Though it may occur at any age, including in children, it is most often observed in women between 30 and 60 years of age. The highest prevalence from one study was found in the elderly members of the community.Those that already have an autoimmune disease are at greater risk of developing Hashimotos as the diseases generally coexist with each other. Common diseases seen coexisting with Hashimotos include celiac disease, multiple sclerosis, type 1 diabetes, vitiligo, and rheumatoid arthritis.Congenital hypothyroidism affects 1 in 3500-4000 newborns at birth and is a version of intellectual disability that can be treated if caught early, but can be hard to diagnose given that symptoms are minimal at a young age. Congenital hypothyroidism is generally caused by defects of the thyroid gland, but for most cases in Europe, Asia, and Africa, the iodine intake can cause hypothyroidism in newborns. Geographic influence of dietary trends
Diets consisting of low or high iodine intake determine a populations risk of developing thyroid-related disorders. It is more common in regions of high iodine dietary intake, and among people who are genetically susceptible. Geography plays a large role in which regions have access to diets with low or high iodine. Iodine levels in both water and salt should be heavily monitored in order to protect at-risk populations from developing hypothyroidism.Geographic trends of hypothyroidism vary across the world as different places have different ways of defining disease and reporting cases.
Risk factors
The strong genetic component is borne out in studies on monozygotic twins, with a concordance of 38–55%, with an even higher concordance of circulating thyroid antibodies not in relation to clinical presentation (up to 80% in monozygotic twins). Neither result was seen to a similar degree in dizygotic twins, offering strong favour for high genetic aetiology. Medications that influence thyroid function
Certain medications or drugs have been associated with altering and interfering with thyroid function. Of these drugs, there are two main mechanisms of interference that they can have.One of the mechanisms of interference is when a drug alters thyroid hormone serum transfer proteins. Estrogen, tamoxifen, heroin, methadone, clofibrate, 5-flurouracile, mitotane, and perphenazine all increase thyroid binding globulin (TBG) concentration. Androgens, anabolic steroids such as danazol, glucocorticoids, and slow release nicotinic acid all decrease TBG concentrations. Furosemide, fenoflenac, mefenamic acid, salicylates, phenytoin, diazepam, sulphonylureas, free fatty acids, and heparin all interfere with thyroid hormone binding to TBG and/or transthyretin.The other mechanism that medications can utilize to interfere with thyroid function would be to alter extra-thryoidal metabolism of thyroid hormone. Propylthiouracil, glucocorticoids, propanolol, iondinated contrast agents, amiodarone, and clomipramine all inhibit conversion of T4 and T3. Phenobarbital, rifampin, phenytoin and carbamazepine all increase hepatic metabolism. Finally, cholestryamine, colestipol, aluminium hydroxide, ferrous sulphate, and sucralfate are all drugs that decrease T4 absorption or enhance excretion. HLA genes
The first gene locus associated with autoimmune thyroid disease was major histocompatibility complex (MHC) region on chromosome 6p21. It encodes HLAs.