Sacroiliac joint dysfunction is known to cause low back pain, but diagnosing can be hard for some doctors. Especially those that do not have a great deal of experience in sacroiliac joint pain. However, chiropractors specialize in this area as the SI joint is an important part of the musculoskeletal system.
SI joint dysfunction and pain can involve�one or both joints.
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Other terms associated with SI joint dysfunction are sacroiliitis or degenerative sacroiliitis.
Low back pain may be SI joint-related, so how to start the conversation with your doctor?
Things to Remember Before Appointment
Diagnosing sacroiliac joint-related pain begins before your first appointment with a doctor or chiropractor.
Three things to do before your appointment can help make the visit highly productive.
I. Know your medical history
If you have an existing spinal condition, it can definitely affect SI joint dysfunction
Any recent trauma, like an auto accident or fall?
Pregnant?
Think about these before, because they can help a doctor identify links or cause of Sacroiliac joint dysfunction.
II. Know the symptoms
Make it a point to know the symptoms so you can explain them in full detail.
Dull pain
Achy
Stiff
If you need to, write them down.
Common symptoms:
Low back pain
Pain that travels through:
Hips
Buttocks
Thighs
Groin
Pain when pressing on the Sacroiliac joints�
Stiffness or electrical burning sensations in the pelvis
Know when the symptoms get worse and when they go away. For example:
The pain usually increases when:
Standing
Walking for extended periods
Climbing stairs
Getting/rising up from a seated position
And the pain usually goes away when lying down.
III. Write down questions for your doctor.
Think about what you want your doctor to understand and the pain you are going through.
Write down questions and take them with you.
This questions could be like:
Is this pain caused by a sacroiliac joint problem?
Why rule out sacroiliac joint dysfunction?
How long does it take for the treatment/s to take effect?� �
Is the treatment plan for long sustained relief or short-term relief?
The Appointment
Ask your doctor to examine you for sacroiliac joint dysfunction.
Low back pain research shows the sacroiliac joint, is a definite cause of low back pain.
This problem affects� 30-34% of patients with low back pain.
A doctor can diagnose sacroiliac joint dysfunction based on medical history and a physical exam.
The physical exam, which can include performing specific maneuvers/movements to re-create the pain in a controlled manner, to help confirm a diagnosis.
Physical tests can initiate sacroiliac joint pain and help diagnose low back pain that is being caused by sacroiliac joint dysfunction.
Fortin finger test, which means pressing down near the sacroiliac joints
If three out of five tests produce pain, then more than likely you have sacroiliac joint dysfunction.
Dialogue with your doctor/chiropractor
It�s normal to feel overwhelmed during a doctor’s visit, especially if you have a�condition that is hard-to-diagnose.
Talk with your doctor, their voice should not be the only one heard, this is your body and your health that’s at stake.
Your information is essential to help with an accurate diagnosis.
If your doctor doesn’t feel comfortable or feels they don’t have enough experience in diagnosing sacroiliac joint pain, then ask for a referral to a spine specialist/chiropractor that is comfortable and does have the experience in diagnosing sacroiliac joint pain.
There are a number of treatments for sacroiliac joint dysfunction, including pain medication, epidural steroid injection, and surgery. However, chiropractic care is non-invasive and does not have the unpleasant, sometimes harmful side effects of pain meds. It is safe and effective and treats the entire body instead of just the part that hurts.
Low Back Pain Treatment | El Paso, Tx
Low back pain which gradually influenced his quality of life was developed. David Garcia was unable to walk as his symptoms worsened and his back pain became excruciating. He first visited Dr. Alex Jimenez, a chiropractor in El Paso, TX, following a recommendation from his sister. Dr. Jimenez managed to supply David Garcia with all the aid he deserved for his low back pain, restoring his well-being. David Garcia clarifies the wonderful service Dr. Alex Jimenez and his team have given him to offer him relief from his painful symptoms and he highly recommends chiropractic care as the non-surgical pick for low back pain, among other health problems.
NCBI Resources
Patients who experience lower back pain never want to deal with it again, but�it can flare up periodically. According to the�National Institute of Neurological Disorders and Stroke, roughly 20% of those who suffer from low back pain will eventually deal with it chronically. This can cause frustration, primarily when it affects mobility.
Before you run screaming in horror to the medicine cabinet, one of the best reasons to participate in chiropractic treatment is that it helps reduce the chance of a recurrence. By working on the total body and getting it in the best shape possible, the patient is stronger and more balanced to handle their workload and other strenuous activities. Chiropractors also impart advice on how to minimize the chances of re-aggravating the lower back.
