The most common causes of TBI which result in ER visits include slip-and-fall accidents, blows to the head, and automobile accidents. Abrupt forces which jolt the brain violently within the skull, such as shock waves from explosions, which can also cause TBI. Traumatic brain injury can also result from bullet wounds or other injuries which penetrate the skull and brain. �
Doctors characterize traumatic brain injury as mild, moderate, or severe depending on whether the injury causes unconsciousness, how long it lasts, and other symptoms. Although most traumatic brain injuries are characterized as mild because they’re not considered life-threatening, even a mild TBI can have serious and long-lasting effects if left untreated. � Resulting from an impact to the head which interrupts brain function, TBI is a threat to cognitive health in two ways: �
The effects of traumatic brain injury, which may be long-lasting or even permanent, can include unconsciousness, inability to recall the event, confusion, difficulty learning new information, trouble speaking, unsteadiness, lack of coordination, and health issues associated with vision or hearing, among other common symptoms.
TBI may increase the risk of developing Alzheimer’s disease or dementia, years after the injury takes place.
According to the Centers for Disease Control and Prevention (CDC), approximately 2.8 million TBI-associated ER visits, hospitalizations, and deaths occurred in 2013, the latest year for which information is available. The purpose of the following article is to discuss traumatic brain injury (TBI) and its connection with Alzheimer’s disease and other health issues. �
Contents
Traumatic Brain Injury Causes
Slip-and-fall accidents are the most common cause of traumatic brain injury, where falls pose a potentially serious risk factor for older adults. According to a CDC special report evaluating data from several federal agencies, approximately 56,000 seniors are hospitalized every year as a result of head injuries sustained in falls. A serious TBI from a slip-and-fall accident may ultimately result in long-term cognitive changes and reduced ability to function as well as overall mood changes. �
About 775,000 older adults have traumatic brain injury-related disability. Measures to reduce the risk of falls include: �
Using a walker or other assistive device to compensate for mobility problems, muscle weakness or poor balance.
Having your vision checked regularly and using glasses or contact lenses that correct for changes.
Working with your doctor to watch for medication side effects or interactions among drugs you�re taking.
Avoiding household hazards, such as clutter, loose rugs or poor lighting.
Automobile accidents are another common cause of traumatic brain injury (TBI). People can reduce the risk of being involved in an auto accident by keeping their vehicle in good condition, following the rules of the road, and buckling their seat belt. Wearing a helmet and when biking, inline skating, or playing contact sports can also help protect the head from TBI. �
TBI Symptoms
The severity of symptoms for traumatic brain injuries largely depends on whether the injury is mild, moderate, or severe. Mild traumatic brain injury (TBI), also known as a concussion, can either not cause unconsciousness or can cause unconsciousness which lasts for 30 minutes or less. Mild traumatic brain injury (TBI) symptoms may include: �
Inability to remember the traumatic event immediately before or up to 24 hours after
Confusion and disorientation
Difficulty learning new information
Headache
Dizziness
Blurry vision
Nausea and vomiting
Ringing in the ears
Trouble speaking coherently
Mood changes or changes in sleeping patterns
These symptoms will commonly manifest at the time of the TBI or soon after, however, these may sometimes not develop till several days or even weeks following the traumatic event. Mild TBI symptoms are generally temporary and these will clear up within hours, days, or weeks following the traumatic even, however, they can occasionally last several months or longer. �
Moderate traumatic brain injury can cause unconsciousness which lasts more than 30 minutes but less than 24 hours and severe traumatic brain injury can cause unconsciousness for more than 24 hours. Symptoms of moderate and severe traumatic brain injury are similar to those of mild traumatic brain injury but these are more serious and longer-lasting. �
In all types of TBI, cognitive changes are the most common symptoms. The ability to learn and remember new information is also frequently affected. Other commonly affected cognitive skills include the ability to pay attention, organize thoughts, plan effective strategies for completing tasks and activities, and/or make sound judgments. More severe changes in cognitive skills may develop years after the traumatic event where the person may appear to have recovered from the previous TBI. �
TBI Diagnosis
Evaluations performed by healthcare professionals to help diagnose traumatic brain injury (TBI) generally include: �
Questions about the traumatic event
Analysis of the person’s level of consciousness and confusion
Neurological tests to analyze memory and thinking, vision, hearing, touch, balance, and reflexes
Let your doctor know if you are taking any drugs and/or medications, especially blood thinners, because they can increase the chance of complications. Also, inform your healthcare professional if you drink alcohol or take illicit drugs. �
Depending on the cause of the TBI and the severity of symptoms, brain imaging with computed tomography (CT) may be necessary to determine if there�s swelling or bleeding in the brain. If you experience a traumatic brain injury, it should be noted in your permanent medical record and mentioned whenever familiarizing a new doctor with your medical history. �
Traumatic Brain Injury Treatment
The most serious traumatic brain injuries commonly require specialized hospital care and can also need several months of rehabilitation. Most traumatic brain injuries are mild and can be treated with either a short hospital stay for observation or at-home monitoring followed by outpatient rehabilitation, if necessary. Treatment of dementia in a person with a history of traumatic brain injuries varies depending on the type of dementia diagnosed. Treatment strategies for Alzheimer’s disease or another type of dementia are ultimately the same for people with and without a history of traumatic brain injury. �
Alzheimer’s disease and other types of dementia which may occur as a long-term result of traumatic brain injury (TBI) are progressive health issues which worsen over time. As with all types of dementia, they can affect a person’s quality of life, shorten lifespan, and complicate the effort to manage other health issues effectively. However, because other types of dementia, such as CTE, are considerably new for researchers and healthcare professionals, clinical guidelines for diagnosis and treatment do not exist. Several research studies are underway to gain further insight into the patterns of TBI and Alzheimer’s disease which may be implicated in CTE and to develop strategies for prevention, diagnosis, and treatment. �
As previously mentioned in the article above, Alzheimer�s disease and other types of dementia which may occur as a long-term result of traumatic brain injury (TBI) are progressive health issues which may ultimately worsen over time. As with all types of dementia, these can affect quality of life, shorten life span, and complicate the effort to manage other health issues effectively. It’s essential for patients and healthcare professionals to diagnose and treat a traumatic brain injury to prevent further health issues in the future, including Alzheimer’s disease and dementia. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
According to research studies, TBI is ultimately associated with Alzheimer�s disease and other types of dementia. Doctors commonly characterize traumatic brain injury as mild, moderate, or severe depending on whether the previous traumatic event causes unconsciousness, how long it lasts, and other well-known symptoms. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. 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 �
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.
