RURAL REPORTER

Last updated12:12, September 4 2017

LIC

A good looker, and the best performing bull at LIC is Sierra, a kiwicross bull. The 7-year-old bull might have 100,000 daughters in the next few years.

Father's Day was on Sunday, and many families got together,but there wasone super dad who foundit a struggle meeting all his offspring.

Sierra, one of LIC's top bulls, has fathered 1700 daughters (milking dairy cows).

"We expect that he will have 12,000 more daughters entering the national herd this year, and predict a further 100,000 over the next few years," said Simon Worth, LIC's livestock selection manager.

Farmers needed top quality genetics to get their cows producing top quality heifers in New Zealand and internationally.He said LIC owned24 of the top 30 artificial breeding (AB) bulls in the country, including Sierra - its top kiwicross bull.

READ MORE:

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*Genetics company LIC sells off its deer improvement business

"Bulls like Sierra are shaping the future of dairying in New Zealand. Our bulls provide three out of every four cows in the country, contributing $300 million towards the economy each year," said Dave Hale, LIC's national artificial breeding manager.

During the peak dairy cow mating season in spring LIC collectedsemen from its 73 elite bulls seven days a week, at itsNewstead farm near Hamilton.

Up to five million semen straws will be processed between now and Christmas, with the co-op's exclusive long last liquid semen diluent (LIC proprietary technology) enabling one bull ejaculate to average 7000 fresh semen straws for insemination.

Straws are sentfresh to a team of 775 AB technicians all over the country, for insemination into cows as early as that same afternoon. Top AB technicians inseminate up to 10,000 cows a year, or200-300 a day.

On the peak day in spring 120,000 semen straws are dispatched nationally, internationally the co-op exports one million frozen straws worldwide year-round.

"While only seven years old, Sierra is definitely one of our super dad bulls. Without them Kiwis probably wouldn't have their morning lattes," said Hale.

-Stuff

Read more:
Artificial breeding bulls in demand as farmers improve genetics - Stuff.co.nz

September 4, 2017

People with a specific variation in the CLOCK gene have more migraines under financial stress. This work, the first time that the genetics of circadian rhythms has been shown to have an effect on migraine, is presented at the ECNP conference in Paris.

Migraine is a serious and debilitating neurological disease affecting 1 billion people worldwide. Migraine has been estimated to cause a financial cost of around 27 billion every year in the European Union, and $17 billion every year in the USA. In the UK, 1 in 4 women and 1 in 12 men are migraine sufferers.

The background of migraine is highly complex involving a large number of genes and their interaction with environmental effects, and acting via multiple pathways in the central nervous system. Variations of circadian genes (which affect how the body controls and responds to environmental changes -- such as changes in light) have previously been shown to affect mood disorders, so it was thought it would be interesting to see if they were associated with migraine.

The group of researchers from Hungary and the UK checked 999 patients from Budapest and 1350 from Manchester, for two variants (single nucleotide polymorphisms, SNPs) of the CLOCK gene, and how these are associated with migraine. The CLOCK gene has an important role in regulating many rhythmic patterns of the body, including body temperature or level of cortisol, the primary stress hormone. They found that there was no significant direct connection between the gene and migraine, but when they factored in stress (financial stress, measured by a financial questionnaire), they showed that the investigated gene variants increased the odds of having migraine type headaches in those subjects who suffered from financial hardship by around 20%. (odds ratio -- see abstract for details).

The researchers looked at functional single nucleotide polymorphisms within the CLOCK gene that are able to influence how much protein is transcribed from the gene. Because this protein controls the body clock machinery these variants may impair processes that can prevent migraine in the face of stress.

Researcher Daniel Baksa (Semmelweis University, Budapest) said:

"This work does not show what causes migraine -- there is no single cause -- but it does show that both stress and genetics have an effect. In the work presented here, we were able to show that stress -- represented by financial hardship -- led to an increase in migraine in those who have a particular gene variant. What we need to do now is to see if other circadian gene variants in association with different stress factors cause the same effect.

The strength of our study is that we saw the same effect in two independent study groups, in Budapest and Manchester, so we think it is a real effect. The investigated gene variants are present in around 1/3 of the population, so they are common variants with small effect size. Our results shed light on one specific mechanism that may contribute to migraine. What it does mean is that for many people, the stress caused by financial worries can physically affect you. Migraine involves a huge health and financial burden each year, so any steps we can take to help patients understand their condition will be really welcome."

Commenting, Professor Andreas Reif (University Hospital, Frankfurt) said:

"This is a really interesting study on the interaction of genetics with stress in migraine. The studied gene is involved in the circadian system, which has previously been shown to be implicated in mental disorders such as bipolar disorder, which intriguingly is comorbid with migraine. Thus, this study might provide a clue how these diseases might be linked on the genetic level which is interesting as such. But even beyond this, the study demonstrates how an environmental risk factor exerts its effect only in the presence of a given genetic risk factor. This has not been done to a great extent in migraine, making this study an exciting new lead."

Read more here:
Genetics of circadian rhythms found to have effect on migraine - News-Medical.net

Its a beautiful, sunny, fall-esque day here on Long Island, and I have something personal to share with you. After a nuclear stress test taken earlier in the week, my dads cardiologist recommended he check himself into the hospital on Thursday to have an angiogram. My dads had a couple of heart attacks in the past, and while his doctor didnt think it was anything too too serious, he wanted to make sure.

The angiogram showed a 99% blockage in one of his arteries. Because of this, three stents were put in to open it up. An additional stent is being put in as we speak, and if all goes well, he should be out by tomorrow. My dad is in good spirits and looks pretty good, so Im very optimistic that this will be the last we hear of this for a while.

That being said, something I heard his doctor tell him disturbed me quite a bit. Somehow, the topic of genetics came up in the conversation. My father was essentially told that this was all genetic, there was nothing he could do to improve his condition, and that once he gets out and he rests for about a week, he can resume all regular life activities.

The cardiac wing of the hospital was also feeding him garbage for his heart, like bread (derived from grains, which are inflammatory) and margarine (a trans fat, which is bad for the heart) but we wont even get into that today

While I know genetics can play a role in the acquisition of several diseases, theres a new study called EPIGENETICS. The premise behind this field of study is that based upon your chosen environment and your personal lifestyle habits, you can manipulate your genetic code, and either keep a negative genetic trait like heart disease dormant, or you can completely REVERSE that genes expression, and thus, never develop a hereditary disease in the first place!

Ive heard plenty of would-be clients over the years use genetics as an excuse for their being overweight. My parents, grandparents, aunts and uncles were all fat, so this is just something I have to deal with!

Often, when somebody is overweight, its due to poor diet. Plain and simple. Theres a small percentage of the population that has hormonal imbalances, and thus, theres a bit more to it than that. That being said, most hormone issues can be regulated (and even corrected!) by certain dietary strategies that will get those levels back to normal, and then enable them to both function and lose weight normally.

When the folks who blame genetics review their nutrition with me, Ill tell you one thing: It aint just geneticsIf its even genetics, at all! Their diets tend to be comprised of excessive amounts of sugar, grains and processed foods, which, when ingested in large quantities as they were in these instances, are ALL linked to an increased risk of obesity, Type-2 Diabetes, heart disease, various forms of cancer, and even neurological diseases like Parkinsons and Alzheimers!!

Whether youre dealing with weight issues, whether youre diabetic, or whether youre even suffering from a heart condition like my dad is, youre rarely too far gone!!! There are healthy dietary changes you can make that will not only help you in regulating these conditions, but also help in the REVERSAL of many of these conditions.

Moral of the Story: I was highly DISTURBED to hear this explanation given to my dad. Its never too late to change and improve the quality of your life. The question is: Whatre you going to do to change your circumstances?

pete@weightlossbypete.com

P.S. If you feel you need more help on the nutritional side, then youre definitely going to want to invest in my Food Guide and Healthy Recipe Book!

The Food Guide lays out the three phases of nutrition I use with my Permanent Weight Loss clients. Phase 1 gets you in the habit of making healthier choices, while Phase 2 really cleans up the frequency with which you eat healthier. Phase 3 is a strict macronutrient breakdown that will help expedite the process of weight loss, all while improving your health and making your body a well-oiled machine!

My Healthy Recipe Book includes 72 recipes spanning breakfast,lunch, dinner, snacks, appetizers and desserts. Im constantly adding to it, but these recipes are easy to make, simple and enable you to have your cake and eat it, too!

Normally, I sell each of these books for $10 a piece, but because Im feeling generous today, you can get BOTH for just $13.99!:-)

Excerpt from:
Weight Loss Tip: It Ain't Just About Genetics! - HuffPost

Twenty-five per cent of Australian adults are estimated to be clinically obese. The common view is that obesity is a self-inflicted condition. But one Melbourne clinic is challenging that perception.

Austin Health Obesity Physician, Professor Joe Proietto says he treats obesity as a chronic genetic disease.

"The view that obesity is genetic is controversial, however the evidence is very strong that there is a genetic predisposition to obesity," said Professor Proietto.

In a new SBS documentary Obesity Myth, doctors are trying to treat patients through a combination of diet, medication and surgery, tailored specifically for their genetic make-up.

Professor Proietto believes the environment has far less bearing on weight than genetics.

But Sydney University Obesity Research Director, Dr Nick Fuller says blaming genetics is only going to make the obesity crisis worse.

"We are finding more and more genes that contribute to obesity but genetics are not the reason for the increase in prevalence of obesity," said Dr Fuller.

Dr Fuller believes dieting is not the most effective solution.He believes weight loss should happen slowly, to trick the body into believing it is at a new set weight point.

"They need to lose a small amount of weight before the usual response to weight loss kicks in and maintain that weight so they can reprogram their set weight before going on to lose weight," said Dr Fuller.

Helene Jagdon has been trying to lose weight for 30 years. She has tried every fad diet and training regime in the book.

Only in the last few years under Dr Fuller's strategy has she been able to lose 14 kilograms and keep it off.

"He didn't make us feel like we were on a diet, he was just guiding us to what foods we can eat and not really saying what foods we can't eat.

"He was just saying if you feel like having a laksa, have a laksa, but maybe limit it to one takeaway treat in a week," said Ms Jagdon.

Now sitting at a comfortable 68 kilograms, Helene has maintained her passion for cooking and is inspiring people half her age to lose weight without dramatically changing their lives.

Preview: The Obesity Myth

The three-part documentary series The Obesity Myth starts September 4 on SBS at 7.30pm.

More here:
Could genetics be the reason behind obesity? - SBS

Rush Neurologist Gian Pal, MD, MS, the primary investigator for the National Institute of Health-funded clinical study Parkinson disease and DBS: cognitive effects in GBA mutation carriers. Credit: Rush Photo Group

In the first ever clinical investigation involving genetic screening for Parkinson's disease, researchers are testing whether the presence of a specific genetic mutation identifies which patients are the best candidates for deep brain stimulation surgery, and whether neurologists should perform that procedure differently based on that genetic information.

"We are at a very promising time in Parkinson's disease (PD) research. Finding the connections between the vast amounts of genetic data and cognitive data we are gathering will allow us to tailor future therapies based on genetic biomarkers," said Rush neurologist Gian Pal, MD, MS, the primary investigator for the National Institute of Health-funded clinical study "Parkinson disease and DBS: cognitive effects in GBA mutation carriers"

Deep brain stimulation (DBS) is a surgical procedure in which a battery-operated medical device implanted in the brain delivers electrical stimulation to specific areas in the brain that control movement, thus altering the abnormal signals that cause many PD motor symptoms.

DBS is typically used for individuals whose symptoms cannot be adequately controlled with medication and has proven to dramatically improve motor function and potentially reduce medication burden for many PD patients.

Research suggests that patients who carry a mutation in the glucocerebrosidase (GBA) gene may respond differently to DBS than those who do not carry the mutation. These GBA mutation carriers compose 10-17 percent of subjects undergoing DBS, and typically have higher deposits of alpha-synuclein protein in the brain. Abnormal accumulation of alpha-synuclein is thought to be a key reason for the development and progress ion of PD. These higher levels of alpha-synuclein in patients with the GBA mutation carriers may translate to even more problems with thinking, movement, behavior, and mood than expected in typical PD. Dr. Pal and colleagues are hoping to understand how DBS affects motor function and cognition in these GBA mutation carriers over time.

"If we can determine how GBA mutation carriers respond to DBS, we can better counsel patients on expectations from the surgery, and potentially target a different region of the brain to maximize the benefit and minimize side effects from the surgery. This would be the first time that genetics would inform a clinical decision in the field of PD"

"Deep brain stimulation is a tremendous option for many Parkinson's disease patients, but not all," said Pal, who is developing a programmatic line of research involving genetics and surgical treatments for PD at the Rush Parkinson's Disease and Movement Disorders Program.

The Rush Parkinson's Disease and Movement Disorders Program is one of the largest and oldest such centers in the country, treating more than 2,000 patients annually. Rush has been a longstanding Parkinson's Disease Foundation Center of Excellence, based on decades of clinical and research excellence, and is now also recognized as a National Parkinson Foundation Center of Excellence as well.

Explore further: Drug discovery: Alzheimer's and Parkinson's spurred by same enzyme

Read more:
Rush testing if genetic clues identify best candidates for Parkinson's surgery - Medical Xpress

Brian J. O'Roak, Ph.D., assistant professor of molecular and medical genetics, OHSU, January 4, 2017. Credit: OHSU/John Valls

Autism spectrum disorder affects approximately one out of every 68 children in the United States. Despite expansive study, the origin and risk factors of the complex condition are not fully understood.

To better understand the root causes, an international team led by researchers at OHSU in Portland, Oregon has applied a new systematic analysis to a cohort of 2,300 families who have a single child affected with autism. The study focused on identifying and characterizing low-lying genetic mutations that may have been missed in previous research, given these mutations are only present in a fraction of the bulk DNA of an individual.

Known as postzygotic mosaic mutations, or PMMs, these genetic changes occur after the conception of the human zygote during the development cycle of a fetus. An individual will contain a mosaicor assortmentof mutated and non-mutated cells with the level of mosaicism depending on the time and location of the mutation's occurrence. This emerging class of genetic risk factors has recently been implicated in various neurologic conditions, however, their role in more complex disorders, such as autism, has been unclear.

Autism risk due to unexpected mosaic mutations

By comparing genetic sequencing data of these familiespart of the Simons Simplex Collection, a permanent repository of precisely characterized genetic samplesthe research team determined that approximately 11 percent of previously reported new mutations affecting a single DNA base, which were thought to have be present at the time of human conception, actually show evidence of the mutation occurring during the development process.

"This initial finding told us that, generally, these mosaic mutations are much more common than previously believed. We thought this might be the tip of a genetic iceberg waiting to be explored," said the study's principal investigator Brian O'Roak, Ph.D., an assistant professor of molecular and medical genetics in the OHSU School of Medicine.

To investigate this possibility, a custom approachleveraging next generation sequencing and molecular barcodes - was developed to both identify these low-level mutations, and also validate that they are, in fact, real and not technological artifacts. With this more sensitive method, the rate of potentially PMMs increased to 22 percent of the new mutations present in children.

The researchers then compared the rates of PMMs that result in different predicted effects on the genome in affected children and their unaffected siblings. This lead to an unexpected finding that so-called "silent" mosaic mutations were enriched in the affected children, contributing risk to approximately 2 percent of the individuals with autism in this cohort. These types of mutations are generally believed to be neutral, as they don't alter the genetic coding of proteins. However, the team found evidence that these mutations might actually be altering how genetic messages are stitched together.

The study also found preliminary evidence that mosaic mutations that alter the protein code of genes essential for development, or genes that resist mutations, are also enriched in individuals with autism. This contributes risk to an additional 1 to 2 percent of individuals with autism. Many of the PMMs occurred in some of the most highly validated autism risk genes identified to date, further suggesting that these mutations are contributing to autism genetic risk. Due to this, the research team believes that overall, mosaic mutations may contribute to autism risk in 3 to 4 percent of this cohort.

Understanding the timeline and location of mosaic mutations

Determining exactly when and where these mutations are occurring during development is challenging. The PMMs identified were present in 10 to 75 percent of the cells examined from the children's blood, suggesting that they likely occurred early in development. However, the exact timeline was not known.

By leveraging the unique family design of the Simons Simplex Collection cohort, O'Roak's team analyzed the parents' genomes and discovered that 6.8 percent of the supposedly "new" mutations present in children at conception could actually be traced back to a PMM that occurred early in the development of their parent. These mutations were generally present in 20 to 75 percent of the parents' blood cells, providing indirect evidence that many of the PMMs occurring in children did in fact happen very early during development and that they likely contribute mosaicism across the body, including in the brain.

"In addition to a need for broader research focused on the role that mosaicism plays in autism and related disorders, our data argue that physicians should be requiring more sensitive testing of both children and parents, when a new disorder-related genetic mutation is identified," O'Roak said. "These mutation can go from being in a few percent of the cells of a parent to 100 percent of the cells of a child. If present, at even low levels in the parents, the risk of additional children receiving this mutation is dramatically increased."

"Exonic mosaic mutations contribute risk for Autism Spectrum Disorder" published today in The American Journal of Human Genetics.

Explore further: Late-breaking mutations may play an important role in autism

More information: Deidre R. Krupp et al. Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder, The American Journal of Human Genetics (2017). DOI: 10.1016/j.ajhg.2017.07.016

Visit link:
Study identifies new genetic risk factor for developing autism spectrum disorder - Medical Xpress

Nanoparticles (orange) deliver temporary gene therapy to immune cells (blue) to give them disease-fighting tools. (Fred Hutch Illustration / Kimberly Carney)

CAR T immunotherapies are all the rage in the medical community, reprogramming a patients immune system to fight cancer. For some patients, theyve produced near-miraculous recoveries, and they could be a huge breakthrough in cancer treatment.

The business community is taking note as well: Kite Pharma, a biotech company developing these therapies, announced a deal to be acquired for $11.9 billion on Monday, sending stock prices of Seattle immunotherapy developer Juno Therapeuticsskyrocketing.

But there are still giant pitfalls to using the therapies on a large scale because they are incredibly complex and expensive to produce. Researchers from Seattles Fred Hutchinson Cancer Research Center are taking the problem head-on with new hit-and-run gene editing technology.

In a study published Wednesday in the journal Nature Communications, researchers led by Dr.Matthias Stephan reported they have developed a nanoparticle delivery system that can temporarily alter cells so they are able to fight cancer and other diseases.

The best part? The treatment is a powder that just needs to be mixed with water to activate and even better, it could be an essential breakthrough in making cutting-edge medical technology affordable for patients.

Stephan told GeekWire in a previous piece on the technology that his goal is to make immunotherapy so easy to access that it replaces chemotherapy as the front-line treatment for cancer.

What I envision is like the Walgreens flu shot scenario, or you go to your doctor and you get hepatitis B shot, he said at the time. You go there every Friday, and thats it.

We realized in order to outcompete chemotherapy, we have to design something that is at least as affordable and can be manufactured at large scale by one biotech company and shipped out to local infusion centers, Stephan said. At the moment, CAR T cell therapies must be made individually for each patient in specialized labs.

Heres how the new tech works: The nanoparticles designed by Stephan and his team act like shipping containers for bundles of mRNA, the molecules that tell cells how to build disease-fighting proteins. The nanoparticles also have molecules attached to the outside to help them find the right kind of cells, like a shipping label on a package.

When the mRNA is delivered to the cell, it prompts the cell to grow disease-fighting features, like the chimeric antigen receptor in CAR T cells that help them identify and kill cancer.Researchers said the technology could potentially be used to develop treatments for HIV, diabetes and other immune-related diseases.

In the short run, the tech could help researchers discover new treatments and therapies in the lab. It could one day be used in hospitals and clinics around the world, but will first need to undergo extensive clinical trials to ensure the tech is effective and safe to use in humans.

View post:
New 'hit-and-run' gene editing tool temporarily rewrites genetics to treat cancer and HIV - GeekWire

Clay Siegall

Seven years after Copenhagen-based Genmab inked a collaboration deal with Seattle Genetics, the US biotech has decided to opt-in on a development partnership.

The pact struck in 2010 gave Genmab rights to Seattle Genetics antibody-drug conjugate tech so it could work on a new approach for its HuMax-TF antibody targeting the tissue factor antigen. A year later they struck a deal giving Seattle Genetics an opt-in on tisotumab vedotin, now in several Phase I/II studies for solid tumors, including recurrent cervical cancer.

Whatever data that early program has produced was good enough to persuade Seattle Genetics to agree to share the development costs and any profits 50/50.

Seattle Genetics has run into a series of late-stage mishaps over the past year. The biotech was forced to scrap a Phase III study of vadastuximab and halt a slate of other trials as researchers puzzled out what caused an imbalance of deaths between the drug and control arms. Just a few weeks before the June imbroglio, Seattle Genetics was also forced to throw the towel in on a $2 billion deal to collaborate with Immunomedics, further limiting its late-stage effort. Seattle Genetics mainstay franchise drug did score a win on frontline Hodgkin lymphoma at the end of H1, but the gain was so marginal that some analysts fretted it looked like the kind of small advantage that may not be worth much commercially.

Our ADC partnership with Genmab has generated promising Phase I/II data for tisotumab vedotin in patients with recurrent cervical cancer. As Seattle Genetics opts into co-development of this clinical program, we add another potential product to our strong pipeline, said Seattle Genetics CEO Clay Siegall.

Full-text daily reports for those who discover, develop, and market drugs. Join 17,000+ biopharma pros who read Endpoints News by email every day.

Read the original here:
Seven years in the making, Seattle Genetics picks up early option on Genmab's ADC effort - Endpoints News

August 30, 2017

Scientists have discovered a network of genes and genetic regulatory elements in the lining of the intestines that has stayed remarkably the same from fishes to humans. Many of these genes are linked to human illnesses, such as inflammatory bowel diseases, diabetes, and obesity.

The findings, which appear in the journal PLOS Biology, establish the fish as an experimental platform for studying how this ancient genetic information -- distilled over 420 million years of evolution -- controls the development and dysfunction of the intestine.

"Our research has uncovered aspects of intestinal biology that have been well-conserved during vertebrate evolution, suggesting they are of central importance to intestinal health," said John F. Rawls, Ph.D., senior author of the study and associate professor of molecular genetics and microbiology at Duke University School of Medicine. "By doing so, we have built a foundation for mechanistic studies of intestinal biology in non-human model systems like fish and mice that would be impossible to perform in humans alone."

The intestine serves a variety of important functions that are common to all vertebrates. It takes up nutrients, stimulates the immune system, processes toxins and drugs, and provides a critical barrier to microorganisms. Defects in the intestinal epithelial cells lining the intestine have been implicated in a growing number of ailments, including inflammatory bowel diseases, colorectal cancer, food allergy, diabetes, obesity, malnutrition and infectious diarrheas.

For decades, scientists have relied on animal models to gather information on intestinal epithelial cells that could help combat human diseases. But it wasn't clear just how alike these cells were across multiple species.

In this study, Rawls and his team used a comparative biology approach to tackle that question. Research associate Colin R. Lickwar, Ph.D., and colleagues generated genome-wide data from intestinal epithelial cells in four evolutionarily distant species: zebrafish, stickleback fish, mouse and human. Lickwar then created maps for each of the species depicting not only the activity level of all of the genes, but also the location of specific genetic sequences or regulatory elements that flipped those genes on and off.

Lickwar was surprised to find a striking amount of similarity between the different vertebrate species. He identified a common set of genes -- an intestinal epithelial cell signature -- some of which had shared patterns of activity in specific regions along the length of the intestine. What's more, many of the genes included in this conserved signature had previously been implicated in a variety of human diseases. Lickwar and Rawls wondered if this conserved genetic signature was controlled by regulatory elements that might also be shared between species.

To test if this was the case, they took various regulatory elements from fish, mice, and humans and stuck them into the zebrafish. Because zebrafish are transparent organisms, the researchers could look under the microscope for patterns of color to tell whether a green fluorescent protein or red fluorescent protein, which they had inserted along with the regulatory element, had been flipped on in the intestine. They found that the regulatory switches transplanted from the other species worked in zebrafish, indicating a remarkable level of conservation.

"Our findings suggest that intestinal epithelial cells use an ancient core program to do their job in the body of most vertebrates," said Lickwar, who is lead author of the study. "Now that we have identified this core program, we can more easily translate results back and forth between humans and zebrafish."

Continue reading here:
Genetics of digestion stayed remarkably the same from fishes to humans, research shows - News-Medical.net

August 29, 2017

Studies have shown that an early age of drinking initiation (ADI) increases the chance of developing an alcohol use disorder (AUD). There is limited evidence that ADI differs across ethnic groups. This study examined whether the pathway from ADI to AUD symptoms by early adulthood is influenced by two factors: ethnicity and having the alcohol metabolizing gene variant allele, ALDH2*2. This allele produces an inactive enzyme that leads to higher levels of acetaldehyde during alcohol metabolism, which are associated with unpleasant effects after drinking alcohol and a decreased risk for an AUD.

Researchers examined 604 college students recruited from the University of California, San Diego: 214 of Korean ancestry (107 men, 107 women), 200 of European ancestry (106 men, 94 women), and 190 of Chinese ancestry (99 women, 91 men), each with both biological parents having the same heritage. Participants were genotyped for the ALDH2*2 variant allele and completed a self-report assessment.

The effect of ADI as a risk factor for developing AUD symptoms varied with both ethnicity and ALDH2*2 status. ADI was not associated with AUD symptoms in Korean-Americans with an ALDH2*2 allele or in Chinese-Americans regardless of ALDH2*2 status. This indicates that being Korean (and having the protective ALDH2*2 allele) or Chinese buffered the risk for developing AUD symptoms associated with an early ADI. Although an earlier ADI places some individuals at risk to develop AUD symptoms, the path from ADI to AUD symptoms is complex and can be modified by other factors.

Link:
Pathway from ADI to AUD symptoms influenced by ethnicity and genetics - News-Medical.net