Spinal Flexion/Forward Bending – How am I damaging my back?

With so many people suffering from low-back-pain, there’s been a lot of talk about proper body mechanics. Are you bending at the hips or at the waist? Is your back straight and knees bent when you lift? What kind of macro or microdamage are you actually doing to your spine every time you forward bend? We spend most of our time seated, which means that our spine is in a prolonged state of slight flexion. Sitting for more than half your day increases your chances of developing serious chronic diseases, such as diabetes, obesity, and yes back pain. Flexion may be beneficial in some cases of back pain where the person suffers from spinal stenosis, as slight flexion can widen the central canal and intervertebral foramen that have become narrowed. Let’s review the biomechanics of forward bending.

I’m going to focus on the lumbar spine, as this is the area where most people will experience pain. When a motion segment, which is the functional spinal unit, is in flexion most of the resistance comes from the intervertebral ligaments. During the first few degrees of flexion, there is some resistance from ligamentum flavum (this is the one to look at concerning central spinal stenosis, but more on that later) and from the posterior annulus of the intervertebral disc. At about fifty percent flexion, the intervertebral disc offers more resistance than the posterior ligaments. at this point, the posterior annulus of the disc is under tension and the anterior annulus is under compression. In full flexion, approximately thirty eight percent of resistance comes from the capsular ligament of the zygapophyseal (facet) joints, twenty-nine percent form the intervertebral disc, nineteen percent from the interspinous and supraspinous ligaments, and thirteen percent from ligamentum flavum. In full flexion, pressure in the nucleus increases by up to 110%!

Upon rising in the morning, the intervertebral discs have higher water content, which will increase intradiscal pressure and disc resistance during flexion. Prolonged loading throughout the day expels water from the disc, giving it some slack, which increases range of flexion. So your discs are more prone to injury earlier in the day because of the increased disc height.

Studies suggest that the discs and ligaments more strongly resist spinal flexion motion than the muscle length. So while back exercises are extremely important, we really need to focus on the health of our ligaments and discs!

The supraspinous and interspinous ligaments are the first to sustain damage in flexion injuries. If lateral bending is combined with forward flexion – oblique axis, then the contralateral zygapophyseal joint capsule can be sprained. In flexion injuries involving more forceful forward bending moments, the ligaments are grossly damaged and fail to protect the intervertebral disc allowing the posterior annulus to fail. The outer annulus has nociception thanks to the sinuvertebral nerve, which can be a source of diffuse discogenic pain. Once the annulus fails, this allows the inner annulus to pull the cartilaginous (hyaline cartilage) endplate free from the subchondral bone as it is pulled axially. This is a plausible example of how bone and cartilage fragments end up in herniated material.

Sustained flexion reduces the motion segments resistance to bending, as ligaments and muscles become relaxed. The ligamentous structures surrounding the spine have a high collagen content, which limits their extensibility. The ligamentum flavum is an exception, it contains a high percentage of elastin, which allows it to contract during extension (backward bending) and to elongate during flexion (forward bending). If ligamentum flavum becomes hypertrophied it can lead to central canal stenosis, causing bilateral thigh pain that is aggravated by extension, such as when you’re in an upright standing position. Hypertrophy of ligamentum flavum is the result of fibrosis, in most cases. This is due to accumulated mechanical stress, especially along the dorsal aspect of the LF. Hypertrophied ligamentum flavum is associated with zygapophyseal facet hypertrophy. Viscoelastic deformities of the disc are much slower, as fluid must be expelled to create more flexion. As a result, rapid flexion is more likely to damage the disc and ligaments than is slow forward bending to the same degree.

Bending forward to reach objects that are not directly in front of you is coupled by axial rotation. This can compress the ipsilateral zygapophyseal joint while stretching the capsule of the contralateral zygapophyseal joint. The intertransverse ligaments are stretched the most by lateral bending, followed by ligamentum flavum and the capsular ligaments. The capsular ligaments of the zygapophyseal joints are strained the most during rotation.

Slouching! Your mother told you to sit up straight, but did you listen? No! Now you’ve got back pain, forward head carriage, and possibly even a dowager’s hump. We’ll discuss Janda’s Crossed Syndromes another time… Just know that slouching when seated, imposes a backward rotation of the pelvis while the entire trunk is flexed; this puts a tremendous strain on the iliolumbar ligaments. Iliolumbar ligament pain is generally located around the posteromedial iliac crest, but may refer pain down the leg leading people to believe that they have sciatica.

Sitting puts more pressure on your spine than standing or lying down. Your intervertebral discs require movement for diffusion to take place. Disruption of diffusion is the precursor to degenerative changes in the spine. Please refer to one of my previous posts on disc metabolism to learn more about the nutrition of the IVD. As previously mentioned, sitting for prolonged periods can damage your spine and lead to disc degeneration and eventual disc herniation.

You’re going to have to sit, so what to do?

See the source image
  • Take mini-breaks every 20 minutes from the desk. Set an alarm if you need to as a reminder. Drink plenty of water so you have an excuse to get up and use the restroom. Walk around and stretch when you’re talking on the phone.
  • Proper workstation ergonomics: Straight back, straight wrists, monitor at proper eye level, lumbar support, feet flat on floor
  • Practice some back extension poses, like bird-dog, cobra, and bridge pose to counterbalance all the flexion.

The above are just a few suggestions. There are many yoga and Pilate’s exercises that are great for people who have low-back-pain. Ask a therapist or trainer who is certified in Corrective Exercise to help you come up with a strengthening and lengthening plan that is right for you. Lengthening the shortened, hypertonic hip flexors, strengthening the inhibited glutes and multifidi are just some of the many exercises that you may need to focus on to help alleviate your low-back-pain and take control of your back.

