February 23, 2017 Joel Eissenberg, Ph.D., is professor of biochemistry and molecular biology at Saint Louis University. Credit: Saint Louis University

Thanks to recent scientific advances and plunging costs in genetic sequencing, consumers now can order simple, inexpensive, mail-in genetic tests to learn more about health risks, inherited traits and ancestry. But, is it a good idea to bypass your doctor's office when it comes to interpreting health risks?

New technology means grappling with new questions of ethics, best practices and access to information. In an article published in Missouri Medicine, Joel Eissenberg, Ph.D., professor of biochemistry and molecular biology at Saint Louis University, explores questions that stem from these advances, which have the effect of separating the physician-patient relationship from access to new personal health data.

Some companies offer DNA tests via a mail-in saliva sample. Once the sample is tested, the company provides consumers with a report showing whether they are a carrier for any of over 35 diseases, as well as information about traits and ancestry. Participants might learn, for example, that they carry a genetic variation for cystic fibrosis or hereditary hearing loss. Carriers may pass along these genetic variations to a child, who could develop the condition if both parents carry and pass on the variation.

Other tests might find that a consumer carries a genetic variation that increases the risk of breast cancer or Alzheimer's disease. In the case of breast cancer, preventive measures, like regular screening via mammography or preventive surgery, may offer a chance to limit the risk of developing cancer. On the other hand, there is no proven medical treatment for Alzheimer's disease.

In the article, Eissenberg notes several areas of concern for consumers as they attempt to interpret their personal information without the help of a physician or genetic counselor, including a limited understanding of genetics, confusion about disease risk and anxiety caused by new information in the absence of guidance from a medical professional.

Eissenberg concludes, however, that individuals should be able to access their own personal genome data.

"In an open society, maximizing autonomy is a virtue," Eissenberg said. "Knowledge is power."

He notes that, in many ways, we've already moved along the path of patient-initiated testing, with digital thermometers, blood pressure cuffs, blood sugar monitors and pregnancy testing kits that give the public direct access to health information.

In theory, understanding genetic risk could help guide life decisions, such as encouraging regular cancer screenings, a healthy diet and exercise to offset some genetic risks for some illnesses. (Though, some research has found that communicating DNA-based disease risk has little or no effect on smoking and physical activity.)

"At its best, direct-to-consumer genomics testing could eventually become like other forms of home medical testing - another way for people to take personal control of their health and wellness," Eissenberg said.

At the same time, he urges caution in how these tests are marketed, noting that currently they are not able to offer useful predictions or recommendations for many diseases.

"Today, however, genomics testing to assess risk for complex diseases rests on a weak foundation of clinical validation. Thus, in most cases, genomics data cannot serve as a guide to action."

Finally, while Eissenberg does not believe medical paternalism is warranted in restricting access to direct-to-consumer tests, he shares several instances in which consumers may benefit from consulting with their physician or a genetic counselor: to prepare for adverse news, to help interpret risk, to prescribe a risk response and to counsel caution in over interpretation.

But the bottom line?

"It is important to stress that genetic risk is not the same as genetic destiny," Eissenberg said.

Explore further: Customers who receive genetic health data not alarmed by results, find information useful

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Direct-to-consumer genomics: Harmful or empowering? - Medical Xpress

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Boehringer Ingelheim's North American headquarters located in Ridgefield, CT.

Boehringer Ingelheim's North American headquarters located in Ridgefield, CT.

BI announces COPD collaboration with Weill Cornell Medicine

RIDGEFIELD Boehringer Ingelheim announced a collaboration with Weill Cornell Medicine to identify new treatment approaches for chronic obstructive pulmonary disease, also known as COPD, with the hopes of halting or reversing the progression of the disease.

The three-year collaboration combines Weill Cornell Medicines Department of Genetic Medicines understanding of chronic airway diseases and use of novel therapeutic concepts for airway repair with BIs knowledge in the discovery and development of new therapies for respiratory diseases.

It is the second collaboration between BI and Weill Cornell Medicine, following prior work in inflammatory bowel disease.

The scientists at Weill Cornell Medicine and Boehringer Ingelheim will work hand in hand to translate new discoveries into drug discovery and development programs at Boehringer Ingelheim, Dr. Clive R. Wood, senior corporate vice president, Discovery Research at BI, said in a release.

The new collaboration is an excellent example of our unique partnering approach and our focus on early innovation, underscoring our ambition to develop the next generation of medical treatments for patients with COPD.

Chronic lower respiratory diseases, which include COPD, are the third leading cause of death in the United States. Approximately 15 million Americans have been told by a health care provider that they have COPD, BI officials said.

The goal of the new treatment is to help patients keep as active as possible and improve their overall quality of life, BI officials said.

Our continuous search for molecular drivers of chronic obstructive airway diseases has revealed novel repair mechanisms that warrant further investigation of their potential as therapeutic approaches, Dr. Ronald G. Crystal, chairman of Genetic Medicine at Weill Cornell Medicine and lead investigator in the new collaboration, said in a release.

BI is based in Ridgefield and employs about 2,500 people locally.

cbosak@hearstmediact.com; 203-731-3338

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BI announces COPD collaboration with Weill Cornell Medicine - Danbury News Times

February 22, 2017 by Kristin Samuelson Flickr photo by Benjamin Watson

A new Northwestern Medicine study found evidence suggesting how neural dysfunction in a certain region of the brain can lead to obsessive and repetitive behaviors much like obsessive-compulsive disorder (OCD).

Both in humans and in mice, there is a circuit in the brain called the corticostriatal connection that regulates habitual and repetitive actions. The study found certain synaptic receptors are important for the development of this brain circuit. If these receptors are eliminated in mice, they exhibit obsessive behavior, such as over-grooming.

This is the first strong evidence that supports the biological basis for how these genes that code for these receptors might affect obsessive or compulsive behaviors in humans. By demonstrating that these receptors have this role in development, researchers down the line will have a target to develop treatments for obsessive-compulsive behavior.

"Variations in these receptor genes are associated with human neurodevelopmental disorders, such as autism and neuropsychiatric disorders such as OCD," said lead author Anis Contractor, associate professor of physiology at Northwestern University Feinberg School of Medicine. "People with OCD are known to have abnormalities in function of corticostriatal circuits."

The study was published February 21 in the journal Cell Reports. The findings shed light on the importance of these receptors in the formation of the corticostriatal circuits, Contractor said.

"A number of studies have found mutations in the kainate receptor genes that are associated with OCD or other neuropsychiatric and neurodevelopmental disorders in humans," said Contractor, who also is an associate professor of neurobiology at the Weinberg College of Arts and Sciences at Northwestern. "I believe our study, which found that a mouse with targeted mutations in these genes exhibited OCD-like behaviors, helps support the current genetic studies on neuropsychiatric and neurodevelopmental disorders in humans."

The traits of OCD the mice in the study exhibited included over-grooming, continuously digging in their bedding and consistently failing a simple alternating-choice test in a maze.

The study is titled, "Complete Disruption of the Kainate Receptor Gene Family Results in Corticostriatal Dysfunction in Mice."

Explore further: Gene loss creates eating disorder-related behaviors in mice

More information: Jian Xu et al. Complete Disruption of the Kainate Receptor Gene Family Results in Corticostriatal Dysfunction in Mice, Cell Reports (2017). DOI: 10.1016/j.celrep.2017.01.073

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OCD-like behavior linked to genetic mutation - Medical Xpress - Medical Xpress

Crowd control: Nearly 4 percent of people carry at least one genetic variant tied to a serious medical condition.

brainmaster / Getty Images

Most adults with genetic variants tied to certain conditions, such as heart disease or cancer, go undiagnosed, according to a study of more than 50,000 people1.

The variants silence leaves these people unaware of their risk of developing the conditions later in life, says lead investigator David Carey, director of the Weis Center for Research at Geisinger Health System in Danville, Pennsylvania.

Careys team looked for genetic variants associated with 27 chronic conditions. The list of conditions does not include autism, but does include tuberous sclerosis complex. As many as half of all people with tuberous sclerosis complex have autism. Other teams are studying the same population to gauge the effects of variants linked to autism.

