Do thyroid problems lead to decreased brain function or the onset of dementia?

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In addition, each study used different doses of levothyroxine with specific tools for evaluating cognition. The majority of published articles assessed only limited aspects of cognitive function. According to Samuels et al., his cross-sectional study of 20 euthyroid and 34 treated hypothyroid patients with LT-4 showed decreased health status, psychological function, working memory, and motor learning compared to euthyroid controls 32. According to an online survey of hypothyroid patients, 60%of those who received an LT-4 drug experienced increased memory problems 55. Alzheimer’s disease (AD) has received significant attention by the medical world because it accounts for the majority of dementia cases (Katzman, 2008). In an attempt to unravel the mysteries of AD etiology and progression, some researchers sought to find an association with prior or concurrent medication use.

This website does not provide, and should not be used for, medical advice, diagnosis, or treatment. You should consult with your healthcare providers when making decisions regarding your health. For the analysis and data extraction, we finalized the free full-text papers that met the above requirements. The study also showed that patients who were women were more likely to have low TSH levels and be overtreated. The authors declare no conflicts of interest or financial interests in any product or service mentioned in this article including grants, employment, gifts, stock holdings, or honoraria.

Statistical Analysis

Hypothyroidism alters the expression of synaptic proteins involved in acetylcholine release 37. One of the mechanisms by which LT-4 recovers cognitive function could be increased cholinergic activity 38. GABA inhibits the release of TSH from the pituitary gland, while thyroid hormones affect multiple components of the GABA system. Thyroid hormone deficiency may cause disruptions in the GABA synthesizing enzyme, resulting in lower GABA content in the hippocampus 17,39.

• Expression of significant components in the MAPK/ERK-CREB and Ca2+/Calmodulin pathways, which are crucial for synaptic plasticity, decreases in the hypothyroid state and restored after thyroid hormone supplementation (68).
• These studies suggest that there may be a loss of acetylcholine due to TRH depletion, the elevation of acetylcholinesterase activity or other reasons yet to be explored in the hyperthyroid state, leading to cognitive impairment.
• Given the theoretically increased risk of cognitive decline with thyroid dysfunction, it is conceivable that thyroid diseases can contribute to the pathophysiology of AD.
• A few animal studies reported a 30% reduction in proliferating neurons in the hippocampus without thyroid hormone 24.

A reanalysis of eight case-control studies exposed a significantly heightened risk of AD in patients with hypothyroidism (26). We found a nonsignificant trend suggesting that baseline thyroid dysfunction may also be related in some way to more rapid time to diagnosis of DAT. All referenced reports that found no association relied on cross-sectional analysis, eventually citing a lack of extensive follow-up as a weakness.

Thyroid hormones can also affect adult hippocampal neurogenesis by stimulating the proliferation, survival and differentiation of dentate granule cell progenitors (67). Expression of significant components in the MAPK/ERK-CREB and Ca2+/Calmodulin pathways, which are crucial for synaptic plasticity, decreases in the hypothyroid state and restored after thyroid hormone supplementation (68). Meanwhile, antithyroid drug administration led to a reduction in serum BDNF levels and a developmental delay in primary hippocampal neurons in rats, and the addition of BDNF can rescue this synthroid vasculitis variation (69).

• Past research has focused on relationships between dementias and a broad spectrum of drug classes, including estrogens (Slooter et al., 1999), antidepressants (Mayeux and Sano, 1999), antihypertensives (Yasar et al., 2006), and statins (Hayden et al., 2005).
• Lisinopril is used to help lower blood pressure in people who have high blood pressure.
• Referral by a primary care physician or other health professional accounts for approximately 20% of participants.
• Several processes, such as obesity, leptin resistance, inflammation, chronic illness, prescription medications (and so on), limit how well your body can turn T4 into T3.
• We tested the Cox proportional hazards assumption by adding the interaction term between hormone level and age to the model.

• Imaging studies revealed levothyroxine’s reversible effect on cerebral blood flow, brain function, cortical excitability, and brain metabolic activity 17,28,48-50.
• However, we must admit that the exact mechanisms and the sequence of events between thyroid dysfunction and AD have not yet been convincingly concluded.
• In addition to cognitive decline, too much thyroid hormone is linked to other health risks, including atrial fibrillation (AFib)—an irregular heartbeat that can lead to blood clots and stroke—and a risk of fractures (especially in older women), according to Cooper.

And this is one of the reasons why prescription medications have negative side effects. But, they differ from hormones in one very important way, they are not natively found inside of the body which means they are a foreign substance. While hormones do require a prescription to obtain from your pharmacy, they are not the same as prescription medications. There is also a big difference between the use of hormones and the use of prescription medications. If your body can’t convert T4 into T3, then it will build up a large store of free T4 with inadequate or low levels of T3. Free T3 should be differentiated from other thyroid lab tests and measurements including TSH (which is commonly used), Free T4, and thyroid antibodies.

This sudden drop in thyroid medication may cause symptoms such as weight gain, increased fatigue, hair loss, cold intolerance, and so on. I’ve discussed the side effects which can occur when you stop taking your thyroid medication on my blog before and I would encourage you to read this post for more information. That means most people experience negative side effects when taking thyroid medication because they are not taking enough or because they are taking too much. Sometimes you can experience mild side effects such as stomach upset or nausea which is related to fillers and binders in your thyroid medication, but these are infrequent.

1. The effect of hyperthyroidism on AD

The dose was titrated until the suppression of TSH with the same proportion of dose adjustments in the placebo. Two studies compared pre- and post-treated hypothyroid patients with age and sex-matched euthyroid controls 16,17. Two studies assessed the post-treatment effect on hypothyroid patients without controls 18,19. Thyroid function tests were conducted on all patients and controls before and after the replacement of LT-4 in all studies 16-21. The most common and precocious are neurocognitive alterations (memory and attention difficulties), followed by depression.

The clinical presentation includes cognitive, attention, and mood disorders such as depression, which in many cases point to hippocampal dysfunction 24. Cognitive impairments include poor recall, slow thought process, acalculia, impaired motor learning, and visuospatial abilities leading to pseudo dementia 30-34. The thyroid hormone has an outstanding role in neuron regulation in the adult brain.