Back Clinic Nerve Injury Team. Nerves are fragile and can be damaged by pressure, stretching, or cutting. Injury to a nerve can stop signals to and from the brain, causing muscles not to work properly and losing feeling in the injured area. The nervous system manages a great majority of the body’s functions, from regulating an individual’s breathing to controlling their muscles as well as sensing heat and cold. But, when trauma from an injury or an underlying condition causes nerve injury, an individual’s quality of life may be greatly affected. Dr. Alex Jimenez explains various concepts through his collection of archives revolving around the types of injuries and condition which can cause nerve complications as well as discuss the different form of treatments and solutions to ease nerve pain and restore the individual’s quality of life.
The information herein is not intended to replace a one-on-one relationship with a qualified healthcare professional or licensed physician and is not medical advice. We encourage you to make your own health care decisions based on your research and partnership with a qualified health care professional. Our information scope is limited to chiropractic, musculoskeletal, physical medicines, wellness, sensitive health issues, functional medicine articles, topics, and discussions. We provide and present clinical collaboration with specialists from a wide array of disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system. Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and support, directly or indirectly, our clinical scope of practice.* Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.
We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
Neurological diseases, including well-known neurodegenerative disorders like Alzheimer’s disease (AD) and Parkinson’s disease (PD) as well as other rare health issues, such as Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS), affect millions of people worldwide. Unfortunately, these are estimated to increase due to the aging population. Currently, there is no treatment available for any neurodegenerative disorder. Treatments for symptoms are available for several neurological diseases, such as PD and HD, but the therapeutic benefits are limited. Although the causes and symptoms for these health issues are different for each neurodegenerative disorders, their molecular pathogeneses share common underlying factors and characteristics, including excessive levels of reactive oxygen species (ROS), mainly due to mitochondrial impairment, neuroinflammation, and disturbances in protein homeostasis (proteostasis). This increases the possibility of developing a universal treatment that will focus on targeting the common triggers of neurological diseases. �
Nrf2 Activation Pathways and the Human Brain
The transcription factor, Nrf2, regulates the main endogenous defense mechanism against oxidative and xenobiotic stress and inflammation. Nrf2 also plays a fundamental role in the management of mitochondrial function and cellular proteostasis, which suggests the possible benefits of Nrf2 to control neurodegenerative disorders. When under stress, Nrf2 activates the transcriptional upregulation of a large network of cytoprotective genes that allow adaptation and survival. The levels and activity of Nrf2 are controlled through ubiquitination and proteasomal degradation mediated by several ubiquitin ligase systems, including Keap1-Cul3/Rbx1, ?-TrCP-Cul1, and Hrd1. Keap1 is the most well understood key regulator of Nrf2. �
Keap1 functions as a primary sensor for electrophiles and oxidants, which chemically change certain cysteines in Keap1, leading to conformational changes that protect Nrf2 from Keap1-associated degradation. Subsequently, Nrf2 will accumulate and then translocate to the nucleus where it binds as a heterodimer with a small Maf transcription factor to antioxidant response elements in the promoter of its target genes to activate the expression of a large network of detoxification, antioxidant, and anti-inflammatory genes as well as other genes involved in the clearance of damaged proteins. Of particular interest is also the upregulation of genes responsible in the biosynthesis and the regeneration of glutathione (GSH), a major intracellular antioxidant. Moreover, Nrf2 also suppresses proinflammatory responses through transcriptional repression and it is involved in the regulation of mitochondrial function. Keap1 and p62/SQSTM1 are Nrf2-associated proteins and main regulators of negative and positive feedback loop mechanisms. In addition, p62 targets Keap1 for selective degradation through autophagy, therefore contributing to the sustained Nrf2 activation response. �
Aging has been associated with the increase in ROS and chronic inflammation, which suggests a loss of adaptability and/or impairment of Nrf2 signaling, which are particularly pronounced in age-dependent neurodegenerative disorders. Surprisingly, rare mutations in SQSTM1 can cause susceptibility to the human neurodegenerative disorder, ALS as well as frontotemporal lobar degeneration, and are associated with muted Nrf2 activation responses in clinical trials. Research studies suggest a reciprocal correlation and show negative effects of mutant disease-related proteins on Nrf2 signaling, thus suggesting the inhibition of the Nrf2 pathway as a possible mechanism underlying neurodegeneration and health issues. �
Nrf2 Activation for Neurodegenerative Disorders
ALS, an adult-onset neurodegenerative disorder caused by the selective death of motor neurons in the brain and spinal cord, is commonly characterized by progressive muscle weakness and atrophy which is generally considered to be fatal, typically within 5 years of diagnosis. ALS has a predominant sporadic ALS form with no apparent genetic component, however, approximately 5 to 10 percent of cases show an autosomal dominant inheritance pattern or familial form of the disease, known as fALS, with is known to cause gene mutations. The symptoms of sporadic ALS and familial ALS are similar, which suggests the involvement of common pathogenic mechanisms, including oxidative stress and neuroinflammation. �
Research studies show that oxidative stress and neuroinflammation should be the key therapeutic targets of Nrf2 signaling in ALS. Genetic research studies in ALS mouse models have shown a considerable therapeutic effect of increased Nrf2 levels in astrocytes, the main GSH producers for neurons. Furthermore, Nrf2 signaling is fundamental for controlling neuroinflammation in ALS through the management of the effects of activated microglial cells on overall neuronal survival. Consistent with the therapeutic potential of Nrf2 signaling, treatment with small molecule activators, including the extremely potent cyanoenone triterpenoids, has ultimately shown efficacy in research study mouse ALS models. �
The neuroprotective potential of Nrf2 activation has been evaluated in experiments utilizing genetic mouse HD models. HD is an autosomal dominant and highly penetrant neurodegenerative disorder, which results from the pathological expansion of a trinucleotide CAG repeats encoding polyglutamines in HTT protein. Brains from patients with HD usually show marked striatal and cortical atrophy at the time of diagnosis. Once motor or other symptoms become apparent, generally throughout midlife, the affected individuals become increasingly disabled over the course of 15 to 25 years before eventually succumbing to the effects of severe physical and mental deterioration, according to evidence from research studies. �
Complex pathogenic mechanisms have been shown in HD, however, excessive oxidative stress has been recognized as a fundamental driver of pathology. The harmful role of oxidative stress has been described in both HD patients and in experimental clinical trial models and it is potentially due to the neuronal sensitivity of an excess in ROS. The levels of several Nrf2-dependent antioxidant proteins, including glutathione peroxidases, catalase, and superoxide dismutase 1, are increased in human HD brains as compared with non-disease controls, suggesting a partial activation of Nrf2 defense signaling yet insufficient enough to block progressive neurodegeneration. Pharmacological activation of Nrf2 results in the broad antioxidant effects of HD in mouse brains and ameliorates the neurological phenotype. Increased expression of several key inflammatory mediators has been shown in the blood, the striatum, the cortex, and the cerebellum from postmortem patient HD tissues, however, neuroinflammation in HD patients seems to be less pronounced than in ALS or PD patients. �
Neurological Disease Treatment with Nrf2 Activation
Finally, the neurological phenotype of the most common neurological disease and neurodegenerative disorder, PD, can be challenged by Nrf2 activation. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra and the profound reduction of dopamine in the striatum. Currently available dopaminergic treatments offer relief from several symptoms but these only address the motor manifestations. Multiple genetic and environmental factors have been suggested in the etiology of PD, however, like ALS, the majority of the clinical cases are sporadic. The discovery that the environmental neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes Parkinson’s disease in humans, led to the development of the MPTP mouse model of disease, which to date, remains one of the most highly utilized animal models of sporadic PD, including the evaluation of drug efficiency. Nrf2 activators showed neuroprotective effects in MPTP mice, which are associated with a reduction of oxidative damage and neuroinflammation. The identification of causative mutations in SNCA, the gene encoding ?-synuclein (aSyn), developed genetic mouse PD models, in which daily oral delivery of the Nrf2 activator dimethyl fumarate (DMF) protected nigral dopaminergic neurons against aSyn toxicity. �
Although oxidative stress and neuroinflammation are pathological hallmarks of AD, a therapeutic role of Nrf2 signaling has developed more slowly, perhaps due to the complexity of disease pathogenesis and readouts of efficiency. Nonetheless, there is a number of recent research studies that demonstrate the efficiency of Nrf2 activators in AD mouse models. � DMF, a U.S. FDA-approved drug (Tecfidera, Biogen-Idec) for the treatment of relapsing multiple sclerosis, activates Nrf2 through the regulation of the Keap1 sensor. DMF is of seemingly low potency and specificity, which prevents neurodegeneration. Drug-like molecules with a similar mechanism of action or with the ability of direct interference with the Keap1/Nrf2 interaction are emerging. The data demonstrate the feasibility to develop Nrf2 activators for treatment. �
In summary, although the causes and symptoms of neurological diseases are different, neurodegenerative disorders share similar molecular mechanisms, which could be regulated and managed with Nrf2 activators. Moreover, targeting Nrf2 signaling may offer a safe and effective treatment approach for a variety of these health issues. Because pharmacological Nrf2 activation targets the broad mechanisms of these health issues, all neurodegenerative conditions would be eligible for treatment. Furthermore, the main goal is to develop noninvasive oral treatment(s) for patients under the supervision of healthcare professionals, which targets both sporadic and familial patients. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
Neurological diseases, including well-known neurodegenerative disorders like Alzheimer’s disease (AD) and Parkinson’s disease (PD) as well as other rare health issues, such as Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS), affect millions of people worldwide. Unfortunately, these are estimated to increase due to the aging population. Currently, there is no treatment available for any neurodegenerative disorder. Treatments for symptoms are available for several neurological diseases, such as PD and HD, but the therapeutic benefits are limited. Although the causes and symptoms for these health issues are different for each neurodegenerative disorders, their molecular pathogeneses share common underlying factors and characteristics, including excessive levels of reactive oxygen species (ROS), mainly due to mitochondrial impairment, neuroinflammation, and disturbances in protein homeostasis (proteostasis). This increases the possibility of developing a universal treatment that will focus on targeting the common triggers of neurological diseases. �
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References: �
Dinkova-Kostova, Albena T, et al. �Activation of Nrf2 Signaling as a Common Treatment of Neurodegenerative Diseases.� Activation of Nrf2 Signaling as a Common Treatment of Neurodegenerative Diseases | Neurodegenerative Disease Management, 23 May 2017, www.futuremedicine.com/doi/full/10.2217/nmt-2017-0011#.
