We thank Dr. Ross (1) for her comments on our recent paper on cognition and type 1 diabetes (2). We agree that many questions remain open with regard to the etiology underlying impaired cognitive performance in patients with type 1 diabetes.
Although it seems clear that the underlying pathophysiology is a multifactorial process, the exact nature and the relative contribution of different underlying mechanisms is not yet understood. Indeed, outside the field of diabetes, there is growing evidence for a possible protective role of long-chain polyunsaturated fatty acids (LCPUFAs) on cognitive function (3). However, until now the possible role of altered fatty acid profiles on cognition in type 1 diabetic patients has not been systematically investigated and, as such, was beyond the scope of our meta-analysis. The profile of cognitive disturbances (e.g., reduced overall cognitive performance and lowered processing speed) in middle-aged persons with lowered intake of ω-3 LCPUFAs (3) resembles the cognitive pattern described in our meta-analysis (2).
Still, one has to notice that this cognitive profile is not unique for lowered levels of LCPUFAs but has, for example, also been described in studies addressing cognitive performance in normal aging (4). Therefore, the possible protective role of LCPUFAs warrants further investigation.
A first step would be to examine the relation between LCPUFA levels, as well as other potentially relevant etiologic factors that are discussed in our review (2), and impaired cognition in patients with type 1 diabetes. Considering the limited effect sizes of cognitive impairments found in our meta-analysis and the relatively large interindividual variation, this will require large, preferentially prospective, population-based study designs. Also, highly sensitive neuropsychological tests should be used in order to detect even subtle cognitive changes.
