Pilates or yoga can work wonders and always stretch before physical exercise.
Get fit – no regular physical activity can lead to serious conditions and possibly chronic pain.
Exercise benefits all, even some light walking around the neighborhood is enough. Just get moving!
Playing a sport could be a way to keep active. Remember, in order for any exercise to work is that it is done regularly.
Strength training is important, just as its name implies strength training builds muscle and reduces muscle imbalances.
It�s never too late to increase strength and flexibility.
Look at activities that you and your friends/family can enjoy and make doing them a regular thing.
A�chiropractor�is the ideal�medical professional to consult with for any unexplained pain in the musculoskeletal system. They are highly qualified professionals that their specialty is treating conditions like lower back pain and they are very affordable. If you or a loved one have pain in the lower back, give us a call. We�re here to help!
Understand *FOOT PRONATION* & How to Correct it with Orthotics | El Paso, TX (2019)
Foot pronation is the natural movement that occurs during foot landing while walking or running. Foot pronation also occurs while standing, and in this instance, it is the amount in which the foot rolls inward toward the arch. Foot pronation is normal, however, excessive foot pronation can cause a variety of health issues, including bad posture. The following video describes the 5 red flags of excessive foot pronation, which can ultimately affect a person’s overall health and wellness. Dr. Alex Jimenez can help diagnose and treat excessive foot pronation. Patients recommend Dr. Alex Jimenez and his staff as the non-surgical choice for excessive foot pronation health issues.
When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. �
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease associated with the degeneration of motor neurons which ultimately determine the length of the health issue. ALS is considered fatal several years after it begins. It is hypothesized that L-glutamate excitotoxicity plays a role in the motor neuron death in ALS because cells demonstrate increased levels of calcium-permeable AMPA receptors and low levels of calcium-binding proteins. Compared to the utilization of AMPA and kainate, and L-HCA, in the spinal cord of rats, treatment with NMDA spared motor neurons suggests that NMDA excitotoxicity may actually not play a fundamental role in ALS. However, NMDA receptor-mediated excitotoxicity in motor neurons was demonstrated in chick embryo organotypic slice cultures. Electrophysiological research studies suggested that transient hyperexcitability of motor nerves in the presymptomatic phase of ALS in mice transgenic for the G93A mutation of human SOD1 is associated with hereditary ALS. Additionally, cortical hyperexcitability was recorded in familial and sporadic ALS patients with the onset of symptoms in familial ALS mutation carriers. Moreover, the only approved drug and/or medication utilized for ALS, which increases survival by 2 to 3 months, acts as an inhibitor of both NMDA and kainate receptors together with quickly upregulating EAAT activity in synaptosomes, according to several research studies. �
In autopsied spinal cords from patients with ALS, several groups demonstrated a decrease in EAAT2 and not in EAAT1 protein expression in the gray matter of regions with considerable motor neuron loss. In addition, both L-glutamate uptake and EAAT2 immunoreactivity, as demonstrated by Western blotting, were demonstrated to be quantitatively decreased in postmortem tissue of ALS patients, particularly in the spinal cord, the tissue which is most commonly affected by the health issue. Additionally, it has been demonstrated that as a possible effect of EAAT2 downregulation, L-glutamate amounts are increased in the CSF in patients with ALS. However, this outcome measure couldn’t be replicated by other research studies. �
The downregulation of EAAT2 in human ALS is demonstrated in several animal models of ALS, including transgenic mice expressing human SOD1 containing the G93A mutation which causes hereditary ALS or transgenic rats expressing the same mutation. Surprisingly, “whereas Bendotti demonstrated a late decrease in EAAT2 expression at the time when the mice had already become symptomatic,” research studies demonstrated fluctuations in EAAT2 expression at the presymptomatic stage. The ?-lactam antibiotic ceftriaxone (Cef) promotes the production of EAAT2 in cultured murine spinal cord slices and in neuron/astrocyte co-cultures. In addition, it caused EAAT2 expression from the spinal cords of wild-type and mutant G93A mSOD1 Tg mice, which has been associated with a decrease in motor neuron loss, weight reduction, and other ALS-like symptoms as well as an increase in survival, compatible with the hypothesis that EAAT2 loss contributes to chronic excitotoxicity in this mouse model. Just recently, a significant decrease in EAAT2 immunoreactivity had been demonstrated in a separate bark model for ALS, rats expressing ALS-inducing mutant TAR DNA binding protein 43 in astrocytes only. Surprisingly, the research studies demonstrated that when measured by microdialysis, the extracellular L-glutamate and L-aspartate concentrations increase while the L-glutamate clearance capability decrease in the cerebral cortex of G93A mSOD1 Tg mice, however, this region doesn’t show overt pathology nor downregulation of EAAT1 when evaluated. �
Taken together these research studies support the view that there is a downregulation of EAAT2 in both human ALS patients and animal models of ALS. However, while some animal research studies suggest that EAAT2 downregulation occurs before motor neuron loss, others are compatible with the hypothesis that the downregulation of EAAT2, the astroglial expression of which is associated with the existence of neurons, is a consequence of neurodegeneration in neurological diseases. �
Furthermore, EAATs decrease extracellular L-glutamate, extracellular cerebral L-glutamate is upregulated in a variety of brain regions from the cystine/glutamate antiporter system x?c. XCT, one particular subunit of program x?c, was demonstrated to be differentially regulated and maintained in mouse models of ALS. Research studies demonstrated that the uptake of radiolabelled cystine was upregulated in spinal cord slices of presymptomatic G93A mSOD1 Tg mice at the age of 70 days but not in 55 or 100 days and not in symptomatic 130 day-old mice which also determined that the upregulation of cystine uptake at day 70 was because of system x?c activity utilizing the system x?c inhibitor sulfasalazine (SSZ). It needs to be considered, however, that cystine can also be hauled by EAATs. Therefore, as evidence about the SSZ-sensitivity of cystine uptakes were not demonstrated for days 100 and 130, the differential cystine uptake demonstrated in this research study at the older ages could rather be a result of decreased EAAT action. By comparison, research studies with rtPCR demonstrated a strong growth in xCT mRNA levels in G37R mSOD1 Tg mice on the beginning of symptoms, which has been further increased as symptoms improved. Moreover, it was demonstrated that xCT was primarily demonstrated in spinal cord microglial cells. Microglia revealed xCT mRNA upregulation in the presymptomatic stage. Taken together, these outcome measures suggest the system x?c is upregulated in animal models of ALS. However, the evidence is lacking about whether this is true for human cases of ALS. Nevertheless, further research studies revealed that the mRNA levels of CD68, a marker of microglial activation, were associated with xCT mRNA expression in postmortem spinal cord tissue of individuals with ALS, demonstrating that neuroinflammation in humans is also ultimately associated with xCT upregulation. �
Beyond the dysregulation of L-glutamate and L-aspartate levels by EAAT downregulation or system x?c upregulation, pathways that indirectly regulate and maintain glutamatergic neurotransmission also have been suggested to participate in motor neuron degeneration in ALS. D-Serine levels have been shown to become considerably increased from the spinal cord of G93A mSOD1 Tg mice. Starting at disease onset and ongoing during the course of this symptomatic phase, D-serine increases NMDA excitotoxicity in motor neurons. The upregulation of D-serine at the spinal cord was duplicated by other research studies. Downregulation of this D-serine metabolizing enzyme DAO in the reticulospinal tract has been demonstrated as the main mechanism for D-serine upregulation in the spinal cord in ALS mice. In addition, genetic inactivation of DAO in mice has been associated with motor neuron degeneration and a deficiency in the D-serine generating enzyme serine racemase prolonged survival in G93A mSOD1 Tg mice although it hastened neurodegenerative disease onset. A heterozygous mutation of DAO has been demonstrated to be separate from the ALS phenotype in a large family with hereditary ALS. However, this continues to be the only family determined where a DAO mutation is associated with ALS. �
Concerning the other amino acid co-agonist of the NMDA receptor, glycine, an increase in the CSF levels in patients with ALS was demonstrated by one group, however, it couldn’t be replicated by other research studies. Several research studies also determined that KYNA levels are upregulated in the CSF of bulbar ALS patients as well as those in end-stage ALS. Independently, it was revealed that tryptophan and KYN levels are increased in the CSF from ALS patients as compared to controls. Additionally, IDO was proven to be expressed in neurons and spinal cord microglia from patients with ALS, indicating that microglial activation may increase the conversion of tryptophan in ALS into KYN, among others. �
Multilayered evidence suggests that increased glutamatergic neurotransmission is within ALS and may ultimately cause neurodegeneration in neurodegenerative diseases, as shown in Figure 3. Downregulation of EAAT2 in astrocytes and upregulation of program x?forecast in the context of microglial activation was repeatedly documented. NMDA receptors by D-serine may also play a role in dysregulation. Moreover, the kynurenine pathway seems to be triggered in ALS. �
�
In many research studies, evidence and outcome measures have demonstrated that chronic excitotoxicity may be associated with a variety of neurodegenerative diseases, including AD, HD, and ALS, ultimately causing neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to outline what may cause excitotoxicity in neurodegenerative diseases. We will discuss these in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD). – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
In the article above, we outlined what is known about the pathways which may cause excitotoxicity in neurodegenerative diseases. We also discussed that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
Sacroiliac joint dysfunction is known to cause low back pain, but diagnosing can be hard for some doctors. Especially those that do not have a great deal of experience in sacroiliac joint pain. However, chiropractors specialize in this area as the SI joint is an important part of the musculoskeletal system.
SI joint dysfunction and pain can involve�one or both joints.
�
Other terms associated with SI joint dysfunction are sacroiliitis or degenerative sacroiliitis.
Low back pain may be SI joint-related, so how to start the conversation with your doctor?
Things to Remember Before Appointment
Diagnosing sacroiliac joint-related pain begins before your first appointment with a doctor or chiropractor.
Three things to do before your appointment can help make the visit highly productive.
I. Know your medical history
If you have an existing spinal condition, it can definitely affect SI joint dysfunction
Any recent trauma, like an auto accident or fall?
Pregnant?
Think about these before, because they can help a doctor identify links or cause of Sacroiliac joint dysfunction.
II. Know the symptoms
Make it a point to know the symptoms so you can explain them in full detail.
Dull pain
Achy
Stiff
If you need to, write them down.
Common symptoms:
Low back pain
Pain that travels through:
Hips
Buttocks
Thighs
Groin
Pain when pressing on the Sacroiliac joints�
Stiffness or electrical burning sensations in the pelvis
Know when the symptoms get worse and when they go away. For example:
The pain usually increases when:
Standing
Walking for extended periods
Climbing stairs
Getting/rising up from a seated position
And the pain usually goes away when lying down.
III. Write down questions for your doctor.
Think about what you want your doctor to understand and the pain you are going through.
Write down questions and take them with you.
