Louis Pasteur’s germ theory has become a curse!
Why does pH balance or pH homeostasis define good health?
pH Homeostasis is a bit like balancing the books in accounting. It is maintained by balancing inputs with outputs.
How well we adapt in health and sickness is largely a function of the pH homeostatic mechanism.
The body’s chemistry response to such subtle changes that a negative thought, an acidic food or drink, or eating too much food can be a problem for maintaining balance.
Doctors prescribed diet, rest, sleep, exercise, and salt baths!
Ultimately, you are the one who has to take charge.
How Does She Do IT?
The singer and dancer is currently prepping for her first Las Vegas residency — which begins Aug. 13 at the Flamingo Hotel and Casino — and she’s putting in the hard work, starting each day before the sun and going until late at night.
“It’s very physically intense,” Abdul tells PEOPLE. “I get up at 6 and I work with my trainer for an hour and a half. Then I go to rehearsals at about a quarter to 9. We do a warm-up and then we dance. We go from about 9:45 until 7 p.m., and we take one day off.”
The “Opposites Attract” singer has to treat her body well to keep going day after day.
“I do a lot of stretching,” she says. “When I’m with my trainer I’m doing Pilates, I’m doing a lot of back and core work. Even though I’m dancing all day I often do straight cardio just so that I’m conditioning my body. And after each performance I usually get in an ice-cold tub. It’s not fun! It shocks your body, but it helps with inflammation.”
Abdul also watches what she eats, partially because of the hours spent dancing, and partially due to her history with reflex sympathetic dystrophy(RSD), a type of chronic pain after an injury or surgery.
“When you have RSD, the best thing to do is lower your acidity to slow inflammation, so I follow a low alkaline diet,” she says. “I don’t like following diets but I try to keep the acidity down because that’s what causes flares up in my body. But I’m really blessed; I’m in remission and I’ve been in remission for years now.”
Dr. Robert O Young discovered many years that you cannot have inflammation without acid. He has stated, “acid is inflammation and inflammation is acid.”
Where do acids come from?
According to Dr. Young acids come from, “what you eat, what you drink, what you breathe, what you think and what you believe.”
To learn more about an alkaline lifestyle and diet read, The pH Miracle, revised and updated. www.drrobertyoung.com and http://www.phmiracleproducts.com
The New England quarterback’s alkaline diet has many rules to keep people on track as they attempt this new lifestyle.
Just in time for the Super Bowl!
1. Consume mainly alkaline foods – At least 80%!
2. Pay attention to portion sizes. The plate should include two palm sizes of vegetables and one-palm size of protein
3. Stop eating two to three hours before bed
4. You cannot combine protein and complex carbs for a meal
5. Cannot eat fruit alone
6. Little to no carbs for breakfast
7. Eat foods based on seasons
8. Consume 20oz of alkaline water at a pH of 9.5 right when you wake up
9. If you cannot give up coffee then limit caffeine intake to 200mg (two cups of coffee)
10. No soda, carbonation, milk, dairy, fruit juices, sweetened drinks, and alcohol!
Giving it a try! Toronto-based fitness trainer Keltie O’Connor shared with her followers how she attempted the alkaline diet!
Before the pH Alkaline diet Keltie admitted she was bloated!
After 30 days on the pH Alkaline Diet no more digestive problems and bloating!
To learn more about the pH Miracle lifestyle read The pH Miracle, revised and updated.
To order the pH Miracle Alkaline Lifestyle and Diet book go to: https://www.amazon.com/Robert-O.-Young/e/B001ILKCSU/ref=sr_tc_2_0?qid=1547305442&sr=1-2-ent
Which Lifestyle and Diet Did YOU Follow in 2018!
Dr. Young’s pH Miracle Alkaline Lifestyle and Diet
Victoria Beckham keeps her slender physique in shape by following the pH Alkaline Lifestyle and Diet, recommended by Robert O. Young PhD. This plan means you ingest ONLY alkaline foods and liquids to keep your acidic levels in your blood, interstitial fluids, intracellular fluids at an alkaline pH between 7.35 and 7.45. All of these fluids can be tested with the Full-Body 3-D Bio-Electro Scan and the non-invasive blood testing of the chemistry, including pH of the blood, stomach, intestines and interstitial fluids.
To learn more about these non-invasive medical tests click here: (http://www.universalmedicalimaging.com/index.html
The following chart lists some of the acidic foods on the pH Miracle Alkaline Diet to eliminate completely or eat sparingly:
The following chart lists some of the foods you can eat freely on the pH Miracle alkaline diet:
The supermodel Elle Macpherson stated that following a plant-based pH Miracle alkaline lifestyle and diet and taking supplements have helped her look younger than her 54 years. (wwwijuicenow.com and http://www.phoreveryoung,com)
“When I turned 50 I realized things I did in my 20s weren’t working anymore,” Macpherson said. “I follow a plant-based alkaline diet, focusing on healthy, whole food. I take green powder and protein powder every day, and I drink three liters of water a day.” (www.ijuicenow.com, http://www.phoreveryoung.com)
So where does a 6’7″ man who weighs over 270 pounds get his protein from? Tony Robbins eats broccoli! Over 50 percent of the calories from steamed organic broccoli comes from protein. It is important to note that the body does not build muscle from protein – it builds it from red blood cells. Muscle, bone, and all organs and glands are made from red blood cells NOT protein! Tony is a strong advocate and walking testimony of Dr. Young’s alkaline lifestyle and diet which he teaches from the stage at ALL his events.
Prince Harry and Meghan follow the pH Miracle Alkaline Lifestyle and Diet. In fact it was Meghan who introduced Harry to the alkaline lifestyle.
So what keeps Tom Brady so healthy, fit and strong at the age of 41 and still playing NFL Football? The answer is the pH Miracle alkaline lifestyle and diet!
The Vegan Diet
Beyonce is a big fan of Marcos Borges 22 days of Vegan program which is a vegan meal service. Although not a full vegan, the singer ordered in the service to get in shape for Coachella. “The benefits of a plant-based diet need to be known,” Beyoncé said. “We should spend more time loving ourselves, which means taking better care of ourselves with good nutrition and making healthier food choices.”
The following are just a few of the foods I recommend that you can eat freely when following an Vegan Diet as outlined in The pH Miracle revised and updated book and The pH Miracle for Weight Loss – http://www.phoreveryoung.com
The Ancient Grains Diet
To keep her energy levels at an all-time high, Angelina Jolie snacks on ancient grains such as quinoa, chia seeds, millet, buckwheat and spelt. “She’s into eating products made from ancient grains and raves about their health benefits,” a source told Marie Claire. “She claims they provide her with nutrients she can’t find anywhere else, plus shinier skin.”
The wonderful benefits of ancients grains like quinoa, millet, buckwheat and spelt, they are low in carbohydrate (sugar) and higher in protein. Keep in mind though I only recommend these grains sparingly and no more than 10 grams of protein daily.
Remember, all body cells, including bone and muscle are made from blood NOT protein. And blood is made from chlorophyll (green foods), unsaturated oil, alkaline water and mineral salts or sodium, potassium, magnesium and calcium.
The Paleo Diet
Jessica Biel credits her super svelte physique down to the Paleo diet. Heavily endorsed by Pete Evans, the diet works on the ethos you go back to eating like a caveman and eradicate dairy, grains and legumes from your diet. “Eating Paleo just leans you down and slims you up and takes that little layer of fat and water-weight right off your body,” says Jessica. “I do a lot of cooking at home using fresh fish or lean meat like chicken and vegetables,” she adds.
The Paleo diet will provide short term benefits but long term damage from ALL the acidic foods from dairy, legumes and grains such as wheat. You are better off with both short and long term benefits by sticking with a diet that does not cause eventual gland, organ and tissue damage. That diet would be low carbohydrate, low protein and liberal amounts of healthy unsaturated oil, like hemp seed, flax seed, broccoli seed, carrot seed, cabbage seed, just to name a few.
The Atkins Diet
Kim Kardashian lost 25 kilos in 11 months on the Atkins diet, which is a high acidic protein, low carb diet. “ Anyone who has had kids knows your body changes, and it’s hard to get your body back in shape,” she said. “It takes so much determination, and mental and physical power and energy.”
Unfortunately this diet also has short term benefits with long term damage, especially to the intestinal villi if you are ingesting animal protein which does not digest (unless you juice the animal flesh). Maybe that is why Kim looks bloated in the lower abdominal area. It is important to stay away from this diet unless your protein sources are from green plants such as avocado, broccoli and buckwheat.
Check out the above list of foods to avoid and especially avoid animal sources for safe and healthy weight loss.
The World’s Number 1 Lifestyle and Diet for Health, Energy, Vitality, Fitness & Beauty!
