Does Diet Influence the Retinal Microvasculature in Children?
To the Editor:
The retinal microvasculature is anatomically and physiologically similar to the cerebral microcirculation, and may thus serve as a surrogate marker for small vessel disease in the brain that predisposes people to the development of stroke.1 The recent article by Kaushik and associates reports that higher glycemic index and lower cereal fiber diet are associated with stroke mortality in persons 50 years and older.2 An interesting finding was that 50% of this association was explained by a corresponding association between high glycemic index and low cereal fiber diet with larger retinal venular caliber, suggesting that the relationship of diet and stroke may be partly mediated by the microcirculation. This is further supported in another analysis of the same cohort in which decreased fish consumption was shown to be associated with similar retinal vascular caliber changes and stroke risk.3
A high glycemic index and low cereal fiber diet may contribute to vascular dysfunction through the formation of advanced glycation end products. However, many systemic diseases (eg, diabetes, hypertension) and eye diseases (eg, diabetic retinopathy, glaucoma) can also affect the state of the retinal microvasculature, and their influence cannot be completely controlled for by statistical modeling.2 Studying the retinal microvasculature in healthy children minimizes confounding by these systemic factors and is therefore an ideal approach for assessing the physiological influence of diet on the microcirculation. We analyzed the relationship between dietary factors and retinal vascular caliber in 823 healthy Singapore Chinese schoolchildren aged 12.8 (±0.8) years who underwent retinal photography and computerized measurement of retinal vascular caliber similar to Kaushik et al.4 Diet was assessed by interviewers using a validated semiquantitative food-frequency questionnaire adapted for teenagers.5 Linear regression models were constructed to assess the association of dietary constituents with retinal vascular caliber, after adjusting for age, gender, body mass index and mean arterial blood pressure. The results revealed no significant associations between any of the dietary constituents, including fiber and sugar intake, and retinal arteriolar or venular caliber (Table).
Our findings in Singapore Chinese teenagers appear to contrast with Kaushik et al’s study in older white adults and suggest that the microvascular effects of diet may be evident only in later life. This would be consistent with a possible cumulative dose-dependent effect of diet on the retinal vasculature over time. Clearly, additional studies are needed to verify our hypothesis. Further prospective evaluation of our cohort may shed more light into these mechanisms.
Baker ML, Hand PJ, Wang JJ, Wong TY. Retinal signs and stroke: revisiting the link between the eye and brain. Stroke. 2008; 39: 1371–1379.
Kaushik S, Wang JJ, Wong TY, Flood V, Barclay A, Brand-Miller J, Mitchell P. Glycemic index, retinal vascular caliber, and stroke mortality. Stroke. 2009; 40: 206–212.
Cheung N, Tong L, Tikellis G, Saw SM, Mitchell P, Wang JJ, Wong TY. Relationship of retinal vascular caliber with optic disc diameter in children. Invest Ophthalmol Vis Sci. 2007; 48: 4945–4948.