L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the following article, we will discuss the general principles of L-glutamate signaling in the brain. Then, we will demonstrate this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discuss their possible physiological functions in the human brain. �
Contents
Glutamate Signaling in the Brain
According to research studies, the human brain has about a 6 to 7 ?mol/g wet weight of L-glutamate. L-glutamate, together with glutamine, is one of the most abundant free amino acids in the central nervous system (CNS). More than five decades ago, several research studies demonstrated that L-glutamate has an excitatory response on nerve cells. Since then, its role as an excitatory neurotransmitter as well as its cerebral metabolism has been evaluated in numerous research studies. �
L-glutamate is commonly found throughout synaptic vesicles in the presynaptic terminal through the process of vesicular glutamate transporters. Additionally, several of the L-glutamate in the vesicles may develop by a vesicle-associated aspartate amino-transferase from 2-oxoglutarate utilizing L-aspartate as the amino group donor. During the depolarization of the presynaptic membrane, L-glutamate is released into the synaptic cleft and connects to ionotropic glutamate receptors, known as iGluRs, at the postsynaptic membrane, as shown in Figure 1. According to research studies, iGluRs are characterized as ligand-gated ion channels which include receptors of the ?-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), kainate, and N-methyl-D-aspartic acid (NMDA) types. While AMPA and kainate receptors primarily regulate and maintain sodium influx, NMDA receptors actually have a high calcium conductivity. Moreover, the activation of NMDA receptors plays a fundamental role in synaptic plasticity and learning. In contrast to the other iGluRs, the activity of NMDA receptors is ultimately restricted by an Mg+2 block at the regular membrane potential, however, the ion channel is immediately unblocked by membrane depolarization which eliminates Mg+2 from the pore. Furthermore, NMDA receptors are tetramers that have two NR1 subunits and two NR2 or NR3 subunits, according to several research studies. �
Additionally to iGluRs, there are also eight isoforms of metabotropic glutamate receptors (mGluRs) which belong to the family of G-protein-coupled receptors, where they don’t develop ion channels but instead signal through a variety of second messenger systems. L-glutamate-associated depolarization causes a postsynaptic excitatory potential which eases the development of an action potential at the axon hillock. The glutamatergic synapse is activated by astrocytic processes that demonstrate high levels of excitatory amino acid transporters (EAATs). There are five different EAATs, EAAT1 to 5, of which EAAT1 and 2 are the primary astrocytic EAATs, whereas EAAT3 shows a predominantly neuronal expression. Approximately 90 percent of the L-glutamate transport is regulated and maintained by EAAT2 such as GLT-1 in rodent models. These transporters then co-transport 2 or 3 molecules of Na+ and a proton with each molecule of L-glutamate or L-aspartate together with the counter-transport of a K+ ion. Therefore, by utilizing the electrochemical gradient of these ions throughout the plasma membrane as an energy source, the transporters are able to safely and effectively accumulate L-glutamate and L-aspartate in cells against their sudden intra- to extracellular concentration gradients. This allows the brain to control a very low extracellular L-glutamate concentration in the low micromolar range. It is generally believed that L-glutamate taken up by astrocytes is turned to glutamine by the enzyme glutamine synthetase, the glutamine is then released, taken up by neurons and turned to L-glutamate, where it is ultimately utilized once again for neurotransmission. �
Extrasynaptic Glutamate in the Brain
Aside from the essential role of L-glutamate as the primary excitatory neurotransmitter released from glutamatergic presynapses, as previously mentioned above, it has become evident that L-glutamate receptors outside the synaptic cleft also play an essential role in brain physiology. In the cerebellum, it was demonstrated by evaluating AMPA receptor-mediated currents in Bergmann glia that synaptically released L-glutamate concentrations can reach extrasynaptic concentrations of up to 190 ?M while concentrations in the synaptic cleft can exceed 1 mM. Moreover, several mGluRs have been shown to demonstrate a different localization in proximity to the postsynaptic density which would allow them to immediately recognize L-glutamate escaping from the synaptic cleft, as shown in Figure 1. However, current research studies have demonstrated that iGluRs, especially of the NMDA type, are also found at extrasynaptic regions in the neuronal cell membrane. Utilizing light and electron microscopy, other research studies also demonstrated that extrasynaptic NMDA receptors gather at different regions of close contact in the dendritic shaft with axons, axon terminals, or astrocytic processes. The proportion of extrasynaptic NMDA receptors was estimated to be as high as 36 percent of the dendritic NMDA receptor pool in rat hippocampal slices. Although extrasynaptic NMDA receptors were associated with similar scaffolding proteins as synaptic NMDA receptors, an in vitro research study suggested that extrasynaptic and synaptic NMDA receptors may ultimately activate different downstream signaling pathways with a variety of results, including the suppression of CREB activity by extrasynaptic NMDA receptor activation as well as activation by synaptic NMDA receptors. Furthermore, NMDA receptors localized extrasynaptically on dendritic shafts connect extrasynaptic L-glutamate as well as regulate and maintain Ca2+ influx during the elimination of the Mg+2 block by dendrite depolarization throughout the backfiring of action potentials. Research studies demonstrated that L-glutamate release from astrocytes can activate slow inward currents through extrasynaptic NMDAR receptors in CA1 neurons which can also be ultimately synchronized. The mechanisms through which glial cells release L-glutamate as well as how the extrasynaptic L-glutamate concentrations are controlled are vital towards understanding how the activity of extrasynaptic NMDA receptors is controlled. �
Different mechanisms through which astrocytes can release L-glutamate have been suggested, including vesicular L-glutamate release and non-vesicular release through anion channels as well as connexin hemichannels and release through the cystine/glutamate antiporter system x?c. Several research studies strongly suggest that vesicular release from astrocytes plays a minor role because the Ca+2-associated release of L-glutamate was still present in astrocytes created from dominant-negative SNARE mice where vesicular release can be blocked by doxycycline withdrawal. System x?c is a cystine/glutamate antiporter which is characterized as heterodimeric amino acid transporters, made up of xCT as the specific subunit and 4F2hc as the promiscuous heavy chain. This transporter is demonstrated in the brain, especially in astroglial and microglial cells, as shown in Figure 1. The fact that extrasynaptic L-glutamate levels in different regions of the human brain are downregulated by approximately 60 percent to 70 percent in xCT knock out mice, research studies demonstrated that system x?c releases L-glutamate into the extrasynaptic space and suggests that this transporter is essential in the regulation of extrasynaptic L-glutamate levels. This is further supported by the observation that when measured by in vivo microdialysis, the increase in extrasynaptic L-glutamate developed by EAAT inhibitors is neutralized by blocking system x?c while blocking neuronal vesicular L-glutamate release is ineffective. Further research studies are still required. �
Taken together, glutamatergic neurotransmissions don’t simply happen through classical excitatory synapses but also through extrasynaptic L-glutamate receptors, as shown in Figure 1. Finally, the levels of extrasynaptic L-glutamate are determined, at least partially, by glial non-vesicular L-glutamate release, as also shown in Figure 1. However, the regulation of extrasynaptic L-glutamate levels, as well as its temporal-spatial dynamics and its effect on neuronal function, neurodegeneration, and behavior, are far from being fully understood by researchers, healthcare professionals, and patients. �
Glutamate, together with aspartate, is one of the main excitatory neurotransmitters in the human brain. Although it plays a fundamental role in the overall structure and function of the 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 neurological diseases. The following article describes the role of glutamate in the human brain. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the article above, we discussed the general principles of L-glutamate signaling in the brain. Then, we demonstrated this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discussed their possible physiological functions in the human brain. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
Myofascial syndrome, what is it? You’re probably thinking I don’t have that, but more than likely, you have.
Myo means muscle and fascia refer to the tissue bands that cover and connect the muscles/organs.
Tightness
Twitching areas
Painful knots
In the neck/back, then myofascial pain syndrome could be the cause.
Myofascial syndrome is a very common condition. It affects about 44 million people in the United States.
Contents
Trigger Points The Areas Where Pain Can Develop
Myofascial pain is associated with trigger points. These are areas that can become tender and stiff inside muscle tissue that reduce the range of motion.
Myofascial pain syndrome can happen when you have several active trigger points.
Trigger points are often referred to as knots because they feel tight and balled up compared to the softer relaxed surrounding muscle/s.
If the muscle becomes tight, it can cut off its blood supply, that can trigger:
Muscle tenderness
Pain
Spasm
Tightness
Trigger points can form all over the body which includes:
Neck
Mid-back
Low back
Common characteristics of trigger points are that they cause pain that travels or spreads to the surrounding area. For example, shoulder pain can radiate across the upper back.
The muscles can also twitch when touched.
Pretty much everyone has trigger points, but not all triggers cause symptoms.
Dormant or latent��trigger points can reduce the range of motion but only cause pain when directly palpated or compressed,
Active trigger points are painful any time, even when at rest.
Lifestyle factors like:
Stress
Poor posture
Can make a dormant trigger point become active.
Trigger Point Causes in the Spine
Spinal injury or trauma can result in myofascial pain syndrome, but lifestyle factors usually have a hand in the condition.
Poor posture over a long period, for example, sleeping in an awkward position can cause physical muscular stress on the spinal muscles.
Mental and emotional stress can present itself through muscle tension that helps the development of trigger points.
The trapezius muscle, that extends from the back of the neck down the shoulders and upper back, is the most common site of spinal trigger points and myofascial pain because of the significant amount of pressure that the muscle has to bear and its susceptibility to whiplash.
The Difference Myofascial Syndrome and Fibromyalgia
Because myofascial syndrome is linked to triggering points, fibromyalgia and its tender points bring out a comparison of the two.
Myofascial pain syndrome and fibromyalgia are two distinct conditions, and the table below outlines the primary differences.
Because they are unique conditions, there is a possibility to develop both conditions.
Doctor(s) can help craft a treatment approach that addresses the pain of both trigger points and tender points.
Diagnosis can be difficult
Myofascial pain syndrome is common but can be difficult to diagnose.
The challengingreasons behind diagnosing include:
Scientists are not sure how these trigger points cause pain.
The condition is often confused for other spinal disorders and conditions.
An example is having low back pain caused by myofascial syndrome in the lumbar spine. But low back pain brought on by arthritis can cause similar pain. That’s when the cause needs to be carefully and properly assessed.
There is no standard test for myofascial pain syndrome diagnosis yet.
There�s no standard diagnosing protocol but manual palpation or use of the hands to feel for:
Tenderness
Twitching
Tightness around the area
Is the most common way doctors diagnose the condition.
Some doctors might only utilize manual palpation but ultrasound is emerging as a diagnostic tool for myofascial pain syndrome.
Ultrasound produces clean images of the soft tissues and shows the active trigger points.
