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Like, Share, Tweet Facebook. Do you order from outside the EU? Then place your order on Bik-Bik. Sale Vitals by Vitaminedesk. De zuivere 14 stammen van Bio-Kult. The study included 25, men aged 50 years and older and women aged 55 years and older who had no history of cancer, and most had adequate serum 25 OH D levels at baseline.

Rates of breast, prostate, and colorectal cancer did not differ significantly between the vitamin D and placebo groups. However, normal-weight participants had greater reductions in cancer incidence and mortality rates than those who were overweight or obese.

A few studies have examined the effect of vitamin D supplementation on specific cancers. Below are brief descriptions of studies of vitamin D and its association with, or effect on, breast, colorectal, lung, pancreatic, and prostate cancers.

Breast cancer Some observational studies support an inverse association between 25 OH D levels and breast cancer risk and mortality, but others do not [ ]. The Women's Health Initiative clinical trial randomized 36, postmenopausal women to receive IU vitamin D 3 plus 1, mg calcium daily or a placebo for a mean of 7 years [ 96 ]. The vitamin D 3 and calcium supplements did not reduce breast cancer incidence, and 25 OH D levels at the start of the study were not associated with breast cancer risk [ 97 ].

In a subsequent investigation for 4. Colorectal cancer A large case-control study included 5, individuals who developed colorectal cancer and whose 25 OH D levels were assessed a median of 5. Levels of 75 to less than The association was substantially stronger in women. In the Women's Health Initiative clinical trial described above , vitamin D 3 and calcium supplements had no effect on rates of colorectal cancer. Another study included 2, healthy individuals aged 45 to 75 years who had had one or more serrated polyps precursor lesions to colorectal cancer that had been removed [ ].

These participants were randomized to take 25 mcg 1, IU vitamin D 3 , 1, mg calcium, both supplements, or a placebo daily for 3—5 years, followed by an additional 3—5 years of observation after participants stopped the treatment.

Vitamin D alone did not significantly affect the development of new serrated polyps, but the combination of vitamin D with calcium increased the risk almost fourfold. The VITAL trial found no association between vitamin D supplementation and the risk of colorectal adenomas or serrated polyps [ ]. Lung cancer A study of cohorts that included 5, participants who developed lung cancer and 5, matched controls found no association between serum 25 OH D levels and risk of subsequent lung cancer, even when the investigators analyzed the data by sex, age, race and ethnicity, and smoking status [ ].

Pancreatic cancer One study comparing men who developed pancreatic cancer to matched controls found no relationship between serum 25 OH D levels and risk of pancreatic cancer [ ]. Another study that compared male smokers in Finland with pancreatic cancer to matched controls found that participants in the highest quintile of 25 OH D levels more than Prostate cancer Research to date provides mixed evidence on whether levels of 25 OH D are associated with the development of prostate cancer.

Several studies published in suggested that high levels of 25 OH D might increase the risk of prostate cancer. This U-shaped association was most pronounced for men with the most aggressive forms of prostate cancer. A case-control analysis of 1, cases of prostate cancer and 1, controls found no associations between 25 OH D levels and prostate cancer risk [ ]. Since , however, several published studies and meta-analyses have found no relationship between 25 OH D levels and prostate cancer risk [ , ].

For example, an analysis was conducted of 19 prospective studies that provided data on prediagnostic levels of 25 OH D for 13, men who developed prostate cancer and 20, control participants [ ]. Vitamin D deficiency or insufficiency did not increase the risk of prostate cancer, and higher 25 OH D concentrations were not associated with a lower risk.

Several studies have examined whether levels of 25 OH D in men with prostate cancer are associated with a lower risk of death from the disease or from any cause.

One study included 1, men treated for prostate cancer whose plasma 25 OH D levels were measured 4. Among the participants who died 41 deaths were due to prostate cancer , 25 OH D levels were not associated with risk of death from prostate cancer or any cause [ ]. However, a meta-analysis of 7 cohort studies that included 7, men with prostate cancer found higher 25 OH D levels to be significantly associated with lower mortality rates from prostate cancer or any other cause [ ]. For men with prostate cancer, whether vitamin D supplementation lengthens cancer-related survival is not clear.

Conclusions about vitamin D and cancer The USPSTF stated that, due to insufficient evidence, it was unable to assess the balance of benefits and harms of supplemental vitamin D to prevent cancer [ ]. Taken together, studies to date do not indicate that vitamin D with or without calcium supplementation reduces the incidence of cancer, but adequate or higher 25 OH D levels might reduce cancer mortality rates.

Further research is needed to determine whether vitamin D inadequacy increases cancer risk, whether greater exposure to the nutrient can prevent cancer, and whether some individuals could have an increased risk of cancer because of their vitamin D status over time.

Cardiovascular disease Vitamin D helps regulate the renin-angiotensin-aldosterone system and thereby blood pressure , vascular cell growth, and inflammatory and fibrotic pathways [ ]. Vitamin D deficiency is associated with vascular dysfunction, arterial stiffening, left ventricular hypertrophy, and hyperlipidemia [ ]. For these reasons, vitamin D has been linked to heart health and risk of CVD. Observational studies support an association between higher serum 25 OH D levels and a lower risk of CVD incidence and mortality.

For example, a meta-analysis included 34 observational studies that followed , participants mean age greater than 50 years for 1. The results showed that baseline serum 25 OH D levels were inversely associated with total number of CVD events including myocardial infarction, ischemic heart disease, heart failure, and stroke and mortality risk [ ]. Another large observational study that followed , adults from Denmark for 0—7 years found that levels of 25 OH D that were low about Other meta-analyses of prospective studies have found associations between lower vitamin D status measured by serum 25 OH D levels or vitamin D intakes and an increased risk of ischemic stroke, ischemic heart disease, myocardial infarction, and early death [ , ].

In contrast to the observational studies, clinical trials have provided little support for the hypothesis that supplemental vitamin D reduces the risk of CVD or CVD mortality. For example, a 3-year trial in New Zealand randomized 5, adults mean age Vitamin D supplementation had no effect on the incidence rate of myocardial infarction, angina, heart failure, arrhythmia, arteriosclerosis, stroke, venous thrombosis, or death from CVD.

Similarly, the VITAL clinical trial described above found that vitamin D supplements did not significantly decrease rates of heart attacks, strokes, coronary revascularization, or deaths from cardiovascular causes [ 91 ].

High serum cholesterol levels and hypertension are two of the main risk factors for CVD. The data on supplemental vitamin D and cholesterol levels are mixed, as shown in one meta-analysis of 41 clinical trials in a total of 3, participants mean age 55 years. The results of this analysis showed that 0. Studies of the effects of vitamin D supplements on hypertension have also had mixed findings. In contrast, another meta-analysis of 30 clinical trials in 4, participants mean age Another meta-analysis of genetic studies in , participants primarily adults found that a low vitamin D status increased blood pressure and hypertension risk in people with genetic variants associated with low endogenous production of 25 OH D [ ].

Depression Vitamin D is involved in various brain processes, and vitamin D receptors are present on neurons and glia in areas of the brain thought to be involved in the pathophysiology of depression [ ]. A systematic review and meta-analysis of 14 observational studies that included a total of 31, adults mean age ranging from Clinical trials, however, do not support these findings. For example, a meta-analysis of 9 trials with a total of 4, adult participants diagnosed with depression or depressive symptoms found no significant reduction in symptoms after supplementation with vitamin D [ ].

They also had different study durations 5 days to 5 years , mean participant ages range, 22 years to 75 years , and baseline 25 OH D levels; furthermore, some but not all studies administered concurrent antidepressant medications.

Three trials conducted since that meta-analysis also found no effect of vitamin D supplementation on depressive symptoms. Most participants had minimal or mild depression, had a low mean baseline 25 OH level of The groups showed no significant differences in the incidence and recurrent rates of depression, clinically relevant depressive symptoms, or changes in mood scores.

Overall, clinical trials did not find that vitamin D supplements helped prevent or treat depressive symptoms or mild depression, especially in middle-aged to older adults who were not taking prescription antidepressants.

No studies have evaluated whether vitamin D supplements may benefit individuals under medical care for clinical depression who have low or deficient 25 OH D levels and are taking antidepressant medication.

Multiple sclerosis MS is an autoimmune disease of the central nervous system that damages the myelin sheath surrounding and protecting nerve cells in the brain and spinal cord.

This damage hinders or blocks messages between the brain and body, leading to clinical features, such as vision loss, motor weakness, spasticity, ataxia, tremor, sensory loss, and cognitive impairment [ , ]. Some people with MS eventually lose the ability to write, speak, or walk.

The geographical distribution of MS around the world is unequal. Few people near the equator develop the disease, whereas the prevalence is higher further north and south. This uneven distribution has led to speculation that lower vitamin D levels in people who have less sunlight exposure might predispose them to the disease [ ].

Many epidemiological and genetic studies have shown an association between MS and low 25 OH D levels before and after the disease begins [ ].

Observational studies suggest that adequate vitamin D levels might reduce the risk of contracting MS and, once MS is present, decrease the risk of relapse and slow the disease's progression [ ].

One study, for example, tested 25 OH D levels in 1, women in Finland an average of 9 years before their MS diagnosis and compared their outcomes with those of 2, similar women who did not develop MS [ ].

More than half the women who developed MS had deficient or insufficient vitamin D levels. Two earlier prospective studies of similar design—one in the United States with non-Hispanic White individuals [ ] and the other with individuals in northern Sweden [ ]—found that levels of 25 OH D greater than No clinical trials have examined whether vitamin D supplementation can prevent the onset of MS, but several have investigated whether supplemental vitamin D can help manage the disease.

A Cochrane review analyzed 12 such trials that had a total of participants with MS; the reviewers judged all of these trials to be of low quality [ ]. Overall, vitamin D supplementation, when compared with placebo administration, had no effect on relevant clinical outcomes, such as recurrent relapse or worsened disability.

Experts have reached no firm consensus on whether vitamin D can help prevent MS given the lack of clinical trial evidence [ ]. In addition, studies have not consistently shown that vitamin D supplementation tempers the signs and symptoms of active MS or reduces rates of relapse. Type 2 diabetes Vitamin D plays a role in glucose metabolism.

It stimulates insulin secretion via the vitamin D receptor on pancreatic beta cells and reduces peripheral insulin resistance through vitamin D receptors in the muscles and liver [ ]. Vitamin D might be involved in the pathophysiology of type 2 diabetes through its effects on glucose metabolism and insulin signaling as well as its ability to reduce inflammation and improve pancreatic beta-cell function [ , ].

Observational studies have linked lower serum 25 OH D levels to an increased risk of diabetes, but their results might have been confounded by the fact that many participants were overweight or obese and were therefore more predisposed to developing diabetes and having lower 25 OH D levels [ 1 ]. A review of 71 observational studies in adults with and without type 2 diabetes from 16 countries found a significant inverse relationship between vitamin D status and blood sugar levels in participants who did and did not have diabetes [ ].

In contrast to observational studies, clinical trials provide little support for the benefits of vitamin D supplementation for glucose homeostasis. In the 54 participants who completed the study, vitamin D supplementation did not improve insulin sensitivity or insulin secretion in comparison with placebo.

Vitamin D had no significant effects on glucose homeostasis, insulin secretion or resistance, or hemoglobin A1c levels a measure of average blood sugar levels over the previous 2—3 months , irrespective of the study population, vitamin D dose, or trial quality. Several trials have investigated whether vitamin D supplementation can prevent the transition from prediabetes to diabetes in patients with adequate 25 OH D levels, and all have had negative results. In a trial in Norway, men and women aged 25—80 years mean age 62 years with prediabetes received mcg 20, IU vitamin D 3 or a placebo each week for 5 years [ ].

The results showed no significant differences in rates of progression to type 2 diabetes; in serum glucose, insulin, or hemoglobin A1c levels; or in measures of insulin resistance. The largest trial to date of vitamin D supplements for diabetes prevention randomized 2, men and women aged 25 years and older mean age 60 years with prediabetes who were overweight or obese mean BMI of Vitamin D did not significantly prevent the development of diabetes in comparison with placebo.

Studies have also assessed the value of vitamin D supplementation for managing diabetes, and they have found that the vitamin offers limited benefits. One meta-analysis of 20 clinical trials compared the effects of 0. However, the supplementation had no significant effects on fasting blood glucose, hemoglobin A1c, or fasting insulin levels. Clinical trials to date provide little evidence that vitamin D supplementation helps maintain glucose homeostasis, reduces the risk of progression from prediabetes to type 2 diabetes, or helps manage the disease, particularly in vitamin D-replete individuals.

Weight loss Observational studies indicate that greater body weights are associated with lower vitamin D status, and obese individuals frequently have marginal or deficient circulating 25 OH D levels [ ]. However, clinical trials do not support a cause-and-effect relationship between vitamin D and weight loss.

A systematic review and meta-analysis of 15 weight-loss intervention studies that used caloric restriction, exercise, or both, but not necessarily vitamin D supplementation or other treatments, found that people who lost weight had significantly greater increases in serum 25 OH D levels than those who maintained their weight [ ].

