RETRACTED: Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses

Sofianopoulou, Eleni; Kaptoge, Stephen; Afzal, Shoaib; Jiang, Tao; Gill, Dipender; Gundersen, Thomas E.; Bolton, Thomas; Allara, Elias; Arnold, Matthew; Mason, Amy M.; Chung, Ryan; Pennells, Lisa; Shi, Fanchao; Sun, Luanluan; Willeit, Peter; Forouhi, Nita G.; Langenberg, Claudia; Sharp, Stephen J.; Panico, Salvatore; Engström, Gunnar; Melander, Olle; Tong, Tammy Y.N.; Pérez-Cornago, Aurora; Norberg, Margareta; Johansson, Ingegerd; Katzke, Verena; Srour, Bernard; Sánchez, María José; Redondo‐Sánchez, Daniel; Olsen, Anja; Dahm, Christina C.; Overvad, Kim; Brustad, Magritt; Skeie, Guri; Moreno‐Iribas, Conchi; Onland‐Moret, N. Charlotte; Schouw, Yvonne T. van der; Tsilidis, Konstantinos K.; Heath, Alicia K.; Agnoli, Claudia; Krogh, Vittorio; Boer, Ian H. de; Kobylecki, Camilla J; Çolak, Yunus; Zittermann, Armin; Sundström, Johan; Welsh, Paul; Weiderpass, Elisabete; Aglago, Elom K.; Ferrari, Pietro; Clarke, Robert; Boutron, Marie-Christine; Severi, Gianluca; MacDonald, Conor James; Providência, Rui; Masala, Giovanna; Ros, Raul Zamora; Boer, Jolanda M. A.; Verschuren, W M Monique; Cawthon, Peggy M.; Schierbeck, Louise Lind; Cooper, Cyrus; Schulze, Matthias B.; Bergmann, Manuela M.; Hannemann, Anke; Kiechl, Stefan; Brenner, Hermann; Schoor, Natasja M. van; Albertorio, Juan R; Sacerdote, Carlotta; Linneberg, Allan; Kårhus, Line Lund; Huerta, José María; Imaz, Liher; Joergensen, Christel; Ben‐Shlomo, Yoav; Lundqvist, Annamari; Gallacher, John; Sattar, Naveed; Wood, Angela; Wareham, Nicholas J.; Nordestgaard, Børge G.; Angelantonio, Emanuele Di; Danesh, John; Butterworth, Adam S.; Burgess, Stephen

doi:10.1016/s2213-8587(21)00263-1

Cited by 172 publications

(140 citation statements)

References 31 publications

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“…No significant effect of genetically lower 25OHD concentrations on overall or cause-specific mortality was found in several studies summarized in a recent review [23]. However, combining a large MR study (n = 386,406) with real measurements of calcifediol (n = 500,962) [47] confirmed:…”

Section: Mortalitymentioning

confidence: 97%

“…Moreover, even the MR studies dealing with a large number of SNPs cannot predict more than a 10% variation in serum calcifediol and thus cannot predict the lifelong consequences of more severe vitamin D deficiency. However, a UK Biobank study combining measurements of serum calcifediol and MR revealed that genetically low serum calcifediol and low measured serum calcifediol increased overall, including cardiovascular mortality [ 47 ].…”

Section: Extra-skeletal Consequences Of Calcifediol Deficiencymentioning

confidence: 99%

See 1 more Smart Citation

Calcifediol (25OH Vitamin D3) Deficiency: A Risk Factor from Early to Old Age

Bouillon

LʼAbbate

Rosero³

2022

Nutrients

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Vitamin D deficiency is the main cause of nutritional rickets in children and osteomalacia in adults. There is consensus that nutritional access to vitamin D can be estimated by measuring serum concentrations of 25OHD and vitamin D deficiency can thus be considered as calcifediol deficiency. However, the threshold for vitamin D/calcifediol sufficiency remains a matter of debate. Vitamin D/calcifediol deficiency has been associated with musculoskeletal effects but also multiple adverse extra-skeletal consequences. If these consequences improve or if they can be treated with vitamin D supplementation is still unclear. Observational studies suggest a higher infection risk in people with low calcifediol levels. There is also a consistent association between serum calcifediol and cardiovascular events and deaths, but large-scale, long-term intervention studies did not show any benefit on cardiovascular outcomes from supplementation, at least not in subjects without clear vitamin D deficiency. Cancer risk also did not change with vitamin D treatment, although there are some data that higher serum calcifediol is associated with longer survival in cancer patients. In pregnant women, vitamin D supplementation decreases the risk of pre-eclampsia, gestational diabetes mellitus, and low birth weight. Although preclinical studies showed that the vitamin D endocrine system plays a role in certain neural cells as well as brain structure and function, there is no evidence to support a beneficial effect of vitamin D in neurodegenerative diseases. Vitamin D supplementation may marginally affect overall mortality risk especially in elderly subjects with low serum calcifediol concentrations.

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Section: Mortalitymentioning

confidence: 97%

Section: Extra-skeletal Consequences Of Calcifediol Deficiencymentioning

confidence: 99%

Calcifediol (25OH Vitamin D3) Deficiency: A Risk Factor from Early to Old Age

Bouillon

LʼAbbate

Rosero³

2022

Nutrients

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show abstract

“…The primary reasons for MRA failure are likely to include the fact that total SNP-induced variation in 25(OH)D has often been less than 25(OH)D assay variance [134] and that genome-wide association studies' (GWAS) analyses of the total percentage of SNP effects are made on the 25(OH)D data as a whole, although such data is non-linear with much of it lying in the low and high plateaus of the 25(OH)D-health outcome relationships, a problem that the GWAS analysis of 25(OH)D data stratified for different ranges of 25(OH)D efficacy might overcome [135]. That this is the case for mortality rates was shown in two recent articles, one [10] where GWAS serum 25(OH)D concentration was stratified at <10 ng/mL, 10-20 ng/mL, 20-30 ng/mL, and >30 ng/mL and significantly increased risk was only present at 25(OH)D <10 ng/mL for all-cause mortality, cardiovascular mortality, and non-CVD and non-cancer mortality with trends for increases in risk for stroke and cancer mortality. The other [12], using genetic increases in serum 25(OH)D calculated for 100 equal strata of measured serum 25(OH)D showed similar results for CVD with risk reduction for increases in 25(OH)D values up to ~20 ng/mL.…”

Section: Types Of Studies Strengths and Weaknessesmentioning

confidence: 99%

A Narrative Review of the Evidence for Variations in Serum 25-Hydroxyvitamin D Concentration Thresholds for Optimal Health

et al. 2022

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Vitamin D3 has many important health benefits. Unfortunately, these benefits are not widely known among health care personnel and the general public. As a result, most of the world’s population has serum 25-hydroxyvitamin D (25(OH)D) concentrations far below optimal values. This narrative review examines the evidence for the major causes of death including cardiovascular disease, hypertension, cancer, type 2 diabetes mellitus, and COVID-19 with regard to sub-optimal 25(OH)D concentrations. Evidence for the beneficial effects comes from a variety of approaches including ecological and observational studies, studies of mechanisms, and Mendelian randomization studies. Although randomized controlled trials (RCTs) are generally considered the strongest form of evidence for pharmaceutical drugs, the study designs and the conduct of RCTs performed for vitamin D have mostly been flawed for the following reasons: they have been based on vitamin D dose rather than on baseline and achieved 25(OH)D concentrations; they have involved participants with 25(OH)D concentrations above the population mean; they have given low vitamin D doses; and they have permitted other sources of vitamin D. Thus, the strongest evidence generally comes from the other types of studies. The general finding is that optimal 25(OH)D concentrations to support health and wellbeing are above 30 ng/mL (75 nmol/L) for cardiovascular disease and all-cause mortality rate, whereas the thresholds for several other outcomes appear to range up to 40 or 50 ng/mL. The most efficient way to achieve these concentrations is through vitamin D supplementation. Although additional studies are warranted, raising serum 25(OH)D concentrations to optimal concentrations will result in a significant reduction in preventable illness and death.

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“…The reversal on the role of a vitamin D deficiency in dental disease etiology was opposite of clinical trial evidence and may still cause harm. Fluoride, regardless of its effectiveness in preventing dental caries, does not prevent the increased chronic disease mortality associated with vitamin D deficiency [7,8].…”

Section: Introductionmentioning

confidence: 99%

How a Nutritional Deficiency Became Treated with Fluoride

Hujoel

2021

Nutrients

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Ignoring evidence on causes of disease such as smoking can harm public health. This report explores how public health experts started to ignore evidence that pediatric vitamin D deficiencies are associated with dental caries. Historical analyses show that an organization of clinical specialists, the American Dental Association (ADA), initiated this view. The ADA was a world-leading organization and its governing bodies worked through political channels to make fluoride a global standard of care for a disease which at the time was viewed as an indicator of vitamin D deficiencies. The ADA scientific council was enlisted in this endeavor and authorized the statement saying that “claims for vitamin D as a factor in tooth decay are not acceptable”. This statement was ghost-written, the opposite of what the ADA scientific council had endorsed for 15 years, and the opposite of what the National Academy of Sciences concluded. Internal ADA documents are informative on the origin of this scientific conundrum; the ADA scientific council had ignored their scientific rules and was assisting ADA governing bodies in conflicts with the medical profession on advertising policies. The evidence presented here suggests that professional organizations of clinical specialists have the power to create standards of care which ignore key evidence and consequently can harm public health.

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RETRACTED: Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses

Cited by 172 publications

References 31 publications

Calcifediol (25OH Vitamin D3) Deficiency: A Risk Factor from Early to Old Age

Calcifediol (25OH Vitamin D3) Deficiency: A Risk Factor from Early to Old Age

A Narrative Review of the Evidence for Variations in Serum 25-Hydroxyvitamin D Concentration Thresholds for Optimal Health

How a Nutritional Deficiency Became Treated with Fluoride

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