NSAID Use and Chronic Low-Back-Pain

Willow bark has been used for pain relief for thousands of years. Hippocrates wrote about willow bark as a remedy for pain and fever around 500 BCE. The active ingredient of willow bark, salicylic acid, was first isolated in the 1820s. Aspirin (acetylsalicylic acid) was developed from salicylic acid in 1897 by Felix Hoffman of Bayer. Aspirin became available to the public without a prescription in 1915, making it one of the first synthetic over-the-counter medications. It wasn’t until 1971 that Aspirin’s mechanism of action was discovered by pharmacologist, Dr. John Vane. He found that aspirin and other similar drugs inhibit prostaglandin synthesis. Prostaglandins are hormone-like compounds, known as lipid autocoids, that are produced in various bodily tissues as needed. They play an important role in regulating bodily functions, such as pain, fever, inflammation, blood clotting, blood pressure (smooth muscle contraction and kidney filtration rates), stomach acid secretion, and mucus production.
More specifically, Vane discovered that these drugs inhibit the enzyme known as cyclooxygenase (COX), which is needed for prostaglandin synthesis. Vane was awarded the Nobel Prize in Physiology for his discovery.

Even though salicylic acid is the constituent isolated from willow bark for the development of acetylsalicylic acid (Aspirin), there are other natural chemicals in white willow bark that work synergistically with salicylic acid. One such chemical compound is miyabeacin, which contains two salicin groups, and is shown to be effective in treating many types of cancers. Other salicinoids in willow may prove to enhance the overall therapeutic benefits of this miraculous herb.

Following the revelation of aspirin’s mechanism of action, other NSAIDs (non-steroidal anti-inflammatory drugs) like ibuprofen and naproxen were developed in the 1950s and 1970s. The term non-steroidal was important to differentiate them from corticosteroids, another class of anti-inflammatory drugs, that have significant deleterious side-effects.
The 1990s led to the discovery of two COX enzyme isoforms. Cox-1 is involved in bodily functions, while COX-2 is primarily responsible for pain and inflammation. NSAIDs are not selective about which COX enzymes that they inhibit. Hello selective inhibitors! Celebrex enters the market in 1998 as a COX-2 inhibitor. The goal was to reduce the gastrointestinal side-effects of NSAIDs by only inhibiting one of the COX isoforms. They worked fantastically well for pain and inflammation relief, but unfortunately, COX-2 inhibitors were found to have an increased risk of cerebrovascular and cardiovascular events.

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are a common treatment for short-term, or acute, Low-Back-Pain (LBP) as well as other pain disorders often associated with inflammation. However, their long-term use for chronic pain, as in LBP conditions lasting longer than 3 months, may paradoxically contribute to persistent or worsening pain.

History of NSAIDs

Impaired Healing and Tissue Degeneration

Inflammation is a vital part of our body’s healing process. It works by clearing out damaged or diseased cells and stimulating tissue repair. NSAIDs work by inhibiting cyclooxygenase enzymes called COX-1 and COX-2, which are responsible for producing pro-inflammatory chemicals called prostaglandins. This is why NSAIDs can alleviate pain that is caused by inflammation. Unfortunately, long-term suppression of inflammation hinders tissue repair and regeneration. NSAIDs may also hinder bone healing and negatively affect the outcome of surgical fusions. For conditions like chronic LBP or osteoarthritis, which involves tissue damage, this can mean that the underlying problem is not resolved. NSAIDs can disrupt the balance of pro-resolving mediators (SPMs), which are integral for halting the inflammatory cascade and promoting tissue repair. These mediators (resolvins, protectins, and maresins) are needed for the transition from a pro-inflammatory state of tissue repair to the resolution of inflammation with regenerated tissue.

Research shows that long-term use of NSAIDs may actually accelerate degenerative processes, such as cartilage degradation in osteoarthritis. This can worsen conditions like LBP, which is often associated with degenerative discs and facet joints.

Rebound Pain and Sensitization

Rebound pain can occur if pain pathways are constantly suppressed, leading to a complex interplay between discomfort and the body’s response mechanisms. When the use of pain medications or treatments is halted, the pain can return even more severely if a tolerance has developed over time. This phenomenon can be particularly challenging for individuals who have dealt with chronic pain, as they may find themselves facing not only the original pain but also intensified sensations that were previously masked.

