Genetic influence on medication response

Do you experience many of the side effects described in the package insert? Or does a medicine actually do less than you expected? That may be due to your genes, because everyone is unique, after all. personal medicine test

The personal medicine test, a medication response test (also known as a pharmacogenetic test), determines how your body breaks down medicines based on your DNA. With these results, your healthcare provider can make better informed decisions about which medicine suits you best and at what dose/strength.

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Determination of 34 genes involved in drug processing.
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  • fewer side effects on medications
  • whether statins may be suitable for you
  • which antidepressant may suit you
  • whether you're a worrier or a warrior
  • whether anticonceptive pills might work less effectively or even need to be avoided
  • which medications for high blood pressure suit you best
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Effect of genes on medication in certain conditions

Depression and Anxiety
More than one million people use an antidepressant, although it does not work sufficiently well in about 30 to 50% of the cases. The search for the right agent in the right dosage can take months. During that time, the side effects are often violent, which seriously affects self-confidence, or confidence in the doctor and in the treatment.

Do you recognize this and do you have problems finding the right medicine for depression or anxiety disorder? Then take a DNA test. Your DNA regulates how your body deals with medicines. Our DNA test shows the activity per gene and which medicines are processed by each gene. This way you can immediately see which medicine may be more appropriate.
Medicines are usually an important part of the treatment of psychosis. These medicines are called 'antipsychotics'. They affect the functioning of nerve cells in the brain. Antipsychotics help you to get out of psychosis. Antipsychotics have no curative effect; they do not eliminate the cause of the psychosis or solve underlying problems. The medication ensures that anxiety and agitation are muffled. This can help you regain control of your life. Antipsychotics often come with many side effects and it can often take a long time before it is clear whether they also help against the psychotic symptoms.

Do you have trouble finding a suitable medicine? Then take a DNA test. Your DNA regulates how your body deals with medicines. Our DNA test shows the activity per gene and which medicines are processed by each gene. This way you can immediately see which medicine may be more appropriate.
High Blood Pressure
High blood pressure is a leading cause of cardiovascular disease, heart failure, strokes, kidney problems and brain damage. In addition to factors such as diet and smoking, blood pressure is largely (30% to 60%) determined by hereditary predisposition. Your doctor or general practitioner determines in consultation with you which medicines you will receive to treat high blood pressure. There are different types of medication to lower blood pressure.

You will often be prescribed more than one kind. That often works better and you have less chance of side effects. Unfortunately, only a small number of patients with hypertension control blood pressure with the appropriate drug therapy. Research into differences in DNA can then be used as a tool to improve the treatment of blood pressure.
High Cholesterol
Statins are indicated for the prevention of cardiovascular disease and are among the most commonly prescribed classes of medication. However, not all patients respond favorably to statins, and some do not achieve their cholesterol lowering goals. In addition, a significant number of patients experiences adverse effects. Muscle inflammation, muscle weakness, and liver abnormalities are the most commonly reported side effects of statins, often leading to poor compliance or statin discontinuation.

A pharmacogenetic test, such as the personal medicine test, can provide an opportunity for the patient to weigh up the potential benefits against the potential risks of a statin together with his practitioner. The choice of a statin and its dosage can be adjusted to your DNA.

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Do you see yourself here? ...then order a DNA test for yourself.

There is an enzyme that is responsible for 95% of the breakdown of caffeine. Does our test show that you have a slow variant of this enzyme? Now you know better why you are awake for so long after a cup of coffee.
High Cholesterol
By a lower activity of certain enzymes, statins (simvastatin, ...) can be removed too slowly from the body. Then the medicine accumulates and that can explain severe side effects. So show the results to your doctor.
In people with inactive variants of the BCHE gene, muscle relaxants, which are used in emergency situations (operations), can last too long making independent breathing only possible later. A dose adjustment resolves this.
Blood Clotting
This test determines how your blood clotting is controlled. Maybe wound healing takes a little longer with you? Then at a later age you may also have less need for anticoagulants in the prevention of blood clots?

Your DNA influences the result

Your DNA determines how you respond to medication. Your genes have a huge influence on the way a medicine is taken up, divided into the body and broken down again. They can therefore be responsible for the differences in response to a medication. Your genes determine whether your body breaks down a drug too slowly, normally or too quickly, which can result in unpleasant side effects or no effect at all.

A pharmacogenetic test shows the activity of the different involved enzymes and gives information about the type of medicine that suits you and the corresponding dose.

