What Are Those Miracle Drugs Really Doing to Your Insides?
Historically pharmacy and pharmaceuticals related to healing originated from plants and knowledge of their use that developed over the ages from prehistoric times (Ellis, 2000). The Arabs established the first drug stores in the world in Baghdad around 754 AD. Their research and pharmaceutical science included some two thousand medicinal herbs to be used in specific treatments (Hadzovic, 1997).
Over time the pharmacy tradition spread to Europe. In the Middle Ages, pharmacy and healing herbs often operated under the purview of the various monastic orders. The monastery of Olimje in Slovenia, founded by the Pauline monks, has the third oldest pharmacy in Europe after Paris and Dubrovnik. Over time, healing herbs and herbalist monks gave way to physicians, modern-day pharmacies and many small drug companies.
DISEASE TREATMENT WITH NUTRITION
Although in 1601 some physicians understood that lemons and limes could prevent scurvy, the idea that a substance in the diet could prevent certain diseases did not register with the medical experts for hundreds of years. Pellagra is a good example of a deficiency disease that can be eliminated with proper nutrition. In 1915, eleven thousand deaths from pellagra were reported in the southern U.S. and just two years later there were more than 170,000 cases. Dr. Goldberger showed that he could eliminate the disease by improving the diet in 1918. But despite this knowledge, people continued to die from pellagra in large numbers, even into the 1950s.
Why did people continue to fall victim to a disease that was entirely preventable? Pasteur’s and Koch’s postulates regarding germ theory, namely that microbes cause all diseases, were widely accepted. Medical doctors believed that the nutritional diseases of rickets, beriberi and others were caused by a microorganism.
The victims of pellagra were poor and mostly black Americans living in the South. Their diet consisted largely of maize which contained no tryptophan, the precursor of niacin (vitamin B3) (Mahan, 2004). In Europe, maize was introduced from the Americas after the voyages of Columbus and other explorers and soon came into the food supply. In Italy, Spain and other countries, many poor peasants died from pellagra because of a steady diet of maize polenta made from milled maize. American Indians knew how to prepare maize properly to preserve or enhance the nutrients. The traditional method of preparing maize calls for soaking the grain in lime water which releases the niacin that is bound up in the grain, improves the quality of the amino acids (Fallon, 2001), and significantly reduces the molds that can infect maize. The Indians also mixed it with many kinds of other foods and therefore were not niacin-deficient and victims of pellagra (Jacob, 2007).
In fact the health of America was at such a low state at the turn of the twentieth century that almost one-third of World War I new recruits were rejected for a range of more than two hundred diseases. Young draftees were rejected for rickets, pellagra, goiter and many other diseases. The uproar that ensued led to food fortification programs, widely claimed to solve the problem (Markel, 2005).
It wasn’t until 1941 that the Food and Nutrition Board, part of the National Academy of Sciences, addressed the issue of nutrition’s role in disease and issued the first RDAs (required daily allowances) in 1941. The panel set the lower limits of nutrients needed to prevent diseases such as beriberi, rickets, pellagra, scurvy and others. In 1997 the Food and Nutrition Board created the DRIs (dietary reference intakes), a complicated four-level set of guidelines that tries to put some substance into the amounts of nutrients required for health at different ages: the updated RDAs; the tolerable, nutrient levels which could be harmful if exceeded; the EAR, an estimate average requirement, which meets the needs of 50 percent of people with that level of consumption; and AI, adequate intake, a value similar to the RDAs.
According to Ross Pelton, RPh, PhD, CCN, the author of Drug Induced Nutrient Depletion, RDAs represent the “minimum wage of nutrition.” He says that the government has been promoting the RDAs for over fifty years as guidelines that will meet the needs of healthy individuals. “Could this be the reason why the United States has the highest level of technology and the highest rate of disease?” he asks. “It is important for people to realize that the RDAs have nothing to do with optimal heath and wellness. In most cases nutrient intake for optimal health is far beyond the RDAs” (Pelton, 2001).
ENTER MIRACLE DRUGS
At about the time that the Food and Nutrition Board got around to establishing RDAs, the drug penicillin started to make headlines. When it came into use shortly after World War II, it was referred to as a “miracle drug” (Bynum, 2006).
In the United States, these erstwhile “miracle drugs” have left a legacy of disease and death. Adverse drug reactions or ADRs are one of the leading causes of death in the U.S., accounting for over one hundred thousand deaths and one and one-half million hospitalizations a year. An additional three-quarters of a million people a year develop an adverse reaction after they are hospitalized. An ADR is a serious reaction to a drug that has been prescribed by a physician. As statistics show, taking prescription drugs is a high-risk behavior (Lazarou J, 1998).
