Clinic Wellness Team. A key factor to spine or back pain conditions is staying healthy. Overall wellness involves a balanced diet, appropriate exercise, physical activity, restful sleep, and a healthy lifestyle. The term has been applied in many ways. But overall, the definition is as follows.
It is a conscious, self-directed, and evolving process of achieving full potential. It is multidimensional, bringing together lifestyles both mental/spiritual and the environment in which one lives. It is positive and affirms that what we do is, in fact, correct.
It is an active process where people become aware and make choices towards a more successful lifestyle. This includes how a person contributes to their environment/community. They aim to build healthier living spaces and social networks. It helps in creating a person’s belief systems, values, and a positive world perspective.
Along with this comes the benefits of regular exercise, a healthy diet, personal self-care, and knowing when to seek medical attention. Dr. Jimenez’s message is to work towards being fit, being healthy, and staying aware of our collection of articles, blogs, and videos.
Vascular biology, endothelial and vascular smooth muscle as well as cardiac dysfunction play a primary role in hypertension, cardio-vascular disease and target organ damage. Nutrient-gene interactions and epigenetics are predominant factors in promoting positive and negative effects in cardiovascular health and hypertension. In a series of research studies correlated to cardiovascular disease and hypertension, Dr. Mark C. Houston, MD, discussed the role that vascular biology and nutraceuticals play in relation to treatment of hypertension and cardiovascular disease.
What is the cause of cardiovascular disease and hypertension?
Vascular disease can appropriately be described as the balance between vascular injury and vascular repair (Figure 1). The endothelium is strategically found to be closely associated to the bloodstream as well as the vascular smooth muscle and it is also in charge of discharging a variety of substances in order to preserve vascular homeostasis and health (Figures 2 and 3). Numerous irritations which can provoke damage or harm to the endothelium, can lead to endothelial dysfunction, or ED, and can cause hypertension and other cardiovascular diseases.
Hypertension might be a hemodynamic indication of a damaged or injuried endothelium and vascular smooth muscle which could be connected to definite inflammation responses, oxidative stress and immune dysfunction of the arteries leading to ED, vascular and cardiac smooth muscle disorder, loss of arterial elasticity together with reduced arterial compliance and increased systemic vascular resistance. Hypertension is a significant outcome of the interaction between environmental factors and genetics. Macronutrients and micronutrients are crucial in the regulation of blood pressure, or BP, following target organ damage, or TOD. Nutrient-gene interactions, subsequent gene expression, epigenetics, oxidative stress, inflammation and autoimmune vascular dysfunction have positive or negative influences on vascular biology in humans. Endothelial activation with endothelial dysfunction and vascular smooth muscle breakdown, or VSMD, can ultimately trigger and continue to stimulate the development and growth of hypertension.
Macronutrient and micronutrient deficiencies are extremely common in the general population and may be even more common in individuals with hypertension and cardiovascular disease associated with genetics, environmental factors and even prescription drug and medication usage. These deficiencies have an enormous impact on cardiovascular health issues, such as hypertension, myocardial infarction, or MI, stroke and renal disease. The diagnosis and treatment of those deficiencies will reduce BP and improve ED, vascular biology and health, as well as cardiovascular function.
Epidemiology
Epidemiology,�the branch of medicine that deals with the incidence, distribution, and possible control of diseases and other factors relating to health, emphasizes the role of diet and related nutritional intake when it comes to hypertension and cardiovascular disease. The transition from the Paleolithic diet to our modern diet has produced an outbreak of nutritionally-related diseases (Table 1). Hypertension, atherosclerosis, coronary heart disease, or CHD, MI, congestive heart failure, or CHF, cerebro-vascular accidents, or CVA, renal disease, type 2 diabetes mellitus, or T2DM, metabolic syndrome, or MS, and obesity are several examples of those diseases. Table 1 contrasts intake of nutrients included during the Paleolithic Era and modern time, involved in the regulation of blood pressure, or BP. An unnatural and unhealthy nutritional selection process has been established by evolution from a pre-agricultural, hunter-gatherer milieu into an agricultural, refrigeration society. In sum, diet has changed more than our genetics can adapt.