However, more research is needed to secure its place as a diagnostic method and tool.
A personal or primary care doctor can diagnose myofascial syndrome, but they may refer you to a pain specialist or a spine specialist like:
Doctors and researchers are still learning about myofascial syndrome, therefore, treatment options differ from doctor to doctor.
But most doctors do support a multidisciplinary treatment approach that is, using a variety of therapies and employing lifestyle changes to manage trigger point pain and prevent it from coming back.
Below are common treatments for myofascial pain syndrome.
Release Therapy
Myofascial release is a broad treatment option that consists of manual or instrument-guided therapydesigned to release the muscles and fascia by use of applying pressure.
There are different release therapies, such as:
Practitioners and clinicians are trained in myofascial release therapy, including:
Massage therapists
Physical therapists
Chiropractors
Physiatrists
The goal is the same:
Put pressure on the trigger point and release it.
Myofascial release technique might sound like a massage, but it is a distinct method compared to massage.
Massage moves muscles up and down,� myofascial release utilizes direct pressure into the stiff fascia and muscle.
Repeated pressure on the tight areas is not soothing, and patients tell of soreness during and after the treatment.
Once the trigger point loosens up, blood flow and nerve function begin to return to the area.
Then the pain is gone, hallelujah!
Additional Care Options
Myofascial release therapy is just one option for trigger point pain.
Other common treatments to manage spine-related pain include:
Home
If you know the location of the trigger points you can treat them at home with simple tools.
Rolling the trigger point over a:
Foam roller
Golf ball
Tennis ball
Can help loosen any of the tight areas.
Over-the-counter medication
If doctor-approved, then taking an over-the-counter pain reliever like acetaminophen (Tylenol) or ibuprofen (Motrin, Advil) can help with spine pain and allow daily activities.
Physical therapy
Physical therapy like:
Massage
Chiropractic
Heat
Electrical stimulation
Ultrasound
There are also stretches/exercises to keep muscles warm and flexible to help any future trigger points from forming.
Massage therapy
Licensed massage therapists practice myofascial release therapy, but also include other forms of massage
Deep tissue massage
Swedish massage
Can also help relieve trigger point pain.
Massage can also help to relax, and this is very important in preventing myofascial pain syndrome.
Also, learn how to keep stress and anxiety in check, and avoid tension that can turn into trigger points.
Dry needling/acupuncture
While both therapies use needles, dry needling and acupuncture are different treatments that can reduce the pain.
There is not a lot of research on dry needling like acupuncture, but it can help increase blood flow to the trigger point area.Acupuncture means inserting needles into specific points on the body.
These needles help stimulate the body’s energy and help in sending signals to the nervous system to release chemicals into the body to help with the pain, which means less pain.
Trigger point injections
If any of these treatments don’t seem to be working, then you might want to talk to your doctor about trigger point injections.
Trigger point injections can help relieve pain, and a doctor usually recommends them to be done along with a physical therapy/chiropractic treatment program.
Keep the Pain Away & Prevention
Many people who have trigger points or myofascial pain syndrome in their spine have knots and tightness throughout their back and neck.
To prevent myofascial pain syndrome one needs to practice a healthy lifestyle that promotes good spine health.
Stretching and exercising regularly can help keep stress under control and prevent tension from building up, which makes it harder for trigger points to activate and cause pain.
El Paso Chiropractic Back Pain Therapy
Andres “Andy” Martinez first came to see Dr. Alex Jimenez in Push Fitness after undergoing back pain and knee issues. Following a period of physical therapy and rehabilitation, Andy became engaged in Crossfit, where he learned everything he needed to know about health and wellness from the coaches at Push. Andres Martinez expresses how grateful he is to receive the amount of care he does against the staff and he clarifies how much his perspective of fitness has shifted from the first time he walked into Push Fitness. Andy has seen a family at Push who led him to a healthy, clean life and both the trainers and staff mean everything to Andres Martinez.
NCBI Resources
The knots you have probably felt in your muscles or had others identify are also known as trigger points. These tight spots are often sensitive to the touch and can be found in any muscle in your body. As they develop, they may produce symptoms like numbness, burning, weakness, pain, and tingling. Trigger points are caused by trauma to the body, such as an accident in a car or during athletics. They can also be caused by more mild, long-term trauma, such as working at a desk without proper ergonomics or making a repetitive motion over a long period of time. Chiropractors are not only good at finding trigger points, but they are also good at treating them.
For people who love drinking diet sodas, recent research studies have found that diet drinks can increase the risk of stroke and dementia. Although diet drinks have been previously advertised as a much more healthier, low-calorie alternative than regular carbonated drinks, a closer look at the results of these recent research studies ultimately suggests otherwise. �
One research study, consisting of 2,888 participants, ages 45 and older, in the Framingham Heart Study, asked for diet entries to be filled out up to three times within a seven-year period. According to the research study, participants who said they drank one diet soda a day were roughly twice as likely to have a stroke within the next decade than individuals who didn’t drink diet soda. Drinking regular, sugar-sweetened carbonated drinks did not seem to increase the risk of stroke. �
However, these types of research studies have only been able to prove an association between diet drinks, stroke, and dementia. “Also, only 97 people (about 3 percent) had strokes during the follow-up, which means that only two or even three of those strokes may be associated to drinking diet soda,” stated Dr. Kathryn Rexrode, an associate professor of medicine at Harvard-affiliated Brigham and Women’s Hospital which co-authored a research study on soda intake and stroke risk. �
Contents
Risk of Stroke Associated with Diet Drinks
The research study found a slightly increased risk of stroke in people who drank more than one soda per day, whether or not it contained any type of artificial sweetener. Although the research study didn’t particularly show a considerable increase in stroke risk, that doesn’t necessarily suggest that they’re a better option than diet sodas. Research studies have shown that drinking carbonated drinks may lead to weight gain, diabetes, high blood pressure, heart disease, and stroke, ” she stated. �
As a matter of fact, researchers believe that one possible explanation as to why regular, sugar-sweetened carbonated drinks weren’t associated with stroke in the recent research study is a phenomenon known as the survival bias. In this instance, it would mean that individuals who drink a lot of carbonated drinks may have died from health issues such as heart disease. �
Conversely, diet drinks may be associated with an increased risk of stroke due to a variety of health issues known as reverse causation. In an attempt to be healthier, individuals who are overweight or have diabetes may be more inclined to select diet drinks over regular drinks. Their increased risk of stroke may come from their health issues rather than their drink option. “We may ultimately only be measuring the residual effect of weight gain, obesity, and diabetes,” says Dr. Rexrode. �
Artificial Sweeteners and Stroke
� Although researchers need further evidence to determine why artificial sweeteners may increase stroke risk, there are other reasons as to why these should be avoided. Research studies show that artificial sweeteners can make individuals crave sugary, high-calorie meals, therefore, decreasing the artificial sweetener’s purpose of cutting your total calorie consumption. �
Moreover, many researchers believe that people who use these artificial sweeteners, which can be many times sweeter than sugar, can come to find naturally sweet foods, such as fruits, to be less appealing and less-sweet foods, such as vegetables, to be entirely unpalatable. Furthermore, individuals may be missing out on the many nutrients found in fresh, natural foods. �
“I encourage my patients to stop drinking soda and other sugar-sweetened carbonated drinks regularly to prevent empty calories,” she says. “However, if someone says that they can’t do without soda in the morning to wake up, I will encourage them to switch to diet soda.” Water is a much better choice, however. “There are plenty of ways to make it more attractive, both visually and taste-wise.” She adds. Try flavoring sparkling or flat water or add crushed mint, cucumber, or frozen fruit. �
Risk of Dementia Associated with Diet Drinks
In another research study, people who drank diet soda were associated with an increased risk of developing dementia. “The research study can’t prove a connection between drinking habits and health issues, however, it does strongly suggest an association,” Stated Dr. Matthew Pase, neurology fellow at Boston University School of Medicine and contributing author. �
The initial research study evaluated food questionnaires, MRI scans, and cognitive tests of approximately 4,000 people ages 30 and up. Researchers found that individuals who consumed over three diet sodas per week were more likely to have memory problems, a reduced brain volume, and a smaller hippocampus, an area of the brain used in memory and learning. In the research study, drinking a minimum of one diet soda per day was also associated with a reduced brain volume. �
During a second research study, the researchers tracked two different groups of adults for ten years. According to the research study, out of almost 3,000 adults over age 45, approximately 97 adults suffered a stroke during that time and from almost 1,500 adults over age 60, approximately 81 adults developed Alzheimer’s disease or another type of dementia. �
Past research studies have connected diet drinks to an increased risk of weight gain and stroke. Researchers believe that artificial sweeteners may ultimately affect the human body in many different ways, such as by transforming gut bacteria and tricking the brain into craving more calories. This is the first-time diet sodas have been associated with dementia. Because people with diabetes drink more diet soda, researchers believe that the health issue may partly explain the rise in dementia, although not completely. When people with diabetes were excluded from the research study, the association stayed. �
As stated by the United States Department of Agriculture, Americans consumed 11 million metric tons of sugar in 2016, much of it in the form of sugary, sweetened carbonated drinks. Because it would have been difficult to measure total sugar consumption from all type of different food sources, the research study focused on sugary, sweetened carbonated drinks. �
A growing number of research studies suggest that diet drinks may not be a safe alternative to sugary, sweetened drinks. Even small causal effects can have much bigger consequences on health, given the popularity of both diet and regular sodas. The research study concluded that both glucose and artificially sweetened soft drinks “may be hard on the brain.” �
Diet soda is basically a mixture of carbonated water, natural or artificial sweetener, colors, flavors, and other food additives. Although diet drinks generally have very few to no calories, these essentially have no significant nutritional value. Many research studies have demonstrated that drinking diet soda is associated with an increased risk of stroke and dementia. Researchers have also found that diet drinks can cause a variety of other health issues. It’s essential for to avoid drinking too much diet soda. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Recent research studies have found that diet drinks are associated with an increased risk of stroke and dementia. Although diet drinks are advertised as a much more healthier, low-calorie alternative than regular carbonated drinks, a closer look at the results of these recent research studies ultimately suggests otherwise. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Corliss, Julie. �Does Drinking Diet Soda Raise the Risk of a Stroke?� Harvard Health Blog, 31 July 2017, www.health.harvard.edu/blog/drinking-diet-soda-raise-risk-stroke-2017073112109.
MacMillan, Amanda. �A Daily Diet Soda Habit May Be Linked to Dementia.� Health.com, 21 Apr. 2017, www.health.com/alzheimers/diet-soda-linked-to-dementia-stroke.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download�
* All of the above XYMOGEN policies remain strictly in force.
