This is alot of info, don't try to read it all at once, come back to it over a few sessions. This a truly helpful herb. And its one of a few that can give you energy when you are sooooo exhausted, and things aren't helping. Its non stimulant, and helps clean the liver....

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Red Reishi (Ganoderma Lucidum), commonly known as Ling Zhi in Chinese, is a herbal mushroom known to have miraculous health benefits.

It has been used in Japan and China for over 2,000 years and thus making it the oldest mushroom known to have been used as medicine. Since ancient times, the Reishi mushroom was reserved for emperors and royalties. It has been revered as nature’s rarest and most beneficial herb. In the Superior category of Shen Nung Ben Cao Jing, the oldest and most famous medical text on Oriental herbal medicine, red Reishi is ranked as the number one herb, ahead of ginseng, because of its following qualities:

1. It is non-toxic and can be taken daily without producing any side effects.

2. When it is taken regularly, it can restore the body to its natural state, enabling all organs to function normally.

3. Immune modulator - regulates and fine tunes the immune system.
What are the benefits of Reishi?

Red Reishi is primarily composed of complex carbohydrates called water-soluble polysaccharides, triterpeniods, proteins and amino acids. Researchers have identified that water-soluble polysaccharides are the most active element found in Red Reishi that have anti-tumour, immune modulating and blood pressure lowering effects.

Another major active ingredient found in Red Reishi are triterpenes , called ganoderic acids. Preliminary studies indicated that ganoderic acids help alleviate common allergies by inhibiting histamine release, improve oxygen utilization and improve liver functions. Triterpenes are bitter in taste and the level of the triterpene content contained in a product can be determined by the bitterness.

Regular consumption of red Reishi can enhance our body's immune system and improve blood circulation, thus improving better health conditions. Generally, Reishi is recommended as an adaptogen, immune modulator, and a general tonic. Red Reishi is also used to help treat anxiety, high blood pressure, hepatitis, bronchitis, insomnia, and asthma. A full list of reported benefits can be found here.
Is there any evidence?

A considerable number of studies in Japan , China , USA , and the UK in the past 30 years have shown that the consumption of red Reishi has been linked to the treatment of a vast range of diseases, common ailments, and conditions. From asthma to zoster, the applications of red Reishi seem to be related to a multitude of body organs and systems.

However, most of the scientific research that has been conducted appears to strongly support red Reishi's role as a normalizing substance - a nutritional supplement that can yield medical benefits through its normalization and regulation of the body's organs and functions.

The role of Red Reishi in maintaining a healthy lifestyle can best be explained through the Traditional Chinese Medicine (TCM) point of view because none of the known active components taken alone is as more effective than the consumption of Reishi itself. Whereas Western medicine focuses on the “cure” after the disease has already occurred, TCM, established through over 2,000 years of human observation, focuses on disease prevention by sustaining the right balance within the body through proper nutrition, exercise, and meditation. Reishi is an important adaptogenic herb in TCM in helping the body maintain this balance and also restore the balance when one is sick
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Inhibitory Effects of Components from Ganoderma lucidum
on the Growth of Human Immunodeficiency Virus (HIV)
and the Protease Activity
Research Institute for Wakan-Yaku (Traditional Sino-Japanese Medicines)
Toyama Medical and Pharmaceutical University
Masao Hattori
1) Sahar El-Mekkawy, Meselhy and R. Meselhy
Abstract : A new highly oxygenated triterpene has been isolated from the methanol extract of the fruiting bodies of Ganoderma lucidum together with twelve known compounds. The structures of the isolated compounds were determined by spectroscopic means including 2D-NMR. Ganoderiol F and ganodermanontriol were found active as anti-HIV with an inhibitory concentration of 7.8 m g/ml for both, and ganoderic acid B, ganoderiol B, ganoderic acid Cl, 3b -5a -dihydroxy-6b -methoxyergosta-7,22-diene, compound 1, ganoderic acid H and ganoderiol A were moderately active inhibitors against HIV-1 PR with a 50% inhibitory concentration of 0.17 mM.