Long-term reliance on NSAIDs without allowing the body to heal or addressing the underlying cause can allow central sensitization or a hypersensitive pain response to develop. This happens when the body becomes accustomed to the constant presence of pain relief medications, leading to altered pain processing pathways in the nervous system. After long-term use of NSAIDs, individuals may find themselves in a cycle where they experience heightened pain sensitivity, making even mild stimuli feel unbearable.

Masking Underlying Issues

By effectively alleviating pain, NSAIDs may delay proper diagnosis and treatment of the root cause of the back pain. This may allow the underlying cause of back pain to progress, while also hindering your body’s own healing capabilities. This leads to more severe pain and possibly more problems and reduced mobility.

Masking the pain can possibly cause individuals to put off physical therapy or corrective exercises that would help balance their body’s biomechanics and make ergonomic adjustments to help align their spine and prevent further injury or degeneration. Over time, neglecting the root cause of pain can create compensatory patterns in movement, which may inadvertently exacerbate existing problems and lead to further injuries.

Adverse Effects

• Gastrointestinal problems, such as gastritis, ulcers, bleeding, heartburn, and SIBO are not uncommon and can even be life-threatening complications of NSAID use.

• Cardiovascular risks include heart attack, stroke and hypertension.

• NSAIDs decrease kidney function and also lead to fluid retention. This is because NSAIDs block prostaglandin synthesis, which alters the kidneys’ ability to regulate electrolytes. This is made worse for individuals with pre-existing heart conditions.
• NSAIDs are ototoxic, meaning they can lead to hearing loss. Tinnitus may be one of the first warning signs. If stopped soon enough, some of the damage may be reversed.

Suppressing Inflammation

Suppression of inflammation, especially during the acute phase of pain, may actually be counterproductive to long-term pain relief and lead to longer healing time or suppression of tissue repair. Research suggests that icing a sprain, especially in the acute phase, actually hinders healing by reducing blood flow and delaying the body’s inflammatory healing response. Some studies show that prolonged icing may even cause further tissue harm. The RICE protocol has now been updated to include movement, which promotes circulation and healing. Movement, rather than rest, yields greater results for recovery. Our bodies were designed to heal, inflammation (via circulation) is part of this miraculous process of tissue healing and regeneration.

Specialized pro-resolving mediators (SPMs) are endogenous lipid molecules (as mentioned earlier) that are crucial in limiting acute inflammation and the prevention of chronic inflammation. SPMs are very different than NSAIDs and steroids, as they don't suppress the immune system, but rather promote the resolution of inflammation. NSAIDs can interfere with this natural process, potentially leading to chronic inflammation, delayed healing, and the need for chronic use of analgesics.

                                                               Movement Is Medicine

Movement is vital to the healing process. Muscle contraction helps pump blood and lymph throughout the body, delivering oxygen and nutrients to tissues to promote recovery and resolve inflammation. Regular movement promotes flexibility and prevents stiffness. Movement also helps our cells take-up glucose and stay insulin sensitive; this reduces the risk of developing metabolic complications from sedentarism or bed rest. Stretching can reduce adhesion formation from injuries, enhance circulation and also helps the myofascial tissues stay pliable for smoother movement.

Mechanical spinal decompression alleviates disc compression and improves circulation by creating a negative pressure within the intervertebral discs. This innovative therapy not only helps retract bulging and herniated discs, but it also significantly alleviates nerve compression, providing much-needed relief from pain and discomfort. As the negative pressure is generated, it encourages the movement of essential fluids, nutrients, and oxygen back into the discs, thus promoting healing and reducing inflammation. Furthermore, this process can enhance overall spinal health by restoring proper alignment and function to the vertebrae, leading to improved mobility and quality of life for individuals suffering from various spinal conditions, making it an effective non-surgical option worth considering.

Even gentle activity helps increase circulation, which improves blood flow to injured tissues. Blood carries oxygen, nutrients, and growth factors that are vital for tissue remodeling and waste removal. Stagnant waste and inflammatory mediators prolong the inflammatory phase and hinder the healing process.
Movement is essential for proper lymphatic drainage, which flushes out inflammatory byproducts from the injured site. 

