34 hot topic(s) found with the query "Vitamin d"
Comprehensive evaluation of smoking exposures and their interactions on DNA methylation
TT Hoang et al, EBiomedicine, January 9, 2024
(Posted: Jan 10, 2024 8AM)
From the abstract: "Smoking impacts DNA methylation, but data are lacking on smoking-related differential methylation by sex or dietary intake, recent smoking cessation (<1 year), persistence of differential methylation from in utero smoking exposure, and effects of environmental tobacco smoke (ETS). We meta-analysed data from up to 15,014 adults across 5 cohorts with DNA methylation measured in blood using Illumina's EPIC array for current smoking (2560 exposed), quit < 1 year (500 exposed), in utero (286 exposed), and ETS exposure (676 exposed). We also evaluated the interaction of current smoking with sex or diet (fibre, folate, and vitamin C)."
Cord blood DNA methylation signatures associated with preeclampsia are enriched for cardiovascular pathways: insights from the VDAART trial.
Hanna M Knihtilä et al. EBioMedicine 2023 11 104890
(Posted: Nov 29, 2023 9AM)
From the abstract: "Preeclampsia has been associated with maternal epigenetic changes, in particular DNA methylation changes in the placenta. It has been suggested that preeclampsia could also cause DNA methylation changes in the neonate. We examined DNA methylation in relation to gene expression in the cord blood of offspring born to mothers with preeclampsia. This study included 128 mother-child pairs who participated in the Vitamin D Antenatal Asthma Reduction Trial (VDAART), where assessment of preeclampsia served as secondary outcome. We found that preeclampsia is related to differential cord blood DNA methylation signatures of cardiovascular pathways, including the apelin signaling pathway. "
International electronic health record-derived post-acute sequelae profiles of COVID-19 patients
HG Zhang et al, NPJ Digital Medicine, June 29, 2022
(Posted: Jun 29, 2022 7PM)
We leveraged electronic health record (EHR) data from 277 international hospitals representing 414,602 patients with COVID-19, 2.3 million control patients without COVID-19 in the inpatient and outpatient settings, and over 221 million diagnosis codes to systematically identify new-onset conditions enriched among patients with COVID-19 during the post-acute period. Compared to inpatient controls, inpatient COVID-19 cases were at significant risk for angina pectoris (RR 1.30, 95% CI 1.09–1.55), heart failure (RR 1.22, 95% CI 1.10–1.35), cognitive dysfunctions (RR 1.18, 95% CI 1.07–1.31), and fatigue (RR 1.18, 95% CI 1.07–1.30). Relative to outpatient controls, outpatient COVID-19 cases were at risk for pulmonary embolism (RR 2.10, 95% CI 1.58–2.76), venous embolism (RR 1.34, 95% CI 1.17–1.54), atrial fibrillation (RR 1.30, 95% CI 1.13–1.50), type 2 diabetes (RR 1.26, 95% CI 1.16–1.36) and vitamin D deficiency (RR 1.19, 95% CI 1.09–1.30).
Man whose genetic condition went undiagnosed for 36 years is awarded £2.5m.