INTRODUCTION

Over the past decade, substantial progress has been made in defining strategies for the treatment of human immunodeficiency virus (HIV) disease, the cause of acquired immunodeficiency syndrome (AIDS) , where natural products can serve as a source of structurally novel chemicals that are worth investigating as specific inhibitors of HIV as well as its essential enzymes, protease (PR) and reverse transcriptase (RT).

Ganoderma lucidum (Japanese name: Reishi) is one of the valuable crude drugs, which has long been used in China and Japan as a traditional Chinese medicine or a folk medicine for the treatment of various kinds of diseases1). Several biologically active triterpenes and sterols have been isolated from this mushroom and proved effective as cytotoxic2,3), antiviral4) and anti-inflammatory agents5,6). Besides, polysaccharides and glycoproteins possessing hypoglycemic7,8) and immunostimulant9-13) activities have also been isolated from its water extract. In the course of our continuing search for natural products as anti-HIV agents, the MEOH extract of the fruiting bodies was found to be moderately active against HIV-1 as well as its essential enzyme, protease (PR). Therefore this extract was selected for further fractionation. When subjected to bioassay-guided fractionation, the extract yielded several active compounds. This paper describes the isolation of thirteen compounds, and their inhibitory effects against HIV-1 and its enzyme PR.



RESULTS AND DISCUSSION
Isolation and structure determination of compounds isolated from Ganoderma lucidum

Bioactivity-guided fractionation of the MEOH extract enriched the anti- HIV and HIV-PR inhibitory effects in two fractions, B and C. Final purification of the active compounds was achieved by repeated column chromatography and HPLC to give thirteen compounds, 4, 5, 8 and 9 in fraction B, and 1-3, 6, 7 and 12 in fraction C. Three compounds (10, 11 and 13) were also obtained from fraction A. The structures of the known compounds were identified on the basis of their spectroscopic properties when compared with those reported for ganoderic acids A (2) 14-16), B (3)14-16), Cl (4)16,17) and ganoderic acid H (5)18,19), ganoderiols A (6)20) B (7)20)and F (8)21) , and ganodermanontriol (9)20), (all were previously isolated from the same mushroom). Besides, ergosterol (10), ergosterol peroxide (11, previously isolated from the sponge Ascidia nigra) 22), cerevisterol (12)23,24) and 3b -5a -dihydroxy-6b -methoxyergosta-7,22-diene (13) (both were previously isolated from the mushroom Agaricus blazei)24)

Compound 1 was obtained as an amorphous powder, [a ]D + 55.5° (CHCI3). A molecular formula Of C32H46O9 was estimated from a molecular ion at m/z 574 [M] + in its mass spectrum (MS). The ultra violet (UV) absorption (254 nm) and the infrared (IR) bands (1700 and 1660 cm-1) suggested the presence of a conjugated ketone (acid carbonyl stretching at 1750 cm-1 was also seen). The proton nuclear magnetic resonance (1H NMR) spectrum of 1 analyzed by the aid of 1H 1H shift correlated spectroscopy (COSY) and heteronuclear multiple quantum coherence (HMQC) experiments showed signals for seven methyls

Fig.1
Structures of compounds isolated from the MeOH extract of the fruiting bodies of Ganoderma Luciderm

(including two as doublet at (d 0.96 and 1.22), and three methine protons at d 3.20 (dd, J = 10.5 and 5 Hz), 4.80 (dd, J = 8.5 and 4.5 Hz) and 5.62 (s). In addition, a singlet at d 2.26 for an ester methyl was also seen (Fig. 1). The carbon-13 nuclear magnetic resonance (13 C NMR) and driven equilibrium Fourier transformation (DEPT) spectra demonstrated signals characteristic for eight methyls, seven methines (including three oxymethines at d 66.2, 77.3 and 79.1), and eleven quaternary carbons (including five carbonyls at d 170.2, 179.6, 193.0, 199.0 and 206.1) (Table 1). These data suggested a highly oxygenated lanostane-type triterpene close to the respective structures of 3, 5 and ganoderic acids G (15)18), and K (16)25). However, the chemical shift difference between C-8 and C-9 (about 6.0 ppm) in 1 and 5 relative to that reported for 3 and 14 (about 16.5 ppm), suggested a substitution pattern in rings B and C similar to that of 5. The mass spectrum (Fig. 2a) displayed prominent fragment ions at m/z 513 corresponding to the loss of an acetoxyl group (as acetic acid) from the molecule, and successive losses of 18 mass units (m/z 496 and 478) indicated the presence of two hydroxyl groups. The fragment ions m/z 417 [a]+ and 115[e]+ (resulted from the cleavage between C-22 and C-23) suggested the same side chain as in related ganoderic acids.