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. �
Food Sensitivity for the IgG & IgA Immune Response
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with food sensitivities. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs. �
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.
How often do you feel unclear thoughts or concentration and brain fog? How often do you experience pain, discomfort, and/or inflammation? How often do you feel mental and physical fatigue after eating meals? Inflammation is an essential immune response, however, chronic inflammation, especially in the brain and the joints, can cause a variety of health issues. Fortunately, there are many natural remedies that can help reduce inflammation, including turmeric or curcumin. �
Turmeric, sometimes known as Indian saffron or the golden spice, is a tall plant that grows in Central America and Asia. The turmeric that we commonly see on shelves and in spice cabinets is made of the ground roots of the plant. Moreover, the bright yellow color of processed turmeric has inspired many cultures to use it as a dye. Ground turmeric is also the main ingredient in curry powder. Capsules, powders, teas, and extracts are several ways that turmeric is available commercially. �
Curcumin is the active ingredient found in turmeric and it has many powerful biological properties. Ayurvedic medicine, a traditional Indian system of treatment, recommends utilizing turmeric for a variety of health issues, including chronic pain and inflammation. Western medicine has started to evaluate the use of turmeric as a pain reliever. �In the following article, we will discuss the health benefits and risks of turmeric as well as how these can affect overall health and wellness. �
Health Benefits of Turmeric
According to the Arthritis Foundation, research studies in which turmeric has been utilized helped reduce chronic inflammation in the clinical trial participants. The anti-inflammatory properties of turmeric, or curcumin, may help reduce arthritis joint pain and discomfort. Together with other supplements, such as an Nrf2 activator, research studies have shown that these can reduce inflammatory cytokines by dampening NF-?B activity and down-regulating COX, LOX, iNOS, matrix metalloproteiases, INF-a, and interleukines-1, 2, 6, 8, 12 as well as chemokines. The Arthritis Foundation suggests taking capsules of 400 to 600 milligrams (mg) of turmeric or curcumin up to three times per day for chronic pain and inflammation. �
Many researchers and healthcare professionals believe that turmeric may not only be efficient at reducing inflammation but it may also be safe and effective as a chronic pain reliever. As previously mentioned, the spice is reputed to help relieve arthritis as well as fibromyalgia symptoms. Research tudies seem to support the utilization of turmeric for pain relief, with one source noting that it seemed to work as well as ibuprofen (Advil) in people with arthritis. Although dosing recommendations seem to vary, those who participated in the research study took 800 mg of turmeric in capsules, each day. �
Turmeric has also recently been getting a lot of attention because of its antioxidant abilities. The antioxidant effects of turmeric appear to be so powerful that it may even help stop or prevent your liver from being damaged by toxins. This could be good news for people who take strong medicines for diabetes or any other health issues that may damage their liver through long-term utilization. Curcumin has also shown great promise as a type of cancer treatment. Research studies suggest that curcumin can have protective effects against pancreatic cancer, prostate cancer, and multiple myeloma. �
Turmeric is utilized in curry powder is because it helps add a delicious element to foods. However, turmeric can also play a fundamental role in the digestive process of that food. Because of its antioxidant and anti-inflammatory properties, turmeric can help promote healthy digestion. It’s utilized in ayurvedic medicine as a digestive system healing agent. Today, Western medicine has started to evaluate how turmeric, or curcumin, can help with gut inflammation as well as gut permeability, two measures of your digestive efficiency. Turmeric is even being explored as a possible treatment approach for irritable bowel syndrome (IBS). Turmeric can have many health benefits but curcumin supplements may also have several health risks. �
Health Risks of Turmeric
The same healing agents in turmeric that support healthy digestion can unfortunately also cause irritation when consumed in large amounts. Several research study participants looking at the utilization of turmeric as a type of cancer treatment had to drop out of the clinical trial because their digestive system was so negatively affected by the spice. Turmeric stimulates the stomach to produce more gastric acid. Although this can help with digestion, it can negatively affect digestion for others. �
Turmeric’s purifying properties may also make you bleed more easily. It’s not completely understood why this happens. However, people who take blood-thinning medicines, such as warfarin (Coumadin) should avoid consuming large doses of turmeric or curcumin.�
Researchers and healthcare professionals hypothesize that turmeric’s other benefits, including its capability to lower blood pressure and cholesterol, may have something to do with how turmeric affects your blood. Furthermore, researchers and healthcare professionals believe that the way curcumin is extracted from turmeric can be the cause of this health issue. Approximately 95 percent of curcumin in the U.S. is extracted by carcinogenic solvents. �
You may have also heard that eating foods seasoned with curry can stimulate labor. Although there’s little evidence to back up this claim, research studies suggest that turmeric can help ease symptoms of PMS. But perhaps, there may be some truth behind the old wives’ tale. Because of its blood-thinning effects alone, however, pregnant women are recommended to avoid taking turmeric supplements. Adding small amounts of turmeric as a spice to food or meals shouldn’t be a problem. �
The Takeaway of Turmeric
It appears that there are many health benefits to including turmeric as a part of your regular diet. The golden spice supports a healthy immune system, helps relieve chronic pain, and can even help promote healthy digestion, among other health benefits. However, because of some of its health risks and side effects, turmeric or curcumin may not be worth taking for several people. It’s essential to utilize caution when deciding whether turmeric is something you may want to try. As with any alternative treatment option, talk with your doctor before you utilize turmeric to treat any health issue. If you want to buy a turmeric or curcumin supplement, then there is an excellent selection online with thousands of great customer reviews. �
Turmeric, or curcumin, is a powerful, natural remedy which has been demonstrated to have many health benefits, especially for chronic pain and inflammation, among others. However, too much of the powerful, golden spice can also have several health risks and side effects. It’s fundamental to talk to a healthcare professional to discuss if turmeric or curcumin is a good treatment option. Turmeric, or curcumin, can be utilized for a variety of health issues, including arthritis and fibromyalgia. Make sure to talk to a doctor before using turmeric or curcumin supplements. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
How often do you feel unclear thoughts or concentration and brain fog? How often do you experience pain, discomfort, and/or inflammation? How often do you feel mental and physical fatigue after eating meals? Inflammation is an essential immune response, however, chronic inflammation, especially in the brain and the joints, can cause a variety of health issues. Fortunately, there are many natural remedies that can help reduce inflammation, including turmeric or curcumin. �
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
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. �
Food Sensitivity for the IgG & IgA Immune Response
Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with food sensitivities. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs. �
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.
How often do you feel more susceptible to pain, discomfort, and inflammation? Rheumatoid arthritis (RA) is an autoimmune disease that affects about 0.5 to 1.0 percent of the adult population throughout the world. Evidence suggests that the autonomic nervous system (ANS) plays a fundamental role in the management of an abnormal immune response and inhibition of inflammation. The ANS regulates cytokine production through the cholinergic anti-inflammatory pathway, including the efferent vagus nerve, the neurotransmitter ACh, and its receptors (?7 nicotinic ACh receptor, ?7 nAChR). �
Turmeric, or curcumin, has historically been utilized as a spice and a medicinal herb in India and China. Evidence suggests that curcumin affects diverse bioactivities. In recent years, a variety of research studies have shown that consuming curcumin considerably ameliorated collagen-induced arthritis (CIA). A clinical trial has shown that curcumin is a safe and effective natural remedy for RA patients. However, pharmacokinetic research studies have shown that its bioavailability can be very poor which raises the question, how does curcumin, or turmeric, produce an anti-inflammatory effect? �
Curcumin, the Gut-Brain Axis, and Inflammation
Researchers believe that they have found how curcumin, or the natural phenol compounds found in turmeric, can ultimately help reduce inflammation. Curcumin-containing turmeric is commonly given to horses by their owners due to its perceived anti-inflammatory properties. As a matter of fact, researchers have shown the ability of curcuminoids to reduce inflammation in aging horses. In one research study, researchers writing in the Journal of Neuroinflammation described their findings with rats that had collagen-induced arthritis to learn more about the performance of curcumin. The research team stated that several research studies had shown that taking curcumin by mouth reduced collagen-induced arthritis. �
During another clinical trial, the findings had shown that curcumin was safe and effective for patients with rheumatoid arthritis. However, the research study had also shown that its bioavailability was poor, which raised questions about how curcumin produced its anti-inflammatory effect. They then evaluated whether the gut-brain axis was involved in its therapeutic action. The researchers found that curcumin reduced collagen-induced arthritis through the gut-brain axis by controlling the function of the cholinergic system. The cholinergic system consists of nerve cells that utilize the neurotransmitter acetylcholine. It is associated with cognition, memory, selective attention, and emotional processing. �
The research study team believes that targeting the gut cholinergic anti-inflammatory pathway could be a promising treatment approach for rheumatoid arthritis patients as well as with other inflammatory disorders, such as irritable bowel syndrome, characterized by an imbalanced autonomic nervous system. Previous research studies also suggested that curcumin activated its effects in a gut-dependent way. The gut is a sensory organ, which sends signals from the lumen to the central nervous system, which in turn sends signals to peripheral tissues or organs. Surprisingly, recent research studies ultimately show that curcumin has regulatory effects on the gut microbiota in several circumstances and that the gut microbiota is involved in the development of arthritis. �It is possible that curcumin affects the cholinergic anti-inflammatory pathway through the gut-brain axis via modulation of the gut microbiota�, stated the research study team. �
How Turmeric Changes the Gut Microbiome
Further research studies are still required to continue to explain the turmeric paradox: efficacy despite poor bioavailability. One possible hypothesis as to how curcumin and turmeric change the gut microbiome, according to the first human clinical research study evaluating its effects, is that the gastrointestinal effects of the spice may have wider-reaching systemic effects. Previous research studies show that curcumin can considerably alter gut microbiota where these alterations of the composition and/ or metabolic activity of gut bacteria may in part explain the therapeutic benefits of curcumin. �
To demonstrate how curcumin alters gut bacteria in humans, a research study involved a group of people taking turmeric (3000 mg turmeric root plus 3.75 mg black pepper�derived extract of piperine alkaloid [BioPerine]), curcumin (3000 mg of curcumin [Curcumin C3 Complex] plus 3.75 mg BioPerine) or placebo, twice daily for 8-weeks. Utilizing gut microbial DNA sequencing it was found that both turmeric and curcumin changed the gut microbiota in a highly similar manner, with the research study team suggesting that curcumin may drive the majority of changes observed in turmeric-treated subjects. �
Overall, turmeric and curcumin increased bacterial species richness. Surprisingly, although the gut microbiota response was highly individual, there were several concordances in response to turmeric/ curcumin. �Responsive� subjects had a similar microbial signature involving uniform increases in species of polysaccharide-degrading and hydrogen-consuming bacteria. �
�This research study in healthy subjects has potentially raised more intriguing questions than it has fully answered and emphasizes the complexity of human intervention research studies intending to evaluate the effects of these potentially powerful herbal medicines,� stated the research study investigators. One hypothesis they suggest is that individual variations in turmeric absorption may result in the observed variations in prebiotic-like effects. �Future research studies that include a larger human cohort will clarify whether the responsive microbiota we identified here is representative and whether less prevalent response signatures in our data may be clearly defined with additional participants,� they concluded. �
If there is definitely a fundamental role of the gut microbiome in regulating individual responses to turmeric and/ or curcumin more research studies in this field could help support the understanding of its health benefits in the context of personalized nutrition, especially for rheumatoid arthritis (RA) patients, among patients with inflammatory health issues. �
Turmeric, or curcumin, is a powerful, natural remedy which has been demonstrated to have many health benefits, especially for brain health. According to many research studies, turmeric or curcumin can help reduce inflammation associated with rheumatoid arthritis (RA), among that of other inflammatory diseases. Although further research studies are still required to establish this as a fact, the current findings suggest that curcumin, or turmeric, is a safe and effective treatment for chronic inflammation. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal. �
How often do you feel more susceptible to pain, discomfort, and inflammation? Rheumatoid arthritis (RA) is an autoimmune disease that affects about 0.5 to 1.0 percent of the adult population throughout the world. Evidence suggests that the autonomic nervous system (ANS) plays a fundamental role in the management of an abnormal immune response and inhibition of inflammation. The ANS regulates cytokine production through the cholinergic anti-inflammatory pathway, including the efferent vagus nerve, the neurotransmitter ACh, and its receptors (?7 nicotinic ACh receptor, ?7 nAChR). �
Turmeric, or curcumin, has historically been utilized as a spice and a medicinal herb in India and China. Evidence suggests that curcumin affects diverse bioactivities. In recent years, a variety of research studies have shown that consuming curcumin considerably ameliorated collagen-induced arthritis (CIA). A clinical trial has shown that curcumin is a safe and effective natural remedy for RA patients. While research studies show that its bioavailability can be very poor,� curcumin or turmeric produces an anti-inflammatory effect by ultimately affecting the gut-brain axis and changing the gut microbiome. �
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
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.
How often do you get fatigued after meals? How often do you have difficulty falling into deep, restful sleep? How often do you feel more susceptible to pain? Chronic brain inflammation can cause numerous symptoms which are commonly associated with a wide variety of neurological diseases. Fortunately, researchers and healthcare professionals have found a natural remedy that can help improve chronic brain inflammation and it can provide many more health benefits: turmeric. �
For centuries, researchers and healthcare professionals alike have been studying the many health benefits of turmeric. In recent decades, however, research studies are attempting to verify the claims of our ancestors by testing turmeric in numerous clinical trials. Curcumin has been shown to have a wide variety of healing properties and practical uses. However, can turmeric improve chronic brain inflammation? In this article, we will discuss the benefits of turmeric for brain health. �
Turmeric and Brain Health
Turmeric, or curcumin, supplements have shown tremendous potential towards the safe and effective treatment of a variety of health issues. Research studies show that turmeric can help relieve arthritis and joint pain, lower blood pressure, and even enhance skincare. Turmeric may also ultimately help improve allergy symptoms and it may also help promote weight loss. �
New evidence from several research studies also suggests that turmeric may provide considerable health benefits for overall brain health, including the prevention of neurological diseases. Curcumin contains neuroprotective properties that can help preserve mental acuity. Therefore, turmeric may have the ability to boost memory function, reduce brain fog, and enhance overall cognition. Before we evaluate the research studies, we will discuss memory and brain fog in a bit more detail. �
Understanding Memory and Brain Fog
The lack of mental clarity is commonly associated with the inability to focus, poor levels of concentration, and memory problems. Best known as brain fog, or mental fatigue, this is a collection of symptoms related to reduced brain function rather than a single health issue.�The brain is an extremely complex organ. The extent with which turmeric can help depends on the cause of your brain fog, which we will discuss shortly. First, let�s review several core functions of the human brain. �
The brain acquires knowledge by using the senses as well as by experiences and thinking in what we know as cognition. Cognition ultimately includes memory, problem-solving, and decision making, among other brain functions.�
The brain is also capable of storing and recalling information. Memory is the collection of this data saved over time by neural connections in the brain. Information in the brain is made up of short-term memory and long-term memory.
The brain also other functions that work together with memory. The way we learn mainly includes how we acquire knowledge as well as how this information is remembered in the future. Learning can include changing these skills.
Brain plasticity, also known as neuroplasticity, is the way a person’s brain will change throughout their life. This helps make synapses stronger and/or weaker and it can ultimately help improve a person’s learning and memory capabilities.�
Turmeric and Brain Health: Benefits of Curcumin
One research study evaluated the effects of turmeric, or curcumin, on cognition and mood in a group of healthy, elderly individuals. The clinical trial included 60 subjects ranging between the ages of 60 and 85 years old, which consumed a 400 mg dose of curcumin. The research study was a double-blinded, placebo-controlled, and randomized clinical trial. �
One hour post-administration, researchers found considerable performance improvements in working memory tasks and sustained attention span compared to the placebo group. After four additional weeks of treatment, the turmeric, or curcumin, group experienced reduced psychological stress-induced fatigue, enhanced mood, and a better sense of calmness. �
Finally, the research study showed improvements in overall alertness and contentedness. Turmeric ultimately appears that it can also help enhance memory, focus, and concentration as well as cognition in elderly populations, among others. �
There are several mechanisms of action that turmeric takes on the human body to help prevent cognitive impairment. Turmeric reduces chronic low-grade systemic inflammation, enhances antioxidant activity, and reduces oxidative stress. �
By fighting free radicals in the human body, turmeric has also shown the potential to preserve neuronal integrity, which can inhibit the progression of cognitive decline. Furthermore, these processes demonstrate an innate ability to slow down brain aging and reduce brain fog symptomology caused by aging and disease, decreasing the risk or neurological diseases. �
Turmeric may also improve DHA, or docosahexaenoic acid, synthesis. DHA is the fatty acid most closely associated with brain health, brain development, and neuroprotection. If you have a DHA deficiency, you leave yourself at risk of developing several cognitive disorders, including anxiety, memory problems, inability to focus, etc. Researchers have found that turmeric increases multiple enzymes responsible for the synthesis of DHA from its precursor, alpha-lipoic acid, or ALA. �
According to research studies, another way in which curcumin can help improve brain health is by reducing the neurotoxicity caused by fluoride. It�s well-known that fluoride may have adverse effects on mental health and other core biological functions. Researchers performed a clinical trial testing curcumin�s neuroprotective health benefits on a group of mice. �
The results of the research study showed that fluoride increased lipid peroxidation, or LPO, a major cause of damage to cell membranes. In addition, fluoride also increased the number of neurodegenerative cells present in the hippocampus. With 30 days of curcumin administration from the research study, there was a considerable decrease in neurodegeneration and LPO. �
A second animal research study utilized curcumin to evaluate its effects on cognition and neurogenesis in a group of aged rats. Neurogenesis refers to the process of developing new neurons in the brain. Following the 12-week treatment period, researchers in the research study were ultimately able to demonstrate increased cognition and neurogenesis in the rats. �
The treated group also experienced enhanced spatial and non-spatial memory. These results suggest that turmeric may affect neuronal development, neurotransmission, synaptic plasticity, and signal transduction, among other brain functions. �
Additionally, another fundamental protein for cognition is the brain-derived neurotrophic factor, or BDNF, which promotes the growth and maturation of brain cells or, neurons. According to research studies, turmeric has shown that it can considerably help improve BDNF levels in people with premenstrual syndrome or PMS, diabetes, and obesity. �
The last research study we will look at further supports the hypothesis of utilizing turmeric to improve memory and reduce brain fog. A group of chronically stressed rats were given turmeric throughout a 20-day treatment period. �
Following turmeric administration, there was a notable reversal of impaired hippocampal neurogenesis, followed by increases in serotonin receptors and BDNF. The results of the research study ultimately suggest that turmeric, or curcumin, may overcome stress-induced abnormalities in the brain that can inhibit cognitive function, among other brain functions. �
Turmeric, or curcumin, is a powerful, natural remedy which has been demonstrated to have many health benefits, especially for brain health. Regarded as an antioxidant with anti-cancer, antidepressant, and anti-aging properties, turmeric can do much more than improve memory and brain fog. According to many research studies, turmeric or curcumin can help reduce brain inflammation or neuroinflammation by blocking the production of proinflammatory cytokines. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
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The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
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How often do you get fatigued after meals? How often do you have difficulty falling into deep, restful sleep? How often do you feel more susceptible to pain? Chronic brain inflammation can cause numerous symptoms which are commonly associated with a wide variety of neurological diseases. Fortunately, researchers and healthcare professionals have found a natural remedy that can help improve chronic brain inflammation and it can provide many more health benefits: turmeric. �
For centuries, researchers and healthcare professionals alike have been studying the many health benefits of turmeric. In recent decades, however, research studies are attempting to verify the claims of our ancestors by testing turmeric in numerous clinical trials. Curcumin has been shown to have a wide variety of healing properties and practical uses. However, can turmeric improve chronic brain inflammation? In this article, we will discuss the benefits of turmeric for brain health. �
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
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Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
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How often do you feel agitated, easily upset, and nervous between meals? How often do you depend on coffee to keep yourself going?How often do you have difficulty concentrating before eating? Inflammation is an essential reaction of the human body. It’s triggered by the immune system to protect us from injury, infection, and/or illness. However, what happens if there is too much inflammation in the human body? And, what happens if there is too much inflammation in the brain?
Neuroinflammation can cause a variety of health issues, such as anxiety, stress, depression, brain fog, fatigue, and even lethargy, among other well-known symptoms. Fortunately, there is one natural remedy that can help tremendously reduce inflammation and improve brain function. According to research studies, curcumin can help combat neuroinflammation. The purpose of the article below is to discuss the anti-inflammatory effects of curcumin in microglia, brain health, and wellness.
Anti-inflammatory Effects of Curcumin in Microglial Cells
Abstract
Lipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the underlying signaling pathways are largely unidentified. Here, we investigated curcumin�s anti-neuroinflammatory properties in LTA-stimulated BV-2 microglial cells. Inflammatory cytokine tumor necrosis factor-? [TNF-?, prostaglandin E2 (PGE2), and Nitric Oxide (NO] secretion in LTA-induced microglial cells were inhibited by curcumin. Curcumin also inhibited LTA-induced inducible NO synthases (iNOS) and cyclooxygenase-2 (COX-2) expression. Subsequently, our mechanistic studies revealed that curcumin inhibited LTA-induced phosphorylation of mitogen-activated protein kinase (MAPK) including ERK, p38, Akt, and translocation of NF-?B. Furthermore, curcumin induced hemeoxygenase (HO)-1HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression in microglial cells. Inhibition of HO-1 reversed the inhibition effect of HO-1 on inflammatory mediators released in LTA-stimulated microglial cells. Taken together, our results suggest that curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses. � Keywords:curcumin, neuroinflammation, TLR2, HO-1, microglial cells
Introduction
Chronic neuroinflammation plays an important role in various neurodegenerative diseases, including AD, Parkinson�s disease (PD), Huntington�s disease (HD), stroke, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) (Spangenberg and Green, 2017). Neuroinflammation is interceded by the activation of microglia, the prime effector cells and resident immune cells of the CNS (Nakagawa and Chiba, 2015). Microglial cells can be activated in response to neuronal death or neuronal damage induced by neuroinflammatory responses or by extracellular toxins, such as bacteria and pathogens (Larochelle et al., 2015). In neuroinflammation, activated microglia releases various kinds of cytokines, chemokines, reactive oxygen species, and reactive nitrogen species for the development and maintenance of inflammatory responses (Moss and Bates, 2001). Excessive production of these inflammatory mediators could cause neuronal damage and death. Accumulated evidence suggests that control of microglial activation could attenuate the severity of neurodegenerative disease (Perry et al., 2010). Therefore, the development of anti-neuro-inflammatory agents for the inhibition of microglial activation could be beneficial for the treatment of neurodegenerative diseases.