Excitotoxicity is characterized as an acute insult which causes nerve cell death due to the excessive activation of iGluRs. Acute excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue. �
With brain ischemia, L-glutamate-associated and L-aspartate-associated excitotoxicity happen within minutes due to the growth in extracellular cerebral L-glutamate as well as L-aspartate. Because these are also energy-dependent, the abrupt loss of energy due to the shut down of blood flow can ultimately breakdown the neuronal and astroglial membrane. In neurons, membrane depolarization contributes to vesicular discharge. Additionally, energy degradation may even cause a change in their action, therefore, causing L-glutamate and L-aspartate to activate and affect ionic homeostasis which can interrupt EAAT action. The activation of L-glutamate/L-aspartate contributes to excitotoxicity through the over-activation of iGluRs of the NMDA type as demonstrated by the efficiency of NMDA antagonists in animal models of transient cerebral ischemia. �
In TBI, the mechanical tissue damage and the disruption of the blood-brain barrier can trigger acute secondary neurodegeneration, which, together with neuroinflammation and oxidative stress, is associated with L-glutamate activation from intracellular compartments and, therefore, by acute excitotoxicity. Moveover, acute application of the NMDA antagonist MK801 following TBI ameliorates neuronal loss and long-term behavioral abnormalities, among others. �
In status epilepticus, continuing the synchronized activity of excitatory neuronal networks as well as the continuous breakdown of restricting mechanisms is the main source of L-glutamate and L-aspartate activation. As the severity of synchronous activity depends upon the involvement of nerve cells into a neuronal system as well as the capability of a neural cell to withstand excess glutamate mainly depends on the expression pattern of iGluRs, a somewhat restricted and maturation-associated degeneration of neuronal populations which is ultimately caused by prolonged epileptic seizures. The significance of excitotoxicity in status epilepticus is shown as NMDA antagonists, such as ketamine, decrease adrenal loss. �
Excitotoxicity in Neurological Diseases
Because EAATs were discovered to be down-regulated in a variety of central nervous system (CNS) health issues and L-glutamate, as well as L-aspartate, clearance can ultimately affect the excitotoxicity of neurological diseases, many healthcare professionals have decided to determine substances which cause EAAT2, or the main EAAT in the brain and most commonly shown to be downregulated. This has demonstrated substances which shows astrocytic EAAT2 expression both in vitro and in vivo research studies. Several of these have also demonstrated protective properties in animal models of neurological diseases. Cef is one of the most evaluated compounds and it has been analyzed in AD, HD, and ALS models with positive outcomes. However, none of the substances has been extensively researched for its capability to interact with other neuroprotective pathways. Cef has also been demonstrated to promote EAAT2 expression but also to trigger the transcription factor Nrf2, which results in the transcription of a wide array of genes involved in cytoprotection and antioxidant protection. Because oxidative stress is believed to play an essential role in many, if not all, neurological diseases, this pathway may account for the neuroprotection caused by Cef. Furthermore, xCT, which can be one of the downstream targets of Nrf2, has been demonstrated to be upregulated by Cef in vitro and in vivo. Another in vitro EAAT2-promoting substance, MS-153, efficiently protected against secondary neurodegeneration after traumatic brain injury as well as through mechanisms other than EAAT2 upregulation. Evidence of concept experiments which demonstrate the increased stimulation through iGluRs in neurodegenerative diseases needs manipulations of their neurotransmitter physiology. �
Glud1 Tg mice demonstrate a model of excitotoxicity associated with enhanced synaptic L-glutamate activation with restricted neuronal loss. However, this animal model of glutamatergic neurotransmission has not yet been utilized to analyze if Glud1 over-expression aggravates the phenotype of mouse models in neurological diseases. Another version involves the EAAT2-deficient mouse. Homozygous EAAT2 knock-out mice have health issues associated with premature death because of epilepsy as well as hippocampal and focal cortical atrophy. Heterozygous EAAT2 knock-out mice, however, develop normally and show only mild behavioral abnormalities. This mouse model of moderate glutamate hyperfunction has been utilized in a collection of evidence of principle research studies which demonstrated the fundamental role of glutamate. ALS mice, which have both the G93A mSOD1 mutation and a decreased quantity of EAAT2 (SOD1(G93A)/EAAT2�), revealed an increase in the speed of motor decline accompanied by earlier motor neuron loss when compared with single mutant G93A mSOD1 Tg mice. A decrease in survival was also demonstrated in these mutant mice. When crossed with transgenic mice expressing mutations of the human amyloid-? protein precursor and presenilin-1 (A?PPswe/PS1?E9), partial loss of EAAT2 unmasked spatial memory deficits in 6-month-old mice expressing A?PPswe/PS1?E9. These mice demonstrated an increase in the ratio of detergent-insoluble A?42/A?40 demonstrating that shortages in glutamate transporter function ultimately cause premature pathogenic processes associated with AD. By comparison, the phenotype of the R6/2 HD mouse model wasn’t changed in mice which had only one EAAT2 allele. Further research studies are still necessary for further evidence. �
As a complement to these research studies, transgenic mice which over-express EAAT2 in astrocytes through the GFAP promoter has also been developed. EAAT2/G93A mSOD1 double Tg mice demonstrated moderate amelioration of their ALS-like phenotype with a statistically significant (14 times ) delay in grip power decrease and loss of motor neurons as well as a decrease in other occasions, such as caspase-3 activation and SOD1, although not at the beginning of paralysis, weight loss or an extended life span when compared with monotransgenic G93A mSOD1 littermates. Exactly the same EAAT2 transgenic mouse model was utilized to evaluate the effect of improved astrocytic L-glutamate and L-aspartate uptake by cross-breeding with an animal model of AD, A?PPswe/Ind mice. Increased EAAT2 protein levels considerably increased and improved overall cognitive functioning, restored synaptic ethics, and decreased amyloid plaques in those AD mice. �
In mice in which genetically engineered regulation and management of xCT causes a lack in the glutamate/cystine antiporter system x?c, the obvious decrease of extrasynaptic L-glutamate is associated with the tremendous resistance of dopaminergic neurons against 6-hydroxydopamine-induced neurodegeneration, perhaps as a consequence of reduced excitotoxicity. However, microglial activation has also been demonstrated to be modulated by system x?c deficiencies leading to a more neuroprotective phenotype which offers an explanation for the protective effect of xCT deletion in this circumstance. �
Therefore, genetic variations encourage the role of chronic excitotoxicity in neurodegenerative diseases, particularly AD and ALS. These models all represent life-long changes in glutamatergic neurotransmission. These models can’t determine if the utilization of drugs and/or medications can directly affect glutamate levels throughout the neurodegenerative process and/or be protective. Both evaluation and analysis of EAAT2-inducing medicine for the progression of inducible mouse models and their interaction with other signaling pathways is still warranted by researchers and healthcare professionals. �
In many research studies, evidence and outcome measures have demonstrated that glutamate dysregulation and excitotoxicity in many neurological diseases, including AD, HD, and ALS, ultimately lead to neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to discuss and demonstrate the role that glutamate dysregulation and excitotoxicity plays on neurodegenerative diseases. The mechanisms for excitotoxicity are different for every health issue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Metabolic Assessment Form
The following Metabolic Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptom groups listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
Excitotoxicity is characterized as an acute insult which causes cell death due to the excess activation of iGluRs. Excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
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Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
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If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
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Autoimmune disease is the disease of the modern era. It is a condition where the body�s immune system mistakenly attacks the body. Since the body�s immune system usually guards against bacteria and viruses, it can sense the foreign cells and send out fighter cells to attack them. When it�s an autoimmune disease, however, the immune system starts to make mistakes to certain parts of the body. It starts attacking the joints, the skin, or the musculoskeletal system as foreign cells and attacking them. The immune system releases autoantibody proteins to attack the healthy cells, thus causing autoimmune disease in the body.
What Triggers the Activation of the Autoimmune Mechanism?
Surprisingly, the body�s antibodies go through a process by cleaning up the old and damaged cells, so that way, new healthy cells can grow and replace the old cells. Although if the body has an excessive number of antibodies in their system, it can cause the individual to have an autoimmune disease. Research has shown that a part of the autoimmune ecology, the influence of environmental exposure can not only develop autoimmune disorder but shape the function of the immune system.
Another study stated that approximately 30% of all autoimmune diseases come from genetic disposition while 70% is due to environmental factors, including toxic chemicals, dietary components, gut dysbiosis, and infections in the body. So some of the ecological factors that are included are adjuvants (immunostimulant effects). These are typically used in vaccines to produce a more effective immunization reaction.
Researchers stated that molecular mimicry is one of the mechanisms, where a foreign antigen shares a sequence or structural similarities with self-antigens. This means that any infections that can initiate and maintain autoimmune responses can lead to specific tissue damage in the body. It is a phenomenon that molecular mimicry and cross-reactivity are identical. Cross-reactivity is significant when it comes to food allergies and is often responsible for many disorders. It affects the scope of the disease, the reliability of diagnostic testing, and has implications for any current and potential therapies.
Common and Rare Autoimmune Diseases
The primary function of the immune system is to repair the body with new cells. Individuals with an autoimmune disease will have many chronic illnesses that are both common and rare when they are being diagnosed. Below is a list of autoimmune diseases that range from common to some of the rarer autoimmune conditions an individual may experience.
Rheumatoid arthritis (RA)
Rheumatoid arthritis is when the immune system is attacking the joints. This attack causes redness, warmth, soreness, and stiffness. It�s one of the most common autoimmune diseases that is found in women but can affect men and elderly people as well. Studies have shown that if a family member has rheumatoid arthritis, it is likely that other family members may have an increased chance of developing this autoimmune disease. The signs and symptoms of rheumatoid arthritis can vary depending on the severity of the inflamed joints, potentially causing them to deform and shift out of place.��
Lupus
Lupus is a systemic autoimmune disease that occurs when an individual�s immune system starts attacking their own tissue and organs. Even though lupus is difficult to diagnose because it often mimics other ailments, it can cause inflammation to different body systems. These body systems include the joints, skin, kidneys, blood cells, brain, heart, and lungs. A distinctive sign of lupus is a facial rash that resembles butterfly wings unfolding across booth cheek.
Ehlers-Danlos Syndrome (EDS)
EDS (Ehlers-Danlos Syndrome) is a rare autoimmune disease that causes soft connective tissues to be fragile in the body. This autoimmune disease is still new for doctors; however, there is always more research to be done about this disease. The symptoms can vary from mild skin and joint hyperlaxity to severe physical disability and life-threatening vascular complications. One of the most common symptoms is joint hypermobility. This disease can cause the joints to be unstable or loose, and it can cause the body�s joints to have frequent dislocations and pain.
Polymyalgia Rheumatica
Polymyalgia rheumatica is an inflammatory musculoskeletal disorder that is most common in elderly adults. This disease causes muscle pain and stiffness around the joints, most commonly occurring in the morning.�It also shares similarities with another disease known as giant cell arteritis. If an individual has polymyalgia rheumatica, they can have the symptoms of giant cell arteritis as well. The symptoms are inflammation in the lining of the arteries. The two factors that can cause the development of polymyalgia rheumatica are genetics and environmental exposure that can increase the chances of having the disorder.
Ankylosing spondylitis
Ankylosing spondylitis is an autoimmune inflammatory disease that can cause some of the vertebrae in the spine to fuse over time. When this happens, the fusing makes the spine less flexible and causes the body to be in a hunched-forward posture. It is most common for men, and there are treatments to lessen the symptoms and possibly slow down the progression of the disease.
Celiac disease
Celiac disease is an autoimmune disease that occurs in about 1% of individuals. This disease makes the individual have an inflammatory reaction to the intestinal permeability barrier from eating gluten found in wheat, rye, and barley. Studies show that patients with celiac disease and autoimmune disease have to be on a gluten-free diet to heal the gut. Symptoms can include bloating, digestive issues, inflammation, and skin rashes.
Conclusion
Mechanisms of an autoimmune disease can be caused by genetics or induced by environmental factors. This can cause an individual to have problems in their body related to inflammation.�There are many autoimmune diseases�that can affect the body from the most common to some of the rarer kinds and it can have lasting effects.
In honor of Governor Abbott’s declaration, October is Chiropractic Health Month. To learn more about the proposal on our website.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References:
Anaya, Juan-Manuel, et al. �The Autoimmune Ecology.� Frontiers in Immunology, Frontiers Media S.A., 26 Apr. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4844615/.
Bonds, Rana S, et al. �A Structural Basis for Food Allergy: the Role of Cross-Reactivity.� Current Opinion in Allergy and Clinical Immunology, U.S. National Library of Medicine, Feb. 2008, www.ncbi.nlm.nih.gov/pubmed/18188023.
Clinic Staff, Mayo. �Ankylosing Spondylitis.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 7 Mar. 2018, www.mayoclinic.org/diseases-conditions/ankylosing-spondylitis/symptoms-causes/syc-20354808.
Clinic Staff, Mayo. �Lupus.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 25 Oct. 2017, www.mayoclinic.org/diseases-conditions/lupus/symptoms-causes/syc-20365789.
Clinic Staff, Mayo. �Polymyalgia Rheumatica.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 23 June 2018, www.mayoclinic.org/diseases-conditions/polymyalgia-rheumatica/symptoms-causes/syc-20376539.
Cusick, Matthew F, et al. �Molecular Mimicry as a Mechanism of Autoimmune Disease.� Clinical Reviews in Allergy & Immunology, U.S. National Library of Medicine, Feb. 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3266166/.
De Paepe, A, and F Malfait. �The Ehlers-Danlos Syndrome, a Disorder with Many Faces.� Clinical Genetics, U.S. National Library of Medicine, July 2012, www.ncbi.nlm.nih.gov/pubmed/22353005.
Schmidt, Zsuzsa, and Gyula Po�r. �Polymyalgia Rheumatica Update, 2015.� Orvosi Hetilap, U.S. National Library of Medicine, 3 Jan. 2016, www.ncbi.nlm.nih.gov/pubmed/26708681.
Scott, David L, et al. �Rheumatoid Arthritis.� Lancet (London, England), U.S. National Library of Medicine, 25 Sept. 2010, www.ncbi.nlm.nih.gov/pubmed/20870100.
Vojdani, Aristo, et al. �Environmental Triggers and Autoimmunity.� Autoimmune Diseases, Hindawi Publishing Corporation, 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4290643/.
SIBO (small intestinal bacterial overgrowth) is defined as 105 up to 106 organisms of bacteria in the small intestines. It is highly relevant to remember that the abundance of bacteria in the small intestine that has SIBO, are healthy bacteria that live in the gastrointestinal tract. It means that the bacteria in the digestive tract is either missed or dislocated and is in the wrong place in the small intestines. While SIBO still remains a poorly understood disease, it is frequently implicated to be the cause of chronic diarrhea and malabsorption. Individuals who have SIBO can also suffer from many chronic illnesses. This includes unintended weight loss, nutritional deficiencies, and osteoporosis.
SIBO and IBS
Studies have indicated that 84% of individuals that has IBS (irritable bowel syndrome) will have SIBO. SIBO is one of the causes of leaky gut, and leaky gut is one of the triad factors that can lead the body to have an autoimmune disease. Health care professionals that diagnose individuals who have SIBO can link the virus to other health problems that the individual may have. Studies have mentioned that when LPS (lipopolysaccharide) is moving from the large intestines to the small intestines, it can contribute to developing intestinal inflammation. With LPS, it can cause an increase of intestinal tight junction permeability or leaky gut.
So SIBO will release LPS into the gut, causing the leaky gut to the gut system in the body. Another study showed that autoimmune diseases are always a triad of a few different things. To have an autoimmune disease, you have to have the gene to get the disease. Although most people know that if they have a gene, doesn�t mean that they will have an autoimmune disease. Even if they don�t have an autoimmune disease, there�s an environmental trigger that will come on and creates an epigenetic change. This will cause the gene in the human body to be expressed.
So the first two factors of the autoimmune disease, are a genetic factor and an environmental factor, the third and final factor is intestinal permeability. So if the primary two factors that are causing disruption to the intestinal permeability, they will prevent the intestinal permeability to actually heal itself. With all three elements being linked to autoimmune disease and SIBO, it will cause the body to have the leaky gut syndrome and health problems to individuals.
So when doctors are diagnosing the patient that has SIBO, they will do a lactulose breath test. What this test does, is that it will indicate that the patient has IBS bloating, and it is causing them discomfort in their gut. Research stated that the lactulose breath test shows the correlation between the pattern of the bowel movements and the type of excreted gas in the stomach. So for anyone that is positive with IBS and takes the breath test, they will understand the consequences of the factors that are leading to the SIBO disease and causing leaky gut.
How do we get SIBO?
With the understanding of what SIBO is, we can see that SIBO is not the only cause of irritable bowel syndrome, but the big player of the syndrome. So taking a step back, we have to discuss what the MMG (Migrating Motor Complex) is before we go further in explaining the pathogenesis of the SIBO disease. Migrating motor complexes are waves of electrical activity that is sweeping through the intestines in a regular cycle. It often happens when a person is fasting, therefore with MMG, we can look at the acute gastroenteritis in the body.
With acute gastroenteritis, the body has some sort of severe infection like bloating, diarrhea, constipation, or a variety of things that are infectious to the gut; however, they are self-limiting. Healthcare professionals who see patients with these acute infections can see that most of the bacteria can cause gastroenteritis, pile up, and release CTD (cytolethal distending toxin). What CTD does is that it will create a reaction against vinculin; which regulates the ICC (interstitial cells of Cajal) and the ICC then regulates the migrating motor complex.
So when the CTD releases toxins in the gut, it causes a reaction to a molecular mimicry reaction. That reaction causes the body to create antibodies to fight against that toxin but through molecular mimicry. CTD looks exactly like vinculin and cross-reacts with the antibodies, So now those antibodies are attacking vinculin, thus damaging the ICC. Since the MMC clears the intestinal tract, when a person is fasting, and the CTD is damaging the intestines, SIBO is created since the body can not flush out the bacteria.
Studies have shown that there are many ways to get SIBO, it can happen by either food poisoning, abdominal surgery, or low stomach acid. Another thing to mention is that mostly 70% of SIBO is caused by food poisoning. Most people who had to suffer from food poisoning don�t realize that SIBO is already in their gut. So the research states that small bowel motility disorders can be the predispose development of SIBO since the bacteria may not be effectively swept from the bowel into to colon.
Treating SIBO
There are many ways to treat SIBO, healthcare professionals can suggest these treatments to their patients who have SIBO and start restoring their intestinal barrier in the long haul. So here are some of the procedures that can help the body and treat SIBO.
Pharmaceuticals: If a patient has constipation and is taking rifaximin if the symptoms are not clearing up, adding another medication with rifaximin for 14 days may help in battling SIBO. It will take a bit longer, but it will help clear the SIBO out of the gut.
Herbal Treatment: With herbal treatments, there are many ways to help treat SIBO naturally. It can be berberine containing herbs, oil of oregano, neem, garlic, Lactobacillus plantarum, Lauricidin, and Antrantil. These herbal treatments can naturally help to fight against SIBO, and studies show that 46% of patients feel a lot better in a short amount of time.
Conclusion
So SIBO is a bacterial disease that can disrupt the gastrointestinal tract and cause the leaky gut to the body. It will cause inflammation and can be in an individual�s body through three factors like genetics, environmental triggers, and food poisoning. It can be treated through pharmaceuticals and herbal treatments prescribed by doctors.� In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month, learn more about this proposal on our website and read what the proposal is all about. The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References:
Bezine, Elisabeth, et al. �The Cytolethal Distending Toxin Effects on Mammalian Cells: a DNA Damage Perspective.� Cells, MDPI, 11 June 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4092857/.
Brown, Kenneth, et al. �Response of Irritable Bowel Syndrome with Constipation Patients Administered a Combined Quebracho/Conker Tree/M. Balsamea Willd Extract.� World Journal of Gastrointestinal Pharmacology and Therapeutics, Baishideng Publishing Group Inc, 6 Aug. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4986399/.
Chedid, Victor, et al. �Herbal Therapy Is Equivalent to Rifaximin for the Treatment of Small Intestinal Bacterial Overgrowth.� Global Advances in Health and Medicine, Global Advances in Health and Medicine, May 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4030608/.
Dukowicz, Andrew C, et al. �Small Intestinal Bacterial Overgrowth: a Comprehensive Review.� Gastroenterology & Hepatology, Millennium Medical Publishing, Feb. 2007, www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/.
Endo, EH, and Dias Filho. �Antibacterial Activity of Berberine against Methicillin-Resistant Staphylococcus Aureus Planktonic and Biofilm Cells.� Austin Journal of Tropical Medicine & Hygiene, 19 Feb. 2015, austinpublishinggroup.com/tropical-medicine/fulltext/ajtmh-v1-id1005.php.
Fasano, Alessio, and Terez Shea-Donohue. �Mechanisms of Disease: the Role of Intestinal Barrier Function in the Pathogenesis of Gastrointestinal Autoimmune Diseases.� Nature News, Nature Publishing Group, 1 Sept. 2005, www.nature.com/articles/ncpgasthep0259.
Ghonmode, Wasudeo Namdeo, et al. �Comparison of the Antibacterial Efficiency of Neem Leaf Extracts, Grape Seed Extracts and 3% Sodium Hypochlorite against E. Feacalis – An in Vitro Study.� Journal of International Oral Health: JIOH, International Society of Preventive and Community Dentistry, Dec. 2013, www.ncbi.nlm.nih.gov/pubmed/24453446.
Guo, Shuhong, et al. �Lipopolysaccharide Regulation of Intestinal Tight Junction Permeability Is Mediated by TLR4 Signal Transduction Pathway Activation of FAK and MyD88.� Journal of Immunology (Baltimore, Md. : 1950), U.S. National Library of Medicine, 15 Nov. 2015, www.ncbi.nlm.nih.gov/pubmed/26466961.
Lin, Henry C. �Small Intestinal Bacterial Overgrowth: a Framework for Understanding Irritable Bowel Syndrome.� JAMA, U.S. National Library of Medicine, 18 Aug. 2004, www.ncbi.nlm.nih.gov/pubmed/15316000.
Preuss, Harry G, et al. �Minimum Inhibitory Concentrations of Herbal Essential Oils and Monolaurin for Gram-Positive and Gram-Negative Bacteria.� Molecular and Cellular Biochemistry, U.S. National Library of Medicine, Apr. 2005, www.ncbi.nlm.nih.gov/pubmed/16010969.
Sienkiewicz, Monika, et al. �The Antibacterial Activity of Oregano Essential Oil (Origanum Heracleoticum L.) against Clinical Strains of Escherichia Coli and Pseudomonas Aeruginosa.� Medycyna Doswiadczalna i Mikrobiologia, U.S. National Library of Medicine, 2012, www.ncbi.nlm.nih.gov/pubmed/23484421.
Soifer, Luis Oscar, et al. �Comparative Clinical Efficacy of a Probiotic vs. an Antibiotic in the Treatment of Patients with Intestinal Bacterial Overgrowth and Chronic Abdominal Functional Distension: a Pilot Study.� Acta Gastroenterologica Latinoamericana, U.S. National Library of Medicine, Dec. 2010, www.ncbi.nlm.nih.gov/pubmed/21381407/.
The Nrf2 cell defense creates a pathway that provides protection against oxidative stress and disorders. It plays a vital role in maintaining cellular homeostasis and keeping each cell strand in check. Without the Nrf2 cell defense, oxidative stress can be excessive and directly cause or contribute to many common diseases. This includes cancer, osteoporosis, inflammatory bowel diseases, and neurodegeneration. Studies show that even oxidative stress can contribute to insulin resistance and multiple sclerosis.
Certain foods that are beneficial to the Nrf2 cell structure, due to their antioxidative properties; can enhance the Nrf2 cell gene gradually. Researchers studied that dietary sources that contain antioxidants flavonoids, fermented food and drinks that contain lactobacilli, and sulforaphane from cruciferous vegetables; are the contributors to aid the Nrf2 cell structure. With these certain foods in a person�s diet, it can be beneficial to combating oxidative stress and preventing oxygen toxicity from producing in the bloodstream.
Legumes: Soybeans and other soy products, chickpeas, mung beans
With these types of antioxidant foods, they can help aid the body by lowering the stress compound naturally without the usage of medications. There are ways to get the nutrients of the different food groups to support the body and activate the Nrf2 pathways. Fermented foods that contain lactobacilli can express and activate the gene pathway.
Let�s start with Lactobacillus plantarum and Lactobacillus brevis. These two are the good bacteria that are found in traditional vegetables, fruit, and fermented malt whiskey. They help the body by breaking down the food that is being consumed, absorbing the nutrients, and fighting off the harmful organisms that are causing discomfort to the gut. When these two bacteria are expressing PAD (phenolic acid derivatives) and being introduced to a caffeic acid; the results are astonishing.
Studies indicate that particular strains of lactobacilli can biotransform the caffeic acid to potently activate the Nrf2 pathways from an inactive precursor. �So let�s say that if an individual is stressed and then they eat some food. Suddenly they feel a bit better after eating, that is because of the Nrf2 pathways mixed with the enhanced lactobacilli in their food helped neutralized the stress compound in the body.
With sulforaphane in cruciferous vegetables, it can help with the Nrf2 pathways. Since cruciferous plants have natural fighting properties against cancer, they have a good source of phytonutrients and the sulforaphane combined.
Here are some of the cruciferous vegetables that can help the Nrf2 pathway in the body.
Arugula
Bok choy
Broccoli
Brussels sprouts
Cabbage
Cauliflower
Kale
Radish
Turnips
These vegetables are nutritious when they are eaten raw or cooked. Sulforaphane in the many cruciferous plants has been linked to many health benefits such as improving heart health and digestion. This compound has an inactive form of glucoraphanin, but when it comes in contact with myrosinase, it releases the glucosinolates. This means that when the cruciferous vegetables are either damaged, cut, chopped or chewed on, the myrosinase enzymes are activated and turning into sulforaphane.
Studies have even been shown that sulforaphane can prevent cancer cell growth by releasing antioxidants and detoxifying enzymes that protect carcinogens, which are substances that can cause cancer.
How the Nrf2 Cell Activates
The various molecules in them can exhibit a robust activation in the Nrf2 defense system. Researchers have studied that the Nrf2 defense pathway can provide natural protection against oxidative stress and chemical toxicity through relatively small electrochemical co-factors called Nrf2 activators.
These activators actually amplify the effect of ROS (reactive oxygen species) by cycling through oxidation-reduction reactions and liberating Nrf2 in the human endothelial cells. Since the human body can get sick from stress, it is essential to eat foods that can fight off the harmful organisms. Nrf2 cells do regulate the oxidative stress by releasing itself into the body�s system. It is crucial to make sure that good, nutritious food that is beneficial in helping the Nrf2 cells by doing it naturally.
With a person�s hectic lifestyle gets in the way, they start to feel overly stressed. The body begins to develop chronic ailments that can harm not only the outside of the body but the inside as well. When individuals go to see health care professional for any chronic diseases that they may have, they will be informed of remedies to help aid them the best way they can. Individuals can find ways to deal with the stress hormone and calm it down through functional medicine. So when the body develops oxidative stress, it will affect the organ system, the nerve system, and the neurological system.
With the Nrf2 cells, the cell structure goes towards the oxidative stress compound and put a stop to it. And with the nutritious food that is available to aid the Nrf2 cell more. When we can calm down our anxious mind through the use of functional medicine and by eating healthy, organic, whole foods; we are actually repairing the body from the inside out.
Conclusion
As stated from the beginning, the Nrf2 cell helps the body by protecting it against oxidative stress. When we add nutritious food into the collection, it is aiding the Nrf2 cells a whole lot. Since the entire body needs the nutrients from the different food groups to assist not only the Nrf2 cells but to all crucial organs that need the nutrient sources to function correctly. The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References
Bryan, Holly K, et al. �The Nrf2 Cell Defence Pathway: Keap1-Dependent and -Independent Mechanisms of Regulation.� Biochemical Pharmacology, U.S. National Library of Medicine, 15 Mar. 2013, www.ncbi.nlm.nih.gov/pubmed/23219527.
Coyle, Daisy. �Sulforaphane: Benefits, Side Effects, and Food Sources.� Healthline, 26 Feb. 2019, www.healthline.com/nutrition/sulforaphane.
Prochaska, H J, et al. �On the Mechanisms of Induction of cancer-protective Enzymes: a Unifying Proposal.� Proceedings of the National Academy of Sciences of the United States of America, U.S. National Library of Medicine, Dec. 1985, www.ncbi.nlm.nih.gov/pubmed/3934671.
Senger, Donald R., et al. �Activation of the Nrf2 Cell Defense Pathway by Ancient Foods: Disease Prevention by Important Molecules and Microbes Lost from the Modern Western Diet.� PLOS ONE, Public Library of Science, 17 Feb. 2016, journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0148042.
Su, Xuling, et al. �Anticancer Activity of Sulforaphane: The Epigenetic Mechanisms and the Nrf2 Signaling Pathway.� Oxidative Medicine and Cellular Longevity, Hindawi, 6 June 2018, www.ncbi.nlm.nih.gov/pubmed/29977456.
