The researchers say in fact that what children were eating in those days before primary school has more of an effect than the chicken nuggets they ate at lunchtime.
The researchers from the Institute of Education, at the University of London say they have found that children who ate a diet of junk food at the age of three, made less progress in school between the ages of six and ten.
Junk food was defined as highly processed foods, 'take-aways' and foods high in fat and sugar, such as crisps, sweets and fizzy drinks.
The researchers say the 25% of children who ate the most junk food at age three were 10% less likely to achieve the expected levels of improvement between the ages of six and ten, compared with the rest of the children.
They say children ™s diet at later ages appears to have less impact on their school attainment.
The research is based on detailed information from the 'Children of the 90s' study, which has been following the development of 14,000 children since birth in 1991-2, which allowed researchers to adjust the statistics to take account of factors such as low income or poor housing.
The researchers say even after adjustments were made for such factors, the association remained between poor diet at three and comparatively slow progress at school several years later.
Researcher Dr. Pauline Emmett says they are confident that this is a robust association which indicates that early eating patterns have effects that persist over time, regardless of later changes in diet.
Dr. Emmett says it is therefore very important for children to eat a well-balanced diet from an early age if they are to get the best out of their education.
The research is published in the Journal of Epidemiology and Community Health.
Another animal model is providing insight into the impact of early life stressors or low socioeconomic status on cardiovascular disease. Research again found that, as with people, these animals have normal blood pressure as pups. But as stressed adult rats, they have higher pressure increases and a delayed recovery unless they are missing an endothelin receptor gene. "It cures it," says Dr. Jennifer Pollock. "This early life stressor is being mediated through the endothelin pathway." Her postdoctoral fellow, Dr. Analia Loria, found these early life stressor models also have more constrictive blood vessels because they are more sensitive to angiotensin. New studies will further test the endothelin connection and see if a high-fat diet makes things worse by increasing oxidative stress.
Wildlife biologists have found naturally occurring models. Rat pups whose mother builds a nest far from a food source and so must be gone foraging several hours each day, are more anxious. Neurobiologists have shown animals separated from their moms for long periods can't run through mazes well and tend to back off in competition for food, Dr. Jennifer Pollock says. "We took that to mean their blood pressure could also be hyper reactive. Sure enough, that is what we found."
"This has a lot of implications for earlier detection of risk-increasing environmental exposures and what you can do about it," says Dr. Treiber, a clinical child psychologist and program project leader. "If you can't alter the environment that quickly in life, you know now where they are headed and maybe you can preempt it pharmacogenetically."
In the diverse group of some 600 young people he's been following for 17 years, Dr. Treiber has found that, as with the general population, some already are obese and/or hypertensive at the average age of 25. He'll continue to follow and annually assess them over the next five years in an effort to better understand how stress contributes to hypertension. "What we are doing is looking at chronic environmental stress in combination with some bad candidate genes that are stress activated," says Dr. Treiber. He's thinking that, as with rats, genetic predisposition and stress can doom people with normal pressures to hypertension. They'll look at blood pressure reactivity, recovery, sodium secretion, measure the footprints left by oxidative stress and the levels of the stress hormone cortisol. They'll look at early indicators of cardiovascular disease, such as enlargement of the pumping chamber of the heart and signs of carotid artery disease. "If you have a tendency to have high blood pressure or if you are obese, we can see the inner layer of the carotid getting thicker than normal people your age," says Dr. Gaston Kapuku, cardiologist and cardiovascular researcher at the Georgia Prevention Institute and a project core leader.
America's current obesity and type 2 diabetes epidemic also has them looking at insulin, glucose and cholesterol levels and whether fat exacerbates all the factors they are following, which they believe it does.
One reason the Georgia Prevention Institute was founded was to identify risk factors for cardiovascular disease, says Dr. Harshfield. In his 10 years at the institute, the agenda has shifted from looking at precursor development of adult hypertension to identifying mechanisms causing pediatric hypertension, a disease that didn't exist when most hypertension textbooks were written, he says.
"Our ultimate goal, of course, is prevention," he says. "But when we can't do that, we want to give physicians ways to determine precisely the cause or causes of your hypertension and optimal ways to target your disease."
The MCG Department of Biostatistics, chaired by Dr. Varghese George, is designing the studies for the Program Project grant to ensure scientifically validity and managing data for all the program projects.
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