Why Doesn’t the Brain Lose Weight, When Obese People Diet?

Abstract

Objective: As has been shown recently, obesity is associated with brain volume deficits. We here used an interventional study design to investigate whether the brain shrinks after caloric restriction in obesity. To elucidate mechanisms of neuroprotection we assessed brain-pull competence, i.e. the brain’s ability to properly demand energy from the body. Methods: In 52 normal-weight and 42 obese women (before and after ≈10% weight loss) organ masses of brain, liver and kidneys (magnetic resonance imaging), fat (air displacement plethysmography) and muscle mass (dual-energy X-ray absorptiometry) were assessed. Body metabolism was measured by indirect calorimetry. To investigate how energy is allocated between brain and body, we used reference data obtained in the field of comparative biology. We calculated the distance between each woman and a reference mammal of comparable size in a brain-body plot and named the distance ‘encephalic measure’. To elucidate how the brain protects its mass, we measured fasting insulin, since ‘cerebral insulin suppression’ has been shown to function as a brain-pull mechanism. Results: Brain mass was equal in normal-weight and obese women (1,441.8 ± 14.6 vs. 1,479.2 ± 12.8 g; n.s.) and was unaffected by weight loss (1,483.8 ± 12.7 g; n.s.). In contrast, masses of muscle, fat, liver and kidneys decreased by 3–18% after weight loss (all p < 0.05). The encephalic measure was lower in obese than normal-weight women (5.8 ± 0.1 vs. 7.4 ± 0.1; p < 0.001). Weight loss increased the encephalic measure to 6.3 ± 0.1 (p < 0.001). Insulin concentrations were inversely related to the encephalic measure (r = –0.382; p < 0.001). Conclusion: Brain mass is normal in obese women and is protected during caloric restriction. Our data suggest that neuroprotection during caloric restriction is mediated by a competent brain-pull exerting cerebral insulin suppression.

Stress habituation, body shape and cardiovascular mortality

“…Thus, updating the probabilities of the competing hypothesis with the help of Krieger's data gave a huge boost to the brain-pull hypothesis. Adding further evidence from experiments using state-of-the-art technology, including magnet resonance imaging and spectroscopy (Peters et al, 2011;Kubera et al, 2013;Oltmanns et al, 2008;Goodman et al, 1984;Muhlau et al, 2007) and positron-emission-tomography (Kuzawa et al, 2014), more and more increased the likelihood of the brain-pull hypothesis being true. Now, that the conventional view advocating the null hypothesis has become increasingly unlikely, it seems promising to look at the 'obesity paradox' observations in the light of brain-pull mechanisms.…”

Rise in Plasma Lactate Concentrations with Psychosocial Stress: A Possible Sign of Cerebral Energy Demand

“…We have recently shown that a competent brain-pull, i.e. the brain’s ability to properly demand energy from the body, functions to preserve brain mass when obese people diet [3]. By contrast, an incompetent brain-pull will lead to build-ups in the cerebral supply chain culminating in obesity and type 2 diabetes [2].…”

Glucagon-like peptide-1 analogs against antipsychotic-induced weight gain: potential physiological benefits

“…To our knowledge, weight loss has not been associated with changes in brain volume. In the available study addressing this issue, only global brain volume was assessed [63], thereby rendering the possibility that weight loss may still have a regional effect on brain volume. Nevertheless, some of the cognitive deficits associated with elevated BMI (that is, memory and attention/executive functioning) may be reversed after intentional weight loss [64].…”