Microglia express pattern recognition receptors (PRR) that can bind to pattern-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) such as lipopolysaccharide (LPS) and lipoteichoic acid (LTA), respectively (Jack et al., 2005). TLRs, a major class of PRRs, play a crucial role in host defense by inducing innate immune responses. Increasingly, studies have indicated that TLR2 agonist LTA is involved in the pathogenesis of CNS infectious diseases and can induce neuronal damage (Neher et al., 2011). Inhibition of TLR2 activation attenuates microglial cell activation and amyloid ? accumulation in the brain (McDonald et al., 2016; Hossain et al., 2017). Signal transduction via TLR2 is mediated by different adaptor proteins, including MyD88, which promotes downstream signaling via MAPK and NF-?B activation leading to the expression of inflammatory mediators (Larochelle et al., 2015).
Inflammatory and oxidative molecules are very potent activators of Keap-Nrf2 (NF-E2-related factor 2), which induces the expression of Phase II detoxification enzymes to adapt to the oxidative stress condition (Rojo et al., 2010). Usually, Nrf2 acts in an inactive form. Upon stimulation, Nrf2 separates from Keap1 and translocates into the nucleus, where it binds to the antioxidant response element (ARE) to activate the transcription of antioxidant genes for cytoprotection (Ma, 2013; Cho et al., 2015). One of the Nrf2-regulated genes is heme oxygenase-1 (HO-1), which has an ARE sequence in its promoter region. Recently, HO-1 has been reported to be a predominant factor in controlling oxidative stress and inflammatory responses in neurodegenerative diseases (Schipper et al., 2009). HO-1 is the first inducible rate-limiting enzyme in the degradation of heme into by-products. HO-1 may provide neuroprotection or neurotoxic effect because of the balance between the beneficial and toxic effects of heme and heme products (Mancuso et al., 2010). One by-product of HO-1, Bilirubin, has been demonstrated to protect neurons from oxidative stress in vivo and in vitro. Bilirubin can be oxidized to biliverdin by scavenging peroxyl radicals (Chen, 2014). It has been suggested that HO-1, biliverdin, and CO have anti-inflammatory properties (Jazwa and Cuadrado, 2010). Another study has suggested that mice lacking HO-1 were vulnerable to pro-inflammatory stimuli and developed chronic inflammation due to reduced iron levels (Chora et al., 2007). Furthermore, a recent study suggested that the up-regulation of the Nrf2 and HO-1 pathways significantly inhibited the inflammatory reaction in activated microglia (Kim et al., 2016). Nrf2 inhibited microglial hyperactivation by suppressing p38 MAPK and the NF-?B signaling pathway (Kim B.W. et al., 2013). Knockdown of Nrf2 in mice was shown to be hypersensitive to neuroinflammation, as indicated by an increase in the inflammatory markers iNOS, IL-6, and TNF-? (Rojo et al., 2010). Consequently, Nrf2 and HO-1 have been considered as important therapeutic targets for neurodegenerative diseases (Koh et al., 2011; Zhang et al., 2014).
Curcumin, the main curcuminoid isolated from Curcuma longa L. (turmeric) has been used for centuries in Southeast Asia both as a medicinal remedy and as food (Kunnumakkara et al., 2017). Curcumin, demethoxycurcumin, bisdemethoxycurcumin, ar-turmerone, ?-turmerone, and ?-turmerone are the major bioactive compounds found in C. longa. In modern pharmacological studies, C. longa constituents, particularly curcumin, have shown promising pharmacological activities due to its anti-neuroinflammatory, neuroprotective, chemopreventive, immunomodulatory, and potentially chemotherapeutic effects (Garcia-Alloza et al., 2007; Zhou et al., 2017). A previous study showed that curcumin inhibited LPS-induced inflammatory responses in RAW264.7 macrophages, suggesting a potential role of curcumin in anti-Gram-negative bacterial infection (Zhou et al., 2017) and both in vivo and in vitro research have shown that curcumin exhibits anti-inflammatory effects (Garcia-Alloza et al., 2007; Prakobwong et al., 2011; Parada et al., 2015; Li et al., 2016). Furthermore, curcumin has also been reported to promote the development of the M2 microglial phenotype in an HO-1-dependent manner and reduce iNOS induction, protecting microglial cells against oxidative stress (Parada et al., 2015). In the present study, we investigated whether curcumin could affect LTA-induced microglial activation. The TLR2 ligand LTA is a major constituent of the cell wall of Gram-positive bacteria. We show that curcumin exhibits anti-inflammatory and antioxidant effects in LTA-stimulated BV2 microglia through activation of HO-1/Nrf2/ARE cytoprotective mechanisms.
Materials and Methods
Materials
Curcumin and other reagents were purchased from Sigma (C7727, >80%, St. Louis, MO, United States). Protoporphyrin IX (SnPP) and antibodies directed against HO-1 (sc-390991) – Nrf2 (sc-722), TATA-binding protein (TBP; sc-74595), ?-tubulin (sc-134237), and ?-actin (sc-130065) – were purchased from Santa Cruz Biotechnology, Inc., (Dallas, TX, United States). Antibodies directed against iNOS (13120) – phosphorylated (p)-MAPK (9910s), MAPK (9926), protein kinase B (Akt; 4685), p-Akt (13038), and an NF-?B pathway kit (9936) – were purchased from Cell Signaling Technology, Inc., (Danvers, MA, United States). LTA was obtained from InvivoGen (tlrl-pslta,Toulouse, France). Additionally, JNK inhibitor (JNK inhibitor II; 420119), Akt inhibitor (wortmannin; 12-338), ERK inhibitor (PD98059, 513000), and p38 inhibitor (SB230580, 559395) were purchased from EMD Millipore (Billerica, MA, United States). The cell culture medium, DMEM, and fetal bovine serum (FBS) were purchased from Gibco BRL (now Invitrogen Corporation, Carlsbad, CA, United States).
Cell Culture
Mouse BV-2 microglial cells were purchased from ATCC. Cells were cultured in DMEM supplemented with 10% heat-inactivated FBS and 0.1% penicillin-streptomycin (BioSource International, Camarillo, CA, United States) at 37�C in a humidified atmosphere of 5% CO2 and 95% air.
Cell Viability Assay
The cytotoxicity of curcumin was assessed using a microculture [3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT)-based colorimetric assay. Cells were incubated in 24-well plates at a density of 5 � 105 cells per well. The MTT solution (5 ml of 5 mg/ml) was added to each well (final concentration 62.5 mg/ml). After incubation for 3 h at 37�C in 5% CO2, the supernatant was removed and the formazan crystals produced in viable cells were solubilized with 150 ml of dimethylsulfoxide (DMSO). The absorbance of each well was then read at 570 nm using a microplate reader (Wallac 1420; PerkinElmer, Inc., Boston, MA, United States).
Measurement of Nitrite Concentration
NO synthesis in cell cultures was measured by the Griess method with microplate. To measure nitrite, 100-?l aliquots were removed from the conditioned medium and incubated with an equal volume of the Griess reagent [1% sulfanilamide/0.1%N-(1-naphthyl)-ethylenediaminedihydrochloride/2.5% H3PO4] at room temperature for 10 min. The nitrite concentration was determined by measuring the absorbance at 540 nm with a Vmax 96-well microplate spectrophotometer (Molecular Devices, Menlo Park, CA, United States). Sodium nitrite was used as a standard.
Measurement of TNF-? and PGE2 Concentration
The cells were incubated first with various concentrations of curcumin for 1 h and then with LTA for 16 h. Following 24 h incubation, TNF-? and PGE2 levels were quantified in the culture media using an enzyme-linked immunosorbent assay (ELISA) kit (R&D Systems, Minneapolis, MN, United States) according to the manufacturer�s instructions.
Preparation of Nuclear Extract
BV-2 microglial cells were washed three times with cold PBS and collected in 3000 ?l PBS using centrifugation at 800 �g for 5 min (4�C). The cell pellets were suspended in buffer A [10 mM HEPES-KOH (pH 7.9); 1.5 mM MgCl2; 10 mM KCl; 0.5 mM dithiothreitol (DTT); 0.2 mM protease inhibitor (PI)] and incubated for 5 min on ice. Buffer B [10 mM HEPES-KOH (pH 7.9); 1.5 mM MgCl2; 420 mM NaCl; 0.2 mM EDTA; glycerol 25% v/v; 0.1 mM DTT; 0.2 mM PI] was added to the cell extract and was incubated on ice for 5 min prior to centrifugation at 11,000 �g for 1 min at 4�C. Nuclear proteins were extracted with the addition of complete lysis buffer B [10 mM HEPES-KOH (pH 7.9); 1.5 mM MgCl2; 10 mM KCl; 0.5 mM DTT; 0.2 mM PI; 25% (w/v) glycerin; 420 mM NaCl; 0.2 mM EDTA] for 30 min at 4�C with occasional vortexing. Following centrifugation at 11,000 �g for 5 min at 4�C, the supernatants were collected and stored at -70�C.
