Hashimoto's, Graves' Disease, and Hyperthyroidism.
Development Processes of Thyroid Diseases, Immune Attacks, and Treatment Approaches
Graves' and Hashimoto's diseases are conditions that affect thyroid functions, arising from the immune system attacking the body's own tissues. Although there is a widespread belief in society that iodine use directly causes these diseases, this statement can be considered entirely incorrect. Iodine alone is not seen as the cause of these diseases; to understand these processes, one must first examine how and why the immune system attacks thyroid tissue.
When the immune system is activated by viral infections, severe stress, bacterial factors, certain chemical cosmetics, or neurotoxins, it can lose the ability to recognize the self-signals within thyroid cells. In this situation, the immune system perceives thyroid tissue as foreign and launches an attack. In Hashimoto's, this attack occurs directly within the tissue, leading to cell destruction. The excess hormone released from the destroyed tissue initially elevates T3 and T4 levels, causing a temporary hyperthyroid episode. If necessary precautions are not taken and attacks continue, the cells eventually die, becoming unable to produce hormones, and the condition transforms into hypothyroidism.
The situation in Graves' disease is different. Here too, there is an immune system attack, but the thyroid tissue begins to produce thyroxine hormone non-stop, without regard to TSH stimulation from the pituitary. In Graves', tissue destruction or a shift to hypothyroidism is generally not observed; on the contrary, there is a constant state of hyperthyroidism. This condition can lead to a toxic state, progressing with symptoms such as severe weight loss, palpitations, brain fog, hair loss, and tremors.
In treatment processes, corticosteroid drugs to suppress the immune system and special drug groups used for hyperthyroidism treatment can be preferred. Medications like methimazole and propylthiouracil aim to stop new hormone production by suppressing the thyroxine peroxidase (TPO) enzyme in thyroid cells. Propylthiouracil group drugs, unlike others, can be prioritized in acute crises as they also prevent the conversion of T4 to T3 in blood levels.
In Hashimoto's patients, the presence of anti-TPO antibodies is investigated during diagnosis. Initially, instead of drugs that directly suppress thyroid functions, the process can be managed with supportive measures that balance the immune system, control heart rate, or have a calming effect. If a significant portion of the thyroid tissue has been destroyed, external thyroid hormone support may become a necessity, as the body will lack hormones.
In Graves' patients, high-dose medication and heart rate control are essential due to the constant hyperthyroidism. In cases where it cannot be controlled by medication and is accompanied by goiter (thyroid enlargement), surgical intervention may be considered. Before surgery, methods such as high-dose iodine application may be used to prevent blood flow to the thyroid tissue and dilation of blood vessels.
In conclusion, iodine intake alone does not cause Hashimoto's or Graves' disease. These diseases are more associated with factors that confuse the immune system, such as prolonged fasting, severe stress, and neurotoxic effects. The immune system's failure to recognize its own tissues can affect not only the thyroid but also other organs like the kidneys, liver, or lungs. Therefore, it is recommended to consult specialist physicians to correctly differentiate thyroid problems and manage the appropriate process.