Thyroid & Autoimmune Disease:
- Autoimmune thyroid disease
- Environmental factors
- Endogenous factors
- Accelerator hypothesis
- Selenium intake
- Iodine intake
The thyroid gland plays a major role in the human body; it produces the hormones necessary for appropriate energy levels and an active life. These hormones have a critical impact on early brain development and somatic growth. At the same time, the thyroid is highly vulnerable to autoimmune thyroid diseases (AITDs). They arise due to the complex inter- play of genetic, environmental, and endogenous factors, and the specific combination is required to initiate thyroid autoimmunity. When the thyroid cell becomes the target of autoimmunity, it interacts with the immune system and appears to affect disease progression. It can produce different growth factors, adhesion molecules, and a large array of cytokines. Preventable environmental factors, including high iodine intake, selenium deficiency, and pollutants such as tobacco smoke, as well as infectious diseases and certain drugs, have been implicated in the development of AITDs in genetically predisposed individuals. The susceptibility of the thyroid to AITDs may come from the complexity of hormonal synthesis, peculiar oligoelement requirements, and specific capabilities of the thyroid cell’s defense system. An improved understanding of this interplay could yield novel treatment pathways, some of which might be as simple as identifying the need to avoid smoking or to control the in- take of some nutrients.
Special Clinic News & Events
The thyroid gland is important in the human body because of its ability to produce hormones necessary for appropriate energy levels and an active life. These molecules have pleiotropic effects, playing critical roles in early brain development, somatic growth, bone maturation, and the mRNA synthesis of more than 100 proteins that constantly regulate each and every bodily function.
At the same time, the thyroid is highly vulnerable to autoimmune diseases. The incidence of chronic autoimmune thyroiditis (CAT) and Graves’ disease (GD) has in- creased dramatically over the past few decades, afflicting up to 5% of the general population. In children, CAT is the most common cause of acquired hypothyroidism in non-endemic goiter areas.
Initial studies on the association between early fetal nutrition and the pathogenesis of autoimmune thyroid diseases (AITDs) resulted in controversial data. In twin studies, Phillips et al.  found that among monozygotic twins the smaller twin had higher levels of thyroid per- oxidase (TPO) antibodies. However, these data were not confirmed in another twin study in which a larger cohort was analyzed . The ‘accelerator hypothesis’ and the influence of rapid childhood growth due to energy-dense food and adipokine imbalance have not been investigated in childhood AITDs. In both type 1 and type 2 diabetes, the accelerator hypothesis proposes a critical influence of obesity as an exogenous factor contributing to disease; even in a population of children with type 1 diabetes, the fattest presented with disease the earliest (evidence of true acceleration) . With regard to AITDs, other accelerators in addition to obesity include low selenium (Se) and a high iodine intake. Obese children are hyperleptinemic, and leptin, with its numerous functions including the promotion of cell-mediated immune responses, is a good candidate for contributing to the pathogenesis of autoimmune diseases. Obese children have been found to have increased interferon (IFN)- -secreting T helper cells and altered thyroid structure and hormonal status [4–8].
Autoimmunity is generally considered to be only a cause of disease; nevertheless, human T cell repertoires naturally comprise autoimmune lymphocytes. Autoimmune T cells can help heal damaged tissues, indicating that natural autoimmunity can also contribute to health and benefit self-maintenance . The immune system makes its decisions and acts by integrating multiple signals in an ongoing dialog with tissues. It is likely that the tissue itself provides signals that trigger the type of inflammation that is required for tissue self-maintenance and repair [9, 10].
Autoimmune disorders result from a complex interplay of genetic, environmental, and endogenous factors (fig. 1), and a combination of these factors is required to initiate thyroid autoimmunity [11, 12]. Recent advances in genome-wide studies have made it possible to efficient- ly identify complex disease-associated genes. Using both the candidate gene approach and whole-genome linkage studies, 6 AITD susceptibility genes have been identified and confirmed; the first group includes the immunomodulatory gene products HLA-DR, CD40, cytotoxic T lymphocyte-associated factor (CTLA-4), and protein tyrosine phosphatase 22 (PTPN22), and the second group includes the thyroid-specific gene products thyroglobulin (Tg) and thyroid-stimulating hormone receptor (TSHR). Genetic factors predominate, accounting for approximately 80% of the likelihood of developing AITDs, whereas at least 20% is due to environmental factors (fig. 1). In recent years, a number of excellent reviews have been published on the genetic background of AITDs [13, 14].
An increased frequency of AITDs is reported in Turner syndrome (TS) and in other nondisjunctional chromosomal disorders such as Down and Klinefelter syndromes. The theory that maternal autoimmunity may lead to the preferential survival of a fetus with chromosomal aneuploidy is attractive but remains unproven . The most prevalent autoimmune disorder in TS appears to be CAT, with a reported thyroid autoantibody incidence of 30– 50%. Hypothyroidism of autoimmune origin is so common in TS that almost every other TS woman will prob- ably develop hypothyroidism, and it increases with age [16, 17].
