When Doctors say “It’s genetic”, they are often wrong

Dr Sundhya Raman
7 min readMar 3, 2021

People often think that their high blood pressure/diabetes/cholesterol is something they inherited from a parent.

And doctors will re-affirm that these things are genetic.

But they are most usually wrong.

What they mean in most cases is that it is ‘epigenetic’

I am not being pedantic. The reason that this matters is that our genetic code is fixed. But our epigenetics can be altered by our behaviours. The majority of those illnesses we – and often even our doctors – think of as being ‘genetic’ are not.

They are within our control!

‘Epigenetics‘ explains a great deal about why we all have different risks of disease, as well as how and why we can shift that risk through our behaviours.

To explain what epigenetics is, let me take you on a brief tour of

1) the life of honey bees, and

2) a tale from World War II

I promise they are both relevant to epigenetics!

The humble honey bee

Honey bees live in colonies with a very specific social structure.

They are composed of a single fertile ‘queen’, a few thousand male ‘drone’ bees who’s sole function is to mate and then die (imagine that!), and tens of thousands of sexually sterile female ‘worker’ bees who pretty much do everything; care for the young bee larvae, clean and guard the hive, forage for food and make beeswax and honey.

A queen bee will place an egg in each cell of a honeycomb. If the egg is fertilised it will become a female, if it is unfertilised it will become a male.

So what have honey bees got to do with epigenetics?

Humour me for a bit longer.

The most remarkable thing is what differentiates the queen bee from all of the other female bees. It all comes down to what she is fed.

Whilst all the baby larvae are fed royal jelly for 3 days, after this it is ONLY the queen-to-be that is fed exclusively on royal jelly.

She becomes much bigger than the other bees, she has a sting that is smooth, and most significantly she develops functioning ovaries and thus becomes the only fertile female amongst her sisters.

So whilst every female bee is genetically the same, mothered by the same queen bee, some of the genes become activated in the single larva that has been selected to become a new queen. In other words, the environment (feeding the larva royal jelly) made it look different, behave differently and have different abilities.

What is also amazing is that if the queen is somehow lost to the hive, some of the usually sterile worker bees become fertile – an external event (Queen absence), influences an internal, reproductive capability (fertility).

How?

Hongerwinter

It is September 1944 and a military operation codenamed ‘Operation Market Garden’ is underway. Despite declaring itself neutral from the onset of the conflict, the Netherlands has been occupied by Nazi Germany since May 1940.

The German occupation had begun relatively peaceably, but as the long war rages on, the Dutch are asked to make greater and greater sacrifices to their invaders.

Operation Market Garden aims to liberate nine bridges in Nazi-occupied Netherlands to create a route for the Allied forces to invade Germany via it’s Northern border.

The operation is a mixed success; the South of the country is liberated, however the forces are unable to secure a bridge across the river Rhine into Northern Germany.

From a scientific point of view however, what ensues has been a game changer in our understanding of genetics and human physiology.

The densely populated Northern and Western parts of the country experienced what is known in Dutch history as the ‘Hongerwinter’ (Hunger Winter); German blockade of food supplies and an early and severe winter which froze food transport via canals led to a famine in the region.

Food rations fell to under 1000 calories per day, and as low as 580 calories in the mid-winter.

The famine ended in the spring of 1945 when the Germans surrendered to the Allied forces.

But the Hongerwinter is a unique example of famine occurring in a modern, developed country, where an entire geographical population experienced a single period of malnutrition in the context of an established healthcare system.

After the famine, records were kept of birth weights and other health measures, and this meant that decades later the repercussions of this discrete event on the population have been well studied.

In particular we now know that if mothers were in their second or third trimester of pregnancy during the Hongerwinter, their babies were born small.

This makes sense because babies do most of their growing in the womb towards the latter part of pregnancy and since their mothers were starving they didn’t have the resources to grow to their full potential in the womb.

For babies who were conceived during the Hongerwinter the story was different.

These babies who‘s mothers were only starved in the first trimester of pregnancy were born a normal birth weight.

Again this makes sense given that a foetus’s growth happens during the latter part of pregnancy.

But when all of these babies were followed up over the next several decades a surprising finding emerged.

The small babies remained small despite a normal food environment for the next several decades of their lives. What is more, they had lower rates of obesity than the general population.

Four Generations of the Hongerwinter Study. Source (hongerwinter.nl/onderzoek/?lang=en)

The later conceived, normal birthweight babies however had the opposite effect; although at birth they appeared healthy, as time went on they had higher rates of obesity, higher fat levels in their blood, higher rates of schizophrenia and they died at a younger age than average for the population.

Even more remarkable, whatever happened to change the health outcomes of these two sets of babies continued into their children – the next generation inherited the same protection and risks! How could this be and why?

The answer lies in a whole new field of understanding how our genes work called ‘epigenetics’.

This environmental control of genes is what we call ‘epigenetics’ and it explains how living things adapt to short term changes in the environment.

Our genetic code is very stable and takes a huge amount of time to change -thousands of years. So how do we make the frequent changes we need to survive in environments that alter at a more rapid rate than this?

We can differ in how we switch on and off our genes by our behaviours, but also it seems by the information we gain from our mothers and grandmothers about the likely environment we are born into.

The types of food we eat, the amount we sleep, the amount of exercise we take, whether we smoke, our stress levels – these can all lead to little tags being added to our genes saying ‘I can be switched on’ or ‘I’m not available’.

Why is this the case?

In the case of honey bees, their survival depends on co-operating as a group. They need to make sacrifices for the greater good of the hive.

In the second scenario, genes that suggested that there was a shortage of food and more fat needed to be stored may have been activated in the baby to improve their survival.

What does this mean for us now?

When we see that some illnesses like diabetes and high blood pressure ’run in families’ it is sometimes because of the genetic code. But far more often it is not the code itself but the tags that have been added to the codes.

In practice this means that we can alter our risk of disease by giving different signals about the outside environment to our DNA.

We would be doing this for ourselves, and also for our children and grandchildren.

What superheroes we are!

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Dr Sundhya Raman

Co-founder of My Wellness Doctor (www.mywellnessdoctor.co.uk) Lifestyle Medicine Physician, Scientist, Parent, Gardener, Foodie.