See the source image
See the source image

See the source image

Let me know what exercises and stretches help alleviate your back pain. What tricks do you use to improve your posture and sit less? How do you unload your spine? Do you use an inversion table or other form of traction? Let me know below!

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Posted by on January 10, 2019 in Uncategorized


Joint Stability

Joint Stability

Happy New Year; wishing you a healthy and prosperous 2019!

Hilton’s Law – “The same trunks of nerves whose branches supply the groups of muscles moving a joint furnish also a distribution of nerves to the skin over the insertion of the same muscles; and the interior of the joint receives its nerves from the same source.”
Hilton also stated “Every fascia of the body has a muscle attached to it, and that every fascia throughout the body must be considered as a muscle.”
So many things to take into consideration when studying the joints ROM and limitation of movement. Look at the disorganization of the foot and ankle complex in Charcot arthropathy or even joint instability in flaccid paralysis. Think of how the ligaments are not limiting the ROM to prevent dislocation. A healthy, well-innervated joint/limb will not have excessive ROM, even in a relaxed state. It is only by reciprocal innervation and inhibition of muscles, whereby the agonist contracts sending an impulse to the antagonist to relax, that movement is even possible.
Knee extension is not stopped by the PCL or ACL, but by tension in these ligaments causing a reflex signal to the knee flexors to contract. This is how the joint capsule and associated ligaments work along with tendons to protect the joints.

Myotatic reflex, or stretch reflex, is a muscle contraction in response to a sudden stretch. When a muscle elongates, the muscle spindle is stretched which results in a monosynaptic reflex. This action helps keep our joints stable. As bones and tendons do not typically pull muscles, the rapid stretch stimulates muscle spindle activity to protect the joint from being distracted.

Noxious stimuli can also increase muscle spindle activity. This is thought to be what drives the pain-spasm-pain cycle in those who suffer from many chronic pain syndromes.  Likewise, this can also lead to a reduction of joint ROM. Joints love movement as it helps stimulate the production of synovial fluid and intraarticular nutrition and waste removal. Movement is necessary for hyaline cartilage health.

Reciprocal inhibition can be altered by having a hypertonic agonist, which will decrease neural input to the antagonist. This alters the force-couple relationship creating synergistic dominance, which leads to faulty movement patterns, poor neuromuscular coordination and proprioception, and arthrokinetic dysfunction. This altered joint motion leads to more pain which can further alter muscle recruitment and motor control, eventually causing joint damage.

Are the ligaments really responsible for joint stability in otherwise healthy joints, or is it altered proprioception and neuromuscular control?

Let’s briefly discuss the specialized neurons called mechanoreceptors. – StretchReflx

Two afferent receptors of muscles and tendons (tenomuscular mechanoreceptors) are: Golgi Tendon Organs, embedded  within the musculotendinous junction, stimulates muscle relaxation after prolonged tension. Muscle Spindles, located within the skeletal muscles, respond to sudden stretch, thus stimulating muscle contraction.

There are two primary joint receptors located within the joint and surrounding ligaments: Ruffini Endings, located on flexion side of joint capsule, respond to extreme joint motion into extension with rotation – they protect joint stability. Pacinian Corpuscles are located throughout the joint capsule, joint, and periarticular tissue; they respond to compressive forces across the joint during movement. Another less discussed articular mechanoreceptor is Golgi-Mazzoni Corpsucles; located within the joint capsule and is activated by compression.

Ligamentous receptors are myelinated and can transmit sensory information regarding joint position to the CNS, they inhibit continued agonist contraction to decrease tension on the ligament. They have been classified into four types. Type II are thickly encapsulated, medium diameter, conical corpuscles believed to provide joint sensation and proprioception, particularly at the beginning of movement; they have a low threshold, rapid adaption and are dynamic. Type III are larger in diameter, thinly encapsulated fusiform corpuscles with high threshold activated by extreme dynamic ROM, slow adapting.  Type I  are thinly encapsulated globular corpuscles with a small diameter and a low threshold, slow adapting both static and dynamic – they are constantly firing to provide proprioception, even at rest . Type IV contain plexuses and free nerve endings, they are very small in diameter, have a high threshold and are responsible for nociception.

My 17 year old autistic son has proprioception dysfunction – which is common in children with ASD and other forms of sensory processing disorders. As a result he holds himself in awkward postures and finds it difficult to follow along with a Pilate’s exercise routine as he is unaware of whether or not his legs are straight or pelvis is aligned with his shoulders, etc.  If you’ve seen kids with ASD constantly kick their feet or flap their hands, that’s just a method they are using to stimulate proprioceptive feedback. They may have difficulty isolating body parts and movements for coordinated tasks. Neuromuscular control is a struggle, as their internal feedback is lacking. Our internal feedback is what allows us to modify movements to achieve joint stability.

Now that you understand how important proprioception is for neuromuscular control, you can imagine how standing or sitting in awkward, unbalanced, misaligned postures can damage the kinetic chain. Foot and ankle complex disorders such as pronation distortion are very common, as is an uneven lumbosacral junction, then there’s scoliosis accompanied by the classic rib hump and uneven shoulder girdle with head tilt. This example is a proprioceptive disorder with origins in the CNS. So what about peripheral neuropathic disorders? As mentioned earlier, in cases of Charcot arthropathy, or neuropathic arthropathy, which is a progressive denervation induced degeneration of the foot and ankle joints that leads to eventual deformity. Without the proper proprioceptive feedback the ligaments fail to withstand abnormal arthrokinematics. This is why it is so important to perform regular exams of diabetic patient’s feet. sensory-examination Diabetes is the most common cause of neuropathic arthropathy leading to this type of foot and ankle joint disorder, but peripheral nerve (lower motor neuron) injury or even brain or spinal cord (upper motor neuron) injuries may be a causal factor. There are even congenital disorders that cause analgesia (CIP). Heavy metal poisoning can also destroy afferent proprioceptive fibers.

