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Vitamins But don’t mix these Vitamins together Magnesium and calcium When these minerals are taken at the same time, they may not be quite as effective, says Tod Cooperman, MD, president of consumer labs, an independent testing company focused on health and nutrition products in White Plains, New York. “Taking large amounts of minerals with other minerals will reduce absorption,” he says. In essence, the minerals compete with one another, and both lose out. Maximize your benefits by taking any mineral supplements at least two hours apart.  Zinc and copper Among zinc’s many benefits, enhanced immunity ranks high. You might turn to the mineral for help in staving off or shortening the duration of common colds, but you should know that zinc interferes with copper absorption. Some people need to take copper due to conditions that cause copper deficiency. If you must take copper and also take zinc, space the two out by at least two hours, Dr. Cooperman says. High doses of zinc taken over the long term (50 mg or more per day for 10 weeks or longer) can also cause copper deficiency. “This is something you can talk to your doctor about,” he says.  Iron and green tea You need iron to help distribute oxygen to cells—it’s vital for your energy. But if you mix it with green tea, black tea, or curcumin supplements, your body won’t absorb the mineral. It’s OK to drink green tea beverages—such as matcha—just don’t do it with your iron supplements, Dr. Cooperman says; spread the two apart by a couple of hours. Fish oil and gingko biloba Omega-3 fish oil supplements may tame inflammation and improve your mood, but when you take these supplements with herbs that thin the blood—such as ginkgo biloba or garlic—they may prevent clotting and can lead to uncontrolled bleeding, Dr. Cooperman says. To be safe, split them up by at least two hours.  Melatonin and other sedating herbs You can easily overdo herbs or supplements with sedative properties. These include melatonin, valerian, ashwagandha, kava, and St. Johns’s Wort: “When taken together, they can cause too much sleepiness,” Dr. Cooperman says. Always read the labels to find out what you can expect from supplements. Red yeast rice and niacin If you are one of the 95 million Americans with high cholesterol, you might like the idea of taking a natural supplement to lower your levels. Two possible pills that lower cholesterol levels—red yeast rice and niacin—don’t play well together. “Doubling up doesn’t increase the benefits and may be harmful to the liver,” says Todd Sontag DO, a family medicine specialist with Orlando Health Physician Associates in Florida. When prescription cholesterol-lowering drugs are added to the mix, your risks can increase. Be sure you’re aware of niacin flush and what you can do about this potential side effect. Vitamins A, D, E, and K If you take vitamin K with other fat-soluble vitamins such as A, D, or E, you may not be absorbing as much as you would by taking them at different times, Dr. Cooperman says. “If you take a multivitamin don’t worry, but if you are K deficient and need extra K, take it two hours apart from the other fat-soluble vitamins,” he says. Believe it or not, vitamin K is one of the nutrients even nutritionists don’t get enough of. Potassium and calcium Again, these necessary minerals will compete for absorption by the body, meaning you get less of each when you take them together, warns Dr. Cooperman. People who labor or exercise in humid climates or have digestive issues can fall short on potassium; if you need to take both supplements, be sure to space them out by a few hours, he advises. Don’t miss these signs your body is running low on key vitamins. St. John’s wort and antidepressants You need to be wary of over the counter or prescription drugs that can interact poorly with supplements, says Robert Glatter, MD, an assistant professor of emergency medicine at Northwell Health in New York City. For example, St. John’s wort may cause fever, confusion, and anxiety if it’s taken with other antidepressants. Antidepressants and St John’s wort both increase levels of the feel-good brain chemical serotonin. “This can cause serotonin syndrome and in severe cases, it may lead to muscle rigidity and seizures,” he says. CoQ10 and your diabetes meds CoQ10 is a powerful compound that helps your heart. Dr. Glatter warns that “CoQ10 can also lower blood sugar, and if you are taking other diabetes drugs, you run the risk of developing low blood sugar,” he says. CoQ10 can also lower blood pressure. “In combination with blood pressure medications, this can cause dangerously low blood pressure,” he says. “This can happen out of the blue, often after you have been taking CoQ10 for six to eight weeks, and it could precipitate a fall or head injury.” Watch out for these other symptoms of low blood pressure. Garlic and OTC or Rx blood thinners Garlic thins out the blood, and if you take a daily baby aspirin or a blood thinner such as Coumadin (warfarin), it could be risky, Dr. Glatter says. “It can cause bleeding episodes after a fall or injury, and there’s a high risk of internal bleeding,” he says. His advice: Be careful and make sure your doctor knows exactly what you are taking and why. “Just because something is natural doesn’t mean it is risk-free.” Garlic isn’t the only supplement that can up your bleeding risk. Ginkgo biloba, fish oil, ginger, feverfew, vitamin E, and white willow bark are also on the list. Make sure you know the super-important questions to ask before you take prescription medications. Vitamin K and blood thinners Some vitamins and supplements can interfere with blood-thinning blood pressure drugs, Dr. Glatter says. Vitamin K—even in foods such as kale, lettuce, broccoli, and chickpeas—can counteract a blood thinner’s benefits. This is one of the more common food-drug reactions. Echinacea, a popular cold remedy, may decrease the effectiveness of blood thinners, and increase stroke risk, Dr. Glatter says. “This is a big one to be aware of.” These are some other foods you shouldn’t eat with certain medications. Antibiotics and iron Taking antibiotics—especially those in the tetracycline family—along with iron supplements can dampen the effects of the antibiotics, making them less likely to work, Dr. Glatter says. Spacing out the two will help.

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.

How much is enough?? Personally I believe it is a very important aspect of fighting cancer. Muscle mass is required for the body to move effectively and when the body is not getting enough energy from food it resorts to taking it from fat stores and then from muscles. Many people know that standard oncology treatments of Chemotherapy have side effects that compromise health due to loss of appetite, nausea and fatigue. This is when the body starts to feed on itself. I advocate, and always will, as a Cancer survivor for Natural Cures that don't have the side effects and allow a person to exercise effectively to maintain important muscle mass. For those people who take the standard treatments they must understand how the body works during their fight against cancer and realise that standard treatments not only rob your body of "quality of life" but also rob your body of important muscle mass. Exercise is important to maintain health free of Cancer! What is Physical Exercise and Cancer Physical activity is defined as any movement that uses skeletal muscles and requires more energy than resting. Physical activity can include walking, running, dancing, biking, swimming, performing household chores, exercising, and engaging in sports activities. A measure called the metabolic equivalent of task, or MET, is used to characterize the intensity of physical activity. One MET is the rate of energy expended by a person sitting at rest. Light-intensity activities expend less than 3 METs, moderate-intensity activities expend 3 to 6 METs, and vigorous activities expend 6 or more METs. Sedentary behavior is any waking behavior characterized by an energy expenditure of 1.5 or fewer METs while sitting, reclining, or lying down ( 1 ). Examples of sedentary behaviors include most office work, driving a vehicle, and sitting while watching television. A person can be physically active and yet spend a substantial amount of time being sedentary. What is known about the relationship between exercise and cancer risk? Evidence linking higher physical activity to lower cancer risk comes mainly from observational studies , in which individuals report on their physical activity and are followed for years for diagnoses of cancer. Although observational studies cannot prove a causal relationship, when studies in different populations have similar results and when a possible mechanism for a causal relationship exists, this provides evidence of a causal connection. There is strong evidence that higher levels of physical activity are linked to lower risk of several types of cancer. Bladder cancer: In a 2014 meta-analysis of 11 cohort studies and 4 case-control studies, the risk of bladder cancer was 15% lower for individuals with the highest level of recreational or occupational physical activity than in those with the lowest level ( 5 ). A pooled analysis of over 1 million individuals found that leisure-time physical activity was linked to a 13% reduced risk of bladder cancer. Breast cancer: Many studies have shown that physically active women have a lower risk of breast cancer than inactive women. In a 2016 meta-analysis that included 38 cohort studies, the most physically active women had a 12–21% lower risk of breast cancer than those who were least physically active. Physical activity has been associated with similar reductions in risk of breast cancer among both premenopausal and postmenopausal women. Women who increase their physical activity after menopause may also have a lower risk of breast cancer than women who do not. Colon cancer: In a 2016 meta-analysis of 126 studies, individuals who engaged in the highest level of physical activity had a 19% lower risk of colon cancer than those who were the least physically active. Endometrial cancer: Several meta-analyses and cohort studies have examined the relationship between physical activity and the risk of endometrial cancer (cancer of the lining of the uterus. In a meta-analysis of 33 studies, highly physically active women had a 20% lower risk of endometrial cancer than women with low levels of physical activity. There is some evidence that the association is indirect, in that physical activity would have to reduce obesity for the benefits to be observed. Obesity is a strong risk factor for endometrial cancer. Esophageal cancer: A 2014 meta-analysis of nine cohort and 15 case–control studies found that the individuals who were most physically active had a 21% lower risk of esophageal adenocarcinoma than those who were least physically active. Kidney (renal cell) cancer: In a 2013 meta-analysis of 11 cohort studies and 8 case–control studies, individuals who were the most physically active had a 12% lower risk of renal cancer than those who were the least active. A pooled analysis of over 1 million individuals found that leisure-time physical activity was linked to a 23% reduced risk of kidney cancer. Stomach (gastric) cancer: A 2016 meta-analysis of 10 cohort studies and 12 case–control studies reported that individuals who were the most physically active had a 19% lower risk of stomach cancer than those who were least active. There is some evidence that physical activity is associated with a reduced risk of lung cancer. However, it is possible that differences in smoking, rather than in physical activity, are what explain the association of physical activity with reduced risk of lung cancer. In a 2016 meta-analysis of 25 observational studies, physical activity was associated with reduced risk of lung cancer among former and current smokers but was not associated with risk of lung cancer among never smokers. For several other cancers, there is more limited evidence of an association. These include certain cancers of the blood, as well as cancers of the pancreas, prostate, ovaries, thyroid, liver, and rectum. How might physical activity be linked to reduced risks of cancer? Exercise has many biological effects on the body, some of which have been proposed to explain associations with specific cancers. These include: Lowering the levels of sex hormones, such as estrogen, and growth factors that have been associated with cancer development and progression [breast, colon] Preventing high blood levels of insulin, which has been linked to cancer development and progression [breast, colon] Reducing inflammation Improving immune system function Altering the metabolism of bile acids, decreasing exposure of the gastrointestinal tract to these suspected carcinogens [colon] Reducing the time it takes for food to travel through the digestive system, which decreases gastrointestinal tract exposure to possible carcinogens [colon] Helping to prevent obesity, which is a risk factor for many cancers What is known about the relationship between being sedentary and the risk of cancer? Although there are fewer studies of sedentary behavior and cancer risk than of physical activity and cancer risk, sedentary behavior—sitting, reclining, or lying down for extended periods of time (other than sleeping)—is a risk factor for developing many chronic conditions and premature death. It may also be associated with increased risk for certain cancers. How much physical activity is recommended? The U.S. Department of Health and Human Services Physical Activity Guidelines for Americans, 2nd edition, released in 2018, recommends that, for substantial health benefits and to reduce the risk of chronic diseases, including cancer, adults engage in 150 to 300 minutes of moderate-intensity aerobic activity, 75 to 100 minutes of vigorous aerobic activity, or an equivalent combination of each intensity each week. This physical activity can be done in episodes of any length. muscle-strengthening activities at least 2 days a week balance training, in addition to aerobic and muscle-strengthening activity Is physical activity beneficial for cancer survivors? Yes. A report of the 2018 American College of Sports Medicine International Multidisciplinary Roundtable on Physical Activity and Cancer Prevention and Control concluded that exercise training and testing are generally safe for cancer survivors and that every survivor should maintain some level of physical activity. The Roundtable also found strong evidence that moderate-intensity aerobic training and/or resistance exercise during and after cancer treatment can reduce anxiety, depressive symptoms, and fatigue and improve health-related quality of life and physical function strong evidence that exercise training is safe in persons who have or might develop breast-cancer-related lymphedema some evidence that exercise is beneficial for bone health and sleep quality insufficient evidence that physical activity can help prevent cardiotoxicity or chemotherapy-induced peripheral neuropathy or improve cognitive function, falls, nausea, pain, sexual function, or treatment tolerance In addition, research findings have raised the possibility that physical activity may have beneficial effects on survival for patients with breast, colorectal, and prostate cancers. Breast cancer: In a 2019 systematic review and meta-analysis of observational studies, breast cancer survivors who were the most physically active had a 42% lower risk of death from any cause and a 40% lower risk of death from breast cancer than those who were the least physically active. Colorectal cancer: Evidence from multiple epidemiologic studies suggests that physical activity after a colorectal cancer diagnosis is associated with a 30% lower risk of death from colorectal cancer and a 38% lower risk of death from any cause. Prostate cancer: Limited evidence from a few epidemiologic studies suggests that physical activity after a prostate cancer diagnosis is associated with a 33% lower risk of death from prostate cancer and a 45% lower risk of death from any cause. There is very limited evidence for beneficial effects of physical activity on survival for other cancers, including non-Hodgkin lymphoma, stomach cancer, and malignant glioma. What additional research is under way on the relationship between physical activity and cancer? Findings from observational studies provide much evidence for a link between higher levels of physical activity and lower risk of cancer. However, these studies cannot fully rule out the possibility that active people have lower cancer risk because they engage in other healthy lifestyle behaviors. For this reason, clinical trials that randomly assign participants to exercise interventions provide the strongest evidence because they eliminate bias caused by pre-existing illness and attendant physical inactivity. To confirm the observational evidence and define the potential magnitude of the effect, several large clinical trials are examining physical activity and/or exercise interventions in cancer patients and survivors. These include the Breast Cancer Weight Loss (BWEL) trial in newly diagnosed breast cancer patients, the CHALLENGE trial in colon cancer patients who have recently completed chemotherapy, and the INTERVAL-GAP4 trial in men with metastatic, castrate-resistant prostate cancer. Many additional questions have yet to be answered in several broad areas of research on physical activity and cancer: What are the mechanisms by which physical activity reduces cancer risk? What is the optimal time in life, intensity, duration, and/or frequency of physical activity needed to reduce the risk of cancer, both overall and for specific sites? Is sedentary behavior associated with increased risk of cancer? Does the association between physical activity and cancer differ by age or race/ethnicity? Does physical activity reduce the risk of cancer in people who have inherited a genetic variant that increases cancer risk?