The value lies in the huge population, all captured within the same healthcare system. Its really fantastic, says Dan Arking, associate professor of genetic medicine at Johns Hopkins University in Baltimore, Maryland, who was not involved in the new work.

The variants in the study are clinically significant: Some increase the risk of the linked condition by up to 70 percent. But variants interact with many other genetic and environmental factors, and these interactions may cause the conditions features to be more or less severe or even absent.

People used to say anytime there is a [spontaneous] variant or something really rare, that it must cause disease, says Arking. The new study instead suggests that, on the contrary, some rare variants have weak ties to conditions such as autism, he says. The results appeared 23 December in Science2.

Carey and his team looked at data from the MyCode Community Health Initiative, launched in 2007 by Geisinger Health System in central Pennsylvania. MyCode researchers have collected DNA samples and up to 14 years worth of medical records from the participants.

The researchers probed the 50,726 participants genomes for inserted or deleted sequences, and for single nucleotide variants, called SNVs, in the code. Their analysis revealed that each individual harbors about 21,409 SNVs, consistent with findings from previous studies.

The researchers then narrowed their analysis to 76 genes known to contribute to life-threatening conditions such as cancer or cardiovascular disease. The list includes three genes tied to tumor growth and to autism: PTEN, TSC1 and TSC2. (Clinicians are obligated to counsel individuals with variants in any of these 76 genes.)

Nearly 4 percent of the general population carries variants in at least one of these genes, the researchers found. But more than one-third of these people show no symptoms and have no family history of the linked condition. For example, most of the individuals who carry a variant linked to an inherited condition that causes high cholesterol have normal cholesterol levels, according to a second study by Careys team in the same issue of Science.

The findings could mean the individual will develop the condition later in life or not, Carey says. Other variants in her genome might mitigate the risk, he says.

We generally look at one gene at a time, but we have about 20,000 genes and they all work in concert, Carey says. Were not sophisticated enough yet to be able to tease out all the genetic interactions, but we know that they exist.

Last year, another team of researchers used the MyCode data to show that genetic changes tied to autism also crop up in many people without the condition. At the 2016 American Society of Human Genetics annual meeting in Vancouver, Canada, last year, they presented results showing that about 2,000 of the MyCode participants carry large deletions or duplications of genetic material associated with autism, intellectual disability or schizophrenia. But less than 5 percent of this group has received treatment for any of the conditions.

The finding suggests that genetic variants can confer features so subtle that they go unrecognized well into adulthood. Researchers could study this group to understand the mildest end of the autism spectrum.

This cohort could help us describe the full picture of autism, the breadth of the phenotype, says Christa Lese Martin, director of the Autism and Developmental Medicine Institute at Geisinger Health System in Lewisburg, Pennsylvania. Martin was a lead investigator on the autism study but was not involved in the new work.

About 125,000 people have enrolled in MyCode so far. By early next year, researchers expect to have sequencing data for 90,000 of the individuals.

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Many people with harmful genetic variants show no ill effects ... - Spectrum

Personalized medicine, which involves tailoring health care to each persons unique genetic makeup, has the potential to transform how we diagnose, prevent and treat disease. After all, no two people are alike. Mapping a persons unique susceptibility to disease and targeting the right treatment has deservedly been welcomed as a new power to heal.

The human genome, a complete set of human DNA, was identified and mapped a decade ago. But genomic science remains in its infancy. According to Francis Collins, the director of the National Institutes of Health, It is fair to say that the Human Genome Project has not yet directly affected the health care of most individuals.

Its not that there havent been tremendous breakthroughs. Its just that the gap between science and its ability to benefit most patients remains wide. This is mainly because we dont yet fully understand the complex pathways involved in common chronic diseases.

I am part of a research team that has taken on the ambitious goal of narrowing this gap. New technologies are allowing us to probe DNA, RNA, proteins and gut bacteria in a way that will change our understanding of health and disease. Our hope is to discover novel biological markers that can be used to diagnose and treat common chronic conditions, including Alzheimers disease, heart disease, diabetes and cancer.

But when it comes to preventing the leading causes of death which include chronic diseases, genomics and precision medicine may not do as much as we hope.

Chronic diseases are only partially heritable. This means that the genes you inherit from your parents arent entirely responsible for your risk of getting most chronic diseases.

The estimated heritability of heart disease is about 50 percent. Its 64 percent for Type 2 diabetes mellitus, and 58 percent for Alzheimers disease. Our environment and lifestyle choice are also major factors; they can change or influence how the information coded in our genes is translated.

Chronic diseases are also complex. Rather than being controlled by a few genes that are easy to find, they are weakly influenced by hundreds if not thousands of genes, the majority of which still elude scientists. Unlocking the infinite combinations in which these genes interact with each other and with the environment is a daunting task that will take decades, if ever, to achieve.

While unraveling the genomic complexity of chronic disease is important, it shouldnt detract from existing simple solutions. Many of our deadliest chronic diseases are preventable. For instance, among U.S. adults, more than 90 percent of Type 2 diabetes, 80 percent of coronary arterial disease, 70 percent of stroke and 70 percent of colon cancer are potentially avoidable.

Smoking, weight gain, lack of exercise, poor diet and alcohol consumption are all risk factors for these conditions. Based on their profound impact on gene expression, or how instructions within a gene are manifested, addressing these factors will likely remain fundamental in preventing these illnesses.

A major premise behind personalized medicine is that empowering patients and doctors with more knowledge will lead to better decision-making. With some major advances, this has indeed been the case. For instance, variants in genes that control an enzyme that metabolizes drugs can identify individuals who metabolize some drugs too rapidly (not giving them a chance to work), or too slowly (leading to toxicity). This can lead to changes in medication dosing.

When applied to prevention, however, identifying our susceptibility at an earlier stage has not aided in avoiding chronic diseases. Research challenges the assumption that we will use genetic markers to change our behavior. More knowledge may nudge intent, but that doesnt translate to motivating changes to our lifestyle.

A recent review found that even when people knew their personal genetic risk of disease, they were no more likely to quit smoking, change their diet or exercise. Expectations that communicating DNA-based risk estimates changes behavior is not supported by existing evidence, the authors conclude.

Increased knowledge may even have the unintended consequence of shifting the focus to personal responsibility while detracting from our joint responsibility for improving public health. Reducing the prevalence of chronic diseases will require changing the political, social and economic environment within which we make choices as well as individual effort.

Perhaps the most awaited hope of the genomic era is that we will be able to develop targeted treatments based on detailed molecular profiling. The implication is that we will be able to subdivide disease into new classifications. Rather than viewing Type 2 diabetes as one disease, for example, we may discover many unique subtypes of diabetes.

This already is happening with some cancers. Patients with melanoma, leukemia or metastatic lung, breast or brain cancers can, in some cases, be offered a molecular diagnosis to tailor their treatment and improve their chance of survival.

We have been able to make progress in cancer therapy and drug safety and efficacy because specific gene mutations control a persons response to these treatments. But for complex, chronic diseases, relatively few personalized targeted treatments exist.

Customizing treatments based on our uniqueness will be a breakthrough, but it also poses a challenge: Without the ability to test targeted treatments on large populations, it will make it infinitely harder to discover and predict their response.

The very reason we group people with the same signs and symptoms into diagnoses is to help predict the average response to treatment. There may be a time when we have one-person trials that custom tailor treatment. However, the anticipation is that the timeline to getting to such trials will be long, the failure rate high and the cost exorbitant.

Research that takes genetic risk of diabetes into account has found greater benefit in targeting prevention efforts to all people with obesity rather than targeting efforts based on genetic risk.

We also have to consider decades of research on chronic diseases that suggest there are inherent limitations to preventing the global prevalence of these diseases with genomic solutions. For most of us, personalized medicine will likely complement rather than replace one-size-fits-all medicine.

Where does that leave us? Despite the inherent limitations to the ability of genomic medicine to transform health care, medicine in the future should unquestionably aspire to be personal. Genomics and molecular biosciences will need to be used holistically in the context of a persons health, beliefs and attitudes to fulfill their power to greatly enhance medicine.

