Milk thistle Cushings Disease

[Barbarossa]

Hey Guys,

I am taking Milk thistle since 3 weeks against pituitary tumor aka Cushings Disease and
it doesn’t work anymore against my symptoms(anxiety, more relaxed, blood pressure, weight loss) for a few days.
I take 1500 mg per day.
Could be this a sign of adaptation of my body or tolerance against it?

Could I try a higher dosage? Studies show a 1500 mg dosage for humane but I don’t know if I can go higher..

I really need help…

 

[HighT]

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[Peachy]

Do you think the main reason it was working was its effects on the liver? Maybe use it in combination with or alternating with other herbs that help with liver function?

Offhand, ones I’d research - dandelion, burdock, hibiscus (blood pressure), medicinal mushrooms

 

[cs3000]

Hey Guys,

I am taking Milk thistle since 3 weeks against pituitary tumor aka Cushings Disease and
it doesn’t work anymore against my symptoms(anxiety, more relaxed, blood pressure, weight loss) for a few days.
I take 1500 mg per day.
Could be this a sign of adaptation of my body or tolerance against it?

Could I try a higher dosage? Studies show a 1500 mg dosage for humane but I don’t know if I can go higher..

I really need help…

I've seen cyproheptadine can cause rebound increase in cortisol in cushings (if taken in high doses)
so if going off it has to be stopped slowly in this case , tapered off

Rebound elevation of Cortisol following cyproheptadine withdrawal in Cushing’s disease from a pituitary macroadenoma - Journal of Endocrinological Investigation

A 44-year-old female with Cushing’s disease associated with a pituitary macroadenoma was treated with cyproheptadine, 24 mg per day, after partial surgical resection of the tumor. A large residual tumor remained. There was no clear suppression of serum and urinary Cortisol during therapy, but...

link.springer.com

btw Vitamin A high dose might help you out

New Insights in Cushing Disease Treatment With Focus on a Derivative of Vitamin A

Cushing’s disease (CD) is an endocrine disorder originated by a corticotroph tumor. It is linked with high mortality and morbidity due to chronic hypercortisolism. Treatment goals are to control cortisol excess and achieve long-term remission, ...

www.ncbi.nlm.nih.gov

A first clinical human study demonstrated clinical and biochemical effectiveness in 5/7 patients treated with RA for a period of up to 12 months. In a recent second clinical trial, 25% of 16 patients achieved eucortisolemia, and all achieved a cortisol reduction after 6- to 12-month treatment.

normal ACTH-secreting cells express COUP-TFI, but tumoral cells do not (112). Corticotroph normal cells do not respond to RA treatment and this may be attributed to the fact that they express the inhibitory factor COUP-TFI. In fact, when tumoral cells responding to RA are transfected with a COUP-TFI expression vector, the response to RA is abolished (112). In 34 specimens of human pituitary adenomas, 29 expressed COUP-TFI but only 5 of them presented expression of COUP (122). This interesting difference between normal/tumoral COUP-TFI expression makes this protein a promising biomarker of a possible response of the cells to RA action

if u tolerate vitamin D, it can help balance out bone resorption effects

dose of retinoic acid = 10mg increased up to 80mg daily
https://pubmed.ncbi.nlm.nih.gov/22851491/

A marked decrease in UFC levels was observed in five patients; mean UFC levels on retinoic acid were 22-73% of baseline values and normalization in UFC was achieved in three patients. Plasma ACTH decreased in the first month of treatment and then returned to pretreatment levels in responsive patients whereas no clear-cut pattern could be detected for serum cortisol. Blood pressure, glycemia, and signs of hypercortisolism, e.g. body weight and facial plethora, were ameliorated to a variable extent on treatment. Patients reported only mild adverse effects, e.g. xerophthalmia and arthralgias.

Conclusions: Long-term treatment with retinoic acid proved beneficial and well tolerated in five of seven patients with Cushing's disease. This represents a novel, promising approach to medical treatment in Cushing's disease.

idk the dose conversion of retinol to retinoic acid if u cant find retinoic acid directly, or conversion of retinyl palmitate to retinoic acid
it might be 10x higher retinol dose needed? so 100mg+. liver is highest natural source but supplementation needed for those doses

 

[cs3000]

@Barbarossa Found this and remembered your post

alongside the vitamin A,

Ursolic acid decreases ACTH secretion in pituitary tumor cells. and it crosses the blood brain barrier
Ursolic acid suppresses growth and adrenocorticotrophic hormone secretion in AtT20 cells as a potential agent targeting adrenocorticotrophic hormone-producing pituitary adenoma

edit: problem is it has very low oral availability so i dont even think there would be effect orally?
holy basil has ursolic acid there's standardized products
maybe sublingual ursolic acid would work? if it can be tolerated on tissue
https://examine.com/supplements/ursolic-acid/research/
in humans high amounts stayed at low microgram/ml concentrations even when injected
took 20 - 40 micro mole in the cell study. which is like 0.45mg/ml. so way higher. no good.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647049/

AtT20 cells, incubated for 48 and 96 h with these carotenoids. We observed a decrease in cell viability caused by the lycopene and beta-carotene treatments. Also, carotenoids induced apoptosis after 96 h. Lycopene and beta-carotene decreased the secretion of ACTH in AtT20 cells in a dose-dependent manner.
These results show that lycopene and beta-carotene were able to negatively modulate events related to the malignant phenotype of AtT-20 cells, through a mechanism that could involve changes in the expression of connexin 43, Skp2 and p27kip1; and suggest that these compounds might provide a novel pharmacological approach to the treatment of Cushing’s disease.

Most carotenoids are lipophilic with the ability to cross the blood-brain barrier