We know more about the minor details of AITDs, but the main question remains unanswered: why is the thyroid so prone to autoimmune disease? This review seeks to emphasize the role of the thyroid cell per se in AITDs and to focus attention on preventable exogenous factors.
Thyroid Cell Specificity
The thyroid cell produces a variety of immunologically active factors (table 1) and has complex nutrient requirements for hormonal synthesis and function (table 2), both of which influence susceptibility to AITDs. Thus, the thyroid cell is not just the innocent victim of an unchecked and disordered immune system. It is increasingly obvious that the target cells interact with the immune system, often in ways that seem defensive and protective, yet they can go awry and exacerbate autoimmunity under particular circumstances .
In most human autoimmune diseases, the events that trigger autoimmunity remain elusive. Most importantly, it is unclear whether autoimmunity results primarily from an immune defect, is secondary to target organ alterations, or both. The thyroid shows increased iodine uptake and oxidation prior to lymphocytic infiltration concomitant with decreased thyroid epithelial cell proliferation in vitro. Modifying thyroid function influences the development of thyroid autoimmunity . The thyroid cell, unlike other epithelial cells in the endocrine system, is unique because it releases hormonal products on its basal surface instead of its apical surface, thus allowing for the trafficking of precious iodine twice across the cell.
Thyroid cells are capable of producing different factors (table 1), including IGF I, IGF II, and EGF, that can stimulate angiogenesis. The half-life of these molecules is short and they induce only local (non-systemic) effects. Stimulated thyroid follicular cells secrete several growth factors . The expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-3 (LFA-3) by thyroid cells is enhanced by IFN- , tumor necrosis factor (TNF), and interleukin (IL)-1. Thyroid cells express CD44, which acts as a homing receptor for hyaluronan, mediates leukocyte rolling (the first step in tissue homing), and may (like ICAM-1) induce lymphocyte activation under certain circumstances. Thyroid cells are now known to produce many cytokines (especially after stimulation with IL-1), including IL-1, IL-6, IL-8, IL-12, IL-13, and IL-15 . Activated lymphocytes can produce TSH, which could have a variety of implications .
Low dose tolerance can easily be broken, and the thyroid is not well tolerated by the immune system. Auto- antigens in AITDs, as in other autoimmune endocrine diseases, include tissue-specific membrane receptors, enzymes, and secreted hormones. Mixed cellular and anti- body autoimmune responses are likely pathogenic to some degree. Circulating anti-Tg autoantibodies are also found in GD and CAT, as are autoantibodies to triiodothyronine (T3) and thyroxine (T4). The human (h) TSHR is the primary antigenic target in autoimmune hyperthyroidism . The TPO autoantibody seems unlikely to have much pathogenic importance as it has limited access to TPO in vivo due to its location inside the cell. Further- more, anti-TPO autoantibodies do not inhibit the activity of the enzyme. Thus, their clinical value is principally to document thyroid gland autoimmunity. However, TPO may act as a hidden antigen because it is not adjacent to the vasculature.
In humans, excess thyroid hormone results in the attenuation of natural killer (NK) cell activity, which in theory could lead to the continuation of an autoimmune disorder. Upon return to a euthyroid status and the resulting normalization of NK activity, a reversion to control of the abnormal immune reaction would occur with perpetuation of GD. Additionally, an anti-idiotype might function as an agonist for the original antigen. Thus, an antibody to an antibody (anti-idiotype) to TSH might bind to the TSHR and stimulate the thyroid . A more likely hypothesis is that anti-idiotypic antibodies are rarely produced at a detectable level. Hodkinson et al.  recently found a positive association between thyroid hormone concentration and NK-like T cells in the elderly. This relationship has not been investigated in young patients.
Antigen Presentation By The Thyroid Cell
Bottazzo et al.  first suggested that antigen presentation by HLA-DR-expressing thyroid cells may be a critical aspect of thyroid autoimmune disease. It quickly became apparent that the only stimulus able to induce MHC class II expression on thyroid cells was the T cell cytokine IFN- . Normal cells respond exactly the same as AITD thyroid cells to IFN- , and in animal models of AITDs class II expression on thyroid cells is always followed by the appearance of lymphocytes in the gland. In addition to inducing MHC class II expression, IFN- increases MHC class I expression on thyroid cells, thus allowing potential for the recognition of thyroid cells by cytotoxic CD8+ T cells .
It is possible that direct antigen presentation by the thyroid cell itself may occur in individuals who inherit thyroid-reactive T cells; such a circumstance would effectively bypass the classical macrophage-processing mechanism. The HLA-DR antigen-expressing thyroid cell may be as effective as the macrophage at presenting thyroid- specific antigens to the immune system , but the thyroid cell is incapable of supplying the costimulatory signals that professional antigen-presenting cells (APCs) do . Any stimulus that causes increased DR expression on thyrocytes, such as IFN- produced by T cells in response to infection, combined with increased TSH stimulation may allow thyrocytes to function as APCs. Although thyroid cells may perform this function poorly, they are numerous and localized in one area, therefore allowing for increased production of the already established normally occurring low levels of antibodies .