For safe and effective weight loss or weight gain read The pH Miracle for Weight Loss by Robert O Young PhD – http://www.phoreveryoung.com or on amazon.com at: https://www.amazon.com/gp/product/0446694703/ref=dbs_a_def_rwt_hsch_vapi_taft_p1_i1
Maryanne lost over 150 pounds in less than a year following The pH Miracle for Weight Loss.
Scott Jacobs lost over 100 pounds in 12 weeks following The pH Miracle for Weight Loss lifestyle and diet plan.
Ryan Marcotte lost 31 pounds of fat and gained 11 pounds of muscle in 12 weeks following Dr. Robert O. Young’s pH Miracle Lifestyle and Diet!
Donna lost over 100 pounds following Dr. Robert O. Young’s pH Miracle Lifestyle and Diet! See Donna’s before and after pictures below as she shows her new found energy doing the splits on the Jump Sport Rebounder.
To learn more about the pH Miracle Lifestyle and Diet and Dr. Robert O. Young go to: http://www.drrobertyoung.com
Eating Avocado Seeds Can Help Fight Cancer (and 4 Other Health Benefits) – http://www.ijuicenow.com
The avocado seed and more important the avocado seed oil contains anti-tumor properties, especially the potent antioxidants called flavonols. In a 2013 study published in the journal, Pharmaceutical Biology, researchers from the University of Antioquia in Medellin, Colombia found that the oil from avocado fruit and seeds caused leukemia cells to self-destruct.
In a more recent study published in the peer-reviewed journal Cancer Research, researchers discovered that a compound found in avocado seed extract called avocatin B was effective phytochemical against acute myeloid leukemia cells. In total, study researchers tested 800 natural health products against the human acute myeloid leukemia cells.
Avocado Seed Oil Overview – http://www.ijuicenow.com
Avocados are, by far, my favorite food; in fact, I try to eat at least one avocado every day. The green, creamy fruit can pretty much go with anything. I add half an avocado to my morning smoothie and another half to my salad at dinnertime…and if I have a craving for tomato and avocado, I love making homemade guacamole!
Like most people, I use to toss the avocado seed in the garbage. But it turns out avocado seeds and avocado seed oil are not only healthy, but they have even been used in traditional medicine for centuries.
Is It Safe to Eat Avocado Seeds?
“Wait a minute,” some may say. “Aren’t fruit seeds and oil are toxic?” Well, fruit seeds from cherries, plums, and apricots contain the toxic chemical cyanide, and large quantities of these seeds can lead to vomiting, dizziness, and even death. But that is not the case with the avocado seed and avocado seed oil. http://www.ijuicenow.com
Avocado seeds and oil contain tannins, which are mildly toxic; however, you would have to consume several before you’d notice any negative health effects. In a 2013 study published in the Scientific World Journal, researchers concluded that the avocado seed oil was safe and it did not show any human toxicity.
5 Healthy Benefits of Eating Avocado Seeds and Oil
We know avocados are loaded with folate, vitamin B, and healthy fats. But avocado seeds and oil are nutrient-rich as well. The avocado seed is a beneficial source of bioactive phytochemicals.
It contains fatty acids, triterpenes, phytosterols, and glucosides from abscisic acid. The avocado seed also contains 70% of the avocado’s antioxidant content. The antioxidant phytochemicals in avocado seeds include proanthocyanidins and flavonols. The avocado seed is also considered one of the best sources of soluble fiber.
What are the health benefits of eating avocado seeds and oil?
They contain antifungal, antibiotic, antimicrobial, insecticidal, larvicidal, amoebicidal, giardicidal, hypolipidemic, and antihypertensive properties. Eating avocado seeds also has other valuable health benefits.
1. Avocado Seeds and Oil Help Fight Cancer
The avocado seeds and oil contain anti-tumor properties, especially the potent antioxidants called flavonols. In a 2013 study published in the journal Pharmaceutical Biology, researchers from the University of Antioquia in Medellin, Colombia found that extract from avocado fruit and seeds caused leukemia cells to self-destruct.
In a more recent study published in the peer-reviewed journal Cancer Research, researchers discovered that a compound found in avocado seed extract called avocatin B was effective against acute myeloid leukemia cells. In total, study researchers tested 800 natural health products against the human acute myeloid leukemia cells.
2. Avocado Seeds and Oil Benefits the Heart
In a 2012 study published in the journal Plant Foods for Human Nutrition, avocado seed flour reduced the total cholesterol and LDL (low-density lipoprotein) cholesterol levels in mice. Researchers also suggested that avocado seeds could offer protection against arterial plaque formation.
The dietary fiber found in avocado seeds is linked with lower cholesterol. The fiber will bind to the cholesterol in the intestinal tract and prevent it from being absorbed. Other research shows that avocado seeds can help improve high cholesterol and hypertension. It can also help fight inflammation and diabetes.
3. Avocado Seed Oil Aids Digestive
Eating avocado seeds can also help with digestion. South Americans once used avocado seeds for treating gastric ulcers, severe diarrhea (dysentery), acute diarrhea, and other digestive problems. The antioxidants and fiber found in the avocado seed are beneficial for digestion.
4. Avocado Seed Oil Strengthens the Immune System
A strong immune system is a great way to prevent disease. Avocado seeds and skins contain greater antioxidant levels, including proanthocyandins and catehchins.
They have anti-inflammatory properties that reduce stiffness, swelling, joint pain, and diseases. The anti-inflammatory effects also help strengthen the immune system and prevent the expulsion of dietary and metabolic acids called cold or flu.
In an in-vitro study, published in the journal Revista de Sociedade Brasileira de Medicina Tropical in 2009, researchers found that the antifungal and antibiotic effects of avocado seed extract could inhibit harmful pathogens such as candida, along with other fungi. Fungal and candida infections are related to a weakened immune system.
5. Avocado Seed Oil Helps Reduce Wrinkles
Evidence shows that avocado seed oil can increase collagen in the skin, which reduces the appearance of wrinkles. Avocado seed oil is also used to treat acne flare-ups.
How to Extract the Avocado Seed
To safely remove the avocado seed from the avocado:
- Cut the avocado by slicing around the pit in order to cleanly remove the seed.
- Insert your knife tip into the pit, twist, and gently pull.
- Finally, remove the avocado seed from the knife.
- Simply put the avocado seed into a plastic bag and then crush it with a hammer (or a blunt object).
- Combine the crushed seed and blended avocado seeds in an Vitamix blender with iJuice Avocado Seed Oil with your favorite smoothie ingredients, such as avocado meat and dark leafy green vegetables, like spinach and kale. If you have a high-powered blender such as a Vitamix, you will not need to crush the avocado seed first, but you will need to add alkaline water.
Recipe for the Perfect Avocado Seed & Oil Green Smoothie
- 1/2 organic avocado seed
- 1/2 organic avocado
- 1 tsp of iJuice organic avocado oil – http://www.ijuicenow.com
- 5 drops of iJuice organic avocado seed oil – http://www.ijuicenow.com
- 1 cup of organic almond milk or water
- 1 scoop of iJuice Super Greens powder
- 1 scoop of iJuice Super Chlorophyll
- 1 cup of organic spinach
- 1 cup of organic kale
- 1 to 2 organic English cucumber
- 1 small piece of organic ginger (grated) or 1 to 2 drops of iJuice organic Ginger oil
- Smash or grade the seed, blend all of the ingredients together until smooth, and enjoy your avocado seed green goddess smoothie!
Do you want another green smoothie recipe? You’re in luck—this next recipe also contains flaxseed and red leaf lettuce:
- 1/2 organic avocado seed
- 1 tsp of iJuice organic avocado oil
- 5 to 10 drops of iJuice organic avocado seed oil
- 2 1/2 cups of water or almond milk
- 1/2 to 3/4 of an organic mango
- 3 tablespoons of ground flaxseed
- 3/4 of a head of red leaf lettuce
- Be sure to crush your avocado seed and blend in a Vitamix all of the ingredients until smooth.
- Serve and enjoy!
Other Uses for the Avocado Seed
Besides adding nutrition to your green alkaline smoothies, the avocado seed and oil has a plethora of other uses. Here are some of my favorites:
- Guacamole saver: Keep your guacamole from going bad in the refrigerator by placing the avocado seed or a few drops of iJuice avocado seed oil in your dip.
- Homemade face mask: The avocado seed and/or oil can also make a great face mask exfoliator. All you need to do is dry the seeds, grind them up in a Vitamix, and add them to a homemade face mask recipe.
- Avocado seed tea: The avocado seed and/or oil makes a great tea. Simply boil the seed for approximately 30 minutes or add a few drops of iJuice Avocado Seed oil to your tea.
