Can we control the genetic information we pass on to our children?

NathanEvery parent wants to provide whatever they can to help their child grow up happy and healthy. Most people will immediately think of things like a safe place to live, healthy food to eat, a good education, and so on. However, the very first thing that a parent provides is something much more fundamental: the genes that determine the biological makeup of their child. As I have written about before in this blog post, our gene DNA sequences determine the functions of the proteins, cells, tissues and organs that biologically define us. But we can’t change our DNA sequences (at least not yet, though maybe one day it will be possible through genome editing technology such as CRISPR/Cas9), so is there any way of controlling the genetic information we pass on to our children?

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Your blood can reveal your risk for heart disease

Researcher at CERG, Anja ByeWhen you visit your general practitioner you can get your blood analyzed for cholesterol and triglycerides, to get an idea of your risk for cardiovascular disease. With additional information about BMI, smoking habits and blood pressure, this can be used to calculate your 10-year risk for cardiovascular disease. There are several risk prediction calculators available today that general practitioners can use the before they give advice and prescriptions to their patients. This risk calculators predicts the 10-year risk for dying form cardiovascular disease, and includes information on age, gender, smoking habits, systolic blood pressure and total cholesterol.

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Cas9: the gene hacker that bites DNA

Jose Bianco MoreiraEvolutionary pressures forced all living species to adapt to challenging and hostile environments. Giraffes developed long necks that enable them to reach more food on top of trees, birds can fly to escape dangers from ground level and humans became smart enough to domesticate their previous predators. These characteristics evolved over millions of years as a result of random DNA mutations, which somehow conferred survival advantage to an organism that would then pass this “good mutation” to the next generations. Although these DNA alterations (mutations) are necessary for the evolution of species, their random nature sometimes gives rise to unwanted characteristics. This is the case of genetic diseases that have haunted humanity for centuries.

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We hear about them all the time, but what is a gene?

Nathan ScrimeourWe hear about them all the time – this gene causes a disease, or that gene is important for normal heart function. Most people could tell you that your genes are made of something called DNA, that you inherit them from your parents and pass them on to your children, and that they determine much of who you are and what you look like. But how do we get from genes to an entire organism, and what control do we have over our genes?

To answer these questions, we need a basic understanding of what is known as the “central dogma” of biology, which describes the one way flow of genetic information. While the reality is more complex than this, the flow can be simplified as such:

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What is your cholesterol? – Know your number!

Elisabeth Vesterbekkmo. Foto: BERRE ASFamilial Hypercholesterolaemia (FH) is the most common of all severe familial disorders and its hallmark is high LDL-cholesterol in plasma. The disease is carried by one out of 200-300 persons in Europe – that is to say a total of about 2 million people in Europe carry FH. The disease is present from early childhood, but is carried without symptoms until the third or fourth decade in life, when heart disease will appear. If untreated, 50 percent of men will have had their first heart attack before the age of 50 years, and women before 55 years. To carry FH is to carry a ticking bomb that, if untreated, will cause cardiac disease or death.

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Why do some people get fitter than others?

Two women running outdoorThe response to exercise training is often described in general terms, with the assumption that the group average represents a typical response for most individuals. However, in reality, it is more common for individuals to show a wide range of responses to identical exercise programs. In 1999, a large study published by Claude Bouchard and colleagues, reported that 20 % of us show little or no gain in maximal oxygen consumption (VO2max) with exercise training. This is a concern, since a high VO2max is associated with decreased rates of cardiovascular morbidity and mortality. Exploring the phenomenon of high responders and low responders following the same exercise program may provide helpful insights into mechanisms of training adaptation and methods of training prescription.

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Genetics and cardiovascular disease

Picture of DNAIn Western world, cardiovascular disease (CVD) is among the leading cause of premature death and a major cause of disability. Over the years, the knowledge of CVD risk factors clustering and their multiplicative interactions to promote CVD risk has led to the development of multivariable risk prediction algorithms to use in primary care settings. The guidelines for CVD prevention recommend that an individual’s risk of CVD is estimated by combining different risk factors into a numeric estimate of risk. Most of these risk prediction algorithms include well-known CVD risk factors such as: age, sex, hypertension, cholesterol, smoking, family history of CVD and diabetes mellitus. A variety of risk prediction algorithms are available, as charts, tables, computer programmes, and web-based tools.

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Tailored exercise for your DNA

DNA blåLes dette innlegget på norsk her!

Several research reports state that our genes play an important role in how each of us responds to different types of exercise. The first major study that showed variation in training response was published in 1980. In this study, 720 individuals participated in a training program that lasted five months, and the researchers measured the maximal oxygen uptake (the best measure of fitness) before and after the exercise period. Surprisingly, they saw a huge difference in changes of oxygen uptake. A few actually decreased while others increased tremendously.

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Er vi fanget av genene våre?

Foto: Geir Mogen

Den varslede epidemien av overvekt og fedme er over oss med full kraft og over 1 million nordmenn er i dag overvektige mens tallet på verdensbasis har passert 1.4 milliarder. Det er veldig usannsynlig at forandring i gener har bidratt til den eksplosive utviklingen, men bak tallene er det samtidig store individuelle forskjeller. Mange opplever at de legger på seg lettere enn andre uten at man ser en opplagt årsak. Faktisk er den arvelige komponenten til overvekt estimert til å være på mellom 40-70 % og bare et enkelt gen kan gjøre at et individ lagrer 200 ekstra kalorier per dag og øker risikoen for fedme med 20-30 %.

Men arv og miljø opererer sjelden uavhengig av hverandre og denne uka ble det publisert en stor studie som bidrar ytterligere til vår forståelse av hvordan det komplekse samspillet mellom gener og livsstil påvirker risikoen for overvekt. Over 12.000 amerikanske kvinner og menn deltok i studien som er publisert i anerkjente Circulation. Hos disse identifiserte forskerne hele 32 såkalte «fedmegener», dvs. genetiske varianter som man vet disponerer for overvekt, og de kalkulerte ved hjelp av disse en samlet genetisk risikoprofil for hver enkelt deltaker. Dette var relativt vanlige gener som de fleste av oss bærer med oss i større eller mindre grad, ikke sjeldne genmutasjoner man ser i enkelte tilfeller av sykelig overvekt. Deltakerne ble fulgt opp i to år og som forventet økte vekten proporsjonalt med hvor genetisk disponert de var.

Når forskerne gikk dypere i materialet og undersøkte effekten av fysisk aktivitet og inaktiv tid på fedmerisikoen oppdaget man derimot samspillet mellom gener og aktivitetsnivå var av stor betydning. Stillesitting, målt som antall timer deltakerne oppga å se på TV hver dag forsterket effekten av genetisk disposisjon for fedme betydelig. Innflytelsen av genene alene var 50 % høyere for de som satt fire timer eller mer foran skjermen daglig. Den gode nyheten var derimot at et relativt moderat nivå av fysisk aktivitet på fritiden i betydelig grad reduserte effekten av fedmegenene.

Forskerne estimerte at forskjellen i vektoppgang mellom de som var maksimalt heldige med genene (ingen genetisk disposisjon for overvekt) og de som var maksimalt uheldige (hadde alle kjente genetiske disposisjoner) ble halvert for hver time daglig gange, eller hver halvtime med jogging. På den andre siden økte forskjellen med 25 % for hver andre time deltakerne tilbragte i sofaen.

Altså er det særlig viktig, hvor urettferdig det enn høres ut, å redusere stillesittende aktivitet og øke fysisk aktivitet for de som er arvelig disponert for overvekt. Akkurat hvordan fysisk aktivitet overvinner effekten av fedmegenene vet man ikke i detalj, men mye tyder på at regelmessig fysisk aktivitet trigger forandring i genuttrykk slik at de helsefremmende blir mer aktive mens man undertrykker de som er relatert til vektoppgang. Det er også verdt å merke seg at betydningen av stillesittende TV-tid og fysisk aktivitet var uavhengig av hverandre, altså var begge deler innflytelsesrike faktorer.

Vi kan altså ikke forandre genene våre, men det ser ut til at vi i stor grad kan påvirke innflytelsen de har på oss. Derfor er det beste rådet fortsatt, uansett genetisk utgangspunkt, å følge helsemyndighetenes anbefalinger for kosthold og fysisk aktivitet, samt redusere tiden foran tv-en.

Skrevet av Bjarne Nes, Stipendiat CERG.