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Overview of thyroid gland:
- The thyroid gland produces two hormones, T3 (triiodothyronine) and T4 (thyroxine)
- TSH (Thryoid Stimulating Hormone) is released by the pituitary gland to tell the thyroid to make more T3 and T4
- Hypothyroidism is when your thyroid gland is underactive, in blood tests this can show as a high TSH level and low T3/T4 level
- Hyperthyroidism is the opposite.
Effects of Ashwhaganda
- Ashwhaganda has many effects that may be usefull in heightmaxxing however, I am only going to discuss effects that have an effect on the thyroid hormones
- It is well known Ashwhaganda decreases stress and decreases cortisol levels. It also acts as something called a "GABA mimetic". This is means it has a calming effect on your brain. GABA is the prominent inhibitory neurotransmitter in the brain, it promotes relaxation, calmness and sleep
- In a clinical study following 50 people, ashwhaganda was shown to increase levels of T3 and T4 in the blood while decreasing TSH. This trial was a double blind RCT so it's results are likely legit. The dose used was the common 600mg dose too. It is likely it achieves this effect by lowering corisol.
Relationship between thyroid hormones and IGF-1
- IGF-1 is vital if you want to heightmax. You can increase your HGH all you want by gymmaxxing or injecting it or taking peptides etc, but if IGF-1 is not being synthesised in the liver or if your bones are not responding to it - NOTHING WILL HAPPEN
This is claiming that without thyroid hormones, IGF1 synthesis will be limited, so you will have lower IGF1 levels to start of with even if you are dosing HGH. And most importantly: ". Cartilage response to IGF1 and osteoblastic/osteoclastic bone remodeling are also regulated by thyroid hormones." This means if you have hypothyroidism, or even subclinical hypothyroidism your bones will simply not respond to the IGF and you will not grow even if your growth plates are still open.TH potentiate GH stimulation of the synthesis and action of insulin-like growth factor 1 (IGF1) and stimulation of the production of different growth factors (epidermal growth factor, nerve growth factor, and erythropoietin). Cartilage response to IGF1 and osteoblastic/osteoclastic bone remodeling are also regulated by thyroid hormones.
Subclinical hypothyroidism is defined by either borderline high TSH with normal T3/T4 levels or TSH. Unfortunatly many doctors will not treat subclinical hypothyroidism even if you are showing symptomps despite latest evidence saying to treat it. [4]. Alot of people have subclinical hypothryoidism without knowing it.> Even in subclinical hypothyroidism, a condition of mild thyroid failure, growth velocity in children is suboptimal.
Relationship between thyroid hormones and growth plate closure
This is a very important section. Hopefully this emphasises the importance of taking an aromatase inhibitor in your stack. That same research paper has the following claim:> The process of longitudinal bone growth is governed by a complex network of endocrine signals, including growth hormone, IGF1, glucocorticoid, thyroid hormone, oestrogen, androgen, vitamin D and leptin ([Nilsson et al., 2005](https://www.intechopen.com/chapters/42441#B23)). The growth plate consists of three principal layers: the resting zone, proliferative zone and hypertrophic zone. In hypothyroid animals, the proliferative and hypertrophic zones are decreased in height, and chondrocyte proliferation, chondrocyte hypertrophy and vascular/bone cell invasion are affected. In addition, the normal columnar organisation of the growth plate is disrupted (Stivens et al., 2000). Some of the sceletal effects appear to be due to direct action on the growth plate. Growth plate chondrocytes express thyroid hormone receptor (TR) isoforms TR-α, α-1,and β. Most cases of thyroid hormone resistance in humans are caused by dominant-negative mutations of the TR-β gene, which may also affect TR-α function and show variable sceletal effects ([Takeda et al., 1992](https://www.intechopen.com/chapters/42441#B37), [Nilsson et al., 2005](https://www.intechopen.com/chapters/42441#B23)).
