Cancer Adjuvant Therapy Protocol


The good news is that many of the 4 million people being treated for cancer in America will survive the disease and go on to live full and productive lives.

While the numbers that survive are far too low (about 44%), many of the more than 1500 daily cancer deaths occur because patients and their families are unaware of the depth of the resources currently available. Unfortunately, some die avowing they would never resort to natural medicine, while others are interested but lack the expertise to implement the program to their best advantage. Regrettably, some turn to alternative care fairly late in the course of the disease process, weakening the probability of recovery.

Mainstream medicine (relying upon surgery, chemotherapy, and radiation) may initially appear successful, but the harbingers of the disease process are less often addressed. Conventional cancer treatments are not for those individuals who are frail in body or spirit. For the past 30 years, cancer therapies have experienced tremendous setbacks because of an associated toxic response, resulting in significant numbers of treatment-induced deaths rather than disease-induced fatalities. Awareness regarding historic numbers of unsuccessful outcomes has forced patients to look for alternatives to bolster survival odds. Many who use alternative therapies report doing so without their oncologist's knowledge, fearful of verbal castigation or rejection by a physician (Richardson 2000).

The University of Texas's M.D. Anderson Cancer Center (Houston) found that 99.3% of patients had heard of complementary medicine, and 68.7% of patients reported having used at least one unconventional therapy (Richardson 2000). About 75% of the patients surveyed, however, yearned for more information concerning complementary medicine and about one-half of those participating in the survey wanted the information to come from their physician.

Until most recently, major medical schools relegated only a few hours to nutritional education out of the hundreds of academic hours required to complete medical school. The exclusion began when Abraham Flexner (commissioned to correct inequities occurring in medical schools) penned the Flexner Report of 1910. His contribution, entitled Medical Education in the United States and Canada, closed smaller medical schools and forced those that survived to adopt a uniform curriculum that excluded nutritional courses. Thus, some physicians emerged from medical schools, scoffing at the concept of nutrition influencing health or overcoming disease.

Sir William Osler (1849-1919), chief physician at Johns Hopkins's School of Medicine, drilled into students that medical research must be validated and replicated to be good medicine. This led to controlled experiments (as randomized, controlled trials) that became the backbone of orthodox supremacy. Nutritional protocols often used multiple nutrients, a difficult model to apply in clinical trials. Testing a single nutraceutical denied the patient full support of nutritional pharmacology, an injustice when treating a seriously ill patient. In addition, trials are expensive to conduct and early natural healers (by and large) did not represent an affluent subset of society.

But, ever so slowly, the medical scene is being revolutionized. According to the American College for Advancement in Medicine, physicians (in many cases) are showing eagerness to learn more about natural medicine and how to best implement it into their practice (Corbin et al. 2002). Scientists, teaching at nutritional seminars, report attendees are often medical doctors, a vast departure from years past.

PREVENTING AND CONTROLLING CANCER

While some individuals will be reading this protocol looking for help managing a malignancy, others will be focusing upon prevention and recurrence. The alphabetical list that follows provides quick guidelines for structuring a program, highlighting major nutrients in the prevention and treatment of cancer.

These recommendations should not be implemented individually in aggressive cancers without careful consultation of the remainder of the material. Cancer patients (and physicians) should be deliberate about reading the entirety of this protocol in order to avoid missing information that could prove to be lifesaving. Note: It is important that the reader also consult the protocols entitled Cancer Treatment: The Critical Factors and Cancer: Should Patients Take Dietary Supplements?

The dosages required for treating cancer (which are considerably larger than those required for prevention) can change the effects that a nutrient has on the body. The risk is multidirectional. Overdosing or underdosing, as well as a lack of patient awareness regarding the full potential of natural pharmaceuticals, hampers recovery.

THE CRITICAL IMPORTANCE OF SCHEDULED BLOOD TESTS

It is important to measure the successes or losses in regard to treatment-associated tumor response. Evaluating tumor markers in the blood or tumor imagery provides a basis forcalculating the regression of the disease. In addition, tumor markers provide direction for introducing other therapies if failures are evidenced.

