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National Library of Medicine Abstract This year, more than 1 million Americans and more than 10 million people worldwide are expected to be diagnosed with cancer, a disease commonly believed to be preventable. Only 5–10% of all cancer cases can be attributed to genetic defects, whereas the remaining 90–95% have their roots in the environment and lifestyle. The lifestyle factors include cigarette smoking, diet (fried foods, red meat), alcohol, sun exposure, environmental pollutants, infections, stress, obesity, and physical inactivity. The evidence indicates that of all cancer-related deaths, almost 25–30% are due to tobacco, as many as 30–35% are linked to diet, about 15–20% are due to infections, and the remaining percentage are due to other factors like radiation, stress, physical activity, environmental pollutants etc. Therefore, cancer prevention requires smoking cessation, increased ingestion of fruits and vegetables, moderate use of alcohol, caloric restriction, exercise, avoidance of direct exposure to sunlight, minimal meat consumption, use of whole grains, use of vaccinations, and regular check-ups. In this review, we present evidence that inflammation is the link between the agents/factors that cause cancer and the agents that prevent it. In addition, we provide evidence that cancer is a preventable disease that requires major lifestyle changes. INTRODUCTION After sequencing his own genome, pioneer genomic researcher Craig Venter remarked at a leadership for the twenty-first century conference, “Human biology is actually far more complicated than we imagine. Everybody talks about the genes that they received from their mother and father, for this trait or the other. But in reality, those genes have very little impact on life outcomes. Our biology is way too complicated for that and deals with hundreds of thousands of independent factors. Genes are absolutely not our fate. They can give us useful information about the increased risk of a disease, but in most cases they will not determine the actual cause of the disease, or the actual incidence of somebody getting it. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not driven directly by the genetic code” This statement is very important because looking to the human genome for solutions to most chronic illnesses, including the diagnosis, prevention, and treatment of cancer, is overemphasized in today’s world. Observational studies, however, have indicated that as we migrate from one country to another, our chances of being diagnosed with most chronic illnesses are determined not by the country we come from but by the country we migrate to. In addition, studies with identical twins have suggested that genes are not the source of most chronic illnesses. For instance, the concordance between identical twins for breast cancer was found to be only 20%. Instead of our genes, our lifestyle and environment account for 90–95% of our most chronic illnesses. Cancer continues to be a worldwide killer, despite the enormous amount of research and rapid developments seen during the past decade. According to recent statistics, cancer accounts for about 23% of the total deaths in the USA and is the second most common cause of death after heart disease. Death rates for heart disease, however, have been steeply decreasing in both older and younger populations in the USA from 1975 through 2002. In contrast, no appreciable differences in death rates for cancer have been observed in the United States. By 2020, the world population is expected to have increased to 7.5 billion; of this number, approximately 15 million new cancer cases will be diagnosed, and 12 million cancer patients will die. These trends of cancer incidence and death rates again remind us of Dr. John Bailer’s May 1985 judgment of the US national cancer program as a “qualified failure,” a judgment made 14 years after President Nixon’s official declaration of the “War on Cancer.” Even after an additional quarter century of extensive research, researchers are still trying to determine whether cancer is preventable and are asking “If it is preventable, why are we losing the war on cancer?” In this review, we attempt to answer this question by analyzing the potential risk factors of cancer and explore our options for modulating these risk factors. Cancer is caused by both internal factors (such as inherited mutations, hormones, and immune conditions) and environmental/acquired factors (such as tobacco, diet, radiation, and infectious organisms; Fig.  1 ). The link between diet and cancer is revealed by the large variation in rates of specific cancers in various countries and by the observed changes in the incidence of cancer in migrating. For example, Asians have been shown to have a 25 times lower incidence of prostate cancer and a ten times lower incidence of breast cancer than do residents of Western countries, and the rates for these cancers increase substantially after Asians migrate to the West Genes and Environment The role of genes and environment in the development of cancer. A The percentage contribution of genetic and environmental factors to cancer. The contribution of genetic factors and environmental factors towards cancer risk is 5–10% and 90–95% respectively. B Family risk ratios for selected cancers. The numbers represent familial risk ratios, defined as the risk to a given type of relative of an affected individual divided by the population prevalence. The data shown here is taken from a study conducted in Utah to determine the frequency of cancer in the first-degree relatives (parents + siblings + offspring). The familial risk ratios were assessed as the ratio of the observed number of cancer cases among the first degree relatives divided by the expected number derived from the control relatives, based on the years of birth (cohort) of the case relatives. In essence, this provides an age-adjusted risk ratio to first-degree relatives of cases compared with the general population. C Percentage contribution of each environmental factor. The percentages represented here indicate the attributable-fraction of cancer deaths due to the specified environmental risk factor. The importance of lifestyle factors in the development of cancer was also shown in studies of monozygotic twins. Only 5–10% of all cancers are due to an inherited gene defect. Various cancers that have been linked to genetic defects are shown in Fig.  2 . Although all cancers are a result of multiple mutations, these mutations are due to interaction with the environment. Genetic Cancers Genes associated with risk of different cancers. These observations indicate that most cancers are not of hereditary origin and that lifestyle factors, such as dietary habits, smoking, alcohol consumption, and infections, have a profound influence on their development. Although the hereditary factors cannot be modified, the lifestyle and environmental factors are potentially modifiable. The lesser hereditary influence of cancer and the modifiable nature of the environmental factors point to the preventability of cancer. The important lifestyle factors that affect the incidence and mortality of cancer include tobacco, alcohol, diet, obesity, infectious agents, environmental pollutants, and radiation. RISK FACTORS OF CANCER Tobacco Smoking was identified in 1964 as the primary cause of lung cancer in the US Surgeon General’s Advisory Commission Report, and ever since, efforts have been ongoing to reduce tobacco use. Tobacco use increases the risk of developing at least 14 types of cancer (Fig.  3 ). In addition, it accounts for about 25–30% of all deaths from cancer and 87% of deaths from lung cancer. Compared with nonsmokers, male smokers are 23 times and female smokers 17 times more likely to develop lung cancer. The carcinogenic effects of active smoking are well documented; the U. S. Environmental Protection Agency, for example, in 1993 classified environmental tobacco smoke (from passive smoking) as a known (Group A) human lung carcinogen . Tobacco contains at least 50 carcinogens. For example, one tobacco metabolite, benzopyrenediol epoxide, has a direct etiologic association with lung cance. Among all developed countries considered in total, the prevalence of smoking has been slowly declining; however, in the developing countries where 85% of the world’s population resides, the prevalence of smoking is increasing. According to studies of recent trends in tobacco usage, developing countries will consume 71% of the world’s tobacco by 2010, with 80% increased usage projected for East Asia. The use of accelerated tobacco-control programs, with an emphasis in areas where usage is increasing, will be the only way to reduce the rates of tobacco-related cancer mortality. Cancer types How smoking contributes to cancer is not fully understood. We do know that smoking can alter a large number of cell-signaling pathways. Results from studies in our group have established a link between cigarette smoke and inflammation. Specifically, we showed that tobacco smoke can induce activation of NF-κB, an inflammatory marker. Thus, anti-inflammatory agents that can suppress NF-κB activation may have potential applications against cigarette smoke. We also showed that curcumin, derived from the dietary spice turmeric, can block the NF-κB induced by cigarette smoke. In addition to curcumin, we discovered that several natural phytochemicals also inhibit the NF-κB induced by various carcinogens. Thus, the carcinogenic effects of tobacco appear to be reduced by these dietary agents. A more detailed discussion of dietary agents that can block inflammation and thereby provide chemopreventive effects is presented in the following section. Alcohol The first report of the association between alcohol and an increased risk of esophageal cancer was published in 1910. Since then, a number of studies have revealed that chronic alcohol consumption is a risk factor for cancers of the upper aerodigestive tract, including cancers of the oral cavity, pharynx, hypopharynx, larynx, and esophagus, as well as for cancers of the liver, pancreas, mouth, and breast (Fig.  3 ). Williams and Horn, for example, reported an increased risk of breast cancer due to alcohol. In addition, a collaborative group who studied hormonal factors in breast cancer published their findings from a reanalysis of more than 80% of individual epidemiological studies that had been conducted worldwide on the association between alcohol and breast cancer risk in women. Their analysis showed a 7.1% increase in relative risk of breast cancer for each additional 10 g/day intake of alcohol. In another study, Longnecker et al ., showed that 4% of all newly diagnosed cases of breast cancer in the USA are due to alcohol use. In addition to it being a risk factor for breast cancer, heavy intake of alcohol (more than 50–70 g/day) is a well-established risk factor for liver and colorectal cancers. There is also evidence of a synergistic effect between heavy alcohol ingestion and hepatitis C virus (HCV) or hepatitis B virus (HBV), which presumably increases the risk of hepatocellular carcinoma (HCC) by more actively promoting cirrhosis. For example, Donato et al . reported that among alcohol drinkers, HCC risk increased linearly with a daily intake of more than 60 g. However, with the concomitant presence of HCV infection, the risk of HCC was two times greater than that observed with alcohol use alone (i.e., a positive synergistic effect). The relationship between alcohol and inflammation has also been well established, especially in terms of alcohol-induced inflammation of the liver. How alcohol contributes to carcinogenesis is not fully understood but ethanol may play a role. Study findings suggest that ethanol is not a carcinogen but is a cocarcinogen. Specifically, when ethanol is metabolized, acetaldehyde and free radicals are generated; free radicals are believed to be predominantly responsible for alcohol-associated carcinogenesis through their binding to DNA and proteins, which destroys folate and results in secondary hyperproliferation. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P-4502E1, which is associated with enhanced production of free radicals and enhanced activation of various procarcinogens present in alcoholic beverages; a change in metabolism and in the distribution of carcinogens, in association with tobacco smoke and diet; alterations in cell-cycle behavior such as cell-cycle duration leading to hyperproliferation; nutritional deficiencies, for example, of methyl, vitamin E, folate, pyridoxal phosphate, zinc, and selenium; and alterations of the immune system. Tissue injury, such as that occurring with cirrhosis of the liver, is a major prerequisite to HCC. In addition, alcohol can activate the NF-κB proinflammatory pathway , which can also contribute to tumorigenesis. Furthermore, it has been shown that benzopyrene, a cigarette smoke carcinogen, can penetrate the esophagus when combined with ethanol. Thus anti-inflammatory agents may be effective for the treatment of alcohol-induced toxicity. In the upper aerodigestive tract, 25–68% of cancers are attributable to alcohol, and up to 80% of these tumors can be prevented by abstaining from alcohol and smoking. Globally, the attributable fraction of cancer deaths due to alcohol drinking is reported to be 3.5%. The number of deaths from cancers known to be related to alcohol consumption in the USA could be as low as 6% (as in Utah) or as high as 28% (as in Puerto Rico). These numbers vary from country to country, and in France have approached 20% in males. Diet In 1981, Doll and Peto estimated that approximately 30–35% of cancer deaths in the USA were linked to diet (Fig.  4 ). The extent to which diet contributes to cancer deaths varies a great deal, according to the type of cancer. For example, diet is linked to cancer deaths in as many as 70% of colorectal cancer cases. How diet contributes to cancer is not fully understood. Most carcinogens that are ingested, such as nitrates, nitrosamines, pesticides, and dioxins, come from food or food additives or from cooking. Diet and cancer Cancer deaths (%) linked to diet as reported by Willett Numerous outdoor air pollutants such as PAHs increase the risk of cancers, especially lung cancer. PAHs can adhere to fine carbon particles in the atmosphere and thus penetrate our bodies primarily through breathing. Long-term exposure to PAH-containing air in polluted cities was found to increase the risk of lung cancer deaths. Aside from PAHs and other fine carbon particles, another environmental pollutant, nitric oxide, was found to increase the risk of lung cancer in a European population of nonsmokers. Other studies have shown that nitric oxide can induce lung cancer and promote metastasis. The increased risk of childhood leukemia associated with exposure to motor vehicle exhaust was also reported. Indoor air pollutants such as volatile organic compounds and pesticides increase the risk of childhood leukemia and lymphoma, and children as well as adults exposed to pesticides have increased risk of brain tumors, Wilm’s tumors, Ewing’s sarcoma, and germ cell tumors. In utero exposure to environmental organic pollutants was found to increase the risk for testicular cancer. In addition, dioxan, an environmental pollutant from incinerators, was found to increase the risk of sarcoma and lymphoma. Long-term exposure to chlorinated drinking water has been associated with increased risk of cancer. Nitrates, in drinking water, can transform to mutagenic N-nitroso compounds, which increase the risk of lymphoma, leukemia, colorectal cancer, and bladder cancer. Radiation Up to 10% of total cancer cases may be induced by radiation, both ionizing and nonionizing, typically from radioactive substances and ultraviolet (UV), pulsed electromagnetic fields. Cancers induced by radiation include some types of leukemia, lymphoma, thyroid cancers, skin cancers, sarcomas, lung and breast carcinomas. One of the best examples of increased risk of cancer after exposure to radiation is the increased incidence of total malignancies observed in Sweden after exposure to radioactive fallout from the Chernobyl nuclear power plant. Radon and radon decay products in the home and/or at workplaces (such as mines) are the most common sources of exposure to ionizing radiation. The presence of radioactive nuclei from radon, radium, and uranium was found to increase the risk of gastric cancer in rats. Another source of radiation exposure is x-rays used in medical settings for diagnostic or therapeutic purposes. In fact, the risk of breast cancer from x-rays is highest among girls exposed to chest irradiation at puberty, a time of intense breast development. Other factors associated with radiation-induced cancers in humans are patient age and physiological state, synergistic interactions between radiation and carcinogens, and genetic susceptibility toward radiation. Nonionizing radiation derived primarily from sunlight includes UV rays, which are carcinogenic to humans. Exposure to UV radiation is a major risk for various types of skin cancers including basal cell carcinoma, squamous cell carcinoma, and melanoma. Along with UV exposure from sunlight, UV exposure from sunbeds for cosmetic tanning may account for the growing incidence of melanoma. Depletion of the ozone layer in the stratosphere can augment the dose-intensity of UVB and UVC, which can further increase the incidence of skin cancer. Low-frequency electromagnetic fields can cause clastogenic DNA damage. The sources of electromagnetic field exposure are high-voltage power lines, transformers, electric train engines, and more generally, all types of electrical equipments. An increased risk of cancers such as childhood leukemia, brain tumors and breast cancer has been attributed to electromagnetic field exposure. For instance, children living within 200 m of high-voltage power lines have a relative risk of leukemia of 69%, whereas those living between 200 and 600 m from these power lines have a relative risk of 23%. In addition, a recent meta-analysis of all available epidemiologic data showed that daily prolonged use of mobile phones for 10 years or more showed a consistent pattern of an increased risk of brain tumors. PREVENTION OF CANCER The fact that only 5–10% of all cancer cases are due to genetic defects and that the remaining 90–95% are due to environment and lifestyle provides major opportunities for preventing cancer. Because tobacco, diet, infection, obesity, and other factors contribute approximately 25–30%, 30–35%, 15–20%, 10–20%, and 10–15%, respectively, to the incidence of all cancer deaths in the USA, it is clear how we can prevent cancer. Almost 90% of patients diagnosed with lung cancer are cigarette smokers; and cigarette smoking combined with alcohol intake can synergistically contribute to tumorigenesis. Similarly, smokeless tobacco is responsible for 400,000 cases (4% of all cancers) of oral cancer worldwide. Thus avoidance of tobacco products and minimization of alcohol consumption would likely have a major effect on cancer incidence. Infection by various bacteria and viruses is another very prominent cause of various cancers. Vaccines for cervical cancer and HCC should help prevent some of these cancers, and a cleaner environment and modified lifestyle behavior would be even more helpful in preventing infection-caused cancers. The first FDA approved chemopreventive agent was tamoxifen, for reducing the risk of breast cancer. This agent was found to reduce the breast cancer incidence by 50% in women at high risk. With tamoxifen, there is an increased risk of serious side effects such as uterine cancer, blood clots, ocular disturbances, hypercalcemia, and stroke. Recently it has been shown that a osteoporosis drug raloxifene is as effective as tamoxifen in preventing estrogen-receptor-positive, invasive breast cancer but had fewer side effects than tamoxifen. Though it is better than tamoxifen with respect to side effects, it can cause blood clots and stroke. Other potential side effects of raloxifene include hot flashes, leg cramps, swelling of the legs and feet, flu-like symptoms, joint pain, and sweating. The second chemopreventive agent to reach to clinic was finasteride, for prostate cancer, which was found to reduce incidence by 25% in men at high risk. The recognized side effects of this agent include erectile dysfunction, lowered sexual desire, impotence and gynecomastia . Celecoxib, a COX-2 inhibitor is another approved agent for prevention of familial adenomatous polyposis (FAP). However, the chemopreventive benefit of celecoxib is at the cost of its serious cardiovascular harm . The serious side effects of the FDA approved chemopreventive drugs is an issue of particular concern when considering long-term administration of a drug to healthy people who may or may not develop cancer. This clearly indicates the need for agents, which are safe and efficacious in preventing cancer. Diet derived natural products will be potential candidates for this purpose. Diet, obesity, and metabolic syndrome are very much linked to various cancers and may account for as much as 30–35% of cancer deaths, indicating that a reasonably good fraction of cancer deaths can be prevented by modifying the diet. Extensive research has revealed that a diet consisting of fruits, vegetables, spices, and grains has the potential to prevent cancer . The specific substances in these dietary foods that are responsible for preventing cancer and the mechanisms by which they achieve this have also been examined extensively. Various phytochemicals have been identified in fruits, vegetables, spices, and grains that exhibit chemopreventive potential , and numerous studies have shown that a proper diet can help protect against cancer. Below is a description of selected dietary agents and diet-derived phNumerous outdoor air