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Nerve Injury

Nerve Injury: Nerves are fragile and can be damaged by pressure, stretching, or cutting. Injury to a nerve can stop signals to and from the brain, causing muscles not to work properly, and a loss of feeling in the injured area.The nervous system manages a great majority of the functions of the body, from regulating an individual’s breathing to controlling their muscles as well as sensing heat and cold. But, when trauma from an injury or an underlying condition causes nerve injury, an individual’s quality of life may be greatly affected. Dr. Alex Jimenez explains various concepts through his collection of archives revolving around the types of injuries and condition which can cause nerve complications as well as discuss the different form of treatments and solutions to ease nerve pain and restore the individual’s quality of life. For more information, please feel free to contact us at (915) 850-0900 or text to call Dr. Jimenez personally at (915) 540-8444.


Functional Neurology: Brain Fog and Vision Problems

Functional Neurology: Brain Fog and Vision Problems

Have you been experiencing noticeable variations in your mental speed? Do you suffer from pain, discomfort, and inflammation? Have you been experiencing fatigue, especially after meals or exposure to chemicals, scents, or pollutants? If you answered yes to any of the previous questions, you may be experiencing brain fog, unclear thoughts or concentration.  

 

Brain fog is a well-known symptom associated with a variety of health issues. It can affect many brain functions, including memory and concentration. It can occur as a result of poor lifestyle habits, including stress, an unhealthy diet, and lack of sleep, or due to other health issues, including multiple sclerosis and chronic fatigue syndrome. Moreover, brain fog can be accompanied by other symptoms like vision problems. In the following article, we will discuss brain fog and vision problems.  

 

What is Brain Fog?

 

Brain fog can make a person feel as if the processes of thinking, understanding, and remembering are not working as they should. It can affect memory, the ability to process and understand information, visual and spatial skills, the ability to calculate and solve problems as well as executive functioning. If these essential brain functions don’t work efficiently, it can become challenging to understand, focus, and even remember simple things. It can ultimately lead to stress and fatigue.  

 

A variety of health issues can lead to brain fog. People with multiple sclerosis (MS) may experience changes in their ability to make decisions as well as to process and recall information. These changes are generally mild or moderate and they do not affect a person’s ability to live independently. However, they can be frustrating and these can make it difficult to complete regular tasks. Fibromyalgia can also affect a person’s concentration and memory. Chronic fatigue syndrome (CFS) is another chronic, or long-term, health issue that can result in brain fog, fatigue, and other symptoms, such as vision problems.  

 

Changes to a person’s hormone levels can also affect brain function, especially during pregnancy or menopause. A 2013 research study found that hormonal changes throughout a woman’s menopausal transition made it difficult for women to learn or retain new information and to focus on challenging everyday tasks. Hypothyroidism and Hashimoto’s disease can cause hormone imbalances. Memory and thinking problems similar to brain fog are also common in thyroid disorders.  

 

Depression is a mood disorder that affects how a person thinks and feels. Problems with memory, focus, and decision-making can contribute to brain fog. There may also be problems with sleeping and a lack of energy, which can make concentrating and completing everyday tasks much more challenging. Stress and anxiety can also make it difficult to think clearly.  

 

Vision Problems and Brain Fog

 

Many people with brain fog due to multiple sclerosis (MS) or chronic fatigue syndrome (CFS) also experience vision problems. Healthcare professionals believe that vision problems associated with CFS and other health issues are caused due to brain dysfunction rather than eye dysfunction. Our brain constantly transmits signals into our eyes which allows us to know where we are as well as what it is that you’re seeing. The brain is also in charge of controlling the eye reflexes, including pupil dilation due to light and dark changes. However, these brain and eye functions may not work properly with brain fog.  

 

Most frequently, patients with brain fog experience vision problems where their environment appears to be blurry or it seems to be foggy. According to Dr. Peter Rowe, director of the Chronic Fatigue Clinic at Johns Hopkins Children’s Center in Baltimore, these vision problems most frequently occur when standing up, making the patients also feel lightheaded.  

 

Furthermore, other vision problems that CFS and MS patients commonly experience with brain fog, ultimately include:  

 

  • Difficulty when focusing on objects, generally those which are close up
  • Inability to see objects in peripheral vision, as though they have tunnel vision
  • Dizziness and being unable to look at moving objects without feeling dizzy
  • Seeing an excess amount of “floaters” and/or “flashes of light” in their vision
  • Intolerant to light or feeling discomfort in bright rooms and outdoors in the sunshine
  • Feeling as though the eyes are dry or as though they’re itchy, gritty, or burning

 

Proper Health Care with Brain Fog and Vision Problems

 

People with brain fog and vision problems associated with CFS, MS, or any other health issue will commonly visit an optometrist or ophthalmologist. However, an eye exam will generally return as “normal”. In addition, prescription lenses may not help because of rapid vision changes. If you do wear glasses, tints may ultimately help reduce sensitivity to light.  

 

Because blurred or foggy vision is the most common problem associated with brain fog, researchers and healthcare professionals believe that improving blood flow to the brain can help improve symptoms. Treating any underlying health issues and/or practicing proper lifestyle habits, such as eating a healthy diet, engaging in exercise or physical activity, and sleeping properly can help promote proper blood flow to the brain and ultimately improve brain fog and vision problems.  

 

Blurry or foggy vision, among other vision problems, are frequently believed to be a temporary symptom and are more associated with lightheadedness and blood flow to the brain. You may need to see a cardiologist or a neurologist to treat lightheadedness or dizziness. If you have chronic fatigue syndrome (CFS), multiple sclerosis (MS), or any other health issue where you find that you can’t tolerate bright light, you should wear sunglasses when you’re outdoors in the sunshine.  

 

El Paso Chiropractor Staff and Doctor

Brain fog commonly includes feelings of confusion and disorientation, where it can make a person have difficulty thinking, understanding, and even remembering basic information. Brain fog is a symptom, rather than a single disorder, associated with vision problems and other health issues like CFS and MS. Researchers and healthcare professionals believe that because brain fog can ultimately affect brain function, it can also affect essential eye reflexes responsible for these well-known vision problems, among other symptoms, including fatigue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Neurotransmitter Assessment Form

 

Neurotransmitter Assessment Form AE260 (1)

 

The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms 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.  

 

Have you been experiencing noticeable variations in your mental speed? Do you suffer from pain, discomfort, and inflammation? Have you been experiencing fatigue, especially after meals or exposure to chemicals, scents, or pollutants? Brain fog is a symptom that can affect many brain functions, including memory and concentration. It can also be accompanied by other symptoms like vision problems. In the article above, we discussed brain fog and vision problems.   The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or 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:  

 

  • Sissons, Claire. “Brain Fog: Multiple Sclerosis and Other Causes.” Medical News Today, MediLexicon International, 12 June 2019, www.medicalnewstoday.com/articles/320111.php#1.
  • Orenstein, Beth W. “When Chronic Fatigue Syndrome Harms Vision.” EverydayHealth.com, Everyday Health, 4 March 2010, www.everydayhealth.com/chronic-fatigue-syndrome/vision-problems.aspx.

 


 

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

 

Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Brain Fog, Depression, and Fatigue

Functional Neurology: Brain Fog, Depression, and Fatigue

Are you constantly feeling exhausted? Have you been noticing any mood changes? Do you struggle to focus on regular tasks? Brain fog, which often includes depression and fatigue, is a health issue that can have consequences on all facets of your life.  

 

Why Depression Causes Fatigue

 

Depression is just one of the most frequent mental health issues in the United States. Some symptoms, which may stem from depression, are excessive feelings of guilt, hopelessness, insomnia, and fatigue as well as brain fog, among others.  

 

Depression, brain fog, and fatigue, or chronic tiredness, can frequently go hand in hand. It is a vicious cycle: brain fog makes you spend energy for you to make it through the day, which in turn, makes you feel even more tired when you also have depression. Then when you’re feeling unproductive, it worsens your depression even more and it can affect your sleep.  

 

The direction of causality has not been ascertained but researchers have found definite links between inflammation, brain fog, and depression. These links can go beyond just the cognitive and psychological aspects of depression and brain fog.  

 

Other health issues that can involve autoimmune and/or inflammatory processes also correlate with brain fog, including chronic fatigue syndrome, fibromyalgia, or rheumatoid arthritis. Therefore, several healthcare professionals and researchers now believe that inflammation may be a significant origin of depressive symptoms, although not the sole one.  

 

Understanding Brain Fog

 

We hear the term brain fog a lot nowadays but what exactly is brain fog? Brain fog isn’t a health issue on its own but rather a symptom of several different health issues. It’s a collection of symptoms, such as lack of motivation, irritability, inability to focus, and memory problems. It may generally feel like you’re losing control of your brain or your overall health and wellness.  

 

If you’ve ever experienced brain fog, you will know that its intensity may differ from day to day, even from one moment to the other. It may also ultimately feel almost as if the exterior world is moving too quickly for you to keep up with it.  

 

It can also become extremely frustrating if you can’t recall an ideal word during a conversation or in the event that you forget if you’ve locked the door in the morning. You must understand that it’s brain fog and know that it’s not who you really are. However, with long-standing depression, it may also begin to feel as if you’ve just become lethargic and slow.  

 

Health issues, such as brain fog, can be caused by several different physical and mental health issues. It can be difficult to explain to others that you’re feeling fatigued since it’s often simply mistaken for being tired after a long day of work.  

 

But fatigue is much more than just being tired. People experiencing fatigue feel tired even after mild exertion. Getting through an average day appears to be a marathon. And waking up feeling unrefreshed is a major indicator that your feelings of fatigue can possibly be a much more intricate health issue associated with inflammation, brain fog and depression.  

 

Why Depression Causes Brain Fog

 

Because brain fog can be an indication of many different health issues and not just depression, the relationship between both is not entirely clear. Depression disturbs the balance of the “feel good” chemicals in the brain, known as dopamine, which can also result in a chronic sense of sadness and lack of health and wellness. But that is not the whole story.  

 

Your upbringing can also set you up with a lack of self-compassion, which the helplessness of brain fog amplifies. Research studies show that these states can relate to elevated inflammatory chemicals that make you feel much more brain fog.  

 

Another cause of brain fog includes depression medicines, like antidepressants. The purpose of these drugs and/or medications is to relieve depression symptoms and re-establish the balance of chemicals in the brain.  

 

However, these medicines appear to contribute to brain fog as a side-effect due to the biochemical changes which they cause in the mind. If you feel that your antidepressants may be the actual culprit, it may be well worth monitoring when you experience a brain fog episode. Tracking your symptoms, in general, can help you figure out ways to counter brain fog.  

 

Research shows that depression negatively affects the brain’s reward system by changing the amount of dopamine, a neurotransmitter involved in feelings of pleasure, reward, and motivation. A reward system that is disrupted can ultimately make it difficult to find the point in spending some energy to perform or participate in regular everyday activities.  

