[* Read before the S.G. & O. Society, 19th Anniversary Convention, A.I.A., June 29, 1953, Swampscott, Mass.]
RUSSEL STUART MAGEE, M.D., F.A.C.S.
Journal of the Amer. inst. of Homoeo. May, 1954.
Iodides are rapidly fixed by the thyroid gland, at first in an inorganic state, By a process of enzymic oxidation idothyroglobulin is formed.
Thyroxin is an amino – acid compound. If radio – active iodine is used as an indicator, the tagged iodine can be determined roughly. In eight hours after ingestion, the thyroid cell shows its highest value for combined or thyroxin iodine, while from 40 to 48 hours are needed to give the greatest yield of thyroxin. Twenty per cent of a tracer dose is still present in the gland at the end of ten days.
It has been determined that the thyroid follicle proceeds through the stages of:
2. Colloid release
3. Partial collapse
This metamorphosis of the cell is constantly proceeding, the nucleus changing in its position and the cytoplasm becoming granular throughout this cycle. Secretion takes place toward the lumen of the follicle, which begins to fill white colloid having a high thyroxin content.
This cycle varies in time from a period of 19 hours to 21 days. The activity of this cycle depends upon widely diverse influences, such as food, emotional state, mental and physical activity, surrounding temperature, season of the year, barometric pressure, childhood, senescence, and so forth. When a variation in one or more of these external conditions indicates a changing need for the thyroid hormone, the mechanisms by which this is achieved depend upon the interactivity of nervous, glandular and chemical factors.
Nervous impulses from the brain stimulate the anterior pituitary which produces its thyroid stimulating hormone and the following results: (1) an hypertrophy and hypertrophy and hyperplasia of the cells, (2) an increase in their secretory activity, and (3) a quickened release of thyroid hormone from the interfollicular colloid.
This response is altered by the amount of iodine available and by the amount of thyroid hormone formed. If there is an iodine deficiency, then both the previously normal and previously hyperplastic gland evidence an increased ability to iodine and convert it into an organic form. The cells of both these types of gland become more active and increase in size, with increased vascularity.
In the case of the initially normal gland, a prolonged deficiency will produce a simple colloid type of goiter. In the hyperplastic type of gland, pre – existing evidences of an increased activity of the thyroid cells are accentuated, and blood protein – bound iodine remains at a high level for a considerable time after the iodine deficiency is established. In as much as a deficiency in iodine gives rise to an increased production of thyrotropic hormone, it is probable that the above effects are mediated by way of the anterior pituitary.
When iodine in small amounts is fed to patients with simple colloid goiter an increase in metabolism follows. If, however, the metabolic rate is already increased, as in hyperthyroidism, the moderate intake of iodine, brings about a decrease.
This decrease in the metabolism of the hyperthyroid individual, following the administration of iodine, is secondary to a decrease in the capacity of the gland to fix iodine and to convert it into an inorganic form. The manufacture of hormone – rich colloid is blocked. The ability of the gland to store colloid is enhanced, and as a result, the protein bound iodine of the blood decreases toward normal.