Western Blot Analysis
BV-2 cells were harvested in an ice-cold lysis buffer (1% Triton X-100; 1% deoxycholate; 0.1% sodium dodecyl sulfate). The protein content of the cell lysates was subsequently determined using Bradford reagent (Bio-Rad Protein Assay Kit I5000001; Bio-Rad Laboratories, Inc., Hercules, CA, United States). Total proteins in each sample (50 ?g) were separated by 7.5% SDS-PAGE and transferred to polyvinylidene difluoride membranes. Following blocking of the non-specific binding sites with 5% non-fat milk at room temperature for 30 min, the membranes were incubated with primary antibodies directed against iNOS (1:500), p-Akt (1:1,000), p-MAPK (1:1,000), MAPK (1:1,000), p-p65, p65 (1:500), p-I?B?, I?B? (1:1,000), HO-1 (1:1,000), Nrf2 (1:1,000), TBP (1:3,000), ? (1:1,000), HO-1 (1:1.0), and actin (1:3,000) for 16 h at 4�C. This was followed by incubation with horseradish peroxidase-conjugated anti-rabbit (sc-2768; 1:5,000) or anti-mouse (sc-2371; 1:5,000) secondary antibodies (Santa Cruz Biotechnology, Inc.) at room temperature for 1 h. Tubulin was used as the loading control for each lane. The proteins were visualized using an enhanced chemiluminescence detection kit (GE Healthcare, Chicago, IL, United States). Following washing with PBS with Tween-20, the protein bands were visualized using the Gel Docsed as the loading control for each lane. The proteins were visualized using a Quant 350 analyzer (GE Healthcare).
Real-Time RT-PCR
Total RNA was isolated from cells using an RNA spin miniRNA isolation kit (GE Healthcare, Uppsala, Sweden) according to the manufacturer�s instructions. cDNA was synthesized from 1 ?g of total RNA using Maxime RT PreMix (Takara, Gyeonggi-do, Japan) and anchored oligo-dT15-primers. Real-time PCR was performed using a Chromo4TM instrument (Bio-Rad) and SYBR Green Master Mix (Applied Biosystems, Foster City, CA, United States). Relative amounts of target mRNA were determined using the comparative threshold (Ct) method by normalizing target mRNA Ct values to those for ?-actin (Ct). Prime sequences used in the study were shown in Table ?1.
Statistical Analysis
Data are expressed as the mean (standard deviation, SD). Each experiment was repeated at least three times. Statistical analysis was performed using the Statistical Package for GraphPad Prism software (version 16.0) to determine significant differences. We used either Student�s t-test or one-way analysis of variance (ANOVA) followed by Dunn�s post hoc tests for analyses. P-values < 0.05 were considered statistically significant.
Results
Curcumin Did Not Affect Cell Viability
Cell viability experiments were carried out to determine whether concentrations of curcumin used in this study affected the viability of BV2 microglia. Figure ?1 shows that curcumin at the concentration range of 5�20 ?M, together with or without 5 ?g/ml LTA, did not produce cytotoxicity in BV2 microglia. Therefore, we used these concentrations of curcumin for further study.
Curcumin Prevented the Production of Neuroinflammatory Molecules in LTA-Activated BV2 Microglia
To investigate the effects of curcumin on the secretion of inflammatory cytokines, BV2 cells were treated with LTA in the presence and absence of curcumin for 24 h. Curcumin was not removed before LTA addition. Release of NO, PGE2, and TNF-? were significantly and dose-dependently reduced by curcumin (Figures 2A�C). Furthermore, LTA increased the mRNA expression of iNOS and COX-2. Incubation with curcumin suppressed the mRNA expression of COX-2 and iNOS in BV2 microglial cells stimulated by LTA in a concentration-dependent manner (Figures 2D, E).
Curcumin Suppressed LTA-Induced Activation of NF-?B in BV-2 Microglial Cells
The genes encoding inflammatory protein expression in response to microglial activation were under the transcription control of NF-?B. Therefore, we examined the effect of curcumin on the activation of NF-?B in LTA-stimulated microglial cells. The results showed that LTA induced a characteristic increase in the phosphorylation of I?B?. Following pre-treatment with curcumin, levels of p-I?B? were significantly reduced in a concentration-dependent manner (Figure ?3 and Supplementary Figure S1). Consistently, the nuclear translocation of the NF-?B p65 subunit induced by LTA was also attenuated by pre-treatment with curcumin. Taken together, curcumin likely attenuates the expression of neuroinflammatory molecules by suppressing the nuclear translocation and activation of NF-?B. Quantification with statistical analysis was provided as supporting data.
Curcumin Inhibited LTA-Induced Activation of p38, and ERK MAPK in BV-2 Microglial Cells
Apart from NF-?B, MAPKs are also upstream modulators of neuroinflammatory molecules in microglial cells. Previous studies showed that curcumin antagonized LPS-induced MAPKs phosphorylation in microphage (Yang et al., 2008; Kunnumakkara et al., 2017). To investigate whether curcumin inhibits neuroinflammation through regulating MAPKs, we examined its effects on LTA-induced MAPK phosphorylation. BV-2 microglial cells were pre-treated with different concentrations of curcumin for 3 h and were then stimulated with LTA for 1 h. As shown in Figure ?4A and Supplementary Figure S2, curcumin inhibited LTA-induced ERK, p38, and Akt phosphorylation. However, up to 20 ?M curcumin did not affect LTA-induced JNK phosphorylation. MAPKs pathway has been reported to mediate the production of cytokines, chemokine, and other neuroinflammatory molecules. Therefore, we next investigated the role of ERK, p38, JNK, and Akt in BV2 cells� neuroinflammatory molecule production using the ERK, p38, JNK, and Akt inhibitors. However, only the p38 inhibitor SB203580 significantly decreased LTA-induced release of NO and mRNA expression levels of iNOS (Figures 4B, C). Although phosphorylation of JNK was not inhibited by curcumin, the JNK inhibitor II significantly inhibited LTA-induced NO release (Figure ?4B). The results suggest that MAPKs� signaling pathways are involved in curcumin�s anti-neuroinflammatory effects in LTA-stimulated microglial. Quantification with statistical analysis is provided as supporting data.
Inhibition of HO-1 Signaling Abolished Curcumin�s Inhibitory Effect on Neuroinflammatory Responses
HO-1 acts as an anti-inflammatory and antioxidant modulator in microglia (Schipper et al., 2009). Western blot and RT-PCR analyses showed that curcumin upregulated HO-1 expression at the protein and mRNA levels, as shown in Figures 5A�D and Supplementary Figure S3. The expression of HO-1 mRNA and protein was maximally increased in BV-2 microglial cells treated with 20?M curcumin for 4 h and 8 h respectively. Furthermore, curcumin increased Nrf2 nuclear translocation within 1 h and prolonged its nuclear translocation state to 2 h (Figures 5E, F and Supplementary Figure S3). Next, we investigated whether curcumin-induced HO-1 mediated an anti-neuroinflammatory response in LTA-stimulated BV-2 microglial cells. We treated cells with the HO-1 inhibitor SnPP. We then evaluated curcumin�s effect on LTA-induced NO and TNF-? release. Treatment with SnPP significantly suppressed curcumin-mediated inhibition of NO and TNF-a release (Figures 5G, H). Taken together, these results reveal that curcumin-dependent HO-1 and Nrf-2 signal activation plays a crucial role in downregulating neuroinflammatory responses. Quantification with statistical analysis is provided as supporting data.