The precise connectivity of 1 was established by interpretation of HMBC data summarized in Table 1. Long-range correlations between H-5 and C-7 (or C-9); H32 and C-8; H-19 and C-9; and H-12 and C-11 confirmed the diketone substitution at C-7 and C-11. Correlations between H-18 and C-12, and H-12 and a carbonyl carbon signal at d 170.2 (IR 1730cm-1) revealed the connectivity of the acetoxyl group at C-12. Since H-5 and H-29 were coupled to C-3, a hydroxyl group was concluded to be located at C-3. On the other hand, the 1H-1H correlations between H-15 and H16a and H-16b led to the presence of the other hydroxyl group at C-15.

The relative stereochemistry of 1 was confirmed by measuring the NOESY and nuclear Oberhauser effect (NOE) difference spectra as shown in Fig. 2b. The spatial correlations observed between H-3, H-30 and H-5 confirmed the configuration of the hydroxyl group at C-3, which was equatorially oriented (ddd, J = 10.5, 5, 5 Hz). Similarly, b -configuration of the acetoxyl group at C-12 was inferred from the correlations observed between H-12 and the proton signal at d 1.49 (H-32). Appreciable enhancement of H-15 upon irradiation of H-32, vice versa, with no evidence of spatial correlation with H-18 or long-range correlations (in 1H 1H COSY) between H-15 and H-32, confirmed the G-configuration of a hydroxyl group at C-15. Correlations between H-17 and H-32, and H-18 and a proton signal at d 2.24 (H-20) confirmed the configurations at C-17 and C-20, respectively. What remained to be established was the stereochemistry at C-25, which was
Table 1. NMR Spectral Data of Compound 1 (in CDCI3)

atom 13 C 1 H HMBC

1 33.1 t
2 27.2 t 1.70, 1.64
3 77.3 d 3.20 ddd (10.5, 5, 5) C-2, C-5
4 40.3 s
5 51.2 d 1.56 dd (1 3.5, 3.5) C-3, C-7, C-9
6 36.6 t 2.65, 2.54 C-7, C-8
7 199.0 s
8 145.6 s
9 151.7 s
10 39.0 s
11 193.0 s
12 79.1 d 5.62 s C-9, C-11, C-17
13 47.9 s
14 58.5 s
15 66.2 d 4.80 dd (8.5, 4.5)
16 48.5 t 2.46, 2.30
17 44.6 d 2.55 C-20
18 12.1 q 0.96 s C-12, C-17
19 17.9 q 1.27 s C-5, C-9
20 29.4 d 2.24 C-23
21 21.5 q 0.96 d (6) C-17, C-22
22 38.0 t 2.75, 1,92
23 206.1 s
24 46.6 t 2.40, 2.80
25 35.1 d 2.91 C-23
26 179.6 s
27 17.1 q 1.22 d (7) C-26
30 27.8 q 1.03 s C-3, C-5
31 15.5 q 0.85 s C-3, C-5
32 20.9 q 1.49 s C-8, C-13, C-15
CH3CO 170.2 s
CH3CO 21.2 q 2.26 s C-12


suggested to be R, when compared with that of ganoderic acid H (3, given the name ganoderic acid C by Hirotani et al)25) having the same side chain which was confirmed by X-ray.
Fig. 2 a) Proposed mass fragmentation pattern of Compound 1.

b) Sterostructure for 1 as indicated by difference NOE and NOESY spectra.


Table 2. Inhibitory Activities of Compounds from Ganoderma lucidum against Protease and Proliferation of HIV-1
Item
HIV-1 PR
IC50 (mM)


IC (m g/ml)
HIV-1
CC (m g/ml)

MeOHext


47.7*


31.3#


125#
Compound (1)
0.19

NE

> 1000
Ganododeric acid A (2)
NE

(1000)

> 1000
Ganododeric acid B (3)
0.17

NE

> 1000
Ganoderic acid CI (4)
0.18

NE

> 1000
Ganoderic acid H (5)
0.20

NE

> 1000
Ganoderiol A (6)
0.23

NE

> 1000
Ganoderiol B (7)
0.17

(7.8)

500
Ganoderiol F (8)
0.32

7.8

15.6
Ganodermanontriol (9)
NE

7.8

15.6
Ergosterol (10)
NE

7NE

1000
Ergosterol peroxide (11)
NT

NE

15.6
Cerevisterol (12)
NE

NE

31.3
3b -5a -dihydroxy-6-B-methoxy

ergosta-7,22-dienne (13)

0.18

NE

15.6

IC, the minimum concentration for complete inhibition of HIV-1 induced CEP in MT-4 cells by microscopic observation. CC, the minimum concentration for appearance of MT-4 cell toxicity by microscopic observation. NE, not effective. ( ) , concentration at which weak anti-HIV-1 activity was observed.* %Inhibition at 100m g/ml. #As m g/ml

Inhibitory effects of isolated compounds on HIV and its enzymes

Investigation of anti-HIV and PR-inhibitory activities of the isolated compounds (1-13) yielded some compounds with moderate activities (Table 2). In the primary screening test for anti-HIV activity, compounds 8 and 9 were found to inhibit HIV1 induced cytopathic effect (CPE) in MT-4 cells with a 100% inhibitory concentration (IC) value of 7.8 m g/ml for both compounds, and the IC value for both was a half of the respective cytotoxic concentration (CC) value.

As for HIV-1 PR inhibitory effects, the PR activity was determined by analysing the hydrolysates of a synthetic substrate in the presence or absence of the isolated compounds using high performance liquid chromatography (HPLC) method. Of the tested compounds, 3 and 7 were found to be the most active against HIV-1 PR enzyme with an IC50 of 0.17 mM for both compounds. Other compounds such as ganoderiol B, ganoderic acid Cl, 3b -5a -dihydroxy-6,b -methoxyergosta-7,22-diene, compound 1, ganoderic acid H and ganoderiol A inhibited the enzyme activity in a similar extent.

In the present experiment, we found that D7(8),D 9(11)-lanostadiene-type triterpenes had relatively strong anti-HIV activity. On the other hand, D8(9) -lanostene-type triterpenes and ergostane-type compounds 10-12 had no inhibition of HIV-induced cytopathic effects. As to HIV-protease, we could not obtain any conclusive findings on the structure-activity relationship. Lanostane-type triterpenes showed IC50 of 0.17-0.32 mM, while ergosterol derivatives had no inhibitory activity. However, it was reported that synthetic cosalane and its derivatives had an anti-HIV effect as well as inhibitory effects on RT and PR27) . Several triterpenes have been described as antiviral compounds. Glycyrrhizin displays some limited activity against a whole range of viruses including HIV-128). Salaspermic acid29) and suberol (a lanostane-type)30) inhibit HIV-1 in H9 cells in the upper micromolar range. Bile acid derivatives were found slightly active (at 10-4 M) against HIV-1 in MT-4 cells31). Betulinic acid derivatives (lupane-type) have been described as potent inhibitors of the cytopathogenicity of HIV-1 in CEM 4 and MT-4 cells without affecting HIV-1 RT or PR activity32).

When compared with other triterpenes reported, compounds 8 and 9 can be used as leads to develop other related compounds with potential anti-HIV activity. This subject will be of particular interest to be investigated in the future.

REFERENCES
1. Hanssen, H. P. (1988) Dtsch Apoth Ztg 128, 789-792.

2. Toth, J. 0., Luu, B. and Ourisson, G. (1983) Tetrahedron Letters 24, 1081-1084.

3. Kohda, H., Tokumoto, W., Sakamoto, K., Fujii, M., Hirai, Y., Yamasaki, K., Komoda, Y., Nakamura, H. Ishihara, S. and Uchida, M (1985) Chem. Pharm. Bull. 33, 1367-1373.

4. Lindequist, U., Lesnau, A., Teuscher, E. and Pilgrim, H. (1989) Pharmazie 44, 579-580.

5. Tasaka, K., Akagi, M., Miyoshi, K., Mio, M. and Makino, T. (1988) Agents Actions 23, 153-156.

6. Tasaka, K., Mio, M., lzushi, K., Akagi, M. and Makino, T. (1988) Agents Actions 23, 157-160.

7. Hikino, H. and Mizuno, T. (1989) Planta Medica 55, 358.

8. Hikino, H., Ishiyama, M., Suzuki, Y. and Konno, C. (1989) Planta Medica 55, 423-428.

9. Lei, L., S. and Lin, Z.,B. (1993) Yao-Hsueh-Hseuh-Pao 28, 577-582.

10. Lei, L., Lin, Z., Chen, Q., Li, R. and lie, Y. (1993) Zhongguo Yaolixue Yu Dulixue Zashi 7, 183.

11. Kino, K., Yamashita, A., Yamaoka, K., Watanabe, J., Tanaka, S., Ko, K., Shimizu, K. and Tsuno, H. (1989) J. Biol. Chem. 264, 472-478.

12. Kino, K., Sone, T., Watanabe, J., Yamashita, A., Tsuboi, H., Miyama, H and Tsuno, H. (1985) Int. J. Immunopharmacol. 13, 109-1115.

13. He, Y., Li, R., Chen, Q., Lin, Z., Xia, D. and Ma, L. (1992) d. Chin. Pharm. Sci. 1, 79-81.

14. Kubota, T., Asaka, Y., Miura, 1. and Mori, H. (1982) Helv. Chim. Acta 65, 611-619.

15. Kikuchi, T., Matsuda, S., Murai, Y. and Ogita, Z. (1985) Chem. Pharm. Bull. 33, 2628-

16. Kikuchi, T., Kanmi, S., Kadota, S., Murai, Y., Tsubuno, K. and Ogita, Z. (1986) Chem. Pharm. Bull. 34, 3695-3712.

17. Nishitoba, T., Sato, H., Kasai, T., Kawagishi, H. and Sakamura, S. (1985) Agric. Biol. Chem. 49, 1793-1798.

18. Kikuchi, T., Kanmi, S., Kadota, S., Murai, Y., Tsubuno, K. and Ogita, Z. (1986) Chem. Pharm. Bull. 34, 4018-4029.

19. Kikuchi, T., Matsuda, S., Murai, Y. and Ogita, Z. (1985) Chem. Pharm. Bull. 33, 26242627.

20. Sato, H., Nishitoba, T., Shirasu, S., Oda, K. and Sakamura, S. (1986) Agric. Biol. Chem. 50, 2887-2890.

21. Nishitoba, T., Oda, K., Sato, H., and Sakamura, S. (1988) Agric. Biol. Chem. 52, 367-372.

22. Gunatilaka, A. A. L., Gopichand, Y., Schmitz, F. J. and Djerassi, C. (1981) J. Org. Chem. 46, 3860-3866.

23. Iorizzi, M., Minale, L. and Riecio, R. (1988) J. Nat. Prod. 51, 1098-1103.

24. Kawagishi, H., Katsumi, R., Sazawa, T., Mizuno, T., Hagiwara, T. and Nakamura, T. (1988) Phytochemistry 27, 2777-2779.

25. Morigawa, A., Kitabataki, K., Fujimoto, Y. and Ikekawa, N. (1986) Chem. Pharm. Bull. 34, 3025-3028.

26. Hirotani, M., Furuya, T. and Shiro, M. (1985) Phytochemistry 24, 2055-2061.

27. Cushman, M., Golebiewski, W. M., MeMahon, J. B., Buckheit, R. W. J., Clanton, D. J., Weislow, 0., Haugwitz, R. D., Bader, J., Graham, L. and Rice, W. G. (1994) J. Med. Chem. 37, 4030-3050.

28. Pompei, R., Flore, 0., Marccialis, M. A., Pani, A. and Loddo, B. (1979) Nature 218, 689-690.

29. Chen, K., Shi, Q., Kashiwada, Y., Zhang, D.-C., Hu, C.-Q., Jin, J.-Q., Nozaki, H., Kilkuskie, R. E., Tramontano, E., Cheng, Y. C., MaPhail, D. R. and Lee, K.-H. (1992). Nat. Prod. 55, 340-346.

30. Li, H.-Y., Sun, N.-J., Kashiwada, Y., Sun, L., Snider, J. V., Cosentino, L. M. and Lee, K.-H. (1993) J. Nat. Prod. 56, 1130-1133

31. Baba, M., Schols, D., Nakashirna, ll., Pauwels, R. Parmentier, G. Meijer, D. K. F. and DeClercq, E. (1989) J. Acquired Immune Defic. Syndr. 2, 264-271.

32. Evers, M., Poujade, C., Soler, F., Ribeill, Y., James, C., Lelievre, Y., Gueguen, J.-C., Reisdorf, D., Morize, I., Pauwels, R., DeClercq, E., Henin, Y., Bousseau, A., Mayaux, J.-F., LePecq, J.-B. and Dereu, N. (1996) J. Med. Chem. 39, 1059-1068.
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Ganoderma has been recognized traditionally and scientifically as potentially useful in the treatment of cancer, but there is a notable discrepancy with the public's frequent impression that Ganoderma may be a cure for cancer and the lack of clinical trials demonstrating such efficacy. We intend to summarize the extent of available theoretical, experimental and clinical data for the use of Ganoderma supplementation in cancer and outline its indications, especially in the context of clinical results from bioactively similar polysaccharide derived biological response modifiers (BRM's) from other fungi (Mizuno 1996).

EXPERIMENTAL EVIDENCE OF GANODERMA'S POTENTIAL IN CANCER TREATMENT

Ikekawa et al. (1968) first reported on the efficacy of soluble extracts from Ganoderma in inhibiting transplanted sarcoma 180 in mice. This host-dependent antitumor activity has been subsequently confirmed to be from the polysaccharide fractions of Ganoderma (Sasaki et al., 1971). Multiple similar studies subsequently confirms this observation and antitumor efficacy of Ganoderma has been demonstrated from various species, at different stages of growth and using different solvents for extraction and different routes of administration. Antitumor activity has been demonstrated in vitro as well as in syngeneic tumor systems in animals. However, no human trials of Ganoderma against cancer in peer reviewed journals nor any controlled clinical trials in humans have yet been conducted or published.

From a theoretical point of view, it is important to note that other fungal polysaccharides of comparable structure and function as those found in Ganoderma have undergone rigorous clinical trials, including Lentinan, Sizofilan, PSK (Krestin), and PSP. Since it is now increasingly clear that immunostimulatory bioactivity from most beta-glucan based compounds function via a similar beta-glucan receptor (Czop 1985), it has been possible to hypothesize that Ganoderma polysaccharides should function similarly (Chang, 1996). Clinical effects of various glucan based BRM's should therefore be comparable. Results from Lentinan, Sizofilan, PSK and PSP human trials demonstrated the efficacy of these glucan BRM's in prolonging survival in recurrent or advanced gastric and colon cancer, lung cancer and gynecologic cancers. Data from such bioactively comparable compounds all suggest improved quality of life or survival for cancer patients may be possible with Ganoderma supplementation.



INDICATIONS AND EVIDENCE SUPPORTING THE USE OF
GANODERMA SUPPLEMENTATION IN CANCER

Whilst some efficacy of Ganoderma in cancer is undoubted, it remains important to specify the various indications and cite the evidence to support its use. This can be discussed under four different circumstances:
A. As a supplement during chemotherapy or radiotherapy to reduce side-effects such as fatigue, loss of appetite, hair loss, bone marrow suppression and risk of infection. There are studies demonstrating Ganoderma's efficacy against fatigue (Yang 1994), hair loss (Miyamoto et al. 1985), and bone marrow suppression (Jia et al. 1993) and the presence of similar clinical evidence for other glucan BRM's applied in the setting of cancer chemotherapy or radiotherapy (Shi 1993) lends further support to the supplementation of Ganoderma in combination with cytotoxic cancer therapies. The recommended dose should be in the range of five to ten grams of fruiting body or equivalent per day (Chang 1994).

B. As a supplement for cancer patients to enhance survival and reduce likelihood of metastasis. While only anecdotal data exists that Ganoderma supplementation may enhance survival of cancer patients, this survival advantage has been demonstrated for a number of comparable glucan BRM'S. Specifically, Lentinan use in advantage at 1, 2, 3 and 4 years in a randomized control trial (Taguchi 1987). Sizofilan given together with chemotherapy enhanced survival of cervical cancers irrespective of stage in a prospective randomized controlled trial (Inoue et al. 1993), significantly enhanced survival (P < .01) in lung cancer patients (Honma 1982) and improved five year survival of head and neck cancer from 73.4 to 86.7% was noted in another small study (Kimura et al. 1994). More appropriate for comparison to Ganoderma is perhaps and PSK or PSP, which are orally administered. Mitomi et al. (1994) found significantly improved survival and disease-free survival (P=0.013) in resected colorectal cancer given PSK supplementation over three years when compared to control in a multi-center randomized controlled trial. In an animal model, Ganoderma has been demonstrated to effectively prevent metastasis (Lee 1984), and these results are comparable to those of Lentinan (Suga 1994). Other glucan BRM's have been demonstrated to effectively prevent or suppress pulmonary metastasis of methylcholanthrene-induced sarcomas, human prostate cancer DU145M, and lymphatic metastasis of mouse leukemia P388 (Kobayashi et al. 1995). The recommended dose should be five to ten grams or more of fruiting body or equivalent per day, with a linear enhancement in efficacy expected up to 30 grams per day (Chang 1994).

C. As a supplement for cancer patients to improve quality of life. Again, only anecdotal information exists for Ganoderma in this situation but other oral glucan derivatives such as PSP has been found to be useful in improving quality of life in cancer patients (Yao 1993). Significantly, Ganoderma supplementation was noted to decrease pain in cancer patients (Kupin 1994). The recommended dose would be five to ten grams of fruiting body or equivalent per day (Chang 1994).

D. As a supplement for the prevention of occurrence or recurrence of cancer. Since immune stimulation, especially Natural Killer (NK) and Cytotoxic Lymphocyte (CTL) activation may be effective in the immune prevention of cancer by enhanced immune surveillance (Lotzova 1985), and Ganoderma has been demonstrated to enhance NK and CTL activity when administered orally (Won et al. 1989), it is thus a candidate for prevention of the occurrence or recurrence of cancer. Stavinoha et al. demonstrated the efficacy of Ganoderma in the preventing the progression of microadenomatous growths in animals (Stavinoha 1993), and the efficacy of other glucan BRM's in primary and secondary cancer prevention have been similarly demonstrated in vitro, in vivo and in clinical trials.

CONCLUSION

Although Ganoderma and its derivatives are not pharmaceuticals and have not undergone rigorous clinical trials to be tested against cancer, there is abundant in vitro, animal and indirect clinical evidence to support its supplemental use in cancer. Standardization in bioactive polysaccharide content and dosages will be necessary to assure its rational use, and clinical trials in select cancers with defined endpoints will confirm its efficacy.


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