How often do you have a hard time remembering your appointments? Has it become harder for you to learn new things? How often do you feel you have something that must be done? Or even, how often do you feel more susceptible to pain?�Research studies have demonstrated that brain fog may be associated with Alzheimer’s disease. In the following article, we will discuss how midlife systemic inflammatory markers have ultimately been associated with late-life brain volume. �
Midlife Systemic Inflammatory Markers are Associated with Late-life Brain Volume
Abstract
Objective: To clarify the temporal relationship between systemic inflammation and neurodegeneration, we examined whether a higher level of circulating inflammatory markers during midlife was associated with smaller brain volumes in late-life using a large biracial prospective cohort study.
Methods: Plasma levels of systemic inflammatory markers (fibrinogen, albumin, white blood cell count, von Willebrand factor, and Factor VIII) were assessed at baseline in 1,633 participants (mean age 53 [5] years, 60% female, 27% African American) enrolled in the Atherosclerosis Risk in Communities Study. Using all 5 inflammatory markers, an inflammation composite score was created for each participant. We assessed episodic memory and regional brain volumes, using 3T MRI, 24 years later.
Results: Each SD increase in midlife inflammation composite score was associated with 1,788 mm3 greater ventricular (p = 0.013), 110 mm3 smaller hippocampal (p = 0.013), 519 mm3 smaller occipital (p = 0.009), and 532 mm3 smaller Alzheimer disease signature region (p = 0.008) volumes, and reduced episodic memory (p = 0.046) 24 years later. Compared to participants with no elevated (4th quartile) midlife inflammatory markers, participants with elevations in 3 or more markers had, on average, 5% smaller hippocampal and Alzheimer disease signature region volumes. The association between midlife inflammation and late-life brain volume was modified by age and race, whereby younger participants and white participants with higher levels of systemic inflammation during midlife were more likely to show reduced brain volumes subsequently.
Conclusions: Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging.
Introduction
� Although elevated levels of inflammatory markers have been found in the blood,1 CSF,2 and brain parenchyma3 of individuals with cognitive impairment and Alzheimer disease (AD), it remains unclear whether this heightened inflammatory state is driving neurodegenerative changes. If low-grade systemic inflammation does play a causal role in AD and other neurodegenerative diseases, a heightened inflammatory response during midlife would be expected to increase one’s risk for pathologic brain changes much later. Although cross-sectional studies have demonstrated a link between elevated inflammatory markers and reduced brain volume in older adults,4,�7 it remains unclear whether systemic inflammation during midlife, before the onset of significant age- and disease-related neurologic changes, is associated with brain volume loss later in life. � The goal of the current study was to examine how midlife plasma markers of inflammation relate to late-life brain volume among a biracial community sample of older adults. To this end, we examined the relationship between 5 markers of systemic inflammation measured during midlife and MRI measures of regional brain volume 24 years later in the Atherosclerosis Risk in Communities (ARIC) Study cohort. We tested the hypothesis that greater midlife systemic inflammation is associated with smaller brain volumes in regions most susceptible to AD-related atrophy and reduced episodic memory in older adulthood. Based on cross-sectional evidence suggesting that race, sex, and age may modify the association between inflammatory markers and brain volume,5,8,9 the current study also examined the modifying effects of each of these demographic characteristics. �
Methods
� Study population. The ARIC study, an ongoing community-based prospective study, enrolled 15,792 middle-aged adults (45�65 years of age at baseline).10 Participants were selected by probability sampling in 4 US communities: Washington County, Maryland; Forsyth County, North Carolina; northwestern suburbs of Minneapolis, Minnesota; and Jackson, Mississippi. Following the baseline visit in 1987�1989 (visit 1), participants were seen at 3 more visits, approximately 3 years apart until 1996�1998 (visit 4), and at the fifth visit in 2011�2013 (visit 5). � At visit 5, a subset of 1,978 participants was selected to undergo brain MRI scans.11 Participants were selected to undergo a brain MRI based on previous participation in the ARIC Brain MRI Ancillary Study and standard safety exclusion criteria. In addition, all participants with evidence of cognitive impairment at visit 5 and an age-stratified random sample of participants without evidence of cognitive impairment were recruited. The participation rate among eligible individuals selected to undergo brain MRI was approximately 81%. A detailed description of the MRI sampling strategy is provided in the e-Methods at Neurology.org. We excluded participants with poor imaging quality (n = 6), neurologic disease (i.e., stroke, multiple sclerosis) (n = 80), missing inflammatory biomarker data (n = 38), missing covariates (n = 215), and race other than white or African American (n = 6). Participants who met criteria for dementia (5%, n = 83) were excluded from the primary analyses. � Standard protocol approvals, registrations, and patient consents. The ARIC study protocol has been approved by the institutional review boards at each participating center. All participants gave written informed consent at each study visit. � Inflammatory markers. Plasma levels of 4 acute-phase reactants�fibrinogen, albumin, von Willebrand factor (VWF), and Factor VIII (FVIII)�and white blood cell (WBC) count were used to measure systemic inflammation.12 Using standard protocols, study technicians drew fasting blood, centrifuged samples, and froze plasma blood samples at ?70�C until the samples were analyzed.13 Fibrinogen (mg/dL), albumin (g/dL), VWF (% of standard), and FVIII activity (% of standard) measured at visit 1 were analyzed in an ARIC research laboratory in accordance with a standardized protocol.13,14 WBC count was determined from whole anticoagulated blood using an automated particle Coulter Counter within 24 hours of venipuncture. Repeated testing revealed interassay coefficients of variation below 8% for fibrinogen, albumin, FVIII, and WBC, and 17%�19% for VWF.15,16 � Brain MRI. MRI scans were conducted using a 3T MRI scanner.11 Magnetization-prepared rapid gradient echo (MPRAGE), axial T2* gradient recalled echo, axial T2 fluid-attenuated inversion recovery, and axial diffusion tensor imaging sequences were obtained. Freesurfer (surfer.nmr.mgh.harvard.edu) was used to measure brain volume from MPRAGE sequences.17 Total brain and ventricular volume, lobar volume (frontal, temporal, parietal, occipital), AD signature region volume (i.e., the combined volume of the parahippocampal, entorhinal, inferior parietal lobules, hippocampus, and precuneus),18 hippocampal volume, and total intracranial volume were evaluated for the current study. � Episodic memory. Episodic memory was assessed at visit 5, concurrent with the brain MRI, using the delayed word recall test (DWR). DWR is a test that requires participants to learn and recall a list of 10 words following a delay period.19 Participants were scored based on the total number of words correctly recalled. � Covariates. Race, sex, years of education attained (less than high school, high school/General Equivalency Development/vocational school, or any college), cigarette smoking status (current/former/never), average weekly alcohol consumption (grams), and previous cancer diagnosis were self-reported. A random zero sphygmomanometer was used to calculate sitting diastolic and systolic blood pressure. Second and third blood pressure measurements were averaged for the current analyses. Hypertension was defined as systolic blood pressure >140 mm Hg, diastolic blood pressure >90 mm Hg or use of hypertensive medication. Body mass index was calculated using recorded height and weight (kg/m2). Coronary heart disease was defined as self-reported coronary bypass, balloon angioplasty, angioplasty of one or more coronary artery, or myocardial infarction. Medications used in the previous 2 weeks were recorded. The presence of chronic inflammatory conditions (e.g., arthritis, lupus, gout) was assessed by patient self-report of physician diagnosis at visit 4. History of regular anti-inflammatory medication use (e.g., nonsteroidal anti-inflammatory drug, arthritis medication) was assessed at visit 5. All other variables were assessed at visit 1. Dementia diagnosis was adjudicated at visit 5 by an expert committee using cognitive, imaging, and functional data.20 � Total cholesterol and triglycerides were measured using enzymatic methods,21,22 and low-density lipoprotein using the Friedewald equation.23 Serum glucose was measured using the hexokinase method. Diabetes was defined as a fasting glucose ?126 mg/dL or a nonfasting glucose ?200 mg/dL, current use of diabetes medication or insulin, or participant report of physician-diagnosed diabetes. APOE genotype (0, 1, or 2 ?4 alleles) was assessed using the TaqMan assay (Applied Biosystems, Foster City, CA). � Statistical analysis. We examined systemic inflammation as both a continuous and categorical exposure measure. A continuous inflammation composite Z score was created using the 5 inflammatory markers. WBC count was log-transformed to correct for skewness. Each inflammatory biomarker was converted to a standardized Z score such that the group mean was zero with an SD of 1. The mean of the 5 Z scores was calculated to generate an inflammation composite Z score. Because albumin decreases in response to inflammation, albumin values were multiplied by ?1 before being included in the composite Z score. With few exceptions, the intercorrelations between inflammatory markers were within an optimal range, between 0.2 and 0.4; composite score item�test correlations, principal component factor loadings, and Cronbach ? (0.61) were satisfactory for our purposes (table e-1). For each participant, we also created a categorical measure of systemic inflammation by computing the number of inflammatory marker Z scores in the highest quartile (?75%tile) and trichotomizing this number (0, 1�2, or 3�5). � Participant characteristics were compared using an analysis of variance or ?2 tests. Multivariable linear regression was used to assess the association between continuous and categorical inflammation variables and measures of brain volume and episodic memory. Brain volume analyses were adjusted for total intracranial volume, and all analyses included the covariates described in the previous section. Interaction terms or stratification were used to evaluate the modifying effects of age, race, and sex. � Sensitivity analyses were performed excluding participants who reported regular anti-inflammatory medication use during follow-up and including participants who met criteria for dementia. For all analyses, sampling weights were incorporated to account for the ARIC brain MRI sampling strategy. Thus, all results represent estimates for the entire ARIC visit 5 study population. Because the associations between inflammation markers and specific regions of interest (ROIs) are correlated, we did not adjust for multiple comparisons. A 2-sided p-value <0.05 designated statistical significance. All analyses were conducted using Stata Version 14 (StataCorp, College Station, TX). �
Results
� Study population characteristics. A total of 1,633 participants (baseline mean age 52.8 [5.3] years, 27% African American, 60% women, 46% college or professional degree) were included in the study sample. The time between baseline assessment and follow-up MRI scan was 24 (1) years; the average age at follow-up was 76.5 (5.4) years. As shown in table 1, a higher inflammation composite score at baseline was associated with older age, female sex, African American race, and increased levels of a number of cardiovascular risk factors. � Inflammatory markers and brain volume. Each SD increase in inflammation composite score at baseline was associated with a 532 mm3 smaller AD signature region volume (95% confidence interval [CI] ?922 to ?141), a 519 mm3 smaller occipital lobe volume (CI ?906 to ?132), a 110 mm3 smaller hippocampal volume (CI ?196 to ?24), and a 1,788 mm3 larger ventricular volume (CI 371 to 3,205) at follow-up (table 2). We found the estimated effect of a 1 SD increase in inflammation composite score during midlife on occipital lobe, ventricular, and hippocampal volume to be similar to the effect associated with possession of a single APOE ?4 allele in our multivariable regression analyses. No association was found for the total brain, frontal lobe, temporal lobe, or parietal lobe volume (ps > 0.071). Our findings did not change meaningfully after excluding participants who regularly used anti-inflammatory medication during the follow-up period (table e-2) and after including participants who met the criteria for dementia at visit 5 (table e-3). For descriptive purposes, associations between individual inflammatory markers and AD signature region volume are provided in a table e-4. � An assessment of linear trend revealed that compared to individuals with 0 elevated (?75th %tile) inflammatory biomarkers at baseline (reference), those with 1�2 and 3�5 elevated biomarkers had lower AD signature region (p trend = 0.001), occipital lobe (p trend = 0.007), and hippocampal volume (p trend = 0.041) 24 years later (figure 1). Compared to the reference group, participants with 3 or more elevated markers demonstrated 5.3% smaller AD signature region volumes, 5.7% smaller occipital lobe volumes, and 4.6% smaller hippocampal volumes, on average. However, this pattern was not statistically supported for the total brain, ventricular, frontal lobe, temporal lobe, and parietal lobe volume (p trends >0.072). The modifying effects of age, race, and sex. A significant age-by-inflammation composite score interaction was found for the AD signature region, occipital lobe, and hippocampal volume (table 2). Because a reversal of association was observed at age 60 (figures 2, e-1, and e-2), we stratified the sample into young-midlife and old-midlife subgroups (<60/? 60). As displayed in table 2, the associations between higher midlife inflammation composite score and lower AD signature region, occipital lobe, and hippocampal volume at follow-up were significantly stronger among participants who were 60 or younger at baseline compared to those who were older than 60. A marginal race-by-inflammation composite score interaction was found for occipital lobe volume, whereby a higher midlife inflammation composite score was associated with lower occipital lobe volume among white, but not African American, participants (table 3). No interactions with sex were found (table e-5). � Inflammatory markers and episodic memory. Late-life episodic memory, which was associated with hippocampal and AD signature region volume after controlling for age (partial rs > 0.21, ps < 0.001), was reduced among participants with higher levels of the inflammation composite score. Each SD increase in inflammation composite score was associated with a ?0.08 SD performance decrement on the DWR after adjusting for covariates (CI ?0.15 to 0.00; p = 0.046). Similarly, a higher number of elevated inflammatory biomarkers at baseline was associated with reduced DWR performance (p trend = 0.009; figure 1). �
Discussion