Supplements are essential as we take them for our overall health. Since we can�t produce supplements naturally, we make it in pill form or eat whole, nutritious food. When we don�t take our supplements, our bodies will not function properly, and we can have a severe health risk. In the last article, we took a look at what vitamins does to our micronutrients in our bodies to perform functional and healthy. Today we will discuss what some supplement that will help our micronutrients in our bodies.
Contents
The Supplements
Since supplements can come in many types of foods and can be found as pills in whole food stores in the vitamin section.� Here are some of the leading supplements to ensure that your body’s micronutrients are getting the essentials to promote a long healthy life.
Vitamin K1 and K2
Vitamin K is known for its role in blood clotting. With vitamin K1 and K2, they can provide the health benefits that will help you from getting a blood clot. Vitamin K was accidentally discovered in the 1920s and 1930s after researchers found that animals having a restricted diet leads to excessive bleeding.
Vitamin K1 (phylloquinone) is found in plants foods like leafy green vegetables. With K2, it is found in fermented foods and animal products. Vitamin K2 (menaquinones) can be produced by gut bacteria and help promote a healthy gut. These two vitamins are fat-soluble that share the same chemical structure and have different effects on your health.
Vitamin K1 can be absorbed quickly than vitamin K2 and can stay in the bloodstream for hours. Vitamin K1 is transported primarily to and used by the liver. Even though vitamin K1 is mostly found in plant foods, here are some of the food sources that are caulked filled with this vitamin and amazing when cooked.
Kale
Collard greens
Spinach
Turnip greens
Broccoli
Brussel sprouts
Vitamin K2 is mostly found in animal products that contain fat. Even though it provides fatty compounds, vitamin K2�s long side-chain allows it to circulate the blood longer than K1 can remain in the blood for days.� Here are some fermented food sources and animal products that vitamin K2 as MK-10 and MK-11.
Natto
Pork sausage
Hard cheeses
Porkchop (with the bone)
Chicken (leg/thigh)
Soft cheeses
Egg yolk
Calcium
Calcium is one of the most essential supplements that is for all living organisms. It is found naturally in many foods and added to certain products like supplements. Calcium promotes bone health, and without it, bone density can happen when we don�t take in the supplement. It also helps regulate muscle contractions, including the beating of the heart muscle. When that happens, calcium helps the proteins in the muscle to carry out the work of the contraction. Here are some of the foods and drinks that are richly filled with calcium.
Milk
Cheese
Yogurt
Seaweed
Beans
Figs
Tofu
Manganese
Manganese is an essential supplement for your brain and nervous system as well as many of your body�s enzyme system. Our body stores up to 20 mg of manganese in our kidneys, liver, pancreas, and bones. In a 2011 study, manganese helps form an antioxidant enzyme called SOD (superoxide dismutase). It helps break down one of the most dangerous free radicals called superoxide; into smaller components that are not harmful. Researchers also suggested that SOD is beneficial as a therapeutic agent for inflammatory diseases. Small amounts of manganese are present in these food sources.
Raw pineapple and pineapple juice
Pinto beans
Spinach
Black and green teas
Sweet potato
Almonds
Instant oatmeal
Copper
Copper is an essential trace supplement that is necessary for survival. It is found in all the body tissues and plays a vital role in making red blood cells, maintaining nerve cells and the immune system. When you have sufficient copper in your diet, it may help prevent cardiovascular diseases and osteoporosis. Copper deficiency is a rare case, but low levels of copper can lead to anemia, loss of skin pigmentation, thyroid problems, and the rare disease Menkes disease. Since copper is found in a wide variety of foods, here are some excellent food sources that contain it.
Oysters and other shellfish
Whole grains
Cocoa
Black pepper
Organ meats (liver and kidneys)
Potatoes
Dried fruit
Chromium
Also known as chromium picolinate, this supplement does serve several vital functions in the body. Chromium can improve your body�s blood sugar by impacting on the hormone insulin. Several studies indicate that people with diabetes take the chromium supplement to improve their blood sugar. While another study researched that people who are overweight or obese, taking the chromium supplement can lose weight.
Iron
Iron is one of the essential supplements that are vital to the human body. It helps hemoglobin function properly by transporting oxygen in the blood. Iron also plays a huge role as it functions in a variety of other vital processes in the body. With iron�s health benefits, the supplement can promote a healthy pregnancy, regulate body temperature, preserve universal energy and focus, help the gastrointestinal process, and support the immune system.
When we don�t get enough iron in our system, we do suffer from anemia, which causes fatigue, heart palpitations, pale skin, and breathless. So it is crucial that when we eat iron-rich foods so that way, we won�t have that deficiency. There are two types of dietary iron that we consumed, and they are known as heme and non-heme. These two forms are both animal source food and plant food, and here are what the food sources contain.
Canned clams
Cooked Pacific oysters
Beef liver
Lean ground beef
Cooked spinach
Dark chocolate
Firm tofu
Medium baked potato
Magnesium
Magnesium is an essential mineral that is found in the earth, sea, plants, animals, and humans. In our body, there is about 60% of magnesium in our bones. While the rest is in the muscles, soft tissues, and fluids, including blood. Magnesium helps to prevent problems with our bones, the cardiovascular system, diabetes and fights depression.
The recommended intake amount to take magnesium is 300-420mg per day for men and 310-320mg per day for women. We can get it from both food sources and supplements, here are some of the food sources that contain magnesium.
Dark chocolate (70-85% cocoa)
Cashews
Quinoa, cooked
Avocado
Spinach, boiled
Mackeral
Selenium
Selenium is an essential supplement that can help contribute thyroid hormone metabolism, process a healthy immune system, and protect against oxidative damage and infections in the body. Selenium deficiency is rare, but the supplement can be found in whole grains and animal products than fresh fruits and vegetables. Here are some of the food sources that contain selenium.
Brazil nuts
Tuna
Brown rice
White bread
Egg
Halibut
Omegas
The Omega supplements are very well known, especially Omega-3; which can help us with our brain, eyes, and immune health. Without the supplement, it can lead to reduced energy, loss of attention and concentration, dry, irritated skin problems, and many more symptoms. It is mostly found in fish and seafood as well as some vegetables and seed oils. Here are some of the omega supplements to help promote a healthy body.
DPA (docosapentaenoic acid): This omega supplement is the most influential on reducing inflammation and helping people who are profiled for cardiac risk.
EPA (eicosapentaenoic acid): This omega supplement is vital to boost the brain and moods.
LA (linoleic acid): This omega supplement can�t be synthesized in the body, but does help fight cancer. It is needed to help out with omega 3 and is primarily found in beef.
Conclusion
Granted that these are only some of the supplements here that can help your body function properly. There are many supplements and vitamins out there in the world that are in both pill and food form to help our bodies grow and overall makes us healthier. These supplements and vitamins help us by making sure that our bodies don�t get sick and suffer from chronic diseases that we may encounter. So go out there and enjoy some whole, nutritious food that oozing with beneficial vitamins and supplements.
Cites:
Almquist, H J. �Early History of Vitamin K.� OUP Academic, Oxford University Press, 1 June 1975, academic.oup.com/ajcn/article-abstract/28/6/656/4716361?redirectedFrom=fulltext.
Beulens, Joline W J, et al. �The Role of Menaquinones (Vitamin K?) in Human Health.� The British Journal of Nutrition, U.S. National Library of Medicine, Oct. 2013, www.ncbi.nlm.nih.gov/pubmed/23590754.
Brinton, Eliot A, and R Preston Mason. �Prescription Omega-3 Fatty Acid Products Containing Highly Purified Eicosapentaenoic Acid (EPA).� Lipids in Health and Disease, BioMed Central, 31 Jan. 2017, www.ncbi.nlm.nih.gov/pubmed/28137294.
Calder, Philip C. �Docosahexaenoic Acid.� Annals of Nutrition & Metabolism, U.S. National Library of Medicine, 2016, www.ncbi.nlm.nih.gov/pubmed/27842299.
DeLoughery, Thomas G. �Iron Deficiency Anemia.� The Medical Clinics of North America, U.S. National Library of Medicine, Mar. 2017, www.ncbi.nlm.nih.gov/pubmed/28189173.
Di Bona, Kristin R, et al. �Chromium Is Not an Essential Trace Element for Mammals: Effects of a �Low-Chromium� Diet.� Journal of Biological Inorganic Chemistry: JBIC: a Publication of the Society of Biological Inorganic Chemistry, U.S. National Library of Medicine, Mar. 2011, www.ncbi.nlm.nih.gov/pubmed/21086001.
Fu, Xueyan, et al. �Measurement of Multiple Vitamin K Forms in Processed and Fresh-Cut Pork Products in the U.S. Food Supply.� Journal of Agricultural and Food Chemistry, U.S. National Library of Medicine, 8 June 2016, www.ncbi.nlm.nih.gov/pubmed/27191033.
Goodson, Amy. �10 Evidence-Based Benefits of Manganese.� Healthline, Healthline Media, 31 Aug. 2018, www.healthline.com/nutrition/manganese-benefits.
Gr�ber, Uwe, et al. �Magnesium in Prevention and Therapy.� Nutrients, MDPI, 23 Sept. 2015, www.ncbi.nlm.nih.gov/pubmed/26404370.
Harshman, Stephanie G, et al. �Vegetables and Mixed Dishes Are Top Contributors to Phylloquinone Intake in US Adults: Data from the 2011-2012 NHANES.� The Journal of Nutrition, Oxford University Press, July 2017, www.ncbi.nlm.nih.gov/pubmed/28566528.
Kaur, Gunveen, et al. �Short Update on Docosapentaenoic Acid: a Bioactive Long-Chain n-3 Fatty Acid.� Current Opinion in Clinical Nutrition and Metabolic Care, U.S. National Library of Medicine, Mar. 2016, www.ncbi.nlm.nih.gov/pubmed/26808265.
Li, Chang, and Hai-Meng Zhou. �The Role of Manganese Superoxide Dismutase in Inflammation Defense.� Enzyme Research, SAGE-Hindawi Access to Research, 2011, www.ncbi.nlm.nih.gov/pmc/articles/PMC3185262/.
Megan Ware, RDN. �Copper: Health Benefits, Recommended Intake, Sources, and Risks.� Medical News Today, MediLexicon International, 23 Oct. 2017, www.medicalnewstoday.com/articles/288165.php.
Naughton, Shaan S, et al. �Linoleic Acid and the Pathogenesis of Obesity.� Prostaglandins & Other Lipid Mediators, U.S. National Library of Medicine, Sept. 2016, www.ncbi.nlm.nih.gov/pubmed/27350414.
Newman, Tim. �Calcium: Health Benefits, Foods, and Deficiency.� Medical News Today, MediLexicon International, 21 Aug. 2017, www.medicalnewstoday.com/articles/248958.php.