Type of Cancers and the Tumor Marker Used for Assessment
Type of Cancer
Tumor Marker Blood Test
Ovarian cancer
CA 125
Prostate cancer
PSA, PAP, prolactin, testosterone, and others
Breast cancer
CA 27.29, CEA, alkaline phosphatase, and prolactin (or CA 15-3 rather than the CA 27.29)
Colon, rectum, liver, stomach, and other organ cancers CEA and GGTP
Pancreatic cancer
CA 19.9, CEA, and GGTP
Leukemia, lymphoma, and Hodgkin's disease
CBC with differential, immune cell differentiation and leukemia profile

It is also important to evaluate the effectiveness of immune-boosting therapies and guard against anemia and therapeutic toxicities. At a minimum, a monthly complete CBC chemistry test that includes assessment of hematocrit, hemoglobin, and liver and kidney function should be done in all cancer patients undergoing treatment.

An immune cell test should be performed bimonthly, measuring total blood count, CD4 (T-helper), CD4/CD8 (T-helper-to-T-suppressor) ratio, and NK (natural killer) cell activity. Also consider tests measuring cortisol levels (Cortisol am and pm) and HCG (human chorionic gonadotropin), a hormone that may be elevated 10-12 years prior to a diagnosis of cancer. For information regarding test availability call (800)208-3444.

COMPLEMENTARY THERAPIES

When describing the various complementary cancer therapies, it is not possible to endorse one supplement, hormone, or drug over another. We have provided as much evidence as space allows so that patients and their physicians can evaluate what approach may be suited for the individual situation.

A great deal of effort has been made to identify therapies that are substantiated in published scientific literature or that provide a cancer patient with the opportunity to experiment with cutting-edge treatment strategies. The focus of our effort has been to identify potentially lifesaving therapies that have been overlooked by mainstream oncology. We also attempt to discuss both positive and negative studies when applicable.

The Life Extension Foundation can assume no responsibility for treatment or outcome, apart from a self-assigned duty to stay abreast of the most promising of therapies and to share the data with members. No warranties (expressed or implied) accompany the material; neither is the information intended to replace medical advice. As always, each reader is urged to consult professional help for medical problems, especially those involving cancer. All supplements, drugs, and hormones are listed alphabetically and not in order of importance.

Alpha-Lipoic Acid--is a powerful antioxidant that regulates gene expression and preserves hearing during cisplatin therapy
Lester Packer, Ph.D. (scientist and professor at the Berkeley Laboratory of the University of California), refers to lipoic acid as the most powerful of all the antioxidants; in fact, Packer says that if he were to invent an ideal antioxidant, it would closely resemble lipoic acid (Packer et al. 1999). Alpha-lipoic acid claims anticarcinogenic credits because it independently scavenges free radicals, including the hydroxyl radical (a free radical involved in all stages of the cancer process and linked to an increase in the likelihood of metastasis).

Lipoic acid is unselfish, that is, it increases the efficacy of other antioxidants, regenerating vitamins C and E, coenzyme Q10, and glutathione for continued service. In fact, lipoic acid boosts the levels of glutathione by 30-70%, particularly in the lungs, liver, and kidney cells of laboratory animals injected with the antioxidant. In addition to being one of the most powerful free-radical scavengers, glutathione also tempers the synthesis of damaging cytokines and adhesion molecules by influencing the activity of NF-kB, a transcription factor (Exner et al. 2000). Note: A great deal of material relating to NF-kB is presented in the protocol Cancer Treatment: The Critical Factors.

Alpha-lipoic acid appears to be capable of amending an old adage: Genes are our destiny. By regulating gene expression, a new genetic road map emerges, one that is steered away from familial weaknesses and toward a healthier forecast (Busse et al. 1992). Lipoic acid can downregulate genes that accelerate cancer without inducing toxicity. So responsive are cancer cells that laboratory-induced cancers literally soak up lipoic acid, a saturation that increased the lifespan of rats with aggressive cancer by 25% (Karpov et al. 1977).