The human genetic makeup is approximately 99.9 percent that of our Paleolithic ancestors, however our nutritional, vitamin and mineral intakes have vastly changed. The macronutrient and micronutrient variations, oxidative stress from radical oxygen species, or ROS, and radical nitrogen species, or RNS, and inflammatory mediators, such as cell adhesion molecules, or CAMs, cytokines, signaling molecules and autoimmune vascular dysfunction of T cells and B cells, have contributed to the greatest prevalence of hypertension and other cardiovascular diseases through complex nutrient-gene interactions, epigenetic and nutrient-caveolae interactions and nutrient responses with pattern recognition receptors from the endothelium (Figure 4). A decrease in endothelin coupled with endothelial activation, increase in angiotensin II and nitric oxide bioavailability can cause coronary artery disease and vascular disease as well as hypertension. Poor nutrition, together with obesity and a sedentary lifestyle have led to an exponential increase in nutritionally-related ailments. In particular, the high Na+/K+ ratio of contemporary diets has contributed to hypertension, CVA, CHD, MI, CHF and renal disorder as have the relatively low intake of omega-3 PUFA, increase in omega-6 PUFA, saturated fat and trans fatty acids.
Pathophysiology
Vascular biology plays a major role in the initiation and perpetuation of hypertension. Oxidative stress (both ROS and RNS), inflammation and autoimmune vascular dysfunction (both T cells and B cells) are the primary pathophysiologic and functional mechanisms that cause cardiovascular disease (Figure 5). All three of them are closely interconnected and provide the absolute combination that leads to cardiovascular disease, or CVD, vascular smooth muscle and cardiac dysfunction, hypertension, vascular disease, atherosclerosis and endothelial dysfunction, or ED.
Hypertension is not a disease but is the proper and continuous, unregulated reaction with an exaggerated outcome of the infinite irritations to the blood vessel following environmental-genetic expression patterns and downstream disturbances in which the vascular system is the innocent bystander. This really becomes a maladaptive vascular response that was initially meant to provide vascular defense to the endothelial insults (Figure 6). Hypertension is a vasculopathy, characterized by ED, structural remodeling, vascular inflammation, improved stiffness, decreased distensibility and loss of elasticity. These insults are biomechanical (BP, heartbeat, blood circulation, oscillatory flow, turbu-lence, enhancement, pulse wave velocity and reflected waves) and biohumoral or biochemical which includes all the non-mechanical causes like metabolic, endocrine, nutritional, toxic, infectious and other etiologies.
In addition to the connections for endocrine and nutritional causes of hypertension, infections and toxins can increase blood pressure as well. Various toxins, such as mercury, polychlorinated biphenyls, lead, cadmium, arsenic and iron, also increase BP and CVD. Numerous microbial organisms have also been implicated in hypertension and CHD. All of these irritations lead to the altered vascular structure and function that manifests clinically as hypertension. Patients with hypertension have abnormal microvasculature in the form of inward eutrophic remodeling of the tiny resistance arteries leading to impaired vasodilatory capacity, increased cardiovascular disease, increased media to lumen ratio, decreased maximal organ perfusion and decreased flow reserve, particularly in the heart with decreased coronary flow reserve. Significant functional structural microvascular impairment occurs even before the individual’s blood pressure begins to increase in normotensive offspring of the patients with hypertension, as evidenced by endothelial dysfunction, diminished vasodilation, forearm vascular resistance, diastolic dysfunction, increased left ventricular mass index, increased septal and posterior wall thickness and left untreated hypertrophy. Therefore, the processes underlying the circulatory issues are associated to a vascular phenotype of hypertension that may be determined by early life programming and imprinting which may be compounded by cerebral aging.
In conclusion, vascular biology, endothelial and vascular smooth muscle as well as cardiac dysfunction play a primary role in hypertension, cardio-vascular disease and target organ damage. Then, the epidemiology, or the incidence, distribution, and possible control of diseases and other factors relating to health, emphasizes the role of diet and related nutritional intake when it comes to hypertension and cardiovascular disease. And finally, oxidative stress, inflammation and autoimmune vascular dysfunction are the primary pathophysiologic and functional mechanisms that cause cardiovascular disease. Hypertension is an indication of cardiovascular issues which should be addressed by a healthcare professional.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
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.
Introduction
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. [1] 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 [2]. 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) [3]. 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 [9]. 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 [15]. 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 [11].
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 [18]. 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 [19]. 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 [11]. Activated lymphocytes can produce TSH, which could have a variety of implications [20].
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 [21]. 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 [22]. A more likely hypothesis is that anti-idiotypic antibodies are rarely produced at a detectable level. Hodkinson et al. [23] 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. [24] 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 [11].
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 [25], but the thyroid cell is incapable of supplying the costimulatory signals that professional antigen-presenting cells (APCs) do [11]. 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 [12].
Environmental Factors
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).
Iodine
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 [27].
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 [29].
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 [30]. 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 [31]. 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.
Selenium
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 [32]. 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 [35].
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. [37] 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. [38] 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.
Environmental Pollutants
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 [27]. 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 [41]. 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 [44] 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 [45].
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].
Infections
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 [27].
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. [46] 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 [21]. 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 [49]. Inflammation induced by viral infections or by pollutants can modify cell signaling pathways and influence T cell activity and cytokine secretion profiles [26].
Drugs
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 [27]. Thyroid antibodies disappeared from the circulation 6 months after amiodarone discontinuation [32].
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) [32].
Stress
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 [27].
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. [52] 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 [55]. 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 [32]. 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 [42]. 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 [57]. 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 [59].
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 [48]. 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 [60].
Conclusion
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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Thyroid diseases, such as hypothyroidism and hyperthyroidism, both caused by the altered function of the thyroid gland found in the neck, have been reported to develop due to a variety of factors. Among these factors, however, research studies have recently found a connection between the use of pesticides and thyroid disease.
What is the connection between thyroid disease and pesticides?
One of the most recent research studies, published in the American Journal of Epidemiology (AJE), discovered that exposure to fungicides and organochlorine pesticides increased the rate of hypothyroidism among women by 20 and 40 percent, respectively. Thyroid disease is most often diagnosed in women than in men.
Thyroid Disease and Pesticides
Thyroid disease can ultimately affect overall health and wellness, manifesting in symptoms of fatigue, weight fluctuations and mental issues. Some thyroid diseases, like Hashimoto’s thyroid disease and Graves’ disease, are autoimmune thyroid diseases which cause the body’s own cells to attack the thyroid gland.
Researchers in the University of Nebraska Medical Center derived these figures from clinical information collected from the Agricultural Health Study (AHS), conducted in North Carolina and Iowa between 1993 and 1997.
All those enrolled in the AHS were the female partners of agricultural workers. Nearly seven percent of them reported suffering from hypothyroidism, or underactive thyroid function. The typical speed of the disorder among Americans is five percent, according to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). In the AJE, several agricultural chemical classes weren’t associated with hypothyroidism or hyperthyroidism. These comprised of fumigants herbicides, organophosphates, pyrethroids and carbamate.
However, any exposure to organochlorine pesticides or fungicides resulted in a greater rate of hypothyroidism. Pesticides are an extremely toxic class of neurotoxins which includes DDT, as stated by the University of Connecticut Center for Environmental Health. This exposure can affect the proper function of an otherwise healthy thyroid.
Other studies have made similar associations between pesticides and thyroid disorder. A 1998 study published in the journal Environmental Health Perspectives found that 10 percent of pesticides analyzed from the U.S. Environmental Protection Agency were carcinogenic in laboratory rodents.
A 2003 report in the Journal of Occupational and Environmental Medicine found that polychlorinated biphenyls (PCBs) – compounds used to dilute pesticides, seem to impact the volume, hormone levels and the incidence of nodules in the thyroid glands of individuals most exposed to PCBs.
Hypothyroidism slows down many of the human body’s functions, leading to fatigue, weight reduction, brittle hair and constipation, the NIDDK reports. The report adds that women are more likely to develop the illness. If you begin to notice any of the above symptoms, be sure to seek immediate medical attention in order to diagnose the presence of any thyroid disease and begin a proper treatment plan to correct the thyroid hormone disbalance.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
The thyroid diseases, hyperthyroidism and hypothyroidism, are important to take care of in pregnancy, and unfortunately, they can occur relatively frequently. The thyroid gland is an organ found in the neck which releases hormones that regulate your metabolism, heart and nervous system, weight, body temperature, and many different processes within the body.
What are the risks of thyroid disease in pregnancy?
During pregnancy, in case you have preexisting hyperthyroidism or hypothyroidism, you may require more medical attention to control these conditions, particularly in the first trimester. Pregnancy may cause symptoms much like those common in these thyroid disases, in the first trimester. Should you experience palpitations, weight loss, and persisting vomiting, you should contact your doctor.
Untreated thyroid diseases in pregnancy may lead to early birth, preeclampsia (a severe increase in blood pressure), miscarriage, and low birth weight among other problems. It’s very important to talk to your healthcare professional if you have some background of hyperthyroidism or hypothyroidism so you may be monitored before, and during pregnancy and have your treatment adjusted if needed.
Symptoms of Thyroid Disease in Pregnancy
Hyperthyroidism
Symptoms of hyperthyroidism may mimic those of normal pregnancy, such as an increased heart rate, sensitivity to warm temperatures, and exhaustion. Additional symptoms of hyperthyroidism include the following:
Irregular heartbeat
Nervousness
Severe nausea or vomiting
Slight tremor
Trouble sleeping
Weight loss or low weight gain for a typical pregnancy
Hypothyroidism
Symptoms of hypothyroidism, such as extreme tiredness and weight gain, can be easily confused with normal symptoms of pregnancy. Other symptoms include:
Constipation
Difficulty concentrating or memory problems
Sensitivity to cold temperatures
Muscle cramps
Causes of Thyroid Disease in Pregnancy
The most common cause of maternal hyperthyroidism during pregnancy is the autoimmune disease Grave’s disease. In this disorder, the body makes an antibody (a protein created by the body when it thinks a virus or bacteria has invaded) called thyroid-stimulating immunoglobulin (TSI) which causes the thyroid to make an excessive amount of thyroid hormone.
The most frequent cause of hypothyroidism is the autoimmune disorder called Hashimoto’s thyroiditis. In this condition, the body attacks the thyroid gland cells, leaving the thyroid without enzymes and cells to make enough thyroid hormones.
Diagnosis of Thyroid Disease in Pregnancy
Hyperthyroidism and hypothyroidism in pregnancy are identified based on symptoms, physical examination, and blood tests to measure levels of thyroid-stimulating hormone (TSH) and thyroid hormones T4, and for hyperthyroidism, additionally T3.
Treatment of Thyroid Disease in Pregnancy
For women who require treatment for hyperthyroidism, an antithyroid medication that interferes with the production of thyroid hormones is utilized. This medication is usually PTU or propylthiouracil for your first trimester, and methimazole can be used also, following the first trimester, if necessary. In cases in which women don’t respond to these drugs or have unwanted effects from the remedies, surgery to remove part of the thyroid could be critical. After you give birth, hyperthyroidism can get worse at the first 3 weeks, and your physician may have to raise the dose of medicine.
Hypothyroidism is treated with a synthetic (artificial) hormone called levothyroxine, which is comparable to the hormone T4 made by the thyroid. Your doctor will continue to monitor your thyroid function tests every 4-6 months and will adjust the dose of your levothyroxine in diagnosis of pregnancy. In case you have hypothyroidism and are taking levothyroxine, it’s important to notify your physician once you know so that the dose of levothyroxine can be increased to accommodate the increase in thyroid hormone replacement, you are pregnant. Because the calcium and iron in prenatal vitamins can block the absorption of thyroid hormone in the human body, you should not take your vitamin.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
“More children and teens than ever seem to have hypothyroidism, a thyroid gland which does not produce enough thyroid hormone”, says pediatric endocrinologist Andrew J. Bauer, MD, medical director of Medical Center at Children’s Hospital of Philadelphia. An underactive thyroid can even put on grip on and interfere with normal growth and development. Additionally, the fatigue hypothyroidism in children and infants causes can ultimately hinder performance at school and leave kids without enough energy for sports and play.
What should we known about hypothyroidism in children?
“We used to think that one or two in 100 kids and adolescents would develop hypothyroidism, but today it looks like two to three in 100 do,” states Dr. Bauer, co-author of a current review of childhood thyroid ailments for pediatricians and family physicians published in JAMA Pediatrics. “We don’t know the entire extent of hypothyroidism in young men and women in the United States, but numbers seem to be increasing along with levels of other autoimmune conditions. We do not know why. It may be that more children as well as teens are being analyzed, so we’re finding it.
The “hygiene hypothesis”, that residing in clean surroundings early in life can throw away the immune system, is just another potential explanation.” Here’s what parents should know about this thyroid condition:
Hypothyroidism is Common in Children
Routine testing at birth uncovers hypothyroidism in one of every 1,500-3,000 newborns. The cause is a problem with the growth of the thyroid gland, the gland found at the base of the neck. “Early identification and treatment of thyroid hormone deficiency is crucial to ensure normal physical growth and normal brain growth,” Dr. Bauer says. “Screening for thyroid disease should be a part of all newborn screening programs in America.”
But, hypothyroidism may also develop later in childhood or the teen years. The risk is four times higher in girls than in boys. And people with a family history of autoimmune disorders or who have Turner syndrome, Down syndrome, type 1 diabetes or autoimmune disease may also be at risk of developing hypothyroidism.
The most typical cause of this “obtained” hypothyroidism is: An immune system assault on cells in the thyroid gland. Additional factors that could damage the thyroid gland or its capacity to produce thyroid hormones include radiation for cancers of the head and throat, some drugs (including lithiumion, some epilepsy medications and chemotherapy drugs called tyrosine kinase inhibitors) and, infrequently, iodine deficiency. Thanks to “iodized” salt (fortified with iodine) as well as the pure iodine in milk products, eggs and fish, this nourishment problem is comparatively rare in the U.S.
Symptoms Can Hide in Plain Sight
Tiredness, constipation, feeling cold and dry hair and skin are red signs but doctors and parents may not suspect that a sluggish thyroid as these indicators are common complaints of life, not specific to thyroid disorder. A slow-down in development, a delay in growing at puberty and, for women, irregular periods, are symptoms that are key.
“Delays in diagnosing thyroid problems are also common in children and adolescents with hyperthyroidism (a thyroid gland that produces too much thyroid gland) because of the cross-over in behaviour that is similar to anxiety and/or attention deficit disorders,” Dr. Bauer says. “We are also seeing the flip side –more parents legitimately concerned about their child’s fatigue or weight want to know if it’s a thyroid issue. If parents are concerned–especially if their child is not growing well, isn’t going through puberty when they ought to be, or if they develop unexplained and consistent indications or signs consistent with hypo- or hyperthyroidism — it is well worth mentioning to the doctor.”
Weight Gain and Obesity in Children
“Weight gain and obesity are seldom caused by hypothyroidism in children and adolescents,” Dr. Bauer says. “Parents wonder if a thyroid issue is the cause, particularly when they’re doing all they can to help a kid eat a healthy diet and be active. Children with hypothyroidism may sometimes look as if they’re carrying a few extra pounds because they’re not getting taller. But the majority of the time, it’s being overweight that can lead to changes in thyroid hormone levels.”
Extra body fat may increase levels of the hormone leptin, which then increases levels of thyroid stimulating hormone when the thyroid is currently working normally. That could look like subclinical hypothyroidism. “With weight loss, thyroid stimulating hormone levels return to normal,” Dr. Bauer says
Parents Can Check from Home
An enlarged thyroid gland is an important clue to hypothyroidism and hyperthyroidism. “Along with other ailments, it can help your doctor determine whether it is worthwhile performing thyroid testing,” Dr. Bauer explains. “But you can have hypothyroidism with no enlarged thyroid gland.” Parents can do the basic test ” he says. “We don’t encourage parents to attempt to become physicians, but with your child appear at the ceiling while you look at their neck is a fairly easy. If you are able to see the overview of the thyroid gland in this place, then the thyroid is enlarged.”
The thyroid gland is situated at the base of the neck. It extends about an inch. Check by simply looking at this area of the neck in three places to determine if there is an enlarged thyroid:
While your child looks straight using their chin parallel to the floor.
While your son or daughter looks up with her head and her chin pointing upward so that her neck is extended.
As she looks up while she swallows.
About Thyroid Disease Treatment
Doctors diagnose hypothyroidism by assessing for symptoms, taking a family history, analyzing a child’s thyroid gland and analyzing levels of thyroid-stimulating hormone (TSH) and free T4 (free thyroxine). High TSH and T4 can mean hypothyroidism. Amounts of anti-thyroid antibodies, which may be elevated, may also get checked. “If a child or adolescent has hypothyroidism, the typical treatment is levothyroxine–artificial thyroid hormone to replace hormones the thyroid isn’t producing in large-enough amounts,” Dr. Bauer says.
The dose is customized for each child, so that thyroid hormone levels remain within a healthy range. Your child’s physician will recheck his or her thyroid every three to six months before she or he reaches full height–after a change in dose with more checks. “This should look after delays in growth and puberty, stop learning delays, improve energy levels and receive a young man’s life back to normal,” Dr. Bauer says.