Methylene Blue Methylene Blue : This synthetic compound has been making waves in the health and wellness world for its potential benefits to humans. Clinical studies suggest that it may improve cognitive performance , including memory tasks, and even alleviate symptoms of certain conditions caused by cerebral hypoperfusion by increasing cerebral blood flow. Methylene blue treatment is known for enhancing blood circulation, improving oxygen levels, boosting cognition, and reducing inflammation. Methylene blue (MB) is used as a textile dye but has since found its way into medicine. In recent years, studies have shown that MB can increase cell oxygen utilization, which could lead to improved energy levels and cognitive function. Additionally, MB enhances cerebral blood flow, aiding in memory tasks and retrieval. It has also shown promise in protecting against brain damage. A research article in the Journal of Alzheimer’s Disease showed that participants with mild cognitive impairment who took a 30 mg dose of MB daily for six months showed significant improvements in memory recall and attention compared to those who took a placebo, according to clinical studies. Another paper in the Journal of Psychopharmacology found that MB improved reaction time and accuracy on cognitive tasks in healthy adults, possibly due to its effect on cerebral blood flow. MB may also benefit individuals with brain damage, but further research is needed. But it’s not just cognitive performance that MB may benefit from. Clinical studies suggest it could also help mental health conditions such as depression and cerebral hypoperfusion. Additionally, research shows that MB may increase serotonin levels, which could positively affect mood and overall well-being. Furthermore, MB has potential benefits in conditions such as Parkinson’s disease, sepsis, and other illnesses. However, the optimal dose and form of MB for different disease conditions are under study. It’s important to note that while MB shows promise as a potential treatment option , individuals should always consult their healthcare provider before trying new supplements or treatments. Some forms of MB are light-sensitive and can cause skin discoloration if not used properly. Health Benefits of Methylene Blue Boosts Hemoglobin Levels in the Blood Methylene blue (MB) is a medication used for various health conditions, including treating methemoglobinemia, where the blood cannot carry oxygen effectively. Recent studies suggest that MB can also help increase hemoglobin levels in the blood. Low hemoglobin levels can lead to anemia, causing fatigue, weakness, and shortness of breath. Anemia is linked to other health complications. In a paper in “The Journal of Clinical Investigation,” researchers found that administering methylene blue (MB) increased hemoglobin levels and improved oxygen delivery in mice with anemic conditions. Another study on human subjects showed similar results, suggesting that mb may benefit individuals with low hemoglobin levels. Potential to Lower Blood Pressure High blood pressure is a common disease that affects millions worldwide, leading to heart attack and stroke. Recent studies suggest that methylene blue (MB) may lower blood pressure. A paper in the journal “Hypertension” found that methylene blue (MB) reduced high blood pressure in rats by increasing nitric oxide production. Nitric oxide improves blood flow by relaxing blood vessels and lowering overall blood pressure. Another study conducted on human subjects showed similar results. Participants who took methylene blue (MB) had significantly better systolic and diastolic blood pressure than those who took a placebo. More studies are ongoing to understand how methylene blue affects blood pressure regulation in humans, becoming a promising treatment option for Hypertension. MB could potentially offer hope for those struggling with high blood pressure. Neuroprotective Effects on the Brain Methylene blue (MB) has a neuroprotective effect on the brain and is used to treat neurodegenerative diseases such as Alzheimer’s and Parkinson’s. It has shown potential in inhibiting tau formation, a key factor in the pathology of Alzheimer’s disease, suggesting it may help manage cognitive decline associated with the disease. One research article published in the prestigious journal Nature discovered that methylene blue (MB) could stop toxic proteins from accumulating in the brains of mice suffering from Alzheimer’s disease. Another study involving human participants found that methylene blue (MB) could enhance brain function in people with mild cognitive impairment. Methylene blue (MB) may also have potential as a treatment for traumatic brain injury (TBI). A paper in the Journal of Neurotrauma found that administering MB after a TBI reduced brain swelling and improved neurological outcomes in rats. Research is ongoing to understand how methylene blue affects brain health entirely; these findings suggest that it may benefit individuals at risk for or suffering from neurodegenerative diseases or traumatic brain injuries. MB may be a promising treatment option for these conditions. Therapeutic Uses of Methylene Blue Treatment for Methemoglobinemia Methylene blue (MB) is a medication used to treat methemoglobinemia , in which the blood cannot carry oxygen properly. When someone has methemoglobinemia, MB can alleviate symptoms such as shortness of breath, fatigue, and cyanosis (a bluish tint to the skin). MB can effectively restore the oxygen-carrying capacity of hemoglobin molecules chemically altered due to exposure to certain medications or chemicals, or it can be inherited. Methylene blue (MB) converts abnormal hemoglobin molecules into normal ones that can carry oxygen effectively. It does this by acting as an acceptor electron and reducing the iron in the hemoglobin molecule from its ferric (Fe3+) state back to its ferrous (Fe2+) state. This allows oxygen to bind more effectively and improves tissue oxygenation. Photodynamic Therapy for Cancer and Skin Conditions In addition to treating methemoglobinemia, methylene blue (MB) is used in photodynamic therapy (PDT) for certain types of cancer and skin conditions. PDT involves administering a photosensitizing agent like MB and exposure to specific wavelength light energy. The photosensitizer absorbs light energy and undergoes a chemical reaction that generates reactive oxygen species, which can destroy nearby cells. Methylene blue (MB) is effective in PDT for various types of cancer, including bladder, breast, and head and neck cancers. It is used successfully in treating acne vulgaris and other dermatological conditions with the help of MB. Medication Reversal and Vasoplegic Syndrome (VS) Treatment in Nursing Methylene blue (MB) has other therapeutic uses as a medication reversal agent and treatment option for Vasoplegic syndrome (VS) in nursing settings. Patients may sometimes receive vasopressor medications like epinephrine or norepinephrine to increase blood pressure during surgery or other medical procedures. Sometimes, these medications can cause VS, where the blood vessels become dilated, and blood pressure drops dangerously low. Methylene blue (MB) reverses the effects of vasopressors and restores normal vascular tone. It works by inhibiting nitric oxide synthase, an enzyme that produces nitric oxide, which causes vasodilation. By inhibiting this enzyme, MB can constrict blood vessels and increase blood pressure. In nursing settings, methylene blue (MB) may also treat septic shock or other conditions where vasodilation causes dangerously low blood pressure. MB is typically administered intravenously and requires careful monitoring of vital signs. Methylene Blue Benefits: Anti-Aging Properties Antioxidant Properties of Methylene Blue Methylene blue is a compound that possesses antioxidant properties. Antioxidants help neutralize free radicals and prevent damage to cells that contribute to aging. By reducing oxidative stress in the body, methylene blue may help combat the effects of aging. Studies have shown that methylene blue (MB) can effectively reduce cellular damage caused by free radicals . In one mb study, researchers found that methylene blue protected cells from damage caused by hydrogen peroxide, a type of free radical. Another mb study found that methylene blue was able to reduce oxidative stress in the brains of mice. Cognitive Function and Memory Improvement As we age, our cognitive function and memory may decline. However, studies have suggested that MB, or methylene blue, can improve these functions. Methylene blue has shown potential for memory enhancement by increasing ATP production in the brain, which can improve memory and focus while preventing age-related cognitive decline. Older adults on MB improved their cognition compared to those not taking the supplement. Another study investigated the effects of methylene blue on memory in rats. The researchers found that rats given methylene blue could remember objects they had seen before better than rats who did not receive the supplement. Potential for Lifespan Extension Methylene blue (MB) also has the potential to extend the lifespan of certain organisms. In one study, researchers found that adding small amounts of MB to the diet of fruit flies increased their lifespan by up to 40 percent. While more research is ongoing on humans, these findings suggest that methylene blue (MB) may have anti-aging benefits beyond improving cognitive function and memory. Cognitive Benefits of Methylene Blue Improving Cognitive Function in Individuals with Cognitive Impairment Methylene blue (MB), a medication used to treat methemoglobinemia, has been found to have cognitive benefits. Studies have shown that MB can improve cognitive function in individuals with cognitive impairment. In one study, 14 patients with Alzheimer’s disease were given MB for four weeks. The results showed that MB improved their cognitive function and slowed down the progression of the disease. Additionally, MB has been shown to mitigate cognitive deficits and neuronal loss associated with chronic cerebral hypoperfusion, highlighting its potential neuroprotective and therapeutic effects in neurodegenerative diseases like Alzheimer’s. Increasing Cerebral Blood Flow Cerebral hypoperfusion is when decreased blood flow to the brain causes brain damage and other neurological problems. Methylene blue (MB) increases cerebral blood flow , which can help counteract cerebral hypoperfusion and prevent brain damage. Enhancing Memory Retrieval in Memory Tasks Low methylene blue (MB) doses enhance memory retrieval in memory tasks. Participants in the research were given either a low dose of mb or a placebo before taking part in a memory task. The results showed improved performance in those on MB compared to those who had taken the placebo. Improving Mental Health and Alleviating Symptoms of Depression Methylene blue (MB) has been found to increase serotonin levels, which may improve mental health and alleviate symptoms of depression. In the context of depression, methylene blue is considered a potent antidepressant due to its ability to increase key neurotransmitters like norepinephrine, serotonin, and dopamine. This regulation can also impact related conditions such as anxiety and bipolar disorder. Serotonin regulates mood, sleep, appetite, and other bodily functions. Low levels of serotonin are present in those with depression and anxiety disorders. High methylene blue (MB) doses can lead to serotonin syndrome, a potentially dangerous condition characterized by excessive serotonin activity. Therefore, taking methylene blue (MB) only under medical supervision is crucial. How Methylene Blue Combats Oxidative Stress and Neuroinflammation Methylene blue is a powerful agent in the fight against oxidative stress and neuroinflammation, both implicated in the progression of brain diseases. Here’s how it works: Targeting Mitochondria : The compound specifically targets mitochondria, the energy powerhouses of cells. By enhancing mitochondrial function, methylene blue helps reduce oxidative damage, a key factor in neuroinflammation. Reducing Oxidative Damage : Through its antioxidant properties, methylene blue minimizes the harmful effects of free radicals. These molecules are notorious for damaging cells and tissues, leading to inflammation and other harmful processes in the brain. Mitigating Inflammation : By lowering oxidative stress, methylene blue indirectly reduces inflammation in the brain. This dual action helps mitigate the behavioral symptoms often associated with aging and neurodegenerative diseases. In summary, methylene blue provides a comprehensive approach to protecting the brain by improving mitochondrial function, reducing oxidative damage, and lowering inflammation levels. Potential Medical Uses of Methylene Blue Methylene Blue: A Long-Standing Medical Dye Methylene blue (MB) has been used in medical procedures for over 100 years. It stains tissues during surgeries and diagnostic procedures, allowing doctors to better visualize and differentiate between different tissue types. However, recent research has shown that mb may have potential medical uses beyond its traditional role as a dye. Treating Methemoglobinemia with Methylene Blue One of the most promising methylene blue (MB) uses is treating methemoglobinemia. This condition occurs when too much methemoglobin is in the blood, which prevents oxygen from binding to hemoglobin and being transported throughout the body. This leads to shortness of breath, fatigue, and cyanosis (a bluish tint to the skin). In very severe cases, it can be life-threatening. Methylene blue (MB) works by converting methemoglobin back into normal hemoglobin, allowing oxygen to be transported throughout the body again. This makes it an effective treatment for methemoglobinemia, especially when other MB treatments have failed or are unavailable. However, it’s important to note that methylene blue should only be used under medical supervision. While it is generally safe when used correctly, it can cause adverse effects such as headaches, nausea, vomiting, and confusion. Vasoplegic Syndrome Treatment with Methylene Blue Another potential use for methylene blue is in the treatment of Vasoplegic syndrome. This condition occurs when blood vessels become dilated and cannot constrict properly, leading to low blood pressure and improved blood flow to vital organs such as the brain and kidneys. Methylene blue restores proper blood vessel function through its effects on nitric oxide signaling pathways, making it an effective treatment for Vasolegic syndrome. However, as with methemoglobinemia, methylene blue should only be used under medical supervision. It interacts with certain medications, causing adverse effects such as low blood pressure and shortness of breath. FDA Approval for Methylene Blue While methylene blue has shown promise in treating various medical conditions, it’s important to note that the FDA has restricted its use in diagnostic procedures. While doctors may use methylene blue off-label to treat certain conditions, there is limited research on its safety and effectiveness. When considering methylene blue, it’s crucial to understand how it may interact with other substances, including alcohol and tobacco. Before starting treatment, inform your healthcare provider about all medications you are currently taking. This includes prescription drugs, over-the-counter products, and any dietary supplements. Methylene blue can interact with certain substances, potentially altering its effectiveness or increasing the risk of side effects. For instance, consuming alcohol while using methylene blue can diminish its therapeutic effects and may also heighten side effects such as dizziness or nausea. Similarly, smoking tobacco can influence how the body processes methylene blue, potentially requiring dosage adjustments. Here’s a checklist to ensure safety: Prescription Medications: Verify any potential reactions, particularly if you are on MAO inhibitors or serotonergic drugs. Over-the-Counter Drugs: Include common pain relievers, cold medications, and antacids. Dietary Supplements: Herbal supplements and vitamins should not be overlooked. Alcohol and Tobacco: Disclose your consumption habits to account for possible interactions. Being transparent with your healthcare professional about your lifestyle and medication use is essential for minimizing risks and optimizing the effectiveness of methylene blue treatment. Mechanism of Action of Methylene Blue Methylene Blue Affects Mitochondrial Function Methylene blue is a medication used for many years in various medical fields. One of these effects is on mitochondrial energy metabolism. Mitochondria are cell organelles that produce energy; methylene blue enhances this process. Methylene blue can improve mitochondrial respiration and reduce oxidative stress, improving overall cellular health by stimulating the electron transport chain (ETC), a series of proteins located within the inner membrane of mitochondria. This stimulation increases the production of ATP, which is the primary energy source for cellular processes. The Drug Has an Effect on Monoamine Oxidase Another mechanism by which methylene blue provides therapeutic benefits is through its effect on monoamine oxidase (MAO). MAO is an enzyme that down neurotransmitters such as serotonin and dopamine, which play essential roles in mood regulation. Methylene blue is helpful as a potential treatment for neurodegenerative diseases such as Alzheimer’s due to its ability to protect against neuronal damage caused by oxidative stress. Methylene blue inhibits MAO activity, increasing these neurotransmitters’ levels in the brain. This increase can positively affect mood disorders such as depression and anxiety. Methylene Blue’s Mechanism of Action Involves Mitochondria As mentioned earlier, methylene blue’s mechanism of action involves mitochondria. Specifically, it works by donating electrons to complex IV within the ETC. This donation helps restore proper mitochondrial function and enhances ATP production. Methylene blue can act as an antioxidant within mitochondria by scavenging free radicals that cause oxidative damage. Methylene blue can improve overall cellular health and function by reducing oxidative stress within cells’ powerhouse organelles. The Drug’s Impact on Mitochondrial Function is Linked to Its Therapeutic Benefits The impact of methylene blue on mitochondrial function is crucial to its therapeutic benefits. As mentioned earlier, mitochondria are responsible for producing energy within cells. By enhancing this process, methylene blue can provide many benefits. For example, studies have shown that methylene blue can improve cognitive function in individuals with neurodegenerative diseases such as Alzheimer’s. The drug has been a potential treatment for sepsis due to its ability to enhance mitochondrial respiration and reduce oxidative stress. Role of Methylene Blue in Treating Neurological Disorders Methylene Blue Provides Neuroprotection Against Various Diseases Methylene blue is a synthetic compound used for various medical purposes. A promising application is its potential to treat neurological disorders. Research has shown that methylene blue can cross the blood-brain barrier, enhancing brain function, cognition, and emotional regulation. It provides neuroprotection against multiple diseases, including Alzheimer’s and Parkinson’s. Methylene Blue May Improve Cognitive Function in Animal Models Studies have found that methylene blue may improve cognitive function in animal models of Alzheimer’s and Parkinson’s diseases. This indicates that it could be a potential treatment option for these conditions. The way methylene blue improves cognitive function has yet to be fully understood. Further Research is ongoing to determine the Effectiveness of Humans. While research has shown promising results for using methylene blue as a treatment option for neurological disorders, further research is needed to determine its effectiveness in humans. Clinical trials are underway to investigate methylene blue’s use for treating Alzheimer’s disease. How Methylene Blue Assists in Treating Traumatic Brain Injury (TBI) Methylene blue plays a crucial role in the management of traumatic brain injury (TBI) through several mechanisms. Reduces Brain Swelling: This compound helps decrease brain edema, which is the swelling that often accompanies TBIs. By minimizing edema, methylene blue can alleviate pressure and improve overall brain function. Mitigates Inflammation: It works to suppress inflammation in the brain, providing a protective effect against further damage that often follows an initial brain injury. Enhances Oxygen Supply: By improving oxygen delivery to brain cells, methylene blue supports cellular recovery, which is vital for healing after a TBI. This enhanced oxygenation aids in restoring cognitive functions and promoting brain health. Overall, methylene blue shows considerable potential in supporting recovery by addressing multiple aspects of brain injury and promoting a conducive environment for healing. Effects of Methylene Blue on Stroke Treatment Methylene blue is garnering attention for its potential benefits in stroke therapy. Research suggests that it plays a significant role in treating ischemic strokes, which occur when a blood clot obstructs the flow of blood and oxygen to the brain. Key Benefits: Reduction of Brain Lesion Volume: Studies, particularly those conducted on animals, have demonstrated that methylene blue administered over the long term can significantly decrease the size of brain lesions. This effect is particularly notable in the chronic phase following a stroke. Neuroprotective Properties: Methylene blue exhibits neuroprotective effects, potentially safeguarding brain cells from the damage typically associated with strokes. This could lead to better recovery outcomes and reduced disability. Overall, while methylene blue’s primary approved use is for treating methemoglobinemia, its promising effects on stroke treatment highlight its potential as a valuable therapeutic option in this area. Further research could clarify its role in human stroke recovery. Methylene Blue Dye: A Diagnostic Tool for Abnormal Cells Detecting Blood Disorders Methylene blue dye has been used as a diagnostic tool to identify abnormal cells in the body, including blood disorders. Clinical trials have shown that methylene blue can detect blood disorders such as G6PD deficiency and phosphate dehydrogenase deficiency. Due to enzyme deficiencies, red blood cells cannot function properly in these disorders. When a patient is given methylene blue, it causes the red blood cells to become oxidized and appear darker under a microscope. This helps doctors identify which type of enzyme deficiency the patient may have. Identifying Cancer Cells Evidence suggests that methylene blue can also identify cancer cells in the body. In one study, researchers found that when methylene blue was injected into tumors in mice, it caused the tumors to turn blue and become more visible during surgery. This allowed surgeons to remove more of the cancer and improve patient outcomes. Diagnosing Shock and Kidney Dysfunction A systematic review found that methylene blue is helpful as a diagnostic tool for shock and kidney dysfunction caused by ifosfamide, a chemotherapy drug. Ifosfamide can damage the kidneys and cause shock in some patients. By administering methylene blue, doctors can determine if the patient’s symptoms are due to ifosfamide toxicity or other causes. Benefits of Methylene Blue for Skin Health Reducing Inflammation Methylene blue is a versatile compound used in various medical applications, including treating malaria and methemoglobinemia. However, recent studies show it can also improve skin health by reducing inflammation and protecting cells. Chronic inflammation causes eczema, psoriasis, and rosacea. Methylene blue acts as an anti-inflammatory agent by inhibiting the production of pro-inflammatory cytokines. These cytokines are responsible for triggering inflammation in the body. Additionally, methylene blue’s antioxidant properties help in protecting cells from oxidative damage, which is integral to preventing various chronic diseases and enhancing overall health. Methylene blue can help reduce inflammation and prevent skin damage by blocking their production. This property makes it an effective ingredient in skincare products that treat inflammatory skin conditions. Antibacterial Properties Another benefit of methylene blue for skin health is its antibacterial properties. Acne is caused by bacteria that live on the skin’s surface and clog pores. It eliminates several types of bacteria that cause acne and other skin conditions. Methylene blue disrupts the bacterial cell membrane and inhibits its growth. This makes it an effective treatment against acne and other bacterial infections on the skin. Because methylene blue targets only bacterial cells and not healthy cells, it has no adverse effects on the surrounding tissue. Reducing Fine Lines and Wrinkles Aging causes loss of skin elasticity due to decreased collagen production, leading to fine lines and wrinkles that make us look much older. Methylene blue may help reduce signs of aging by improving the blood flow of blood to the skin and stimulating mitochondrial function in cells, and increasing energy production in tissues. When applied topically on the skin, this increases blood flow, helping improve overall skin health and reducing facial fine lines and wrinkles. Anticancer Properties Methylene blue may also have anticancer properties that could benefit skin health. Recent research indicates that methylene blue could be used in cancer treatment because it prompts cancer cells to self-destruct. Moreover, methylene blue inhibits angiogenesis, forming new blood vessels that supply nutrients to cancer cells. By preventing the growth of these blood vessels, methylene blue can help slow down or even stop cancer cell growth. Effectiveness of Methylene Blue in Treating Infections Methylene Blue as an Alternative to Antibiotics in Treating Fungal Infections and Nail Fungus Methylene blue is a synthetic compound used for years as a dye in various industries. Significant medical benefits are seen, including its effectiveness in treating various infections. One of the most notable benefits of methylene blue is its ability to act as an alternative to antibiotics in treating fungal infections and nail fungus. Different fungi cause fungal infections and can affect various body parts, including the skin, nails, and hair. These infections can be challenging to treat because they often require long-term use of antifungal medications that can cause side effects such as liver damage. However, methylene blue is effective against some fungi, including Candida albicans, which cause thrush and other yeast infections. Nail fungus affects millions of people worldwide and can cause thickened, discolored nails that are painful and difficult to manage. The traditional treatment for nail fungus involves taking oral antifungal medications for several months or even up to a year. In addition to being effective against fungal infections, methylene blue has also been found to help treat nail fungus. Methylene blue offers an alternative treatment option for nail fungus that is safe and effective, promoting healthy tissue regeneration around the infected area. Healthcare Providers Should Determine Methylene Blue’s Potency and Doses. While methylene blue has shown promising results in treating various infections, it’s essential to note that healthcare providers should always determine its potency and doses. This is because methylene blue can cause allergic reactions in some people, and it’s essential to ensure that the correct dosage is administered for each specific condition. One of the most common uses of methylene blue is in treating malaria. Malaria is a parasitic infection affecting millions worldwide, primarily in tropical regions. Methylene blue is effective against malaria by inhibiting the parasite’s growth responsible for generating the condition. Methylene blue is also effective in treating Lyme disease, a condition marked by rash, fever, joint pain, and fatigue. It offers potential healing against this infection. Finally, methylene blue has also been effective in treating septic shock. Septic shock is a severe medical condition which an infection causes a dangerous drop in blood pressure. If not addressed quickly, this condition can cause the failure of multiple organs. Methylene blue helps by raising blood pressure and decreasing inflammation. Future Potential Applications of Methylene Blue Methylene Blue in Clinical Studies Methylene blue is a versatile compound used for decades as a dye, medication, and laboratory reagent. Researchers have been exploring its potential future applications in clinical trials in recent years. Scientists are currently investigating the use of methylene blue in cancer treatment. Various studies have found that it can effectively destroy cancer cells in lab conditions. However, more research is required to understand its potential benefits for human patients. Methylene blue also shows potential in treating brain diseases like Alzheimer’s and Parkinson’s. Animal studies have demonstrated that it can lower oxidative stress and inflammation in the brain, contributing significantly to these diseases. Additionally, methylene blue can accelerate the recovery of metabolically defective brain cells when combined with red light therapy. Now, researchers are working to see if these results can be applied to human treatments. Potential Side Effects While methylene blue has many potential benefits, side effects must be considered. For example, high doses of methylene blue can cause nausea, vomiting, headache, and confusion. However, most people who take methylene blue do not experience any severe side effects. Researchers are more closely addressing potential side effects by studying methylene blue’s chemical properties. By understanding how it interacts with different tissues and organs in the body, they hope to develop safer and more effective treatments. Animal Studies Animal studies have been essential in advancing our understanding of how methylene blue works and its potential applications. For example, researchers have used animal models to investigate whether methylene blue can improve cognitive function after traumatic brain injury or stroke. In one study published in 2019[1], rats were given saline or methylene blue injections before being subjected to a simulated stroke. The rats who received the methylene blue had significantly better outcomes than those who received saline, suggesting that methylene blue may be a promising treatment for stroke in humans. Chemical Studies Methylene blue is a complex compound with many chemical properties that make it useful for various applications. Researchers are studying these properties to better understand how methylene blue can be used in medicine and other fields. One area of interest is using methylene blue as a photosensitizer in photodynamic therapy (PDT). PDT is a cancer treatment involving light to activate drugs that kill cancer cells. Methylene blue is an effective photosensitizer, and researchers are exploring ways to enhance its effectiveness in this application. Following Ongoing Research As research into methylene blue continues, new potential applications will likely emerge. Whether it’s treating cancer, neurodegenerative diseases, or other conditions, scientists are excited about this versatile compound’s possibilities. However, it’s important to remember that much more research is needed before any new treatments can be developed. In the meantime, researchers will continue following the latest developments in the methylene blue study and working towards a better understanding of its chemical properties and potential benefits. Methylene blue is a compound studied for its various health benefits. From its therapeutic uses to its anti-aging properties, methylene blue has many potential applications in medicine and beyond. Health Benefits of Methylene Blue One of the most significant benefits of methylene blue is its ability to improve mitochondrial function . Mitochondria are the powerhouses of our cells, responsible for producing energy that fuels all cellular processes. By enhancing blood circulation and increasing cellular oxygen consumption, methylene blue may help protect against age-related decline, improve cognitive function, and reduce oxidative stress, promoting overall health. Therapeutic Uses of Methylene Blue Methylene blue has also been used therapeutically in a variety of contexts. For example, it can be used as an antidote for cyanide poisoning or as a treatment for methemoglobinemia, a condition where the blood cannot carry oxygen effectively. Anti-aging Properties of Methylene Blue As mentioned earlier, methylene blue’s ability to improve mitochondrial function may also have anti-aging effects . Studies have shown that it can improve cognitive function in older adults and even extend lifespan in specific animal models. Cognitive Benefits of Methylene Blue In addition to its anti-aging effects, methylene blue may also have cognitive benefits. It may enhance memory recall and improve attention span in healthy individuals and those with cognitive impairment. Potential Medical Uses of Methylene Blue Beyond these specific benefits, there is also potential for methylene blue to be helpful in various medical contexts. For example, it is beneficial as a treatment for neurodegenerative diseases like Alzheimer’s or Parkinson’s. Mechanism of Action of Methylene Blue The mechanism by which methylene blue exerts these various effects has yet to be fully understood, but likely to involve multiple pathways within cells and tissues. Role of Methylene Blue in Treating Neurological Disorders One area where research on methylene blue is up-and-coming is in treating neurological disorders. Studies have shown that it can improve symptoms in individuals with Alzheimer’s disease and may also be effective in treating depression. Use of Methylene Blue as a Diagnostic Tool Methylene blue is a diagnostic tool commonly used to stain cells for microscopy or identify leaks in surgical procedures. Benefits of Methylene Blue for Skin Health Methylene blue benefits skin health as well. It can help reduce inflammation and improve wound healing, making it helpful in treating conditions like acne or eczema. Effectiveness of Methylene Blue in Treating Infections Finally, methylene blue may also be effective at treating certain infections. Studies have shown that it can inhibit the growth of bacteria and viruses, making it a potentially useful treatment option. Methylene blue has many potential benefits across a wide range of applications. We will learn more about this fascinating compound and its uses as research continues. Exploring Methylene Blue as an Alternative to NAD+ Therapy for Cancer Patients Methylene blue has emerged as a potential alternative to NAD+ therapy for cancer patients, particularly those unable to undergo the latter treatment. This compound plays a crucial role by facilitating the oxidation of NADH, a process that increases NAD levels in the body. NAD, or nicotinamide adenine dinucleotide, is a vital coenzyme that bolsters metabolism and supports various bodily functions, including brain and heart health. Benefits for Cancer Patients One of the significant advantages of methylene blue is its ability to mitigate some side effects commonly associated with chemotherapy and radiation. While NAD+ therapy has shown potential in supporting cellular health, it poses a risk for certain cancer patients as it might contribute to the proliferation of cancer cells. Given these considerations, methylene blue is a promising option, offering similar benefits without some of the potential drawbacks of NAD+ therapy. This makes it a viable alternative for enhancing the quality of life for cancer patients undergoing traditional treatments. Renal Impairment Considerations In patients with kidney issues, adjust methylene blue doses: Mild to moderate impairment: No dose change needed Severe impairment: Use caution, consider dose reduction Dialysis patients: Give after dialysis sessions We closely monitor renal function and adjust as needed. Methylene blue can affect certain lab tests, so we interpret results carefully. Adjustments for Hepatic Impairment Mild impairment: No dose adjustment required Moderate to severe impairment: Reduce dose by 50% Monitor liver function tests regularly We watch for signs of toxicity, such as nausea or confusion. In some cases, we may need to use alternative treatments. Taking methylene blue orally changes the conformation of hemoglobin in RBCs to help it carry oxygen more efficiently, promotes oxygen release into tissues so it can be utilized more easily, helps clear senescent cells, increases mitochondrial biogenesis, and works as a monoamine oxidase inhibitor (MAO-I) which leads to increases in dopamine, norepinephrine, and serotonin. Phew! Are you keeping up? This compound is doing a lot and has a large therapeutic range… from 4 to 210 mg (<0.5 to 3 mg/kg). Even at doses >3 mg/kg, when methylene blue is no longer an electron donor and becomes purely oxidative, there may be a role for it in cancer and sepsis. But that’s a huge therapeutic range. How do you know what dose is best for you? Dosing and proper use of methylene blue The key point is to distinguish what kind of dosing helps acutely (i.e., for a disease or condition) vs. what dosing will help optimize health or a more chronic condition. And also to be aware of the significant dangers of taking too much methylene blue at high doses for long periods, including the risk of methemoglobinemia in susceptible individuals and other side effects. Let’s chat about the risks of higher-dose methylene blue Methylene blue and the disruption of GI biofilms One concern with higher-dose methylene blue, typically greater than 1 mg/kg body weight, is that it may disrupt natural and healthy gastrointestinal biofilms, leading to issues with your gut lining and gut microbiota. Biofilms are a collective of one or more types of microorganisms that can grow on many different surfaces. They produce an extracellular polymeric substance (EPS), which gives the surface a film-like/sticky consistency. A fully functioning biofilm structure is comprised of microbial cells and EPS, has a defined architecture, and provides an optimal environment for the exchange of genetic material between cells of the same and different phyla, otherwise known as trans-kingdom interactions. Microorganisms that form biofilms include bacteria, fungi, and protists. In the gut, biofilms naturally grow, both at the epithelial surface and in the lumen as mucin-attached and food particle-attached colonies. Communities of microbes that form biofilms are usually more resilient to stress and are well-known to keep surfaces like your mouth and gut healthy. This includes enhancing immune system function. They also function as a physical barrier to the intestinal lining. There are, however, times when these biofilms can become pathologic, such as in dental plaques or with certain bacterial infections, like Bartonella. When this occurs, biofilms can protect pathogenic bacteria and can be difficult for the host defense system to identify. This is where methylene blue can be very effectively used at higher doses, especially when combined with other synergistic therapies, such as photodynamic therapy. High doses may be dangerous due to methylene blue's half-life. Here’s why… Methylene blue — whether IV, oral, or in troche form — is almost 100% bioavailable, meaning that almost all the methylene blue you take in gets into your bloodstream. How long methylene blue stays in your body depends on its half-life. This is defined as the time it takes for one-half of the amount of ingested methylene blue to leave your body. The half-life of IV methylene blue is 24 hours. The half-life of oral methylene blue is 4 to 6 hours (this half-life, of note, is a critical factor to consider when there are missed doses or when increasing the dose to twice or three times daily). Let’s take the example of a 100 mg oral methylene blue dose with a half-life of 6 hours: Imagine you take your dose at 8 am… half-life #1: 50 mg left in your body at 2 pm (i.e., 6 hours later) half-life #2: 25 mg left in your body at 8 pm (i.e., another 6 hours later) half-life #3: 12.5 mg left in your body at 2 am half-life #4: 6.25 mg left in your body at 8 am This means that if you take 100 mg of methylene blue at 8 am, you'll still have 6.25 mg of methylene blue in your body 24 hours later. Even if we assume that the methylene blue half-life is 4 hours, then there would be 3.125 mg of methylene blue left in your body at 8 am the next day. Either way, 100 mg daily methylene blue taken daily will continue to build up in your system, and this buildup could lead to adverse effects, especially when the cumulative dose reaches 3 mg/kg or greater. High doses of methylene blue and the risk of gastric ulceration? While higher doses of methylene blue may help treat some disease processes, it may cause a higher risk of gastric ulceration over the long term. In addition, there has been some discussion about whether methylene blue requires gastric acid for activation (as an argument against using methylene blue buccal troches), but this is not the case. After all, IV methylene blue is 100% bioavailable and completely bypasses the GI system (including any gastric acid). Using methylene blue with G6PD deficiency Although rare, a higher dosage, definitely greater than 3 mg/kg and possibly >1 mg/kg if used IV, methylene blue may also cause hemolysis (the destruction of red blood cells) in those with G6PD deficiency, an inherited blood disorder. At lower doses and with oral formulations, this would be rare, but caution is still advised. Methylene Blue's Cellular Mechanisms: 8 Reasons Why Low-Dose Methylene Blue is a Biohacker’s Delight MB is an electron donor and acceptor, both donating and accepting electrons. After absorption in the buccal mucosa (e.g., in a troche), oral ingestion, or IV administration, MB concentrates in tissues with the most mitochondria (e.g., the brain, where it readily crosses the blood-brain barrier, the heart, the liver, and kidneys). It is at low doses that MB makes (blue) magic happen. Here are the 8 most promising ways it works: MB donates electrons to the electron transport chain (ETC) and increases adenosine triphosphate (ATP) production. This effect can occur in the presence or absence of oxygen. Forgot how the ETC works? Watch this video (start at 1 minute). MB enhances the function of cytochrome oxidase (complex IV), making it work faster and more efficiently. This leads to increased oxygen consumption and increased ATP production, especially in the most metabolically active cells like the nerve cells in memory regions of the brain! MB stimulates glucose metabolism in conditions without oxygen and increases the amount of NAD+ + produced by mitochondria. The greater the amount of NAD+, the younger your cells remain/become due to sirtuin activation (see David Sinclair’s book Lifespan for more information). In red blood cells, low-dose MB changes the configuration of the iron (heme) in hemoglobin, the molecule in a red blood cell that carries oxygen. This improves the oxygen-carrying capacity of hemoglobin, which leads to increased ATP production from the ETC. Low-dose MB also functions as a powerful antioxidant as it scavenges the mitochondria and cytosol for free electrons to accept and neutralize. On the macro level, this is how MB may be neuroprotective and even reverse skin damage (see below). Low-dose MB also has antidepressant effects, functioning as a monoamine oxidase (MAO) inhibitor. Inhibiting MAO prevents monoamine neurotransmitter breakdown (dopamine, melatonin, and serotonin), which leads directly to increases in these neurotransmitters. Low-dose MB may also function as a cholinesterase inhibitor, increasing the amount of acetylcholine available, a neurotransmitter in the brain responsible for arousal, attention, memory, and motivation. Low-dose MB combined with certain spectrums of light (UV, primarily) may also be anti-infective against viruses. Amazingly, there are 4 distinct ways MB increases cellular energy (ATP) production, three of which are related to its direct effects on the mitochondria. Are you paying attention yet? Moderate to High Doses of Methylene Blue At moderate doses (4 to 10 mg/kg in most studies), MB becomes a pro-oxidant and facilitates the generation of singlet oxygen and peroxide radicals, especially in the presence of certain spectrums of light. This is likely the way MB works against septic shock (via nitric oxide synthase inhibition) and possibly in cancer treatment synergy. At high doses (>10 mg/kg), MB can have harmful oxidative effects. Methylene Blue Safety MB is a very safe drug, especially when taken at low doses and when purity/potency is tested. The most common (and harmless… and awesome?) side effect of MB is blue urine. Because of the potential risk of serotonin syndrome (a life-threatening condition), do not combine MB with SSRIs, SNRIs, or drugs that increase serotonin levels except under the very close supervision of a provider. For all you psychonauts out there considering MB, certain psychedelic substances like MDMA and psilocybin increase serotonin, and the vine in ayahuasca ceremonies has MAOI properties like MB... so be mindful of what you are stacking/ingesting and wait at least 24 hours before having MB and these compounds. Are you pregnant or breastfeeding? Please don’t take MB. It is contraindicated (e.g., it ain't good for the babies on board). At high doses (>10 mg/kg), MB may cause a litany of potential side effects including hypertension, methemoglobinemia (a condition it treats at low doses), dizziness, gastrointestinal distress, affect readings of a pulse oximeter, induce hemolytic anemia in patients with a genetic condition called G6PD, and more. Don't Drink Fish Tank Cleaner, Please! Go Beyond USP! Whatever you do... please do NOT drink fish tank cleaner. Although it has MB in it to treat fish fungal infections, fish tank MB is not only diluted with water to around 2% purity, it also contains a lot of impurities and heavy metals such as arsenic, aluminum, cadmium, and lead. Industrial- and chemical-grade MB can also consist of up to 11% of impurities as well. Your safest choice is USP (pharmaceutical grade) MB, but even that can have impurities. This is why it’s important not only to ensure your MB is USP but that it also has testing that documents its purity and potency. However, even USP-grade MB can contain the aforementioned impurities. This is why the MB you are consuming must come with documentation of purity and potency along with a USP designation! Methylene Blue, Infrared Light, and the Mitochondria in the Brain Holy synergy! Although methylene blue and red light are administered in very different ways, they both seem to share a mechanism of action: enhancing the ETC in the mitochondria [1]. Methylene blue has a bio chemical effect, while NIR light has a bio physical effect. While methylene blue donates electrons , NIR light donates photons . Methylene blue is administered orally and reaches the brain through the bloodstream, whereas infrared light is applied transcranially. But in the end, they both enhance cellular metabolism and oxygen consumption to produce energy and, therefore, have neuroprotective effects against cognitive decline. Adverse Effects and Precautions Methylene blue can cause several side effects and has important safety considerations. We’ll cover the most common issues, serious reactions, drug interactions, and special population factors to be aware of. Common Side Effects: Methylene blue often causes blue or green urine. This is normal and not harmful. Some people may experience: Headache Dizziness Nausea Skin discoloration Sweating Feeling hot These effects are usually mild and go away on their own. Methylene blue can also cause pain in the arms or legs and change how things taste. Serious Adverse Reactions While rare, methylene blue can cause more serious problems: Anaphylaxis (severe allergic reaction) Serotonin syndrome (when combined with certain medications) Hemolytic anemia in people with G6PD deficiency We must watch for signs of these reactions, which can include: Trouble breathing Swelling of the face, lips, and tongue Confusion, agitation, fever Muscle stiffness or twitching Rapid heart rate Seek medical help right away if these occur. Drug Interactions Methylene blue can interact dangerously with some medicines. It should not be used with: SSRIs (like Prozac, Zoloft) SNRIs (like Effexor, Cymbalta) MAO inhibitors (like Nardil, Parnate) These combos can cause serotonin syndrome, a potentially life-threatening condition. Other drugs may also interact. We always check with a doctor or pharmacist before using methylene blue with other medications. Specific Population Considerations Some groups need extra caution with methylene blue: Pregnancy: We use it only if needed. Not enough studies exist on its safety for unborn babies. Breastfeeding: It may pass into breast milk. We discuss risks with a doctor. G6PD Deficiency: Can cause severe anemia. We avoid use or use with extreme caution. Cancer: May interfere with some cancer treatments. We consult an oncologist before use. Methylene blue can also cause photosensitivity. We advise patients to protect their skin from sun exposure while using it. Safety Guidelines and Monitoring Safety is key when using methylene blue. We need to watch for side effects and make sure it’s working right. Let’s look at some important things to keep in mind. Monitoring Therapy Effectiveness We must check how well methylene blue is working. Pulse oximetry helps us track oxygen levels in the blood. This shows if the medicine is doing its job. We should also watch vital signs closely. These include: Blood pressure Heart rate Breathing rate Temperature Regular blood tests are important too. They help us see if methemoglobin levels are going down. We might need to adjust the dose based on these results. It’s crucial to keep an eye on urine color. Methylene blue can turn urine blue or green. This is normal, but can be alarming if you’re not expecting it. Identifying and Managing Hypersensitivity Reactions We must be alert for signs of allergic reactions. These can happen even if you’ve taken methylene blue before without problems. Symptoms to watch for include: Skin rash or hives Itching Swelling, especially of the face or throat Trouble breathing If any of these occur, we need to stop the treatment right away. Seek medical help immediately. Some people might have a more serious reaction called anaphylaxis. This is rare but can be life-threatening. We must have emergency medicines on hand just in case. Blue Dye Precautions Methylene blue is a dye as well as a medicine. This means it can stain skin and other surfaces. We should wear gloves when handling it. If it gets on your skin, wash it off right away with soap and water. Be careful with clothing and bedding. The dye can stain these items, too. Use old or dark-colored sheets if possible. Methylene blue can interfere with some medical tests. We need to tell any healthcare provider about its use before getting tests done. It’s also important to avoid certain foods and drinks that are blue or green. These might make it hard to spot changes in urine color. FAQs Is methylene blue safe to use? Yes, when used appropriately, methylene blue is generally considered safe. Can I take methylene blue supplements? Yes, there are dietary supplements available that contain methylene blue. Does methylene blue have any side effects? Possible side effects include nausea, vomiting, and headache. How does methylene blue work in the body? Methylene blue (MB) is a fascinating compound with a range of applications in medicine. The exact mechanism of methylene blue works has yet to be fully understood, but likely to involve multiple pathways within cells and tissues. Primarily, it is known for treating methemoglobinemia, a rare blood condition that affects how blood delivers oxygen throughout the body. By enhancing cellular and mitochondrial function in the brain, methylene blue can improve cognition and mood. It also plays a role in combating infectious diseases and reducing inflammation, showcasing its versatility. Notably, MB can serve as an alternative to NAD+ therapy for cancer clients, underscoring its potential in diverse therapeutic contexts. How It Works: Oxygen Delivery: Methylene blue helps convert red blood cells into a form that can carry and release oxygen effectively. This process is crucial for treating methemoglobin levels greater than 30% or when symptoms persist despite oxygen therapy. Administration: Health professionals must oversee its use, typically administering it via injection to ensure proper dosage and effectiveness. Methylene blue’s multifaceted role in medical treatments highlights its significance, making it a valuable tool in both routine and complex healthcare scenarios. What medical conditions might benefit from treatment with methylene blue? Methylene blue shows promise as a potential treatment option for neurodegenerative diseases like Alzheimer’s or Parkinson’s disease. This promising compound works by targeting mitochondria-related changes commonly seen in these brain disorders. Many brain diseases, including Alzheimer’s, are characterized by inflammation, decreased oxygen levels, and an impaired balance of mitochondrial processes such as fission and fusion. These are critical factors in maintaining healthy brain cell function. Researchers are optimistic that methylene blue can address these issues at a cellular level. By doing so, it potentially stabilizes or even reverses some of the detrimental changes associated with neurodegeneration. This broad approach not only highlights its potential for Alzheimer’s but suggests it could benefit other brain conditions as well.

Epoch Health Article A Natural Sweetener That Could Combat COVID, Diabetes, and Cancer One significant benefit of monk fruit is that it can manage blood sugar and lipid levels, it might have antiviral and anti-cancer effects. Following in stevia’s footsteps, monk fruit has gained widespread attention as a natural sweetener. One significant benefit of this sweetener is that it can manage blood sugar and lipid levels. It also might have antiviral effects against COVID-19 and even anti-cancer properties. Monk fruit is also known as luo han guo, and its fruit resembles a small melon on the outside. Ancient Chinese people have used it for centuries as a natural sweetener and traditional medicine. According to a review article in Frontiers in Pharmacology, monk fruit contains various nutritious compounds, including mogrosides, vitamin C, trace elements, linolenic acid, and other unsaturated fatty acids. “Monk fruit does actually contain natural sugars. Those are mainly fructose and glucose. However, unlike most fruit, the natural sugars from monk fruit aren’t really responsible for the sweetness. Instead, the intense sweetness comes from a group of compounds called mogrosides,” Taylor Wallace, an adjunct associate professor at the Friedman School of Nutrition Science and Policy at Tufts University and CEO at the Think Healthy Group LLC, said in an interview with The Epoch Times. “The extracted mogrosides from monk fruit, obtained through processing, don’t necessarily contain fructose or glucose. So these are very similar compounds to what you would see in other high-intensity sweeteners,” Mr. Wallace said. Mogrosides are 200 to 350 times sweeter than sucrose, and monk fruit sweetener is essentially derived from mogrosides. Mogrosides account for about 1.2 percent of the fresh monk fruit and 3.8 percent of dried fruit powder, according to a review published in Molecules. “Mogroside, as a natural sweetener derived from plants, is a series of molecules, and the taste of these molecules is different,” Nate Yates, vice president of the Global Sugar Reduction Platform at Ingredion Inc., told The Epoch Times. Mogroside V is the most abundant of the compounds, and ripe monk fruit is exceptionally sweet because of its high content of mogroside V, according to the Molecules review.  “After further refinement and extraction, the taste is more pure and pleasant,” Mr. Yates said. Monk Fruit Sugar’s Anti-Diabetic Effects Like stevia, monk fruit sugar is a zero-calorie sweetener. It is often described as having a taste similar to that of cane sugar, which is a high-calorie sweetener. In a randomized controlled trial published by the International Journal of Obesity in 2017, 30 healthy men were asked to consume a standardized breakfast, and one hour before lunch, they were provided beverages containing sucrose, aspartame, stevia, or monk fruit sweetener. They were then allowed to choose their lunch from the options provided, and their dinner was recorded. In addition, blood draws and appetite measures were conducted at various points throughout the study. The results showed that those who consumed beverages containing sucrose experienced an increase in blood sugar and insulin levels within an hour before a meal, and those who consumed beverages containing one of the other sweeteners, including monk fruit, did not. After subsequent monitoring, the researchers concluded that natural sweeteners, including monk fruit sweetener, had the most negligible effect on post-meal blood sugar levels and insulin secretion compared with sucrose.  A recent systematic review and meta-analysis conducted by Canadian researchers showed that in the short term, like water, beverages sweetened with non-caloric artificial or natural sweeteners didn’t affect metabolism and endocrine function. There is currently limited human research on monk fruit sweeteners, unlike on stevia. However, numerous cellular models and animal experiments have indicated that mogrosides provide various beneficial effects for both Type 1 and Type 2 diabetes, according to a review published in the journal Foods. Mogrosides have been shown to regulate lymphocyte antigens in Type 1 diabetic mice and exhibit therapeutic effects on symptoms. Monk fruit extract can also alleviate and repair damage to pancreatic beta cells and promote insulin secretion, according to the Frontiers in Pharmacology review. According to the Molecules review, mogrosides have been found to effectively reduce blood sugar and lipid levels in people with Type 2 diabetes. In a study involving mice with diabetes, those given monk fruit extract or mogrosides experienced significant decreases in fasting blood sugar, glycated serum protein, and insulin resistance. The treatment also resulted in a reduction in LDL cholesterol and an increase in HDL cholesterol levels. Additionally, mogrosides can alleviate symptoms of diabetic nephropathy, according to the Frontiers in Pharmacology review. Monk fruit beverages, made from monk fruit powder and water, have already been granted patent registrations in China. The review published in Frontiers in Pharmacology suggested that such drinks are suitable for treating diabetes. Moreover, according to the Foods review, the flavonoid compounds found in monk fruit can significantly lower blood sugar levels and protect the pancreas, while the polysaccharides can ameliorate lipid disorders and reduce plasma glucose levels. Potential Benefits of Monk Fruit Against COVID-19 Monk fruit, a natural sweetener, has long been used in traditional Chinese medicine (TCM) to treat cough, sore throat, bronchitis, and asthma. According to the Frontiers in Pharmacology review, records of its effectiveness in relieving phlegm, alleviating pain, clearing heat, and moisturizing the lungs—to use some terms from TCM—can be traced back 2,000 years. “In particular, during the summer, it is recommended to consume monk fruit when experiencing symptoms such as sore throat, throat discomfort, or cough,” Jonathan Liu, a professor of Chinese medicine at Georgian College and the director of Liu’s Wisdom Healing Centre in Canada, told The Epoch Times. A study published in Frontiers in Endocrinology in 2022 demonstrated that mogroside V can effectively target multiple sites of COVID-19, potentially helping treat those infected with the virus. Mogrosides can also inhibit the release of inflammatory factors, effectively suppressing and reducing pulmonary fibrosis. According to the Molecules review, numerous animal studies have demonstrated that monk fruit extract can significantly inhibit cough and enhance sputum excretion. It also possesses anti-inflammatory properties and can help manage asthma. Additionally, mogrosides show a protective effect against acute lung injury. Anti-Cancer, Anti-Inflammatory, and Antioxidant Properties Mogrosides Exhibit Anti-Cancer Properties Mogrosides exhibit comprehensive anti-cancer activities, as evidenced by various experiments. According to the review in Foods, they can inhibit the invasion and migration of lung cancer cells, induce cell apoptosis, and impede the proliferation of colorectal and laryngeal cancer cells. Moreover, mogrosides can disturb the growth cycle of pancreatic cancer cells and cause cell death. According to the Frontiers in Pharmacology review, monk fruit extract has also been found to have inhibitory effects on liver cancer. Additionally, mogrosides can help inhibit the toxicity of carcinogens, according to a paper published in Cancer Letters. For instance, they can help prevent skin cancer induced by exposure to certain chemicals, according to commentary published in Future Medicinal Chemistry. Animal studies mentioned in the Cancer Letters paper have shown that phytochemicals in monk fruit can even directly kill tumor cells. Monk Fruit Benefits the Brain and Nervous System Mogrosides can alleviate neuroinflammation in brain cells and help manage Alzheimer’s disease, according to the Molecules review. They can also reduce memory impairments and prevent hippocampus apoptosis. In addition, animal studies mentioned in the Foods review have shown that mogrosides can effectively improve schizophrenic behaviors in mice and modulate partial permanent impairment of the nervous system. Monk Fruit Acts as an Antioxidant The Molecules review states that mogrosides are antioxidant agents, enabling them to scavenge reactive oxygen species and protect cells. They can also inhibit DNA oxidative damage, thereby slowing the aging process. Additionally, mogrosides demonstrate significant protective effects against exercise-induced tissue damage, including cardiac injury. The Foods review indicated they could also improve nonalcoholic fatty liver disease by preventing liver fat accumulation and inhibiting lipid peroxidation. In addition, the flavonoids and polysaccharides found in monk fruit also show vigorous antioxidant activity. Who Should Avoid Consuming Monk Fruit Sugar? “Monk fruit sweetener seems to be fairly safe, though it undergoes an artificial extraction process,” Mr. Wallace said. According to the information published by the U.S. Food and Drug Administration, monk fruit extract is classified as “generally recognized as safe.” However, no specific acceptable daily intake has been established for monk fruit extract, which is typical because evidence of the ingredient’s safety is established for amounts well above that needed to achieve the desired effect in food. According to TCM, monk fruit is considered to have a slightly cold nature and is associated with minimal side effects. However, Mr. Liu advised that people with cold constitutions, such as those who frequently experience loose stools, have a large, pale tongue, or exhibit prominent tooth marks on the edges of the tongue, may want to avoid monk fruit consumption. In addition, monk fruit belongs to the Cucurbitaceae family, which includes common plants such as cucumber, zucchini, pumpkin, and melon. Therefore, people allergic to these foods are more likely to be allergic to monk fruit.

Normal and cancer cells

Epoch Health Article Coping with Cancer If you've been diagnosed with cancer, Coping with Cancer & knowing what to expect, and making plans for how to proceed can help make this stressful time easier. Learning that you have cancer can be hard. Some people say they felt anxious, afraid, or overwhelmed when they were first diagnosed. If you aren't sure what to do to cope, here are 11 ideas to help you deal with a cancer diagnosis. Get the facts about your cancer diagnosis and try to get as much basic, useful information as you can. This will help you to make decisions about your care. Write down your questions and concerns. Bring them with you when you see your healthcare provider. By Mayo Clinic Staff Learning that you have cancer can be hard. Some people say they felt anxious, afraid, or overwhelmed when they were first diagnosed. If you aren't sure what to do to cope, here are 11 ideas to help you deal with a cancer diagnosis. Get the facts about your cancer diagnosis Try to get as much basic, useful information as you can. This will help you to make decisions about your care. Write down your questions and concerns. Bring them with you when you see your healthcare provider. You may ask: • What kind of cancer do I have? • Where is the cancer? • Has it spread? • Can my cancer be treated? • What is the chance that my cancer can be cured? ( I advocate for Natural treatments and Oncologists will never say "Cured" G. R.) • What other tests or procedures do I need? • What are my treatment options? ( Natural Treatments do not have side effects and are effective ) • How will the treatment benefit me? • What can I expect during treatment? ( Totally dependent on treatment given ) • What are the side effects of the treatment? ( There are many and dependent on the treatment they give. No side effects with natural products ) • When should I call my health care provider? • What can I do to prevent my cancer from coming back? ( Keep your immune system built up and take the Natural Treatments ) • How likely are my children or other family members to get cancer? ( Depends on the type of cancer cell line ) • What happens if I don't get treatment? ( if you do not take any treatments of any type the cancer will spread and you will most likely die from it! ) Some of the views expressed here are from the standpoint of Cancer Institutes and current Medical advice. I went with a natural protocol and lived with Quality of life. I do take a maintenance dose 3-4 times a week to keep the cancer from recurring as well. We ALL have a choice to make as we need to change words (Them to "Me" and They to "I") Consider bringing a family member or friend with you to your first few appointments. They can help you remember what you hear. Think about how much you want to know about your cancer. Some people want all the facts and details. This helps them be part of the decision-making process. Others want to learn the basics and leave details and decisions to their healthcare providers. Think about which works best for you. Let your healthcare team know what you'd like. Keep the lines of communication open Have honest, two-way communication with your loved ones, healthcare providers, and others. You may feel alone if people try to protect you from bad news by not talking about it. Or you might feel alone or less supported if you try to look strong and not share your feelings. If you and others show your real emotions, you can help support each other. Anticipate possible physical changes The best time to plan for changes to your body is right after your cancer diagnosis and before you begin treatment. Prepare yourself now so that you'll be able to deal with everything later. Ask your healthcare provider what may change. Medicines may make you lose your hair. Advice from experts about clothing, makeup, wigs, and hairpieces may help you feel more comfortable and attractive. Insurance often helps pay for wigs and other devices to help you adapt. Consider joining a cancer support group. Members can provide tips that have helped them and others. Also, think about how treatment will affect your daily life. Ask your provider whether you will be able to continue your usual routine. You may need to spend time in the hospital or have many medical appointments. If your treatment will make it hard to perform your daily duties, make arrangements for this. Plan ahead for your finances. Figure out who will do routine household chores. If you have pets, ask someone to take care of them. Maintain a healthy lifestyle A healthy lifestyle can improve your energy level. Choose a healthy diet. Get enough rest. These tips will help you manage the stress and fatigue of the cancer and its treatment. If you can, have a consistent daily routine. Make time each day to exercise, get enough sleep, and eat meals. Exercise and participating in activities that you enjoy also may help. People who get exercise during treatment not only deal better with side effects but also may live longer. Let friends and family help you Your friends and family can run errands, take you to appointments, prepare meals, and help you with household chores. This can give those who care about you a way to help during a difficult time. Also urge your family to accept help if it's needed. A cancer diagnosis affects the entire family. It also adds stress, especially to the ones who take care of you. Accepting help with meals or chores from neighbors or friends can help your loved ones from feeling burned out. Review your goals and priorities Figure out what's really important in your life. Find time for the activities that are most important to you and give you the most meaning. Check your calendar and cancel activities that don't meet your goals. Try to be open with your loved ones. Share your thoughts and feelings with them. Cancer affects all of your relationships. Communication can help lower the anxiety and fear that cancer can cause. Try to maintain your lifestyle Keep your lifestyle, but be open to changing it. Take one day at a time. It's easy to forget to do this during stressful times. When the future is not sure, organizing and planning may suddenly seem like too much work. Consider how your diagnosis will impact your finances Many unexpected financial issues can happen after a cancer diagnosis. Your treatment may require time away from work or home. Consider the costs of medicines, medical devices, traveling for treatment, and parking fees at the hospital. Many clinics and hospitals keep lists of resources to help you financially during and after your cancer treatment. Talk with your healthcare team about your options. Questions to ask include: Will I have to take time away from work? If I do, what will happen to my benefits? Will my friends and family need to take time away from work to be with me? Will my insurance pay for these treatments? ( Natural vs Clinical ) Will my insurance cover the cost of medicines? How much will I have to pay? If insurance won't pay for my treatment, are there programs that can help? Do I qualify for disability benefits? How does my diagnosis affect my life insurance? Who do I call to talk about what my insurance will cover? Talk to other people with cancer It can be hard for people who have not had cancer to understand how you're feeling. It may help to talk to people who have been in your situation. Other cancer survivors can share their experiences. They can tell you what to expect during Clinical vs Natural treatment . Talk to a friend or family member who has had cancer. Or connect with other cancer survivors through support groups. Ask your healthcare provider about support groups in your area. Online message boards also bring cancer survivors together. Reach out to friends or neighbors who have had a serious illness. Ask them how they dealt with these complex issues. Fight stigmas Some old stigmas about cancer still exist. Your friends may wonder if your cancer is contagious. Co-workers may doubt you're healthy enough to do your job. Some may avoid you because they're afraid to say the wrong thing. Many people will have questions and concerns. Determine how you'll deal with others. In general, others will follow what you do. Remind friends that cancer shouldn't make them afraid to be around you. Develop your own ways to deal with cancer Just as each person's cancer treatment is different, so are the ways of dealing with cancer. Ideas to try: Practice ways to relax. Share your feelings honestly with family, friends, a spiritual adviser, or a counselor. Keep a journal to help organize your thoughts. When faced with a difficult decision, list the pros and cons of each choice. Find a source of spiritual support. Set aside time to be alone. Remain involved with work and leisure activities as much as you can. Be ready to say no. This is the time to focus on you. What helped you through rough times before your cancer diagnosis can help ease your worries now. This may include a close friend, a religious leader, or a favorite activity. Turn to these comforts now. Also, be open to trying new ways to deal with your cancer. Learning that you have cancer can be hard. Some people say they felt anxious, afraid, or overwhelmed when they were first diagnosed. If you aren't sure what to do to cope, here are 11 ideas to help you deal with a cancer diagnosis. Get the facts about your cancer diagnosis Try to get as much basic, useful information as you can. This will help you to make decisions about your care. Write down your questions and concerns. Bring them with you when you see your healthcare provider. You may ask: What kind of cancer do I have? Where is the cancer? Has it spread? Can my cancer be treated? What is the chance that my cancer can be cured? What other tests or procedures do I need? What are my treatment options? How will the treatment benefit me? What can I expect during treatment? What are the side effects of the treatment? When should I call my healthcare provider? What can I do to prevent my cancer from coming back? How likely are my children or other family members to get cancer? What happens if I don't get treatment? Consider bringing a family member or friend with you to your first few appointments. They can help you remember what you hear. Think about how much you want to know about your cancer. Some people want all the facts and details. This helps them be part of the decision-making process. Others want to learn the basics and leave details and decisions to their healthcare providers. Think about which works best for you. Let your healthcare team know what you'd like. Keep the lines of communication open Have honest, two-way communication with your loved ones, healthcare providers, and others. You may feel alone if people try to protect you from bad news by not talking about it. Or you might feel alone or less supported if you try to look strong and not share your feelings. If you and others show your real emotions, you can help support each other. Anticipate possible physical changes The best time to plan for changes to your body is right after your cancer diagnosis and before you begin treatment. Prepare yourself now so that you'll be able to deal with everything later. Ask your healthcare provider what may change. Medicines may make you lose your hair. Advice from experts about clothing, makeup, wigs, and hairpieces may help you feel more comfortable and attractive. Insurance often helps pay for wigs and other devices to help you adapt. Consider joining a cancer support group. Members can provide tips that have helped them and others. Also, think about how treatment will affect your daily life. Ask your provider whether you will be able to continue your usual routine. You may need to spend time in the hospital or have many medical appointments. If your treatment will make it hard to perform your daily duties, make arrangements for this. Plan for your finances. Figure out who will do routine household chores. If you have pets, ask someone to take care of them. Maintain a healthy lifestyle A healthy lifestyle can improve your energy level. Choose a healthy diet and get enough rest. These tips will help you manage the stress and fatigue of cancer and its treatment. If you can, have a consistent daily routine. Make time each day to exercise, get enough sleep, and eat meals. Exercise and participating in activities that you enjoy also may help. People who get exercise during treatment not only deal better with side effects but also may live longer. Let friends and family help you Your friends and family can run errands, take you to appointments, prepare meals and help you with household chores. This can give those who care about you a way to help during a difficult time. Also urge your family to accept help if it's needed. A cancer diagnosis affects the entire family. It also adds stress, especially to the ones who take care of you. Accepting help with meals or chores from neighbors or friends can help your loved ones from feeling burned out. Review your goals and priorities Figure out what's really important in your life. Find time for the activities that are most important to you and give you the most meaning. Check your calendar and cancel activities that don't meet your goals. Try to be open with your loved ones. Share your thoughts and feelings with them. Cancer affects all of your relationships. Communication can help lower the anxiety and fear that cancer can cause. Try to maintain your lifestyle Keep your lifestyle, but be open to changing it. Take one day at a time. It's easy to forget to do this during stressful times. When the future is not sure, organizing and planning may suddenly seem like too much work. Consider how your diagnosis will impact your finances Many unexpected financial issues can happen after a cancer diagnosis. Your treatment may require time away from work or home. Consider the costs of medicines, medical devices, traveling for treatment, and parking fees at the hospital. Many clinics and hospitals keep lists of resources to help you financially during and after your cancer treatment. Talk with your healthcare team about your options. Questions to ask include: Will I have to take time away from work? If I do, what will happen to my benefits? Will my friends and family need to take time away from work to be with me? will my insurance pay for these treatments? Will my insurance cover the cost of medicines? How much will I have to pay? If insurance won't pay for my treatment, are there programs that can help? Do I qualify for disability benefits? How does my diagnosis affect my life insurance? Who do I call to talk about what my insurance will cover? Develop your own ways to deal with cancer Just as each person's cancer treatment is different, so are the ways of dealing with cancer. Ideas to try: Practice ways to relax. Share your feelings honestly with family, friends, a spiritual adviser, or a counselor. Keep a journal to help organize your thoughts. When faced with a difficult decision, list the pros and cons of each choice. Find a source of spiritual support. Set aside time to be alone. Remain involved with work and leisure activities as much as you can. Be ready to say no. This is the time to focus on you. What helped you through rough times before your cancer diagnosis can help ease your worries now. This may include a close friend, a religious leader, or a favorite activity. Turn to these comforts now. Also, be open to trying new ways to deal with your cancer. Mayo Clinic Above all else explore Natural Treatments. Personally I would rather enjoy a quality of life many traditional treatments for cancer will rob from you. Chemotherapy, while affecting some people more than others is usually pretty hard on a person, and nausea, vomiting, hair loss, infections, and tiredness are common. The drugs they use are NOT selective and do kill healthy cells just as readily as they do cancer cells, and this is something that natural treatments do not do. natural treatments are usually readily available in North America and vary depending on which country you live in. Natural treatments are cheaper by far than traditional treatments and other than a rare allergy in some people they are very well tolerated. These are personal choices of course so do your research. I have given an impressive list of natural cancer treatments and in the Ivermectin, Fenbendazole, Mebendazole, and Hydroxychloroquine treatments I have linked to Research studies showing their efficacy and by viewing these studies in full you are presented with an extensive list of citations to studies that also reference them.

NIH Article Historically, pandemics were often interpreted as something more significant than microbes as viruses or bacteria—many cultures viewed them as manifestations of moral failings. The Black Death, known as “The Great Mortality,” killed an estimated 15 million people between 1347 and 1350. It is rated as the worst pandemic recorded of plagues in human history. At the time, the Black Death was seen as a warning of God's wrath for man's moral corruption. As recorded in the book, “The Great Mortality,” one of the most widely circulated public documents—a Heavenly Letter–during the Black Death period, read, “O ye of little faith ... Ye have not repented of your sins ... therefore I have sent against you the Saracens and heathen people, earthquake, famine, beasts ...” Christians were persecuted throughout the Roman Empire two millennia earlier, beginning in the 1st century A.D. In 64 A.D., Roman emperor Nero initiated a brutal persecution of Christians, wrongly blaming them for a catastrophic fire in Rome. He inflicted severe torture, using Christians as prey for wild beasts and burning them alive as human torches. Over time, 10 Roman emperors, from Nero, Domitian, Trajan, to Diocletian, continued this persecution, with the most severe persecution occurring under Diocletian’s reign from 303 to 312 A.D. According to historical records, Ancient Rome was frequently plagued by pandemics, with roughly one significant disease outbreak occurring every 10 to 20 years. One of the biggest pandemics, “The Antonine Plague,” began in 165 A.D. The pandemic was reported to be smallpox, and it contributed to the empire’s decline. When comparing COVID-19 with the historical plagues in Rome, similarities appear. The COVID-19 pandemic occurred in 2019 when the Chinese regime was not only cracking down on Christian churches and believers but also continuing the 25-year-long persecution of Falun Gong, a traditional belief counting 100 million adherents based on moral values of truthfulness, compassion, and forbearance. Like Christianity and other religious belief systems, Falun Gong is based on moral values of truthfulness, compassion, and forbearance. Ever since the CCP took rule of the Chinese mainland in 1949, the totalitarian government has rid people of their freedom of spiritual belief and violated their basic human rights. Independent investigations have revealed that the Chinese regime has been killing prisoners of conscience, primarily Falun Gong practitioners, and forcibly harvesting their organs—in many cases—these horrors occur while they are still alive. The location where COVID-19 originated from and hit most severely is China, suggesting the main issue is closely linked with China. Black plague

Epoch Health Article Stevia has recently become one of the most popular natural sugar substitutes. Sugar is known to raise blood sugar levels, but stevia can actually lower them. In fact, it was even used to treat diabetes in ancient times. Stevia is also known as honey leaf, sweet leaf, or sweet herb. According to a paper published in Nutrition Today, it belongs to the sunflower (Asteraceae) family and is native to southern Brazil and northern Paraguay. The indigenous Guaraní people have been using stevia to sweeten their food and beverages for centuries. According to a 2019 meta-analysis published in Nutrients, they have also used it for medicinal purposes, such as treating diabetes. Stevia’s sweetness mainly comes from steviol glycosides, which are about 200 to 300 times sweeter than sucrose. High-purity stevia extracts contain 95 percent or more steviol glycosides, according to the Nutrition Today paper. A 2023 study published in Molecules found eight different types of steviol glycosides that occur naturally in stevia leaves, with stevioside being the most abundant. Because of its commercial potential and pharmacological properties, stevia has attracted widespread attention from the food and scientific community. As a result, stevia plantations can now be found in many regions around the world. Stevia’s glycemic index (GI) and calorie content are zero (pdf). The glycemic index measures how quickly and to what extent a food increases blood sugar levels, also called blood glucose levels, with glucose being the standard at a GI value of 100. Modern research has found that stevia exhibits anti-diabetic activity. Stevia not only increases insulin secretion and activity but also reduces insulin resistance. It also inhibits or reduces the liver’s production of glucose, which helps maintain healthy blood sugar levels. Additionally, the stevioside and steviol found in stevia help to regulate the activity of certain enzymes, preventing blood sugar from dropping too low and causing hypoglycemia. Researchers from the University of Florida conducted an experiment in which 31 adult participants fasted for 12 hours and ate the same breakfast. Twenty minutes before lunch and dinner, they were given tea and snacks containing sucrose, aspartame, or stevia, without knowing which type of sugar they were ingesting. They were then free to eat lunch and dinner as they wished. Their hunger and satiety levels were evaluated hourly, and blood tests were conducted. All participants completed three days of food tests.  The results showed that participants who consumed stevia had significantly lower blood sugar levels right after lunch than those who consumed sucrose, and they had no significant fluctuations. “It would suggest that compared to other types of sweeteners, stevia could be beneficial in helping people keep their glucose levels under control or in a healthy range after eating,” study co-author Stephen Anton, a professor in the Department of Physiology and Aging at the University of Florida who has a doctorate in clinical and health psychology, told The Epoch Times. “Compared to sucrose and aspartame, stevia could lead to better post-meal metabolic states.” Moreover, participants who consumed stevia and aspartame had a significantly lower total caloric intake. Although participants who consumed stevia before meals didn’t obtain calories from it, they didn’t compensate for the calorie difference by consuming more during lunch or dinner compared with those who consumed high-calorie sucrose. Furthermore, their satiety levels were similar. A randomized, controlled trial on diabetic patients published in the Journal of the Science of Food and Agriculture in 2016 further demonstrated the blood sugar-lowering effect of stevia. Twenty patients with Type 2 diabetes were randomly divided into two groups, one taking 1 gram of dried stevia leaf powder daily and the other not taking any. The experiment was conducted over 60 days. The results showed that taking dried stevia leaf powder significantly reduced the fasting and postprandial blood sugar levels of these diabetic patients. “I see that using stevia as a sugar substitute can bring about a huge change,” said Per Bendix Jeppesen, an associate professor in the department of endocrinology and diabetes at Aarhus University in Denmark who is currently studying stevia extract as an anti-diabetic drug and as a healthy sweetener. “It is a game changer,” he told The Epoch Times. That’s because the main component of stevia has positive effects on the human endocrine system, especially for people with diabetes. In addition to studying stevia’s effectiveness and extraction techniques, Mr. Jeppesen is involved in related experiments on anti-diabetic drugs. Modern people tend to engage in too little physical activity, consume too much food, and eat diets that are high in sugar and fat. “Stevia could be a very good substitute for the sugar that we are consuming too much of,” Mr. Jeppesen said. “By adding stevia, it could really enhance public health, as the calorie intake would decrease when we consume less sugar.” Effects on Metabolism, Blood Pressure, and Blood Lipids In addition to controlling postprandial blood sugar and other anti-diabetic effects, stevia can lower blood pressure and blood lipids. Steviol glycosides found in stevia can regulate the level of calcium in the blood, which can lead to vasodilation and reduced arterial contraction, both of which contribute to lowering blood pressure, according to the 2023 Molecules study. Researchers in Taiwan conducted a randomized, double-blind, placebo-controlled trial on hypertensive patients in which 174 hypertensive patients were divided into two groups. One group took steviol glycoside capsules three times a day, each containing 500 milligrams of steviol glycoside, while the other group took a placebo. Two years later, those who took steviol glycoside showed significant improvements in their blood pressure. Their systolic blood pressure decreased from an average of 150 to 140 mm Hg, and their diastolic blood pressure decreased from an average of 95 to 89 mm Hg. Notably, the beneficial effects of steviol glycosides on hypertensive patients were observed approximately one week after the start of the experiment and continued throughout the entire study. Additionally, the group taking steviol glycosides had significantly improved overall quality of life scores, as measured by a survey. The Nutrients meta-analysis included seven studies and nine randomized controlled trials involving 462 participants. The analysis revealed that compared with taking a placebo, steviol glycosides significantly reduced systolic blood pressure by 6.32 mm Hg and diastolic blood pressure by 3.6 mm Hg. Additionally, there were nonsignificant reductions in body mass index, fasting blood sugar, and total cholesterol. Stevia can also lower blood lipids. A review study showed that consuming stevia extract can significantly increase the level of high-density lipoprotein (“good” cholesterol) and reduce the levels of total cholesterol, triglycerides, and low-density lipoprotein (“bad” cholesterol). Anti-Inflammatory and Antioxidant Properties Stevia contains more than 100 compounds, many of which benefit our health. In addition to natural sweeteners and various trace elements, stevia contains terpenes, sterols, tannins, volatile acids, flavonoids, vitamins, enzymes, organic acids, and polysaccharides, all of which have biological activity. According to the Molecules study, steviol glycosides have been found to suppress and control factors that trigger cell inflammation. They also play a protective role in the liver by preventing inflammation and have been shown to enhance the body’s innate immune system. In addition, steviol glycosides exhibit antioxidant properties. The study published in Molecules in 2023 demonstrated that they can protect heart cells from damage caused by hydrogen peroxide, resulting in increased vitality and improved antioxidant capacity. They can also prevent oxidative DNA damage in the liver and kidneys. Minimal Side Effects According to a paper published in the Experimental and Clinical Sciences (EXCLI) Journal, Paraguayans have been consuming stevia continuously for more than 1,500 years with almost no adverse effects reported. Additionally, a review study indicates that most reports on stevia consumption don’t suggest any adverse events. According to the U.S. Food and Drug Administration (FDA), highly purified steviol glycosides are generally recognized as safe (GRAS). But stevia leaf and crude stevia extract are not considered GRAS “due to inadequate toxicological information.” They are subject to food additive regulations, not dietary ingredients and dietary supplements, FDA said. In other countries like Japan, Australia, and Brazil, stevia leaf-derived products are approved for use as sweeteners in food. They are used in a variety of foods, including teas.  The acceptable daily intake of steviol glycosides, as defined by the U.S. Food and Drug Administration and the European Food Safety Authority, is 4 mg per kg body weight, or about 1.8 mg per pound. Mr. Jeppesen stated that these agencies took more than 10 years to conduct rigorous evaluations before listing stevia as a food additive. However, stevia extracts has been widely used as a sweetener in Japan since the 1980s. An earlier rat study mentioned in the EXCLI Journal suggested that stevia might affect the fertility of experimental animals. However, Mr. Jeppesen said that the final results of these studies generally weren’t accepted. How to Choose Stevia Sweetener Despite stevia’s benefits, not all stevia products available for sale are high quality. Some products have been found to contain artificial sweeteners sodium saccharin and sodium cyclamate. In addition, crude stevia extracts may have a higher allergenic potential than high-purity stevia sweeteners containing at least 95 percent of steviol glycosides.  Because stevia is so sweet, most stevia products found in supermarkets are blended formulas. Steviol glycosides generally account for only about 1 percent of powdered products, while the remaining ingredients are usually sugar alcohols such as erythritol and xylitol. Certain products may also contain a combination of steviol glycosides and cane sugar or raw sugar. Liquid-based stevia products mainly contain water and may also contain some preservatives such as alcohol. Colorless and transparent products are formulated using steviol glycosides as raw materials; products that are green in color are more likely to be directly extracted from the stevia plant. Mr. Jeppesen recommended choosing products that combine soluble fiber and steviol glycosides for a calorie-free sweet taste and additional fiber intake. Also, the application and preparation methods of these products are similar to those of sugar, making them a practical alternative for use in cooking. Some stevia products have a metallic or bitter taste from the stevioside compound. Mr. Jeppesen said that the taste of steviol glycoside products would continue to improve as extraction technology advances. In fact, the aftertaste of metallic or bitter flavors can now be eliminated. In the future, there will be more and more steviol glycoside products available to choose from.

Healthline Article Purpose of review This article recounts the history of the diet-heart hypothesis from the late 1950s to the current day, with revelations that have never been published in the scientific literature. Insights include the role of authorities in launching the diet hypothesis, including a potential conflict of interest for the American Heart Association; several crucial details regarding studies considered influential to the hypothesis; irregularities in the scientific reviews on saturated fats, for both the 2015 and 2020 Dietary Guidelines for Americans; and possible conflicts of interest on the relevant subcommittee reviewing saturated fats for the 2020 Dietary Guidelines Advisory Committee. Information obtained via the Freedom of Information Act (FOIA) on emails from the 2015 process is published here for the first time. These findings are highly relevant to the 2025–2030 Dietary Guidelines process, now underway, which has plans for a new review on saturated fats. Recent findings Recent findings include shortcomings in the scientific review processes on saturated fats, for both the current 2020–2025 Dietary Guidelines for Americans and the previous edition (2015–2020). Revelations include the fact the 2015 Advisory Committee acknowledged, in an e-mail, the lack of scientific justification for any specific numeric cap on these fats. Other, previously unpublished findings include significant potential financial conflicts on the relevant 2020 guidelines subcommittee, including the participation of plant-based advocates, an expert who promotes a plant-based diet for religious reasons, experts who had received extensive funding from industries, such as tree nuts and soy, whose products benefit from continued policy recommendations favoring polyunsaturated fats, and one expert who had spent more than 50 years of her career dedicated to ‘proving’ the diet-heart hypothesis. Summary The idea that saturated fats cause heart disease, called the diet-heart hypothesis, was introduced in the 1950s, based on weak, associational evidence. Subsequent clinical trials attempting to substantiate this hypothesis could never establish a causal link. However, these clinical trial data were largely ignored for decades, until journalists brought them to light about a decade ago. Subsequent re-examinations of this evidence by nutrition experts have now been published in >20 review papers, which have largely concluded that saturated fats do not affect cardiovascular disease, cardiovascular mortality, or total mortality. The current challenge is for this new consensus on saturated fats to be recognized by policymakers, who, in the United States, have shown marked resistance to the introduction of the new evidence. In the case of the 2020 Dietary Guidelines, experts have been found even to deny their evidence. The global re-evaluation of saturated fats that has occurred over the past decade implies that caps on these fats are not warranted and should no longer be part of national dietary guidelines. Conflicts of interest and longstanding biases stand in the way of updating dietary policy to reflect the current evidence. Keywords:  dietary guidelines, food policy, polyunsaturated fats, saturated fats INTRODUCTION The concept that saturated fat causes cardiovascular disease by raising serum cholesterol is called the ‘diet-heart hypothesis’, a highly influential idea that has been a lynchpin of nutrition policy for some 60 years. This hypothesis remains today a foundation of public health policy, with nearly all dietary guidelines worldwide recommending a cap on saturated fat consumption as a primary measure of protection against heart disease. Over the past 12 years, however, there has been a major shift in scholarly understanding of these fats, with now >20 review papers, by independent teams of scientists, on the whole concluding that saturated fats do not affect major cardiovascular outcomes, including heart attacks, strokes or cardiovascular mortality, or total mortality. National dietary guidelines have not recognized this new thinking on saturated fats, however, and continue to promote policies based on outdated or insufficient evidence.  KEY POINTS HISTORICAL PERSPECTIVE ON DIETARY SATURATED FAT The diet-heart hypothesis was first proposed in the 1950s by Ancel Keys, a physiologist at the University of Minnesota with an interest in nutrition. Keys based his idea on a handful of small feeding experiments conducted on humans together with some animal data suggesting that high blood cholesterol caused fatty deposits of the type thought to clog arteries and cause heart attacks. Keys had further observed, on travels through post-War Europe, that less wealthy populations in Sardinia, Naples, and Spain, appeared to suffer lower rates of heat attacks while consuming diets low in saturated fat-rich foods, such as meat and dairy. Keys postulated that saturated fat and cholesterol caused heart disease – his diet-heart hypothesis – whose claims he asserted in no fewer than 20 papers in 1957 and 1958. Keys has been widely described by his colleagues as having a highly persuasive, even aggressive, personality, and these attributes may have in part allowed him to ensure that his idea edged out competing hypotheses to become the dominant paradigm explaining cardiovascular disease for the next 70 years. One authority whom Keys successfully won over was Paul Dudley White, an influential cardiologist and the personal doctor for President Dwight D. Eisenhower. When Eisenhower suffered the first of several heart attacks, in September 1955, Keys’ ideas were elevated by White into the national spotlight. With the President hospitalized, the nation became laser-focused on the question of what caused heart disease, a relatively new and terrifying condition that had been rare in the early 1900s yet had risen by the 1950s to become the country's leading cause of death. White made it clear that diet was to blame. Under his guidance, Eisenhower undertook a new regimen, low in cholesterol and saturated fats. As charted in news headlines across the nation, Eisenhower shunned butter for polyunsaturated margarine and ate melba toast for breakfast. The second authority that came to adopt the diet-heart hypothesis was ultimately more enduring in its influence. This was the American Heart Association (AHA), the nation's largest nonprofit organization and long a respected leader in the field of heart disease. White had been an AHA founder, and Eisenhower hosted fundraisers for the group in the White House. Throughout the 1950s, the AHA had resisted giving advice on heart disease prevention, citing a lack of evidence, yet in 1960, Keys was appointed to the group's nutrition committee, and one year later, although no greater evidence could be cited, he had convinced his colleagues to recommend his idea as official AHA policy. Thus, from 1961 on, the AHA recommended that all men (and subsequently women) decrease their consumption of saturated fat, replacing these fats whenever possible with polyunsaturated vegetable oils, as the most promising measure of protection against heart disease. The 1961 AHA advice to limit saturated fat is arguably the single most influential nutrition policy ever published, as it came to be adopted first by the U.S. government, as official policy for all Americans, in 1980, and then by governments around the world as well as the World Health Organization. It is worth noting that the AHA had a significant conflict of interest, since in 1948, it had received $1.7 million, or about $20 million in today's dollars, from Procter & Gamble (P&G), the makers of Crisco oil. This donation was transformative for the AHA, propelling what was a small group into a national organization; the P&G funds were the ‘bang of big bucks’ that ‘launched’ the group, according to the organization's official history. Vegetable oils such as Crisco have reaped the benefits of this recommendation ever since, as Americans increased their consumption of these oils by nearly 90% from 1970 to 2014. THE SEVEN COUNTRIES STUDY The Seven Countries Study (SCS), led by Keys, was for many decades considered the bedrock data for the diet-heart hypothesis. Launched in 1957, the study was larger and more ambitious than any U.S. nutrition study to date. By 2004, according to one estimate, SCS had already been cited more than one million times. The SCS followed some 12 770 men in 16 locations within seven countries, including Italy, Greece, Yugoslavia, Finland, the Netherlands, the United States, and Japan. Keys, due to his worldwide travels, knew that choosing these countries was likely to confirm his hypothesis. He did not include, for instance, places like Germany, Switzerland, and France, where people ate a great deal of saturated fat yet experienced rates of heart disease similarly low to those included in the SCS. Keys’ selection of nations has given rise to the critique that he ‘cherry-picked’ countries to ‘prove’ his hypothesis. While defenders of the SCS have attempted to dismiss this allegation], it remains true that Keys used a non-random approach for the selection of countries in SCS, allowing for the introduction of bias. In 1975, when Keys published his results in a special issue of an AHA journal, he found as he had hoped: a strong correlation between the consumption of saturated fat and deaths from heart disease. The SCS was a groundbreaking study in its scope: one of its accomplishments was simply to demonstrate that people living in different nations really did suffer vastly different rates of heart attacks and that therefore the disease could potentially be prevented. Subsequent analyses of the SCS have found numerous shortcomings in the data, however. For instance, Keys sampled dietary data from only 3.9% of the men, which is fewer than 500 total participants, or about 30 per location. Further, he used unvalidated and non-standardized methods of dietary evaluation that differed across groups. On Crete, one of the dietary samples was taken during the period of Lent, which was strictly observed under the Greek Orthodox church and would have banned ‘all animal foods. Saturated fats were therefore very likely undercounted in this population, yet Keys downplayed this issue in his report and concluded that the excellent health of the Cretans could be credited to their low consumption of these fats. The failure to adjust for the Lent data was a ‘remarkable and troublesome omission,’ wrote researchers in  Public Health Nutrition  in 2005, yet this analysis took place long after the diet-heart hypothesis had become solidified as public policy. In 1989, a re-analysis of the SCS data by some of the original study researchers found that coronary mortality best correlated not with saturated fats, as originally reported, but with ‘sweets,’ defined as sugar products and pastries. Possibly the correlation would have been even stronger if the ‘sweets’ category had included chocolate, ice cream, and soft drinks, but researchers said data on these items were too difficult to combine. Ultimately, the principal limitation of the SCS data was that they could only show an association, not a cause-and-effect relationship. The results of the SCS have never been independently analyzed, and most subsequent studies using similar approaches have failed to confirm its conclusions, as described below. STUDIES ON SATURATED FATS Governments around the world, including the United States, Norway, Finland, and Australia, among other countries, recognized the need for more rigorous, clinical trial data that could establish a causal relationship between saturated fat and heart disease. Large, randomized, controlled clinical trials (RCTs) were undertaken in the 1960s and 1970s, in which saturated fats were replaced by polyunsaturated fats from vegetable oils. Altogether, these ‘core’ trials tested the diet-heart hypothesis on about 67,000 people and were especially important, because they assessed long-term clinical outcomes, that is, ‘hard endpoints,’ such as heart attacks and death. These outcomes are considered more reliable for making public health policy compared to studies that use ‘intermediary endpoints,’ such as cholesterol or inflammatory measures, whose value for predicting cardiovascular events is disputed. These trials provided surprisingly little support for the diet-heart hypothesis. Dramatic reductions in the consumption of saturated fats had successfully lowered the participants’ cholesterol, by an average of 29 mg/dl, ‘indicating a high level of compliance’ among subjects, according to one analysis, yet the expected reductions in either cardiovascular or total mortality were not observed in most trials. In other words, although diet could successfully lower blood cholesterol, this reduction did not appear to translate into long-term cardiovascular gains. By the time these results emerged, however, Keys’ hypothesis had already gained widespread acceptance among his colleagues, including, importantly, leadership at the National Institutes of Health (NIH). By the late 1960s, a bias in favor of the diet-heart hypothesis was strong enough that researchers with contrary results found themselves unable or unwilling to publish their results. For instance, the largest test of the diet-heart hypothesis, the Minnesota Coronary Survey, involving 9057 men and women over 4.5 years, tested a diet of 18% saturated fat against controls eating 9%, yet did not find any reduction in cardiovascular events, cardiovascular deaths, or total mortality. Although the study had been funded by the NIH, the results were not published for 16 years, after the principal investigator, Ivan Frantz, had retired. Frantz is reported to have said that there was nothing wrong with the study; ‘We were just disappointed in the way it came out’. Frantz's decision not to publish his results on time resulted in these contradictory data not being considered for another 40 years. Other results that went unpublished were from one of the most famous heart disease investigations ever undertaken, the Framingham Heart Study, begun in 1948. Vanderbilt University professor George Mann led a dietary investigation, collecting detailed food-consumption data from 1049 subjects. When he calculated the results in 1960, it was very clear that saturated fat was  not  related to heart disease. Concerning the incidence of coronary heart disease and diet, the authors concluded, simply, ‘No relationship found’. However, not until 1992 did a Framingham study leader publicly acknowledge the study's findings on fat. ‘In Framingham, Mass, the more saturated fat one ate. … the  lower  the person's serum cholesterol… and [they] weighed the  least ,’ wrote William P. Castelli, one of the Framingham directors, in an informal commentary. As a consequence of the nonpublication or disregard of study findings contrary to the diet-heart hypothesis, the idea that saturated fat had possibly been unduly vilified for decades not seriously considered by most nutrition experts. RECONSIDERATION OF THE TRIALS ON SATURATED FATS Reviews and books critical of the diet-heart hypothesis were not unknown in the 1960s and 1970s, including a publication by a former editor of the  Journal of the American Heart Association  and articles by other prominent scientists. They argued that the hypothesis was not supported by the available data and was contradicted by numerous observations. Over time, however, these critics were effectively marginalized and silenced. Not until the 2000s did this science again come to light, mainly through the work of journalist Gary Taubes. The first comprehensive compilation of arguments about why saturated fats are not bad for health was published by this author, also a journalist. The earliest formal analyses of the early data on saturated fats were led by Ronald M. Krauss, a cardiologist and nutrition expert, and published in two papers in the  American Journal of Clinical Nutrition  in 2010. Krauss experienced formidable hurdles in the peer-review process, evidently due to widespread resistance to re-evaluating a long-standing hypothesis. A colleague of Keys attempted to rebut these papers, yet soon thereafter, other scientists joined Krauss in reassessing the same data. Results from the core trials have now been analyzed extensively by scientists worldwide, including by the prestigious Cochrane group, most recently in 2020. Altogether, >20 review papers, including umbrella reviews, have been published, with the vast majority concluding that the data from randomized, controlled trials do not provide consistent or adequate evidence for continued recommendations limiting the intake of saturated fat. A few reviews have had findings to the contrary, yet these have mainly been explained by the inclusion of one trial, called the Finnish Mental Hospital Study, which lacked proper randomization, among other problems, and was therefore excluded in more recent reviews. The finding in Cochrane 2020 of an effect on cardiovascular events disappeared when subjected to a sensitivity analysis inside the report, in which studies that had not successfully reduced saturated fats were excluded. Reviews that have focused on LDL-cholesterol have ignored the far more definitive, long-term outcomes of cardiovascular events and mortality. Overall, therefore, despite extensive testing of the diet-heart hypothesis, the data do not support continued advice to restrict these fats for the prevention of heart disease. The findings from observational or epidemiological studies constitute less robust data since these studies are usually limited to demonstrating associations rather than cause-and-effect relationships. However, substantial epidemiological findings that contradict a hypothesis provide reasonable evidence that the hypothesis may be in error. Data from the largest epidemiological cohort study ever conducted, called Prospective Urban Rural Epidemiology (PURE), provides this type of contradictory evidence regarding the diet-heart hypothesis. PURE followed individuals aged 35–70 years, from 2003 to 2013, in 18 countries with a median follow-up of 7 4 years. The PURE investigators found that saturated fat was not associated with the risk of myocardial infarction or cardiovascular disease mortality and was significantly associated with lower total mortality as well as lower risk of stroke. This last finding, on stroke, is particularly significant, as it is consistent with other observational studies, and saturated fat is the only type of fat found to have a positive effect on this important cardiovascular health outcome. Further, nine reviews of the observational data conducted since 2010 have found no significant associations between the consumption of these fats and coronary heart disease. Epidemiological data of this quality and magnitude meaningfully contribute to the understanding of the relationship between saturated fats and cardiovascular disease. These data reinforce the findings from the more rigorous, clinical trial data, described above. Despite these extensive findings disproving a relationship between saturated fats and heart disease, speculation about the diet-heart hypothesis continues. For instance, the AHA journal  Circulation  published findings of an association between linoleic fatty acid, a prominent component of vegetable oils, and a lower incidence of cardiovascular events and mortality. However, this finding is based on nonstandardized, country-level (ecological) data, which is generally regarded to be among the lowest-quality types of evidence. U.S. DIETARY GUIDELINES ON SATURATED FATS The U.S. government was the first in the world to recommend saturated fat restriction. The United States Senate Select Committee on Nutrition and Human Needs published the Dietary Goals for the United States in 1977, which recommended that the public ‘reduce saturated fat consumption to account for about 10% of total energy intake. The report was heavily influenced by experts from the AHA and was written by a single Senate staffer with no background in science or nutrition. An early draft of the report further recommended that people ‘decrease consumption of meat,’ based on its saturated fat content. This advice was revised to read: ‘choose meats … which will reduce saturated fat intake’, leading to an emphasis in favor of ‘lean meat.’ Some observers have interpreted this revision to be exclusively due to the interference of the meat industry, yet a 2014 article in the  American Journal of Public Health  that examined the Senate committee process in detail concludes that ‘a lack of scientific consensus was the principal reason for the change in language on meat. This latter interpretation also reflects the absence of rigorous data linking saturated fats to heart disease, as described above. The Dietary Goals led to the establishment of a policy, co-issued by the U.S. Departments of Agriculture and Health and Human Services (USDA-HHS), called the Dietary Guidelines for Americans (DGA), first published in 1980 and every 5 years since. The inaugural edition of the guidelines included advice to ‘Avoid too much fat, saturated fat, and cholesterol’ but did not include a specific numerical cap on saturated fats. The 1990 guidelines and all subsequent editions have included the target of limiting these fats to 10% of total calories or less. According to U.S. law, the DGA must reflect ‘the preponderance of the scientific and medical knowledge which is current at the time the report is prepared’. The subject of saturated fats presents a unique difficulty, however, since the original core trials concluded before the guidelines began. A review of all the DGA expert reports found that none of the expert committees appointed to review the science for each new edition of the guidelines had ever undertaken a direct, systematic review of these core trials on saturated fats. The guidelines had simply inherited the widely held view that saturated fats were linked to cardiovascular disease without its novel review of the science. A growing awareness of the core trials from the year 2010 onwards should arguably have spurred one of the subsequent Dietary Guidelines Advisory Committees (DGACs) to initiate a systematic review of these major trials, yet none has occurred. The 2015 DGAC decided at a late stage in the DGA process to undertake a new review of saturated fats, in response to the publication of a review paper on this topic, with authors including professors from Cambridge and Harvard Universities, and a prominent article in the  Wall Street Journal  on the same topic. Both publications suggested a lack of evidence linking saturated fats to heart disease. The DGAC's decision to initiate a review of saturated fats was revealed in emails obtained through a request made under the Freedom of Information Act and reflects a discomfort among some DGAC members that these publications ‘contradict[ed] the AHA conclusions’ on saturated fats. DGAC Vice-Chair, Alice Lichtenstein, a Tufts University scientist who had also twice chaired the AHA nutrition committee, suggested in an E-Mail to other DGAC members that they set a numerical cap on saturated fats, even though, she wrote, ‘There is no magic/data for the 10% number or 7% number that has been used previously’. The 2015 DGAC analysis of saturated fats resulting from this e-mail exchange was a narrative, nonsystematic review of seven external review papers. Two analyses of this 2015 DGAC review found it to have omitted at least one paper with null findings on saturated fat while inappropriately including other papers that supported advice to promote vegetable oils over saturated fats. In one instance, the DGAC included a paper that looked exclusively at linoleic acid, not saturated fats. In another instance, a review paper was included that relied heavily on the Finnish Mental Hospital Study, whose data, for reasons discussed above, had been deemed unreliable. The result was a DGAC review that did not provide a balanced or thorough evaluation of the external review papers current at the time the 2015 report was prepared. The 2015 DGAC concluded that the evidence for a relationship between saturated fats and heart disease was ‘strong.’ For the 2020 guidelines, the DGAC also conducted a review of saturated fats. A recent analysis of the studies included in this review found that 88% did  not  support a link between these fats and heart disease. Due to a new rule introduced by the USDA for this guidelines process, the 2020 DGAC was not allowed to examine external review papers and was therefore unable to consider any of the approximately 20 review papers described above. Top experts in the field attempted to introduce this evidence via written comments submitted formally to the USDA, in addition to meeting with the relevant senior staff members at both HHS and USDA and submitting a letter to members of Congress. Among the external review papers was now a 2021 ‘State of the Art Review,’ in the highly regarded  Journal of the American College of Cardiology , whose authors included 4 members of previous DGACs, and which found that there is ‘no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent cardiovascular disease or reduce mortality.’ The paper was named one of the top 100 articles of 2021 by the journal's editor-in-chief, yet this and other reviews were ultimately not considered in the 2020 DGAC review on saturated fats. The DGAC final report makes no mention of any shift in scientific thinking on these fats and concludes that the evidence linking them to heart disease is ‘strong.’ An analysis of the 2020 DGAC subcommittee in charge of the saturated fat review found numerous intellectual, financial, and even religious conflicts of interest that may have contributed to a bias against saturated fats. For instance, one member was found to have chaired five vegetarian conferences from 1997 to 2018, which might reflect a bias against saturated fats, since a more liberal policy towards these fats would inevitably allow for greater consumption of animal foods. This member was also found to have been receiving funds from seven soy and tree nut industry groups, which stand to benefit commercially when guidelines favor the type of fats (polyunsaturated) commonly found in these foods. Another member had spent the last 50 years of her career working as a lead investigator on some of the government's largest trials attempting to show that fat and saturated fats are bad for health. A third member is part of a vegetarian activist group that has condemned the evolving science of saturated fats. These and other interests continue to influence the scientific debate on saturated fats. In conclusion, the DGA process has never systematically reviewed either the ‘core trials’ on saturated fats directly or the subsequent external review papers of those trials. The major change in thinking on saturated fats that has occurred among independent teams of scientists globally over the past 12 years has therefore not been reflected in U.S. nutrition policy. As a result, the Dietary Guidelines must be considered outdated on this topic. CONCLUSION For decades following the introduction of the diet-heart hypothesis, many scientists were unaware of the lack of evidence for this theory. However, the rediscovery of rigorous clinical trials testing this hypothesis and the subsequent publication of multiple review papers on these data have provided a new awareness of the fundamental inadequacy of the evidence to support the idea that saturated fats cause heart disease. The observed resistance against considering this new science by successive DGACs can potentially be seen as reflecting longstanding biases in the field and the influence of vested interests. Until the recent science on saturated fats is incorporated into the U.S. Dietary Guidelines, the policy on this topic cannot be seen as evidence-based. https://pmc.ncbi.nlm.nih.gov/articles/PMC9794145/