Cimetidine (Tagamet) pros and cons

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Cimetidine (Tagamet)

Histamine (H2) receptor antagonists (such as cimetidine) became popular in

the late 1970s to treat gastrointestinal ulcers and other benign conditions

of the stomach, esophagus, and duodenum. In 1985, the Life Extension

Foundation announced that cimetidine had merit (as a cancer adjunctive).

Since then, many studies have been published encouraging the use of

cimetidine as a means of disabling tumors and expanding survival rates.

The four stages of malignant cancer are determined by the spread of the

cancer cells. This classification helps physicians develop a treatment plan

specific to each individual cancer. (Anatomical Chart Company 2002®,

Lippincott & Wilkins)

Researchers reporting in Digestion were motivated to do a full literature

search to determine the pathways through which cimetidine impacts cancer.

They concluded that cimetidine appeared to deliver a significant advantage

through a three-pronged mechanism involving (1) inhibition of cancer cell

proliferation, (2) stimulation of lymphocyte activity by inhibition of

T-cell suppressor function, and (3) inhibition of histamine's activity as a

growth factor (Siegers et al. 1999).

In a Japanese study, a total of 64 colorectal cancer patients (who had

earlier undergone surgery) were evaluated for the effects of cimetidine on

survival and disease recurrence. The cimetidine arm of the study received

800 mg a day of cimetidine along with 200 mg a day of 5-fluorouracil

(5-FU); the control group received only 5-FU. The treatment was initiated 2

weeks following surgery and terminated 1 year later. Strikingly beneficial

effects were noted: The 10-year survival rate for patients treated with

cimetidine/5-FU was 84.6%, whereas that of the control group (5-FU alone)

was only 49.8% (Matsumoto et al. 2002).

The same team of researchers then evaluated the effect of cimetidine on a

particularly aggressive form of colon cancer (Dukes grade C). The

cumulative 10-year survival rate of the cimetidine-treated group was

consistently 84.6%, whereas that of the control group was only 23.1%. (Less

virulent strains (Dukes A or responded less well to cimetidine treatment.)

According to researchers from the Fujita Health University and the Nagoya

City University Medical School, cimetidine treatment is particularly

effective in patients whose tumors express higher levels of A and

X antigens (i.e., breast and pancreatic cancers, as well as about 70%

of colon cancers). A and X antigens are cell surface ligands

that adhere to a molecule in the blood vessels called E-selectin. (Ligand

comes from the Latin word ligare, meaning that which binds.)

The adhesion of the cancer cell to vascular endo-thelial cells expressing

E-selectin is a key step in invasion and metastasis. Cimetidine improved

patient outcome by inhibiting the expression of E-selectin, thus abolishing

the binding site for continued cancer growth and metastasis. The 10-year

cumulative survival rate of the cimetidine group displaying antigens

was 95.5%, whereas the control group was only 35.1% (Matsumoto et al.

2002). Comment: Patients are well advised to undergo antigen

determinations for optimal therapy and a more favorable outcome. Contact

Impath Laboratories at 521 West 57 Street, New York, NY 10019, Telephone:

(800) 447-5816, for information regarding testing.

Researchers recently unearthed another mechanism through which cimetidine

offers cancer protection. Cimetidine enhanced cell-mediated immunity by

improving suppressed dendritic cell function (Kubota et al. 2002).

Dendritic cells capture foreign invaders and carry the antigen to lymph

nodes and spleen. The " hand-delivered " antigen shows the immune system

exactly what it has to fight. A more in-depth explanation regarding

dendritic cells appears in a separate protocol entitled Cancer Vaccines.

In a study conducted at the Institute of Psychiatry (London), the growth

inhibitory effects of cimetidine were assessed on five cell lines derived

from human brain tumors of different tissue types and grades of malignancy.

Each cell line was treated with cimetidine 24 hours before analysis.

Cimetidine significantly inhibited cell proliferation in three of five cell

lines, which indicates the apparent dependence of these cells on histamine

stimulation (Finn et al. 1996).

Because we do not wish the reader to interpret positive material as a

universal ameliorant for all cancers, the following findings are noted:

Fred Hutchinson Cancer Research Center researchers explored whether

cimetidine exerted a cancer-preventive effect on prostate and breast

cancers by tracking 48,512 individuals from 1977-1995. Unfortunately, the

study concluded showing that cimetidine did not influence the risk of

female breast cancers; in addition, the researchers concluded that there

was little evidence to support the previously hypothesized preventive

effect of cimetidine on the risk of prostate cancers (Rossing et al. 2000).

The Department of Hematology (University of Newcastle, U.K.) found that

cimetidine reduced by about 30% the bioavailability of melphalan (Alkeran)

in multiple myeloma patients, the standard treatment for the disease

(Sviland et al. 1987).

A total of 132 male rats were evaluated for immune status after ingesting

cimetidine to forestall a diagnosis of gastric cancer. In the

cimetidine-fed group, 19 of 48 developed cancer, versus 12 of 43 in the

control group. The Norwegian researchers concluded that cimetidine had no

significant immune-modulating effects on the development of gastric cancer

in rodents (Hortemo et al. 1999).

While cimetidine shows efficacy in treating certain cancers, it has not

been shown to prevent them. A suggested cimetidine dosage for cancer

patients is 800 mg (taken at night). Do not supplement with cimetidine

without physician awareness; the drug can interact with several medications

(such as digoxin, theophylline, phenytoin, warfarin, and lidocaine),

increasing or decreasing drug potency.