Thornton Jacqui et al. BMJ (Clinical research ed.) 2022 1 o238
(Posted: Jan 29, 2022 11AM)
A man with a rare, progressive, genetic condition who was only diagnosed aged 36 once his sister was found to have a milder form of the disease has been awarded £2.5m in a High Court settlement. The brother, who cannot be identified, was finally diagnosed with the disorder methylmalonic acidemia type CblA after his sister fought as an adult for a diagnosis herself and then paid for private tests which showed he had the same condition. If spotted early enough, the metabolic condition can be treated with a lifetime regime of intramuscular vitamin B12 injections, which can avoid the development of clinical symptoms
Genomics elucidates both common and rare disease aetiology
A McNeil, EJHG, November 26, 2021
(Posted: Nov 28, 2021 10AM)
We close the year with a range of interesting and informative papers. Birth defects (congenital anomalies) affect many thousands of neonates every year; yet the aetiology of many of them remains unresolved. A new paper reviews what is known about the genomic basis of congenital diaphragmatic hernia (CDH). Around 10% of cases of CDH are associated with a copy number variant. Implicated pathways include NRF2 and vitamin A homeostasis. In contrast to common malformations, the genetic basis of rare disease continues to be elucidated with more and more causal genes identified annually
The effect of circulating zinc, selenium, copper and vitamin K1 on COVID-19 outcomes: a Mendelian randomization study
MK Sobczyk et al, MEDRXIV, October 19, 2021
(Posted: Oct 20, 2021 4AM)
The causal effect of serum vitamin D concentration on COVID-19 susceptibility, severity and hospitalization traits: a Mendelian randomization study
Z Cui et al, MEDRXIV, March 13, 2021
(Posted: Mar 14, 2021 10AM)
Genetically predicted serum vitamin D and COVID-19: a Mendelian randomization study
BK Patchen et al, MEDRXIV, February 1, 2021
(Posted: Feb 02, 2021 11AM)
Adolescent-Onset and Adult-Onset Vitamin-Responsive Neurogenetic Diseases: A Review.
Mandia Daniele et al. JAMA neurology 2021 Jan
(Posted: Jan 12, 2021 11AM)
Vitamin-responsive neurogenetic diseases represent a group of rare conditions that are probably underdiagnosed in adults and may have a dramatic response to treatment when started early in the course of the disease. In this review, main features of the adult-onset forms are defined are provided.
Folic Acid Information
CDC, January 2020
(Posted: Jan 05, 2020 11AM)
Folic acid is a B vitamin. If a woman has enough folic acid in her body before and during pregnancy, it can help prevent major birth defects of the baby’s brain and spine. Women need 400 micrograms (mcg) of folic acid every day.
The causal role of circulating vitamin D concentrations in human complex traits and diseases: a large-scale Mendelian randomization study
X Jiang et al, BIOXIV, December 2019
(Posted: Dec 30, 2019 10AM)
Our MR analyses did not convincingly support a causal effect of circulating 25(OH)D on complex traits and diseases examined here. Our results may inform ongoing and future randomized clinical trials of vitamin D supplementation. Future studies are warranted to prioritize the most promising target diseases for vitamin D intervention.
Role of vitamin D in disease through the lens of Mendelian randomization—Evidence from Mendelian randomization challenges the benefits of vitamin D supplementation for disease prevention
D Manousaki et al, IJE, September 2019
(Posted: Sep 21, 2019 1PM)
Two studies add to the increasing repertoire of Mendelian randomization papers exploring the causal role of vitamin D on a variety of health outcomes. Indeed, among 62 Mendelian randomization papers for vitamin D published over the past 8?years, evidence supporting a causal role of vitamin D was provided only for a limited number of outcomes.
Polymorphisms in the vitamin D receptor gene are associated with reduced rate of sputum culture conversion in multidrug-resistant tuberculosis patients in South Africa.
Magee Matthew J et al. PloS one 2017 12(7) e0180916
(Posted: Jul 19, 2017 8AM)
The influence of genetic susceptibility and calcium plus vitamin D supplementation on fracture risk
Y Wang et al, AJCN< April 2017
(Posted: Apr 24, 2017 3PM)
Toward personalized calcium and vitamin D supplementation
Roberto Civitelli, AJCN, April 2017
(Posted: Apr 24, 2017 9AM)
The epigenetic role of vitamin C in health and disease.
Camarena Vladimir et al. Cellular and molecular life sciences : CMLS 2016 Feb
(Posted: Feb 13, 2016 11AM)
Vitamin D and Risk of Multiple Sclerosis: A Mendelian Randomization Study
LE Mokry et al. PLoS Medicine, August 25, 2015
(Posted: Aug 25, 2015 3PM)
Vitamin D and prostate cancer prognosis: a Mendelian randomization study.