But from time to time, that the “brain fog” or exhaustion of hypothyroidism does not fully lift with levothyroxine, ” he notes. “If that is true for your child, it is worth asking the physician whether adding a second thyroid gland, known as T3, could be advantageous,” Dr. Bauer says. “We are beginning to see advantages for many adults and kids utilizing combined T3 and T4 therapy, although, this approach remains controversial and additional research into this approach is required.” This is probably the primary reason why some patients feel better on ‘natural’ thyroid hormone — it is not that it’s a ‘natural’ product when compared with a ‘synthetic’ product but that the ‘natural’ variant of thyroid gland has both T3 and T4 from the formulation.
Meanwhile, some parents detect a sudden “side effect” of therapy: Kids who were silent and relatively inactive today have lots of energy, and may be more interested in playing and just running over sitting down to do homework. “There are usually kids with severe hypothyroidism who get all their assignments done and do not get distracted as they were too tired to do much else but sit around,” Dr. Bauer says. “Following treatment, all of a sudden you have got a typical eight-year-old who is full of energy. It may be an alteration for the patient and the parents.”
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Hypothyroidism is the most common kind of thyroid disorder in children. It occurs when the thyroid gland is underactive and doesn’t produce enough thyroid hormone to satisfy the needs of the body.
Why is thyroid health important for children?
Thyroid function is essential for children and infants, whose bodies and brains rely on adequate levels of thyroid hormone. Hypothyroidism can result in disability and development failure. Congenital hypothyroidism, which is present at birth, and acquired hypothyroidism, which develops after birth, usually during late childhood or adolescence.
Congenital hypothyroidism
Congenital hypothyroidism affects 1 in 1,500-3,000 babies in the U.S. every year. Approximately, 10 to 20 percent of the time it is inherited, although the illness has been recorded to occur for no known reason.
The disease can result from insufficient maternal iodine consumption during pregnancy, but that is rare in the U.S., where dietary iodine is usually sufficient (iodine is added to table salt and can be present in seafood and milk). Rarely, medications for treating overactive thyroid may lead to congenital hypothyroidism, although the condition resolves without any effects. Still, it’s important for women to get their own thyroid function checked during pregnancy.
Congenital hypothyroidism is among the most common and preventable causes of cognitive disability. Since most newborns show no indications of it, the condition is normally detected during routine newborn screening, which will be mandatory at U.S. hospitals. Checks for congenital hypothyroidism and a number of other congenital disorders. Parents who choose home birth should be sure to secure the screening for their newborns.
Blood samples may show low levels of T4 (thyroxine), a hormone secreted from the thyroid, and/or high levels of TSH (thyroid stimulating hormone), which is released by the pituitary gland.
If the identification is supported through thyroid evaluations, teens have to be treated as rapidly as possible with synthetic thyroid gland, which should be provided as a pill. It should not be given with soy formula or calcium or iron supplements, which may decrease absorption of replacement hormone. Thyroid hormone replacement should also not be given in liquid form, which is unstable.
Most babies will have to take replacement hormone for the rest of their lives, but around 30 percent only require treatment for the first 3 decades of life and might have a transient form. In all cases, checkups and early treatment with a pediatric endocrinologist are important to help ensure normal growth and mind development. Children with congenital hypothyroidism are monitored during the first few years of existence.
Some data have revealed that the prevalence of congenital hypothyroidism is 100 percent higher in Hispanic newborns and 44 percent higher in Asians. The prevalence has also been proven to be 30 percent lower in newborns compared to whites. Infants with Down syndrome include a 10-fold increased incidence of congenital hypothyroidism.
Acquired Hypothyroidism
Acquired hypothyroidism develops during late childhood or adolescence, typically after arrival. The condition is common, affecting 1 in 1,250 kids. About 4.6 percent of the U.S. population age 12 and older has hypothyroidism, as stated by the National Health and Nutrition Examination Survey (NHANES?III).
Hormones produced by the thyroid perform several functions during youth including regulating metabolism and maintaining normal growth and bone growth.
Acquired hypothyroidism in children and teens’ usual cause is an autoimmune disorder called Hashimoto’s thyroiditis, in which the thyroid is attacked by the immune system, interfering with an gland’s ability and causing inflammation. (Hashimoto’s is also the chief cause of hypothyroidism in adults at the U.S.)
Less frequently, Candida can originate from the thyroid or from the pituitary, in case the gland fails to produce enough thyroid gland. Certain medications (like lithium) can decrease thyroid hormone production, and too much or too little iodine in the diet can lead to hypothyroidism, as can radiation exposure and infiltrative disease.
