Recovery of Hunger Sensations Associated with Low Preprandial Blood Glucose: An Easy Exit from Diabetes?

Abstract

Background: Obesity, diabetes, asthma, autism, birth defects, dyslexia, attention deficit-hyperactivity disorder and schizophrenia have increased in children in the last half century. These increases may depend on the widespread, well known error in energy balance: the unremitting addition of fat at any will (decision) to eat. In most (60%) but not all people, the decision arises as conditioned before energy exhaustion of the energy available from previous meals. After meal suspension for few hours (up to 48 hours), healthy subjects identified the arousal of sensations of hunger that we named Initial Hunger (IH). After this identification, subjects distinguished IH from conditioned sensations before subsequent meals by mental comparison of the current arousal with the remembered IH. BG decreased to 76.6 ± 3.7 mg/dL and hunger sensations (Initial hunger, IH) arose spontaneously and corresponded to the complete exhaustion of the previous meals. Objective: Not Insulin Dependent (NID) diabetic people differ from fattening people in this: after meal suspension, they do not develop any hunger sensation nor the associated low blood glucose (BG). Methods: Meal suspension lets IH arise and after no arousal, reduction of energy intake. The two subjects consumed meals that provided at least 20 grams of animal protein and up to one kg of not-starchy vegetable (NSV) for 6 to 12 months. At reappearance of IH, we implemented an Initial Hunger Meal Pattern (IHMP). Results: We tried to implement IHMP training in two obese (BMI of 39 and 33) adults out of two consecutive recruitments of subjects who showed high fasting BG. We found an absence of BG decline to 76.6 ± 3.7 mg/dL and an absence of any hunger sensation after eating suspension. Both subjects lost 13% - 20% of their body weight and recovered 76.6 ± 3.7 mg/dL of BG and hunger sensations, i.e., went off diabetes. IHMP maintained the decreased body weight in the subsequent months. Conclusion: Diabetes develops for inveterate conditioned intake (when previous energy intake has not been fully exhausted before meals), excessive fattening (with presumed excessive post-absorption emission of fatty acids from fatty tissues), permanent loss of BG decline to 76.6 ± 3.7 mg/dL and permanent loss of physiological signals of hunger. A healthy, non-diabetic life may be recovered by painless loss of weight up to 20%. The body weight remained stable by implementing IHMP at reappearance of hunger sensations. This costs accurate energy intake planning instead of hunger endurance.