Discussion
Microglia, the major resident macrophages of the CNS, has been reported to be the main effector cells in mediating neuroinflammation and selective neuronal death (Perry et al., 2010). Microglial cells increase the production of neuroinflammatory molecules after exposure to activators such as LPS and LTA via their surface receptors, TLR4 and TLR2, respectively (Perry and Holmes, 2014; Hossain et al., 2017). Increased expression and activation of TLR2 is associated with the progression of neurodegenerative diseases, such as PD and dementia (Dzamko et al., 2017). For example, activation of TLR2 could upregulate ?-synuclein in PD brains and play important roles in the pathogenesis of PD brains (Roodveldt et al., 2013). In addition, Kim C. et al. (2013) also showed that neurodegeneration was attenuated by either knockout or knockdown of TLR2 in rodent PD models. Thus, controlling TLR2-mediated microglia activation and neurotoxicity has been suggested as an important therapeutic approach to treating neurodegenerative diseases. A potential agent in this process could be curcumin, which has been shown to exert neuro-protective and anti-inflammatory effects in various experiment models (Parada et al., 2015; Li et al., 2016). Curcumin is a highly lipophilic natural compound. A previous study has well demonstrated that curcumin is able to cross the blood�brain barrier and that it is mainly concentrated in the hippocampus in the brain (Tsai et al., 2011). Some studies reported that curcumin inhibited HIV-1 gp120-induced neuronal damage and provided anti-neuroinflammatory effects in LPS-induced microglia (Gong et al., 2012). This protective effect of curcumin seems to be dependent on its anti-inflammatory actions. Curcumin could protect neurons against microglia-mediated neurotoxicity while becoming inefficient under microglia-depleted conditions (Park et al., 2001; Yang et al., 2008; Parada et al., 2015). Similar studies in peripheral cells also showed the anti-inflammatory effects of curcumin. Using RAW 264.7 murine macrophages, studies have shown that curcumin inhibited PGE2, NO, and TNF-? release following LPS stimulation (Pae et al., 2008). However, the effects of curcumin on TLR2-induced neuroinflammation in microglial cells are not fully understood.
Regulation of the signaling pathways in activated microglia is important in maintaining CNS homeostasis because deregulated neuroinflammatory responses can result in the death of adjacent neurons through the release of inflammatory molecules, such as cytokines, chemokines, NO, and ROS (Perry and Holmes, 2014; Spangenberg and Green, 2017). For example, excessive NO synthesis under endotoxins results in the formation of reactive nitrogen species and neuronal cell death (Perry et al., 2010). PGE2 has also been shown to contribute to neuronal death through activation of the MAPK/ERK pathway in microglia (Xia et al., 2015). In this present study, we showed that curcumin inhibited the secretion of inflammatory mediators TNF-?, NO, and PGE2, and expression of iNOS and COX-2 in BV2 microglia stimulated with LTA. We further showed that curcumin attenuated these effects of LTA without altering cell survival, suggesting that curcumin is safe and could be considered as a potential therapeutic agent in neuroinflammation.
NF-?B is the main transcription factor which plays critical roles in regulating redox homeostasis. NF-?B is considered the master regulator of microglial inflammatory responses to neuronal injury (Acharyya et al., 2007). Recent studies showed that NF-?B activation controlled the expression of inflammatory molecules, such as NO, PGE2, and TNF-?, and IL-1b production (Acharyya et al., 2007). Therefore, modulation of NF-?B activation is considered a critical way to control microglial activation. The activation of the NF-?B signaling pathway is mediated by the I?B protein. The phosphorylation of I?B results in NF-?B dissociation, which leads to the induction of inflammatory mediators. In this study, it was shown that curcumin produced dual inhibition of phosphorylation and degradation of I?B?, as well as nuclear translocation of p65, suggesting that this agent could stabilize NF-?B in the microglial cytoplasm following stimulation with LTA in BV-2 microglial cells.
In mammalian cells, MAPKs signaling pathways, including ERK, JNK, and p38, contribute to the production of a wide variety of neuroinflammatory mediators (Chantong et al., 2014). In this present study, pre-treatment with curcumin decreased the phosphorylation of p38 and ERK. Furthermore, the p38 inhibitor SB203580 significantly reduced the secretion of NO and the mRNA expression of the key pro-inflammatory gene, iNOS. These results suggested that curcumin initiated the anti-neuroinflammatory effects in LTA-stimulated BV-2 microglial cells, partially through inhibition of p38 MAPK activation. The PI3K/Akt-dependent signaling pathway promotes inflammatory responses in microglia. The involvement of the Akt pathway has been shown in the expression of inflammatory mediators in microglia through the activation of NF-?B in microglia (Lo et al., 2015). Curcumin suppressed the phosphorylated Akt, the downstream target of PI3K. However, the PI3K inhibitor wortmannin did not show any inhibitory effect on the secretion of NO or the mRNA expression of iNOS. Taken together, these data suggest that the anti-neuroinflammatory effect of curcumin occurs mainly through inhibiting the NF-?B and MAPKs signaling.
We also identified the intracellular pathway that negatively regulates the inflammatory-molecule expression in microglial cells. Nrf2 is a redox-sensitive transcription factor that regulates microglial inflammatory responses to brain infections. The effect of Nrf2 has been described in different in vivo models where knockdown of Nrf2 in mice enhanced vulnerability to asthma or emphysema (Ma, 2013). Moreover, the TLR2/TLR4 agonist promoted inflammatory responses in Nrf2 KO mice compared to WT mice (Kong et al., 2011). In the current study, we showed that curcumin increased the expression of Nrf2 and its downstream protein HO-1. HO-1 is a key signaling molecule implicated in the regulation of inflammatory and oxidative responses. The HO-1 gene has an ARE sequence in its promoter region, which is a binding site for the transcription factor Nrf2. Several studies have proposed that NF-?B interrupts the Nrf-2-ARE signaling pathway because many compounds that induced HO-1 and Nrf2 signaling incidentally repressed NF-?B activation (Li et al., 2016). HO-1 expression was essential for the microglial specific cytoprotective effect (Parada et al., 2015). Several studies have also shown an inverse correlation between HO-1 and inflammatory mediator secretion (Chora et al., 2007; Parada et al., 2015). In agreement, we observed that curcumin alone induced the expression of HO-1 in microglial cells. Furthermore, the HO-1 inhibitor abrogated curcumin anti-inflammatory effect in BV-2 microglial cells.
Conclusion
This study demonstrated that curcumin had anti-inflammatory activity in LTA-stimulated microglial cells that may through inhibiting NF-?B and p38 MAPK activation, and may induce the expression of Nrf2 and HO-1 (Figure ?6). Furthermore, curcumin does not have cytotoxic effects in BV-2 microglial cells at its anti-inflammatory dose. Curcumin may have therapeutic potential for some neuroinflammation-associated disorders caused by Gram-positive bacteria.
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Curcumin, or turmeric, is a powerful anti-inflammatory which has been demonstrated to have many health benefits. Regarded as an antioxidant with anti-cancer, antidepressant, and anti-aging properties, curcumin can do much more than heal wounds and enhance memory. According to research studies, curcumin or turmeric can help reduce neuroinflammation or brain inflammation. This powerful anti-inflammatory can block the production of proinflammatory cytokines and promote overall well-being. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
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The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue.
In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal.
How often do you feel agitated, easily upset, and nervous between meals? How often do you depend on coffee to keep yourself going?How often do you have difficulty concentrating before eating? Inflammation is an important response of the human body. It’s activated by the immune system to guard us against injury, infection, and/or illness. However, what happens if there is too much inflammation in the human body? And, what happens if there is too much inflammation in the brain?�
Brain inflammation can cause a variety of health issues, such as anxiety, stress, depression, brain fog, fatigue, and even lethargy, among other common symptoms. Fortunately, there is one natural remedy that can help greatly reduce neuroinflammation and improve brain function. According to research studies, curcumin can combat brain inflammation. The purpose of the article above was to discuss the anti-inflammatory effects of curcumin in microglia and brain well-being
The following article has been referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
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.
How high is your stress level? How often do you feel overwhelmed? Anxiety is a well-known health issue that is, unfortunately, often misunderstood, especially when it manifests other misunderstood symptoms like brain fog. � Brain fog is commonly associated with reduced thinking and processing while anxiety is frequently associated with racing thoughts that can make people overly cautious as well as worries that can keep people awake, wired, and restless. How does anxiety cause brain fog? The purpose of the following article is to understand brain fog associated with anxiety. �
How Does Brain Fog with Anxiety Happen?