Which genes are exactly being tested?

Our pharmacogenetic test checks the following genes: ABCB1, ABCG2, ALDH2, BCHE, COMT, CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2D6-enhancer, CYP2E1, CYP3A4, CYP3A5, CYP3A7, CYP4F2, DPYD, F2, F5, G6PD, GRIK4, GSTP1, HLA-B*1502, IFNL3, MT-RNR1, MTHFR, NAT2, NUDT15, OPRM1, SLCO1B1, TPMT, UGT1A1 and VKORC1.

A gene that allows for a transport protein. Among other things, it transports medicines from the brain and kidneys, for example.

ABCG2 encodes a transport protein present in the liver, intestines, kidneys, and blood-brain barrier. Its function is to pump out potentially harmful substances, such as medicines, from cells, serving as a defence mechanism.

The ALDH2 gene codes for ALDH2, which stands for Aldehyde Dehydrogenase 2, an important enzyme involved in alcohol metabolism. Aldehyde Dehydrogenase 2 is responsible for the breakdown of a toxic substance, acetaldehyde.

A gene that produces an enzyme that helps protect the body against certain toxic substances by breaking them down before they reach the nerves.

COMT is involved in the conversion of certain "stress" hormones such as dopamine and adrenaline, but also, for example, certain female hormones.

CYP1A2 is part of a large family, the cytochrome P450 enzymes. They are primarily in the liver. This group is involved in the metabolism of approximately 60% of the drugs. 8 to 10% of this is converted by this gene, CYP1A2.

CYP2B6 is part of a large family, the cytochrome P450 enzymes. This group is involved in the metabolism of approximately 60% of the drugs. About 4% of the 200 most commonly prescribed and used medicines, including mainly antiviral drugs, are broken down by CYP2B6.

CYP2C8 is part of a large family, the cytochrome P450 enzymes. This group is involved in the metabolism of about 60% of the drugs. This enzyme accounts for 7% of the total CYP enzyme content in the liver.

CYP2C9 is part of a large family, the cytochrome P450 enzymes. This group is involved in the metabolism of approximately 60% of the drugs. About 10%-20% of all medicines are (partly) converted by CYP2C9.

CYP2C19 is part of a large family, the cytochrome P450 enzymes. This group is involved in the metabolism of approximately 60% of the drugs. Approximately 8% of all medicines are (partly) converted by CYP2C19, including, for example, antidepressants, stomach agents (the proton pump inhibitors) and anticoagulants.

CYP2D6 is part of the cytochrome P450 enzymes, these are enzymes that mainly work in the liver and cause the breakdown of many different substances in the body. This gene is involved in at least 25% of medicines prescribed by doctors, such as antidepressants, antipsychotics, opioids, tamoxifen, antiarrhythmics.

CYP2E1 is part of the cytochrome P450 enzymes, these are enzymes that work primarily in the liver and to a lesser extent in the brain, lungs and kidneys. They cause the breakdown of many different substances in the body.

CYP3A4 is part of the cytochrome P450 enzymes. This enzyme is one of the most important CYP enzymes because it is responsible for processing around 45-60% of the prescribed medicines.

CYP3A5 is part of the cytochrome P450 enzymes, these are enzymes that work primarily in the liver and to a lesser extent in the brain, lungs and kidneys. They cause the breakdown of many different substances in the body.

CYP3A7 is part of a large family, the cytochrome P450 enzymes. They are mainly found in the liver. This group is involved in the metabolism of approximately 60% of the drugs. CYP3A7 is primarily expressed in the fetal liver and is responsible for metabolizing a wide range of substances, including pharmaceutical drugs, steroids, and environmental toxins.

CYP4F2 regulates the bioavailability of vitamin E and vitamin K. Variations in CYP4F2 that affect the bioavailability of vitamin K also affect the dosage of vitamin K antagonists such as warfarin or acenocoumarol.

This gene plays a central role. It is involved in the degradation of the uracil and thymine molecules. These are building blocks of the DNA and the related RNA.

The F2 gene contains instructions for making a protein called prothrombin. This is a clotting factor that is important for blood clotting.

The F5 gene contains instructions for making a protein called coagulation factor V (5). This is a clotting factor that is important for blood clotting.

The G6PD gene provides instructions for making an enzyme called glucose-6-phosphate dehydrogenase. This enzyme plays a vital role in red blood cells. Variations in this gene lead to G6PD deficiency manifested as acute haemolytic anemia.