This questions could be like:
Is this pain caused by a sacroiliac joint problem?
Why rule out sacroiliac joint dysfunction?
How long does it take for the treatment/s to take effect?� �
Is the treatment plan for long sustained relief or short-term relief?
The Appointment
Ask your doctor to examine you for sacroiliac joint dysfunction.
Low back pain research shows the sacroiliac joint, is a definite cause of low back pain.
This problem affects� 30-34% of patients with low back pain.
A doctor can diagnose sacroiliac joint dysfunction based on medical history and a physical exam.
The physical exam, which can include performing specific maneuvers/movements to re-create the pain in a controlled manner, to help confirm a diagnosis.
Physical tests can initiate sacroiliac joint pain and help diagnose low back pain that is being caused by sacroiliac joint dysfunction.
Fortin finger test, which means pressing down near the sacroiliac joints
If three out of five tests produce pain, then more than likely you have sacroiliac joint dysfunction.
Dialogue with your doctor/chiropractor
It�s normal to feel overwhelmed during a doctor’s visit, especially if you have a�condition that is hard-to-diagnose.
Talk with your doctor, their voice should not be the only one heard, this is your body and your health that’s at stake.
Your information is essential to help with an accurate diagnosis.
If your doctor doesn’t feel comfortable or feels they don’t have enough experience in diagnosing sacroiliac joint pain, then ask for a referral to a spine specialist/chiropractor that is comfortable and does have the experience in diagnosing sacroiliac joint pain.
There are a number of treatments for sacroiliac joint dysfunction, including pain medication, epidural steroid injection, and surgery. However, chiropractic care is non-invasive and does not have the unpleasant, sometimes harmful side effects of pain meds. It is safe and effective and treats the entire body instead of just the part that hurts.
Low Back Pain Treatment | El Paso, Tx
Low back pain which gradually influenced his quality of life was developed. David Garcia was unable to walk as his symptoms worsened and his back pain became excruciating. He first visited Dr. Alex Jimenez, a chiropractor in El Paso, TX, following a recommendation from his sister. Dr. Jimenez managed to supply David Garcia with all the aid he deserved for his low back pain, restoring his well-being. David Garcia clarifies the wonderful service Dr. Alex Jimenez and his team have given him to offer him relief from his painful symptoms and he highly recommends chiropractic care as the non-surgical pick for low back pain, among other health problems.
NCBI Resources
Patients who experience lower back pain never want to deal with it again, but�it can flare up periodically. According to the�National Institute of Neurological Disorders and Stroke, roughly 20% of those who suffer from low back pain will eventually deal with it chronically. This can cause frustration, primarily when it affects mobility.
Before you run screaming in horror to the medicine cabinet, one of the best reasons to participate in chiropractic treatment is that it helps reduce the chance of a recurrence. By working on the total body and getting it in the best shape possible, the patient is stronger and more balanced to handle their workload and other strenuous activities. Chiropractors also impart advice on how to minimize the chances of re-aggravating the lower back.
Excitotoxicity is characterized as an acute insult which causes nerve cell death due to the excessive activation of iGluRs. Acute excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue. �
With brain ischemia, L-glutamate-associated and L-aspartate-associated excitotoxicity happen within minutes due to the growth in extracellular cerebral L-glutamate as well as L-aspartate. Because these are also energy-dependent, the abrupt loss of energy due to the shut down of blood flow can ultimately breakdown the neuronal and astroglial membrane. In neurons, membrane depolarization contributes to vesicular discharge. Additionally, energy degradation may even cause a change in their action, therefore, causing L-glutamate and L-aspartate to activate and affect ionic homeostasis which can interrupt EAAT action. The activation of L-glutamate/L-aspartate contributes to excitotoxicity through the over-activation of iGluRs of the NMDA type as demonstrated by the efficiency of NMDA antagonists in animal models of transient cerebral ischemia. �
In TBI, the mechanical tissue damage and the disruption of the blood-brain barrier can trigger acute secondary neurodegeneration, which, together with neuroinflammation and oxidative stress, is associated with L-glutamate activation from intracellular compartments and, therefore, by acute excitotoxicity. Moveover, acute application of the NMDA antagonist MK801 following TBI ameliorates neuronal loss and long-term behavioral abnormalities, among others. �
In status epilepticus, continuing the synchronized activity of excitatory neuronal networks as well as the continuous breakdown of restricting mechanisms is the main source of L-glutamate and L-aspartate activation. As the severity of synchronous activity depends upon the involvement of nerve cells into a neuronal system as well as the capability of a neural cell to withstand excess glutamate mainly depends on the expression pattern of iGluRs, a somewhat restricted and maturation-associated degeneration of neuronal populations which is ultimately caused by prolonged epileptic seizures. The significance of excitotoxicity in status epilepticus is shown as NMDA antagonists, such as ketamine, decrease adrenal loss. �
Excitotoxicity in Neurological Diseases