Transarticular ligaments provide more than just support for the joint, they also send sensory output which improves arthrokinematics to prevent joint damage. Proprioception is important for kinesthesia, dynamic stabilization of the joints and neuromuscular control to prevent musculoskeletal injury, especially of the joints. Neuromuscular and sensory testing should be part of our routine evaluation. Neuromuscular and proprioceptive retraining should be incorporated into treatment plans to help restore joint stability.




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Posted by on January 1, 2019 in Uncategorized


Disc Height and Compression

Just a quick share from a topic I posted about on Facebook earlier this week. More to come later – as I’m trying to complete an awesome course on neuroscience right now and have some assignments that require my attention.


The motion segment on the left has a healthy disc while the one on the right has lost disc height. Compressive force is resisted predominantly by the vertebral bodies and the intervertebral discs (IVD), but approximately 15-20% is resisted by the zygapophysial (facet) joints. IVD narrowing of just 1-3 mm increases the load on the facet joints and may cause extra-articular impingement of the inferior articular process on the lamina below (see picture on the right). When IVD height loss is even more severe, as with those suffering from degenerative disc disease (DDD), up to 70% of the compressive load can act upon the facet joints in lordotic postures.
The IVD has higher compressive strength than the adjacent vertebrae. Compressive loading is more likely to damage the vertebral endplate than the IVD. As discussed in some of my previous blog postings, the vertebral endplate is important for IVD health. DDD is associated with endplate sclerosis and loss of IVD height. This of course may lead to stenosis and other painful conditions such as zygapaphysial arthropathy, which affects up to 15% of people with chronic low back pain.
It’s never too soon to start taking care of your back!
The VerteCore Lift is like Viagra for your back, it gets you up and keeps you going!


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Posted by on October 15, 2018 in Uncategorized


Delayed Onset Muscle Soreness (DOMS) – Quit Blaming Lactic Acid!

Did you know that muscle cells will live for your entire life? New cells are only synthesized after traumatic disruption of the cell membrane. Muscle mass increase is not due to new cell formation (known as hyperplasia), but from muscle cell hypertrophy.

Exercise and protein influence muscle adaptation. The half life of contractile proteins is between 7-15 days, allowing for adaptation more rapidly than other tissues.  The type of exercise is also important in muscle adaptation. Endurance training produces the greatest changes to type I (slow twitch) fibers.  Strength and power training primarily alters type II (fast twitch) fibers. Strength training does not create more type II muscle fibers, but causes a transformation. The diameter and length of the muscle changes in response to mechanical loading, specifically eccentric contractions for lengthening. This mechanically-induced hypertrophy is caused by changes in gene expression which increases protein synthesis (e.g. actin and myosin) and the activity of myokinase to bump up the ATP/ADP ratio.

Muscle fibers lengthen due to the addition of new sarcomeres at the musculo-tendinous junctions, this is achieved by eccentric contractions. Stretching allows for creep of the collagenous tissues, but the effects are only temporary.

Physical inactivity will lead to rapid muscle atrophy. Protein synthesis decreases within just hours of bedrest. If your muscle is immobilized in a shortened position then its length and girth will both be reduced. The ratio of collagen to contractile protein begins to increase which will cause stiffness and loss of joint range of motion.

Fortunately, muscles respond quite well to exercise and rehabilitate nicely. Increases in proprioception, neuromuscular activation, recruitment and hypertrophy are all factors at play in strength training and rehabilitation. In some cases, myofascial adhesions and trigger points are addressed before progressing to hypertrophy in corrective exercise programs.

Exertion damage to the muscle cell membrane and repair leads to muscle hypertrophy, specifically eccentric contractions. Damage to the sarcoplasmic reticulum effects calcium homeostasis which doesn’t allow for efficient contraction or excitation of the muscle cells. This is why we may feel weaker for a day or two following an intense work-out. The disruption of the cell membrane allows creatine kinase and histamine into extracellular spaces where they stimulate nociceptors and increase blood vessel permeability. This results in what we know as DOMS (delayed onset muscle soreness) and swelling 24-72 hours after exercise. leg-dayDOMS

Biopsies show muscle damage within an hour of completing exercise, but the damage worsens over the next few days. The damage that occurs following exercise is initiated by non-lysosomal proteinases (e.g. caplain) and other pro-inflammatory mediators. Macrophages and other phagocytes clean up the debris and release proteases that break down the damaged myofibrils. Cytokines are released by the phagocytes which stimulate proliferation of satellite cells. Satellite cells differentiate into myoblasts which fuse to form myotubes that will repair damaged cells or possibly develop into new cells if the muscle cells are too damaged. This repair process results in muscle hypertrophy, and takes place over days or weeks depending on the extent of damage. Collagenous tissue will also regenerate, and can over proliferate if the damage is severe. This leads to scar formation, and possibly myofascial adhesions, which will alter normal muscle function.

Lactic acid has wrongfully been given a bad reputation. Lactic acid is removed from the muscles within 30 minutes of rest after you exercise. Lactate is actually involved in the metabolism of every cell, not just muscle cells.