Some children are at greater risk for example those with disorders like Down syndrome of Hashimoto’s; people having other diseases like type 1 diabetes; and people who have received radiation for cancer therapy. Hashimoto’s runs in families and can be more prevalent in females than men.
The others appear only in kids while some symptoms of Hashimoto’s in older children and adolescents are similar to those in adults. These include slowed rate of growth, delayed puberty and delayed tooth development. Another common sign is an enlarged thyroid gland (goiter). Studies have shown that there is an obvious goiter found in nearly 40 percent of kids with autoimmune thyroiditis.
Hypothyroidism symptoms which children and adolescents have with adults in common include: fatigue, constipation, rough, dry skin and hair, and weight gain, even though the majority of weight gain experienced by adolescents and children isn’t due to thyroid disease.
Acquired hypothyroidism can be diagnosed with blood tests. Usually TSH levels are high and T4 levels are low. Both levels are low. Normal ranges for T4 and TSH are somewhat different in children than in adults, so it is important to speak with a pediatric endocrinologist.
Just like congenital hypothyroidism, obtained hypothyroidism is treated typically in the form of a once-daily pill. Side effects may include difficulty falling asleep, headache and restless sleep and result from overtreatment.
There’s no cure for either kind of hypothyroidism but hormone replacement is considered safe and effective. With appropriate use of drugs and intimate follow-up using a pediatric endocrinologist, children can expect to live a healthy life. Kids might be monitored more frequently if there are concerns about their adhering to the pill regimen.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Hypothyroidism, or underactive thyroid function, is a commonly reported thyroid disease. There are many common symptoms which characterize the presence of hypothyroidism, although a diagnosis is required for treatment.
Can hypothyroidism be left untreated?
Hypothyroidism can progress and cause a great number of complications if left untreated. Getting regular screenings to ensure an early diagnosis and knowing the symptoms of hypothyroidism will prevent the onset of the complications. The list below is a group of common complications which can occur if hypothyroidism isn’t treated properly.
Birth Defects
If you are pregnant and have a thyroid disorder like hypothyroidism, your child may have a higher risk of developing birth defects than babies born to healthy mothers. Infants born to women with untreated thyroid illnesses might have mental and physical growth issues since thyroid hormones are vital for brain growth. Fortunately, if such problems are addressed shortly after the birth, the child may experience a normal, healthy development. An abbreviated thyroid function test is part of the newborn screen. This includes a panel of blood tests performed to exclude diseases.
Goiter
An excessive stimulation can cause the thyroid gland to expand to the point where you’ve got a bulge on your neck when your thyroid over exerts itself in an effort to make an adequate amount of hormones. This is known as a goiter.
Heart Problems
Hypothyroidism in its mildest forms, can affect the health of your heart. An underactive thyroid can boost your chance of developing heart disease because it raises levels of “bad” cholesterol. Too much bad cholesterol can result in atherosclerosis, or hardening of the arteries, which can increase your risk of heart attacks and strokes. Hypothyroidism can result in the buildup of fluid around the heart, medically referred to as pericardial effusion, which might make it harder for the heart to pump blood, affecting its overall function and that of the body.
Infertility
Hypothyroidism can affect ovulation and decrease the chances of conceiving, if thyroid hormone levels are too low. Even with appropriate treatment for hypothyroidism, such as that of thyroid hormone replacement therapy, there is not any guarantee that the woman will be fully fertile.
Mental Health Issues
If left untreated the signs of hypothyroidism can have a toll on the body and mind of the individual. Mild hypothyroidism can cause mild forms of depression. However, the symptoms of hypothyroidism may increase over time. This can directly affect your psychological condition, and your depression may intensify as an outcome. Moreover, untreated hypothyroidism has been associated with a decrease in psychological functioning.
Myxedema
Myxedema is the term for extreme hypothyroidism which occurs if the disease has progressed for a very long time with no treatment. Since it’s highly unlikely that you wouldn’t seek treatment and wouldn’t recognize the signs, Myxedema is quite rare. This kind of hypothyroidism is life threatening. Your metabolism can slow down to the point at which you would fall into a coma. If you experience symptoms such as extreme fatigue or cold intolerance, associated symptoms of myxedema, seek medical treatment from a healthcare professional immediately.
The real key to preventing the complications of hypothyroidism is to understand the disease’s symptoms and seek proper medical intervention. Hypothyroidism is manageable and it does not need to interfere with your life.
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By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
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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].
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 [18]. 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.
Iodine