While initial inflammation is crucial, prolonged or unresolved inflammation can be deleterious. Controlled movement can help regulate the inflammatory response by promoting a healthy transition to the proliferation and remodeling phases of healing. In fact, studies show isometric contractions can provide immediate and sustained pain relief for up to 45 minutes or several hours in some cases. Movement also helps with healthy scar formation and collagen organization. Controlled movement provides mechanical stress that helps align collagen fibers in a more functional pattern. Gentle stretching can help reduce adhesions and increase flexibility and range of motion. 
Fibroblasts are also stimulated by mechanical stress, this is called mechanotransduction. Tension, compression, and shear forces translates mechanical stimuli into biochemical signals within cells. Fibroblasts, when responding to mechanical stress, will produce more collagen and extracellular matrix components. Movement also helps restore proprioception, which is often impaired after tendon or ligament injuries.
Motion is lotion for the joints. Movement encourages the synovial tissue to produce more fluid to lubricate the articular surfaces of the joints. Synovial fluid delivers nutrients to the articular cartilage, which would otherwise have no way of receiving nutrition, as it is avascular.
Immobility can lead to joint and muscle stiffness and possibly even contractures.

It is important that you control your movements, as too much or the wrong type of movements may reinjure the tissue. Healing a herniated disc requires different movements than trying to resolve pain from a low-back sprain or spinal stenosis. There are no one-size fits all approaches when it comes to physical or manual medicine. Follow the advice of your healthcare professionals who can assess your specific situation and guide you on the appropriate timing and intensity of your activities. A functional medicine practitioner, manual osteopath, physical therapist, or holistic manual therapist may help guide you on the journey to healing and pain resolution! 

 

Watch Your Gait!

Observing your client’s gait and stance is an important part of the examination that can help guide you to the correct treatment protocol.

You may identify clues to neurological problems (e.g., Parkinson’s, hemiparesis, cerebellar disease) or neuromusculoskeletal conditions (e.g., spinal stenosis causing NIC, hip or knee arthralgia). You may also recognize clues to your client’s emotional status.

Depressed clients may have a shorter stride with weak push-off, forward head carriage and internally rotated and protracted shoulders.

Remember, the assessment starts before the interview.

Some fundamental reasons for gait abnormalities include: pain, decreased joint range-of-motion, muscle weakness, and abnormal neuromuscular limb control.

Abnormal limb control may result from spasticity, rigidity, proprioceptive problems, cerebellar or cerebral disorders. The children that I treat with ASD often have proprioception abnormalities and may have difficulty with body positioning. This may affect gait, stance, and even lead to spinal curvatures, as the transversospinalis muscles (semispinalis, multifidus, and rotatores) are very important for proprioception of the spinal motion segments.

Is the gait symmetric or asymmetric? Pain, joint hypomobility, and muscle weakness tend to be unilateral, therefore would likely cause asymmetric gaits.

Spasticity or rigidity caused by hemiplegia would be asymmetric, however, if it were caused from paraplegia would be symmetric.

Antalgic gait (painful gait) has a characteristic short contralateral step after bearing weight on the affected side. You can replicate this cadence by walking around with a pebble in one of your shoes. There is also distinctive features to this gait, depending upon whether the pathology is in the foot and ankle, knee, or hip.

If the pain is coming from the foot, the client may bear weight abnormally or unevenly. For example, only placing the heel or lateral metacarpal down during stance or push-off.

Clients with knee pain may not extend or flex their knee fully during stride.

Coxalgic gait, may be seen in patients with hip pain, as an excessive lateral shift of the client’s upper body toward the weight bearing side. The trunk leans while the ipsilateral arm abducts (lateral lurch). This reduces the activation of the hip abductors (gluteus medius, minimus and tensor fascia latae), whose role is to stabilize the upper body during swing of the contralateral leg and/or one-legged stance.

When activated, the hip abductors can add an additional 400 pounds of pressure on the femoral head. Leaning over the affected hip during stance balances their center of gravity over the painful limb and avoids activating the hip abductors for stabilization. Using a cane contralateral to the diseased hip can reduce the pressure placed on the femoral head and allow for gait improvement.