Sports massage is a great way to decrease DOMS; reduce recovery time, increase circulation, release adhesions and muscle tension, reduce edema, and increase range of motion. As an added perk it helps you sleep better by lowering cortisol levels and anxiety. Researchers discovered via biopsy that even a 10 minute massage (post a 70 minute intense cycling session) to the lower extremity reduces inflammation in quadricep muscle tissue and encourages the muscle to produce more mitochondria. Mitochondria dysfunction is associated with muscle atrophy and insulin resistance. So massage isn’t just beneficial for recovering athletes, but also for those who are suffering from chronic inflammatory conditions such as poly/dermato/inclusion-body myositis, necrotizing autoimmune myopathy, muscular dystrophy and even insulin resistant diabetes. Surprisingly – the massage did not help clear lactic acid from the exhausted muscles (go figure).

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Posted by on September 25, 2018 in Uncategorized


Compilation of Some of My Recent Postings on Musculoskeletal Wellness, With an Emphasis on Spine Health.

Keeping a strong and agile spine is important, but our intervertebral discs are often overlooked until we’re diagnosed with degenerative disc disease (DDD), or a bulging or herniated disc. This is often accompanied with low-back-pain and radiculopathy. Spine health is a topic that I’ve discussed a lot, but going a little deeper into the histology, pathophysiology and biomechanics of back pain can help shed some light on exactly why this happens.

Intervertebral Disc Nutrition:
The lumbar IVD’s are avascular. Their blood supply is limited to tiny vessels that spread over the external surface of the annulus, derived from the external arteries that supply adjacent vertebral bodies and other arteries from within the vertebral bodies, which are seperated from the disc by the vertebral endplates and subchondral bone.
The IVD’s rely on diffusion for nutrition; approximately 50% is from the vessels around the periphery of the annulus and the other remaining is from diffusion through the vertebral endplates, which are frequently damaged as a result of DDD and compressive loads.
Nutrients such as glucose and oxygen pass into the disc down concentration gradients. Waste, such as lactic acid, leave the disc via the reverse, however passage is slow and limited because of the density of proteoglycans in the disc.
Nutrition is greatly improved and aided by movement. Movement causes bulk flow of water into and out of the disc, and this bulk flow carries nutrients with it.
The VerteCore Lift® keeps movement possible while decompressing IVD’s, thus allowing an influx of nutrition to aid in healing, widening stenotic IVF, mobilizing fixated zygapophyseal (facet) joints, while also allowing herniated or bulging disc material to be retracted or resorbed.

The Aging Spine and Low-Back-Pain:                                                                                                 Osteopenia is hormone-related bone weakening, when this advances to a level at which fractures are sustained doing normal everyday activities it is called osteoporosis. This is commonly seen in post-menopausal women. Reduced physical activity and loading is also a causative factor in the loss of bone density. Trabeculae bone is affected more than cortical bone. Vertebral bodies contain a lot of trabecula bone, which makes them susceptible to degeneration from osteoporosis. Fracture of the vertically arranged trabeculae that support the vertebral body’s cartilaginous endplates, which serve as an interface between the vertebral body and the discs, are common. Endplates are particularly susceptible to damage, as they must be porous enough to allow capillary transport for disc metabolism, yet strong enough to prevent vertebral fractures. The end plate distributes intradiscal pressures onto the adjacent vertebrae, which prevents the pressurized disc from bulging into the underlying trabecular bone. During compression, the pressurized nucleus causes the end plate to become stretched. Endplate damage or sclerosis can be a source of low-back-pain. End plate innervation has been studied over the last decade and has been identified as a potential pain generator.

The endplate is extremely important for disc nutrition. Blood vessels and marrow spaces provide channels for glucose and oxygen to enter and waste to exit. Nutrients pass through the disc matrix primarily by diffusion. Mechanical disc compression creates convective fluid flow by which larger solutes are moved.

The aging endplate will thin and calcify due to a decrease in content of proteoglycan and collagen. By the time we are 80, proteoglycan content will decrease by approximately 1/2.  Type 1 collagen and water simultaneously decrease significantly as well. These changes are associated with disc degeneration and are consistent with markers of chondrocyte hypertrophy (elevated type X collagen expression). Hydrostatic pressure is an important regulator of chondrocyte function. The accumulation of end plate damage can cause focal weakness which progresses into circumferential fissures. End plate sclerosis impedes nutrient transport to the nucleus of the IVD and may provoke inflammatory responses within the disc or vertebra.

A normal disc has peripheral innervation, which means only the outer layers of the annulus are innervated by the sinu-vertebral nerve. Annular tears often create discogenic pain, which are often a source of LBP. However, the vertebrae are well innervated, particularly the periosteum. But of particular interest, the bone marrow receives the greatest number of sensory fibers! This is purportedly for modulation of hemopoiesis and bone metabolism. This means bone pain may be felt from elevated interosseous pressures even when the pathology is confined within the marrow; this pain can be ameliorated when bone innervation is ablated after procedures such as vertebroplasty. Vertebral bone marrow lesions appear to be related to inflammatory chemicals produced by the disc cells, which trigger an autoimmune response. These nucleus derived cytokines can sensitize nerves and promote new nerve growth via NGF. Lactic acid or other anaerobic metabolic by products can also irritate end plate nerves.  Endplate damage (Schmorl nodes, fractures, calcifications, avulsions & erosions) is associated with bone marrow lesions and disc degeneration. Calcification and sclerosis at the vertebral rim may result form repeated compressive trauma. Endplate fracture is often followed by the vertical herniation of the nucleus tissue into the vertebral body. This displaced tissue along with the calcified shell around it are called Schmorl’s nodes.