Schurgers, Leon J, et al. �Vitamin K-Containing Dietary Supplements: Comparison of Synthetic Vitamin K1 and Natto-Derived Menaquinone-7.� Blood, U.S. National Library of Medicine, 15 Apr. 2007, www.ncbi.nlm.nih.gov/pubmed/17158229.
Serefko, Anna, et al. �Magnesium in Depression.� Pharmacological Reports: PR, U.S. National Library of Medicine, 2013, www.ncbi.nlm.nih.gov/pubmed/23950577.
Suksomboon, N, et al. �Systematic Review and Meta-Analysis of the Efficacy and Safety of Chromium Supplementation in Diabetes.� Journal of Clinical Pharmacy and Therapeutics, Centre for Reviews and Dissemination (UK), June 2014, www.ncbi.nlm.nih.gov/pubmed/24635480.
Tian, Hongliang, et al. �Chromium Picolinate Supplementation for Overweight or Obese Adults.� The Cochrane Database of Systematic Reviews, John Wiley & Sons, Ltd, 29 Nov. 2013, www.ncbi.nlm.nih.gov/pubmed/24293292.
Yasui, K, and A Baba. �Therapeutic Potential of Superoxide Dismutase (SOD) for Resolution of Inflammation.� Inflammation Research: Official Journal of the European Histamine Research Society … [Et Al.], U.S. National Library of Medicine, Sept. 2006, www.ncbi.nlm.nih.gov/pubmed/17122956.
Cervical radiculopathy happens when a pinched nerve in the neck (cervical spine) causes pain.
Radicular pain can extend beyond the neck and radiate down:
The shoulders
Arms
Fingers
This type of nerve compression also causes:
Weakness
Numbness
Tingling
Reflex problems
The neck consists of 8 pairs of nerves that control several motor (strength) and sensory (feel) functions.
The cervical nerve roots at the top send movement and feeling signals to the head and neck, and the nerves at the bottom enable motor and sensory function to the arms and hands.
If one or more of the spinal nerves in the neck gets pinched, it can disturb its ability to function correctly.
This results in radiating pain in the neck and other areas of the body.
This condition can affect anyone but usually affects middle-aged adults.
Men also tend to develop cervical radiculopathy more than women.
Contents
Causes
The natural aging process on the spine is what usually causes cervical radiculopathy.
The spine goes through the aging process just like the rest of the body and even more as it is the basis of our structure.
This process can lead to several degenerative spinal disorders, that include:
Cervical spondylosis (osteoarthritis)
Spinal stenosis
Herniated discs
When nerve passageways begin to narrow, intervertebral discs begin to protrude,� and bone spurs, caused by these disorders can put pressure on the nerves in the neck.
The condition can also be caused by a traumatic injury to the neck like whiplash or sports injury.
Rarely is it caused by an infection or spinal tumor.
Symptoms
The primary symptom is pain radiating from the neck down to the:
Shoulders
Arms
Hands
Fingers
The above is an example of sensory function, which is related to feeling.
In addition to sensory symptoms, radiculopathy can also cause motor dysfunction.
Motor dysfunction relates to muscles and movement.
Reflex changes in the neck and upper body and weakness are examples of motor dysfunction.
Diagnosis
A spine specialist/chiropractor has several tools to diagnose cervical radiculopathy.
First and foremost your medical history will be reviewed and then will be:
Asked to describe symptoms
A physical exam will be conducted�to recreate the pain in a controlled manner in the:
Neck
Shoulder
Arms
Example: Spurling�s maneuver, which gently rotates the head, while applying gentle pressure.
Once the information from the medical history and physical exam are done,��imaging tests such as an MRI�may be ordered so they can pinpoint the location of the nerve compression.
MRI scans show the soft tissues in the spine, including the nerves.
The doctor may request a pair of diagnostic tests called electromyogram (EMG) and nerve conduction exam if there are significant upper nerve arm and neck pain.
These tests help understand if there is nerve damage, the cause of the damage and if the symptoms are related to the nerve damage.
EMG and nerve conduction tests are usually performed together to help in the diagnosis.
Emergency Symptoms
Once the spine specialist confirms the diagnosis, they will develop a treatment plan to relieve the nerve compression or prevent it from getting worse.
Most cases are taken care of with non-surgical treatment, however, if the following occurs you should contact your doctor:
Neck pain does not improve with treatment in the time your doctor expects.
Pain worsens regardless of treatment
Or you develop new:
Numbness
Weakness in the
Neck
Arms
Upper body
Develop fever
If you experience symptoms in the lower body like:
Weakness in the leg
Difficulty walking
Lack of bowel/bladder function, then seek medical attention immediately.
These symptoms may indicate cervical myelopathy, a more severe condition.
Cervical myelopathy is the compression of the spinal cord.
When the spinal cord gets compressed, it can generate widespread spine issues and usually requires surgery.
Treatment Cervical Radiculopathy
Like most types of spine pain, a doctor will recommend trying one or more conservative treatments first.
Conservative treatments are nonsurgical means.
It�s important to understand that just because a treatment is considered conservative does not mean it is ineffective.
In fact, it�s quite the opposite. Most people with nerve compression in their neck respond well to conservative therapies.
Though research on the efficacy of conservative treatments for cervical radiculopathy has produced mixed results, findings show that these therapies help eliminate pain and other nerve-related symptoms (like numbness and muscle weakness) in 40-80% of people.
The following are the most common conservative treatments:
Over-the-counter medications, like acetaminophen (Tylenol) or nonsteroidal anti-inflammatory medications(ibuprofen, Motrin)
Prescription medications, like steroids (prednisone), neuropathic agents (gabapentin, pregabalin), and muscle relaxants (baclofen, cyclobenzaprine)
Cervical spinal traction, that can be performed during physical therapy
Avoiding strenuous activity, but don’t avoid all activity, as too much rest can exacerbate the injury and extend the recovery time
These conservative treatments can go on for 6 to 8 weeks. If there is no improvement or it gets worse, then a doctor may want to step you up to the next level.
This may include steroid injections.
Spinal Injections
Cervical epidural steroid injections are considered a second-line treatment for radiculopathy that is not responding to conservative therapy. These injections send a dose of anti-inflammatory medicine into a specific nerve root�s that can relieve pain.
The number of injections differs from patient to patient. A doctor will make recommendations based on the condition and response to the first injection.
If the first injection reduces the pain and symptoms, a second or third injection might not be necessary unless symptoms recur.
If more than one is needed, they are given 3 weeks between each injection.
Injections can help manage pain and inflammation, but cannot strengthen or improve the flexibility of the cervical muscles.
Because of this, a doctor may prescribe physical therapy, chiropractic or an exercise program to condition the neck muscles.
Surgery Considered
When surgery is needed it is considered a last resort option. This is not a guaranteed solution and there are risks and complications.
Different types of surgical approaches are available. These procedures can be performed minimally invasively in a hospital setting or an outpatient surgery center.
Discussing options with a doctor and whether you are a candidate for minimally invasive surgery or not, along with other types of surgery e.g. artificial disc, is a discussion that is different for everybody, as some patients have existing medical conditions that can increase risks and complications.
Anterior cervical discectomy and fusion (ACDF)
This approach is the most widely used surgical approach.
The surgeon makes an incision through the front of the neck and removes the damaged intervertebral disc, fills the empty space with spacers to restore the height and attaches spinal instrumentation (plate, screws) for stabilization.
A bone graft is then packed into and around the body spacers for bone ingrowth and healing.
Posterior cervical foraminotomy
Here, the surgeon accesses one or more levels of the cervical spine with an incision in the back of the neck.
Foraminotomy decompresses the nerve root by removing whatever is compressing the nerve like a bone or soft tissue.
The procedure opens/widens the neural foramen or the nerve passageway where the nerve exits the spinal canal.
Cervical artificial disc replacement (C-ADR)
Here an artificial disc device is implanted in the empty disc space.
C-ADR is like a shock absorber and enables healthy movement the way that an actual disc does.
Conclusion
A compressed nerve in your neck can lead to radiating pain. This pain can make it almost unbearable to do simple tasks, even moving the neck from side to side or just opening a jar. Conservative treatment like chiropractic and exercise can ease the pain of this condition and restore function. Fortunately, surgery is rarely necessary.
El Paso, TX Neck Pain Chiropractic Treatment
Alfonso J. Ramirez now retired, found follow-up treatment with Dr. Alex Jimenez for his neck pain. Mr. Ramirez experienced chronic pain and headaches, but after receiving chiropractic care, he found relief from his symptoms. Ever since that time, Alfonso Ramirez has continued to maintain the alignment of his backbone with Dr. Jimenez. Mr. Ramirez is grateful for the chiropractic care he’s received for his neck pain and for his knee and shoulder pain. Alfonso J. Ramirez recommends Dr. Alex Jimenez as the non-invasive pick for neck pain.
NCBI Resources
Approximately two-thirds of the population being affected by neck pain at any time throughout their lives. Pain that originates in the cervical spine, or upper spine, can be caused by numerous other spinal health issues. Joint disruption in the neck can generate a variety of other common symptoms, which include headaches, head pain, and migraines. Neck pain affects about 5 percent of the global population, according to statistics.
Mostly everyone takes their vitamins in any shape and form. It can be from the foods that we eat to the supplements and vitamins pills that we make throughout the day. We can get the boost of micronutrients in our bodies with vitamins and foods. It can help with our diets when we are trying to get a head start in our healthy lifestyle change through healthy, nutritious, whole foods. Without it, it can cause our bodies to react differently with ailments. For example, a person has a healthy lifestyle, but they are feeling out of place in their daily lives; it might be due to their low levels of the vitamins they are not taking. We will be taking a look at the micronutrition in vitamins and supplements in this two-part series for the body.
Contents
The Vitamins
Vitamins are essential for the body since we can�t produce them naturally. When we feel sluggish or horrible, it might be due to the low vitamin intake that we are missing to make us feel better. Here are some of the vitamins that can help your body if you feel a bit weak in life.
Vitamin A
Vitamin A is a fat-soluble compound that is an essential nutrient for the body. It is stored in the liver for later use and is transferred to the tissues when needed. Vitamin A helps maintain the integrity and function of all surface tissues and the eyes. Vitamin A has two forms which are retinol and retinyl esters and provitamin A carotenoids. Retinol and retinyl esters health benefits can help prevent macular degeneration to your eyes, and with the provitamin A carotenoids can have potent antioxidants to fight off free radicals in your body.
Deficiencies: Having a Vitamin A deficiency can lead to blindness in the eyes of some people. Anyone who has a deficiency in Vitamin A can have skin issues like hyperkeratosis and acne. Not only that, but it can increase any infections as well as have pregnancy complications for pregnant women.
Food Sources: Here are some of the foods that are very rich with vitamin A that are all carotenoid-rich in both animals and plants.
Egg yolks
Beef liver
Cod liver oil
Salmon
Sweet potatoes
Carrots
Dandelion greens
Cabbage
Vitamin B
All B vitamins are water-soluble, and your body can�t store them. They are used to reduce fatigue and boost your mood. There are 8 B vitamins are vital and have many essential functions for maintaining good health.
B1 (thiamine):Thiamine helps our bodies metabolism by helping convert nutrients into energy. Some food sources include pork, sunflower seeds, and wheat germ.
B2 (riboflavin): Riboflavin converts food into energy and acts as an antioxidant in the body. Some of the food sources that are high in riboflavin are organ meats, beef, and mushrooms.
B3 (niacin):Niacin plays a role in cellular signaling, metabolism and DNA productions, as well as repairs it as well. Some food sources include chicken, tuna, and lentils.
B5 (pantothenic acid): Like other B vitamins, pantothenic acid helps our bodies obtain energy from the food we eat. It also involves hormone and cholesterol production. Some food sources include liver, fish, yogurt, and avocado.
B6 (pyridoxine):Pyridoxine helps produces red blood cells in the body. It helps create amino acid metabolism and neurotransmitters for the body. Foods that are highly rich with this vitamin are chickpeas, salmon, and potatoes.
B7 (biotin):Biotin is highly essential for carbohydrate and fat metabolism and can regulate gene expression in the body. The best food sources that contain biotin are yeast, eggs, salmon, cheese, and liver.
B9 (folate): Our bodies need folate for cell growth, amino acid metabolism, the formation of red and white blood cells as well as proper cell division. Folate can be found in foods like leafy greens, liver, beans and in supplements like folic acid.
B12 (cobalamin): One of the best- known of all the B vitamins, B12 is vital for neurological function, DNA production, and red blood cell count. It can be found naturally in animal food sources like meats, eggs, seafood, and dairy.
Deficiencies: Even though taking the B vitamins are essential, there are side effects to taking a high dose of the vitamin, especially B3 and B6. Some of the side effects include vomiting, high blood sugar levels, skin lesions, nerve damage, and even liver damage.
Vitamin C
Vitamin C is one of the most essential vitamins since it can�t be produced by the body. It has so many roles and has been linked to many impressive health benefits. It can help boost antioxidant levels, reduce high blood pressure, and heart disease risk. It can protect your body against any gout attacks and reduce your risk of dementia while improving your iron absorption and boosting your immunity.
Deficiencies: When you don�t take enough vitamin C, it can raise up your blood sugar. Without it, you can develop scurvy if you don�t have enough of vitamin C in your system. You can get really sick, and your immune system will be shot if you don�t take vitamin C.
Food Sources: The most common way to get vitamin C in your body is through citrus fruit. There are lots of foods that contain vitamin C and are very delicious.
Red and green peppers
Oranges and orange juice
Kiwi
Guava
Broccoli
Strawberries
Brussel sprouts
Tomato juice
Cantaloupe
Vitamin D3
Also known as the sunshine vitamin, vitamin D3 is essential for maintaining healthy bones and teeth. It can support the immune system, brain, and nervous system by keeping it healthy. It will even regulate insulin levels and help managing diabetes. However, vitamin D3 can be synthesized to our body whenever sunlight hits our skin.
Deficiencies: Even though the body can create vitamin D, there many reasons that vitamin D deficiency can occur. If a person has a darker skin color and uses sunscreen to reduce the absorption of UVB (ultraviolet radiation B) rays from the sun. They can stop the production of vitamin D. Some of the symptoms of vitamin D deficiency include getting sick more, fatigue, muscle pain, and depression. And if it continues for long periods, it can lead to obesity, diabetes, hypertension, chronic fatigue syndrome, fibromyalgia, and osteoporosis, just to name a few.
Food Sources: There are a few foods that contain vitamin D naturally. And for vitamin D3 it is mostly animal produced.
Salmon
Sardines
Egg yolk
Shrimp
Milk (fortified)
Cereal (fortified)
Yogurt (fortified)
Vitamin E
Vitamin E is one of the most essential nutrients that is available as a dietary supplement and can occur naturally in foods. It is an antioxidant that can help protect your cells damage and is fat-soluble. Researchers have investigated that vitamin E can be used as a treatment for various degenerative diseases, including high blood pressure, heart disease, and cancer. It is a rare case for a vitamin E deficiency; however, it is a rare condition that is being researched.
Since Vitamin E is the most common nutrient found in most foods, here are some of the foods, including cooking oils that are exceptional.
Wheat Germ Oil
Sunflower seeds
Almonds
Hazelnut Oil
Goose meat
Peanuts
Mango
Conclusion
So with these vitamins, it can help your body feel so much better in the long run. Without them, our bodies will have various health problems that can hurt us in the long haul. When we take these vitamins, our bodies began to heal properly, and we can see that our moods are a bit better. We can have normal functions without the vitamins because we eat the food that contains them, but when we need that extra boost of energy, vitamins are the way to go.
Cites:
Basavaraj, K H, et al. �Diet in Dermatology: Present Perspectives.� Indian Journal of Dermatology, Medknow Publications, 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC2965901/.
Chiu, Zelia K, et al. �Patterns of Vitamin D Levels and Exposures in Active and Inactive Noninfectious Uveitis�Patients.� Ophthalmology, U.S. National Library of Medicine, 11 July 2019, www.ncbi.nlm.nih.gov/pubmed/31519386.
Choi, Hyon K, et al. �Vitamin C Intake and the Risk of Gout in Men: a Prospective Study.� Archives of Internal Medicine, U.S. National Library of Medicine, 9 Mar. 2009, www.ncbi.nlm.nih.gov/pubmed/19273781.
Ettarh, R R, et al. �Vitamin C Lowers Blood Pressure and Alters Vascular Responsiveness in Salt-Induced Hypertension.� Canadian Journal of Physiology and Pharmacology, U.S. National Library of Medicine, Dec. 2002, www.ncbi.nlm.nih.gov/pubmed/12564647.
Institute of Medicine (US) Panel on Micronutrients, Unknown. �Vitamin A.� Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc., U.S. National Library of Medicine, 1 Jan. 1970, www.ncbi.nlm.nih.gov/books/NBK222318/.
Martel, Julianna L. �Vitamin B1 (Thiamine).� StatPearls [Internet]., U.S. National Library of Medicine, 14 Aug. 2019, www.ncbi.nlm.nih.gov/books/NBK482360/.
Megan Ware, RDN. �Vitamin D: Health Benefits, Facts, and Research.� Medical News Today, MediLexicon International, 13 Nov. 2017, www.medicalnewstoday.com/articles/161618.php.
Meyer-Ficca, Mirella, and James B Kirkland. �Niacin.� Advances in Nutrition (Bethesda, Md.), American Society for Nutrition, 16 May 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4863271/.
N/A, Unknown. �Office of Dietary Supplements – Vitamin E.� NIH Office of Dietary Supplements, U.S. Department of Health and Human Services, 0AD, ods.od.nih.gov/factsheets/VitaminE-HealthProfessional/.
O’Leary, Fiona, and Samir Samman. �Vitamin B12 in Health and Disease.� Nutrients, Molecular Diversity Preservation International, Mar. 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC3257642/.
Ozuguz, Pinar, et al. �Evaluation of Serum Vitamins A and E and Zinc Levels According to the Severity of Acne Vulgaris.� Cutaneous and Ocular Toxicology, U.S. National Library of Medicine, June 2014, www.ncbi.nlm.nih.gov/pubmed/23826827.
Pham-Huy, Lien Ai, et al. �Free Radicals, Antioxidants in Disease and Health.� International Journal of Biomedical Science : IJBS, Master Publishing Group, June 2008, www.ncbi.nlm.nih.gov/pubmed/23675073.
Senoo, Haruki, et al. �Hepatic Stellate Cell (Vitamin A-Storing Cell) and Its Relative–Past, Present and Future.� Cell Biology International, U.S. National Library of Medicine, Dec. 2010, www.ncbi.nlm.nih.gov/pubmed/21067523.
Wong, Cathy. �Benefits of Vitamin C You May Not Know About.� Verywell Health, Verywell Health, 17 July 2019, www.verywellhealth.com/the-benefits-of-vitamin-c-supplements-89083.