See the article here:

Soon, Medication Will be Custom Tailored to Your Specific Genetics - Futurism

Personalized medicine, which involves tailoring health care to each persons unique genetic makeup, has the potential to transform how we diagnose, prevent and treat disease. After all, no two people are alike. Mapping a persons unique susceptibility to disease and targeting the right treatment has deservedly been welcomed as a new power to heal.

The human genome, a complete set of human DNA, was identified and mapped a decade ago. But genomic science remains in its infancy. According to Francis Collins, the director of the National Institutes of Health, It is fair to say that the Human Genome Project has not yet directly affected the health care of most individuals.

Its not that there havent been tremendous breakthroughs. Its just that the gap between science and its ability to benefit most patients remains wide. This is mainly because we dont yet fully understand the complex pathways involved in common chronic diseases.

I am part of a research team that has taken on the ambitious goal of narrowing this gap. New technologies are allowing us to probe DNA, RNA, proteins and gut bacteria in a way that will change our understanding of health and disease. Our hope is to discover novel biological markers that can be used to diagnose and treat common chronic conditions, including Alzheimers disease, heart disease, diabetes and cancer.

But when it comes to preventing the leading causes of death which include chronic diseases, genomics and precision medicine may not do as much as we hope.

Many diseases arent due only to genetics

Chronic diseases are only partially heritable. This means that the genes you inherit from your parents arent entirely responsible for your risk of getting most chronic diseases.

The estimated heritability of heart disease is about 50 percent. Its 64 percent for Type 2 diabetes mellitus, and 58 percent for Alzheimers disease. Our environment and lifestyle choice are also major factors; they can change or influence how the information coded in our genes is translated.

Chronic diseases are also complex. Rather than being controlled by a few genes that are easy to find, they are weakly influenced by hundreds if not thousands of genes, the majority of which still elude scientists. Unlocking the infinite combinations in which these genes interact with each other and with the environment is a daunting task that will take decades, if ever, to achieve.

While unraveling the genomic complexity of chronic disease is important, it shouldnt detract from existing simple solutions. Many of our deadliest chronic diseases are preventable. For instance, among U.S. adults, more than 90 percent of Type 2 diabetes, 80 percent of coronary arterial disease, 70 percent of stroke and 70 percent of colon cancer are potentially avoidable.

Smoking, weight gain, lack of exercise, poor diet and alcohol consumption are all risk factors for these conditions. Based on their profound impact on gene expression, or how instructions within a gene are manifested, addressing these factors will likely remain fundamental in preventing these illnesses.

Will more knowledge be more power?

A major premise behind personalized medicine is that empowering patients and doctors with more knowledge will lead to better decision-making. With some major advances, this has indeed been the case. For instance, variants in genes that control an enzyme that metabolizes drugs can identify individuals who metabolize some drugs too rapidly (not giving them a chance to work), or too slowly (leading to toxicity). This can lead to changes in medication dosing.

When applied to prevention, however, identifying our susceptibility at an earlier stage has not aided in avoiding chronic diseases. Research challenges the assumption that we will use genetic markers to change our behavior. More knowledge may nudge intent, but that doesnt translate to motivating changes to our lifestyle.

A recent review found that even when people knew their personal genetic risk of disease, they were no more likely to quit smoking, change their diet or exercise. Expectations that communicating DNA-based risk estimates changes behavior is not supported by existing evidence, the authors conclude.

Increased knowledge may even have the unintended consequence of shifting the focus to personal responsibility while detracting from our joint responsibility for improving public health. Reducing the prevalence of chronic diseases will require changing the political, social and economic environment within which we make choices as well as individual effort.

What about treating chronic diseases?

Perhaps the most awaited hope of the genomic era is that we will be able to develop targeted treatments based on detailed molecular profiling. The implication is that we will be able to subdivide disease into new classifications. Rather than viewing Type 2 diabetes as one disease, for example, we may discover many unique subtypes of diabetes.

This already is happening with some cancers. Patients with melanoma, leukemia or metastatic lung, breast or brain cancers can, in some cases, be offered a molecular diagnosis to tailor their treatment and improve their chance of survival.

We have been able to make progress in cancer therapy and drug safety and efficacy because specific gene mutations control a persons response to these treatments. But for complex, chronic diseases, relatively few personalized targeted treatments exist.

Customizing treatments based on our uniqueness will be a breakthrough, but it also poses a challenge: Without the ability to test targeted treatments on large populations, it will make it infinitely harder to discover and predict their response.

The very reason we group people with the same signs and symptoms into diagnoses is to help predict the average response to treatment. There may be a time when we have one-person trials that custom tailor treatment. However, the anticipation is that the timeline to getting to such trials will be long, the failure rate high and the cost exorbitant.

Research that takes genetic risk of diabetes into account has found greater benefit in targeting prevention efforts to all people with obesity rather than targeting efforts based on genetic risk.

We also have to consider decades of research on chronic diseases that suggest there are inherent limitations to preventing the global prevalence of these diseases with genomic solutions. For most of us, personalized medicine will likely complement rather than replace one-size-fits-all medicine.

Where does that leave us? Despite the inherent limitations to the ability of genomic medicine to transform health care, medicine in the future should unquestionably aspire to be personal. Genomics and molecular biosciences will need to be used holistically in the context of a persons health, beliefs and attitudes to fulfill their power to greatly enhance medicine.

Sharon Horesh Bergquist, Physician, teacher, researcher in preventive medicine and healthy aging, Emory University

See original here:

Personalized medicine may do more to treat rather than prevent ... - Salon

According to an international team of researchers led by University College London and Kings College London, the discovery of a molecular switch that causes the mucosal inflammatory diseases ulcerative colitis, Crohns disease, and celiac disease, could lead to effective new treatments for these autoimmune conditions. The discovery is reported in the journal PLoS Genetics.

According to Soderquest et al, T-bet plays an important role in coordinating the bodys immune responses. Image credit: Werbe Fabrik.

For the first time, researchers have a specific target for the treatment of these life-changing conditions by identifying an immune molecule called T-bet (TBX21) as the key control point that regulates the genetic risk in specific diseases.

Our research outlines a specific focus for the development of new treatments for these diseases which have such a profound effect on sufferers, explained Kings College London Professor Graham Lord, co-senior author on the study.

In the study, Prof. Lord and his colleagues examined how genetic variation affects T-bet binding to DNA, as a key regulatory mechanism in the immune response.

Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) that may be causative for autoimmune diseases, the researchers said.

The majority of these polymorphisms are located within non-coding distal regulatory elements.

It is considered that these genetic variants contribute to disease by altering the binding of regulatory proteins and thus gene expression, but whether these variants alter the binding of lineage-specifying transcription factors has not been determined.

The researchers found that T-bet binding sites are specifically enriched in genetic variants associated with the mucosal autoinflammatory diseases.

They also identified genetic variants that alter T-bet binding and gene expression.

We show that SNPs associated with the mucosal inflammatory diseases Crohns disease, ulcerative colitis and celiac disease, but not rheumatoid arthritis or psoriasis, are enriched at T-bet binding sites, the authors said.

Furthermore, we identify disease-associated variants that alter T-bet binding in vitro and in vivo.

Our results suggest that genetic polymorphisms may predispose individuals to mucosal autoimmune disease through alterations in T-bet binding, they said.

Other disease-associated variants may similarly act by modulating the binding of lineage-specifying transcription factors in a tissue-selective and disease-specific manner.

_____

K. Soderquest et al. 2017. Genetic variants alter T-bet binding and gene expression in mucosal inflammatory disease. PLoS Genet 13 (2): e1006587; doi: 10.1371/journal.pgen.1006587

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'Molecular Switch' that Causes Mucosal Autoimmune Diseases Discovered - Sci-News.com

Updated March 05, 2016.

Definition: In genetic variation, the genes of organisms within a population change. Gene alleles determine distinct traits that can be passed on from parents to offspring. Gene variation is important to the process of natural selection. The genetic variations that arise in a population happen by chance, but the process of natural selection does not. Natural selection is the result of the interactions between genetic variations in a population and the environment. The environment determines which variations are more favorable. More favorable traits are thereby passed on to the population as a whole.