GRIK4 codes for a protein that transmits signals from the neurotransmitter glutamate in the brain. Not much can be said for certain about this gene yet, but variations in this gene are associated with how your body responds to anti-depressants.

The GSTP1 gene encodes the enzyme glutathione S-transferase Pi 1. It belongs to the glutathione S-transferase (GST) family of enzymes, which are involved in the detoxification and elimination of a wide range of toxic compounds, including carcinogens, drugs, and environmental pollutants. GSTP1 is primarily found in the liver.

HLA-B is an important part of the immune system. It belongs to a family of genes, the HLA complex. It helps the immune system to distinguish between your own proteins and proteins from an intruder, such as a bacterium or a virus.

IFNL3 is a gene that codes for a cytokine. Cytokines are important signal proteins in the immune system. When a threat is detected in your body, many cytokines are activated, which can trigger the immune response.

MT-RNR1 is a gene located in humans’ mitochondrial DNA (mtDNA). It encodes a vital RNA molecule, which is an essential component of the mitochondrial ribosome. Mitochondrial ribosomes are responsible for synthesizing proteins within the mitochondria, the cellular organelles that produce energy. Mutations or alterations in the MT-RNR1 gene can lead to mitochondrial disorders and hearing loss.

The MTHFR gene encodes the enzyme methylenetetrahydrofolate reductase. This enzyme is involved in folic acid metabolism. This folic acid metabolism is essential for the production of DNA and protein synthesis, which in turn are essential for all bodily functions.

The NAT2 gene encodes the enzyme N-acetyltransferase 2. It is primarily expressed in the liver, playing a crucial role in the metabolism of various drugs, chemicals, and environmental compounds.

The NUDT15 gene encodes the enzyme nudix hydrolase 15. Just like TPMT, it is involved in the detoxification of the body. NUDT15 is mainly found in the liver and is also present in other tissues involved in drug metabolism, such as the intestines and bone marrow.

The OPRM1 gene contains instructions for making a protein called the mu (μ) opioid receptor. This is a normal part of our body and is called the opioid system and it is a system where pain, reward but also addiction are regulated.

This SLCO1B1 gene contains the instructions for making a protein called organic anion-transporting polypeptide 1B1 or OATP1B1. It influences the transport of substances in the body. The protein is found in liver cells where it transports compounds from the blood to the liver so that they can be removed from the body.

The TPMT gene encodes the enzyme thiopurine S-methyl transferase. Just like COMT (also a methyl trasferase), TPMT is involved in the detoxification of the body. TPMT is mainly found in the liver and kidneys and is less common in the brain and lungs.

This gene belongs to a family of genes that provide instructions for making enzymes called UDP glucuronosyl transferases. These enzymes carry out a reaction called glucuronidation: this process is a convenient way for the body to make various substances more water-soluble and in this way easier to transport through the body or to remove from the body via urine or bile relief (from the liver).

This gene codes for an enzyme in the liver that plays a key role in the vitamin K cycle. Vitamin K plays an important role in helping to make a blood clot and thus preventing excessive bleeding.

In the news...

Articles from newspapers and renowned organizations describing the value of pharmacogenetic testing and impact on personal health.
Some articles are not in English (we recommend you to use your browser translation feature to read them).

Fran Lowry (06-06-2019)
Genetic testing may help identify the best antidepressant

Pharmacogenetic testing can help physicians choose with greater precision the most effective antidepressant for their patients with major depressive disorder (MDD). A study examining the utility of such tests showed that remission, response and relief of depressive symptoms were greater in patients whose care was guided by such tests, compared to patients who received treatment as usual, without genetic accompaniment. “Pharmacogenetic testing will not tell us in advance which antidepressant is most effective for a patient, at least not at the moment. But such tests help us know which medicines may be incorrect, not the best choice or incorrect only for a particular patient”, said researcher John F. Greden, MD, executive director, University of Michigan Comprehensive Depression Center and Rachel Upjohn Professor of Psychiatry, Ann Arbor. Pharmacogenetic testing is not yet routinely used by physicians as a way to improve outcomes for patients with MDD. “There is a lot of skepticism about such tests, there is confusion, people are amazed about this, but there are reasons for this. For example, early studies and publications on pharmacogenetics studied small numbers of genes and variants and had small sample sizes and short follow-up duration. But such tests have come a long way since the early days”, said Greden. "Knowing how to use pharmacogenetic data helps physicians make choices that bring about response and remission", he added.