As far too many Americans and Texans know, chronic pain remains a huge public health problem and one of the most prevalent reasons why people seek medical care. Chronic pain negatively impacts many aspects of a person�s life as well as the lives of their families, friends, and caregivers. It is essential that patients understand all treatment options for various types of pain.
Chiropractors are highly skilled professionals who are dedicated to providing safe and effective physician-level health care to patients suffering from back pain. Chiropractic care focuses on disorders of the musculoskeletal system and the nervous system as well as promotes a hands-on, non-drug approach to pain management and healthy lifestyles. Their expertise in the prevention, care, and rehabilitation of back, neck, joint, and head pain is critical for treating patients with various pains and disorders and can save the public from the physical and financial tolls of other treatment options. As a first line of defense against pain, chiropractors� services can help individuals heal naturally without the need for drugs or surgery.
At this time, I encourage all Texans to learn more about the vital role that chiropractors play in the health care field and how chiropractic services can benefit their lives. I commend Texas chiropractors for their commitment and efforts to improve the quality of life for all Texans by promoting effective pain management and healthy lifestyles.
Therefore, I, Greg Abbott, Governor of Texas, do hereby proclaim October 2019, to be
Chiropractic Health Month
in Texas, and urge the appropriate recognition whereof.
In official recognition whereof, I hereby affix my signature this the 18th day of September 2019.
� Governor of Texas
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NCBI Resources
Do you have back, shoulder, neck, leg pain, headaches, or stress? Pain medications work for only so long and don�t fix the problem. A chiropractor can help your symptoms. A chiropractic adjustment means that a chiropractor physically/manually adjusts the vertebrae in the spine. This procedure creates positive effects without the stress or invasiveness of surgery. A chiropractic adjustment�can be a great way to improve multiple areas of the body, along with improving overall health with non-invasive treatment.
Previous research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity on neurons. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain (0.96-1.62 ?mol/gram wet weight), their extracellular concentrations in the cortex as measured by microdialysis (1.62 ?M for L-aspartate and 9.06 ?M for L-glutamate) and their supply according to immunohistochemistry suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. EAATs which play a fundamental role in the uptake of all vesicular released L-glutamate in the central nervous system (CNS) also requires the utilization of L-aspartate. L-aspartate is perhaps as less essential as L-glutamate connected to the total excitatory activity associated with iGluRs. Along with its role as a neurotransmitter, as previously mentioned, L-aspartate is also necessary as a substrate for aspartate amino-transferase which turns into 2-oxoglutarate and L-glutamate to transport to the cortical vesicles of glutamatergic neurons which may also consequently and indirectly increase L-glutamate release. �
Other Molecules in Glutamate Signaling
One characteristic which distinguishes NMDA receptors from different iGluRs is that the activation of NMDA receptors needs the connection of a co-agonist to the glycine binding region of the receptor. By way of instance, in the retina and in the spinal cord, the origin of glycine may spillover out of glycinergic inhibitory synapses. But, in different regions of the brain with increased NMDA receptor expression, such as the hippocampal formation, reactions associated with strychnine-sensitive glycine receptors are missing, at least in adult neurons, demonstrating the absence of glycinergic inhibitory neurotransmissions. But, glycine is found in the extracellular fluid of the hippocampus at baseline amounts of roughly 1.5 ?M, which is similar to the saturation of the glycine binding region of the NMDA receptor, although these may be up- and down-regulated. The origin of extracellular glycine in the hippocampus can be neurons which release glycine through the alanine-serine-cysteine amino acid transporter 1 (asc-1). But, glycine release by astrocytes that is stimulated by depolarization and kainate, has also been demonstrated. Further research studies are required to ultimately show these outcome measures. �
Even in previous research studies of the NMDA receptor and its co-activation by glycine revealed that D-amino acids, particularly D-serine, are nearly as powerful as glycine. Only several years after, it became obvious that D-serine is found in rat and human brains at roughly one-third of their concentration of L-serine having an absolute concentration of more than 0.2 ?mol/g brain tissue. Utilizing an antiserum for D-serine, research studies demonstrated that D-serine from the brain is only found in astrocytes and its supply fits the expression of NMDA receptors. In addition, the same researchers demonstrated that D-serine is released from cultured astrocytes when exposed to L-glutamate or kainate. The abundance of D-serine is found by the degrading enzyme D-amino acid oxidase (DAO) which reveals increased expression in the hindbrain where D-serine levels are reduced as well as the synthetic enzyme serine racemase which creates D-serine from L-serine. D-Serine appears to be stored in cytoplasmic vesicles in astrocytes and it can be released by exocytosis. Long-term potentiation is dependent upon D-serine release from astrocytes in hippocampal slices, suggesting that this amino acid definitely plays a fundamental role in glutamatergic neurotransmission through NMDA receptors. Additionally in hippocampal slices, research studies found, utilizing D-serine and glycine degrading enzymes, which D-serine functions as a co-transmitter for synaptic NMDA receptors on CA1 neurons likewise which glycine functions as the endogenous co-agonist for extrasynaptic NMDA receptors. Synaptic NMDA receptors of dentate gyrus neurons utilize glycine rather than D-serine as the co-agonist. �
Taken collectively, multilayered outcome measures show that L-aspartate doesn’t simply function as an agonist on NMDA receptors but also glycine and D-serine play fundamental roles in glutamatergic neurotransmission in the human brain. But, other molecules also have been demonstrated to be relevant modulators of glutamatergic neurotransmission. �
Glutamate Activated by Other Molecules
