Thyroid hormone (TH) regulates the body's metabolism and iodine, a vital trace mineral, is vital for TH synthesis. As a TH biosynthesis catalyst, iodine has a substantial role in our health. When there is a modest iodine deficit, the thyroid gland grows autonomously, resulting in thyrotoxicosis. Those who consume excessive iodine risk developing hypothyroidism and thyroid autoimmunity. A transient hyperthyroid condition may rapidly increase iodine consumption. Iodine deficiency is common across the globe, and provision of supplementary iodine, in forms such as iodized salt or vegetable oil, has many benefits. Vegetarians, for instance, may not consume adequate amounts of iodine in some countries with high iodine content. Reduced dietary iodine intakes may be a consequence of efforts to reduce salt intakes to prevent hypertension. In addition, iodine consumption is decreasing in many countries, even among those where endemic goiter has previously been eradicated, leading to the re-emergence of iodine-deficiency-related disorders such as goiter. This review will discuss how iodine can contribute to the development of thyroid disease.
Background
Menopause is a biological process when a woman’s reproductive capability is no longer functional. A naturally or artificially caused premenopausal is known as early menopause occurs between the ages 40–45, which substantially impacts fertility and disease influenced by genetic plus environmental factors and their interactions. Women in early menopause are at greater risk of cardiovascular disease, general mortality, neurological disorders, osteoporosis, mental illness, and other problems.
Main body
A PubMed search of the electronic literature database yielded articles on early menopause and disease etiology. Several unique genes were identified, such as ESR1, ESR2, CYP1B1, BRSK1, HK3, andTMEM150B are associated with early menopause, and research focused on case-control, cohort, and cross-sectional studies are finding novel predisposition loci for early menopause.
Conclusion
The current study’s focus is to understand better the genetic aspects of early menopause. This knowledge will help researchers enhance EM etiology and identify biomarkers that may detect early development of the disease, allowing women at risk to begin family planning earlier.
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