The Microbiota-Gut-Brain Axis Heart Shunt Part I: The French Paradox, Heart Disease and the Microbiota

It has been well established that a vegetarian and polyphenol-rich diet, including fruits, vegetables, teas, juices, wine, indigestible fiber and whole grains, provide health-promoting phytochemicals and phytonutrients that are beneficial for the heart and brain. What is not well-characterized is the affect these foods have when co-metabolized within our dynamic gut and its colonizing flora. The concept of a heart shunt within the microbiota-gut-brain axis underscores the close association between brain and heart health and the so-called French paradox offers clues for understanding neurodegenerative and cerebrovascular diseases. Moreover, oxidation-redox reactions and redox properties of so-called brain and heart-protective foods are underappreciated as to their enhanced or deleterious mechanisms of action. Focusing on prodromal stages, and common mechanisms underlying heart, cerebrovascular and neurodegenerative diseases, we may unmask and understanding the means to better treat these related diseases

DNA damage in children and adolescents with cardiovascular disease risk factors

The risk of developing cardiovascular disease (CVD) is related to lifestyle (e.g. diet, physical activity and smoking) as well as to genetic factors. This study aimed at evaluating the association between CVD risk factors and DNA damage levels in children and adolescents. Anthropometry, diet and serum CVD risk factors were evaluated by standard procedures. DNA damage levels were accessed by the comet assay (Single cell gel electrophoresis; SCGE) and cytokinesis-blocked micronucleus (CBMN) assays in leukocytes. A total of 34 children and adolescents selected from a population sample were divided into three groups according to their level of CVD risk. Moderate and high CVD risk subjects showed significantly higher body fat and serum CVD risk markers than low risk subjects (PO risco de desenvolver doença cardiovascular (DCV) está relacionado ao estilo de vida (por exemplo, dieta, atividade física e tabagismo), bem como a fatores genéticos. Este estudo teve como objetivo avaliar a associação entre fatores de risco cardiovascular e os níveis de danos ao DNA em crianças e adolescentes. Antropometria, dieta e fatores de risco para DCV foram avaliados através de procedimentos padrão. Níveis de danos no DNA foram avaliados através do ensaio cometa (eletroforese de célula única; EC) e do teste de micronúcleos em leucócitos. Um total de 34 crianças e adolescentes, selecionados a partir de uma amostra populacional, foram divididos em três grupos, de acordo com seu nível de risco de DCV. Indivíduos com níveis moderado e alto risco para DCV apresentaram de forma significativa maiores níveis de gordura corporal e de marcadores séricos de risco cardiovascular que indivíduos de baixo risco (P <0,05). Indivíduos de alto risco também mostraram um aumento significativo de danos ao DNA, de acordo com o EC, mas não de acordo com o teste de micronúcleos, do que indivíduos de risco baixo e moderado. A vitamina C consumida foi inversamente correlacionada com os danos ao DNA avaliados pelo EC, e o número de micronúcleos foi inversamente correlacionado com a ingestão de ácido fólico. Os resultados obtidos indicam um aumento de danos no DNA que pode ser consequente do estresse oxidativo em indivíduos jovens com fatores de risco para DCV, indicando que o nível de danos no DNA pode auxiliar na avaliação do risco de DCV

Leaky Gut, Leaky Brain?

&lsquo;Leaky gut&rsquo; syndrome, long-associated with celiac disease, has attracted much attention in recent years and for decades, was widely known in complementary/alternative medicine circles. It is often described as an increase in the permeability of the intestinal mucosa, which could allow bacteria, toxic digestive metabolites, bacterial toxins, and small molecules to &lsquo;leak&rsquo; into the bloodstream. Nervous system involvement with celiac disease is know to occur even at subclinical levels. Gluten and gluten sensitivity are considered to trigger this syndrome in individuals genetically predisposed to celiac disease. However, the incidence of celiac disease in the general population is quite low. Nevertheless, increased public interest in gluten sensitivity has contributed to expanded food labels stating &lsquo;gluten-free&rsquo; and the proliferation of gluten-free products, which further drives gluten-free lifestyle changes by individuals without frank celiac disease. Moreover, systemic inflammation is associated with celiac disease, depression, and psychiatric comorbidities. This mini-review focuses on the possible neurophysiological basis of leaky gut; leaky brain disease; and the microbiota&rsquo;s contribution to inflammation, gastrointestinal, and blood-brain barrier integrity, in order to build a case for possible mechanisms that could foster further &lsquo;leaky&rsquo; syndromes. We ask whether a gluten-free diet is important for anyone or only those with celiac disease

Leaky Gut, Leaky Brain?

&lsquo;Leaky gut&rsquo; syndrome, long-associated with celiac disease, has attracted much attention in recent years and for decades, was widely known in complementary/alternative medicine circles. It is often described as an increase in the permeability of the intestinal mucosa, which could allow bacteria, toxic digestive metabolites, bacterial toxins, and small molecules to &lsquo;leak&rsquo; into the bloodstream. Nervous system involvement with celiac disease is know to occur even at subclinical levels. Gluten and gluten sensitivity are considered to trigger this syndrome in individuals genetically predisposed to celiac disease. However, the incidence of celiac disease in the general population is quite low. Nevertheless, increased public interest in gluten sensitivity has contributed to expanded food labels stating &lsquo;gluten-free&rsquo; and the proliferation of gluten-free products, which further drives gluten-free lifestyle changes by individuals without frank celiac disease. Moreover, systemic inflammation is associated with celiac disease, depression, and psychiatric comorbidities. This mini-review focuses on the possible neurophysiological basis of leaky gut; leaky brain disease; and the microbiota&rsquo;s contribution to inflammation, gastrointestinal, and blood-brain barrier integrity, in order to build a case for possible mechanisms that could foster further &lsquo;leaky&rsquo; syndromes. We ask whether a gluten-free diet is important for anyone or only those with celiac disease

Implication of Oncogenic Signaling Pathways as a Treatment Strategy for Neurodegenerative Disorders - Contemporary Approaches.

Recent evidence has associated the aberrant, proximal re-expression of various cell cycle control elements with neuronal cell vulnerability in Alzheimer\u27s and Parkinson\u27s diseases, as a common chronic neurodegeneration. This phenomenon associated with oncogenic transduction pathway activation has attracted the interest of scientists all over the world for a few years now. The purpose of this paper is to outline areas of research related to oncogenic factors or medicines in the context of potential applications for future treatment of the above mentioned chronic and, largely, incurable diseases

Vitamin C mediates chemical aging of lens crystallins by the Maillard reaction in a humanized mouse model

Senile cataracts are associated with progressive oxidation, fragmentation, cross-linking, insolubilization, and yellow pigmentation of lens crystallins. We hypothesized that the Maillard reaction, which leads browning and aroma development during the baking of foods, would occur between the lens proteins and the highly reactive oxidation products of vitamin C. To test this hypothesis, we engineered a mouse that selectively overexpresses the human vitamin C transporter SVCT2 in the lens. Consequently, lenticular levels of vitamin C and its oxidation products were 5- to 15-fold elevated, resulting in a highly compressed aging process and accelerated formation of several protein-bound advanced Maillard reaction products identical with those of aging human lens proteins. These data strongly implicate vitamin C in lens crystallin aging and may serve as a model for protein aging in other tissues particularly rich in vitamin C, such as the hippocampal neurons and the adrenal gland. The hSVCT2 mouse is expected to facilitate the search for drugs that inhibit damage by vitamin C oxidation products