Brain fog is a symptom rather than a single health issue. It�s described as the sensation that your brain isn’t functioning properly. Anxiety involves symptoms of overthinking, excessive worrying, imagining negative outcomes, and fear. � Brain fog and anxiety happens because the symptoms of one health issue can ultimately cause the symptoms of the other health issue and vice versa. This can also worsen both conditions. Brain fog and anxiety can cause an infinite loop. �
Anxiety involves �what-ifs,� ruminations, and negative thinking
This can then lead to mental exhaustion or fatigue
Fatigue can also develop brain fog
Brain fog can in turn increase anxiety because it feels frightening, worrisome
Increased anxiety causes this cycle to repeat, seemingly endlessly
Brain fog associated with anxiety may vary from person to person. Several people will experience it often while others will experience it less frequently. It can also come and go quickly, or it can ultimately last for days, weeks, and even months. � Evaluating the symptoms and the causes of brain fog and anxiety will provide insights that can be used for treatment. �
Symptoms of Brain Fog with Anxiety
Brain fog and anxiety share a common symptom, frequently referred to as fatigue or tiredness. Brain fog, anxiety, and fatigue are well-known symptoms that are often connected. However, fatigue is believed to be at the heart of brain fog and anxiety. � Anxiety appears to take control of our entire brain and aggravates thoughts, emotions, and behaviors. Living in a state of constant anxiety is exhausting. Moreover, anxiety can cause sleeping problems. Fatigue can lead directly to brain fog. � Common symptoms of brain fog, anxiety, and fatigue can ultimately include: �
Difficulty concentrating and focusing
Muddled, unclear thoughts
Short-term memory problems
Difficulty reasoning logically
Trouble processing, storing, and retrieving information
Living in a fog that makes grasping comments, instructions, and conversations challenging
The vague sense that you just feel �off� but can�t do anything about it
Causes of Brain Fog with Anxiety
The brain fog that occurs with anxiety can have several causes, including: �
The�symptoms of anxiety, as previously discussed above
The brain�s mental, physical, and emotional response to anxiety
Stress as well as stress hormones and other substances or chemicals.
Understanding the cause of brain fog with anxiety can increase awareness of why these health issues can develop. � The brain�s own reaction to anxiety can also make it feel tired and foggy. The fight-or-flight response is an automatic fear response. The brain reacts in response to an extreme stressor to prepare to either stay and fight or run away to safety. �
Activity in the cortex, the area of rational thinking, decreases, which leads to the inability to think properly
Activity in the hippocampus, the area responsible for learning and memory, is suppressed, causing confusion
Activity in the amygdala accelerates to keep you hypervigilant and ready to leap before you look
The brain also controls the production of hormones in reaction to stress and anxiety. Cortisol, adrenaline, and norepinephrine travel through the brain and the body to keep you alert and ready for action but when these hormones are triggered for too long or in quantities that are too high, they overwhelm and exhaust the brain, causing brain fog. �
Treatment for Brain Fog and Anxiety
The best treatment for brain fog associated with anxiety is to treat it at its source. It’s essential to understand the symptoms of both brain fog and anxiety as well as take steps to reduce other symptoms like fatigue. Furthermore, know what is causing your symptoms so you can ultimately make positive changes to reduce them or even eliminate them, including: �
Develop stress management strategies
Take measures to increase the amount and quality of sleep
Address your anxiety, either with a therapist or other qualified healthcare professional
Listen to your body and brain; participate and engage in exercise, yoga, mindfulness, and meditation
� Brain fog and anxiety can be difficult. But by actively working on them, you can reduce both and promote overall well-being. �
Anxiety can commonly cause a variety of symptoms, including brain fog. Although it may seem like brain fog and anxiety are two separate as well as different health issues, they are frequently connected. Both anxiety and brain fog can cause concentration, focus, and memory problems, and stress is considered to be one of the most well-known causes of brain fog associated with anxiety. Treatment for anxiety and brain fog often involves treating the underlying source of the health issues. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal. �
How high is your stress level? How often do you feel overwhelmed? Anxiety is a well-known health issue that is, unfortunately, often misunderstood, especially when it manifests other misunderstood symptoms like brain fog. � Brain fog is commonly associated with reduced thinking and processing while anxiety is frequently associated with racing thoughts that can make people overly cautious as well as worries that can keep people awake, wired, and restless. How does anxiety cause brain fog? The purpose of the following article is to understand brain fog associated with anxiety. �
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
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.
How often do you feel you have something that must be done? How often do you have difficulty concentrating before eating? Do you suffer from headaches and/or migraines? Head pain is commonly characterized by a variety of symptoms, including pain and discomfort, photophobia or light sensitivity, dizziness, lethargy, and mood changes. However, one of the most common symptoms of head pain is brain fog, which also causes its own variety of symptoms. In the following article, we will discuss brain fog associated with head pain and pressure as well as the common cause of brain fog and headache/migraine. �
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Many patients will commonly visit healthcare professionals reporting mild or moderate head pain and pressure as well as a variety of other symptoms, such as brain fog, fatigue, and even vision problems, among others.� The patients frequently experience a “constant cloud” over their brain and they generally never have a clear head or mental clarity. Many patients will commonly report numerous other symptoms, including poor short-term memory, detachment from reality, sharp pain and discomfort in the head, and ringing in the ears. Many others report anxiety, caused or worsened by the symptoms. �
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Brain Fog and Head Pain
The first approach towards characterizing brain fog associated with head pain is to make sure it’s not caused by a secondary headache or a headache with an identifiable cause. Several types of head pain are more severe than others, such as giant cell arteritis or inflammation of the arteries that run along the temples, raised blood pressure or hypertension,�brain hemorrhage, brain infections like encephalitis, increased pressure in the fluid of the brain or raised intracranial pressure, and brain tumors. Less severe types of head pain include�carbon monoxide poisoning, taking too many painkillers or medication-overuse headache, disorders of the joints of the jaw or temporomandibular joint disorders, dental problems, and sinus infections or sinusitis. Below, we will discuss several of the most common causes of brain fog associated with head pain.
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Causes of Brain Fog and Head Pain
Researchers and healthcare professionals have offered their own hypotheses for why brain fog occurs with head pain, based on their own knowledge and experiences. They believe that brain fog and head pain occur due to epilepsy, overactive parathyroid glands or hyperparathyroidism, overactive thyroid gland or thyrotoxicosis, and brain circulation problems. Researchers and healthcare professionals also suggest it could be due to a vitamin B12 deficiency. Fortunately, the utilization of CT and MRI brain scans, heart tracing, EEG and blood tests, can be utilized to rule out many of these health issues.
Moreover, several health issues require specific tests and evaluations. These include tests for lupus or an inflammatory disorder, magnesium deficiency, zinc deficiency,�Lyme disease or an infection resulting from a tick bite, and postural tachycardia syndrome or an increase in heart rate on standing. Many researchers and healthcare professionals also recommend a detailed examination and investigation of a misalignment or subluxation of the neck or cervical spine. �
If all these tests and evaluations return as normal, then the next approach towards characterizing brain fog associated with head pain is to make sure it’s not caused by a primary headache or a headache without an underlying secondary cause. Primary headaches are diagnosed in 9 out of 10 cases of head pain and pressure. The most common types of primary headaches include tension-type headache,�migraine, and daily persistent headache. Diagnosis depends on the pattern of symptoms as well as examinations and investigations to rule out underlying causes. Although there are specific treatment options for several primary headaches like migraines, in many instances, treatment is frequently a matter of trial and error. �
Furthermore, despite the best efforts of researchers and healthcare professionals as well as comprehensive examinations and investigations, many people who suffer from brain fog associated with head pain and pressure are still left without any explanation for their symptoms. Researchers and healthcare professionals have a name even for this type of brain fog-related head pain known as medically unexplained symptoms or MUS. This ultimately means exactly what reads as: no one is denying that the person has the symptoms, but doctors have been unable to find a medical condition to explain them. �
Several people with MUS undoubtedly do have stress, anxiety, and even depression whether as a result of the symptoms or as a cause of the symptoms. Researchers and healthcare professionals recommend continuing to pursue psychological support if you have brain fog and head pain, as this may help to relieve a potential cause as well as helping to cope with the symptoms. Cognitive-behavioral therapy�would be ideal for this purpose, as would�mindful awareness, a technique that would arm people with a way of deflecting their mind away from their troubling symptoms, improving overall well-being. �
Brain fog can make people feel as if they’re not able to focus or concentrate accordingly and it’s commonly accompanied by head pain, fatigue and even vision problems. While brain fog is a symptom rather than a single health issue, it can be a cause or be caused by other underlying health issues. Head pain and pressure can have a variety of symptoms on its own but head pain-related brain fog has a whole different variety of symptoms. Understanding brain fog associated with head pain and pressure as well as what you can do about the symptoms can help manage brain fog symptoms and promote overall brain health and wellness. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal. �
How often do you feel you have something that must be done? How often do you have difficulty concentrating before eating? Do you suffer from headaches and/or migraines? Head pain is commonly characterized by a variety of symptoms, including pain and discomfort, photophobia or light sensitivity, dizziness, lethargy, and mood changes. However, one of the most common symptoms of head pain is brain fog, which also causes its own variety of symptoms. In the following article, we will discuss brain fog associated with head pain and pressure as well as the common cause of brain fog and headache/migraine. �
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
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.
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