Jacqueline Howard (02-06-2019)
Pancreatic cancer therapy sheds light on the disease's ties to BRCA mutation

Researchers have long known that several cancers, other than breast and ovaries, are associated with harmful mutations in BRCA1 and BRCA2, including ovarian cancer, prostate cancer, and pancreatic cancer. A new study, presented at the annual meeting of the American Society for Clinical Oncology in Chicago, describes a treatment approach specific to patients with metastatic pancreatic cancer who had a BRCA1 or BRCA2 mutation.

D. Primorac, L. Bach-Rojecky (03-05-2019)
Could a personalized approach to therapy end the war on pain?

Chronic pain affects about 20% of the adult population worldwide and is a huge burden on those affected, with a significant negative impact on their quality of life, daily functioning and work productivity. While looking for an explanation of the inter-individual variability in pain perception and drug-induced pain relief, scientists have sought to find the answers in the genes. As of this publication, researchers have identified at least six genes or gene clusters (mostly associated with opioid, adrenergic, and catecholamine pathways) that may be related to pain development. Many physicians already have experience with the great advantage of implementing pharmacogenomics in their daily practice. Dosage adjustments according to a patient's genotype to optimize medicine therapy have been implemented in relevant clinical guidelines and in summaries of product characteristics (SmPC) for particular medicines and medicine classes. Accordingly, translating genomic data is becoming increasingly important in clinical practice in understanding differences in the effect of medications during the treatment of pain.

Sonya Collins (28-02-2019)
Danger abounds when meds and your genes don’t mix

This month, Karen Daggett celebrated 10 years of life she thought she wouldn't have. On Valentine's Day 2009, she didn't feel well enough to have a dinner with a couple of friends on Marco Island, Florida. But her husband insisted that she go with him and Daggett is grateful for that. “If I had stayed [alone] that night, I probably would have died”, she said. Different genes tell the body how to break down different medicines. A variant in one of those genes can affect how you process one, some, or all of the medicines for which the gene is responsible. Some gene variants can make you so sensitive to a medicine that you only need a dosage half as much as most people to get the same effect. Another variant could mean that you need twice as much. Yet another one could cause you to have a potentially fatal reaction to certain medications.

Ellen de Visser (02-01-2019)
How genetic research can prevent serious side effects from chemotherapy

The number of cancer patients who become seriously ill or even die from the commonly used chemo medication 5-FU can be drastically reduced by testing all patients genetically beforehand and then adjusting the dose if necessary. A Dutch study among 1100 patients in seventeen hospitals now provides definitive proof of this. The main explanation for this has been known for years. 5-FU, which is given by infusion or by pill, is broken down by an enzyme in the liver to an inactive substance. Only 8 percent of all people have a genetic variation that makes that enzyme inactive or less active. The consequence: the medicine is broken down too slowly or not at all, so that the level of active substance in the blood remains high and the medicine has the chance to seriously affect healthy tissues. In this study, the DNA was searched for the four most common variations that reduce or disable the activity of the enzyme involved. In the 85 patients with one of the variations studied, the dose of the cancer medication was adjusted and they received a quarter to half less. The number of patients with serious side effects halved, as described in "The Lancet Oncology". personal medicine tests not only those 4 variations, but also many others, the results of which you can take to your treating doctor.

Matilde Capi, Giovanna Gentile, Luana Lionetto, Gerardo Salerno, Fabiola Cipolla, Martina Curto, Marina Borro & Paolo Martelletti (26-10-2018)
Pharmacogenetic considerations for migraine therapies

Migraine is a very common neurological condition with a complex background. Remarkably, there are different reactions to the medicines used for migraines. The ineffective response and degree of side effects are common problems in patients. Several studies show that this condition has an important and complex genetic component related to medicine treatment. Many polymorphisms of genes involved in medication metabolism have been analyzed. These studies show many gene variations, especially on CYP450 (which metabolizes 90% of the medicines) and are the most suitable starting point for both current and future migraine therapy. Pharmacogenetics promise to help find a pharmacological therapy based on the patient's unique genetic characteristics.

Bennie Mols - VPRO (2018)
A look at Estonian pioneering work on personalized medicine

DNA analysis is the future of personalized medicine. In Estonia, citizens can already receive free genetic screening and tailored health advice, but what about the protection of that data?
In March of this year, the Estonian government announced that it is spending five million euros to offer 100000 citizens free genetic screening in the remainder of 2018. Since then, the registrations of interested Estonians have been pouring in every week. "We are going to get those hundred thousand before Christmas", says Professor Andres Metspalu on the phone. Metspalu is director of the Estonian Genome Center at the University of Tartu. The genetic material of the Estonians is stored in the biobank of its center. Estonia has an ideal, says the geneticist: "And we call that ideal: precision prevention". On Sunday, VPRO Tegenlicht (a Dutch channel) will delve deeper into this Estonian ideal with the episode "Conquest of our DNA".

