Caloric Intake, Dietary Lifestyles, Macronutrient Composition, and Alzheimer' Disease Dementia

Alzheimer's disease is a devastating neurodegenerative condition currently affecting over 5 million elderly individuals in the United States. There is much evidence suggesting that certain dietary lifestyles can help to prevent and possibly treat Alzheimer's disease. In this paper, we discuss how certain cardiovascular and diabetic conditions can induce an increased susceptibility for Alzheimer's disease and the mechanisms through which this occurs. We further discuss how the consumption of certain foods or food components can help to reduce one's risk for Alzheimer's disease and may possibly be developed as a therapeutic agent

Ketogenic diets: neurodegenerative and rare diseases

Treballs Finals de Grau de Farmàcia, Facultat de Farmàcia i Ciències de l'Alimentació, Universitat de Barcelona, 2020. Tutor/a: Escolano Miron, Maria CarmenThe ketogenic diet (KD) is a high-fat, low-carbohydrate, and moderate-protein diet that was first described in 1921, with the goal of mimicking the anticonvulsant effects of fasting. KD causes an increased ketone bodies production, allowing the brain to obtain an alternative fuel to glucose. Recently, its clinical use has expanded notoriously, as well as scientific interest, due to its possible positive effects on various diseases. Based on a bibliographic research, this work aims to analyse the current information on KD and its variants, in addition to review some studies that assess its application in two illnesses: glucose transporter type 1 deficiency syndrome (GLUT1DS) and Alzheimer's disease (AD), as examples of rare and neurodegenerative illness, respectively. On one hand, GLUT1DS is an encephalopathy with a wide spectrum of manifestations, with seizures being the most common. In this disorder, KD-derived ketone bodies represent an efficient alternative energy source. On the other hand, AD is the most frequent cause of dementia and its incidence is expected to increase in the coming decades. Currently, there is no cure, so the neuroprotective effects of ketone bodies may decrease the mitochondrial dysfunction, oxidative stress, and neuroinflammation present in AD. Although overall, both the reported cases of GLUT1DS and preclinical and clinical studies in AD demonstrate clinical benefits with KDs, more research is needed to better understand their role in diverse diseases.La dieta cetogénica (DC) es una dieta alta en grasas, baja en carbohidratos y moderada en proteínas que fue descrita por primera vez en 1921, con el objetivo imitar los efectos anticonvulsivos del ayuno. La DC provoca un aumento en la producción cuerpos cetónicos, permitiendo al cerebro obtener un combustible alternativo a la glucosa. Recientemente su uso clínico se ha expandido notoriamente, así como también el interés científico, por sus posibles efectos positivos en diversas enfermedades. A partir de una búsqueda bibliográfica, este trabajo pretende analizar la información actual de la DC y sus variantes, y revisar algunos estudios que evalúen su aplicación en dos enfermedades: el síndrome de deficiencia del transportador de glucosa tipo 1 (SDGLUT1) y la enfermedad de Alzheimer (EA), como ejemplos de enfermedad rara y neurodegenerativa, respectivamente. Por una parte, el SDGLUT1 es una encefalopatía con un amplio espectro de manifestaciones, siendo las crisis convulsivas las más comunes. En esta enfermedad, los cuerpos cetónicos representan una eficaz fuente alternativa de energía. Por otra parte, la EA es la causa más común de demencia y se prevé que su incidencia aumente en las próximas décadas. Actualmente, no existe una cura, por tanto, los efectos neuroprotectores de los cuerpos cetónicos podrían disminuir la disfunción mitocondrial, estrés oxidativo y neuroinflamación presentes en la EA. Aunque en general, tanto los casos reportados de SDGLUT1 como los estudios preclínicos y clínicos en EA, demuestran beneficios clínicos con las DCs, se necesita más investigación para comprender mejor su papel en diversas enfermedades

Advanced glycation end products and age-related diseases in the general population

In this thesis, epidemiological, nutritional, and gut microbiome related studies are presented to illustrate the relation of advanced glycation end products (AGEs) with age-related diseases. The studies are embedded in the Rotterdam Study, a cohort of the Dutch general population of middle-aged and elderly adults. The amount of skin AGEs measured as SAF was used as a representative of the long-term AGE burden. Chapter 1 gives an overview of the whole thesis (Section 1.1) and gives a brief introduction to AGEs and their implications in disease pathophysiology. Chapter 2 focuses on the interplay of AGEs in the skin and clinical and lifestyle factors, and Chapter 3 concerns the link of skin and dietary AGEs with age-related diseases. Chapter 4 discusses the interpretations and implications of the findings, major methodological considerations, and pressing questions for future research

Targeting microbiota : What do we know about it at present?

Publisher Copyright: © 2019 by the authors. Licensee MDPI, Basel, Switzerland.The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host’s organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut–liver axis. The gut–liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut–brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood–brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut–liver axis and gut–brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.publishersversionPeer reviewe