pollutants such as PAHs increase the risk of cancers, especially lung cancer. PAHs can adhere to fine carbon particles in the atmosphere and thus penetrate our bodies primarily through breathing. Long-term exposure to PAH-containing air in polluted cities was found to increase the risk of lung cancer deaths. Aside from PAHs and other fine carbon particles, another environmental pollutant, nitric oxide, was found to increase the risk of lung cancer in a European population of nonsmokers. Other studies have shown that nitric oxide can induce lung cancer and promote metastasis. The increased risk of childhood leukemia associated with exposure to motor vehicle exhaust was also reported. Indoor air pollutants such as volatile organic compounds and pesticides increase the risk of childhood leukemia and lymphoma, and children as well as adults exposed to pesticides have increased risk of brain tumors, Wilm’s tumors, Ewing’s sarcoma, and germ cell tumors. In utero exposure to environmental organic pollutants was found to increase the risk for testicular cancer. In addition, dioxan, an environmental pollutant from incinerators, was found to increase the risk of sarcoma and lymphoma. Long-term exposure to chlorinated drinking water has been associated with increased risk of cancer. Nitrates, in drinking water, can transform to mutagenic N-nitroso compounds, which increase the risk of lymphoma, leukemia, colorectal cancer, and bladder cancer. Radiation Up to 10% of total cancer cases may be induced by radiation, both ionizing and nonionizing, typically from radioactive substances and ultraviolet (UV), pulsed electromagnetic fields. Cancers induced by radiation include some types of leukemia, lymphoma, thyroid cancers, skin cancers, sarcomas, lung and breast carcinomas. One of the best examples of increased risk of cancer after exposure to radiation is the increased incidence of total malignancies observed in Sweden after exposure to radioactive fallout from the Chernobyl nuclear power plant. Radon and radon decay products in the home and/or at workplaces (such as mines) are the most common sources of exposure to ionizing radiation. The presence of radioactive nuclei from radon, radium, and uranium was found to increase the risk of gastric cancer in rats. Another source of radiation exposure is x-rays used in medical settings for diagnostic or therapeutic purposes. In fact, the risk of breast cancer from x-rays is highest among girls exposed to chest irradiation at puberty, a time of intense breast development. Other factors associated with radiation-induced cancers in humans are patient age and physiological state, synergistic interactions between radiation and carcinogens, and genetic susceptibility toward radiation. Nonionizing radiation derived primarily from sunlight includes UV rays, which are carcinogenic to humans. Exposure to UV radiation is a major risk for various types of skin cancers including basal cell carcinoma, squamous cell carcinoma, and melanoma. Along with UV exposure from sunlight, UV exposure from sunbeds for cosmetic tanning may account for the growing incidence of melanoma. Depletion of the ozone layer in the stratosphere can augment the dose-intensity of UVB and UVC, which can further increase the incidence of skin cancer. Low-frequency electromagnetic fields can cause clastogenic DNA damage. The sources of electromagnetic field exposure are high-voltage power lines, transformers, electric train engines, and more generally, all types of electrical equipments. An increased risk of cancers such as childhood leukemia, brain tumors and breast cancer has been attributed to electromagnetic field exposure. For instance, children living within 200 m of high-voltage power lines have a relative risk of leukemia of 69%, whereas those living between 200 and 600 m from these power lines have a relative risk of 23%. In addition, a recent meta-analysis of all available epidemiologic data showed that daily prolonged use of mobile phones for 10 years or more showed a consistent pattern of an increased risk of brain tumors. PREVENTION OF CANCER The fact that only 5–10% of all cancer cases are due to genetic defects and that the remaining 90–95% are due to environment and lifestyle provides major opportunities for preventing cancer. Because tobacco, diet, infection, obesity, and other factors contribute approximately 25–30%, 30–35%, 15–20%, 10–20%, and 10–15%, respectively, to the incidence of all cancer deaths in the USA, it is clear how we can prevent cancer. Almost 90% of patients diagnosed with lung cancer are cigarette smokers; and cigarette smoking combined with alcohol intake can synergistically contribute to tumorigenesis. Similarly, smokeless tobacco is responsible for 400,000 cases (4% of all cancers) of oral cancer worldwide. Thus avoidance of tobacco products and minimization of alcohol consumption would likely have a major effect on cancer incidence. Infection by various bacteria and viruses is another very prominent cause of various cancers. Vaccines for cervical cancer and HCC should help prevent some of these cancers, and a cleaner environment and modified lifestyle behavior would be even more helpful in preventing infection-caused cancers. The first FDA approved chemopreventive agent was tamoxifen, for reducing the risk of breast cancer. This agent was found to reduce the breast cancer incidence by 50% in women at high risk. With tamoxifen, there is an increased risk of serious side effects such as uterine cancer, blood clots, ocular disturbances, hypercalcemia, and stroke. Recently it has been shown that a osteoporosis drug raloxifene is as effective as tamoxifen in preventing estrogen-receptor-positive, invasive breast cancer but had fewer side effects than tamoxifen. Though it is better than tamoxifen with respect to side effects, it can cause blood clots and stroke. Other potential side effects of raloxifene include hot flashes, leg cramps, swelling of the legs and feet, flu-like symptoms, joint pain, and sweating. The second chemopreventive agent to reach to clinic was finasteride, for prostate cancer, which was found to reduce incidence by 25% in men at high risk. The recognized side effects of this agent include erectile dysfunction, lowered sexual desire, impotence and gynecomastia . Celecoxib, a COX-2 inhibitor is another approved agent for prevention of familial adenomatous polyposis (FAP). However, the chemopreventive benefit of celecoxib is at the cost of its serious cardiovascular harm . The serious side effects of the FDA approved chemopreventive drugs is an issue of particular concern when considering long-term administration of a drug to healthy people who may or may not develop cancer. This clearly indicates the need for agents, which are safe and efficacious in preventing cancer. Diet derived natural products will be potential candidates for this purpose. Diet, obesity, and metabolic syndrome are very much linked to various cancers and may account for as much as 30–35% of cancer deaths, indicating that a reasonably good fraction of cancer deaths can be prevented by modifying the diet. Extensive research has revealed that a diet consisting of fruits, vegetables, spices, and grains has the potential to prevent cancer . The specific substances in these dietary foods that are responsible for preventing cancer and the mechanisms by which they achieve this have also been examined extensively. Various phytochemicals have been identified in fruits, vegetables, spices, and grains that exhibit chemopreventive potential , and numerous studies have shown that a proper diet can help protect against cancer. Below is a description of selected dietary agents and diet-derived phytochytochemicals that have been studied extensively to determine their role in cancer prevention. A diet we should eat! Fruits, vegetables, spices, condiments and cereals with potential to prevent cancer. Fruits include 1 apple, 2 apricot, 3 banana, 4 blackberry, 5 cherry, 6 citrus fruits, 7 dessert date, 8 durian, 9 grapes, 10 guava, 11 Indian gooseberry, 12 mango, 13 malay apple, 14 mangosteen, 15 pineapple, 16 pomegranate. Vegetables include 1 artichok, 2 avocado, 3 brussels sprout, 4 broccoli, 5 cabbage, 6 cauliflower, 7 carrot, 8 daikon 9 kohlrabi, 10 onion, 11 tomato, 12 turnip, 13 ulluco, 14 water cress, 15 okra, 16 potato, 17 fiddle head, 18 radicchio, 19 komatsuna, 20 salt bush, 21 winter squash, 22 zucchini, 23 lettuce, 24 spinach. Spices and condiments include 1 turmeric, 2 cardamom, 3 coriander, 4 black pepper, 5 clove, 6 fennel, 7 rosemary, 8 sesame seed, 9 mustard, 10 licorice, 11 garlic, 12 ginger, 13 parsley, 14 cinnamon, 15 curry leaves, 16 kalonji, 17 fenugreek, 18 camphor, 19 pecan, 20 star anise, 21 flax seed, 22 black mustard, 23 pistachio, 24 walnut, 25 peanut, 26 cashew nut. Cereals include 1 rice, 2 wheat, 3 oats, 4 rye, 5 barley, 6 maize, 7 jowar, 8 pearl millet, 9 proso millet, 10 foxtail millet, 11 little millet, 12 barnyard millet, 13 kidney bean, 14 soybean, 15 mung bean, 16 black bean, 17 pigeon pea, 18 green pea, 19 scarlet runner bean, 20 black beluga, 21 brown spanish pardina, 22 green, 23 green (eston), 24 ivory white, 25 multicolored blend, 26 petite crimson, 27 petite golden, 28 red chief. Phytochemical structures Phytochemicals derived from fruits, vegetables, spices, condiments and cereals with potential to prevent cancer. 