Proper exercise and nutrition can help counter the effects of osteopenia. Exercising early in life can increase bone mass to help counter normal age-related bone loss. An athletic trainer, PT, nutritionist, and other health and wellness specialists can collectively help you determine the best protocol for your bone health. Frequently loaded bone can increase by 40% in just 6 weeks, whereas 8 weeks of disuse or bedrest leads to a 10-15% loss of bone. Cytokines can decrease or increase bone mass. Growth factors stimulate hypertrophy, whereas interleukins reduce bone mass. Wolf’s law states that the architecture adapts to best resist the forces that are applied to it.

Vertebral endplates are composed of hyaline cartilage as are facet articulations of the zygapophyseal joints. Cartilage contains a scarcity of chondrocytes, but is avascular. Hyaline cartilage is mainly composed of water, collagen, and proteoglycans. Proteoglycans are molecules that have a protein core, with side chains of glycosaminoglycan (GAG), chondroitin sulphate and keratin sulphate. The most common proteoglycan, aggrecan (90%), combines with hyaluronan to form huge aggregates. GAG attract water electrostatically, so the main role of proteoglycans is to attract and hold on to water. Collagen and proteoglycans work together to help resist deformation. Nutrients reach chondrocytes across the matrix by diffusion or bulk fluid flow. Metalloproteases (MMPs) are enzymes produced by the chondrocytes that control matrix breakdown. Chondrocyte activity is controlled by cytokines, which can be produced locally or from more distant cells. Chondrocyte activity is also influenced by mechanical loading. Moderate, cyclic loading tends to stimulate synthesis, but prolonged static loading slows synthesis. Physical activity leads to thicker and stiffer cartilage, whereas inactivity has the opposite effect. If cartilage is cut it does not heal, possibly because the surrounding cells die. If an injury penetrates the cartilage through to the subchondral bone, then fibrous tissue can grow from the bone to fill in the injury site. However, this does not integrate well with the surrounding cartilage and degeneration will result.

The number of live chondrocytes die with age. Advanced glycation end products will also stiffen the tissue and inhibit proteoglycan synthesis, this is due to low oxygen concentrations in the tissue. Increased stiffness makes the tissue brittle and vulnerable to injury. This contradicts the old belief of wear and tear degeneration or fatigue damage accumulating. It is well known today that osteoarthritis is mainly a result of metabolic disease/syndrome with an association of a type 2 collagen defect. However, aging cells are less responsive to mechanical stimuli than younger cells. Osteoarthritis (OA) is characterized by cartilage thinning & fibrillation and hypertrophy of the subchondral bone with osteophytes forming around the joint margins or possibly even sclerosis. Almost 90% of everyone over 40 will be affected by zygapophyseal joint OA.

Physical inactivity also reduces muscle mass. Inactivity induces atrophy, with protein synthesis falling within hours. Sitting really is the new smoking (but smoking is bad for your back too, that’s in a different blog post)! If the muscle is immobilized in a shortened position, then its length is reduced along with its girth and the proportion of collagen to contractile protein ratio increases. The muscle becomes stiffer and less extensible, also decreasing range of motion at the joint it acts upon. Complete immobilization of the leg reduces quadriceps by 15-20% in just 6 weeks, with the most loss from type I fiber atrophy resulting from a reduction in protein synthesis rather than an increase in catabolism.  Sarcopenia is age related loss of muscle strength and mass. It is greater in those who are less physically active.


The functional difference between tendons and ligaments is that tendons transmit tensile force in one direction (muscle to bone) and ligaments must resist force from many directions to keep bones from dislocating. This is reflected in the direction and orientation of their collagen fibers. Both tendons and ligaments have a blood supply, but is poorly vascularized. They have a variety of nerve endings which monitor stretch and pain. These tissues have approximately a 15% stretch capacity before failure. One built in safety mechanism is that they have crimped collagen fibers that gradually straighten under high tensile forces. Fibroblasts are responsible for the turnover of this collagen. Tendons and ligaments are able to strengthen or weaken in response to mechanical loading, but strengthening will be at a slower pace due to the sparse vascularization. This is why over-training will often affect the musculo-tendinous. The type and magnitude of mechanical loading influences the matrix. Fatigue injuries often occur from repetitive overloading, remember tendons take time to heal!  New fibers are typically weaker and thinner, as they are laid down in a disorganized crimped structure.

Interspinous ligament injuries (neck or back sprain) are common among athletes and after whiplash injury. I have seen many clients with LBP that is associated with iliolumbar ligament sprain. The iliolumbar ligament has the tasking job of attaching and stabilizing our ilium to the lumbar spine. Bending and twisting the spine, especially under load or repetitively, are common causes for iliolumbar ligament sprain. Sitting for long periods will often exacerbate the symptoms. The iliolumbar ligaments can refer pain to the pelvis, sacroiliac joint, groin, hip (near the greater trochanter) and across the low back around the L4/L5 region. The ligamentum flavum is of special interest to me. It often becomes hypertrophic and buckles with disc degeneration and can cause narrowing, or stenosis, of the vertebral canal. With age and degenerative changes, it’s fibers become more calcified and its elastin content fails.

I’ve already discussed the fibrocartilage IVD’s (intervertebral discs) and their metabolism and blood supply, but is worth mentioning again. As previously mentioned, smaller metabolites are moved by diffusion, while larger molecules are transported primarily by bulk fluid flow. Physical activity is needed for this transport to occur (as has been demonstrated by imaging following the movement of dye), this is one reason why inactivity and bed rest is no longer recommended for patients with back pain.