Hip extension toward the end of stance is normally 20 degrees, this will be limited if the hip is painful or has reduced ROM.

Joint immobility is another cause of abnormal gait. One commonly seen is plantar flexion contracture. This may be due to plaster immobilization or reduced ambulation for a period. You may notice your client places the forefoot and midfoot abnormally during initial stance, or lifts the heel too early or leans forward to compensate. During swing phase the patient may have trouble with their toes clearing the floor, may drag their foot to clear it, lean contralaterally, contralateral vaulting or steppage.

A simple ROM assessment can identify immobility in the hips, knees or ankles.

Weakness in certain muscles may manifest as a specific gait abnormality. Gait typical of gluteus maximus and quadricep weakness is not as prevalent as it was when poliomyelitis and diphtheria numbers were higher.

Trendelenburg gait is seen with weakness in the gluteus medius and minimus. These two muscles are hip abductors and supports the contralateral pelvis from dropping excessively during single-leg stance. Damage to the superior gluteal nerve can cause neuromuscular weakness, this may be the result of a complication during hip arthroplasty using the lateral approach. Improperly given intermuscular gluteal injection can also damage the superior gluteal nerve. Congenital hip dislocation can cause abductor weakness. Coxa vara, which includes varus and retroversion of the proximal femur, displaces the greater trochanter superiorly and shortens the abductor muscles making them more horizontal as opposed to vertical. This reduces their ability to abduct the hip and stabilize the contralateral pelvis during one-leg stance.

If the hip abductors are weak bilaterally, the client will waddle like a duck. If the weakness is unilateral, the client will have a slight lean towards the affected side during stance and a hinge-like sway of the ipsilateral shoulder and contralateral pelvis.

Trendelenburg’s sign is a test where the client is asked to stand on one leg with the other hip flexed to 90 degrees. If the abductor strength is normal, the contralateral buttock elevates, but if the muscles are weak, the contralateral buttock falls. If the client has severe genu verum, you may get a false positive.

Gluteus maximus gait is a result of weak hip extension. The trunk lurches backwards (trunk extension) during heel strike and early stance on the weakened side, which places the center of gravity behind the acetabulofemeral joint. This removes the need for the gluteus maximus to contract, extending the hip.

 

Flu is in the Air!

What’s Causing your cold or flu-like symptoms?

There have been many respiratory viruses circulating this season. They seem to have fully launched in early October, with high numbers of influenza B being diagnosed in early November and throughout December. According to health officials, the flu usually peaks sometime between late December and February.

Often times, other viral infections are mistakenly referred to as the flu. Your nurse or doctor can diagnose you with type A or B influenza with a rapid nasal or throat swab. Your healthcare provider can make the diagnosis based on clinical presentation as well.

Rhinovirus is thought to be responsible for up to 50% of cold viruses. However, WebMD states it is more like 10-40% – that’s a pretty large range. The rhinovirus proliferates in temperatures around 32-35 Celsius (approximately 89-95 Fahrenheit), which is the temperature inside your upper respiratory tract – convenient.

There are 3 species of the RNA rhinovirus (A,B,C) differentiated by their serotype (surface proteins), of the genus Enterovirus and belong to the Picornaviridae family. This is meant to be an easy breakdown, so that’s as much as I’m delving into virology with you guys. Oh, except to point out how entirely small they are, they’re approximately 1/3- 1/4 the size of the influenza virus.

Rhinovirus is most prevalent in the fall (Sept./ Oct.) and spring (March/April). They are transmitted via aerosols of respiratory droplets and contaminated surfaces, this includes hands, handles and shopping carts. The virus can survive up to 3 hours outside a host.

Symptoms of the rhinovirus include: sore throat, runny or congested nose, pain or pressure in the sinuses, sneezing, cough, watery eyes; and sometimes may include body aches, mild fatigue, headache, weakness and loss of appetite. Extreme fatigue and fever are not common with this virus. In children and susceptible adults, this virus may lead to otitis media. This is why proper sinus drainage techniques are important.

The incubation period for the rhinovirus is anywhere between 12 hours to 4 days, with most being 2 days. Symptoms may last up to 2 weeks.