- Grow an avocado plant: You can also grow an avocado seed into a decorative houseplant.
- Natural food additive: The antioxidant phytochemicals are thought to make avocado seeds a healthy food additive. In a 2011 study published in the Journal of Agricultural and Food Chemistry, researchers concluded that the antimicrobial and antioxidant effects of avocado seeds may help with food spoilage prevention.
“Could avocados hold the key to treating leukemia?” PubMed Health, National Center for Biotechnology Information web site, June 17, 2015; http://www.ncbi.nlm.nih.gov/pubmedhealth/behindtheheadlines/news/2015-06-17-could-avocados-hold-the-key-to-treating-leukaemia/
For more healthy alkaline juice, smoothie and soup recipes using avocado seed and oil read, The pH Miracle revised and updated and The pH Miracle for Cancer – http://www.phoreveryoung.com
What Is Alkaline Water?
The pH (potential hydrogen ions or protons) scale runs from zero to fourteen with 7 being the med-point. A liquid with a pH of less than 7 is considered acid unless it donates more base or electrons than acids or protons. A basic or alkaline substance that contributes more electrons than protons is referred to as an electron donor and is considered alkaline regardless of the ph of the substance on the pH scale. For example your tap water is generally mixed with chlorine making the water base or alkaline at a pH of 7 or above. Because tap water contains other acidic substances such as antibiotics (acids), hormones (acids) and heavy metals this makes tap water a hydrogen or proton donor and is considered acidic to the stomach, blood and interstitial fluids of the Interstitium (the fluids that surround every human cell in the body).
(This illustration shows the compartments of interstitial fluids of the Interstitium)
When the body builds up acids in the interstitial fluids this is when you feel low energy, fatigue, start gaining weight and are at risk for serious health challenges such as diabetes and cancer.
These negative health effects are completely avoidable by just drinking pure, reduced electro-rich alkaline water and eating organic green electron-rich alkaline vegetables and fruit such as lemon, lime, tomato, green pepper, avocado, cucumber, spinach, parsley, broccoli, and peppermint leaf, just to name a few. To learn more about acidic and alkaline foods read, The pH Miracle, revised and updated – http://www.phoreveryoung.com
Importance Of Alkalinity
The foods we eat, the liquids we drink, the air that we breath and the thoughts that we have can determine our overall pH levels and has been the basis of my research for 40 years.
Dr. Otto Warburg of Germany, received two Nobel Prizes in 1931 and 1952 for discovering that all cancer cells and tumors are bathed in an acidic interstitial fluid environment and suggested this was the cause of cancer. He also managed to prove that cancer cannot thrive in an alkaline, electron-rich environment where the pH level in the interstitial fluids is 7.36 to 7.4.
According to Dr. Warburg, acidosis (excess of hydrogen ions or protons) is not only connected to the development of cancer, but it was also the cause of cancer and other diseases like osteoporosis, diabetes and heart disease.
Here is the special anti-acid or alkalizing, electron-donor beverage you can drink every day prevent the build-up into the acid holding compartments in the Interstitium.
1 organic lemon
1/2 organic cucumber
1/4 of organic ginger root
1/2 cup of organic peppermint leaf
Before you cut the organic ginger, peel a small amount of it.
Slice up all the ingredients and add one glass of alkaline, electron-rich water.
Do not throw the ingredients after one use if you want to get the most out of them.
If you keep adding new alkaline, electron-rich water, they will last around three days.
Drink the alkaline, electron-rich water first thing in the morning in order to receive the optimum results!
How Does It Work?
Organic lemon possesses numerous alkalizing, electron-donor properties. Organic lemon is high in potassium bicarbonate making it inherently alkaline and an electron-donor. It is also a powerful disinfectant and antibacterial compound which helps in the treatment of numerous conditions from bad breath to cholera, and has even 22 anti-cancer properties the most important being bicarbonates of sodium and potassium.
To learn more about preventing cancer and other diseases and for great alkaline, electron-rich recipes read, The pH Miracle for Cancer:
You register and attend the next medical conference where Robert O Young PhD will be speaking go to:
To learn more about the research and findings of Dr. Robert O. Young go to: http://www.drrobertyoung.com
“The cure for cancer is NOT found in its treatment but is found in its prevention” – Dr. Robert O. Young
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” (http://indiatoday.digitaltoday.in/index.php?
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 (1–4). 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% (5). 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 (6). 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 (6).
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 (7). 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 (http://www.dietandcancerreportorg/?p=ER).
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 (8). 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 (9, 10), these mutations are due to interaction with the environment (11, 12).
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 (13). 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
Smoking was identified in 1964 as the primary cause of lung cancer in the US Surgeon General’s Advisory Commission Report (http://profiles.nlm.nih.gov/NN/Views/AlphaChron/date/10006/05/01/2008), 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.
(http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts_and_Figures_2008.asp accessed on 05/01/2008).
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.
(http://cfpub2.epa.gov/ncea/cfm/recordisplay.cfm?deid=2835 accessed on 05/01/2008).
Tobacco contains at least 50 carcinogens. For example, one tobacco metabolite, benzopyrenediol epoxide, has a direct etiologic association with lung cancer (14). 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.
(http://www.fao.org/DOCREP/006/Y4956E/Y4956E00.HTM accessed on 01/11/08)
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.
Cancers that have been linked to alcohol and smoking
Percentages represent the cancer mortality attributable to alcohol and smoking in men and women as reported by Irigaray et al. (see 13).
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 (15,16). 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 (15). In addition to curcumin, we discovered that several natural phytochemicals also inhibit the NF-κB induced by various carcinogens (17). 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.
The first report of the association between alcohol and an increased risk of esophageal cancer was published in 1910 (18). 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 (18–21), as well as for cancers of the liver, pancreas, mouth, and breast (Fig. 3). Williams and Horn (22), 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 (23). In another study, Longnecker et al., (24) 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 (25) and colorectal (26,27) 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. (28) 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 (29). 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 (30), which can also contribute to tumorigenesis (31). Furthermore, it has been shown that benzopyrene, a cigarette smoke carcinogen, can penetrate the esophagus when combined with ethanol (32). 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 (33). Globally, the attributable fraction of cancer deaths due to alcohol drinking is reported to be 3.5% (34). 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 (18).
In 1981, Doll and Peto (21) 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 (35). 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.
Cancer deaths (%) linked to diet as reported by Willett (see 35)
Heavy consumption of red meat is a risk factor for several cancers, especially for those of the gastrointestinal tract, but also for colorectal (36–38), prostate (39), bladder (40), breast (41), gastric (42), pancreatic, and oral (43) cancers. Although a study by Dosil-Diaz et al., (44) showed that meat consumption reduced the risk of lung cancer, such consumption is commonly regarded as a risk for cancer for the following reasons. The heterocyclic amines produced during the cooking of meat are carcinogens. Charcoal cooking and/or smoke curing of meat produces harmful carbon compounds such as pyrolysates and amino acids, which have a strong cancerous effect. For instance, PhIP (2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridine) is the most abundant mutagen by mass in cooked beef and is responsible for ~20% of the total mutagenicity found in fried beef. Daily intake of PhIP among Americans is estimated to be 280–460 ng/day per person (45).
Nitrites and nitrates are used in meat because they bind to myoglobin, inhibiting botulinum exotoxin production; however, they are powerful carcinogens (46). Long-term exposure to food additives such as nitrite preservatives and azo dyes has been associated with the induction of carcinogenesis (47). Furthermore, bisphenol from plastic food containers can migrate into food and may increase the risk of breast (48) and prostate (49) cancers. Ingestion of arsenic may increase the risk of bladder, kidney, liver, and lung cancers (50). Saturated fatty acids, trans fatty acids, and refined sugars and flour present in most foods have also been associated with various cancers. Several food carcinogens have been shown to activate inflammatory pathways.
According to an American Cancer Society study (51), obesity has been associated with increased mortality from cancers of the colon, breast (in postmenopausal women), endometrium, kidneys (renal cell), esophagus (adenocarcinoma), gastric cardia, pancreas, prostate, gallbladder, and liver (Fig. 5). Findings from this study suggest that of all deaths from cancer in the United States, 14% in men and 20% in women are attributable to excess weight or obesity. Increased modernization and a Westernized diet and lifestyle have been associated with an increased prevalence of overweight people in many developing countries (52).
Various cancers that have been linked to obesity. In the USA overweight and obesity could account for 14% of all deaths from cancer in men and 20% of those in women (see 51).
Studies have shown that the common denominators between obesity and cancer include neurochemicals; hormones such as insulinlike growth factor 1 (IGF-1), insulin, leptin; sex steroids; adiposity; insulin resistance; and inflammation (53).
