Sarah Rice BSC. (Hons), Mcoptom (UK), MHP, NNP
Import
A recent study by Vranjić et al. (2025) It reviews the complex interaction between the function of the ketogenic diet (KD) and the thyroid, underlining metabolic, hormonal, immune and individual factors mediated in this relationship (1).
The relationship between metabolic health and the function of the thyroid is complex and two-way, where the non-thyroid disease describes the condition by which the hypothalamic-hypotharoid-thyroid system and the metabolism of the thyroid hormone is abnormal due to non-thyroid. Studies indicate that glycemic control and function of the thyroid are interconnected, with abnormal TSH concentrations that occur in a slightly controlled type 2 diabetes and an increased risk of autoimmune thyroid disease occurring in type 1 diabetes (2, 3). The two -way relationship between obesity and thyroid disease also reflects this complexity (3). Insulin resistance is involved in the development of thyroid and disease dysfunction, where the highest levels of insulin circulation can cause increased proliferation of the thyroid and inversely resistance to insulin and type 2 diabetes. This complex relationship extends to the effect of nutritional ketosis on metabolic pathways, which can regulate thyroid hormones (1).
A metabolic advantage to healthy people?
A shortening Looking at the effect of nutritional KETA on healthy participants, they used three weeks of iso-Iso-Iso-Crossover, comparing a low-carbohydrate diet with a low-fat carbohydrate diet (5). They found that the KD led to greater weight loss, without any change in the metabolic rate of rest (RMR). Compared to pre-order levels, the TSH and T4 creature were unchanged, while the T3 plasma concentration was significantly lower after the KD diet (T3 unchanged on the low fat diet). Nutritional ketosis can contribute to a metabolic advantage through the effect of thyroid hormones on the metabolic pathways associated with storage and energy costs, including lipid metabolism and carbohydrates. Thyroid hormones mediate the metabolic rate and adaptive thermogenesis, playing an important role in determining body weight. An interesting observation was that the displacement of the hormones that occurred in this study is similar to the effect observed in the cold exposure, suggesting that dietary ketosis leads to similar changes to the metabolic effect of brown adipose tissue as shown with cold stimulation (5).
Improvements in Hashimoto’s thyroiditis using TCR
Hashimoto (HT) thyroiditis is an autoimmune endocrine condition and the most common form of thyroiditis. At its core, HT is an inflammatory disorder with basic characteristics, including the production of pro -imemic cytokines (TNF-alfa, interleukin-6) that leads to an increase in extracellular levels and water retention, which is observed as an increase in water supply. Research suggests potential TCR benefits for thyroiditis through mechanisms that include reducing inflammation and improving insulin sensitivity, which help improve metabolic indicators in this population.
In this study by Huang et al. (2024)Magnetic resonance scans were used to assess the synthesis of the thyroid to determine dietary effects. After 6 months, it was observed that patients in the group of reduced carbohydrates had significant reductions in thyroid water content, along with a decrease in thyroid antibodies (TPOAB and TGAB) (6).
Thyroid hormone regulation under KD
KD changes several hormonal pathways: Leeptin and insulin levels are decreasing, reducing the activity of the secretion of Th and TSH and Deiodinase, while cortisol is increasing transiently during early adjustment, possibly suppressing the HPT axis. Ghrelin may increase, but its effect is small compared to leptin and cortisol (1). Adequate protein is important for the synthesis of hormones and fat quality can also affect inflammation and function of the thyroid. The absorption of germs and nutrients, paying attention to selenium, iodine and zinc, are other important components of a successful dietary approach (1).
KD leads to reduced tropythyronine circulation (T3) levels, often without a compensatory increase in thyroid stimulation hormone (TSH), indicating a non -pathological, adaptive regulation of thyroid activity (1). This decrease is mainly due to the reduced deiodinase activity, resulting from lower levels of insulin and glucose, which prevents thyroxin (T4) converting to active T3. The reverse T3 can be increased by further reducing the availability of active thyroid hormone. These changes mimic the normal response to fasting or calorie restriction and are generally not related to obvious hypothyroidism, in the absence of symptoms. In fact, studies show firmly TSH that remains in the range during nutritional icing despite a decrease in T3 (1) concentration.