Traumatic brain injury (TBI) is one of the most common causes of disability and death among the general population, especially in young adults. Additionally, TBI is associated with a variety of neurodegenerative diseases, such as Alzheimer�s disease (AD) and Parkinson�s disease (PD). It is essential for patients and healthcare professionals to understand the pathophysiological mechanisms of traumatic brain injury and neurodegenerative diseases to diagnose factors which may ultimately cause neurodegeneration associated with TBI as well as determine possible treatment approaches. �
Oxidative stress, neuroinflammation, and glutamatergic excitotoxicity have previously been associated with TBI and neurodegenerative diseases. As a matter of fact, oxidative stress is believed to be an essential pathological mechanism which connects TBI to neurodegenerative diseases. Research studies have demonstrated that reactive oxygen species and their subsequent byproducts may play a role as novel fluid markers for the identification and monitoring of cellular damage. These reactive oxygen species can also serve as a suitable treatment approach to ultimately help reduce the risk of neurodegenerative diseases and promote quality of life for people suffering from TBI and other health issues. �
Contents
Pathogenesis of TBI and Neurodegenerative Diseases
Several research studies have demonstrated the development of neurodegenerative diseases following TBI. Previous research studies have also shown a three times higher prevalence of PD following TBI. Likewise, the prevalence of AD has also been shown to be higher following TBI. Moreover, traumatic brain injury has been demonstrated to be a risk factor for ALS with several research studies demonstrating an increased risk of neurological diseases in professional Italian soccer players. A case-control research study of ALS patients in the United States also found an increased risk of ALS with repeated TBI. However, it currently appears unlikely that a single occurrence of TBI could considerably affect the risk of ALS. Additionally, chronic traumatic encephalitis (CTE), a tau pathology, has been demonstrated in NFL players and professional athletes which suffer from repeated TBI. Because of the prevalence of neurodegenerative diseases and other health issues appears to increase after TBI, it is relevant to discuss the pathogenesis of TBI and neurodegenerative diseases. �
In several research studies, TBI patients and TBI animal models have been shown to demonstrate characteristic pathological mechanisms in key proteins, indicating the disruption of axonal transport due to axonal injury. The accumulated proteins which result in protein neuropathy include A?, ?-synuclein, and tau protein. These abnormal proteins are specifically interesting because it is well-known that A? protein aggregation is an essential pathological factor of AD, ?-synuclein protein aggregation is an important characteristic of PD, and tau protein aggregation is fundamental in the pathogenesis of CTE and AD. Surprisingly, these protein neuropathological changes occur in all three proteins through oxidative stress-associated free radicals and reactive aldehydes which are commonly increased following TBI. Additionally, the reactive aldehyde byproducts of lipid peroxidation have been demonstrated to result in further lipid peroxidation. Provided that these pathological proteins can also cause the development of free radicals through excitotoxicity or changes in mitochondrial ion balance. Because reactive aldehydes can cause further lipid peroxidation and protein carbonylation, it is possible that oxidative stress also plays a key role in a self-propagating cycle of lipid peroxidation, protein carbonylation, and neurodegenerative protein aggregation. Further research studies are still necessary to determine these outcome measures. �
TBI patients and TBI animal models have also demonstrated behavioral signs and symptoms, such as post-TBI dementia which resembles AD, post-TBI motor deficits which offer evidence of post-TBI brain tissue damage in the region of the hippocampus thus, resembling brain tissue damage in AD, and damage in the basal ganglia thus, resembling the brain tissue damage which occurs in PD. Functional magnetic resonance imaging (fMRI) research studies have also shown transient and persistent neuropathological functional changes in the brain of TBI patients which may contribute to the development of chronic neurodegenerative diseases. These changes observed in post-injury patients suggest that TBI could cause the initial tissue damage which resembles or results in processes in the pathophysiology of neurodegenerative diseases. �
Based on the essential role which oxidative stress plays in post-TBI secondary injury and in the pathophysiology of neurodegenerative diseases, it is possible that oxidative stress is a key process in connecting TBI to the increased prevalence of neurodegenerative diseases. Furthermore, oxidative stress may serve as a therapeutic, diagnostic, or prognostic marker in evaluating the risks of long term neurological diseases following TBI which can help determine a proper treatment approach. �
Treatment of TBI and Neurological Diseases
Considering the considerable risks caused by TBI, it is clear that there is a need for effective methods and techniques for early diagnosis and treatment of TBI patients to ultimately reduce the prevalence of post-TBI neurological sequelae. Currently, the diagnosis of TBI is primarily based on the patient’s provided history and clinical observations. Several clinical systems have been developed for the evaluation of mTBI, which is the most common type of clinical TBI, including the Sports Concussion Assessment Tool and Military Acute Concussion Evaluation. However, these assessments are made to be utilized immediately after injury and, as such, quickly decreasing in sensitivity with delayed evaluation. Moreover, the Glasgow Coma Scale has been utilized for decades and allows for both quick and constant communication of the patient’s condition nevertheless, the currently accepted threshold score of 13 may not be adequate to exclude visible abnormalities on computed tomography imaging which require neurosurgical intervention. Due to these outcome measures in current diagnostic methods and techniques, civilian and military work-groups have recommended the development of fluid or imaging-based biomarkers for the diagnosis of mTBI to ultimately determine the most appropriate treatment approach. �
Several substances and proteins have been suggested to play an essential role as fluid biomarkers, including glial fibrillary acidic protein (GFAP), calcium-binding protein S100B, and tau protein. In most cases, the presence of these biomarkers demonstrates a blood-brain barrier disruption within the central nervous system. These proteins have been demonstrated to be acutely increased following TBI in human participants, however, these currently face challenges of low specificity, poor correlation with the development of post-concussive symptoms, and poor correlation with imaging abnormalities. �
Provided the key role of oxidative stress and neuroinflammation in secondary neuronal injury and neurodegeneration, it is possible that the results of these processes may also serve as suitable biomarkers. As previously mentioned, plasma levels of several oxidative stress and inflammation-associated markers have been demonstrated to be increased in serum up to 42 days following multiple blast injuries and as early as one day following a single injury. Furthermore, lipid peroxidation products, such as acrolein and 4-hydroxynonenal, have also been demonstrated to be associated not only in TBI secondary injury but also in other types of neuronal health issues, such as spinal cord injury and ischemia-reperfusion injury. Provided that these peroxidation products are not only a cause of damage but also able to cause the modification of biomacromolecules where it is possible that measured increases may be able to demonstrate not only present damage but also continued secondary injury. Treatment of oxidative stress could help as a possible prophylactic treatment to decrease the risk of post-TBI neurodegeneration. Direct supplementation with endogenous antioxidants, such as glutathione and superoxide dismutase, has not demonstrated considerable benefits because these do not easily cross the blood-brain barrier. However, the glutathione precursor N-acetylcysteine has demonstrated several acute benefits in both animal and human research studies. Additionally, focusing on substances of the oxidative cascade, such as reactive aldehydes, has been demonstrated as a possible treatment due to the more lengthened half-lives of these substances when compared to ROS. However, despite the lengthened increase of inflammatory and oxidative byproducts, trials of antioxidant therapies have generally favored acute treatment, often within hours of the TBI, suggesting that acute treatment is appropriate. �
Considering the essential role of post-TBI oxidative stress in the development and progression of chronic neurodegenerative diseases, diagnosis and treatment of this process seem to be promising for the management and regulation of neurodegenerative diseases following TBI. Provided their connection to oxidative stress, inflammatory markers, and lipid peroxidation byproducts could serve as surrogate biofluid markers. Finally, antioxidant treatment strategies can help neutralize perpetuation of cellular and molecular damage and decrease risks of long-term neurological sequelae. �
As previously mentioned in the article above, oxidative stress seems to be the key pathological mechanism connecting neuroinflammation and glutamatergic excitotoxicity in both TBI and neurodegenerative diseases. Due to the increased prevalence of TBI and neurodegenerative diseases, the development of new safe and effective, early diagnosis and treatment approaches is fundamental for overall health and wellness. Many healthcare professionals can improve symptoms and health issues associated with TBI and neurodegenerative diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
TBI is associated with a variety of neurodegenerative diseases, such as Alzheimer�s disease (AD) and Parkinson�s disease (PD). It is essential for patients and healthcare professionals to understand the pathophysiological mechanisms of traumatic brain injury and neurodegenerative diseases to diagnose factors which may ultimately cause neurodegeneration associated with TBI as well as determine possible treatment approaches. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. 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 �
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.
