Anna Casajoana

Is Trabecular Bone Score Valuable In Bone Microstructure Assessment After Gastric Bypass In Women With Morbid Obesity

Introduction: The effects of bariatric surgery on skeletal health raise many concerns. Trabecular bone score (TBS) is obtained through the analysis of lumbar spine dual X-ray absorptiometry (DXA) images and allows an indirect assessment of skeletal microarchitecture (MA). The aim of our study was to evaluate the changes in bone mineral density (BMD) and alterations in bone microarchitecture assessed by TBS in morbidly obese women undergoing Roux-en-Y gastric bypass (RYGB), over a three-year follow-up. Material/Methods: A prospective study of 38 morbidly obese white women, aged 46.3 ± 8.2 years, undergoing RYGB was conducted. Biochemical analyses and DXA scans with TBS evaluation were performed before and at one year and three years after surgery. Results: Patients showed normal calcium and phosphorus plasma concentrations throughout the study. However, 25-hydroxyvitamin D (25(OH)D3) decreased, and 71% of patients had a vitamin D deficiency at three years. BMD at femoral neck and lumbar spine (LSBMD) significantly decreased 13.53 ± 5.42% and 6.03 ± 6.79%, respectively, during the three-year follow-up; however Z-score values remained above those for women of the same age. TBS was within normal ranges at one and three years (1.431 ± 106 and 1.413 ± 85, respectively), and at the end of the study, 73.7% of patients had normal bone MA. TBS at three years correlated inversely with age (r = −0.41, p = 0.010), body fat (r = −0.465, p = 0.004) and greater body fat deposited in trunk (r = −0.48, p = 0.004), and positively with LSBMD (r = 0.433, p = 0.007), fat mass loss (r = 0.438, p = 0.007) and lean mass loss (r = 0.432, p = 0.008). In the regression analysis, TBS remained associated with body fat (β = −0.625, p = 0.031; R2 = 0.47). The fracture risk, calculated by FRAX® (University of Sheffield, Sheffield, UK), with and without adjustment by TBS, was low. Conclusion: Women undergoing RYGB in the mid-term have a preserved bone MA, assessed by TBS.

Weight loss in the healthy elderly might be a non-cognitive sign of preclinical Alzheimer’s disease

Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´s Disease Neuroimaging Initiative (mean follow-up 50.5±30.5 months). Subjects were classified according to body weight trajectory into a weight loss group (WLG; relative weight loss ≥ 5%) and a non-weight loss group (non-WLG; relative weight loss < 5%). Linear mixed effects models were used to estimate the effect of body weight changes on ADAS-Cognitive score across time. Baseline CSF tau/AΔ42 ratio and AV45 PET uptake were compared between WLG and non-WLG by analysis of covariance. Atrophy maps were compared between groups at baseline and longitudinally at a 2-year follow-up using Freesurfer. WLG showed increased baseline levels of cerebrospinal fluid tau/AΔ42 ratio, increased PET amyloid uptake and diminished cortical thickness at baseline. WLG also showed faster cognitive decline and faster longitudinal atrophy. Our data support weight loss as a non-cognitive manifestation of pre-clinical AD.

Obesity and Alzheimer’s disease, does the obesity paradox really exist? A magnetic resonance imaging study

Mid-life obesity is an established risk factor for Alzheimers disease (AD) dementia, whereas late-life obesity has been proposed as a protective state. Weight loss, which predates cognitive decline, might explain this obesity paradox on AD risk. We aimed to assess the impact of late life obesity on brain structure taking into account weight loss as a potential confounder. We included 162 elderly controls of the Alzheimers Disease Neuroimaging Initiative (ADNI) with available 3T MRI scan. Significant weight loss was defined as relative weight loss ≥5% between the baseline and last follow-up visit. To be able to capture weight loss, only subjects with a minimum clinical and anthropometrical follow-up of 12 months were included. Individuals were categorized into three groups according to body mass index (BMI) at baseline: normal-weight (BMI<25 Kg/m2), overweight (BMI 25-30 Kg/m2) and obese (BMI>30 Kg/m2). We performed both an interaction analysis between obesity and weight loss, and stratified group analyses in the weight-stable and weigh-loss groups. We found a significant interaction between BMI and weight loss affecting brain structure in widespread cortical areas. The stratified analyses showed atrophy in occipital, inferior temporal, precuneus and frontal regions in the weight stable group, but increased cortical thickness in the weight-loss group. In conclusion, our data support that weight loss negatively confounds the association between late-life obesity and brain atrophy. The obesity paradox on AD risk might be explained by reverse causation.

