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Autoimmune Thyroid Diseases Associated with Infections | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Chiropractic

Autoimmune thyroid diseases, such as Hashimoto’s thyroid disease and Graves’ disease, are several of the most prevalent causes behind thyroid gland dysfunction. Autoimmune thyroid diseases, or AITDs, occur when the human body’s own immune system attacks and damages a healthy thyroid gland. It’s this autoimmune assault on the thyroid which can, over time, lead to the overactive or the underactive function of the buttefly-shaped gland in our neck.

What other factors can cause autoimmune thyroid diseases?

According to numerous research studies, autoimmune thyroid diseases can be caused due to a variety of factors. Environmental factors like iodine intake and selenium deficiency can alter the balanced metabolism of chemicals in the human body necessary for the proper function of the thyroid gland. Additionally, environmental factors such as exposure to environmental pollutants and toxins have been linked to the interference of efficient thyroid hormone secretion.

Autoimmune Thyroid Disease & Infection

One autoimmune thyroid disease trigger, however, is often overlooked by healthcare professionals; infection. Researchers today still do not fully understand how�infections trigger autoimmune diseases, however because our immune systems are so complicated and every disease is unique, it’s very likely that there are a number of variables. Recent studies have identified three theories which explain the links between infections and AITDs.

Molecular Mimicry

Autoimmune thyroid diseases triggered by molecular mimicry are virtually hypothesized to occur when the infection is structurally similar to that of the thyroid gland. Therefore, once the network of defense cells, tissues and organs activates, the immune system proceeds to strike the infection and attacks your thyroid gland.

Bystander Activation

In this circumstance, the immune system activates when a virus or bacteria invades the thyroid gland and sends cells into your thyroid to destroy the infection. While these cells are currently all attacking the bacteria or virus, it injures the thyroid gland. More cells are signaled by the inflammation to the thyroid gland where they often continue to attack.

Cryptic Antigens

You can think about this as the “hijacking theory” where an infection (usually due to a virus) hijacks the thyroid cells’ DNA to hide from your immune system. The immune system is intelligent enough to detect the virus anyway, and strikes the virus as well as the thyroid cells it is hiding in.

AITDs as a Response to Infection

In certain individuals, autoimmunity is the price to be paid for the eradication of an infectious agent. Infections are implicated in the pathogenesis of endocrine, and nonendocrine diseases. Either fungal or viral diseases may represent a risk factor for the evolution of AITDs. Viruses have long been suspected as etiological agents in a variety of health disorders, uncluding autoimmune thyroid disease; furthermore, a trigger of AITDs, infecting the thyroid or immune cells, was demonstrated in an avian model. This potential remains unproven although viruses may be agents in AITDs.

An increased frequency of antibodies to the influenza B virus has been observed in a group of patients with thyrotoxicosis. Virus-like particles have been discovered in the thyroid of chickens together with similar particles. Serological evidence of staphylococcal and streptococcal disorders were described in a few patients with AITDs.

Some of the strongest evidence linking infectious agents to AITDs’ induction has been the institution of Yersinia enterocolitica disease with thyroid disorder. This Gram-negative coccobacillus commonly causes diarrhea along with a number of abnormalities that indicate disorder, including arthritis, arthralgias, erythema nodosum, carditis, glomerulonephritis, and iritis. Weiss et al. demonstrated that Y. enterocolitica needed a saturable, hormone-specific binding site for its mammalian TSH that resembled the receptor for TSH from the human thyroid gland.

An immune response against a viral antigen that shares homology with the TSHR might be the inductive event that ultimately leads to autoimmunity. A substantial association between AITDs and hepatitis C has also been found. Antibody titers are shown to increase in patients with the hepatitis C virus, and these patients were more susceptible to AITDs than were hepatitis B sufferers. These patients must be screened for autoimmune thyroid disease.

Infection might induce an autoimmune response by various mechanisms, such as polyclonal T cell activation by microbial superantigens mimicry, and thyroid expression of human leukocyte antigens. Inflammation can alter cell signaling pathways and influence T cell activity and cytokine secretion profiles.