As a doctor who practices functional medicine, Dr. Jimenez utilizes the Neural Zoomer Plus. This is a blood test that analyzes neurological autoantibodies which offer very specific antibody-to-antigen recognition. The Neural Zoomer Plus tests the reactivity an individual has to 48 neurological antigens. These neurological antigens may be related to neurological disease and can help individuals assess the presence of a neurological condition.There are 48 markers that are measured and they can be summed up and categorized into 7 larger groups. These groups include demyelination antigens, blood-brain barrier disruption, optical and autonomic nervous system disorders, peripheral neuropathy, neuromuscular disorders, brain autoimmunity, brain inflammation, and infections. (For a full list of the markers that the Neural Zoomer Plus measures, click here).�The truth of the matter is that autoimmune disorders affect 5-10% of the general population and can target virtually and structure within the central or peripheral nervous system. Symptoms of an autoimmune disorder involving the CNS/PNS include but are not limited to:�
Cognitive decline
Memory loss
Ataxia
Balance problems
Neuropathy
Alzheimer’s disease
Multiple sclerosis
Encephalitis
Muscle spasms
Huntington’s disease
Epilepsy
Parkinson’s disease
Dementia�
Myasthenia gravis
Muscle stiffness/rigidity�
Optical decline
Neuromyelitis Optica
History of concussion
Autism
PANDAS/ANDAS/OCD
Demyelinating diseases�
�Having the tools to prevent a disease or disorder can be life-changing. With the ability to assess these markers, the rate of cognitive decline can steadily reduce. If you suffer from any of the above symptoms, the Neural Zoomer Plus may be right for you.
The intention of having our patients complete a Neural Zoomer Plus is to help us detect an individual’s IgA, IgG, and IgM sensitivity to antigens, down to the peptide level. Once we receive the results, not only do we have a resource that aids in the early detection of neurological diseases, but we also have a path. This path allows us to create a personalized prevention plan that will focus on the patient along with their lifestyle. – Kenna Vaughn, Senior Health Coach�
The usage of integrated functional medicine is essential when it comes to our bodies overall health. Local practitioners and health coaches, talk with patients on what seems to bother them. Sometimes it is a simple adjustment, but mostly it�s what�s causing them problems on the inside. Some patients have inflammation around their intestinal epithelial barriers, and it can cause a leaky gut.
In the previous article, we talked about what the microbiomes do in our intestines and what is their functions are in the intestinal epithelial barrier. However, today we will discuss what the immunoglobulins antibodies do with proteins and peptides in the intestinal permeability. As well as explaining what the Lectin Zoomer and the Dairy Zoomer does when a patient has a food sensitivity and needs testing in a two-part series about the intestinal permeability and food zoomers.
Contents
Immunoglobulins
The first thing that we need to know is that immunoglobulins are immune-mediated reactions. So anything that involves the immune system will cause a hypersensitivity reaction to one or more food or foreign proteins, and their presence can be of one or more types of immunoglobulins.
There are 3 terms of hypersensitivities that can be involved with immunoglobulins:
Allergies are the ones that are most common and are associated with anaphylaxis. Patients can have a very severe and acute immediate reaction to specific allergens like food or environmental like pollen or a bee sting.
Non-allergies, sensitivity reactions involved either chemical mediators or antibody reactions.
Food intolerances are non-immune-mediated reactions, and a good example is Lactose Intolerance or a bile salt deficiency. These can make somebody who has a food intolerance, can�t digest fat.
These three terms are often mistaken and used interchangeably clinically, but they are entirely different since they are not interchangeable. Especially when it comes to sensitivities and intolerances because those two commonly get used in place of each other, but they are totally different.
If you are testing your patient�s immunoglobulins, remember that antibodies are particular to each type of foreign substances and can be in three types of hypersensitivity. Antibodies will only bind an react to the specific proteins of the foreign material but not to the substance�s extract. The most common ones are type 3, where it involves IgG, IgA, and IgM. This type can tell us what cells and mechanisms are involved.
Type 3 Hypersensitivity Mechanisms
Here are the types of mechanisms that are involved with Type 3 immunoglobulins.
Antigens are a foreign protein that is present and is recognized as a threat or non-self.
Antibodies will bind to the antigen to neutralize or keep it from linking to anywhere else in the body. This is where the immune complex is formed.
Immune complexes insert themselves into the small blood vessel, joints, tissues, and glomeruli, causing symptoms to the body.
They are far more capable of interacting with complement proteins to form medium-sized complexes; which has an excess amount of antigens that are high pathogenic.
However, once the immune complex is in the tissue, it can induce an inflammatory response and cause damage to the body. This damage is the result of the action of cleaved complement anaphylatoxins, which can mediate a mast cell degranulation.
With the recruitment of inflammatory cells in the tissue, it can lead to tissue damage through phagocytosis.
IgA and IgG
In a previous article, we mentioned the mechanics of the intestinal permeability. However, we going to discuss what IgA antibodies and IgG antibodies do to the gut and to the entire body.
IgA Antibodies
IgA antibodies are found in the body where there is a mucosal lining around the areas like the nose, breathing passages, digestive tract, ears, eyes, and vaginal region. These surfaces are exposed to the outside of the environment either by air, food, or other foreign substances regularly.
IgA antibodies actually protect the body surfaces that are exposed to outside foreign substances, and these antibodies can be found in saliva, tears, and blood.
In the gut, however, it can bind to the mucosal layer on the top of the intestinal epithelial cells to form a barrier to neutralizing threats before they reach the cell. And that is very important, especially since IgA is like an insurance policy for your gut.
IgA antibodies are considered as non-inflammatory. Which means that they don�t stimulate inflammatory processes in the body like IgG does. They do, however, create a mucosal response to a foreign antigen, and it is usually microbial (ex., bacteria, yeast, viruses, parasites) or microbial toxins. They can also generate a response to pollutants, toxins, and recognized undigested food as a foreign protein.
In the intestinal lumen, IgA can be indicative of an immune response stimulated by T-b cell interaction. So a healing intervention, if a patient has an abundance of IgA antibodies may need to target TH1 and TH2 balance so it can regulate T-reg production.
IgG Antibodies
IgG antibodies are found in all body fluids. They happen to be the smallest but the most common of all antibodies as they make-ups about 75% to 80% of antibodies found throughout the entire body. These antibodies are essential as they fight against bacterial and viral infections, and they are the only type that can cross the placenta.
They do indicate exposure to a specific antigen, but they don�t always necessarily indicate active inflammation; however, they can contribute to it in a dose-independent.
Why measure IgA and IgG?
So why do we measure IgA and IgG? Surprisingly some people don�t produce as much or any IgA antibodies, and therefore, local practitioners would not know if their patients have formed a reactivity to an antigen if they don�t check their IgG levels.