L-homocysteate (L-HCA) has structural similarities with L-glutamate. The non-protein amino acid is an oxidation product of homocysteine that is biosynthesized from methionine in the elimination of its own terminal methyl group and it is also an intermediate of the transsulfuration pathway by which methionine may be converted to cysteine through cystathionine. Early research studies demonstrated that this amino acid can cause calcium influx in cultured neurons as safely and effectively as L-glutamate. Moreover, L-HCA revealed an increased affinity for NMDA receptors when compared to other iGluRs in binding assays associated with its capacity to cause NMDA receptor antagonist-inhibitable excitotoxicity and sodium influx. Additionally, L-HCA can trigger mGluR5 as efficiently as L-glutamate. L-HCA is found in the brain, however, the concentrations were demonstrated to be approximately 500-fold lesser than those of L-glutamate and even 100-fold lesser when compared to those of L-aspartate in different regions of the rat brain. Throughout potassium-induced stimulation, L-HCA discharge is triggered from brain slice preparations as demonstrated for L-aspartate and L-glutamate although the absolute release of HCA is approximately 50-fold lesser. Surprisingly, HCA is a very efficient competitive inhibitor of cystine and L-glutamate uptake through the cystine/glutamate antiporter system x?c, the activity that regulates and manages the extracellular extrasynaptic L-glutamate concentrations in the brain. Therefore, the impact of L-HCA on the activation of NMDA and other L-glutamate receptors may also rely on the L-HCA-induced trigger of L-glutamate through system x?c. L-HCA may play an important role in the overall stimulation of L-glutamate receptors. Nevertheless, this can change tremendously under certain conditions, e.g., in patients with high-dose methotrexate therapy, an anticancer drug which, by restricting dihydrofolate reductase, limits the tetrahydrofolate-catalyzed recycling of methionine from homocysteine. Here, L-HCA concentrations of more than 100 ?M have been demonstrated from the cerebrospinal fluid whereas L-HCA was undetectable in control subjects. Further research studies are still required to determine these outcome measures. �
Further endogenous small molecules which are believed to affect L-glutamate signaling include several intermediates of tryptophan metabolism, as shown in Figure 2. Through the activity of indoleamine 2,3-dioxygenase (IDO) or tryptophan 2,3-dioxygenase (TDO), tryptophan is turned into N-formyl-L-kynurenine which is later turned into kynurenine (KYN) by formamidase. Three pathways, two of which connect at a subsequent step, result in further metabolism. First, through the activity of kynurenine aminotransferase (KAT), KYN is converted into kynurenic acid (KYNA). KYN can also be converted to 3-hydroxykynurenine (3HK) by kynurenine monooxygenase (KMO), which can subsequently be utilized as a substrate by kynureninase for the synthesis of 3-hydroxyanthranilic acid (3HANA). Additionally, utilizing KYN as a substrate, kynureninase develops anthranilic acid (ANA), which by non-specific hydroxylation may also be converted to 3HANA. According to research studies, 3HANA finally functions as a substrate for the generation of quinolinic acid (QUIN). �
The tryptophan concentration in the rat brain is roughly 25 nmol/g wet weight and approximately 400-fold less than L-glutamate and 100-fold less than L-aspartate. The demonstrated brain levels of kynurenines are even lower with 0.4-1.6 nmol/g for QUIN, 0.01-0.07 nmol/ml for KYNA, and 0.016 nmol/g for 3HANA. Approximately 40 percent of brain KYN is locally synthesized. The metabolites of tryptophan demonstrate differential binding to plasma proteins and their transport through the barrier which is quite different. KYN and 3HK are carried through the large neutral amino acid carrier system L. Kynurenines seem to penetrate the human brain by passive diffusion. Additionally, KYNA, 3HANA, and especially ANA bind to serum proteins which then ultimately restrict and limit their diffusibility across the blood-brain barrier. �
Research studies demonstrated that QUIN, when ionophoretically utilized in rat cells, caused neuronal firing which has been prevented by an NMDA receptor antagonist, suggesting that QUIN may function as an NMDA receptor agonist. However, the EC50 for QUIN to trigger NMDA receptor currents has been shown to be roughly 1000-fold higher than the EC50 of L-glutamate. Intracerebral injection of QUIN was proven to cause ultrastructural, neurochemical, and behavioral changes similar to those caused by NMDA receptor agonists. The fact that QUIN concentrations are about 5000- to 15,000-fold lower than cerebral L-glutamate concentrations makes it unlikely that modulation of NMDA receptor signaling by QUIN plays an essential role. KYNA was demonstrated to function as an NMDA receptor antagonist. But, although infusion with the KMO inhibitor Ro 61-8048 improved cerebral extracellular KYNA concentrations 10-fold, this didn’t result in an inhibition of NMDA-mediated neuronal depolarization, a finding which challenges the belief that KYNA at near-physiological amounts directly modulates NMDA receptors. In comparison, increased KYNA in the brain induced from the KMO inhibitor JM6 decreased the extracellular cerebral L-glutamate concentration. Additionally, KYNA levels from the extracellular cerebral fluid have been associated with L-glutamate levels suggesting that even at physiological or near physiological levels, KYNA modulates L-glutamate metabolism. Both the activation of the G-protein-coupled receptor GPR35 and the inhibition of presynaptic ?7 nicotinic acetylcholine receptors are suggested in the KYNA-induced reduction in L-glutamate release. To summarize, although QUIN and L-HCA are present in the human brain, their concentrations discuss against them with roles in regulating and maintaining neurotransmission. In contrast, even though the pathways have to be defined in greater detail, evidence supports levels and the opinion that discharge can be modulated by KYNA and neurotransmission. �
Glutamate, together with aspartate and other molecules, are several of the main excitatory neurotransmitters in the human brain. Although these play a fundamental role in the overall structure and function of the central nervous system, including the brain and the spinal cord, excessive amounts of other molecules can ultimately trigger glutamate receptors. Excess glutamate can cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurological diseases. The following article describes how other molecules can activate glutamate receptors. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
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