In conclusion, research studies have shown that autoimmune thyroid diseases may also be the response of environmental factors such as infections. Infections can lead to AITDs when the human body’s own immune system attacks and damages the thyroid gland cells in addition to those of bacteria and viruses. Ultimately, treating bacterial and viral infections can be an essential way to prevent autoimmune thyroid disease or complications.

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.

Thyroid Disease, Environmental Pollutants & Toxins | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Chiropractic

The thyroid gland is a large, butterfly-shaped gland located at the base of the neck. Although it may seem insignificant in nature, this ductless gland is fundamental for the human body’s overall function. The thyroid gland secretes an essential collection of thyroid hormones which aid in the growth and development of the systems through the rate of metabolism.

What is the purpose of the thyroid gland?

The continuous release of thyroid hormones activate numerous bodily functions, including proper heart and digestive function, muscle control, brain growth and development, bone maintenance and even body temperature.

As important as the thyroid gland is, however, the human body’s own immune system can sometimes attack and damage a healthy thyroid gland, a condition medically referred to as autoimmune thyroid disease. Autoimmune thyroid diseases, or AITD’s, such as Hashimoto’s thyroid disease and Graves’ disease can ultimately alter the overall function of the body. Autoimmune thyroid disease is believed to have no apparent cause, but, research studies have hypothesized that exposure to environmental pollutants and toxins can bring an onset of AITD’s.

Environmental Pollutants and Toxins

The exposure to environmental pollutants and toxins have been previously implicated in the induction of autoimmune thyroid diseases throughout various research studies. Similar studies have also linked AITD’s to other environmental factors, such as iodine intake and selenium deficiency. However, in cases where autoimmune thyroid disease cannot be attributed to diet and nutrition, healthcare professionals have suspected the influence of other environmental factors.

Polyhalogenated biphenyls are commonly used compounds with a variety of applications. Polybrominated biphenyls are flame retardant, and polychlorinated biphenyls, or PCB’s, are used as lubricants, adhesives, inks, and plasticizers. PCB’s are known to accumulate in rivers and lakes and then in the adipose tissue of fish and humans. AITD’s might be triggered by these compounds by interfering with iodide transport, causing oxidative stress. There is proof that thyroid hormone levels in rat pups decrease with exposure to perinatal PCB’s. In adults, adolescents, and children from such areas, the concentration of PCB’s in blood samples negatively correlated with levels of circulating thyroid hormones.

Populations with long-term exposure to PCB’s have increased prevalences of antibodies, which can be linked to the increased effects of these compounds in the environment. Pollutants and toxins from heavy industry and auto emissions, in addition to coal pollution and agricultural fungicides, are also implicated in development of AITD’s.

Smoking is associated with an increased risk of developing Graves’ disease, an autoimmune thyroid disease which causes hyperthyroidism, an overactive thyroid gland, as well as a remission rate after thionamide treatment. Even more striking is the impact of smoking on Graves’ orbitopathy, which tends to become more serious in smokers. Smoking might contribute to the pathogenesis of Graves’ disease by altering the structure of the thyrotropin receptor, making it more immunogenic and causing the creation of thyrotropin antibodies that react with retroorbital tissue.

Smoking increases antigens by cells that are damaged and induces the polyclonal activation of T and B cells. Hypoxia can play a part in Graves’ orbitopathy when cultured under hypoxic conditions because retrobulbar fibroblasts show a significant increase in proliferation and glycosaminoglycan production. The impacts of smoking on thyroid function in fetuses or infants that are 1-year-old offer insight into the interrelationship between smoking and autoimmune thyroid disease. The latter study found that the mothers and fathers of babies whose had higher cord serum levels of Tg and thiocyanate than did infants whose parents did not smoke. The result observed in adolescents exposed to passive smoking could be due to direct stimulation of sympathetic nervous activity from smoking in addition to the increase in thyroid hormone secretion. The association of smoking with chronic autoimmune thyroiditis is less well-defined.

In conclusion, various research studies have demonstrated that exposure to environmental pollutants and toxins, including smoking, may have a connection with autoimmune thyroid diseases. While the thyroid gland is virtually an essential part of the function of the human body, it can no doubt be sensitive to environmental factors.