| Summary: | The effect of glucose on memory has been investigated for in excess of 25 years, with some consensus generated amongst the literature indicating that glucose has a facilitating effect. However, the robustness of the glucose effect has been questioned, with a considerable body of evidence reporting no glucose facilitation of memory. It has been suggested that glucoregulatory control may be a key mediating factor of the glucose effect. Glucoregulatory control and cognitive functioning are intrinsically linked, with cognitive impairments a common feature in populations presenting with poor glucoregulatory control such as diabetics, Alzheimer‘s disease sufferers, schizophrenics and the elderly. Although again the evidence has proven contradictory, with evidence to suggest that both better and poorer glucoregulators are more / less susceptible to the glucose effects on cognition. Verbal declarative memory has been reported to be the most reliably enhanced aspect of memory to benefit from a glucose effect. However, it is not yet clear whether verbal declarative memory as a whole is being facilitated, or whether the different phases of memory (encoding, consolidation, retrieval etc.) are differentially targeted. Consequently the primary aim of this thesis was to evaluate the effect of glucoregulatory control and glucose, on the different phases of verbal declarative memory. This was achieved through the use of novel paradigms employed previously within the cognitive sciences literature. Chapter 2 addressed a secondary aim of this thesis; investigating the current gap in the literature pertaining to the effect of glucose administration on cognition in children. Chapter 3 investigated the types of recognition (recollection and familiarity) that were made subsequent to a glucose load, using the 'remember/know' paradigm. Chapter 4 investigated encoding efficiency during the item method directed forgetting paradigm, in which participants actively attempt to forget specific stimuli through cessation of encoding. In chapters 5 and 6 the potential mediation of inhibition processes was explored, with both semantically related (Retrieval Induced Forgetting paradigm) and orthographically similar but semantically unrelated stimuli (Memory Blocking Effect paradigm). The tentative evidence presented in this thesis indicates that glucoregulatory control may mediate the glucose facilitation effect during the encoding phase, with better regulators seemingly benefiting from greater encoding benefits than poorer following glucose. Glucose was not observed to influence inhibition processes, or types of recognitions made. However, better glucoregulators exhibited more efficient adaptive inhibition (overcoming inhibition of blocking items to continue searching the lexicon and increased inhibition of semantically related competing stimuli). Administration of glucose did not mediate cognition in children, with the exception of an impairment of performance on a challenging reaction time task following 20 g of glucose. Memory phases are seemingly differentially affected by glucose administration, with the effect mediated by glucoregulatory control. Utilising the paradigms employed here (or similar) to investigate a range of populations presenting with cognitive decline/glucoregulatory control, would further allow the glucose and glucoregulatory effects on the different phases of memory to be further disentangled.
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