Nutritional deficiencies and bone metabolism after endobarrier in obese type 2 patients with diabetes

Endobarrier® is a minimally invasive, reversible endoscopic treatment for obesity. It provokes malabsorption along 60 cm of the small intestine, which can contribute to the development of vitamin deficiencies and to changes in bone mineral density (BMD). To determine the prevalence of nutrient deficiencies, changes in body composition and BMD during the first year after Endobarrier® placement. Twenty-one patients with type 2 diabetes met inclusion criteria. Levels of vitamins, micro and macronutrients were assessed prior and at 1, 3 and 12 months post-operatively. DEXA was performed before and 12 months after implant. Nineteen patients completed the 12 months follow-up. Vitamin D deficiency was the most prevalent finding before Endobarrier® implant. The percentage of patients with severe deficiency decreased from 19 to 5% at 12 months after supplementation. Microcytic anaemia was initially present in 9.5% of patients and increased to 26.3% at 12 months. Low ferritin and vitamin B12 levels were observed in 14.2 and 4.8% of patients before the implant and worsened to 42 and 10.5%. Low concentrations of magnesium and phosphorus were also common but improved along the study. A significant but not clinically relevant decrease in BMD of 4.14 ± 4.0% at the femoral neck was observed at 12 months without changes in osteocalcin levels. Vitamin deficiencies are common after Endobarrier® implant. It is therefore important to screen patients prior to and at regular intervals after the implant, and to encourage adherence to diet counselling and supplementation.

WEIGHT LOSS MIGHT BE A NON-COGNITIVE SIGN OF PRECLINICAL ALZHEIMER'S DISEASE

Background: Patients who had a cerebrovascular event are at higher risk of developing vascular dementia, especially in older age. However, some patients appear resilient to cognitive impairment even at advanced age. One possible explanation is that they have resistance to small vessel disease, particularly white matter hyperintensities (WMH) detectable on MRI. We studied the relevance of WMH to cognition in relation to age in patients who had a TIA/non-disabling stroke, particularly the older-old (>80). Methods: 570 consecutive patients with recent TIA/nondisabling stroke from the Oxford Vascular Study underwent multimodal MRI and cognitive assessment with the Montreal Cognitive Assessment scale (MoCA). They were divided into two age groups (<80, N1⁄4461; 80, N1⁄4109) and three cognitive groups according to their MoCA score: no vascular cognitive impairment (NoCI, MoCA>24, N1⁄4384), mild vascular cognitive impairment (MildVCI, MoCA1⁄420-24, N1⁄4143) or severe vascular cognitive impairment (SevereVCI, MoCA<20, N1⁄443). WMHwere automatically segmented on FLAIR images using BIANCA (Griffanti et al., Neuroimage 2016) and the relative WMH volumes calculated. A two-way between groups factorial ANOVA was performed on the WMH volumes to test the interaction between age and cognition. Voxel-wise correlational analyses were then performed on the binarised, normalized, smoothed maps of WMH using non-parametric permutation test in FSL to explore if lower MoCA score would be associated with higher probability of WMH in different localization in the younger relative to the older-old patients. Results:A 2x3 between-group factorial ANOVA on WMH volumes showed significant main effects of age (F1⁄429.04, p<0.001) and cognitive group (F1⁄45.71, p1⁄40.004), and a significant age/cognition interaction (F1⁄44.67,p1⁄40.010), in that differences across cognitive groups were significant in the younger but not in the olderold group. Accordingly, the voxel-wise analysis showed a significant negative correlation (voxel-corrected p<0.05) between WMH probability and MoCA score in the younger group only, mainly in periventricular frontal areas (figure). Conclusions: WMH in patients aged 80 years with TIA/minor stroke is unrelated to cognition suggesting that the presence of WMH (i) does not undermine resilience to dementia in the older-old and (ii) should not prompt consideration of a diagnosis of vascular cognitive impairment in the older old.