Cancer Prevention: Vitamin D and Breast Cancer

Jacob Schor ND, FABNO

January 2008

The term preventive medicine is frequently misused.

Most things referred to as preventive medicine are actually only screening routines intended to detect disease at an earlier stage but that do not prevent disease development.

I am writing today about a preventive strategy for cancer. In writing this I single out one particular racial group who can benefit more from this information than others.  I understand that some prefer that the world be colorblind.  Yet it would seem irresponsible not to bring up race when the information could be potentially life saving.

 Vitamin D is the hormone we make in our skin in response to sunlight exposure.  It offers a range of benefits including protection against cancer.  Our diets are nearly useless at providing adequate amounts of vitamin D and most Americans have much lower than ideal levels.  Our primary source is from sun exposure.  The darker a person’s complexion, the less vitamin D they make during an identical time period of sun exposure compared to someone with a lighter complexion.

Last June, Lappe and his colleagues published the results of a prospective study on vitamin D in women in the American Journal of Clinical Nutrition.  Up to this publication, although many observational and epidemiologic studies suggested vitamin D supplementation would significantly lower cancer risk, often by 50%, no prospective trial had been published.  This June paper was the first randomized prospective controlled trial to test the theory.

The study was conducted in Nebraska, at approximately the same latitude as we are with similar sun exposure. The results obtained in Nebraska should apply to women in Colorado.

The study was conducted over a four-year period and was a double-blind, randomized placebo-controlled trial.  This is the gold standard for scientific research. In total, 1179 healthy postmenopausal women aged older than 55 years old took part. They were randomly assigned to take calcium alone, calcium and 1,000 IU of vitamin D or a placebo.

If we discount cancers that were diagnosed in the first 12 months of the study, a period too short to expect a decrease in risk, the results are astounding.

In years 2, 3 and 4, the relative risk of getting cancer dropped in the women taking calcium and vitamin D to 0.232 compared to the control group.  Expressed in simpler English, taking vitamin D and calcium lowered these women’s risk of being diagnosed with cancer by 77%.

Prior publications had suggested we should have expected results like this.  Still the magnitude of the protection is striking.  This is the study that convinced the Canadian Cancer Society to tell Canadians to start taking vitamin D.

Another paper published in December’s edition of the same journal tells us that African-American women are at high risk of vitamin D deficiency.  When it comes to vitamin D, skin color matters.  The darker a person’s complexion, the less light penetrates and the less vitamin D is made.

Researchers in Mineola, New York, recruited 208 post menopausal black women for a three-year study in which half of them received daily doses of vitamin D.  After two years of supplementation at 800 IU per day, twice the RDA, only 88% had reached the targeted blood level determined by the researchers.  It wasn’t until they jumped their daily dose to 2,000 IU per day for a year that the remaining women reached the targeted blood levels.

If African American women have a difficult time keeping their vitamin D levels high enough to protect against cancer, might their cancer rates be higher than women with lighter complexions?

A January 2008 article in the British Journal of Cancer tells us that in London, black women develop breast cancer twenty years younger than white women. The black patients were diagnosed with breast cancer at an average age of 46 while the white patients were diagnosed at an average age of 67.

The researchers also found that survival was poorer among black women with smaller tumors. The tumors in the younger black women were more likely to be aggressive, and a higher proportion of tumors were basal, the kind less likely to respond to cancer treatments like Herceptin.

Black women who get breast cancer are more likely than white women to die from it. “Ninety percent of white women who are diagnosed with breast cancer will live at least five years, but only 76 percent of black women with breast cancer will live five years, according to the American Cancer Society.”

The Center for Disease Control’s weekly publication tells us that from, “1980 through 1987, cervical cancer mortality rates for black women were consistently more than twice those for white women. Although the rates for both races declined during that period (for black women, from 10.1 to 7.6 per 100,000; for white women, from 3.6 to 2.9 per 100,000), the black-white rate ratio remained stable (2.8 in 1980 compared with 2.6 in 1987).”   Repeating that information but in English, black women are almost three times as likely to die of cervical cancer than white women.

It’s not only black women that don’t have low vitamin D levels.  A study published last year measuring vitamin D in Hawaiians found that more than half of them had substandard levels of vitamin D. Actually 51% were below the minimum level of 30 ng/ml set by researchers.   This is striking as this minimum level is well below the 60 or 75 ng/ml target level set by other experts as being ideal. 

One would think putting these three tracks of information together would be a no brainer.  Let me summarize: 

  • Having adequate vitamin D lowers a woman’s risk of cancer by 77%.
  • Many women, but especially black women, have trouble making and maintaining adequate vitamin D.
  • Black women are at greater risk of dying of cancer than white women.

Explain this to your fifth grader and see what they can figure out.  Given this information, can you think of a simple way to lower cancer rates, especially among black women?

We live in a country where health policies are driven by market and economic concerns not by intelligent planning.  No drug company or medical equipment manufacturer has an incentive to push for vitamin D screening.  But for mammograms or cholesterol testing or Statin drug prescribing, there are clear profit incentives. It is the potential for profit that drives much of our health care policies.


A drug company cannot patent vitamin D.  It is sold over the counter and is cheap.  The cost of a year’s worth of supplemental vitamin D is measured in dollars.  There is no profit in selling it.  There is no financial incentive to test for or sell vitamin D aside from the potential to decrease human suffering that does not show up on a balance sheet.

The only way we will see vitamin D become part of a national cancer prevention strategy will be through public policy not free market initiative. 

None of the healthcare proposals being brought before the Colorado Legislature address the real issue; our current healthcare model is one of disease treatment. Its policies are modeled to maximize profits for investors. Some suggest that it would be cheaper to invest in disease prevention.  That is true only if you are measuring profits in reducing morbidity and mortality and increasing quality of life. If vitamin D cuts cancer rates in half, screening at risk populations for deficiency could change health care costs significantly.  Reducing costs means reducing profits and well, I’d better stop here for fear I write something I may later regret.

Am J Clin Nutr.  2007 Jun;85(6):1586-91.

Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial.

Lappe JM , Travers-Gustafson D , Davies KM , Recker RR , Heaney RP .

Osteoporosis Research Center , Creighton University , Omaha , NE.

BACKGROUND: Numerous observational studies have found supplemental calcium and vitamin D to be associated with reduced risk of common cancers. However, interventional studies to test this effect are lacking. OBJECTIVE: The purpose of this analysis was to determine the efficacy of calcium alone and calcium plus vitamin D in reducing incident cancer risk of all types. DESIGN: This was a 4-y, population-based, double-blind, randomized placebo-controlled trial. The primary outcome was fracture incidence, and the principal secondary outcome was cancer incidence. The subjects were 1179 community-dwelling women randomly selected from the population of healthy postmenopausal women aged >55 y in a 9-county rural area of Nebraska centered at latitude 41.4 degrees N. Subjects were randomly assigned to receive 1400-1500 mg supplemental calcium/d alone (Ca-only), supplemental calcium plus 1100 IU vitamin D(3)/d (Ca + D), or placebo. RESULTS: When analyzed by intention to treat, cancer incidence was lower in the Ca + D women than in the placebo control subjects (P < 0.03). With the use of logistic regression, the unadjusted relative risks (RR) of incident cancer in the Ca + D and Ca-only groups were 0.402 (P = 0.01) and 0.532 (P = 0.06), respectively. When analysis was confined to cancers diagnosed after the first 12 mo, RR for the Ca + D group fell to 0.232 (CI: 0.09, 0.60; P < 0.005) but did not change significantly for the Ca-only group. In multiple logistic regression models, both treatment and serum 25-hydroxyvitamin D concentrations were significant, independent predictors of cancer risk. CONCLUSIONS: Improving calcium and vitamin D nutritional status substantially reduces all-cancer risk in postmenopausal women. This trial was registered at as NCT00352170.

PMID: 17556697 [PubMed - in process]

British Journal of Cancer (2008) 98, 277-281.

doi:10.1038/sj.bjc.6604174 Published online 8 January 2008

Early onset of breast cancer in a group of British black women

R L Bowen1, S W Duffy2, D A Ryan3, I R Hart1 and J L Jones1

1Centre for Tumour Biology, Institute of Cancer and CR-UK Clinical Centre, Barts and The London, Queen Mary's School of Medicine and Dentistry, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK

2Cancer Research UK, Centre for Epidemiology, Mathematics and Statistics, Wolfson Institute of Preventive Medicine, Charterhouse Square, London EC1M 6BQ, UK

3Department of Histopathology, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK

Correspondence to: Dr RL Bowen, E-mail:

Ethics Committee Approval: St Mary's REC, 06/Q0403/162

Revised 21 November 2007; accepted 30 November 2007; published online 8 January 2008

Since there are no published data on breast cancer in British black women, we sought to determine whether, like African-American women, they present at a younger age with biologically distinct disease patterns. The method involved a retrospective review of breast cancer to compare age distributions and clinicopathological features between black women and white women in the UK, while controlling for socioeconomic status. All women presented with invasive breast cancer, between 1994 and 2005, to a single East London hospital. Black patients presented significantly younger (median age of 46 years), than white patients (median age of 67 years (P=0.001)). No significant differences between black and white population structures were identified. Black women had a higher frequency of grade 3 tumours, lymph node-positive disease, negative oestrogen receptor and progesterone receptor status and basal-like (triple negative status) tumours. There were no differences in stage at presentation; however, for tumours of 2 cm, black patients had poorer survival than white patients (HR=2.90, 95% CI 0.98-8.60, P=0.05). Black women presented, on average, 21 years younger than white women. Tumours in younger women were considerably more aggressive in the black population, more likely to be basal-like, and among women with smaller tumours, black women were more than twice as likely to die of their disease. There were no disparities in socioeconomic status or treatment received. Our findings could have major implications for the biology of breast cancer and the detection and treatment of the disease in black women.

Erin Allday. Breast cancer mortality studied in black women. San Francisco Chronicle

Friday, May 18, 2007

MMWR WeeklyApril 20, 1990 / 39(15);245-246,248

J Clin Endocrinol Metab. 2007 Jun;92(6):2130-5. Epub 2007 Apr 10.Click here to read Links

    Low vitamin D status despite abundant sun exposure.

    Binkley N, Novotny R, Krueger D, Kawahara T, Daida YG, Lensmeyer G, Hollis BW, Drezner MK.

    University of Wisconsin Osteoporosis Research Program, Madison, WI 53705, USA.

    CONTEXT: Lack of sun exposure is widely accepted as the primary cause of epidemic low vitamin D status worldwide. However, some individuals with seemingly adequate UV exposure have been reported to have low serum 25-hydroxyvitamin D [25(OH)D] concentration, results that might have been confounded by imprecision of the assays used. OBJECTIVE: The aim was to document the 25(OH)D status of healthy individuals with habitually high sun exposure. SETTING: This study was conducted in a convenience sample of adults in Honolulu, Hawaii (latitude 21 degrees ). PARTICIPANTS: The study population consisted of 93 adults (30 women and 63 men) with a mean (sem) age and body mass index of 24.0 yr (0.7) and 23.6 kg/m(2) (0.4), respectively. Their self-reported sun exposure was 28.9 (1.5) h/wk, yielding a calculated sun exposure index of 11.1 (0.7). MAIN OUTCOME MEASURES: Serum 25(OH)D concentration was measured using a precise HPLC assay. Low vitamin D status was defined as a circulating 25(OH)D concentration less than 30 ng/ml. RESULTS: Mean serum 25(OH)D concentration was 31.6 ng/ml. Using a cutpoint of 30 ng/ml, 51% of this population had low vitamin D status. The highest 25(OH)D concentration was 62 ng/ml. CONCLUSIONS: These data suggest that variable responsiveness to UVB radiation is evident among individuals, causing some to have low vitamin D status despite abundant sun exposure. In addition, because the maximal 25(OH)D concentration produced by natural UV exposure appears to be approximately 60 ng/ml, it seems prudent to use this value as an upper limit when prescribing vitamin D supplementation.

    PMID: 17426097 [PubMed - indexed for MEDLINE]