 

Insomnia, which is distinguished by difficulty falling or staying asleep, is closely related to depression. This usually means that the probability of depression raises since it deprives us of the physical repairs of sleep and power. And having depression, in turn, makes it difficult to get a good night’s sleep because of the cycle of unwanted thoughts. The end-product is, as you may have guessed, unbeatable tiredness or fatigue. After all, brain fog, depression, and fatigue all seem to be connected.  

 

El Paso Chiropractor Staff and Doctor

Brain fog is closely associated with both depression and fatigue. Being open and honest about your symptoms can be a fundamental step in your recovery process. Although inflammation is the human body’s immune response to injury, infection, or illness, too much inflammation can actually cause a variety of health issues. Evidence from research studies has demonstrated that inflammation can ultimately be associated with brain fog, depression, and even fatigue symptoms. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Neurotransmitter Assessment Form

Neurotransmitter Assessment Form AE260 (1)

 

The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms 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.  

 

Are you constantly feeling exhausted? Have you been noticing any mood changes? Do you struggle to focus on regular tasks? Brain fog, which includes depression and fatigue, is a problem that can affect your overall health and wellness. 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  

 


 

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

  Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Understanding Inflammation and Brain Fog

Functional Neurology: Understanding Inflammation and Brain Fog

Is your memory noticeably declining? Are you having a hard time remembering names and phone numbers? Or is your ability to focus noticeably declining? If you’ve experienced any of these situations, you may ultimately be experiencing brain fog.  

 

What is Brain Fog?

 

Brain fog is not a health issue but rather a symptom of other injuries or conditions. It is a cognitive dysfunction involving:  

 

  • memory problems
  • lack of mental clarity
  • poor concentration
  • inability to focus

 

Several people can also experience brain fog as mental fatigue. Based on the seriousness of brain fog, it may ultimately interfere with work, school, or any other regular tasks. However, it doesn’t have to be a permanent problem in your lifetime.  

 

What Causes Brain Fog?

 

There are many reasons why brain fog happens. By identifying the underlying reason, you may fix the health issue.  

 

Stress

 

Chronic stress can raise blood pressure, weaken the immune system, and trigger anxiety, depression, and other mood changes. It can also result in fatigue. It becomes more difficult to think, reason, and focus when your mind is tired.  

 

Lack of Sleep

 

Poor sleep quality may also interfere with how well your brain works. Try to get between 8 to 9 hours of sleep each night. Lack of sleep, or sleeping too little. may ultimately lead to poor concentration and cloudy thoughts, among other symptoms.  

 

Hormonal Changes

 

Hormonal changes can also activate brain fog, including increased levels of estrogen and the growth of the hormones progesterone. Memory can also be affected by hormonal changes and may cause short-term cognitive impairment.  

 

Similarly, a drop in estrogen levels during menopause can cause forgetfulness, poor concentration, and cloudy thinking.  

 

Diet

 

Diet may also play a part in brain fog. Vitamin B-12 supports healthy brain function and a vitamin B-12 deficiency can result in brain fog. Similar to food allergies or sensitivities, brain fog can also develop after eating particular foods, including:  

 

  • MSG
  • aspartame
  • peanuts
  • dairy

 

Eliminating trigger foods out of your diet and consuming more anti-inflammatory foods can ultimately improve symptoms.  

 

Medications

 

If you begin to experience brain fog whilst taking any types of drugs and/or medications, talk to your doctor. Brain fog may be a side effect. Reducing your dosage or switching to different medications may also help improve your symptoms.   Moreover, brain fog can also happen after certain cancer treatments. This is most commonly known as the chemo brain.  

 

Other Health Issues

 

Other health issues associated with inflammation, fatigue, or changes in blood sugar levels, can also cause brain fog as well as mental fatigue. By way of instance, brain fog is a symptom of chronic fatigue syndrome, which involves mental fatigue.   People who have fibromyalgia can also experience brain fog. Other health issues that may cause brain fog includes:  

 

  • anemia
  • depression
  • diabetes
  • Sjögren syndrome
  • migraines
  • Alzheimer’s disease
  • hypothyroidism
  • autoimmune diseases, such as lupus, arthritis, and multiple sclerosis
  • dehydration

 

Brain Fog Diagnosis and Treatment

 

Talk to your doctor if you have a persistent absence of clarity that worsens or doesn’t improve. A test can’t diagnose brain fog. Brain fog may indicate an underlying problem. Your doctor will conduct a physical examination and discuss your:  

 

  • mental health
  • diet
  • level of physical activity
  • current medications or supplements

 

You should tell your doctor about any other symptoms you may have. By way of instance, people with hypothyroidism may also have weight gain, dry skin, and hair loss. Blood work can also help identify brain fog. A blood test can also determine:  

 

  • abnormal glucose levels
  • poor liver, kidney, and thyroid function
  • nutritional deficiencies
  • infections
  • inflammatory diseases

 

Based on the results, your doctor will decide whether to investigate the diagnosis further. Diagnostic tools may include imaging tests to look within the body, such as X-rays, MRI, or CT scans. The doctor can also conduct allergy testing or a sleep study to check for a sleeping disorder. Keeping a food diary can help you determine if your diet contributes to brain fog.  

 

Brain fog treatment is dependent upon the cause. By way of instance, if you are anemic, iron supplements may boost your production of red blood cells and reduce your brain fog. If you’re diagnosed with an autoimmune disorder, your doctor may suggest a corticosteroid or alternative medication to help decrease inflammation or to suppress the immune system.  

 

Furthermore, relieving brain fog may ultimately be an easy matter of simply correcting a nutritional deficiency, altering medications, or even improving the quality of your sleep. Home remedies to help improve brain fog can include:  

 

  • sleeping 8 to 9 hours per night
  • managing stress by knowing your limitations and avoiding excessive alcohol and caffeine
  • exercising
  • strengthening your brainpower (try volunteering or solving brain puzzles)
  • finding enjoyable activities
  • increasing your intake of protein, fruits, vegetables, and healthy fats

 

El Paso Chiropractor Staff and Doctor

Brain inflammation has been associated with a variety of symptoms, including brain fog. Inflammation is an essential function of the immune system, however, excess brain inflammation, can cause brain fog and a variety of other symptoms. In the following article, inflammation and brain fog, can be caused due to a variety of causes. Although brain fog may be a frustrating symptom, relief is possible with proper treatment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Neurotransmitter Assessment Form

Neurotransmitter Assessment Form AE260 (1)

 

The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms 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.  

 

Has it become harder for you to learn new things? How often do you have a hard time remembering your appointments? Or is your temperament generally getting worse? If you’ve experienced these situations, you may have brain fog. 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  

 


 

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

Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

 

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Brain Inflammation and Depression

Functional Neurology: Brain Inflammation and Depression

According to the World Health Organization, depression is one of the main causes of disability worldwide. Moreover, approximately 30 percent to 60 percent of patients don’t respond to the currently available antidepressant treatments. That means that about 40 percent to 70 percent of patients aren’t being helped by existing antidepressant treatments. One region of research studies can ultimately shed some light on why many patients are not helped by antidepressants.  

 

Neuroinflammation and Mood Changes

 

Increasing evidence from these research studies shows that brain inflammation can aggravate or even increase symptoms of depression. Inflammation is a fundamental part of the immune system. When the human body is affected by toxins, bacteria, viruses, or parasites, the immune system recruits cells, proteins, and other structures, to attack these invaders. The main purpose is to indicate the injured body parts so that we can pay more attention. Inflammation makes affected body parts reddish, swollen, and hot. After the injury isn’t localized, then the nervous system can become inflamed. Neuroinflammation can ultimately contribute to “mood changes.” These can also include cognitive, physical, and behavioral changes.  

 

Generally, people with depression experience sleepiness, fatigue, slow response time, cognitive impairments, and loss of sexual desire. This collection of changes causes people to want to get more sleep to heal themselves and remain isolated so as to not spread infections. However, prolonged inflammation can wreak havoc in the human body and it can increase the risk of depression and other illnesses. Increased evidence shows the link between brain inflammation and depression.  

 

By way of instance, markers of inflammation are increased in people who suffer from depression in contrast to non-depressed types, according to research studies. Furthermore, indicators of inflammation may also predict the intensity of gastrointestinal tract symptoms associated with depression. A research study that examined twins which share 100 percent of the same genes found that the twin who had a greater CRP concentration, a common measure of inflammation, was more prone to develop depression five years later. Doctors also noticed that cancer and Hepatitis C patients treated with IFN-alpha treatment, which increases the human body’s inflammatory response, also suffered from depression later in life.  

 

This treatment increased the discharge of pro-inflammatory cytokines, which increased the reduction of appetite, sleep disturbances, anhedonia or lack of enjoyment, cognitive impairment, and suicidal ideation, according to research studies. The incidence of depression in these patients has increased. Additionally, these results provided further evidence for the connection between inflammation and depression. Subsequent, careful research studies also demonstrated that the increase in the prevalence of depression in patients treated with IFN-alpha was not only due to the previously presented problem.  

 

Depression and Brain Inflammation in Functional Neurology

 

Utilizing a very simple way of injecting healthy subjects with immune system invaders, researchers found higher levels of depressive symptoms from the ones who were more vulnerable compared to the placebo group. The subjects that were provided with an inflammatory response complained of symptoms, such as negative mood, anhedonia, sleep disturbances, social withdrawal, and cognitive impairments. The link between inflammation and depression is much more powerful for patients that don’t respond to current antidepressant treatments. Various studies have revealed that treatment-resistant patients tend to have elevated inflammatory aspects circulating at baseline compared to responsive ones.  

 

This is clinically significant because a clinician can utilize CRP levels, which are part of a regular physical exam, to predict the treatment response to antidepressants. In one research study, they found that increased levels of an inflammation molecule before treatment predicted poor response to antidepressants. There are environmental factors that cause inflammation and increase the risk of depression, including stress, low socioeconomic status, or even a troubled childhood. Additionally, an increased inflammatory response leads to greater sensitivity to stress. The result was reported in research studies in mice.  

 

By way of instance, mice that have gone under chronic unpredictable stress have higher levels of inflammation markers. Surprisingly, there are individual differences that make some mice resistant to stress, therefore, initiating a calmer immune response. Depression is a heterogeneous disorder. Each individual’s struggle is unique given their youth, genetics, the sensitivity of their immune system, other existing bodily illnesses, and their current status in society. Being around the disadvantageous end of the dimensions disrupts our immune system and causes chronic inflammation.  

 

The mind is very responsive to those circulating inflammatory markers and initiates “illness behavior”. When the inflammation is prolonged by stressors or other vulnerabilities, the illness behavior becomes depression. If you are a healthcare professional working with people that have depression, it’s fundamental to look at the health of the patients’ immune systems. If you are a patient experiencing an exaggerated immune disorder (e.g., arthritis), don’t discount the depressive symptoms that you might be experiencing. If you are currently suffering from depression, prevent anything that might exacerbate your reaction. After all, treating the root of the health issue may ultimately improve depression.  