Of special interest to me as a manual pain management therapist specializing in neuromuscular therapy and spine health (just had to throw this one in):

The relationship between the ventral rami and the psoas major muscle (simplified):
The ventral rami of the lumbar spinal nerves enter the substance of the psoas major, upon exiting their intervertebral foramina, thus forming the lumbar plexus. Deep branches of the lumbar plexus innervate the psoas & quadratus lumborum. From the lateral surface of the psoas, emerge the iliohypogastric & ilioinguinal nerves which supply the muscles & skin of the lower abdominal wall & groin. Also emerging from the lateral surface of the psoas is the lateral cutaneous nerve of the thigh. The genitofemoral nerve, from the ventral surface of the psoas, supplies the cremaster muscle. The femoral nerve emerges from the lateral psoas surface and the obturator nerve from the medial surface. The lumbosacral trunk also arises from the medial surface. The lumbosacral trunk provides fibers for L4 & L5 spinal nerves to the sacral plexus, which innervates the lower limb.
Back pain associated with neurological abnormalities in the lower abdominal wall or proximal thigh may imply secondary involvement of nerves in pathological processes affecting the psoas.


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Posted by on April 8, 2018 in Uncategorized


The Affects of Chronic Stress on Our Body and How Hormones Play a Key Role

Various hormones decline as we age:
Growth Hormone, Testosterone & DHEA decline as much as 50% from age 25-50, and then another 50% decline by age 75.
Estrogen declines approximately 30% from age 25-50, and will continue to slowly decline thereafter.  pathway-of-estrogen-and-progesterone-formation
Progesterone will have a steep decline (about 75%) from age 35-50, and will continually decline thereafter.
Melatonin takes a drastic and continual decline after the age of 40.

Researchers have long known that the aging process is related to a decline in hormones that begins after development ceases and then accelerates as we enter our fifth decade of life. Decline in hormone production can also result from physical and emotional stress. Youthful hormones can be found in people over 70, while suboptimal levels are commonly seen in teenagers.

Hormones influence our metabolism, enzyme production, regulate DNA and RNA production and the subsequent synthesis of cell proteins, and influence energy production of the mitochondria. Hormones also regulate your body’s stress response, kidney function, blood sugar, cognition, mood, bone and muscle health, menstruation, and sexual function.

Chronic stress amongst younger individuals can result in hormone levels of a 70 year old. This is said to be one reason that stress ages you.

Stress affects the body in so many ways (I’ll try to be brief):

Musculoskeletal  pain-spasm-pain

When the body is stressed, muscles tense. Think about that. Chronic stress leads to chronic muscle tension, which leads to myofascial pain, tension-type and migraine headaches, decrease in joint mobility and range of motion, TMJD, etc. Relaxation techniques like meditation, massage therapy, breathing exercises, and yoga are effective ways of reducing muscle tension. Cognitive behavioral therapy may also be beneficial.


When we’re stressed we tend to take shallow, rapid chest breaths that seem to never make their way to the belly. This stresses our accessory muscles of respiration which can pull our shoulders and head forward and down. Acute stress can even trigger an asthma attack or hyperventilation. Diaphragmatic (belly) breathing exercises have been shown to improve the quality of life among patients with asthma. Working with a therapist or taking a pranayama class to develop relaxation and breathing strategies can help.


Stress hormones (adrenaline, noradrenaline and cortisol) can elevate blood pressure. Heart rate and stroke volume = cardiac output. Heart rate and stroke volume are influenced the nervous system and hormones. Cortisol (which is released during the stress response by our sympathetic nervous system) increases our heart rate in preparation to jump into action – to fight or flee. Epinephrine is then released to constrict certain blood vessels (so we don’t bleed out from our battle wounds), while increasing blood flow to our skeletal muscles so we can run or fight. It increases heart rate and contraction force, thus increasing output and blood pressure.

Chronic stress can contribute to hypertension, stroke and hearth attack. Repeated acute stress and chronic stress can contribute to inflammation in the circulatory system, which is shown to aid the formation of atherosclerosis, resulting in hypertension and eventually left ventricular hypertrophy. This is one way that stress is linked to having a heart attack. Estrogen appears to help blood vessels respond better to stress, which is why post-menopausal women are at greater risk for the effects of stress related heart-disease.

Endocrine  HPAaxis

The Hypothalamus-Pituitary-Adrenal (HPA) Axis is our central stress-response system. The hypothalamus releases corticotropin-releasing hormone (CRH), also known as corticotropin-releasing factor (CRF).  CRH acts on the anterior pituitary, which releases adrenocorticotropic hormone (ACTH). ACTH binds to receptors on the adrenal cortex which stimulates the release of cortisol. There is a negative feedback loop that signals the  hypothalamus, then the pituitary and finally the adrenals to calm down production of these stress-hormones and return the body to homeostasis once the stressful situation is over.

But what happens if the stress-response doesn’t turn off? When cortisol and epinephrine are released, the liver produces more glucose in preparation to fight or run. For those who are insulin resistant, the extra glucose can cause hyperglycemia – which can lead to Type 2 Diabetes. Chronic stress can also increase Reverse T3 (RT3), or reverse triiodothyronine, an inactive form of T3 which can prevent the active T3 from getting into cells. Emotional, physical or biological stress increases cortisol which can cause a higher ratio of T4 to be converted into RT3 instead of the much needed T3.

I promised I wouldn’t drag this out, so I’m not going to spell out the implications of having low thyroid levels, but weight gain, low energy and thinning hair is just the surface.


Besides the usual over or undereating when we’re stressed, which can cause gastric acid and enzyme imbalances, some people increase alcohol or tobacco intake. Comfort foods are generally starchy and/or processed, which can contribute to obesity, cancer and diabetes.