Surprisingly, some IgG antibodies are not an indicator of actual inflammation or disease process. Some IgG antibodies are formed in response to a protein as sort of a tracker in the body but do not elicit a reaction. However, IgA antibody is coupled with IgG to indicate a bit stronger immune response to an antigen in some cases.
IgA and IgG in the Protein Level
IgA and IgG testing in the protein level is what the food sensitivity tests are looking at. They look for the whole protein, which is the extract level. All food sensitivity test looks for residues of carbohydrate and lipid-based particles. It�s not pure protein but that what the test does, it seems for the reactive compound. Some of the strengths are that the test gives an acute measure of IgG and IgA to a specific protein. It can also be suitable for associating Type 3 reactions involving IgG and IgA complexes, and if the IgG is pathogenic, then it will be beneficial.
Some of the weaknesses are that IgG can be a protective antibody, and it may be a good thing. It means that the immune system is handling it and there�s nothing necessarily wrong about that. IgG and IgA antibodies represent whole proteins being presented to the immune system can it also be an indicator that a patient may have a lack of sufficient digestive capacity when many food sensitivities are being detected.
IgG and IgA in the Peptide Level
When IgG and IgA are being tested at the peptide level, this is where the food zoomer test focuses on. This is because there is a high level of antibodies specificity, cross-reactivity is minimized if not completely eliminated. The concept of foods that are cross-react, for example, gluten, might cross-react to other foods that are similarly shaped in their molecular structure, then you should eliminate the gluten out of your diet as well as the foods that are in contact with them.
However, if the antibodies to gluten are being picked up at the peptide level, then it won�t look at those foods that are being cross-reactive to gluten. The antibodies will only bind to the individual peptides than the whole protein. This will be a more accurate assessment of whether or not that the patient is sensitive to the foods their body is reacting to.
What is Loss of Oral Tolerance?
Loss of oral tolerance is a term used to describe the phenomenon of someone developing a sensitivity, whether it is accompanied by symptoms or not, and it�s usually a commonly consumed or semi-regularly consumed food. When that happens, there is a production of inflammatory cytokines and antibodies that will respond to the continued exposure to the food.
For the inflammatory responses to be eliminated, patients have to remove the offending food for about 3 to 4 weeks if IgA antibodies are present or 3 to 6 months if the IgG antibodies are present as well. This is the only way for the antibodies to disappear, and the intestinal permeability can heal. But the disappearance of antibodies does not guarantee that oral tolerance has been established. If you are retesting a patient and if the antibodies are gone, that indicates that the patient has done an excellent job in eliminating that food from their diet. However, the only way to know is to reintroduce the food and retest after a few months, just to make sure that no antibodies are being produced after the intestinal barrier has been fully healed.
Conclusion
All in all, that is what the intestinal permeability does when we have IgA and IgG antibodies and what do they do when there is food sensitivity in the body.� However, it is crucial that our patients understand that we here at Injury Medical Clinic, take the time to study what causes inflammation in our patients and using integrated functional medicine to make sure that their intestines are being healed naturally. In the next article, we will discuss the difference between peptides and proteins, and about the Lectin and Dairy Zoomer.
Pelvic tilts to gently awaken the transverse abdominals
Side-stretching helps� expand the spine
Stretching the sides of your body allows for space between the ribs.
It alleviates back pain and improves breathing.
As pregnancy advances, the middle area of your body can feel tighter.
This is one reason you may feel out of breath.
My massage therapist shared a stretch that helps to open up this space.
Sit cross-legged and raise both arms toward the ceiling
Put your right hand down and, with the left hand, reach over toward the right side of the room
Repeat on the opposite side
Take deep breaths
The goal is to reach up and over to improve breathing.
Legs up the wall
Your legs, knees, and feet will begin to feel the effects of added bodyweight and pressure.
A restorative yoga pose that involves placing a yoga mat or blanket as a back cushion next to a wall.
Lie on the floor against the wall
Let your legs climb up the wall
Stretch arms outward and turn your palms up
Take deep breaths
This reverses the blood flow and gives your joints a much-needed break.
Hang out and enjoy.
If the back of your legs feel like it’s too much to stretch all the way up, bring the soles of your feet together and let the knees butterfly out to the sides.
Make it a Daily habit
It can be a struggle to do daily stretches and exercises, especially as things get crazier and busier.
But this is what makes these home exercises/tips work.
Get into the habit to make it more personal and make body-care a top priority.
Children and life will try to take over but your wellness needs to come first before the care of others.
Living with back pain is something I would not recommend trying. Instead, see a chiropractor/doctor and learn these exercises and more tips so you can work out the discomfort/pain whenever it presents and enjoy your pregnancy to the fullest.
Lower Back Pain Pregnancy Chiropractic Treatment El Paso, TX
Truide Torres, office supervisor, first considered chiropractic care with Dr. Alex Jimenez throughout her pregnancy as a consequence of her lower back pain. Mrs. Torres experienced aggravating symptoms throughout different stages of her pregnancy, which led her to seek a pure remedy strategy for her well-being, particularly because of her child in the womb. After Truide Torres began chiropractic therapy with Dr. Alex Jimenez, she recovered her overall well-being and managed to go back to her first state of well-being. As a professional manager, Truide Torres additionally receives regular chiropractic care for any lower back pain that might occur as a result of her occupation. Mrs. Truide expresses how important it is to keep her spinal care and she recommends Dr. Alex Jimenez as the non-surgical pick for several health difficulties.
Low back pain, or LBP, is a normal health problem between the muscles, nerves, and bones of the spine. Pain could differ, often called a dull persistent pain or any sudden sharp sense. Low back pain could be classified by length and severity, including acute (pain lasting less than 6 weeks ), sub-chronic (6 to 12 months ), or chronic (over 12 weeks ). The status could be further categorized together with the inherent causes as both bodily, non-mechanical, or referred pain. The signs of lower back pain may generally improve in a couple of weeks, but a few instances may require further treatment. In virtually all episodes of lower back pain, a certain underlying cause is not identified or properly cared for, and health care professionals might feature it to muscle or joint strain.
What’s Afoot
The human body is an intricate machine, and everything is connected so when something goes wrong in one area, it can cause problems in other areas. The back carries a lot of the stress in the body so when there is a problem with the hips, knees, or a foot dysfunction, the spine can bear at least some of the brunt of the pain and other effects.
NCBI Resources
Chiropractic a preferred treatment for pregnancy low back pain. The chiropractor may perform a spinal subluxation to bring the spine back into alignment and the body back into balance. Regular chiropractic care�and following the doctor�s instructions can help greatly decrease low back pain for the mom to be so that she can better enjoy the excitement and joy of her pregnancy.
The Neural Zoomer Plus is a blood test that is designed to test 48 neurological antigens. When testing for these antigens, the results these markers find can help physicians determine if a patient is at risk for neurological conditions later on. To view last week’s article containing a full list of the signs and 48 markers, click here.�
When a patient comes to us with concerns, we listen very intently and make sure our patient’s concerns are addressed. More often than not, patients reveal they are having issues that relate to neurological declines, such as, muscle spasms or memory loss. With symptoms like these, the patient is referred to get a Neural Zoomer Plus.�
Once we receive the results back, it is compiled into a large report. From here, we assess it and go through all of the markers with an additional team of clinicians. An example of a few of the markers tested in a Neural Zoomer Plus is below. One can see that this patient has an elevated �Anti-Voltage gated potassium channel�. Anti- Voltage-gated potassium channels are responsible for multiple cellular processes such as cell growth and differentiation.�
After analyzing the data, we take these findings and create a treatment protocol that is specific to each patient and their lifestyle. Due to the fact that this patient shows an elevation in specific markers, there are certain adjustments we make in order to help prevent or reverse the cognitive and physical effects of neurological disorders.�
The first step we take is to change the diet of the patient. Many foods are not properly digested, leading to gut inflammation, which further leads to �leaky gut� which then enters the bloodstream and into the blood-brain barrier, causing neurological decline. In order to reverse these effects, we want to make sure the gut is getting the proper nutrients from foods that will not cause inflammation. For this patient, we recommend the Wahls Protocol.�
The second step we take is to usually get the patient involved in a more active lifestyle. By having this patient start to exercise with activities like yoga, it can improve the state of mind and their mind-body connection.�
The third step is usually nutraceuticals. These are supplements that will naturally help the body and brain with no addictive or harsh chemicals. With every patient, the nutraceuticals and amount needed vary depending on their specific body. For this case, we recommend:��
N-acetyl-L-cysteine:� (NAC) is a precursor to glutathione, the body�s most important cellular�antioxidant. NAC supplements have been shown to increase cellular glutathione levels.
Vitamins B12, B6, and folate: These are metabolic cofactors important for cellular metabolism and maintenance of all tissue cell types, but particularly important to nerve cells. Deficiencies in�B12 or folate can raise homocysteine levels, which have been associated with a higher risk for�vascular disease and dementia.
Alpha Lipoic Acid:� (ALA) is an essential cofactor in normal cellular metabolism and cellular�energy production.
Vitamin C and vitamin E: Can reverse symptoms caused by vitamin C and E�deficiencies.
As mentioned before, each patient is different and their lab work shows varying needs. However, with the Neural Zoomer Plus, we are able to get ahold of these symptoms, create a personalized treatment plan, and get them under control.�
As one can see, the data and knowledge we gain from these tests are truly eye-opening and give us an early advantage to help reverse or aid in prevention methods. We take the needs and concerns of every patient very seriously and work extremely hard to figure out the right method of treatment for them. Our goal is to help ensure that this lifestyle change is as smooth and easy on the patient as possible so they can get back to enjoying the activities they love and spending time with loved ones. The transition into a new lifestyle can be stressful, but with the information we gain from the tests, the knowledge we use from the doctor, and the willingness to change from the patient, we are set up to be the best team you can have to get your life back! – Kenna Vaughn, Senior Health Coach�
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases. �
An understanding of the mechanisms underlying TBI and neurodegenerative diseases is fundamental to determine the possible connection between these health issues, to allow the safe and effective diagnosis and treatment. In the following article, we discuss the pathological mechanisms of neurodegenerative diseases and how they’re associated with traumatic brain injury (TBI), including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
Contents
Pathological Mechanisms of Neurodegenerative Diseases
Although many neurological diseases may have different symptoms, AD, PD, and ALS have several common characteristics. Each neurodegenerative disease is caused by genetic risk factors, however, most cases are idiopathic or unknown. The pathological mechanisms of these health issues are ultimately characterized by the degeneration of brain cells or neurons together with several common symptoms. Moreover, abnormal clusters or dysfunction of the substances amyloid-? (A?), ?-synuclein, and superoxide dismutase (SOD1) are generally found in AD, PD. Although the exact pathological mechanisms of neurodegenerative diseases have not been fully determined, it has been suggested that oxidative stress, glutamatergic excitotoxicity, and neuroinflammation play fundamental roles in neurological diseases such as AD, PD, and ALS. �
AD has a tremendous prevalence among older adults which can greatly decrease their rate of survival and their overall quality of life. In 2008, as many as 24 million people worldwide had dementia, where most had AD, a number which is expected to double every 20 years as the population ages. The pathological mechanisms of AD include the presence of neuritic plaques and the loss of cholinergic neurons or brain cells in the human brain, however, the underlying risk factors leading to these events are still unclear. Neurodegeneration in AD is believed to happen due to the accumulation of amyloid ?-peptide (A?) in plaques in the brain tissue however its aggregation and toxicity are still completely misunderstood. �
Research studies have demonstrated that oxidative stress may play a fundamental role in the pathogenesis of AD because of increased neurotoxic markers of lipid peroxidation, such as 4-hydroxynonenal, in human participants, increased brain protein oxidation in AD, increased nuclear DNA oxidation in the brain of AD patients, 30 percent increased activity of the free radical scavenging enzyme SOD-1 in cell lines of AD patients, and considerable evidence that beta amyloid creates free radical peptides. In addition, it has been demonstrated that free radicals and lipid peroxidation caused by A? can ultimately result in neuronal death in AD. In vitro and animal research studies have demonstrated that the antioxidant effect of cannabinoids was able to prevent neurodegeneration in the neurological disease, suggesting the role of oxidative stress in AD. �
Neuroinflammation has also been associated wit A? toxicity which has likewise been connected to oxidative stress by inflammatory cytokine activity. The purpose of inflammation is to restore cellular homeostasis and balance redox equilibrium, however, inflammation changes with co-localized A? deposits, inflammatory-related proteins, and activated microglial cells in AD. Microglia and astroglia recognize misfolded proteins which can trigger an immune response that may be responsible for the progression and severity of the neurodegenerative disease. The microglial cells promote A? clearance and support neuroprotective properties in early stages of AD, but as the health issue progresses, inflammatory cytokines downregulate A? clearance genes and promote A? accumulation, ultimately causing neurodegeneration. Moreover, cytokines can trigger the creation of arachidonic acid which aggravates neurodegeneration by increasing extracellular levels of glutamate, known to cause excitotoxicity in AD as well as causing the creation of superoxide free radicals which are responsible for cellular death. Furthermore, research studies suggest that non-enzymatically glycated tau causes oxidative stress which results in cytokine gene expression and release of A?-peptide in AD, demonstrating pathological mechanisms between cytokines and oxidative stress which causes the progression and severity of AD. In addition, oxidative damage from reactive oxygen species and lipid peroxidation products, such as 4-hydroxy-2-nonenal (HNE), can restrict glutamate transporters, causing a decreased glutamate uptake that is fundamental for neuronal survival, an increased glutamate concentration in the synaptic cleft, and subsequent excitotoxicity which ultimately causes neurodegeneration in AD. �
Neurodegenerative Diseases in Functional Neurology
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repeated blunt force impacts to the head with the transfer of acceleration and deceleration forces to the brain or repetitive mild traumatic brain injuries, although the central pathological mechanisms for the development of neurodegeneration in CTE has not been discovered. CTE has been associated with behavioral and personality changes, parkinsonism, and dementia. Research studies demonstrated similarities between CTE and Alzheimer�s disease but these were different in the predominance of tau protein deposition over amyloid. The tau protein deposition in CTE has been previously demonstrated to restrict kinesin-dependent transport of peroxisomes and the loss of peroxisomes makes the cells vulnerable to oxidative stress, ultimately causing neurodegeneration. This tau protein deposition, which occurs in AD, also restricts the transport of amyloid precursor protein (APP) in axons or dendrites, causing its accumulation in the cell body. Along with tau proteins, portions of TDP43, a nuclear RNA/DNA binding protein which controls the transcription of thousands of genes, have been demonstrated in AD, PD, ALS, and CTE, which cause the misfolding of SOD1, affecting the surrounding cells with free-radical damage. The research studies have also demonstrated the purpose of oxidative stress in CTE neurodegeneration and in other neurological diseases. �
Chronic inflammation has also been demonstrated in CTE and AD, which is believed to aggravate neurodegeneration and, as previously mentioned, it is ultimately associated with oxidative stress though inflammatory cytokines. Moreover, it has been demonstrated that after the initial head trauma in CTE, microglia activate and release toxic levels of cytokines and excitotoxins, such as glutamate, where the excitotoxins restrict phosphatases, resulting in hyperphosphorylated tau, neurotubule dysfunction, and neurofibrillary tangle deposition, all of which are fundamental factors of CTE. Research studies have also demonstrated a synergy between proinflammatory cytokines and glutamate receptors which increase reactive oxygen species and worsens neurodegeneration in the injured brain associated with TBI and neurological diseases. �
Parkinson�s disease is the second most prevalent neurodegenerative disease with a prevalence of approximately 0.3 percent of the older adult population. PD is characterized by the development of ?-synuclein rich Lewy bodies and subsequent death of the dopaminergic neurons of the substantia nigra. Several genetic risk factors have also been demonstrated, including mutations to the ubiquitin-proteasome system. Although the pathological mechanisms which trigger dopaminergic degeneration in non-hereditary PD are still unclear, it has been suggested that oxidative modification or carbonylation of the lysine-rich N-terminus and the non-amyloid factor of ?-synuclein may ultimately cause an ?-synuclein aggregation. �
The reactive carbonyls created as secondary products in oxidative stress have been demonstrated to develop lysine adducts and promote ?-synuclein aggregation in vitro. Additionally, animal models of PD utilizing agents, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, have demonstrated the increased development of superoxide in dopaminergic cells associated with the cortex. Furthermore, mitochondrial localization of ?-synuclein has been demonstrated to promote oxidative stress in vitro. Neuroinflammation is believed to be a partial cause for the oxidative stress in PD with activated microglial cells demonstrated in the substantia nigra and striatum of deceased PD patients. Activated microglia were also demonstrated in rhesus monkeys up to 14 years after model induction. In addition, glutamatergic excitotoxicity is believed to play a fundamental role in PD. Rotigotine, an FDA approved dopamine receptor agonist, has been suggested to improve the efficiency of glutamate transporter 1 (GLT-1) and has been demonstrated to support neuroprotection against glutamatergic excitotoxicity in dopaminergic cell culture as well as a variety of other functions in the human brain in Parkinson’s disease. �
ALS is a fatal neurodegenerative disease characterized by the death of motor neurons in the central nervous system (CNS) and it is the most common motor neuron disease. Approximately 10 percent of all ALS cases have been associated with genetic causes while the majority are idiopathic or of unknown cause. Mutations affecting superoxide dismutase (SOD1) are responsible for almost 20 percent of all familial cases, however, this is responsible for only 2 percent of all overall cases. Despite the characterized mutations, the exact pathological mechanisms of ALS have yet to be fully determined. �
Research studies utilizing SOD1 mutant mouse models have demonstrated the development of SOD1 aggregates. Given the fundamental role of SOD1 in detoxification of superoxide radicals, it has been previously mentioned that loss of function could cause increased cellular exposure to reactive oxygen species, however, this hypothesis has been challenged by outcome measures in the normal development of SOD1 deficient mice in the absence of considerable traumatic injuries. Furthermore, research studies demonstrated that SOD1 mutant animals ultimately demonstrated no considerable improvement in symptomatic progression with knockout or coexpression of wild type SOD1 which suggests that the mutation results not in the loss of function but rather in the gain of toxic properties. Research studies in rats and human patients suggest that, similar to ?-synuclein and A?, SOD1 mutation cause the development of potentially cytotoxic protein aggregates even in patients without SOD1 mutations. Additionally, the catalysis changes achieved by several mutant variants causes decreased astroglial reuptake of glutamate through restriction of GLT-1. Riluzole, an FDA approved treatment for ALS, has been suggested to help improve glutamatergic excitotoxicity with increased glutamate uptake through GLT-1 and blockade of sensitive channels. Oxidative stress is also involved in neuronal death and in the progression of ALS. �
Given its fundamental role in maintaining and regulating damage from neuroinflammation and excitotoxicity, it is possible that oxidative stress also plays a fundamental role in the pathophysiology of AD, PD, and ALS in a similar fashion to TBI. As such, addressing oxidative stress in neurodegeneration could serve as an effective treatment strategy in neuroprotection. �
Conclusion
Despite the prevalence of TBI the significant neurological sequelae associated with such injuries, diagnosis, and treatment of TBI remains greatly misunderstood. In addition, the causing factors connected to TBI and neurodegenerative diseases, such as AD, PD, ALS, and CTE, have not been fully determined. Several processes, including oxidative stress and neuroinflammation, have also been found to be common between secondary TBI and several neurodegenerative diseases. In particular, oxidative stress appears to be the key mechanism connecting neuroinflammation and glutamatergic excitotoxicity in both TBI and neurological diseases. It is possible that the oxidative cascade caused by TBI ultimately causes and results in the characteristic pathologies of neurodegenerative diseases through oxidation or carbonylation of essential proteins. �
Due to the high prevalence of TBI and neurodegenerative diseases, the development of new safe and effective treatment approaches for TBI is fundamental. Given the essential role that oxidative stress plays in connecting secondary injury and neurodegeneration, detection of ROS and key byproducts could serve as a method or technique for the diagnosis and treatment of potential cellular damage. Finally, these reactive species may serve as a viable therapeutic target for reducing long-term neurodegenerative disease risk following TBI, helping to reduce the disability and death as well as improve the quality of life of individuals in the United States that suffer from traumatic brain injury (TBI) and other health issues. �
TBI is among one of the most common causes of disability and death among the general population in the United States. According to a variety of research studies, mild, moderate, and severe traumatic brain injury has been associated with neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, as well as a variety of other neurodegenerative diseases. It is fundamental to understand the pathophysiological mechanisms of neurodegenerative diseases while further research studies are still required to determine the association between TBI and neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may cause a variety of neurodegenerative diseases and health issues, such as Alzheimer’s disease (AD). The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. 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 �
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.
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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.
When we look at our patients, we try to figure out what is causing their ailments from living their best lives. Some practitioners would prescribe medications to alleviate pain. While other practitioners will start trying to figure out what is causing the patient to have these ailments. Here at Injury Medical Clinic, we talk to our patients about the importance of functional medicine and how it can benefit them. In this article, we will be discussing Connective Tissue Disorder and how it is linked to wheat-related disorders.
Contents
What is Connective Tissue Disorder?
CTD (Connective Tissue Disorder) is an autoimmune disorder that can affect the connective tissues such as the collagen and elastin in our skins. This disease is highly inflammatory and can occur alongside with other autoimmune diseases, and it is common if families have a history of Connective Tissue Disorder.
About 3% of the population has a connective tissue disorder, and it is most likely to occur in women than men. In fact, women who are diagnosed with connective tissue disorder have a ration of 10:1, compared to men.
CTD includes (but is not limited to) the following conditions:
Systemic Lupus Erythematosus (SLE): SLE is a widespread and chronic autoimmune condition, for unknown reasons, can cause the immune system to attack the body�s own tissue and organs, including joints, kidneys, heart, lungs, brain, blood, and skin.
Sjogren�s Syndrome: This autoimmune disease causes white blood cells to attack moisture-producing glands, such as the tear ducts and salivary glands. This can make it very difficult for the body to produce tears and saliva.
Systemic sclerosis (scleroderma): This condition causes the skin and connective tissue to harden and tighten.
Rheumatoid arthritis (RA): RA is a chronic inflammatory condition and an autoimmune disorder that can generally affect the lining of the joints, but mostly in the hands and feet. Rheumatoid arthritis causes painful swelling that can eventually lead to deformity and erosion in the joints and bones.
Polymyositis: This is a persistent inflammatory muscle disease that causes weakness in the skeletal muscles, which can affect your body movement.
Dermatomyositis: This is an uncommon inflammatory disease that is marked by muscle weakness and can cause a distinctive skin rash.
These conditions can group together and can be very hard to diagnose because of the research and many tests that the patient is taking. Surprisingly, the average patient suffers from symptoms for 3.6 years before meeting diagnostic criteria. And the systems alone are difficult to classify, and often mimic or overlap other conditions. Some of the symptoms include hair loss, muscle pain, numbness or tingling, inflammation, low-grade fever, weakness and fatigue, joint pain, sensitive skin, and rashes.
Increased Need For Advanced Testing and Early Diagnosis
Sadly though, patients wait longer when they have these conditions, and it can worsen in the process as it takes years to get diagnosed for CDT. Practitioners can use treatments on their patients, but the medications act as a band-aid to mask the symptoms, but it does not adequately address the root causes of the disease. Sometimes the symptoms can progress faster than the current diagnostic test. So if you want to make sure your patients have any autoimmune diseases, run a diagnostic test on them, so you can detect early stages of the disease and start treating them so it can go away.
ENA and ANA
Extractable nuclear antigen (ENA) is a blood test that looks for antibodies to about 6 or 7 different proteins in the body.Antinuclear antibody (ANA) is used as an initial test that can help evaluate a person for an autoimmune disorder that can affect many tissues and organs throughout the body. It is most often used when practitioners are diagnosing patients for systemic lupus erythematosus.
Surprisingly ENA can be more predictive than ANA. However, patients were followed for 2 years, and about 20% of those patients developed positive ENA.
Vibrant Wellness Wheat Zoomer
In�a�previous article, we talked about gluten sensitivity and introduced the wheat zoomer. What the Vibrant Wheat Zoomer does is that it actually runs a test on your microbiomes to determine if you have a wheat sensitivity or a gluten sensitivity. It can actually detect IgG and IgA antibodies as well as detecting if your body has the celiac disease and intestinal permeability.� It pairs well with the Vibrant Gut Zoomer, and here at Injury Medical, we use the Wheat Zoomer on our patients to inform them about what is causing them to have gut inflammation or even leaky gut.
Celiac Disease and Wheat Allergens
Celiac Disease and Wheat Allergens is an autoimmune disorder in genetically susceptible individuals, and it affects about 1% of the population. In a previous article, we mentioned the hidden problems that gluten does to the body. And surprisingly, any wheat-related disorders can exist on a spectrum, this includes wheat allergy, gluten sensitivity, and wheat sensitivity.
When a person, has the celiac disease, having any traces of wheat can actually upset their intestinal permeability and causing them to have a leaky gut.
The Connection to CTD and Celiac Disease
But how do connective tissue disorder and celiac disease are connected? Well, surprisingly, Rheumatoid arthritis (RA) and celiac disease (CD) share multiple aspects in epidemiology and clinical manifestations. Both disorders have been proven to be influenced by comparable environmental factors and a recent incidental surge of associated antibodies. Even though they have different depositions, both of them are mediated by endogenous enzymes that target different tissues and organs.
Conclusion
However through functional medicine; local chiropractors and health coaches here at Injury Medical Clinic, strive to understand what do our patients need to make their bodies feel better. If we can use functional medicine to prevent leaky gut at the early stages and help our patients with any ailments that they may have, then we can gently push them into the right direction of exercising throughout the week (even if it is about thirty minutes) and eating nutritious, whole, organic foods; as well as, preventing their ailments coming back then their bodies can finally heal.
Piriformis syndrome will cause dull, mild pain in the low back, buttocks and can radiate down the leg.
Hip pain attributed to avascular necrosis will be severe and constant.
Sacroiliac joint pain could be attributed to the hip and the low back because the sacroiliac joints connect the sacrum in the spine to the hip bones.
Symptoms that the Spine Is the Root
Where groin pain is a sign that the pain is linked to the hip when the pain is above the waistline and travels down the body usually indicates a low back issue.
Among the most common degenerative conditions that affect the lumbar spine are:
Herniated discs
Spinal stenosis
Spondylolisthesis
Pain is caused by irritating the low back nerves, which result in pain shooting down the leg/s and:
Weakness
Numbness
Reduced range of motion
Arthritis of the spine brings on pain usually when first getting out of bed or rising up after sitting.
It usually improves after beginning to move.
Spinal stenosis or nerve pressure compression pain worsens with prolonged standing or walking, while relief comes with sitting.
Getting to the Root
When there is pain in the lower body and are not sure whether it’s the back or hip, the first course of action is to visit your doctor or a chiropractor.
They will review your medical history and perform a series of physical exams, such as various movements to get an idea of what is going on.
Your primary doctor may refer you to a doctor/chiropractor who specializes in hip or spinal conditions to make an accurate diagnosis.
The doctor will ask you to describe the:
Pain
Location
When it worsens
When it’s relieved
What the pain feels like (e.g., sharp, dull).
The doctor may have you perform various movements to observe your biomechanics.
The goal is to determine what movements trigger the pain.
For both spine and hip pain, surgery is rarely necessary and only utilized as the last-resort option.
Labrum Tear Hip Treatment El Paso, TX Chiropractor
Andrew Hutchinson turned into chiropractic care and Crossfit rehab after suffering a high ankle sprain and a hip labrum tear for which he moved through with surgery to repair it. After being bedridden for weeks so as to correctly recuperate, Andrew Hutchinson transitioned to chiropractic care and Crossfit rehab to regain his strength, freedom, and flexibility before returning to perform. Although he has suffered other sports accidents, Andrew Hutchinson continues to trust in chiropractic care and Crossfit rehab to keep his spine properly aligned and maintain overall health and wellbeing.
Labrum tears in athletes may occur from a single event or recurring trauma. Running may lead to labrum tears as a result of labrum being used more for weight-bearing and taking excessive forces while at the end-range motion of the leg. Sporting activities are likely causes, especially the ones that require frequent hip rotation or pivoting to some wealthy femur as in ballet or hockey. Continuous hip rotation places increased pressure on the capsular tissue and injury to the iliofemoral ligament. This then causes hip instability placing increased stress on the labrum and resulting in a cool labrum tear.
What’s Afoot
Muscle imbalances in the hip, such as tight hip flexors, can cause low back pain � or at least contribute to it. When the hip flexor muscles are too tight, it causes what is known as an anterior pelvic tilt. In other words, the muscles cause an anterior pull on the pelvis. This affect posture and throws the entire lower body out of alignment. It can also affect the knees and feet if left untreated.
