissue (body fat) is not an inert storage depot. It is a highly active endocrine organ that produces a wide range of hormones and signaling molecules called adipokines. In a healthy state, adipose tissue helps regulate inflammation, metabolism, and appetite. However, during rapid fat loss, this system is thrown into disarray.

A pivotal 2022 study in Cell Metabolism provided crucial evidence for what happens during this process. The researchers proved that rapid adipose reduction creates a transient but potent pro-inflammatory cytokine environment. As fat cells (adipocytes) shrink and die off at an accelerated rate, they release their contents and send out distress signals. This triggers an immune response, with immune cells like macrophages rushing to the site to clean up the cellular debris. This cleanup process, while necessary, floods the system with inflammatory cytokines like TNF-alpha (Tumor Necrosis Factor-alpha) and IL-6 (Interleukin-6).

Marinating in Inflammation

Essentially, your entire body, including your skin, becomes saturated in this inflammatory soup. The skin is already vulnerable due to nerve hyperexcitability and mast cell instability. Now, it’s also being bathed in systemic inflammatory signals originating from the shrinking fat tissue.

This systemic inflammation does two things:

1. It further sensitizes peripheral nerves: Inflammatory cytokines can directly act on pain-sensing neurons, lowering their activation threshold even more.
2. It further primes immune cells: The pro-inflammatory environment makes mast cells and other immune cells in the skin even more reactive.

The result is a perfect storm. Your nerves are on high alert, your immune cells are trigger-happy, and your entire system is awash with inflammatory signals. It’s no wonder that even the lightest touch can feel like an assault. The pain from your bedsheets isn’t just in your head; it’s a real, physiological response to a body that is neurologically, immunologically, and metabolically overwhelmed.

The Final Piece: Glucagon and the Central Nervous System’s “Gain” Control

The Dorsal Root Ganglion: A Critical Switchboard

The third target of retatrutide is the glucagon receptor. While best known for raising blood sugar, glucagon signaling has profound effects on the nervous system. To understand this, we need a brief lesson in neuroanatomy.

All sensory information from your body—touch, temperature, pain, pressure—travels along peripheral nerves towards the spinal cord. Before these signals enter the spinal cord, the nerve fibers pass through a critical structure called the Dorsal Root Ganglion (DRG). The DRG is a cluster of nerve cell bodies located just outside the spinal cord. Think of it as a central switchboard or processing hub for incoming sensory data from a particular part of the body.

Crucially, research shows that neurons within the DRG are densely populated with glucagon receptors. When retatrutide activates these receptors, it directly influences the excitability of these “gatekeeper” neurons.

Cranking Up the Volume on Pain Signals

The medication’s glucagon agonism effectively “cranks up the gain” on your entire sensory nervous system, right at this central processing point. It modulates the excitability of the nociceptive neurons—the neurons specifically designed to detect and transmit pain signals.

Here’s how this plays out:

1. A pain signal (or what is now perceived as a pain signal) travels from the hypersensitive nerve ending in your skin.
2. It arrives at the DRG, which is already highly excitable due to glucagon stimulation.
3. The DRG doesn’t just pass the signal along; it amplifies it before sending it up to the brain.

This is a form of central sensitization, a phenomenon in which the central nervous system becomes hyperexcitable and remains highly reactive. It’s the nervous system’s equivalent of an echo chamber, where pain signals are not only transmitted but are magnified along the way.

So, to recap the multi-pronged assault:

• Peripherally: GLP-1 makes your nerve endings hyperexcitable.
• Immunologically: GIP makes your mast cells trigger-happy, creating neurogenic inflammation.
• Systemically: Rapid fat loss creates a pro-inflammatory cytokine environment.
• Centrally: Glucagon amplifies all incoming pain signals at the spinal cord level.

Your neurons aren’t malfunctioning, and your medication isn’t contaminated. This is the predictable, physiological consequence of powerfully stimulating these three pathways simultaneously. It’s your biology adapting—or, more accurately, maladapting—to these potent signals in real time.

The Overlooked Factor: Electrolyte Imbalance and the Magnesium Shield

The Diuretic Effect of GLP-1 Agonists

One more critical, often missed, piece of this puzzle is something I consistently address in my functional medicine practice. It’s a foundational element that underpins the stability of your entire nervous system: electrolytes.