Stress can trigger inflammatory bowel flare-ups and lead to the development of peptic ulcers.  Stress also negatively affects the absorption of nutrients and bowel motility. Our food digests better when we are at rest and our parasympathetic nervous system is active.



Chronic stress can result in adrenal dysfunction, sometimes referred to as adrenal fatigue.  Symptoms of adrenal dysfunction can include: weight gain, depression, anxiety, blood sugar dysregulation, cravings (especially salty foods or sweets), lethargy, low sex drive, PMS, brain fog, bowel movement dysfunction, orthostatic hypotension, myofascial pain, frequent infections (cold and flu), palpitations, increase in allergies, and an intolerance to handling routine stressors. The list could go on…

Since nutritional deficiencies can be a direct result of stress or even a causal factor of increased stress, maintaining a healthy diet is very important. Stress, cigarettes and alcohol can deplete our vitamin C and B reserves. When under stress our need for certain nutrients actually increases. Vitamin C, E, A, B-Complex, Zinc, Selenium and Magnesium are essential nutrients  that many people lack in their SAD (standard American Diet) diet, and can also play a role in hormone synthesis and metabolism. Good quality water also has an effect on the oxygenation of our tissues. So drink wisely!

Environmental factors can also cause hormonal imbalance. endocrine-disruptors Radiation, heavy metals, fluoride, phthalates, glyphosate, xenoestrogens in pesticides, BPA, ingredients in cosmetics, hormones in food, etc…

Complimentary and Alternative health practitioners are excellent resources for helping you handle stress and developing a wellness routine to help bring harmony and balance back to your body and life. Many practitioners offer biochemical analysis and hormone testing with nutraceutical and/or botanical  protocols.  Bodywork therapy can help alleviate myofascial pain, headaches, relieve stress, promote well-being and activate the parasympathetic nervous system to promote “rest and digest” and increase lymphocytic immune activity. Yoga, Pilates, and Corrective Exercise can condition the body, correct postural distortions, improve balance and proprioception, increase core stability, and improve flexibility and joint range of motion.

Managing stress in a healthy manner can help harmonize hormones and greatly improve quality of life. Contact Sharon for your consultation & wellness plan, and be stress-less in 2018!








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Posted by on January 1, 2018 in Uncategorized


Essential Oils for Sensory Processing Dysregulation and Autism

Autism is the most prevalent childhood disability in the United States. According to the DSM-5, abnormal sensory responses are included in the core diagnostic criteria; although not everyone with sensory dysregulation will have autism. An accepted, evidence-based, complimentary therapy for children with ASD is massage therapy. Massage is safe, nurturing, and can enhance sensory integration. Unfortunately, massage is difficult to apply on the go. However, aromatherapy is safe, effective, easy to use and discreet.

Studies have identified an abnormal tactile pattern that is specific to children with ASD. This includes painful withdrawal from normal touch (allodynia) and hyposensitivity to injurious stimuli (hypoesthesia). Some of my favorite massage modalities used to improve stereotypical autistic behavior include: Thai Traditional Massage, CranioSacral Therapy, and Qigong Massage. When combined with aromatherapy, the therapeutic actions are greatly enhanced.

Children with ASD have a dysfunctional sensory system. Sometimes one or more senses will be over or under reactive to stimulation. Such sensory problems may lead to behaviors such as spinning, rocking, and hand-flapping. Although the receptors for these senses are located in the peripheral nervous system, it is believed that the problem originates in the central nervous system.

Sensory integration normally focuses on tactile, vestibular, and proprioceptive senses. These senses interconnections begin to form before birth and continue developing as the person matures and interacts with their environment. One sense that is often forgotten about is olfaction.

A study comparing typically developing children to those with ASD showed that there is pronounced difference in sniff response to various pleasant verses unpleasant odors. The study found that the sniff response was highly predictive of the social affect component of autism, but not the restrictive and repetitive behavior component. So, to put it simply, the sniff-response measure is reflective of the mechanism involved with social impairment that is at the heart of ASD symptoms.
It only makes sense that we should treat all aspects of the sensory realm and not just those affecting the repetitive and restrictive behaviors that massage therapy is so good at. Over the last several years I have taken quite an interest in the use of essential oils, so I finally decided to enroll in an in-depth course and gain clinical certification to further my knowledge and repertoire. I was narrowing down schools when by chance I happened upon Heart of Herbs. After reading Demetria Clark’s biography and reviewing the quality of the courses that she offers, I enrolled that day. One of the many reasons that I began using essential oils was for my son’s behavioral problems, that I would later find out was part of the stereotypical autistic behavior that occurs due to sensory dysregulation.

Essential oils are not perfumes or fragrant oils, which contain artificial ingredients and possibly phthalates (which are very dangerous). Essential oils are derived from real plants and contain the true essence of the plant they came from. Just like any other therapy, aromatherapy should be individualized. Not all children with autism have the same sensory or biochemical needs. If you’ve seen one child with autism, you’ve seen one child with autism.

Many children with ASD have digestive problems. Historically, peppermint has been used to soothe digestive complaints. One study has shown that enteric coated peppermint oil capsules were effective in relieving symptoms of IBS. I’m not recommending the use of peppermint oil internally for children, but diluted properly abdominal massage with peppermint may help relieve some of the digestive troubles that children with ASD so frequently suffer with. Dr. William Dember, of the University of Cincinnati Psychology Department, discovered in a research study that inhaling peppermint oil increased mental accuracy of the students by up to 28%. In 2006, Dr. Bryan Raudenbush from Wheeling Jesuit University found that drivers exposed to peppermint were less frustrated, anxious and fatigued; they also stayed more alert! Dr. Raudenbush found that peppermint increased oxygen saturation and blood flow to the brain. This is one reason to carefully screen individuals, as the increased blood flow is the result of an increase in blood pressure! My son, who often gets stress/tension headaches and dizziness, finds relief from inhaling peppermint oil. – Always follow safety precautions when using essential oils.

