Nutrients in our Formulas
Contact your health-care provider immediately if you suspect that you have a medical problem. Glutathione is the most powerful internal antioxidant and liver protector. Breathing deeply is always a simple but effective way to treat a weak nervous system. Severe shortage results in death; critical toxemia develops from unmetabolized carbohydrate fragments. Thank you Babette in Oh. Displayed content is offered by businesses which have been compensated.
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Amazon Drive Cloud storage from Amazon. Alexa Actionable Analytics for the Web. AmazonGlobal Ship Orders Internationally. Amazon Inspire Digital Educational Resources. Amazon Rapids Fun stories for kids on the go. Substances that may cause overactivity or induction of the P- enzymes: The family of P enzyme systems is quite diverse, with specific enzyme systems being inducible by particular drugs, toxins or metabolites.
It is this characteristic that has allowed the development of special tests to check the function of the various pathways - see liver tests. The substrate is the substance that is acted upon by the enzyme.
Theophylline, caffeine, phenacetin, acetaminophen, Lidocaine, erythromycin, cyclosporin, ketoconazole, testosterone, estradiol, cortisone, Alprenolol, bopindolol, carvedilol, metoprolol, propranolol , Amitriptyline, clomipramine, desipramine, nortriptyline , Codeine, dextrometh- orphan, ethylmorphine, 4-methoxyamphetamin Family Phenytoin, ibuprofen, naproxen, oxicam drugs, S-warfarin, Diazepam, hexobarbitone, imipramine, omeprazole, alcohol, chlorzoxazone, enflurane.
The liver's third role in detoxification involves a two-step enzymatic process for the neutralization of unwanted chemical compounds. These not only include drugs, pesticides, and toxins from the gut, but also normal body chemicals such as hormones and inflammatory chemicals e. Phase I enzymes directly neutralize some chemicals, but most are converted to intermediate forms that are then processed by phase II enzymes.
These intermediate forms are much more chemically active and therefore more toxic. If the phase II detoxification systems are not working adequately, these intermediates can cause substantial damage, including the initiation of carcinogenic processes. Phase I detoxification of most chemical toxins involves a group of enzymes which, collectively, have been named cytochrome P Some enzymes make up the cytochrome P system.
Each enzyme works best in detoxifying certain types of chemicals, but with considerable overlap in activity among the enzymes. The activity of the various cytochrome P enzymes varies significantly from one individual to another, based on genetics, the individual's level of exposure to chemical toxins, and his or her nutritional status. Since the activity of cytochrome P varies so much, so does an individual's risk for various diseases.
This variability of cytochrome P enzymes is seen in the variability of people's ability to detoxify the carcinogens found in cigarette smoke and helps to explain why some people can smoke with only modest damage to their lungs, while others develop lung cancer after only a few decades of smoking. Patients with underactive phase I detoxification will experience caffeine intolerance, intolerance to perfumes and other environmental chemicals, and an increased risk for liver disease, while those with an overactive system will be relatively unaffected by caffeine drinks.
One way of objectively determining the activity of phase I is to measure how efficiently a person detoxifies caffeine. Using this test, a surprising fivefold difference in the detoxification rates of apparently healthy adult has been discovered.
When cytochrome P metabolizes a toxin, it chemically transforms it to a less toxic form, makes it water-soluble, or converts it to a more chemically active form. Caffeine is an example of a chemical directly neutralized by phase I. Making a toxin water-soluble allows its excretion by the kidneys. Transforming a toxin to a more chemically reactive form makes it more easily metabolized by the phase II enzymes.
A significant side-effect of phase I detoxification is the production of free radicals as the toxins are transformed--for each molecule of toxin metabolized by phase I, one molecule of free radical is generated. Without adequate free radical defenses, every time the liver neutralizes a toxin exposure, it is damaged by the free radicals produced. The most important antioxidant for neutralizing the free radicals produced in phase I is glutathione.
Glutathione is required for one of the key phase II detoxification processes. When high levels of toxin exposure produce so many free radicals from phase I detoxification that the glutathione is depleted, the phase II processes dependent upon glutathione stop.
Recent research shows that the cytochrome P enzyme systems are also found in other parts of the body, especially the brain cells. Inadequate antioxidants and nutrients in the brain result in an increased rate of neuron damage, such as seen in Alzheimer's and Parkinson's disease patients. As with all enzymes, the cytochrome Ps require several nutrients to function, such as copper, magnesium, zinc and vitamin C. A considerable amount of research has found that various substances activate cytochrome P while others inhibit it.
Good picture of Phase I activities: Good picture of Phase I enzymes: The term "induce" can be misleading as it refers to anything that fires up the system - those that are harmful which need processing, and those which arent harmful and activate processing. Cytochrome P is induced by some toxins and by some foods and nutrients. Obviously, it is beneficial to improve phase I detoxification in order to eliminate toxins as soon as possible.
This is best accomplished by providing the needed nutrients and non-toxic stimulants while avoiding those substances that are toxic. However, stimulation of phase I is contraindicated if the patient's phase II systems are underactive.
Drugs and environmental toxins activate P to combat their destructive effects, and in so doing, not only use up compounds needed for this detoxification system but contribute significantly to free radical formation and oxidative stress. Among foods, the brassica family, i. One such compound is indolecarbinol, which is also a powerful anti-cancer chemical. It is a very active stimulant of detoxifying enzymes in the gut as well as the liver. The net result is significant protection against several toxins, especially carcinogens.
This helps to explain why consumption of cabbage family vegetables protects against cancer. Oranges and tangerines as well as the seeds of caraway and dill contain limonene, a phytochemical that has been found to prevent and even treat cancer in animal models. Limonene's protective effects are probably due to the fact that it is a strong inducer of both phase I and phase II detoxification enzymes that neutralize carcinogens. In general, inhibition of detoxification is not desired.
In the case of Gilbert's Syndrome, there is an exception to Phase 1 inhibitors, as at a certain level it can allow Phase II detox to keep up with it. Many substances inhibit cytochrome P This situation can cause substantial problems as it makes toxins potentially more damaging because they remain in the body longer before detoxification.
For example, grapefruit juice decreases the rate of elimination of drugs from the blood and has been found to substantially alter their clinical activity and toxicity. Curcumin, the compound that gives turmeric its yellow color, is interesting because it inhibits phase I while stimulating phase II. This effect can be very useful in preventing certain types of cancer. Curcumin has been found to inhibit carcinogens, such as benzopyrene found in charcoal-broiled meat , from inducing cancer in several animal models.
It appears that the curcumin exerts its anti-carcinogenic activity by lowering the activation of carcinogens while increasing the detoxification of those that are activated. Curcumin has also been shown to directly inhibit the growth of cancer cells. As most of the cancer-inducing chemicals in cigarette smoke are only carcinogenic during the period between activation by phase I and final detoxification by phase II, curcumin in the turmeric can help prevent the cancer-causing effects of tobacco.
Those exposed to smoke, aromatic hydrocarbons, and other environmental carcinogens will probably benefit from the frequent use of curry or turmeric.
The activity of phase I detoxification enzymes decreases in old age. Aging also decreases blood flow through the liver, further aggravating the problem. Lack of the physical activity necessary for good circulation, combined with the poor nutrition commonly seen in the elderly, add up to a significant impairment of detoxification capacity, which is typically found in aging individuals. This helps to explain why toxic reactions to drugs are seen so commonly in the elderly.
Phase II reactions include sulfation and glucuronidation, which are key to human detoxification, along with glutathione conjugation, methylation, amino acid conjugation, and acetylation.
Phase II detoxification typically involves biochemical conjugation, in which various enzymes in the liver attach small chemical moieties to the toxin. The conjugation reaction neutralizes toxins and reactive intermediates left over from Phase I detoxification. Enzyme quantity can be influenced by dietary components. Green tea and products found in red wine grapes encourage glucuronidation and glutathione conjugation enzymes, respectively.
Foods rich in limonene, a monoterpene found in citrus peel, dill weed oil, and caraway oil, can increase UDPGT activity and encourage the glucuronidation mechanism. Many commonly used substances--for example, aspirin, menthol, synthetic vanilla, acetaminophen, morphine, diazepam, digitalis, benzoates, and some hormones--are detoxified through the glucuronidation pathway. Beta-glucuronidase, regarded as a dangerous enzyme, interferes with the glucuronidation process, allowing toxic levels of drugs and contaminants to accumulate.
Older individuals appear particularly susceptible to increased beta-glucuronidase formation because of long-term exposure to toxic agents. Gilbert's syndrome is a benign hereditary condition characterized by hyperbilirubinemia serum bilirubin level 1. The Gilbert's syndrome patient typically complains of loss of appetite, malaise, and fatigue, symptoms often identifiable with liver dysfunction.
This is called the conjugation pathway, whereby the liver cells add another substance eg. This makes the toxin or drug water-soluble, so it can then be excreted from the body via watery fluids such as bile or urine. Major Phase II pathways include glutathione, sulfate, glycine, and glucuronide conjugations. Individual xenobiotics and metabolites usually follow one or two distinct pathways. Again, this makes testing of the various pathways possible by challenging with known substances.
The conjugation molecules are acted upon by specific enzymes to catalyse the reaction step. Through conjugation, the liver is able to turn drugs, hormones and various toxins into excretable substances. For efficient phase two detoxification, the liver cells require sulphur-containing amino acids such as taurine and cysteine.
The nutrients glycine, glutamine, choline and inositol are also required for efficient phase two detoxification. Eggs and cruciferous vegetables eg. Thus, these foods can be considered to have a cleansing action. Glutathione is the most powerful internal antioxidant and liver protector. Phase II reactions may follow Phase I for some molecules or act directly on the toxin or metabolite.
Good picture of Phase II conjugation reactions: Phase II detoxification typically involves conjugation in which various enzymes in the liver attach small chemicals to the toxin. This conjugation reaction either neutralizes the toxin or makes the toxin more easily excreted through the urine or bile.
Phase II enzymes act on some toxins directly, while others must first be activated by the phase I enzymes. There are essentially six phase II detoxification pathways: In order to work, these enzyme systems need nutrients both for their activation and to provide the small molecules they add to the toxins. In addition, they utilize metabolic energy to function and to synthesize some of the small conjugating molecules.
Thus, mitochondrial dysfunction, such as found in chronic fatigue syndrome, a magnesium deficiency or physical inactivity, can cause phase II detoxification to slow down, allowing the build-up of toxic intermediates. Glutathione, vitamin B6 Amino acid conjugation: Cysteine, methionine, molybdenum Acetylation: Brassica family foods cabbage, broccoli, Brussels sprouts ; limonene-containing foods citrus peel, dill weed oil, caraway oil Amino acid conjugation: Lipotropic nutrients choline, methionine, betaine, folic acid, vitamin B12 Sulfation: Cysteine, methionine, taurine Acetylation: Fish oils, cigarette smoking, birth control pills, Phenobarbital, limonene-containing foods.
Inhibition of phase II detoxification is not desired, especially in those with Gilbert's Syndrome, as these enzymes are already inhibited. Selenium deficiency, vitamin B2 deficiency, glutathione deficiency, zinc deficiency Amino acid conjugation: Low protein diet Methylation: Folic acid or vitamin B12 deficiency Sulfation: Non-steroidal anti-inflammatory drugs e.
Vitamin B2, B5, or C deficiency Glucuronidation: Glucuronidation is a major phase II detoxification pathway in which the sugar moiety of UDP-glucuronic acid is covalently linked to a xenobiotic or endobiotic, facilitating its removal from the body in the urine or bile. The directed excretion of glucuronides from the lumen of the endoplasmic reticulum ER to the plasma membrane and the exterior of the cell is an important regulated process.
Impaired excretion leads to liver damage. Specific transporters for excretion of glucuronides have been implicated in lever cell function in ER and bile canaliculus.
Polycyclic aromatic hydrocarbons, steroid hormones, some nitrosamines, heterocyclic amines, some fungal toxins, and aromatic amines. It also removes "used" hormones, such as estrogen and T4 thyroid hormone that are produced naturally by the body.
Many of the commonly prescribed drugs are detoxified through this pathway. It also helps to detoxify aspirin, menthol, vanillin synthetic vanilla , food additives such as benzoates, and some hormones.
Glucuronidation appears to work well, except for those with Gilbert's syndrome--a relatively common syndrome characterized by a chronically elevated serum bilirubin level 1. The condition is usually without serious symptoms, although some patients do complain about loss of appetite, malaise, and fatigue typical symptoms of impaired liver function.
The main way this condition is recognized is by a slight yellowish tinge to the skin and white of the eye due to inadequate metabolism of bilirubin, a breakdown product of hemoglobin. The activity of UDPGT is increased by foods rich in the monoterpene limonene citris peel, dill weed oil, and caraway oil. Methionine, administered as SAM, has been shown to be quite beneficial in treating Gilbert's syndrome.
Glucuronidation is a major inactivating pathway for a huge variety of exogenous and endogenous molecules, including drugs, polluants, bilirubin, androgens, estrogens, mineralocorticoids, glucocorticoids, fatty acid derivatives, retinoids and bile acids.
These enzymes are primarily found in the endoplasmic reticulum of many tissues, with the liver being, quantitatively, the most significant site of glucuronidation. In addition to a wide tissue distribution of UGTs, different isozymes can be preferentially expressed in specific tissues. Furthermore, polymorphic expression of certain UGTs has also been observed 2.
Of these three families UGT1 and UGT2 have been shown to catalyze the glucuronidation of a wide variety of xenobiotic substrates, with UGT1 being more active in the glucuronidation of amines 3,4. Aryl- and alkylamines, sulfonamides, heterocyclic amines and hydroxylated compounds have all been reported to undergo glucuronidation in many animal species and humans. The primary function of UGTs is to eliminate substrates from the body via urine and feces by catalyzing the formation of hydrophilic glucuronide conjugates 5.
UGT detoxifies many xenobiotics. The UGT1 family specializes in processing amines, arylamines and alkylamines, sulfonamides, heterocyclic amines and hydroxylated compounds. UDP-glucuronosyltransferases UGTs belong to a superfamily of microsomal enzymes responsible for glucuronidation of numerous endogenous and exogenous compounds including bilirubin, hormones, various drugs as well as environmental carcinogens.
Glucuronidation predominantly serves as a pathway for elimination of the different glucuronidated compounds. Seventeen human UGT transcripts have been identified thus far, and the UGT proteins are differentially expressed in a wide-range of human tissues.
Most of the UGTs are expressed in the liver as well as other extrahepatic tissues; however, some are exclusively extrahepatic Table 1. The tissue specific regulation of UGTs ensures a unique complement of UGT proteins to various tissues, and defines the capacity of each tissue's ability to eliminate or inactivate various exogenous and endogenous substrates.
A primary phase II detoxification route is conjugation with glutathione a tripeptide composed of three amino acids--cysteine, glutamic acid, and glycine. Glutathione conjugation produces water-soluble mercaptates which are excreted via the kidneys.
The elimination of fat-soluble compounds, especially heavy metals like mercury and lead, is dependent upon adequate levels of glutathione, which in turn is dependent upon adequate levels of methionine and cysteine. When increased levels of toxic compounds are present, more methionine is utilized for cysteine and glutathione synthesis. Methionine and cysteine have a protective effect on glutathione and prevent depletion during toxic overload. This, in turn, protects the liver from the damaging effects of toxic compounds and promotes their elimination.
Glutathione is also an important antioxidant. This combination of detoxification and free radical protection, results in glutathione being one of the most important anticarcinogens and antioxidants in our cells, which means that a deficiency is cause of serious liver dysfunction and damage.
Exposure to high levels of toxins depletes glutathione faster than it can be produced or absorbed from the diet. This results in increased susceptibility to toxin-induced diseases, such as cancer, especially if phase I detoxification system is highly active. Disease states due to glutathione deficiency are not uncommon.