Because EAATs were discovered to be down-regulated in a variety of central nervous system (CNS) health issues and L-glutamate, as well as L-aspartate, clearance can ultimately affect the excitotoxicity of neurological diseases, many healthcare professionals have decided to determine substances which cause EAAT2, or the main EAAT in the brain and most commonly shown to be downregulated. This has demonstrated substances which shows astrocytic EAAT2 expression both in vitro and in vivo research studies. Several of these have also demonstrated protective properties in animal models of neurological diseases. Cef is one of the most evaluated compounds and it has been analyzed in AD, HD, and ALS models with positive outcomes. However, none of the substances has been extensively researched for its capability to interact with other neuroprotective pathways. Cef has also been demonstrated to promote EAAT2 expression but also to trigger the transcription factor Nrf2, which results in the transcription of a wide array of genes involved in cytoprotection and antioxidant protection. Because oxidative stress is believed to play an essential role in many, if not all, neurological diseases, this pathway may account for the neuroprotection caused by Cef. Furthermore, xCT, which can be one of the downstream targets of Nrf2, has been demonstrated to be upregulated by Cef in vitro and in vivo. Another in vitro EAAT2-promoting substance, MS-153, efficiently protected against secondary neurodegeneration after traumatic brain injury as well as through mechanisms other than EAAT2 upregulation. Evidence of concept experiments which demonstrate the increased stimulation through iGluRs in neurodegenerative diseases needs manipulations of their neurotransmitter physiology. �
Glud1 Tg mice demonstrate a model of excitotoxicity associated with enhanced synaptic L-glutamate activation with restricted neuronal loss. However, this animal model of glutamatergic neurotransmission has not yet been utilized to analyze if Glud1 over-expression aggravates the phenotype of mouse models in neurological diseases. Another version involves the EAAT2-deficient mouse. Homozygous EAAT2 knock-out mice have health issues associated with premature death because of epilepsy as well as hippocampal and focal cortical atrophy. Heterozygous EAAT2 knock-out mice, however, develop normally and show only mild behavioral abnormalities. This mouse model of moderate glutamate hyperfunction has been utilized in a collection of evidence of principle research studies which demonstrated the fundamental role of glutamate. ALS mice, which have both the G93A mSOD1 mutation and a decreased quantity of EAAT2 (SOD1(G93A)/EAAT2�), revealed an increase in the speed of motor decline accompanied by earlier motor neuron loss when compared with single mutant G93A mSOD1 Tg mice. A decrease in survival was also demonstrated in these mutant mice. When crossed with transgenic mice expressing mutations of the human amyloid-? protein precursor and presenilin-1 (A?PPswe/PS1?E9), partial loss of EAAT2 unmasked spatial memory deficits in 6-month-old mice expressing A?PPswe/PS1?E9. These mice demonstrated an increase in the ratio of detergent-insoluble A?42/A?40 demonstrating that shortages in glutamate transporter function ultimately cause premature pathogenic processes associated with AD. By comparison, the phenotype of the R6/2 HD mouse model wasn’t changed in mice which had only one EAAT2 allele. Further research studies are still necessary for further evidence. �
As a complement to these research studies, transgenic mice which over-express EAAT2 in astrocytes through the GFAP promoter has also been developed. EAAT2/G93A mSOD1 double Tg mice demonstrated moderate amelioration of their ALS-like phenotype with a statistically significant (14 times ) delay in grip power decrease and loss of motor neurons as well as a decrease in other occasions, such as caspase-3 activation and SOD1, although not at the beginning of paralysis, weight loss or an extended life span when compared with monotransgenic G93A mSOD1 littermates. Exactly the same EAAT2 transgenic mouse model was utilized to evaluate the effect of improved astrocytic L-glutamate and L-aspartate uptake by cross-breeding with an animal model of AD, A?PPswe/Ind mice. Increased EAAT2 protein levels considerably increased and improved overall cognitive functioning, restored synaptic ethics, and decreased amyloid plaques in those AD mice. �
In mice in which genetically engineered regulation and management of xCT causes a lack in the glutamate/cystine antiporter system x?c, the obvious decrease of extrasynaptic L-glutamate is associated with the tremendous resistance of dopaminergic neurons against 6-hydroxydopamine-induced neurodegeneration, perhaps as a consequence of reduced excitotoxicity. However, microglial activation has also been demonstrated to be modulated by system x?c deficiencies leading to a more neuroprotective phenotype which offers an explanation for the protective effect of xCT deletion in this circumstance. �
Therefore, genetic variations encourage the role of chronic excitotoxicity in neurodegenerative diseases, particularly AD and ALS. These models all represent life-long changes in glutamatergic neurotransmission. These models can’t determine if the utilization of drugs and/or medications can directly affect glutamate levels throughout the neurodegenerative process and/or be protective. Both evaluation and analysis of EAAT2-inducing medicine for the progression of inducible mouse models and their interaction with other signaling pathways is still warranted by researchers and healthcare professionals. �
In many research studies, evidence and outcome measures have demonstrated that glutamate dysregulation and excitotoxicity in many neurological diseases, including AD, HD, and ALS, ultimately lead to neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to discuss and demonstrate the role that glutamate dysregulation and excitotoxicity plays on neurodegenerative diseases. The mechanisms for excitotoxicity are different for every health issue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Metabolic Assessment Form
The following Metabolic Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptom groups listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
Excitotoxicity is characterized as an acute insult which causes cell death due to the excess activation of iGluRs. Excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
Autoimmune disease is the disease of the modern era. It is a condition where the body�s immune system mistakenly attacks the body. Since the body�s immune system usually guards against bacteria and viruses, it can sense the foreign cells and send out fighter cells to attack them. When it�s an autoimmune disease, however, the immune system starts to make mistakes to certain parts of the body. It starts attacking the joints, the skin, or the musculoskeletal system as foreign cells and attacking them. The immune system releases autoantibody proteins to attack the healthy cells, thus causing autoimmune disease in the body.
What Triggers the Activation of the Autoimmune Mechanism?