Genetic variation occurs mainly through DNA mutation, gene flow (movement of genes from one population to another) and sexual reproduction. Due to the fact that environments are unstable, populations that are genetically variable will be able to adapt to changing situations better than those that do not contain genetic variation.

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Genetic Variation: Causes and Examples

The future of medicine is here and a genetic test may be able to determine if a person will have a bad reaction to certain medicine or not respond to certain drugs at all.

A R3500 test called the mygeneRx created by Johannesburg company DNAlysis can analyse your DNA and look at the genetic variation in genes that control drug-using enzymes.

These enzymes can allow a drug to be metabolized (used) by the body so fast that it gets rid of the medicine before it has time to work or very slowly so the body can have difficulty eliminating the drug.

The slow metabolism rate could lead to an overdose and unintended side effects.

The test which uses a swab from your cheek only looks at a personal response to 150 medications used for pain heart disease high cholesterol and depression.

But experts warn that genetic testing to determine how a person will respond to medication is not yet advanced enough to help the average patient.

University of Kwazulu-Natal Pharmacology lecturer Andy Gray said: I certainly would not recommend blanked testing its an exploitation of the worried well with questionable clinical benefits.

Dr Mamoonah Chaudhry Postdoctoral Fellow at the University of Pretorias Institute for Cellular and Molecular Medicine explained the field of individual testing is known as pharmacogenomics and can help warn of a persons likelihood to have bad reactions to a drug.

She said the personalized medicine approach will help reduce mortality and morbidity due to adverse (bad) drug reactions.

Chaudhry however warned that current genetic tests were not advanced enough to be used widely to guide doctors on what medication to prescribe.

Most of the (laboratories) only test for a few genetic markers as also indicated in this test which are not enough for personalized treatment.

But Chaudhry said it did show a change in thinking about medication.

The idea of one size fits all has changed over the time and a personalized medicine approach has emerged.

Pharmacist Shafrudeen Amod said the 150 drugs the test looks at were too few and cause for concern.

If the aim of pharmacogenomics is to optimise drug therapy then this test represents a science at its infancy and the test is being prematurely released Amod said.

Amod also said the medications effect was never just related to a patients genes.

There are various reasons patients may not respond to a medication ranging from something as simple as not taking the medicine to complex drug interactions. Similarly side effects to medications range from minor to major Amod said.

Gray said there were genetic variabilities that affected how people reacted to some drugs such as warfarin which is used to stop blood-clotting and the common pain killer codeine where some people get high from it.

Some people on certain drugs such as warfarin may benefit from this testing Gray suggested.

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Genetic test to determine reaction to medicine is on the market ... - SowetanLIVE

WOBURN, Mass.--(BUSINESS WIRE)--

Courtagen Life Sciences, Inc., an innovative molecular information company, announced today that it has launched Avantra Genetics, a division of the company dedicated to providing advanced genomic information for functional medicine practices. Patients suffering from functional disorders may experience symptoms such as pain, fatigue, numbness or sensations and gastrointestinal distress that can be severe, chronic or debilitating. These disorders are often difficult to diagnose and treat, but may have a genetic origin or influence.

Physicians practicing functional, integrative, or naturopathic medicine have been early adopters of personalized medicine and the use of personal genetic information to help guide diet and lifestyle choices, said Brian McKernan, CEO of Courtagen Life Sciences. Our new Avantra Genetics tests provide genomic information focused on biological pathways important to these functional medicine clinicians.

Courtagens Avantra Genetics division launches two genomic information-only tests for migraines and abdominal pain, with additional tests following later this year. The tests focus on genes in pathways of interest to functional medicine clinicians who want to better understand their patients with the signs, symptoms and indications of pain. The tests cover genes associated with, but are not limited to, celiac disease and lactase deficiency for abdominal pain, and coenzyme Q10 deficiency and dystonia associated with migraines. Also included are selections of common variants reported to be associated with general wellness. These genomic informative reports provide features such as links to literature and databases for the variants identified in the individual tested.

To learn more, visit Courtagen on Facebook, Twitter, and Instagram and Avantra Genetics on Facebook and Twitter.

About Courtagen Life Sciences, Inc.

Courtagen Life Sciences, Inc., located in Woburn, MA, is a CLIA/CAP certified molecular information company focused on the diagnosis of a range of neurological, endocrine, and functional disorders associated with the central, peripheral, and autonomic nervous systems, including the endocannabinoid receptor system. Courtagen operates a highly sophisticated Next Generation DNA Sequencing, bioinformatics, and clinical interpretation business that helps physicians elucidate the linkages between the genotypes and phenotypes of various diseases, which may be treated with a host of therapies, including pharmaceutical drugs and medical cannabis. For more information, please visit http://www.courtagen.com/.

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Courtagen Launches New Avantra Genetics Division to Provide ... - Yahoo Finance

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Dermatology - Stanford University School of Medicine

Boehringer Ingelheim recentlyannounced a collaboration with Weill Cornell Medicine to identify new treatment approaches forchronic obstructive pulmonary disease (COPD)in order to develop novel treatments that could possibly halt or even reverse the progression of the disease process. The new, three-year collaboration combines Weill Cornell Medicines Department of Genetic Medicines unique understanding of chronic airway diseases and experience in the investigation of novel therapeutic concepts for airway repair with Boehringer Ingelheims expertise in the discovery and development of new therapies for respiratory diseases. This collaboration is the second collaboration between Boehringer Ingelheim and Weill Cornell Medicine, following prior work in inflammatory bowel disease (IBD).

Chronic lower respiratory diseases, which include COPD, are the third leading cause of death in the United States,and approximately 15million Americans have been told by a healthcare provider that they have COPD.It cannot be cured and current treatment approaches focus on bronchodilation, reducing symptoms and preventing exacerbations to decelerate the downward spiral of the disease.The goal is to help patients keep as active as possible and overall, improve their quality of life.

Our continuous search for molecular drivers of chronic obstructive airway diseases has revealed novel repair mechanisms that warrant further investigation of their potential as therapeutic approaches, said Dr. Ronald G. Crystal, Chairman of Genetic Medicine at Weill Cornell Medicine and lead investigator in the new collaboration. We will look to further expand our knowledge about progressive airway destruction in close collaboration with Boehringer Ingelheim and focus on promising therapeutic concepts with the potential to slow down or halt progressive airway damage in patients with COPD.

We are delighted to work with Dr. Crystal at Weill Cornell Medicine, who is one of the leading scientists in severe progressive airway diseases worldwide, said Dr. Clive R. Wood, Senior Corporate Vice President, Discovery Research at Boehringer Ingelheim. The scientists at Weill Cornell Medicine and Boehringer Ingelheim will work hand in hand to translate new discoveries into drug discovery and development programs at Boehringer Ingelheim. The new collaboration is an excellent example of our unique partnering approach and our focus on early innovation, underscoring our ambition to develop the next generation of medical treatments for patients with COPD.

Boehringer Ingelheim is combining a focus on cutting-edge science with a long-term view enabling the company to create a stable environment for the development of the next generation of medical breakthroughs. This new project adds another building block in this long-term strategy to improve the lives of patients with high unmet medical needs.

Weill Cornell's Office of BioPharma Alliances and Research Collaborations negotiated the three-year collaboration.The offices mission is to proactively generate, structure and market translational research alliances with industry in order to advance promising research projects that have commercial potential. For more information, contact Larry Schlossman atlas2041@med.cornell.eduor at 212-746-6909.

About Boehringer Ingelheim in Respiratory

Boehringer Ingelheim has over 90 years of heritage in respiratory disease. Since 1921 the company has emerged as a leader in this disease area and has launched several treatments in a range of respiratory conditions including asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung cancer. Boehringer Ingelheims focus is on improving the quality of life of patients suffering from debilitating respiratory diseases and enabling them to maintain a more independent life.

About Boehringer Ingelheim Pharmaceuticals, Inc. Boehringer Ingelheim Pharmaceuticals, Inc., based in Ridgefield, CT, is the largest U.S. subsidiary of Boehringer Ingelheim Corporation.

Boehringer Ingelheim is one of the worlds 20 leading pharmaceutical companies.Headquartered in Ingelheim, Germany, the company operates globally with 145affiliates and more than 47,000 employees.Since its founding in 1885, the family-owned company has been committed to researching, developing, manufacturing and marketing novel treatments for human and veterinary medicine.

Boehringer Ingelheim is committed to improving lives and providing valuable services and support to patients and their families. Our employees create and engage in programs that strengthen our communities. To learn more about how we make more health for more people, visit ourCorporate Social Responsibility Report.

In 2015, Boehringer Ingelheim achieved net sales of about $15.8B (14.8billioneuros). R&D expenditure corresponds to 20.3 percent of its net sales.

SOURCE: Boehringer Ingelheim Pharmaceuticals, Inc.

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Boehringer Ingelheim And Weill Cornell Medicine Announce New ... - Clinical Leader

February 16, 2017 Credit: UNIGE

When a child is conceived, he or she receives DNA from both parents. The child's own genome thus consists of a maternal and a paternal genome. However, some genesabout 100 out of the 20,000 encoded genes are exclusively expressed either from the maternal or from the paternal genome, with the other copy of the gene remaining silent. We know that these imprinted genes are more likely to lead to serious genetic diseases, such as PraderWilli or Angelman syndrome. Researchers at the University of Geneva (UNIGE), Switzerland, have devised a new technique, based on a combination of biology and bioinformatics, to quickly and accurately detect the imprinted genes expressed in each of the cell types that constitute the human organs. This major breakthrough will improve our understanding and diagnosis of genetic diseases. The study can be read in full in the American Journal of Human Genetics.

The research team, led by Professor Stylianos Antonarakis from the Department of Genetic Medicine and Development in the Faculty of Medicine at UNIGE, focused on genomic imprinting. This is a set of genes exclusively expressed from the genetic code inherited either from the father (the paternal allele) or from the mother (maternal allele). Why is there so much interest in the identification of the imprinted genes? Because if a deleterious mutation affects the functional allele, it cannot be compensated by the expression of the second silent allele, likely causing a serious genetic disease. The goal, therefore, is to determine the imprinted genes in all cell types of human body tissues that are liable to cause these kind of diseases.

Until recently, millions of cells were analysed together without distinction. "We have now developed a new technique with a better resolution, known as Human Single-Cell Allele-Specific Gene Expression," explains Christelle Borel, UNIGE researcher. "The process can be used to simultaneously examine the expression of the two alleles, paternal and maternal, of all known genes in each individual cell. The method is fast and can be carried out on thousands of single cells with the utmost precision using next-generation sequencing technology." The heterogeneity of each tissue of the body is thus analysed in detail while searching for imprinted genes in disease-relevant tissue. The individual's genome is sequenced, as is the genome of both parents, in order to identify the parental origin of the alleles transcribed in the person's single cell.

Each cell is unique

Federico Santoni, first author of the study and researcher at UNIGE and HUG (Geneva University Hospitals) further explains, "We establish the profile of the allelic expression for thousands of genes in each single cell. We then process this data with a novel computational and statistical framework to identify the specific signature of each imprinted gene, enabling us to accurately record them." This new technique redefines the landscape of imprinted genes by examining all cell types, and can be applied to all tissues affected by diseases, such as cardiac and brain tissue. Moreover, the scientists have discovered novel imprinted genes and demonstrated that some were restricted to certain tissues or cell types.

This technique focuses on the specific characteristics of each individual by treating each cell as a single entity. This concept, called Single-cell Genomics, is part of an emerging field that is assuming an all-important role at UNIGE, which sees it as the future of medicine that will be personalised rather than generalised. Thanks to the technique pioneered by UNIGE researchers, it will be possible to identify new disease causing genes and to adapt a specific and targeted treatment for individual patients.

Explore further: Expanding the brain: Research identifies more than 40 new imprinted genes

More information: Federico A. Santoni et al. Detection of Imprinted Genes by Single-Cell Allele-Specific Gene Expression, The American Journal of Human Genetics (2017). DOI: 10.1016/j.ajhg.2017.01.028

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Stepping up the hunt for genetic diseases - Medical Xpress

February 16, 2017 by Sharon Horesh Bergquist, The Conversation What could genomic medicine do in the future? Credit: http://www.shutterstock.com

Personalized medicine, which involves tailoring health care to each person's unique genetic makeup, has the potential to transform how we diagnose, prevent and treat disease. After all, no two people are alike. Mapping a person's unique susceptibility to disease and targeting the right treatment has deservedly been welcomed as a new power to heal.

The human genome, a complete set of human DNA, was identified and mapped a decade ago. But genomic science remains in its infancy. According to Francis Collins, the director of the National Institutes of Health, "It is fair to say that the Human Genome Project has not yet directly affected the health care of most individuals."

It's not that there haven't been tremendous breakthroughs. It's just that the gap between science and its ability to benefit most patients remains wide. This is mainly because we don't yet fully understand the complex pathways involved in common chronic diseases.

I am part of a research team that has taken on the ambitious goal of narrowing this gap. New technologies are allowing us to probe DNA, RNA, proteins and gut bacteria in a way that will change our understanding of health and disease. Our hope is to discover novel biological markers that can be used to diagnose and treat common chronic conditions, including Alzheimer's disease, heart disease, diabetes and cancer.

But when it comes to preventing the leading causes of death which include chronic diseases, genomics and precision medicine may not do as much as we hope.

Many diseases aren't due only to genetics

Chronic diseases are only partially heritable. This means that the genes you inherit from your parents aren't entirely responsible for your risk of getting most chronic diseases.

The estimated heritability of heart disease is about 50 percent. It's 64 percent for Type 2 diabetes mellitus, and 58 percent for Alzheimer's disease. Our environment and lifestyle choice are also major factors; they can change or influence how the information coded in our genes is translated.

Chronic diseases are also "complex." Rather than being controlled by a few genes that are easy to find, they are weakly influenced by hundreds if not thousands of genes, the majority of which still elude scientists. Unlocking the infinite combinations in which these genes interact with each other and with the environment is a daunting task that will take decades, if ever, to achieve.

While unraveling the genomic complexity of chronic disease is important, it shouldn't detract from existing simple solutions. Many of our deadliest chronic diseases are preventable. For instance, among U.S. adults, more than 90 percent of Type 2 diabetes, 80 percent of coronary arterial disease, 70 percent of stroke and 70 percent of colon cancer are potentially avoidable.

Smoking, weight gain, lack of exercise, poor diet and alcohol consumption are all risk factors for these conditions. Based on their profound impact on gene expression, or how instructions within a gene are manifested, addressing these factors will likely remain fundamental in preventing these illnesses.

Will more knowledge be more power?

A major premise behind personalized medicine is that empowering patients and doctors with more knowledge will lead to better decision-making. With some major advances, this has indeed been the case. For instance, variants in genes that control an enzyme that metabolizes drugs can identify individuals who metabolize some drugs too rapidly (not giving them a chance to work), or too slowly (leading to toxicity). This can lead to changes in medication dosing.

When applied to prevention, however, identifying our susceptibility at an earlier stage has not aided in avoiding chronic diseases. Research challenges the assumption that we will use genetic markers to change our behavior. More knowledge may nudge intent, but that doesn't translate to motivating changes to our lifestyle.

A recent review found that even when people knew their personal genetic risk of disease, they were no more likely to quit smoking, change their diet or exercise. "Expectations that communicating DNA-based risk estimates changes behavior is not supported by existing evidence," the authors conclude.

Increased knowledge may even have the unintended consequence of shifting the focus to personal responsibility while detracting from our joint responsibility for improving public health. Reducing the prevalence of chronic diseases will require changing the political, social and economic environment within which we make choices as well as individual effort.

What about treating chronic diseases?

Perhaps the most awaited hope of the genomic era is that we will be able to develop targeted treatments based on detailed molecular profiling. The implication is that we will be able to subdivide disease into new classifications. Rather than viewing Type 2 diabetes as one disease, for example, we may discover many unique subtypes of diabetes.

This already is happening with some cancers. Patients with melanoma, leukemia or metastatic lung, breast or brain cancers can, in some cases, be offered a "molecular diagnosis" to tailor their treatment and improve their chance of survival.

We have been able to make progress in cancer therapy and drug safety and efficacy because specific gene mutations control a person's response to these treatments. But for complex, chronic diseases, relatively few personalized targeted treatments exist.

Customizing treatments based on our uniqueness will be a breakthrough, but it also poses a challenge: Without the ability to test targeted treatments on large populations, it will make it infinitely harder to discover and predict their response.

The very reason we group people with the same signs and symptoms into diagnoses is to help predict the average response to treatment. There may be a time when we have one-person trials that custom tailor treatment. However, the anticipation is that the timeline to getting to such trials will be long, the failure rate high and the cost exorbitant.

Research that takes genetic risk of diabetes into account has found greater benefit in targeting prevention efforts to all people with obesity rather than targeting efforts based on genetic risk.

We also have to consider decades of research on chronic diseases that suggest there are inherent limitations to preventing the global prevalence of these diseases with genomic solutions. For most of us, personalized medicine will likely complement rather than replace "one-size-fits-all" medicine.

Where does that leave us? Despite the inherent limitations to the ability of genomic medicine to transform health care, medicine in the future should unquestionably aspire to be "personal." Genomics and molecular biosciences will need to be used holistically in the context of a person's health, beliefs and attitudes to fulfill their power to greatly enhance medicine.

Explore further: Gene variants associated with body shape increase risk of heart disease, type 2 diabetes

This article was originally published on The Conversation. Read the original article.

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Personalized medicine may do more to treat rather than prevent chronic diseases - Medical Xpress

INGELHEIM, Germany--(BUSINESS WIRE)--

Boehringer Ingelheim today announced a collaboration with Weill Cornell Medicine to identify new treatment approaches for chronic obstructive pulmonary disease (COPD) in order to develop novel treatments that could possibly halt or even reverse the progression of the disease process. The new, three-year collaboration combines Weill Cornell Medicines Department of Genetic Medicines unique understanding of chronic airway diseases and experience in the investigation of novel therapeutic concepts for airway repair with Boehringer Ingelheims expertise in the discovery and development of new therapies for respiratory diseases. This collaboration is the second collaboration between Boehringer Ingelheim and Weill Cornell Medicine, following prior work in inflammatory bowel disease (IBD).

Chronic lower respiratory diseases, which include COPD, are the third leading cause of death in the United States, and approximately 15 million Americans have been told by a healthcare provider that they have COPD. It cannot be cured and current treatment approaches focus on bronchodilation, reducing symptoms and preventing exacerbations to decelerate the downward spiral of the disease. The goal is to help patients keep as active as possible and overall, improve their quality of life.

Our continuous search for molecular drivers of chronic obstructive airway diseases has revealed novel repair mechanisms that warrant further investigation of their potential as therapeutic approaches, said Dr. Ronald G. Crystal, Chairman of Genetic Medicine at Weill Cornell Medicine and lead investigator in the new collaboration. We will look to further expand our knowledge about progressive airway destruction in close collaboration with Boehringer Ingelheim and focus on promising therapeutic concepts with the potential to slow down or halt progressive airway damage in patients with COPD.

We are delighted to work with Dr. Crystal at Weill Cornell Medicine, who is one of the leading scientists in severe progressive airway diseases worldwide, said Dr. Clive R. Wood, Senior Corporate Vice President, Discovery Research at Boehringer Ingelheim. The scientists at Weill Cornell Medicine and Boehringer Ingelheim will work hand in hand to translate new discoveries into drug discovery and development programs at Boehringer Ingelheim. The new collaboration is an excellent example of our unique partnering approach and our focus on early innovation, underscoring our ambition to develop the next generation of medical treatments for patients with COPD.

Boehringer Ingelheim is combining a focus on cutting-edge science with a long-term view enabling the company to create a stable environment for the development of the next generation of medical breakthroughs. This new project adds another building block in this long-term strategy to improve the lives of patients with high unmet medical needs.

Weill Cornell's Office of BioPharma Alliances and Research Collaborations negotiated the three-year collaboration.The offices mission is to proactively generate, structure and market translational research alliances with industry in order to advance promising research projects that have commercial potential. For more information, contact Larry Schlossman at las2041@med.cornell.edu or at 212-746-6909.

For references and notes to editors, please visit:

http://www.boehringer-ingelheim.com/press-release/weill-cornell-collaboration-develop-next-generation-copd-treatments

View source version on businesswire.com: http://www.businesswire.com/news/home/20170215005565/en/

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Boehringer Ingelheim and Weill Cornell Medicine announce new ... - Yahoo Finance

Although common, male baldness can have negative psychological effects and some studies have even linked it to a handful of serious illnesses. New research identifies the genetic variants involved in the condition, which could eventually enable researchers to predict a person's chances of hair loss.

Male baldness - also referred to as androgenetic alopecia or male pattern baldness (MPB) - affects a significant number of people in the United States, as the condition accounts for over 95 percent of all hair loss in men.

According to the American Hair Loss Association, two thirds of U.S. adults will be affected by MPB to a certain degree by the age of 35, and around 85 percent of men will have experienced significant hair loss by the age of 50.

A lot of these men are seriously affected by the condition, which can have a negative effect on a person's self-image, as well as on their interpersonal relationships.

Additionally, some genetic studies have even associated MPB with negative clinical outcomes such as prostate cancer and cardiovascular disease.

A new study - led by Saskia Hagenaars and David Hill of the University of Edinburgh in the United Kingdom - explores the genetic basis for the condition. The findings were published in the journal PLOS Genetics.

Scientists analyzed the genomic and health data of more than 52,000 men enrolled in the UK Biobank - an international health resource offering health information on more than 500,000 individuals.

The team located more than 250 independent genetic regions linked to severe hair loss.

The researchers split the 52,000 participants into two groups: a so-called discovery sample of 40,000 people and a target sample of 12,000 individuals. Based on the genetic variants that separated those with no hair loss from those with severe hair loss, the team designed an algorithm aimed to predict who would develop MPB.

The algorithmic baldness predictor is based on a genetic score, and although accurate predictions are still a long way off, the results of this study might soon enable researchers to identify subgroups of the population that are particularly prone to hair loss.

In the present study, researchers found that 14 percent of the participants with a submedian genetic score had severe MPB, and 39 percent had no hair loss. By contrast, 58 percent of those scoring in the top 10 percent on the polygenic score had moderate to severe MPB.

Co-lead author Saskia Hagenaars - a Ph.D. student at the University of Edinburgh's Centre for Cognitive Aging and Cognitive Epidemiology - comments on the findings:

"We identified hundreds of new genetic signals," Hagenaars says. "It was interesting to find that many of the genetics signals for male pattern baldness came from the X chromosome, which men inherit from their mothers."

The study's other lead author, Dr. David Hill, notes that the study did not collect data on the age of baldness onset, but only on hair loss pattern. However, he adds that, "we would expect to see an even stronger genetic signal if we were able to identify those with early-onset hair loss."

To the authors' knowledge, this is the largest genetic study of MPB to date.

The study's principal investigator, Dr. Riccardo Marioni, from the University of Edinburgh's Centre for Genomic and Experimental Medicine, explains the significance of the findings:

"We are still a long way from making an accurate prediction for an individual's hair loss pattern. However, these results take us one step closer. The findings pave the way for an improved understanding of the genetic causes of hair loss."

Learn how a drug promises robust new hair growth.

More here:

Genetic basis for male baldness identified in large-scale study - Medical News Today

Sharon Horesh Bergquist, Associated Press Published: February 15, 2017 9:20 PM CDT

Sharon Horesh Bergquist, Emory University

(THE CONVERSATION) Personalized medicine, which involves tailoring health care to each persons unique genetic makeup, has the potential to transform how we diagnose, prevent and treat disease. After all, no two people are alike. Mapping a persons unique susceptibility to disease and targeting the right treatment has deservedly been welcomed as a new power to heal.

The human genome, a complete set of human DNA, was identified and mapped a decade ago. But genomic science remains in its infancy. According to Francis Collins, the director of the National Institutes of Health, It is fair to say that the Human Genome Project has not yet directly affected the health care of most individuals.

Its not that there havent been tremendous breakthroughs. Its just that the gap between science and its ability to benefit most patients remains wide. This is mainly because we dont yet fully understand the complex pathways involved in common chronic diseases.

I am part of a research team that has taken on the ambitious goal of narrowing this gap. New technologies are allowing us to probe DNA, RNA, proteins and gut bacteria in a way that will change our understanding of health and disease. Our hope is to discover novel biological markers that can be used to diagnose and treat common chronic conditions, including Alzheimers disease, heart disease, diabetes and cancer.

But when it comes to preventing the leading causes of death which include chronic diseases, genomics and precision medicine may not do as much as we hope.

Chronic diseases are only partially heritable. This means that the genes you inherit from your parents arent entirely responsible for your risk of getting most chronic diseases.

The estimated heritability of heart disease is about 50 percent. Its 64 percent for Type 2 diabetes mellitus, and 58 percent for Alzheimers disease. Our environment and lifestyle choice are also major factors; they can change or influence how the information coded in our genes is translated.

Chronic diseases are also complex. Rather than being controlled by a few genes that are easy to find, they are weakly influenced by hundreds if not thousands of genes, the majority of which still elude scientists. Unlocking the infinite combinations in which these genes interact with each other and with the environment is a daunting task that will take decades, if ever, to achieve.

While unraveling the genomic complexity of chronic disease is important, it shouldnt detract from existing simple solutions. Many of our deadliest chronic diseases are preventable. For instance, among U.S. adults, more than 90 percent of Type 2 diabetes, 80 percent of coronary arterial disease, 70 percent of stroke and 70 percent of colon cancer are potentially avoidable.

Smoking, weight gain, lack of exercise, poor diet and alcohol consumption are all risk factors for these conditions. Based on their profound impact on gene expression, or how instructions within a gene are manifested, addressing these factors will likely remain fundamental in preventing these illnesses.

A major premise behind personalized medicine is that empowering patients and doctors with more knowledge will lead to better decision-making. With some major advances, this has indeed been the case. For instance, variants in genes that control an enzyme that metabolizes drugs can identify individuals who metabolize some drugs too rapidly (not giving them a chance to work), or too slowly (leading to toxicity). This can lead to changes in medication dosing.

When applied to prevention, however, identifying our susceptibility at an earlier stage has not aided in avoiding chronic diseases. Research challenges the assumption that we will use genetic markers to change our behavior. More knowledge may nudge intent, but that doesnt translate to motivating changes to our lifestyle.

A recent review found that even when people knew their personal genetic risk of disease, they were no more likely to quit smoking, change their diet or exercise. Expectations that communicating DNA-based risk estimates changes behavior is not supported by existing evidence, the authors conclude.

Increased knowledge may even have the unintended consequence of shifting the focus to personal responsibility while detracting from our joint responsibility for improving public health. Reducing the prevalence of chronic diseases will require changing the political, social and economic environment within which we make choices as well as individual effort.

Perhaps the most awaited hope of the genomic era is that we will be able to develop targeted treatments based on detailed molecular profiling. The implication is that we will be able to subdivide disease into new classifications. Rather than viewing Type 2 diabetes as one disease, for example, we may discover many unique subtypes of diabetes.

This already is happening with some cancers. Patients with melanoma, leukemia or metastatic lung, breast or brain cancers can, in some cases, be offered a molecular diagnosis to tailor their treatment and improve their chance of survival.

We have been able to make progress in cancer therapy and drug safety and efficacy because specific gene mutations control a persons response to these treatments. But for complex, chronic diseases, relatively few personalized targeted treatments exist.

Customizing treatments based on our uniqueness will be a breakthrough, but it also poses a challenge: Without the ability to test targeted treatments on large populations, it will make it infinitely harder to discover and predict their response.

The very reason we group people with the same signs and symptoms into diagnoses is to help predict the average response to treatment. There may be a time when we have one-person trials that custom tailor treatment. However, the anticipation is that the timeline to getting to such trials will be long, the failure rate high and the cost exorbitant.

Research that takes genetic risk of diabetes into account has found greater benefit in targeting prevention efforts to all people with obesity rather than targeting efforts based on genetic risk.

We also have to consider decades of research on chronic diseases that suggest there are inherent limitations to preventing the global prevalence of these diseases with genomic solutions. For most of us, personalized medicine will likely complement rather than replace one-size-fits-all medicine.

Where does that leave us? Despite the inherent limitations to the ability of genomic medicine to transform health care, medicine in the future should unquestionably aspire to be personal. Genomics and molecular biosciences will need to be used holistically in the context of a persons health, beliefs and attitudes to fulfill their power to greatly enhance medicine.

This article was originally published on The Conversation. Read the original article here: http://theconversation.com/personalized-medicine-may-do-more-to-treat-rather-than-prevent-chronic-diseases-71474.

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Personalized medicine may do more to treat rather than prevent chronic diseases - NewsOK.com

Posted: Feb. 15, 2017 8:00 am Updated: Feb. 15, 2017 3:09 pm

NEW YORK (AP) The Associated Press is teaming up with the Howard Hughes Medical Institute's Department of Science Education to expand its coverage of science, medicine and health journalism.

The initial collaboration includes two pilot projects. With the first project, AP will create and distribute a series of stories, profiles, videos and graphics focusing on genetic medicine. The second project will look at a variety of science topics in the news that will help readers stay current on the latest science research and make informed decisions on topics ranging from the environment, to public health.

"This collaboration brings wider attention and new storytelling tools to evidence-based, factual science," AP Executive Editor Sally Buzbee said.

HHMI, based in Chevy Chase, Maryland, supports the advancement of biomedical research and science education. The organization's origin dates back to the late 1940s when a small group of physicians and scientists advised Hughes. The medical institute was created in 1953.

The primary purpose of the organization is to promote human knowledge in the field of the basic sciences and its effective application for the benefit of mankind, according to its charter. In fiscal 2016, it provided $663 million in U.S. biomedical research and $86 million in grants and other support for science education.

HHMI's Department of Science Education, the largest private, nonprofit supporter of science education in the country, will provide funding for the AP projects. The funding will allow AP to increase the amount of science-related stories it provides to news organizations and add more journalists to support its current science reporting team. HHMI will also offer expert background information and educational material.

While the AP will receive funding and utilize HHMI's expertise when crafting its content, it maintains full editorial control of published material.

"We're proud to stand shoulder to shoulder with the world's most respected news organization to ensure that the best evidence around important scientific topics is presented clearly and distributed widely," said Sean B. Carroll, vice president of HHMI's Department of Science Education.

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AP, HHMI collaborate on expanded science, health coverage - New Jersey Herald

Editing human genes that would be passed on for generations could make sense if the diseases are serious and the right safeguards are in places, a scientific panel says.

Scientists could be allowed to make modifications in human DNA that can be passed down through subsequent generations, the National Academy of Sciences and the National Academy of Medicine say.

Such a groundbreaking step should only be considered after more research and then only be conducted under tight restrictions, the academies write in a highly anticipated report released Tuesday. Such work should be reserved to prevent serious diseases and disabilities, it says.

The academies determined that new gene-editing techniques had made it reasonable to pursue such controversial experiments down the road, though not quite yet.

"It is not ready now, but it might be safe enough to try in the future," R. Alta Charo, a bioethicist at the University of Wisconsin-Madison who co-chaired the committee, said. "And if certain conditions are met, it might be permissible to try it."

That conclusion counters a long-standing taboo on making changes in genes in human sperm, eggs or embryos because such alterations would be inherited by future generations. That taboo has been in place partly because of fears that mistakes could inadvertently create new diseases, which could then become a permanent part of the human gene pool.

Another concern is that this kind of genetic engineering could be used to make genetic modifications for nonmedical reasons.

For example, scientists could theoretically try to create designer babies, in which parents attempt to select the traits of their children to make them smarter, taller, better athletes or to have other supposedly superior attributes.

Nothing like that is currently possible. But even the prospect raises fears about scientists essentially changing the course of evolution and creating people who are considered genetically superior, conjuring up the kind of dystopian future described in movies and books like Aldous Huxley's Brave New World.

"These kinds of scenarios used to be science fiction; they used to be seen as far-off hypotheticals," says Marcy Darnovsky, who runs the Center for Genetics and Society, a genetic watchdog group. "But actually, right now, I think they're urgent social justice questions."

She says, "we're going to be creating a world in which the already privileged and affluent can use these high-tech procedures to make children who either have some biological advantages" or are perceived to have biological advantages. "And the scenario that plays out is not a pretty one."

But Charo says the report clearly states that any attempt to create babies from sperm, eggs or embryos that have had their DNA edited could only be tried someday under very tightly controlled conditions and only to prevent devastating medical disorders.

"We said, 'Use it for serious diseases and serious conditions only period,'" Charo says. "We simply said, 'No enhancement.' "

But Darnovsky is skeptical that line will hold. "I don't think there's any way to keep that genie in the bottle," he says.

The report, however, was praised by many scientists.

"It's important to be extraordinarily cautious on technologies that could leave a permanent mark on the human population for all generations to come," says Eric Lander, who runs the Broad Institute at the Massachusetts Institute of Technology and Harvard University. "But it's important to try to help people. I think they've been very thoughtful about how you should balance those things."

The report acknowledges that it may be difficult in the future to draw a line between using gene-editing to prevent or treat disease and using it for enhancement. Gene-editing designed to prevent or treat the muscle disease muscular dystrophy, for example, could theoretically be used to try to make healthy people stronger.

Prominent Harvard geneticist George Church agrees. "The report is very clearly broad," he says. "It could include a lot of things people consider enhancement. I think it will be case by case and there will be some people will be consider enhancement that some people will consider preventive medicine."

For example, if scientists figure out how to makes changes that boost thinking abilities to stave off dementia in Alzheimer's patients by making them slightly above average or considerably above average, he says, "that might be considered enhancement or it might be considered preventive medicine."

Scientists have been able to edit the DNA in the cells of humans and other creatures for decades. But the academies commissioned the report after scientists developed powerful new gene-editing techniques in recent years, such as CRISPR-Cas9, that make it much easier and faster.

That raised the possibility that gene editing might be used to treat many diseases and possibly even to prevent many devastating disorders from occurring in the first place by editing out genetic mutations in sperm, eggs and embryos. That could potentially prevent a wide range of diseases, including breast cancer, Tay-Sachs, sickle cell anemia, cystic fibrosis and Huntington's disease.

As a result, the academies assembled a 21-member committee of scientists, bioethicists, lawyers, patient advocates, biotech entrepreneurs and others to conduct a far-reaching investigation that involved more than year of study.

The resulting report stresses that because the technology is so new, it would be unsafe for anyone to even begin studies to try to create babies from sperm, eggs or embryos that have had their DNA edited before conducting much more research.

The committee also says no clinical trials of gene editing should be allow unless:

"It would be essential for this research to be approached with caution, and for it to proceed with broad public input," the 261-page report states.

The report notes that the Food and Drug Administration is barred from reviewing "research in which a human embryo is intentionally created or modified to include a heritable genetic modification." Federal funding of such research is also prohibited.

Many other countries have signed an international convention prohibiting this kind of gene editing.

But the report aims to provide guidance for those countries where it's not prohibited or in those where the prohibitions would be lifted. The FDA ban, for example, could expire or be reversed.

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Scientific Panel Says Editing Heritable Human Genes Could Be OK In The Future - NPR

Newswise Downers Grove, Ill. (Feb. 14, 2017) A pioneer on the frontier of genetic medicine and his team at one of the nations top-five medical research schools have joined forces with FAST (Foundation for Angelman Syndrome Therapeutics) to develop a treatment for the rare disorder Angelman syndrome.

Researcher James M. Wilson, M.D., Ph.D., has been working for three decades to develop effective strategies to treat and cure genetic diseases. Wilson directs the Orphan Disease Center (ODC) in the Perelman School of Medicine at the University of Pennsylvania, which focuses on making rare disease research a priority.

The partnership with FAST is a natural.

Angelman syndrome is a neuro-genetic disorder affecting one in every 15,000 individuals, totaling about 490,000 people worldwide. It is often misdiagnosed as autism or cerebral palsy. AS is generally diagnosed in children within their first two years of life and is characterized by debilitating seizures, balance and motor impairments, and a lack of speech. But Angelman syndrome is not a degenerative disease. Rather, it is caused by a lack of function of a single gene, and scientists like Wilson believe that symptoms of the disorder could be reversed using gene therapy.

FAST is a nonprofit organization founded by Paula Evans, an Illinois mother whose daughter was diagnosed with Angelman syndrome. FAST raises money to fuel cutting-edge research and takes an active role in drug development to treat, and ultimately cure, the disorder. Through Evans leadership, FAST has built relationships with researchers at multiple universities. Wilson and Penns Orphan Disease Center is the latest research laboratory to join the FAST team.

FAST will provide funding to Wilson and his team to develop an effective gene therapy strategy for the treatment of Angelman syndrome.

By combining the Orphan Disease Centers experience in novel therapeutics with the tremendous progress made by FAST and its families, caregivers and scientists, Wilson said, we have set the stage for a very aggressive and exciting research and development plan.

FASTs partnership with Wilson and his team is an important milestone for the Angelman community. Wilson has emerged as a leader in the field of gene therapy and continues to be at the forefront of genetic innovation. Two years ago, Wilson was recognized as one of 12 leading pioneers in cell and gene research with the Pioneer Award given by Human Gene Therapy, a peer-reviewed journal of the medical research community. George Dickson of the University of London, Surrey, recently heralded Wilsons work, saying: His unparalleled contributions to the adenoviral and AAV vector fields over more than 25 years have been profound and seminal.

Wilson has focused his lab on the development of novel virus-like particles called vectors that can carry replacement genes into the body, one of which has been used to treat a rare form of pancreatitis and became the first gene therapy product approved in the Western hemisphere. The ODC is currently developing novel gene therapy approaches for more than 20 rare diseases.

Wilsons decision to take on Angelman syndrome as his next project is significant news for the gene therapy community and families affected by Angelman syndrome.

All of the board members of FAST are parents who are working toward breakthrough treatments for our children, said FAST Chief Scientific Officer Dr. Allyson Berent. To have an accomplished visionary researcher developing a potential gene therapy treatment for AS indicates we are closer than ever to our ultimate goal. Dr. Wilson and the team at Penn have such a successful track record in the field of gene therapy, and we are beyond enthusiastic that, for our children, the time is now.

Wilson agrees that there are reasons to be hopeful. We are entering a remarkable era of gene therapy research that will accelerate its development, he said. After 30 years of science, we have the technology and know-how to safely and efficiently transfer genes into human cells. Our goal is to develop a gene therapy for AS to replace the gene in children who are lacking a functional copy.

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About FAST FAST (Foundation for Angelman Syndrome Therapeutics) is a Section 501(c)(3) nonprofit research organization singularly focused on funding research that holds the greatest promise of treating Angelman syndrome. FAST is the largest, non-governmental funder of Angelman-specific research. Paula Evans, the mother of a young girl with Angelman syndrome, founded FAST in 2008. The foundation is based in Downers Grove, Ill.

The cost of developing gene therapy is significant. FAST has launched an aggressive fundraising campaign to support this development program. Please visit the Cure Angelman Now initiative at CureAngelman.org to see how you can play a role in curing Angelman syndrome.

Angelman Syndrome Angelman syndrome (AS) is a rare neuro-genetic disorder that affects roughly one in 15,000 individuals about 490,000 people worldwide. Individuals with Angelman syndrome generally have balance issues, motor impairment and debilitating seizures. Some people with AS never walk. Most do not speak. Anxiety and disturbed sleep can be serious challenges among those with AS. While individuals with Angelman syndrome have a normal lifespan, they require continuous care and are unable to live independently. Typical characteristics of AS are not usually evident at birth. People with the disorder have feeding difficulties as infants and noticeable delayed development around 6-12 months of age. They need intensive therapies to help develop functional skills. In most cases, Angelman syndrome isn't genetically inherited. AS affects every race and both genders. It is often misdiagnosed as autism or cerebral palsy. For more information about Angelman syndrome, please visit CureAngelman.org.

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Penn gene therapy pioneer teams up with FAST in race ... - Newswise - Newswise (press release)