� Using a large community sample, we demonstrated that a higher level of systemic inflammatory markers measured during midlife is independently associated with lower regional brain volume and reduced episodic memory 24 years later among older adults without dementia. Similarly, participants who had elevations in a larger number of 5 inflammatory markers during midlife were found to have lower regional brain volumes and reduced episodic memory in late-life in a dose-response manner. For several brain regions, including the hippocampus, the effect of a 1 SD increase in midlife inflammation composite score was comparable to that of possessing a single APOE ?4 allele during late life. Whereas age and race were found to modestly modify the relationship between midlife inflammation and late-life regional brain volume, the previously reported modifying effect of sex was supported. � Although cross-sectional evidence from the Framingham5 study and several other population-based8,9 studies suggests an association between brain volume and inflammation in older adults, the temporal relationship between inflammation and brain volume loss is still not well-understood. As a result, whether heightened systemic inflammation constitutes a potential cause or consequence of neurodegeneration and brain atrophy remains unclear. Because the pathophysiologic processes driving neurodegeneration and brain volume loss begin decades before the onset of frank cognitive decline,24 it is essential to determine how biological processes that take place during middle adulthood relate to neurologic outcomes later in life. By demonstrating that an elevation in plasma inflammatory markers during midlife is independently associated with smaller regional brain volumes, larger ventricular volume, and reduced episodic memory in late life, the current findings provide support for a potential causal, rather than associative, role of systemic inflammation in late-life neurodegeneration (i.e., atrophy) and resulting cognitive decline. The current findings align closely with those from the neurocardiovascular literature, which have found associations between midlife blood pressure,25 cholesterol,26 and diabetes27 and adverse neurologic and cognitive outcomes in older adulthood. The contributing role of systemic inflammation to subsequent neurodegenerative processes has been demonstrated previously by animal studies,28 but had not yet been supported by a large prospective MRI study. � The current results suggest that several demographic factors modify the relationship between midlife inflammation and late-life brain volume. Younger individuals with elevated levels of inflammation (particularly participants in their 40s) were more likely to display lower brain volumes decades later, supporting the idea that elevated systemic inflammation earlier in life may make individuals especially vulnerable to neurodegenerative brain changes as they age. Although we expected stronger effects would emerge within the African American group, given the greater burden of systemic disease29 and dementia,30 the associations between inflammation and brain volume were generally weaker among African Americans. A previous study that examined the moderating effects of race found similar results in a cross-sectional analysis of older adults without dementia.8 � Circulating levels of acute-phase reactants, such as those used in the current study, change in parallel with an inflammatory response as a result of signaling from inflammatory cytokines such as interleukin-6 and tumor necrosis factor-?.12 Cytokines in the periphery have the potential to induce a pro-inflammatory neurotoxic state within the CNS through multiple routes, including activation of endothelial cells of the blood-brain barrier,31 activation of macrophage in circumventricular organs,32 and signaling of the afferent vagus nerve.33 In addition to providing support for a pathogenic role of systemic inflammation in neurodegenerative disease, the present findings indicate that elevations in commonly assayed inflammatory proteins may serve as markers of risk for future neurodegenerative changes and cognitive decline. Although we did not examine all brain regions in our analysis, our assessment of 7 representative ROIs suggests that brain regions vulnerable to atrophy, amyloid deposition, and metabolic abnormalities in the earliest phases of AD may be more vulnerable to volume loss associated with heightened midlife inflammation. This pattern of neuroanatomic specificity has been supported by previous cross-sectional studies of older adults without dementia.4,7,�9,34 � In the context of the current findings, several alternative explanations should be considered. First, it remains possible that elevated systemic inflammation may simply serve as a marker of another pathologic process linked to neurodegeneration (e.g., oxidative stress). Second, it is possible that the biological processes causing brain atrophy to trigger a protective neuroimmune response, which increases peripheral inflammation. Third, the associations found here may be an effect of residual or unmeasured confounding. Despite these caveats, the contributory role of systemic inflammation has been supported by a sizable body of literature implicating peripheral inflammatory signaling in neurodegenerative processes such as neural apoptosis,35 ?-amyloid formation,36 and neuronal tau phosphorylation.37 � Strengths of the current study include the prospective study design, length of follow-up, detailed assessment of potentially confounding variables, large sample size, and the inclusion of a large African American sample. However, the current findings should be interpreted within the context of several limitations. Although the acute-phase reactants used in the present study represent components of the innate immune system, several of these proteins are implicated in another closely related physiologic process, such as hemostasis, which may also influence brain volume. Evaluating inflammatory biomarkers that have greater biological specificity in future prospective studies will allow for stronger inferences about the contributing role of systemic inflammation. Interpretation of the current findings is also limited by the measurement of inflammatory markers at a single time point, as it is unclear whether a single measurement can adequately capture inflammation chronicity. The relatively high interassay variability of VWF also increases the likelihood of exposure misclassification; however, this possibility is mitigated by the use of the inflammation composite score. We found that participants who dropped out and participants who died before visit 5 had significantly higher levels of midlife inflammation, were older, had greater levels of medical comorbidity at baseline, and were more likely to be African American38 (table e-6). As a result, selective attrition may have biased results in the direction of the null hypothesis, particularly for African American and older participants. Finally, our interpretation of the contributory role of inflammation in neurodegeneration rests on the assumption that brain volume loss occurred after inflammatory markers were assessed. Although evidence suggests that this is likely the case (brain volume loss accelerates after age 60 years39), this cannot be confirmed without the assessment of change over time. � Despite these limitations, the current study provides insights into the connection between midlife systemic inflammation and late-life brain volume loss. These findings provide support for inflammation’s early pathogenic role in the development of neurodegenerative brain changes associated with late-life cognitive decline, AD, and other forms of dementia. �
Is inflammation the final trip wire for Alzheimer’s disease?� Research studies have demonstrated that neuroinflammation is considered to be the main epigenetic trip wire for the genetic predisposition of Alzheimer’s disease or AD. Moreover, patients with inflammation can also develop a variety of symptoms, including brain fog which can make thinking, understanding, and remembering basic information challenging. Neuroinflammation can cause brain fog and other other well-known health issues, including Alzheimer’s disease and other neurological diseases. – 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. � Have you been experiencing noticeable variations in your mental speed? Do you suffer from pain, discomfort, and inflammation? Have you been experiencing fatigue, especially after meals or exposure to chemicals, scents, or pollutants?�Brain fog can cause a variety of symptoms, including memory and concentration as well as vision problems. According to the research study above, midlife inflammation and brain fog may be associated with Alzheimer’s disease. � 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
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Physical therapists or PT’s are healthcare professionals that help treat/rehabilitate patients of all ages with various types of injuries.
