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Obesity has been linked to numerous health and nutritional problems, including impaired iron metabolism, a common cause of anemia. We aimed to determine the prevalence of anemia, iron deficiency (ID), and iron deficiency anemia (IDA) among women aged 20–49 years based on body mass index (BMI) status. We used measures of iron status and body mass index from the 2001–2006 National Health and Nutrition Examination Survey (NHANES). Mean serum ferritin, erythrocyte protoporphyrin, and soluble transferrin receptor were higher, while those of serum iron, percent transferrin saturation, and mean cell volume (MCV) were lower in women with obesity than those with normal weight (all p < 0.016). ID based on the ferritin model was 12.5 ± 1.0% vs. 22.9 ± 1.6% (p < 0.001); 9.0 ± 0.9% vs. 20.0 ± 1.3% (p < 0.001) based on the MCV model; and 8.1 ± 1.0% vs. 10.5 ± 1.2% (p > 0.05) based on the BII model for women with normal weight and women with obesity, respectively. Anemia prevalence was 5.5 ± 0.8% (normal) vs. 9.3 ± 1.0% (obese) (p = 0.005). The IDA estimates based on the ferritin and MCV models were similar but higher than that from the BII model (p < 0.001). Generally, the prevalence rates of ID and anemia (and IDA) were higher for women with obesity, but the method used to define deficiency mattered. The choice of iron indices is important for estimating ID and IDA in populations with obesity.

Objective: Increased stress and cortisol are important risk factors for cardiovascular diseases, including cerebrovascular disease. The present study used an experimental speech task to determine the relationship between inhibitory control and cortisol response to social stress. We hypothesized that poorer inhibitory control would predict larger cortisol response to the stressor. Method: Participants were 42 women with overweight/obesity recruited for larger project examining the impacts of weight stigma on inflammation. The computerized Stroop Color-Word and Go/No-Go assessed baseline inhibitory control and other neurocognitive factors. Higher scores indicate better performance. After a baseline blood sample, participants were randomized and asked to give a speech (1 = stigma, 0 = neutral). Subsequent blood draws were taken at 30-, 60-, and 90-minutes post-speech. Area under the curve was calculated to represent total cortisol increase. Results: Analyses, controlling for speech condition and BMI, revealed that cortisol reactivity to the speech task was predicted by both Stroop Color-Word (β = −0.42, p = 0.007) and Interference (β = −0.35, p = 0.022) scores, as well as Go/No-Go Hits (β = −0.33, p = 0.04) and Omissions (β = −0.34, p = 0.03), but not Commissions (β = −0.038; p = 0.81). Conclusions: The pattern of results suggests that individuals with lower inhibitory control experienced a greater cortisol output after the stressor. In this context, individuals who were better able to ignore irrelevant social aspects of the speech experienced a smaller cortisol reaction than the individuals who could not ignore them. To reduce risk for cerebrovascular disease, clinical interventions should focus on the practice of ignoring irrelevant stressors to promote more adaptive biological responses to stress.

Adverse childhood experiences (ACEs) may predict markers of neurocognitive performance (i.e., executive function; EF) and brain health/plasticity (i.e., brain-derived neurotropic factor; BDNF). This pilot examined the magnitude of effects between: 1) ACES and EF performance, 2) ACEs and BDNF levels, and 3) EF performance and BDNF levels. We hypothesize that higher ACEs will be associated with poorer EF scores and lower BNDF levels and that lower EF scores will be associated with lower BDNF levels. Given the pilot nature of the study, an emphasis is placed on effect size vs. significance. Participants were 36 middle-aged women enrolled in the NICE SPACES trial (age=31.4 years, BMI=34.2, racially minoritized=37.9%). ACES were quantified using the 10-item Adverse Childhood Experiences Scale. EF was measured using the fluid cognition composite from the NIH Toolbox – Cognition Battery. BDNF was estimated using proBDNF levels estimated from serum collected via venipuncture. Higher ACEs levels were not directly associated with EF scores (b = 0.03, p = .854); but did show a meaningful negative beta coefficient with BDNF levels (b = -0.34, p = .053). EF scores and BDNF showed a positive coefficient that did not reach significance (b = .26, p = .122). In a modest pilot of middle-age women, higher ACEs were associated with lower BDNF, indicating greater adversity in childhood is linked to lower neurotrophins levels in adulthood. The lower BDNF levels may help explain poorer performance on cognitive tasks. Larger follow-up studies in more powered samples are warranted given the size of detected coefficients.

This review paper will discuss the recent literature examining the relationship between obesity and neurocognitive outcomes, with a particular focus on cognitive changes after bariatric surgery. Obesity is now recognized as an independent risk factor for adverse neurocognitive outcomes, and severely obese persons appear to be at even greater risk. Bariatric surgery is associated with rapid improvements in cognitive function that persist for at least several years, although the mechanisms underlying these improvements are incompletely understood. Assessment of cognitive impairment in bariatric surgery patients is challenging, and improved methods are needed, as poorer performance on neuropsychological tests of memory and executive function leads to poorer clinical weight outcomes. In addition to its clinical importance, further study in this area will provide key insight into obesity-related cognitive dysfunction and clarify the possibility of an obesity paradox for neurological outcomes.