Often referred to as C1-C7, with the “C” indicating cervical, and the numbers 1-7 indicate the level.
C1 is closest to the skull
C7 is closest to the thoracic chest/rib cage area
The cervical spine is particularly susceptible to degenerative problems because:
Highly mobile with a broad range of motion
Supports the skull
Neck anatomy is complex
Many degenerative problems, including osteophytes or bone spurs, can develop.
Neck Pain Symptoms
Several symptoms can occur and indicate the presence of a degenerative condition:
Neck pain
Pain around the back of the shoulder area
Arm pain, numbness, or weakness
Difficulty with hand dexterity or walking
Conditions That Affect the Neck
The degenerative process begins in any of the joints in the spine, but over time it can cause changes in the other joints.
An example is an intervertebral disc�where:
The disc narrows and the normal movement becomes altered, and the adjacent joints are subjected to force and pressure, which can lead to degenerative arthritis joint inflammation.
Spondylosis or spinal osteoarthritis causing pain in the neck is common. The pain can radiate, or spread, into the shoulder/s or down the arm/s. Arm pain or weakness caused by a bone spur compressing a spinal nerve root can also occur.
Diagnosing Cervical Spine Conditions
Once examined one or more symptoms are likely to be present.
The doctor will ask the patient questions to learn the history of the patient.
A thorough evaluation of the patient will be conducted, including tests to identify the cause of pain and symptoms.
A neurologic examination is performed to rule out neurological disorders
Shoulder examination will also be done to ensure that the symptoms originate from the neck
Diagnostic tests
X-rays for:
Narrow intervertebral disc space
Anterior osteophytes or bone spurs
Spondylosis (ie, arthritis) of the facet joints
Osteophytes created from the uncovertebral joints
CT Scans or computed tomography can show bone changes associated with degenerative spondylosis. Osteophytes can be observed and evaluated.
CT does not provide an optimal evaluation but can sometimes show disc herniations.
MRI magnetic resonance imaging is a powerful tool for cervical spondylosis.
MRI can help doctors identify:
Disc herniation
Osteophytes
Joint arthrosis a type of osteoarthritis
MRI is best for soft disc herniation/s.
Myelogram/CT can be utilized in complex cases that involve multi-level spinal diseases.
It is very useful in delineating bone spurs from safe disc herniations.
Discography is used diagnostically when viewing the lumbar/low back and thoracic/mid-back spine, but using it in cervical spine imagery is debated among doctors.
Treatment Options
After the tests have been performed, a custom treatment plan is created.
Nonsurgical Neck Pain Treatment
Nonsurgical treatment of cervical degenerative disease has been proven to provide excellent results in over 85% of patients.
A multi-disciplinary approach:
Immobilization of the neck�to reduce motion can be beneficial during acute episodes of pain.
Physical therapy (PT) and Chiropracticcan be useful to decrease muscle spasms and return motion.
Non-surgical treatment provides positive long-term pain and symptom relief.
Surgery
A surgeon is likely to consider surgery for a disorder if one or more of the following criteria are met:
Nonsurgical care has been tried and has not worked
Spinal cord dysfunction
Arm pain or weakness (neurological symptoms) that do not go away
Depending on the diagnosis, surgical procedures can vary:
One type of surgery is the removal of the bone spur(s)
Cervical spinal fusion that joins two or more vertebrae
But the surgical procedure is based on the way you the patient wants to go, the diagnosis, general health, and what the spine surgeon recommends.
The surgeon will explain the recommended procedure to you clearly.
Most of the time the preferred approach is anterior or from the front interbody fusion.
A cervical plate could be placed over the interbody device or graft to stabilize the neck. This can avoid the need for a brace after.
A posterior approach from the back of the spine is considered when a disc has herniated laterally or to the side.
Things You Can Do
Cervical spine disorders can be diagnosed�and treated more accurately with today’s advancing technology.
With the guidance and treatment of an expert medical team, patients can expect to see a definite improvement in their condition and symptoms.
El Paso, TX Neck Pain Chiropractic Treatment
Sandra Rubio discusses the symptoms, causes, and treatments of neck pain. Headaches, migraines, dizziness, confusion, and weakness in the upper extremities are a few of the typical symptoms. Trauma from an accident, such as that from an automobile accident or a sports injury, or an aggravated illness because of improper posture can commonly cause neck pain and other ailments. Dr. Alex Jimenez uses spinal alterations and manual manipulations, one of other chiropractic treatment techniques like deep-tissue massage, to reestablish the alignment of the cervical spine and improve neck pain. Chiropractic care with Dr. Alex Jimenez is your non-surgical choice for restoring general patient well-being.
Neck pain is a frequent health issue, with roughly two-thirds of the people being influenced by neck pain at any time throughout their lifetimes. Numerous other health issues can cause pain arising in the upper back, or the spine. Neck pain can result emanating from the vertebrae, or because of muscular tightness in both the neck and the upper back. Joint disruption in the neck causes migraines, and headache, as does joint disturbance at the trunk, or can generate a variety of other symptoms. Neck pain affects about 5 percent of the worldwide population as of 2010, based on figures.
NCBI Resources
A chiropractor evaluates the spine as a whole because other regions of the�neck (cervical), mid-back (thoracic) and low back (lumbar)�can be affected as well. Along with treating the spine as a whole, chiropractic medicine treats the entire person and not just a specific symptom/s. Chiropractors may�educate on nutrition, stress management, and lifestyle goals in addition to treating neck pain.