Vigorous handwashing, not touching your face and other hygiene practices are amongst your best avoidance techniques.

Coronavirus, is a RNA virus active during winter and early spring. This virus has 6 known human species and is responsible for about 20% of colds. It is way larger than the rhinovirus, in fact it is one of the largest RNA viruses. They primarily attack the upper respiratory tract and the gastrointestinal tract, but can also attack the lower respiratory tract.

The coronavirus is typically more severe than the rhinovirus. Incubation period is from 2-10 days, with a mean of 5 days. Symptoms are flu-like in nature, or milder, depending on which species you are infected with. Symptoms may consist of: fever of 100 or above, muscle aches, headache, diarrhea, followed by the onset of a sore and swollen throat and adenoids, dry-cough, dyspnea and possibly even pneumonia during the advanced stage. This virus can cause viral pneumonia or viral bronchitis, or lead to a secondary infection of bacterial pneumonia or bacterial bronchitis – especially if coughs are non-productive. This virus is notorious for exacerbating asthma.

An interesting finding that commonly occurs with this virus is lymphopenia (low lymphocytes). As a result, coronavirus antibodies usually don’t last very long and you may become re-infected. Also, antibodies for one strain will not give you immunity to a different circulating strain.

One of the coronaviruses more dangerous forms is referred to as SARS (severe acute upper respiratory infection) or SARSCoV. You may remember the much publicized outbreak in Asia. SARSCoV in its most severe form may cause pulmonary, cardiac and hepatic failure. During the SARS epidemic in Asia, approximately half of all people infected over 65 died. The viral genetic sequence was mapped from infected patients in Toronto in 2013. Animals like dogs, cats, chickens, rodents and racoons are also susceptible. One circulating theory is that this virus actually evolved to infect humans from bats. Thanks a lot Ozzy!

An interesting tidbit for you fellow nerds out there, the primary receptor site for SARSCoV is angiotensin-converting enzyme 2 (ACE2). In a healthy respiratory tract, the SARSCoV may be removed by mucociliary clearance, and thus gain access to the gastrointestinal tract. Diarrhea is commonly observed in patients with SARS.

MERS, is another type of coronavirus (Middle East Respiratory Syndrome) and was first recognized in 2012 in the – you guessed it- Middle East. Cases of this strain seem to be linked to individuals who have traveled to the Arabian Peninsula. MERCoV is fatal in approximately 30-40% of people who contract it. As RNA viruses (like the coronavirus) constantly mutate, there are major concerns this virus could become pandemic. This strain has been found in camels and bats, so it probably also has a zoological origin . Quit kissing your pets!

The coronavirus is spread in the same manner as the rhinovirus. The same precautions apply. Oh yeah, don’t kiss your pet. Ferrets can catch human colds, don’t get your ferret sick.

Yes, that’s me kissing Honey. Give me a break, I was only 16!

RSV/HRSV (Human Respiratory Syncytial Virus/Human Orthopneumovirus) is a major cause of lower respiratory tract infections. It is a medium sized RNA virus. Most all children will have had this virus by age 3. Approximately 3% of those infected will develop bronchiolitis. In fact, the CDC believes this virus is responsible for the majority of bronchiolitis and pneumonia in children younger than 1.

Young adults may be re-infected every 5 to 7 years. The incubation for RSV is 4 to 6 days. The virus is usually prevalent during the flu season. In adults, the symptoms are usually mild and typical of the common cold. People with asthma, the elderly or who are immunocompromised are more likely to become seriously ill. In those, the virus may start off like the common cold, but then develop into bronchiolitis and/or pneumonia as the virus works its way from the nasal passages, the throat and then the lungs. The virus usually lasts for 2-8 days, however, symptoms may linger for 3 weeks. I find this especially true in asthmatic children.

One interesting tidbit about the RSV virus, is that it has 2 separate genes encoding for nonstructural proteins that suppress the host’s innate immunity. There are approximately 10 known strains and the genome was sequenced in 1997.

The virus spreads like the aforementioned two. It can survive for 5 hours on hard surfaces. Staying home when sick and handwashing is strongly advised. Your healthcare provider can test for RSV using a nasal swab. Oxygen saturation or a chest radiograph may also be used to assess for lung congestion.

