A biochemical approach to decreasing muscle pain with food and hormones.

pain and hormones

pain and hormones

A biochemical approach to decreasing muscle pain is often the last place most people look and that includes many pain specialists. Modulating pain and hormones through food and other variables can create some impressive results. Aches and pains are a common theme in every day living. Some people seek to push themselves harder with excessive training schedules, others spend more time in a seated position and other factors contribute to tissue not responding the way that it should. Pain and the concept of nociception is a system of feedback for the body that is protective in essence. You touch something you shouldn’t; first pain kicks in to remove you from the painful stimulus (lasts less than 0.1 seconds), after that and depending on severity of damage second pain kicks in.

First pain and second pain (both reside in the anterolateral system or ALS) utilise different chemical messengers and another factor for this form of feedback is that other nociceptive factors like touch, visual, auditory and other sensations of stress can be part of the problematic feedback if not resolved. All of these have the capacity to interrupt optimal motor control and functioning of joints and soft tissues and affect hormone profiles. Even a bad smell can create neurological chaos.

Another less well known aspect (in therapy based settings) of disruptive function in muscle tissue are the effects of hormones that may lead to decreased feed back and be responsible for pain. Hypothyroidism affects muscle tissue via energy and neurological deficiencies.

Hypothyroidism results in

Slower peripheral and central nerve conduction velocity Lower body temperature is a factor creating slowed velocity Decreased active cell transport in the cerebral cortex Decreased flux of sodium and calcium for contraction/relaxation Poor production of energy for contraction/relaxation Decreases depolarisation of action potential

cold body

cold body

In a nutshell a colder, slower body leads to a decreased   coordinated body that has a hard time contracting and relaxing muscle tissue. This can lead to increased incidence of injury and pain.

A slowed heart rate is a sign of hypothyroidism and the bradychardia (slowed heart rate) should serve the purpose of describing the decreased rate of function throughout all muscle tissue. Thyroid hormone can improve both rate of contraction and relaxation in both fast and slow twitch muscles but also exerts a cardio protective role on blood vessels and bowel function via smooth muscle tissue. The documented symptoms of hypertension and constipation along with the neuromuscular actions tend to resolve with adequate thyroid hormone (Gao, Zhang, Zhang, Yang, & Chen, 2013).

Prior to initiating thyroid therapy it’s essential to rule out functionally hypothyroid states induced by diet, stress, excess exercise and other environmental factors. Many clients often present with lowered temperature, with cold hands, feet and nose, altered bowel, sleep and emotional function, which can often be resolved with appropriate energy and decreased intestinal irritants.

Chronic pain increases cortisol production which decreases thyroid hormone production (Samuels & McDaniel, 1997) as does fasting or calorie restriction which induces a decrease in available T3 (thyroid hormone) (Hulbert, 2000).

This gives us two approaches 1) to reduce pain with appropriate therapy and to ensure that adequate energy modulates the suppression of excess cortisol and increases available thyroid for tissue organisation and recovery.

Hormones also affect tendons; diabetics and poor insulin profiles appear to create disorganised tendon structure but this may be a factor related to decreased available thyroid hormone. Hypothyroidism decreases available T3 within tendons, which can decrease growth, structure, and collagen production and create hypoxia of tissue leading to calcification.

Estrogen, although necessary for growth of tissue can often be found in excess creating problematic growth. Estrogen is also well known to decrease thyroid hormone and can provide an explanation why more females then men tend to be hypothyroid. The decrease in both thyroid hormone and progesterone can increase muccopolysacharides, which increase pressure in tissues, creating puffy, oedema like states. The swelling can be linked to many pain states which include carpal tunnel, which can be resolved with progesterone and thyroid in the absence of physical therapy. Progesterone also appears to induce myelination of nerves (surrounds and allows nerve conduction) and decreases inflammation (Milani et al 2010).

Energy production remains  a most potent form of therapy for decreasing pain, optimising rehabilitation and restoring tissue function.


  1. Gao, N., Zhang, W., Zhang, Y., Yang, Q., & Chen, S. (2013). Carotid intima-media thickness in patients with subclinical hypothyroidism: A meta-analysis. Atherosclerosis, 227(1), 18–25.

  2. Hulbert, A. (2000). Thyroid hormones and their effects: a new perspective. Biological Reviews of the Cambridge Philosophical Society, 75(4), 519–631.

  3. Milani, P., Mondelli, M., Ginanneschi, F., Mazzocchio, R., & Rossi, A. (2010). Progesterone - new therapy in mild carpal tunnel syndrome? Study design of a randomized clinical trial for local therapy. Journal of Brachial Plexus and Peripheral Nerve Injury, 5(1).


  5. Samuels, M. H., & McDaniel, P. A. (1997). Thyrotropin levels during hydrocortisone infusions that mimic fasting- induced cortisol elevations: A clinical research center study. Journal of Clinical Endocrinology and Metabolism, 82(11), 3700–3704.

Can a bad smell create pain, dysfunction and weakness?

