The Functions of AHCC

3-1 Effect of AHCC on the Immune System

Carcinogenesis and Immune Response in Cancer

The body is composed of billions of cells, which are all subject to free radical damage and mutations caused by various carcinogens.  Free radicals and carcinogens cause cells to become mutated and abnormal.  The immune surveillance system plays a critical role in prevention of cancer by recognizing the formation of these abnormal cells.  T-cells in particular are valuable for their ability to distinguish the mutated cells from normal cells.  Yet, when the immune system is suppressed, the mutated carcinoma cells are not recognized by the immune surveillance system and the cells grow uncontrollably and become cancerous.

Cancer cells release several kinds of immune suppressive factors, which inhibit antigen and macrophage activity.  T-cells in a suppressed immune system do not recognize cancer cells.  The suppressed macrophage cells fail to produce IL-12 and thus the Th0 cells cannot proliferate or differentiate into Th1/Th2 cells.  The suppressed Th1 cells cannot exert their anti-tumor effects which include production of IL-2 and IFN-?.  Finally, the anti-cancer immune response fails when the proliferation of CTL, LAK or NK cells fails.

Cancer is a disease of the immune system whereby immune suppression allows cancerous cells to not be recognized and grow uncontrollably.  Thus, reversing and restoring the suppressed immune system should be a very important part of cancer treatment.

AHCC : The Most Effective Product to Enhance Immune Response in Cancer Treatment

AHCC restores and reverses a suppressed immune status by stimulating and activating the immune system and finally wiping out cancerous cells. The mechanism of AHCC in enhancement of immune system is described in the following figure.

1)  Basic Research

Enhanced Macrophage Proliferation and Activity

The Institute for Genetic Medicine at Hokkaido University found that the macrophage population harvested from AHCC peritoneal treated rats increased twice as much as rats in the control group, for both normal rats and in tumor-bearing rats.  This result demonstrated that AHCC increased the proliferation and activation of macrophages.

(The 4th Symposium of AHCC Research Association, Jun. 1997).

Increased Cytokine Expression in the Splnocytes of Tumor Bearing Mice Treated with AHCC and its Fraction

AHCC was extracted and separated into low and high molecular fractions.  The fractions were evaluated in tumor bearing mice for their effects on cytokine expression.  The result showed that AHCC, used as a whole molecule, increased IL-2 and TNF-a expression, while AHCC’s low molecular fraction was the strongest enhancer for the IL-12 expression in the splenocytes of the tumor-bearing mice.  Furthermore, AHCC and its fractions were found to inhibit the immune suppressive cytokine TGF-ß expression derived from tumor tissue.

(The 6th Symposium of AHCC Research Association, Nov. 1998)

Improvement of Chemotherapy-Induced Immune Suppression by AHCC

Chemotherapy is a main therapy for cancer but it often induces some serious side effect such as immune suppression.  When the immune system is suppressed, infections result, and then cancerous cells proliferate further.  Therefore, it is very important to improve the immune suppression induced by chemotherapy during cancer treatment.  

The Institute for Genetic Medicine in Hokkaido University evaluated the effects of AHCC on its ability to lessen immune suppression induced by UFT chemotherapy.  Results showed that the UFT treated group had weakened NK activity; yet, the UFT+AHCC group had less suppression of NK activity.  This result suggested that AHCC reversed chemotherapy-induced immune suppression.

In addition, testing was done to determine AHCC’s effects on chemotherapy-induced inhibition of macrophage activity.  The macrophages (PEC) were harvested from breast cancer bearing rats treated with UFT or UFT+AHCC.  The nitrogen oxide (NO) production was measured from the culture supernatants of the macrophages.  Result showed that the NO production in the UFT+AHCC treated group was higher than that in UFT only treated group.  This suggested that AHCC restored the chemotherapy-induced inhibition of macrophage activity.

(Anti-cancer Drugs, 1998, 9, 343-350)

2) Clinical Research

AHCC as an Immunotherapy for Cancer Patients

Dr. Uno (Comfort Medical Foundation, Japan) reported that AHCC exerted its anti-tumor effect by improving the relationship between the cancer and its host.  As shown in Figure, the serum of 47 cancer patients administered with AHCC showed gradual increases in IL-12 levels. 

AHCC + PSK was also administered to 520 cancer patients not treated with chemotherapy or BRM agents.  The dose of AHCC was 6g/day, and that of PSK was 3g/day.  Before the AHCC treatment began, IL-12 levels were 7.8 pg/ml (an undetectable level).  Yet, they reached normal level after 2 to 4 months of AHCC treatment.  In result, AHCC treatment increased IFN-? level as seen by IL-12 pattern.  

The therapeutic effects of AHCC were shown in Table.  Several parameters were evaluated including CR (complete response), PR (partial response), NC (No change) and PD (progressive disease).  The patients were selected to be subjects only if they could undergo 6 months of treatment.  The results showed that AHCC treatment lead to improvements in PR (49.7%), CR (8%), and Quality of Life (60 %).

 (Biotherapy, 2000, 14 (3), 303 - 307).

The Clinical Effectiveness of AHCC Treatment in Cancer Patients with Progressive or Metastasized Cancers: An Observation of Immune Parameters.

Dr. Gye Hoon Ahn et al (OK-Chem Hospital, Korea) evaluated the immune parameters from patients with progressive cancers.  All the patients were diagnosed as either Stage III (3 patients) or stage IV (9 patients) by roentgenological image and pathological examination.  The types of cancers ranged from breast, gastric, lung, liver, uterine, and ovarian.  Of the 12 cases, 9 cases were treated with AHCC and the other three cases were treated with AHCC plus shark cartilage.  The immune parameters were examined every two months.  There were no side effects found in any of the patients.

Results showed that a one-month administration of AHCC caused an increase in NK activity, which lasted up to six months.  CD4 count increased smoothly while CD8 count was found to decrease gradually.  The CD4/CD8 ratio significantly increased after 8 months of AHCC treatment.  As for clinical efficacy, there were 3 cases of tumor regression.  The result also suggested that AHCC restored the immune suppression in the patients who underwent chemotherapy.  

(The 8th International Symposium of AHCC Research Association, Aug. 2000)

In summary, the results of the basic and clinical research indicated AHCC is a powerful anti-tumor substance, which works by activating and enhancing the cells of the immune system.  The powerful immune regulating effects of AHCC could be used in a variety of immune related diseases.

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