The virus can spread from apes to humans, but not the reverse. Hmmm…

So, the flu isn’t the only virus spiking right now. The CDC stated that more then 2 million children under 5 are diagnosed with RSV every year. It also hits the elderly pretty hard as well.

Adenoviruses (HAdV) are medium sized DNA viruses. Their name is derived from the tissue it was originally isolated from, the human adenoids. In humans, there are more than 50 serotypes broken down into 7 species (A-G).

The adenovirus most commonly causes respiratory illness, but depending on the serotype can affect any mucous membrane. Symptoms from respiratory involvement may range from common cold-like illness to pneumonia, croup and bronchitis. Cystitis and gastroenteritis may also occur. Conjunctivitis is very common with this virus.

Respiratory illness is most likely caused by the B or C species. Conjunctivitis may be caused by B and D and Gastroenteritis by F and G species. Adenovirus can also cause cystitis. Men are vulnerable to urethritis caused from the adenovirus, this is referred to as non-gonococcal urethritis (NGU).

Several adenoviruses may be somewhat responsible for obesity, or adipogenesis, in cells. The serotype HAdV-D-36 is the one most studied as it pertains to human obesity, diabetes, and enteritis; although serotypes A-31, C-5, and D-9,36, and 37 are all associated with obesity in humans and animals. AD-36 antibodies in the blood are associated with the presence of obesity.

HAdV is spread by respiratory droplets or fecal oral route. Some types may even reside in your tonsils, adenoids and/or intestines and be asymptomatic for years while shedding. Inadequately chlorinated pools may be responsible for febrile disease with conjunctivitis “pool fever” (pharyngoconjunctival fever). Your child may present with high fever, sore throat, conjunctivitis without pus, enlarged cervical lymph nodes, headache, fatigue and malaise. The incubation period for this particular illness is 5-9 days, so you may not associate the sickness with your child’s swimming event at a public pool.

In 2007, an outbreak of the adenovirus was coined “Boot Camp Flu”, as it spread through the Air Force Base in San Antonio. One trainee died from the virus.

Most people recover well from the HAdV, however necrotizing pneumonia (which results in something similar to patients with bronchiectasis), bronchiolitis obliterans (bronchioles are replaced by scar tissue) have been known to occur. HAdV-14 is dubbed the “killer cold”, due to the high amount of hospitalizations and associated death.

Adenovirus respiratory infections are more common in the late winter and early spring. However, depending upon the strain may be circulating in the early summer, or year round. These viruses are responsible for approximately 10% of childhood fevers. Nearly every child will have had at least one type of adenovirus by age 10. You may have immunity of one or more types of the adenovirus, but there are certainly more out there.

Alcohol based sanitizers are not effective at killing HAdV. Essentially, any bodily fluid may spread the virus. You may spread the virus for months after recovering. It can survive for many hours to days on surfaces.

Parainfluenza/Human Parainfluenza (HPIV) is a RNA virus, of which there are four major serotypes. The parainfluenza virus is between 150-250 nm in diameter, whereas the flu virus is 80-120 nm.

Parainfluenza virus is the 2nd leading cause of hospitalization in children under 5 with respiratory illness, #1 is RSV. This is the virus that comes to mind when a child has croup (laryngotracheobronchitis). Croup is caused from the large scale production of IgE antibodies which mediate the release of histamine in the trachea. Each year in the US, 5 million children are hospitalized for lower respiratory infections, parainfluenza types 1-3 are responsible for up to 1/3 of these infections.

Overall symptoms may include: rhinitis, red swollen eyes, bark-like cough, noisy breathing, hoarseness, rattling felt in the chest, wheezing, fever, decreased appetite, vomiting and diarrhea. It is also associated with febrile seizures, so keep an eye on your child’s temp. In rare cases, parainfluenza may lead to viral meningitis and Guillain-Barre’ Syndrome.

75% of children older than 5 have antibodies to parainfluenza-1. As this is a RNA virus, it mutates over time and re-infection can occur. You may also become infected with Type-2 or 3 after becoming immune to Type-1.

Parainfluenza Type 1 (HPIV-1) is the most common cause of croup!