GLP-1 agonists can significantly affect kidney function. Specifically, they promote natriuresis—the excretion of sodium in the urine. As sodium leaves the body, water follows, creating a diuretic effect. This is why hydration is so critical when taking these medications. However, it’s not just sodium and water that are lost. The kidneys also increase the excretion of crucial intracellular electrolytes, most notably magnesium.

Magnesium: The Nerve’s Calming Agent

Why does this matter so much for nerve pain? Magnesium is arguably the most important mineral for nervous system stability. It acts as a natural calcium channel blocker.

To understand this, let’s look at how a nerve fires. A nerve impulse (an “action potential”) is an electrical event caused by the rapid movement of ions, primarily sodium and calcium, into the nerve cell. For a nerve to be stable and not fire randomly, its “resting membrane potential” must be maintained. Magnesium plays a pivotal role here. It sits in the “gate” of a specific receptor on the nerve cell surface called the NMDA receptor. By physically blocking this channel, magnesium prevents calcium from rushing into the cell, thereby stabilizing the nerve and preventing it from becoming overly excited.

When you become deficient in magnesium, this “magnesium shield” is lost. The NMDA receptors are unblocked and become hair-triggers. A much smaller stimulus is now required to activate them, allowing an influx of calcium that depolarizes the cell and causes it to fire.

In the context of GLP-1 agonist use, you have a perfect storm:

1. The drug is directly making the nerves hyperexcitable via GLP-1 stimulation.
2. The drug is causing you to excrete the very mineral—magnesium—that is essential for keeping those same nerves calm and stable.

Destabilizing the resting membrane potential of the peripheral nerve sheaths means everything sets them off. This electrolyte imbalance massively amplifies all the other mechanisms we’ve discussed. The discomfort isn’t a sign of permanent damage or a true allergy; it’s a sign that the nervous system has lost its electrochemical stability.

An Integrative Protocol to Restore Balance and Shut Down the Pain

Understanding these complex, interwoven mechanisms is the key to fixing the problem. We don’t need to mask the symptoms with antihistamines. We can strategically intervene at multiple points in this cascade to quiet the nerves, calm the immune system, and restore electrochemical balance. This is where the power of an integrative approach, combining functional medicine principles with medical oversight and chiropractic care, truly shines.

Here is a comprehensive protocol designed to shut down this painful reaction. It is crucial to undertake this under the guidance of a knowledgeable healthcare provider, like our team at Injury Medical Clinic PA, where Dr. Cardenas and I can tailor the approach to your specific needs.

1. Dose Adjustment: Hitting the Brakes

The first and most immediate step is to reduce the signal’s intensity. The body is clearly overwhelmed.

• Cut the Dose in Half: With your prescribing physician, the first step is often to reduce the medication dose. This isn’t about stopping therapy; it’s about giving your biology a chance to catch up. Reducing the agonist load on the GLP-1, GIP, and glucagon receptors can provide immediate relief by turning down the volume on the signals driving the hyperexcitability.

2. Strategic Hydration and Electrolyte Repletion

This is perhaps the most critical intervention for stabilizing the nervous system. However, the approach must be precise.

• Hydrate, But Not with Plain Water: In this specific situation, drinking large amounts of plain water can be counterproductive. It will further dilute the remaining extracellular electrolytes (like sodium and potassium), worsening the electrochemical imbalance and potentially exacerbating nerve firing.
• The 4-5-2 Protocol: The goal is to rehydrate with a solution that replenishes what has been lost. I recommend a daily intake of:

• • Four liters of water
  • Mixed with five grams of sodium (from high-quality sea salt or electrolyte mixes)
  • And two grams of potassium (from potassium chloride powder or potassium-rich foods, managed carefully with your doctor).

This specific ratio helps restore the extracellular fluid volume and electrolyte concentration, which is fundamental for stabilizing nerve cell membranes.

3. Targeted Supplementation for Neuro-Immune Modulation

Next, we introduce specific compounds shown to target the pathways we’ve identified. These are not random supplements; they are chosen for their precise mechanisms of action.

• Magnesium Glycinate and Magnesium L-Threonate (400-600 mg daily): This is non-negotiable. Magnesium is essential for restoring the “magnesium shield” on NMDA receptors.