When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. �
Contents
Huntington’s Disease
Huntington’s disease (HD) is as an inherited, fatal neurodegenerative disease which is caused by a trinucleotide (CAG) repeat expansion in the coding region of the huntingtin (htt) gene which is associated with the degeneration of the GABAergic medium-sized spiny neurons (MSN) in the striatum, although other brain regions can also ultimately be affected as the health issue progresses. HD is identified as a movement disorder with co-morbid cognitive and psychiatric symptomatology. Both mutant htt RNA together with the encoded protein which includes a polyglutamine repeat expansion is believed to cause the complicated changes in cellular metabolism which occurs in mitochondrial dysfunction and oxidative stress. �
Early research study findings which demonstrated that excitotoxicity may play a fundamental role in HD were based upon the observation that an injection of their KYN metabolite and NMDA receptor agonist QUIN, in addition to L-glutamate and kainate, in the striatum of rats caused neuronal degeneration. Another research study determined that QUIN, as compared to NMDA and kainate, causes selective degeneration of the MSNs instead of neuronal death, which tremendously resembles the pathology of HD. Moreover, NMDA receptors have been shown to be hyperactive and striatal neurons from different HD mouse models, such as a yeast artificial chromosome (YAC) which leads to over-expression of full-length htt with elongated polyglutamine repeats as well as R6/2 mice over-expressing htt exon 1 with elongated polyglutamine repeats in addition to in knock-in mice with greater CAG repeats inserted from the mouse htt gene, were demonstrated to be sensitized to excitotoxicity in vitro. Furthermore, in vivo, a sensitization to an excitotoxin injection into the striatum was only demonstrated in the transgenic YAC model of HD, whereas mice overexpressing mutant htt exon 1, R6/1 and R6/2 mice, or N171-82Q mice overexpressing mutant exon 1 and components of exon 2 or the so-called “shortstop” mouse expressing human N-terminal htt encoded by exon 1 and 2 with a 128 CAG repeat below the htt promoter, produced somewhat of a resistance to striatal excitotoxin injection during the aging process. This neuroprotection isn’t necessarily for NMDA receptor agonists, however, it can help different neurotoxic insults and may be an adaptive response to cellular stress. �
Rat MSN release increased levels of NR2A- and NR2B-containing NMDA receptors compared to interneurons in the striatum. NR1 and NR2B mRNA expression in the neostriatum of HD patients has been demonstrated to considerably decrease which is associated with the loss of these neurons. In addition, NMDA receptor-mediated pathways in MSN were determined to be tremendously sensitive to the NR2B-specific inhibitor ifenprodil. In HEK293 cells, overexpression of mutant htt increased NMDA receptor-mediated pathways and aggravated NMDA-induced cell release only when NR2B- but not when NR2A-containing NMDA receptors were co-expressed. One possible explanation for the increase in NR2B-containing NMDA receptor expression from HD models is that an extended polyglutamine repeat in htt decreases its connection to PSD95, a postsynaptic density protein included in NMDA and kainate receptor clustering, ultimately causing a greater response of PSD95 together with the NR2B subunit. Recently, research study findings suggest that not only does the subunit composition but also the localization of NMDA receptors may play a fundamental role in the NMDA receptor activity. Another research study showed that in severe striatal slice preparations from YAC transgenic mice utilizing 128 CAG repeats, extrasynaptic NMDA receptors, especially those with NR2B, are considerably increased compared to pieces from wild-type mice and YAC mice expressing htt with 18 CAG repeats. As expected from in vitro research studies, this change was associated with decreased CREB phosphorylation. The increased percentage of NR2B-containing extrasynaptic NMDA receptors was demonstrated to be associated with increased extrasynaptic localization of PSD95. One pathway which may cause the sensitization to excitotoxic stimulation downstream of the activation of extrasynaptic NMDA receptors was identified as activation of p38 MAPK. Taken multilayered evidence suggests that mutant htt results in sensitization of MSN into glutamate excitotoxicity through the redistribution of NMDA receptors from subunits to extrasynaptic sites. �
The activation of extrasynaptic NMDA receptors in acute striatal brain slices can be effectively shown in YAC mice utilizing 128 CAG repeats through spillover of synaptic glutamate by restricting EAATs. As a result, it may be determined that decreased EAAT expression may increase the activation of NMDA receptors. Surprisingly, within situ-hybridization, research studies discovered a decrease in astrocytic EAAT2 mRNA expression in the neostriatum of all HD patients. As compared to wild-type mice, however, no changes in protein expression were found to be decreased in synaptosomes of YAC mice overexpressing human htt utilizing 128 CAG repeats. The researchers determined that a decrease in EAAT2 activity from the YAC model of HD was caused by decreased palmitoylation of the transporter. In R6/2 mice, others discovered decreased EAAT2 mRNA and protein expression associated with decreased EAAT2 in synaptosomes or acute cortico-striatal pieces. However, extracellular striatal glutamate concentrations have been shown to be similar to those of wild-type control mice and a decreased glutamate clearance capability in the R6/2 mice demonstrated by therapy with EAAT inhibitors or glutamate. A putative explanation for this finding could be a decrease in glutamate release through system x?c and in xCT, the subunit of system x?c which has been demonstrated at the striatum of R6/2 mice in the mRNA and protein levels. �
As previously mentioned, the injection of the KYN metabolite QUIN in supraphysiological concentrations was utilized as an early animal model of HD. This caused further research studies of KYN metabolism in HD. Surprisingly, the QUIN precursor 3HK aggravates neurodegeneration from the QUIN HD version while KYNA is protective. Research studies discovered that in early-stage HD, compared to control and end-stage HD, neostriatal 3HK and QUIN concentrations were considerably upregulated. Another research study discovered that KYNA levels decreased in autopsied HD striata with the CSF of HD patients when compared with controls. The first enzyme of this KYN pathway, IDO, is triggered from the striatum of both YAC mice with 128 CAG repeats. Mice deficient in IDO are less sensitive to intrastriatal QUIN injection. Evaluation of KYN metabolites from three different mouse models of HD, R6/2 mice, YAC128 mice as well as HdhQ92 and HdhQ111 knock-in mice in various brain regions, suggested age-dependent activation of their KYN pathway. However, the detailed pattern of metabolite changes was different among the versions with increased 3HK in cortex, striatum, and cerebellum in R6/2 mice whereas mice expressing full-size mutant htt demonstrated an extra cortical and striatal upregulation of QUIN. Moreover, treatment of R6/2 mice with a non-blood brain barrier permeable KMO inhibitor, JM6, which indirectly improved cerebral extracellular KYNA concentrations by 50 percent, has been associated with a decrease in extracellular cerebral L-glutamate, decreased neurodegeneration and prolonged survival. Further research studies are still required for further evidence. �
Taken collectively, the research studies support the view that in HD there is a redistribution of both NMDA receptors, especially those containing NR2B, which can activate signaling pathways which boost neurodegeneration, as shown in Figure 5. There is not any evidence that cerebral L-glutamate levels are grossly increased in HD. This might be explained by the fact that even though EAAT2 and KYNA may be downregulated, there is also a downregulation of system x?c action. As only very high levels of QUIN activated NMDA receptors, this KYN metabolite is unlikely to contribute to the excitotoxic load. �
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
[wp-embedder-pack width=”100%” height=”1050px” download=”all” download-text=”” attachment_id=”72423″ /] � 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. �
In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal. �
In the article above, we outlined what is known about the pathways which may cause excitotoxicity in neurodegenerative diseases. We also discussed that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. 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. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
The thyroid is a small, butterfly-shaped gland that is located in the anterior neck producing T3 (triiodothyronine) and T4 (tetraiodothyronine) hormones. These hormones affect every single tissue and regulate the body�s metabolism while being part of an intricate network called the endocrine system. The endocrine system is responsible for coordinating many of the body’s activities. In the human body, the two major endocrine glands are the thyroid glands and the adrenal glands. The thyroid is controlled primarily by TSH (thyroid-stimulating hormone), which is secreted from the anterior pituitary gland in the brain. The anterior pituitary gland can stimulate or halt the secretion to the thyroid, which is a response only gland in the body.
Since the thyroid glands make T3 and T4, iodine can also help with the thyroid hormone production. The thyroid glands are the only ones that can absorb the iodine to help hormone growth. Without it, there can be complications like hyperthyroidism, hypothyroidism, and Hashimoto�s disease.