Surprisingly, the body�s antibodies go through a process by cleaning up the old and damaged cells, so that way, new healthy cells can grow and replace the old cells. Although if the body has an excessive number of antibodies in their system, it can cause the individual to have an autoimmune disease. Research has shown that a part of the autoimmune ecology, the influence of environmental exposure can not only develop autoimmune disorder but shape the function of the immune system.
Another study stated that approximately 30% of all autoimmune diseases come from genetic disposition while 70% is due to environmental factors, including toxic chemicals, dietary components, gut dysbiosis, and infections in the body. So some of the ecological factors that are included are adjuvants (immunostimulant effects). These are typically used in vaccines to produce a more effective immunization reaction.
Researchers stated that molecular mimicry is one of the mechanisms, where a foreign antigen shares a sequence or structural similarities with self-antigens. This means that any infections that can initiate and maintain autoimmune responses can lead to specific tissue damage in the body. It is a phenomenon that molecular mimicry and cross-reactivity are identical. Cross-reactivity is significant when it comes to food allergies and is often responsible for many disorders. It affects the scope of the disease, the reliability of diagnostic testing, and has implications for any current and potential therapies.
Common and Rare Autoimmune Diseases
The primary function of the immune system is to repair the body with new cells. Individuals with an autoimmune disease will have many chronic illnesses that are both common and rare when they are being diagnosed. Below is a list of autoimmune diseases that range from common to some of the rarer autoimmune conditions an individual may experience.
Rheumatoid arthritis (RA)
Rheumatoid arthritis is when the immune system is attacking the joints. This attack causes redness, warmth, soreness, and stiffness. It�s one of the most common autoimmune diseases that is found in women but can affect men and elderly people as well. Studies have shown that if a family member has rheumatoid arthritis, it is likely that other family members may have an increased chance of developing this autoimmune disease. The signs and symptoms of rheumatoid arthritis can vary depending on the severity of the inflamed joints, potentially causing them to deform and shift out of place.��
Lupus
Lupus is a systemic autoimmune disease that occurs when an individual�s immune system starts attacking their own tissue and organs. Even though lupus is difficult to diagnose because it often mimics other ailments, it can cause inflammation to different body systems. These body systems include the joints, skin, kidneys, blood cells, brain, heart, and lungs. A distinctive sign of lupus is a facial rash that resembles butterfly wings unfolding across booth cheek.
Ehlers-Danlos Syndrome (EDS)
EDS (Ehlers-Danlos Syndrome) is a rare autoimmune disease that causes soft connective tissues to be fragile in the body. This autoimmune disease is still new for doctors; however, there is always more research to be done about this disease. The symptoms can vary from mild skin and joint hyperlaxity to severe physical disability and life-threatening vascular complications. One of the most common symptoms is joint hypermobility. This disease can cause the joints to be unstable or loose, and it can cause the body�s joints to have frequent dislocations and pain.
Polymyalgia Rheumatica
Polymyalgia rheumatica is an inflammatory musculoskeletal disorder that is most common in elderly adults. This disease causes muscle pain and stiffness around the joints, most commonly occurring in the morning.�It also shares similarities with another disease known as giant cell arteritis. If an individual has polymyalgia rheumatica, they can have the symptoms of giant cell arteritis as well. The symptoms are inflammation in the lining of the arteries. The two factors that can cause the development of polymyalgia rheumatica are genetics and environmental exposure that can increase the chances of having the disorder.
Ankylosing spondylitis
Ankylosing spondylitis is an autoimmune inflammatory disease that can cause some of the vertebrae in the spine to fuse over time. When this happens, the fusing makes the spine less flexible and causes the body to be in a hunched-forward posture. It is most common for men, and there are treatments to lessen the symptoms and possibly slow down the progression of the disease.
Celiac disease
Celiac disease is an autoimmune disease that occurs in about 1% of individuals. This disease makes the individual have an inflammatory reaction to the intestinal permeability barrier from eating gluten found in wheat, rye, and barley. Studies show that patients with celiac disease and autoimmune disease have to be on a gluten-free diet to heal the gut. Symptoms can include bloating, digestive issues, inflammation, and skin rashes.
Conclusion
Mechanisms of an autoimmune disease can be caused by genetics or induced by environmental factors. This can cause an individual to have problems in their body related to inflammation.�There are many autoimmune diseases�that can affect the body from the most common to some of the rarer kinds and it can have lasting effects.
In honor of Governor Abbott’s declaration, October is Chiropractic Health Month. To learn more about the proposal on our website.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References:
Anaya, Juan-Manuel, et al. �The Autoimmune Ecology.� Frontiers in Immunology, Frontiers Media S.A., 26 Apr. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4844615/.
Bonds, Rana S, et al. �A Structural Basis for Food Allergy: the Role of Cross-Reactivity.� Current Opinion in Allergy and Clinical Immunology, U.S. National Library of Medicine, Feb. 2008, www.ncbi.nlm.nih.gov/pubmed/18188023.
Clinic Staff, Mayo. �Ankylosing Spondylitis.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 7 Mar. 2018, www.mayoclinic.org/diseases-conditions/ankylosing-spondylitis/symptoms-causes/syc-20354808.
Clinic Staff, Mayo. �Lupus.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 25 Oct. 2017, www.mayoclinic.org/diseases-conditions/lupus/symptoms-causes/syc-20365789.
Clinic Staff, Mayo. �Polymyalgia Rheumatica.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 23 June 2018, www.mayoclinic.org/diseases-conditions/polymyalgia-rheumatica/symptoms-causes/syc-20376539.
