[Lotus]

I just think god made some people men and we aren't meant to look female and grow breasts, while people like you are made to grow breasts and any method will make your chest grow.

I agree in part with the former, but the latter is a garbage statement...and a copout. 

You should do more research before claiming reishi is poisonous. Reishi mushroom extract is Hepatoprotective...meaning it protects the liver. Reishi protects the liver mainly from its polysaccharides, antioxidants and free radical-scavenging activity. Here's only two studies (of many) on hepatoprotective activity of reishi. 

Hepatoprotective Activity and the Mechanisms of Action of Ganoderma lucidum (Curt.:Fr.) P. Karst. (Ling Zhi, Reishi Mushroom) (Aphyllophoromycetideae) 

Yihuai Gao, Min Huang, Zhi-Bin Lin, Shufeng Zhou 

International Journal of Medicinal Mushrooms 5 (2), 2003 

Herbal medicines are always considered to be a safe and useful approach for the treatment of chronic hepatopathy. Ganoderma lucidum (Curt.: Fr.) P. Karst.[(Ling Zhi, Reishi mushroom)(Aphyllophoromycetideae)], a highly ranked medicinal mushroom in Oriental traditional medicine, has been widely used for the treatment of chronic hepatopathy of various etiologies. Data from in vitro and animal studies indicate that G. lucidum extracts (mainly polysaccharides or triterpenoids) exhibit protective activities against liver injury induced by toxic chemicals (eg, CCl 4) and Bacillus Calmette-Guerin (BCG) plus lipopolysaccharide (LPS). G. lucidum also showed anti–hepatitis B virus (HBV) activity in a duckling study. Recently, a randomized placebo-controlled clinical study showed that treatment with G. lucidum polysaccharides for 12 weeks reduced hepatitis B e antigen (HBeAg) and HBV DNA in 25%(13/52) patients with HBV infection. The mechanisms of the hepatoprotective effects of G. lucidum have been largely undefined. However, accumulating evidence suggests several possible mechanisms. These include antioxidant and radical-scavenging activity, modulation of hepatic Phase I and II enzymes, inhibition of b-glucuronidase, antifibrotic and antiviral activity, modulation of nitric oxide production, maintenance of hepatocellular calcium homeostasis, and immunomodulating effects. G. lucidum could represent a promising approach for the management of various chronic hepatopathies. Further studies are needed to explore the kinetics and mechanisms of action of G. lucidum constituents with hepatoprotective activities.
https://www.researchgate.net/publication...eae_Review


Hepatoprotective Effects of Mushrooms

6.2. Triterpenoids, Polysaccharides and Peptides from Ganoderma lucidum 

The most studied mushroom with respect to hepatoprotective effects is Ganoderma lucidum. This fact is not surprising because G. lucidum is, indubitably, the most studied medicinal mushroom. Approximately 400 chemical substances have been isolated from G. lucidum, which include mainly polysaccharides, triterpenoids, nucleosides, ergosterols, fatty acids, proteins/peptides, and trace elements. Particularly polysaccharide and triterpenoid components in G. lucidum have been proposed as the bioactive constituents responsible for the protective activities against toxin-induced liver injury [105,106,107]. In a broad review about the hepatoprotective properties of G. lucidum, Gao et al. [106] collected evidence to suggest possible molecular mechanisms to explain its hepatoprotective actions. Among these mechanisms, the authors include antioxidant and radical-scavenging activity, modulation of hepatic Phase I and II enzymes, inhibition of β-glucuronidase, antifibrotic and antiviral activity, modulation of nitric oxide production, maintenance of hepatocellular calcium homeostasis, and immunomodulatory effects. 

Data from in vitro and animal studies indicate that G. lucidum extracts, mainly polysaccharides or triterpenoids, exhibit protective activities against liver injury induced by toxic chemicals (e.g., CCl4) and Bacillus Calmette-Guerin (BCG) plus lipopolysaccharide (LPS). The fungus also showed antihepatitis B-virus (HBV) activity in a duckling study. Recently, a randomized placebo-controlled clinical study showed that treatment with G. lucidum polysaccharides for 12 weeks reduced hepatitis B e antigen (HBeAg) and HBV DNA by 25% (13/52) in patients with HBV infection. The mechanisms of the hepatoprotective effects are still undefined. Evidence suggests that antioxidant and radical scavenging activity, modulation of hepatic phase I and II enzymes, inhibition of b-glucuronidase, antifibrotic and antiviral activity, modulation of nitric oxide production, maintenance of hepatocellular calcium homeostasis, and immunomodulatory effects might be involved [107]. 

The effects of total triterpenoids extracts from G. lucidum on two different experimental liver injury models induced by carbon tetrachloride and d-galactosamine were extensively studied in mice [35,40,108,109]. Administration of the extract (80 mg/kg) significantly inhibited the increase of serum ALT and liver triglyceride levels in the models, effects similar to those of malotilate, a known reference substance for this kind of protective effects [110]. The G. lucidum extract also antagonized the decrease of the SOD activity and the GSH content and inhibited the increase of the MDA content in the carbon tetrachloride and d-galactosamine liver-injured mice. It could equally improve the histopathological changes. These observations are likely to indicate that triterpenoids isolated from G. lucidum have a powerful protective effect against liver damage induced by carbon tetrachloride and d-galactosamine. Their hepatoprotective effects were perhaps related to the ability to increase the activity of free radical scavenging enzymes and, thus, to raise the ability of antioxidation. It should be stressed that ganoderic acid (Figure 2), one of the triterpenoids found in G. lucidum, was proven to be a potent inhibitor of β-glucuronidase activity, an indicator of hepatic damage [111]. 

The hepatoprotective activity of peptides from Ganoderma lucidum was evaluated against d-galactosamine (d-GalN)-induced hepatic injury in mice. G. lucidum peptides were administered via gavage daily for two weeks at doses of 60, 120 and 180 mg/kg, respectively. The d-GalN-induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (AST, ALT) in serum, by the increased MDA levels in the liver, and by significant decreases in the activity of SOD and in the GSH level in the liver. Pretreatment of mice with G. lucidum peptides maintained these parameters at their normal values. These biochemical results were supplemented by histo-pathological examination of liver sections. The best hepatoprotective effects of the G. lucidum peptides were observed after treatment with the dose of 180 mg/kg as deduced from the biochemical parameters and liver histopathological examinations. Results of this study revealed that the G. lucidum peptides can produce a significant diminution of the d-GalN-induced hepatocellular injury [40].

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6270077/#!po=30.5310


If you don't have SHBG tested you won't be able to determine how much free E2 (or its percentage) is available to bind in tissues. You can actually have normal range E2 but low free E2, thus a very small percentage of free E2 is available to make a significant impact on breast growth or feminization. 

Total estradiol (or even total T) only paints a partial picture...ask your doctor for this test. There's no reason or excuse why you shouldn't ask. I believe there's nothing else to discuss here until you have test results to share.