A New Model Discussing Interleukin-10
The primary reason people go to chiropractors is for the complaint of spinal pain. A recent review of the chiropractic profession, published in the prestigious journal Spine, shows that 93% of chiropractic patients initially seek chiropractic care for spinal pain complaints: 63% for low back pain and 30% for neck pain. Patient satisfaction with their chiropractic care is exceptionally high (1).
Pain is an electrical signal interpreted by one’s brain. The electrical signal is brought to the brain by a nerve (2). All nerves, including the pain nerves, have a threshold. Nerves will not send their electrical signal unless that threshold is met.
Again, before any nerve generates the electrical signal to send to the brain, it must first reach threshold. As an example, for the brain to perceive sound, the sound must be great enough to reach the threshold of the sound nerve. Otherwise, the subject would not hear it.
Pain nerves also have a threshold. As an analogy, touching one’s skin over a muscle will reach threshold for the touch nerve. The subject becomes aware of the touch. But there is no pain because the pain nerve has a higher threshold than the touch nerve.
However, if greater amounts of pressure are applied, the pressure nerve will reach threshold, and the subject will become aware of both touch and pressure.
If even greater amounts of pressure are applied, the threshold of the pain nerve will be reached, and the subject will feel touch, pressure, and pain.
Measuring a patient’s pain threshold has been described for more than forty years (4, 5, 6). The device to do this is called a pressure pain threshold device, or an algometer. An algometer is defined as (7):
“An algometer is a specialized, handheld force gauge used to objectively measure pain sensitivity, specifically identifying the minimum pressure (pressure-pain threshold) or force that induces pain. It operates by applying pressure to soft tissues or joints to quantify tenderness, commonly used to evaluate conditions like fibromyalgia, musculoskeletal disorders, or trigger points.”
Traditionally and at present, the perception of pain is linked to inflammation (8, 9). Inflammation reduces the threshold of the pain nerve. This means that more inflammation causes more pain, and reduced inflammation reduces pain.
A published example of this concept is provided by Sota Omoigui, MD, the medical director of the Los Angeles Pain Clinic. In his article from 2007 he states (9):
The Biochemical Origin of Pain:
The Origin of All Pain is Inflammation and the Inflammatory Response
“Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome.”
“The key to treatment of Pain Syndromes is an understanding of their inflammatory profile.”
“Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response.”
“Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response.”
“Activation of pain receptors, transmission and modulation of pain signals, neuro-plasticity and central sensitization are all one continuum of inflammation and the inflammatory response.”
“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”
This perspective agrees with Vert Mooney’s address when he was elected President of the International Society for the Study of the Lumbar Spine. His address was published in the journal Spine, and titled (10):
Where Is the Pain Coming From?
“In the United States in the decade from 1971 to 1981, the numbers of those individuals disabled from low-back pain grew at a rate 14 times that of the population growth. This is a greater growth of medical disability than any other. Yet this growth occurred in the very decade when there was an explosion of ergonomic knowledge, labor-saving mechanical assistance devices, and improved diagnostic equipment. We apparently could not find the source of pain.”
“Anatomically the motion segment of the back is made up of two synovial joints and a unique relatively avascular tissue found nowhere else in the body – the intervertebral disc. Is it possible for the disc to obey different rules of damage than the rest of the connective tissue of the musculoskeletal system?”
“Mechanical events can be translated into chemical events related to pain.”
“Mechanical activity has a great deal to do with the exchange of water and oxygen concentration [in the disc].”
An important aspect of disc nutrition and health is the mechanical aspects of the disc related to the fluid mechanics.
The pumping action maintains the nutrition and biomechanical function of the intervertebral disc. Thus, “research substantiates the view that unchanging posture, as a result of constant pressure such as standing, sitting or lying, leads to an interruption of pressure-dependent transfer of liquid. Actually, the human intervertebral disc lives because of movement.”
“The fluid content of the disc can be changed by mechanical activity.”
“In summary, what is the answer to the question of where is the pain coming from in the chronic low-back pain patient? I believe its source, ultimately, is in the disc. Basic studies and clinical experience suggest that mechanical therapy is the most rational approach to relief of this painful condition.”
This perspective that spinal motion activates a pump that disperses the accumulation of chemicals that cause pain is very important to the chiropractic profession.
