Hypothyroidism and slow metabolism are related. The pituitary gland in the brain is responsible for sleep, food cravings, stress and sex/thyroid hormones. It regulates thyroid hormones.
Thyroid hormone (TH) is required for normal development as well as regulating metabolism in the adult. The thyroid hormone receptor (TR) isoforms, α and β, are differentially expressed in tissues and have distinct roles in TH signaling. Local activation of thyroxine (T4), to the active form, triiodothyronine (T3), by 5′-deiodinase type 2 (D2) is a key mechanism of TH regulation of metabolism. D2 is expressed in the hypothalamus, white fat, brown adipose tissue (BAT), and skeletal muscle and is required for adaptive thermogenesis. The thyroid gland is regulated by thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH). In addition to TRH/TSH regulation by TH feedback, there is central modulation by nutritional signals, such as leptin, as well as peptides regulating appetite. The nutrient status of the cell provides feedback on TH signaling pathways through epigentic modification of histones. Integration of TH signaling with the adrenergic nervous system occurs peripherally, in liver, white fat, and BAT, but also centrally, in the hypothalamus. TR regulates cholesterol and carbohydrate metabolism through direct actions on gene expression as well as cross-talk with other nuclear receptors, including peroxisome proliferator-activated receptor (PPAR), liver X receptor (LXR), and bile acid signaling pathways. TH modulates hepatic insulin sensitivity, especially important for the suppression of hepatic gluconeogenesis.
A. Hypothalamic-Pituitary-Thyroid Axis
TH is secreted from the thyroid gland under the regulation of the hypothalamic-pituitary axis (). TRH, secreted from the hypothalamus, acts upon the pituitary gland, binding to G protein-coupled TRH receptors on the thyrotrope, resulting in an increase in intracellular cAMP, and subsequent thyrotropin (TSH) release ( ). Hormone signals that have modulatory effects on TSH secretion include dopamine ( ), somatostatin ( ), and leptin ( ), which function as a point of central regulation of thyroid hormone release ( ). TSH secretion, and its sensitivity to TRH stimulation, is affected by renal failure, starvation, sleep deprivation, depression, and hormones, including cortisol, growth hormone, and sex steroids ( , ).
The importance of the adrenergic nervous system in central TRH/TSH regulation is being increasingly recognized (). The combination of central nutritional and hormonal signals, including leptin, adrenergic signaling, and cortisol, integrate information regarding overall nutritional status, circadian rhythms, as well as acute stress, to modulate thyroid hormone production ( , ). A central regulator of circadian rhythms, the RevErbAα/RevErbAβ nuclear receptors, are activated by BMAL-1, which then suppresses BMAL-1 transcription ( ). RevErbAα is transcribed from the strand opposite the TRα gene and binds heme.
TSH binds to a G protein-coupled TSH receptor on the thyroid follicular cell, stimulating the production and release of TH. T4, a prohormone, is the primary secretory product of the thyroid gland, which utilizes MCT8 for secretion (). Local conversion of T4 to T3
, by D2, provides negative feedback at the level of both thyrotrophs in the pituitary and tanycytes in the hypothalamus (, , ). This results in reduction in TRH and TSH secretion in response to adequate tissue levels of TH. Polymorphisms in the D2 gene have been associated with interindividual variation in the TSH-free T4 “set point” ( ).
. Ashwaganda: This supplement may increase both thyroxine (T4) and its more potent counterpart, active thyroid hormone (T3). Ashwaganda appears to boost thyroid function without influencing the release of the TSH, indicating that it works directly on the thyroid gland and other body tissues. This is good news, since thyroid problems most often occur within the thyroid gland itself, or in the conversion of T4 into T3 in tissues outside the thyroid gland. Take 750-1,000 mg twice a day. Ashwaganda is my favourite choice for supporting the thyroid when stress is also a concern.
2. L-Tyrosine: The amino acid tyrosine is necessary for the production of thyroid hormone in the body. It takes four weeks to reach full effectiveness, so starting this at the beginning of a weight-loss program is a good idea. Seeing as tyrosine increases the production of both dopamine and thyroid hormone, it could give you just the boost you need to push past your plateau. The recommended dose is 1,000 mg on rising, before breakfast. Do not take this supplement if you have high blood pressure.
3. Coconut oil: Not all fats are created equal and by the same token, not all fats are unhealthy. One way to boost a sluggish thyroid is to consume non-hydrogenated coconut oil. This is a medium-chain saturated fat that promotes healthy weight loss and is thought to naturally stimulate the thyroid. Unlike olive oil, it has a high heat tolerance so you can actually use it to cook your food, or include a tablespoon in your morning smoothies for a summer-fresh taste.