What does your thyroid gland do to your metabolism and energy?
A properly functioning thyroid directly determines your energy expenditure, weight and cholesterol. If you suffer from persistent fatigue, feeling cold or unexplained weight gain, it is worthwhile asking your GP for a blood test.
Your thyroid produces two hormones: T4 and T3. T4 is the storage form; in tissues such as muscles it is converted into the active T3. T3 is one of the biggest drivers of your resting metabolism: it determines how much energy your cells burn while you are doing nothing. Too little T3 measurably lowers your energy expenditure. You notice this as fatigue, feeling cold and weight gain1,2,3.
The enzyme that converts T4 into T3 also plays a role in heat production in the cold. In brown adipose tissue and muscles it can increase local T3 availability, releasing extra heat. In newborns and small mammals this has been well demonstrated. In adult humans brown adipose tissue is present only in limited amounts and muscles likely play a larger role. How significant this effect is in daily life is not yet fully understood1,4.
T3 also governs fat metabolism: both fat breakdown and fat storage, and through the liver the production and clearance of cholesterol. This explains why people with an underactive thyroid (hypothyroidism) typically have elevated cholesterol1,2.
The thyroid does not work alone. The brain directs the thyroid via two intermediate stations to produce T3 and T4. During prolonged fasting or severe stress that activity decreases. The appetite centre in the brain also responds to thyroid hormones, but how large that effect is in practice in humans has not yet been sufficiently studied5,6,1,2.
Even a mild, symptom-free underactivity in which your blood values are already slightly abnormal can lower your resting metabolism and thereby contribute to weight gain. Conversely, excess body weight can disrupt thyroid function through inflammatory substances released from fat tissue. It is therefore not a simple one-way street2. Finally, one small study involving 28 people examined the AIP diet in the autoimmune condition Hashimoto's disease. Symptoms and weight improved, but the results were contradictory. The study is too small to base practical recommendations on7.
Three sources are review articles on thyroid hormone physiology (PMID 24692351, 34574358, 4363889). The remainder are mechanistic studies or a small intervention study (n=28). There are no large randomised trials or meta-analyses. The basic physiology surrounding T3, T4 and resting metabolism is well supported. The influence on appetite and the role of the T4-to-T3-converting enzyme in adult humans are less certain.