Humans are exposed to an abundant amount of synthetic chemicals through our environment. These chemicals have the potential to disrupt our physiology, particularly thyroid function, due to the numerous biological processes that thyroid hormones are involved in. This article will focus on environmental toxicity and its contribution to low thyroid function, or hypothyroidism.
Low thyroid function can significantly affect humans in all stages of life, from gestation to adulthood. While the thyroid gland develops at around 7 weeks gestation, it is not considered fully functioning until birth. However, thyroid hormone receptors are present in the fetal brain as early as the first trimester, so it is not surprising that endocrine-disrupting chemicals have an impact on neurodevelopment. Studies have shown that both maternal hypothyroidism and congenital hypothyroidism contribute to motor and cognitive deficits in children. Persistent organic pollutants (POPs) like polychlorinated biphenyls (PCB’s) and polybrominated diphenyl ethers (PBDEs) have been shown to not only reduce circulating levels of thyroid hormone, but to directly influence thyroid hormone-mediated communication between brain cells, thus disrupting brain development.
POPs are found in pesticides, flame retardants and solvents. Because they are lipophilic (they love fat) and resistant to environmental degradation, they have the tendency to bio accumulate in human and animal tissue. Many POPs are organochlorine compounds (OCs) that share a similar chemical structure to triiodothyronine (T3) and thyroxine (T4), the primary thyroid hormones. One theory of how OC’s can disrupt thyroid function is that they compete with T3 and T4 for binding proteins, thus displacing thyroid hormones through excretion.
A study on the Faroe Islands in Scandinavia followed children from birth up to 5 ½ years of age and assessed the OC content of their mother’s serum and breast milk. The subjects exposed to high OC content from their mothers had lower levels of resin triiodothyronine uptake (T3RU), a measure of thyroid function.
Low thyroid function can also be the result of an autoimmune disease. While environmental toxins can directly inhibit thyroid function, they may also stimulate autoimmunity, thus indirectly inhibiting thyroid function. While 70 – 80% of autoimmune thyroid disease is a result of genetics, the remaining 20 – 30% is thought to be due to environmental exposure. One theory proposes that toxins like POPs accelerate the autoimmune process in already genetically susceptible individuals. A study in male factory workers exposed to polyhalogenated biphenyls showed an increased incidence of antimicrosomal thyroid antibodies and hypothyroidism, indicative of an autoimmune process. Another study showed higher rates of Hashimoto’s thyroiditis and the presence of anti-thyroid antibodies in subjects living close to a petrochemical complex in Brazil. POPs such as polycyclic aromatic hydrocarbons, furans, dioxins, and toluene are found in petrochemicals and can cause immunotoxicity by affecting cellular signaling mechanisms to induce autoimmunity.
Another probable source of thyroid disrupting chemicals is the water supply. One study measured nitrate levels in well water used by an Amish population in Pennsylvania. Nitrate is an agricultural chemical found in water supplies in rural regions. It shares a similar chemical structure to iodine (a substance needed by the thyroid to make hormones) and can compete with iodine for uptake in the thyroid gland, thus contributing to reduced production of thyroid hormones. The study in Pennsylvania revealed clinical hypothyroidism in the women in the population but not the men. This result parallels the greater overall prevalence of hypothyroidism in females.
Low levels of pharmaceutical drugs can also be found in the water supply. This is due to people flushing unneeded medications down the toilet or just through drugs being passed through people’s urine and feces. Some pharmaceuticals remain even after water treatment plants clean sewage water. One study looked at Lithium levels in the urine of women in the Argentinean Andes. These women were not taking Lithium as a therapeutic medication but were likely exposed to it through the water supply. The amounts of Lithium in their urine paralleled the concentrations in patients’ urine that were on a maintenance dose of the drug. Side effects of long-term Lithium therapy include hypothyroidism and goiter. Not surprisingly, the women in the Argentinean Andes showed decreased thyroid hormones, consistent with lab findings of patients on long-term Lithium therapy.
If low thyroid function is a result of environmental toxicity levels, the naturopathic approach is to treat the cause of this dysfunction through detoxification protocols. A main reason for the bioaccumulation of toxins is due to their affinity for the fat in our bodies so maintaining a healthy body weight with an emphasis on lean muscle is one way to reduce toxic burden. Regular exercise stimulates sweating and lipolysis (fat breakdown), two factors important in detoxification. Hydrotherapy techniques that encourage sweating such as sauna therapy and hot baths also mobilize toxins from the tissues. Emphasis on a diet rich in organic produce and low in animal products also reduces exposure to POPs.
From a public health standpoint, recognition needs to be placed on the correlation between environmental toxicity and disease. More stringent regulations should be imposed on industry and public utilities. Until this happens, it can only be expected that the prevalence of thyroid disease will increase.
References
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