HPIV-2 causes croup along with other upper and lower respiratory tract illnesses.

HPIV-3 is can cause bronchiolitis and/or pneumonia.

HPIV-4 is further subdivided into 4a and 4b and is predominantly associated with upper respiratory symptoms that are milder.

Again, mode of transmission is from droplets and secretions. The virus may remain infectious for more than an hour on surfaces. Don’t touch your face, nose, mouth or eyes when out and about. Thorough hand washing is your best defense. The parainfluenza has an incubation period of approximately 2-6 days. It is biennial, with large outbreaks of croup in the fall occurring in odd-numbered years. 2019 was our year. Happy 2020!

Influenza, aka “the flu”, is all the talk right now. There are 4 types of this RNA virus.

Influenza A is the virus that you hear about in birds and some mammals. Wild birds are thought to be the harbinger of this virus. There are many subtypes of influenza A based upon their surface proteins (serotype), such as H1N1, H1N2, H2N2, etc.. They will have an H number and an N number. There are at least 18 H antigens and 11 N antigens.

Influenza B is not as pandemic, since only humans, ferrets and seals can be infected. However, this season has had an unusually high number of people testing positive for this strain. Influenza B mutates 2-3 times slower than type A, so the chance that the vaccine will match up for the B strain is greater. However, it mutates enough that the strain may be different before the season is over and you will catch the mutated strain regardless of being vaccinated for the old strain. Therefore, you will not have immunity to the virus after it has mutated.

Influenza C mutates even more slowly than B. It can infect humans, dogs and swine. Type C is usually associated with milder symptoms than Type A or B.

Type D is known to infect swine and cattle, no known human infections from this virus have been reported.

Symptoms of the influenza virus usually start with body aches and chills followed by high fever, runny nose, sore throat, muscle and joint aches, headache, coughing, and fatigue. Influenza may occasionally present like sepsis in young people and delirium or confusion in the elderly.

The incubation period is usually 1-4 days. The virus lasts about a week, but symptoms may persist for more than 2 weeks. Diarrhea and vomiting may occur in children. (Gastroenteritis is the virus responsible for what most people call the “stomach-flu” or “24 hour bug”).

Some may develop viral pneumonia, or a secondary bacterial pneumonia or sinus infection. Anytime your child or loved one has dyspnea, cyanosis, confusion, inability to stay hydrated, or chest pain please seek emergency medical assistance. I know that you know, but I still wanted to emphasize it.

I would love to go on and discuss other viruses, as they are extremely fascinating, but alas I promised to only talk about flu and cold-like viruses.

There are a lot of good nutraceutical and botanical supplements that support a healthy immune system and may even hasten your recovery from some of these nasty bugs. For more information on that consult with your Functional Medicine Practitioner or Naturopath.

 

You Can Heal a Degenerative Intervertebral Disc!

Degenerative disc disease (DDD) is a major cause of low back pain (LBP). One of the most important factors in the development of DDD is vertical loading, which can activate an enzymatic process facilitating disc degeneration. When a disc is compressed, the hydrostatic pressure within the nucleus rises and increases tensile stress in the outer annulus restraining the nucleus. The annulus bulges outwards, which reduces disc height.

The endplates are pressed together from this compressive force. However, due to the high water content of the nucleus it is incompressible. As a result, the endplates bulge into the vertebral bodies. Thus, when the motion segment is axially compressed, or under pure axial compression with torsion or axial compression and flexion, the endplate fails before the annulus.

Endplate sclerosis has been implicated in the genesis of intervertebral (IVD) disc prolapse.

Segmental instability can occur is the second phase of DDD if preventative measures are not sought. Back surgery, such as microdiscectomies and laminectomies can accelerate this phase of degeneration. The 3 phases described in DDD are temporary dysfunction, unstable phase or instability, and finally secondary stabilization.

In the first stage, temporary dysfunction, early signs of degeneration can only be seen on a T2 weighted MRI. Disc signal loss, or desiccation, will appear as a black IVD with loss of height and changes in contour of the annulus.

If preventative measures aren’t taken, then progression to phase two – instability – will occur. Structural changes occur in the collagen of the annulus during this phase, reducing its tensile strength. Proteoglycans are also decreasing, leading to decreased water content that results in reduced IVD height which causes laxity. Laxity of these restraining structures is what causes the instability.

So, what is instability? It simply means, excess or abnormal movement at a particular spinal segment. So the structures that restrain this segment have been damaged, which is usually caused by the IVD becoming decompressed – losing its hydrostatic pressure – like deflating a tire. Pain during this phase may arise from damage to the endplates, nerve root compression from IVD prolapse, facet joint arthropathy, or simply inflammation caused by the biochemical mediators. The facet arthropathy, coupled with the hypermobility can lead to degenerative retrolisthesis or degenerative scoliosis. Flexion/extension studies are performed to assess stability.

IVD’s can also lose water from sustained compression. Diffusion of water cannot take place in a compressed disc. A loss of water = loss of disc height, which creates slack leading to excess movement and instability. The neural arches are closer together, creating stress within the articular pillar and leading to facet hypertrophy and arthrosis. Due to the increased motion segment movement, osteophytes develop. This takes us to the secondary stability phase. Osteophyte formation increases the stability of the degenerated motion segment, which is phase three.

As a recap, IVD prolapse or endplate fracture (or both) decompresses the nucleus, which reduces the disc height and creates slack in the intervertebral ligaments. This allows the motion segment to have excess, or unwanted, movement. This is usually accompanied by call-mediated (MMP-2) degenerative changes. This is seen as degradation and restructuring of the annulus by metalloproteinases. There are targeted functional medicine approaches that help prevent this type of degradation and collagen shift.

Posture is important for not only normal IVD loading, but also nutrition. The IVD is avascular, so it relies on diffusion from the vessels around the periphery of the annulus and through the endplate. Impaired diffusion and metabolite transfer is strongly associated with DDD. Good posture is very important for proper diffusion and the influx of fluid. IVD glucose uptake is important for proteoglycans of the nucleus to survive and therefore, maintain water content. (I have a whole article dedicated to disc metabolism, please read it for more information.)

Successful metabolite diffusion into the disc is based on the distance to the nearest blood supply, as describe above. This is dependent on diffusion pathway distance. Flexed postures, such as slouching, increases the length of the posterior annulus by approximately 50%, and compresses the anterior annulus by 30%. Posture also affects fluid flux within discs, which is important for the transport of larger molecules which have a slower diffuse rate. Fluid expulsion is increased in a flexed or extended disc. Fluid expelled under disc loading returns once the load is reduced, bringing the influx of metabolites with it. Cadaveric studies show that metabolic transport via fluid flux is increased when flexed postures are alternated with extension (lordotic) postures.

I warn my clients about overworking the abdominal muscles, especially the rectus and obliques. Abdominal muscles that are shortened will cause a flexion curve of the spine, increasing IVD pressure and reducing the exchange of metabolites. Muscles can generate passive tension when their resting length is shortened. This is why I love yoga for LBP! Increasing tonus of the transverse abdominis and the multifidus is what we want to achieve to create better spinal stability. Certain Pilates and yoga exercises are great for this. (Please read my blog post on yoga and Pilates for back pain.)

Mobile, active, decompression reduces the compression the IVD’s allowing micro and macro molecules to diffuse via the influx of water. This helps restore disc height to alleviate nerve root compression by allowing prolapsed disc material to be reabsorbed. This negative intradiscal pressure creates a vacuum, allowing metabolites and fluid into the desiccated disc. The glucose that is brought back into the disc helps nourish the anulus allowing it to regenerate. T2 weighted MRI images have shown the after-effects of IVD unloading and the return of water content and regeneration.

You can heal a degenerative disc. Your body is miraculous, all it needs are the proper tools to assist it. The VerteCore Lift can help unload your IVD’s allowing your body to do the rest! It is the only wearable that comfortably allows you to remain active, which increases circulation and thus diffusion – allowing for restoration of disc height. Give your body what it needs to heal, before allowing surgery or drugs to foreclose your options.

 

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?

• 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.

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!

 

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. –

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. 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.

 

 

 

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!

 

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.

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).

 

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.

 

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.  
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  

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.

Respiratory

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.

Cardiovascular

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  

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.

Gastrointestinal

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. 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!