Category Archives: Pharmacogenomics

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Pharmacogenomics, also called PGx, combines the science of how medications work (pharmacology) with the science of how genetic differences can influence health (genomics).Inova is pleased to offer the MediMap PGx test to adults and children, as well asto newbornsdelivered atInova Womens Hospital.

MediMap is part of the standard package of services offered to all babies born at Inova Womens Hospital located at Inova Fairfax Medical Campus, and it is therefore performed at no additional cost. Inova is the only health system in the U.S. that provides this optional pharmacogenomics test to newborns as part of our standard package of care. More info about MediMap for newborns

Inova is pleased to announce that we will be offering theMediMap test to adults and children in the near future.More info about MediMap for adults and children

Until recently, most medicines have been developed and prescribed to patients in a one size fits all approach. PGx testing informs your physician about your, or your childs, genetic makeup to help determine which medications to use or the amount prescribed. PGx testing may also reduce side-effects.

MediMap is a one-time genetic test that may indicate how a person will respond to some prescription medications. The test helps guide healthcare providers to better medication choices and doses for their patients. MediMap testing provides information to more effectively manage illnesses and improve their health.

Cant find what you are looking for? Please call us at 1-844-GENOME-4U (1-844-436-6634) or email us at geneinfo@inova.org.

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Pharmacogenetics is the study of inherited genetic differences in drug metabolic pathways which can affect individual responses to drugs, both in terms of therapeutic effect as well as adverse effects.[1] The term pharmacogenetics is often used interchangeably with the term pharmacogenomics which also investigates the role of acquired and inherited genetic differences in relation to drug response and drug behavior through a systematic examination of genes, gene products, and inter- and intra-individual variation in gene expression and function.[2]

In oncology, pharmacogenetics historically is the study of germline mutations (e.g., single-nucleotide polymorphisms affecting genes coding for liver enzymes responsible for drug deposition and pharmacokinetics), whereas pharmacogenomics refers to somatic mutations in tumoral DNA leading to alteration in drug response (e.g., KRAS mutations in patients treated with anti-Her1 biologics).[3]

Much of current clinical interest is at the level of pharmacogenetics, involving variation in genes involved in drug metabolism with a particular emphasis on improving drug safety. The wider use of pharmacogenetic testing is viewed by many as an outstanding opportunity to improve prescribing safety and efficacy. Driving this trend are the 106,000 deaths and 2.2 Million serious events caused by adverse drug reactions in the US each year.[4][unreliable medical source?] As such ADRs are responsible for 5-7% of hospital admissions in the US and Europe, lead to the withdrawal of 4% of new medicines, and cost society an amount equal to the costs of drug treatment.[5]

Comparisons of the list of drugs most commonly implicated in adverse drug reactions with the list of metabolizing enzymes with known polymorphisms found that drugs commonly involved in adverse drug reactions were also those that were metabolized by enzymes with known polymorphisms (see Phillips, 2001).

Scientists and doctors are using this new technology for a variety of things, one being improving the efficacy of drugs. In psychology, we can predict quite accurately which anti-depressant a patient will best respond to by simply looking into their genetic code.[citation needed][dubious discuss] This is a huge step from the previous practice of adjusting and experimenting with different medications to get the best response. Antidepressants also have a large percentage of unresponsive patients and poor prediction rate of ADRs (adverse drug reactions). In depressed patients, 30% are not helped by antidepressants. In psychopharmacological therapy, a patient must be on a drug for 2 weeks before the effects can be fully examined and evaluated. For a patient in that 30%, this could mean months of trying medications to find an antidote to their pain. Any assistance in predicting a patients drug reaction to psychopharmacological therapy should be taken advantage of. Pharmacogenetics is a very useful and important tool in predicting which drugs will be effective in various patients.[6] The drug Plavix blocks platelet reception and is the second best selling prescription drug in the world, however, it is known to warrant different responses among patients.[7]GWAS studies have linked the gene CYP2C19 to those who cannot normally metabolize Plavix. Plavix is given to patients after receiving a stent in the coronary artery to prevent clotting.

Stent clots almost always result in heart attack or sudden death, fortunately it only occurs in 1 or 2% of the population. That 1 or 2% are those with the CYP2C19 SNP.[8] This finding has been applied in at least two hospitals, Scripps and Vanderbilt University, where patients who are candidates for heart stents are screened for the CYP2C19 variants.[9]

Another newfound use of pharmacogenetics involves the use of Vitamin E. The Technion Israel Institute of Technology observed that vitamin E can be used to in certain genotypes to lower the risk of cardiovascular disease in patients with diabetes, but in the same patients with another genotype, vitamin E can raise the risk of cardiovascular disease. A study was carried out, showing vitamin E is able to increase the function of HDL in those with the genotype haptoglobin 2-2 who suffer from diabetes. HDL is a lipoprotein that removes cholesterol from the blood and is associated with a reduced risk of atherosclerosis and heart disease. However, if you have the misfortune to possess the genotype haptoglobin 2-1, the study shows that this same treatment can drastically decrease your HDL function and cause cardiovascular disease.[10]

Pharmacogenetics is a rising concern in clinical oncology, because the therapeutic window of most anticancer drugs is narrow and patients with impaired ability to detoxify drugs will undergo life-threatening toxicities. In particular, genetic deregulations affecting genes coding for DPD, UGT1A1, TPMT, CDA and CYP2D6 are now considered as critical issues for patients treated with 5-FU/capecitabine, irinotecan, mercaptopurine/azathioprine, gemcitabine/capecitabine/AraC and tamoxifen, respectively. The decision to use pharmacogenetic techniques is influenced by the relative costs of genotyping technologies and the cost of providing a treatment to a patient with an incompatible genotype. When available, phenotype-based approaches proved their usefulness while being cost-effective.[11]

In the search for informative correlates of psychotropic drug response, pharmacogenetics has several advantages:[12]

The first observations of genetic variation in drug response date from the 1950s, involving the muscle relaxant suxamethonium chloride, and drugs metabolized by N-acetyltransferase. One in 3500 Caucasians has less efficient variant of the enzyme (butyrylcholinesterase) that metabolizes suxamethonium chloride.[13] As a consequence, the drugs effect is prolonged, with slower recovery from surgical paralysis. Variation in the N-acetyltransferase gene divides people into "slow acetylators" and "fast acetylators", with very different half-lives and blood concentrations of such important drugs as isoniazid (antituberculosis) and procainamide (antiarrhythmic). As part of the inborn system for clearing the body of xenobiotics, the cytochrome P450 oxidases (CYPs) are heavily involved in drug metabolism, and genetic variations in CYPs affect large populations. One member of the CYP superfamily, CYP2D6, now has over 75 known allelic variations, some of which lead to no activity, and some to enhanced activity. An estimated 29% of people in parts of East Africa may have multiple copies of the gene, and will therefore not be adequately treated with standard doses of drugs such as the painkiller codeine (which is activated by the enzyme). The first study using Genome-wide association studies (GWAS) linked age-related macular degeneration (AMD) with a SNP located on chromosome 1 that increased ones risk of AMD. AMD is the most common cause of blindness, affecting more than seven million Americans. Until this study in 2005, we only knew about the inflammation of the retinal tissue causing AMD, not the genes responsible.[9]

One of the earliest tests for a genetic variation resulting in a clinically important consequence was on the enzyme thiopurine methyltransferase (TPMT). TPMT metabolizes 6-mercaptopurine and azathioprine, two thiopurine drugs used in a range of indications, from childhood leukemia to autoimmune diseases. In people with a deficiency in TPMT activity, thiopurine metabolism must proceed by other pathways, one of which leads to the active thiopurine metabolite that is toxic to the bone marrow at high concentrations. Deficiency of TPMT affects a small proportion of people, though seriously. One in 300 people have two variant alleles and lack TPMT activity; these people need only 6-10% of the standard dose of the drug, and, if treated with the full dose, are at risk of severe bone marrow suppression. For them, genotype predicts clinical outcome, a prerequisite for an effective pharmacogenetic test. In 85-90% of affected people, this deficiency results from one of three common variant alleles.[14] Around 10% of people are heterozygous - they carry one variant allele - and produce a reduced quantity of functional enzyme. Overall, they are at greater risk of adverse effects, although as individuals their genotype is not necessarily predictive of their clinical outcome, which makes the interpretation of a clinical test difficult. Recent research suggests that patients who are heterozygous may have a better response to treatment, which raises whether people who have two wild-type alleles could tolerate a higher therapeutic dose.[15] The US Food and Drug Administration (FDA) have recently deliberated the inclusion of a recommendation for testing for TPMT deficiency to the prescribing information for 6-mercaptopurine and azathioprine. The information previously carried the warning that inherited deficiency of the enzyme could increase the risk of severe bone marrow suppression. It now carries the recommendation that people who develop bone marrow suppression while receiving 6-mercaptopurine or azathioprine be tested for TPMT deficiency.[citation needed]

A polymorphism near a human interferon gene is predictive of the effectiveness of an artificial interferon treatment for Hepatitis C. For genotype 1 hepatitis C treated with Pegylated interferon-alpha-2a or Pegylated interferon-alpha-2b (brand names Pegasys or PEG-Intron) combined with ribavirin, it has been shown that genetic polymorphisms near the human IL28B gene, encoding interferon lambda 3, are associated with significant differences in response to the treatment.[16] Genotype 1 hepatitis C patients carrying certain genetic variant alleles near the IL28B gene are more probable to achieve sustained virological response after the treatment than others, and demonstrated that the same genetic variants are also associated with the natural clearance of the genotype 1 hepatitis C virus.[17]

Despite the many successes, most drugs are not tested using GWAS. However, it is estimated that over 25% of common medication have some type of genetic information that could be used in the medical field.[18] If the use of personalized medicine is widely adopted and used, it will make medical trials more efficient. This will lower the costs that come about due to adverse drug side effects and prescription of drugs that have been proven ineffective in certain genotypes. It is very costly when a clinical trial is put to a stop by licensing authorities because of the small population who experiences adverse drug reactions. With the new push for pharmacogenetics, it is possible to develop and license a drug specifically intended for those who are the small population genetically at risk for adverse side effects. [19]

The ability to test and analyze an individuals DNA to determine if the body can break down certain drugs through the biochemical pathways has application in all fields of medicine. Pharmacogenetics gives those in the health care industry a potential solution to help prevent the significant amount of deaths that occur each year due to drug reactions and side effects. The companies or laboratories that perform this testing can do so acrossed all categories or drugs whether it be for high blood pressure, gastrointestinal, urological, psychotropic or anti-anxiety drugs. Results can be presented showing which drugs the body is capable of breaking down normally versus the drugs the body cannot break down normally. This test only needs to be done once and can provide valuable information such as a summary of an individuals genetic polymorphisms, which could help in a situation such as being a patient in the emergency room.[20]

As the cost per genetic test decreases, the development of personalized drug therapies will increase.[21] Technology now allows for genetic analysis of hundreds of target genes involved in medication metabolism and response in less than 24 hours for under $1,000. This a huge step towards bringing pharmacogenetic technology into everyday medical decisions. Likewise, companies like deCODE genetics, Navigenics and 23andMe offer genome scans. The companies use the same genotyping chips that are used in GWAS studies and provide customers with a write-up of individual risk for various traits and diseases and testing for 500,000 known SNPs. Costs range from $995 to $2500 and include updates with new data from studies as they become available. The more expensive packages even included a telephone session with a genetics counselor to discuss the results.[9]

Pharmacogenetics has become a controversial issue in the area of bioethics. It's a new topic to the medical field, as well as the public. This new technique will have a huge impact on society, influencing the treatment of both common and rare diseases. As a new topic in the medical field the ethics behind it are still not clear. However, ethical issues and their possible solutions are already being addressed.

There are three main ethical issues that have risen from pharmacogenetics. First, would there be a type equity at both drug development and the accessibility to tests.[22] The concern of accessibility to the test is whether it is going to be available directly to patients via the internet, or over the counter. The second concern regards the confidentiality of storage and usage of genetic information.[23] Thirdly, would patients have the control over being tested.

One concern that has risen is the ethical decision health providers must take with respect to educating the patient of the risks and benefits of medicine developed by this new technology. Pharmacogenetics is a new process that may increase the benefits of medicine while decreasing the risk. However clinicians have been unsuccessful in educating patients regarding the concept of benefits over risk. The Nuffield Council reported that patients and health professionals have adequate information about pharmacogenetics tests and medicine.[23] Health care providers will also encounter an ethical decision in deciding to tell their patients that only certain individuals will benefit from the new medicine due to their genetic make-up.[22] Another ethical concern is that patients who have not taken the test be able to have access to this type of medicine. If access is given by the doctor the medicine could negatively impact the patient's health. The ethical issues behind pharmacogenetics tests, as well as medicine, are still a concern and policies will need to be implemented in the future.

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Pharmacogenetics - Wikipedia

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Attention deficit-hyperactivity disorder (ADHD) is a very common and heterogeneous childhood-onset psychiatric disorder, affecting between 3% and 5% of school age children worldwide. Although the neurobiology of ADHD is not completely understood, imbalances in both dopaminergic and noradrenergic systems have been implicated in the origin and persistence of core symptoms, which include inattention, hyperactivity, and impulsivity. The role of a genetic component in its etiology is strongly supported by genetic studies, and several investigations have suggested that the dopamine transporter gene (DAT1; SLC6A3 locus) may be a small-effect susceptibility gene for ADHD. Stimulant medication has a well-documented efficacy in reducing ADHD symptoms. Methylphenidate, the most prescribed stimulant, seems to act mainly by inhibiting the dopamine transporter protein and dopamine reuptake. In fact, its effect is probably related to an increase in extracellular levels of dopamine, especially in brain regions enriched in this protein (i.e. striatum). It is also important to note that dopamine transporter densities seem to be particularly elevated in the brain of ADHD patients, decreasing after treatment with methylphenidate. Altogether, these observations suggest that the dopamine transporter does play a major role in ADHD. Among the several polymorphisms already described in the SLC6A3 locus, a 40 bp variable number of tandem repeats (VNTR) polymorphism has been extensively investigated in association studies with ADHD. Although there are some negative results, the findings from these reports indicate the allele with ten copies of the 40 bp sequence (10-repeat allele) as the risk allele for ADHD. Some investigations have suggested that this polymorphism can be implicated in dopamine transporter gene expression in vitro and dopamine transporter density in vivo, even though it is located in a non-coding region of the SLC6A3 locus. Despite all these data, few studies have addressed the relationship between genetic markers (specifically the VNTR) at the SLC6A3 locus and response to methylphenidate in ADHD patients. A significant effect of the 40 bp VNTR on response to methylphenidate has been detected in most of these reports. However, the findings are inconsistent regarding both the allele (or genotype) involved and the direction of this influence (better or worse response). Thus, further investigations are required to determine if genetic variation due to the VNTR in the dopamine transporter gene is able to predict different levels of clinical response and palatability to methylphenidate in patients with ADHD, and how this information would be useful in clinical practice.

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Frequently Asked Questions About Pharmacogenomics

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Pharmacogenomics uses information about a person's genetic makeup, or genome, to choose the drugs and drug doses that are likely to work best for that particular person. This new field combines the science of how drugs work, called pharmacology, with the science of the human genome, called genomics.

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Until recently, drugs have been developed with the idea that each drug works pretty much the same in everybody. But genomic research has changed that "one size fits all" approach and opened the door to more personalized approaches to using and developing drugs.

Depending on your genetic makeup, some drugs may work more or less effectively for you than they do in other people. Likewise, some drugs may produce more or fewer side effects in you than in someone else. In the near future, doctors will be able to routinely use information about your genetic makeup to choose those drugs and drug doses that offer the greatest chance of helping you.

Pharmacogenomics may also help to save you time and money. By using information about your genetic makeup, doctors soon may be able to avoid the trial-and-error approach of giving you various drugs that are not likely to work for you until they find the right one. Using pharmacogenomics, the "best-fit" drug to help you can be chosen from the beginning.

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Doctors are starting to use pharmacogenomic information to prescribe drugs, but such tests are routine for only a few health problems. However, given the field's rapid growth, pharmacogenomics is soon expected to lead to better ways of using drugs to manage heart disease, cancer, asthma, depression and many other common diseases.

One current use of pharmacogenomics involves people infected with the human immunodeficiency virus (HIV). Before prescribing the antiviral drug abacavir (Ziagen), doctors now routinely test HIV-infected patients for a genetic variant that makes them more likely to have a bad reaction to the drug.

Another example is the breast cancer drug trastuzumab (Herceptin). This therapy works only for women whose tumors have a particular genetic profile that leads to overproduction of a protein called HER2.

The U.S. Food and Drug Administration (FDA) also recommends genetic testing before giving the chemotherapy drug mercaptopurine (Purinethol) to patients with acute lymphoblastic leukemia. Some people have a genetic variant that interferes with their ability to process the drug. This processing problem can cause severe side effects and increase risk of infection, unless the standard dose is adjusted according to the patient's genetic makeup.

The FDA also advises doctors to test colon cancer patients for certain genetic variants before administering irinotecan (Camptosar), which is part of a combination chemotherapy regimen. The reasoning is that patients with one particular variant may not be able to clear the drug from their bodies as quickly as others, resulting in severe diarrhea and increased infection risk. Such patients may need to receive lower doses of the drug.

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Much research is underway to understand how genomic information can be used to develop more personalized and cost-effective strategies for using drugs to improve human health.

In 2007, the FDA revised the label on the common blood-thinning drug warfarin (Coumadin) to explain that a person's genetic makeup might influence response to the drug. Some doctors have since begun using genetic information to adjust warfarin dosage. Still, more research is needed to conclusively determine whether warfarin dosing that includes genetic information is better than the current trial-and-error approach.

The FDA also is considering genetic testing for another blood-thinner, clopidogrel bisulfate (Plavix), used to prevent dangerous blood clots. Researchers have found that Plavix may not work well in people with a certain genetic variant.

Cancer is another very active area of pharmacogenomic research. Studies have found that the chemotherapy drugs, gefitinib (Iressa) and erlotinib (Tarceva), work much better in lung cancer patients whose tumors have a certain genetic change. On the other hand, research has shown that the chemotherapy drugs cetuximab (Erbitux) and panitumumab (Vecitibix) do not work very well in the 40 percent of colon cancer patients whose tumors have a particular genetic change.

Pharmacogenomics may also help to quickly identify the best drugs to treat people with certain mental health disorders. For example, while some patients with depression respond to the first drug they are given, many do not, and doctors have to try another drug. Because each drug takes weeks to take its full effect, patients' depression may grow worse during the time spent searching for a drug that helps.

Recently, researchers identified genetic variations that influence the response of depressed people to citalopram (Celexa), which belongs to a widely used class of antidepressant drugs called selective serotonin re-uptake inhibitors (SSRIs). Clinical trials are now underway to learn whether genetic tests that predict SSRI response can improve patients' outcomes.

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Yes. Besides improving the ways in which existing drugs are used, genome research will lead to the development of better drugs. The goal is to produce new drugs that are highly effective and do not cause serious side effects.

Until recently, drug developers usually used an approach that involved screening for chemicals with broad action against a disease. Researchers are now using genomic information to find or design drugs aimed at subgroups of patients with specific genetic profiles. In addition, researchers are using pharmacogenomic tools to search for drugs that target specific molecular and cellular pathways involved in disease.

Pharmacogenomics may also breathe new life into some drugs that were abandoned during the development process. For example, development of the beta-blocker drug bucindolol (Gencaro) was stopped after two other beta-blocker drugs won FDA approval to treat heart failure. But interest in Gencaro revived after tests showed that the drug worked well in patients with two genetic variants that regulate heart function. If Gencaro is approved by the FDA, it could become the first new heart drug to require a genetic test before prescription.

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Last Updated: May 2, 2016

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The U.K. has the same problem with its health care system as North America. Only days before Dr. Roses spoke at a scientific meeting in London, the National Health Service reported that the total cost of drugs had soared by 50 percent in the previous three years, from $2.3 billion a year to an annual cost to the taxpayer of $7.2 billion.

An announcement by GSK the previous week promoted a line up of 20 or more new drugs under development that boasted potential earnings of up to $1 Billion (?600m) a year.

Dr. Roses is an academic geneticist originally from Duke University in North Carolina. In his talk he cited figures on how well different classes of drugs work in real patients. And he probably knew just what he was doing - heralding the "brave new world" of genetic engineering and genomics. When you want to promote a new therapy, you have to prove that the previous one is not doing the job or that the new modality at least improves on existing technology. Roses was doing just that when he talked about drugs for Alzheimer's disease working in less than one third of patients, and cancer chemotherapy being effective in less than one in four. Drugs for migraines, osteoporosis, and arthritis do somewhat better and work in about half the patients. His final analysis was that more than 90 percent of drugs work in only 30 to 50 percent of people. That's way less than the placebo effect!

The reason that drugs work effectively, on average, in less than one half of patients according to Dr. Roses, is because their genetic makeup interferes with the medicine in some unknown way. Some people thought it was a gaffe but others admitted that: "Roses is a smart guy and what he is saying will surprise the public but not his colleagues. He is a pioneer of a new culture within the drugs business based on using genes to test for who can benefit from a particular drug."

Roses is on a mission to promote his field of "pharmacogenomics", which applies human genetics to drug development by "identifying "responders", or people who benefit from the drug, with a simple and cheap genetic test that can be used to eliminate those nonresponders who might benefit from another drug. It may be the trend in medicine but it does fly in the face of an industry that markets drugs to the masses, not a select few.

Are we ready to leap into pharmacogenomics when we haven't even mastered nutrition? The late Dr. David Horrobin, a psychopharmacologist and a pioneer in the field of essential fatty acids, asked the quintessential question in his article, "Why do we not make more medical use of nutritional knowledge? How an inadvertent alliance between reductionist scientists, holistic dietitians and drug-oriented regulators and governments has blocked progress." He was probably frustrated with being misquoted so often over the years, thus he made his point perfectly clear in the unwieldy title of his paper.

Dr. Horrobin, a brilliant researcher, questioned whether there was "Something Rotten at the Core of Science?" in a 2001 issue of Trends in Pharmacological Sciences. Commenting on an analysis of the medical journal peer review system and a U.S. Supreme Court decision which questioned the authority of peer review, Dr. Horrobin concluded that, "Far from filtering out junk science, peer review may be blocking the flow of innovation and corrupting public support of science."

Horrobin and a handful of scientists have complained about the peer review process for decades, to no avail. A crack in the armor began in earnest when two researchers, Rothwell and Martyn, laboriously evaluated reviews of papers submitted to two neuroscience journals. They performed a statistical analysis on the correlations among reviewers' recommendations. They concluded that none of the reviewers seemed to agree on anything! Horrobin lamented that, "The core system by which the scientific community allots prestige (in terms of oral presentations at major meetings and publication in major journals) and funding is a nonvalidated charade whose processes generate results little better than does chance. Given the fact that most reviewers are likely to be mainstream and broadly supportive of the existing organization of the scientific enterprise, it would not be surprising if the likelihood of support for truly innovative research was considerably less than that provided by chance."

Horrobin noted that scientists often become angry because the public rejects the results of the scientific process. However, the Rothwell and Martyn report indicates that the public may be on the right track and is waiting for science to do more than just state its superiority but actually put itself to objective evaluation. Dr. Horrobin found that in the midst of the rejection of science by the public there is also the fact that pharmaceutical research is failing. The annual number of new chemical entities submitted for approval is steadily declining. Horrobin concluded that drug companies are merging because of failure; it is not a measure of success.

In his field of psychopharmacology, Dr. Horrobin said he was able to find no improvement in the treatment of depression and schizophrenia in the past forty years. "Is it really a success that 27 of every 100 patients taking the selective 5HT reuptake inhibitors stop treatment within six weeks compared with the 30 of every 100 who take a 1950's tricyclic antidepressant compound?"

Of course, I say my Future Health Now! online lifestyle and wellness program is the future of medicine, not genetic engineering. William Leiss is past President of the Royal Society of Canada and a widely sought after advisor on the social and ethical implications of "risk controversies and public policy." In an interview available online, Leiss attempts to warn government and the public about galloping technology. Dr. Leiss says there is an unresolved tension between two competing aspects of the scientific revolution in the modern world.

There is a battle between inventive science, the creation of products, and transformative science, which results in cultural change. Inventive science goes from triumph to triumph virtually uncontested and is bolstered by unlimited funding. Even though Francis Bacon in the 1600s championed inventions as a way of improving the human race, it was not until the end of the 1800s that Bacon's dream was realized. The first inventions were in the field of chemistry.

Transformative science was championed in the 1700s as a way of not just understanding and overcoming nature but as an important new way of organizing the basis of social institutions, promoting universal education and rendering social policies and institutes more humane and just.

Dr. Leiss reminds us of the many risks we have overcome through advancement in invention and transformative science. Where would we be if it were not for the many products that have advanced the world through childbirth morality, infant and childhood mortality, infectious diseases, malnutrition, personal security, accidents, birth control, and the treatment of mental disorders reflected in an increase in average lifespan? Bacon would be happy that we have achieved results far beyond what he had expected, however, Leiss is afraid we don't know when to put the brakes on technology. He also asks why have we accepted without challenge most new inventions that have darkened our door?

When it comes to genetic engineering, affecting our very DNA, proponents envision programming perfection in humans, doubling the human lifespan, and developing entirely new life forms once scientists have mastered the necessary genome that will sustain human life.

Leiss thinks that by the late 19th century, the products of science began to be more important than improvement of society through transformative science. He reminds us that World War II brought us extremely close to nuclear war and changed the world immeasurably. But Leiss feels the final frontier is biotechnology that is capable of "modifying" genes at the embryo stage. For neurodegenerative diseases like Huntington's Chorea, this treatment could be a miracle. But what is to stop scientists from enhancing normal performance and creating super geniuses, super athletes, super entertainers, or super politicians. Many questions are yet to be asked. How will these changes affect the gene pool? What about the notion of extending human life? Leiss, with tongue firmly incheek, speculates about a 200year life span and spending the last 100 years of life on cruise ships!

Dr. Epstein, a professor of environmental and occupational medicine at The School of Public Health, University of Chicago, spoke at The Lighthouse in New York on November 11, 2001. He said that this century has seen the emergence of new technologies: petrochemicals developed around 1940 with new methods of fractional distillation creating 1 billion pounds in 1940, 50 billion by 1950 and now an annual production of 900 billion pounds; a second concern is nuclear technology and fuel; a third is genetic engineering, an emerging technology with the potential for irreversible health effects.

Epstein says these technologies outstrip any social mechanism that would try to control them. Therefore, we have a complex set of factors, which add up to seeing the actual abolition and desecration of democratic structure by corporate influences on national and government levels. Most journalists in a kneejerk reaction cheer on the technologies, says Dr. Epstein, and furthermore, they never see a carcinogen they don't like.

Less than six months after Dr. Roses made his startling announcement that 90 percent of drugs only work on 3050 percent of the population, GlaxoSmithKline sponsored a special edition of the wellknown scientific journal, Nature. It was called "Nature: Insight on Human Genomics and Medicine" and GSK defined the parameters of the journal as follows:

1. Pharmacogenetics exploring the genetic basis for drug response to find the right medicine for the right patient.

2. Disease Genetics - studying patient populations with common disease: asthma, depression, COPD, osteoarthritis, early onset heart disease, and migraine in order to identify disease susceptibility genes.

3. Genomics/Proteomics understanding the functions of genes, proteins, and their complex interactions to discover and validate new drug targets and biomarkers.

4. Bioinformatics combining biology, genetics, statistics, and computer.

Exerpted and edited from Death by Modern Medicine: Seeking Safe Solutions, eBook. Dr. Carolyn Dean.

About the author: About the Author: Carolyn Dean MD ND is The Doctor of the Future. She is a medical doctor and naturopathic doctor in the forefront of the natural medicine revolution since 1979. She is working on several patents on novel products including the iCell in RnA Drops. Dr. Dean is a leading expert in magnesium and she has created a picometer, stabilized-ionic form of magnesium, called ReMag that's 100% absorbed at the cellular level and non-laxative making it one of the only magnesiums that can be taken in therapeutic amounts with no side effects. ReLyte is her multiple mineral product that is also completely absorbed at the cellular level and contains the 9 minerals necessary for supporting proper thyroid function. RnA Drops help make perfect cells via RNA through Chromosome 14 affecting DNA. ReNew, which is highly concentrated RnA Drops is a powerful skin serum and ReAline is a safe detox formula with methylated B's, l-taurine and dl-methionine (the precursor to glutathione), all available at http://www.RnAReSet.com Dr. Dean is the author/coauthor of 33 health books (print and eBooks) and 106 Kindle books including The Magnesium Miracle, Death by Modern Medicine, IBS for Dummies, IBS Cookbook for Dummies, The Yeast Connection and Women's Health, Future Health Now Encyclopedia, Death by Modern Medicine, Everything Alzheimers, and Hormone Balance. She is on the Medical Advisory Board of the non-profit educational site - Nutritional Magnesium Association (www.nutritionalmagnesium.org). Dr. Dean has a free online newsletter and a valuable online 2-year wellness program called Completement Now! at http://www.drcarolyndean.com/fhn. She also runs a busy telephone consulting practice and has a weekly radio show Mondays at 4pm PST on http://www.achieveradio.com. Find out more at http://www.drcarolyndean.com, http://www.drcarolyndeanlive.com, http://www.RnAReSet.com, and http://www.howionic.com.

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Pharmacogenomics, the next frontier in medicine ...