Trummer Olivia et al. World J Urol 2015 Jul 25.
(Posted: Aug 21, 2015 10AM)
Vitamin D metabolism genes in asthma and atopy.
Morales Eva et al. Mini Rev Med Chem 2015 May 18.
(Posted: May 23, 2015 9AM)
Vitamin K supplementation for cystic fibrosis.
Jagannath Vanitha A et al. Cochrane Database Syst Rev 2015 CD008482
(Posted: May 02, 2015 4PM)
The role of telomeres and vitamin D in cellular aging and age-related diseases.
Pusceddu Irene et al. Clin. Chem. Lab. Med. 2015 Mar 21.
(Posted: May 01, 2015 9AM)
Prevalence of vitamin d deficiency in sickle cell disease: a systematic review.
Nolan Vikki G et al. PLoS ONE 2015 (3) e0119908
(Posted: Apr 01, 2015 1PM)
Vitamin D binding protein genotype variants and risk of chronic obstructive pulmonary disease: a meta-analysis.
Horita Nobuyuki et al. Respirology 2015 Feb (2) 219-25
(Posted: Mar 27, 2015 5PM)
Vitamin D-binding protein gene polymorphisms and chronic obstructive pulmonary disease susceptibility: A meta-analysis.
Xie Xinming et al. Biomed Rep 2015 Mar (2) 183-188
(Posted: Mar 27, 2015 5PM)
Genetic Associations with Plasma B12, B6, and Folate Levels in an Ischemic Stroke Population from the Vitamin Intervention for Stroke Prevention (VISP) Trial.
Keene Keith L et al. Front Public Health 2014 112
(Posted: Mar 16, 2015 9AM)
Hemochromatosis
From NHLBI health topic site
(Posted: Jan 11, 2014 11AM)
What Is
Hemochromatosis (HE-mo-kro-ma-TO-sis) is a disease in which too much iron builds up in your body (iron overload). Iron is a mineral found in many foods.
Too much iron is toxic to your body. It can poison your organs and cause organ failure. In hemochromatosis, iron can build up in most of your body's organs, but especially in the liver, heart, and pancreas.
Too much iron in the liver can cause an enlarged liver, liver failure, liver cancer, or cirrhosis (sir-RO-sis). Cirrhosis is scarring of the liver, which causes the organ to not work well.
Too much iron in the heart can cause irregular heartbeats called arrhythmias (ah-RITH-me-ahs) and heart failure. Too much iron in the pancreas can lead to diabetes.
If hemochromatosis isn't treated, it may even cause death.
Overview
The two types of hemochromatosis are primary and secondary. Primary hemochromatosis is caused by a defect in the genes that control how much iron you absorb from food. Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload.
Most people who have primary hemochromatosis inherit it from their parents. If you inherit two hemochromatosis genes?one from each parent?you're at risk for iron overload and signs and symptoms of the disease. The two faulty genes cause your body to absorb more iron than usual from the foods you eat.
Hemochromatosis is one of the most common genetic disorders in the United States. However, not everyone who has hemochromatosis has signs or symptoms of the disease.
Estimates of how many people develop signs and symptoms vary greatly. Some estimates suggest that as many as half of all people who have the disease don't have signs or symptoms.
The severity of hemochromatosis also varies. Some people don't have complications, even with high levels of iron in their bodies. Others have severe complications or die from the disease.
Certain factors can affect the severity of the disease. For example, a high intake of vitamin C can make hemochromatosis worse. This is because vitamin C helps your body absorb iron from food.
Alcohol use can worsen liver damage and cirrhosis caused by hemochromatosis. Conditions such as hepatitis also can further damage or weaken the liver.
Outlook
The outlook for people who have hemochromatosis largely depends on how much organ damage they have at the time of diagnosis. Early diagnosis and treatment of the disease are important.
Treatment may help prevent, delay, or sometimes reverse complications of the disease. Treatment also may lead to better quality of life.
For people who are diagnosed and treated early, a normal lifespan is possible. If left untreated, hemochromatosis can lead to severe organ damage and even death.
?Acquired hemochromatosis
?Classical hemochromatosis
?Genetic hemochromatosis
?Genetic iron poisoning
?Hereditary hemochromatosis
?Iron overload disease
?Primary hemochromatosis
?Secondary hemochromatosis
Pernicious Anemia
From NHLBI health topic site
(Posted: Jan 11, 2014 11AM)
What Is
Pernicious anemia (per-NISH-us uh-NEE-me-uh) is a condition in which the body can't make enough healthy red blood cells because it doesn't have enough vitamin B12.
Vitamin B12 is a nutrient found in some foods. The body needs this nutrient to make healthy red blood cells and to keep its nervous system working properly.
People who have pernicious anemia can't absorb enough vitamin B12 from food. This is because they lack intrinsic (in-TRIN-sik) factor, a protein made in the stomach. A lack of this protein leads to vitamin B12 deficiency.
Other conditions and factors also can cause vitamin B12 deficiency. Examples include infections, surgery, medicines, and diet. Technically, the term "pernicious anemia" refers to vitamin B12 deficiency due to a lack of intrinsic factor. Often though, vitamin B12 deficiency due to other causes also is called pernicious anemia.
This article discusses pernicious anemia due to a lack of intrinsic factor and other causes.
Overview
Pernicious anemia is a type of anemia. The term "anemia" usually refers to a condition in which the blood has a lower than normal number of red blood cells. In pernicious anemia, the body can't make enough healthy red blood cells because it doesn't have enough vitamin B12.
Without enough vitamin B12, your red blood cells don't divide normally and are too large. They may have trouble getting out of the bone marrow?a sponge-like tissue inside the bones where blood cells are made.
Without enough red blood cells to carry oxygen to your body, you may feel tired and weak. Severe or long-lasting pernicious anemia can damage the heart, brain, and other organs in the body.
Pernicious anemia also can cause other problems, such as nerve damage, neurological problems (such as memory loss), and digestive tract problems. People who have pernicious anemia also may be at higher risk for weakened bone strength and stomach cancer.
Outlook
The term ?pernicious? means ?deadly.? The condition is called pernicious anemia because it often was fatal in the past, before vitamin B12 treatments were available. Now, pernicious anemia usually is easy to treat with vitamin B12 pills or shots.
With ongoing care and proper treatment, most people who have pernicious anemia can recover, feel well, and live normal lives.
Without treatment, pernicious anemia can lead to serious problems with the heart, nerves, and other parts of the body. Some of these problems may be permanent.
Other Names
Pernicious anemia is one of two major types of "macrocystic" or "megaloblastic" anemia. These terms refer to anemia in which the red blood cells are larger than normal. (The other major type of macrocystic anemia is caused by folic acid deficiency.)
Rarely, children are born with an inherited disorder that prevents their bodies from making intrinsic factor. This disorder is called congenital pernicious anemia.
Vitamin B12 deficiency also is called cobalamin deficiency and combined systems disease.
Stomach (Gastric) Cancer Prevention (PDQ®)–Health Professional Version
(Posted: Jan 11, 2014 11AM)
Overview
Note: Separate PDQ summaries on Stomach (Gastric) Cancer Screening, Gastric Cancer Treatment, and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
Who Is at Risk?