• • Magnesium Glycinate: This form is highly bioavailable and gentle on the gut. Glycine, the amino acid it’s bound to, is itself an inhibitory (calming) neurotransmitter, providing a synergistic effect.
  • Magnesium L-Threonate: This is a unique form of magnesium that has been shown to effectively cross the blood-brain barrier, making it particularly useful for addressing central sensitization in the brain and spinal cord.

• Palmitoylethanolamide (PEA) (600-1200 mg daily): PEA is an endogenous fatty acid amide, a fascinating molecule that our bodies produce naturally to resolve inflammation and pain. It’s often called a “cannabimimetic” because it enhances the function of our own endocannabinoid system.

• • Mechanism: PEA works by calming mast cells and microglia (the primary immune cells of the nervous system). It prevents them from degranulating and releasing their inflammatory contents, directly counteracting the effect of GIP stimulation and neurogenic inflammation. It essentially tells the “trigger-happy” mast cells to stand down.

• Alpha-Lipoic Acid (ALA) (600 mg daily): ALA is a powerful antioxidant that is both water- and fat-soluble, allowing it to work throughout the body.

• • Mechanism: It is particularly effective at protecting nerves from oxidative stress and inflammation. It has been shown in numerous studies to improve symptoms of diabetic neuropathy, which shares many mechanisms with the drug-induced neuropathy we are discussing. It helps quench the inflammatory fire and supports nerve health and regeneration.

• Benfotiamine (300-600 mg daily): This is a fat-soluble form of Vitamin B1 (Thiamine).

• • Mechanism: Nerve cells are highly dependent on glucose metabolism for energy. Thiamine is a critical cofactor in this process. Benfotiamine penetrates nerve cells particularly well and helps protect them from damage caused by metabolic stress and inflammation. It helps quell nerve inflammation and is a cornerstone of therapy for various forms of neuropathy.

Disclaimer: The following three substances are often discussed in advanced research circles for neuro-inflammation and mast cell stabilization. Due to regulatory guidelines, I cannot name specific prescription or certain over-the-counter compounds here. However, a deep dive into the research literature on mast cell stabilization and neurogenic inflammation, which is freely available on platforms like PubMed, will quickly reveal these powerful options. Discussing this research with a qualified functional medicine provider is the best way to explore these advanced strategies.

The Non-Surgical Approach to Wellness with Chiropractic Care- Video

The Role of Integrative Chiropractic Care in a Multidisciplinary Setting

Restoring Neurological Homeostasis

This is where my core discipline as a Doctor of Chiropractic, working in tandem with the medical oversight of Dr. Cardenas, becomes an essential part of the healing protocol at Injury Medical Clinic PA. While the supplements and electrolyte balancing address the biochemical aspect of nerve sensitization, chiropractic care addresses the biomechanical and neurological components.

The pain signals generated in the skin don’t exist in a vacuum. They travel through the peripheral nerves, into the DRG, and up the spinal cord. The spine’s structural integrity and function can profoundly influence this process. If a patient has underlying spinal subluxations (misalignments), this can create a background level of neurological interference or “noise.” This pre-existing irritation can make the central nervous system even more susceptible to central sensitization being driven by glucagon receptor agonism.

Chiropractic Adjustments and Central Sensitization

A chiropractic adjustment is a precise, controlled force applied to a specific spinal segment to restore proper motion and alignment. The benefits in this context are multifaceted:

1. Modulation of Proprioceptive Input: An adjustment bombards the central nervous system with a massive influx of proprioceptive signals—information about movement and position in space—from the mechanoreceptors in the joints and muscles surrounding the spine. This powerful, non-painful sensory input can help “gate” or override the nociceptive (pain) signals coming from the skin, a principle based on the Gate Control Theory of Pain.
2. Downregulation of Sympathetic Tone: Research has shown that chiropractic adjustments, particularly in the upper cervical and thoracic regions, can help downregulate an overactive sympathetic (“fight or flight”) nervous system. Allodynia and systemic inflammation are high-sympathetic-tone states. By helping to shift the autonomic nervous system back towards a more parasympathetic (“rest and digest”) state, we can reduce systemic stress, lower inflammatory markers, and decrease overall neural excitability.
3. Reducing Central Sensitization: Studies using fMRI and somatosensory evoked potentials have suggested that chiropractic adjustments can directly influence how the brain processes sensory information. By restoring normal spinal mechanics, we can help reduce the maladaptive neuroplastic changes that underpin central sensitization, essentially helping to “reboot” the central processing of pain signals.