A report from the University of Sydney showed that alpha-lipoic acid was preferentially toxic to leukemia cells lines (Jurkat and CCRF-CEM cells). The selective toxicity of lipoic acid to Jurkat cells was credited (in part) to the antioxidant's ability to induce apoptosis. Packer also published promising news, showing lipoic acid activated (by nearly 100%) an enzyme (caspase) that kills leukemia cells. Other researchers showed that lipoic acid acted as a potentiator, amplifying the antileukemic effects of vitamin D. It is speculated that lipoic acid delivers much of its advantage by inhibiting NF-kB and the appearance of damaging cytokines (Sokoloski et al. 1997; Zhang et al. 2001). Finding that lipoic acid can differentiate between normal and leukemic cells charts new courses in treatment strategies to slow or overcome the disease (Packer et al. 1999).

As with all antioxidants, the appropriateness of using lipoic acid with chemotherapy arises. Animal studies indicate that alpha-lipoic acid decreased side effects associated with cyclophosphamide and vincristine (chemotherapeutic agents) but did not hamper drug effectiveness (Berger et al. 1983). More recently, other scientists showed that a combination of alpha-lipoic acid and doxorubicin resulted in a marginally significant increase in survival of leukemic mice (Dovinova et al. 1999). Nonetheless, the definitive answer regarding coupling antioxidants with conventional cancer therapy is complex. Factors, such as type of malignancy, as well as the nature of the cytotoxic chemical and even the time of day the agents are administered, appear to influence outcome (please consult the protocol Cancer: Should Patients Take Dietary Supplements to learn more about the advisability of antioxidant therapy during conventional treatments).

To its credit, lipoic acid appears able to counter the hearing loss and deafness that often accompanies cisplatin therapy. Depreciated hearing occurs as free radicals, produced as a result of treatment, plunder the inner ear; lipoic acid preserves glutathione levels and thus prevents deafness (Rybak et al. 1999).

A suggested alpha-lipoic acid dosage for healthy individuals is from 250-500 mg a day. Degenerative diseases usually require larger dosages (sometimes as much as 500 mg 3 times a day). Packer, in his book The Antioxidant Miracle, recommends taking biotin supplements with alpha-lipoic acid when the daily intake exceeds 100 mg. (Alpha-lipoic acid may compete with biotin and interfere with biotin's activities in the body.) Hyperalertness and insomnia are also associated with mega dosages.

A positive study conducted by a team of German researchers showed that arginine contributed significantly to immune function by increasing levels of white blood cells. Scottish scientists added that dietary supplementation with arginine in breast cancer patients enhanced NK cell activity and lymphokine cytotoxicity (Brittenden et al. 1994). (Lymphokines are chemical factors produced and released by T-lymphocytes that attract macrophages to a site of infection or inflammation in preparation for attack.) Various researchers have shown that increasing arginine increases neutrophils (white blood cells that remove bacteria, cellular debris, and solid particles), significantly upgrading host defense (Muhling et al. 2002).

Apart from enhancing immune function, arginine increases a number of amino acids, creating the possibility of an amino acid imbalance. Oversupplying some amino acids while undersupplying others is thought to destabilize the tumor. All cells, both healthy and diseased, have amino acid requirements; if not met, the cell is significantly handicapped (Muhling et al. 2002). Amino acid manipulation has been applied in oncology for decades with varying degrees of success.

Interesting studies have emerged regarding arginine or arginine analogs in cancer treatment. For example, infusions of arginine significantly reduced the incidence of liver and lung metastasis in laboratory mice. Earlier research found that supplemental arginine altered the number of tumor-infiltrating lymphocytes in human colorectal cancer, offering important implications for new strategies in cancer treatment (Heys et al. 1997). Though many factors are involved (including appropriate dosages), Japanese researchers found that arginine induced apoptosis in pancreatic (AR4-2J) cells, inhibiting cell proliferation (Motoo et al. 2000).