Personal
Work
Sports
Auto Accidents
A primary care physician, physiatrist, orthopaedist, spine surgeon, or neurosurgeon may refer an individual to a physical therapist as part of a non-surgical�treatment plan.
A physical therapy program may be an integral part of your after-care following surgery.
Some treatments are done prior to active therapeutic exercise.
Conditions therapists treat
Sciatica
Whiplash
Rheumatoid arthritis
Degenerative disc disease
Spondylosis (spinal arthritis)
Post spine surgery therapy
Therapists want to help patients rebuild strength, flexibility, and endurance after any type of intense surgery, as well as help with any specific physical necessities related to post-surgery.
Team Care
Therapists often work directly for or with a doctor/chiropractor to coordinate a treatment plan.
A doctor may send the therapist:
Diagnosis
Current medications
Imaging/scan results
During the consultation, the physical therapist talks about medical history, diagnosis, and symptoms.
This can include:
Conditions
Medications being taken
Diet
Supplements
Type of Pain like:
Acute
Chronic
Episodic
The location of the pain that will also include:
Severity
Type
Factors that decrease or increase pain
Training
Physical therapists have completed an accredited physical therapy program and passed a required state licensing examination.
Therapists graduate with a Doctor of Physical Therapy (DPT) degree.
The American Board of Physical Therapy Specialties through a series of classes/tests therapists can become board-certified specialists in specific areas like:
Orthopedics
Pediatrics
Geriatrics
Sports
These are just a few, but there are many areas of specialization.
Physical Therapist
Many states allow individuals to go to a physical therapist without a referral from a doctor.
Definitely ask your doctor for a recommendation, but also think about what you want in a therapist.
Male or female physical therapist, which is right for you
Take Charge
Physical therapists are valuable healthcare professionals and members of the medical community.
Physical therapy can be challenging but don’t let that get you down, because they will help get you back to optimal health, along with building a stronger, healthier body.
Whiplash Massage Therapy El Paso, TX Chiropractor
Physical therapist Sandra Rubio describes how whiplash-associated disorders resulting from an automobile accident can cause symptoms of neck pain.
An injury to the cervical spine can damage the complex structures of the neck, including:
Vertebrae
Intervertebral discs
Soft tissues
Tendons
Ligaments
Muscles
Neck pain can come from various structures in the neck including vascular, nerve, airway, digestive, and musculature or it can originate from other areas of the human body.
Most cases can be treated with assistance or using self-help suggestions and techniques.
NCBI Resources
Physical therapy includes both active and passive treatments. Passive treatments help to unwind the body and the physique. As an individual does not need to actively participate, they�re known as passive. A physical treatment program may begin with treatments that are passive, but the goal is to get into treatments that are more active.
If you are experiencing any of these situations, then you might be experiencing problems with your stomach acid pH balance.
The pH Balance of the Stomach
The stomach produces gastric acids that help breakdown the food contents that a person eats. With the gastric acids, studies stated that its role is diverting the bile and pancreatic juice from the intestines. With humans, the stomach plays a significant role as a biological filter with moderate lifestyle changes. Whether it changes in a person’s diet, hygiene, and medical interventions can alter the stomach’s pH levels.
With the stomach acidity in the body, it is a double-edged sword. High acidity in the stomach can prevent pathogen exposure, but it can also decrease the likelihood of recolonization of beneficial microbes. Low acidity in the stomach is more likely to be colonized by pathogens and can cause gastric infections.
Acid Reflux
Acid reflux is a common condition that features a burning pain in the lower chest area, and it occurs when stomach acid flows back up into the food pipe. Diseases that are the result of acid reflux is one of the most common gut complaints from individuals and seen by hospital departments in the United States. The stomach contains hydrochloric acid that helps breakdown food and protects it from pathogens such as bacteria.
Even though the lining of the stomach is specially adapted to protect it from hydrochloric acid, the esophagus is not protected from this powerful acid. The gastroesophageal sphincter is a ring of muscle that generally acts as a valve that lets food into the stomach but does not let the food back up into the esophagus. When it fails, the stomach contents will regurgitate into the esophagus, and the symptoms of acid reflux will be felt.
One of the risk factors that acid reflux causes that are not preventable are hiatal hernia. This hernia causes a hole in the diaphragm that allows the upper part of the stomach to enter the chest cavity. Other risk factors include:
Obesity
Smoking (active or passive)
Low levels of physical exercise
Certain medication
Poor diet
Some of the symptoms that acid reflux creates can cause heartburn, and it is uncomfortable when the sensation travels up to the neck and throat. When an individual lays down or bends over, it tends to get the worst and can last for several hours. Some of the symptoms caused by acid reflux include:
Heartburn
Sour taste in the mouth
Regurgitation
Dyspepsia
Difficulty swallowing
Sore throat
Dry cough
Asthma symptoms
Hypochlorhydria
Hypochlorhydria is the medical term for low levels of stomach acid. Individuals with hypochlorhydria are unable to produce enough hydrochloric acid in their stomach and may experience digestive issues, nutritional deficiencies, and gastrointestinal infections.
Some of the common causes of hypochlorhydria are:
Age: Aging can make the stomach produce less acid in the body. A 2013 review stated that adults over the age of 65 are more susceptible to develop that hypochlorhydria.
Stress: Even though everyday stress does not have much effect on the production of stomach acid, chronic stress, however, can contribute to hypochlorhydria.
Medication: Individuals that use long-term antacids or other medication for acid reflux or heartburn may decrease the stomach acid that the body produces.
Bacterial Infection: A bacteria called Helicobacter pylori is a widespread, yet under-appreciated pathogen that can alter the host physiology and subvert the host immune response. It is the primary cause of peptic ulcers and gastric cancers while contributing to a low level of stomach acid.
Zinc deficiency: Zinc is a necessary mineral for stomach acid production. A lack of this mineral can contribute to hypochlorhydria to the body.
Stomach surgery: Surgical procedures like gastric bypass surgery can reduce the amount of the stomach produces.
