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Journal of Neurology, Neurosurgery, and... Dec 2023Nutritional peripheral neuropathies are a global problem, heavily influenced by geopolitical, cultural and socioeconomic factors. Peripheral neuropathy occurs most... (Review)
Review
Nutritional peripheral neuropathies are a global problem, heavily influenced by geopolitical, cultural and socioeconomic factors. Peripheral neuropathy occurs most frequently secondary to B-vitamin deficiencies, which is suspected to increase in years to come due to the popularity of vegan and vegetarian diets and increased use of bariatric surgery.This review will focus on the common B-vitamins for which a causal link to peripheral neuropathy is more established (vitamins B, B, B, B and B). We will review the historical human and animal data on which much of the clinical descriptions of vitamin deficiencies are based and summarise current available tools for accurately diagnosing a nutritional deficiency. We will also review recently described genetic diseases due to pathogenic variants in genes involved in B-vitamin metabolism that have helped to inform the phenotypes and potential causality of certain B-vitamins in peripheral neuropathy (B and B).Endemic outbreaks of peripheral neuropathy over the last two centuries have been linked to food shortages and nutritional deficiency. These include outbreaks in Jamaican sugar plantation workers in the nineteenth century (Strachan's syndrome), World War two prisoners of war, Cuban endemic neuropathy and also Tanzanian endemic optic neuropathy, which remains a significant public health burden today. An improved understanding of lack of which vitamins cause peripheral neuropathy and how to identify specific deficiencies may lead to prevention of significant and irreversible disability in vulnerable populations.
Topics: Animals; Humans; Peripheral Nervous System Diseases; Vitamin B Complex; Avitaminosis; Malnutrition; Thiamine; Vitamin A; Optic Nerve Diseases
PubMed: 37536924
DOI: 10.1136/jnnp-2022-329849 -
Metabolism: Clinical and Experimental Jul 2023Recent research has revealed causes other than aging that may induce sarcopenia in young people, contrary to the long-studied age-dependent reduction in muscular mass... (Review)
Review
Recent research has revealed causes other than aging that may induce sarcopenia in young people, contrary to the long-studied age-dependent reduction in muscular mass and function. The risk of sarcopenia begins in early adulthood, resulting in exaggerated muscle dysfunction in later life. Despite its clinical significance, research on youth-onset sarcopenia is still in its infancy. Due to a paucity of epidemiologic data and standardized criteria for sarcopenia in youth, determining the prevalence of sarcopenia in the young population remains challenging. Based on the evidence, >1 in every 10 young adults of most ethnicities is estimated to have sarcopenia. This review summarizes the possible etiologies of sarcopenia in young populations, including metabolic syndrome, physical inactivity, inadequate nutrition, inherent and perinatal factors, vitamin D deficiency, endocrinopathy, an imbalance of gut microbiota, neuromuscular diseases, organ failure, malignancy, and other inflammatory disorders. This is the first review of the current knowledge on the importance, prevalence, diagnosis, and causes of sarcopenia in youth.
Topics: Young Adult; Humans; Adolescent; Adult; Sarcopenia; Aging; Metabolic Syndrome; Vitamin D Deficiency; Muscle, Skeletal
PubMed: 37080353
DOI: 10.1016/j.metabol.2023.155557 -
The Journal of Steroid Biochemistry and... Jul 2023In this review, we summarize the most recent advances in vitamin D cancer research to provide molecular clarity, as well as its translational trajectory across the... (Review)
Review
In this review, we summarize the most recent advances in vitamin D cancer research to provide molecular clarity, as well as its translational trajectory across the cancer landscape. Vitamin D is well known for its role in regulating mineral homeostasis; however, vitamin D deficiency has also been linked to the development and progression of a number of cancer types. Recent epigenomic, transcriptomic, and proteomic studies have revealed novel vitamin D-mediated biological mechanisms that regulate cancer cell self-renewal, differentiation, proliferation, transformation, and death. Tumor microenvironmental studies have also revealed dynamic relationships between the immune system and vitamin D's anti-neoplastic properties. These findings help to explain the large number of population-based studies that show clinicopathological correlations between circulating vitamin D levels and risk of cancer development and death. The majority of evidence suggests that low circulating vitamin D levels are associated with an increased risk of cancers, whereas supplementation alone or in combination with other chemo/immunotherapeutic drugs may improve clinical outcomes even further. These promising results still necessitate further research and development into novel approaches that target vitamin D signaling and metabolic systems to improve cancer outcomes.
Topics: Humans; Vitamin D; Proteomics; Vitamins; Neoplasms; Vitamin D Deficiency; Antineoplastic Agents; Receptors, Calcitriol
PubMed: 37054849
DOI: 10.1016/j.jsbmb.2023.106308 -
Annals of Medicine Dec 2023Children's Vitamin D (VitD) fortification and supplementation are diminishing due to less outdoor exercise and insufficient VitD intake (low exogenous intake and... (Review)
Review
Children's Vitamin D (VitD) fortification and supplementation are diminishing due to less outdoor exercise and insufficient VitD intake (low exogenous intake and endogenous malabsorption induced by gastrointestinal disease). Consequently, children in many developed countries suffer from VitD deficiency, which may contribute to many paediatric disorders. Our review briefly introduced the metabolic process of VitD, summarized the role of VitD in paediatric diseases such as autism, obesity, rickets and asthma. We sought to identify the link between VitD deficiency and these diseases.
Topics: Child; Humans; Vitamin D Deficiency; Vitamin D; Vitamins; Obesity; Nutritional Status
PubMed: 36495273
DOI: 10.1080/07853890.2022.2154381 -
BMJ (Clinical Research Ed.) Nov 2023
Topics: Humans; Vitamin B 12; Vitamin B 12 Deficiency; Vitamins
PubMed: 37984968
DOI: 10.1136/bmj-2022-071725 -
Bioscience Reports Oct 2023Thiamine (thiamin, B1) is a vitamin necessary for proper cell function. It exists in a free form as a thiamine, or as a mono-, di- or triphosphate. Thiamine plays a...
Thiamine (thiamin, B1) is a vitamin necessary for proper cell function. It exists in a free form as a thiamine, or as a mono-, di- or triphosphate. Thiamine plays a special role in the body as a coenzyme necessary for the metabolism of carbohydrates, fats and proteins. In addition, it participates in the cellular respiration and oxidation of fatty acids: in malnourished people, high doses of glucose result in acute thiamine deficiency. It also participates in energy production in the mitochondria and protein synthesis. In addition, it is also needed to ensure the proper functioning of the central and peripheral nervous system, where it is involved in neurotransmitter synthesis. Its deficiency leads to mitochondrial dysfunction, lactate and pyruvate accumulation, and consequently to focal thalamic degeneration, manifested as Wernicke's encephalopathy or Wernicke-Korsakoff syndrome. It can also lead to severe or even fatal neurologic and cardiovascular complications, including heart failure, neuropathy leading to ataxia and paralysis, confusion, or delirium. The most common risk factor for thiamine deficiency is alcohol abuse. This paper presents current knowledge of the biological functions of thiamine, its antioxidant properties, and the effects of its deficiency in the body.
Topics: Humans; Thiamine; Thiamine Deficiency; Korsakoff Syndrome; Wernicke Encephalopathy; Vitamin B Complex; Malnutrition
PubMed: 37389565
DOI: 10.1042/BSR20230374 -
Vnitrni Lekarstvi 2023Osteomalacia with characteristic histomorphometric, radiographic, laboratory and clinical features is a prominent syndrome of disturbed bone mineralisation in adulthood....
Osteomalacia with characteristic histomorphometric, radiographic, laboratory and clinical features is a prominent syndrome of disturbed bone mineralisation in adulthood. From an etiological point of view, osteomalacia is usually caused by substrate (calcium, phosphate) deficiency, presence of excess mineralization inhibitors or deficiency or ineffectivness of mineralization facilitator (vitamin D). In proportion to the high number of congenital and acquired causes of osteomalacia, its clinical and laboratory picture is heterogeneous and rarely fully expressed. The treatment of a particular case is determined by the cause of osteomalacia and may (but does not necessarily) include correction of the underlying disease, administration of calcium and various forms of vitamin D, as well as orthopaedic interventions. For some of the hereditary forms, biological or replacement therapy is prospectively available. The article attempts to cover the whole range of osteomalacia variants, mentioning a fact discussed only in recent years - the occurrence of oligosymptomatic, incompletely expressed forms.
Topics: Humans; Osteomalacia; Calcium; Vitamin D; Vitamin D Deficiency; Syndrome; Vitamins
PubMed: 37468295
DOI: 10.36290/vnl.2023.048 -
The Journal of Clinical Endocrinology... Sep 2023Long COVID is an emerging syndrome affecting 50% to 70% of COVID-19 survivors that still lacks predicting factors.
CONTEXT
Long COVID is an emerging syndrome affecting 50% to 70% of COVID-19 survivors that still lacks predicting factors.
OBJECTIVE
Due to the extraskeletal effects of vitamin D, we retrospectively assessed the association between 25(OH) vitamin D levels and long COVID in COVID-19 survivors 6 months after hospitalization.
METHODS
Long COVID was defined according to NICE guidelines. Fifty long COVID and 50 non-long-COVID subjects matched on a 1:1 basis were enrolled from an outpatient clinic post-COVID cohort seen from August to November 2020. Therapies/comorbidities affecting calcium/vitamin D/bone metabolism, and/or admission to the intensive care unit during hospitalization were exclusion criteria. 25(OH) Vitamin D was measured at hospital admission and 6 months after discharge.
RESULTS
We observed lower 25(OH) vitamin D levels, evaluated at follow-up, in subjects with long COVID than those without (20.1 vs 23.2 ng/mL, P = .03). Regarding the affected health areas evaluated in the entire cohort, we observed lower 25(OH) vitamin D levels in those with neurocognitive symptoms at follow-up (n = 7) than those without (n = 93) (14.6 vs 20.6 ng/mL, P = .042). In patients presenting vitamin D deficiency (<20 ng/mL), both at admission and at follow-up (n = 42), those affected by long COVID (n = 22) presented lower 25(OH) vitamin D levels at follow-up than those not affected (n = 20) (12.7 vs 15.2 ng/mL, P = .041). In multiple regression analyses, lower 25(OH) vitamin D levels at follow-up were the only variable significantly associated with long COVID in our cohort (P = .008, OR 1.09, CI 1.01-1.16).
CONCLUSION
COVID-19 survivors with long COVID have lower 25(OH) vitamin D levels than matched patients without long COVID. Our data suggest that vitamin D levels should be evaluated in COVID-19 patients after hospital discharge. The role of vitamin D supplementation as a preventive strategy of COVID-19 sequelae should be tested in randomized controlled trials.
Topics: Humans; COVID-19; Post-Acute COVID-19 Syndrome; Retrospective Studies; Vitamin D; Vitamin D Deficiency; Vitamins; Survivors
PubMed: 37051747
DOI: 10.1210/clinem/dgad207 -
Advances in Food and Nutrition Research 2024The role of vitamin D in the prevention of chronic diseases including cancer, has received a great deal of attention during the past few decades. The term "Cancer"... (Review)
Review
The role of vitamin D in the prevention of chronic diseases including cancer, has received a great deal of attention during the past few decades. The term "Cancer" represents multiple disease states with varying biological complexities. The strongest link between vitamin D and cancer is provided by ecological and studies like observational, in preclinical models. It is apparent that vitamin D exerts diverse biological responses in a tissue specific manner. Moreover, several human factors could affect bioactivity of vitamin D. The mechanism(s) underlying vitamin D initiated anti-carcinogenic effects are diverse and includes changes at the muti-system levels. The oncogenic environment could easily corrupt the traditional role of vitamin D or could ensure resistance to vitamin D mediated responses. Several researchers have identified gaps in our knowledge pertaining to the role of vitamin D in cancer. Further areas are identified to solidify the role of vitamin D in cancer control strategies.
Topics: Humans; Vitamin D; Neoplasms; Animals; Vitamin D Deficiency
PubMed: 38777419
DOI: 10.1016/bs.afnr.2023.12.002 -
International Journal of Molecular... Jul 2023Exclusive breastfeeding is considered the ideal food in the first six months of life; however, paradoxically, vitamin D content in human breast milk is clearly low and... (Review)
Review
Exclusive breastfeeding is considered the ideal food in the first six months of life; however, paradoxically, vitamin D content in human breast milk is clearly low and insufficient to obtain the recommended intake of 400 IU daily. This article summarizes the extraordinary metabolism of vitamin D during pregnancy and its content in human breast milk. The prevalence of hypovitaminosis D in pregnant women and/or nursing mothers and its potential maternal-fetal consequences are analyzed. The current guidelines for vitamin D supplementation in pregnant women, nursing mothers, and infants to prevent hypovitaminosis D in breastfed infants are detailed. Low vitamin D content in human breast milk is probably related to active changes in human lifestyle habits (reduced sunlight exposure).
Topics: Infant; Female; Humans; Pregnancy; Vitamin D; Breast Feeding; Dietary Supplements; Vitamins; Vitamin D Deficiency; Rickets; Milk, Human
PubMed: 37569256
DOI: 10.3390/ijms241511881