However, a meta-analysis of 12 vitamin D supplementation trials including 5 in which body composition measurements were primary outcomes found that vitamin D supplements without calorie restriction did not affect body weight or fat mass when the results were compared with those of placebo [ ]. Overall, the available research suggests that consuming higher amounts of vitamin D or taking vitamin D supplements does not promote weight loss. Excess amounts of vitamin D are toxic.

Because vitamin D increases calcium absorption in the gastrointestinal tract, vitamin D toxicity results in marked hypercalcemia total calcium greater than Hypercalcemia, in turn, can lead to nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.

In extreme cases, vitamin D toxicity causes renal failure, calcification of soft tissues throughout the body including in coronary vessels and heart valves , cardiac arrhythmias, and even death. Vitamin D toxicity has been caused by consumption of dietary supplements that contained excessive vitamin D amounts because of manufacturing errors, that were taken inappropriately or in excessive amounts, or that were incorrectly prescribed by physicians, [ ].

Experts do not believe that excessive sun exposure results in vitamin D toxicity because thermal activation of previtamin D 3 in the skin gives rise to various non-vitamin D forms that limit formation of vitamin D 3.

Some vitamin D 3 is also converted to nonactive forms [ 1 ]. However, other, shorter from 24 weeks to 5 years clinical trials of vitamin D supplementation alone or with calcium in adults found greater risks of hypercalcemia and hypercalciuria, but not of kidney stones [ , ].

While acknowledging that signs and symptoms of toxicity are unlikely at daily intakes below mcg 10, IU , the FNB noted that even vitamin D intakes lower than the ULs might have adverse health effects over time. Vitamin D supplements may interact with several types of medications. A few examples are provided below.

Individuals taking these and other medications on a regular basis should discuss their vitamin D intakes and status with their healthcare providers. Statins Statin medications reduce cholesterol synthesis. Because endogenous vitamin D is derived from cholesterol, statins may also reduce vitamin D synthesis [ ].

These medications can reduce calcium absorption and impair vitamin D metabolism [ ]. Thiazide diuretics Thiazide diuretics e. The combination of these diuretics with vitamin D supplements which increase intestinal calcium absorption might lead to hypercalcemia, especially among older adults and individuals with compromised renal function or hyperparathyroidism [ , , ]. The federal government's Dietary Guidelines for Americans notes that "Because foods provide an array of nutrients and other components that have benefits for health, nutritional needs should be met primarily through foods.

In some cases, fortified foods and dietary supplements are useful when it is not possible otherwise to meet needs for one or more nutrients e. For more information about building a healthy dietary pattern, refer to the Dietary Guidelines for Americans and the U. Department of Agriculture's MyPlate.

We encourage you to talk to your healthcare providers doctor, registered dietitian, pharmacist, etc. Any mention in this publication of a specific product or service, or recommendation from an organization or professional society, does not represent an endorsement by ODS of that product, service, or expert advice.

Updated: August 17, History of changes to this fact sheet. Find ODS on:. Strengthening Knowledge and Understanding of Dietary Supplements. Health Information Health Information. Vitamin D Fact Sheet for Consumers. Vitamin D. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, Jones G.

Modern Nutrition in Health and Disease, 11th ed. Intestinal absorption of vitamin D: A systematic review. Nutr Rev ; Vitamin D assays and the definition of hypovitaminosis D. Br J Clin Pharmacol ; Screening for vitamin deficiency in adults: U.

Preventive Services Task Force recommendation statement. Ann Intern Med ; It should not be construed to indicate that use of the drug is safe, appropriate, or effective for you. Consult your healthcare professional before using this drug. Vitamin D is a fat-soluble vitamin which plays an important role in regulating calcium, phosphorus and minerals in the body and for promoting normal bone development.

Vitamin D supplements are used to treat and prevent vitamin D deficiencies rickets ; to regulate parathyroid hormone; to prevent and treat muscle cramps; to treat certain types of calcium and phosphate disorders. Take this medication orally as directed. Swallow tablets and capsules whole.

Do not crush or chew them. Blended with prebiotic fiber to enhance absorption. A popular flowering herb used traditionally to help support your body's natural resilience and aid faster recovery. Vitamin C plays an important role in enhancing immune cell functions to boost our body's natural defenses.

Evidence suggests that it can reduce the incidence and duration of the common cold as well as aid prevention by regular use. Our Vitamin D3 also known as the sunshine vitamin' is sourced from Lichens and is the most efficient source of Vitamin D. It is well studied in its vital role as a key modulator to both innate and adaptive immunity.