Vitamin E or tocopherol is a fat-soluble vitamin functioning as an antioxidant, protecting the cell membrane. As with all vitamins, the body does not form vitamin E. It solely forms from photosynthetic processes of plants, and therefore must be consumed from outside sources in small quantities. It is found abundantly in olive and sunflower oils, as well as nuts, soybeans, avocados, wheat, and green leafy vegetables.
In the present study, we examined the effect of high fructose-induced metabolic syndrome (MetS) on tissue vitamin E and lipid peroxide (LPO) levels in rats. Feeding of a diet containing 60% fructose (HFD) to Wistar rats for 2, 4, and 6 wk caused week-dependent increases in HOMA-IR score and serum insulin, triglyceride, total cholesterol, and free fatty acid concentrations. Each week HFD feeding increased serum vitamin E concentration. Six-week HFD feeding reduced vitamin E status (the serum ratio of vitamin E/triglyceride+total cholesterol). Four- and 6-wk HFD feeding increased serum LPO concentration. Two-week HFD feeding increased liver, heart, kidney, and skeletal muscle (SM) vitamin E contents and decreased white adipose tissue (WAT) vitamin E content. Four- and 6-wk HFD feeding further reduced WAT vitamin E content without affecting the increased kidney and SM vitamin E contents. Six-week HFD feeding reduced the increased liver and heart vitamin E contents below the level of non-HFD feeding. Four-week HFD feeding increased heart and WAT LPO contents. Six-week HFD feeding increased liver LPO content and further increased heart and WAT LPO contents. Kidney and SM LPO contents remained unchanged. These results indicate that HFD-rats with early MetS have increased liver, kidney, heart, and SM vitamin E contents and decreased WAT vitamin E content under unchanged tissue LPO content and vitamin E status, while HFD-fed rats with progressed MetS have both decreased liver, heart, and WAT vitamin E contents under increased tissue LPO content and disrupted vitamin E status.
“E-cigarettes” are a class of consumer devices designed to deliver drugs, primarily nicotine or marijuana oils, to the lung by vaporization. Regulation of the devices in the United States is relatively minimal, and research on both epidemiology and potential toxicity has focused on nicotine devices. In 2019, an outbreak of an acute respiratory illness in the United States was traced back to the contamination of e-cigarette fluids with vitamin E acetate, which had been used to disguise the dilution of marijuana oils. The outbreak, termed “e-cigarette or vaping associated lung injury” by the U.S. Centers for Disease Control, was characterized by pulmonary infiltrates and hypoxia, which usually required hospitalization and, often, admission to ICUs. The syndrome sickened >2,600 people, mostly young men, and killed >50 people before it began to abate 6 months later. No current regulations exist to prevent a similar event with the same or different chemical contaminants. Absent such regulation, respiratory practitioners should be prepared to evaluate, identify, and treat future cases of acute lung toxicity from e-cigarettes.
Background: Vitamins are commonly used in the prevention of major cardiovascular disease. However, the efficacy and optimum choice remain controversial.
Objective: To compare and rank the relative efficacy among all available vitamin preparations for cardiovascular disease through a network meta-analysis.
Methods: Eligible studies were identified by searching PubMed, Embase, Medline, Cochrane library and Web of Science for randomized controlled trials. A random effects model was applied within a frequentist framework.
Results: Forty-two articles (45 comparisons, 384,248 participants), including nine vitamin interventions, were identified. Vitamin D had the highest probability of being ranked best in effectiveness (0.84 [0.72, 0.98]) on prevention of cardiovascular events. With regard to reducing death of cardiovascular disease rate, vitamin E was considered better efficacy.
Conclusions: Vitamin B, D and E could reduce the incidence of cardiovascular events to varying degrees. At the same time, the combination of vitamins can not show improvement on the efficacy.
When the dairy cow is fed grass with a naturally high vitamin E content, the milk’s content of vitamin E is higher than when the cow is primarily fed feed containing synthetic vitamin E, finds new research.
Nonalcoholic fatty liver disease (NAFLD) has emerged as the leading liver disease globally. NAFLD patients can have a progressive phenotype, non-alcoholic steatohepatitis (NASH) that could lead to cirrhosis, liver failure and cancer. There is a close bi-directional relationship between NAFLD and type 2 diabetes mellitus (T2DM); NAFLD increases the risk for T2DM and its complications whereas T2DM increases the severity of NAFLD and its complications. The large global impact of NAFLD and T2DM on healthcare systems requires a paradigm shift from specialty care to early identification and risk stratification of NAFLD in primary care and diabetes clinics. Approach to diagnosis, risk stratification and management of NAFLD is discussed. In addition to optimizing the control of coexisting cardiometabolic comorbidities, early referral of NAFLD patients at high risk of having NASH or significant fibrosis to hepatology specialist care may improve management and allow access for clinical trials. Lifestyle modifications, vitamin E, pioglitazone and metformin are currently available options that may benefit patients with T2DM and NAFLD. The burst of clinical trials investigating newer therapeutic agents for NAFLD and NASH offer hope for new, effective and safe therapies in the near future.
Abstract
The pathogenesis of celiac disease (CD) is complex and has not been fully elucidated. It has been postulated that oxidative stress, because of an increase in the concentration of reactive oxygen species and antioxidant capacity reduction, is one of the processes possibly involved in gliadin toxicity. Oxidative imbalance induced by gliadin peptides in enterocytes leads to the activation of the transcription of proinflammatory cytokines and enzymes, such as inducible nitric oxide synthase (iNOS), which in turn causes an increased production of nitric oxide (NO) metabolites favoring oxidative stress. Based on the our previous study, we hypothesized that persistent nitrosative stress despite gluten-free diet (GFD) may be responsible for persistent histopathologic changes and that GFD is only partially able to improve oxidative imbalance. Hence, serum NO levels seem to be useful as a marker of treatment efficacy, and alterations in these levels could indicate CD activity. It is possible that oral antioxidant supplementation may decrease the toxic effects of peptides. In the current study, we aimed to evaluate the effect of treatment with oral vitamin E on oxidative imbalance in adult patients with CD on GFD. For that purpose, we assessed the fasting plasma levels of nitrate as a marker of endogenous NO production and oxidative stress. Moreover, we monitored the individual components of antioxidant capacity. To the best of our knowledge, this is the first study evaluating the effects of oral vitamin E supplementation on oxidative imbalance in patients with CD.
The main findings of this project include the following: the amount of RRR-alpha-tocopherol, a natural form of vitamin E, accounts for more than 75 percent of the total alpha-tocopherol in breast milk and umbilical cord blood; Xanthophyll is of the highest amount compared with any other carotenoid to promote fetuses’ and infants’ visual development.
An interesting analytical challenge still exists for measuring vitamin E in foods. In the US, the FDA defines declarable vitamin E as alpha‑tocopherol where there is both a very bioactive naturally‑occurring form, and a less bioactive man‑made form.1 The FDA requires manufacturers to make and keep written records to verify the amount of both forms1 because there is no recognised analytical method that differentiates between the two. Until a method is developed and internationally recognised, the lab needs to have access to those records to properly calculate the amount placed in a nutritional facts panel.
Many people struggle to quit smoking cigarettes to prevent and slow lung diseases, such as chronic obstructive pulmonary disorder.
Nicotine is such an addictive substance that in a desperate attempt to get healthy many people turned to e-cigarettes, which delivered the nicotine in a vapor instead of smoke. But instead of getting healthier, these former smokers got worse. In addition, healthy, young people started experimenting with recreational vaping, and despite their health and youth, they, too, developed serious lung problems.
Why did this happen? What went wrong?