1 diosgenin, 2 glycyrrhizin, 3 glycyrrhetinic acid, 4 18-β-glycyrrhetinic acid, 5 oleandrin, 6 oleanolic acid, 7 betulinic acid, 8 lupeol, 9 guggulsterone, 10 celastrol, 11 ursolic acid, 12 acetyl-11-keto-β-boswellic acid, 13 1’-actoxychavicol acetate, 14 α-lipoic acid 15 yakuchinone A, 16 yakuchinone B, 17 curcumin, 18 gingerol, 19 resveratrol, 20 piceatannol 21 genistein, 22 capsaicin, 23 dibenzoylmethane, 24 piperine, 25 kahweol, 26 indiruibin-3’-monoxime, 27 caffeic acid phenethyl ester, 28 emodin, 29 eugenol, 30 linalol, 31 quinic acid, 32 garcinol, 33 sesamin, 34 theaflavin-3,3’-digallate, 35 sanguinarine, 36 silymarin, 37 mangostin, 38 mangiferin, 39 butein, 40 berberine, 41 glabridin, 42 myricetin, 43 carnosol, 44 β-lapachone, 45 evodiamine, 46 wogonin, 47 apigenin, 48 (-)-epigatechin, 49 tanshinones IIA, 50 tanshinones I, 51 (-)-epicatechin gallate, 52 epigallocatechin gallate, 53 carnosol, 54 zerumbone, 55 sulforaphane, 56 phytic acid, 57 allicin, 58 benzyl isothiocyanate, 59 baicalin, 60 ascorbic acid, 61 anethole, 62 indole 3-carbinol, 63 phenyl isothiocyanate, 64 thymoquinone, 65 plumbagin, 66 γ-tocotrienol, 67 lutein, 68 β-cryptoxanthine, 69 β-carotene, 70 lycopene, 71 α-tocoperol. Fruits and Vegetables The protective role of fruits and vegetables against cancers that occur in various anatomical sites is now well supported . In 1966, Wattenberg proposed for the first time that the regular consumption of certain constituents in fruits and vegetables might provide protection from cancer. Doll and Peto showed that 75–80% of cancer cases diagnosed in the USA in 1981 might have been prevented by lifestyle changes. According to a 1997 estimate, approximately 30–40% of cancer cases worldwide were preventable by feasible dietary means. Several studies have addressed the cancer chemopreventive effects of the active components derived from fruits and vegetables. More than 25,000 different phytochemicals have been identified that may have potential against various cancers. These phytochemicals have advantages because they are safe and usually target multiple cell-signaling pathways. Major chemopreventive compounds identified from fruits and vegetables includes carotenoids, vitamins, resveratrol, quercetin, silymarin, sulphoraphane and indole-3-carbinol. Carotenoids Various natural carotenoids present in fruits and vegetables were reported to have anti-inflammatory and anticarcinogenic activity. Lycopene is one of the main carotenoids in the regional Mediterranean diet and can account for 50% of the carotenoids in human serum. Lycopene is present in fruits, including watermelon, apricots, pink guava, grapefruit, rosehip, and tomatoes. A wide variety of processed tomato-based products account for more than 85% of dietary lycopene. The anticancer activity of lycopene has been demonstrated in both in vitro and in vivo tumor models as well as in humans. The proposed mechanisms for the anticancer effect of lycopene involve ROS scavenging, up-regulation of detoxification systems, interference with cell proliferation, induction of gap-junctional communication, inhibition of cell-cycle progression, and modulation of signal transduction pathways. Other carotenoids reported to have anticancer activity include beta-carotene, alpha-carotene, lutein, zeaxanthin, beta-cryptoxanthin, fucoxanthin, astaxanthin, capsanthin, crocetin, and phytoene. Resveratrol The stilbene resveratrol has been found in fruits such as grapes, peanuts, and berries. Resveratrol exhibits anticancer properties against a wide variety of tumors, including lymphoid and myeloid cancers, multiple myeloma, and cancers of the breast, prostate, stomach, colon, and pancreas. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; induction of apoptosis via Fas/CD95, p53, ceramide activation, tubulin polymerization, mitochondrial and adenylyl cyclase pathways; up-regulation of p21 p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL, and cellular inhibitor of apoptosis proteins; activation of caspases; suppression of nitric oxide synthase; suppression of transcription factors such as NF-κB, AP-1, and early growth response-1; inhibition of cyclooxygenase-2 (COX-2) and lipoxygenase; suppression of adhesion molecules; and inhibition of angiogenesis, invasion, and metastasis. Limited data in humans have revealed that resveratrol is pharmacologically safe. As a nutraceutical, resveratrol is commercially available in the USA and Europe in 50 µg to 60 mg doses. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential chemopreventive and therapeutic agents for cancer. Quercetin The flavone quercetin (3,3′,4′,5,7-pentahydroxyflavone), one of the major dietary flavonoids, is found in a broad range of fruits, vegetables, and beverages such as tea and wine, with a daily intake in Western countries of 25–30 mg. The antioxidant, anti-inflammatory, antiproliferative, and apoptotic effects of the molecule have been largely analyzed in cell culture models, and it is known to block NF-κB activation. In animal models, quercetin has been shown to inhibit inflammation and prevent colon and lung cancer. A phase 1 clinical trial indicated that the molecule can be safely administered and that its plasma levels are sufficient to inhibit lymphocyte tyrosine kinase activity. Consumption of quercetin in onions and apples was found to be inversely associated with lung cancer risk in Hawaii. The effect of onions was particularly strong against squamous cell carcinoma. In another study, an increased plasma level of quercetin after a meal of onions was accompanied by increased resistance to strand breakage in lymphocytic DNA and decreased levels of some oxidative metabolites in the urine. Silymarin The flavonoid silymarin (silybin, isosilybin, silychristin, silydianin, and taxifolin) is commonly found in the dried fruit of the milk thistle plant Silybum marianum . Although silymarin’s role as an antioxidant and hepatoprotective agent is well known, its role as an anticancer agent is just emerging. The anti-inflammatory effects of silymarin are mediated through suppression of NF-κB-regulated gene products, including COX-2, lipoxygenase (LOX), inducible NO synthase, TNF, and IL-1. Numerous studies have indicated that silymarin is a chemopreventive agent in vivo against various carcinogens/tumor promoters, including UV light, 7,12-dimethylbenz(a)anthracene (DMBA), phorbol 12-myristate 13-acetate, and others. Silymarin has also been shown to sensitize tumors to chemotherapeutic agents through down-regulation of the MDR protein and other mechanisms. It binds to both estrogen and androgen receptors and down-regulates prostate specific antigen. In addition to its chemopreventive effects, silymarin exhibits activity against tumors (e.g., prostate and ovary) in rodents. Various clinical trials have indicated that silymarin is bioavailable and pharmacologically safe. Studies are now in progress to demonstrate the clinical efficacy of silymarin against various cancers. Indole-3-carbinol The flavonoid indole-3-carbinol (I3C) is present in vegetables such as cabbage, broccoli, brussels sprout, cauliflower, and daikon artichoke. The hydrolysis product of I3C metabolizes to a variety of products, including the dimer 3,3′-diindolylmethane. Both I3C and 3,3′-diindolylmethane exert a variety of biological and biochemical effects, most of which appear to occur because I3C modulates several nuclear transcription factors. I3C induces phase 1 and phase 2 enzymes that metabolize carcinogens, including estrogens. I3C has also been found to be effective in treating some cases of recurrent respiratory papillomatosis and may have other clinical uses. Sulforaphane Sulforaphane (SFN) is an isothiothiocyanate found in cruciferous vegetables such as broccoli. Its chemopreventive effects have been established in both in vitro and in vivo studies. The mechanisms of action of SFN include inhibition of phase 1 enzymes, induction of phase 2 enzymes to detoxify carcinogens, cell-cycle arrest, induction of apoptosis, inhibition of histone deacetylase, modulation of the MAPK pathway, inhibition of NF-κB, and production of ROS. Preclinical and clinical studies of this compound have suggested its chemopreventive effects at several stages of carcinogenesis. In a clinical trial, SFN was given to eight healthy women an hour before they underwent elective reduction mammoplasty. Induction in NAD(P)H/quinone oxidoreductase and heme oxygenase-1 was observed in the breast tissue of all patients, indicating the anticancer effect of SFN. Teas and Spices Spices are used all over the world to add flavor, taste, and nutritional value to food. A growing body of research has demonstrated that phytochemicals such as catechins (green tea), curcumin (turmeric), diallyldisulfide (garlic), thymoquinone (black cumin) capsaicin (red chili), gingerol (ginger), anethole (licorice), diosgenin (fenugreek) and eugenol (clove, cinnamon) possess therapeutic and preventive potential against cancers of various anatomical origins. Other phytochemicals with this potential include ellagic acid (clove), ferulic acid (fennel, mustard, sesame), apigenin (coriander, parsley), betulinic acid (rosemary), kaempferol (clove, fenugreek), sesamin (sesame), piperine (pepper), limonene (rosemary), and gambogic acid (kokum). Below is a description of some important phytochemicals associated with cancer. Catechins More than 3,000 studies have shown that catechins derived from green and black teas have potential against various cancers. A limited amount of data are also available from green tea polyphenol chemoprevention trials. Phase 1 trials of healthy volunteers have defined the basic biodistribution patterns, pharmacokinetic parameters, and preliminary safety profiles for short-term oral administration of various green tea preparations. The consumption of green tea appears to be relatively safe. Among patients with established premalignant conditions, green tea derivatives have shown potential efficacy against cervical, prostate, and hepatic malignancies without inducing major toxic effects. One novel study determined that even persons with solid tumors could safely consume up to 1 g of green tea solids, the equivalent of approximately 900 ml of green tea, three times daily. This observation supports the use of green tea for both cancer prevention and treatment ( 78 ). Curcumin Curcumin is one of the most extensively studied compounds isolated from dietary sources for inhibition of inflammation and cancer chemoprevention, as indicated by almost 3000 published studies. Studies from our laboratory showed that curcumin inhibited NF-κB and NF-κB-regulated gene expression in various cancer cell lines. In vitro and in vivo studies showed that this phytochemical inhibited inflammation and carcinogenesis in animal models, including breast, esophageal, stomach, and colon cancer models. Other studies showed that curcumin inhibited ulcerative proctitis and Crohn’s disease, and one showed that curcumin inhibited ulcerative colitis in humans. Another study evaluated the effect of a combination of curcumin and piperine in patients with tropical pancreatitis. One study conducted in patients with familial adenomatous polyposis showed that curcumin has a potential role in inhibiting this condition. In that study, all five patients were treated with curcumin and quercetin for a mean of 6 months and had a decreased polyp number (60.4%) and size (50.9%) from baseline with minimal adverse effects and no laboratory-determined abnormalities. The pharmacodynamic and pharmacokinetic effects of oral Curcuma extract in patients with colorectal cancer have also been studied. In a study of patients with advanced colorectal cancer refractory to standard chemotherapies, 15 patients received Curcuma extract daily for up to 4 months. Results showed that oral Curcuma extract was well tolerated, and dose-limiting toxic effects were not observed. Another study showed that in patients with advanced colorectal cancer, a daily dose of 3.6 g of curcumin engendered a 62% decrease in inducible prostaglandin E2 production on day 1 and a 57% decrease on day 29 in blood samples taken 1 h after dose administration. An early clinical trial with 62 cancer patients with external cancerous lesions at various sites (breast, 37; vulva, 4; oral, 7; skin, 7; and others, 11) reported reductions in the sense of smell (90% of patients), itching (almost all patients), lesion size and pain (10% of patients), and exudates (70% of patients) after topical application of an ointment containing curcumin. In a phase 1 clinical trial, a daily dose of 8,000 mg