Contents
Thyroid Influences on The Body Systems
The thyroid can help metabolize the body, such as regulating heart rate, body temperature, blood pressure, and brain function. Many of the body�s cells have thyroid receptors that the thyroid hormones respond to. Here are the body systems that the thyroid helps out.
Cardiovascular System and the Thyroid
Under normal circumstances, the thyroid hormones help increase the blood flow, cardiac output, and heart rate in the cardiovascular system. The thyroid can influence the heart�s �excitement,� causing it to have an increasing demand for oxygen, therefore increasing the metabolites. When an individual is exercising; their energy, their metabolism, as well as their overall health, feels good.
The thyroid actually strengthens the heart muscle, while decreasing the external pressure because it relaxes the vascular smooth muscle. This results in a decrease of arterial resistance and diastolic blood pressure in the cardiovascular system.
When there is an excess amount of thyroid hormone, it can increase the heart�s pulse pressure. Not only that, the heart rate is highly sensitive to an increase or decrease in the thyroid hormones. There are a few related cardiovascular conditions listed below that can be the result of an increased or decreased thyroid hormone.
Metabolic Syndrome
Hypertension
Hypotension
Anemia
Arteriosclerosis
Interestingly, iron deficiency can slow the thyroid hormones as well as increase the production of the hormones causing problems in the cardiovascular system.
The Gastrointestinal System and the Thyroid
The thyroid helps the GI system by stimulating carbohydrate metabolism and fat metabolism. This means that there will be an increase in glucose, glycolysis, and gluconeogenesis as well as an increased absorption from the GI tract along with an increase in insulin secretion. This is done with an increased enzyme production from the thyroid hormone, acting on the nucleus of our cells.
The thyroid can increase the basal metabolic rate by helping it increase the speed of breaking down, absorbing, and the assimilation of the nutrients we eat and eliminate waste. The thyroid hormone can also increase the need for vitamins for the body. If the thyroid is going to regulate our cell metabolism, there has to be an increased need for vitamin cofactors because the body needs the vitamins to make it function properly.
Some conditions can be impacted by thyroid function, and coincidentally can cause thyroid dysfunction.
Abnormal cholesterol metabolism
Overweight/underweight
Vitamin deficiency
Constipation/diarrhea
Sex Hormones and the Thyroid
The thyroid hormones have a direct impact on ovaries and an indirect impact on SHBG (sex hormone-binding globulin), prolactin, and gonadotropin-releasing hormone secretion. Women are dramatically more affected by thyroid conditions than men due to hormones and pregnancy. There is also another contributing factor that women share, their iodine vitals and their thyroid hormones through the ovaries and the breast tissue in their bodies. The thyroid can even have either a cause or contribution to pregnancy conditions like:
Precocious puberty
Menstrual issues
Fertility issues
Abnormal hormone levels
HPA Axis and the Thyroid
The HPA axis�(Hypothalamic-Pituitary-Adrenal Axis) modulates the stress response in the body. When that happens, the hypothalamus releases the corticotropin-releasing hormone, it triggers the ACH (acetylcholine hormone) and the ACTH (adrenocorticotropic hormone) to act on the adrenal gland to release cortisol. Cortisol is a stress hormone that can lower inflammation and increase carbohydrate metabolism in the body. It can also trigger a cascade of �alarm chemicals� like epinephrine and norepinephrine (fight or flight response). If there is an absence of lowered cortisol, then the body will desensitize for the cortisol and the stress response, which is a good thing.
When there is a higher level of cortisol in the body, it will decrease the thyroid function by lowering the conversion of the T4 hormone to T3 hormone by impairing the deiodinase enzymes. �When this happens, the body will have a less functional thyroid hormone concentration, since the body can�t tell the difference of a hectic day at work or running away from something scary, it can either be very good or horrible.
Thyroid Problems in the Body
The thyroid can produce either too much or not enough hormones in the body, causing health problems. Down below are the most commonly known thyroid problems that will affect the thyroid in the body.
Hyperthyroidism: This is when the thyroid is overactive, producing an excessive amount of hormones. It affects about 1% of women, but it�s less common for men to have it. It can lead to symptoms such as restlessness, bulging eyes, muscle weakness, thin skin, and anxiety.
Hypothyroidism: This is the opposite of hyperthyroidism since it can�t produce enough hormones in the body. It is often caused by Hashimoto�s disease and can lead to dry skin, fatigue, memory problems, weight gain, and a slow heart rate.
Hashimoto�s disease: This disease is also known as chronic lymphocytic thyroiditis. It affects about 14 million Americans and can occur in middle-aged women. This disease develops when the body�s immune system mistakenly attacks and slowly destroys the thyroid gland and its ability to produce hormones. Some of the symptoms that Hashimoto�s disease causes are a pale, puffy face, fatigue, enlarged thyroid, dry skin, and depression.
Conclusion
The thyroid is a butterfly-shaped gland located in the anterior neck that produces hormones that help function the entire body. When it doesn�t work correctly, it can either create an excessive amount or decrease the number of hormones. This causes the human body to develop diseases that can be long term.
In honor of Governor Abbott’s proclamation, 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:
America, Vibrant. �Thyroid and Autoimmunity.� YouTube, YouTube, 29 June 2018, www.youtube.com/watch?feature=youtu.be&v=9CEqJ2P5H2M.
Clinic Staff, Mayo. �Hyperthyroidism (Overactive Thyroid).� Mayo Clinic, Mayo Foundation for Medical Education and Research, 3 Nov. 2018, www.mayoclinic.org/diseases-conditions/hyperthyroidism/symptoms-causes/syc-20373659.
Clinic Staff, Mayo. �Hypothyroidism (Underactive Thyroid).� Mayo Clinic, Mayo Foundation for Medical Education and Research, 4 Dec. 2018, www.mayoclinic.org/diseases-conditions/hypothyroidism/symptoms-causes/syc-20350284.
Danzi, S, and I Klein. �Thyroid Hormone and the Cardiovascular System.� Minerva Endocrinologica, U.S. National Library of Medicine, Sept. 2004, www.ncbi.nlm.nih.gov/pubmed/15282446.
Ebert, Ellen C. �The Thyroid and the Gut.� Journal of Clinical Gastroenterology, U.S. National Library of Medicine, July 2010, www.ncbi.nlm.nih.gov/pubmed/20351569.
Selby, C. �Sex Hormone Binding Globulin: Origin, Function and Clinical Significance.� Annals of Clinical Biochemistry, U.S. National Library of Medicine, Nov. 1990, www.ncbi.nlm.nih.gov/pubmed/2080856.
Stephens, Mary Ann C, and Gary Wand. �Stress and the HPA Axis: Role of Glucocorticoids in Alcohol Dependence.� Alcohol Research: Current Reviews, National Institute on Alcohol Abuse and Alcoholism, 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3860380/.
Wallace, Ryan, and Tricia Kinman. �6 Common Thyroid Disorders & Problems.� Healthline, 27 July, 2017, www.healthline.com/health/common-thyroid-disorders.
