Medically driven food prohibitions

Medically driven food prohibitions

(compiled from NORD [])

Disease/Syndrome Causative Food Cause Comment
Disaccharide intolerance Sucrose, dextrins Autosomal recessive trait characterized by the deficiency or absence of enzymes sucrase and isomaltase in the intestine. Attacks characterized by bloating and diarrhea.
Favism Broadbean (Vicia fava) X-linked recessive trait resulting in low amounts of glucose-P-dehydrogenase. Several subtypes known. Hemolytic anemia may result from consumption of offending foods.
Galactosemia Galactose and lactose (dairy products) Autosomal recessive trait with low levels of any one of three enzymes directly responsible for galactose metabolism. High levels of galactose in the blood results in hepatomegaly, cirrhosis, and renal failure. Infant mortality is ~75%.
Gluten intolerance Wheat, barley, gluten containing foods Autoimmune disease Sensitivity to storage protein (gliadin) in some grains.
Lactose intolerance Dairy products Inborn error of metabolism—low or no lactase enzyme in the intestine. Lactase is required to cleave lactose (a disaccharide of galactose and glucose). Bloating and diarrhea may develop.
Ornithine transcarbamylase deficiency Dietary nitrogen (primarily meat) X-linked recessive disorder resulting in low production of hepatic ornithine transcarbamylase interrupting the urea cycle and leading to accumulation of ammonia. Although usually first seen in neonates, there may be an adult onset.
Citrullinemia is another genetic disease affecting the urea cycle.
Phenylketonuria (PKU disease) Phenylalanine in foods Autosomal recessive trait characterized by inadequate hepatic phenylalanine hydroxylase. Leads to accumulation of phenylpyruvate which may accumulate in the brain and lead to seizures, mental retardation, etc.Products containing phenylalaine must be labeled.
Refractory sprue Wheat, barley and rye Autoimmune disorder triggered by gliadin, a gluten storage protein. Unlike common celiac sprue, adherence to a gluten-free diet may not cause symptoms to abate.
Trimethylaminuria Fish Autosomal recessive resulting in low production of flavin containing monoxygenase enzyme 3 (FMO3). Fish odor syndrome. Failure to breakdown trimethylamine, a build of which results in a fish odor.
Very long chain Acyl CoA dehydrogenase deficiency (LCAD) Very long chain fatty acids Autosomal recessive trait resulting from a mutation in the HADHA gene. Prevents mitochondrial metabolism of very long chain fatty acids.

Other medically driven prohibitions include food allergies, the most common of which are to milk, egg, fish, crustacean shellfish, tree nuts, wheat, peanuts and soybeans which account for 90% of all food allergies in the US. The Food Allergen Labeling and Consumer Protection Act of 2004 (FALCPA), effective January 1, 2006, requires labeling of any product containing these ingredients or a protein derived from one of these offending foods or incidental additives or flavors derived therefrom. Exceptions are limited to any highly refined oil derived from a major food allergen (e.g., peanut or soybean oil) or any food ingredient exempt from labeling under a petition or notification process specified in the law [].

There are also a number of food-drug interactions, the consumption of one interfering with the metabolism of the other, which may result in an enhanced or abated effect of the drug (Table 2).

Food drug interactions

Used with permission from Kotsonis and Burdock []

Enzyme or Transporter Food Drug
CYP1A2 Caffeine, theophylline, grapefruit juice (naringen and furanocourmarins bergmottin and dihydroxybergamotin), grape juice, cruciferous vegetables, apiaceous vegetables, cooked meat Clozapine, fluvoxamine, imipramine
CYP2E1 Watercress and possibly other isothiocyanate-containing cruciferous vegetables; polyunsaturated fatty acids (corn oil, menhaden oil) Ethanol, halothane, enflurane
CYP3A4 Grapefruit, orange juice, red wine, possibly other polyphenol-containing substances, St. Johns wort, garlic Ketoconazole, cyclosporine, erythromycin, protease inhibitors, HMG-CoA reductase inhibitors
UGT and GST Brussels sprouts, cabbage, watercress, broccoli Acetaminophen, oxazepam, morphine, ibuprofen
P-glycopeptide and OATP Vegetables, fruit juice, St. Johns wort Digoxin, cyclosporine, parvastatin

Toxin Incorporation during Growth, Storage or Processing

Environmental contaminants

Selenium in grain

Selenium (Se) enters the food chain via plant and microorganism conversion of inorganic selenium to organically bound forms []. Selenium toxicity (i.e., selenosis), caused by excessive selenium intake, has occurred on a large scale in seleniferous regions in China as the result of increased consumption of selenium-containing foods (approximate daily intake of 3–6.5 mg Se/day) []. The most common symptoms of selenosis are loss of hair, deformity, and loss of nails. Other reported symptoms include increased blood selenium levels, diarrhea, fatigue, a garlic-like odor of the breath and bodily secretions, irritability, peripheral neuropathy, and skin lesions []. Selenium intake levels that cause selenosis have not yet been well defined. Studies in China suggest that approximately 3–5 mg/day (0.05–0.08 mg/kg/day) will cause selenosis. Residents of seleniferous regions in South Dakota who consumed approximately 700 µg selenium/day (0.01 mg/kg/day) showed no symptoms of selenosis. The EPA has proposed an oral reference dose (RfD) of 0.005 mg/kg bw/day, or 350 µg/day [].

Methyl mercury in seafood

Exposure to elemental mercury is relatively rare, although was once an occupational disease of hat manufacturers as elemental mercury was used for the curing of animal pelts. Inhalation of the mercury fumes led to mental deterioration and subsequently named “mad hatter syndrome” [].

Of interest to food toxicology, is the methyl derivative, methyl mercury, formed by bacterial action in an aquatic environment from anthropogenic and natural sources of elemental mercury. Anthropogenic sources include burning of coal (which contains mercury), chloralkali process and other sources of elemental mercury into aquatic environments. In the case of Minamata, Japan, there was a direct discharge of methyl mercury into the environment.

Methyl mercury exposure may cause neurological paresthesias, ataxia, dysarthria, hearing defects and death. Developmental delays have been documented in children borne of mothers exposed to methyl mercury []. Other than direct exposure to methyl mercury, exposure usually comes about as the result of methyl mercury becoming incorporated into the food chain, moving up as each predator consumes the smaller and less fortunate animal.

Near the peak of the food chain, methyl mercury becomes concentrated in fish including, bonito (Sarda spp.), halibut (Hippoglossus spp.), mackerel (Scomberomorus spp.), marlin (Makaira spp.), shark (all species), swordfish (Xiphias gladius), and bluefin tuna (Thunnus spp.). The selection of these species was based on historical data on levels of methyl mercury found in fish consumed in the U.S. The selection was also based on an FDA action level of 1.0 ppm in the edible portion of fish []. However, the allowable level of mercury depends on whether the mercury was “added”; that is, did the presence of mercury arise from an anthropogenic source (i.e., was the fish caught in an area known for mercury discharge), or was not added and the result of mercury naturally present in the environment [].

Naturally formed substances

β-Thujone

Thujone, a monoterpene ketone, is the primary constituent of essential oils derived from a variety of plants, including sage (Salvia officinalis), clary (Salvia sclarea), tansy (Tanacetum vulgare), wormwood (Artemisia spp. and white cedar (Thuja occidentalis L.) []. Essential oils from these plants are used in herbal medicines, as flavorings in alcoholic drinks and fragrances throughout the world. Thujone is potentially toxic and the presence of alpha- or beta-thujone in food and beverages is regulated by law in several countries. In the US, thujone as an isolated substance is banned as an ingredient to be added to food and many of the natural thujone-containing plant oils (e.g., wormwood, white cedar, oak moss (Evernia prunastri) and tansy) are used as flavorings in food under the condition that the finished food is thujone-free []. Absinthe (made from wormwood) contains significant levels of thujone and is available in Spain, Denmark and Portugal. Wormwood itself is a popular flavoring for vodka in Sweden, while vermouth, chartreuse, and Benedictine all contain small levels of thujone []. Sage oil is used to provide the characteristic flavor in sausages, meats, condiments and sauces, and contains approximately 20–30% thujone (alpha- and beta-) [,].

Both alpha- and beta-thujone act as noncompetitive blockers of the gamma-aminobutyric acid (GABA)-gated chloride channel []. The essential oils of sage, hyssop (Hyssopus officinalis L.), and cedar all contain thujone and have been cited to have caused central nervous system effects characterized by tonic-clonic or solely clonic convulsions []. Thujone is believed to be the toxic agent in absinthism, a syndrome produced by the chronic use of absinthe, made from the essence of wormwood. The syndrome is characterized by addiction, hyperexcitability and hallucinations. The debilitating illnesses suffered by Vincent Van Gogh and Henri de Toulouse-Lautrec have been linked to absinthism, while the toxicity of thujone was a major factor in banning absinthe in the early 1900s []. A published case report detailed a male subject that drank about 10 mL of essential oil of wormwood (believing it was absinthe) and became agitated, incoherent and disoriented, subsequently developing renal failure []. The no observable effect limit (NOEL) for convulsions in subchronic toxicity studies in female rats was 5 mg/kg bw/day []. Detoxification of thujone is thought to occur via CYP450-dependent oxidation and subsequent glucuronidation and excretion []. The FDA limits exposure to β-thujone from Artemisia spp., when used as a natural flavoring substance or natural substance used in conjunction with flavors (21 CFR 182.20).

Prussic acid in cherry, apple and peach pits

Prussic acid (also known as hydrocyanic acid, hydrogen cyanide, or cyanide) is formed when cyanogenic glycosides found in leaves, cherry, apple and peach pits, oak moss and other plant tissues are damaged and come into contact with beta-glycosidase or emulsion enzymes. The enzymes release the cyanide from the glycoside, and the cyanide prevents the body’s cells from utilizing oxygen, resulting in cellular necrosis and tissue damage. The mucous membranes and blood are bright red as they are oxygenated, but the cells in the tissues cannot utilize the oxygen. Clinical signs of prussic acid poisoning include rapid breathing, trembling, incoordination and in extreme cases, respiratory and/or cardiac arrest []. Many fruit trees contain prussic acid glycosides in the leaves and seeds, but only negligible levels are present in the fleshy parts of the fruit []. In the west African tropics, cassava is consumed as a dietary staple and inappropriate handling of the cassava prior to processing and consumption can result in a chronic form of cyanide poisoning termed “tropical ataxic neuropathy”, the result of demyelinization of the optic, auditory, and peripheral nerve tracts [].

Prussic acid as found in flavoring ingredients is limited to 25 ppm in cherry pits (Prunus avium L. or P. cerasus L.), cherry laurel leaves (Prunus laurocerasus L.), elder tree leaves (Sambucus nigra L.), and peach leaves (Prunus persica (L.) Batsch) (21 CFR 172.510); although the extract of bitter almond (Prunus amygdalus Batsch, Prunus armeniaca L., or Prunus persica (L.) Batsch) must be prussic acid free (21 CFR 182.20). There are no FDA regulations or guidelines restricting the presence of prussic acid in apple seed (Malus spp.), probably because extracts of these seeds have no economic value as flavor ingredients.

Hypericin in St. John’s wort

St. John’s wort (Hypericum perforatumFigure 1) is an herbal thought to alleviate symptoms of depression, and standardized extracts of St. John’s wort are consumed typically in tablet or capsule form. The major active antidepressive constituents in St. John’s wort are thought to be hyperforin and hypericin [,]. The mechanism of action is not fully understood, but may involve inhibition of serotonin (5-HT) reuptake, similar to conventional antidepressive drugs. In this manner, hyperforin and hypericin taken in conjunction with other serotonin reuptake inhibitors may contribute to serotonin syndrome, a potentially life-threatening elevation of serotonin in the central nervous system. Hyperforin is also known to induce cytochrome P450 enzymes CYP3A4 and CYP2C9, which can lead to increased metabolism of certain drugs and decreased clinical response [].

Goitrogens (glucosinolates) in Brassica spp.

Certain raw foods have been found to contain substances that suppress the function of the thyroid gland by interfering with the uptake of iodine, an essential nutrient in growth, cognitive function, and hormonal balance. A lack of functional iodine is known to result in cognitive deficiencies (e.g., Cretinism). The decrease in iodine uptake causes the thyroid gland to enlarge, forming a goiter. Foods that have been identified as goitrogenic include spinach, cassava, peanuts, soybeans, strawberries, sweet potatoes, peaches, pears, and vegetables in the Brassica genus, which include broccoli, brussels sprouts, cabbage, canola, cauliflower, mustard greens, radishes, and rapeseed []. Goiter has also been attributed to the consumption of large quantities of uncooked kale or cabbage.

High temperatures (i.e., cooking) inactivate the goitrogenic substances, collectively termed glucosinolates. Cassava (Manihot esculenta) is an essential dietary source of energy in the tropics, but contains high levels of linamarin, a glucosinolate. Cassava must be properly processed-dried, soaked in water or baked to effectively reduce the linamarin content []. Glucosinolates are sulfur-containing substances that are metabolized in the body by thioglucosidase to form thiocyanate, isothiocyanate, nitriles and sulfur. Under certain conditions the isothiocyanates undergo cyclization to form goitrins, increasing their potent goitrogenic activity. The oils from rapeseed (Brassica napus) must be analyzed for potential goitrins to circumvent potential goitrogenic activity when consuming these oils []. No FDA regulations were located for permissible concentrations of glucosinolates in human food. Glucosinolates (calculated as epi-progoitrin) and goitrin are limited to not more than 4% and 0.1% (respectively) of the seed meal of Crambe abyssinica (Crambe meal) obtained after the removal of the oil and used as an animal feed ingredient (21 CFR 573.310).

 Erucic acid in rape

Rape (Brassica napus L. or Brassica campestris L.) is an annual herb of the mustard family native to Europe and is grown in the United States because it produces oil-rich seeds for cooking oil []. Rapeseed oil had been used for hundreds of years as oil for lamps and more recently as machine oil lubricant. Widespread use of rapeseed oil as a food ingredient was not considered until the late 1940s and 50s. However, early studies found that feeding high levels of rapeseed oil to rats significantly increased cholesterol levels in the adrenal glands and lipidosis in the cardiac tissue [,]. This effect was also noted in chickens, ducks and turkeys fed high levels of rapeseed oil, resulting in growth retardation, mortality, and a thickening of the epicardium and increased fibrous tissue in different areas of the myocardium []. Erucic acid was identified as the causative agent of these effects of rapeseed oil. Erucic acid is a long-chain fatty acid with one unsaturated carbon-carbon bond (C22:1). High levels of erucic acid have been liked to fatty deposit formation in heart muscle in animals []. Erucic acid is poorly oxidized by the mitochondrial β-oxidation system, especially by the myocardial cells, which results in an accumulation of erucic acid, producing myocardial lipidosis which has been reported to reduce the contractile force of the heart []. Although myocardial lipidosis due to erucic acid consumption has not been confirmed in humans, animal feeding studies confirmed the formation of myocardial lipidosis in a variety of animal species in a dose-dependent manner, which has been the standard assessment by government agencies of potential adverse effects in humans. Canola oil is obtained from Canola (Canadian oil, low acid), a rapeseed variety that was conventionally bred in the late 1970s in Canada to contain reduced levels of erucic acid and glucosinolates [,]. The FDA limits the amount of erucic acid in Canola oil to no more than 2% of the component fatty acids (21 CFR 184.1555).

Furocoumarins

Furocoumarins represent a family of natural food constituents with phototoxic and photomutagenic properties. They are found mainly in plants belonging to the Rutaceae (e.g., citrus fruits) and Umbelliferae(e.g., parsnip, parsley, celery, carrots) families. Furocoumarins are produced in response to stress, to aid plants in defense against viruses, bacteria, fungi, insects and animals, and are regarded as natural pesticides []. Concentrations may also increase after exposure to UV radiation, changes in temperature, prolonged storage, or treatment with hypochlorite or copper sulfate (Chaudhary et al., as cited in Wagstaff 1991 [], p. 270 and Beier et al., as cited in Ashwood-Smith [], p. 916).

The three most active furocoumarins in producing photodermatitis are psoralen, 5-methoxypsoralen (5-MOP, bergapten), and 8-methoxypsoralen (8-MOP, xanthotoxin or methoxsalen) []. In the presence of near UV light (320–380 nm), these three linear furocoumarins can form adducts with DNA and DNA-crosslinks. The consequences of these photoadditions to cells are cell death, mutations and chromosome aberrations []. In the presence of ultraviolet A radiation, 5-MOP and 8-MOP produce skin tumors in experimental animals. At a chronic dose of 37.5 mg/kg bw/day in the diet, 8-MOP produces increased incidences of tubular cell hyperplasia, adenomas, and adenocarcinomas of the kidney and carcinomas of the Zymbal gland in rats []. Cases of skin cancer have been reported in patients treated with 8-MOP and long-wave ultraviolet light for treatment of psoriasis or mycosis fungoides [,]. IARC has classified 5-MOP and 8-MOP plus ultraviolet radiation in group A (probably carcinogenic in humans) and in group 1 (carcinogenic to humans), respectively [,].

Citrus fruits, especially grapefruit, produce a variety of chemicals in their peels that may have adverse interactions with drugs. Typically, citrus fruit juice is produced utilizing the whole fruit, including the peel. One chemical found in the peel is bergamottin (also known as bergamot), a natural furanocoumarin that is known to inhibit some isoforms of the cytochrome P450 enzyme (CYP) 3A4 []. Inhibition of this enzyme prevents oxidative metabolism of certain drugs, resulting in an elevated concentration of a drug in the bloodstream []. Bergamot and other chemicals in citrus (e.g., lime, grapefruit, orange, lemon) oils [] are also phototoxic, causing significant toxicity to the skin when exposed to sunlight []. 5-Methoxypsoralen, the most phototoxic constituent of bergamot oil, showed mutagenic activity in bacterial assays and clastogenic effects in mammalian cells in culture when exposed to UV light [].

Celery reportedly contains 100 ppb psoralens (100 micrograms/kg) and parsnips as much as 40 ppm (40 mg/kg) []. The estimated dietary intake of furocoumarins for people eating furocoumarin-containing foods (est. 80% of the population) is 1.31 mg/day [], which is approximately 0.022 mg/kg bw/day for a 60 kg human. This is approximately 1000-fold lower than the 13-week dietary no observable adverse effect level (NOAEL) for liver toxicity in the rat (25 mg 8-MOP/kg bw/day) and 1700-fold lower than the dietary dose that has been shown to induce cancer in rats (37.5 mg/kg). Therefore, the risk of developing liver toxicity or cancer due to ingestion of psoralens in the diet is low.

In humans, the phototoxic threshold dose of furocoumarin mixtures after dietary exposure is of the order of 10 mg 8-MOP plus 10 mg 5-MOP, which is equivalent to about 15 mg 8-MOP per person. This phototoxic threshold dose is not reached by the consumption of celery roots and other conventional vegetables under normal dietary habits, which result in intake of approximately 2–8 mg furocoumarins per person []. Therefore, ordinarily dietary exposure to psoralens is not considered to be a significant risk for development of photodermatitis, albeit the margin of safety is low []. There are no FDA regulations or guidelines specific to the presence of furocoumarins in food.

4.2.7. Amylase inhibitors

Naturally occurring inhibitors of α-amylase are found in aqueous extracts of wheat, rye and kidney beans. The physiological role of α-amylase inhibitors in plants is not well understood, but may protect them against insect infestation. In mammals, some amylase inhibitors have been shown to attenuate the normal increase in blood glucose that occurs after ingestion of starch. However, since α-amylase inhibitors have been shown to be inactivated by gastric acid, pepsin or pancreatic proteinases, their potential as “starch blockers” is limited []. α-Amylase inhibitors were once added to foods as “starch blockers” to limit carbohydrate absorption for the purpose of weight loss; however, the FDA later determined that at least this use of α-amylase inhibitors was as drug, and they were consequently taken off the market [].

α-Amylase inhibitor protein is a major allergen (referred to as Asp o 2) that has been implicated in the development of occupational toxicity known as “baker’s asthma disease” []. Although α-amylase inhibitor protein is naturally found in wheat flour, it is also found in flour in which α-amylase from Aspergillus oryzae has been added to enhance carbohydrate fermentation by yeast []. Consequently, α-amylase inhibitor protein can be potentially found in baked products that are derived from sources other than wheat. Cases of food allergy have been reported in people ingesting bread containing α-amylase inhibitor protein. Symptoms of allergy include sneezing, rhinorrhea, oropharyngeal itching, hoarseness, cough and dyspnea [].

High α-amylase inhibitor activity against human salivary α-amylase has been found in wheat flour (590 units/g), whole wheat flour (351 units/g) and whole rye flour (186 units/g). Bread baking reduces the activity by 80–100%, depending on type. The activity in uncooked spaghetti (248 units/g) is reduced more than 98% by 15 minutes of boiling. Boiling of red beans for 1.5 hours reduces activity to undetectable levels []. However, α-amylase has been shown to retain some allergenic activity when heated to 200 °C (Baur et al., as cited in Phadia AB 2010 [], p. 2).

Lectins in legumes

Lectins are a group of glycoproteins that are present in high levels in legumes (e.g., black beans, soybeans, lima beans, kidney beans and lentils) and grain products [,]. Lectins can reversibly bind to carbohydrates without altering their covalent structure []. The ability of lectins to bind to and agglutinate red blood cells is well known and used for blood typing—hence the lectins are commonly called hemagglutinins. Lectins also can bind avidly to mucosal cells and interfere with nutrient absorption from the intestine []. Because the ability of the lectins to cause intestinal malabsorption is dependent on the presence of enteric bacteria, it has been hypothesized that lectins may also produce toxicity by facilitating bacterial growth in the GI tract [].

Lectins isolated from black beans can produce growth retardation when fed to rats at 0.5% of the diet, and lectin from kidney beans causes death within two weeks when fed to rats at 0.5% of the diet. Soybean lectin produces growth retardation when fed to rats at 1% of the diet. The castor bean lectin ricin (one of the most toxic natural substances known) is notorious for causing deaths of children, and has been used as an instrument of bioterrorism [].

Phytohaemagglutinin (PHA) is a lectin found in significant quantities (as much as 2.4–5% of total protein) in legumes such as red or white kidney beans, green beans and fava beans. PHA has a number of different properties, including the ability to induce mitosis, affect membrane transport and permeability to proteins, and agglutinate red blood cells. Rats fed a diet containing 6% PHA exhibit weight loss, associated with malabsorption of lipid, nitrogen and vitamin B12 []. PHA from red kidney beans inhibits sodium and chloride absorption in the rabbit ileum, indicating that PHA can affect electrolyte transport in the gut []. Symptoms of toxicity to PHA in humans such as nausea, vomiting, or diarrhea occur within three hours of ingestion. Recovery generally occurs within four or five hours of onset [].

There are no FDA regulations or guidelines restricting the presence of lectins in food, but the FDA does provide recommended cooking practices prior to consuming legumes. Concentrations of PHA (and other lectins) are higher in uncooked than cooked beans. A raw, red kidney bean can contain up to 70,000 hemagluttinating units (hau). Most lectins are reduced by moist, but not dry heat. Therefore, steaming or boiling causes a significant reduction in concentrations of lectins in beans. Boiling for at least ten minutes has been shown to reduce hau in beans by 200-fold. Because cooking temperatures under 176 °F do not destroy lectin, use of slow cooking and/or a crockpot is not advised for cooking beans [].

Anti-thiamine compounds

Substances that act on the availability of vitamins are commonly referred to as antivitamins. These include materials that can cause a deficiency of vitamins by competing with vitamins in various metabolic reactions as the result of similar chemical structure or destroying or decreasing the effects of a vitamin by modifying the molecular conformation or by forming a complex [].

Thiaminase cleaves thiamine (vitamin B1) at the methylene linkage, rendering it biologically inactive. Activity of thiaminase requires a cosubstrate—usually an amine or sulfhydryl-containing protein such as proline or cysteine. Thiaminase is found in fish, crab, clams and in some fruits and vegetables such as blueberries, black currants, red beets, Brussels sprouts and red cabbage [].

Thiamine is an essential vitamin involved in energy production. Thiamine deficiency is associated with impaired pyruvate utilization, resulting in a shortage of cellular ATP. In humans, thiamine deficiency may lead to weakness and weight loss. Severe thiamine deficiency produces “beri-beri”, a disease characterized by anorexia, cardiac enlargement, and muscular weakness leading to ataxia []. Cooking destroys thiaminases in fish and other sources. There are no FDA regulations or guidelines specific to the presence of thiaminase in food.

 Pyrrolizidine alkaloids

Pyrrolizidine alkaloids (PAs) are found in some plants of the Apocyanacae, Asteraceae, Boraginaceae, Compositae (Senecionae and Eupatoriae), Fabaceae, Leguminosae (Crotalaria), Rannuculaceae and Scrophulariaceae families. Herbs such as comfrey root and leaf (Symphytum spp.) (Figure 2), coltsfoot leaf and flower (Tussilago farfara) and borage leaf (Borago officinale), and several species of Eupatoriumtypically contain high levels of PAs. Humans are exposed to PAs through the accidental contamination of foodstuffs and intentional ingestion of PA-containing vegetables and herbal medicines. Serious incidences of illness have been reported in people consuming cereal grains that are contaminated with the seeds of PA-containing plants []. PAs are also present in milk from cows and goats and in honey [].

Published by

connie dello buono

Health educator, author and enterpreneur motherhealth@gmail.com or conniedbuono@gmail.com ; cell 408-854-1883 Helping families in the bay area by providing compassionate and live-in caregivers for homebound bay area seniors. Blogs at www.clubalthea.com Currently writing a self help and self cure ebook to help transform others in their journey to wellness, Healing within, transform inside and out. This is a compilation of topics Connie answered at quora.com and posts in this site.

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