Emily Pond (07-09-2018)
Combinatorial pharmacogenetics useful in treatment for depression

The use of pharmacogenomics in the treatment of major depressive disorder (MDD) is supported by study data published in the Journal of Psychiatry Research. Researchers designed an open-label prospective study to examine the efficacy of pharmacogenomics for patients with MDD in both psychiatric and primary care settings. Pharmacogenomic testing was performed for all patients at baseline (N=1871), using genomic DNA isolated from buccal swabs. Medications were classified as congruent or incongruent via genotyping results. Depressive symptoms were assessed at baseline and then at 8 to 12 weeks’ follow-up using the Beck Depression Inventory (BDI).

Batya Swift Yasgur (30-05-2018)
Pharmacogenetics in psychiatry: promising developments and potential pitfalls

Finding an effective and tolerable antidepressant for a particular patient can take a long time. During this time, patients are exposed to ineffective medications with potential adverse effects and the harmful effects of the depression itself. The reasons for a negative response to antidepressants can be complex, but genetic components are clearly relevant. The use of pharmacogenetics in antidepressant treatments is therefore intended to improve remission rates of depression and reduce its adverse effects.

Robert H. Shmerling (12-01-2018)
Genetic testing to predict medication side effects

Statins are commonly prescribed medicines in the Netherlands. Statins are the first choice for doctors. On average, about 50% of patients stop taking statin medicines. This has several causes. No improvement is felt and/or there are side effects and/or publicity is believed in which the effect is called into question. Often about 25% start again with another statin medicine. Other 25%, however, choose not to use a statin medicine anymore, because of the unpleasant side effects. A study was conducted in Chicago with patients who had stopped taking statin medicines. They had a DNA test and on the basis of this a statin medicine that matched the DNA profile found was prescribed. Almost 60% of this group was ready to continue with the new medication. After 8 months the cholesterol levels were lower. Only 33% of the control group, where the DNA test was not taken, was willing to start using statin medication again.

VIG (14-04-2017)
Medicines very poorly adapted to the patient's DNA

In 200000 medication prescriptions in 2016, the dose would have been adjusted if pharmacists had been able to request the DNA profile for medicine degradation. According to the KNMP, this is evident from figures from the SFK, presented at the jubilee conference.

ZonMw (06-04-2017)
Pharmacogenetics essential for tailor-made treatment

Today, the treatment of patients is increasingly looking at unique genetic and biological characteristics. This makes it possible to set up a closely tailored treatment at an individual level. This is called personalized medicine. Pharmacogenetics - part of personalized medicine - makes it possible to determine whether or not a particular medicine is effective in an individual patient or whether it may cause side effects that could lead to hospitalization or even death.

J. Kitzmiller, E. Mikulik, A. Dauki, C. Murkherjee, J. Luzum (03-10-2016)
Pharmacogenomics of statins: understanding susceptibility to adverse effects

Statins are a cornerstone of the pharmacological treatment and prevention of atherosclerotic cardiovascular disease. Atherosclerosis is a predominant cause of death and morbidity worldwide. Statins are among the most commonly prescribed classes of medicines, and their prescribing indications and target populations have been significantly expanded in the official guidelines recently published by the US and European expert panels. However, adverse effects of statin pharmacotherapy lead to significant costs and morbidity and can lead to non-adherence and discontinuation of therapy. Statin-associated muscle symptoms occur in circa 10% of patients on statins and are the most commonly reported adverse reaction associated with statin pharmacotherapy. Significant clinical and non-clinical research efforts are focused on determining whether genetics can provide meaningful insight into the risk of statin adverse effects in an individual patient. This contemporary review of the relevant clinical research on polymorphisms in several key genes influencing statin pharmacokinetics (eg. transporters and metabolizing enzymes), statin efficacy (eg. medicine targets and pathways) and end-organ toxicity (eg. myopathy pathways) highlights several promising pharmacogenomic candidates. However, SLCO1B1 521C is currently the only clinically relevant pharmacogenetic test with regard to statin toxicity and its relevance is limited to simvastatin myopathy.

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