Thyroid Disorder and Dizziness in Humans: History
Please note this is an old version of this entry, which may differ significantly from the current revision.
Subjects: Physiology

The regulation of thyroid hormone production is under the control of the hypothalamic–pituitary–thyroid (HPT) axis. TRH (Thyrotropin-Releasing Hormone), which is synthesized and secreted by the neurons of the paraventricular nuclei of the hypothalamus, stimulates the release of TSH (Thyroid-Stimulating Hormone) by the pituitary gland. TSH binds to its membrane receptor in the thyroid follicular cells and triggers the synthesis and secretion of the following thyroid hormones: Thyroxine (Tetraiodothyronine, T4) and T3 (Triiodothyronine). When the concentration of T4 and T3 in the blood increases, a negative feedback loop is set up to inhibit the pituitary response to TRH and decrease TSH secretion.

  • thyroxine
  • thyroid hormones
  • thyroid axis
  • vestibular system
  • vestibular compensation

1. A Vestibular Modulation of the Thyroid Axis?

In a quite interesting way, gravity influences thyroid cells (for review: [28]). Indeed, thyroid carcinoma cells cultured at 0 g to simulate microgravity strongly reduce the secretion of free T4 and T3 [29]. These data are in agreement with the decrease in T4 and T3 levels of astronauts after a space flight [30,31,32,33]. Morphological examination of the thyroid glands of rats exposed to a space flight has shown histological changes indicating a reduction in thyroid activity [34,35]. Conversely, in rats subjected to hypergravity, T3 production is increased [36]. These different effects have not been characterized precisely and further studies are needed to clarify the role of gravity on thyroid function. It is possible that the vestibular system, activated by terrestrial gravity, has connections to the thyroid gland.
Researchers can make an interesting analogy between the data concerning the impact of microgravity on thyroid function and the effects of space flight on the muscles involved in posture. Since the mid-1970s, it has been recognized that spaceflight induces substantial muscle atrophy, particularly in the antigravity and postural muscles [37]. Indeed, previous studies have shown in rats a loss of muscle mass of the soleus muscle of about 30% in microgravity [38,39,40,41]. In addition, microgravity exposure produces structural changes in soleus muscle with a shift to a faster phenotype, correlated with a significant decrease in type 1 and 2A fibers and an increase in 2X and 2B fibers, as well as changes in myosin heavy chain isoforms [42]. Given the influence of gravity on the thyroid system, it cannot be ruled out that the alteration of the soleus muscle (related to its underutilization) in a hypogravity environment also involves this hormonal component [43]. Indeed, the crew of the International Space Station devotes an average of 2.5 h per day to physical exercise; however, even this is not sufficient to compensate for the effects of continuous exposure to microgravity on the muscular system [44]. These results suggest the involvement of additional mechanisms in the alteration of antigravity muscles in microgravity. Considering the presence of TH receptors in skeletal muscles and the involvement of TH in the regulation of muscle tone [45], it is very likely that the histological alterations of the soleus muscle observed in astronauts or rats in microgravity result from the hypofunction of the thyroid gland in microgravity. This point is developed further in Section 5.7 below.
At the central level, researchers can also assume connections between the vestibular nuclei and the neurons of the hypothalamus responsible for TRH release. Indeed, the neurons that synthesize and release TRH are located in the paraventricular nucleus (PVN) of the hypothalamus [46]. Electrical and caloric stimulation of vestibular pathways elicits a response in PVN neurons in guinea pigs [47,48]. Retrograde tracing has also demonstrated the presence of a direct vestibulo-paraventricular projection in rats [49] and a paraventricular-vestibular pathway has also been described [50]. These neuroanatomical pathways support the link between the vestibular system and the stress axis or hypothalamic–pituitary–adrenal axis [51,52]. The interaction between the vestibular system and thyroid axis remains unexplored. The vestibular syndrome after unilateral vestibular deafferentation activates the stress axis [53,54]. It would be interesting to demonstrate that a change in vestibular system activity generated either by the stimulation of vestibular receptors or by their suppression activates the thyroid axis as is the case for the stress axis and the neuronal histaminergic axis [55].

2. Thyroid Disorder and Dizziness in Humans

Despite the histopathological parameter correlated with Meniere’s disease (endolymphatic hydrops: dilation of the membranous labyrinth of the inner ear) [56,57], its etiopathogenesis remains uncertain and multifactorial. Autoimmune factors, trauma, viral infection, genetic predisposition, hormonal disorder, and metabolic factors could contribute to the development of Meniere’s disease [58]. The possible correlation between hypothyroidism and Meniere’s disease was proposed over 40 years ago. Powers and colleagues reported hypothyroidism in 17% of 98 patients with Meniere’s disease [59]. A recent study of 5410 hypothyroid patients demonstrates that subjects with hypothyroidism have a greater risk of developing Meniere’s disease than euthyroid subjects [60]. Bhatia and colleagues report that symptoms of vertigo were observed in 29.1% of patients with hypothyroidism [61]. More recently, Kim et al. demonstrated that both hypo- and hyperthyroidism were related to Meniere’s disease [62]. The attenuation of Meniere’s disease after thyroxine supplementation of hypothyroid patients is controversial. In Powers’ study, only 3 of 97 patients had an improvement in symptoms after thyroxine treatment [59]. In another study, 12 of 35 hypothyroid patients were found to have Meniere’s disease and all 12 patients reported subjective improvement in symptoms after 12 weeks of thyroxine treatment [63]. According to Lin’s population-based study, the overall incidence of Meniere’s disease was lower in hypothyroid patients who received thyroxine treatment compared to those who did not; however, the difference was not significant [60].
Other studies have focused more specifically on the links between vertigo and autoimmune hypothyroidism, such as Hashimoto’s thyroiditis (for review: [64]). Indeed, inflammatory diseases (such as Hashimoto’s: chronic autoimmune inflammation of the thyroid causing hypothyroidism) could cause a cross-immune reaction against inner ear cells and impair cochlear and vestibular functions. Following this reasoning and considering the inflammatory basis of Hashimoto’s thyroiditis, it is possible to find a relationship between the two diseases. In support of this hypothesis, Kim et al. studied the composition of the endolymphatic sac in a group of 13 patients with Meniere’s disease and found the presence of immunoglobulins, proving the possibility of immune reactions in the labyrinth [65]. Fattori and colleagues report that the prevalence of anti-thyroid autoantibodies was significantly higher in the group of Meniere’s disease patients (38%) than in the two control groups (7% in a healthy control group, and 12% in a group of non-Meniere’s disease patients). These data on 50 Meniere’s patients indicate a close relationship between autoimmune thyroid disease and Meniere’s disease [66]. This study reinforces the hypothesis of a possible pathogenic role of autoimmunity in the development of Meniere’s disease [66]. These data have been confirmed by other teams and confirm that patients with Meniere’s disease or benign paroxysmal positional vertigo (BPPV) are potential candidates to develop Hashimoto’s thyroiditis and vice versa [67,68,69].

This entry is adapted from the peer-reviewed paper 10.3390/ijms24129826

This entry is offline, you can click here to edit this entry!
Video Production Service