People at elevated risk for gastric cancer include elderly patients with atrophic gastritis or pernicious anemia, patients with sporadic gastric adenomas,[1] familial adenomatous polyposis,[2] or hereditary nonpolyposis colon cancer,[3] and immigrant ethnic populations from countries with high rates of gastric carcinoma.[4,5] Workers in the rubber and coal industries are also at increased risk.[6]
Risk factors for gastric cancer include the presence of precursor conditions such as chronic atrophic gastritis and intestinal metaplasia, pernicious anemia, and gastric adenomatous polyps. Genetic factors include a family history of gastric cancer, Li Fraumeni syndrome, and Type A blood type.[6] Environmental factors include low consumption of fruits and vegetables; consumption of salted, smoked, or poorly preserved foods; cigarette smoking; and radiation exposure.[6-8]
There is consistent evidence that Helicobacter pylori infection, also known as H. pylori infection, of the stomach is strongly associated with both the initiation and promotion of carcinoma of the gastric body and antrum and of gastric lymphoma.[9-11] The International Agency for Research on Cancer classifies H. pylori infection as a cause of noncardia gastric carcinoma and gastric low-grade B-cell mucosa-associated lymphoid tissue or MALT lymphoma (i.e., a Group 1 human carcinogen).[12,13]
Compared with the general population, people with duodenal ulcer disease may have a lower risk of gastric cancer.[14]
Interventions for Reduction of Stomach (Gastric) Cancer Risk
Smoking cessation
Based on solid evidence, smoking is associated with an increased risk of stomach cancer.[15-17] The 2004 Surgeon General?s report identifies cigarette smoking as a cause of stomach cancer, with an average relative risk (RR) in former smokers of 1.2 and in current smokers of 1.6.[18] Compared with persistent smokers, the risk of stomach cancer decreases among former smokers with time since cessation. This pattern of observations makes it reasonable to infer that cigarette smoking prevention or cessation would result in a decreased risk of gastric cancer.
Magnitude of Effect: A systematic review and meta-analysis showed a 60% increase in gastric cancer in male smokers and a 20% increase in gastric cancer in female smokers compared with nonsmokers.[15]
Study Design: Evidence obtained from case-control and cohort studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.
H. Pylori infection eradication
Based on solid evidence, H. pylori infection is associated with an increased risk of gastric cancer. A meta-analysis of seven randomized studies, all conducted in areas of high-risk gastric cancer and all but one conducted in Asia, suggests that treatment of H. pylori may reduce gastric cancer risk (from 1.7% to 1.1%; RR = 0.65; 95% confidence interval, 0.43?0.98).[19] Only two studies assessed gastric cancer incidence as the primary study outcome, and two different studies were double blinded. It is unclear how generalizable the results may be to the North American population.
In the initial report from a clinical trial, 3,365 randomized subjects were followed in an intention-to-treat analysis; it was shown that short-term treatment with amoxicillin and omeprazole reduced the incidence of gastric cancer by 39% during a period of 15 years following randomization, with similar but not statistically significant reductions for gastric cancer mortality.[20]
Magnitude of Effect: Risk of cancer may be reduced; effect on cancer mortality is not known.
Study Design: Randomized controlled trials of H. pylori eradication.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.
Interventions With Inadequate Evidence as to Whether They Reduce the Risk of Stomach (Gastric) Cancer
Diet
Based on fair evidence, excessive salt intake and deficient dietary consumption of fresh fruits and vegetables are associated with an increased risk of gastric cancer. Dietary intake of vitamin C contained in vegetables, fruits, and other foods of plant origin is associated with a reduced risk of gastric cancer. Diets high in whole-grain cereals, carotenoids, allium compounds, and green tea are also associated with a reduced risk of this cancer. However, it is uncertain if changing one's diet to include more vegetables, fruits, and whole grains would reduce the risk of gastric cancer.
Magnitude of Effect: Small, difficult to determine.
Study Design: Cohort or case-control studies.
Internal Validity: Good.
Consistency: Small number of studies.
External Validity: Fair (populations vary greatly in their underlying nutritional status). Cancer
Cystic Fibrosis
From NHLBI health topic site
(Posted: Jan 01, 2014 0AM)
What Is
Cystic fibrosis (SIS-tik fi-BRO-sis), or CF, is an inherited disease of the secretory (see-KREH-tor-ee) glands. Secretory glands include glands that make mucus and sweat.