Wint, Carmella, and Elizabeth Boskey. �Hashimoto’s Disease.� Healthline, 20 Sept. 2018, www.healthline.com/health/chronic-thyroiditis-hashimotos-disease.
Hormone deficiencies and imbalances are more common than one might originally think. Research suggests that “nearly half of the women in the United States have experienced a hormone imbalance” (Grinta, 1) . However, hormone imbalance does not just affect women, “as nearly 35% of males in their seventh decade have lower testosterone levels than younger men”. (McBride, 2)��An imbalance in hormones can cause an array of symptoms and ultimately affect an individuals day to day life.�
Contents
Symptoms�
The symptoms of hormone deficiency might not be as obvious as one could imagine. Some symptoms are small and could be brushed off as stress or lack of sleep, but it is important to look at the symptoms for what they really are. “In women, low estrogen can contribute to:
mood swings
hot flashes
headaches
depression
trouble concentrating
fatigue
irregular or absent periods
increased UTI’s “
(Swns, 3)�
In men, some of the symptoms are similar to those in women, but also include:
decreased bone mass
sleep disturbances
decreased motivations
increased body fat
decreased muscle mass
hair loss
libido
(Wallace, 4)
Solutions�
If these symptoms are affecting an individual’s lifestyle, there are multiple steps that can be taken to diagnose the problem and ultimately reduce symptoms. In today’s medical world, practitioners are able to use integrative techniques towards functional medicine, focusing on the biochemical level. If a patient is seeking solutions, the first step taken is an extensive questionnaire. This allows the doctor to pinpoint the exact symptoms, issues, and gives an insider look as to what direction to head towards first.
An example of the questions asked are as follows:
Once the questionnaire is completed and reviewed, a lab test is needed in order to confirm and view the exact levels the hormones are at. D.U.T.C.H ( Dried Urine Test for Comprehensive Hormones) provides one of the most accurate results. To gain more insight on D.U.T.C.H and how it works, please see last week’s article, linked here.
Testing & Conclusions
Filling out the questionnaire�essentially allows the practitioner to score and rate the severity of the issues. Adding the D.U.T.C.H results to the questionnaire gives the practitioner a factual level and complete understanding of their patient’s sex and adrenal hormones and metabolites.
This further allows the practitioner to diagnose (if necessary) and suggest nutraceuticals to help the patient’s hormone levels return to normal and minimize symptoms. There are many factors and systems involved when it comes to treating hormones and having tests completed that reflect the numbers that need to be adjusted is necessary. A hormone imbalance can easily take charge of an individual’s life, but now is the time to get these symptoms under control and get back to feeling like you used to!
A great place to start is to find a doctor or healthcare provider who will supply you with a full questionnaire and listen to the symptoms you’re having. This condition is fairly common and can be treated! October is Chiropractor Health Month, and we would love to see you and aid in providing treatment if you are experiencing any of these symptoms. Due to the fact that hormones can be complex and affect different body systems, we take the time to really understand and check all aspects before jumping to a conclusion. – Kenna Vaughn, Senior Health Coach
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 .
Bibliography
(1) Ginta, Daniela. �What Are the Symptoms of Low Estrogen in Women and How Are They Treated.� Healthline, 31 Jan. 2017, www.healthline.com/health/womens-health/low-estrogen-symptoms.
(2) McBride, J Abram, et al. �Testosterone Deficiency in the Aging Male.� Therapeutic Advances in Urology, SAGE Publications, Feb. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4707424/.
(3) Swns. �Nearly Half of Women Have Been Affected by a Hormonal Imbalance.� New York Post, New York Post, 22 Feb. 2019, nypost.com/2019/02/22/nearly-half-of-women-have-been-affected-by-a-hormonal-imbalance/.
(4) Wallace, Ryan, and Kathleen Yoder. �12 Signs of Low Testosterone .� Healthline, 25 Apr. 2019, www.healthline.com/health/low-testosterone/warning-signs.
Many patients with peripheral neuropathy often believe that their painful symptoms are irreversible or permanent. However, Dr. John Coppola and Dr. Valerie Monteiro describe that peripheral neuropathy can be treated by treating the underlying source of the painful symptoms. Several patients discuss their painful peripheral neuropathy symptoms and how these affected their overall quality of life.
Moreover, the patients also discuss how Dr. John Coppola and Dr. Valerie Monteiro helped treat their painful peripheral neuropathy symptoms through the use of a variety of treatment methods and techniques. Dr. Alex Jimenez, doctor of chiropractic in El Paso, TX, can help treat painful symptoms associated with peripheral neuropathy. Dr. Alex Jimenez is the non-surgical choice for chiropractic care and peripheral neuropathy treatment.
Contents
Peripheral Neuropathy Recovery Stories | El Paso, TX (2019)
Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves.
The causes of neuropathy, or nerve damage, can vary among individuals and these may be caused by different:
Diseases
Injuries
Infections
Vitamin deficiencies
Neuropathy can also be classified according to the location of the nerves being affected and according to the disease-causing it.
Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest.
Peripheral neuropathy is simply referred to as neuropathy, which is a state that happens when the nerves become damaged or injured, oftentimes simply disturbed.
It�s estimated that neuropathy affects roughly 2.4 percent of the general populace and approximately 8 percent of people older than age 55.
Type
Neuropathy can affect any of the three types of peripheral nerves:
Sensory nerves�transmit messages from sensory organs:
Eyes
Nose
Brain
Motor nerves track the movement of the muscles
Autonomic nerves regulate the involuntary body functions
Sometimes, neuropathy will only impact one nerve. This is medically referred to as mononeuropathy and instances of it include:
Ulnar neuropathy affects the elbow
Radial neuropathy affects the arms
Peroneal neuropathy affects the knees
Femoral neuropathy affects the thighs
Cervical neuropathy affects the neck
Sometimes, two or more isolated nerves in separate regions of the body can become damaged, injured or disrupted, resulting in mono neuritis multiplex neuropathy.
Most of the time, multiple peripheral nerves malfunction at the same time, a condition called polyneuropathy.
Cause
Neuropathies are often inherited from birth or they develop later in life.
The most frequent inherited neuropathy is the Charcot-Marie-Tooth disease, which affects 1 in 2,500 people in the USA.
Although healthcare professionals are sometimes not able to pinpoint the exact reason for an acquired neuropathy, medically referred to as idiopathic neuropathy.
There are many known causes for them, including:
Systemic diseases – a systemic disease is one that affects the whole body.
Physical trauma
Infectious diseases
Autoimmune disorders
The most frequent systemic cause behind peripheral neuropathy is diabetes, which can lead to chronically high blood glucose levels that harm nerves.
Other systemic issues can cause neuropathy, including:
Kidney disorders permit high levels of nerve-damaging toxic chemicals to flow in the blood
Toxins from exposure to heavy metals include:
Arsenic
Lead
Mercury
Thallium
Drugs/medications, including anti-cancer medications, anticonvulsants, antivirals, and antibiotics
Chemical imbalances because of liver illnesses.
Hormonal diseases, like hyperthyroidism, which disturbs metabolic processes, and potentially induces cells and body parts to exert pressure on the nerves.