Involvement of signaling pathways such as the IGF/insulin/Akt signaling pathway, the leptin/JAK/STAT pathway, and other inflammatory cascades have also been linked with both obesity and cancer (53). For instance, hyperglycemia, has been shown to activate NF-κB (54), which could link obesity with cancer. Also known to activate NF-κB are several cytokines produced by adipocytes, such as leptin, tumor necrosis factor (TNF), and interleukin-1 (IL-1) (55). Energy balance and carcinogenesis has been closely linked (53). However, whether inhibitors of these signaling cascades can reduce obesity-related cancer risk remains unanswered. Because of the involvement of multiple signaling pathways, a potential multi-targeting agent will likely be needed to reduce obesity-related cancer risk.
Worldwide, an estimated 17.8% of neoplasms are associated with infections; this percentage ranges from less than 10% in high-income countries to 25% in African countries (56, 57). Viruses account for most infection-caused cancers (Fig. 6). Human papillomavirus, Epstein Barr virus, Kaposi’s sarcoma-associated herpes virus, human T-lymphotropic virus 1, HIV, HBV, and HCV are associated with risks for cervical cancer, anogenital cancer, skin cancer, nasopharyngeal cancer, Burkitt’s lymphoma, Hodgkin’s lymphoma, Kaposi’s sarcoma, adult T-cell leukemia, B-cell lymphoma, and liver cancer.
Various cancers that have been linked to infection. The estimated total of infection attributable cancer in the year 2002 is 17.8% of the global cancer burden. The infectious agents associated with each type of cancer is shown in the bracket. HPV Human papilloma virus, HTLV human T-cell leukemia virus, HIV human immunodeficiency virus, EBV Epstein–Barr virus (see 57).
In Western developed countries, human papillomavirus and HBV are the most frequently encountered oncogenic DNA viruses. Human papillomavirus is directly mutagenic by inducing the viral genes E6 and E7 (58), whereas HBV is believed to be indirectly mutagenic by generating reactive oxygen species through chronic inflammation (59–61). Human T-lymphotropic virus is directly mutagenic, whereas HCV (like HBV) is believed to produce oxidative stress in infected cells and thus to act indirectly through chronic inflammation (62, 63). However, other microorganisms, including selected parasites such as Opisthorchis viverrini or Schistosoma haematobium and bacteria such as Helicobacter pylori, may also be involved, acting as cofactors and/or carcinogens (64).
The mechanisms by which infectious agents promote cancer are becoming increasingly evident. Infection-related inflammation is the major risk factor for cancer, and almost all viruses linked to cancer have been shown to activate the inflammatory marker, NF-κB (65). Similarly, components of Helicobacter pylorihave been shown to activate NF-κB (66). Thus, agents that can block chronic inflammation should be effective in treating these conditions.
Environmental pollution has been linked to various cancers (Fig. 7). It includes outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons (PAHs); indoor air pollution by environmental tobacco smoke, formaldehyde, and volatile organic compounds such as benzene and 1,3-butadiene (which may particularly affect children); food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins, and other organochlorines; carcinogenic metals and metalloids; pharmaceutical medicines; and cosmetics (64).
Various cancers that have been linked to environmental carcinogens. The carcinogens linked to each cancer is shown inside bracket. (see 64).
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 (64).
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 (64).
Up to 10% of total cancer cases may be induced by radiation (64), both ionizing and non-ionizing, 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.
Non-ionizing 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 sun beds 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 (64).
Fruits, vegetables, spices, condiments and cereals with potential to prevent cancer. Fruits include 1 apple, 2apricot, 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 1artichok, 2 avocado, 3 brussels sprout, 4 broccoli, 5 cabbage, 6 cauliflower, 7 carrot, 8 daikon 9 kohlrabi, 10onion, 11 tomato, 12 turnip, 13 ulluco, 14 water cress, 15 okra, 16 potato, 17 fiddle head, 18 radicchio, 19komatsuna, 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, 18camphor, 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, 22green, 23 green (eston), 24 ivory white, 25 multicolored blend, 26 petite crimson, 27 petite golden, 28 red chief.
Join Robert O Young PhD and Galina Migalko MD in Dubai on December 5th and 6th, 2018 for the Annual Conference on Bacterial, Viral and Infectious Diseases. They will be Key Note Speakers and doing a workshop on the New Biology.
For more information and to register go to: https://bacterialdiseases.infectiousconferences.com/organizing-committee.php
The following is the abstract for Dr. Young’s lecture:
The Dismantling of the Viral Theory
Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner
There is now over 100 years of documented history and research on the Polio virus and whether or not its treatment by inoculation has been successful in eradicating Polio. I am suggesting in this article and in my lecture that there are significant findings based on historical and past and current research, including my own that the viral theory of Polio and possibly other modern-day diseases, such as Post-Polio Syndrome, Polio Vaccine-Induced Paralysis, Legionnaires, CNS disease, Cancer, HIV/AIDS and now Zika may be caused by acidic chemical poisoning from DDT (dichloro-diphenyl-trichloroethane) and other related DDT pesticides, acidic vaccinations, and other factors including lifestyle and dietary factors rather than from a lone infectious virus. I will present ten historical graphs outlining the history of Polio, the production of DDT, BHC, Lead, Arsenic, Polio vaccinations and the author’s theory that chemical poisoning, vaccination, and lifestyle and dietary choices are a more likely causes for the symptoms of Polio, neurological diseases, Cancer, HIV/AIDS and now Zika.
THE POSSIBLE CAUSE OF POLIO, POST-POLIO, CNS, PVIPD, LEGIONNAIRES, AIDS and the CANCER EPIDEMIC – MASS ACIDIC CHEMICAL POISONING?
1. L. N. Kolonel, D. Altshuler, and B. E. Henderson. The multiethnic cohort study: exploring genes, lifestyle and cancer risk. Nat. Rev. Cancer. 4:519–27 (2004) doi:10.1038/nrc1389. [PubMed]
2. J. K. Wiencke. Impact of race/ethnicity on molecular pathways in human cancer. Nat. Rev. Cancer. 4:79–84 (2004) doi:10.1038/nrc1257. [PubMed]
3. R. G. Ziegler, R. N. Hoover, M. C. Pike, A. Hildesheim, A. M. Nomura, D. W. West, A. H. Wu-Williams, L. N. Kolonel, P. L. Horn-Ross, J. F. Rosenthal, and M. B. Hyer. Migration patterns and breast cancer risk in Asian-American women. J. Natl. Cancer Inst.85:1819–27 (1993) doi:10.1093/jnci/85.22.1819. [PubMed]
4. W. Haenszel and M. Kurihara. Studies of Japanese migrants. I. Mortality from cancer and other diseases among Japanese in the United States. J. Natl. Cancer Inst.40:43–68 (1968). [PubMed]
5. A. S. Hamilton and T. M. Mack. Puberty and genetic susceptibility to breast cancer in a case-control study in twins. N. Engl. J. Med.348:2313–22 (2003) doi:10.1056/NEJMoa021293. [PubMed]
6. A. Jemal, R. Siegel, E. Ward, T. Murray, J. Xu, and M. J. Thun. Cancer statistics, 2007. CA Cancer J. Clin.57:43–66 (2007). [PubMed]
7. F. Brayand, and B. Moller. Predicting the future burden of cancer. Nat. Rev. Cancer. 6:63–74 (2006) doi:10.1038/nrc1781. [PubMed]