The two faces of arginine, however, cloud dosing with confidence. The role of nitric oxide (NO), a molecule synthesized from arginine, remains controversial and poorly understood. While a few reports indicate that the presence of NO in tumor cells or their microenvironment is detrimental to tumor-cell survival, and subsequently their metastatic potential, a large body of data suggests that NO actually promotes tumor progression. Illustrative of its fickleness, NO was recently identified as a downstream regulator of prolactin, an inhibitor of apoptosis. The same team of Canadian scientists determined that arginine stimulated proliferation of prolactin-dependent Nb2 lymphoma cells in laboratory rats (Dodd et al. 2000). Researchers from the University of Pittsburgh also found that NO production (by murine mammary adenocarcinoma cells) promoted tumor-cell invasiveness. Introducing NO inhibitors resulted in more positive results, that is, an antitumor, antimetastatic profile (Orucevic et al. 1999).

Ambiguity and nonconformity reduce arginine's role at the present time to adjunctive support with either traditional cancer treatment or fish oil supplementation. A heartening report regarding arginine, fish oil, and doxorubicin therapy appears in this protocol in the section devoted to Essential Fatty Acids (Ogilvie et al. 2000). Nonetheless, the diverse biological properties of L-arginine demand further careful studies, clarifying chemopreventive advantages and endangerments (Szende et al. 2000).

Carotenoids--have antioxidant activity, inhibit cellular proliferation, and offer protection against numerous types of malignancies
Carotenoids, acting as immune enhancers and free-radical scavengers, are important substances in oncology. When using carotenoids for antioxidant and cancer protection, it appears wise to use mixed carotenoids, that is, alpha-carotene, lycopene, zeaxanthin, canthaxanthin, beta-crytoxanthine, and lutein rather than emphasizing only beta-carotene.

The following are illustrative of the worth of mixed carotenoids:

Lycopene offers targeted protection against cancers arising in the prostate (Kucuk et al. 2001), pancreas (Burney et al. 1989), digestive tract (De Stefani et al. 2000), and colon (Nair et al. 2001).

The American Journal of Clinical Nutrition added that individuals seeking broad spectrum colon protection should also include lutein-rich foods in their diet (spinach, broccoli, lettuce, tomatoes, oranges, carrots, celery, and greens) (Slattery et al. 2000).
Canthaxanthin, a less well-known carotenoid, was shown to induce apoptosis and inhibit cell growth in both WiDR colon adenocarcinoma and SK-MEL-2 melanoma cells (Palozza et al. 1998).
Researchers showed that the risk of breast cancer approximately doubled (2.21-fold) among subjects with blood levels of beta-carotene in the lowest quartile, compared with those in the highest quartile. The risk of breast cancer associated with low levels of other carotenoids was similar, that is, a 2.08-fold increased risk if lutein is deficient and a 1.68-fold greater risk if beta-cryptoxanthin is lacking (Toniolo et al. 2001). A Swedish study found that menopausal status has an impact on the protection delivered by carotenoids. Analysis showed that lycopene was associated with decreased breast cancer risk in postmenopausal women, but in premenopausal women, lutein offered greater protection (Hulten et al. 2001).
Leukoplakia (an often precancerous condition marked by white thickened patches on the mucous membranes of the cheeks, gums, or tongue) is responsive to spirulina, a source of proteins, carotenoids, and other micronutrients (Sankaranarayanan et al. 1995). An inverse relationship between beta-carotene and thyroid carcinoma was observed in both papillary and follicular carcinomas (D'Avanzo et al. 1997). A high dietary intake of beta-carotene appears a protective (though modest) factor for the development of ovarian cancer (Huncharek et al. 2001).
Lastly, Japanese researchers showed that all the carotenoids inhibited hepatic (liver) invasion, probably through antioxidant properties (Kozuki et al. 2000).
Historically, men who consume 10 or more servings of tomato products per week reduce their risk of prostate cancer by about 35%. The American Chemical Society (August 2001) reported that 32 (largely African-American) patients diagnosed with prostate cancer and awaiting radical prostatectomy were placed on diets that included tomato sauce, providing 30 mg a day of lycopene. After 3 weeks, mean serum PSA concentrations fell by 17.5%, oxidative burden by 21.3%, DNA damage by 40%, while programmed cell death increased threefold in cancer cells (Holzman 2002). Part of lycopene's protection involves the ability of carotenoids to counteract the proliferation of cancer cells induced by insulin-like growth factors (Agarwal et al. 2000a).

Beta-carotene exhibited a radioprotective effect among 709 children exposed to radiation inflicted by the Chernobyl nuclear accident. It is possible that information gathered from Chernobyl may benefit cancer patients undergoing radiotherapy. For example, the Chernobyl accident showed that irradiation increases the susceptibility of lipids to oxidation and that natural beta-carotene may act as an in vivo lipophilic antioxidant or radioprotective (Ben-Amotz et al. 1998). Therefore, using beta-carotene following radiotherapy may reduce the devastation visited upon tissues during treatment.

Beta-carotene, perhaps the most controversial of the family of carotenoids, has come under attack several times in the past few years. For example, smokers who received synthetic beta-carotene (as a prophylactic) in the CARET study had a higher rate of lung cancer and death than smokers not supplemented. In fact, the study was terminated by the National Cancer Institute (NCI) because of the widespread discrepancy between the two groups. The CARET study is not new, but because it still concerns beta-carotene users, we will attempt to explain the unexpected results of the study.

Dr. Packer described the subjects as "walking time bombs." Many were victims of asbestos exposure or heavy smoking. The form of beta-carotene selected for the study (synthetic versus natural) was also cited as another possible explanation for the negative outcome.

Dr. Leo Galland, M.D. (practitioner and director of the Foundation of Integrated Medicine, New York City), also explains that high-dose beta-carotene (25,000 IU a day) administered to smokers results in a particular pattern of metabolism (Galland 2000). The process is orchestrated as cytochrome p450 (enzymes of the Phase I detoxification system) is summoned into action by tars appearing in cigarette smoke. As beta-carotene is acted on by cytochrome p450, oxidative end products are formed, as well as a generation of toxic derivatives. Simultaneously, vitamins C and A, as well as glutathione, are depleted, severing antioxidant protection. This sequence can damage DNA and increase the likelihood of lung cancer, particularly in an environment with initially high oxidative stress, a profile common to smokers. Without full spectrum antioxidant support, the single dose of beta-carotene produces an oxidative field rather than one of protection. (Comment: As one free radical is neutralized by an antioxidant, another oxidant may be formed. It is well established that vitamin C can serve as a pro-oxidant through the formation of ascorbyl radicals. It is also known that this radical is quenched by vitamin E to yield a tocopheryl radical, which in turn is reduced by the conversion of glutathione to glutathione disulfide. Thus, the full team should always be used, rather than emphasizing single antioxidants.)

Beta-carotene is largely considered nontoxic even at high doses; for example, many cancer therapies recommend large amounts of carrot juice. One large glass of carrot juice can contain 100,000-200,000 IU of provitamin A or carotene. The problem with carrot juice is that it is loaded with fructose (sugar). Cancer cells feed on sugar, and drinking carrot juice induces an insulin spike that fuels cancer cell propagation. Cancer patients should consider natural beta-carotene supplements in lieu of carrot juice. Suggested phytonutrient dosages are from 9-20 mg of sulphoraphane, 10-30 mg a day of lycopene, and 15-40 mg of lutein, along with a mixed carotenoid blend that includes alpha- and beta-carotene. A product called PhytoFood Powder provides potent amounts of sulphoraphane, while carotenoid extracts are available in a variety of encapsulated preparations. Note: Diet: What Should the Cancer Patient Eat, appearing later in this protocol, contains a discussion regarding the value of sulphoraphanes in the diet.

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 Williams & 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 B) 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 Lewis A and Lewis X antigens (i.e., breast and pancreatic cancers, as well as about 70% of colon cancers). Lewis A and Lewis 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 Lewis antigens was 95.5%, whereas the control group was only 35.1% (Matsumoto et al. 2002). Comment: Patients are well advised to undergo Lewis 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.

Note: The Melanoma Center at the University of Pittsburgh Cancer Institute showed a potential role for histamine in cancer immunotherapy. A recently completed Phase II trial of IL-2 versus IL-2 and histamine in patients with metastatic melanoma demonstrated a trend toward a superior survival benefit from IL-2 and histamine for all patients enrolled and a statistically significant survival benefit for patients with hepatic metastasis (Agarwala et al. 2001).

Cancer Adjuvant Therapy Pg (1) (2) (3) (4) (5) (6) (7)

These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease