Correlation between iodine deficiency, thyroid and atherosclerosis

The thyroid, although small, exerts a deep influence on our cardiovascular health through the production of hormones that regulate energy metabolism, lipid and vascular function. At the heart of this report there is iodine, micronutrient indispensable for thyroxin synthesis (T4) and triiodothyronine (T3), thyroid hormones that form multiple physiological processes. When the availability of iodine is inadequate, the production of such hormones is reduced: this state of hypothyroidism can foster numerous pathogenic mechanisms involved in the development of atherosclerosis, the main cause of cardiovascular diseases in the modern world.

Iodine is present in foods, especially in sea fish, dairy products and, in the countries that adopt it, in iodized kitchen rooms. When hiring iodine is insufficient, thyroid cannot synthesize adequate amounts of T4 and T3. In response, the pituitary increases the secretion of thyroid stimulating hormone (TSH), to try to stimulate greater hormonal production. If iodine deficiency persists, conclaimed or subclinical hypothyroidism develops, with systemic consequences that include alterations of lipid metabolism and vascular tone.

An extensive clinical and experimental literature revealed the association between thyroid dysfunction and atherosclerosis. Hypothyroidism, especially when protracted over time, was related to an increase in the risk of develop atherosclerotic plaques in the arteries, resulting in increased cardiovascular risk.

The main ways through which hypothyroidism accelerates athenogenesis are: atherogen dyslipidemia, increased oxidative stress and lipid peroxidation, and endothelial dysfunction associated with chronic inflammation.

In detail, the lipid profile of people with hypothyroidism tends to change in an unfavourable sense: a increase in total cholesterol, above all low density lipoproteins (LDL) and triglycerides, while high density lipoproteins (HDL), often protective, are reduced. This combination promotes the accumulation of fat in the arterial wall and the formation of atherosclerotic plaques, the pathological basis of myocardial infarction and stroke.

Parallel, in hypothyroidism increases oxidative stress, with greater peroxidation of lipids in plasma lipoproteins. The oxidized LDLs are particularly harmful because they are more easily captured by macrophages, forming foam cells, a central element in the genesis of atherosclerotic plaques.

The shortage of thyroid hormones also alters the properties of vascular endothelium, reducing the production of nitric oxide, important vasodilator, and increasing the pro-inflammatory state. This condition promotes arterial rigidity and progression of atherosclerotic lesions.

Already in the early 20th century doctors such as Theodor Kocher noted that arteriosclerosis was more frequent in surgically thyroid private patients, suggesting a causal link between hypothyroidism and vascular pathology. In animal experiments, the use of oral iodines or thyroid extracts has shown protective effects against the development of atherosclerotic plaques, highlighting a possible antioxidant or metabolic role of iodate compounds.

Autoradiographs with radio-idine (I‐131) also documented the presence of iodine in the walls of elastic arteries even many days after injection, suggesting that iodine can play a direct role in vascular structures as well as its endocrine function.

From a nutritional point of view, ensuring an adequate supply of iodine is essential to support a normal thyroid function and avoid metabolic and vascular consequences associated with hypothyroidism. Iodoprophylaxis programmes (e.g. iodized salt) were introduced in many countries to prevent widespread deficiencies and their serious repercussions on health.

In conclusion, the relationship between iodine, thyroid function and atherosclerosis emerges from a complex interweaving of endocrine, metabolic and inflammatory mechanisms. Iodine deficiency, through the development of hypothyroidism, negatively affects the lipid profile and favors inflammatory and oxidative processes that accelerate the formation of atherosclerotic plaques. The nutritional prevention with adequate supply of iodine and attention to thyroid function therefore represent important aspects not only for metabolic health, but also for the prevention of cardiovascular diseases.

Bibliographic references

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