8. P. Lichtenstein, N. V. Holm, P. K. Verkasalo, A. Iliadou, J. Kaprio, M. Koskenvuo, E. Pukkala, A. Skytthe, and K. Hemminki. Environmental and heritable factors in the causation of cancer—analyses of cohorts of twins from Sweden, Denmark, and Finland. N. Engl. J. Med.343:78–85 (2000) doi:10.1056/NEJM200007133430201. [PubMed]
9. K. R. Loeb, and L. A. Loeb. Significance of multiple mutations in cancer. Carcinogenesis. 21:379–85 (2000) doi:10.1093/carcin/21.3.379. [PubMed]
10. W. C. Hahn, and R. A. Weinberg. Modelling the molecular circuitry of cancer. Nat. Rev. Cancer. 2:331–41 (2002) doi: 10.1038/nrc795. [PubMed]
11. L. A. Mucci, S. Wedren, R. M. Tamimi, D. Trichopoulos, and H. O. Adami. The role of gene-environment interaction in the aetiology of human cancer: examples from cancers of the large bowel, lung and breast. J. Intern. Med.249:477–93 (2001) doi:10.1046/j.1365-2796.2001.00839.x. [PubMed]
12. K. Czene, and K. Hemminki. Kidney cancer in the Swedish Family Cancer Database: familial risks and second primary malignancies. Kidney Int.61:1806–13 (2002) doi:10.1046/j.1523-1755.2002.00304.x.[PubMed]
13. P. Irigaray, J. A. Newby, R. Clapp, L. Hardell, V. Howard, L. Montagnier, S. Epstein, and D. Belpomme. Lifestyle-related factors and environmental agents causing cancer: an overview. Biomed. Pharmacother.61:640–58 (2007) doi:10.1016/j.biopha.2007.10.006. [PubMed]
14. M. F. Denissenko, A. Pao, M. Tang, and G. P. Pfeifer. Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53. Science. 274:430–2 (1996) doi:10.1126/science.274.5286.430.[PubMed]
15. R. J. Anto, A. Mukhopadhyay, S. Shishodia, C. G. Gairola, and B. B. Aggarwal. Cigarette smoke condensate activates nuclear transcription factor-kappaB through phosphorylation and degradation of IkappaB(alpha): correlation with induction of cyclooxygenase-2. Carcinogenesis. 23:1511–8 (2002) doi: 10.1093/carcin/23.9.1511. [PubMed]
16. S. Shishodiaand, and B. B. Aggarwal. Cyclooxygenase (COX)-2 inhibitor celecoxib abrogates activation of cigarette smoke-induced nuclear factor (NF)-kappaB by suppressing activation of IkappaBalpha kinase in human non-small cell lung carcinoma: correlation with suppression of cyclin D1, COX-2, and matrix metalloproteinase-9. Cancer Res. 64:5004–12 (2004) doi:10.1158/0008-5472.CAN-04-0206. [PubMed]
17. H. Ichikawa, Y. Nakamura, Y. Kashiwada, and B. B. Aggarwal. Anticancer drugs designed by mother nature: ancient drugs but modern targets. Curr Pharm Des. 13:3400–16 (2007) doi:10.2174/138161207782360500. [PubMed]
18. A. J. Tuyns. Epidemiology of alcohol and cancer. Cancer Res. 39:2840–3 (1979). [PubMed]
19. H. Maier, E. Sennewald, G. F. Heller, and H. Weidauer. Chronic alcohol consumption—the key risk factor for pharyngeal cancer. Otolaryngol. Head Neck Surg.110:168–73 (1994). [PubMed]
20. H. K. Seitz, F. Stickel, and N. Homann. Pathogenetic mechanisms of upper aerodigestive tract cancer in alcoholics. Int. J. Cancer. 108:483–7 (2004) doi:10.1002/ijc.11600. [PubMed]
21. R. Doll, and R. Peto. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J. Natl. Cancer Inst. 66:1191–308 (1981). [PubMed]
22. R. R. Williams, and J. W. Horm. Association of cancer sites with tobacco and alcohol consumption and socioeconomic status of patients: interview study from the Third National Cancer Survey. J. Natl. Cancer Inst.58:525–47 (1977). [PubMed]
23. N. Hamajima et al. Alcohol, tobacco and breast cancer—collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease. Br. J. Cancer. 87:1234–45 (2002) doi:10.1038/sj.bjc.6600596. [PMC free article] [PubMed]
24. M. P. Longnecker, P. A. Newcomb, R. Mittendorf, E. R. Greenberg, R. W. Clapp, G. F. Bogdan, J. Baron, B. MacMahon, and W. C. Willett. Risk of breast cancer in relation to lifetime alcohol consumption. J. Natl. Cancer Inst.87:923–9 (1995) doi:10.1093/jnci/87.12.923. [PubMed]
25. F. Stickel, D. Schuppan, E. G. Hahn, and H. K. Seitz. Cocarcinogenic effects of alcohol in hepatocarcinogenesis. Gut. 51:132–9 (2002) doi:10.1136/gut.51.1.132. [PMC free article] [PubMed]
26. H. K. Seitz, G. Poschl, and U. A. Simanowski. Alcohol and cancer. Recent Dev Alcohol. 14:67–95 (1998) doi:10.1007/0-306-47148-5_4. [PubMed]
27. H. K. Seitz, S. Matsuzaki, A. Yokoyama, N. Homann, S. Vakevainen, and X. D. Wang. Alcohol and cancer. Alcohol Clin. Exp. Res.25:137S–143S (2001). [PubMed]
28. F. Donato, U. Gelatti, R. M. Limina, and G. Fattovich. Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence. Oncogene. 25:3756–70 (2006) doi:10.1038/sj.onc.1209557. [PubMed]
29. G. Poschl, and H. K. Seitz. Alcohol and cancer. Alcohol Alcohol. 39:155–65 (2004) doi:10.1093/alcalc/agh057. [PubMed]
30. G. Szabo, P. Mandrekar, S. Oak, and J. Mayerle. Effect of ethanol on inflammatory responses. Implications for pancreatitis. Pancreatology. 7:115–23 (2007) doi:10.1159/000104236. [PMC free article][PubMed]
31. B. B. Aggarwal. Nuclear factor-kappaB: the enemy within. Cancer Cell. 6:203–208 (2004) doi:10.1016/j.ccr.2004.09.003. [PubMed]
32. M. Kuratsune, S. Kohchi, and A. Horie. Carcinogenesis in the esophagus. I. Penetration of benzo(a) pyrene and other hydrocarbons into the esophageal mucosa. Gann. 56:177–87 (1965). [PubMed]
33. C. La Vecchia, A. Tavani, S. Franceschi, F. Levi, G. Corrao, and E. Negri. Epidemiology and prevention of oral cancer. Oral Oncol.33:302–312 (1997). [PubMed]
34. P. Boffetta, M. Hashibe, C. La Vecchia, W. Zatonski, and J. Rehm. The burden of cancer attributable to alcohol drinking. Int. J. Cancer. 119:884–887 (2006) doi:10.1002/ijc.21903. [PubMed]
35. W. C. Willett. Diet and cancer. Oncologist. 5:393–404 (2000) doi:10.1634/theoncologist.5-5-393.[PubMed]
36. S. A. Bingham, R. Hughes, and A. J. Cross. Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response. J. Nutr.132:3522S–3525S (2002).[PubMed]
37. A. Chao, M. J. Thun, C. J. Connell, M. L. McCullough, E. J. Jacobs, W. D. Flanders, C. Rodriguez, R. Sinha, and E. E. Calle. Meat consumption and risk of colorectal cancer. JAMA. 293:172–182 (2005) doi:10.1001/jama.293.2.172. [PubMed]
38. N. Hogg. Red meat and colon cancer: heme proteins and nitrite in the gut. A commentary on diet-induced endogenous formation of nitroso compounds in the GI tract. Free Radic. Biol. Med.43:1037–1039 (2007) doi:10.1016/j.freeradbiomed.2007.07.006. [PubMed]
39. C. Rodriguez, M. L. McCullough, A. M. Mondul, E. J. Jacobs, A. Chao, A. V. Patel, M. J. Thun, and E. E. Calle. Meat consumption among Black and White men and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort. Cancer Epidemiol. Biomarkers Prev. 15:211–216 (2006) doi:10.1158/1055-9965.EPI-05-0614. [PubMed]
40. R. Garcia-Closas, M. Garcia-Closas, M. Kogevinas, N. Malats, D. Silverman, C. Serra, A. Tardon, A. Carrato, G. Castano-Vinyals, M. Dosemeci, L. Moore, N. Rothman, and R. Sinha. Food, nutrient and heterocyclic amine intake and the risk of bladder cancer. Eur. J. Cancer. 43:1731–1740 (2007) doi:10.1016/j.ejca.2007.05.007. [PubMed]
41. A. Tappel. Heme of consumed red meat can act as a catalyst of oxidative damage and could initiate colon, breast and prostate cancers, heart disease and other diseases. Med. Hypotheses. 68:562–4 (2007) doi:10.1016/j.mehy.2006.08.025. [PubMed]
42. L. H. O’Hanlon. High meat consumption linked to gastric-cancer risk. Lancet Oncol. 7:287 (2006) doi:10.1016/S1470-2045(06)70638-6. [PubMed]
43. T. N. Toporcov, J. L. Antunes, and M. R. Tavares. Fat food habitual intake and risk of oral cancer. Oral Oncol. 40:925–931 (2004) doi:10.1016/j.oraloncology.2004.04.007. [PubMed]