Deficiencies in vitamins, such as E, B1 (thiamine), B6 (pyridoxine), B12, and niacin can be vital for healthy nerves.
Alcohol abuse induces vitamin deficiencies and could harm nerves.
Cancers and tumors can exert damaging pressure on nerve fibers and paths.
Chronic inflammation can damage protective tissues around nerves, which makes them more vulnerable to compression, getting inflamed and swollen.
Blood diseases and blood vessel damage, which may damage or injure nerve tissue by decreasing the available oxygen supply
Symptoms
Depending on the reason and unique to each patient, signs, and symptoms of neuropathy can include:
Symptoms are dependent on autonomic, sensory, or motor nerves or a combination are affected.
Autonomic nerve damage can start a chain reaction of physiological functions like blood pressure or create gastrointestinal problems and issues.
Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while injury to motor nerves affects movement and reflexes.
When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.
Complications
Peripheral�neuropathy�may result in several complications, as a result of disease or its symptoms.
Numbness from the ailment can allow you to be less vulnerable to temperatures and pain, making you more likely to suffer from burns and serious wounds.
The lack of sensations in the feet, for instance, can make you more prone to developing infections from minor traumatic accidents, particularly for diabetics, who heal more slowly than other people, including foot ulcers and gangrene.
Furthermore, muscle atrophy may cause you to develop particular physical disfigurements, such as pes cavus, a condition marked by an abnormally high foot arch, and claw-like deformities in the feet and palms.
Treatment
The first step in neuropathy treatment should be finding the root cause that’s causing the neuropathy.
Treatment of diseases such as:
Diabetes
Guillain-Barre syndrome
Rheumatoid arthritis
Sarcoidosis
Other underlying diseases
Prevents continued nerve damage and in cases heals the damaged nerves.
If you are unaware of any underlying disease that is causing the peripheral neuropathy, make sure to let your doctor know of abnormal symptoms.
Medication
Peripheral neuropathy can be treated with various medications.
The first type used to treat mild symptoms are:
Over-the-counter pain medications
In more severe cases:
Opiates
Narcotic medications
Anti-seizure medications
A doctor may prescribe a lidocaine patch or anti-depressants to relieve symptoms.
Patients should thoroughly discuss�neuropathymedication with a doctor before proceeding.
Chiropractic/Massage/Physical Therapy
Various manual therapies can benefit symptoms in neuropathy treatment.
A therapist or chiropractor will perform various manipulation techniques, and teach exercises and stretches to help improve symptoms combined with increased muscle strength/control.
A therapist may also recommend braces or splints to improve mobility.
Patients should attend all physical therapy sessions to gain maximum benefits.
Acids
Supplements like:
Essential acids called ALA (alpha-Lipoic acid)
GLA (gamma-linolenic acid) and omega-3 fatty acids
These can have a beneficial effect on diabetic peripheral neuropathy.
L-Carnitine
L-carnitine is a substance that the body makes and stores in the:
Liver
Brain
There have been reports that certain diabetics with neuropathy symptoms could regain regular sensation in the limbs when they increased their consumption of carnitine called acetyl-L-carnitine.
Red meat
Peanut butter
Dairy products
Are good dietary sources of this nutrient.
Supplements are also available at health food stores and pharmacies and health/wellness clinics.
Vitamin Supplements
Vitamin deficiencies can result in peripheral neuropathy in some people.
Therefore there needs to be a replenishing of vitamins:
B
B12
E
These can help to decrease symptoms.
Recommended dosages are 300mg daily of vitamin E.
Doses of the different B vitamins differ, but one option for patients is to take a daily B-complex supplement.
Herb Supplements
Herbal remedies are an alternative to explore.
St. John’s Wort, is a herbal supplement that can be taken orally and can reduce the pain.
Topical creams that have capsaicin, which is an anti-inflammatory found in chili peppers, can reduce the burning sensation.
While every type of neuropathy, such as diabetic neuropathy or autoimmune disease-associated neuropathy, develops its own unique group of symptoms, many patients will often report common complaints. Individuals with neuropathy generally describe their pain as stabbing, burning or tingling.
If you experience unusual or abnormal tingling or burning sensations, weakness and/or pain in your hands and feet, it�s essential to seek immediate medical attention in order to receive a proper diagnosis of the cause of your specific signs and symptoms. Early diagnosis may help prevent further nerve injury. Visit http://www.neuropathycure.org.
When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. �
Contents
Alzheimer’s Disease
Alzheimer’s disease (AD) is one of the main causes of dementia among older adults in the United States. Neuropathologically, AD is characterized as neurodegeneration with extracellular senile plaques made up of ? amyloid (A?) and intraneuronal neurofibrillary tangles of aggregated tau, which initially appear in the hippocampus than then spread as the health issue progresses. Prominent microglial cell activation can also be associated with AD. Hereditary types of AD occur due to mutations in the A? precursor protein, A?PP, or in the presenilins, which are part of the multi-protein complex involved in A? generation. The pathophysiology of AD is complicated and a variety of pathways are included in the synaptic and the cellular degeneration in AD, such as abnormalities in signaling pathways through glycogen synthase kinase-3 beta or mitogen-activated protein kinases, cell cycle re-entry, oxidative stress, or decreased transport of trophic factors and adrenal dysregulation. However, evidence suggests that L-glutamate dysregulation plays a critical role in Alzheimer’s disease. �
Research studies demonstrated that primary neurons from transgenic mice overexpressing mutant presenilin are far more sensitive to excitotoxic stimulation in vitro. In vitro, aggregated A? increases both NMDA and kainate receptor-mediated L-glutamate toxicity, perhaps by interrupting neuronal calcium homeostasis. Others have demonstrated that A? can increase neuronal excitability by changing the capacity of glycogen synthase kinase 3? inhibition to decrease NMDA receptor-mediated pathways. Soluble A? oligomers were demonstrated to cause L-glutamate release from astrocytes resulting in dendritic spine loss through over-activation of extrasynaptic NMDA receptors. Moreover, extracellular L-glutamate concentrations were demonstrated to increase in a triple transgenic mouse model of AD, in which a 3-month treatment with the NMDA receptor inhibitor ultimately affected synapse loss. However, further research studies are still required. �
Numerous mouse research studies have demonstrated the consequences of AD-like pathology on EAAT expression and/or function. In acute hippocampal slice preparations, A? was shown to interrupt the clearance of synaptically released L-glutamate by diminishing membrane insertion of EAAT2, a result perhaps mediated by oxidative stress. In aged A?PP23 mice, research studies revealed the downregulation of EAAT2 expression in the frontal cortex and hippocampus, which in the frontal cortex was associated with an increase in xCT expression. These changes were associated with a strong tendency toward improved extracellular L-glutamate amounts as measured by microdialysis. In triple transgenic AD mice expressing the amyloid precursor protein mutations K670N and M671L, the presenilin 1 mutation M146V and the tau P301L mutation, a strong and age-dependent decrease of EAAT2 expression was demonstrated. Restoration of EAAT2 activity in the AD mice following treatment with all the ?-lactam antibiotic Cef was associated with a decrease in cognitive impairment and reduced tau pathology. In human AD brains, decreased expression of EAAT2 protein and a decrease in EAAT action was determined. However,� this outcome measure could not be replicated by other researchers. On the transcriptome level, research studies discovered exon-skipping splice variations of EAAT2 which reduce glutamate transport activity to be upregulated in human AD brains. From the CSF, several groups demonstrated an increase in glutamate concentrations in AD patients where other groups demonstrated absolutely no change or even diminished levels of L-glutamate associated with Alzheimer’s disease. �
In vitro, A? causes L-glutamate discharge from primary microglia through the upregulation of program x?c. Others discovered that it also triggered L-glutamate release from astrocytes through the activation of the ?7 nicotinic acetylcholine receptor. Additionally, xCT, the specific subunit of system x?c is upregulated at the region of senile plaques, possibly in microglial cells, in Thy1-APP751 mice (TgAPP) expressing human APP bearing the Swedish (S: KM595/596NL) and London (L: V6421) mutations after A? injection in the hippocampus. Semiquantitative immunoblot evaluations revealed an upregulation of xCT protein expression in the frontal cortex in elderly A?PP23 mice compared to wild-type controls. �
Postmortem research studies show that KYN metabolism affects AD elevated concentrations of KYNA while also discovered in the basal ganglia of both AD sufferers. Utilizing immunohistochemistry, research studies demonstrated immunoreactivity for both IDO and QUIN upregulated in AD brains, particularly in the vicinity of plaques. A? causes IDO expression in human primary macrophages and microglia. Systemic inhibition of KMO ultimately increases brain KYNA levels and ameliorated the phenotype of a mouse model of AD, indicating an upregulation of KYNA may be an endogenous protective reaction, including the IDO inhibitor, coptisine, decreased microglial, astrocytic activation and cognitive impairment in AD mice. �
Taken together, along with many other harmful changes, there is evidence for chronic excitotoxicity in AD which can be driven by numerous variables, including the central sensitization of both NMDA receptors, a decrease in L-glutamate and L-aspartate reuptake capacity and an increase in glutamate release through system x?c, as shown in Figure 4. Although the KYN pathway seems to be upregulated in AD, no specific conclusions can be drawn regarding glutamatergic neurotransmission from the upregulation of the two QUIN which was neurotoxic and neuroprotective KYNA. �
�
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
In the article above, we outlined what is known about the pathways which may cause excitotoxicity in neurodegenerative diseases. We also discussed that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. 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. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
The gut-brain connection is essential in the body. If an individual has a leaky gut that is causing inflammation, it can send the signal to the brain and it can create problems like neurotransmitter dysfunction to systems that just don�t connect. The leaky gut can lead to brain dysfunction or brain dysfunction can lead to leaky gut. Sometimes an autoimmunity disease in the stomach can lead to a disruption in the mind. Then, brain disruption can also lead to inflammation in the gut. It�s a never-ending loop that the brain and gut can go on forever. Studies have stated that gut microbiota appears to influence the development of emotional behaviors like stress, pain modulation systems, and brain neurotransmitter systems.
Contents
The Brain System to the Gut System
The brain is the main control room that controls the body�s system and how the body should behave. The human brain also contains neuron cells that are found in the central nervous system. With the gut-brain connection, two critical systems help send the signal to the brain and the gut; these are known as the vagus nerve and the neurotransmitters.
The Vagus Nerve
There are approximately 100 billion neurons in the brain, while the gut contains about 500 million neurons, which is connected to the brain through the nerves in the nervous system. The vagus nerve is one of the most significant nerves that send signals back and forth to the brain and the gut. When the body is stressed, the stress signal inhibits the vagus nerve, and it can cause problems to the gut-brain connection. Animal studies have shown that any stress that is in the animal�s body can cause gastrointestinal issues and PTSD. While another study stated that individuals that have IBS (irritable bowel syndrome) have a reduced function of the vagus nerve.
There are ways to reduce the stress hormone so that the vagus nerve can function properly and send the right signals to the gut and the brain. Probiotic foods can help lower the amount of stress hormone in the bloodstream. When that happens, the body can start healing naturally when the stress is reduced; however, if the vagus nerve is damaged, then the probiotic has no effect.
Neurotransmitters
Neurotransmitters are produced chemically in the brain by controlling feelings and emotions in the body. Since the brain and gut are connected to neurotransmitters, the neurotransmitters can create these compounds that help contribute to the body. In the brain, the neurotransmitter can produce serotonin to make the person feel happy and help control their body�s biological clock.
In the gut, there are trillions of microbes that live there, and interestingly researchers stated that serotonin is mainly being produced by the gut system. Another neurotransmitter that is provided in the gut is called GABA (gamma-aminobutyric acid), which helps control the feeling of fear and anxiety. When the brain feels overly anxious or has been through a traumatic experience that has caused them to be fearful, it can cause them to be hypersensitive and can cause a chemical imbalance to the gut, causing inflammation or leaky gut if it is severe.
The Gut System to the Brain System
The gut microbes can produce neurotransmitters to send to the brain, protect the intestinal barrier and the tight junction integrity, regulate the mucosal immune system, and modulates the enteric sensory afferents. The gut microbe produces a lot of SCFA (short-chain fatty acids) that form a barrier between the brain and blood flow called the blood-brain barrier. The blood-brain barrier protects the CNS (central nervous system) from toxins, pathogens, inflammation, injury, and disease.
The gut microbes also metabolize bile and amino acids to help produce other chemicals that affect the brain. When the body is stressed, it can reduce the production of bile acid by gut bacteria and alter the genes that are involved. When that stress is still creating problems in mind, the gut can develop gastrointestinal issues that will destroy the permeability barrier that is protecting the intestines.
The gut-brain connection plays an essential role in the body�s immune system as it controls inflammation and what passes into the body. Since the immune system controls inflammation, if it is turned on for too long, inflammation can occur as well as several brain disorders like depression and Alzheimer�s disease. Stress can even disrupt the gut by causing contractions to the GI tract, make inflammation worse in the intestinal permeability, and making the body more at risk to infections.
When the body starts to alleviate stress, it can naturally heal itself, and the gut-brain connection can begin functioning normally. With changes in a person�s eating habits and lifestyle, it can drastically change a person�s mood and recover from intestinal ailments they may have. If the brain feels right, then the gut feels good as well. They work together side by side to make sure that the body is functioning correctly. When either one is being disrupted, then the body does not function properly.
Conclusion
Therefore, the gut-brain connection is vital to the body. Neurotransmitters and other components that are in both systems work together to make sure that the body is working correctly. When one of the connections is being disrupted, however, the body can develop many chronic illnesses even if the person seems fine. By altering little things like changing a person�s diet and lifestyle, it can help improve the body and bring the balance back to the gut-brain connection.