of curcumin taken by mouth for 3 months resulted in histologic improvement of precancerous lesions in patients with uterine cervical intraepithelial neoplasm (one of four patients), intestinal metaplasia (one of six patients), bladder cancer (one of two patients), and oral leukoplakia (two of seven patients). Results from another study conducted by our group showed that curcumin inhibited constitutive activation of NF-κB, COX-2, and STAT3 in peripheral blood mononuclear cells from the 29 multiple myeloma patients enrolled in this study. Curcumin was given in doses of 2, 4, 8, or 12 g/day orally. Treatment with curcumin was well tolerated with no adverse events. Of the 29 patients, 12 underwent treatment for 12 weeks and 5 completed 1 year of treatment with stable disease. Other studies from our group showed that curcumin inhibited pancreatic cancer. Curcumin down-regulated the expression of NF-κB, COX-2, and phosphorylated STAT3 in peripheral blood mononuclear cells from patients (most of whom had baseline levels considerably higher than those found in healthy volunteers). These studies showed that curcumin is a potent anti-inflammatory and chemopreventive agent. A detailed description of curcumin and its anticancer properties can be found in one of our recent reviews. Diallyldisulfide Diallyldisulfide, isolated from garlic, inhibits the growth and proliferation of a number of cancer cell lines including colon, breast, glioblastoma, melanoma, and neuroblastoma cell lines. Recent studies showed that this compound induces apoptosis in Colo 320 DM human colon cancer cells by inhibiting COX-2, NF-κB, and ERK-2. It has been shown to inhibit a number of cancers including dimethylhydrazine-induced colon cancer, benzo[a]pyrene-induced neoplasia, and glutathione S-transferase activity in mice; benzo[a]pyrene-induced skin carcinogenesis in mice; N-nitrosomethylbenzylamine-induced esophageal cancer in rats; N-nitrosodiethylamine-induced forestomach neoplasia in female A/J mice; aristolochic acid-induced forestomach carcinogenesis in rats; diethylnitrosamine-induced glutathione S-transferase positive foci in rat liver; 2-amino-3-methylimidazo[4,5-f]quinoline-induced hepatocarcinogenesis in rats; and diethylnitrosamine-induced liver foci and hepatocellular adenomas in C3H mice. Diallyldisulfide has also been shown to inhibit mutagenesis or tumorigenesis induced by vinyl carbamate and N-nitrosodimethylamine; aflatoxin B1-induced and N-nitrosodiethylamine-induced liver preneoplastic foci in rats; arylamine N-acetyltransferase activity and 2-aminofluorene-DNA adducts in human promyelocytic leukemia cells; DMBA-induced mouse skin tumors; N-nitrosomethylbenzylamine-induced mutation in rat esophagus; and diethylstilbesterol-induced DNA adducts in the breasts of female ACI rats. Diallyldisulfide is believed to bring about an anticarcinogenic effect through a number of mechanisms, such as scavenging of radicals; increasing gluathione levels; increasing the activities of enzymes such as glutathione S-transferase and catalase; inhibiting cytochrome p4502E1 and DNA repair mechanisms; and preventing chromosomal damage. Thymoquinone The chemotherapeutic and chemoprotective agents from black cumin include thymoquinone (TQ), dithymoquinone (DTQ), and thymohydroquinone, which are present in the oil of this seed. TQ has antineoplastic activity against various tumor cells. DTQ also contributes to the chemotherapeutic effects of Nigella sativa . In vitro study results indicated that DTQ and TQ are equally cytotoxic to several parental cell lines and to their corresponding multidrug-resistant human tumor cell lines. TQ induces apoptosis by p53-dependent and p53-independent pathways in cancer cell lines. It also induces cell-cycle arrest and modulates the levels of inflammatory mediators. To date, the chemotherapeutic potential of TQ has not been tested, but numerous studies have shown its promising anticancer effects in animal models. TQ suppresses carcinogen-induced forestomach and skin tumor formation in mice and acts as a chemopreventive agent at the early stage of skin tumorigenesis. Moreover, the combination of TQ and clinically used anticancer drugs has been shown to improve the drug’s therapeutic index, prevents nontumor tissues from sustaining chemotherapy-induced damage, and enhances the antitumor activity of drugs such as cisplatin and ifosfamide. A very recent report from our own group established that TQ affects the NF-κB signaling pathway by suppressing NF-κB and NF-κB-regulated gene products. Capsaicin The phenolic compound capsaicin (t8-methyl- N -vanillyl-6-nonenamide), a component of red chili, has been extensively studied. Although capsaicin has been suspected to be a carcinogen, a considerable amount of evidence suggests that it has chemopreventive effects. The antioxidant, anti-inflammatory, and antitumor properties of capsaicin have been established in both in vitro and in vivo systems. For example, showed that capsaicin can suppress the TPA-stimulated activation of NF-κB and AP-1 in cultured HL-60 cells. In addition, capsaicin inhibited the constitutive activation of NF-κB in malignant melanoma cells. Furthermore, capsaicin strongly suppressed the TPA-stimulated activation of NF-κB and the epidermal activation of AP-1 in mice. Another proposed mechanism of action of capsaicin is its interaction with xenobiotic metabolizing enzymes, involved in the activation and detoxification of various chemical carcinogens and mutagens. Metabolism of capsaicin by hepatic enzymes produces reactive phenoxy radical intermediates capable of binding to the active sites of enzymes and tissue macromolecules. Capsaicin can inhibit platelet aggregation and suppress calcium-ionophore–stimulated proinflammatory responses, such as the generation of superoxide anion, phospholipase A2 activity, and membrane lipid peroxidation in macrophages. It acts as an antioxidant in various organs of laboratory animals. Anti-inflammatory properties of capsaicin against carcinogen-induced inflammation have also been reported in rats and mice. Capsaicin has exerted protective effects against ethanol-induced gastric mucosal injury, hemorrhagic erosion, lipid peroxidation, and myeloperoxidase activity in rats that was associated with suppression of COX-2. While lacking intrinsic tumor-promoting activity, capsaicin inhibited TPA-promoted mouse skin papillomagenesis. Gingerol Gingerol, a phenolic substance mainly present in the spice ginger ( Zingiber officinale Roscoe), has diverse pharmacologic effects including antioxidant, antiapoptotic, and anti-inflammatory effects. Gingerol has been shown to have anticancer and chemopreventive properties, and the proposed mechanisms of action include the inhibition of COX-2 expression by blocking of the p38 MAPK–NF-κB signaling pathway. A detailed report on the cancer-preventive ability of gingerol was presented in a recent review by Shukla and Singh. Anethole Anethole, the principal active component of the spice fennel, has shown anticancer activity. In 1995, Al-Harbi et al. studied the antitumor activity of anethole against Ehrlich ascites carcinoma induced in a tumor model in mice. The study revealed that anethole increased survival time, reduced tumor weight, and reduced the volume and body weight of the EAT-bearing mice. It also produced a significant cytotoxic effect in the EAT cells in the paw, reduced the levels of nucleic acids and MDA, and increased NP-SH concentrations. The histopathological changes observed after treatment with anethole were comparable to those after treatment with the standard cytotoxic drug cyclophosphamide. The frequency of micronuclei occurrence and the ratio of polychromatic erythrocytes to normochromatic erythrocytes showed anethole to be mitodepressive and nonclastogenic in the femoral cells of mice. In 1996, Sen et al ., studied the NF-κB inhibitory activity of a derivative of anethole and anetholdithiolthione. Their study results showed that anethole inhibited H2O2, phorbol myristate acetate or TNF alpha induced NF-κB activation in human jurkat T-cells studied the anticarcinogenic activity of anethole trithione against DMBA induced in a rat mammary cancer model. The study results showed that this phytochemical inhibited mammary tumor growth in a dose-dependent manner. Nakagawa and Suzuki studied the metabolism and mechanism of action of trans-anethole (anethole) and the estrogenlike activity of the compound and its metabolites in freshly isolated rat hepatocytes and cultured MCF-7 human breast cancer cells. The results suggested that the biotransformation of anethole induces a cytotoxic effect at higher concentrations in rat hepatocytes and an estrogenic effect at lower concentrations in MCF-7 cells on the basis of the concentrations of the hydroxylated intermediate, 4OHPB. Results from preclinical studies have suggested that the organosulfur compound anethole dithiolethione may be an effective chemopreventive agent against lung cancer. Lam et al , conducted a phase 2b trial of anethole dithiolethione in smokers with bronchial dysplasia. The results of this clinical trial suggested that anethole dithiolethione is a potentially efficacious chemopreventive agent against lung cancer. Diosgenin Diosgenin, a steroidal saponin present in fenugreek, has been shown to suppress inflammation, inhibit proliferation, and induce apoptosis in various tumor cells. Research during the past decade has shown that diosgenin suppresses proliferation and induces apoptosis in a wide variety of cancer cells lines. Antiproliferative effects of diosgenin are mediated through cell-cycle arrest, disruption of Ca2+ homeostasis, activation of p53, release of apoptosis-inducing factor, and modulation of caspase-3 activity. Diosgenin also inhibits azoxymethane-induced aberrant colon crypt foci, has been shown to inhibit intestinal inflammation, and modulates the activity of LOX and COX-2. Diosgenin has also been shown to bind to the chemokine receptor CXCR3, which mediates inflammatory responses. Results from our own laboratory have shown that diosgenin inhibits osteoclastogenesis, cell invasion, and cell proliferation through Akt down-regulation, IκB kinase activation, and NF-κB-regulated gene expression. Eugenol Eugenol is one of the active components of cloves. Studies conducted by Ghosh et al . showed that eugenol suppressed the proliferation of melanoma cells. In a B16 xenograft study, eugenol treatment produced a significant tumor growth delay, an almost 40% decrease in tumor size, and a 19% increase in the median time to end point. Of more importance, 50% of the animals in the control group died of metastatic growth, whereas none in the eugenol treatment group showed any signs of cell invasion or metastasis. In 1994, Sukumaran et al . showed that eugenol DMBA induced skin tumors in mice. The same study showed that eugenol inhibited superoxide formation and lipid peroxidation and the radical scavenging activity that may be responsible for its