This is one of the very interesting potential anti-cancer treatments and I am very enthusiast about it. It is relevant for most type of cancers, it is cheap and accessible and can be performed at home, while tracking some of the thyroid hormones via weekly blood tests. Its effectiveness in prolonging life (or even obtaining complete remission) has already demonstrated on humans and published recently, while the theory is 20-30 years old.
As a result, I would strongly suggest to discuss this option with your doctor.
Summary & Mechanism
Hypothalamus sends signals to pituitary gland via the hormone TRH. Pituitary gland than sends the signal to the Thyroid gland via the hormone TSH. As a result Thyroid gland will start producing T4 hormone as well as T3. However, most (95%) of the hormone produced in thyroid is T4 (Thyroxine) while T3 (Triiodothyronine) is produced based on T4 in other organs, but most in the liver. T3 is the active form of thyroid hormone which is produced as a result of one iodine being cleaved from T4.
In a study from 2015, 23 stage IV cancer patients, were treated by inducing hypothyroxinemia, which means lowering thyroid hormone T4 levels. This T4-depleting therapy far exceeded the expected survival in most cases. They achieved this simply by lowering the activity of the thyroid with the help of a common drug and at the same time supplementing the T3, via oral administration of T3 capsules. In case of the patients with low thyroid function, previously on T4 supplementation, they just had to stop T4 supplementation and replace that with T3 capsules. As a result, T3 has been maintained in normal range while T4 was pushed down below the normal range.
Note: About 60% of the T4 is converted into T3, 20% is converted into an inactive form of thyroid hormone known as reverse T3 (irreversible), and the remaining 20% is converted into T3S (T3 sulfate) and T3AC (triiodothyroacetic acid). Reverse T3 can be problematic; even though it is inactive, it will still bind to T3 receptors and block T3 from binding and working its magic on metabolism. Too much or too little cortisol that is produced by the adrenal glands will increase circulating levels of reverse T3. This mechanism is due to suppressed liver detoxification and clearance of reverse T3 from excess cortisol production. Stress can not only cause signs of hypothyroidism but it will also impair the liver€™s ability to detoxify. Cortisol will also suppress TSH production resulting in low thyroid function. (Ref.)
GBM ON L-T4 GBM O L-T4 -3 WEEKS GBM ON L-T4 GBM O L-T4 -On T3 ON L-T4 O L-T4 -3 On T3 HYPOTHYROXINEMIA MEDIATED BY EXOGENOUS 3,5,3′-TRIIODO-L-THYRONINE [T3] IS ASSOCIATED WITH TUMOR RESPONSE IN CANCER PATIENTS: A COMPASSIONATE CARE EXPERIENCE
67 year old woman on L-T4 supplementation pre and post CRANIOTOMY and biopsy -of 3.5×3.5 cm L. parieto-occipital glioblastoma[GBM]. Rapid Performance Status deterioration while on post-operative radiation therapy [3960cGy] and Temodar –From ECOG 1 TO 3[KPS80 to 40] –patient incapacitated No response to high dose dexamethasone. Memory impairment and visual eld loss. MRI showed signicant tumor enlargement, 6X5cm contralateral spread and vasogenic edema. Recovery not expected. Patient’s 75 ug /day L-T4 discontinued –exogenous T3 initiated . After 7 days signicant clinical and neurological improvement-patient become ambulatory. At 3 weeks MRI shows signicantly smaller tumor and decrease in vasogenic edema. CLINICAL COURSE radiation therapy and chemotherapy. L-thyroxine supplementation 88 mcg/day. Exogenous T3 initiated 6.25mcg x 3 /day.
See the above case report.
Preparation & Administration
Methimazole 40€“50 mg/day (single dose or divided doses) and L-T3 5€“6.25 mg 3 times per day were used initially while adjusting doses at 2- to 4-week intervals until serum TSH concentration was reduced to the lower limit of the reference range and FT4 had fallen below reference range and stabilized.The final doses of methimazole ranged from 20 to 50 mg/day in single or divided doses and L-T3 ranged from 5 to 12.5 ug 2 or 3 times per day up to a maximum of 37.5 ug/day. (Ref.)
T3 should be taken on an empty stomach, 2h after food 1h before eating again.
Source & Cost
Methimazole can be bought at online pharmacies on the web
Both are cheap enough to be accessible to anyone.
Synergists & Antagonists
Other relevant links:
1981: Inhibition of Local and Metastatic Hepatoma Growth and Prolongation of Survival after Induction of Hypothyroidism http://cancerres.aacrjournals.org/content/41/8/3040
2013: Thyroid hormone, thyroid hormone receptors, and cancer: a clinical perspective http://erc.endocrinology-journals.org/content/20/2/R19?cited-by=yes&legid=erc;20/2/R19
2015: Medically induced euthyroid hypothyroxinemia may extend survival in compassionate need cancer patients: an observational study. http://www.ncbi.nlm.nih.gov/pubmed/25410096
Cancer Cell Gene Expression Modulated from Plasma Membrane Integrin Î±vÎ²3 by Thyroid Hormone and Nanoparticulate Tetrac. http://www.ncbi.nlm.nih.gov/pubmed/25628605
Integrin Î±vÎ²3-Targeted Cancer Therapy http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901818/
Spontaneous remission of cancer–a thyroid hormone dependent phenomenon? http://www.unboundmedicine.com/medline/citation/10697597/Spontaneous_remission_of_cancer__a_thyroid_hormone_dependent_phenomenon
Mitotane Treatment in Patients with Adrenocortical Cancer Causes Central Hypothyroidism. http://www.ncbi.nlm.nih.gov/pubmed/26221968
Thyroid hormones and cancer: clinical studies of hypothyroidism in oncology http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.658.2074&rep=rep1&type=pdf Accumulating clinical evidence may justify new, broadly-based controlled studies in cancer patients of the possible contribution of thyroid hormone to tumor behavior
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