In honor of Governor Abbott’s proclamation, 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:
Anguelova, M, et al. �A Systematic Review of Association Studies Investigating Genes Coding for Serotonin Receptors and the Serotonin Transporter: I. Affective Disorders.� Molecular Psychiatry, U.S. National Library of Medicine, June 2003, www.ncbi.nlm.nih.gov/pubmed/12851635.
Bravo, Javier A, et al. �Ingestion of Lactobacillus Strain Regulates Emotional Behavior and Central GABA Receptor Expression in a Mouse via the Vagus Nerve.� Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 20 Sept. 2011, www.ncbi.nlm.nih.gov/pubmed/21876150.
Carabotti, Marilia, et al. �The Gut-Brain Axis: Interactions between Enteric Microbiota, Central and Enteric Nervous Systems.� Annals of Gastroenterology, Hellenic Society of Gastroenterology, 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/.
Daneman, Richard, and Alexandre Prat. �The Blood-Brain Barrier.� Cold Spring Harbor Perspectives in Biology, Cold Spring Harbor Laboratory Press, 5 Jan. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4292164/.
Herculano-Houzel, Suzana. �The Human Brain in Numbers: a Linearly Scaled-up Primate Brain.� Frontiers in Human Neuroscience, Frontiers Research Foundation, 9 Nov. 2009, www.ncbi.nlm.nih.gov/pmc/articles/PMC2776484/.
Lucas, Sian-Marie, et al. �The Role of Inflammation in CNS Injury and Disease.� British Journal of Pharmacology, Nature Publishing Group, Jan. 2006, www.ncbi.nlm.nih.gov/pmc/articles/PMC1760754/.
Mayer, Emeran A, et al. �Gut/Brain Axis and the Microbiota.� The Journal of Clinical Investigation, American Society for Clinical Investigation, 2 Mar. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4362231/.
Mayer, Emeran A. �Gut Feelings: the Emerging Biology of Gut-Brain Communication.� Nature Reviews. Neuroscience, U.S. National Library of Medicine, 13 July 2011, www.ncbi.nlm.nih.gov/pmc/articles/PMC3845678/.
Mazzoli, Roberto, and Enrica Pessione. �The Neuro-Endocrinological Role of Microbial Glutamate and GABA Signaling.� Frontiers in Microbiology, Frontiers Media S.A., 30 Nov. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC5127831/.
Pellissier, Sonia, et al. �Relationship between Vagal Tone, Cortisol, TNF-Alpha, Epinephrine and Negative Affects in Crohn’s Disease and Irritable Bowel Syndrome.� PloS One, Public Library of Science, 10 Sept. 2014, www.ncbi.nlm.nih.gov/pubmed/25207649.
Rooks, Michelle G, and Wendy S Garrett. �Gut Microbiota, Metabolites and Host Immunity.� Nature Reviews. Immunology, U.S. National Library of Medicine, 27 May 2016, www.ncbi.nlm.nih.gov/pubmed/27231050.
Sahar, T, et al. �Vagal Modulation of Responses to Mental Challenge in Posttraumatic Stress Disorder.� Biological Psychiatry, U.S. National Library of Medicine, 1 Apr. 2001, www.ncbi.nlm.nih.gov/pubmed/11297721.
Yano, Jessica M, et al. �Indigenous Bacteria from the Gut Microbiota Regulate Host Serotonin Biosynthesis.� Cell, U.S. National Library of Medicine, 9 Apr. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4393509/.
Pilates or yoga can work wonders and always stretch before physical exercise.
Get fit – no regular physical activity can lead to serious conditions and possibly chronic pain.
Exercise benefits all, even some light walking around the neighborhood is enough. Just get moving!
Playing a sport could be a way to keep active. Remember, in order for any exercise to work is that it is done regularly.
Strength training is important, just as its name implies strength training builds muscle and reduces muscle imbalances.
It�s never too late to increase strength and flexibility.
Look at activities that you and your friends/family can enjoy and make doing them a regular thing.
A�chiropractor�is the ideal�medical professional to consult with for any unexplained pain in the musculoskeletal system. They are highly qualified professionals that their specialty is treating conditions like lower back pain and they are very affordable. If you or a loved one have pain in the lower back, give us a call. We�re here to help!
Understand *FOOT PRONATION* & How to Correct it with Orthotics | El Paso, TX (2019)
Foot pronation is the natural movement that occurs during foot landing while walking or running. Foot pronation also occurs while standing, and in this instance, it is the amount in which the foot rolls inward toward the arch. Foot pronation is normal, however, excessive foot pronation can cause a variety of health issues, including bad posture. The following video describes the 5 red flags of excessive foot pronation, which can ultimately affect a person’s overall health and wellness. Dr. Alex Jimenez can help diagnose and treat excessive foot pronation. Patients recommend Dr. Alex Jimenez and his staff as the non-surgical choice for excessive foot pronation health issues.
When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. �
Contents
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease associated with the degeneration of motor neurons which ultimately determine the length of the health issue. ALS is considered fatal several years after it begins. It is hypothesized that L-glutamate excitotoxicity plays a role in the motor neuron death in ALS because cells demonstrate increased levels of calcium-permeable AMPA receptors and low levels of calcium-binding proteins. Compared to the utilization of AMPA and kainate, and L-HCA, in the spinal cord of rats, treatment with NMDA spared motor neurons suggests that NMDA excitotoxicity may actually not play a fundamental role in ALS. However, NMDA receptor-mediated excitotoxicity in motor neurons was demonstrated in chick embryo organotypic slice cultures. Electrophysiological research studies suggested that transient hyperexcitability of motor nerves in the presymptomatic phase of ALS in mice transgenic for the G93A mutation of human SOD1 is associated with hereditary ALS. Additionally, cortical hyperexcitability was recorded in familial and sporadic ALS patients with the onset of symptoms in familial ALS mutation carriers. Moreover, the only approved drug and/or medication utilized for ALS, which increases survival by 2 to 3 months, acts as an inhibitor of both NMDA and kainate receptors together with quickly upregulating EAAT activity in synaptosomes, according to several research studies. �
In autopsied spinal cords from patients with ALS, several groups demonstrated a decrease in EAAT2 and not in EAAT1 protein expression in the gray matter of regions with considerable motor neuron loss. In addition, both L-glutamate uptake and EAAT2 immunoreactivity, as demonstrated by Western blotting, were demonstrated to be quantitatively decreased in postmortem tissue of ALS patients, particularly in the spinal cord, the tissue which is most commonly affected by the health issue. Additionally, it has been demonstrated that as a possible effect of EAAT2 downregulation, L-glutamate amounts are increased in the CSF in patients with ALS. However, this outcome measure couldn’t be replicated by other research studies. �
The downregulation of EAAT2 in human ALS is demonstrated in several animal models of ALS, including transgenic mice expressing human SOD1 containing the G93A mutation which causes hereditary ALS or transgenic rats expressing the same mutation. Surprisingly, “whereas Bendotti demonstrated a late decrease in EAAT2 expression at the time when the mice had already become symptomatic,” research studies demonstrated fluctuations in EAAT2 expression at the presymptomatic stage. The ?-lactam antibiotic ceftriaxone (Cef) promotes the production of EAAT2 in cultured murine spinal cord slices and in neuron/astrocyte co-cultures. In addition, it caused EAAT2 expression from the spinal cords of wild-type and mutant G93A mSOD1 Tg mice, which has been associated with a decrease in motor neuron loss, weight reduction, and other ALS-like symptoms as well as an increase in survival, compatible with the hypothesis that EAAT2 loss contributes to chronic excitotoxicity in this mouse model. Just recently, a significant decrease in EAAT2 immunoreactivity had been demonstrated in a separate bark model for ALS, rats expressing ALS-inducing mutant TAR DNA binding protein 43 in astrocytes only. Surprisingly, the research studies demonstrated that when measured by microdialysis, the extracellular L-glutamate and L-aspartate concentrations increase while the L-glutamate clearance capability decrease in the cerebral cortex of G93A mSOD1 Tg mice, however, this region doesn’t show overt pathology nor downregulation of EAAT1 when evaluated. �
Taken together these research studies support the view that there is a downregulation of EAAT2 in both human ALS patients and animal models of ALS. However, while some animal research studies suggest that EAAT2 downregulation occurs before motor neuron loss, others are compatible with the hypothesis that the downregulation of EAAT2, the astroglial expression of which is associated with the existence of neurons, is a consequence of neurodegeneration in neurological diseases. �
Furthermore, EAATs decrease extracellular L-glutamate, extracellular cerebral L-glutamate is upregulated in a variety of brain regions from the cystine/glutamate antiporter system x?c. XCT, one particular subunit of program x?c, was demonstrated to be differentially regulated and maintained in mouse models of ALS. Research studies demonstrated that the uptake of radiolabelled cystine was upregulated in spinal cord slices of presymptomatic G93A mSOD1 Tg mice at the age of 70 days but not in 55 or 100 days and not in symptomatic 130 day-old mice which also determined that the upregulation of cystine uptake at day 70 was because of system x?c activity utilizing the system x?c inhibitor sulfasalazine (SSZ). It needs to be considered, however, that cystine can also be hauled by EAATs. Therefore, as evidence about the SSZ-sensitivity of cystine uptakes were not demonstrated for days 100 and 130, the differential cystine uptake demonstrated in this research study at the older ages could rather be a result of decreased EAAT action. By comparison, research studies with rtPCR demonstrated a strong growth in xCT mRNA levels in G37R mSOD1 Tg mice on the beginning of symptoms, which has been further increased as symptoms improved. Moreover, it was demonstrated that xCT was primarily demonstrated in spinal cord microglial cells. Microglia revealed xCT mRNA upregulation in the presymptomatic stage. Taken together, these outcome measures suggest the system x?c is upregulated in animal models of ALS. However, the evidence is lacking about whether this is true for human cases of ALS. Nevertheless, further research studies revealed that the mRNA levels of CD68, a marker of microglial activation, were associated with xCT mRNA expression in postmortem spinal cord tissue of individuals with ALS, demonstrating that neuroinflammation in humans is also ultimately associated with xCT upregulation. �
Beyond the dysregulation of L-glutamate and L-aspartate levels by EAAT downregulation or system x?c upregulation, pathways that indirectly regulate and maintain glutamatergic neurotransmission also have been suggested to participate in motor neuron degeneration in ALS. D-Serine levels have been shown to become considerably increased from the spinal cord of G93A mSOD1 Tg mice. Starting at disease onset and ongoing during the course of this symptomatic phase, D-serine increases NMDA excitotoxicity in motor neurons. The upregulation of D-serine at the spinal cord was duplicated by other research studies. Downregulation of this D-serine metabolizing enzyme DAO in the reticulospinal tract has been demonstrated as the main mechanism for D-serine upregulation in the spinal cord in ALS mice. In addition, genetic inactivation of DAO in mice has been associated with motor neuron degeneration and a deficiency in the D-serine generating enzyme serine racemase prolonged survival in G93A mSOD1 Tg mice although it hastened neurodegenerative disease onset. A heterozygous mutation of DAO has been demonstrated to be separate from the ALS phenotype in a large family with hereditary ALS. However, this continues to be the only family determined where a DAO mutation is associated with ALS. �
Concerning the other amino acid co-agonist of the NMDA receptor, glycine, an increase in the CSF levels in patients with ALS was demonstrated by one group, however, it couldn’t be replicated by other research studies. Several research studies also determined that KYNA levels are upregulated in the CSF of bulbar ALS patients as well as those in end-stage ALS. Independently, it was revealed that tryptophan and KYN levels are increased in the CSF from ALS patients as compared to controls. Additionally, IDO was proven to be expressed in neurons and spinal cord microglia from patients with ALS, indicating that microglial activation may increase the conversion of tryptophan in ALS into KYN, among others. �
Multilayered evidence suggests that increased glutamatergic neurotransmission is within ALS and may ultimately cause neurodegeneration in neurodegenerative diseases, as shown in Figure 3. Downregulation of EAAT2 in astrocytes and upregulation of program x?forecast in the context of microglial activation was repeatedly documented. NMDA receptors by D-serine may also play a role in dysregulation. Moreover, the kynurenine pathway seems to be triggered in ALS. �
�
In many research studies, evidence and outcome measures have demonstrated that chronic excitotoxicity may be associated with a variety of neurodegenerative diseases, including AD, HD, and ALS, ultimately causing neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to outline what may cause excitotoxicity in neurodegenerative diseases. We will discuss these in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD). – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
In the article above, we outlined what is known about the pathways which may cause excitotoxicity in neurodegenerative diseases. We also discussed that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. 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. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
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.�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?
Contents
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.
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine
The thyroid actually 
The thyroid can increase the basal metabolic rate by helping it increase the speed of breaking down, absorbing, and the assimilation of the nutrients we eat and eliminate waste. The thyroid hormone can also increase the need for vitamins for the body. If the thyroid is going to regulate our cell metabolism, there has to be an increased need for vitamin cofactors because the body needs the vitamins to make it function properly.
The thyroid hormones have a direct impact on ovaries and an indirect impact on SHBG (
When there is a higher level of cortisol in the body, it will decrease the thyroid function by lowering the conversion of the T4 hormone to T3 hormone by impairing the deiodinase enzymes. �When this happens, the body will have a less functional thyroid hormone concentration, since the body can�t tell the difference of a hectic day at work or running away from something scary, it can either be very good or horrible.
� 
In the gut, there are trillions of microbes that live there, and interestingly 
The gut microbes also metabolize bile and amino acids to help produce other chemicals that affect the brain. When the body is stressed, it can reduce the production of bile acid by gut bacteria and alter the genes that are involved. When that stress is still creating problems in mind, the gut can develop gastrointestinal issues that will destroy the permeability barrier that is protecting the intestines.
The gut-brain connection plays an essential
�
�
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?
