Thyroid hormone T3 largely determines how much energy your body burns at rest, regulates fat metabolism and cholesterol, and responds to signals about food intake and stress. Both an underactive and an overactive thyroid have measurable consequences for weight and energy levels. The relationship with excess weight also runs in the opposite direction: adipose tissue can disrupt thyroid function.
The thyroid gland produces two hormones, T4 and T3. T4 is the 'storage' form and is converted in tissues such as muscles into the active T3 by an enzyme called D2. T3 is then one of the most important drivers of the resting metabolic rate: it controls how much energy your cells burn at rest. Without sufficient T3, your energy expenditure drops measurably, which can manifest as fatigue, feeling cold and weight gain (PMID 24692351, 34574358, 4363889).
The conversion of T4 to T3 by D2 also plays a role in heat production, for example in cold conditions. In brown adipose tissue and skeletal muscle, this enzyme can increase the local availability of T3, causing extra heat to be generated. In newborns and small mammals this is well established. In healthy adults, brown adipose tissue is only present in limited amounts, and skeletal muscle likely plays a larger role in this adaptation. The mechanism is plausible, but its precise significance for humans has not yet been fully clarified (PMID 24692351, 16283553).
T3 also influences fat metabolism: it directs both fat breakdown and fat storage in fat cells, and regulates the production and removal of cholesterol via the liver. This explains why people with an underactive thyroid (hypothyroidism) often have elevated cholesterol (PMID 24692351, 34574358).
The thyroid is controlled by a chain of brain signals: the hypothalamus releases TRH, which prompts the pituitary gland to produce TSH, which in turn stimulates the thyroid to make T3 and T4. This chain adapts based on the body's energy status: during prolonged fasting or severe stress, thyroid activity decreases. The appetite centre in the brain also responds to T3 and TSH, but how large this effect is in practice in humans has not been sufficiently studied (PMID 27515033, 34745011, 24692351, 34574358).
Even a mild, 'silent' underactivity of the thyroid (subclinical hypothyroidism, where a person has few or no symptoms but TSH is already slightly elevated) can already lower the resting metabolic rate and thereby contribute to weight gain. Importantly, the relationship also works in the other direction: excess weight can disrupt thyroid function through inflammatory substances released by adipose tissue. It is therefore not a simple one-way street (PMID 34574358).
Finally, there is one small study (28 people with the autoimmune condition Hashimoto's disease) that investigated the so-called AIP diet. The results were mixed: symptoms and weight improved, but the two antibodies examined showed contradictory responses. The study is too small and too short to base any practical recommendations on (PMID 37772528).
Three of the sources are review articles/overview studies on thyroid hormone physiology (PMID 24692351, 34574358, 4363889). The remaining sources are mechanistic studies or a small intervention study (n=28). No large RCTs or meta-analyses are included in the supplied claims. The basic physiology (T3/T4 and resting metabolism) is well supported; the appetite-related effects and the role of D2 in adult humans are less certain.