44. O. Dosil-Diaz, A. Ruano-Ravina, J. J. Gestal-Otero, and J. M. Barros-Dios. Meat and fish consumption and risk of lung cancer: A case-control study in Galicia, Spain. Cancer Lett.252:115–122 (2007) doi:10.1016/j.canlet.2006.12.008. [PubMed]
45. S. N. Lauber, and N. J. Gooderham. The cooked meat derived genotoxic carcinogen 2-amino-3-methylimidazo[4,5-b]pyridine has potent hormone-like activity: mechanistic support for a role in breast cancer. Cancer Res.67:9597–0602 (2007) doi:10.1158/0008–5472.CAN-07-1661. [PubMed]
46. D. Divisi, S. Di Tommaso, S. Salvemini, M. Garramone, and R. Crisci. Diet and cancer. Acta Biomed. 77:118–123 (2006). [PubMed]
47. Y. F. Sasaki, S. Kawaguchi, A. Kamaya, M. Ohshita, K. Kabasawa, K. Iwama, K. Taniguchi, and S. Tsuda. The comet assay with 8 mouse organs: results with 39 currently used food additives. Mutat. Res.519:103–119 (2002). [PubMed]
48. M. Durando, L. Kass, J. Piva, C. Sonnenschein, A. M. Soto, E. H. Luque, and M. Munoz-de-Toro. Prenatal bisphenol A exposure induces preneoplastic lesions in the mammary gland in Wistar rats. Environ. Health Perspect.115:80–6 (2007). [PMC free article] [PubMed]
49. S. M. Ho, W. Y. Tang, J. Belmonte de Frausto, and G. S. Prins. Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4. Cancer Res.66:5624–32 (2006) doi:10.1158/0008-5472.CAN-06-0516.[PMC free article] [PubMed]
50. A. Szymanska-Chabowska, J. Antonowicz-Juchniewicz, and R. Andrzejak. Some aspects of arsenic toxicity and carcinogenicity in living organism with special regard to its influence on cardiovascular system, blood and bone marrow. Int. J. Occup. Med. Environ. Health. 15:101–116 (2002). [PubMed]
51. E. E. Calle, C. Rodriguez, K. Walker-Thurmond, and M. J. Thun. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 348:1625–1638 (2003) doi:10.1056/NEJMoa021423. [PubMed]
52. A. Drewnowski, and B. M. Popkin. The nutrition transition: new trends in the global diet. Nutr. Rev.55:31–43 (1997). [PubMed]
53. S. D. Hursting, L. M. Lashinger, L. H. Colbert, C. J. Rogers, K. W. Wheatley, N. P. Nunez, S. Mahabir, J. C. Barrett, M. R. Forman, and S. N. Perkins. Energy balance and carcinogenesis: underlying pathways and targets for intervention. Curr. Cancer Drug Targets. 7:484–491 (2007) doi:10.2174/156800907781386623. [PubMed]
54. A. Nareika, Y. B. Im, B. A. Game, E. H. Slate, J. J. Sanders, S. D. London, M. F. Lopes-Virella, and Y. Huang. High glucose enhances lipopolysaccharide-stimulated CD14 expression in U937 mononuclear cells by increasing nuclear factor kappaB and AP-1 activities. J. Endocrinol.196:45–55 (2008) doi:10.1677/JOE-07-0145. [PubMed]
55. C. H. Tang, Y. C. Chiu, T. W. Tan, R. S. Yang, and W. M. Fu. Adiponectin enhances IL-6 production in human synovial fibroblast via an AdipoR1 receptor, AMPK, p38, and NF-kappa B pathway. J. Immunol.179:5483–5492 (2007). [PubMed]
56. P. Pisani, D. M. Parkin, N. Munoz, and J. Ferlay. Cancer and infection: estimates of the attributable fraction in 1990. Cancer Epidemiol. Biomarkers Prev.6:387–400 (1997). [PubMed]
57. D. M. Parkin. The global health burden of infection-associated cancers in the year 2002. Int. J. Cancer. 118:3030–3044 (2006) doi:10.1002/ijc.21731. [PubMed]
58. S. Song, H. C. Pitot, and P. F. Lambert. The human papillomavirus type 16 E6 gene alone is sufficient to induce carcinomas in transgenic animals. J. Virol.73:5887–5893 (1999). [PMC free article] [PubMed]
59. B. S. Blumberg, B. Larouze, W. T. London, B. Werner, J. E. Hesser, I. Millman, G. Saimot, and M. Payet. The relation of infection with the hepatitis B agent to primary hepatic carcinoma. Am. J. Pathol.81:669–682 (1975). [PMC free article] [PubMed]
60. T. M. Hagen, S. Huang, J. Curnutte, P. Fowler, V. Martinez, C. M. Wehr, B. N. Ames, and F. V. Chisari. Extensive oxidative DNA damage in hepatocytes of transgenic mice with chronic active hepatitis destined to develop hepatocellular carcinoma. Proc. Natl. Acad. Sci. U S A. 91:12808–12812 (1994) doi:10.1073/pnas.91.26.12808. [PMC free article] [PubMed]
61. A. L. Jackson, and L. A. Loeb. The contribution of endogenous sources of DNA damage to the multiple mutations in cancer. Mutat. Res.477:7–21 (2001) doi:10.1016/S0027-5107(01)00091-4. [PubMed]
62. N. De Maria, A. Colantoni, S. Fagiuoli, G. J. Liu, B. K. Rogers, F. Farinati, D. H. Van Thiel, and R. A. Floyd. Association between reactive oxygen species and disease activity in chronic hepatitis C. Free Radic. Biol. Med.21:291–5 (1996) doi:10.1016/0891–5849(96)00044-5. [PubMed]
63. K. Koike, T. Tsutsumi, H. Fujie, Y. Shintani, and M. Kyoji. Molecular mechanism of viral hepatocarcinogenesis. Oncology. 62(Suppl 1):29–37 (2002) doi:10.1159/000048273. [PubMed]
64. D. Belpomme, P. Irigaray, L. Hardell, R. Clapp, L. Montagnier, S. Epstein, and A. J. Sasco. The multitude and diversity of environmental carcinogens. Environ. Res.105:414–429 (2007) doi:10.1016/j.envres.2007.07.002. [PubMed]
65. Y. S. Guan, Q. He, M. Q. Wang, and P. Li. Nuclear factor kappa B and hepatitis viruses. Expert Opin. Ther. Targets. 12:265–280 (2008) doi:10.1517/14728126.96.36.1995. [PubMed]
66. S. Takayama, H. Takahashi, Y. Matsuo, Y. Okada, and T. Manabe. Effects of Helicobacter pylori infection on human pancreatic cancer cell line. Hepatogastroenterology. 54:2387–2391 (2007). [PubMed]
67. K. A. Steinmetz, and J. D. Potter. Vegetables, fruit, and cancer prevention: a review. J. Am. Diet Assoc.96:1027–1039 (1996) doi:10.1016/S0002–8223(96)00273-8. [PubMed]
68. P. Greenwald. Lifestyle and medical approaches to cancer prevention. Recent Results Cancer Res.166:1–15 (2005). [PubMed]
69. H. Vainio, and E. Weiderpass. Fruit and vegetables in cancer prevention. Nutr. Cancer. 54:111–42 (2006) doi:10.1207/s15327914nc5401_13. [PubMed]
70. L. W. Wattenberg. Chemoprophylaxis of carcinogenesis: a review. Cancer Res. 26:1520–1526 (1966).[PubMed]
71. B. B. Aggarwal, and S. Shishodia. Molecular targets of dietary agents for prevention and therapy of cancer. Biochem. Pharmacol.71:1397–1421 (2006) doi:10.1016/j.bcp.2006.02.009. [PubMed]
72. H. Nishino, M. Murakosh, T. Ii, M. Takemura, M. Kuchide, M. Kanazawa, X. Y. Mou, S. Wada, M. Masuda, Y. Ohsaka, S. Yogosawa, Y. Satomi, and K. Jinno. Carotenoids in cancer chemoprevention. Cancer Metastasis Rev.21:257–264 (2002) doi:10.1023/A:1021206826750. [PubMed]
73. K. B. Harikumar, and B. B. Aggarwal. Resveratrol: A multitargeted agent for age-associated chronic diseases. Cell Cycle. 7:1020–1037 (2008). [PubMed]
74. G. L. Russo. Ins and outs of dietary phytochemicals in cancer chemoprevention. Biochem. Pharmacol. 74:533–544 (2007) doi:10.1016/j.bcp.2007.02.014. [PubMed]
75. R. Agarwal, C. Agarwal, H. Ichikawa, R. P. Singh, and B. B. Aggarwal. Anticancer potential of silymarin: from bench to bed side. Anticancer Res. 26:4457–98 (2006). [PubMed]
76. E. G. Rogan. The natural chemopreventive compound indole-3-carbinol: state of the science. In Vivo. 20:221–228 (2006). [PubMed]
77. N. Juge, R. F. Mithen, and M. Traka. Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cell Mol Life Sci. 64:1105–27 (2007) doi:10.1007/s00018-007-6484-5. [PubMed]
78. L. Chen, and H. Y. Zhang. Cancer preventive mechanisms of the green tea polyphenol (−)-epigallocatechin-3-gallate. Molecules. 12:946–957 (2007). [PMC free article] [PubMed]
79. P. Anand, C. Sundaram, S. Jhurani, A. B. Kunnumakkara, and B. B. Aggarwal. Curcumin and cancer: An “old-age” disease with an “age-old” solution. Cancer Lett. in press (2008). [PubMed]
80. F. Khanum, K. R. Anilakumar, and K. R. Viswanathan. Anticarcinogenic properties of garlic: a review. Crit. Rev. Food Sci. Nutr.44:479–488 (2004) doi:10.1080/10408690490886700. [PubMed]
81. G. Sethi, K. S. Ahn and B. B. Aggarwal. Targeting NF-kB activation pathway by thymoquinone: Role in suppression of antiapoptotic gene products and enhancement of apoptosis. Mole Cancer Res. in press (2008). [PubMed]
82. Y. J. Surh. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem. Toxicol.40:1091–1097 (2002) doi:10.1016/S0278-6915(02)00037-6. [PubMed]
83. Y. Shukla, and M. Singh. Cancer preventive properties of ginger: a brief review. Food Chem. Toxicol.45:683–690 (2007) doi:10.1016/j.fct.2006.11.002. [PubMed]
84. M. M. al-Harbi, S. Qureshi, M. Raza, M. M. Ahmed, A. B. Giangreco, and A. H. Shah. Influence of anethole treatment on the tumour induced by Ehrlich ascites carcinoma cells in paw of Swiss albino mice. Eur. J. Cancer Prev.4:307–318 (1995) doi:10.1097/00008469-199508000-00006. [PubMed]
85. C. K. Sen, K. E. Traber, and L. Packer. Inhibition of NF-kappa B activation in human T-cell lines by anetholdithiolthione. Biochem. Biophys. Res. Commun.218:148–53 (1996) doi:10.1006/bbrc.1996.0026.[PubMed]
86. R. A. Lubet, V. E. Steele, I. Eto, M. M. Juliana, G. J. Kelloff, and C. J. Grubbs. Chemopreventive efficacy of anethole trithione, N-acetyl-L-cysteine, miconazole and phenethylisothiocyanate in the DMBA-induced rat mammary cancer model. Int. J. Cancer. 72:95–101 (1997) doi:10.1002/(SICI)1097-0215(19970703)72:1<95::AID-IJC14>3.0.CO;2-9. [PubMed]
87. Y. Nakagawa, and T. Suzuki. Cytotoxic and xenoestrogenic effects via biotransformation of trans-anethole on isolated rat hepatocytes and cultured MCF-7 human breast cancer cells. Biochem. Pharmacol.66:63–73 (2003) doi:10.1016/S0006-2952(03)00208-9. [PubMed]
88. S. Lam, C. MacAulay, J. C. Le Riche, Y. Dyachkova, A. Coldman, M. Guillaud, E. Hawk, M. O. Christen, and A. F. Gazdar. A randomized phase IIb trial of anethole dithiolethione in smokers with bronchial dysplasia. J. Natl. Cancer Inst.94:1001–1009 (2002). [PubMed]
89. S. Shishodia, and B. B. Aggarwal. Diosgenin inhibits osteoclastogenesis, invasion, and proliferation through the downregulation of Akt, I kappa B kinase activation and NF-kappa B-regulated gene expression. Oncogene. 25:1463–1473 (2006) doi:10.1038/sj.onc.1209194. [PubMed]
90. R. Ghosh, N. Nadiminty, J. E. Fitzpatrick, W. L. Alworth, T. J. Slaga, and A. P. Kumar. Eugenol causes melanoma growth suppression through inhibition of E2F1 transcriptional activity. J. Biol. Chem.280:5812–5819 (2005) doi:10.1074/jbc.M411429200. [PubMed]
91. K. Sukumaran, M. C. Unnikrishnan, and R. Kuttan. Inhibition of tumour promotion in mice by eugenol. Indian J. Physiol. Pharmacol.38:306–308 (1994). [PubMed]
92. K. Imaida, M. Hirose, S. Yamaguchi, S. Takahashi, and N. Ito. Effects of naturally occurring antioxidants on combined 1,2-dimethylhydrazine- and 1-methyl-1-nitrosourea-initiated carcinogenesis in F344 male rats. Cancer Lett.55:53–59 (1990) doi:10.1016/0304-3835(90)90065-6. [PubMed]
93. M. Pisano, G. Pagnan, M. Loi, M. E. Mura, M. G. Tilocca, G. Palmieri, D. Fabbri, M. A. Dettori, G. Delogu, M. Ponzoni, and C. Rozzo. Antiproliferative and pro-apoptotic activity of eugenol-related biphenyls on malignant melanoma cells. Mol Cancer. 6:8 (2007) doi:10.1186/1476-4598-6-8.[PMC free article] [PubMed]
94. S. S. Kim, O. J. Oh, H. Y. Min, E. J. Park, Y. Kim, H. J. Park, Y. Nam Han, and S. K. Lee. Eugenol suppresses cyclooxygenase-2 expression in lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells. Life Sci. 73:337–348 (2003) doi:10.1016/S0024–3205(03)00288-1. [PubMed]
95. H. P. Deigner, G. Wolf, U. Ohlenmacher, and J. Reichling. 1¢-Hydroxyeugenol- and coniferyl alcohol derivatives as effective inhibitors of 5-lipoxygenase and Cu(2+)-mediated low density lipoprotein oxidation. Evidence for a dual mechanism. Arzneimittelforschung. 44:956–961 (1994). [PubMed]
96. C. J. Rompelberg, M. J. Steenwinkel, J. G. van Asten, J. H. van Delft, R. A. Baan, and H. Verhagen. Effect of eugenol on the mutagenicity of benzo[a]pyrene and the formation of benzo[a]pyrene-DNA adducts in the lambda-lacZ-transgenic mouse. Mutat. Res.369:87–96 (1996) doi:10.1016/S0165-1218(96)90052-X. [PubMed]
97. D. P. Richardson. The grain, the wholegrain and nothing but the grain: the science behind wholegrain and the reduced risk of heart disease and cancer. Nutr. Bull.25:353–360 (2000) doi:10.1046/j.1467-3010.2000.00083.x.
98. H. E. Miller, F. Rigelhof, L. Marquart, A. Prakash, and M. Kanter. Antioxidant content of whole grain breakfast cereals, fruits and vegetables. J. Am. Coll. Nutr.19:312S–319S (2000). [PubMed]
99. J. L. Slavin, D. Jacobs, and L. Marquart. Grain processing and nutrition. Crit. Rev. Food Sci. Nutr.40:309–326 (2000) doi:10.1080/10408690091189176. [PubMed]
100. L. Chatenoud, A. Tavani, C. La Vecchia, D. R. Jacobs, Jr, E. Negri, F. Levi, and S. Franceschi. Whole grain food intake and cancer risk. Int. J. Cancer. 77:24–8 (1998) doi:10.1002/(SICI)1097-0215(19980703)77:1<24::AID-IJC5>3.0.CO;2-1. [PubMed]
101. D. R. Jacobs, Jr, L. Marquart, J. Slavin, and L. H. Kushi. Whole-grain intake and cancer: an expanded review and meta-analysis. Nutr. Cancer. 30:85–96 (1998). [PubMed]
102. L. Marquart, K. L. Wiemer, J. M. Jones, and B. Jacob. Whole grains health claims in the USA and other efforts to increase whole-grain consumption. Proc. Nutr. Soc.62:151–160 (2003) doi:10.1079/PNS2003242. [PubMed]
103. M. Eastwood, and D. Kritchevsky. Dietary fiber: how did we get where we are? Annu. Rev. Nutr.25:1–8 (2005) doi:10.1146/annurev.nutr.25.121304.131658. [PubMed]
104. A. McIntyre, P. R. Gibson, and G. P. Young. Butyrate production from dietary fibre and protection against large bowel cancer in a rat model. Gut. 34:386–391 (1993) doi:10.1136/gut.34.3.386.[PMC free article] [PubMed]
105. J. L. Slavin, D. Jacobs, L. Marquart, and K. Wiemer. The role of whole grains in disease prevention. J. Am. Diet Assoc.101:780–5 (2001) doi:10.1016/S0002-8223(01)00194-8. [PubMed]
106. K. S. Ahn, G. Sethi, K. Krishnan, and B. B. Aggarwal. Gamma-tocotrienol inhibits nuclear factor-kappaB signaling pathway through inhibition of receptor-interacting protein and TAK1 leading to suppression of antiapoptotic gene products and potentiation of apoptosis. J. Biol. Chem.282:809–820 (2007) doi:10.1074/jbc.M610028200. [PubMed]
107. F. H. Sarkar, S. Adsule, S. Padhye, S. Kulkarni, and Y. Li. The role of genistein and synthetic derivatives of isoflavone in cancer prevention and therapy. Mini Rev. Med. Chem.6:401–407 (2006) doi:10.2174/138955706776361439. [PubMed]
108. K. W. Lee, H. J. Lee, Y. J. Surh, and C. Y. Lee. Vitamin C and cancer chemoprevention: reappraisal. Am. J. Clin. Nutr.78:1074–1078 (2003). [PubMed]
109. B. A. Ingraham, B. Bragdon, and A. Nohe. Molecular basis of the potential of vitamin D to prevent cancer. Curr. Med. Res. Opin.24:139–149 (2008) doi:10.1185/030079907X253519. [PubMed]
110. F. W. Booth, M. V. Chakravarthy, S. E. Gordon, and E. E. Spangenburg. Waging war on physical inactivity: using modern molecular ammunition against an ancient enemy. J. Appl. Physiol.93:3–30 (2002).[PubMed]
111. G. A. Colditz, C. C. Cannuscio, and A. L. Frazier. Physical activity and reduced risk of colon cancer: implications for prevention. Cancer Causes Control. 8:649–67 (1997) doi:10.1023/A:1018458700185.[PubMed]
112. A. R. Shors, C. Solomon, A. McTiernan, and E. White. Melanoma risk in relation to height, weight, and exercise (United States). Cancer Causes Control. 12:599–606 (2001) doi:10.1023/A:1011211615524.[PubMed]
113. A. Tannenbaum, and H. Silverstone. The initiation and growth of tumors. Introduction. I. Effects of underfeeding. Am. J. Cancer. 38:335–350 (1940).