 

El Paso Chiropractor Staff and Doctor

Brain inflammation has been associated with a variety of signs and symptoms, including mood changes like anxiety and depression. Inflammation in the brain can also cause a variety of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. Inflammation is an essential function of the immune system, however, excess brain inflammation, can cause anxiety, depression, and other health issues. In the following article, inflammation and mood changes, such as depression, can cause a variety of symptoms, including fatigue and cognitive impairment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

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.  

 

According to the World Health Organization, depression is one of the main causes of disability worldwide. Moreover, approximately 30 percent to 60 percent of patients don’t respond to the currently available antidepressant treatments. That means that about 40 percent to 70 percent of patients aren’t being helped by existing antidepressant treatments. One region of research studies can ultimately shed some light on why many patients are not helped by antidepressants. 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:  

  1. Haapakoski, R., Mathieu, J., Ebmeier, K.P., Alenius, H., Kivimäki, M., 2015. Cumulative meta-analysisofinterleukins6 and 1β,tumournecrosisfactorα and C-reactive protein in patients with major depressive disorder. Brain Behav.Immun. 49,206.  
  2. Hodes GE, Pfau ML, Leboeuf M, Golden SA, Christoffel DJ, Bregman D et al (2014). Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress. Proc Natl Acad Sci USA 111: 16136–16141.  
  3. Krishnan V, Nestler EJ (2008). The molecular neurobiology of depression. Nature 455: 894–902.  
  4. Lotrich, F.E., Rabinovitz, M., Gironda, P., Pollock, B.G., 2007. Depression following pegylated interferon-alpha: characteristics and vulnerability.J.Psychosom.Res.63, 131–135.https://doi.org/10.1016/j.jpsychores.2007.05.013.  
  5. O’Brien, S.M., Scully, P., Fitzgerald, P., Scott, L.V., Dinan, T.G., 2007a. Plasma cytokine profiles in depressed patients who fail to respond to selective serotonin reuptake inhibitor therapy. J. Psychiatr. Res. 41, 326e331.  
  6. Tianzhu, Z., Shihai, Y., Juan, D., 2014. Antidepressant-like effects of cordycepin in a mice model of chronic unpredictable mild stress. Evid. Based Complement. Altern. Med. 2014, 438506.

 


 

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

 

Neural Zoomer Plus | El Paso, TX Chiropractor

 

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: What Causes Inflammation and Brain Fog?

Functional Neurology: What Causes Inflammation and Brain Fog?

Of all of the wide array of health issues that healthcare professionals talk to their patients about, there is one which is tremendously overlooked and not taken seriously: brain fog. Many people suffer from brain fog and fatigue and unfortunately, many people are left to fend for themselves when it comes to this health issue. Patients describe feeling as if they’re living in a haze, their lives passing them by. Instead of being engaged in the present moment, patients describe feeling as though they’re seeing life from a distance. Their thinking is no longer sharp, and their brilliant minds are sidelined.  

 

Why do health issues like these fall through the cracks of conventional medicine? This may be because there’s currently no definitive treatment available for brain fog. The purpose of the following article is to discuss the causes of inflammation and brain fog. Understanding the reasons for this type of health issue may hopefully help shine a new light on future treatments.  

 

Brain Fog and Inflammation

 

Inflammation is an essential part of the immune system. We need inflammation to protects us from injury, infection, and illness. However, as with everything else in the human body, it is all about balance. An excessive amount of inflammation can cause the blood-brain barrier (BBB) to become more permeable, leading to brain inflammation. Neuroinflammation is sometimes known as “leaky brain syndrome” and this inflammatory oxidative stress (OS) in the hypothalamus of the brain is ultimately believed to be the root cause of brain fog, among other neurological diseases, such as Alzheimer’s disease.  

 

Hidden Causes of Inflammation and Brain Fog

 

“Brain fog”, however, is very much considered to be a general term for the actual health issue. The name tells you exactly what it is (diminished brain function), however, it doesn’t exactly tell you what’s causing the brain inflammation in the first place. Let’s dig deeper into the reasons for brain fog. We will describe the main causes of brain fog, according to researchers.  

 

Thyroid Problems

 

Every cell in the human body depends on thyroid function to be healthy and to be able to operate at full capacity. Thyroid hormone imbalances have been demonstrated to cause inflammatory reactions. The thyroid functions by receiving the proper messages in the brain during the hypothalamic-pituitary-thyroid (HPT) axis. Therefore, if the hypothalamus is inflamed, it can cause dysfunction in the brain-thyroid axis. The final result? A vicious cycle of inflammation.  

 

Adrenal Fatigue

 

As you’ve got the brain-thyroid axis, you also have the brain-adrenal (HPA) axis. Dysfunctions of the hormonal circadian rhythm are known as an adrenal disorder. During fatigue, your stress hormone cortisol can be found all over the region and this imbalance can stress out your system. The same as thyroid problems, brain fog can be both the cause and the consequence of adrenal fatigue because of the brain-hormone connection, among other essential functions in the body.  

 

Viral Infections

 

Low-grade chronic viral infections, such as Epstein-Barr virus (EBV), are connected to a wide array of inflammatory ailments like chronic fatigue syndrome. The brain needs vitamin D to flourish and EBV has been demonstrated to actually block the body from utilizing it. Viral infections, if left untreated, can also trigger excess inflammation, leading to many health issues.

 

Leaky Gut Syndrome

 

The gut and the brain are unmistakenly connected, they are even formed from the exact same fetal tissue when you’re growing in your mother’s uterus. According to a variety of research studies, leaky gut syndrome is associated with an increase in gut toxins, known as LPS, which have been demonstrated to affect inflammation and brain fog.  

 

Candida Overgrowth

 

Researchers state that excess yeast in the microbiome, by way of instance, candida overgrowth, can also ultimately increase the inflammatory cells IL-1, IL-6, and TNF, which may contribute to too much inflammation in the human brain and body.  

 

Histamine Intolerance

 

Several people, especially people with all of the gut problems mentioned above, are more prone to experiencing something known as histamine intolerance. This happens when the body does not break down the cell histamine and it causes a discharge of superoxide, a well-known free radical which brings about a lot of inflammation and other health issues.  

 

Inflammatory Foods

 

Inflammatory foods high in sugar, gluten (wheat, rye, barley, spelt, and oats), or casein (dairy products) are a problem for many men and women. Free radical harm can triple by higher blood glucose levels from these inflammatory foods.  

 

Toxins

 

Toxins like mold and heavy metals are just two overlooked factors that can contribute to brain fog in patients.  

 

Poor Sleep

 

If you’re not sleeping properly at night, you don’t need me to tell you that it affects your brain health. The antioxidant glutathione, which increases stress from the hypothalamus, can ultimately cause brain fog due to a lack of sleep.  

 

Methylation Impairments

 

Methylation is a big biochemical superhighway that happens 1 billion times every second in the human body. It makes your brain healthy and it can help detox your body. People who have hereditary methylation problems may often have a difficult time detoxing and their body may ultimately not be able to regulate or manage inflammation, including neuroinflammation.  

 

El Paso Chiropractor Dr. Alex Jimenez

Brain inflammation has been associated with a variety of signs and symptoms, including brain fog. Inflammation in the brain can also cause a variety of neurological diseases, such as Alzheimer’s disease. Inflammation is an essential function of the human body, however, too much brain inflammation, can cause brain fog and other health issues. In the following article, inflammation and brain fog can be caused by a variety of factors, including leaky gut syndrome and inflammatory foods, among others. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

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.  

 

Of all of the wide array of health issues that healthcare professionals talk to their patients about, there is one which is tremendously overlooked and not taken seriously: brain fog. Many people suffer from brain fog and fatigue and unfortunately, many people are left to fend for themselves when it comes to this health issue. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .  

 

Curated by Dr. Alex Jimenez  

 

References:

  • Cole, William. “Here’s Exactly What To Do About Brain Fog: A Functional Medicine Expert Explains.” Mindbodygreen, Mindbodygreen, 17 Feb. 2017, www.mindbodygreen.com/0-28772/heres-exactly-what-to-do-about-brain-fog-a-functional-medicine-expert-explains.html.

 


 

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

  Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Signs and Symptoms of Brain Inflammation in Functional Neurology

Signs and Symptoms of Brain Inflammation in Functional Neurology

Inflammation is the human body’s natural response to injury, infection, or illness. However, too much inflammation can affect your overall health and wellness, especially when you have inflammation in the brain. Brain inflammation can even affect your mental and emotional well-being. Understanding the causes and symptoms of inflammation in the brain can help determine the best treatment option. Dr. Santosh Kesari describes that brain inflammation can be due to various reasons, including toxins like tobacco or alcohol, diabetes, hypertension, infections, trauma, aging, diet, and stress.  

 

“Some inflammation is acute, short-lasting, and possibly reversible but other types of inflammation are chronic and continue to cause brain damage,” Dr. Kesari states. “These may be cumulative and not readily reversible, such as Alzheimer’s disease.” With an overactive immune system, such as in people who have multiple sclerosis or encephalitis which is inflammation in the brain, several people may already be genetically predisposed to experience brain inflammation. Severe inflammation can lead to a variety of symptoms, it may also result in coma, brain damage, or death. The following 7 signs and symptoms may indicate inflammation in the brain. Make sure to seek immediate medical attention if brain inflammation is suspected.  

 

Brain Fog

 

If we’re talking about chronic inflammation caused by exposure to toxins or due to poor lifestyle habits, brain fog, as well as decreased cognitive abilities, can be some signs and symptoms of inflammation in the brain. You may ultimately lose your train of thought constantly when you have brain fog and you’ll frequently have trouble focusing on your regular tasks and daily activities. As Dr. Carolyn Dean, author of 365 Ways to Boost Your Brain Power, states, restricting dairy consumption or foods that can cause inflammation, smoking, and alcohol, may help improve these signs and symptoms of brain fog.

 

Mood Changes

 

As soon as your brain is inflamed, you may also experience signs and symptoms of depression. This type of brain inflammation is generally associated with poor lifestyle habits. As a nutritional therapist and health coach, Christina Tsiripidou informs us that eating meals that are high in proteins or altered proteins as well as low in veggies and fats, can contribute to brain inflammation. Not getting enough sleep and stress can also make these signs and symptoms worse.  

 

Fatigue

 

When your brain has inflammation, you may not only experience brain fog but you may also experience fatigue which commonly accompanies it. According to Caleb Wellness, Health and Backe Expert for Maple Holistics, small modifications in diet and lifestyle habits can be very powerful. Besides curbing your sugar and caffeine intake, it’s important to eat foods which are full of B vitamins and fatty acids. “Besides providing you with a much-needed energy boost, these types of foods also function by minimizing inflammation, which has been linked to increased brain fog and other health issues,” Backe says.  

