1.
Links between metabolic syndrome and the microbiome.
Gildner, TE
Evolution, medicine, and public health. 2020;2020(1):45-46
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Metabolic syndrome (MetS) is a cluster of co-occurring pathological conditions, characterised by insulin resistance, abdominal obesity, hypertension and dyslipidaemia One possible factor contributing to MetS risk is change in microbiome composition. Diets high in processed foods appear to alter microbiome composition in ways that promote higher fat mass and insulin resistance. Additionally, a sedentary lifestyle decreases microbiome diversity, elevating inflammation and metabolic disease risk. Research on how the microbiome responds to modest, attainable changes in diet and physical activity will help identify which dietary adjustments and exercise types have the greatest potential to protect patients from MetS.
Abstract
Metabolic syndrome (MetS) is a cluster of harmful conditions which occur together, such as insulin resistance, abdominal obesity, and hypertension. The global prevalence of MetS is growing rapidly, with some estimates suggesting over one billion people worldwide experience increased morality and disease rates linked with this syndrome. One possible factor contributing to MetS risk is changes in microbiome composition. Approximately 100 trillion bacteria and other microbes reside in the human intestinal tract, collectively termed the gut microbiome. Humans and microbes share a long evolutionary history, with many of these microbes influencing human health outcomes. However, environmental conditions have changed dramatically with human technological innovations; many of these changes (e.g., diets high in processed foods and sedentary lifestyles) appear to impact human-microbe relationships. In general, recent changes in diet and activity patterns have been linked to decreased microbiome diversity, elevating inflammation and metabolic disease risk and likely promoting the development of MetS. Targeting patient diet or exercise patterns may therefore help doctors better treat patients suffering from MetS. Still, additional work is needed to determine how the microbiome responds to changes in patient activity and diet patterns across culturally and biologically diverse human populations.
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Metabolic profiling distinguishes three subtypes of Alzheimer's disease.
Bredesen, DE
Aging. 2015;7(8):595-600
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The causes of Alzheimer’s Disease (AD) remain incompletely defined and there are currently no truly effective drug therapies available. However, there is growing evidence that disordered blood glucose management and hormonal changes and deficiencies, amongst other things, are implicated in symptom onset. Optimising these various metabolic processes, therefore, may be used as a comprehensive way to avoid cognitive decline or achieve cognitive improvements in symptomatic individuals. This report provides the metabolic results of 3 case studies and suggests 3 different types of AD classification, depending on the individual metabolic profile. Further studies are required to elaborate on the metabolic profiles suggested in this report, however Nutrition Practitioners working with cognitive decline, can use this report as a basis for individualised nutrition protocols to optimise metabolic processes in clients with cognitive decline.
Abstract
The cause of Alzheimer's disease is incompletely defined, and no truly effective therapy exists. However, multiple studies have implicated metabolic abnormalities such as insulin resistance, hormonal deficiencies, and hyperhomocysteinemia. Optimizing metabolic parameters in a comprehensive way has yielded cognitive improvement, both in symptomatic and asymptomatic individuals. Therefore, expanding the standard laboratory evaluation in patients with dementia may be revealing. Here I report that metabolic profiling reveals three Alzheimer's disease subtypes. The first is inflammatory, in which markers such as hs-CRP and globulin:albumin ratio are increased. The second type is non-inflammatory, in which these markers are not increased, but other metabolic abnormalities are present. The third type is a very distinctive clinical entity that affects relatively young individuals, extends beyond the typical Alzheimer's disease initial distribution to affect the cortex widely, is characterized by early non-amnestic features such as dyscalculia and aphasia, is often misdiagnosed or labeled atypical Alzheimer's disease, typically affects ApoE4-negative individuals, and is associated with striking zinc deficiency. Given the involvement of zinc in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling, this syndrome of Alzheimer's-plus with low zinc (APLZ) warrants further metabolic, genetic, and epigenetic characterization.