BookPDF Available

CULTURA NUTRICIONAL Y ARTE MÉDICO: LA MAS RÁPIDA SOLUCIÓN PARA DISMINUÍR LA POBREZA (Primera Versión, Marzo de 2001)

Authors:

Abstract and Figures

PARTE UNO:  Resumen: SITUACIÓN ACTUAL DE LA MALNUTRICIÓN Y LA ENFERMEDAD  INTRODUCCIÓN  LA RESISTENCIA A ENFERMAR: Educar en Nutrición para una Salud Optima generadora de Riqueza  Referencias Bibliográficas PARTE DOS: DESARROLLO DEL PROYECTO NUTRICION-PAIS  Justificación 1. Nutrición y Genes: el papel de la regulación Hormonal 2. Nutrición y Conducta 3. Nutrición: Terapia Preventiva y Recuperativa 4. Desmitificación en Nutrición 5. Nutrición y Desarrollo  ESTRATEGIAS DE EDUCACIÓN EN SEGURIDAD ALIMENTARIA
Content may be subject to copyright.
A preview of the PDF is not available
ResearchGate has not been able to resolve any citations for this publication.
Article
Full-text available
Background Evidence on the relationship between fruit and vegetable consumption (FV) and mental health in adolescence is sparse and inconsistent. Social determinants of FV include ethnicity, family environments and economic disadvantage. We investigated the relationship between FV and mental health in the British multi-ethnic Determinants of Adolescents (now young Adult) Social well-being and Health (DASH) longitudinal study. Methods A longitudinal study of 4683 adolescents living in London at age 11–13 years and followed up at 14–16 years. FV was measured using validated questions on the number of portions consumed daily. Mental health was measured by the Strengths and Difficulties Questionnaire as mean Total Difficulties Score (TDS) and by classification as a ‘probable clinical case’ (TDS > 17). Social measures included ethnicity, parenting and socioeconomic circumstances. Multilevel modelling was used to investigate the association between FV and mental health throughout adolescence. Results Low FV was common among adolescents, with approximately 60–70% of adolescents reporting < 5 portions/day and 20–30% reporting < 1 portion/day. In late adolescence, most ethnic minority groups reported lower FV than their White peers. In fully adjusted models, < 1 portion/day remained a significant correlate with mean TDS (Coef: 0.55, 0.29–0.81, P < 0.001) and TDS > 17 (Odds Ratio: 1.43, 1.11–1.85, P = 0.007). Gender- or ethnic-specific effects were not observed. Low parental care partly attenuated the association between FV and mental health. Conclusions Low FV is a longitudinal correlate of poor mental health across adolescence. A focus on FV in parenting interventions could yield interrelated benefits across developmental outcomes given its importance to both physical and socioemotional health. Electronic supplementary material The online version of this article (10.1186/s12966-019-0780-y) contains supplementary material, which is available to authorized users.
Article
Full-text available
Background Diabetes is a risk factor for cognitive impairment, but whether there is also a link between pre-diabetes and cognitive dysfunction is not yet fully established. The aim of this observational study was to investigate associations between pre-diabetes/diabetes and cognitive test results, and also between glucose levels measured during the Oral Glucose Tolerance Test (OGTT) and cognitive outcomes. Methods During 2007–2012, in all 2994 people (mean age 72 years), residing in Malmö, Sweden, underwent a clinical examination including the OGTT, cardiovascular measurements including carotid-femoral pulse wave velocity (c-f PWV) and two cognitive tests, the Mini Mental State Examination (MMSE), measuring global cognitive function, and A Quick Test of Cognitive Speed (AQT), measuring processing speed and executive functioning. Regression analyses were performed to investigate associations between: (a) categories of normal or impaired glucose metabolism, and (b) OGTT measurements, respectively, as exposure variables and cognitive test results as outcomes. Adjustments were made for demographics, lifestyle factors and cardiovascular risk factors. Results Participants with pre-diabetes and diabetes scored slightly worse cognitive test results compared to the control group. Results of participants with a long disease duration of diabetes since the baseline examination 13 years earlier were poorer (mean AQT test time 17.8 s slower than controls, p < 0.001). Linear associations were found between fasting and 2-h glucose and cognitive outcomes in the whole population, but also in a sub-analysis including only individuals without diabetes (for 2-h glucose and MMSE results: B = − 2.961, p = 0.005). Associations were stronger for older or less physically active individuals. When adjusting for cardiovascular risk factors, most correlations were non-significant. Conclusions Pre-diabetes and diabetes are associated with minor deficits in global cognitive function, processing speed and executive functioning. Long-standing diabetes is associated with bigger deficits. There appears to be a continuous inverse correlation between glucose levels and cognitive test results, also for people without diabetes. Associations are stronger in older and less physically active individuals. Cardiovascular factors are important mediating factors in the pathway between diabetes and cognitive dysfunction.