A number of environmental factors have been implicated in the development of AITD in genetically predisposed individuals, including high iodine intake, Se deficiency, pollutants such as tobacco smoke, infectious dis- eases, certain drugs, and physical and emotional stress [26–30]. Herein, we focus on these preventable triggers. Individual susceptibility suggests that, in addition to genetics, some endogenous factors are also important to the development of AITDs, such as growth spurts in childhood, puberty, pregnancy, menopause, aging, and gender (fig. 1, 2).
Dietary iodine plays an important role in the expression of AITDs. Epidemiological studies have suggested that AITDs are more common in areas of iodine sufficiency than in areas of iodine deficiency and that general increases in AITDs occur in parallel with increases in dietary iodine. CAT is less common in countries with a low iodine intake .
The thyroid requires the right amount of iodine. Either too much or too little causes problems. Too little io- dine brings all of the adaptive immune mechanisms of the thyroid into play, but despite these responses iodine deficiency disorders may still result. Too much iodine also affects the thyroid. Protective mechanisms include diminished trapping of iodide by the thyroid and de- creased iodide organification. In experimental thyroiditis several types of Tg epitopes have been found, including some containing iodine and/or hormones as well as some conformational epitopes. Experimentally increasing the iodination of Tg makes the protein more antigen- ic [28, 31]. Optimally, the iodine intake of a population should be kept within a relatively narrow interval that prevents iodine disorders, but not higher .
The mechanism of action of iodine in contributing to thyroid autoimmunity is not clear. Iodine may stimulate B lymphocytes to increase the production of immunoglobulin and thus induce AITDs by enhancing the activity of lymphocytes that have been primed by thyroid- specific antigens . Iodine may enhance the antigen- presenting capabilities of macrophages, resulting in increased macrophage activity and enhanced lymphocyte stimulation. In addition, a high iodine intake in- creases the iodine content of the Tg molecule, which may increase its immunogenicity . Lastly, iodine may provoke thyroid follicular cells to become APCs and thus potentiate AITDs by turning genetically predisposed normal thyrocytes into antigen-presenting thyrocytes.
Table 2 shows several minerals and trace elements that are essential for normal thyroid hormone metabolism. The role of these elements in childhood AITDs has not been well investigated.
The second factor that has been strongly implicated in the development of autoimmune thyroiditis is the trace element Se. Se is a constituent of selenoproteins (SePs), in which it is incorporated as selenocysteine. Relevant actions of Se and SePs include antioxidant effects, appropriate functioning of the immune system, antiviral effects, influence on fertility, and a beneficial effect on mood . Se deficiency is thought to be involved in the pathogenesis of autoimmune thyroiditis by lengthening the duration and exacerbating the severity of the disease; these effects may occur via reduced activity of the SeP glutathione peroxidase, which leads to an increased production of hydrogen peroxide. Another important class of SePs are the iodothyronine selenodeiodonases D1 and D2, which are responsible for producing biologically active T3 via 5 -deiodination in extrathyroidal tissues [33, 34].
Combined Se and iodine deficiencies lead to myxedematous cretinism. Adequate Se nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage from excessive iodine exposure. In regions having severe combined deficiencies of iodine and Se, it is mandatory to normalize the Se supply before the initiation of iodine supplementation to prevent hypothyroidism .
In celiac disease, the inability to absorb Se may modulate SeP gene expression and promote intestinal mucosal damage, and this deficiency could additionally predispose to complications such as AITDs [34, 36].
Derumeaux et al.  discovered an inverse association between Se status and thyroid volume and echo- structure in French adults and concluded that Se may protect against AITDs. Duntas et al.  found beneficial effects when treating patients with autoimmune thyroiditis with selenomethionine for 6 months due to its ability to reduce anti-TPO antibodies. In the group treat- ed with LT4 combined with Se, these effects were very prominent in the first 3 months and were further sustained after 6 months of treatment. A striking majority of the patients reported an improvement in mood and well-being.
Various environmental toxins and pollutants have been implicated in the induction of AITDs.
Polyhalogenated biphenyls are commonly used com- pounds with a wide variety of industrial applications. Polybrominated biphenyls are flame retardant, and polychlorinated biphenyls (PCBs) are used as lubricants, adhesives, inks, and plasticizers. PCBs are known to accumulate in lakes and rivers and subsequently in the adipose tissue of fish and humans . These compounds might trigger AITDs by interfering with iodide transport and inducing oxidative stress. There is evidence that peri- natal PCB exposure decreases thyroid hormone levels in rat pups. In adults, adolescents, and children from highly PCB-exposed areas, the concentration of PCBs in blood samples negatively correlated with levels of circulating thyroid hormones [39, 40]. Populations with long-term exposure to PCBs have increased prevalences of anti-TPO antibodies, which is probably related to the immunomodulatory effects of PCBs. Pollutants from car emissions and heavy industry as well as coal pollution and agricultural fungicides are also implicated in AITD development [26, 27].
Smoking is associated with an increased risk of developing GD and with a reduced remission rate after thionamide treatment. Even more striking is the effect of smoking on Graves’ orbitopathy, which tends to be more severe in smokers [32, 41]. Smoking might contribute to the pathogenesis of GD by altering the structure of the thyrotropin receptor, making it more immunogenic and leading to the production of thyrotropin receptor-stimulating antibodies that react strongly with retroorbital tissue . Smoking induces the polyclonal activation of B and T cells and increases presentation of antigens by damaged cells. Hypoxia may play a role in Graves’ orbitopathy because retrobulbar fibroblasts show a significant increase in proliferation and glycosaminoglycan production when cultured under hypoxic conditions [42, 43]. The effects of parental smoking on thyroid function in fetuses or 1-year-old infants  provide additional insight into the interrelationship between smoking and thyroid dysfunction. The latter study found that infants whose mothers and fathers smoked had higher cord serum concentrations of Tg and thiocyanate than did infants whose parents did not smoke. The clinical picture observed in adolescents exposed to passive smoking could be due to direct stimulation of sympathetic nervous activity by nicotine in addition to the smoking-induced increase in thyroid hormone secretion .
The association of smoking with CAT is less well defined. Although a relationship with autoimmune hypothyroidism or postpartum thyroiditis has been reported, this finding was not supported by meta-analysis of the published papers [32, 45].
In some individuals, autoimmunity is the price that must be paid for the eradication of an infectious agent. Infections have been implicated in the pathogenesis of several autoimmune, endocrine, and non-endocrine diseases. Either viral or bacterial infections might represent a risk factor for the development of AITDs. Viruses have long been suspected as etiological agents in many auto- immune diseases, including AITDs; moreover, a viral cause of AITDs, infecting either the thyroid or immune cells, has been demonstrated in an avian model. Although viruses may be likely etiological agents in human AITDs, this possibility remains unproven [25, 27, 30].
An increased frequency of antibodies to the influenza B virus has been observed in a group of patients with thyrotoxicosis. In addition, virus-like particles have been found in the thyroids of chickens with autoimmune thyroiditis, with similar particles detected in the thyroids of humans. Serological evidence of prior staphylococcal and streptococcal illnesses has been described in a few patients with AITDs .
Some of the strongest evidence linking infectious agents to the induction of AITDs has been the association of Yersinia enterocolitica infection with thyroid disease. This Gram-negative coccobacillus commonly causes diarrhea along with a variety of abnormalities that suggest autoimmune disease, including arthralgias, arthritis, erythema nodosum, carditis, glomerulonephritis, and iritis. Weiss et al.  demonstrated that Y. enterocolitica had a saturable, hormone-specific binding site for the mammalian TSH that resembled the receptor for TSH in the human thyroid gland.
An immune response against a viral antigen that shares homology with the TSHR may be the inductive event that ultimately leads to TSHR autoimmunity . A significant association between hepatitis C and AITDs has been found. Anti-TPO antibody titers have been shown to increase at the end of treatment with IFN- in patients with the hepatitis C virus, and these patients were more susceptible to AITDs than were hepatitis B patients. These patients should be screened for autoimmune thyroiditis before and after IFN treatment [47, 48].
Infection might induce an autoimmune response by various mechanisms, such as molecular mimicry, polyclonal T cell activation by microbial superantigens, and increased thyroid expression of human leukocyte anti- gens . Inflammation induced by viral infections or by pollutants can modify cell signaling pathways and influence T cell activity and cytokine secretion profiles .
Several drugs have been implicated in the pathogenesis of AITDs. Amiodarone is an iodine-containing drug with diverse effects on thyroid function. Serum titers of TPO antibodies are elevated in approximately half of the patients who develop amiodarone-induced hypothyroid- ism. Amiodarone has also been shown to affect T cell function . Thyroid antibodies disappeared from the circulation 6 months after amiodarone discontinuation .
Lithium, a psychopharmaceutical and well-known goitrogen, has been shown to inhibit thyroid hormone release. Antithyroid antibodies are found more frequently in psychiatric patients on lithium therapy than in similar psychiatric patients treated with other drugs. Lithium-induced increases in serum TSH concentrations might enhance autoantigen expression on the surface of thyrocytes, thereby exacerbating autoimmune responses [32, 50].
Other agents involved in thyroid autoimmunity are IL-2 (thyroid autoimmune phenomena with or without hypothyroidism), IFN- (thyroid dysfunction, hypothyroidism, and occurrence of thyroid autoantibodies), highly active antiretroviral therapy (HAART; possible occurrence of thyroid autoimmune phenomena and dysfunction), and Campath-1H, a humanized monoclonal antibody targeting the CD52 antigen on lymphocytes and monocytes that is used after transplantation (occurrence of GD) .
Although numerous anecdotal reports have associated the onset of AITDs, and particularly GD, with stressful events, objective evidence has been difficult to obtain. Both psychological stress, such as bereavement, and physical stress, such as trauma or major illness, have been implicated .
Neuroendocrine immune mechanisms responsible for the putative effects of stress on the onset and course of GD are poorly defined, but they might include activation of the HPA axis (although this should cause immunosuppression) and a shift from a Th1 (cell-mediated) immune response to a Th2 (humoral) immune response [32, 51].
Additionally, heat shock proteins (HSPs), which are well-known stress proteins, could share epitopes with the TSHR. Heufelder et al.  found that high levels of HSP- 72 expression in AITDs may reflect a state of chronic cellular stress, but this finding could also indicate an immunomodulatory function of HSP-72 in AITDs. HSPs are ubiquitous, highly conserved proteins that are expressed in response to a wide variety of physiological and environmental insults. They allow cells to survive otherwise lethal conditions. HSPs have been postulated to be critical antigens in both autoimmune diseases and experimental models of autoimmunity [53, 54].
Improving stress by the prolonged use of bromazepam has been shown to increase the remission rate of hyper- thyroidism after a thionamide course . The relation- ship between stress and CAT is less evident. Graves’ patients might be stressed because of hyperthyroidism and not hyperthyroid because of stress, whereas CAT patients are not stressed because they are euthyroid or hypothyroid . Whatever the mechanism of action, stress may cause decompensation in a genetically susceptible individual and lead to the induction or exacerbation of an AITD.
Pregnancy And Postpartum
AITDs tend to be more frequent in women. The reason for this gender-related difference is not clear and is not explained by the additional X chromosome in females . The possibility that genes responsible for immune responses are located on the X chromosome has been considered but not confirmed. Sex steroids could modify immune responses by acting directly on immune cells. Estrogens are well-known stimulators of TSH secretion, which could enhance HLA-DR expression. Parity per se does not seem to play a significant role [32, 56].
The accumulation of fetal cells in the maternal thyroid gland during pregnancy (painless postpartum thyroiditis) may induce autoimmune thyroiditis . Pregnancy is accompanied by a suppression of the immune system with a shift in the Th1/Th2 balance towards Th2 immunity, a process that is aimed at protecting the fetus. A possible link between pregnancy and the postpartum occurrence of AITDs might be represented by fetal microchimerism. Fetal cells pass into the maternal circulation and may persist in the maternal blood. Microchimerism of presumed fetal origin has been shown in thyroid tissue specimens of women with previous pregnancies, particularly in those with AITDs. The persistence of activated intrathyroidal fetal cells might influence thyroid autoimmunity in genetically susceptible women by modulating or even initiating maternal immune responses in a graft- versus-host reaction upon termination of pregnancy-re- lated immune suppression. It cannot presently be ruled out, however, that intrathyroidal fetal cells are only innocent bystanders and do not participate in triggering or exacerbating thyroid autoimmune responses [32, 54, 58]. Mothers who have given birth to sons have thyroidal Y chromosome-positive cells more frequently if they are affected by either CAT or GD than if they have thyroid adenomas .
The presence of elevated TPO antibodies in about 10% of pregnant women is associated with an increased risk of miscarriage, gestational thyroid dysfunction, and postpartum thyroiditis . Maternal-to-fetal transfer of TSHR antibodies with polyclonal activity and a different half-life can lead to a transient perinatal thyroid dysfunction, opposite to a maternal one .
A rapidly growing body of evidence on the interplay between genetic, environmental, and endogenous factors has expanded our knowledge of the complex etiopathogenesis of AITDs. Autoimmune thyroid disorders are examples of common diseases in which immunogenetic factors play an important role.
The thyroid cell itself appears to play a major role in disease progression by interacting with the immune system. The complexity of hormonal synthesis, unique oligoelement requirements, and the specific capabilities of the thyroid cell defense system probably make the thyroid prone to AITDs. The initial insult to the human thyroid gland that activates the onset of AITDs remains un- known and seems to be strongly individual. Understand- ing more about the interaction between genes and the environment could yield entirely novel pathways, some of which might be as simple as identifying the need to avoid smoking or to control the intake of particular nutrients. Evidence for many causal agents is, however, scarce, and more data are certainly required. We believe that it is particularly important to draw attention to this problem in pediatric patients. Lessons learned from the enigmatic questions raised in AITD studies could clarify the pathogenesis of other organ-specific autoimmune disorders.
L. Saranac S. Zivanovic B. Bjelakovic H. Stamenkovic M. Novak B. Kamenov Pediatric Clinic, University Clinical Center, Nis, Serbia
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MEET THE STAFF
These canons of professional ethics are based upon fundamental principles of moral and professional behavior and recommended for all doctors of chiropractic and chiropractic assistants. The following basic principles should be guiding factors in the practice of chiropractic and upheld at all times:
Consider the well-being of the patient. The primary effort and ultimate goal is for the greatest good of our patients.
- Dr. Alexander D. Jimenez D.C., C.C.S.TChief Clinical DirectorPhone: 9155408444Email: email@example.com
Specializing in Severe Pain: Sciatica, Neck-Back Pain, Whiplash, Headaches, Knee Injuries, Sport Injuries, Dizziness, Poor Sleep, Arthritis. We use advanced proven therapies focused on optimal mobility, health, fitness, and structural conditioning. We use Patient Focused Diet Plans, Specialized Chiropractic Techniques, Mobility-Agility Training, Cross-Fit Protocols and the "PUSH System" to treat patients suffering from various injuries and health problems.
Message from: Dr. Alex Jimenez D.C., C.C.S.T
( Biography and my promise to you )
My name is Dr. Alex Jimenez, I am Chiropractic Doctor specializing in advanced therapies focused on total joint health, strength training and complete fitness conditioning. We use patient Focused Diet Plans, Advanced Chiropractic Techniques, Agility Training, Cross-Fit and the PUSH System to treat patients suffering from various injuries and health problems. Our goal too is to help your body heal itself naturally. When your body is truly healthy, you will arrive at your fitness level and proper weight efforlessly. We want to help educate you on how to live a new and improved lifestyle. Our doctors have spent over 25+ years researching and testing methods with thousands of patients. We strive to create fitness and better the body through researched methods and total programs...
My goal too is to help the body heal itself naturally. When your body is truly healthy and balanced, you will move pain free and ultimatly arrive at your optimal fitness levels and proper weight effortlessly. We want to help educate you on how to live a new and improved lifestyle. Our doctors have spent over 25 years researching and testing methods with thousands of patients. We strive to create fitness and better the body through researched methods and total programs. These programs are natural, and use the body's own ability to achieve goals of improvement, rather than introducing harmful chemicals, controversial hormone replacement, surgery, or addictive drugs. We want you to live a life that is fulfilled with more energy, positive attitude, better sleep, less pain, proper body weight and educated on how to maintain this way of life.
The focus on spinal and skeletal adjustments is what makes doctors of chiropractic unique in their approach to treating patients with spinal complaints. This hallmark chiropractic adjustment, however, is not the only procedure a chiropractor may employ in managing a patient's care. I am very proud to bring my patients a variety of treatment options beyond the typical scope of care. With the advances in physical therapies and modalities we bring El Paso option that better aid in the rehabilitation process. Tissue healing is a wonderful process that begins the moment an injury occurs. How the injury is managed determine the final outcome in terms of healing. It is critical we implement immediate procedures as soon as we can in order to gain optimal recovery. The old day of let it rest until it gets better is not the only option.
Letting it rest may even be an irresponsible approach considering what we now know. The implementation of active and movement based treatments have clearly shown increased and improved outcomes in many instances.
As a doctors focused on the greater good for a patient, we must assess each patient individually and apply the appropriate protocols. It is also very important to denote, that El Paso has fine doctors in many specialties of healing and repair. The direct relationship we have with specialist of these disciplines is clearly what allows us to bring the highest quality of care to our patients.
My promise to my patients is clear for all to read here. I, with Gods help, will do what ever it takes to assist you in your recovery. I too will draw upon all the specialist in this town to find you the collaborative care that is required with the disorders being tended to.
With Great Regards to you.Read moreRead lessEducation:
Affiliations and Certifications:
- Texas Chiropractic Association
- Chiropractic Care
- Physical Therapy
- Strength Training
- Crossfit Doctor
- Return to Competition Rehabilitation
- Truide TorresExecutive Director / Patient LiasonPhone: 9152526149Email: firstname.lastname@example.org
Director: Patient Relations Advocate Dept.
Truide has been working for the past 20 years in claims resolutions. She works hand in hand with patients and is availible to resolve dispute resolutions.
Truide Torres (Bio)
Driven by the passion of doing what is in the best interest of the patient, I wake up every morning with the drive to help those in need. The claims process for health care is full of pits, valleys and difficult obstacles designed to strike fear in those in need. My duty is to do what is within the confines of the law, "what ever it takes" to get those involved to pay attention to those who need help. That is what I am honored to do for our patients.
Personally, I have seen great injustices transpire on those that do NOT have a voice. Whether, a language barrier or just not knowing the rules. My job is to find out how I can help. If I personally can not help, I will find the right sources to open the possibilities. I get the job done.
As a wife and mother of 2 children, 3 dogs and 2 Cats. My passion is for God, Family and the mission of serving my fellow man.
