Vitamin D and cancer

A variety of studies have suggested that vitamin D protects against cancer. This seemingly intuitive proposition is supported by neither epidemiological nor molecular evidence. In fact, the very opposite is true. This article reviews why this body of research is most likely incorrect – or at the very least, much more complicated than articles in the popular media would have a person believe.

Latitude studies - The “latitude studies” are observational, as opposed to interventional, studies, which use ambient solar UV radiation as a proxy for latitude and vitamin D status. For these studies, researchers compare rates of certain major cancers - most notably breast, colorectal and prostate cancer - to rates of sunlight exposure. This group of research has the liability of being wildly inconsistent. The choice to publish research on a specific latitude gradient may be a better proxy for a researcher's bias.
Interventional studies - While some randomized controlled trials have suggested that consuming vitamin D reduces rates of cancer, larger and more carefully controlled studies show no such effect.
Studies of vitamin D status - Many of the studies examining the relationship between vitamin D status and incidence of cancer argue that low levels of 25-D contribute to cancer. This conclusion has been invalidated by larger well-controlled studies. Although the immune system works to downregulate 25-D (25-hydroxyvitamin D) in inflammatory diseases such as cancer, very high levels of 25-D are a clear indication of regular supplementation. Studies suggest that consuming large amounts of vitamin D predispose a person to increased incidence of cancer.
Observational studies – Some case control studies have found that vitamin D intake seems to increase incidence of certain types of cancer.

According to the Marshall Pathogenesis, alteration of vitamin D metabolism by a pathogenic microbiota prevents any benefit from vitamin D supplementation.

Latitude studies

Main article: Latitude studies in cancer

Main article: Vitamin D and cancer

A number of studies have suggested that sunlight exposure, and the resulting cutaneous synthesis of vitamin D, might have a beneficial influence for certain major cancers, most notably breast, colorectal and prostate cancer. These studies have been based either on using ambient solar UV radiation as a proxy for latitude in those studies looking at the geographical incidence and/or mortality of cancer, or case–control studies using questionnaires in which individuals are asked to recall previous sun exposure. However, this data is not consistent. There are any number of counterexamples in which there is an “inverse latitude gradient.”

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Randomized controlled trials of vitamin D intake

While some randomized controlled trials have suggested that consuming vitamin D reduces rates of cancer, larger and more carefully controlled studies show no such effect. Lappe et al published work, conducted over four years, that seemingly showed vitamin D might lower the incidence of colorectal cancer.¹⁾ The study had participants take 1,100 IU’s of vitamin D over the course of four years, a time that corresponds to the period when the short-term immunosuppressive effects of the steroid would be at its strongest.

Lappe opted to discard the data of subjects who developed cancer during the first year of the study. The rationale was that cancers during the first year would have been present but undiagnosed at entry. Of the 50 people who developed cancer during the four-year study, 13 were removed based on this premise, and only 37 cases of cancer were actually analyzed. But the 13 people who developed cancer during the first year were likely to be the study participants with the highest loads of the Th1 pathogens. They would have been the people to suffer the most from the negative impact of elevated 25-D on the immune system. If data from the 13 participants would have been included in the study, the results would have undoubtedly reflected much less of a “benefit” from vitamin D. Even the researchers admit that “their conclusion was strengthened by both the observational, substantial improvement in risk reduction when cancers occurring early in the trial were excluded.”

Another problem with Lappe's study is that it did not randomize participants on the basis of the stated primary outcome of the paper.²⁾ As far as epidemiological research goes, this is a no-no, and is the equivalent of “moving the goalposts.” Nor did it report losses to follow-up for each intervention group separately

In a similar study looking at a larger cohort and over a longer period of time, Chlebowski et al. found no such effect.³⁾

In our study we found absolutely no indication of an effect of calcium or vitamin D [on cancer] — zero. And that’s over a seven-year period. It was a much larger study and a much longer study.

Jacques Rossouw, MD, National Institutes of Health ABC News

A second study by the Women’s Health Initiative found no reduction in risk of breast cancer among postmenopausal women supplementing with 1000 mg calcium and 440 IUs of vitamin D.⁴⁾ Researchers at the American Cancer Society conducted a study on 68,567 postmenopausal women and found that “neither use of supplemental calcium nor vitamin D intake was associated with [breast cancer] risk.”⁵⁾ And researchers at the Northern California Cancer Center found no association between dietary vitamin D intake during adolescence and subsequent breast cancer risk.⁶⁾

A 2011 systematic review of prospective studies assessing the association of vitamin D intake with the risk of colorectal cancer that vitamin D intake increased risk of colorectal cancer,⁷⁾ thus directly contradicting Lappe's study.

Cohort studies are no more likely to show a long-term positive effect of vitamin D intake, The Iowa Women's Health study showed vitamin D intake seemed to protect against breast cancer in the first five years after it was taken. However, the effect began to reverse between years five and ten and was completely lost after year ten, trending towards an opposing effect.⁸⁾

Longitudinal studies (those lasting decades) examining the relationship between long-term intake of vitamin D and incidence of cancer are lacking. Those that have measured incidence of various other diseases, including atopy, allergic rhinitis, and brain lesions, have found that vitamin D intake increases the rate of these diseases. There is no reason to think cancer would be substantially different.

Vitamin D status studies

A number of vitamin D studies point to low levels of the inactive metabolite, 25-D, as playing a causative role in the incidence of cancer. Large, well-controlled studies have not been able to verify this claim.

A recent study by the National Cancer Institute - the first study to look at the relationship between measured vitamin D in the blood and subsequent total cancer deaths - failed to show an association between baseline vitamin D status and overall cancer risk in men, women, non-Hispanic whites, non-Hispanic blacks, Mexican Americans, and in persons younger than 70 or 70 years or older.⁹⁾ The study analyzed data from 16,818 subjects.

When asked by a correspondent from CBS News if vitamin D can reduce the risk of cancer, said the following:

I don’t believe vitamin D is the answer. I wish it was as simple as saying ‘If you take vitamin D, cancer will be cured. I don’t think it’s that simple.

David Fishman, M.D, Head of the National Ovarian Cancer Early Detection Program at New York University

Evidence that vitamin D intake increases incidence of cancer

An underreported body of research shows that levels of 25-D sufficiently high enough to suggest heavy supplementation are consistent with higher rates of cancer. Stolzenberg-Solomon et al tracked a cohort of men over the course of 16 years for pancreatic cancer.¹⁰⁾ They found that over this time period, high 25-D levels greater than 26 ng/ml were associated with a three-fold increased risk for the cancer. It is noteworthy that according to molecular modeling research, 26 ng/ml is near the range when 25-D significantly shuts off the Vitamin D Receptor, particularly when it is already partially blocked by bacterial proteins.

Contrary to expectations, subjects with higher prediagnostic vitamin D status had an increased pancreatic cancer risk compared with those with lower status…. Our results are intriguing and may provide clues that further the understanding of the etiology of this highly fatal cancer.

Rachael Stolzenberg-Solomon, et al. ¹¹⁾

Researchers at the Chinese Academy of Medical Sciences in China found a similar association between excessive vitamin D intake and esophageal and gastric cancers in men. Male subjects with levels of 25-D in the range of 48.7 ng/ml (which once again suggests heavy supplementation) were much more likely to develop one of the two forms of cancer.¹²⁾ A 2011 case control study found that those in the highest 25% of vitamin D intake compared to those in the lowest 25% were significantly more likely to develop oesophageal adenocarcinoma.¹³⁾

The following research by Freedman DM, Looker AC, Abnet CC, Linet MS, Graubard BI remains unpublished

Abstract Vitamin D has been hypothesized to protect against cancer. We followed 16,819 participants in NHANES III from 1988 through 2006, expanding upon an earlier NHANES III study (1988-2000). Using Cox proportional hazard regression models, we examined risk related to baseline serum 25-hydroxyvitamin D (25(OH)D) for total cancer mortality, in both sexes, and by racial/ethnic groups, as well as for site-specific cancers. Because serum was collected in the south in cooler months and the north in warmer months, we examined associations by collection season (“summer/higher latitude” and “winter/lower latitude”). We identified 884 cancer deaths during 225,212 person-years. Overall cancer mortality risks were unrelated to baseline 25(OH)D status in both season/latitude groups, and in non-Hispanic whites, non-Hispanic blacks, and Mexican-Americans. In men, risks were elevated at higher levels (e.g., for ≥100 nmol/L, RR= 1.85 (95% CI=1.02-3.35) compared to <37.5 nmol/L).

Observational studies

One Norway-based study surveyed over 50,000 participants for their intake of dietary vitamin D and then compared those results to their later risk of cutaneous malignant melanoma. The researchers found that female subjects who consumed cod liver oil, which is high in vitamin D, were significantly more likely to later be diagnosed with melanoma.¹⁴⁾

A 2010 study showed that multivitamin use may be correlated with increased risk of breast cancer.¹⁵⁾ In 1997, 35,329 Swedish cancer-free women completed a self-administered questionnaire that solicited information on multivitamin use as well as other breast cancer risk factors. During a mean follow-up of 9.5 years, 974 women were diagnosed with incident breast cancer.

Patient reports

I have avoided the sun since severe sunburn at age 10. Cancer was found in my left breast some time before MP was available. It was controlled by surgery followed by radiotherapy and Tamoxifen.

I first had lumpectomy, followed by complete breast removal and removal of some lymph nodes, because the cancer was beginning to spread into the lymph system.

While on MP, a “pre-cancerous” patch on my left arm changed and I was referred to a dermatologist for surgery, but he preferred to watch and wait as the possible cancer was on an arm with lymphoedema.

I am glad he took pictures, as the possible cancer continued to change and then disappeared entirely.
Good old MP, when followed as precisely as I was doing at that time.
Sallie Q

I just posted this abstract to the site. This is the largest (16,819 patients) and longest (1988-2006) retrospective study I have seen on cancer mortality rates and 25D levels and, significantly, was produced by the NCI. It's a preprint so this is going to create some big time waves when it comes out…. XXXXX

Cancer Res. 2010 Sep 16. [Epub ahead of print]

Serum Vitamin D and Cancer Mortality in the NHANES III Study (1988-2006).¹⁷⁾ Freedman DM, Looker AC, Abnet CC, Linet MS, Graubard BI.

Division of Cancer Epidemiology and Genetics, National Cancer Institute.

Abstract Vitamin D has been hypothesized to protect against cancer. We followed 16,819 participants in NHANES III from 1988 through 2006, expanding upon an earlier NHANES III study (1988-2000). Using Cox proportional hazard regression models, we examined risk related to baseline serum 25-hydroxyvitamin D (25(OH)D) for total cancer mortality, in both sexes, and by racial/ethnic groups, as well as for site-specific cancers. Because serum was collected in the south in cooler months and the north in warmer months, we examined associations by collection season (“summer/higher latitude” and “winter/lower latitude”). We identified 884 cancer deaths during 225,212 person-years. Overall cancer mortality risks were unrelated to baseline 25(OH)D status in both season/latitude groups, and in non-Hispanic whites, non-Hispanic blacks, and Mexican-Americans. In men, risks were elevated at higher levels (e.g., for ≥100 nmol/L, RR= 1.85 (95% CI=1.02-3.35) compared to <37.5 nmol/L). Athough risks were unrelated to 25(OH)D in all women combined, risks significantly decreased with increasing 25(OH)D in the summer/higher latitude group (for ≥100 nmol/L, RR= 0.52 (95% CI=0.25-1.15) compared to <37.5 nmol/L, P-trend=0.03, based on continuous values). We also observed a suggestion of an inverse association with colorectal cancer mortality(P-trend=0.09) and a positive association with lung cancer mortality among males (P-trend=0.03). Our results do not support a the hypothesis that 25(OH)D is associated with reduced cancer mortality. Although cancer mortality in females was inversely associated with 25(OH)D in the summer/higher latitude group, cancer mortality at some sites was increased among men with higher 25(OH)D. These findings argue for caution before increasing 25(OH)D levels to prevent cancer.

Integrate here, then consider including some of these studies under rickets.

J Natl Med Assoc. 2009 Dec;101(12):1310-2. Black-white differences in cancer risk and the vitamin D hypothesis.¹⁸⁾ Frost P. Comment on: J Natl Med Assoc. 2008 Sep;100(9):1040. PMID: 20070025

To the Editor: A recent letter to the editor noted that serum vitamin D levels are lower in black Americans than in white Americans. The letter writer then suggested that this difference could explain racial disparities in cancer incidence, mortality, and survival.1

This hypothesis attributes the low vitamin D levels of black Americans to their dark skin, which is presumably less able to produce this vitamin in the temperate zone. There is thus a mismatch between current and ancestral environments. At all latitudes the skin must have enough melanin to block harmful solar UV while letting in enough UVB for vitamin D synthesis. Since the tropical zone has intense year-round sunlight, even very dark skin can produce sufficient vitamin D for the body’s needs. This adaptive compromise becomes unbalanced, however, when dark-skinned humans move to the temperate zone. Their skin now screens out too much UVB and produces too little vitamin D.

The above hypothesis has 2 flaws. First, dark skin does not seriously limit vitamin D production. While it is true that a single UVB exposure of moderate intensity will produce less vitamin D in black skin than in white skin, the difference narrows with longer exposure time, since white skin cuts back production after 20 minutes in the sun.2 Even in England, where sunlight is relatively weak, vitamin D levels show similar spring and summer increases in Asian, West Indian, and European adolescents.3

Second, serum vitamin D levels are low even in dark-skinned humans who still inhabit the tropical zone. In a study from Hawaii, vitamin D status was assessed in visibly tanned young adults who averaged 22.4 hours per week of unprotected sun exposure. Yet 51% had levels below the current recommended minimum of 30 ng/mL.4 In a study from south India, levels were below 20 ng/mL in 44% of the men and 70% of the women. The subjects are described as “agricultural workers starting their day at 0800 and working outdoors until 1700 with their face, chest, back, legs, arms, and forearms exposed to sunlight.”5 In a study from Saudi Arabia, levels were below 10 ng/mL in, respectively, 35%, 45%, 53%, and 50% of normal male university students of Saudi, Jordanian, Egyptian, and other origins.6

Tropical humans seem to compensate for this lower level of production by converting more vitamin D to its active form. Although a single UVB exposure produces less vitamin D3 in black subjects than in whites, the difference narrows after liver hydroxylation to 25-OHD and disappears after kidney hydroxylation to 1,25-(OH)2D. The active form of vitamin D is thus kept at a constant level regardless of skin color.7,8 It is no paradox, then, that nearly half of black Americans are classified as vitamin D deficient and yet few show signs of calcium deficiency, which would be a logical symptom. Indeed, this population has “a lower prevalence of osteoporosis, a lower incidence of fractures and a higher bone mineral density than white Americans, who generally exhibit a much more favorable vitamin D status.”9 A similar picture emerges from a survey of East African immigrant children in Australia, among whom 87% had vitamin D levels below 20 ng/mL and 44% below 10 ng/mL. None had rickets, the usual sign of vitamin D deficiency in children.10

In sum, humans have adapted to the tropical zone by producing less vitamin D and converting more to its active form. Outside the tropical zone, humans have come to produce more and convert less. Why this difference in adaptation? Perhaps the seasonal variation in UVB at higher latitudes favors producing as much vitamin D as possible in summer in order to have a reserve for winter, ie, “making hay while the sun shines.” This high production for future use may have selected for a lower conversion rate.

What effects, then, can we expect from artificially raising the vitamin D levels of black Americans? Keep in mind that we are really talking about a hormone, not a vitamin. This hormone interacts with the chromosomes and may gradually shorten their telomeres if concentrations are too low or too high.11 Similarly, cancer risk increases if concentrations are too low or too high. Prostate cancer is least likely when vitamin D levels vary between 16 and 24 ng/mL—a range of values below the current recommended minimum of 30 ng/ mL.11 This optimal range may require greater compliance from humans of tropical origin, such as black Americans, because their bodies are less adapted to wide seasonal variation in vitamin D levels.

If this optimal range is continually exceeded, the long-term effects may look like those of aging. Genetically modified mice with high vitamin D activity show premature aging, as indicated by retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism, and short lifespan.11-13 Similar accelerated aging has been noted in rachitic German children who were given high oral doses of vitamin D after World War II.11

It is possible that these negative effects coexist with the positive effects claimed by vitamin D proponents. In the case of black Americans, however, positive effects are attested by only 2 studies. One study found that the intensity of solar UVB inversely correlates with mortality rates for breast, colon, esophageal, gastric, and rectal cancers among black Americans.14 This is essentially a latitude effect: cancer rates are higher in northern states than in southern states. Northern states, however, not only receive less solar UVB but also have more manufacturing, particularly heavy industries that use synthetic chemicals. On a county-by-county basis, there is a clear association between higher cancer mortality and the presence of chemical, automobile, and machinery manufacturing.15

A second study found that cancer incidence and mortality correlate in black men with an index of vitamin D deficiency.16 The index is based on 4 risk factors: residence in the northeastern United States, low dietary intake of vitamin D, high body mass, and low physical activity (a marker of outdoor sun exposure). Three of the 4 factors, however, are closely tied to other factors that are known to increase cancer risk independently of vitamin D status, ie, proximity to heavy industry,15 obesity,17 and lack of exercise.18 The authors go on to state that among subjects who gave blood samples, the serum vitamin D level was higher in black men with 1 risk factor (21.6 ng/mL) than in black men with 2 risk factors (17.2 ng/mL). This is a small and probably insignificant difference. By comparison, white Americans can range from 48.8 ng/mL in late summer to 29.6 ng/L in late winter.19 The authors do not state whether the vitamin D levels inversely correlated with cancer risk, probably because the correlation was not significant.

Despite this weak evidence, support is growing for vitamin D supplementation. A National Institutes of Health–funded study will investigate the benefits of supplementation over 5 years in a sample that includes 5000 black Americans, the hope being to bring their disease rates down to those of other Americans.20 Possible negative effects will also be studied. Nonetheless, such effects may escape notice if they are long-term and mimic those of aging.

Peter Frost, PhD peter_frost61z@globetrotter.qc.ca c/o Bernard Saladin d’Anglure, PhD Département d’anthropologie Université Laval Québec (Québec) G1K 7P4 Canada

1. Grant WB. Differences in vitamin-D status may explain black-white differences in breast cancer survival rates. J Natl Med Assoc. 2008;100:1040. 2. Holick MF. Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications. Bone. 1995;17:107S-111S. 3. Ellis G, Woodhead JS, Cooke WT. Serum-25hydroxyvitamin-D concentrations in adolescent boys. Lancet. 1977;1:825-828. 4. Binkley N, Novotny R, Krueger D, et al. Low vitamin D status despite abundant sun exposure. J Clin Endocr Metab. 2007;92:2130 –2135. 5. Harinarayan CV, Ramalakshmi T, Prasad UV, et al. High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians. Am J Clin Nutr. 2007;85:1062-1067. 6. Sedrani SH. Low 25-hydroxyvitamin D and normal serum calcium concentrations in Saudi Arabia: Riyadh region. Ann Nutr Metab. 1984;28:181-185. 7. Matsuoka LY, Wortsman J, Haddad JG, et al. Racial pigmentation and the cutaneous synthesis of vitamin D. Arch Dermatol. 1991;127:536-538. 8. Matsuoka, LY, Wortsman J, Chen TC, et al. Compensation for the interracial variance in the cutaneous synthesis of vitamin D. J Lab Clin Med. 1995;126:452-457. 9. Robins AH. The evolution of light skin color: role of vitamin D disputed. Am J Phys Anthropol. 2009;139:447-450. 10. McGillivray G, Skull SA, Davie G, et al. High prevalence of asymptomatic vitamin-D and iron deficiency in East African immigrant children and adolescents living in a temperate climate. Arch Dis Child. 2007;92:1088-1093. 11. Tuohimaa P. Vitamin D and aging. J Steroid Biochem. 2009;114:78-84. 12. Ignat M, Teletin M, Tisserand J, et al. Arterial calcifications and increased expression of vita- min D receptor targets in mice lacking TIF1a. PNAS. 2009;105:2598-2603. 13. Keisala T, Minasyan A, Lou Y-R, et al. Premature aging in vitamin D receptor mutant mice. J Steroid Biochem. 2009;115:91-97. 14. Grant WB. Lower vitamin-D production from solar ultraviolet-B irradiance may explain some differences in cancer survival rates. J Natl Med Assoc. 2006;98:357-364. 15. Hoover R, Mason TJ, McKay FW, et al. Cancer by county: New resource for etiologic cues. Science. 1975;189:1005-1007. 16. Giovannucci E, Liu Y, Willett WC. Cancer incidence and mortality and vitamin D in black and white male health professionals. Cancer Epidem Biomar. 2006;15:2467-2472. 17. Calle EE, Rodriguez C, Walker-Thurmond K, et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of US adults. N Engl J Med. 2003;348:1625-1638. 18. Friedenreich CM, Orenstein MR. Physical activity and cancer prevention: Etiologic evidence and biological mechanisms. J Nutr. 2002;132:3456S-3464S. 19. Barger-Lux J, Heaney RP. Effects of above average summer sun exposure on serum 25-hydroxyvitamin D and calcium absorption. J Clin Endocr Metab. 2002;87:4952-4956. 20. Cooney E. Brigham study to test vitamin D, fish oil supplements. Boston Globe. June 23, 2009.

The evolution of light skin color: role of vitamin D disputed.¹⁹⁾

Robins AH.

Department of Medicine, Division of Pharmacology, University of Cape Town Medical School, Observatory, South Africa 7925. ashley.robins@uct.ac.za PMID: 19425095 [PubMed - in process]

Cancer and vitamin D 15225775

Vitamin D and Cancer: Existing Evidence Shows No Clear BenefitZosia Chustecka Authors and Disclosures Print This Email this Share

March 31, 2011‚Äî The idea that vitamin D reduces both cancer incidence and mortality, which stems from observational studies, is biologically plausible and has been promulgated with widespread enthusiasm. But the evidence is “inconsistent and inconclusive as to causality,” say vitamin D experts who were on the Institute of Medicine (IOM) panel that recently published a definitive report on vitamin D and health outcomes.

Although the IOM report covered all aspects of vitamin D and its effects on health, a new pronouncement ‚Äî published online March 23 as a Perspective in the New England Journal of Medicine ‚Äî focuses specifically on cancer.

“Given that the potential role of vitamin D in cancer prevention has been widely touted, many people were surprised that cancer-related considerations didn't figure prominently” in the IOM report, write the authors, headed by JoAnn Manson, MD, DrPH, from the Department of Medicine at Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

“The committee's comprehensive review of the evidence regarding vitamin D's role in preventing cancer, however, revealed that the research is inconsistent and doesn't establish a cause‚Äìeffect relationship,” they explain.

Most of the evidence is derived from laboratory studies, ecologic correlation, and observation investigations of serum vitamin D levels in association with cancer outcomes. There have been no large-scale randomized clinical trials with vitamin D and cancer as the primary prespecified end point, they noted.

“Existing evidence falls short” of showing clear benefits from vitamin D on cancer, they conclude.

Ongoing trials are assessing the effect of vitamin D supplementation in moderate to high doses for cancer prevention; results from these studies should be available in 5 or 6 years.

Dr. Manson discusses the main points from the IOM report on vitamin D in a Medscape videocast .

N Engl J Med. Published online March 23, 2011.

Vitamin D and Cancer Mortality: Not to be Taken Lightly

Cancer Causes Control. 2011 Mar;22(3):319-40. Epub 2011 Jan 4. Associations of circulating and dietary vitamin D with prostate cancer risk: a systematic review and dose-response meta-analysis. Gilbert R, Martin RM, Beynon R, Harris R, Savovic J, Zuccolo L, Bekkering GE, Fraser WD, Sterne JA, Metcalfe C. School of Social and Community Medicine, University of Bristol, Canynge Hall, 39 Whatley Road, Bristol BS8 2PS, UK. Becky.Gilbert@Bristol.ac.uk Abstract OBJECTIVE: We systematically reviewed and meta-analyzed literature examining associations of vitamin D (dietary intake, circulating 25-hydroxy-vitamin-D (25(OH)D), and 1,25-dihydroxy-vitamin-D (1,25(OH)(2)D) concentrations) with prostate cancer. METHODS: We searched over 24,000 papers from seven electronic databases (to October 2010) for exposures related to vitamin D. We conducted dose-response random-effects meta-analyses pooling the log odds ratio (OR) and 95% confidence intervals (CI) per change in natural units of each exposure. The I(2) statistic quantified between-study variation due to heterogeneity. RESULTS: Twenty-five papers were included. In prospective studies, the OR per 1,000 IU increase in dietary intake was 1.14 (6 studies; CI: 0.99, 1.31; I (2) = 0%) for total prostate cancer and 0.93 (3 studies; 0.63, 1.39; I (2) = 25%) for aggressive prostate cancer. Five case-control studies examined dietary intake, but there was a high degree of inconsistency between studies (I (2) = 49%). The OR per 10 ng/mL increase in 25(OH)D was 1.04 (14 studies; 0.99, 1.10; I (2) = 0%) for total prostate cancer and 0.98 (6 studies; 0.84, 1.15; I (2) = 32%) for aggressive prostate cancer. The OR per 10 pg/mL increase in 1,25(OH)(2)D was 1.00 (7 studies; 0.87, 1.14; I (2) = 41%) for total prostate cancer and 0.86 (2 studies; 0.72, 1.02; I (2) = 0%) for aggressive prostate cancer. CONCLUSION: Published literature provides little evidence to support a major role of vitamin D in preventing prostate cancer or its progression. PMID: 21203822

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¹⁰⁾ , ¹¹⁾

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¹²⁾

Chen W, Dawsey SM, Qiao Y, Mark SD, Dong Z, Taylor PR, Zhao P, Abnet CC. Prospective study of serum 25(OH)-vitamin D concentration and risk of oesophageal and gastric cancers. Br J Cancer. 2007 Jul 2;97(1):123-8. doi: 10.1038/sj.bjc.6603834. Epub 2007 Jun 5.
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