Category Archives: Genetics

Oyster growers hopeful new genetics boost quality – ABC Online

Posted February 23, 2017 16:00:47

Access to superior commercial genetic stock for the first time is boosting morale of New South Wales oyster farmers.

Major disease outbreaks over the past decade have contributed to a steady decline in oyster production and the number of farmers.

Veteran oyster grower Tony Troup said access to new superior stock would finally modernise the industry.

Mr Troup produces about 20,000 dozen Sydney Rock oysters and young oyster spat at his lease at Camden Haven, near Laurieton on the mid north coast of New South Wales.

He said access to new superior stock would finally modernise the industry.

"The breeding program will hopefully bring the oyster industry up into the 21st century," he said.

"We have been relying on basically wild stock for the duration of our industry which is now 150 years old.

"I'm hoping the breeding program will really lift our production and reduce our cost rates."

The young oyster spat used in his hatchery was developed through years of research by the Department of Primary Industries.

It is more resistant to deadly diseases like QX and winter mortality, which have hit the industry hard.

Scientist Michael Dove said a move away from mass breeding using wild oyster stock and to a family breeding program had allowed research to be fast-tracked by years.

"It can shave years off before we actually get the data and with QX we can get that data one year earlier.

"For condition, we can get that data one year earlier than if we bred through the normal part of the season," Mr Dove said.

Select Oyster Company, a company run by NSW Farmers, is now managing the breeding program and distribution of its hatchery stock.

Operations manager Emma Wilkie said it was their job to get the new genetics onto farms.

"The selective breeding program is decades old and the amount of research that has gone into it is phenomenal," she said.

"It is a very sophisticated breeding program and on par with salmon, wheat, cattle and now it is commercial so we are getting the genetics onto the farm."

Despite better stock, there are still perennial challenges with naturally occurring bacteria that can build up in oyster populations.

Biologist Chantal Gionet is a shell fish consultant from the east coast of Canada and has been working with growers to control vibrio.

"Vibrio is an issue for anyone in the world in a hatchery because vibro is natural in the wild.

"When you bring them (oysters) into a closed environment, it's warmer, it will bloom in your tanks. it just promotes growth," Ms Gionet said.

Tony Troup from Camden Haven said Ms Gionet's work on controlling vibrio had made a fantastic difference.

I start the run with something like 100 million oysters and hopefully go to set with 10 to 20 per cent of those.

"They would have been all dead in the first week if she wasn't here," he said.

Tony Troup remains hopeful the industry does have a future.

"If we can get this breeding program really up and going, we will be onto something and the industry will really start to grow."

"I must be an optimist, I've been in the industry now 30 years and I keep thinking it is about to get better, and it still hasn't quite got better yet!"

Topics: fishing-aquaculture, research, marine-biology, laurieton-2443

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Oyster growers hopeful new genetics boost quality - ABC Online

How genetics can uncover links in chronic pain and other conditions – The Conversation UK

Chronic pain can be disabling.

In the recent Global Burden of Disease study, four of the top ten causes of disability worldwide were chronic pain conditions. Chronic pain is defined as pain that lasts beyond normal healing time usually three months and is one of the most common global causes of incapacity. It rarely occurs by itself, however, and is one of the most common conditions to present itself alongside other chronic conditions, such as diabetes and COPD. This increases the overall burden of disability, and the impact of each chronic condition.

The exact reason why some people suffer from several chronic diseases and others dont, is not well understood. However, we have discovered that genetics could partially explain this.

Two of the most common disorders which occur alongside chronic pain are depression and angina. There is already evidence of shared socio-demographic risk factors for all of these conditions, particularly older age and social deprivation, as well as lifestyle factors. However these do not explain all of the shared risk.

In order to investigate a risk within families and a genetic explanation for chronic disease, we examined two major groups, for the co-occurrence of chronic pain, depression and heart disease in individuals and their siblings.

Data from Generation Scotland included 24,000 individuals, recruited in family groups, with data on multiple chronic illnesses, socio-demographic and psychological factors, and blood from which DNA was genetically analysed. When the data was collected, 18% of participants reported chronic pain, 13% had a history of major depressive disorder and 10% had angina.

We looked at the existence of two or three of these conditions in individuals and we found that people with depression were two and a half times more likely to experience chronic pain; while people with both depression and heart disease were nine times more likely to experience chronic pain. It is clear that the existence of one condition increases the chance of an individual having another, or both of the other conditions.

A familial risk was confirmed when we looked at siblings of people affected by these conditions. A sibling of someone with heart disease was twice as likely to have chronic pain, and siblings of those with depression were twice as likely to suffer from heart disease. This suggests that genetics plays a part in these chronic diseases, in addition to known social and demographic factors.

The magnitude of a shared genetic explanation for these chronic conditions was examined by looking at sets of twins. TwinsUK has data on 12,000 identical and non-identical twins from across the UK, of 16-98 years of age. In a sample of 2,902 of these, 20% suffered with chronic pain, 22% had depression and 35% reported a cardiovascular disease.

We compared the rates of occurrence of a condition, and of co-occurrence with another, between identical and non-identical twins. In identical twins, it was consistently more likely that both individuals would be affected, by any of the conditions, than non-identical twins, which further confirms that there is significant genetic contribution. When we examined the co-occurrence of chronic widespread pain and heart disease in our twins we found that the model that best explained the co-occurrence was a combination of both genetic and non-shared environmental factors.

Although there are numerous causes of chronic pain, there are similarities in the socio-demographic factors explaining their development. Recent research shows that there are also similar biological factors present in the development of different types of chronic pain.

For the sufferer, it is the pain itself, rather than the cause, that produces the most distress and disability most chronic pain sufferers had it for more than five years at more than one site. The most common chronic pain, back pain, accounted for 146m years lived with disability in 2013, three times the level of depression.

Overall, 19% of adults in Europe, and 6% in the UK, were found to have significant chronic pain that was intense, severely disabling and limiting. This is similar to the prevalence of conditions such as cancer, heart disease and diabetes.

As well as the issue that chronic pain represents for individuals, its management places an important burden on healthcare services and it impacts on families, society and the economy. Therefore, the finding that a genetic mechanism could help to explain the co-occurence of these conditions is significant to allow further research. The exact genes involved in the occurence and co-occurrence of chronic pain need to be identified, so that we may switch them off at an early stage and try to develop new treatments.

Of course, it will always be important to understand and address the socio-demographic causes of disability and co-occurrence of conditions especially with regards to factors we could change, such as deprivation. However, our research also suggests a new model of chronic disease, based on genetics and biological factors.

Genes are important in determining the risk, both of chronic disease itself, and of co-occurrence of other disabilities. Only a deeper understanding of these factors will allow the development of new preventive and targeted treatments.

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How genetics can uncover links in chronic pain and other conditions - The Conversation UK

Producers seek top genetics at Iowa sale event – Iowa Farmer Today

DES MOINES Rob Long believes spending money on good genetics should not stop because of a lower fed cattle market.

Long, who farms near Creston, sold the top-selling bull at this years. His Simmental bull brought $15,000 to top the breed sale.

With the economy the way it is, its not the time to keep the status quo, Long says. I think we need to focus on the best attributes and buy those bulls that are going to bring value to your operation.

The Southwest Iowa producer says there was a good deal of interest in the bull ahead of the expo.

There was some uniqueness in his pedigree, and that attracted some people, Long says. It showed us that people were still willing to spend money on quality genetics. I think were seeing that this year with this bull.

Commercial producers know spending money on quality genetics will pay off over the long haul, says Kevin Mohrfeld. The West Point producer had the top-selling Angus bull at the expo, bringing $12,000.

Most of our customers are commercial produces, and they are really interested in performance, he says. With prices down, they really want those good genetics.

He says his bull attracted a fair amount of interest from potential buyers ahead of the sale.

They really liked his performance, his overall balance and how his EPDs (expected progeny differences) looked, Mohrfeld says. Weve had the second highest selling bull a couple of times. It was nice to be at the top of the sale this year.

Listed here are complete sale results from this years expo Feb. 12-19.

Angus

The top-selling bull, consigned by Kevin Mohrfeld of West Point, sold for $12,000 to David Deal of Danvers, Ill.

The top-selling female, consigned by Ron Buch of Luzerne, sold for $7,500 to Lyle Olson of Red Oak.

A total of 61 bulls sold for an average price of $4,273. A total of 35 females sold for an average price of $3,325. One embryo lot sold for $3,000.

Charolais

The top-selling bulls, consigned by North Grove Charolais of Grove City, Minn., and Shepherd Charolais of Stuart, sold for $5,500 to Kurt Neff of Blackfoot, Idaho, and Brad Kresak of Milligan, Neb., respectively.

The top-selling female, consigned by North Grove Charolais of Grove City, Minn., sold for $7,500 to Lance Van Roekel of Larchwood.

A total of 43 bulls sold for an average price of $2,990. A total of 36 females sold for an average price of $2,797. Nine embryo lots sold for an average price of $492.

Gelbvieh

The top-selling bull, consigned by Blackhawk Cattle Co./Lazy JV Ranch of Oregon, Ill., sold for $8,400 to Bar Arrow Cattle Co. of Phillipsburg, Kan.

The top-selling female, consigned by Kirkwood Community College of Cedar Rapids, sold for $4,500 to Adelyn Sienknecht of Gladbrook.

A total of 13 bulls sold for an average price of $3,762. A total of 26 females sold for an average price of $2,602.

Hereford

The top-selling bull, consigned by Lorenzen Farms of Chrisman, Ill., sold for $10,200 to Donn Jibben of Fort Worth, Texas.

The top-selling female, consigned by Wiese & Sons of Manning, sold for $7,000 to Express Ranches of Yukon, Okla.

A total of 41 bulls sold for an average price of $3,655. A total of 31 females sold for an average price of $3,347.

Limousin

The top-selling bull, consigned by Deb Vorthmann of Silver City, sold for $5,600 to Vorthmann Limousin of Treynor.

The top-selling female, consigned by Boesch Farms of Indianola, sold for $2,950 to Shelby Skinner of Bolivar, Mo.

A total of 24 bulls sold for an average price of $3,396. A total of nine females sold for an average price of $2,289.

Lowline

The top-selling bull, sold by Swanquist Spring Brook Farm of Lagro, Ind., sold for $1,300 to Randy Larson of Sumner.

The top-selling female, consigned by Reinken Cattle Co. of Boone, sold for $4,400 to Ray Gaskill of Boone.

A total of 16 females sold for an average price of $2,266. One steer sold for a price of $850. Nine semen lots sold for an average price of $228.

Maine-Anjou

The top-selling bull, consigned by Braun Show Cattle of Northwood, sold for $4,100 to Mark Roges of Douds.

The top-selling female, consigned by Jordan Crall of Albia, sold for $4,900 to Jodi Opperman of Manning.

A total of nine bulls sold for an average price of $2,256. A total of 16 females sold for an average price of $1,928.

Miniature Hereford

The top-selling bull, consigned by Smith Mini Herefords of Fairfield, sold for $3,000 to Karly Biddle of Walcott.

The top-selling female, consigned by Allison Gooden of Bloomfield, sold for $5,000 to C & B Farms LLC of Mineral Point, Wis.

A total of four bulls sold for an average price of $2,350. A total of eight females sold for an average price of $4,100. A total of five steers sold for an average price of $830. One flush lot sold for $2,800. Three semen lots sold for an average price of $380.

Red Angus

The top-selling bull, consigned by Ulrich Red Angus of Good Thunder, Minn., sold for $5,800 to Dave Runner of Gilman.

The top-selling female, consigned by Finch Cattle of Kelley, sold for $4,300 to Alex Wilson of Ogden.

A total of 22 bulls sold for an average price of $3,282. A total of 25 females sold for an average price of $2,862.

Three embryo lots sold for an average price of $2,234.

One flush lot sold for $5,000.

Salers

The top-selling bull, consigned by T-Bone Cattle Co. of Osceola, sold for $4,200 to Bill Edwards of Wayland.

The top-selling female, consigned by Barnes Farms of Lamoni, sold for $5,500 to McIvers Happy Acres Farm of Farwell, Minn.

A total of 10 bulls sold for an average price of $2,770. A total of nine females sold for an average price of $2,766.

Shorthorn

The top-selling bull, consigned by Nate Studer Family of Creston, sold for $10,000 to Glenrothes Farm George D. Brown of Beaverton, Ontario.

The top-selling female, consigned by Ryan & Steve Laughlin of Imogene, sold for $5,500 to Kaden Wilson of Creston.

A total of 14 bulls sold for an average price of $4,429. A total of 32 females sold for an average price of $2,527. Five embryo lots sold for an average price of $518. Four semen lots sold for an average price of $201.

Simmental

The top-selling bull, consigned by Rob Long of Creston, sold for $15,000 to Loonan Stock Farm of Corning.

The top-selling female, consigned by GSJG Matt Greiman Family of Goodell, sold for $8,500 to Brittain Cattle of Earlham.

A total of 83 bulls sold for an average price of $3,553. A total of 47 females sold for an average price of $2,878. Fifteen embryo lots sold for an average price of $405. One pregnancy lot sold for $4,200.

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Producers seek top genetics at Iowa sale event - Iowa Farmer Today

Swedroe: Investing Habits Affected By Genetics – ETF.com

Its been well-documented that, on average, retail investors are dumb money. For example, on average, the stocks they buy go on to underperform and the stocks they sell go on to outperform. Investors, sadly, even manage to underperform the very mutual funds in which they invest.

Research from the field of behavioral finance has provided explanations for these poor results. In short, theyre the product of a long list of investment biases exhibited by individual investors. Among these biases are: Investors lack portfolio diversification due to overconfidence and a preference for investing in familiar securities (a home-country bias); they tend to trade too much (overconfidence again); they are reluctant to realize their losses (it is too painful to admit mistakes); they extrapolate recent superior returns into the future (the hot-hands fallacy); and they have a preference for skewness and lottery-type investments (which is explained by prospect theory).

While studies have shown that individual investors, on average, exhibit investment biases, little research has been devoted to uncovering their origins and the differences in them across investors. This, in turn, raises two questions: Are investors genetically endowed with certain predispositions that manifest themselves as investment biases? Or, do investors exhibit biases as a result of parenting or individual-specific experiences or events?

Investment Biases And Genetics

Henrik Cronqvist and Stephan Siegel contribute to the literature on investment biases with their study, The Genetics of Investment Biases, which appeared in the August 2014 issue of the Journal of Financial Economics.

To answer these questions, they used a unique data set, the worlds largest twin registry, the Swedish Twin Registry, and then matched it with detailed data on twins investment behaviors. This enabled them to decompose differences across individuals into genetic versus environmental components.

The decomposition was based on an intuitive insight: Identical twins share 100% of their genes, while the average proportion of shared genes is only 50% for fraternal twins. If identical twins exhibit more similarity with respect to these investment biases than do fraternal twins, then there is evidence that these behaviors are influenced, at least in part, by genetic factors.

The authors database included more than 15,000 sets of twins. Following is a summary of their findings:

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Swedroe: Investing Habits Affected By Genetics - ETF.com

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.

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.

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

Genetics + Family Environment Impact Childhood Obesity – PsychCentral.com

A new international study finds that around 35-40 percent of a childs BMI (Body Mass Index) how fat or thin they are is inherited from their parents.

Investigators say that for the most obese children, the proportion rises to 55-60 percent, thus more than half of their tendency towards obesity is determined by genetics and family environment.

University of Sussex researchers used data on the heights and weights of 100,000 children and their parents across the world, including the U.K., U.S., China, Indonesia, Spain, and Mexico.

Investigators found that the intergenerational transmission of BMI is approximately constant at around 0.2 per parent; i.e., each childs BMI is, on average, 20 percent due to the mother and 20 percent due to the father.

The pattern of results, said lead author Professor Peter Dolton of the University of Sussex, is remarkably consistent across all countries, irrespective of their stage of economic development, degree of industrialization, or type of economy.

Professor Dolton says, Our evidence comes from trawling data from across the world with very diverse patterns of nutrition and obesity, from one of the most obese populations USA to two of the least obese countries in the world, China and Indonesia.

This gives an important and rare insight into how obesity is transmitted across generations in both developed and developing countries.We found that the process of intergenerational transmission is the same across all the different countries.

The findings are published in the journal Economics and Human Biology.

Interestingly, the effect of parents BMI on their childrens BMI depends on what the BMI of the child is. Researchers discovered that consistently, across all populations studied, the parental effect was lowest for the thinnest children and highest for the most obese children.

For the thinnest child their BMI is 10 percent due to their mother and 10 percent due to their father. For the fattest child this transmission is closer to 30 percent due to each parent.

Said Dolton, This shows that the children of obese parents are much more likely to be obese themselves when they grow up the parental effect is more than double for the most obese children what it is for the thinnest children.

These findings have far-reaching consequences for the health of the worlds children. They should make us rethink the extent to which obesity is the result of family factors, and our genetic inheritance, rather than decisions made by us as individuals.

Source: University of Sussex

APA Reference Nauert PhD, R. (2017). Genetics + Family Environment Impact Childhood Obesity. Psych Central. Retrieved on February 22, 2017, from https://psychcentral.com/news/2017/02/21/genetics-family-environment-impact-childhood-obesity/116702.html

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Genetics + Family Environment Impact Childhood Obesity - PsychCentral.com

BRIEF-DE Shaw reports 5 pct passive stake in Myriad Genetics – Reuters

Northern Trust uses blockchain for private equity record-keeping

NEW YORK, Feb 22 Northern Trust Corp has deployed a new blockchain-based system built with International Business Machines Corp to record information on transactions involving private equity funds, in one of the first commercial deployments of the nascent technology.

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BRIEF-DE Shaw reports 5 pct passive stake in Myriad Genetics - Reuters

Jurors In Toxic Tort Litigation Take Genetics Seriously – Law360 (subscription)

Kirk Hartley Can jurors grasp the role of genetics in personal injury claims alleged to arise from exposure to specific chemicals? Can judges grasp the issues well enough to really help expert witnesses present the issues clearly, and to help jurors understand?

Not long ago, we saw the first asbestos trial making explicit reference to a plaintiff with BAP1 mutations and the alleged role of those mutations in the causation story. The point of this article is to provide some more specific information from...

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Jurors In Toxic Tort Litigation Take Genetics Seriously - Law360 (subscription)

Genetics, family set-up play a big role in your tendency to put on weight – Hindustan Times

As per a new study, up to 40% of your body-mass index (BMI) may have been inherited from your parents. The report adds that nearly half of a kids tendency towards obesity is determined by genetics and family environment.

Your obesity worries you? Do you feel guilty every time you have a candy? This research should help you deal with it. A recent study says that up to 40% of your body-mass index may have been inherited from your parents. It adds that more than half of a kids tendency towards obesity is determined by genetics and family environment.

For the most obese children, the proportion rises to 55-60%, researchers said.

The study, led by the University of Sussex in the UK, used data on the heights and weights of 100,000 children and their parents spanning six countries worldwide: the UK, US, China, Indonesia, Spain and Mexico.

The researchers found that the intergenerational transmission of body-mass index (BMI) is almost constant at around 0.2 per parent -- that is each childs BMI on average is around 20% due to the mother and 20% due to the father.

The pattern of results is remarkably consistent across all countries, irrespective of their stage of economic development, degree of industrialisation, or type of economy, said Peter Dolton, Professor at the University of Sussex in the UK.

Our evidence comes from trawling data from across the world with very diverse patterns of nutrition and obesity -- from one of the most obese populations -- the US -- to two of the least obese countries in the world -- China and Indonesia.

This gives an important and rare insight into how obesity is transmitted across generations in both developed and developing countries, said Dolton.

We found that the process of intergenerational transmission is the same across all the different countries, he said.

Up to 40% of your body-mass index (BMI) comes from your parents. (Shutterstock)

The study also shows how the effect of parents BMI on their childrens BMI depends on what the BMI of the child is. Consistently, across all populations studied, they found the parental effect to be lowest for the thinnest children and highest for the most obese children.

For the thinnest child their BMI is 10% due to their mother and 10% due to their father. For the fattest child this transmission is closer to 30% due to each parent.

This shows that the children of obese parents are much more likely to be obese themselves when they grow up - the parental effect is more than double for the most obese children what it is for the thinnest children, said Dolton.

The findings were published in the journal Economics and Human Biology.

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Genetics, family set-up play a big role in your tendency to put on weight - Hindustan Times

Medical genetics – Wikipedia

Medical genetics is the branch of medicine that involves the diagnosis and management of hereditary disorders. Medical genetics differs from human genetics in that human genetics is a field of scientific research that may or may not apply to medicine, while medical genetics refers to the application of genetics to medical care. For example, research on the causes and inheritance of genetic disorders would be considered within both human genetics and medical genetics, while the diagnosis, management, and counselling people with genetic disorders would be considered part of medical genetics.

In contrast, the study of typically non-medical phenotypes such as the genetics of eye color would be considered part of human genetics, but not necessarily relevant to medical genetics (except in situations such as albinism). Genetic medicine is a newer term for medical genetics and incorporates areas such as gene therapy, personalized medicine, and the rapidly emerging new medical specialty, predictive medicine.

Medical genetics encompasses many different areas, including clinical practice of physicians, genetic counselors, and nutritionists, clinical diagnostic laboratory activities, and research into the causes and ixxxxxx nheritance of genetic disorders. Examples of conditions that fall within the scope of medical genetics include birth defects and dysmorphology, mental retardation, autism, and mitochondrial disorders, skeletal dysplasia, connective tissue disorders, cancer genetics, teratogens, and prenatal diagnosis. Medical genetics is increasingly becoming relevant to many common diseases. Overlaps with other medical specialties are beginning to emerge, as recent advances in genetics are revealing etiologies for neurologic, endocrine, cardiovascular, pulmonary, ophthalmologic, renal, psychiatric, and dermatologic conditions.

In some ways, many of the individual fields within medical genetics are hybrids between clinical care and research. This is due in part to recent advances in science and technology (for example, see the Human genome project) that have enabled an unprecedented understanding of genetic disorders.

Clinical genetics is the practice of clinical medicine with particular attention to hereditary disorders. Referrals are made to genetics clinics for a variety of reasons, including birth defects, developmental delay, autism, epilepsy, short stature, and many others. Examples of genetic syndromes that are commonly seen in the genetics clinic include chromosomal rearrangements, Down syndrome, DiGeorge syndrome (22q11.2 Deletion Syndrome), Fragile X syndrome, Marfan syndrome, Neurofibromatosis, Turner syndrome, and Williams syndrome.

In the United States, physicians who practice clinical genetics are accredited by the American Board of Medical Genetics and Genomics (ABMGG).[1] In order to become a board-certified practitioner of Clinical Genetics, a physician must complete a minimum of 24 months of training in a program accredited by the ABMGG. Individuals seeking acceptance into clinical genetics training programs must hold an M.D. or D.O. degree (or their equivalent) and have completed a minimum of 24 months of training in an ACGME-accredited residency program in internal medicine, pediatrics, obstetrics and gynecology, or other medical specialty.[2]

Metabolic (or biochemical) genetics involves the diagnosis and management of inborn errors of metabolism in which patients have enzymatic deficiencies that perturb biochemical pathways involved in metabolism of carbohydrates, amino acids, and lipids. Examples of metabolic disorders include galactosemia, glycogen storage disease, lysosomal storage disorders, metabolic acidosis, peroxisomal disorders, phenylketonuria, and urea cycle disorders.

Cytogenetics is the study of chromosomes and chromosome abnormalities. While cytogenetics historically relied on microscopy to analyze chromosomes, new molecular technologies such as array comparative genomic hybridization are now becoming widely used. Examples of chromosome abnormalities include aneuploidy, chromosomal rearrangements, and genomic deletion/duplication disorders.

Molecular genetics involves the discovery of and laboratory testing for DNA mutations that underlie many single gene disorders. Examples of single gene disorders include achondroplasia, cystic fibrosis, Duchenne muscular dystrophy, hereditary breast cancer (BRCA1/2), Huntington disease, Marfan syndrome, Noonan syndrome, and Rett syndrome. Molecular tests are also used in the diagnosis of syndromes involving epigenetic abnormalities, such as Angelman syndrome, Beckwith-Wiedemann syndrome, Prader-willi syndrome, and uniparental disomy.

Mitochondrial genetics concerns the diagnosis and management of mitochondrial disorders, which have a molecular basis but often result in biochemical abnormalities due to deficient energy production.

There exists some overlap between medical genetic diagnostic laboratories and molecular pathology.

Genetic counseling is the process of providing information about genetic conditions, diagnostic testing, and risks in other family members, within the framework of nondirective counseling. Genetic counselors are non-physician members of the medical genetics team who specialize in family risk assessment and counseling of patients regarding genetic disorders. The precise role of the genetic counselor varies somewhat depending on the disorder.

Although genetics has its roots back in the 19th century with the work of the Bohemian monk Gregor Mendel and other pioneering scientists, human genetics emerged later. It started to develop, albeit slowly, during the first half of the 20th century. Mendelian (single-gene) inheritance was studied in a number of important disorders such as albinism, brachydactyly (short fingers and toes), and hemophilia. Mathematical approaches were also devised and applied to human genetics. Population genetics was created.

Medical genetics was a late developer, emerging largely after the close of World War II (1945) when the eugenics movement had fallen into disrepute. The Nazi misuse of eugenics sounded its death knell. Shorn of eugenics, a scientific approach could be used and was applied to human and medical genetics. Medical genetics saw an increasingly rapid rise in the second half of the 20th century and continues in the 21st century.

The clinical setting in which patients are evaluated determines the scope of practice, diagnostic, and therapeutic interventions. For the purposes of general discussion, the typical encounters between patients and genetic practitioners may involve:

Each patient will undergo a diagnostic evaluation tailored to their own particular presenting signs and symptoms. The geneticist will establish a differential diagnosis and recommend appropriate testing. Increasingly, clinicians use SimulConsult, paired with the National Library of Medicine Gene Review articles, to narrow the list of hypotheses (known as the differential diagnosis) and identify the tests that are relevant for a particular patient. These tests might evaluate for chromosomal disorders, inborn errors of metabolism, or single gene disorders.

Chromosome studies are used in the general genetics clinic to determine a cause for developmental delay/mental retardation, birth defects, dysmorphic features, and/or autism. Chromosome analysis is also performed in the prenatal setting to determine whether a fetus is affected with aneuploidy or other chromosome rearrangements. Finally, chromosome abnormalities are often detected in cancer samples. A large number of different methods have been developed for chromosome analysis:

Biochemical studies are performed to screen for imbalances of metabolites in the bodily fluid, usually the blood (plasma/serum) or urine, but also in cerebrospinal fluid (CSF). Specific tests of enzyme function (either in leukocytes, skin fibroblasts, liver, or muscle) are also employed under certain circumstances. In the US, the newborn screen incorporates biochemical tests to screen for treatable conditions such as galactosemia and phenylketonuria (PKU). Patients suspected to have a metabolic condition might undergo the following tests:

Each cell of the body contains the hereditary information (DNA) wrapped up in structures called chromosomes. Since genetic syndromes are typically the result of alterations of the chromosomes or genes, there is no treatment currently available that can correct the genetic alterations in every cell of the body. Therefore, there is currently no "cure" for genetic disorders. However, for many genetic syndromes there is treatment available to manage the symptoms. In some cases, particularly inborn errors of metabolism, the mechanism of disease is well understood and offers the potential for dietary and medical management to prevent or reduce the long-term complications. In other cases, infusion therapy is used to replace the missing enzyme. Current research is actively seeking to use gene therapy or other new medications to treat specific genetic disorders.

In general, metabolic disorders arise from enzyme deficiencies that disrupt normal metabolic pathways. For instance, in the hypothetical example:

Compound "A" is metabolized to "B" by enzyme "X", compound "B" is metabolized to "C" by enzyme "Y", and compound "C" is metabolized to "D" by enzyme "Z". If enzyme "Z" is missing, compound "D" will be missing, while compounds "A", "B", and "C" will build up. The pathogenesis of this particular condition could result from lack of compound "D", if it is critical for some cellular function, or from toxicity due to excess "A", "B", and/or "C". Treatment of the metabolic disorder could be achieved through dietary supplementation of compound "D" and dietary restriction of compounds "A", "B", and/or "C" or by treatment with a medication that promoted disposal of excess "A", "B", or "C". Another approach that can be taken is enzyme replacement therapy, in which a patient is given an infusion of the missing enzyme.

Dietary restriction and supplementation are key measures taken in several well-known metabolic disorders, including galactosemia, phenylketonuria (PKU), maple syrup urine disease, organic acidurias and urea cycle disorders. Such restrictive diets can be difficult for the patient and family to maintain, and require close consultation with a nutritionist who has special experience in metabolic disorders. The composition of the diet will change depending on the caloric needs of the growing child and special attention is needed during a pregnancy if a woman is affected with one of these disorders.

Medical approaches include enhancement of residual enzyme activity (in cases where the enzyme is made but is not functioning properly), inhibition of other enzymes in the biochemical pathway to prevent buildup of a toxic compound, or diversion of a toxic compound to another form that can be excreted. Examples include the use of high doses of pyridoxine (vitamin B6) in some patients with homocystinuria to boost the activity of the residual cystathione synthase enzyme, administration of biotin to restore activity of several enzymes affected by deficiency of biotinidase, treatment with NTBC in Tyrosinemia to inhibit the production of succinylacetone which causes liver toxicity, and the use of sodium benzoate to decrease ammonia build-up in urea cycle disorders.

Certain lysosomal storage diseases are treated with infusions of a recombinant enzyme (produced in a laboratory), which can reduce the accumulation of the compounds in various tissues. Examples include Gaucher disease, Fabry disease, Mucopolysaccharidoses and Glycogen storage disease type II. Such treatments are limited by the ability of the enzyme to reach the affected areas (the blood brain barrier prevents enzyme from reaching the brain, for example), and can sometimes be associated with allergic reactions. The long-term clinical effectiveness of enzyme replacement therapies vary widely among different disorders.

There are a variety of career paths within the field of medical genetics, and naturally the training required for each area differs considerably. It should be noted that the information included in this section applies to the typical pathways in the United States and there may be differences in other countries. US Practitioners in clinical, counseling, or diagnostic subspecialties generally obtain board certification through the American Board of Medical Genetics.

Genetic information provides a unique type of knowledge about an individual and his/her family, fundamentally different from a typically laboratory test that provides a "snapshot" of an individual's health status. The unique status of genetic information and inherited disease has a number of ramifications with regard to ethical, legal, and societal concerns.

On 19 March 2015, scientists urged a worldwide ban on clinical use of methods, particularly the use of CRISPR and zinc finger, to edit the human genome in a way that can be inherited.[3][4][5][6] In April 2015 and April 2016, Chinese researchers reported results of basic research to edit the DNA of non-viable human embryos using CRISPR.[7][8][9] In February 2016, British scientists were given permission by regulators to genetically modify human embryos by using CRISPR and related techniques on condition that the embryos were destroyed within seven days.[10] In June 2016 the Dutch government was reported to be planning to follow suit with similar regulations which would specify a 14-day limit.[11]

The more empirical approach to human and medical genetics was formalized by the founding in 1948 of the American Society of Human Genetics. The Society first began annual meetings that year (1948) and its international counterpart, the International Congress of Human Genetics, has met every 5 years since its inception in 1956. The Society publishes the American Journal of Human Genetics on a monthly basis.

Medical genetics is now recognized as a distinct medical specialty in the U.S. with its own approved board (the American Board of Medical Genetics) and clinical specialty college (the American College of Medical Genetics). The College holds an annual scientific meeting, publishes a monthly journal, Genetics in Medicine, and issues position papers and clinical practice guidelines on a variety of topics relevant to human genetics.

The broad range of research in medical genetics reflects the overall scope of this field, including basic research on genetic inheritance and the human genome, mechanisms of genetic and metabolic disorders, translational research on new treatment modalities, and the impact of genetic testing

Basic research geneticists usually undertake research in universities, biotechnology firms and research institutes.

Sometimes the link between a disease and an unusual gene variant is more subtle. The genetic architecture of common diseases is an important factor in determining the extent to which patterns of genetic variation influence group differences in health outcomes.[12][13][14] According to the common disease/common variant hypothesis, common variants present in the ancestral population before the dispersal of modern humans from Africa play an important role in human diseases.[15] Genetic variants associated with Alzheimer disease, deep venous thrombosis, Crohn disease, and type 2 diabetes appear to adhere to this model.[16] However, the generality of the model has not yet been established and, in some cases, is in doubt.[13][17][18] Some diseases, such as many common cancers, appear not to be well described by the common disease/common variant model.[19]

Another possibility is that common diseases arise in part through the action of combinations of variants that are individually rare.[20][21] Most of the disease-associated alleles discovered to date have been rare, and rare variants are more likely than common variants to be differentially distributed among groups distinguished by ancestry.[19][22] However, groups could harbor different, though perhaps overlapping, sets of rare variants, which would reduce contrasts between groups in the incidence of the disease.

The number of variants contributing to a disease and the interactions among those variants also could influence the distribution of diseases among groups. The difficulty that has been encountered in finding contributory alleles for complex diseases and in replicating positive associations suggests that many complex diseases involve numerous variants rather than a moderate number of alleles, and the influence of any given variant may depend in critical ways on the genetic and environmental background.[17][23][24][25] If many alleles are required to increase susceptibility to a disease, the odds are low that the necessary combination of alleles would become concentrated in a particular group purely through drift.[26]

One area in which population categories can be important considerations in genetics research is in controlling for confounding between population substructure, environmental exposures, and health outcomes. Association studies can produce spurious results if cases and controls have differing allele frequencies for genes that are not related to the disease being studied,[27] although the magnitude of this problem in genetic association studies is subject to debate.[28][29] Various methods have been developed to detect and account for population substructure,[30][31] but these methods can be difficult to apply in practice.[32]

Population substructure also can be used to advantage in genetic association studies. For example, populations that represent recent mixtures of geographically separated ancestral groups can exhibit longer-range linkage disequilibrium between susceptibility alleles and genetic markers than is the case for other populations.[33][34][35][36] Genetic studies can use this admixture linkage disequilibrium to search for disease alleles with fewer markers than would be needed otherwise. Association studies also can take advantage of the contrasting experiences of racial or ethnic groups, including migrant groups, to search for interactions between particular alleles and environmental factors that might influence health.[37][38]

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