chemopreventive action. Studies conducted by Imaida et al . showed that eugenol enhanced the development of 1,2-dimethylhydrazine-induced hyperplasia and papillomas in the forestomach but decreased the incidence of 1-methyl-1-nitrosourea-induced kidney nephroblastomas in F344 male rats. Another study conducted by Pisano et al . demonstrated that eugenol and related biphenyl ( S )-6,6′-dibromo-dehydrodieugenol elicit specific antiproliferative activity on neuroectodermal tumor cells, partially triggering apoptosis. In 2003, Kim et al . showed that eugenol suppresses COX-2 mRNA expression (one of the main genes implicated in the processes of inflammation and carcinogenesis) in HT-29 cells and lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells. Another study by Deigner et al . showed that 1′-hydroxyeugenol is a good inhibitor of 5-lipoxygenase and Cu(2+)-mediated low-density lipoprotein oxidation. The studies by Rompelberg et al . showed that in vivo treatment of rats with eugenol reduced the mutagenicity of benzopyrene in the Salmonella typhimurium mutagenicity assay, whereas in vitro treatment of cultured cells with eugenol increased the genotoxicity of benzopyrene. Wholegrain Foods The major wholegrain foods are wheat, rice, and maize; the minor ones are barley, sorghum, millet, rye, and oats. Grains form the dietary staple for most cultures, but most are eaten as refined-grain products in Westernized countries. Whole grains contain chemopreventive antioxidants such as vitamin E, tocotrienols, phenolic acids, lignans, and phytic acid. The antioxidant content of whole grains is less than that of some berries but is greater than that of common fruits or vegetables . The refining process concentrates the carbohydrate and reduces the amount of other macronutrients, vitamins, and minerals because the outer layers are removed. In fact, all nutrients with potential preventive actions against cancer are reduced. For example, vitamin E is reduced by as much as 92% Wholegrain intake was found to reduce the risk of several cancers including those of the oral cavity, pharynx, esophagus, gallbladder, larynx, bowel, colorectum, upper digestive tract, breasts, liver, endometrium, ovaries, prostate gland, bladder, kidneys, and thyroid gland, as well as lymphomas, leukemias, and myeloma. Intake of wholegrain foods in these studies reduced the risk of cancers by 30–70%. How do whole grains reduce the risk of cancer? Several potential mechanisms have been described. For instance, insoluble fibers, a major constituent of whole grains, can reduce the risk of bowel cancer. Additionally, insoluble fiber undergoes fermentation, thus producing short-chain fatty acids such as butyrate, which is an important suppressor of tumor formation . Whole grains also mediate favorable glucose response, which is protective against breast and colon cancers. Also, several phytochemicals from grains and pulses were reported to have chemopreventive action against a wide variety of cancers. For example, isoflavones (including daidzein, genistein, and equol) are nonsteroidal diphenolic compounds that are found in leguminous plants and have antiproliferative activities. Findings from several, but not all, studies have shown significant correlations between an isoflavone-rich soy-based diet and reduced incidence of cancer or mortality from cancer in humans. Our laboratory has shown that tocotrienols, but not tocopherols, can suppress NF-κB activation induced by most carcinogens, thus leading to suppression of various genes linked with proliferation, survival, invasion, and angiogenesis of tumors. Observational studies have suggested that a diet rich in soy isoflavones (such as the typical Asian diet) is one of the most significant contributing factors for the lower observed incidence and mortality of prostate cancers in Asia. On the basis of findings about diet and of urinary excretion levels associated with daidzein, genistein, and equol in Japanese subjects compared with findings in American or European subjects, the isoflavonoids in soy products were proposed to be the agents responsible for reduced cancer risk. In addition to its effect on breast cancer, genistein and related isoflavones also inhibit cell growth or the development of chemically induced cancers in the stomach, bladder, lung, prostate, and blood. Vitamins Although controversial, the role of vitamins in cancer chemoprevention is being evaluated increasingly. Fruits and vegetables are the primary dietary sources of vitamins except for vitamin D. Vitamins, especially vitamins C, D, and E, are reported to have cancer chemopreventive activity without apparent toxicity. Epidemiologic study findings suggest that the anticancer/chemopreventive effects of vitamin C against various types of cancers correlate with its antioxidant activities and with the inhibition of inflammation and gap junction intercellular communication. Findings from a recent epidemiologic study showed that a high vitamin C concentration in plasma had an inverse relationship with cancer-related mortality. In 1997, expert panels at the World Cancer Research Fund and the American Institute for Cancer Research estimated that vitamin C can reduce the risk of cancers of the stomach, mouth, pharynx, esophagus, lung, pancreas, and cervix. The protective effects of vitamin D result from its role as a nuclear transcription factor that regulates cell growth, differentiation, apoptosis, and a wide range of cellular mechanisms central to the development of cancer. Exercise/Physical Activity There is extensive evidence suggesting that regular physical exercise may reduce the incidence of various cancers. A sedentary lifestyle has been associated with most chronic illnesses. Physical inactivity has been linked with increased risk of cancer of the breast, colon, prostate, and pancreas and of melanoma. The increased risk of breast cancer among sedentary women that has been shown to be due to lack of exercise has been associated with a higher serum concentration of estradiol, lower concentration of hormone-binding globulin, larger fat masses, and higher serum insulin levels. Physical inactivity can also increase the risk of colon cancer (most likely because of an increase in GI transit time, thereby increasing the duration of contact with potential carcinogens), increase the circulating levels of insulin (promote proliferation of colonic epithelial cells), alter prostaglandin levels, depress the immune function, and modify bile acid metabolism. Additionally, men with a low level of physical activity and women with a larger body mass index were more likely to have a Ki-ras mutation in their tumors, which occurs in 30–50% of colon cancers. A reduction of almost 50% in the incidence of colon cancer was observed among those with the highest levels of physical activity. Similarly, higher blood testosterone and IGF-1 levels and suppressed immunity due to lack of exercise may increase the incidence of prostate cancer. One study indicated that sedentary men had a 56% and women a 72% higher incidence of melanoma than did those exercising 5–7 days per week. Caloric Restrictions Fasting is a type of caloric restriction (CR) that is prescribed in most cultures. Perhaps one of the first reports that CR can influence cancer incidence was published in 1940 on the formation of skin tumors and hepatoma in mice. Since then, several reports on this subject have been published. Dietary restriction, especially CR, is a major modifier in experimental carcinogenesis and is known to significantly decrease the incidence of neoplasms. Gross and Dreyfuss reported that a 36% restriction in caloric intake dramatically decreased radiation-induced solid tumors and/or leukemias. Yoshida et al . also showed that CR reduces the incidence of myeloid leukemia induced by a single treatment with whole-body irradiation in mice. How CR reduces the incidence of cancer is not fully understood. CR in rodents decreases the levels of plasma glucose and IGF-1 and postpones or attenuates cancer and inflammation without irreversible adverse effects. Most of the studies done on the effect of CR in rodents are long-term; however, that is not possible in humans, who routinely practice transient CR. The effect that transient CR has on cancer in humans is unclear. CONCLUSIONS On the basis of the studies described above, we propose a unifying hypothesis that all lifestyle factors that cause cancer (carcinogenic agents) and all agents that prevent cancer (chemopreventive agents) are linked through chronic inflammation . The fact that chronic inflammation is closely linked to the tumorigenic pathway is evident from numerous lines of evidence. Carcinogens & Chemoprotective Agents Carcinogens activate and chemopreventive agents suppress NF-κB activation, a major mediator of inflammation. First , inflammatory markers such as cytokines (such as TNF, IL-1, IL-6, and chemokines), enzymes (such as COX-2, 5-LOX, and matrix metalloproteinase-9 [MMP-9]), and adhesion molecules (such as intercellular adhesion molecule 1, endothelium leukocyte adhesion molecule 1, and vascular cell adhesion molecule 1) have been closely linked with tumorigenesis. Second , all of these inflammatory gene products have been shown to be regulated by the nuclear transcription factor, NF-κB. Third , NF-κB has been shown to control the expression of other gene products linked with tumorigenesis such as tumor cell survival or antiapoptosis (Bcl-2, Bcl-xL, IAP-1, IAP-2, XIAP, survivin, cFLIP, and TRAF-1), proliferation (such as c-myc and cyclin D1), invasion (MMP-9), and angiogenesis (vascular endothelial growth factor). Fourth , in most cancers, chronic inflammation precedes tumorigenesis. Fifth , most carcinogens and other risk factors for cancer, including cigarette smoke, obesity, alcohol, hyperglycemia, infectious agents, sunlight, stress, food carcinogens, and environmental pollutants, have been shown to activate NF-κB. Sixth , constitutive NF-κB activation has been encountered in most types of cancers. Seventh , most chemotherapeutic agents and γ-radiation, used for the treatment of cancers, lead to activation of NF-κB. Eighth , activation of NF-κB has been linked with chemoresistance and radioresistance. Ninth , suppression of NF-κB inhibits the proliferation of tumors, leads to apoptosis, inhibits invasion, and suppresses angiogenesis. Tenth , polymorphisms of TNF, IL-1, IL-6, and cyclin D1 genes encountered in various cancers are all regulated by NF-κB. Also, mutations in genes encoding for inhibitors of NF-κB have been found in certain cancers. Eleventh , almost all chemopreventive agents described above have been shown to suppress NF-κB activation. In summary, this review outlines the preventability of cancer based on the major risk factors for cancer. The percentage of cancer-related deaths attributable to diet and tobacco is as high as 60–70% worldwide. Acknowledgement This research was supported by The Clayton Foundation for Research (to B.B.A.).