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Excitotoxicity is a pathological mechanism seen in a variety of health issues where an excessive synaptic excitation causes neuronal death and is also believed to be caused by the extracellular accumulation of the excitatory neurotransmitter glutamate, which triggers and connects ionotropic N-methyl-D-aspartate glutamatergic receptors (NMDARs) in the brain. Generally, NMDARs regulate and maintain calcium in cells to help manage physiological mechanisms like synaptic plasticity and memory, however, excessive stimulation can ultimately increase intracellular calcium which triggers cell death signaling to activate apoptosis. This pathological mechanism has been suggested in a variety of health issues, such as traumatic brain injury (TBI) and Alzheimer’s disease (AD), where it is extensively examined to understand health issues and treatment approaches. In a stroke, excitotoxicity has been shown to be the main pathological mechanism where neuronal damage happens and it is considered to be a well-known goal for many recent attempts at developing stroke therapeutics. �
Stroke is an acute brain health issue which causes neuronal damage which has currently no safe and effective neuroprotective treatment approaches. Immediately following a stroke, the brain tissue loses blood perfusion and the center of the infarct deteriorates quickly. This then causes milder ischemia and many brain cells or neurons will result in delayed death which can take up to several hours or even days. Research studies show that the mechanism of cell death is mainly NMDA receptor-dependent excitotoxicity. In ischemic areas, extracellular glutamate levels increase while preventing glutamate release, synaptic activity, or NMDAR activation which was capable of limiting cell death in a variety of stroke models. Thus, preventing excitotoxicity is an important treatment approach for reducing brain damage and improving patient outcome measures following a stroke, and this has definitely encouraged extensive efforts towards developing NMDA receptor-based stroke treatment approaches over the last two decades. Unfortunately, these have largely met with rather disappointing results. Several research studies have failed to find the expected efficiency of NMDAR for decreasing brain injuries. The reasons behind the basic research study results and clinical trials are still unknown, however, several reasons have been suggested. These include, but are not limited to, the inability to utilize the correct doses necessary for neuroprotection due to their side-effects, the inability to use the drugs within their neuroprotective windows, poor experimental designs, and heterogeneity in the patient population. However, as we will briefly summarize in the following article, improvement in our understanding of the physiological and pathological mechanisms of NMDAR activation as well as the different pathways connected to different NMDAR subtypes, has allowed researchers to develop new treatment approaches which improve therapeutic windows and increase specificity for death signaling pathways, achieving neuroprotection without interrupting other essential signaling pathways downstream of the NMDAR receptor. �
Contents
Neuroprotectants Targeting NMDAR Subtypes
NMDAR subtypes have different purposes in excitotoxicity and physiology. The NMDAR is a receptor which generally has two GluN1, also known as NR1, subunits as well as two subunits from the GluN2 subfamily (GluN2A-2D, also known as NR2A-2D). In the cortex, the major subpopulations of NMDARs are GluN2A- or GluN2A and 2B-containing receptors. GluN2A-containing receptors are found in synapses whereas GluN2B-containing receptors are found on extrasynaptic membranes. GluN2A- and GluN2B-containing receptors are different from each other because they regulate and manage plasticity, favoring either long-term potentiation (GluN2A) or depression (GluN2B) through a variety of electrophysiological and pharmacological properties as well as signaling proteins. In addition, these receptors play a fundamental role in promoting cell survival (GluN2A) or death (GluN2B) after excitotoxic stimulation. Because GluN2A-containing receptors are mainly focused on synapses while GluN2B-containing receptors are focused to both synaptic and extrasynaptic membranes, when excitotoxic conditions cause glutamate to extend beyond synapses, GluN2B-mediated death signaling becomes stronger in comparison to survival signaling which ultimately results in death. Through a stroke, by way of instance, NMDARs are less likely to favor cell survival and can instead cause detrimental effects by preventing considerable normal physiological purposes. Selfotel, a non-specific NMDAR blocker, was neuroprotective against stroke in vitro and in vivo, however, it ultimately failed to be neuroprotective against stroke in clinical trials by causing a variety of intolerable side-effects. �
Treatment strategies to reduce undesirable side-effects, including glycine site antagonists and NMDAR subtype-specific improvements, was to target the allosteric glycine binding regions on the GluN1 subunits with licostinel and gavestinel instead of directly blocking the receptor. These drug candidates performed well in preclinical examinations, however, they also failed as a result of low efficiency despite minimal side-effect profiles. The negative side-effects were perhaps due to a missed window of time following a stroke that shows which receptor blockers are safe and effective in preventing death. �
Better treatment methods and techniques for reducing unwanted side-effects of NMDAR are to utilize the differences between their variations. By way of instance, the GluN2B-specific inhibitor traxoprodil is neuroprotective in stroke research studies and minimal side-effects, however, it has also failed in clinical trials. Similar to the glycine region antagonists, it possibly needs to be properly regulated and managed to function efficiently. GluN2A agonists should promote cell survival signaling which could allow recovery following a stroke as well as cell survival to prevent passing signaling. As a matter of fact, activation of GluN2A-containing receptors utilizing increased doses of glycine was neuroprotective in an animal model of stroke but further research studies must examine GluN2A activation as a treatment approach in human participants. �
While NMDAR antagonists and modulators are safe and effective at attenuating excitotoxicity in experimental versions, their shortcoming is the challenge in implementing treatment approaches early to coincide with the summit of excitotoxic glutamate release. Stroke patients frequently have no chance of receiving these treatment approaches in time. However, the health issue can be avoided if receptor blockers can be utilized in at-risk populations. One research study has shown that low doses of prophylactic memantine, an NMDAR non-competitive antagonist with few side-effects, can considerably decrease brain injury and functional deficits following a stroke. Whether any medications are tolerable, safe, and effective when taken this way remains to be demonstrated but innovative solutions may nevertheless address how to deliver those drugs. �
One factor apart from those of the failed clinical trials is the interplay of NMDARs in cell survival which may be completely misunderstood. In the last few decades, there has been accumulating evidence that synaptic NMDARs may also cause cell death and GluN2A, as well as GluN2B, do not necessarily have dichotomous functions in excitotoxicity. Further research studies may be required to demonstrate more nuanced receptor inhibitor strategies and to solve this controversy. �
Neuroprotectants Targeting Cell Death Signaling
A treatment approach for NMDAR inhibitors is to focus on the most downstream events for cell death which happen over a much longer time period following receptor activation. A variety of cell death pathways following activation have been determined and several groups have provided proof-of-principle evidence that these pathways can be regulated and managed with the utilization of peptides to ultimately protect brain cells or neurons without any side-effects. �
The oldest reported and most explored peptide strategy in stroke goals is nitrous oxide synthase (nNOS)-mediated cell death. NNOS connects to postsynaptic protein 95 (PSD95) which then connects to the C-terminal tail of the GluN2B subunit. NOS is a calcium-activated enzyme which activates the development of nitric oxide (NO) and its own status in the receptor complex which associates it in proximity to the focused stream of calcium entering activated GluN2B. In a stroke, the excessive calcium influx activates GluN2B-coupled nNOS. An interference peptide is utilized to disconnect the complex to prevent NO development. The peptide, Tat-NR2B9c, is made up of an HIV-1 Tat-derived cell penetration sequence which allows passage through the blood-brain barrier and cell membranes, connected to a copy of the region on the GluN2B for PSD95. The peptide and GluN2B disconnect PSD95, therefore, decoupling nNOS in the local considerable levels of calcium without interrupting the function of the receptor from different pathways. Utilization results in considerable protection against tissue and functional damage with no side-effects in vitro and in vivo after a single dose given before or after ischemia in vivo. The peptide has lately succeeded in Phase II clinical trial where it decreased iatrogenic infarcts during intracranial aneurysm treatment. This is the first time a research study has demonstrated efficiency in humans which also shows authenticity that targeting downstream cell death can be helpful against excitotoxic/ischemic neuronal injuries. �
While the utilization of peptides in a clinical setting is safe and effective, a similar efficiency has been achieved with small molecule drugs which act on the exact same goal and function like the peptides in a laboratory setting. To mimic Tat-NR2B9c, two small molecules, IC87201 and ZL006 have been individually demonstrated to compete at the identical GluN2B-specific connecting region without affecting the connection of PSD95 to other proteins. Additionally, ZL006 imitates the peptide’s neuroprotection without causing any considerable adverse side-effects. By identifying the goals and the specific regions, research studies can simulate small molecule drugs and accelerate their discovery towards excitotoxicity and stroke. �
Other GluN2B-specific pathways have been demonstrated in a similar manner and are showing promise in the stages of development. One such pathway which is triggered following GluN2B activation is the potentiation and recruiting of GluN2B in the cell membrane by death-associated protein kinase 1 (DAPK1). DAPK1 is a protein which connects to calmodulin to activate apoptosis but it is phosphorylated in an inactive form which is incapable of associating cell death and calmodulin. Following excitotoxicity, calcineurin activation dephosphorylates and triggers DAPK1, contributing to cell death. Furthermore, active DAPK1 can connect to and phosphorylate the C-terminal tail of receptors, excitotoxicity, and their function, aggravating calcium influx. A Tat-linked interference peptide which has the C-tail phosphorylation region which is GluN2B managed to block the interaction of active DAPK1 with GluN2B and promote excitotoxicity. Once the peptide was utilized in mice, dubbed Tat-NR2B-CT, it improved the outcome following ischemia. However, Tat-NR2B-CT was only efficient at preventing activity and runaway insertion instead of the downstream apoptotic of DAPK1 signaling. Researchers were also able to connect and guide DAPK1 towards lysosomes by including a sequence in the close of the hindrance peptide to create a degradation peptide. The result has been a serious and temporary fall in busy DAPK1 levels with a corresponding decrease in infarction when administering the peptide hours after ischemia, according to several research studies. �
The c-Jun N-terminal kinase 3 (JNK) acts upon many pathways and is a mediator for cell death in excitotoxicity. JNK interacting protein (JIP) connects and prevents JNK activity through a JNK binding domain (JBD) which spans over 20 residues. When these residues are connected to Tat as from the Tat-JBD20 interrupted peptide, they are capable of limiting JNK activity and preventing cell death in stroke models when administered before or after ischemia. The Tat-JBD20 peptide has also been shown utilizing D-amino acids instead of L-amino acids to withstand degradation by endogenous proteases. Doing so tremendously increases the peptide’s half-life and doesn’t negatively affect its binding affinity and selectivity, demonstrating that this alteration may be utilized for several interference peptides to boost efficiency and bioavailability. �
New targets are always being discovered. While currently, no new stroke treatment approaches are being utilized, a great deal of progress has been made by targeting the processes which occur during stroke towards creating treatment approaches. With the debut of the achievement of degradation and interruption peptides targeting GluN2B-specific passing signaling events, there’s hope that new treatments are on the horizon for health issues which have excitotoxicity. �
Excitotoxicity is the pathological mechanism by which brain cells or neurons are ultimately damaged or eliminated by excessive stimulation from neurotransmitters, including glutamate and other similar substances. This ultimately occurs when the NMDA receptor and the AMPA receptor are overactivated by excitatory neurotransmitter glutamate receptors. This can cause a variety of processes which can damage cell structures, including components of the cytoskeleton, membrane, and DNA. Regulating and managing excitotoxicity can help maintain overall well-being. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Excitotoxicity is a pathological mechanism where an excessive synaptic excitation causes neuronal death and is also believed to be caused by the extracellular accumulation of the excitatory neurotransmitter glutamate, which triggers and connects ionotropic N-methyl-D-aspartate glutamatergic receptors (NMDARs) in the brain. This pathological mechanism has been suggested in a variety of health issues, such as traumatic brain injury (TBI) and Alzheimer’s disease (AD), where it is extensively examined to understand health issues and treatment approaches. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Li, Victor, and Yu Tian Wang. �Molecular Mechanisms of NMDA Receptor-Mediated Excitotoxicity: Implications for Neuroprotective Therapeutics for Stroke.� Neural Regeneration Research, Medknow Publications & Media Pvt Ltd, Nov. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC5204222/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
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Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
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Sometimes low back pain comes out of nowhere, but that sudden twinge in the lower back does have a cause. With some cases, there�s a trigger, like picking up a heavy object/furniture from an awkward position.� But sometimes it can be a mystery and a challenge to diagnose.
It is important to know the cause of lower back pain to figure out the proper treatment plan. Otherwise, one could receive treatment for the wrong diagnosis and possibly exacerbate the existing injury.
Contents
Why do I need to know what triggers my back pain
Knowing what triggers back pain is the first step toward prevention and how to treat it.
Muscle spasms can stop you cold, and so I’m sure you don�t want another one.
Acute Back Pain
Acute low back pain typically comes on suddenly and lasts for a short time.
It often resolves on its own with self-care and a little time.
Back pain that lasts longer than three months, is considered chronic.
Chronic back pain can be more complex and require doctor/spine specialist-directed treatment, like physical therapy.
Lower Back Pain Is Common
Over 90 percent of adults will have some type of low back pain during their life.
It happens to be the number one cause of job disability globally and the leading contributor to missed work.
Lower back pain happens more often, compared to mid or upper back pain because of the location and all of the movement.
The lower back supports the upper body’s weight.
The low back known as the (lumbar spine) absorbs and distributes all of the forces and stress when we move:
Walking
Standing
Rest
Sitting
Sleeping
Spinal and abdominal muscles that are weakened heighten injury risk.
These factors combined make the lower back vulnerable to painful spinal conditions.
Common Triggers
When the lumbar spine:
Muscles
Tendons
Ligaments
And other connective tissues get:
Pulled
Strained
Sprained
Is when lower back pain happens.
Small tears in the disc can also contribute to back pain.
Basically, any number of activity and non-activity can cause damage to the spinal discs depending on the movement.
A study published in Arthritis Care & Research saw 999 people from 300 clinics in Australia, to examine their pain triggers.
The most common triggers include:
Manual tasks performed in an awkward posture
This includes:
Lifting boxes with the back and not bending the knees
Lifting something too heavy
Moderate physical activity
Vigorous physical activity
High intense strength training, long bike rides without proper conditioning, handling people or animals, and picking up children can be triggers and cause injury.
Other triggers include:
Overstretching
Twisting
And Trauma
From:
Falls
Vehicle accidents
Sports
Triggers You Might Not Know About
Although we don’t think about it being Distracted can increase the odds of low back pain.
When we’re not paying attention,� we are more likely to lift and carry something too far from our body or distribute the weight unevenly.Feeling tired and Fatigued is associated with lower back pain.
Getting the proper amount of sleep is vital to restore our bodies to optimal performance.
When we don’t sleep the right amount of hours we make our bodies more susceptible to injury.
Treatment
Thankfully most cases are not serious and typically resolve within a few days to, four weeks healing on its own.
But if not, then there are these conservative treatments that can help you feel better and speed up healing.
Continue to Move Around
Depending on how much pain your body will allow, keep doing regular activities and exercise, as best as you can.
Activity increases blood flow, that moves oxygen and minerals/nutrients through the body.
Activity and movement help reduce muscle tension and inflammation.
Heat/Ice
This will not cure a strain or sprain, but they do help in pain reduction.
Heat helps loosen tight muscles.
This can be done by making warm compresses by soaking a towel in hot water.
Fold it to the size you need and wrap it around your lower back up to 20 minutes.� Then rest, massage and re-apply.
Massage can bring temporary relief from short-term back pain.
If the pain is intense and interferes with daily activities, a chiropractor/physical therapist can offer exercises and stretches to:
Improve posture
Increase mobility
Correct muscle imbalances
Acute lower back pain can stop you cold with its intensity.
Understanding triggers can take steps to maintain a healthy spine and avoid unpleasant surprises.
Medication
Both acetaminophen (Tylenol) and non-steroidal anti-inflammatory drugs (NSAIDs) can relieve pain.
These need to be taken, specifically as directed by your doctor. We’ve seen the opioid crisis going on and now this type of treatment is now a last resort. Various medical associations are now pushing towards natural and alternative therapies before turning to medication.
Prolonged use of NSAIDs (Aleve, Advil) can be associated with an upset stomach, kidney damage and gastrointestinal conditions and bleeding, among other conditions.
Back Pain Specialist | El Paso, Tx
Back pain is one of the most common health issues frequently diagnosed by healthcare professionals. Approximately 80 percent of the population will experience some type of back pain throughout their lifetimes. Because back pain can occur due to a wide array of health issues, diagnosis is essential to follow-up with the proper treatment approach. Dr. Alex Jimenez, chiropractor or doctor of chiropractic in El Paso, TX, utilizes chiropractic care to help treat back pain. Patients describe how their back pain affected their quality of life, and how Dr. Jimenez helped them improve their overall health and wellness with chiropractic. Patients highly recommend Dr. Jimenez and his staff as the non-surgical choice for back pain, among other common health issues.
NCBI Resources
Throbbing, dull and achy, sharp and excruciating. All of these words can be used to describe lower back pain. Unfortunately, lower back pain is a common occurrence in adults. According to the�American Chiropractic Association, low back pain is the single leading cause of disability worldwide, with millions of reported cases every year. Patients who experience lower back pain never want to deal with it again, but�it can flare up periodically. According to the�National Institute of Neurological Disorders and Stroke,�roughly 20% of those who suffer from low back pain will eventually deal with it chronically. This can cause frustration, primarily when it affects mobility.
Today, we will be talking about what does the protein compounds and the peptide compounds do when a patient is being tested for food sensitivity. And we will also discuss what the Lectin and Dairy Zoomer do when a patient has a reaction to those types of food groups. In the last article, we mentioned about immunoglobulins in the intestinal barrier. And what do IgA and IgG antibodies do to the peptide and protein level?
Contents
Proteins vs. Peptides
So let us take a look at proteins and peptides since this is what Vibrant Food Zoomers are actually testing on a patient. Remember that the Food Zoomers are testing the peptides in the whole protein and testing all the links to see what the patient is actually sensitive to the foods they are consuming.
Proteins
Protein is basically abundant biomolecule that is consist of one or more long chains of amino acid residues. Proteins can be found in whole foods like meats and vegetables that can help the muscles in our bodies. In the last article, we talked about how IgA and IgG antibodies are used for food sensitivity testing.
However, there is a limitation of a whole protein food sensitivity testing on a patient. Practitioners do make the assumption that the patient�s gut barrier is functional and intact since there are no signs of a leaky gut syndrome presented in the results. But, if that patient has the leaky gut syndrome, then the food sensitivity test will reflect what the patient has been eating. Another assumption is that the patient�s HCI and digestive enzymes are sufficient for tolerable proteolysis. Which means that those enzymes are breaking down whole proteins into smaller peptides.
Peptides
Peptides are what in protein molecules as they are short chains of amino acids and are linked by the peptide bonds. When they are being tested by the food sensitivity tests, the reproducibility is higher. It doesn�t rely on the excess HCI (hydrochloric acid) or enzymes. What the test eliminates is the cross-reactivity because peptides in proteins are not going to have molecular mimicry to other unrelated proteins.
The antibodies are highly specific to the peptides because they are not going to be generalized or more massive antibodies of proteins since cross-reactivity is eliminated. Another thing is that the peptide test does is that it can measure thousands of peptides in one protein for a full spectrum of reactivity.
When patients are coming in with digestive problems and inflammatory condition/symptoms, practitioners take note that a lot of patients commonly have hypochlorhydria and deficiencies of enzymes and/or bile acids. Most patients sometimes have moderate to severe impairment of the intestinal barrier. When that happens, local doctors discuss with them that they may have to change their diets slowly but surely. And with integrative functional medicine that can occur.� Local practitioners look at their patient�s ailments and start detoxifying their bodies slowly. This helps their bodies heal and recommend them whole, nutritious, organic foods, and supplements to help repair the body naturally. Sometimes medicines can cause disruption to our bodies, however with whole natural foods and specific diets, it can help restore our bodies. Plus making sure that we exercise to make our bodies feel good and look good.
So now that we understand what proteins and peptides do when they are being tested. Let�s take a look at the food zoomers that can help you in case you have a sensitivity to these food groups. These are the Vibrant Lectin Zoomer and the Dairy Zoomer.
Lectin Zoomer
The Lectin Zoomer is consist of a handful of lectins and a handful of aquaporins. The most common lectins that people consume are barley, bell pepper, chickpea, corn, cucumber, potato, etc. And the most common aquaporins that people consume are spinach, soybean, tomato, tobacco, etc.
Difference between Lectins and Aquaporins
The difference between lectins and aquaporins is that lectins are sugar-binding proteins that are found in both animals and plants, which can bind to the carbohydrate structures on cells. While aquaporins are water channels that are found in cavities in both plants and humans. Some aquaporins can cross-react and can lead to primarily neurological symptoms.
How Problematic are Lectins?
Some studies show cell toxicity in humans is done by using extreme cytotoxic lectins. Ricin, for example, is a common biological warfare element that is not from the commonly consumed legumes or grains. It contains cytotoxic lectins and is being consumed by animals like mice or pigs. The assumption is being made that there are similarities with humans and animal gut glycosylation (the process of sugar-binding) in these situations.
Unfortunately, though it hasn�t been demonstrated thoroughly. But lectins have biological activity in the human body. They have been used as a cancer treatment mechanism because they can agglutinate cancer cells. Which means that they produce cytotoxicity to cancer cells and can actually carry chemotherapy across cancer cell membranes.
Even though that is a good thing, lectins can facilitate the bacterial endotoxins across the epithelial barrier and go into the peripheral tissues. And that can cause inflammation to the intestinal epithelial barrier in the small intestines. Animals studies show that raw lectin consumptions can cause hemagglutinating effects, causing inflammation.
But we as humans don�t eat raw lectins because they are cooked, not pressurized cook. Certain foods that are lectins can be eaten raw or cooked. But animal studies stated that they are using for these studies are grain and legume lectins that are raw like beans and grains. But the upside is that lectins can affect the metabolism of nutrients to increase fat loss which is a positive side effect.
Measuring the Sensitivity to Lectins
On the Food Zoomers test, lectins are really not included in each analysis, except for the Wheat Zoomer. Surprisingly, a Food Zoomer may be non-reactive, but whoever is sensitive to a lectin component in the food they eat, may be reactive. So when that happens, it is necessary to eliminate the food temporarily.
If you are sensitive to a particular food, you can have a Food Zoomer and a lectin Zoomer combine. Because if you are sensitive to the food you consume, and it doesn�t show up on the Food Zoomer, but it shows up on the Lectin Zoomer. Then you should eliminate it from your diet for a bit until you retake the test.
Conditions Associated with Lectins
If you do have a lectin sensitivity, here are some of the terms that can affect your body.
Arthritis/rheumatoid arthritis
Connective tissue disorder
Gastrointestinal inflammation
Intestinal permeability
Possible cancer in established cancer patients
Now let�s take a look at the Dairy Zoomer and its functions if you are sensitive to whole dairy products.
Dairy Zoomer
The Dairy Zoomer is a peptide level assessment of the full spectrum of immune response possible to proteins in cow�s milk dairy. What this means that the Dairy Zoomer is only specific to cow�s milk. Since some proteins in cow�s milk are similar enough in the molecular structure to have the same homology to goat or sheep�s milk.
This means that these other kinds of milk may be potential can cause inflammatory in some individuals. The oral challenge for alternative types of fluid may be warranted, but use your best clinical judgment after the intestinal barrier is healed.
What the Dairy Zoomer does is that it takes the milk protein and breaking each individual protein down to its different peptides. If you are wondering if the Dairy Zoomer is a test for lactose intolerance, it is not. Since lactose intolerance is not an immune-based reaction to dairy and does not involve any protein constituents of the food, therefore no antibodies are being generated.
What it is going to test for is the casein and whey proteins in the milk product from all animals, and the ratio of these proteins will vary by species. But all the proteins and milk will generally fall into one of these two proteins.
What to do with the results?
Once your patient comes back after taking the Food Zoomers test, here are some of the things to look for when you are retesting them.
If there are any IgA antibodies still in your patient, warrant an immediate elimination, regardless that it�s moderate or positive.
If there are any Moderate IgG antibodies in your patient, then it should be eliminated in the short term. Then rotate after a 30-60-day elimination and assessing the status of the intestinal permeability to confirm that that gut barrier is no longer �leaky.�
If there is a positive IgG result, then it should be eliminated long term and only reintroduced after 90+ days and confirm of an intact intestinal barrier.
Conclusion
So all in all, food sensitivity combine with the food zoomers test are an excellent way to help your body, especially the intestinal system. The Food Zoomers we used is functional for our patient�s wellness. Because we want to get rid of the excess antibodies and heal our patient�s body through the use of functional medicine.
Many healthcare professionals believe that peripheral neuropathy, which affects the peripheral nerves or the nerves which connect from the brain and spinal cord to the upper and lower extremities, can be permanent or irreversible. However, healthcare professionals like Dr. John Coppola and Dr. Valerie Monteiro have demonstrated that peripheral neuropathy can be treated through the utilization of a variety of treatment methods and techniques.
Dr. Coppola and Dr. Monteiro describe that because peripheral neuropathy can manifest due to a variety of health issues, such as diabetes, treating the underlying cause of a patient’s peripheral neuropathy can help treat their symptoms. The 5 critical keys for defeating peripheral neuropathy are ultimately described to help promote overall health and wellness. Dr. Alex Jimenez, a chiropractor in El Paso, Tx, can help ease symptoms associated with peripheral neuropathy. Dr. Alex Jimenez is the non-surgical choice for peripheral neuropathy.
Contents
Peripheral Neuropathy Relief & Treatment | El Paso, TX (2019)
Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves. The causes of neuropathy, or nerve damage, can vary greatly among each individual and these may be caused by a number of different diseases, injuries, infections, and even vitamin deficiency states. However, neuropathy can most commonly affect the nerves that control the motor and sensory nerves. Because the human body is composed of many different kinds of nerves which perform different functions, nerve damage is classified into several types.
Neuropathy can also be classified according to the location of the nerves being affected and according to the disease-causing it. For instance, neuropathy caused by diabetes is called diabetic neuropathy. Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest as a result. Below we will discuss several specific types of neuropathies clinically treated by chiropractors, physical therapists and physical medicine doctors alike, as well as briefly describing their causes and their symptoms.
Peripheral neuropathy, which is often simply referred to as �neuropathy,� is a state that happens when your nerves become damaged or injured, oftentimes simply disrupted. It�s estimated that neuropathy affects roughly 2.4 percent of the general populace and approximately 8 percent of people older than age 55. However, this quote doesn�t include people affected by neuropathy caused by physical trauma to the nerves.
Types
Neuropathy can affect any of the three types of peripheral nerves:
Sensory nerves, which transmit messages from the sensory organs, eyes, nose to the brain
Motor nerves, which track the conscious movement of the muscles
Autonomic nerves, which regulate the involuntary functions of the body
Sometimes, neuropathy will only impact one nerve. This is medically referred to as mononeuropathy and instances of it include:
Ulnar neuropathy, which affects the elbow
Radial neuropathy, which affects the arms
Peroneal neuropathy, which affects the knees
Femoral neuropathy, which affects the thighs
Cervical neuropathy, which affects the neck
Sometimes, two or more isolated nerves in separate regions of the body can become damaged, injured or disrupted, resulting in mono neuritis multiplex neuropathy. Most often, however, multiple peripheral nerves malfunction at the same time, a condition called polyneuropathy. According to the National Institute for Neurological Disorders and Stroke, or the NINDS, there are over 100 kinds of peripheral neuropathies.
Causes
Neuropathies are often inherited from birth or they develop later in life. The most frequent inherited neuropathy is the neurological disease Charcot-Marie-Tooth disease, which affects 1 in 2,500 people in the USA. Although healthcare professionals are sometimes not able to pinpoint the exact reason for an acquired neuropathy, medically referred to as idiopathic neuropathy, there are many known causes for them, including systemic diseases, physical trauma, infectious diseases, and autoimmune disorders.
A systemic disease is one which affects the whole body. The most frequent systemic cause behind peripheral neuropathy is diabetes, which can lead to chronically high blood glucose levels that harm nerves.
Other systemic issues can cause neuropathy, including:
Kidney disorders, which permit high levels of nerve-damaging toxic chemicals to flow in the blood
Toxins from exposure to heavy metals, including arsenic, lead, mercury, and thallium
Certain drugs and/or medications, including anti-cancer medications, anticonvulsants, antivirals, and antibiotics
Chemical imbalances because of liver ailments
Hormonal diseases, including hyperthyroidism, which disturbs metabolic processes, potentially inducing cells and body parts to exert pressure on the nerves
Deficiencies in vitamins, such as E, B1 (thiamine), B6 (pyridoxine), B12, and niacin, that can be vital for healthy nerves
Alcohol abuse, which induces vitamin deficiencies and might also directly harm nerves
Cancers and tumors that exert damaging pressure on nerve fibers and pathways
Chronic inflammation, which can damage protective tissues around nerves, which makes them more vulnerable to compression or vulnerable to getting inflamed and swollen
Blood diseases and blood vessel damage, which may damage or injure nerve tissue by decreasing the available oxygen supply
Signs and Symptoms
Depending on the reason and unique to each patient, signs, and symptoms of neuropathy can include:
Such signs and symptoms are dependent on whether autonomic, sensory, or motor nerves, as well as a combination of them, are ultimately affected. Autonomic nerve damage can influence physiological functions like blood pressure or create gastrointestinal problems and issues. Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while harm to motor nerves may affect movement and reflexes. When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.
Complications
Peripheral�neuropathy�may result in several complications, as a result of disease or its symptoms. Numbness from the ailment can allow you to be less vulnerable to temperatures and pain, making you more likely to suffer from burns and serious wounds. The lack of sensations in the feet, for instance, can make you more prone to developing infections from minor traumatic accidents, particularly for diabetics, who heal more slowly than other people, including foot ulcers and gangrene.
Furthermore, muscle atrophy may cause you to develop particular physical disfigurements, such as pes cavus, a condition marked by an abnormally high foot arch, and claw-like deformities in the feet and palms.
Neuropathy Treatment
The first step in neuropathy treatment should be finding the root cause that’s causing the neuropathy.
Treatment of diseases such as:
Diabetes
Guillain-Barre syndrome
Rheumatoid arthritis
Sarcoidosis
Other underlying diseases
Prevents continued nerve damage and in some cases heals the damaged nerves.
If you are unaware of any underlying disease that is causing the peripheral neuropathy, make sure to let your doctor know of abnormal symptoms you may be experiencing.
Medication
Peripheral neuropathy can be treated with various medications.
The first type used to treat mild symptoms are:
Over-the-counter pain medications
In more severe cases:
Opiates
Narcotic medications
Anti-seizure medications
A doctor may prescribe a lidocaine patch or anti-depressants, as well to relieve symptoms.
Patients should thoroughly discuss medication for neuropathy treatment with a doctor before proceeding.
Physical Therapy
Physical therapy can benefit symptoms in neuropathy treatment.
A therapist will teach the patient exercises and stretches to help improve symptoms and increase muscle strength/control.
A therapist may also recommend braces or splints to improve mobility.
Patient’s should attend all physical therapy sessions to gain the maximum benefits.
Acids
Supplements like:
Essential acids called ALA (alpha-Lipoic acid)
GLA (gamma-linolenic acid) and omega-3 fatty acids
These can have a beneficial effect on diabetic peripheral neuropathy.
L-Carnitine
L-carnitine is a substance that the body makes and stores in the:
Liver
Brain
There have been reports that certain diabetics with neuropathy symptoms could regain regular sensation in the limbs when they increased their consumption of carnitine called acetyl-L-carnitine.
Red meat
Peanut butter
Dairy products
Are good dietary sources of this nutrient.
Supplements are also available at health food stores and pharmacies and health/wellness clinics.
Vitamins/Minerals
Vitamin deficiencies can result in peripheral neuropathy in some people.
Therefore there needs to be a replenishing of vitamins:
B
B12
E
Can help to decrease symptoms.
Recommended dosages are 300mg daily of vitamin E.
Doses of the different B vitamins differ, but one option for patients is to take a daily B-complex supplement.
Herbal Supplements
Herbal remedies are an alternative to explore.
St. John’s Wort, is a herbal supplement that can be taken orally and can reduce the pain.
Topical creams that have capsaicin, which is an anti-inflammatory found in chili peppers, can reduce the burning sensation.
Traditional Chinese Medicine TCM
Acupuncture can be an effective way to manage peripheral neuropathy.
Acupuncture uses pressure points throughout the body to realign the body’s energy, called the qi or chi.
Also, movement therapy is a way to manage the condition.
Tai chi and yoga can also help:
Align the body
Mind
Encourage relaxation
Distract from the pain
Even if the neuropathy treatment is only temporary, it can still help.
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
Neuropathy can be caused by a variety of injuries and/or aggravated conditions, often manifesting into a plethora of associated signs and symptoms. While every type of neuropathy, such as diabetic neuropathy or autoimmune disease-associated neuropathy, develops its own unique group of signs and symptoms, many patients will often report common complaints. Individuals with neuropathy generally describe their pain as stabbing, burning or tingling in character.
If you experience unusual or abnormal tingling or burning sensations, weakness and/or pain in your hands and feet, it�s essential to seek immediate medical attention in order to receive a proper diagnosis of the cause of your specific signs and symptoms. Early diagnosis may help prevent further nerve injury. Visit www.neuropathycure.org�for more details.
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Myofascial pain is associated with trigger points. These are areas that can become tender and stiff inside muscle tissue that reduce the range of motion.
Myofascial pain syndrome can happen when you have several active trigger points.
Trigger points are often referred to as knots because they feel tight and balled up compared to the softer relaxed surrounding muscle/s.
If the muscle becomes tight, it can cut off its blood supply, that can trigger:
Because they are unique conditions, there is a possibility to develop both conditions.
Doctor(s) can help craft a treatment approach that addresses the pain of both trigger points and tender points.
Vitamin K1 (
Also known as 
When we don�t get enough iron in our system, we do suffer from 
The recommended intake amount to take magnesium is 300-420mg per day for men and 310-320mg per day for women. We can get it from both food sources and supplements, here are some of the food sources that contain magnesium.