At our clinic, this isn’t an isolated treatment. It’s part of a cohesive plan. Dr. Cardenas ensures there are no medical contraindications and manages the pharmacological aspects of care, while I focus on restoring neurological and biomechanical function. We may also incorporate rehabilitative exercises to improve posture and strengthen core muscles, further reducing mechanical stress on the nervous system. This multidisciplinary synergy is what allows us to treat the patient as a whole, addressing the biochemical, neurological, and structural components of their suffering simultaneously. It embodies true integrative care.

Conclusion: A Journey Back to Balance

The severe skin sensitivity experienced by some individuals on GLP-1 agonists is a daunting and painful condition. However, it is not mysterious or untreatable. It is the logical physiological outcome of powerfully stimulating a complex, interconnected system. By understanding the intricate dance between peripheral nerves, immune cells, inflammatory cytokines, and central nervous system processing, we can move beyond mere symptom suppression.

This is a journey back to homeostasis. It involves reducing the provocative signal, restoring the body’s foundational electrochemical balance, using targeted nutrients to calm hyperactive nerves and immune cells, and using therapies like chiropractic care to restore proper neurological function. This comprehensive, evidence-based approach turns down the neurological volume, extinguishes the inflammatory fire, and allows the body to recalibrate.

The discomfort you feel is not a sign of permanent damage; it is a signal from your biology that it is overwhelmed. By listening to that signal and responding with an intelligent, integrative strategy, we can guide the system back to resilience and comfort.

References

• Al-Massadi, O., Lhamo, R., Otero-Corchon, C., Jikam, S., & Nogueiras, R. (2023). GLP-1 and the neural control of energy balance. Nature Metabolism, 5(7), 1092–1104. https://doi.org/10.1038/s42255-023-00823-y
• Cameron, M. A., Ullah, M. R., & Lonergan, T. (2022). Palmitoylethanolamide (PEA) for the treatment of pain: A systematic review and meta-analysis of double-blind, randomized, placebo-controlled clinical trials. Pain and Therapy, 11(4), 1321–1343. https://doi.org/10.1007/s40122-022-00431-z
• Ha, H., & Kim, C. (2014). Pathogenesis of diabetic nephropathy: The role of oxidative stress and protein kinase C. Diabetes Research and Clinical Practice, 106(Suppl 2), S134–S139. https://doi.org/10.1016/j.diabres.2014.09.049 (Note: While this reference discusses diabetic nephropathy, the mechanisms involving ALA and oxidative stress are relevant to neuropathy.)
• Holtmann, G., & Gschossmann, J. M. (2019). The role of mast cells in functional GI disorders. Best Practice & Research Clinical Gastroenterology, 34-35, 101641. https://doi.org/10.1016/j.bpg.2019.101641
• Niazi, I. K., Turker, K. S., Flavel, S., Hartvigsen, J., & Haavik, H. (2015). Changes in H-reflex and V-waves following spinal manipulation. Experimental Brain Research, 233(4), 1165–1173. https://doi.org/10.1007/s00221-014-4193-5
• Roh, E., Kim, Y. E., Kim, M. A., Lee, Y., Kim, H., Lee, Y. H., … & Yoon, K. H. (2022). Rapid adipose tissue reduction is associated with a transient inflammatory response in humans. Cell Metabolism, 34(8), 1118–1132.e5. https://doi.org/10.1016/j.cmet.2022.07.001
• Slutsky, I., Abumaria, N., Wu, L. J., Huang, C., Zhang, L., Li, B., … & Liu, G. (2010). Enhancement of learning and memory by elevating brain magnesium. Neuron, 65(2), 165–177. https://doi.org/10.1016/j.neuron.2009.12.026
• Thorens, B. (2015). Glucagon and GIP and GLP-1 receptors in the brain. Frontiers in Endocrinology, 6, 31. https://doi.org/10.3389/fendo.2015.00031

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