Altered neural inhibition responses to food cues after Roux-en-Y Gastric Bypass.

BACKGROUND: Roux-en-Y gastric bypass (RYGB) surgery is a highly effective weight-loss intervention that often reduces preference and intake of high-energy foods. Research into the neural mechanisms behind this shift has mainly focused on reward processing of food cues. However, the ability to successfully control food intake and thereby weight-loss also depends on inhibitory control capacity. We investigated whether RYGB leads to alterations in neural inhibitory control in response to food cues. METHODS: A food-specific go/no-go task with pictures of high-energy (desserts) and low-energy foods (vegetables), was used to assess neural inhibition responses before and after RYGB with functional magnetic resonance imaging. Data from 18 morbidly obese patients (15 females; age 41 ±â€¯11 years; BMI 42 ±â€¯4 kg/m2 before; BMI 36 ±â€¯4 kg/m2 after) were analysed. Pre- and post-RYGB BOLD fMRI responses were compared for response inhibition towards high- and low-energy foods. Participants were tested in a satiated state. RESULTS: Response inhibition to high-energy foods was associated with increased activation of the right lateral prefrontal cortex (PFC), right medial PFC, dorsolateral PFC, right middle cingulate cortex and the right inferior frontal operculum (involved in inhibitory control), after compared to before surgery. Response inhibition to low-energy foods elicited diminished post- compared to pre-surgery responses in the left superior temporal pole, right parahippocampal gyrus and right hypothalamus (involved in metabolic control). CONCLUSION: Neural changes indicate improved response inhibition towards high-energy food cues, altered influence of metabolic control during response inhibition towards low-energy food cues and a more positive attitude to both high-energy and low-energy food after RYGB. Alterations in neural circuits involved in inhibitory control, satiety signalling and reward processing may contribute to effective weight-loss after RYGB.

The Effect of Obesity on Anti-Xa Concentrations in Bariatric Patients.

BACKGROUND: Morbidly obese patients are at increased risk to develop venous thromboembolism (VTE), especially after bariatric surgery. Adequate postoperative thrombosis prophylaxis is of utmost importance. It is assumed that morbidly obese patients need higher doses of low molecular weight heparin (LMWH) compared to normal-weight patients; however, current guidelines based on relative efficacy in obese populations are lacking. OBJECTIVES: First, we will evaluate the relationship between body weight descriptors and anti-Xa activity prospectively. Second, we will determine the dose-linearity of LMWH in morbidly obese patients. SETTING: This study was performed in a general hospital specialized in bariatric surgery. METHODS: Patients were scheduled for a Roux-en-Y gastric bypass with a total bodyweight (TBW) of ≥ 140 kg. Patients (n = 50, 64% female) received a daily postoperative dose of 5700 IU of nadroparin for 4 weeks. Anti-Xa activity was determined 4 h after the last nadroparin administration. To determine the dose linearity, anti-Xa was determined following a preoperative dose of 2850 IU nadroparin in another 50 patients (52%). RESULTS: TBW of the complete group was 148.5 ± 12.6 kg. Mean anti-Xa activity following 5700 IU nadroparin was 0.19 ± 0.07 IU/mL. Of all patients, 32% had anti-Xa levels below the prophylactic range. Anti-Xa activity inversely correlated with TBW (correlation coefficient - 0.410) and lean body weight (LBW; correlation coefficient - 0.447); 67% of patients with a LBW ≥ 80 kg had insufficient anti-Xa activity concentrations. No VTE events occurred. CONCLUSIONS: In morbidly obese patients, a postoperative dose of 5700 IU of nadroparin resulted in subprophylactic exposure in a significant proportion of patients. Especially in patients with LBW ≥ 80 kg, a higher dose may potentially be required to reach adequate prophylactic anti-Xa levels.

Changes in carotid flow velocity induced by lowering cerebrospinal fluid pressure in normal pressure hydrocephalus.

This is a report of changes in blood flow velocity in the carotid system induced by lumbar puncture in five patients who had clinical and neuroradiological signs of normal pressure hydrocephalus. After lowering cerebrospinal fluid pressure an increase of carotid flow velocity was found on Doppler hematotachography. These changes of carotid blood flow velocity could not be demonstrated in a control group of four patients with normal cerebrospinal fluid dynamics. This method is easy to perform, does not overtax the patient and seems to be indicated for the diagnosis of NPH. It is presented as a new, simple, reproducible aid to the diagnosis of NPH by Doppler hematotachography.