The inflammatory pain-producing chemicals are explored below.
Vert Mooney, MD, was a renowned and respected orthopedic surgeon. He was trained at Columbia University College of Physicians and Surgeons (medical school) and at the University of Pittsburgh (Orthopedic Surgery Residency). He died in 2009.
Dr. Mooney was a founding member of the North American Spine Society (NASS), and he served as NASS President from 1987-1988. He also received the Lifetime Achievement Award in Lumbar Spine Research from the International Society for the Study of the Lumbar Spine in 2008. His area of specialty was advocating for non-surgical approaches to the management of acute and chronic lumbo-pelvic pain and the promotion of interdisciplinary approaches to the prevention, diagnosis, and treatment of lower back spinal problems.
The fact that chiropractors help patients with spine pain syndromes has been unquestioned for more than 40 years. For example, in 1985, orthopedic surgeon W. H. Kirkaldy-Willis stated (11):
“Spinal manipulation, one of the oldest forms of therapy for back pain, has mostly been practiced outside of the medical profession.”
“Over the past decade, there has been an escalation of clinical and basic science research on manipulative therapy, which has shown that there is a scientific basis for the treatment of back pain by manipulation.”
There are several credible theories used to explain why chiropractic care helps people with pain. These include the gate pain theory, activating the suprasegmental descending pain inhibitory system theory, and the dispersion of inflammatory chemicals theory (11, 12, 13, 20, 21).
The Gate Pain Theory
This theory was first proposed in 1962 (12) and updated in 1965 (13). This theory posits that the pain electrical signal to the brain can be blocked (inhibited) by improving the same segmental region mechanical function (small diameter afferents) can be inhibited by non-painful electrical signals arising from other sensory afferents (large diameter afferents).
The perception of pain is dependent upon the balance of activity in large (mechanoreceptor) and small (nociceptive) afferents. (14)
If large myelinated fibers (mechanoreceptors) were selectively stimulated, then normal “balance” of activity between large (mechanoreceptor) and small (nociceptive) fibers would be restored and the pain would be relieved. (14)
“Pain is not simply a direct product of the activity of nociceptive afferent fibers but is regulated by activity in other myelinated afferents that are not directly concerned with the transmission of nociceptive information.” (15)
“The idea that pain results from the balance of activity in nociceptive and non-nociceptive afferents was formulated in the 1960s and was called the gate control theory.” (15)
“Simply put, non-nociceptive afferents ‘close’ and nociceptive afferents ‘open’ a gate to the central transmission of noxious input.” (15)
“The balance of activity in small- and large-diameter fibers is important in pain transmission…” (15)
The Gate Theory of Pain was reviewed and confirmed in 2002 in the British Journal of Anaesthesia (16):
An early application of the Gate Theory to explain the benefits of chiropractic care on pain patients was done by Canadian orthopedic surgeon Kirkaldy-Willis in 1985 (11). Dr. Kirkaldy-Willis notes:
Melzack and Wall proposed the Gate Theory of Pain in 1965, and this theory has “withstood rigorous scientific scrutiny.”
“The central transmission of pain can be blocked by increased proprioceptive input.” Pain is facilitated by “lack of proprioceptive input.” This is why it is important for “early mobilization to control pain after musculoskeletal injury.”
“Increased proprioceptive input in the form of spinal mobility tends to decrease the central transmission of pain from adjacent spinal structures by closing the gate. Any therapy which induces motion into articular structures will help inhibit pain transmission by this means.”
Stretching of facet joint capsules will fire capsular mechanoreceptors which will reflexively “inhibit facilitated motoneuron pools” which are responsible for the muscle spasms that commonly accompany low back pain.
Activating the Suprasegmental Descending Pain Inhibitory System Theory
It has been understood for more than 50 years that the perception of pain is controlled by a spot located at the top of the brainstem (mesencephalon) called the periaqueductal grey matter (17, 18, 19). Stimulating the nerves of the periaqueductal grey matter has shown to reduce or eliminate pain anywhere in the body. Activating this system is known as the Suprasegmental Descending Pain Inhibitory System.
It is now thought that spinal adjusting (specific line-of-drive manipulation) reduces pain by activating this system (20, 21).