I see on the many groups formed on Facebook and Telegram that people really have no idea about the effects of "Long Term" high doses have on our internal organs. This lack of understanding is particularly concerning given the alarming trends in self-medication and the widespread sharing of anecdotal experiences without a solid scientific foundation. Let's take Danny Lemoi as an example, a gentleman from the USA who faced the challenging diagnosis of Lyme disease. In his quest for relief, Danny turned to Ivermectin, believing that it could offer him greater benefits compared to the conventional pharmaceuticals he was prescribed. Unfortunately Danny’s use of Ivermectin on a long term daily basis caused his death from an enlarged heart…twice the size of a normal heart, and caused by Ivermectin use for Lyme disease. NOW, before I go further, I want to emphasize that I do think that Ivermectin is a safe drug; it has a long history of safety and has been used effectively to treat various parasitic infections. However, the caveat here is crucial: Ivermectin is still a drug, and people are abusing it by taking very large doses for an extended period. This misuse can lead to severe complications and unintended health consequences, particularly when individuals self-prescribe without adequate research I take myself as an example to illustrate the complexities involved in treatment decisions. In December of 2023, I received a life-altering diagnosis: cancer that had originated in my left tonsil and had metastasized to the back of my tongue and into the lymph nodes on the left side of my neck. Faced with the oncologists' recommendation of undergoing 37 sessions of radiation and chemotherapy, I chose to forge my own path by developing a personalized treatment protocol. I firmly believe in the potential of natural products and their ability to support our bodies in healing, but similar to pharmaceuticals, some elements of my protocol, such as Ivermectin, can also present opportunities for abuse or misuse. I cured my cancer with the protocol and my faith. But is did so using smaller doses. The case of Danny Lemoi serves as a cautionary tale, and I fear that many individuals are unwittingly placing their lives in jeopardy by following misguided advice. Yes, I utilized Ivermectin alongside Fenbendazole on a daily basis and tailored my dosage to what I felt was appropriate for my specific needs. Concurrently, I incorporated CBD products into my regimen through a tincture I created, along with a carefully considered selection of supplements and dietary adjustments. Importantly, I did not abuse Ivermectin by taking excessively high doses; rather, I adhered to a moderate dosage based on my weight. Specifically, I took a dose of 0.4 mg per kg and, at times, increased it to 0.6 mg per kg of body weight. These doses are relatively small, and I maintained them over a number of months months—three months while actively fighting cancer and three additional months post-treatment to target any residual cancer cells that might remain. I believe, for myself that this low dose was safe as an Ivermetin Dose for Humans. When we examine the side effects and the narratives surrounding them, we can see how easily misinformation can proliferate. The posts regarding Danny Lemoi have taken on a life of their own, influencing many to adopt long-term usage of high-dose Ivermectin without a full understanding of the potential ramifications. Yet, the individuals promoting these ideas are often unaware of the significant risks involved and instead perpetuate the notion that everything is perfectly fine. Unfortunately, the prevailing narrative shared across numerous Facebook groups and Telegram channels is fundamentally flawed. Instead of using Ivermectin as a targeted treatment for cancer and subsequently reducing the dosage significantly once the cancer is gone, many advocates have repeatedly highlighted the "Safety Record" of Ivermectin. By doing so, they inadvertently create the impression that continuous use is totally safe. Ivermectin Paste Ivermectin Oral Liquid Facebook and Ivermectin Dosage While it might seem reasonable to some people to blindly follow the person who, by becoming a top contributor in a Facebook group, elicits an aura of total belief, I encourage people to start to think beyond Facebook posts and do some research for themselves. I have read Facebook posts telling a person that Ivermectin was absolutely a safe drug for them to take, yet the biggest mistake was not asking them 1. Why they wished to take it and 2. What was the current state of their health? It is beyond me how anyone can offer such advice without asking a few simple questions, or better yet, don't suggest nothing. Yes, there are times I have suggested a dose to people based on research I have done, and they have benefited from it with an improvement in their health concern. But I always suggest a lower-than-normal dose, which becomes an even lower dose once the issue has been dealt with. I am not a Doctor or researcher doing scientific studies, I am someone who has a healthy respect for what Ivermectin can do, but lets face the facts. It is still a drug, and it does demand caution. Unfortunately, many people in Danny's Facebook group, Dirt Road Discussions, fail to do so and advocate the use of products like Ivermectin at unsafe levels and for longer than necessary. I can't speak for everyone, and I will not try to influence anyone. I did the research extensively for over 8 months before I wrote my book. The one thing I did NOT do was try to influence anyone to take high doses for an extended period. As I have stated to others is the fact that Ivermectin was only 1 part of over 7 other products I took to beat my cancer, and there are over 22 products in the book. Of those 22 + products, only Ivermectin and Fenbendazole are drugs. The rest are Natural Products that can be safely taken and have been researched as to their effects on cancer. I do not claim any of them other than what research has shown, and I certainly do not claim as to any dose other than what has already been researched. I really do caution people from making outlandish claims about Ivermectin, Febebendazole, or any other repurposed drug. What I see on the Dirt Road Discussion group is, at times, dangerous instructions given by people who are advocating the improper use of a product that they know very little about. Some of the posts are so far from being safe that I do call them out on it with facts taken from researching their claims. I hope that people come to realize that just because someone says something, it does not make it "Fact". I encourage everyone to do more research and form their own opinions instead of listening to or reading the whako posts they see on some Facebook group. I have two groups, and I try to keep my posts relevant and based on facts. If I do post something wrong, I hope others can correct it....but do so based on FACTS! What I use for my Cancer is for "Me," and I encourage everyone to think for themselves, research, and decide what is right for you, without the advice of anyone who just says "It is a totally safe drug to take at high dose rates". I take very low dose rates, and I no longer take it daily...in fact, I only take it 3x a week at most and as stated...a low dose. To get my dose calculator, go to my website Brighter-works.ca and download it for free. Start at 0.2 or 0.4 as I did, and taking any more is a personal decision. I personally have never gone above 0.6 mg per kg, and now I am taking 0.2 mg per kg 3x a week and will just start to take it 2x a week with my other products in a maintenance/prevention dose to negate any chance of cancer recurrence. My feeling is that people need to start researching products instead of blindly following someone's post in a Facebook group. Below is a list of ingredients in the Ivermectin paste: 6.1 List of excipients Hydrogenated Castor Oil Hydroxypropylcellulose Titanium Dioxide (E171) Propylene Glycol Since the product you are using includes the mentioned additives, choosing a liquid form of Ivermectin could be more beneficial, as it only contains purified water as an additive. Purified water is chosen because Ivermectin is hydrophilic, making safe dilution possible. I have used this type of product, and in many countries it is available as an injectable liquid with the same basic properties and form as the Liquid Ivermectin I use at a very low dose several times a week. In Canada, we have a product that can be taken orally, composed of purified water and Ivermectin at the same dose rate as the injectable form, where 1ml of liquid equals 10mg of Ivermectin.

Epoch Health Article If you decide to cut sugar out of your diet, with a few reasonable exceptions, you will experience some unexpected changes. “Your body doesn’t need added sugar,” Dr. Jason Fung, a nephrologist specializing in reversing Type 2 diabetes, told The Epoch Times. Despite that reality, if you’re eating the standard American diet, you’ll likely get a bit of added sugar. If you decide to cut this out of your diet, with a few reasonable exceptions, you will experience some unexpected changes, research finds. Sugar and your Immune System 1. Increased and Sustained Energy “I often call sugars ‘The Great Deceiver,’” said Dr. Becky Gillaspy, a chiropractor and author of the book “Intermittent Fasting Diet Guide and Cookbook,” during an interview with The Epoch Times. She explained that added sugar quickly breaks down into simple sugars, providing a quick burst of energy, “but then it turns around and robs that (energy) from us.” In the first few days of ceasing added sugar intake, we may experience some discomfort. According to Dr. Gillaspy, this is because the body has become accustomed to relying on the quick energy sugar provides and, as a result, exhibits cravings for it, and we see pretty quickly the health effects of sugar. However, the body gradually receives more stable and sustained energy when we shift to obtaining carbohydrates and other nutrients from natural foods and whole grains. Many people find themselves more energetic after quitting sugar for a while. The body quickly adapts and can run on whatever fuel is most available. “Our metabolism switches from being a better sugar burner to being a better fat burner,” said Dr. Gillaspy. This leads to a more sustained energy level, increased metabolic flexibility, and reduced food cravings. “Your body will reset, becoming a body that doesn’t need sugar,” Dr. Fung said. 2. Improved Insulin Sensitivity Stable blood sugar is a natural benefit of quitting sugar, and what’s even better is that quitting also improves insulin resistance. High sugar intake raises blood sugar levels, prompting the pancreas to release more insulin to shuttle sugar into cells, including fat cells. If this is happening often, our cells begin to resist insulin’s demands to take in this sugar, leaving it in the bloodstream where it poses significant health risks  According to a review study (pdf) published in Advances in Clinical and Experimental Medicine in 2019, the prevalence of insulin resistance ranges from 10 percent to 30 percent among different populations. A previous study conducted by the University of Southern California showed that reducing added sugar intake by 40 grams and decreasing calorie intake from added sugar by 5 percent can lead to a 20 percent decrease in insulin secretion. Another study based on the National Health and Nutrition Examination Survey (NHANES) database in the United States revealed that each 8-ounce or 1-cup sugar-sweetened beverage increases insulin resistance by 6 percent. Fasting insulin is one of the markers used to measure insulin resistance. A study involving 2,500 adults showed that those who did not consume sugar-sweetened beverages had lower fasting insulin levels than those who did. 3. Reduced Inflammation and Pain “The best part [of quitting sugar] is no pain,” a photographer named Pat gratefully told Dr. Gillaspy. She used to suffer from severe joint and muscle pain—almost to the point of giving up her photography job, which required standing all day. Now, “the 52-year-old Pat runs literal circles around the 35-year-old former Pat,” Dr. Gillaspy described. Excessive sugar consumption triggers the release of pro-inflammatory substances in the body. A study involving nearly 10,000 adults in England showed that individuals who consumed more added sugar from beverages and tea, coffee, and cereal had higher levels of inflammatory markers in their blood. Research in the field of immunology has indicated an urgent need to understand the impact of excessive sugar intake on the development of human inflammatory diseases. High levels of sugar in the diet can lead to rheumatoid arthritis, multiple sclerosis, psoriasis, inflammatory bowel disease, and low-grade chronic inflammation. 4. Easier Weight Management Losing weight becomes easier after quitting sugar. Jessica Russo, a clinical psychologist in private practice in Philadelphia, mentioned during an interview with The Epoch Times that one of her patients, who had struggled with binge eating and excess weight, lost 10 pounds within a month after cutting out added sugar and other refined carbohydrates. Another individual who successfully lost 54 pounds told Dr. Gillaspy that most of their weight was shed after seriously committing to quitting sugar.  Sugar stimulates insulin secretion, and elevated insulin levels promote fat storage; this is why insulin resistance makes weight loss more challenging. A low-sugar diet leads to lower insulin levels, which, in turn, encourages cells to release fat. A meta-analysis assessing over 60 studies published in the British Medical Journal indicated that reducing dietary sugar intake led to an average weight loss of 0.80 kilogram (approximately 1.76 pounds). Another prospective cohort study involving over 120,000 individuals found that consuming sugar-sweetened beverages resulted in a continuous weight gain of up to 1 pound over four years, while drinking one less sugar-sweetened beverage a day reduced annual weight gain by approximately 25 percent. 5. Enhanced Mental Well-Being Ms. Russo explained that sugar depletes vitamin B, and vitamin B is crucial for the human brain. A deficiency in vitamin B can lead to reduced cognitive clarity and a decline in thinking abilities, which is also one of the reasons sugar consumption can cause irritability. According to Ms. Russo, depression and anxiety are linked to inflammation. Eliminating sugar and reducing inflammation tends to make individuals feel more relaxed and hopeful. We often notice this difference when we pay a bit more attention. Therefore, when feeling down, we can reflect on whether it is due to excessive sugar consumption. A study published in the Frontiers in Public Health in 2023 involving about 16,000 obese American adults revealed that individuals with higher total sugar intake in their diets had a higher prevalence of depressive symptoms. Those with the highest total sugar intake had a 50 percent higher risk of developing depression than those with the lowest, a conclusion corroborated by other meta-analyses and cohort studies. 6. Heightened Taste Sensitivity When people get used to eating fewer sweet foods, they often realize that they do not actually need as much sweetness. “One of the most common things that shocks people when they give up sugar is that they lose their taste for sugar,” said Dr. Gillaspy. Ms. Russo also noted that many individuals find very sweet foods unpleasant in taste after cutting back on their sugar intake. This is because when following a high-sugar diet, the brain’s chemical responses and taste buds can become dulled to sweetness; however, cutting out sugar can restore sensitivity to these organs, allowing us to find satisfaction with smaller amounts of sugar.  “It (giving up sugar) opens up this whole new flavor world for foods that you would have not enjoyed before,” Dr. Gillaspy said, using her own story as an example. When she was younger, she had a strong sugar addiction and was overweight, and foods like Brussels sprouts and sauerkraut would never have been found on her plate. However, after quitting added sugar, she acquired a taste for these ingredients and found them incredibly delicious. 7. Improved or Reversed Fatty Liver Excessive sugar consumption leads to fatty liver, “essentially due to the way fructose is metabolized,” explained Dr. Fung. He said that when referring to sugar, we are usually talking about sucrose, which comprises one glucose molecule and one fructose molecule. While every cell in the body can utilize glucose as an energy source, fructose cannot be used by any cells. Instead, it goes directly to the liver, where some of it is converted into fat. “So fructose, refined sugars, are much worse for you than regular sugar,” emphasized Dr. Fung. They are far worse than empty calories or even regular starch. That is why quitting sugar is crucial in preventing fatty liver disease progression. A study published in Gastroenterology involving children and adolescents showed that when total calorie intake remained the same, reducing added fructose intake over nine consecutive days (controlled at 4 percent of total calories) could decrease the median liver fat percentage from 7.2 percent to 3.8 percent. Furthermore, the conversion of fructose to fat in the liver significantly decreased. In another eight-week trial, restricting dietary sugar intake led to a reduction in the conversion of fructose to liver fat from about 35 percent to about 24 percent. A study published in the British Medical Journal Open in 2017 suggests that reducing added sugar intake by 20 percent could reduce the prevalence of hepatic steatosis, fatty liver disease, cirrhosis, and liver cancer. A 50 percent reduction in intake would have an even more significant proportional effect. 8. Improved Gut Health and Immunity Many may not realize that digestive discomfort or frequent colds could be attributed to excessive sugar consumption. Research suggests that dietary sugar affects immune cells in the gut, leading to the replacement of beneficial bacteria by harmful ones. Furthermore, the body alters the gut microbiota to detoxify the toxins resulting from excessive sugar intake, disrupting the natural balance. This disruption reduces intestinal epithelial integrity and mucosal immunity. Additionally, excessive sugar consumption and high blood sugar levels can increase gut permeability, compromising the gut’s protective barrier and enhancing infection susceptibility. Ms. Russo also pointed out that sugar intake can reduce the body’s zinc levels, which is crucial for the immune system. 9. Improved Skin Health Quitting sugar might be the most straightforward and cost-effective approach to appearing younger and eliminating facial and skin blemishes. Sugar undergoes oxidative reactions with proteins in our bodies, producing advanced glycation end products (AGEs). AGEs are a complex group of substances, and apart from some individual components, they are generally toxic to the body and can accumulate in tissues. Over time, skin problems may arise, such as browning, yellowing, poor elasticity, and deeper wrinkles. AGEs can also cause internal changes in the skin. They hinder wound healing, disrupt skin cell function, induce apoptosis, and trigger inflammation. Quitting sugar not only promotes healthier and more youthful skin but also reduces toxins in the body, thus preventing age-related diseases. AGEs can contribute to age-related diseases, including neurodegenerative disorders, atherosclerosis, and chronic inflammatory conditions. The accumulation of AGEs is accelerated in conditions like insulin resistance and diabetes, leading to a range of comorbidities.

Explore natural cancer cures at Brighter-works Cancer Alternatives Inc. Empower your healing journey with natural cancer cures in Burnaby, BC. Featured Article Highlights Cancer 101 Treatments Alternative Therapies Coping Strategies Research & Development Nutrition Coping Strategies Lifestyle Faith & Spirituality For Loved Ones Cancer 101 Treatments Alternative Therapies Coping Strategies Research & Development Nutrition Coping Strategies Lifestyle Faith & Spirituality For Loved Ones Cancer 101 Treatments Alternative Therapies Coping Strategies Research & Development Nutrition Coping Strategies Lifestyle Faith & Spirituality For Loved Ones Newsletter Sign-Up Join Our Community of Healing and Hope Get the latest on alternative cancer treatments, personal stories, and holistic wellness—delivered straight to your inbox. Email* Yes, subscribe me to your newsletter. Subscribe Search Welcome to Brighter-Works Welcome to Brighter-Works Cancer Alternatives. I’m here to provide you with valuable insights and support as you explore Natural Product Alternatives to the conventional cancer treatments, with their horrible side effects. Whether you’re navigating your own cancer journey, supporting a loved one, or seeking Natural Product Alternatives to Radiation and Chemotherapy, I’m committed to offering the resources and community you need to take charge of your health. Through my blog, I share many different medical conditions and the approach modern medicine takes, but the Natural Alternative products are in my book. This 588 page E-Book, written by a Cancer Survivor, is the most concise and comprehensive look at cancer offered on how to take charge of your own healing with products such as Ivermectin, Fenbendazole, Mebendazole, CBD/CBC/CBGa/THC, Graviola, Brazil's "Mushroom of the Gods", Fucoidan and many more. Vitamins, Herbs and Supplements, as well as smoothy recipes that help to maintain healthy weight and build your immune system. Don't wait....Buy your copy today and embark on a healing journey where you are in control to rid your body of Cancer The Natural Way and become a Cancer Survivor! P.S: Don't forget to download your FREE copy of my Dose Calculator for Ivermectin, I made in an Excel file. Simply input your weight and it will tell you how much Ivermectin you should take, Pill or liquid form, based on how aggressively you may wish to fight your cancer!!! So don't forget to download the free calculator today! Popular Tags cancer (19) 19 posts covid-19 (10) 10 posts HealthyEating (7) 7 posts Faith and Spirituality (6) 6 posts NaturalSweeteners (5) 5 posts SugarAlternatives (5) 5 posts Peripheral Neuropathy (3) 3 posts Plagues in History (3) 3 posts cervical-cancer (2) 2 posts MuscleHealth (2) 2 posts Nutrition (2) 2 posts acid-reflux-and-gerd (1) 1 post Adenocarcinoma (1) 1 post alternative treatments (1) 1 post AlternativeHealing (1) 1 post AlternativeMedicine (1) 1 post AlternativeTherapies (1) 1 post Astragalus (1) 1 post AutoimmuneDisease (1) 1 post AutoimmuneDisorders (1) 1 post BreastCancerAwareness (1) 1 post BreastCancerJourney (1) 1 post BreastCancerSupport (1) 1 post Cancer and Exercise (1) 1 post CancerCareTips (1) 1 post CancerDiagnosis (1) 1 post CancerTherapies (1) 1 post celiac-disease (1) 1 post CognitiveEnhancement (1) 1 post EmpowerCancerJourney (1) 1 post Glaucoma (1) 1 post HER2 Breast Cancer (1) 1 post Ivermectin dosage for humans (1) 1 post Ivermectin dose (1) 1 post Living with Cancer (1) 1 post MethyleneBlueBenefits (1) 1 post Muscles and Cancer (1) 1 post NaturalTherapies (1) 1 post NeuroprotectiveTherapies (1) 1 post StrengthTraining (1) 1 post WomenWarriors (1) 1 post Follow Us Latest News Explore Hope with Brighter-works Cancer Alternatives Whether you’re navigating your own diagnosis or supporting someone you care about, you’ll find hope, and alternative approaches that empower your healing journey. The articles talk about disease and the modern medical approach but do not give the natural protocol or the list of Natural prducts found in the book and available under shop (I make no money from those products under the Shop menu...they are for your benefit, not mine!) Purchase the Book The Latest Articles Find hope, healing, and community at Brighter Works Cancer Alternatives. Stay Informed. Stay Ahead. Your Daily Dose of Reliable News and Insightful Analysis. Promoted Articles

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