 

Headaches And Migraines

 

Occasionally, headaches and migraines can be caused by poor lifestyle habits, but sometimes, it may also be brought on by more serious health issues that may require immediate medical attention. By way of instance, acute headaches can be an indication of inflammation and even swelling in the brain. As Dr. Kesari says, “This is very uncommon and it is generally associated with other neurological signs and symptoms typically due to either mass lesions or illnesses.” Often times, you also can’t really tell if a headache is brought on by a much more serious health issue, so he proposes that you should ultimately consult with your healthcare professional if your headaches last more than usual and they seem unusual.  

 

Neck Stiffness

 

Another more serious sign and symptom of brain inflammation is neck stiffness. As Dr. Dean states, this too can indicate swelling in the brain. Meningitis and encephalitis, which are disorders that cause inflammation around the brain and spinal cord, are often caused by viruses or bacteria. If you’re experiencing neck stiffness accompanied by fever, along with headaches or migraines, make sure to see your healthcare professional right away as this may suggest a serious health issue.  

 

Nausea or Vomiting

 

Encephalitis may give you feelings of nausea, Dr. Dean says. The usual cause of this type of brain inflammation is a viral infection, such as the herpes simplex virus. In reality, brain inflammation due to herpes constitutes 10 percent of all cases of encephalitis in the United States annually. Other common signs and symptoms include a stiff neck, general weakness, and nausea or vomiting. Make sure to talk to your healthcare professional if you notice any of these signs and symptoms.  

 

Vision Problems

 

Healthcare professionals can test your eyes and detect early signs and symptoms of a stroke, a brain tumor, or even Alzheimer’s disease, among other health issues associated with brain inflammation. The brain and the eyes are connected. It is not surprising that when your brain has inflammation, your vision can also ultimately be influenced, Dr. Dean says.   If you’re experiencing any of these signs and symptoms, talk to your healthcare professional. According to Dr. Kesari, the treatment depends on the signs and symptoms. Brain imaging, blood work, and spinal fluid analysis may be needed based on the clinical presentation. For severe symptoms, inflammation is treated with different immunosuppressive treatments including steroids, IVIG, plasmapheresis, and Rituxan. When the source of chronic brain inflammation is lifestyle-related, adjustments to diet, working on stress and also the elimination of habits, such as smoking, may ultimately help.  

 

El Paso Chiropractor Dr. Alex Jimenez

Acute and chronic brain inflammation has been associated with a variety of signs and symptoms, including depression, cognitive, and other mental health issues. Inflammation in the brain can even cause a variety of neurological diseases, such as Alzheimer’s disease. Inflammation is an essential function of the human body, however, too much inflammation, especially in the brain, can alter our overall health and wellness. Make sure to talk to your healthcare professional if you experience any unusual signs and symptoms associated with brain inflammation. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

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.   Inflammation is the human body’s natural response to injury, infection, or illness. However, too much inflammation can affect your overall health and wellness, especially when you have inflammation in the brain. Brain inflammation can even affect your mental and emotional well-being. Inflammation in the brain is associated with neurological disorders. 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  

 


 

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

 

Neural Zoomer Plus | El Paso, TX Chiropractor

 

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Inflammatory Reactions in Functional Neurology

Inflammatory Reactions in Functional Neurology

Inflammatory reactions in the central nervous system (CNS) are currently known to be associated with many neurological disorders. In neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), there is considerable penetration of different leukocyte subsets into the CNS or there is severe activation of microglial cells which increases many inflammatory mediators in the CNS. In acute CNS disorders, including delayed corrosion associated with vasospasm after subarachnoid hemorrhage (SAH), ischemic stroke, spontaneous intracerebral hemorrhage (ICH), and traumatic brain injury (TBI), current evidence from a variety of research studies reveal that inflammation may be a possible target for treatment. Inflammation is becoming a promising region of research study for new treatments.  

 

To speed up the process of translating this information to clinical applications, a number of significant problems have to be addressed as their capacity to continuously identify characteristic cerebral deficits in people with neurodegenerative diseases, the connections of brain injuries to clinical symptoms and genetic diagnosis as well as the level to which the harm respond to various treatment approaches. In this article, findings that address some of these problems are reported by several researchers.  

 

Inflammation and Neurological Disorders

 

In neurodegenerative diseases, a research study reviewed the function of chronic neuroinflammation in the pathogenesis of Alzheimer’s disease (AD). With the glial fibrillary acidic protein-interleukin 6 (GFAP-IL6) transgenic mice model, the researchers demonstrated that this animal model, in which chronic neuroinflammation triggered the expression of the cytokine interleukin-6 (IL-6) in astrocytes, could serve as a great tool for drug and/or medicine discovery and validation in vivo.  

 

Another research study assessed the role of inflammation in the neuropathology of Parkinson’s disease (PD). They supplied a synopsis of current knowledge on the temporal profile of immune reactions in PD and discussed the potential effects of central and peripheral inflammation. The research study utilized TRODAT-1 SPECT to rate leukocyte apoptosis from PD patients and its association with central dopamine neuron loss. The leukocyte apoptosis and striatal dopamine transporter uptake ratios were associated with the duration of the disease and increased severity. The interaction between brain and systemic inflammation may be liable for the neurodegenerative disease progression. Another research study utilized the Longitudinal Health Insurance Database 2000 (LHID2000) to analyze and evaluate the probability of dementia between patients clinically diagnosed with autoimmune rheumatic diseases (ARD) and non-ARD patients during a 5-year follow-up interval. Their findings indicate that patients with and without ARD had comparable risks of developing dementia.  

 

In severe critical CNS diseases, the research study utilized traumatic brain injury (TBI) models to determine whether simvastatin, together with an antioxidant, could cause cerebral vascular endothelial inflammatory responses after traumatic brain injury in rat models. Their findings support that simvastatin combined with an antioxidant could offer neuroprotection and it could possibly be attributed to cerebral vascular inflammatory reactions. The analysis utilized a structural equation modeling to evaluate the predictive value of admission Glasgow Coma Scale (GCS) scores, duration of unconsciousness, neurosurgical intervention, and countercoup lesion associated with the impairment of memory and processing rate functions six months after a TBI. The analysis also revealed that admission GCS score is a tremendous predictor of memory/processing speed dysfunctions after TBI.  

 

One research study investigated serum thiobarbituric acid-reactive substances (TBARS) and free thiol levels in a variety of subtypes of acute ischemic stroke (AIS) where they evaluated their association with clinical results. They discovered that patients with the disease have greater oxidative stress but reduced antioxidant defense compared to those with disease following AIS. Serum TBARS level at the acute phase of a stroke is a predictor for the outcome. Along with other research studies, these aimed to ascertain whether serum adhesion molecules are associated with septic encephalopathy (SE). Their findings reveal that SE suggests higher mortality in nontraumatic patients with sepsis. Serum vascular cell adhesion molecule-1 (VCAM-1) degree on presentation is a much more effective predictor of SE in these patients than lactate concentration and other adhesion molecules on admission, according to research studies.  

 

From the CNS health issues, research studies investigated the relationship between protein expressions of two autophagy markers, LC3B and Beclin-1, with clinical trials in astrocytoma patients. Their results suggest that targeting the cancer stem-like cell in astrocytoma can offer an approach that astrocytoma cancer stem-like cells together with improved autophagy may lead to resistance. Along with another research study, researchers researched DAPK protein expression and promoter hypermethylation in central neurocytoma and oligodendroglioma. Their results demonstrated that repressed expression and DAPK promoter hypermethylation of DAPK protein were prevalent in central neurocytoma than in oligodendroglioma. DAPK promoter hypermethylation can be useful for differential diagnosis between these two types of tumors.  

 

In conclusion, the article above emphasizes several essential research strategies that are making it more evident that neuroinflammation or inflammatory reactions are of translational significance for different types of neurological disorders. The results from these research studies not only enable us to understand the pathogenesis of these disorders but these also show great potential to provide desperately objective biomarkers for analysis and clinical investigation. Knowledge and comprehension of those conditions have contributed to the development of effective treatments, animal models, and innovative tools to characterize these medical conditions and provide better treatment options to patients.  

 

El Paso Chiropractor Dr. Alex Jimenez

Neuroinflammation is ultimately characterized as the inflammation of the nervous tissue. It can commonly occur due to a variety of factors, including toxins, infections, autoimmune diseases, and even traumatic brain injury (TBI). In the central nervous system (CNS), the microglial cells are in charge of activating inflammatory reactions associated with these factors. However, excess microglia activation can ultimately cause a variety of health issues, including neurological diseases, among others. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

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.  

 

Inflammatory reactions in the central nervous system (CNS) are currently known to be associated with many neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). 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

 


 

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

  Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Monosodium Glutamate and Brain Health

Functional Neurology: Monosodium Glutamate and Brain Health

There is plenty of controversies associated with MSG. Researchers believe that the excess consumption of monosodium glutamate can cause asthma, headaches, and even brain health issues. On the other hand, the majority of official sources, including the FDA, claim that MSG is a safe food ingredient. The following article discusses what is monosodium glutamate, or MSG, and its effects on overall health and wellness, exploring both sides of the argument on the food ingredient.  

 

What is Monosodium Glutamate (MSG)?

 

MSG is known as monosodium glutamate. It is a common food ingredient that is utilized to enhance flavor in foods. MSG comes from the amino acid, glutamate or glutamic acid, which is one of the most common amino acids found in nature. Glutamate is a non-essential amino acid, which ultimately means that the human body can naturally produce it. Monosodium glutamate also serves a variety of functions in the human body and it is commonly found in almost all types of foods.  

 

MSG is a white crystalline powder that looks similar to sugar or table salt. It is also made up of a combination of sodium and glutamic acid, known as sodium salt. The glutamic acid in MSG is created by fermenting starches, however, there is no chemical difference between the glutamic acid in monosodium glutamate and that found in natural foods. The glutamic acid in MSG can be easier to absorb because it isn’t bound inside big protein molecules which the body breaks down.  

 

Glutamate in the Human Body

 

Our stomach and gut lining have many glutamate receptors. MSG and other types of glutamate are absorbed through these receptors. Once in the gastrointestinal, or GI, tract, glutamate is broken down as energy or incorporated into other molecules. Glutamate is also an essential neurotransmitter in the brain. However, researchers believe that dietary glutamate is unable to cross the blood-brain barrier, which ultimately suggests that all glutamate from the brain is created there.  

 

Evidence from research studies in mice showed that the blood-brain barrier in newborns is immature and that glutamate can pass into the brain. Increased levels of glutamate injected into newborn mice caused considerable brain damage. A research study showed that increased levels of MSG also cause severe effects in fruit flies, causing premature death. While the levels utilized in these research studies exceeded average daily consumption reported among humans, it is essential to mention that restaurants and food manufacturers are not required to declare the levels of MSG added to their foods.  

 

Is MSG Good or Bad for You?

 

Glutamate, or glutamic acid, functions as a neurotransmitter in the human brain. It is also considered an excitatory neurotransmitter, which means that it stimulates nerve cells to transmit signals. Several people believe that MSG causes excess glutamate in the brain and excess stimulation of the nerve cells. Therefore, MSG has been labeled as an excitotoxin.  

 

Concerns associated with the effects of MSG date as far back as 1969, when a research study found that injecting large doses of MSG into newborn mice caused harmful neurological effects. Since then, a variety of other sources have continued to have this concern with MSG. Another research study showed that increased glutamate activity in the brain can cause harm and large doses of MSG can raise blood levels of glutamate. Aa megadose of MSG increased blood levels by 556%.  

 

However, dietary glutamate should have little to no effect on the human brain because it can’t cross the blood-brain barrier in large amounts. There is not enough evidence to show that MSG acts as an excitotoxin when consumed in normal amounts.  

 

Monosodium Glutamate (MSG) Sensitivity

 

Several people may also experience adverse effects from consuming MSG. This health issue is known as Chinese restaurant syndrome or MSG symptom complex. In one research study, people with self-reported MSG sensitivity consumed either 5 grams of MSG or a placebo where 36.1% reported reactions with MSG compared to 24.6% with placebo. Common symptoms included headaches, flushing, muscle tightness, tingling sensations, numbness, and weakness, among other symptoms.  

 

The threshold dose that causes symptoms seems to be around 3 grams per meal. However, keep in mind that 3 grams is a very high dose, approximately six times the average daily intake of MSG in the United States. It is still unclear why this happens, however, some researchers hypothesize that such large doses of MSG allow trace amounts of glutamic acid to cross the blood-brain barrier and interact with neurons which can cause brain damage, swelling, and injury. Several believe that MSG also causes asthma in susceptible people. In one 32-person research study, 40% of participants experienced an asthma attack with MSG. However, other research studies did not find any relationship between MSG intake and asthma.  

 

Conclusion

 

Depending on who you ask, MSG is either perfectly safe or a dangerous neurotoxin. The truth lies somewhere in between. Evidence indicates that MSG is safe in moderate amounts. However, megadoses may cause harm. If you react adversely to MSG, you shouldn’t eat it. That said, if you don’t experience side effects, there’s no compelling reason to avoid it. Keep in mind that MSG is generally found in processed, low-quality foods — which you should avoid or limit anyway. If you already eat a balanced diet with plenty of whole foods, you shouldn’t have to worry about high MSG intake.  

 

El Paso Chiropractor Dr. Alex Jimenez

The controversy between MSG and brain health has been determined by a variety of research studies. Monosodium glutamate, or MSG, has been utilized as a food ingredient and it is largely consumed by many people in the US on a regular basis today. Although the FDA, or the Food and Drug Administration, categorizes MSG as a safe food ingredient, many research studies have determined that it can cause a variety of brain health issues, including neurological diseases, among other well-known health issues. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

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.   There is plenty of controversies associated with MSG. Researchers believe that the excess consumption of monosodium glutamate can cause asthma, headaches, and even brain health issues. On the other hand, the majority of official sources, including the FDA, claim that MSG is a safe food ingredient. The article discusses what is monosodium glutamate, or MSG, and its effects on overall health and wellness, exploring both sides of the argument on the food ingredient. 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  

 


 

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

 

Neural Zoomer Plus | El Paso, TX Chiropractor

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: MSG and Neurological Diseases

Functional Neurology: MSG and Neurological Diseases

MSG is a food additive which is found in the majority of the industrial foods. It boosts the taste of the food hence attracting customers. There is no value in terms of nutrition and it really does nothing to the eater, however, it can have many effects on foods. MSG is known as an “excitotoxin” or neurotoxin. Research studies have found that it has devastating and degenerative effects on the brain and the nervous system. The neurons or brain cells overstimulate and fatigue to their death. MSG enters the brain through the membranes in the mouth and the throat. It also enters the blood-stream through the digestion of food in the gastrointestinal (GI) tract. MSG “tricks” the human body into believing that it is getting value from these foods.  

 

MSG is not a natural substance found in nature. It’s a man-made chemical from glutamic acid, an amino acid found in proteins. Amino acids do happen naturally in animal cells and in several plant cells. The kinds of amino acids have been processed through the change of this pure form of glutamate. Some of the materials used for this purpose include starches, molasses, and corn. The manipulation procedure generates this type of glutamate. The d-glutamate is not found naturally. The free glutamates can enter the body about eight to ten times faster compared to natural glutamates. Natural glutamate is found in foods such as tomatoes, mushrooms, and milk. Techniques used to manufacture glutamate were not in use before the 1960s. The MSG in use now is not natural. In the article, we will discuss how MSG is associated with neurological diseases.  

 

Research Studies on MSG and Neurological Diseases

 

Research studies indicate that MSG is the reason for neurological diseases like Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis. Neuroscientists have explained that MSG attacks the blood-brain barrier of the neurons which is responsible for the regulation of the fragile chemical exchange inside the brain cells. The chemical exchange process is well balanced and its performance is unquestionable. Under normal conditions, the brain and the entire immune system manage all sorts of toxins, health issues, and stress. A very small amount of poisonous substances can actually make the brain overreact, ultimately resulting in excessive exhaustion and death, according to research studies.  

 

MSG is a leading “excitotoxin” and it is widely known to cause harm to the brain region which governs or controls additional systems from the human body. The damage will seem like a disease in the endocrine system and the immune system. This can be shown in the cases of food cravings, persistent hunger, and unusual sleeping patterns. This normally leads to obesity. MSG is also known to cause migraine headaches, behavioral disorders, depression, asthma attacks, heart problems, arthritis, sinus issues, and digestive issues.  

 

MSG is a neurotoxin which requires an extremely brief time to create a broadly diverse and dramatic effect on the human body. An individual may have a mild dose of a prescription drug and also have favorable effects. However, another individual might take the prescription drug and get sad, have a swollen tongue, stomach disorders, and joint problems. The different parts of the brain affected do govern various body functions. The part which is attacked will depend on the individual. If by way of instance, an individual has had a headache, a genetic pinch in a given portion of the brain, has had a fever that’s attacking regions of the brain, or has had a stroke, then it’s certain that the component of the brain that has been affected will be due to the toxins.  

 

A number of the foods sold are ultimately sold as weight loss promotions to the people. MSG, along with aspartame, is added when food substances, such as fat and sugar, are eliminated from the meals. These excitotoxins have been known to cause obesity and irregular heartbeats. FDA generally allows the labeling of MSG’S as natural flavors, hydrolyzed proteins, and autolyzed yeast, when used as just a partial ingredient in an additive rather than only MSG. Americans now are consuming 160 million lbs of MSG per year. Author and toxicologist Dr, George Schwartz asserts that two tablespoons of MSG on bread could kill a medium-sized dog within a moment. The FDA in 1995 claimed that no one can respond to less than 3 grams of MSG per meal. In spite of their confirmation, they’ve warned that children, pregnant or lactating women, and the elderly should avoid MSG. An extremely sensitive individual can also ultimately react even to under a gram of MSG.  

 

Effects of MSG and Neurological Diseases

 

Research studies have shown that from the late 1950s, an estimated amount of 12 grams per person of MSG was utilized by most Americans each year. These days, taking a look at precisely the same health issue, the quote is between 400 and 500 g per person each year. This is an amount which requires evaluation. The wide usage of MSG arrived in the mid-1970s. It gained much popularity throughout the 1980s with manufacturers of food. Two powerful excitotoxic food additives which took the food sector by storm have been the use of MSG and aspartame. MSG has been broadly associated with a wide assortment of symptoms and health issues. As previously stated, it affects the human body’s neurological system. The same ailments are being reported to be on their rise. The ailments are absolutely unexpected and difficult to describe.  

 

Neurological diseases associated with MSG and numbers of interest released by federal organizations have been recorded in fibromyalgia, which is a growing epidemic. Its patients eliminated aspartame and MSG during the research study conducted by the Florida University which reported complete relief of symptoms. On the other hand, the most cognitive research study was conducted to prove the connection between fibromyalgia and MSG along with several different additives as a common rheumatologic disorder. In this case, 4 patients had been diagnosed for 2 to 17 years with fibromyalgia syndrome. They had undergone various methods of therapy whilst failing to consider MSG as the causative agent. After eliminating aspartame and MSG in their diets, complete or near complete resolution of symptoms diagnosed was listed within months. The subjects were women who had recurring symptoms and multiple comorbidities. It’s therefore indicative that the excitotoxins, present in compounds, such as aspartate and MSG, become excitatory neurotransmitters once ingested and when consumed in excess may lead to neurotoxicity. These 4 patients may, therefore, signify this fibromyalgia syndrome and act as a link to conclusively establish a link to MSG. Therefore, persistent research studies, if carried out on a larger sample, might serve to connect the fibromyalgia syndrome into MSG and aspartame more concretely. Further research studies are required.  

 

Moreover, a research study connected MSG to adrenal adenomas. The hypothalamus which leads damage on the nerves is overstimulated by MSG. The hypothalamus is responsible for directing the pituitary gland’s actions, which can be known as the endocrine gland since it in turn directs the rest of the glands in the human body and their activities such as metabolism, development of reproductive and sex organs and other essential development functions. Statistics have demonstrated that 25 percent of Kenyans have a pituitary adenoma. However, research studies linking pituitary adenomas to MSG have ultimately been inconclusive. Some research studies had depicted this as a disease but have been proven wrong.  

 

About half of the pituitary adenomas secrete prolactin. These can become large over time in the optic nerve, thus, affecting vision. It also prevents ovulation and menses. This prevents pregnancy or conception generally. Furthermore, since prolactin is responsible for lactation, lactation can be caused by secretion in the individual even if they’re male or even when they were not pregnant. Men with these adenomas grow breasts. Since the tumor can only be discovered when it’s big and dangerous unlike in women that are forewarned by the effects on vision or related headaches, this problem is deadly in men. There’s a further need to sponsor more research studies so as to ultimately associate MSG and brain tumors, among others.  

 

Other effects which were attributed to MSG and neurological diseases are headaches and migraines, asthma, and obesity amongst others. In headaches and migraines, an approximate amount of $2.2 billion each year are being spent on drugs and/or medicines that treat head pain. This chronic condition has received a 74 percent increase. Second, asthma associated with the brain was connected to MSG. According to data, there was a decrease of asthma before the mid-eighties. Since then, however, there’s been a 100 percent gain in the rate of death among children and seniors. This prevalence has increased by 600 percent in the last 10 years. FDA has identified that uncontrollable asthma can be caused by MSG, sadly, no measures are taken to take care of the situation. In defects of birth and disorders of production, MSG was identified as a mutagen i.e. mutates fetuses. It’s reputed to cause damage to the development, reproduction, and growth patterns as well as the functions. Such research studies have not been concrete. Other consequences include emotional or neurological disorders. Laboratory research studies demonstrate devastating effects on brain development, including dyslexia, attention deficit, autism, hyperactivity, violent episodes or rage, panic attacks, depression, paranoia, seizures and cerebral palsy. Rats were utilized with this research study. However, human beings are five times more sensitive to MSG than rats.  

 

This topic of ailments in behavior for children is becoming a frequent discussion amongst professionals. These have associated attention deficits, behaviour, and instability to chemical imbalances occurring in the brain. It is now becoming an intense possibility that there’ll be damage caused by excitotoxins in the blood-brain barrier of young brains.  

 

In April 1994, a magazine article confirmed the rising problem of behavioral disorders. The magazine stated that the attention deficit hyperactivity disorder wasn’t in existence. It’s however said that it is currently affecting 3.3 million American kids. This magazine article estimates prominent research studies which 10 years ago stated that symptoms of ADHD and ADD vanished with maturity. Nowadays, however, ADD is the fastest growing diagnostic category for adults. The combination of both excitotoxins i.e. MSG and aspartame came into wide utilization in the 1980s.  

 

El Paso Chiropractor Dr. Alex Jimenez

In the medical field, a controversy as to whether MSG is associated with neurological diseases has been determined. Monosodium glutamate, or MSG, has been utilized as a flavorant in the food industry for approximately 100 years and it is consumed by the masses on a regular basis today. Although the FDA, or the Food and Drug Administration, categorizes MSG as a safe food ingredient, many research studies have determined that it can cause a variety of health issues, including neurodegenerative diseases, among others. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

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.   MSG is a food additive. It boosts the taste of food, attracting customers. There is no nutrition and it really does nothing to the eater, however, it can have many effects on foods. MSG is known as an “excitotoxin” or neurotoxin. Research studies have found that it has devastating and degenerative effects on the brain and the nervous system. 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  

 


 

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

  Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Chronic Excitotoxicity in Neurodegenerative Diseases Part 3

Functional Neurology: Chronic Excitotoxicity in Neurodegenerative Diseases Part 3

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.  

 

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.  

 

El Paso Chiropractor Dr. Alex Jimenez

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

 

  1. 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

 

Neural Zoomer Plus | El Paso, TX Chiropractor

 

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Chronic Excitotoxicity in Neurodegenerative Diseases Part 2

Functional Neurology: Chronic Excitotoxicity in Neurodegenerative Diseases Part 2

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.  

 

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 β amyloid (Aβ) 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 Aβ precursor protein, AβPP, or in the presenilins, which are part of the multi-protein complex involved in Aβ 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 Aβ increases both NMDA and kainate receptor-mediated L-glutamate toxicity, perhaps by interrupting neuronal calcium homeostasis. Others have demonstrated that Aβ can increase neuronal excitability by changing the capacity of glycogen synthase kinase 3β inhibition to decrease NMDA receptor-mediated pathways. Soluble Aβ 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, Aβ 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 AβPP23 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 β-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, Aβ 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 α7 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 Aβ injection in the hippocampus. Semiquantitative immunoblot evaluations revealed an upregulation of xCT protein expression in the frontal cortex in elderly AβPP23 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. Aβ 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.  

 

Figure 4 Potential Mechanisms of Excitotoxicity in AD | El Paso, TX Chiropractor   El Paso Chiropractor Dr. Alex Jimenez

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  

 

  1. 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

 

Neural Zoomer Plus | El Paso, TX Chiropractor

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Chronic Excitotoxicity in Neurodegenerative Diseases

Functional Neurology: Chronic Excitotoxicity in Neurodegenerative Diseases

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.  

 

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 β-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.  

 

Figure 3 Potential Mechanisms for Excitotoxicity in ALS | El Paso, TX Chiropractor  

El Paso Chiropractor Dr. Alex Jimenez

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  

 

  1. 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

 

Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Glutamate Dysregulation and Excitotoxicity

Functional Neurology: Glutamate Dysregulation and Excitotoxicity

Excitotoxicity is characterized as an acute insult which causes nerve cell death due to the excessive activation of iGluRs. Acute excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue.  

 

With brain ischemia, L-glutamate-associated and L-aspartate-associated excitotoxicity happen within minutes due to the growth in extracellular cerebral L-glutamate as well as L-aspartate. Because these are also energy-dependent, the abrupt loss of energy due to the shut down of blood flow can ultimately breakdown the neuronal and astroglial membrane. In neurons, membrane depolarization contributes to vesicular discharge. Additionally, energy degradation may even cause a change in their action, therefore, causing L-glutamate and L-aspartate to activate and affect ionic homeostasis which can interrupt EAAT action. The activation of L-glutamate/L-aspartate contributes to excitotoxicity through the over-activation of iGluRs of the NMDA type as demonstrated by the efficiency of NMDA antagonists in animal models of transient cerebral ischemia.  

 

In TBI, the mechanical tissue damage and the disruption of the blood-brain barrier can trigger acute secondary neurodegeneration, which, together with neuroinflammation and oxidative stress, is associated with L-glutamate activation from intracellular compartments and, therefore, by acute excitotoxicity. Moveover, acute application of the NMDA antagonist MK801 following TBI ameliorates neuronal loss and long-term behavioral abnormalities, among others.  

 

In status epilepticus, continuing the synchronized activity of excitatory neuronal networks as well as the continuous breakdown of restricting mechanisms is the main source of L-glutamate and L-aspartate activation. As the severity of synchronous activity depends upon the involvement of nerve cells into a neuronal system as well as the capability of a neural cell to withstand excess glutamate mainly depends on the expression pattern of iGluRs, a somewhat restricted and maturation-associated degeneration of neuronal populations which is ultimately caused by prolonged epileptic seizures. The significance of excitotoxicity in status epilepticus is shown as NMDA antagonists, such as ketamine, decrease adrenal loss.  

 

Excitotoxicity in Neurological Diseases

 

Because EAATs were discovered to be down-regulated in a variety of central nervous system (CNS) health issues and L-glutamate, as well as L-aspartate, clearance can ultimately affect the excitotoxicity of neurological diseases, many healthcare professionals have decided to determine substances which cause EAAT2, or the main EAAT in the brain and most commonly shown to be downregulated. This has demonstrated substances which shows astrocytic EAAT2 expression both in vitro and in vivo research studies. Several of these have also demonstrated protective properties in animal models of neurological diseases. Cef is one of the most evaluated compounds and it has been analyzed in AD, HD, and ALS models with positive outcomes. However, none of the substances has been extensively researched for its capability to interact with other neuroprotective pathways. Cef has also been demonstrated to promote EAAT2 expression but also to trigger the transcription factor Nrf2, which results in the transcription of a wide array of genes involved in cytoprotection and antioxidant protection. Because oxidative stress is believed to play an essential role in many, if not all, neurological diseases, this pathway may account for the neuroprotection caused by Cef. Furthermore, xCT, which can be one of the downstream targets of Nrf2, has been demonstrated to be upregulated by Cef in vitro and in vivo. Another in vitro EAAT2-promoting substance, MS-153, efficiently protected against secondary neurodegeneration after traumatic brain injury as well as through mechanisms other than EAAT2 upregulation. Evidence of concept experiments which demonstrate the increased stimulation through iGluRs in neurodegenerative diseases needs manipulations of their neurotransmitter physiology.  

 

Glud1 Tg mice demonstrate a model of excitotoxicity associated with enhanced synaptic L-glutamate activation with restricted neuronal loss. However, this animal model of glutamatergic neurotransmission has not yet been utilized to analyze if Glud1 over-expression aggravates the phenotype of mouse models in neurological diseases. Another version involves the EAAT2-deficient mouse. Homozygous EAAT2 knock-out mice have health issues associated with premature death because of epilepsy as well as hippocampal and focal cortical atrophy. Heterozygous EAAT2 knock-out mice, however, develop normally and show only mild behavioral abnormalities. This mouse model of moderate glutamate hyperfunction has been utilized in a collection of evidence of principle research studies which demonstrated the fundamental role of glutamate. ALS mice, which have both the G93A mSOD1 mutation and a decreased quantity of EAAT2 (SOD1(G93A)/EAAT2±), revealed an increase in the speed of motor decline accompanied by earlier motor neuron loss when compared with single mutant G93A mSOD1 Tg mice. A decrease in survival was also demonstrated in these mutant mice. When crossed with transgenic mice expressing mutations of the human amyloid-β protein precursor and presenilin-1 (AβPPswe/PS1ΔE9), partial loss of EAAT2 unmasked spatial memory deficits in 6-month-old mice expressing AβPPswe/PS1ΔE9. These mice demonstrated an increase in the ratio of detergent-insoluble Aβ42/Aβ40 demonstrating that shortages in glutamate transporter function ultimately cause premature pathogenic processes associated with AD. By comparison, the phenotype of the R6/2 HD mouse model wasn’t changed in mice which had only one EAAT2 allele. Further research studies are still necessary for further evidence.  

 

As a complement to these research studies, transgenic mice which over-express EAAT2 in astrocytes through the GFAP promoter has also been developed. EAAT2/G93A mSOD1 double Tg mice demonstrated moderate amelioration of their ALS-like phenotype with a statistically significant (14 times ) delay in grip power decrease and loss of motor neurons as well as a decrease in other occasions, such as caspase-3 activation and SOD1, although not at the beginning of paralysis, weight loss or an extended life span when compared with monotransgenic G93A mSOD1 littermates. Exactly the same EAAT2 transgenic mouse model was utilized to evaluate the effect of improved astrocytic L-glutamate and L-aspartate uptake by cross-breeding with an animal model of AD, AβPPswe/Ind mice. Increased EAAT2 protein levels considerably increased and improved overall cognitive functioning, restored synaptic ethics, and decreased amyloid plaques in those AD mice.  

 

In mice in which genetically engineered regulation and management of xCT causes a lack in the glutamate/cystine antiporter system x−c, the obvious decrease of extrasynaptic L-glutamate is associated with the tremendous resistance of dopaminergic neurons against 6-hydroxydopamine-induced neurodegeneration, perhaps as a consequence of reduced excitotoxicity. However, microglial activation has also been demonstrated to be modulated by system x−c deficiencies leading to a more neuroprotective phenotype which offers an explanation for the protective effect of xCT deletion in this circumstance.  

 

Therefore, genetic variations encourage the role of chronic excitotoxicity in neurodegenerative diseases, particularly AD and ALS. These models all represent life-long changes in glutamatergic neurotransmission. These models can’t determine if the utilization of drugs and/or medications can directly affect glutamate levels throughout the neurodegenerative process and/or be protective. Both evaluation and analysis of EAAT2-inducing medicine for the progression of inducible mouse models and their interaction with other signaling pathways is still warranted by researchers and healthcare professionals.  

 

El Paso Chiropractor Dr. Alex Jimenez

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

Metabolic Assessment Form AE266

 

The following Metabolic Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptom groups listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue.  

 


 

Excitotoxicity is characterized as an acute insult which causes cell death due to the excess activation of iGluRs. Excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .  

 

Curated by Dr. Alex Jimenez  

 

References  

 

  1. 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

  Neural Zoomer Plus | El Paso, TX Chiropractor

 

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Functional Neurology: Other Molecules in Glutamate

Functional Neurology: Other Molecules in Glutamate

Previous research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity on neurons. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain (0.96-1.62 μmol/gram wet weight), their extracellular concentrations in the cortex as measured by microdialysis (1.62 μM for L-aspartate and 9.06 μM for L-glutamate) and their supply according to immunohistochemistry suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. EAATs which play a fundamental role in the uptake of all vesicular released L-glutamate in the central nervous system (CNS) also requires the utilization of L-aspartate. L-aspartate is perhaps as less essential as L-glutamate connected to the total excitatory activity associated with iGluRs. Along with its role as a neurotransmitter, as previously mentioned, L-aspartate is also necessary as a substrate for aspartate amino-transferase which turns into 2-oxoglutarate and L-glutamate to transport to the cortical vesicles of glutamatergic neurons which may also consequently and indirectly increase L-glutamate release.  

 

Other Molecules in Glutamate Signaling

 

One characteristic which distinguishes NMDA receptors from different iGluRs is that the activation of NMDA receptors needs the connection of a co-agonist to the glycine binding region of the receptor. By way of instance, in the retina and in the spinal cord, the origin of glycine may spillover out of glycinergic inhibitory synapses. But, in different regions of the brain with increased NMDA receptor expression, such as the hippocampal formation, reactions associated with strychnine-sensitive glycine receptors are missing, at least in adult neurons, demonstrating the absence of glycinergic inhibitory neurotransmissions. But, glycine is found in the extracellular fluid of the hippocampus at baseline amounts of roughly 1.5 μM, which is similar to the saturation of the glycine binding region of the NMDA receptor, although these may be up- and down-regulated. The origin of extracellular glycine in the hippocampus can be neurons which release glycine through the alanine-serine-cysteine amino acid transporter 1 (asc-1). But, glycine release by astrocytes that is stimulated by depolarization and kainate, has also been demonstrated. Further research studies are required to ultimately show these outcome measures.  

 

Even in previous research studies of the NMDA receptor and its co-activation by glycine revealed that D-amino acids, particularly D-serine, are nearly as powerful as glycine. Only several years after, it became obvious that D-serine is found in rat and human brains at roughly one-third of their concentration of L-serine having an absolute concentration of more than 0.2 μmol/g brain tissue. Utilizing an antiserum for D-serine, research studies demonstrated that D-serine from the brain is only found in astrocytes and its supply fits the expression of NMDA receptors. In addition, the same researchers demonstrated that D-serine is released from cultured astrocytes when exposed to L-glutamate or kainate. The abundance of D-serine is found by the degrading enzyme D-amino acid oxidase (DAO) which reveals increased expression in the hindbrain where D-serine levels are reduced as well as the synthetic enzyme serine racemase which creates D-serine from L-serine. D-Serine appears to be stored in cytoplasmic vesicles in astrocytes and it can be released by exocytosis. Long-term potentiation is dependent upon D-serine release from astrocytes in hippocampal slices, suggesting that this amino acid definitely plays a fundamental role in glutamatergic neurotransmission through NMDA receptors. Additionally in hippocampal slices, research studies found, utilizing D-serine and glycine degrading enzymes, which D-serine functions as a co-transmitter for synaptic NMDA receptors on CA1 neurons likewise which glycine functions as the endogenous co-agonist for extrasynaptic NMDA receptors. Synaptic NMDA receptors of dentate gyrus neurons utilize glycine rather than D-serine as the co-agonist.  

 

Taken collectively, multilayered outcome measures show that L-aspartate doesn’t simply function as an agonist on NMDA receptors but also glycine and D-serine play fundamental roles in glutamatergic neurotransmission in the human brain. But, other molecules also have been demonstrated to be relevant modulators of glutamatergic neurotransmission.  

 

Glutamate Activated by Other Molecules

 

L-homocysteate (L-HCA) has structural similarities with L-glutamate. The non-protein amino acid is an oxidation product of homocysteine that is biosynthesized from methionine in the elimination of its own terminal methyl group and it is also an intermediate of the transsulfuration pathway by which methionine may be converted to cysteine through cystathionine. Early research studies demonstrated that this amino acid can cause calcium influx in cultured neurons as safely and effectively as L-glutamate. Moreover, L-HCA revealed an increased affinity for NMDA receptors when compared to other iGluRs in binding assays associated with its capacity to cause NMDA receptor antagonist-inhibitable excitotoxicity and sodium influx. Additionally, L-HCA can trigger mGluR5 as efficiently as L-glutamate. L-HCA is found in the brain, however, the concentrations were demonstrated to be approximately 500-fold lesser than those of L-glutamate and even 100-fold lesser when compared to those of L-aspartate in different regions of the rat brain. Throughout potassium-induced stimulation, L-HCA discharge is triggered from brain slice preparations as demonstrated for L-aspartate and L-glutamate although the absolute release of HCA is approximately 50-fold lesser. Surprisingly, HCA is a very efficient competitive inhibitor of cystine and L-glutamate uptake through the cystine/glutamate antiporter system x−c, the activity that regulates and manages the extracellular extrasynaptic L-glutamate concentrations in the brain. Therefore, the impact of L-HCA on the activation of NMDA and other L-glutamate receptors may also rely on the L-HCA-induced trigger of L-glutamate through system x−c. L-HCA may play an important role in the overall stimulation of L-glutamate receptors. Nevertheless, this can change tremendously under certain conditions, e.g., in patients with high-dose methotrexate therapy, an anticancer drug which, by restricting dihydrofolate reductase, limits the tetrahydrofolate-catalyzed recycling of methionine from homocysteine. Here, L-HCA concentrations of more than 100 μM have been demonstrated from the cerebrospinal fluid whereas L-HCA was undetectable in control subjects. Further research studies are still required to determine these outcome measures.  

 

Further endogenous small molecules which are believed to affect L-glutamate signaling include several intermediates of tryptophan metabolism, as shown in Figure 2. Through the activity of indoleamine 2,3-dioxygenase (IDO) or tryptophan 2,3-dioxygenase (TDO), tryptophan is turned into N-formyl-L-kynurenine which is later turned into kynurenine (KYN) by formamidase. Three pathways, two of which connect at a subsequent step, result in further metabolism. First, through the activity of kynurenine aminotransferase (KAT), KYN is converted into kynurenic acid (KYNA). KYN can also be converted to 3-hydroxykynurenine (3HK) by kynurenine monooxygenase (KMO), which can subsequently be utilized as a substrate by kynureninase for the synthesis of 3-hydroxyanthranilic acid (3HANA). Additionally, utilizing KYN as a substrate, kynureninase develops anthranilic acid (ANA), which by non-specific hydroxylation may also be converted to 3HANA. According to research studies, 3HANA finally functions as a substrate for the generation of quinolinic acid (QUIN).  

 

Figure 2 Kynurenine Metabolism | El Paso, TX Chiropractor

 

The tryptophan concentration in the rat brain is roughly 25 nmol/g wet weight and approximately 400-fold less than L-glutamate and 100-fold less than L-aspartate. The demonstrated brain levels of kynurenines are even lower with 0.4-1.6 nmol/g for QUIN, 0.01-0.07 nmol/ml for KYNA, and 0.016 nmol/g for 3HANA. Approximately 40 percent of brain KYN is locally synthesized. The metabolites of tryptophan demonstrate differential binding to plasma proteins and their transport through the barrier which is quite different. KYN and 3HK are carried through the large neutral amino acid carrier system L. Kynurenines seem to penetrate the human brain by passive diffusion. Additionally, KYNA, 3HANA, and especially ANA bind to serum proteins which then ultimately restrict and limit their diffusibility across the blood-brain barrier.  

 

Research studies demonstrated that QUIN, when ionophoretically utilized in rat cells, caused neuronal firing which has been prevented by an NMDA receptor antagonist, suggesting that QUIN may function as an NMDA receptor agonist. However, the EC50 for QUIN to trigger NMDA receptor currents has been shown to be roughly 1000-fold higher than the EC50 of L-glutamate. Intracerebral injection of QUIN was proven to cause ultrastructural, neurochemical, and behavioral changes similar to those caused by NMDA receptor agonists. The fact that QUIN concentrations are about 5000- to 15,000-fold lower than cerebral L-glutamate concentrations makes it unlikely that modulation of NMDA receptor signaling by QUIN plays an essential role. KYNA was demonstrated to function as an NMDA receptor antagonist. But, although infusion with the KMO inhibitor Ro 61-8048 improved cerebral extracellular KYNA concentrations 10-fold, this didn’t result in an inhibition of NMDA-mediated neuronal depolarization, a finding which challenges the belief that KYNA at near-physiological amounts directly modulates NMDA receptors. In comparison, increased KYNA in the brain induced from the KMO inhibitor JM6 decreased the extracellular cerebral L-glutamate concentration. Additionally, KYNA levels from the extracellular cerebral fluid have been associated with L-glutamate levels suggesting that even at physiological or near physiological levels, KYNA modulates L-glutamate metabolism. Both the activation of the G-protein-coupled receptor GPR35 and the inhibition of presynaptic α7 nicotinic acetylcholine receptors are suggested in the KYNA-induced reduction in L-glutamate release. To summarize, although QUIN and L-HCA are present in the human brain, their concentrations discuss against them with roles in regulating and maintaining neurotransmission. In contrast, even though the pathways have to be defined in greater detail, evidence supports levels and the opinion that discharge can be modulated by KYNA and neurotransmission.  

 

El Paso Chiropractor Dr. Alex Jimenez

Glutamate, together with aspartate and other molecules, are several of the main excitatory neurotransmitters in the human brain. Although these play a fundamental role in the overall structure and function of the central nervous system, including the brain and the spinal cord, excessive amounts of other molecules can ultimately trigger glutamate receptors. Excess glutamate can cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurological diseases. The following article describes how other molecules can activate glutamate receptors. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

Research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .  

 

Curated by Dr. Alex Jimenez  

 

References  

 

  1. 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

 

Neural Zoomer Plus | El Paso, TX Chiropractor  

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.

 


 

 

Glutamate Toxicity in Functional Neurology

Glutamate Toxicity in Functional Neurology

The term excitotoxicity was first employed to demonstrate the capability of L-glutamate, in addition to structurally-associated amino acids, to destroy nerve cells, a process which has been suggested to occur in acute and chronic health issues of the central nervous system (CNS). Excitotoxicity is caused by the excess stimulation of iGluRs into a characteristic loss of cell bodies and dendrites as well as post-synaptic structures. There is a substantial degree of variation in the sensitivity of nerve cells compared to the variety of iGluRs which is associated with the specific receptors demonstrated on the nerve cells and their metabolisms. The susceptibility of neurons to excitotoxicity can be affected with age.  

 

Acute excitotoxic nerve cell death is believed to occur in reaction to a number of severe insults, including cerebral ischemia, traumatic brain injury (TBI), hypoglycemia, and status epilepticus. However, what about neurodegenerative diseases, such as Alzheimer’s disease? Does chronic excitotoxicity also occur? Could exposure of nerve cells to low but above-average concentrations of L-glutamate, or even glutamatergic neurotransmission through a variety of molecules be involved as previously mentioned, within an extended time period also significantly result in neural cell death? The purpose of the article below is to demonstrate the concepts of acute and chronic glutamate toxicity on the health and wellness of the brain.  

 

Acute and Chronic Glutamate Toxicity

 

Excitotoxicity was initially studied in animals, however, so as to comprehend the mechanisms underlying this procedure, cell culture models were developed. The basic cell culture model of acute excitotoxicity involves the treatment of principal neurons in accordance with L-glutamate or particular iGluRs for a brief time interval (min) and then analyzing downstream events in the time point which is most relevant for the research study. By way of instance, cell death is frequently determined after 24 hours. While these types of research studies are proven to be quite useful for understanding the pathways involved in acute excitotoxicity, it has demonstrated to be far more difficult to evaluate chronic excitotoxicity in culture partially because it is not completely clear how to specify “chronic” in the context of cell culture. Does consistent imply a minimal dose supplied for 24 hours instead of a maximum dose supplied for 5 to 10 minutes or is it more complicated than that?  

 

Among the few research studies which tried to come up with a model of chronic excitotoxicity, it was revealed that it is indeed more complicated with acute and chronic excitotoxicity appearing to be different processes. In this research study, the researchers utilized pure cultures of primary cortical neurons developed from day 14 mouse embryos and treated them after seven and 14 days in culture (DIV). For constant excitotoxicity, the neurons were exposed to L-glutamate or NMDA for 24 hours and for severe excitotoxicity for 10 minutes. In both circumstances, cell death was measured after 24 hours. Surprisingly, the EC50s in their toxicity of L-glutamate were lower for acute toxicity, particularly in the 7 DIV cultures, when compared with the EC50s for chronic toxicity. Additionally, it was discovered that a high cell culture density increased the cells’ sensitivity into excitotoxicity that was acute but not chronic. Further research studies indicated that the lower sensitivity of these neurons to L-glutamate in the chronic excitotoxicity paradigm was due to the stimulation of mGluR1, associated with earlier data on the neuroprotective effects of mGluR1 stimulation, among other important processes.  

 

Further Research Studies for Glutamate Toxicity

 

An alternative approach for understanding chronic glutamate toxicity used organotypic spinal cord cultures in conjunction with L-glutamate uptake inhibitors. These spinal cord cultures, which had been prepared from 8-day-old rat pups, were kept in culture for up to 3 months. Persistent inhibition of L-glutamate uptake utilizing two varieties of uptake inhibitors caused a consistent increase of L-glutamate in the cell culture medium and time period as well as a concentration of dependent motor neuron cell death. The highest concentration of uptake inhibitor increased extracellular L-glutamate levels at least 25-fold and began to kill the cells within 1 week whereas a five-fold lower concentration raised extracellular L-glutamate levels eight-fold and cell death only began after 2 to 3 weeks of treatment. The toxicity was obstructed with non-NMDA but not NMDA receptors as well as by inhibitors of L-glutamate synthesis or release. These research studies ultimately indicate that moderately increased L-glutamate concentrations can also induce toxicity as well as a variety of other health issues.  

 

In vivo approaches to studying excitotoxicity have relied on an approach analogous to that utilized with the spinal cord cultures. In the wide variety of the research studies, a single or multiple EAATs were transiently or permanently genetically eliminated and the effects on brain function were evaluated. During the first few research studies, which utilized rats, chronic intraventricular administration of antisense RNA was utilized to eliminate every one of the 3 primary EAATs (EAAT1, EAAT2, and EAAT3). The loss of either of the glial L-glutamate transporters (EAAT1 and EAAT2) but not the neuronal transporter (EAAT3) caused large increases in extracellular L-glutamate concentrations in the striatum following 7 days as demonstrated by microdialysis (EAAT2, 32-fold increase; EAAT1, 13-fold increase). Treatment with the EAAT1 or EAAT2 antisense oligonucleotides caused a progressive motor impairment whereas epilepsy was produced by the EAAT3 antisense oligonucleotide. The loss of any of the 3 transporters demonstrated clear evidence of neuronal damage in the striatum and hippocampus after 7 days of treatment although the effects of the EAAT1 and EAAT2 antisense oligonucleotides were far more dramatic, consistent with the substantial increases in extracellular L-glutamate brought about by treatment.  

 

Particularly different results were demonstrated with homozygous mice deficient in EAAT2 or EAAT1. Mice deficient in EAAT2 demonstrated sudden and normally deadly seizures with 50 percent dead by 6 weeks of age. Approximately 30 percent of these mice demonstrated selective degeneration in the CA1 area at 4 to  8 weeks of age. L-glutamate amounts in the CA1 region of the hippocampus measured by microdialysis were three-fold greater in the mutant mice as compared with the wild type mice. In contrast, heterozygous EAAT2 knock-out mice have an average lifespan and do not reveal hippocampal CA1 atrophy. However, they exhibit several behavioral abnormalities suggestive of moderate glutaminergic hyperactivity. While mice deficient in EAAT1, that is expressed in cerebellar astrocytes, didn’t reveal changes in cerebellar arrangement or obvious indicators of cerebellar impairment, such as ataxic gait, they had not been able to adapt to difficult motor tasks like rapidly running the rotorod. When taken collectively, these results imply that disruptions in homeostasis which are glutamatergic have a greater impact when they occur in the animal rather than when they are found from conception.  

 

Other Health Issues in Glutamate Toxicity

 

Tuberous sclerosis complex (TSC) is a multi-system genetic disease caused by the mutation of both TSC1 or TSC2 genes, where it is characterized by severe neurodegenerative diseases. Mice with inactivation of the TSC1 gene in glia have a less than 75 percent reduction in the expression and function of EAAT1 and EAAT2 as well as to cause seizures. At 4 weeks of age, prior to the development of seizures in these mice, there was a 50 percent increase in extracellular L-glutamate in the hippocampus of the mutant mice, as determined by microdialysis, which correlated with increases in markers of cell death in neurons in both hippocampus and cortex. Utilizing slices from mice that were 2 to 4 week old, impairments in long-term potentiation were determined, which translated into deficits when mice were analyzed for contextual and spatial memory in the Morris water maze and fear conditioning assays. Further research studies are still necessary for outcome measures.  

 

In the majority of the research studies described above, there was a large increase in extracellular L-glutamate that, when analyzed, caused adverse effects on the role of specific neuronal populations. To ascertain the long-term effects of more moderate increases in extracellular glutamate, further research studies created transgenic (Tg) mice with extra copies of this gene for Glud1, especially in neurons. Mitochondrial 2-oxoglutarate from Glud1 is transported into the cytoplasm of nerve terminals in which it’s converted back into L-glutamate and kept in synaptic vesicles thus leading to the pool of synaptically releasable L-glutamate. Nine-month-old Glud1 Tg mice demonstrated a 10 percent boost in L-glutamate in the hippocampus and striatum relative to wild type mice as determined to utilize magnetic resonance spectroscopy. In addition, 50 percent caused increased L-glutamate release in the striatum. At 12 to 20 months of age, the Glud1 Tg mice revealed significant decreases in the numbers of neurons in the CA1 area of the hippocampus and granule cell layer of the dentate gyrus in addition to an age-dependent loss of the two dendrites and dendritic spines in the hippocampus. There was also a drop in long-term potentiation after high frequency stimulation in hippocampal slices in the mice when compared with the wild type mice. Evaluation of the transcriptome of those Glud1 Tg mice in comparison with wild type mice indicated that long-term moderate increases in cerebral L-glutamate ultimately caused both rapid aging in the level of gene expression combined with compensatory reactions which protected against pressure and/or promoted recovery, among other capabilities.  

 

Conclusion

 

Brain function and nerve cell survival can be affected by excitotoxicity. The results appear to be highly dependent on the degree of L-glutamate increase, however, even a 10 percent growth appears to influence nerve cell survival, particularly in the context of aging indicating that chronic excitotoxicity may be associated with neurodegenerative diseases.  

 

Several toxins which connect to iGluRs and that have also been demonstrated to cause excitotoxicity in cell culture may cause slowly growing neurological health issues in both animals and humans. Surprisingly, each toxin appears to target a particular type of neuron, an effect which may be associated with the pharmacokinetics and ADME properties of the toxins, which have not been analyzed to any great extent. The data from these types of toxins supports the idea that excitotoxicity may play a fundamental role in neurodegenerative diseases as well as in other health issues which exist in humans.  

 

Because iGluRs are demonstrated both from the synapse and in extra-synaptic locations, there has been a great deal of effort devoted to discovering if the region of the receptors impacts the toxicity of molecules. An influential research study with primary neuronal cultures indicated that synaptic and extrasynaptic NMDA receptors have counteracting effects on cell survival with neural cell death being primarily controlled by extrasynaptic NMDA receptors. Nonetheless, these outcome measures have not been reproduced in brain slices or in vivo. Furthermore, many more recent research studies utilizing the exact same primary neuronal culture preparation protocol as the prior research study found either no difference between synaptic and extrasynaptic NMDA receptors in boosting excitotoxicity or discovered that both receptors were needed for cell death. Finally, a variety of research studies that supported the idea that extrasynaptic NMDA receptors promote excitotoxicity relied on the NMDA receptor inhibitor memantine that was originally believed to specifically act on extrasynaptic NMDA receptors. However, more recent research studies demonstrate that memantine can inhibit both synaptic and extrasynaptic NMDA receptors. These results strongly imply that synaptic and extrasynaptic NMDA receptors may contribute to excitotoxicity but the contribution of each depends on the experimental and/or pathological conditions.  

 

El Paso Chiropractor Dr. Alex Jimenez

Glutamate is the primary excitatory neurotransmitter in the brain. Although it plays a fundamental role in the overall structure and function of the central nervous system, excessive amounts of glutamate can ultimately cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurodegenerative diseases. Acute and chronic excitotoxicity treatment currently focuses on decreasing or restricting glutamate receptors or extracellular glutamate. The article above summarizes the available research studies for glutamate toxicity in neurodegenerative diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

Excitotoxicity demonstrates the capability of L-glutamate, as well as structurally-associated amino acids, processes which have been suggested to occur in acute and chronic excitotoxicity. Excitotoxicity is caused by the excess stimulation of iGluRs in cell bodies and dendrites as well as post-synaptic structures. There is a substantial degree of variation in nerve cells compared to iGluRs associated with the receptors demonstrated on the nerve cells and their metabolisms. 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  

 

  1. 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

  Neural Zoomer Plus | El Paso, TX Chiropractor

 

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 Formulas - El Paso, TX

 

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.

xymogen el paso, tx

 

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.