Article
Full-text available
Infectious diseases are associated with disruption of host homeostasis. This can be triggered directly by pathogens or indirectly by host immune-driven resistance mechanisms. Disease tolerance is a defense strategy against infection that sustains host homeostasis, without exerting a direct negative impact on pathogens. The mechanisms governing disease tolerance encompass host metabolic responses that maintain vital homeostatic parameters within a range compatible with survival. Central to this defense strategy is the host's ability to sense and adapt to variations in nutrients, such as iron and glucose. Here we address how host responses regulating iron and glucose metabolism interact to establish disease tolerance and possibly modulate resistance to infection.
Article
Full-text available
The discovery of the ferroportin-hepcidin complex has led to a critical review on the treatment of anemia and anemia of inflammation (AI). Ferroportin, the only known mammalian iron exporter from cells to blood, is negatively regulated by hepcidin, a hormone peptide able to bind to ferroportin, leading to its degradation. Therefore, new efficient therapeutic interventions acting on hepcidin and ferroportin are imperative to manage anemia and AI. Bovine milk derivative lactoferrin (bLf), a glycoprotein able to chelate two ferric ions per molecule, is emerging as a natural anti-inflammatory substance able to modulate hepcidin and ferroportin synthesis through the down-regulation of interleukin-6 (IL-6). Here, an interventional study (ClinicalTrials.gov Identifier: NCT01221844) was conducted by orally administering 100 mg of 20–30% iron-saturated bLf (corresponding to 70–84 μg of elemental iron) twice a day. This treatment was compared with the Italian standard therapy, consisting in the oral administration of 329.7 mg of ferrous sulfate once a day (corresponding to 105 mg of elemental iron). Treatments were carried out on 29 anemic women with minor β-thalassemia (20 pregnant and 9 non-pregnant), 149 women with hereditary thrombophilia (HT) (70 pregnant and 79 non-pregnant) affected by AI and 20 anemic pregnant women suffering from various pathologies. In anemic pregnant and non-pregnant women with minor β-thalassemia, presenting undetectable hepcidin levels, differently from ferrous sulfate management, bLf decreased IL-6 (from 25 ± 8 to 6 ± 3 pg/ml) and increased total serum iron (TSI) (from 54 ± 17 to 80 ± 9 μg/dl). BLf was also more efficient than ferrous sulfate in AI treatment in HT pregnant and non-pregnant women by decreasing both serum IL-6 (from 89 ± 8 to 58 ± 6 pg/ml) and hepcidin (from 115 ± 23 to 65 ± 10 ng/ml), thus increasing hematological parameters, such as the number of red blood cells (RBCs), the concentration of hemoglobin, TSI and serum ferritin. BLf was also efficient in treating anemia in other pathological pregnancies. Taken together all the results, bLf, showing a greater benefit and efficacy than the standard ferrous sulfate management, can be considered as a promising compound in treating anemia and AI through its ability to down-regulate IL-6, thus restoring ferroportin-mediated iron export from cells to blood in a hepcidin-dependent or independent way.