Cusick, Matthew F, et al. �Molecular Mimicry as a Mechanism of Autoimmune Disease.� Clinical Reviews in Allergy & Immunology, U.S. National Library of Medicine, Feb. 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3266166/.
De Paepe, A, and F Malfait. �The Ehlers-Danlos Syndrome, a Disorder with Many Faces.� Clinical Genetics, U.S. National Library of Medicine, July 2012, www.ncbi.nlm.nih.gov/pubmed/22353005.
Schmidt, Zsuzsa, and Gyula Po�r. �Polymyalgia Rheumatica Update, 2015.� Orvosi Hetilap, U.S. National Library of Medicine, 3 Jan. 2016, www.ncbi.nlm.nih.gov/pubmed/26708681.
Scott, David L, et al. �Rheumatoid Arthritis.� Lancet (London, England), U.S. National Library of Medicine, 25 Sept. 2010, www.ncbi.nlm.nih.gov/pubmed/20870100.
Vojdani, Aristo, et al. �Environmental Triggers and Autoimmunity.� Autoimmune Diseases, Hindawi Publishing Corporation, 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4290643/.
SIBO (small intestinal bacterial overgrowth) is defined as 105 up to 106 organisms of bacteria in the small intestines. It is highly relevant to remember that the abundance of bacteria in the small intestine that has SIBO, are healthy bacteria that live in the gastrointestinal tract. It means that the bacteria in the digestive tract is either missed or dislocated and is in the wrong place in the small intestines. While SIBO still remains a poorly understood disease, it is frequently implicated to be the cause of chronic diarrhea and malabsorption. Individuals who have SIBO can also suffer from many chronic illnesses. This includes unintended weight loss, nutritional deficiencies, and osteoporosis.
SIBO and IBS
Studies have indicated that 84% of individuals that has IBS (irritable bowel syndrome) will have SIBO. SIBO is one of the causes of leaky gut, and leaky gut is one of the triad factors that can lead the body to have an autoimmune disease. Health care professionals that diagnose individuals who have SIBO can link the virus to other health problems that the individual may have. Studies have mentioned that when LPS (lipopolysaccharide) is moving from the large intestines to the small intestines, it can contribute to developing intestinal inflammation. With LPS, it can cause an increase of intestinal tight junction permeability or leaky gut.
So SIBO will release LPS into the gut, causing the leaky gut to the gut system in the body. Another study showed that autoimmune diseases are always a triad of a few different things. To have an autoimmune disease, you have to have the gene to get the disease. Although most people know that if they have a gene, doesn�t mean that they will have an autoimmune disease. Even if they don�t have an autoimmune disease, there�s an environmental trigger that will come on and creates an epigenetic change. This will cause the gene in the human body to be expressed.
So the first two factors of the autoimmune disease, are a genetic factor and an environmental factor, the third and final factor is intestinal permeability. So if the primary two factors that are causing disruption to the intestinal permeability, they will prevent the intestinal permeability to actually heal itself. With all three elements being linked to autoimmune disease and SIBO, it will cause the body to have the leaky gut syndrome and health problems to individuals.
So when doctors are diagnosing the patient that has SIBO, they will do a lactulose breath test. What this test does, is that it will indicate that the patient has IBS bloating, and it is causing them discomfort in their gut. Research stated that the lactulose breath test shows the correlation between the pattern of the bowel movements and the type of excreted gas in the stomach. So for anyone that is positive with IBS and takes the breath test, they will understand the consequences of the factors that are leading to the SIBO disease and causing leaky gut.
How do we get SIBO?
With the understanding of what SIBO is, we can see that SIBO is not the only cause of irritable bowel syndrome, but the big player of the syndrome. So taking a step back, we have to discuss what the MMG (Migrating Motor Complex) is before we go further in explaining the pathogenesis of the SIBO disease. Migrating motor complexes are waves of electrical activity that is sweeping through the intestines in a regular cycle. It often happens when a person is fasting, therefore with MMG, we can look at the acute gastroenteritis in the body.
With acute gastroenteritis, the body has some sort of severe infection like bloating, diarrhea, constipation, or a variety of things that are infectious to the gut; however, they are self-limiting. Healthcare professionals who see patients with these acute infections can see that most of the bacteria can cause gastroenteritis, pile up, and release CTD (cytolethal distending toxin). What CTD does is that it will create a reaction against vinculin; which regulates the ICC (interstitial cells of Cajal) and the ICC then regulates the migrating motor complex.
So when the CTD releases toxins in the gut, it causes a reaction to a molecular mimicry reaction. That reaction causes the body to create antibodies to fight against that toxin but through molecular mimicry. CTD looks exactly like vinculin and cross-reacts with the antibodies, So now those antibodies are attacking vinculin, thus damaging the ICC. Since the MMC clears the intestinal tract, when a person is fasting, and the CTD is damaging the intestines, SIBO is created since the body can not flush out the bacteria.
Studies have shown that there are many ways to get SIBO, it can happen by either food poisoning, abdominal surgery, or low stomach acid. Another thing to mention is that mostly 70% of SIBO is caused by food poisoning. Most people who had to suffer from food poisoning don�t realize that SIBO is already in their gut. So the research states that small bowel motility disorders can be the predispose development of SIBO since the bacteria may not be effectively swept from the bowel into to colon.
Treating SIBO
There are many ways to treat SIBO, healthcare professionals can suggest these treatments to their patients who have SIBO and start restoring their intestinal barrier in the long haul. So here are some of the procedures that can help the body and treat SIBO.