Symptoms of hypochlorhydria are related to impaired digestion, increase infection, and reduce the absorption of nutrients from food. Symptoms may include:
Bloating
Burping
Upset stomach
Heartburn
Gas
Indigestion
Undigested food in stool
Neurological issues like numbness, tingling, and vision changes
Conclusion
The stomach is producing gastric acids that help break down food components. When environmental factors are in effect, they can alter the stomach’s pH balance and can disrupt the hydrochloric acid. Since stomach acidity is a double edge sword, it can go back and forth on the pH levels. High acidity in the stomach can cause acid reflux to the esophagus and decrease the likelihood of recolonizing beneficial microbes in the gut. Low acidity in the stomach can cause hypochlorhydria and develop digestive issues, nutrient deficiencies, and gastrointestinal infections. These products can help support the gastrointestinal system, as well as supporting the pH-optimized enzymes in both the gastric and intestinal function in the body.
October is Chiropractic Health Month. To learn more about it, check out Governor Abbott�s proclamation on our website to get full details on this historic moment.
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 .
Reference:
Beasley, DeAnna E, et al. �The Evolution of Stomach Acidity and Its Relevance to the Human Microbiome.� PloS One, Public Library of Science, 29 July 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4519257/.
Britton, Edward, and John T. McLaughlin. �Ageing and the Gut.� Cambridge Core, Cambridge University Press, 12 Nov. 2012, www.cambridge.org/core/journals/proceedings-of-the-nutrition-society/article/ageing-and-the-gut/A85D096755F5F7652C262495ABF302A0/core-reader.
Dix, Megan. �What Is Hypochlorhydria?� Healthline, 12 Mar. 2018, www.healthline.com/health/hypochlorhydria.
Green, G M. �Role of Gastric Juice in Feedback Regulation of Rat Pancreatic Secretion by Luminal Proteases.� Pancreas, U.S. National Library of Medicine, July 1990, www.ncbi.nlm.nih.gov/pubmed/2199966.
Kines, Kasia, and Tina Krupczak. �Nutritional Interventions for Gastroesophageal Reflux, Irritable Bowel Syndrome, and Hypochlorhydria: A Case Report.� Integrative Medicine (Encinitas, Calif.), InnoVision Professional Media, Aug. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4991651/.
Leonard, Jayne. �Hypochlorhydria (Low Stomach Acid): Causes, Symptoms, and Treatment.� Medical News Today, MediLexicon International, 17 July 2018, www.medicalnewstoday.com/articles/322491.php.
MacGill, Markus. �Acid Reflux: Causes, Treatment, and Symptoms.� Medical News Today, MediLexicon International, 13 Nov. 2017, www.medicalnewstoday.com/articles/146619.php.
Ramsay, Philip T, and Aaron Carr. �Gastric Acid and Digestive Physiology.� The Surgical Clinics of North America, U.S. National Library of Medicine, Oct. 2011, www.ncbi.nlm.nih.gov/pubmed/21889024.
Testerman, Traci L, and James Morris. “Beyond the Stomach: An Updated View of Helicobacter Pylori Pathogenesis, Diagnosis, and Treatment.” World Journal of Gastroenterology, Baishideng Publishing Group Inc, 28 Sept. 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4177463/.
Wang, Yao-Kuang, et al. �Current Pharmacological Management of Gastroesophageal Reflux Disease.� Gastroenterology Research and Practice, Hindawi Publishing Corporation, 2013, www.ncbi.nlm.nih.gov/pmc/articles/PMC3710614/.
Is your attention span decreasing? How often do you walk into rooms and forget why? How often do you feel you are not getting enough sleep or rest? If you answered yes to any of the previous questions, you may be experiencing brain fog. Brain fog is a symptom rather than a single condition and it can actually be caused by a very common factor: too much screen time. �
Many people today spend a significant amount of time staring at a screen than ever before. According to the American Optometric Association (AOA), an average office worker in the United States spends a minimum of seven hours a day sitting in front of a computer screen. While other recent research studies have shown that an average American adult spends as much as 11 hours a day looking at some type of screen of some kind, including mobile devices like smartphones. �
In light of this “digital revolution”, however, more and more healthy people in their 20’s, 30’s, and even in their 40’s have started experiencing brain fog, short-term memory loss, and insomnia as well as vision problems, headaches, and migraines. Although there isn’t an abundance of evidence, several research studies have begun to demonstrate the effects of too much screen time on our overall health and wellness. We will discuss why screen time causes brain fog, among other health issues. �
How Screen Time Changes the Brain
Sitting in front of a computer screen or looking at any other type of screen for extended periods of time can ultimately cause brain fog and vision problems, among other health issues because it changes the brain, both behaviorally and structurally. A research study of students in 10 countries showed that many of them feel acute distress if they go without their phones for 24 hours. Also, most people check their phones a minimum of 150 times a day, sending about 100 or more text messages. �
This excessive use of smartphones has been associated with stress, anxiety, and even depression. Neuroscientists have referred to this health issue as “digital dementia,” which ultimately affects important right-brain functions, such as short-term memory, attention, and concentration, in ways that may or may not be reversible if they are not treated properly. �
People who are perceived as having an online game addiction show significant gray matter atrophy in a variety of regions in the brain, including the right orbitofrontal cortex, the bilateral insula, and the right supplementary motor area, when they were evaluated using brain MRI research studies. The regions where volume loss was shown are ultimately in charge of essential cognitive functions, such as planning, prioritizing, organizing, impulse control, and reward pathways. These are also involved in our development of empathy and compassion as well as the translation of physical signals into emotion. �
Several research studies have also shown that too much screen time can also cause long-term vision problems and other eye health issues. According to the American Optometric Association, computer vision syndrome or CVS, also known as digital eye strain, is a complex vision problem associated with tasks and activities that stress the near vision and those that are experienced in relation, or during, the use of the computer, tablet, e-reader, and smartphone. The symptoms include eye strain and ache, dryness, irritation, redness, double or blurred vision, burning, and even neck and shoulder pain. �
Moreover, in 2014, a Harvard Medical School group investigated the biological effects of reading an e-book on a light-emitting device with reading a printed book in the hours before bedtime. The researchers ultimately reported that people who read on the e-book took longer to fall asleep, had less evening sleepiness, decreased melatonin secretion, later timing of their circadian rhythm, and lower next-morning alertness than when reading a printed book. Much of this likely has to do with the fact that e-books and other digital screens emit blue light, which has been shown to interfere with the production of melatonin or the “sleep hormone” which also helps regulate other hormones as well as our circadian rhythms. �
While research studies demonstrating the connection between mood and digital device addiction is still emerging, some recent research studies are starting to associate prolific social media use with the increased risk of anxiety and depression. Many patients report feeling stress, anxiety, and depression caused by spending too much time scrolling through social media, such as Instagram, Facebook, and Twitter feeds. Some even report that “social media detoxes,” where they delete these apps from their smartphones for a few days or weeks, tremendously improved their overall health and wellness. �
How to Prevent Brain Fog from Screen Time
If you find yourself experiencing symptoms such as brain fog, short-term memory loss, vision problems, insomnia, anxiety, depression, headaches, or migraines, make sure to see a healthcare professional for an evaluation first, but then try limiting screen time to six hours per day, avoiding all screens at least one hour before bed and taking the weekends “off” from social media. If you immediately feel better, you have a clear indication of how too much screen time is affecting your brain. �
Several other precautions you can take to prevent the previously mentioned symptoms can include: loading up on nutrients that have been shown to combat brain fog and vision problems like the carotenoid antioxidants zeaxanthin, lutein, and astaxanthin, found in green vegetables and a variety of colorful plant foods similar to these. If you can’t avoid using a computer or other digital device before bed, consider wearing a pair of blue-light-blocking glasses in the evenings, in which several research studies have shown that these can ultimately help restore melatonin production and improve sleep. �
Brain fog can make thinking, understanding, and even remembering basic information challenging. Brain fog is a symptom, rather than a single disorder, commonly associated with vision problems and other health issues like insomnia, anxiety, and even depression. Researchers and healthcare professionals have demonstrated that too much screen time, due to sitting in front of a computer screen or staring at a mobile device for extended periods of time, can ultimately change the brain, causing brain fog and vision problems, among other well-known symptoms. – 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. �
Have you been experiencing noticeable variations in your mental speed? Do you suffer from pain, discomfort, and inflammation? Have you been experiencing fatigue, especially after meals or exposure to chemicals, scents, or pollutants?�Brain fog is a symptom that can affect many brain functions, including memory and concentration. It can also be accompanied by other symptoms like vision problems. Too much screen time can cause brain fog and other health issues. � The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References: �
Sissons, Claire. �Brain Fog: Multiple Sclerosis and Other Causes.� Medical News Today, MediLexicon International, 12 June 2019, www.medicalnewstoday.com/articles/320111.php#1.
Orenstein, Beth W. �When Chronic Fatigue Syndrome Harms Vision.� EverydayHealth.com, Everyday Health, 4 March 2010, www.everydayhealth.com/chronic-fatigue-syndrome/vision-problems.aspx.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
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.
All can help relax muscles, relieve pain and increase mobility.
Proven Reduced Back Pain with *FOOT ORTHOTICS* | El Paso, Tx
Kent S. Greenawalt, President, and CEO of Foot Levelers discuss how custom foot orthotics can help reduce back pain, low back pain, and sciatica.
In a recent research study published by the American Congress of Rehabilitation Medicine (ACRM), researchers demonstrated that Foot Levelers custom foot orthotics help considerably reduce back pain and several of its associated health issues.
The research study also demonstrated that Foot Levelers custom foot orthotics and chiropractic care help tremendously reduce low back pain and sciatica.
Foot Levelers custom foot orthotics and chiropractic care helped improve the patient’s overall health and wellness.
Dr. Alex Jimenez is a chiropractor in El Paso, TX. can help provide these benefits through the utilization of chiropractic care and Foot Levelers custom foot orthotics, among other treatments.
NCBI Resources
Pain in the upper and/or mid-back is not as common as lower back or neck pain. The upper back is called the thoracic spinal column, and it is the most secure part of the spine. The reach of movement in the upper back is limited because of the backbone�s attachments to the ribs (rib cage).
Upper back pain is generally caused by soft tissue injuries, like sprains or strains, muscle tension caused by bad posture, or looking downward for long time spans (eg, texting, mobile phone use).
Pain, tenderness, soreness on the left side, under the rib cage
Nausea or vomiting
Stool undigested, foul-smelling, mucus-like, greasy or poorly formed
If you are experiencing any of these situations, then you might be experiencing pancreatic digestive disorders.
The Pancreas
The pancreas is a gland organ located in the abdomen. It is part of the digestive system, producing insulin and other vital enzymes and hormones that help break down food. It has an endocrine function, due to releasing juices directly into the bloodstream and has an exocrine function that releases juices into the ducts in the body.
One of its many jobs the pancreas does is that it secretes out enzymes into the small intestine and continues to break down that left in the stomach. Another job is that it produces insulin and secretes it into the bloodstream, where it can regulate the body’s glucose or sugar level. When there is a problem with insulin control in the body, it can lead a person to have diabetes. Other health problems include pancreatitis and pancreatic cancer.
Pancreatitis
Pancreatitis is an inflammation in the pancreas. It occurs when the digestive enzymes become activated while irritating the cells in the pancreas. With repeated damages to the pancreas, it can cause either two forms of pancreatitis, which is acute pancreatitis and chronic pancreatitis. Both are very painful and can form scar tissue in the pancreas, causing it to lose its function. A poorly functioning pancreas can cause digestion problems and diabetes. Here are the conditions that can lead to pancreatitis:
Abdominal surgery
Alcoholism
Certain medications
Cystic fibrosis
Gallstones
Obesity
Chronic Pancreatitis
Chronic pancreatitis is a long-term progressive inflammatory disease in the pancreas that can lead to a permanent breakdown of the structure and function of the pancreas in the body. Studies stated that the most common cause of chronic pancreatitis is long term alcohol abuse, it is thought to account for between 70 to 80 percent for all cases, and significantly it affects more men than women.
Common signs and symptoms of chronic pancreatitis include:
Severe upper abdominal pain that is more intense after a meal
Nausea and vomiting
When the disease progresses, the episodes of pain will become more frequent and more severe to individuals. Some individuals eventually suffer from constant abdominal pain, and as chronic pancreatitis progresses, the ability of the pancreas to produce digestive juices will deteriorate, and the following symptoms appear:
Smelly and greasy stool
Bloating
Abdominal cramps
Flatulence
Diabetes
There are numerous complications that an individual can potentially have with chronic pancreatitis. Nutrient malabsorption is one of the most complications since the pancreas is not producing enough digestive enzymes for the body to absorb the nutrients properly, leading to malnutrition. Another possible complication is the development of diabetes, where chronic pancreatitis damages the cells that produce insulin and glucagon to the body. Some individuals will also develop pseudocyst, which is fluid-filled that can form inside or outside the pancreas and can be very dangerous to the body since they can block the essential ducts and blood vessels.
Acute Pancreatitis
Acute pancreatitis is a sudden inflammation of the pancreas. It causes the enzymes to be excessively produced, causing the pancreas gland to be swollen and inflamed. It will make digestion slow down and become painful, making the other body functions be affected as well as making the pancreas be permanently damaged and scarred.
Acute pancreatitis is painful and can develop quickly. It can trigger potentially fatal complications as the mortality rate can range from less than 5 percent to over 30 percent, depending on the severity of the condition and if it reaches to the other organs beyond the pancreas. The most common cause of acute pancreatitis is the production of gallstones in the gallbladder, alcohol misuse, and infections.
When a person has acute pancreatitis, they feel the pain in the lower abdomen and then feel it more gradually as the pain intensified until it is a constant ache. Other symptoms include:
Vomiting and nausea
Diarrhea
Loss of appetite
Pain with coughing, vigorous movements, and deep breathing
Tenderness when the abdomen is touched
Fever
Jaundice, yellowish tinge on the skin and the whites of the eyes
Pancreatic Cancer
Also known as �the silent disease,” pancreatic cancer happens when uncontrolled cell growth begins to form in a part of the pancreas. Tumors develop and interfere with the way the pancreas works. Pancreatic cancer often shows any symptoms until the later stages, and it can be challenging to manage. The signs and symptoms of pancreatic cancer include:
Pain in the upper abdomen that radiates to the back
Unintended weight loss or loss of appetite
Pale or grey fatty stool
Jaundice
New-onset diabetes
Blood clots
Depression
Fatigue
Conclusion
The pancreas is located in the abdomen, and its primary function is to produce insulin and necessary enzymes and hormone to aid the digestion of food. When complications are attacking the pancreas like pancreatic cancer and pancreatitis, it can damage the pancreas to stop producing insulin and can lead to chronic illnesses to spread all over the body. Some products can help support the sugar metabolism that the pancreas creates and offer nutrients and enzymatic cofactors to the gastrointestinal system in the body.
October is Chiropractic Health Month. To learn more about it, check out Governor Abbott�s proclamation on our website to get full details on this historic moment.
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 .
Reference:
Banks, Peter A, et al. �The Management of Acute and Chronic Pancreatitis.� Gastroenterology & Hepatology, Millennium Medical Publishing, Feb. 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC2886461/.
Bartel, Michael. �Acute Pancreatitis – Gastrointestinal Disorders.� MSD Manual Professional Edition, MSD Manuals, July 2019, www.msdmanuals.com/en-gb/professional/gastrointestinal-disorders/pancreatitis/acute-pancreatitis.
Brazier, Yvette. �Acute Pancreatitis: Symptoms, Treatment, Causes, and Complications.� Medical News Today, MediLexicon International, 19 Dec. 2017, www.medicalnewstoday.com/articles/160427.php.
Brazier, Yvette. �Pancreatic Cancer: Symptoms, Causes, and Treatment.� Medical News Today, MediLexicon International, 23 Oct. 2018, www.medicalnewstoday.com/articles/323423.php.
Crosta, Peter. �Pancreas: Functions and Disorders.� Medical News Today, MediLexicon International, 26 May 2017, www.medicalnewstoday.com/articles/10011.php.
Felman, Adam. �Chronic Pancreatitis: Treatments, Symptoms, and Causes.� Medical News Today, MediLexicon International, 19 Dec. 2017, www.medicalnewstoday.com/articles/160459.php.
Health Publishing, Harvard. �Acute Pancreatitis.� Harvard Health, July 2019, www.health.harvard.edu/a_to_z/acute-pancreatitis-a-to-z.
Staff, Mayo Clinic. �Pancreatic Cancer.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 9 Mar. 2018, www.mayoclinic.org/diseases-conditions/pancreatic-cancer/symptoms-causes/syc-20355421.
Staff, Mayo Clinic. �Pancreatitis.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 7 Sept. 2019, www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227.
Have you been experiencing noticeable variations in your mental speed? Do you suffer from pain, discomfort, and inflammation? Have you been experiencing fatigue, especially after meals or exposure to chemicals, scents, or pollutants? If you answered yes to any of the previous questions, you may be experiencing brain fog, unclear thoughts or concentration. �
Brain fog is a well-known symptom associated with a variety of health issues. It can affect many brain functions, including memory and concentration. It can occur as a result of poor lifestyle habits, including stress, an unhealthy diet, and lack of sleep, or due to other health issues, including multiple sclerosis and chronic fatigue syndrome. Moreover, brain fog can be accompanied by other symptoms like vision problems. In the following article, we will discuss brain fog and vision problems. �
What is Brain Fog?
Brain fog can make a person feel as if the processes of thinking, understanding, and remembering are not working as they should. It can affect memory, the ability to process and understand information, visual and spatial skills, the ability to calculate and solve problems as well as executive functioning. If these essential brain functions don’t work efficiently, it can become challenging to understand, focus, and even remember simple things. It can ultimately lead to stress and fatigue. �
A variety of health issues can lead to brain fog. People with multiple sclerosis (MS) may experience changes in their ability to make decisions as well as to process and recall information. These changes are generally mild or moderate and they do not affect a person’s ability to live independently. However, they can be frustrating and these can make it difficult to complete regular tasks. Fibromyalgia can also affect a person’s concentration and memory. Chronic fatigue syndrome (CFS) is another chronic, or long-term, health issue that can result in brain fog, fatigue, and other symptoms, such as vision problems. �
Changes to a person’s hormone levels can also affect brain function, especially during pregnancy or menopause. A 2013 research study found that hormonal changes throughout a woman’s menopausal transition made it difficult for women to learn or retain new information and to focus on challenging everyday tasks. Hypothyroidism and Hashimoto’s disease can cause hormone imbalances. Memory and thinking problems similar to brain fog are also common in thyroid disorders. �
Depression is a mood disorder that affects how a person thinks and feels. Problems with memory, focus, and decision-making can contribute to brain fog. There may also be problems with sleeping and a lack of energy, which can make concentrating and completing everyday tasks much more challenging. Stress and anxiety can also make it difficult to think clearly. �
Vision Problems and Brain Fog
Many people with brain fog due to multiple sclerosis (MS) or chronic fatigue syndrome (CFS) also experience vision problems. Healthcare professionals believe that vision problems associated with CFS and other health issues are caused due to brain dysfunction rather than eye dysfunction. Our brain constantly transmits signals into our eyes which allows us to know where we are as well as what it is that you�re seeing. The brain is also in charge of controlling the eye reflexes, including pupil dilation due to light and dark changes. However, these brain and eye functions may not work properly with brain fog. �
Most frequently, patients with brain fog experience vision problems where their environment appears to be blurry or it seems to be foggy. According to Dr. Peter Rowe, director of the Chronic Fatigue Clinic at Johns Hopkins Children�s Center in Baltimore, these vision problems most frequently occur when standing up, making the patients also feel lightheaded. �
Furthermore, other vision problems that CFS and MS patients commonly experience with brain fog, ultimately include: �
Difficulty when focusing on objects, generally those which are close up
Inability to see objects in peripheral vision, as though they have tunnel vision
Dizziness and being unable to look at moving objects without feeling dizzy
Seeing an excess amount of “floaters” and/or “flashes of light” in their vision
Intolerant to light or feeling discomfort in bright rooms and outdoors in the sunshine
Feeling as though the eyes are dry or as though they’re itchy, gritty, or burning
Proper Health Care with Brain Fog and Vision Problems
People with brain fog and vision problems associated with CFS, MS, or any other health issue will commonly visit an optometrist or ophthalmologist. However, an eye exam will generally return as “normal�. In addition, prescription lenses may not help because of rapid vision changes. If you do wear glasses, tints may ultimately help reduce sensitivity to light. �
Because blurred or foggy vision is the most common problem associated with brain fog, researchers and healthcare professionals believe that improving blood flow to the brain can help improve symptoms. Treating any underlying health issues and/or practicing proper lifestyle habits, such as eating a healthy diet, engaging in exercise or physical activity, and sleeping properly can help promote proper blood flow to the brain and ultimately improve brain fog and vision problems. �
Blurry or foggy vision, among other vision problems, are frequently believed to be a temporary symptom and are more associated with lightheadedness and blood flow to the brain. You may need to see a cardiologist or a neurologist to treat lightheadedness or dizziness. If you have chronic fatigue syndrome (CFS), multiple sclerosis (MS), or any other health issue where you find that you can�t tolerate bright light, you should wear sunglasses when you�re outdoors in the sunshine. �
Brain fog commonly includes feelings of confusion and disorientation, where it can make a person have difficulty thinking, understanding, and even remembering basic information. Brain fog is a symptom, rather than a single disorder, associated with vision problems and other health issues like CFS and MS. Researchers and healthcare professionals believe that because brain fog can ultimately affect brain function, it can also affect essential eye reflexes responsible for these well-known vision problems, among other symptoms, including fatigue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Neurotransmitter Assessment Form
The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �
In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal. �
Have you been experiencing noticeable variations in your mental speed? Do you suffer from pain, discomfort, and inflammation? Have you been experiencing fatigue, especially after meals or exposure to chemicals, scents, or pollutants?�Brain fog is a symptom that can affect many brain functions, including memory and concentration. It can also be accompanied by other symptoms like vision problems. In the article above, we discussed brain fog and vision problems. � The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez �
References: �
Sissons, Claire. �Brain Fog: Multiple Sclerosis and Other Causes.� Medical News Today, MediLexicon International, 12 June 2019, www.medicalnewstoday.com/articles/320111.php#1.
Orenstein, Beth W. �When Chronic Fatigue Syndrome Harms Vision.� EverydayHealth.com, Everyday Health, 4 March 2010, www.everydayhealth.com/chronic-fatigue-syndrome/vision-problems.aspx.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
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.
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
Inflammatory markers and brain volume. Each SD increase in inflammation composite score at baseline was associated with a 532 mm3 smaller AD signature region volume (95% confidence interval [CI] ?922 to ?141), a 519 mm3 smaller occipital lobe volume (CI ?906 to ?132), a 110 mm3 smaller hippocampal volume (CI ?196 to ?24), and a 1,788 mm3 larger ventricular volume (CI 371 to 3,205) at follow-up (table 2). We found the estimated effect of a 1 SD increase in inflammation composite score during midlife on occipital lobe, ventricular, and hippocampal volume to be similar to the effect associated with possession of a single APOE ?4 allele in our multivariable regression analyses. No association was found for the total brain, frontal lobe, temporal lobe, or parietal lobe volume (ps > 0.071). Our findings did not change meaningfully after excluding participants who regularly used anti-inflammatory medication during the follow-up period (table e-2) and after including participants who met the criteria for dementia at visit 5 (table e-3). For descriptive purposes, associations between individual inflammatory markers and AD signature region volume are provided in a table e-4. � 
An assessment of linear trend revealed that compared to individuals with 0 elevated (?75th %tile) inflammatory biomarkers at baseline (reference), those with 1�2 and 3�5 elevated biomarkers had lower AD signature region (p trend = 0.001), occipital lobe (p trend = 0.007), and hippocampal volume (p trend = 0.041) 24 years later (figure 1). Compared to the reference group, participants with 3 or more elevated markers demonstrated 5.3% smaller AD signature region volumes, 5.7% smaller occipital lobe volumes, and 4.6% smaller hippocampal volumes, on average. However, this pattern was not statistically supported for the total brain, ventricular, frontal lobe, temporal lobe, and parietal lobe volume (p trends >0.072). 
The modifying effects of age, race, and sex. A significant age-by-inflammation composite score interaction was found for the AD signature region, occipital lobe, and hippocampal volume (table 2). Because a reversal of association was observed at age 60 (figures 2, e-1, and e-2), we stratified the sample into young-midlife and old-midlife subgroups (<60/? 60). As displayed in table 2, the associations between higher midlife inflammation composite score and lower AD signature region, occipital lobe, and hippocampal volume at follow-up were significantly stronger among participants who were 60 or younger at baseline compared to those who were older than 60. A marginal race-by-inflammation composite score interaction was found for occipital lobe volume, whereby a higher midlife inflammation composite score was associated with lower occipital lobe volume among white, but not African American, participants (table 3). No interactions with sex were found (table e-5). � 
Inflammatory markers and episodic memory. Late-life episodic memory, which was associated with hippocampal and AD signature region volume after controlling for age (partial rs > 0.21, ps < 0.001), was reduced among participants with higher levels of the inflammation composite score. Each SD increase in inflammation composite score was associated with a ?0.08 SD performance decrement on the DWR after adjusting for covariates (CI ?0.15 to 0.00; p = 0.046). Similarly, a higher number of elevated inflammatory biomarkers at baseline was associated with reduced DWR performance (p trend = 0.009; figure 1). �
� 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. �
