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Chemosensory Disorders and Nutrition
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
Carl M. Wahlstrom, Alan R. Hirsch, Bradley W. Whitman
Some primary nutritional deficiency states have also been associated with chemosensory pathology. Hypovitaminosis A induces both hyposmia and hypogeusia that usually resolves within two months with Vitamin A replacement (Sauberlich 1975). The mechanism of the deficit may be a result of epithelial proliferation and drying, which forms a physical barrier that prevents odorants and tastants from reaching their respective receptors (Friedman and Mattes 1991).
Nutrition and Immunity
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Srinivas Denduluri, Ranjit Kumar Chandra
In humans, isolated vitamin A deficiency seldom occurs, and it is usually associated with protein energy malnutrition (PEM). In animals vitamin A deficiency has been shown to depress antibody responses to immunizations and decrease cellular-mediated immunity [18,19]. Vitamin A deficiency in animals resulted in atrophy of spleens and thymuses, with thymic cortices affected mostly and with complete depletion of lymphocytes [18]. The literature on the association between hypovitaminosis A and bacterial and viral infections has been reviewed [20,21], Many pathological mechanisms probably contribute to the increased risk of infection in vitamin A deficiency, including tissue changes and altered specific and nonspecific immunity. Furthermore, infection itself can aggravate vitamin A deficiency.
Nutritional Disorders/Alternative Medicine
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
A number of disease states can be classified under the heading of nutritional disorders, but all relate to the body's supply of or need for one or more nutrients and usually arise from either altered consumption or absorption. Some are usually unintentionally induced, such as the variety of conditions resulting from either an excess (hypervitaminosis) or a deficiency (hypovitaminosis) of the vitamins. Others such as malnutrition are often either economic in origin or arise from an inappropriate diet for other reasons. And some are often considered to be psychological disorders—anorexia nervosa, bulimia, and obesity—although they have been presented in this section since their effects are manifested on the nutritional status of the body.
Efficacy of B-vitamins and vitamin D therapy in improving depressive and anxiety disorders: a systematic review of randomized controlled trials
Published in Nutritional Neuroscience, 2023
Jaqueline G. Borges-Vieira, Camila K. Souza Cardoso
It is valuable to mention three potential risk factors for B vitamins deficiency to be considered in patients experiencing MDD and/or GAD for clinical practice follow-up. The levels of B vitamins may be impacted due to low dietary intake, impaired absorption capacity, or genetic mutations that alter the expression of enzymes involved in the metabolism of B vitamins — in addition to diverse other pathophysiological mechanisms that may occur [37]. First, low dietary vitamin intake may occur because of changes in appetite (undereating or overeating) typical from the clinical course and symptomatology of depression and/or anxiety according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [61]. These responses may be linked to differences in the level of neurocircuit activity (hypoactivation or hyperactivation in response to food) in different brain regions [99]. Also, appetite changes can be a common adverse effect of some SSRIs like sertraline [100] and quetiapine [101]. In any case, hypovitaminosis can be a consequence of either malnutrition or unhealthy overfeeding. Unhealthy dietary pattern (essentially defined as high in refined grains, bread, fat dairy, liquid oils, solid oils, soft drinks, industrial fruit juices, red meats, poultry, processed meats, and sweets) was associated with an increased risk of depression by contributing to a low serum concentration of folate, vitamin B12 [102], and vitamin D [103].
Impact of vitamin deficiency on microbiota composition and immunomodulation: relevance to autistic spectrum disorders
Published in Nutritional Neuroscience, 2021
Roberta Ribeiro, Jacques Robert Nicoli, Gesivaldo Santos, Jane Lima-Santos
Since the first report in the literature by Cannell [50], hypovitaminosis D has been the most studied vitamin deficiency in the development of ASD in utero and in childhood. In a recent cohort study, low levels of vitamin D during pregnancy demonstrated as being strongly related to the increase of ASD risk and cognitive disabilities [51] (Table 1). Furthermore, low levels of vitamin D have been found in the serum of children with ASD and cognitive disabilities [6566–67]. Although the mechanism of vitamin D deficiency correlates with ASD development remains poorly understood, studies in murine models have shown that vitamin D deficiency during pregnancy induces oxidative stress, affects calcium signalization, neurotransmission, and expression of important genes for development of language, intelligence and other cognitive skills, such as the brain-derived neurotrophic factor (BDNF) and forkhead box protein P2 (Foxp2) [6263–64] (Table 1).
Absence of impact of hypovitaminosis C on the bleeding phenotype of primary immune thrombocytopenia: a French prospective multicenter study
Published in Platelets, 2020
Julien Le Marec, Hélène Henique, Emma Rubenstein, Adrien Bigot, Mathieu Puyade, Geoffrey Urbanski, Pierre Lozac’h, Jean-Sébastien Allain, Guillaume Bayer, Olivier Fain, Bertrand Lioger
Overall hemorrhagic symptoms were reported in 19 patients (56%), mainly consisting of cutaneous bleeding (bruising or petechial purpura) or oral bleeding (bullae or gum bleeding). Mean modified Khellaf bleeding score was 2 ± 3. Six patients (18%) had both hypovitaminosis C and bleeding. No difference was found between hypovitaminosis C patients and controls in frequency, severity of bleeding, and in severity of thrombocytopenia (p = 0.61; 0.64; and 0.95, respectively). Conversely, vitamin C concentration was not statistically different between patients with or without hemorrhagic signs (40.2 ± 22.3 µmol/l vs. 41.76 ± 34.9 µmol/l, p = 0.81). No correlation was found between modified Khellaf bleeding score and vitamin C concentration (R2 = 0.00052654, p = 0.89, Supplement 3). Moreover, assessment of malnutrition parameters identified one patient with malnutrition in each group and no difference of BMI or serum albumin concentration between hypovitaminosis C patients and controls (p = 0.58 and 0.47, respectively). A lower consumption of fruit and vegetables was observed in patients with hypovitaminosis C, though the limited number of questionnaires available (53%) does not allow us to draw any conclusion.