TH are critical for normal bone growth and development. In children, hypothyroidism can cause short stature and delayed closure of the epiphyses. Biochemical studies have shown that TH can affect the expression of various bone markers in the serum, reflecting changes in both bone formation and resorption. TH increase alkaline phosphatase and osteocalcin in osteoblasts. Additionally, osteoclast markers such as urinary hydroxiproline, urinary pyridinium, and deoxypyridinium cross-links are increased in hyperthyroid patients. These observations suggest that both osteoblast and osteoclast activities are stimulated by TH ([Yen, 2001](https://www.intechopen.com/chapters/42441#B44)).
This is very information dense so let me summarise:
- Hypothyroidism / Thyroid resistance slows growth plate senesence which leaves the growth plates open for longer
So then why do we not want that? Growth plates being open for longer is good right?Not in this case. Despite our growth plates being open for longer, low T3/T4 levels (or resistance to those hormones) will stop the effect of IGF-1 from taking place.
Also, once your thyroid hormones are working again, you will experience something called "catch up growth", where you will be growing at a much faster rate than normal - HOWEVER your growth plates will shut faster as well. So overall, you will grow less than someone without low levels of T3/T4.
Taking an aromatase inhibitor has been shown to keep the effects of rapid catch up growth while delaying growth plate closure. A dose of 1mg a day of anastrazole is safe to take with normal estrogen levels without experiencing the side effects (as this was used in the case report I am about to link, however it might be different for you)[5] https://doi.org/10.1210/jendso/bvab025
What should you do?
- Before starting your heightmaxxing stack ensure you get your thyroid hormones tested. Ensure T3 and T4 is tested as well as TSH, some doctors, especially in the UK will only test for TSH at first as it saves them money
- If your T3 and T4 is in the lower half of normal and TSH is in the higher half of normal, take ashwhaganda with your heightmaxxing stack, consider taking levothryoxine but that is up to you to look into and decide. As taking too much thyroid hormones can cause a loss in bone density, which is the opposite of what you want for heightmaxxing, ashwhaganda exists as a cheaper, safer and more available alternative.
- If you have hypothyroidism get it treated by a doctor properly while taking HGH + AI at the same time
- If all your values are normal, still take ashwaghanda, you could also take levothryoxine but I would be very catious about this as you dont want to fuck up your thyroid permanetly.
- Make sure you take an aromatase inhibitor.
[1] Pedrón VT, Varani AP, Bettler B, Balerio GN. GABAB receptors modulate morphine antinociception: Pharmacological and genetic approaches. Pharmacol Biochem Behav. 2019 May;180:11-21.
[2] Sharma AK, Basu I, Singh S. Efficacy and Safety of Ashwagandha Root Extract in Subclinical Hypothyroid Patients: A Double-Blind, Randomized Placebo-Controlled Trial. J Altern Complement Med. 2018 Mar;24(3):243-248. doi: 10.1089/acm.2017.0183. Epub 2017 Aug 22. PMID: 28829155.
[3] Saranac L, Stamenkovic H, Stankovic T, et al. (2013) Growth in Children with Thyroid Dysfunction. Current Topics in Hypothyroidism with Focus on Development. InTech. Available at: http://dx.doi.org/10.5772/55017.*
[4] Calissendorff J, Falhammar H. To Treat or Not to Treat Subclinical Hypothyroidism, What Is the Evidence? Medicina (Kaunas). 2020 Jan 19;56(1):40. doi: 10.3390/medicina56010040. PMID: 31963883; PMCID: PMC7022757.
[5] Juanita K Hodax, Lisa Swartz Topor, Shara R Bialo, Jose Bernardo Quintos, Anastrozole Improves Final Adult Height in Severe Hypothyroidism With Rapid Pubertal Progression, _Journal of the Endocrine Society_, Volume 5, Issue 5, May 2021, bvab025, [https://doi.org/10.1210/jendso/bvab025](https://doi.org/10.1210/jendso/bvab025)