Vetiver oil has been used by many children to help with symptoms of ADHD. ASD and ADHD symptoms often overlap to a degree. In fact, many children are initially diagnosed with ADHD before eventually receiving a diagnosis of ASD. Vetiver oil is calming, sedative, and antispasmodic (among other wonderful properties). Vetiver oil can be deeply relaxing and add a sense of security to those experiencing anxiety or fear. Try adding to your massage oil or to your evening bath!

Cedarwood was used by Native Americans to enhance spiritual communication. There are some claims that cedarwood essential oil aromatherapy can promote the release of serotonin, which is a precursor to melatonin. Some texts say that it helps open the pineal gland. Cedarwood has a grounding action on emotions and can help relieve aggression, which is very beneficial for those who are prone to sensory overload (also known as melt downs!).

Lavender oil is my son’s favorite! Lavender essential oil has a calming effect on children with autism. It can help reduce anxiety, emotional distress, aggressive behavior and improve sleep quality while improving mood, concentration and memory. Lavender can help reduce tension headaches that can be a common problem in children with ASD (and their parents). Japanese studies indicate Lavender has an affect on the autonomic, sympathetic, and parasympathetic nervous systems as well as the adrenals. Children with ASD have underactive parasympathetic nervous systems and overactive sympathetic nervous systems. Lavender is one of the most used oils amongst therapists because it has such a wide range of uses and is typically regarded as very safe.

Mandarin essential oil can also help with digestive problems, insomnia and anxiety. It has a sweet citrus scent that is uplifting and can relieve irritability and stress. Blends beautifully with lavender or peppermint. Be aware of photosensitivity and do not use prior to sun exposure. Remember to dilute all essential oils with a carrier, like organic sweet almond, coconut, or olive. (I only use organic essential oils and carriers to avoid pesticide contaminants and interactions.)

Chamomile tea has always helped my son calm down and unwind. I even made chamomile lotion to soothe my daughters eczema, when prescription steroid cream only made it worse. When our nurse practitioner suggested trying chamomile essential oil as well, it was a welcome breath of fresh – aroma! chamomile

Chamomile is one of the most ancient herbs known to mankind. The flowers contain terpenoids and flavonoids contributing to its medicinal properties. Its many indications include: gastrointestinal disorders, insomnia, allergies, eczema and other phlogistic skin conditions, anxiety, depression, hemorrhoids, rheumatic pain, inflammation and muscle spasms. Research shows chamomile induces apoptosis of cancer cells, but not in healthy cells at similar doses. Chamomile has carminative actions, meaning it can help dispel gas. Two clinical trails have proven the efficacy of chamomile for the treatment of colic. Other health benefits were asserted in a study that showed drinking chamomile tea (five cups daily for 2 weeks) boosted the immune system and helped fight infections. Chamomile extracts exhibit benzodiazepine-like hypnotic activity, without the undesirable side-effects of the drug.
– A relatively low percentage of people are sensitive to chamomile and develop allergic reactions. People sensitive to ragweed and chrysanthemums or other members of the Compositae family are more prone to developing an allergy to Chamomile.

Essential oils are extremely potent and should always be diluted with a carrier before topical application to prevent skin irritation. I typically dilute essential oils 3 X more when using them on children, than what I use on healthy adults. If you have any dosage questions please consult with a Certified Aromatherapist or your health and wellness provider. There are also many books available on essential oil applications. A patch test is recommended before using essential oils topically. Essential oils should not be taken internally, unless under the direction of your healthcare provider.

The oils I discussed are only a sampling of many that may be beneficial for those with SPD and ASD. Remember, all children are unique. Not every oil is right for everybody; allow your child to help select the essential oil that they find soothing and appealing.


Sharon Leake is the Managing Director at Holistic Health & Bodywork and Director of Clinical Assessment at VerteCore Technologies. She is a Manual Osteopath, Corrective Exercise Specialist, and Licensed Massage Therapist specializing in orthopedics, neuromuscular therapy, CranioSacral therapy, myofascial release, IASTM, pain management, lymphatic drainage and Eastern modalities such as, Ba Guan, Gua Sha, Ashiatsu and Thai Yoga. Sharon has a degree in Holistic Health and has studied orthomolecular nutrition, metabolic healing, herbal medicine, child development and has received evidence-based training for autism and self-regulation protocols for children with ASD, ADHD, and sensory disorders from the UC Davis Mind Institute.
Keville, K and Green, M, Aromatherapy: A complete Guide to The Healing ArtInternational Journal of Neuroscience: Modulation of Cognitive Performance and Mood by Aromas of Peppermint and Ylang-Ylang
Wheeling Jesuit University: Study Finds That Peppermint and Cinnamon Lower Drivers’ Frustration and Increase Alertness
Srivastava, J.K. and Shankar, E., Chamomile: A herbal medicine of the past with bright future, Molecular Medicine Reports, 2011 Feb 1.
Rozenkrantz, L., Zachor, D. and Sobel, N., A Mechanistic Link between Olfaction and Autism Spectrum Disorder, Journal of Current Biology, Elsevier, 2015 Jul 20


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Posted by on December 16, 2017 in Uncategorized