Contents | eMJA Home     

Med J Aust 2000; 173 Suppl 7 August: S11-S12

Although atherosclerosis usually causes clinical complications such as myocardial infarction or stroke in middle or older age, it is now clear that the disease process actually starts in the first decade of life. Children may develop fatty streaks in their aortas from as young as four years of age, and even in the coronary vessels before age 10 years. In an American urban population, 65% of children aged 12-14 years had fatty streak lesions, while an additional 8% had lesions typical of more advanced atherosclerosis.⁷² These advanced lesions are of particular concern, as they are less easily reversible by risk factor reduction.

The major cardiovascular risk factors can all begin in childhood. These include high cholesterol levels, active or passive smoking, diabetes, obesity, high blood pressure, and a genetic predisposition (positive family history). In 1985, a multicenter cooperative study, the Pathobiological Determinants of Atherosclerosis in Youth (PDAY), was initiated to study the natural history of atherosclerosis, its relationship to risk factors, and the pathobiology of lesion development.⁷³ Pathology laboratories in nine centres collected arteries and tissues from over 2000 persons aged 15-34 years whose deaths were attributed to homicides, accidents, or suicides. Arteries were evaluated for lesions, and risk factors, including serum lipoproteins, serum thiocyanate (smoking), glycohemoglobin (diabetes), thickness of panniculus adiposus (obesity), small renal artery changes (hypertension) and apolipoprotein isoforms (cardiovascular risk), were analysed in a central laboratory. Results from this study have clearly shown that the recognised major risk factors for coronary heart disease are all associated with lesion development in the arteries of these young subjects. Moreover, the risk factors tend to multiply against each other to amplify disease progession. Studies such as this provide strong justification for reducing risk factors in young people.^74,75

Environmental risk factors (poor diet, lack of exercise, obesity, smoking) are at least as prevalent in our young as in other First World countries such as the United States. Many lifestyle habits are established in childhood and adolescence, such as smoking, establishment of a routine level of exercise and dietary preferences. Many of these habits can interact to compound risk. For example, excessive consumption of high-fat processed or fast foods, along with a lack of exercise, may often lead to obesity in children (which is related to hyperlipidaemia), and later to hypertension, diabetes and thereby to atherosclerosis itself. Educating children and parents about the importance of exercise, avoiding smoking and a balanced diet is therefore an important component in primary prevention of cardiovascular disease.⁷⁶ It should be emphasised to parents that passive smoking is also a risk factor for cardiovascular disease.⁷⁷ For children, a balanced diet should include all of the essential food groups to ensure that normal development is supported. Many nutritional studies show that populations that consume more fresh fruit and vegetables tend to have lower rates of cardiovascular disease. Energy requirements should be provided mainly by foods high in complex carbohydrates rather than those high in sugar or fat.

Children in high-risk families, with established early atherosclerosis in close family members, should be screened early. For instance, children from families with diagnosed familial hypercholesterolaemia could be screened from the age of six years. Blood pressure checks at about 18 years of age are recommended if there is a family history of hypertension. In all young people, education about smoking, diet and exercise in primary school and reinforcement at secondary level is important. Children suspected of being overweight should be screened for obesity at 8-10 years of age to indicate any deviation from a normal body mass index, and the screening process should incorporate alert and alarm levels for active intervention.

Several other potential risk factors and markers for disease are the subject of ongoing studies, but are presently at a stage too premature for use in routine testing. These include hyperhomocysteinemia, which shows a strong positive correlation with risk of atherosclerosis,⁷⁸ and folate supplementation, which can lower plasma homocysteine levels. Despite the overwhelming evidence suggesting homocysteine as a significant risk factor, only very recently have studies started to look at whether folate can prevent morbidity and mortality from cardiovascular disease in patients with hyperhomocysteinemia. While some preliminary results indicate that folate therapy may be effective in lowering plasma homocysteine levels and in delaying development of atherosclerosis,⁷⁹ longer-term studies are essential both to extend these findings and to establish the safety of long-term folate treatment, especially in the young.

   to next question...

Readers may print a single copy of these pages for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company
Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>".

<URL: http://www.mja.com.au/> © 2000 Medical Journal of Australia.