Let it be clearly stated... I am here to help. My phone 915-850-0900Read moreRead less
- Daniel AlvaradoExercise PhysiologistPhone: 9152038122Email: email@example.com
Daniel Alvarado is the owner and the top trainer at PUSHasRx® CrossFit Fitness Facility. Since becoming a Trainer Daniel has kept up to date on many continuing educational classes, ensuring that his clients receive the most comprehensive and advanced training. Working directly with the Doctors, he develops and collaborates on care plans that are patient specific. No patient ever gets the same clinical protocol. His expert clinical kinesiology experience spans over 2 decades. He has trained injured patients and NCAA National Champion Athletes. His technical ability to create programs that are clinically sound and second to none. He too has used his physical therapy and recovery experience to take broken top tier athletes into strict recovery protocols assisting them to achieve highly competitive national championships. He certainly will not admit it but, he is a top national champion trainer. Daniel, also develops youth programs that are sport specific to aid young athletes achieve great success. His mastery of clinical recovery is applied applied to all patients and top tier athletes alike. All patient programs are specifically designed with patient focused recovery priorities. He is happily married to beautiful Victoria Alvarado has one child. He enjoys strength training, movies, singing, conducting, writing poetry and being a CrossFit champion. Just a way cool dude. We think you will agree.Read moreRead less
- Dennise AcostaHead Office ManagerPhone: 915-850-0900Email: firstname.lastname@example.org
Dennise has been at Injury Medical & Chiropractic Clinic for four years. Known as the master multi-tasker. Dennise, handles patient care from the moment you walk in the door. She is akin to the air traffic controller. She will assist you in matter requiring clinical preparation and effective inter-office communication. She unifies all department and clinical providers making sure all important information reaches all clinicians in a timely manner. She also loves to work out, stay in shape, watch movies and help people.Read moreRead less
- Sandra MartinezHead Clinical TherapistPhone: 915-850-0900Email: email@example.com
Sandra has been working at Injury Medical & Chiropractic Clinic for over 5 years. As the head Licensed Massage Therapist, she manages and directs critical aspect of clinical care. The patients love her ability to make you laugh while removing those pesky trigger points causing pain. She is able to relax and bring comfort to all she touches. There just simply is no patient that escapes her talented touch. Trained in advance myofascial techniques, she is an integral part of patient recovery. You will never see anything but a kind smile and resolute persona ready to correct your condition and aid in your recovery. She definitely enjoys helping people, has 1 dog and loves movies. She loves flowers too.Read moreRead less
- AlejandraBilling AgentPhone: 915-850-0900Email: firstname.lastname@example.org
Alejandra works in accounts & billing. She is the radar of the bunch. Nothing appears to escape her mind. Highly intelligent and appears not to need a computer for recall of facts. She provides information retrieval for patients and clinical staff. She has been at Injury Medical & Chiropractic Clinic for three years and ready for any task at hand. She performs interoffice communications with attorneys and medical director of ancillary offices. She loves her family and places know how to prioritize well.Read moreRead less
- Mike ContrerasPersonal TrainerPhone: 915-203-8122
Big Mike was born and raised in El Paso and is an excellent personal trainer and CrossFit coach. Mike works hand in hand with each patient’s clinical care plan in order to achieve optimal outcomes. A trusted clinical representative of the PUSHasRx System along with his advance protocols. Mike not only trains the injured and recovering. Mike is a sincere human that has great talent of brining out the best in every individual he works with. He will never admit it, but we will share with you a secret. He with his God given talents trains the greatest athletes and champions in El Paso. Many champions in our community know of his commitment. As a youth, he also played football (wide receiver), basketball, and track at Bel Air High School. Educated in Clinical Human Kinesiology at UTEP and loves playing football and basketball with his little nephews in his free time. Mike has three sisters and one brother, most of which live nearby in El Paso. When he’s not watching the Cowboys or Spurs play, he’s usually lifting, sleeping or watching movies. We are blessed to have this soul on our team.Read moreRead less
- Alexander Isaiah JimenezCollegiate Athletic Consultant & NCAA Wrestling ChampionPhone: 915-820-9443Email: email@example.com
Alexander Isaiah Jimenez leads the power and agility education programs for the high school athletes. While still studying for his medical degree he provides physical performance testing in order to collaborate with clinicians. He is gifted in creating physical performance programs no matter what the clinical presentation is. As national fitness champion and collegiate wrestler, he too understands what performing at high levels entails. He too has had to recover from debilitating injuries only to return better then before an win national titles. He understand how the recovery process is different for clients, patients and extreme athletes. We are blessed to have his counsel.Read moreRead less
- Ethan PadillaPersonal Trainer & Strength CoachPhone: 915-203-8122
