The Fetal Origin of Coronary Heart Disease


dr_duane_graveline_m.d._134By Duane Graveline, MD, MPH

For hundreds of millions of people with heart disease, hypertension and type 2 diabetes, their condition was completely preventable, requiring only improvement in the nutrition of girls and young women.

Babies that are born thin tend to be insulin resistant as children and adults, and are therefore liable to develop insulin resistance syndrome. The apparent severity of their diabetes in the face of elevated insulin levels will greatly frustrate their doctors.

Babies that are born short and fat are thought to be the result of increased maternal blood sugar, with consequent imbalance in the supply of glucose and other nutrients to the fetus, correlating with increased risk of coronary disease as adults.

Studies show that babies whose placentas are disproportionately large in relation to their birth weight tend to have elevated blood pressure as adults. This observation is supported by extensive studies in animals and is believed to correlate with under-nutrition, an adaptive response to extract more nutrients from the mother.

Despite the strong support for epigenetics derived from animal research, this concept has been slow to catch on in clinical application and still rankles many because the mechanism, at least in humans, remains obscure.

Making alterations in the precisely controlled diet of experimental mice that will induce diabetes or cancer in adult mice is one thing. Implying a similar mechanism for coronary artery disease in adult human males is something else entirely, say the critics, so acceptance has come slowly.

But acceptance has caught on in major teaching institutions and is accelerating. The genes that control chronic diseases are now much better understood and the evidence is indisputable—much of hypertension, heart disease and diabetes is brought on by nutritional factors in pregnant women. We need far more emphasis on the importance of proper diet during pregnancy.

Now that a causal relationship has been shown to exist between selected measurements at birth and chronic disease later in life we should be able to discover those gene – environment interactions that reduce this risk of chronic disease.  The tenets of epigenetics—that poor fetal growth and small size at birth are followed by increased risk of coronary artery disease, stroke, hypertension and type 2 diabetes—are now espoused by doctors and research scientists worldwide.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

Recommended reading:

1 Barker DJP, Osmond C, Winter PD, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet 1989;ii:577–80.

2 Barker DJP, Fall C, Osmond C, et al. Fetal and infant growth and impaired glucose tolerance. BMJ 1991;303:1474–5.

3 Law CM, Shiell AW. Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature. J Hypertens.1996;14:935–41.

4 Barker DJP. Fetal origins of coronary heart disease. BMJ 1995;311:171–4.

5 Harding JE, Johnston BM. Nutrition and fetal growth. Reprod Fertil Dev1995;7:539-47.

June 2013


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