Article
Full-text available
The primary stem cells of the cerebral cortex are the radial glial cells (RGC)s, and disturbances in their operation lead to myriad brain disorders in all mammals from mouse to human. Here we found in mice that maternal gestational obesity and hyperglycemia can impair the maturation of RGC fibers and delay cortical neurogenesis. To investigate potential mechanisms, we used optogenetic live imaging approaches in embryonic cortical slices. We found that Ca2+ signaling regulates mitochondrial transport and is crucial for metabolic support in RGC fibers. Cyclic intracellular Ca2+ discharge from localized RGC fiber segments detains passing mitochondria and ensures their proper distribution and enrichment at specific sites such as endfeet. Impairment of mitochondrial function caused an acute loss of Ca2+ signaling, while hyperglycemia decreased Ca2+ activity and impaired mitochondrial transport, leading to degradation of the RGC scaffold. Our findings uncover a novel physiological mechanism indicating pathways by which gestational metabolic disturbances can interfere with brain development.
Article
Full-text available
The central nervous system (CNS) has the highest concentration of lipids in the organism after adipose tissue. Among these lipids, the brain is particularly enriched with polyunsaturated fatty acids (PUFAs) represented by the omega-6 (ω6) and omega-3 (ω3) series. These PUFAs include arachidonic acid (AA) and docosahexaenoic acid (DHA), respectively. PUFAs have received substantial attention as being relevant to many brain diseases, including anxiety and depression. This review addresses an important question in the area of nutritional neuroscience regarding the importance of ω3 PUFAs in the prevention and/or treatment of neuropsychiatric diseases, mainly depression and anxiety. In particular, it focuses on clinical and experimental data linking dietary intake of ω3 PUFAs and depression or anxiety. In particular, we will discuss recent experimental data highlighting how ω3 PUFAs can modulate neurobiological processes involved in the pathophysiology of anxiety and depression. Potential mechanisms involved in the neuroprotective and corrective activity of ω3 PUFAs in the brain are discussed, in particular the sensing activity of free fatty acid receptors and the activity of the PUFAs-derived endocannabinoid system and the hypothalamic–pituitary–adrenal axis.
Article
Full-text available
Background Dietary intake of long-chain omega 3 (n-3) polyunsaturated fatty acids (LCPUFA) represents a putative modifiable risk factor for depression, and a high ratio of omega 6 (n-6) to n-3 LCPUFA is frequently observed in patients with major depressive disorder. Recent reports suggest that the availability of fish and seafood may be associated with lower depression rates. The aim of this study was to investigate associations of fish consumption and LCPUFA levels with depressive symptoms. Methods Participants for this cross-sectional study (n=206) were recruited at a community screening programme in two Torres Strait Islander communities (Mer and Waiben). Depressive symptoms were assessed with the adapted Patient Health Questionnaire-9 (aPHQ-9) and diet with a structured questionnaire. LCPUFA concentrations were measured with a capillary dried blood spot system (PUFAcoat). Logistic and quantile regression modelling was used to test the relationship between seafood consumption, membrane LCPUFAs and depression scores. Results A higher blood n-6/3 LCPUFA ratio was associated with moderate/severe depression scores across both study sites (OR=1.59 (95%CI 1.09-2.34), P = .017). Seafood consumption was higher and the proportion of participants with aPHQ-9 scores above the cut-off for depression was lower on Mer (n = 100) compared with Waiben (n = 106). Higher seafood consumption was associated with lower depression scores on Waiben (B = -0.57 (95%CI -0.98 - -0.16), P = .006) but not on Mer. Conclusions Our findings support an association of n-3 LCPUFA from natural sources with depressive symptoms. The availability of fresh seafood in the local diet may represent a protective factor for depression in this setting.