The older you get, the more you are at risk for ADRs. Studies of the percentage of hospital admissions related to adverse drug reactions found that up to 88 percent of ADR-related hospitalizations in the elderly are preventable and that elderly people are four times more likely to be hospitalized by ADR-related problems than nonelderly (Vestal, 1984).
Studies revealed that almost 30 percent of all emergency department visits were drug-related, including a large proportion due to adverse drug reactions and inappropriate prescriptions. About 70 percent were preventable. (Patel, 2002).
DRUG-NUTRIENT INTERACTIONS
The shockingly high number of people affected by death, illness and suffering related to ADRs is only the tip of the iceberg. Drugs are also involved in drug-nutrient interactions and drug-nutrient depletions.
Drug-induced nutrient depletion refers to the chronic nutrient deficiencies that occur over time through the use of drugs. A major source of information about the effects of drugs on nutrients, Drug Induced Nutrient Depletion Handbook, 2nd edition, by Pelton, LaValle and others, is out of print with no plans for another edition. It is even difficult to find this book in medical libraries.
A drug interaction occurs when a drug or another substance modifies the effect of an ingested drug with an alteration in drug absorption, distribution, biotransformation or excretion. Various types of interactions exist, including drug-drug, drug-nutrient, food-drug, and herb-drug. Adverse effects due to drug interactions are one of the leading causes of death in hospitalized patients (Boullata, 2004).
A drug-nutrient interaction, or DNI, is an interaction resulting from a physical, chemical, physiological, or pathophysiological relationship between a drug and a nutrient involving a single or multiple nutrients, food in general, or nutritional status which is considered clinically significant.
The DNI can change the effect of the drug, leading to malnutrition, provoke a state of altered metabolism or cause a nutrient imbalance (Boullata, 2012). Drugs and nutrients interact because they use the same enzyme systems in the small intestine and liver. Drugs may enhance or inhibit the activities of enzymes, or nutrients may act on drugs (Rolfes, 2006).
One classic and well-known interaction is the interaction between grapefruit juice and simvastatin—grapefruit juice increases bioavailability and makes the simvastatin toxic (Boullata, 2012). Daidzein, a phytoestrogen in soy, increases the bioavailability of theophylline, and further depletes vitamins B1 and B6. Antiepileptic drugs adversely affect vitamin D and K; they affect folate metabolism, biotin status, carnitine status and bone health; and they can cause liver toxicity. Antipsychotic drugs are associated with weight gain, hyperglycemia and elevated lipids (Boullate, 2012; Rolfes, 2006).
Drugs may also cause nutrient depletions by altering the appetite, interfering with taste or smell, inducing nausea and vomiting, causing dry mouth or inflammation in the mouth, changing the acidity of the digestive tract, damaging the cells, binding to nutrients, using similar enzyme systems, competing for transporters, and causing diarrhea (Rolfes, 2006).
Drugs can inhibit specific enzymes which affects the metabolism of other drugs, hormones, vitamins, bile acids and other substances. The most commonly affected are those involving biotransformation of the cytochrome P 450 pathways. The cytochrome P 450 enzyme systems play vital roles in a myriad of reactions in the body, from hormone production to detoxification (Jones, 2005).
YOUR FAVORITE OVER-THE-COUNTER DRUG?
The American College of Cardiology (ACC) and the American Heart Association (AHA) recommend the use of aspirin in low dosages under a doctor’s care for people who have experienced a variety of heart conditions. According to a Bayer Aspirin website, “Aspirin isn’t right for everyone so you should always check with your doctor before beginning an aspirin regimen.” Aspirin is recommended for those who have a heart condition. Does that mean that aging and being elderly are synonymous with having a heart condition? Many elderly people regularly take aspirin on the advice of their doctor “because it is good for their heart.” The Bayer Aspirin website states that taking the aspirin regularly “protects against heart attack and stroke.”
My eighty-six-year-old mother takes Ecotrin every other day: 325 milligrams (mg) of coated aspirin. She does not have a heart condition and never has had a heart attack. The coating is designed to protect the stomach lining which will become inflamed from too many of these drugs. The coating of the aspirin contains 50 mg of aluminum (Olree, 2008). Aluminum has been linked with dementia and senility (Flaten, 2001; Banks and Kastin, 1989).
Aspirin may have significant impact on the nutritional status of users. Nausea, vomiting and induced bleeding can lead to nutritional depletions. Larger doses of aspirin affect carbohydrate metabolism, induce hyperglycemia and deplete muscle glycogen. They inhibit lipolysis, the breakdown of fatty acids from adipose tissue, and may cause liver damage and decreased renal function (Boullata, 2004). Aspirin depletes folic acid, iron, potassium, sodium and vitamin C (Pelton, 2001). Vitamin E taken with aspirin can cause excess bleeding, colitis and damage to the villi of the brush border enzymes and intestinal transport systems. The result is general malabsorption, especially of iron and calcium. This over-the-counter remedy has many dark sides.
For years my mother has also been taking Prilosec, a proton pump inhibitor (PPI), which lowers acid production in the stomach. Her doctor says that she needs it to protect the stomach lining from the aspirin. PPIs are commonly used in the elderly for gastritis, GERD, and to prevent NSAID-induced ulcers. The currently available PPIs are omeprazole (Prilosec), lansoprazole, esomeprazole, rabeprazole and patoprazole (Boullata, 2004).
Despite the Prilosec, my mother’s last endoscopy showed that her stomach and esophagus are inflamed. During that visit, I asked the gastroenterologist if she would be harmed from lowered stomach acid. He told me that she doesn’t need hydrochloric acid, because it is not that important, and he wasn’t going to argue about it. Yet we know that hydrochloric acid in the stomach kicks off digestion and tells the pancreas to do its job. It is an important step in the process of successful digestion. With aging, levels of hydrochloric acid lessen over time. Yet the prescribing of an acid-lowering medication to an aging population with a characteristic low stomach acid production continues by medical professionals.
STOMACH ACID REDUCERS
Pepcid and Zantac are also drugs used to treat ulcer disease and GERD, gastro-esophageal reflux disease. They inhibit gastric acid secretion and raise the gastric pH of the stomach. These effects impair B12 absorption. Raising pH is thought to lead to decreased absorption of calcium, iron, zinc, folic acid, and beta-carotene (Mahan and Escott-Stump, 2004).
Proton pump inhibitors and H2 blockers have been linked with osteoporosis and brittle bones (Briot, 2012; Yang, Lewis, Epstein, & Metz, 2006), and increased risk of Helicobacter pylori infection. H. pylori is strongly associated in many studies with gastritis, duodenal ulcer, gastric cancer and nonulcer dyspepsia (Zhang, 2005; Veldhuyzen van Zanten and Sherman, 1994). There is also cause for concern that PPIs directly induce the pattern of gastritis most associated with increased risk of gastric cancer (McColl, 2004).
During the long course of PPI therapy, my mother was diagnosed with an H. pylori infection. The treatment was a course of antibiotics. At the end of the first week of therapy she experienced severe digestive issues and visited the emergency room where she was detained for several hours. Despite her distress over not being able to complete the therapy, her doctor was not concerned. He recommended no further treatment for the H. pylori. A short time later she began to lose large patches of hair, which was extremely unsightly. After improving her diet and cutting back on the dosage of PPIs , the hair grew back, not of good quality but at least she did not become completely bald.
VITAMIN B12 DEFICIENCY
One of the most serious areas of concern with PPIs is B12 deficiency induced by chronic use of acid-lowering drugs. B12 was first isolated in 1948. Lower levels of stomach acid are associated with inadequate production of intrinsic factor, needed for B12 absorption. B12 deficiency can easily lead to pernicious anemia, a serious and potentially fatal disease in which the blood cells become macrocytic, that is, fewer in number and enlarged (Pelton, 2001).
Pernicious anemia was described in the late ninteenth and early twentieth century. Gastroenterologists at that time believed that the gastric mucosa was the problem and that hydrochloric acid was a remedy. Doctors also prescribed liver and observed that it improved the condition (Bynum, 2006).
B12 plays a central role in the replication of the genetic code. Symptoms of depletion include fatigue, neuropathy, depression, dermatitis and easy bruising. B12 deficiencies in the elderly often cause neuropsychiatric symptoms such as moodiness, confusion, abnormal gait, memory loss, agitation, delusions, dizziness (falling) and hallucinations (Pelton, 2001).
B12-deficient patients display a variety of signs and symptoms: chronic fatigue, weakness, dizziness, burning and numbness, confusion, disturbances in smell and taste, restless legs, tremor, incontinence, paranoia, violence, sore tongue, premature graying of hair, tinnitus, loss of balance and tendency to fall, multiple sclerosis-like symptoms, and others (Pacholok, 2005).
At greatest risk for B12 deficiency are vegetarians, vegans, and those eating macrobiotic diets; the elderly and those who use proton pump inhibitors, H2 blockers such as Zantac, Tagamet, Pepcid; users of antacids such as Maalox, Mylanta, and Tums; patients taking metformin and other biguanides used to treat diabetes; colchicine, used to treat gout, and those undergoing dental procedures with nitrous oxide. Also at risk are women using oral contraceptives; those with autoimmune diseases like celiac disease, and those taking cholestyramine (Questran), a bile acid sequestrant (BAS) to reduce cholesterol (Pacholok, 2005).
BAS are potent depletors of body nutrients. They actively deplete beta-carotene, calcium, folic acid, iron, magnesium, phosphorus, vitamins A, D,E, K and B12, and zinc. Malabsorption of fat soluble vitamins can occur because the absorption is facilitated by bile acids (Boullata, 2004). With prolonged use, many nutrient deficiencies will manifest themselves (Pelton, 2001).
STATINS—BLOCKBUSTER AND HEALTH BUSTER
According to IMS health, simvastatin is the second most prescribed drug in the U.S. with Lipitor coming in thirteenth place. One in four Americans aged forty-five and older takes statin drugs to lower cholesterol and presumably lower the risk of heart attacks (Mercola, 2011).
Serious side effects have been emerging over the years since statins were introduced. The FDA has now announced that statins may increase the risk of type 2 diabetes. This applies to Zocor (simvastatin), Lipitor (atorvastatin) and Crestor (rosuvastatin) (The New York Times, 2011). Statins have been linked with liver damage, muscle weakness, memory loss and confusion (Mercola, 2011).
Statins are involved in major drug-induced nutrient depletions and increase the risk for heart disease because of their method of action. Depleting the body of CoQ10 by blocking the pathway used to produce cholesterol can lead to heart failure, high blood pressure, angina, mitral valve prolapse, loss of cellular energy and increase in free radicals damaging the mitochondria (Pelton, 2001).
The majority of CoQ10 is manufactured by the cells in a complicated seventeen-step process that requires vitamins B2, B3, B5, B6, B12, C, and folic acid (Pelton, 2001).
Statins, which are intended to reduce cholesterol production, increase insulin levels, blood sugar levels and belly fat. The higher the dosage of statins, the higher the diabetes risk. Cholesterol is necessary for the production of vitamin D, sex hormones and bile production. About 25 percent of the brain is cholesterol (Mercola, 2011).
FOLIC ACID
Without folic acid, DNA synthesis is inhibited, cell replication stops and the cell dies. It is necessary for production of red blood cells. A number of drugs deplete folic acid or suppress folic acid activity, such as methotrexate, daraprim, aspirin, cholesytramine, cortisone, prednisone, estrogens, metformin, hydrocodone and aspirin, ibuprofen, and many others (Pelton, 2001).
Folic acid is one of the most common nutrient deficiencies; the vitamin is easily destroyed by light, heat and oxygen. Heavy losses occur during cooking and storage.
Symptoms associated with folic acid include cervical dysplasia, insomnia, nausea, increased infections, anorexia, megaloblastic anemia, birth defects and elevated homocysteine, which is an independent risk factor for heart disease. During pregnancy, the requirements for folic acid are increased and deficiency increases the risk of spina bifida and cleft palate.
Food sources include dark green leafy vegetables, liver, eggs, beets, broccoli, orange juice, cantaloupe and kidney beans (Pelton, 2001).
SELENIUM
Selenium is depleted by several drugs including corticosteroids and some antibiotics. Symptoms include destructive changes in the heart and pancreas, sore muscles, red blood cell fragility, weakened immune system and increased rates of cancers. The primary cause of deficiency is insufficient dietary intake, food processing losses, and lack in soil because it is not added for crop growth.
In addition, selenium is one of the most powerful anticancer agents and has an important role in detoxification. It is a cofactor for glutathione peroxidase, one of most important antioxidant enzymes in our immune system. Selenium is needed for conversion of thyroid hormone from the storage form, T4, to the active form, T3.
Dietary sources include Brazil nuts, whole grains, seafood, garlic, liver, eggs, dairy, and some vegetables (Pelton, 2001).
GLUTATHIONE
Glutathione, a sulfur containing tripeptide, is a critical nutrient in the body. Acetaminophen, hydrocodone with acetaminophen, and oxycodone with acetaminophen deplete glutathione. This depletion results in a decreased capacity for metabolism and excretion of toxic substances.
Glutathione is a critical part of the detoxifying and antioxidant system, important in cancer prevention. It reduces oxidative damage in mitochondria and red blood cells, and free radical damage.
Dietary sources are avocado, tomatoes, spinach, garlic, asparagus, fish, meat, raw milk, fresh unprocessed meat and tomatoes (Pelton, 2001).
BIFIDOBACTERIA AND LACTOBACILLUS
Bifidobacteria are depleted by most antibiotics, causing a condition called dysbiosis. This probiotic is the primary strain of beneficial bacteria in the large intestine. They produce shortchain fatty acids which are the main sources of energy for the colonocytes that line the colon. The short-chain fatty acids produce an acidic environment hostile to the growth of pathogens, yeasts and molds (Pelton, 2001).
Lactobacillus acidophilus is depleted by almost all antibiotics as well.
MAGNESIUM
Magnesium is a cofactor in over three hundred reactions in the body, necessary for transmission of nerve impulses, temperature regulations, detoxification in the liver and formation of bones and teeth. Deficiency is related to atherosclerosis, hypertension, strokes and heart attacks. Deficiency symptoms include insomnia, muscle cramps, kidney stones, osteoporosis, fear, anxiety, and confusion. Low magnesium levels are found in more than 25 percent of people with diabetes. But magnesium shines brightest in cardiovascular health. It alone can fulfill the role of many common cardiac medications: magnesium inhibits blood clots (like aspirin), thins the blood (like Coumadin), blocks calcium uptake (like calcium channel-blocking durgs such as Procardia) and relaxes blood vessels (like ACE inhibitors such as Vasotec) (Pelton, 2001).
Magnesium is depleted by many estrogen compounds such as oral contraceptives, antibiotics, cortisone, prednisone and blood pressure medications (Pelton, 2001).
Food processing, low levels in the soil and modern farming techniques deplete stores of magnesium. For every molecule of sugar we ingest our bodies use fifty-four molecules of magnesium to process it. Alcohol speeds up the excretion of magnesium from the body. Diuretics in coffee and tea (caffeine) also raise excretion levels.
It is difficult to obtain enough magnesium from food because the magnesium content in foods varies widely. Good sources include nuts, legumes, dark green leafy vegetables and some whole grains (Pelton, 2001).
DIABETIC DRUGS
Diabetic drugs such as metformin (Glucophage) used for the management of type 2 diabetes cause malabsorption of B12 with long term therapy, and folic acid deficiency as well (Pelton, 2001).
An increasing frequency of neuropathy was observed in patients treated with oral diabetic sulfonyulureas. The sulfonylureas (phenformin and tolazamide) depleted CoQ10. Research shows that diabetic patients are CoQ10 deficient, and that the drugs used to treat them further deplete the nutrient. This deficiency may create a pancreatic energy deficit that could account for impaired insulin synthesis (Pelton, 2001). It is also important to mention that many diabetic patients are magnesium-deficient and magnesium seems to play a role in neuropathy. Serum magnesium levels can test as normal, and yet there can be an intracellular depletion of magnesium (Boullata, 2004).
ESTROGENS
Oral contraceptives deplete the levels of six nutrients: vitamins B6, B2, B12, folic acid, zinc and vitamin C. Copper levels can be significantly increased. Iron and vitamin K can be elevated. Uterine dysplasia and changes in cervical cells related to oral contraceptives improved with folic acid supplementation. Other side effects include anxiety, decrease of libido, and depression, related to disturbances in the metabolism of tryptophan (Pelton, 2001). Also observed were decreased brain tyrosine concentration, increased triglycerides, ceruloplasin, beta lipoproteins, blood glucose, a decrease in high density lipoproteins HDL (the so-called good cholesterol) and increased low density lipoproteins LDLs (the so-called bad cholesterol).
Data from the national study, NHANES, showed that those women on oral contraceptives had low serum magnesium compared to a control group of non-pregnant women who were not taking oral contraceptives (Pelton, 2001).
WARFARIN
Warfarin (Coumadin), the most widely prescribed anticoagulant in the world, is used to prevent blood clots in patients who have had heart attacks, open heart surgery and a variety of other problems. Patients using warfarin must be closely monitored. Aspirin, tamoxifen, acetaminophen, some antibiotics, statins and many other drugs can increase the risk of serious bleeding when used with warfarin. Warfarin interferes with vitamin K metabolism. The effects of the drug are reduced by vitamin K foods such as green leafy vegetables. When too much warfarin is given or the patient experiences severe bleeding, vitamin K is given as an antidote (Ansell et al., 2004).
CYP2C9, an important P 450 enzyme, metabolizes warfarin and over one hundred other drugs. The gene that directs this enzyme produces many other versions (polymorphisms) and a great deal of inter-individual variability is involved making the use of warfarin not an “exact science.”
CYP4F2 is a critical enzyme for metabolism of vitamin K and vitamin E and affects warfarin metabolism as well (Caldwell, 2008). Garlic and ginger can decrease clotting, which could enhance warfarin’s effects. Bee pollen can increase action of enzymes that regulate warfarin requiring a reduction in the dose (Boullata, 2012). Ginseng, ginkgo biloba, borage (starflower) oil or fish oils have been reported to increase bleeding. Onions, garlic, vitamin E supplements certain herbals like dong quai, will enhance the effects of warfarin leading to less clotting ability (Rolfes, 2006).
Vitamin K plays an essential role in blood clotting and in bone formation. Without vitamin K the bones produce an abnormal protein that cannot bind to the minerals that normally form bones, and bone density is low. Warfarin inhibits the regeneration of the vitamin K cycle. Even small amounts of vitamin K will inhibit warfarin (Rolfes, 2006). Patients are only advised to consume similar amounts of vitamin K daily to keep the level stable (Rolfes, 2006). Many herbs increase the activity of warfarin. These include St. John’s wort, gingko, garlic, ginsing, dong quai and others (Rolfes, 2006).
THE CHALLENGE
In this day of the Standard American Diet (SAD), fast food, and industrial agriculture, finding nutritious food is a challenge. Even organically grown vegetables can be lacking in minerals. Organic farmers are concerned mainly with avoiding chemicals. The best way to get mineral-rich produce is to purchase it from the farmer’s market, your farming neighbors, a local CSA, or grow your own garden using biodynamic practices.
Raw milk from approved farms contains a rich store of nutrients. Look to your local farmer also for pastured beef, chicken and pork. Trying to eat a whole foods diet, with bone broth, homemade beverages, soaked and fermented grains, will go a long way to keeping you healthy. Nourishing Traditions, written by Sally Fallon and Mary Enig, is a rich collection of recipes using traditional methods of food preparation.
Most drugs deplete nutrients, even those drugs we buy over the counter. We have given you a summary here on the actions of drugs on our health. And we are fortunate in our communities to have reference sources at our disposal. Your local library or university library and the Internet have access to information about drugnutrient interactions and drug-nutrient depletion. To remain healthy and energetic, it is necessary to be aware of what drugs do and don’t do. Be proactive. Read and learn about the drugs you are taking, whether you really need them and what nutrients they are compromising, and then do something about it!
REFERENCES
• Ansell, J., Hirsh, J., Poller, L., Bussey, H., Jacobson, A., & Hylek, E. (2004). The pharmacology and management of the vitamin K antagonists: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest, 126(3 Suppl), 204S-233S.
• Banks, W. A., & Kastin, A. J. (1989). Aluminuminduced neurotoxicity: alterations in membrane function at the blood-brain barrier. Neurosci Biobehav Rev, 13(1), 47-53.
• Blaser, M. J. (2006). Who are we? Indigenous microbes and the ecology of human diseases. EMBO Reports 7 (10): 956–60.
• Boullata, J. I. (2012). Drug-Nutrient Interactions: A Broad View with Implications for Practice. Journal of the Academy of Nutrition and Dietetics, 112(4), 506-517.
• Boullata, J. I., & Armenti, V. T. (2004). Handbook of drug-nutrient interactions. Totowa, N.J.: Humana Press.
• Briot, K. (2012). Drug-induced osteoporosis. Rev Prat 62(2), 187-192.
• Brodzy, P.Q. (1977). Zinc status in the vegetarian. Fed Proc, 36, 1139.
• Bynum, W. F. (2006). The Western medical tradition: 1800-2000. Cambridge; New York: Cambridge University Press.
• Caldwell, M. D., Awad, T., Johnson, J. A., Gage, B. F., Falkowski, M., Gardina, P., Burmester, J. K. (2008). CYP4F2 genetic variant alters required warfarin dose. Blood, 111(8), 4106-4112. doi: 10.1182/ blood-2007-11-122010.
• Davenport, C. B., & Love, A. G. (1920). Defects found in drafted men. [S.l.]: Science Press.
• Ellis, L. (2000). Archaeological method and theory : an encyclopedia. New York: Garland Pub.
• Epstein, R. S., Moyer, T. P., Aubert, R. E., DJ, O. K., Xia, F., Verbrugge, R. R., . . . Teagarden, J. R. (2010). Warfarin genotyping reduces hospitalization rates results from the MM-WES (Medco-Mayo Warfarin Effectiveness study). J Am Coll Cardiol, 55(25), 2804-2812.
• Excellus Health Plan. (2011). Medical Policy. Genotyping- Cytochrome P450 (CYP450) for drug metabolism. www.excellusbcbs.com/wps/wcm/connect/75e1a7804e8eb7f59743bfe420b83c88/mp+genotyp_drug+tac+11.pdf?MOD=AJPERES. Accessed May 27, 2011.
• Fallon, S. & Enig, M. (2001). Nourishing Traditions. The Cookbook that Challenges Policially Correct Nutrition and the Diet Dictocrats. Revised Second Edition. Washington, DC: New Trends Publishing.
• Finkelstein, S. N., & Temin, P. (2008). Reasonable Rx : solving the drug price crisis. Upper Saddle River, N.J.: FT Press/Pearson Education.
• Flaten, T. P. (2001). Aluminium as a risk factor in Alzheimer’s disease, with emphasis on drinking water. Brain Res Bull, 55(2), 187-196.
• Fulton, M. M., & Allen, E. R. (2005). Polypharmacy in the elderly: a literature review. J Am Acad Nurse Pract, 17(4), 123-132. doi: 10.111/j.1041-2972.2005.0020.
• Gremo ven. Monastery Olimje. www.gremoven.com/Cerkve/Samostan-Olimje/menu-id-10 – Accessed 5/22/2012.
• Hadzovic, S. (1997). Pharmacy and the great contribution of Arab-Islamic science to its development]. Med Arh, 51(1-2), 47-50.
• Jacob, H.E. (2007). Six Thousand Years of Bread. Its Holy and Unholy History. New York:NY: Skyhorse Publishing.
• Jones, D. S., & Institute for Functional, M. (2005). Textbook of functional medicine. Gig Harbor, WA.: Institute for Functional Medicine.
• Kremers, E., Urdang, G., & Sonnedecker, G. (1976). Kremers and Urdang’s History of pharmacy. Philadelphia: Lippincott.
• Lazarou J, Pomeranz BH, Corey PN. (1998). Incidence of adverse drug reactions in hospitalized patients: A meta-analysis of prospective studies. Journal of the American Medical Association Apr 15. 279: 1200 – 1205.
• Li, Y., Mezei, O., & Shay, N. F. (2007). Human and murine hepatic sterol-12-alphahydroxylase and other xenobiotic metabolism mRNA are upregulated by soy isoflavones. J Nutr, 137(7), 1705-1712.
• Mahan, L. K., & Escott-Stump, S. (2004). Krause’s food, nutrition, & diet therapy. Philadelphia: Saunders.
• Markel,H. & Golden, J. (2005). Successes and Missed Opportunities in Protecting Children’s Health: Critical Junctures in the History of Children’s Health Policy in the United States. Pediatrics 115: sup 3, 1129-1133.
• Mercola, J. (2011). This Drug Causes Diabetes and Robs You of Nutrients. Mercola.com. Take Control of Your Health Newsletter. http://bit.ly/KYDUqo. Accessed May 20, 2012.
• McColl, K. E. (2004). Helicobacter pylori infection and long term proton pump inhibitor therapy. Gut, 53(1), 5-7.
• Nekvindova, J., & Anzenbacher, P. (2007). Interactions of food and dietary supplements with drug metabolising cytochrome P450 enzymes. Ceska Slov Farm, 56(4), 165-173.
• Olree, Richard. (2008). Minerals for the Genetic Code. State College, PA: Pennsylvania Association for Sustainable Agriculture (conference presentation).
• Pacholok, S. M., & Stuart, J. J. (2005). Could it be B12? An epidemic of misdiagnoses.
• Patel, P. & Zed PJ. (2002). Drug-related visits to the emergency department: How big is the problem?. Pharmacotherapy, 22: 915 – 923.
• Pelton, R. (2001). Drug-induced nutrient depletion handbook. Hudson, OH: Lexi-Comp.
• Rolfes, S. R., & Whitney, E. N. (2006). Understanding normal and clinical nutrition. Belmont, CA: Thomson/Wadsworth.
• Ross, A. C., & Zolfaghari, R. (2011). Cytochrome P450s in the regulation of cellular retinoic acid metabolism. Annu Rev Nutr, 31, 65-87. doi: 10.1146/annurevnutr-072610-145127.
• Sakaki, T., Kagawa, N., Yamamoto, K., & Inouye, K. (2005). Metabolism of vitamin D3 by cytochromes P450. Front Biosci, 10, 119-134.
• Stargrove, M. B., Treasure, J., & McKee, D. L. (2008). Herb, nutrient, and drug interactions : clinical implications and therapeutic strategies. St. Louis, Mo.: Mosby/Elsevier.
• Stephens, M. A., Self, T. H., Lancaster, D., & Nash, T. (1989). Hypothyroidism: effect on warfarin anticoagulation. South Med J, 82(12), 1585-1586.
• Tam, T. W., Akhtar, H., Arnason, J. T., Cvijovic, K., Boon, H., Cameron, D. W., . . . Foster, B. C. (2011). Inhibition of human cytochrome p450 metabolism by blended herbal products and vitamins. J Pharm Pharm Sci, 14(1), 1-16.
• Topol, E.J.(2012). The Diabetes Dilemma for Statin Users. New York Times. Published online March 4, 2012. nytimes.com/2012/03/05/opinion/the-diabetes-dilemma-forstatin-users. Accessed 5/23/2012.
• Tuormaa, T. (1995). The Adverse Effects of Zinc Deficiency. Journal of Orthomolecular Medicine, 10(3-4), 149-164.
• van den Bout-van den Beukel, C. J., Koopmans, P. P., van der Ven, A. J., De Smet, P. A., & Burger, D. M. (2006). Possible drug-metabolism interactions of medicinal herbs with antiretroviral agents. Drug Metab Rev, 38(3), 477-514. doi: 10.1080/03602530600754065
• Veldhuyzen van Zanten, S. J., & Sherman, P. M. (1994). Helicobacter pylori infection as a cause of gastritis, duodenal ulcer, gastric cancer and nonulcer dyspepsia: a systematic overview. CMAJ, 150(2), 177-185.
• Vestal RE;, ed. (1984). Drug Treatment in the Elderly. Sydney, Australia: ADIS Health Science Press.
• Weathermon, R., & Crabb, D. W. (1999). Alcohol and medication interactions. Alcohol Res Health, 23(1), 40-54.
• Wikvall, K. (2001). Cytochrome P450 enzymes in the bioactivation of vitamin D to its hormonal form (review). Int J Mol Med, 7(2), 201-209.
• Williams, R. J. (1956). Biochemical individuality; the basis for the genetotrophic concept. New York: Wiley.
• Yang, Y. X., Lewis, J. D., Epstein, S., & Metz, D. C. (2006). Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA, 296(24), 2947-2953.
• Zhang, C., Yamada, N., Wu, Y. L., Wen, M., Matsuhisa, T., & Matsukura, N. (2005). Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer. World J Gastroenterol, 11(6), 791-796.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Summer 2012.
🖨️ Print post
JOHN HO says
Valuable informations !
Nicole Binns says
In my experience, lowering the amount of acid in my stomach CAUSES stomach irritation. I never use antacids. One day I was feeling a little bit sick at work, not badly, and a coworker offered me an antacid. I tried it, just out of curiosity. Shortly after taking it, I developed burning pain in my stomach as though I had ulcers, which lasted for the rest of the day, and I also had acid reflux and burning in my esophagus. I never had either of those symptoms, and they were very unusual for me, and I *never* use any kind of antacids at all, so I knew it was caused by the antacid. It’s my understanding that acid prevents bacteria from growing in the stomach, and without the acid, bacteria grow freely, causing ulcers and irritation (Helicobacter Pylori or whatever else can grow in the stomach). I have heard so many stories of people who have stomach ulcers who are taking antacids like candy. If only they would stop using antacids and let their stomach produce acid, the ulcers would most likely go away. It’s extremely frustrating to watch people you know and love going to doctors, blindly obeying their instructions and using the drugs they prescribe, and being harmed by those very drugs, while refusing to listen to anybody who tells them to just stop going to the doctor. Avoiding doctors is one of the best ways to stay healthy.
Judy McGrath says
smilies/smiley.gif Fascinating information for anyone taking any kind of medication. Much of this applied to me. For example: I was having night cramps in my legs and lower portion of my body. My gastroenterologist researched the matter for me after having asked several doctors over the years. He told me my magnesium was low. I take supplemental magnesium now and the cramps have disappeared. Thank you for sharing this great research. I take meds. for gerd and realize I suffer a B12 deficiency as a result. I’m very tired all the time and fall down at least every 3 weeks though I appear to be healthy and stable at 54. The falling terrifies me. I will increase my B12 and hopefully will stay upright more often.
Dee says
This article should be amended. The word “FOLATE” should be substituted for the words “FOLIC ACID”. FOLIC ACID is toxic to a surprising large portion of the population people with certain genetic mutations. Folic acid can build up to a toxic level.
Sam Barbary says
I’ve always told friends and family, people don’t have elevated cholesterol because their body isn’t making enough Lipitor. My mom’s total cholesterol was over 300. After seeing a Functional Medicine Doctor, it was determined that she was deficient in copper which is essential for hemoglobin production and liver health. Coincidentally, Cholesterol is made in the liver. Once the copper levels were normalized, cholesterol levels decreased to normal levels.