114. S. D. Hursting, J. A. Lavigne, D. Berrigan, S. N. Perkins, and J. C. Barrett. Calorie restriction, aging, and cancer prevention: mechanisms of action and applicability to humans. Annu. Rev. Med.54:131–152 (2003) doi:10.1146/annurev.med.54.101601.152156. [PubMed]
115. M. H. Ross, and G. Bras. Lasting influence of early caloric restriction on prevalence of neoplasms in the rat. J. Natl. Cancer Inst.47:1095–1113 (1971). [PubMed]
116. D. Albanes. Total calories, body weight, and tumor incidence in mice. Cancer Res.47:1987–92 (1987).[PubMed]
117. L. Gross, and Y. Dreyfuss. Reduction in the incidence of radiation-induced tumors in rats after restriction of food intake. Proc. Natl. Acad. Sci. U S A. 81:7596–7598 (1984) doi:10.1073/pnas.81.23.7596. [PMC free article] [PubMed]
118. L. Gross, and Y. Dreyfuss. Prevention of spontaneous and radiation-induced tumors in rats by reduction of food intake. Proc. Natl. Acad. Sci. U S A. 87:6795–6797 (1990) doi:10.1073/pnas.87.17.6795.[PMC free article] [PubMed]
119. K. Yoshida, T. Inoue, K. Nojima, Y. Hirabayashi, and T. Sado. Calorie restriction reduces the incidence of myeloid leukemia induced by a single whole-body radiation in C3H/He mice. Proc. Natl. Acad. Sci. U S A. 94:2615–2619 (1997) doi:10.1073/pnas.94.6.2615. [PMC free article] [PubMed]
120. V. D. Longo, and C. E. Finch. Evolutionary medicine: From dwarf model systems to healthy centenarians? Science. 299:1342–1346 (2003) doi:10.1126/science.1077991. [PubMed]
In September 2017, Brady released his book, The TB12 Method: How to Achieve a Lifetime of Sustained Peak Performance. In this book, Brady detailed exactly what he eats every day. One main feature of his diet is liberal amounts of alkaline foods and liquids.
In the mornings, Brady doesn’t eat a full meal. When he wakes up at 6:00 am, he drinks 20 ounces of alkaline water infused with electrolytes, including sodium, potassium, magnesium and calcium. He then drinks a smoothie and/or juices containing alkalizing grasses, vegetables, fruit, nuts and seeds. Two hours later, he has another glass of alkaline electrolyte-infused water, and a post-workout protein shake. Brady claims to drink somewhere between 12 and 25 glasses of alkaline water per day.
He also heavily encourages snacking. He usually snacks at around 11:00 am, just before lunch. For lunch, Brady will usually have a piece of fatty fish like salmon and a lot of green vegetables. In the afternoon, he may have another protein shake or protein bar, and around 6:00 pm, Brady eats dinner, which, again, consists of mostly green vegetables.
His book provides recipes for green juices, green soups, green salads, and a few carbohydrate recipes such as his pasta dish — which is odd, considering that he supposedly rarely eats carbs. But even Brady treats himself sometimes. He doesn’t often eat dessert, but he does give a recipe for his famous alkaline avocado ice cream.
His book also contains several alkalizing rules for eating. Brady won’t eat carbohydrates and protein together. He recommends eating carbs or protein with green vegetables instead, as he knows that this is better for assimilation and elimination.
Brady’s chef Allen Campbell says that 80 per cent of his diet is green vegetables and the rest of his diet is grass-fed organic steak and wild salmon.
Brady follows what he refers to as an alkaline lifestyle and diet created by Robert O. Young PhD, in order to minimize muscle inflammation caused by the buildup of lactic acid in the interstitial fluids of the Interstitium (see illustration below). This entails limiting ‘acidifying foods,’ which mostly includes starchy foods like potato, pasta, bread and ALL dairy products.
What is even more interesting is the list of acidic foods that Brady doesn’t eat. For Brady, caffeine, white sugar, white flour, dairy, and some nightshade vegetables — eggplant and mushrooms — are completely off the table. He also won’t consume olive oil if it’s used in cooking — but he’ll have it raw. And he won’t eat high sugar fruit, unless it’s in a smoothie.
Since there are profound benefits with Brady’s pH alkaline diet, and it is clearly sustaining his play on the field, there a 100’s of specific health and fitness benefits of the pH alkaline lifestyle and diet which are backed by published scientific evidence.
He claims that limiting acidic foods helps control the body’s pH balance. What one eats, drinks, breaths and thinks has a huge effect on the body fluids, including the blood plasma, interstitial and intracellular fluid pH which is ideal at 7.365.
Brady also knows that the alkaline lifestyle and diet can decrease the lactic acids that causes inflammation in the body, leading to ALL sickness and disease, including connective tissue disorders that can end an athlete’s career.
At 41 years young, which is considered ancient in football years, Brady says he wants to play at least another five years. While he is certainly capable, his pH Miracle lifestyle and diet will be a major reason he WILL achieve HIS goal.
To learn more about the pH alkaline lifestyle and diet read The pH Miracle revised and updated – http://www.phoreveryoung.com
To learn more about the lifestyle and attend a pH Miracle Retreat in Marbella, Spain or Sardenia, Italy, go to: http://www.phmiracleretreat.com
Robert O Young’s CPT, MSc, DSc, PhD, Naturopathic Practitioner shares his work, research and discoveries on the ‘true pH values’ of many alkaline and acidic foods. Dr. Young’s ‘true pH values’ of foods and liquids are listed in his book Sick and Tired. The charts below are a simplified version, based upon testing the whole food before burning the food at high temperatures and then measuring the remaining mineral ash. This is critical to understand, because the FDA determines ‘pH values’ by burning the food at 5000 degrees F to simulate the effects of digestion in the stomach when it combines with the hydrochloric acid. All that remains for determining a ‘pH value’ is a mineral ash, without the consideration of ALL acidic or alkaline components, such as the water, sugar and enzyme content. Thus, this procedure used by the FDA for testing common foods gives a ‘false pH value’. This is the reason you cannot rely upon the ‘pH values’ of the FDA food charts.
Conversely, Dr. Young’s method of testing ‘pH values’ includes all the acidic and alkaline components that are not evaluated by the FDA, such as water, sugar and enzymes. Because these components are included in determining the ‘pH values’, they may be considered more accurate than the ‘pH values’ provided by the FDA.
The following is a simplified version of the “Alkaline-Acid Food Chart” that was taken from the revised and updated pH Miracle book (2010). To find a more comprehensive list of specific ‘pH values’ of the foods listed below, refer to Dr. Young’s book, Sick and Tired.
To learn more about alkaline foods and drinks and for great alkaline recipes, read Sick and Tired, The pH Miracle, and The pH Miracle Revised and Updated www.phoreveryoung.com, www.drrobertyoung.com,www.phmiracleretreat.com, www.ijuicenow.com, www.innerlightblue.com, www.phmlife.com, www.phmiraclestore.com