Article
Full-text available
Physical activity—a lifestyle factor that is associated with immune function, neuroprotection, and energy metabolism—modulates the cellular and molecular processes in the brain that are vital for emotional and cognitive health, collective mechanisms that can go awry in depression. Physical activity optimizes the stress response, neurotransmitter level and function (e.g., serotonergic, noradrenergic, dopaminergic, and glutamatergic), myokine production (e.g., interleukin-6), transcription factor levels and correlates [e.g., peroxisome proliferator-activated receptor C coactivator-1α [PGC-1α], mitochondrial density, nitric oxide pathway activity, Ca2+ signaling, reactive oxygen specie production, and AMP-activated protein kinase [AMPK] activity], kynurenine metabolites, glucose regulation, astrocytic health, and growth factors (e.g., brain-derived neurotrophic factor). Dysregulation of these interrelated processes can effectuate depression, a chronic mental illness that affects millions of individuals worldwide. Although the biogenic amine model has provided some clinical utility in understanding chronic depression, a need remains to better understand the interrelated mechanisms that contribute to immune dysfunction and the means by which various therapeutics mitigate them. Fortunately, convergent evidence suggests that physical activity improves emotional and cognitive function in persons with depression, particularly in those with comorbid inflammation. Accordingly, the aims of this review are to (1) underscore the link between inflammatory correlates and depression, (2) explicate immuno-neuroendocrine foundations, (3) elucidate evidence of neurotransmitter and cytokine crosstalk in depressive pathobiology, (4) determine the immunomodulatory effects of physical activity in depression, (5) examine protocols used to effectuate the positive effects of physical activity in depression, and (6) highlight implications for clinicians and scientists. It is our contention that a deeper understanding of the mechanisms by which inflammation contributes to the pathobiology of depression will translate to novel and more effective treatments, particularly by identifying relevant patient populations that can benefit from immune-based therapies within the context of personalized medicine.
Article
Full-text available
Non-communicable diseases (NSDs) are responsible for two-thirds of all deaths globally, whereas cardiovascular disease (CVD) alone counts for nearly half of them. To reduce the impact of CVD, targeting modifiable risk factors comprised in metabolic syndrome (e.g., waist circumference, lipid profile, blood pressure, and blood glucose) is of great importance. Beneficial effects of fish consumption on CVD has been revealed over the past decades, and some studies suggest that fish consumption may have a protective role in preventing metabolic syndrome. Fish contains a variety of nutrients that may contribute to health benefits. This review examines current recommendations for fish intake as a source of various nutrients (proteins, n-3 fatty acids, vitamin D, iodine, selenium, and taurine), and their effects on metabolic syndrome and the CVD risk factors. Fatty fish is recommended due to its high levels of n-3 fatty acids, however lean fish also contains nutrients that may be beneficial in the prevention of CVD.
Article
Background: Omega-3 polyunsaturated fatty acids, specifically the fish-oil-derived eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been proposed as inflammation-resolving agents via their effects on adipose tissue. Objective: We proposed to determine the effects of EPA and DHA on human adipocyte differentiation and inflammatory activation in vitro. Methods: Primary human subcutaneous adipocytes from lean and obese subjects were treated with 100 μM EPA and/or DHA throughout differentiation (differentiation studies) or for 72 h postdifferentiation (inflammatory studies). THP-1 monocytes were added to adipocyte wells for co-culture experiments. Subcutaneous and visceral adipose explants from obese subjects were treated for 72 h with EPA and DHA. Oil Red O staining was performed on live cells. Cells were collected for mRNA analysis by quantitative polymerase chain reaction, and media were collected for protein quantification by enzyme-linked immunosorbent assay. Results: Incubation with EPA and/or DHA attenuated inflammatory response to lipopolysaccharide (LPS) and monocyte co-culture with reduction in post-LPS mRNA expression and protein levels of IL6, CCL2 and CX3CL1. Expression of inflammatory genes was also reduced in the endogenous inflammatory response in obese adipose. Both DHA and EPA reduced lipid droplet formation and lipogenic gene expression without alteration in expression of adipogenic genes or adiponectin secretion. Conclusions: EPA and DHA attenuate inflammatory activation of in vitro human adipocytes and reduce lipogenesis.