NCBI Resources
Hip flexors can become too tight if the person sits for extended periods of time or engages in activities like cycling and jogging. A chiropractor can guide you through exercises that will help release the tight muscles and stop the micro spams that occur as a result. They will also assess your knees, feet, and ankles to ensure that the issue has not through them out of alignment as well. Correcting the cause of the problem will often correct the associated issues and resolve the pain allowing you to return to your normal activities.
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases. �
A better understanding of the mechanisms underlying TBI and neurodegenerative diseases is ultimately fundamental to determine the possible connection between these health issues to allow safe and effective diagnosis and treatment. In part 1 of the following article, we will discuss the pathological mechanisms of traumatic brain injury (TBI) and how it’s associated with the development of a variety of neurological diseases and other health issues, including Alzheimer’s disease (AD). �
Contents
Pathological Mechanisms of Traumatic Brain Injury
In most instances, TBI is caused by a physical blow to the head during traumatic events, such as falls, automobile accidents, or sports-related accidents, although TBI may also be aggravated by exposure to explosive blasts. TBI can be characterized as mild, moderate, or severe according to the symptoms, such as the length of loss of consciousness and post-traumatic amnesia. Mild TBI (mTBI) is prevalent in the majority of cases, however, it may be difficult to diagnose. This difficulty in diagnosis can be a serious concern as a result of severe consequences like instant impact syndrome or other health issues. �
Damage to the nervous tissue can be characterized as the main injury which happens as a direct effect of a physical blow and secondary injury which happens due to pathophysiological processes subsequent to the traumatic event. The injury process occurs from the rapid acceleration-deceleration of the brain which is believed to harm the brain by causing sheer force within tissue resulting in impact and axonal injury with the cranial wall. These injuries can be contralateral or ipsilateral to the physical blow. In more severe instances, the injury may cause intracranial hypertension and intracranial hemorrhage. This increase in pressure not only damages brain tissue but it also causes potential injury and cerebral hypoperfusion. �
Secondary injury in TBI generally happens several days, weeks, and even months following the traumatic circumstance because of the biochemical changes which occur in the nervous tissue. This harm is often mediated by free radicals and reactive oxygen species (ROS) which develop from ischemia-reperfusion damage, glutamatergic excitotoxicity, or neuroinflammation. After the injury, axonal damage from the sheer force of injury can affect membrane balance. Moreover, uptake of calcium through either membrane disruption or activation of the NMDA and the AMPA receptors by glutamate could ultimately cause mitochondrial dysfunction as well as the overproduction of free radicals and the activation of apoptotic caspase signaling. Following inflammatory processes associated with TBI, such as the activation of microglial cells, can cause oxidative stress through the effects of inflammatory cytokines. These radicals can also cause cellular damage through lipid peroxidation and protein modifications which can overwhelm endogenous antioxidant systems. The secondary products of free radical-mediated lipid peroxidation, such as reactive carbonyl species, can also be electrophilic and can further propagate oxidative damage to biomacromolecules, which can be associated with various neurological diseases. �
Clinical and preclinical research studies have demonstrated the presence of oxidative stress and its byproducts following TBI with both serological and histological methods and techniques. In animal research studies, these products have been demonstrated to continue over a recurrent injury and it may increase following a single traumatic event. Spectroscopic evaluations suggest that the endogenous antioxidants glutathione and ascorbic acid may decrease for 3 to 14 days following the injury. Furthermore, the increase of F2-isoprostane, a lipid peroxidation byproduct, was demonstrated in the cerebrospinal fluid of severe TBI patients with increased levels at 1 day following the injury, however, this was primarily an assessment of alternative treatment and didn’t establish a contrast with healthy controls. Lipid peroxidation products like 4-hydroxynoneal were also found to be elevated in the serum of acute TBI patients needing treatment. Although chronic oxidative stress has not currently been detected following single mild injuries in people, it seems possible that oxidative stress and its associated processes may aggravate or prolong post-concussive symptoms. Given the involvement of oxidative stress in excitotoxicity and reperfusion injury, it’s possible that oxidative stress plays a role in cerebral injury after TBI. �
The pathological mechanisms of secondary TBI are particularly interesting due to the ability to prolong cellular injury beyond the initial traumatic event. Some of these characteristic modifications, such as oxidative stress and excitotoxicity, have also been demonstrated in the pathophysiology of neurodegenerative diseases and other health issues which also suggests a possible pathological mechanistic connection between TBI and neurological diseases. Further research studies of the pathological mechanisms in cerebral diseases and TBI may help determine the factors for neurodegenerative diseases. �
Conclusion
Despite the prevalence of TBI the significant neurological sequelae associated with such injuries, diagnosis, and treatment of TBI remains greatly misunderstood. In addition, the causing factors connected to TBI and neurodegenerative diseases, such as AD, PD, ALS, and CTE, have not been fully determined. Several processes, including oxidative stress and neuroinflammation, have also been found to be common between secondary TBI and several neurodegenerative diseases. In particular, oxidative stress appears to be the key mechanism connecting neuroinflammation and glutamatergic excitotoxicity in both TBI and neurological diseases. It is possible that the oxidative cascade caused by TBI ultimately causes and results in the characteristic pathologies of neurodegenerative diseases through oxidation or carbonylation of essential proteins. �
Due to the high prevalence of TBI and neurodegenerative diseases, the development of new safe and effective treatment approaches for TBI is fundamental. Given the essential role that oxidative stress plays in connecting secondary injury and neurodegeneration, detection of ROS and key byproducts could serve as a method or technique for the diagnosis and treatment of potential cellular damage. Finally, these reactive species may serve as a viable therapeutic target for reducing long-term neurodegenerative disease risk following TBI, helping to reduce the disability and death as well as improve the quality of life of individuals in the United States that suffer from traumatic brain injury (TBI) and other health issues. �
Traumatic brain injury is among one of the most prevalent causes of disability and death among the general population in the United States. According to a variety of research studies, mild, moderate, and severe traumatic brain injury has been associated with neurodegenerative diseases, such as Alzheimer’s disease, as well as a variety of other neurological diseases and health issues. It is fundamental to understand the pathophysiological mechanisms of traumatic brain injury while further research studies are still required to determine the association between TBI and neurodegenerative diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may cause a variety of neurodegenerative diseases and health issues, such as Alzheimer’s disease (AD). The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. 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 �
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
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.
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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.
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About 3% of the population has a connective tissue disorder, and it is most likely to occur in women than men. In fact, women who are diagnosed with connective tissue disorder have a ration of 10:1, compared to men.
CTD includes (but is not limited to) the following conditions:
Sadly though, patients wait longer when they have these conditions, and it can worsen in the process as it takes years to get diagnosed for CDT. Practitioners can use treatments on their patients, but the medications act as a band-aid to mask the symptoms, but it does not adequately address the root causes of the disease. Sometimes the symptoms can progress faster than the current diagnostic test. So if you want to make sure your patients have any autoimmune diseases, run a diagnostic test on them, so you can detect early stages of the disease and start treating them so it can go away.
When a person, has the celiac disease, having any traces of wheat can actually upset their intestinal permeability and causing them to have a leaky gut.
