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Effects of adiposity and metabolic dysfunction on cognition: A review.

ABSTRACT: Obesity and metabolic dysfunction are both correlated with increased rates of cognitive decline. However, because these two conditions often co-occur, it remains unclear whether their cognitive consequences are independent. In this review, we carefully consider literature examining the effects of metabolic dysfunction and increased adiposity on cognition across the lifespan, including only well-controlled studies that attempt to dissociate their effects. We found a total of 36 studies, 17 examining metabolic dysfunction and 19 examining the effects of adiposity. We found evidence from the literature suggesting that increased adiposity and metabolic dysfunction may contribute to deficits in executive function, memory, and medial temporal lobe structures largely independent of one another. These deficits are thought to arise principally from physiological changes associated with inflammation, vascularization, and oxidative stress, among others. Such processes may result from excess adipose tissue and insulin resistance that occur independently and can further exacerbate when the two conditions co-occur. However, we also find it likely that impaired cognition plays a role in behavioral and lifestyle choices that lead to increased adiposity and metabolic dysfunction, which can then perpetuate and augment cognitive decline. We recommend additional prospective and longitudinal studies to examine whether impaired cognition is a cause and/or consequence of these factors.

SUBMITTER: Farruggia MC

PROVIDER: S-EPMC6625347 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Effects of adiposity and metabolic dysfunction on cognition: A review.

Farruggia Michael C MC Small Dana M DM

Physiology & behavior 20190611

Obesity and metabolic dysfunction are both correlated with increased rates of cognitive decline. However, because these two conditions often co-occur, it remains unclear whether their cognitive consequences are independent. In this review, we carefully consider literature examining the effects of metabolic dysfunction and increased adiposity on cognition across the lifespan, including only well-controlled studies that attempt to dissociate their effects. We found a total of 36 studies, 17 examin ...[more]

PMID: 31194997

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Project description:Purpose:Natriuretic peptides (NPs) negatively feedback on the renin-angiotensin-aldosterone system (RAAS) and play a critical role in preserving cardiac structure and maintaining metabolic homeostasis. Well-treated HIV-infected individuals are at risk for fat redistribution and demonstrate evidence of RAAS dysregulation, which relates to metabolic dysfunction. We investigated circulating NPs in relation to RAAS physiology and metrics of body composition in HIV. Methods:We assessed atrial natriuretic peptide, brain natriuretic peptide (BNP), and amino terminal pro B-type natriuretic peptide (NT-proBNP) during acute activation of the RAAS using a low-sodium controlled diet among 20 HIV-infected and 10 non-HIV-infected individuals well phenotyped for body composition. Results:BNP was significantly lower [median, 60 (interquartile range, 44, 152) pg/mL vs 196 (91, 251) pg/mL, respectively; P = 0.04], and serum aldosterone was higher, among HIV-infected than among non-HIV-infected individuals. BNP was significantly and inversely associated with body composition [waist circumference: r = -0.46 (P = 0.04); BMI: r = -0.55 (P = 0.01); body adiposity index: r = -0.49 (P = 0.03)], metabolic indices [total cholesterol: r = -0.44 (P = 0.05), insulin resistance calculated by using homeostatic model assessment: r = -0.44 (P = 0.05); mean arterial pressure: r = -0.44 (P = 0.05)], and serum aldosterone (r = -0.49; P = 0.03) among the HIV-infected group. These relationships were not demonstrated in the non-HIV-infected group. In a four-group comparison stratifying by HIV serostatus and above or below a body mass index (BMI) of 25 kg/m2, BNP decreased significantly across groups; it was highest in non-HIV-infected patients with a BMI <25 kg/m2 and lowest in HIV-infected patients with a BMI ≥25 kg/m2 (overall P = 0.01). Conclusion:Relatively reduced NP, particularly BNP, among HIV-infected individuals with excess adiposity may contribute to reduced suppression of aldosterone and potentially drive aldosterone-mediated metabolic complications. Strategies that target RAAS blockade and/or augment NPs may be useful to reduce cardiometabolic disease among HIV-infected individuals in whom these systems are perturbed.

Project description:BackgroundSome individuals living with obesity may be relatively metabolically healthy, whilst others suffer from multiple conditions that may be linked to adverse metabolic effects or other factors. The extent to which the adverse metabolic component of obesity contributes to disease compared to the non-metabolic components is often uncertain. We aimed to use Mendelian randomisation (MR) and specific genetic variants to separately test the causal roles of higher adiposity with and without its adverse metabolic effects on diseases.MethodsWe selected 37 chronic diseases associated with obesity and genetic variants associated with different aspects of excess weight. These genetic variants included those associated with metabolically 'favourable adiposity' (FA) and 'unfavourable adiposity' (UFA) that are both associated with higher adiposity but with opposite effects on metabolic risk. We used these variants and two sample MR to test the effects on the chronic diseases.ResultsMR identified two sets of diseases. First, 11 conditions where the metabolic effect of higher adiposity is the likely primary cause of the disease. Here, MR with the FA and UFA genetics showed opposing effects on risk of disease: coronary artery disease, peripheral artery disease, hypertension, stroke, type 2 diabetes, polycystic ovary syndrome, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout. Second, 9 conditions where the non-metabolic effects of excess weight (e.g. mechanical effect) are likely a cause. Here, MR with the FA genetics, despite leading to lower metabolic risk, and MR with the UFA genetics, both indicated higher disease risk: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-oesophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism.ConclusionsOur results assist in understanding the consequences of higher adiposity uncoupled from its adverse metabolic effects, including the risks to individuals with high body mass index who may be relatively metabolically healthy.FundingDiabetes UK, UK Medical Research Council, World Cancer Research Fund, National Cancer Institute.

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Effects of adiposity and metabolic dysfunction on cognition: A review.

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Effects of adiposity and metabolic dysfunction on cognition: A review.

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