The Dispersion of Inflammatory Chemicals Theory
As noted above, and as championed by Vert Mooney, MD, an accumulation of inflammatory chemicals lowers the threshold for the pain nerves; and it follows that motion that disperses the accumulation of these chemicals will raise the pain threshold and reduce pain.
This theory is particularly pertinent to discogenic low back pain because:
- The intervertebral disc is the primary source of chronic low back pain.
- The disc does not have a blood supply to deliver anti-inflammatory molecules or to wash away the accumulation of inflammatory pain-producing chemicals
- A mechanistically plausible approach to disperse the inflammatory chemicals of chronic back pain is through motion. Motion pumps the inflammatory chemicals through the porous cartilaginous end-plates into the very vascular vertebral bodies, dispersing their accumulation.
- Chronic back pain patients have reduced segmental mobility and hence they accumulate inflammatory chemicals. Chiropractors have the ability to locate the level and direction of this lack of mobility and to improve it with the delivery of the spinal adjustment, dispersing the chemicals and reducing pain.
Important for this discussion are the findings that the inflammatory chemicals that cause pain, and especially back pain, are primarily categorized into two groups:
Inflammatory Eicosanoids
The best-known inflammatory eicosanoid is prostaglandin E2 (PGE2). PGE2 was the topic of the 1982 Nobel Prize in Medicine or Physiology.
PGE2 is derived from the omega-6 essential fatty acid arachidonic acid. Arachidonic acid is derived from the plant fats found in corn, soy, canola, sunflower, safflower, cottonseed oil, etc. Surprisingly, several of these, especially corn and soy, are subsidized by the US taxpayers.
The primary non-drug management of the pain caused by the inflammatory eicosanoid PGE2 is consumption of high doses of omega-3 essential fatty acids (22, 23, 24).
Inflammatory Cytokines
Cytokines are protein molecules (chemicals) that are produced by immune system cells. Cytokines can be pro-inflammatory or anti-inflammatory.
Interleukins are a category of cytokines. Like cytokines, interleukins can either be pro-inflammatory or anti-inflammatory. Interleukins are abbreviated “IL.”
The best known and understood pro-inflammatory cytokines include:
- Interleukin-6 (IL-6)
- Interleukin-8 (IL-8)
- Interleukin-1 beta (IL-1β)
- Tumor Necrosis Factor-alpha (TNF-alpha)
An excellent discussion to learn about cytokines is found in the 2007 book by attorney Chris Crowley and physician Henry Lodge, MD, titled (25):
Younger Next Year
Live Strong, Fit, and Sexy–Until You’re 80 and Beyond
A more detailed discussion of cytokines is found throughout the 2025 book by neurosurgeon and vagus nerve researcher Kevin Tracey, MD, titled (26):
The Great Nerve:
The New Science of the Vagus Nerve and How to Harness Its Healing Reflexes
Quite important to this discussion is the findings that chronic back pain is coupled to the inflammatory eicosanoid prostaglandin E2 (PGE2) and to the inflammatory cytokine interleukin-6 (IL-6) (27, 28).
A New Model: Interleukin-10
As noted above, there are pro-inflammatory pain-producing cytokines and there are anti-inflammatory cytokines that powerfully inhibit pain. The best understood anti-inflammatory cytokine is interleukin-10 (IL-10). The importance of IL-10 in pain suppression is increasingly being understood.
In their text, attorney Chris Crowley and physician Henry Lodge, MD, make the following statements pertaining to IL-10, that it is (25):
- Anti-Inflammatory
- Regenerative
- Restorative
- It “is the master chemical for repair and growth.”
- It “is the key because growth is the magic you are after.”
- Its effect is to build a “stronger, healthier, younger body.”
In 2020, the journal Frontiers in Immunology published a study titled (29):
IL-27 Counteracts Neuropathic Pain Development Through Induction of IL-10
Neuropathic pain is a difficult type of pain to resolve. The authors of this study note:
“These results provided evidence that IL-27 is a cytokine produced after peripheral nerve injury that counteracts neuropathic pain development through induction of the antinociceptive cytokine IL-10.”
The authors conclude that interventions that increase IL-10 “could emerge as possible therapeutic approaches for the prevention of neuropathic pain development after peripheral nerve injury.”
More recently (2026) the American Association for the Advancement of Science published a study in the journal Science Immunology titled (30):
Monocyte-derived IL-10 Drives Sex Differences in Pain Duration
This assessment included both mouse and 245 human subjects. The objective of this study was to investigate whether IL-10 mediates chronic posttraumatic pain. The human subjects suffered from whiplash injuries.
The authors found:
- The anti-inflammatory cytokine interleukin-10 (IL-10) resolves inflammatory pain.
- Proinflammatory cytokine levels are inversely correlated with IL-10 levels.
The authors stated:
- “Expression of proinflammatory cytokines IL-6, IL-1β, and TNF-alpha was reduced by IL-10.”
- “IL-10 is an important antinociceptive cytokine, with its effect traditionally linked to suppression of inflammation.”
- “Circulating IL-10 levels were negatively correlated with pain severity at 84 days, indicating that higher IL-10 levels were associated with faster pain resolution.”
The Chiropractic Connection
This science and perspective presented here has a lot of relevance for the chiropractic profession and for their patients suffering from pain syndromes. In 2016, the World Federation of Chiropractic award winning paper was published in the Journal of Manipulative and Physiological Therapeutics, titled (31):
Attenuation Effect of Spinal Manipulation on Neuropathic and Postoperative Pain Through Activating Endogenous Anti-Inflammatory Cytokine Interleukin-10 in Rat Spinal Cord
Using animal models, these authors showed that repetitive spinal manipulative therapy “significantly reduced simulated neuropathic and postoperative pain, inhibited or reversed the neurochemical alterations, and increased the anti-inflammatory IL-10 in the spinal cord.” They concluded:
“These findings show that spinal manipulation may activate the endogenous anti-inflammatory cytokine IL-10 in the spinal cord and thus has the potential to alleviate neuropathic and postoperative pain.”
•••••
The science of chiropractic care and the understanding of the physiological benefits of spinal joint adjusting has continually advanced for more than a century. This presentation continues to present relevant updated information that is already being taught in both chiropractic colleges/universities and in post-graduate continuing education classes.
REFERENCES
- Adams J, Peng W, Cramer H, Sundberg T, Moore C; The Prevalence, Patterns, and Predictors of Chiropractic Use Among US Adults; Results From the 2012 National Health Interview Survey; Spine; December 1, 2017; Vol. 42; No. 23; pp. 1810–1816.
- Ambron R; The Brain and Pain: Breakthroughs in Neuroscience; Columbia University Press; New York; 2022.
- Kandel ER, Schwartz JH, Jessell TM; Principles of Neural Science; Fourth Edition; McGraw-Hill; 2000.
- Fischer AA; Pressure Tolerance Over Muscles and Bones in Normal Subjects; Archives of Physical Medicine and Rehabilitation; June 1986; Vol. 67; No. 6; pp. 406-409.
- Fischer AA; Pressure Threshold Meter: Its Use for Quantification of Tender Spots; Archives of Physical Medicine and Rehabilitation; November 1986; Vol. 67; No. 11; pp. 836-838.
- Fischer AA; Pressure Algometry Over Normal Muscles: Standard Values, Validity and Reproducibility of Pressure Threshold; Pain; July 1987; Vol. 30; No. 1; pp. 115-126.
- https://www.merriam-webster.com/medical/algometer; accessed March 31, 2026.
- Omoigui S; The Biochemical Origin of Pain; S.O.T.A. Technologies, Inc.; Hawthorne, CA; 2003.
- Omoigui S; The Biochemical Origin of Pain: The Origin of All Pain is Inflammation and the Inflammatory Response: Inflammatory Profile of Pain Syndromes; Medical Hypothesis; 2007; Vol. 69; No. 6; pp. 1169–1178.
- Mooney V; Where Is the Pain Coming From?; Spine; Vol. 12; No. 8; 1987; pp. 754-759.
- Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985; Vol. 31; pp. 535-540.
- Melzack R, Wall PD; On the nature of cutaneous sensory mechanisms; Brain; June 1962; 85:331-56.
- Melzack R, Wall PD; Pain mechanisms: A New Theory; Science; November 19, 1965; Vol. 150; No. 3699; pp. 971-979.
- Nolte J; The Human Brain; Mosby Year Book, 1993.
- Kandel E, Schwartz J, Jessell T; Principles of Neural Science; McGraw-Hill; 2000.
- Dickenson AH; Gate Control Theory of pain stands the test of time; British Journal of Anaesthesia; June 2022; Vol. 88; No. 6; pp. 755-757.
- Pert CB, Snyder SH; Opiate receptor: Demonstration in Nervous Tissue; Science; March 9, 1973; Vol. 179(4077); pp. 1011-1014.
- Hosobuchi Y, Adams JE, Linchitz R; Pain Relief by Electrical Stimulation of the Central Gray Matter in Humans and its Reversal by Naloxone; Science; July 8, 1977; Vol. 197(4299); pp. 183-186.
- Restak R; The Brain, The Last Frontier; Warner Books; 1979.
- Vicenzino B, Collins D, Wright A; The Initial Effects of a Cervical Spine Manipulative Physiotherapy Treatment on the Pain and Dysfunction of Lateral Epicondylalgia; Pain; November 1996; Vol. 68; No. 1; pp. 69-74.
- Savva C, Giakas G, Efstathiou M; The Role of the Descending Inhibitory Pain Mechanism in Musculoskeletal Pain Following High-velocity, Low Amplitude Thrust Manipulation: A Review of the Literature; Journal of Back Musculoskeletal Rehabilitation; 2014; Vol. 27; No. 4; pp. 377-382
- Maroon JC, Bost JW; Omega-3 Fatty Acids (fish oil) as an Anti-inflammatory: An Alternative toNonsteroidal Anti-inflammatory Drugs for Discogenic Pain; Surgical Neurology; April 2006; Vol. 65; pp. 326–331.
- Cleland LG, James MJ, Proudman SM; Fish oil: What the Prescriber Needs to Know; 2006;Arthritis Research & Therapy; Vol. 8; No. 1; Article 202.
- Goldberg RJ, Katz J; A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain; Pain; May 2007; Vol. 129; No. 1-2; pp. 210-223.
- Crowley C, Lodge H; Younger Next Year: Live Strong, Fit, and Sexy–Until You’re 80 and Beyond; Workman Publishing; New York; 2007.
- Tracey K; The Great Nerve: The New Science of the Vagus Nerve and How to Harness Its Healing Reflexes; Avery; 2025.
- Kang JD, Georgescu HI, McIntyre-Larkin L, Stefanovic-Racic M, Donaldson WF, Evans CH; Herniated Lumbar Intervertebral Discs Spontaneously Produce Matrix Metalloproteinases, Nitric Oxide, Interleukin-6, and Prostaglandin E2; Spine; February 1, 1996; Vol. 21; No. 3; pp. 271-277.
- Kang JD , Stefanovic-Racic M, McIntyre LA, Georgescu HI, Evans CH;Toward a Biochemical Understanding of Human Intervertebral Disc Degeneration and Herniation: Contributions of Nitric Oxide, Interleukins, Prostaglandin E2, and Matrix Metalloproteinases; Spine; May 15, 1997; Vol. 22; No. 10; pp 1065-1073.
- Fonseca MM, Davoli-Ferreira M, Santa-Cecília F, Guimarães RM, Oliveira FFB, Kusuda R, Ferreira DW, Alves-Filho JC, Cunha FQ, Cunha TM; IL-27 Counteracts Neuropathic Pain Development Through Induction of IL-10; Frontiers in Immunology; January 28, 2020; Vol. 10; Article 3059.
- Sim J, O’Guin E, Sugimoto C, Laumet S, and 15 more; Monocyte-derived IL-10 Drives Sex Differences in Pain Duration; Science Immunology; February 20, 2026; Vol. 11; epub.
- Song XJ, Huang ZJ, Song WB, Song XS, Fuhr AF, Rosner AL, Ndtan H, Rupert RL; Attenuation Effect of Spinal Manipulation on Neuropathic and Postoperative Pain Through Activating Endogenous Anti-Inflammatory Cytokine Interleukin-10 in Rat Spinal Cord; Journal of Manipulative and Physiological Therapeutics; January 2016; Vol. 39; No. 1; pp. 42-53.