"Inherited" means the disease is passed from parents to children through genes. People who have CF inherit two faulty genes for the disease?one from each parent. The parents likely don't have the disease themselves.
CF mainly affects the lungs, pancreas, liver, intestines, sinuses, and sex organs.
Overview
Mucus is a substance made by tissues that line some organs and body cavities, such as the lungs and nose. Normally, mucus is a slippery, watery substance. It keeps the linings of certain organs moist and prevents them from drying out or getting infected.
If you have CF, your mucus becomes thick and sticky. It builds up in your lungs and blocks your airways. (Airways are tubes that carry air in and out of your lungs.)
The buildup of mucus makes it easy for bacteria to grow. This leads to repeated, serious lung infections. Over time, these infections can severely damage your lungs.
The thick, sticky mucus also can block tubes, or ducts, in your pancreas (an organ in your abdomen). As a result, the digestive enzymes that your pancreas makes can't reach your small intestine.
These enzymes help break down food. Without them, your intestines can't fully absorb fats and proteins. This can cause vitamin deficiency and malnutrition because nutrients pass through your body without being used. You also may have bulky stools, intestinal gas, a swollen belly from severe constipation, and pain or discomfort.
CF also causes your sweat to become very salty. Thus, when you sweat, you lose large amounts of salt. This can upset the balance of minerals in your blood and cause many health problems. Examples of these problems include dehydration (a lack of fluid in your body), increased heart rate, fatigue (tiredness), weakness, decreased blood pressure, heat stroke, and, rarely, death.
If you or your child has CF, you're also at higher risk for diabetes or two bone-thinning conditions called osteoporosis (OS-te-o-po-RO-sis) and osteopenia (OS-te-o-PEE-nee-uh).
CF also causes infertility in men, and the disease can make it harder for women to get pregnant. (The term "infertility" refers to the inability to have children.)
Outlook
The symptoms and severity of CF vary. If you or your child has the disease, you may have serious lung and digestive problems. If the disease is mild, symptoms may not show up until the teen or adult years.
The symptoms and severity of CF also vary over time. Sometimes you'll have few symptoms. Other times, your symptoms may become more severe. As the disease gets worse, you'll have more severe symptoms more often.
Lung function often starts to decline in early childhood in people who have CF. Over time, damage to the lungs can cause severe breathing problems. Respiratory failure is the most common cause of death in people who have CF.
As treatments for CF continue to improve, so does life expectancy for those who have the disease. Today, some people who have CF are living into their forties or fifties, or longer.
Early treatment for CF can improve your quality of life and increase your lifespan. Treatments may include nutritional and respiratory therapies, medicines, exercise, and other treatments.
Your doctor also may recommend pulmonary rehabilitation (PR). PR is a broad program that helps improve the well-being of people who have chronic (ongoing) breathing problems.
Other Names
?Cystic fibrosis of the pancreas
?Fibrocystic disease of the pancreas
?Mucoviscidosis (MU-ko-vis-ih-DO-sis)
?Mucoviscidosis of the pancreas
?Pancreas fibrocystic disease
?Pancreatic cystic fibrosis
Epidermal nevus vitamin D resistant rickets
From NCATS Genetic and Rare Diseases Information Center
(Posted: Jan 01, 2011 0AM)
Hereditary resistance to anti-vitamin K
From NCATS Genetic and Rare Diseases Information Center
(Posted: Jan 01, 2011 0AM)
Vitamin A embryopathy
From NCATS Genetic and Rare Diseases Information Center
(Posted: Jan 01, 2011 0AM)
Ataxia with vitamin E deficiency
From NCATS Genetic and Rare Diseases Information Center
(Posted: Jan 01, 2011 0AM)
Vitamin B12-responsive methylmalonic acidemia
From NCATS Genetic and Rare Diseases Information Center
(Posted: Jan 01, 2011 0AM)
