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Nutrition in Clinical Practice :... Feb 2024Chronic pancreatitis (CP) is often associated with exocrine pancreatic insufficiency (EPI), which may increase risk for fat-soluble vitamin depletion. Although vitamin D... (Review)
Review
Chronic pancreatitis (CP) is often associated with exocrine pancreatic insufficiency (EPI), which may increase risk for fat-soluble vitamin depletion. Although vitamin D deficiency is widespread among the general population, vitamins A, E, and K deficiencies may more uniquely present in patients with CP. Yet, it is unclear whether fat-soluble vitamin status should be routinely monitored in all patients with CP or limited to those with EPI. The purpose of this review is to describe the laboratory status of vitamins A, E, and K in adult patients with CP and their association with exocrine pancreatic function. Five primary, observational studies met the inclusion criteria for qualitative synthesis. Biochemical deficiencies in fat-soluble vitamins were observed across trials but results varied with respect to whether EPI increased risk. Challenges related to the diagnosis and treatment of EPI along with potential confounders may contribute to the heterogeneity among study results. Although more studies are needed to determine the influence of pancreatic enzyme replacement therapy on fat-soluble vitamin status as well as effective vitamin repletion strategies, clinicians should consider periodically screening for deficiencies in all patients with CP regardless of EPI to avoid associated health effects of vitamin depletion.
Topics: Adult; Humans; Vitamins; Pancreatitis, Chronic; Exocrine Pancreatic Insufficiency; Pancreas; Avitaminosis; Vitamin A; Vitamin K
PubMed: 37840401
DOI: 10.1002/ncp.11082 -
The British Journal of Psychiatry : the... Jun 1990
Review
Topics: Ascorbic Acid Deficiency; Avitaminosis; Folic Acid Deficiency; Humans; Mental Disorders; Vitamin B Deficiency
PubMed: 2207521
DOI: 10.1192/bjp.156.6.878 -
Current Pharmaceutical Design 2018The issue of vitamin deficiency persists to be a major health issue worldwide despite the advancements in medicine. At the same time, the effect of marginal vitamin... (Review)
Review
The issue of vitamin deficiency persists to be a major health issue worldwide despite the advancements in medicine. At the same time, the effect of marginal vitamin deficiency status on physiological processes is proven. However, general methods such as immune-enzyme and fluorescence analysis, microbiological assays, for example, have limitations in vitamin status assessment and are not able to reliably reflect personal vitamin demand. The potential usefulness of modern metabolomics methods in vitamin status assessment is described in this review. These methods can be used for vitamin metabolites detection as well as for comprehensive metabolic phenotyping that makes them even more valuable.
Topics: Avitaminosis; Humans; Metabolomics; Vitamins
PubMed: 30207224
DOI: 10.2174/1381612824666180912142743 -
Handbook of Clinical Neurology 2010The vitamine doctrine: Although diseases resulting from vitamin deficiencies have been known for millennia, such disorders were generally attributed to toxic or... (Review)
Review
The vitamine doctrine: Although diseases resulting from vitamin deficiencies have been known for millennia, such disorders were generally attributed to toxic or infectious causes until the "vitamin doctrine" was developed in the early 20th century. In the late-19th century, a physiologically complete diet was believed to require only sufficient proteins, carbohydrates, fats, inorganic salts, and water. From 1880-1912, Lunin, Pekelharing, and Hopkins found that animals fed purified mixtures of known food components failed to grow or even lost weight and died, unless the diet was supplemented with small amounts of milk, suggesting that "accessory food factors" are required in trace amounts for normal growth. By this time, Funk suggested that deficiencies of trace dietary factors, which he labeled "vitamines" on the mistaken notion that they were "vital amines," were responsible for such diseases as beriberi, scurvy, rickets, and pellagra. Vitamin A deficiency eye disease: Night blindness was recognized by the ancient Egyptians and Greeks, and many authorities from Galen onward advocated liver as a curative. Outbreaks of night blindness were linked to nutritional causes in the 18th and 19th centuries by von Bergen, Schwarz, and others. Corneal ulceration was reported in 1817 by Magendie among vitamin A-deficient dogs fed for several weeks on a diet limited to sugar and water, although he erroneously attributed this to a deficiency of dietary nitrogen (i.e. protein). Subsequently, corneal epithelial defects, often in association with night blindness, were recognized in malnourished individuals subsisting on diets now recognizable as deficient in vitamin A by Budd, Livingstone, von Hubbenet, Bitot, Mori, Ishihari, and others. During World War I, Bloch conducted a controlled clinical trial of different diets among malnourished Danish children with night blindness and keratomalacia and concluded that whole milk, butter, and cod-liver oil contain a fat-soluble substance that protects against xerophthalmia. Early retinal photochemistry: In the 1870s, Boll found that light causes bleaching of the retinal pigment, and suggested that the outer segments of the rods contain a substance that conveys an impression of light to the brain by a photochemical process. Shortly thereafter, Kühne demonstrated that the bleaching process depends upon light, and was reversible if the retinal pigment epithelium was intact. Kühne proposed an "optochemical hypothesis," a prescient concept of photochemical transduction, attributing vision to a photochemical change in visual purple (rhodopsin) with resulting chemical products stimulating the visual cells and thereby conveying a visual image. Vitamin A: In 1913, Ishihara proposed that a "fatty substance" in blood is necessary for synthesis of both rhodopsin and the surface layer of the cornea, and that night blindness and keratomalacia develop when this substance is deficient. That year McCollum and Davis (and almost simultaneously Mendel and Osborne) discovered a fat-soluble accessory food factor (later called "fat-soluble A") distinct from the water-soluble anti-beriberi factor (later called "fat-soluble B"). By 1922 McCollum and colleagues distinguished two vitamins within the fat-soluble fraction, later named vitamins A and D. In 1925 Fridericia and Holm directly linked vitamin A to night blindness in animal experiments using rats, and in 1929 Holm demonstrated the presence of vitamin A in retinal tissue. In the 1930s, Moore, Karrer, Wald, and others established the provitamin role of beta-carotene. Karrer and colleagues isolated beta-carotene (the main dietary precursor of vitamin A) and retinol (vitamin A), and determined their chemical structures. In 1947, Isler and colleagues completed the full chemical synthesis of vitamin A. Modern retinal photochemistry: Beginning in the 1930s, Wald and colleagues greatly elaborated the photochemistry of vision, with the discovery of the visual cycle of vitamin A, demonstration that rhodopsin is decomposed by light into retinal (the aldehyde form of vitamin A) and a protein (opsin), elaboration of the enzymatic conversions of various elements in the rhodopsin system, and discovery that the rhodopsin system is dependent on a photoisomerization of retinal. In 1942, Hecht and colleagues demonstrated that a single photon could trigger excitation in a rod. In 1965, Wald suggested that a large chemical amplification was necessary for this degree of light sensitivity, likely by a cascade of enzymatic reactions. Later studies elaborated this cascade and found that an intermediary in the photoisomerization of retinal interacts with transducin, a G-protein, to activate phosphodiesterases that control cyclic GMP levels, which in turn modulate the release of neurotransmitter from the rod cell. Public health: Although the availability of vitamin A through food fortification and medicinal supplements virtually eliminated ocular vitamin A deficiency from developed countries by the second half of the 20th century, vitamin A deficiency remains a serious problem in developing countries as indicated by global surveys beginning in the 1960s. Millions of children were shown to be vitamin A deficient, with resultant blindness, increased susceptibility to infection, and increased childhood mortality. Beginning in the 1960s, intervention trials showed that vitamin A deficiency disorders could be prevented in developing countries with periodic vitamin A dosing, and in the 1980s and 1990s, large randomized, double-blind, placebo-controlled clinical trials demonstrated the marked efficacy of vitamin A supplementation in reducing childhood mortality.
Topics: Animals; Avitaminosis; History, 19th Century; History, 20th Century; Humans; Malnutrition; Nervous System Diseases; Night Blindness; Vitamin A; Vitamin A Deficiency
PubMed: 19892132
DOI: 10.1016/S0072-9752(08)02129-5 -
Breastfeeding Medicine : the Official... Apr 2020
Topics: Avitaminosis; Dietary Supplements; Double-Blind Method; Female; Humans; Infant; Lactation; Mothers; Vitamin D
PubMed: 32105501
DOI: 10.1089/bfm.2020.0035 -
Duodecim; Laaketieteellinen... 2010Encephalopathy may develop within 1 to 3 weeks upon cessation of thiamine supply. Deficiency of folic acid may require months until encephalopathy develops, whereas this... (Review)
Review
Encephalopathy may develop within 1 to 3 weeks upon cessation of thiamine supply. Deficiency of folic acid may require months until encephalopathy develops, whereas this may take years for vitamin B12 deficiency. It may be harmful for the patient if the impairment of cognitive functions is considered to be due to Alzheimer's disease, even though vitamin deficiency is the cause. Differential diagnosis, however, is not easy. Risk factors for vitamin deficiencies include reduction of body weight, associated surgical procedures and nausea during pregnancy.
Topics: Alzheimer Disease; Cognition Disorders; Diagnosis, Differential; Folic Acid Deficiency; Humans; Risk Factors; Vitamin B 12 Deficiency
PubMed: 21072960
DOI: No ID Found -
Proceedings of the National Academy of... Oct 2018It is proposed that proteins/enzymes be classified into two classes according to their essentiality for immediate survival/reproduction and their function in long-term... (Review)
Review
It is proposed that proteins/enzymes be classified into two classes according to their essentiality for immediate survival/reproduction and their function in long-term health: that is, survival proteins versus longevity proteins. As proposed by the triage theory, a modest deficiency of one of the nutrients/cofactors triggers a built-in rationing mechanism that favors the proteins needed for immediate survival and reproduction (survival proteins) while sacrificing those needed to protect against future damage (longevity proteins). Impairment of the function of longevity proteins results in an insidious acceleration of the risk of diseases associated with aging. I also propose that nutrients required for the function of longevity proteins constitute a class of vitamins that are here named "longevity vitamins." I suggest that many such nutrients play a dual role for both survival and longevity. The evidence for classifying taurine as a conditional vitamin, and the following 10 compounds as putative longevity vitamins, is reviewed: the fungal antioxidant ergothioneine; the bacterial metabolites pyrroloquinoline quinone (PQQ) and queuine; and the plant antioxidant carotenoids lutein, zeaxanthin, lycopene, α- and β-carotene, β-cryptoxanthin, and the marine carotenoid astaxanthin. Because nutrient deficiencies are highly prevalent in the United States (and elsewhere), appropriate supplementation and/or an improved diet could reduce much of the consequent risk of chronic disease and premature aging.
Topics: Animals; Avitaminosis; Dietary Proteins; Humans; Longevity; Models, Biological; United States; Vitamins
PubMed: 30322941
DOI: 10.1073/pnas.1809045115 -
Neoplasma 2008Secondary cancers are among the most threatening long-term health problems of hematopoetic stem cell- transplant (HSCT) patients. There are several lines of evidence... (Review)
Review
Secondary cancers are among the most threatening long-term health problems of hematopoetic stem cell- transplant (HSCT) patients. There are several lines of evidence indicating the possibility of a prolonged Vitamin A deficiency for solid tumor-type secondary cancers: I- Solid tumors such as oral cavity, head/neck region squamous carcinomas, skin cancers and melanomas, where lowered Vitamin A concentrations and chemo-preventing activity of its derivatives (retinoids) are most explicitly proven, arise much more frequently than others. II- Early monitorings: A significant retinol deficiency in HSCT patients is detectable along with a severity of mucositis and the vulnerability to infection. III- Monitoring of other liposoluble vitamins: Vitamin D, a differentiation-inducing vitamin like Vitamin A, showed a sustained decrease. Another similarity of these two vitamins is that they also depend on intestinal absorption and are decreased due to bowel injury by conditioning agents and chronic graft-versus-host disease. IV- Peroxidative reactions and inflammation can directly exhaust retinol levels despite sufficient intake. Considering the similar inhibitory role of Vitamin D analogs (deltanoids) on squamous carcinomas, skin tumors and melanomas, we propose that animal studies and extended vitamin surveillance studies in HSCT patients may unfold a preventive strategy against long-term complications.
Topics: Animals; Avitaminosis; Cell Differentiation; Hematopoietic Stem Cell Transplantation; Humans; Intestinal Absorption; Neoplasms, Second Primary; Retinoids; Vitamin A; Vitamin A Deficiency; Vitamin D Deficiency
PubMed: 18190234
DOI: No ID Found -
Nihon Rinsho. Japanese Journal of... Apr 1993Fat-soluble vitamin deficiency and marginal deficiency of this type of vitamin will be discussed. The trias of vitamin A deficiency is composed of nyctalopia,... (Review)
Review
Fat-soluble vitamin deficiency and marginal deficiency of this type of vitamin will be discussed. The trias of vitamin A deficiency is composed of nyctalopia, xerophthalmia and hyperkeratosis follicularis. Vitamin D deficiency causes rachitis and osteomalacia. In Japan, vitamin D deficiency is more often caused by impaired vitamin D activation due to renal failure, than by a lack of sunbathing or insufficient ingestion of vitamin D from diet. At present, it is quite rare that the physician encounters patients with deficiency of vitamin E or other vitamins. According to surveys of occult vitamin deficiency, the prevalence of marginal fat-soluble vitamin deficiency was lower than that of marginal water-soluble vitamin deficiency. Marginal vitamin deficiency seems to be absent or very rare among healthy individuals. In patients, however, marginal vitamin deficiency is sometimes observed. Since marginal vitamin deficiency can modify the underlying disease or trigger complications, the physician should take adequate measures to prevent the onset of marginal vitamin deficiency in managing patients with various diseases.
Topics: Humans; Vitamin A Deficiency; Vitamin D Deficiency; Vitamin E Deficiency; Vitamin K Deficiency
PubMed: 8483279
DOI: No ID Found -
Hormone and Metabolic Research =... Mar 2023A synergistic interplay between vitamins K and D appears to exist. We aimed to investigate for the first time whether the associations of dietary vitamin K intake and...
A synergistic interplay between vitamins K and D appears to exist. We aimed to investigate for the first time whether the associations of dietary vitamin K intake and circulating 25(OH)D with serum lipoprotein levels are influenced by the existence of deficiency of either or both vitamins K and D. Sixty individuals [24 males, 36(18-79) years old] were examined. Vitamin deficiency of K1 and D were defined as vitamin K1 intake/body weight (BW)<1.00 μg/kg/day and circulating 25(OH)D<20 ng/ml, respectively. In individuals with vitamin K1 deficiency, the vitamin K1 intake/BW correlated positively with high density lipoprotein-cholesterol (HDL-C) (r=0.509, p=0.008) and negatively with serum triglycerides (TG) (r=-0.638, p=0.001), whereas circulating 25(OH)D correlated negatively with TG (r=-0.609, p=0.001). In individuals with vitamin D deficiency, the vitamin K1 intake/BW correlated positively with HDL-C (r=0.533, p=0.001) and negatively with TG (r=-0.421, p=0.009), while circulating 25(OH)D correlated negatively with TG (r=-0.458, p=0.004). The above-mentioned associations of vitamin K1 intake/BW and circulating 25(OH)D with serum lipoproteins were not detected in individuals without vitamin K1 deficiency or the ones without vitamin D deficiency. The vitamin K2 intake/BW correlated negatively with low density lipoprotein-cholesterol (LDL-C) (r=-0.404, p=0.001). In conclusion, the associations of vitamin K1 intake with TG and HDL-C and of circulating 25(OH)D with TG were more pronounced in individuals with deficiency of either or both vitamins K1 and D. Increased dietary vitamin K2 intake was associated with decreased LDL-C.
Topics: Male; Humans; Adolescent; Young Adult; Adult; Middle Aged; Aged; Vitamin K 1; Vitamin K 2; Cholesterol, LDL; Vitamins; Avitaminosis; Vitamin K; Vitamin D Deficiency; Body Weight; Cholesterol, HDL
PubMed: 36848929
DOI: 10.1055/a-2020-2080