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Up to 40 % of Caucasian white persons can't metabolize drugs!

And MDs KNOW and Pharmacists KNOW and the FDA KNOWs and the Chemical Industry KNOWS!! Do they test each person for this before prescribing drugs or before adding them to cosmetics, food, or the other products consumers use?


With the drugs used in psychiatry, (and this is very general) many, are metabolised in the liver by an enzyme system called cytochrome P 450 (and other cytochrome systems). There are genetic, biological differences between individuals, some of whom do not produce certain cytochromes at all. In practice this means that somewhere between 12 and 20% of Caucasians cannot metabolise certain drugs, for example, SSRIs, at all or they do it slowly. Others are fast metabolisers. It is likely that biology accounts for massive drop out rates in clinical rials for both SSRIs and atypicals (up to 50% do not complete the trials and other have Valium co-prescribed and the public is not told.) Statistics about those who could not tolerate drugs do not appear on prescribing information.


Testing for enzyme deficiency - Shorts
Townsend Letter for Doctors and Patients, Dec, 2003 by Jule Klotter
Genetic tests are now available that can help doctors prescribe drugs more effectively and with fewer adverse effects. Doctors know that some people have the intended reaction, some react adversely, and some experience no effect at all. It is often a matter of trial and error. Now, however, genetic testing is available to identify people who are likely to have difficulty with about 25% of all drugs, including Prozac, Paxil, codeine, ibuprofen, THIS IS SPAM TAKE NO NOTICE, Claritin, and propranolol. These folks have variations in the gene responsible for an enzyme needed to metabolize these drugs, known as 2D6. Without 2D6 to break them down, the drugs can build up to toxic levels in the body, causing adverse effects including death. In a case publicized by Fortune (February 17, 2001), a 9-year-old boy with 2D6 deficiency died from a massive overdose of Prozac in 1995. The drug had slowly built up in his body to toxic levels. A Canadian study, published in Clinical Pharmacology and Therapeutics one year later, affirmed that "poor metabolizers appear to be at increased risk for accumulation of fluoxetine and the possible development of fluoxetine-associated toxicity." In addition, people with 2D6 enzyme deficiencies cannot metabolize codeine into morphine, so codeine has little-to-no painkilling effect on them. Between 6% and 10% of Caucasians carry genes that indicate a 2D6 deficiency.


Cytochrome P450 isoforms CYP2D6

CYP2D6 has been studied extensively because it exhibits genetic polymorphism, meaning that distinct population differences are apparent in its expression or activity. Approximately 7 to 10 percent of Caucasians are poor metabolizers of drugs metabolized by CYP2D6.[10] Individuals with normal CYP2D6 activity are termed extensive metabolizers. Ethnic differences are indicated in this genetic polymorphism, since Asians and blacks are less likely than Caucasians to be poor metabolizers.[11,12] Poor metabolizers are at risk for drug accumulation and toxicity from drugs metabolized by this isoform. For example, one patient who suffered cardiotoxicity induced by desipramine (Norpramin) was found to be a poor metabolizer.[13] Poor metabolizers of CYP2D6 substrates are at risk for postural hypotension and antipsychotic side effects such as oversedation, because several antipsychotic agents are metabolized by CYP2D6.[14] In a study of 45 elderly patients five of whom were poor metabolizers) receiving perphenazine, side effects increased fivefold in the poor metabolizers compared with the extensive metabolizers.[15] Conversely, when formation of an active metabolite is essential for drug action, poor metabolizers of CYP2D6 can exhibit less response to drug therapy compared with extensive metabolizers. Codeine is O-demethylated to morphine by CYP2D6, which accounts at least partially for its analgesic effect.[16] Thus, poor metabolizers may have less response to codeine than other persons.


"For a drug that is primarily metabolized by CYP450 2D6 approximately 7% of Caucasians will not be able to metabolize the drug, but the percentage for other RACIAL populations is generally far lower."


Genetic differences

The recently completed map of the human genome has revealed the tremendous genetic variability in the human population. Scientists have identified an estimated 1.4 million specific differences, or polymorphisms, in the human genetic code. Every polymorphism on a human gene is a DNA sequence that differs from one person to the next. Each of these 1.4 million polymorphisms represents a chance for a person to be at risk for a particular disease or uniquely susceptible to the harmful effects of a particular chemical (Stoneking 2001). Put another way, there are now truly 1 million ways that a person could be more or less sensitive to toxic chemicals than his or her neighbor.

Differences in metabolism dramatically influence the toxicity or effectiveness of chemicals and drugs. Metabolism is a function of genetically determined factors including race, age, sex,, and inherent variability (polymorphisms) as well as external factors like diet, disease-state, and exposure to chemical pollutants and heavy metals. One well-characterized genetic variable is the difference in critical metabolic enzyme levels. From 3 to 10 percent of Caucasians "do not have" or "have either low or no activity" of the enzyme (CYP2D6) that metabolizes codeine and the prescribed tricyclic antidepressants (Richelson 1997). Poor functioning, but normally occurring enzyme levels can also make individuals far more vulnerable to toxic chemical exposure. About 30 percent of the population carries a poor version of the enzyme paraoxonase which makes them 11 times more vulnerable to certain neurotoxic insecticides than people with fully functioning paraoxonase. (Schettler 2000).

Chemical absorption

Absorption in the gut may vary by orders of magnitude. While some people who eat mercury contaminated fish absorb 13% of the mercury from their stomach into their blood, others only absorb only 1% (Stern 1997). This means that if two pregnant women eat the same amount of mercury in a fish, one could deliver ten times more mercury to the brain of her developing child.



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