There is evidence that the brain favors consumption of carbohydrates (CHO) rather than fats, this preference resulting in glycolysis-based energy metabolism domination. This metabolic mode, typical for consumers of the “Western diet” (Cordain et al., 2005; Seneff et al., 2011), is characterized by over-generation of reactive oxygen species and advanced glycation products both of which are implicated in many of the neurodegenerative diseases (Tessier, 2010; Vicente Miranda and Outeiro, 2010; Auburger and Kurz, 2011). However, it is not CHO but fat that is often held responsible for metabolic pathologies. This paper, based on analysis of experimental data, offers an opinion that the obesogenic and neurodegenerative effects of dietary fat in the high-fat diets (HFD) cannot be separated from the effects of the CHO compound in them. Since this is not a comprehensive literature review, only essential research results are presented. It is general knowledge that the glucose homeostasis possesses very limited buffering capacities, while energy homeostasis in its fat-controlling part enjoys practically unlimited energy stores. Logically, a control system with a limited buffer should thoroughly defend the “consumption” part. Indeed, existing experimental data (briefly reviewed here later) show important properties of the CHO intake control that is different from or not shown for the fat intake control: (1) A mere oral sensation of CHO elicits physiological anticipation response (cephalic phase) that is either inborn or rapidly conditioned. (2) Oral CHO sensation stimulates reward-specific brain areas. (3) CHO addiction is essentially similar to typical drug addictions. These peculiarities can explain the physiologically and metabolically opposite effects of obesogenic HFD versus the ketogenic diet (KD), which is also HFD but lower in CHO.
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Tanya Zilberter (2011) studied this question.
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