Pharmaceuticals: If a patient has constipation and is taking rifaximin if the symptoms are not clearing up, adding another medication with rifaximin for 14 days may help in battling SIBO. It will take a bit longer, but it will help clear the SIBO out of the gut.
Herbal Treatment: With herbal treatments, there are many ways to help treat SIBO naturally. It can be berberine containing herbs, oil of oregano, neem, garlic, Lactobacillus plantarum, Lauricidin, and Antrantil. These herbal treatments can naturally help to fight against SIBO, and studies show that 46% of patients feel a lot better in a short amount of time.
Conclusion
So SIBO is a bacterial disease that can disrupt the gastrointestinal tract and cause the leaky gut to the body. It will cause inflammation and can be in an individual�s body through three factors like genetics, environmental triggers, and food poisoning. It can be treated through pharmaceuticals and herbal treatments prescribed by doctors.� In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month, learn more about this proposal on our website and read what the proposal is all about. The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References:
Bezine, Elisabeth, et al. �The Cytolethal Distending Toxin Effects on Mammalian Cells: a DNA Damage Perspective.� Cells, MDPI, 11 June 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4092857/.
Brown, Kenneth, et al. �Response of Irritable Bowel Syndrome with Constipation Patients Administered a Combined Quebracho/Conker Tree/M. Balsamea Willd Extract.� World Journal of Gastrointestinal Pharmacology and Therapeutics, Baishideng Publishing Group Inc, 6 Aug. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4986399/.
Chedid, Victor, et al. �Herbal Therapy Is Equivalent to Rifaximin for the Treatment of Small Intestinal Bacterial Overgrowth.� Global Advances in Health and Medicine, Global Advances in Health and Medicine, May 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4030608/.
Dukowicz, Andrew C, et al. �Small Intestinal Bacterial Overgrowth: a Comprehensive Review.� Gastroenterology & Hepatology, Millennium Medical Publishing, Feb. 2007, www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/.
Endo, EH, and Dias Filho. �Antibacterial Activity of Berberine against Methicillin-Resistant Staphylococcus Aureus Planktonic and Biofilm Cells.� Austin Journal of Tropical Medicine & Hygiene, 19 Feb. 2015, austinpublishinggroup.com/tropical-medicine/fulltext/ajtmh-v1-id1005.php.
Fasano, Alessio, and Terez Shea-Donohue. �Mechanisms of Disease: the Role of Intestinal Barrier Function in the Pathogenesis of Gastrointestinal Autoimmune Diseases.� Nature News, Nature Publishing Group, 1 Sept. 2005, www.nature.com/articles/ncpgasthep0259.
Ghonmode, Wasudeo Namdeo, et al. �Comparison of the Antibacterial Efficiency of Neem Leaf Extracts, Grape Seed Extracts and 3% Sodium Hypochlorite against E. Feacalis – An in Vitro Study.� Journal of International Oral Health: JIOH, International Society of Preventive and Community Dentistry, Dec. 2013, www.ncbi.nlm.nih.gov/pubmed/24453446.
Guo, Shuhong, et al. �Lipopolysaccharide Regulation of Intestinal Tight Junction Permeability Is Mediated by TLR4 Signal Transduction Pathway Activation of FAK and MyD88.� Journal of Immunology (Baltimore, Md. : 1950), U.S. National Library of Medicine, 15 Nov. 2015, www.ncbi.nlm.nih.gov/pubmed/26466961.
Lin, Henry C. �Small Intestinal Bacterial Overgrowth: a Framework for Understanding Irritable Bowel Syndrome.� JAMA, U.S. National Library of Medicine, 18 Aug. 2004, www.ncbi.nlm.nih.gov/pubmed/15316000.
Preuss, Harry G, et al. �Minimum Inhibitory Concentrations of Herbal Essential Oils and Monolaurin for Gram-Positive and Gram-Negative Bacteria.� Molecular and Cellular Biochemistry, U.S. National Library of Medicine, Apr. 2005, www.ncbi.nlm.nih.gov/pubmed/16010969.
Sienkiewicz, Monika, et al. �The Antibacterial Activity of Oregano Essential Oil (Origanum Heracleoticum L.) against Clinical Strains of Escherichia Coli and Pseudomonas Aeruginosa.� Medycyna Doswiadczalna i Mikrobiologia, U.S. National Library of Medicine, 2012, www.ncbi.nlm.nih.gov/pubmed/23484421.
Soifer, Luis Oscar, et al. �Comparative Clinical Efficacy of a Probiotic vs. an Antibiotic in the Treatment of Patients with Intestinal Bacterial Overgrowth and Chronic Abdominal Functional Distension: a Pilot Study.� Acta Gastroenterologica Latinoamericana, U.S. National Library of Medicine, Dec. 2010, www.ncbi.nlm.nih.gov/pubmed/21381407/.
The Nrf2 cell defense creates a pathway that provides protection against oxidative stress and disorders. It plays a vital role in maintaining cellular homeostasis and keeping each cell strand in check. Without the Nrf2 cell defense, oxidative stress can be excessive and directly cause or contribute to many common diseases. This includes cancer, osteoporosis, inflammatory bowel diseases, and neurodegeneration. Studies show that even oxidative stress can contribute to insulin resistance and multiple sclerosis.
Certain foods that are beneficial to the Nrf2 cell structure, due to their antioxidative properties; can enhance the Nrf2 cell gene gradually. Researchers studied that dietary sources that contain antioxidants flavonoids, fermented food and drinks that contain lactobacilli, and sulforaphane from cruciferous vegetables; are the contributors to aid the Nrf2 cell structure. With these certain foods in a person�s diet, it can be beneficial to combating oxidative stress and preventing oxygen toxicity from producing in the bloodstream.
Legumes: Soybeans and other soy products, chickpeas, mung beans
With these types of antioxidant foods, they can help aid the body by lowering the stress compound naturally without the usage of medications. There are ways to get the nutrients of the different food groups to support the body and activate the Nrf2 pathways. Fermented foods that contain lactobacilli can express and activate the gene pathway.
Let�s start with Lactobacillus plantarum and Lactobacillus brevis. These two are the good bacteria that are found in traditional vegetables, fruit, and fermented malt whiskey. They help the body by breaking down the food that is being consumed, absorbing the nutrients, and fighting off the harmful organisms that are causing discomfort to the gut. When these two bacteria are expressing PAD (phenolic acid derivatives) and being introduced to a caffeic acid; the results are astonishing.
Studies indicate that particular strains of lactobacilli can biotransform the caffeic acid to potently activate the Nrf2 pathways from an inactive precursor. �So let�s say that if an individual is stressed and then they eat some food. Suddenly they feel a bit better after eating, that is because of the Nrf2 pathways mixed with the enhanced lactobacilli in their food helped neutralized the stress compound in the body.
With sulforaphane in cruciferous vegetables, it can help with the Nrf2 pathways. Since cruciferous plants have natural fighting properties against cancer, they have a good source of phytonutrients and the sulforaphane combined.
Here are some of the cruciferous vegetables that can help the Nrf2 pathway in the body.
Arugula
Bok choy
Broccoli
Brussels sprouts
Cabbage
Cauliflower
Kale
Radish
Turnips
These vegetables are nutritious when they are eaten raw or cooked. Sulforaphane in the many cruciferous plants has been linked to many health benefits such as improving heart health and digestion. This compound has an inactive form of glucoraphanin, but when it comes in contact with myrosinase, it releases the glucosinolates. This means that when the cruciferous vegetables are either damaged, cut, chopped or chewed on, the myrosinase enzymes are activated and turning into sulforaphane.
Studies have even been shown that sulforaphane can prevent cancer cell growth by releasing antioxidants and detoxifying enzymes that protect carcinogens, which are substances that can cause cancer.
How the Nrf2 Cell Activates
The various molecules in them can exhibit a robust activation in the Nrf2 defense system. Researchers have studied that the Nrf2 defense pathway can provide natural protection against oxidative stress and chemical toxicity through relatively small electrochemical co-factors called Nrf2 activators.
These activators actually amplify the effect of ROS (reactive oxygen species) by cycling through oxidation-reduction reactions and liberating Nrf2 in the human endothelial cells. Since the human body can get sick from stress, it is essential to eat foods that can fight off the harmful organisms. Nrf2 cells do regulate the oxidative stress by releasing itself into the body�s system. It is crucial to make sure that good, nutritious food that is beneficial in helping the Nrf2 cells by doing it naturally.
With a person�s hectic lifestyle gets in the way, they start to feel overly stressed. The body begins to develop chronic ailments that can harm not only the outside of the body but the inside as well. When individuals go to see health care professional for any chronic diseases that they may have, they will be informed of remedies to help aid them the best way they can. Individuals can find ways to deal with the stress hormone and calm it down through functional medicine. So when the body develops oxidative stress, it will affect the organ system, the nerve system, and the neurological system.
With the Nrf2 cells, the cell structure goes towards the oxidative stress compound and put a stop to it. And with the nutritious food that is available to aid the Nrf2 cell more. When we can calm down our anxious mind through the use of functional medicine and by eating healthy, organic, whole foods; we are actually repairing the body from the inside out.
Conclusion
As stated from the beginning, the Nrf2 cell helps the body by protecting it against oxidative stress. When we add nutritious food into the collection, it is aiding the Nrf2 cells a whole lot. Since the entire body needs the nutrients from the different food groups to assist not only the Nrf2 cells but to all crucial organs that need the nutrient sources to function correctly. The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References
Bryan, Holly K, et al. �The Nrf2 Cell Defence Pathway: Keap1-Dependent and -Independent Mechanisms of Regulation.� Biochemical Pharmacology, U.S. National Library of Medicine, 15 Mar. 2013, www.ncbi.nlm.nih.gov/pubmed/23219527.
Coyle, Daisy. �Sulforaphane: Benefits, Side Effects, and Food Sources.� Healthline, 26 Feb. 2019, www.healthline.com/nutrition/sulforaphane.
Prochaska, H J, et al. �On the Mechanisms of Induction of cancer-protective Enzymes: a Unifying Proposal.� Proceedings of the National Academy of Sciences of the United States of America, U.S. National Library of Medicine, Dec. 1985, www.ncbi.nlm.nih.gov/pubmed/3934671.
Senger, Donald R., et al. �Activation of the Nrf2 Cell Defense Pathway by Ancient Foods: Disease Prevention by Important Molecules and Microbes Lost from the Modern Western Diet.� PLOS ONE, Public Library of Science, 17 Feb. 2016, journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0148042.
Su, Xuling, et al. �Anticancer Activity of Sulforaphane: The Epigenetic Mechanisms and the Nrf2 Signaling Pathway.� Oxidative Medicine and Cellular Longevity, Hindawi, 6 June 2018, www.ncbi.nlm.nih.gov/pubmed/29977456.
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine
�
