We keep talking about the growing epidemic of obesity with its long term risks of hypertension, cholesterol, diabetes, heart disease and cancer to name just a few. Interesting research has shown that there is a link between maternal smoking and obesity.

The mechanism of this link is not known, but we do know that maternal smoking affects the fetus in several ways.

Nicotine that is inhaled causes narrowing of the blood vessels in the placenta and that leads to under perfusion which means less blood flow and less nutrients and oxygen flowing to the fetus. Carboxyhemoglobin which is increased in smokers also reduces tissue oxygen in the fetus.

Nicotine also suppresses the mom's appetite leading to poor nutrition in the mom and the fetus. In fact, these babies are smaller at birth. But it is as if the physiology of the baby adapts and has impacts later in life that leads to other behaviours. Low birth weight is associated later in life with obesity.

Nicotine is also known to affect the growth and activity in the brain and the peripheral nervous system. This study looks at mechanisms specifically related to nicotine and the brain.

There are nicotinic receptors in the brain and nicotine gets into the fetal circulation and nicotine stays in the fetal circulation for a long time. As a result it can affect the developing brain leading to outcomes later in life. These nicotine receptors modulate neural activity. It is believed that this is what leads to an alteration in the reward system of our brain.

Why some crave dietary fat is complex to understand. Eating behaviour can be looked as an addictive behaviour not dissimilar to craving drugs. Mechanisms in the brain structure help maintain energy balance. As well so called reward related mechanisms in the brain processes how we in a sense relate to food independent of energy status and what we need. This area also processes the responses to illicit drug use.

Research has show that maternal smoking is related to faster weight gain during late puberty. It is also associated with an increased rate of experimentation with drugs of abuse in childhood, adolescence and adulthood. A Canadian study published in this week's Archives of General Psychiatry looked at 378 adolescents studied in late puberty in whom fat intake was assessed as well as assessment of the brain reward system including an area called the amygdala.

Exposure was defined as a mother who smoked more than 1 cigarette daily during the second trimester. Non exposure was no smoking 1 year before and then throughout the pregnancy.

Exposed offspring weighed more than non-exposed and showed a higher inttake of fat. Exposed participants had differences in their MRI studies. They had smaller amygdala volume.

Exposed offspring showed higher alcohol use and drug experimentation but not cigarette smoking. These behaviors did not match up with the amygdala volume so the pathway that drives this outcome may be different. So perhaps there might be a different area of the brain that can be stimulated.

Knowing this, it becomes important to educate these children at risk about better food choices.