Individual volatility
Genetic polymorphisms (eg Dio2 Thr92ala, Apoa2, PPARA) affect individual responses to KD, affecting T3 conversion, fat metabolism and ketogenesis efficiency (1). Gender -based differences are remarkable: women are more susceptible to reproductive and thyroid disorders caused by increased leptin sensitivity and changes in thyroxine binding globin (TBG). Progesterone can also affect the sensitivity of thyroid hormones through changes in body temperature and RMR in a circular manner. During nutritional ketosis, changes in T3 concentration can aggravate the circular characteristics of thyroid metabolism in sensitive women. Changing hormones, such as during the adoption or by using oral contraceptives, may affect laboratory measurements, delivering normal T4 with low free T4 and hypothyroidism symptoms (1).
Thyroid hormone regulation under intermittent fasting
Fluctuations in thyroid hormones during fasting appear to be temporary adjustments, with similar changes observed under carbohydrate restriction conditions (1, 7). The decrease in insulin resistance can improve the sensitivity of thyroid hormones as part of the metabolic improvements that may occur during intermittent fasting as well as the reduction of inflammatory markers, which may have a role in managing thyroiditis.
Conclusion
TCR causes adaptive changes in thyroid hormone metabolism, with possible benefits to inflammation and autoimmunity. Variations in the answers to nutritional changes indicate personalized dietary strategies and proper monitoring of relevant measurements is decisive. Further long -term, controlled studies are needed to clarify the safety and efficacy of TCR in various thyroid phenotypes, especially in the ketogenic range.
Resources
Women are particularly vulnerable to thyroid hormone fluctuations and dysfunction due to circular fluctuations and interactions that occur in response to changes in reproductive hormone. The adoption represents a transitional condition where thyroid hormones can range in response to other hormonal changes. Nutrition Network begins a new lesson where you can find out more about how hormonal fluctuations affect metabolic health: Menopause and Waiting:
Science, Strategies and Life Tools to optimize female hormones.
References
- Vranjić, p. (2025) “Operation of ketogen and thyroid: a delicate act of metabolic balancing”, current issues in Molecular Biology, 47 (9), p. 696 Available in: https://doi.org/10.3390/CIMB47090696.
- Iwamoto, Y. et al. (2022) “Effect of acute metabolic disorder associated with hyperglycaemia on thyroid function parameters in adults”, Borders in endocrinology13, p. 869869 Available in: https://doi.org/10.3389/fendo.2022.869869.
- Cywes, R. et al. (2023) ‘Chapter 3 – endocrine’, in TD Noakes et al. (eds) Ketogenic. Academic Press, pp. 107-203. Available in: https://doi.org/10.1016/B978-0-12-821617-0.00010-3.
- Rezzonico, J. et al. (2008) “Introduction of the thyroid gland as another victim of insulin resistance syndrome”, Thyroid®18 (4), pp. 461-464. Available in: https://doi.org/10.1089/thy.2007.0223.
- Iacovides, S. et al. (2022) Could the ketogenic diet cause shift the function of the thyroid and support a metabolic advantage to healthy participants? A test of randomized controlled controlled pilot ,,,,,,,,,,,,,,,,,,,,,,, PLOS ONE17 (6), p. E0269440. Available in: https://doi.org/10.1371/journal.pone.0269440.
- Huang, X.-S. et al. (2024) “Quantitative evaluation of MRI of the effects of low carbohydrate therapy on Hashimoto’s thyroiditis”, endocrine connections, 1 (AOP). Available in: https://doi.org/10.1530/EC-23-0477.
- Shkorfu, W. et al. (2025) “Intermittent fasting and hormonal regulation: paths for improved metabolic health”, science and nutrition of food, 13 (8), p. E70586. Available in: https://doi.org/10.1002/fsn3.70586.