Ethan was born and raised in El Paso and is one of our most outgoing and friendly coaches. Ethan earned his nickname “rampage Ethan” from his years at El Dorado High School, where he played inside linebacker. He has placed twice in the Strongman Competition and also recently competed in the Desert Games with his fellow PUSH Athletes as a team and placed 4th overall! Ethan is currently pursuing his Bachelor’s Degree in Kinesiology at UTEP. His focus on clients is obvious to all. Ethan is able to manage very large groups of individuals like no other. His awareness of the dangers while exercising is his greatest concern. When he’s not coaching or studying for class, he likes to spend time with his family (who are here in El Paso) or with his weimaraner puppy. Fun fact: Ethan loves any food with sprinkles (especially donuts with sprinkles) and is a diehard Seattle Seahawks fan.Read moreRead less
- AndresRecovery & Nutrition
Andres has been at PUSHasRx for two years. He brought his company Recovery and became the official juicer. Andy will fix you right up. Andres, will make sure that your nutritional recovery programs fits within your standards. Also, there is great care in making sure the nutritional requirement are clinically met. Patients and high performance athletes depend on high performance nutritions. Upon your completion of the physical medicine portion of therapy you will be offered specialized organic recovery drinks and supplementation to help aid in your recovery. You will be confident that from your pushing to recovery, you will be taken care of.Read moreRead less
- Iylene AvalosPUSHasRx TrainerPhone: 915-203-8122
ylene has been working with us for over 4 years. In her spare time she enjoys working out and running. She has 2 dogs and loves movies. Iylene is extremely aware of body mechanics and mindfully watches rehabilitation movements. She is always standing ready to assist and respond to client needs. Her commanding voice is always clear to all, no matter what floor you are on. Iylene is always ready and willing to answer any question you may have regarding fitness and recovery.Read moreRead less
- Rick CanoPersonal Trainier Level VPhone: 915-203-8122
Most early-rising PUSHasRx members know Rick well as a fantastic coach who focuses strongly on form and will always make you laugh. He was born and raised in El Paso and loves to train his athletes and coach CrossFit. Rick is a very diligent, kind and considerate trainer. He is always mindful of client techniques and aware of client goals. When he’s not coaching, Rick loves to work on cars, especially his ’69 Chevelle (his next car will hopefully be a ’69 Charger). He not only became a certified Automotive Mechanic at 17, but while working on his certification at EPCC, he won 1st place in a bench competition when he was 16 (approx. 56 reps at 155#). His favorite movements are clean & jerks and snatches. He loves oreos (eats them every night), loves watching the CrossFit games, and loves his three bulldogs. He spent one year full-time personal training before he started coaching CrossFit two years ago. He is CrossFit Level 1 Certified and hopes to get his Level 2 Certification soon. Rick has competed in several competitions, including WOD for Toys in 2014, where his team placed 1st.Read moreRead less
- Astrid OrnelasBlogger/Research/CuratorPhone: 915-850-0900
Astrid has been at Injury Medical & Chiropractic Clinic for about three years. Astrid has taken her love for writing to an new level. She is a gifted and talented copywriter able to create amazing storylines. She creates content for patient consumption. She is able to bring words to life in a way that perplexes even the elite authors of the day. She loves nutrition and the healing power of clean eating. A naturalist at heart you will never see her eating processed foods that would be contra to clean living. She enjoys movies and creating storylines for Anime.Read moreRead less
- AdamVideographer & Graphics SpecialistPhone: 915-850-0900
Adam has been at Injury Medical & Chiropractic Clinic for about a year. He enjoys designing and various forms of art. A story teller by trade he can see things people don’t see until his masterpieces are revealed. Adam is a director of many medias using the top graphics, audio and video medias to tell the story of our patient. Modest to the core, you would never know what he is about to create. We are blessed to have his talents telling the world about Chiropractic using any and all medias available.Read moreRead less
- Our PassionsEmail: firstname.lastname@example.org
We Welcome You 👊🏻.
Purpose & Passions: I am a Doctor of Chiropractic specializing in progressive cutting-edge therapies and functional rehabilitation procedures focused on clinical physiology, total health, functional strength training and complete conditioning. We focus on restoring normal body functions after neck, back, spinal and soft tissue injuries.
We use Specialized Chiropractic Techniques, Balanced Diet Plans, Agility Training programs, Cross-Fit techniques, the PUSH-Rx Rehabilitation System and a highly specialized program for our Veterans.
We've been blessed to use our methods with thousand of El Pasoans over the last 27 years. This has allowed us to improve health and restore true fitness through researched non-surgical methods and wellness programs. These programs are natural and use the body's own ability to achieve goals of improvement, rather than introducing harmful chemicals, controversial hormone replacement, surgery, or addictive drugs. We want you to live a life that is fulfilled with more energy, positive attitude, better sleep, less pain, proper body weight and informed on how to maintain this way of life.
As an extension to dynamic rehabilitation, we too offer our patients, disabled veterans, athletes, young and elder a diverse portfolio of strength equipment, high performance exercises and advanced agility options. We are very proud to have teamed up with the cities premier therapist and trainers in order to provide high level competitive athletes the option to push themselves to their highest abilities within our facility.
Come learn how to improve your health for yourself and your loved ones.
With a bit of work, we can achieve optimal health together, no matter the age or disability.
Its all about: LIVING, LOVING & MATTERING! 🍎
2 CONVENIENT LOCATIONS:
(LOCATION#1) CENTRAL ELPASO:
6440 Gateway East, Suite B
(LOCATION#2) EAST SIDE ELPASO:
11860 Vista Del Sol, Suite 128
PHONE: 915-850-0900 ✔️Read moreRead less