We know about the feedback of pain and painful stimulus (nociception) and the creation of pain to warn us but what about the effects of noxious and more subtle smells on the nervous system? Over the last few years I have found that nothing ceases to amaze me when it comes to the human body. As it becomes possible to dissect systems and assess interactions of specific stimulus, observing the input/output relationship between stimulus and body. Pain stimulus is observed to be chemical, thermal or mechanical in nature. Please bear with the technicalities before I explain the simplified mechanisms or skip to the last part of the blog, if you get bored!

There are many factors that contribute to a patient’s perception and physical feeling of pain. Pain is the central nervous systems response to an event that has the capacity to injure the tissues of the body. Nociception or pain can be qualified from the following pathways.

The ‘First’ pain is usually a withdrawal mechanism (Nociceptive Withdrawal Reflex or NRA) mediated by the neurotransmitter glutamate and utilises the neospinalthalmic (new pain) tract in the anterolateral system or ALS. This typically lasts less than 0.1 of a second and the signal, suggested to be dampened in the substantia gelatinosa, an area found in the dorsal aspect of the spinal cord. Think about that sharp initial pain experienced causing you to move away from a stimulus, which has been detected by free nerve endings.                               Smelly pain

The ‘Second’ pain is also part of the ALS but is part of the paleospinalthalmic tract (old pain). It typically takes over from the initial first pain/neo. It is mediated by the compound substance P and can be associated with that long, lingering pain experienced from an injury.

In addition to pain, we have the capacity to assess many other features of mechanical distortion such as pressure, stretch and touch. The Dorsal Column Medial Lemniscus or DCML, allows the nervous system to provide adequate feedback to tasks and environmental stimulus.

Another part of the pain detection system is the trigeminal chemosensory system, which has nociceptive/pain and temperature pathways that feedback to cranial nerve five, called the Trigeminal nerve (CNV). When a noxious or toxic substance is processed by the neurons in the mucosal areas of the nose, mouth, eyes and lips it is relayed into the thalamus. The VPMN (or ventral posterior medial nucleus) relays signals to the sensory cortex and provides responses, such as watery eyes, sneezing and withdrawal

When we inspire air with small particles of pollutants, they pass from the lungs into the blood stream. Although the blood brain barrier is supposed to prevent any unwanted chemicals, crossing from the blood to the brain; the Circumventricular organs present an area that does not have the capacity to restrict compounds that can create dis-organisation of neurological signals entering and leaving the brain. The area postrema, also has a chemosensory role to initiate vomiting to deal with exposure to harmful compounds

So let’s have something a little easier on the eyes and brain to read now. For example:

Perhaps you are walking across the road in heavy traffic. Sucking up all the pollutants such as benzene, carbon monoxide and other waste products of burning fossil fuels into your lungs as you find your way from one side of the road to another.

For a few seconds your brain, exposed to the onslaught of pollution, has a hard time processing the compounds that have made their way into areas such as the pineal gland or chemoreceptors that can induce vomiting in response to a noxious stimulus.

You are in a rush and bump into someone, his or her shoulder hitting you firmly in the chest. It was slightly painful but you don’t really notice it, the pain pathway, along with pressure, stretch and touch receptors provided some form of feedback. The brain, perhaps still not capable of processing this feedback due to the short exposure of increased pollutants, is just trying to get on with the milieu of everything else that your body demands of it.

Meanwhile the pectoralis muscle, which is being used with each step that you take, has been exposed to increased pressure, a state of contraction or small window of pain that necessitated a withdrawal reflex. The intrafusal muscle fiber that monitor both stretch and contraction now have increased signal towards sustained contraction due to the chaos of external compounds that entered areas of the brain.

So now we might have some level of muscle dysfunction. We probably don’t even know about it. That level of muscle dysfunction now increases and decreases tension demands to receptors found in the ligaments and tendons. The joint mechanoreceptors have a different signal. The skin exteroreceptors perhaps have a different signal. There’s no pain to remind us of the event. In fact we have now gone to the gym and started doing a bunch of push-ups or gone shopping for food and simply carrying the bag home with that hand and shoulder. This doesn’t create pain, but simply sets the foundation for increased areas of dysfunction from distorted neurological signalling.

The concept of this neurological/chemical chaos is often referred to as ‘brain fog’. It seems to be in the literature for many reasons, blood sugar issues, gluten, estrogen (PMS and menopausal females are particularly susceptible) and other factors. It’s also possible that brain fog can be created from specific food stressors, once again eliciting the same response, proposed in the heavy traffic.

Some might say, how can the body be so fragile? Surely we are more robust than that? But it is possible to create these specific dysfunctions but they can be unravelled. Understanding specific stimulus can give us a solution to what dysfunction exits. We might never find out how it came about but a thorough history taking can help to influence where we assess and how to treat it. This is where a technique like P-DTR or Proprioceptive Deep Tendon Reflex, developed by Dr Jose Palomar is unique and effective at uncovering specific neurological dysfunction.

If emotions, visual, auditory, mechanical, chemical and pain factors perpetuate dysfunction, then using those stimulus can pose an effective form of assessment and treatment.

  1. Palomar, J. Proprioceptive Deep Tendon Reflex: Course Notes.
  2. Purves D et al Neuroscience 5th edition. Sinauer Associates 2012