The bold but unequivocal argument that started with Dr. Peller’s and Dr.
Apperly’s findings continues to gather force today: nonmelanoma skin cancers are relatively easy to detect and treat, unlike lethal colon, prostate, and breast cancer, which we now know are associated with lack of sun exposure. We also know that the sun’s protection against cancer is due to vitamin D. You’ll have to forgive me for sounding a little repetitive with all this research and published works confirming the same or similar conclusions; the statistics can become dizzying, but they are astonishing. All these insights have truly reshaped our view on sunlight as well as given us a reason to view the last decade as a great leap forward in scientific circles.
likely to develop cancers of the breast, ovaries, colon, prostate, bladder, uterus, esophagus, rectum, and stomach.
Based on the statistics available, Grant calculated that in 2002 alone, insufficient sun exposure among Americans caused eighty-five thousand more cases of cancer and thirty thousand more deaths than would have occurred if everyone in the United States had gotten as much sun as people living in the Southwest. Similar observations have been made in Europe.
You may ask, What about the increased rates of melanoma and nonmelanoma skin cancer that would, hypothetically, result from this additional sun exposure?
Grant calculated the additional number of deaths from skin cancer would be three thousand—a tragically high number, but one far smaller than the number of deaths caused by underexposure to sunlight. Recall that most melanomas occur in the least sun-exposed areas, and working outside in the sun all day (what is sometimes referred to as occupational exposure) lowers one’s risk for melanoma.
Certain types of cancer have strong gender associations. Breast cancer affects mostly women, and only men get prostate cancer. Both breast and prostate cancer are strongly influenced—in a preventive manner—by sun exposure.
The Garland brothers and their colleagues and Dr. William Grant have shown that if you start out with a 25-vitamin D of at least 20 nanograms per milliliter, you reduce your risk of developing colorectal, breast, and a wide variety of other cancers by 30 percent to 50 percent. It’s estimated that if you take 1,000 IU of vitamin D per day, you reduce your risk of developing colorectal, breast, prostate, and ovarian cancer by approximately 50 percent.
Cancer also has strong racial associations. It’s well documented that there’s a higher incidence of cancer among African Americans than among Caucasians.
They also have lower survival rates once diagnosed with cancer. Scientists have long hypothesized that this disparity could be due in part to vitamin D status, as vitamin D deficiency is more prevalent and pronounced among African Americans, whose melanin-rich skin absorbs solar UVB radiation and competes with 7-DHC for these vitamin-D producing rays, thus decreasing the amount of vitamin D that can be manufactured in the skin. When Dr. William Grant reported on this in 2006 for the Journal of the National Medical Association ,
stating that lower cancer survival rates could be attributed to lower 25-vitamin D levels in the black community, he even took factors like smoking, alcohol consumption, access to health care, and poverty into consideration.
Large-scale studies performed by researchers at Harvard found that, after adjusting for multiple dietary, lifestyle, and medical risk factors, African American men were at 32 percent greater risk of total cancer incidence and 89 percent greater risk of total cancer mortality than white men. African American men also have been shown to be at an especially high risk of cancer in the digestive tract (colon, rectum, mouth, esophagus, stomach, and pancreas)—the very group of cancers strongly associated with low 25-vitamin D levels. In 2005, at a meeting of the American Association for Cancer Research, Harvard’s lead researcher on these studies, Dr. Edward Giovannucci, a professor of medicine and nutrition, laid out his case in a keynote lecture that had virtually everyone’s ears pricked up. His research suggests that vitamin D might help prevent thirty deaths for each one caused by skin cancer.
Breast Cancer
Here’s a staggering statistic: Women who are deficient in vitamin D at the time they are diagnosed with breast cancer are nearly 75 percent more likely to die from the disease than women with sufficient vitamin D levels. What’s more, their cancer is twice as likely to metastasize to other parts of the body.
In the United States, more than forty thousand women die from breast cancer every year—making it the deadliest killer of women after heart disease. One woman in eight either has or will develop breast cancer in her lifetime. To the more than two hundred thousand women who are diagnosed with this disease each year, there are not only physical consequences but emotional ones too. Self-esteem issues associated with breast cancer can be profound.
There are 214,000 new cases and 41,000 deaths from breast cancer each year in the United States. A 2008 study found that women who had a vitamin D deficiency at the time they were diagnosed with breast cancer were 94 percent more likely to have their cancer spread than women with adequate 25-vitamin D levels in their bodies.
In May 1999, a landmark study by Dr. Esther John, based on the meticulous analysis of breast cancer statistics from the National Health and Nutrition Examination Survey, was published. The results provide extraordinary insight into the relationship between sun exposure and breast cancer. The authors conclude definitively that sun exposure and a vitamin D-rich diet significantly lower the risk of breast cancer.
The John study demonstrates that increased sun exposure alone could potentially reduce the incidence and death rate of breast cancer in the United States by 35 percent to 75 percent. This would mean that the incidence of new cases might be reduced by 70,000 to 150,000 each year and that 17,500 to 37,500 deaths could be prevented. A conservative estimate is that increased sun exposure could prevent 100,000 new cases of breast cancer and 27,500 deaths from this disease. Combining increased sun exposure with a vitamin D-rich diet or supplements could make the disease prevention and death rate figures 150,000 and 38,000, respectively.
In 2007, researchers pooled the results from two studies—the Harvard Nurses’
Health Study and the St. George’s Hospital Study in London—and published a report that said patients with the highest blood levels of 25-vitamin D had the lowest risk of breast cancer. Raising 25-vitamin D levels may prevent up to half of breast and two thirds of colorectal cancer cases in the United States alone. In 2008, Dr. Garland and his colleagues again documented an association among a lack of sunlight exposure, low 25-vitamin D, and breast cancer. These statistics likely replicate in other countries at similar latitudes. Based on his studies, Dr.
William Grant estimates that lack of sun exposure is responsible for approximately 25 percent of the deaths from breast cancer in Europe. Recently, Dr. Julia Knight of the University of Toronto reported that women who had the most sun exposure as teenagers and young adults had a more than 60 percent reduced risk of developing breast cancer compared to women who had the least sun exposure. One can only imagine the excitement that would result if a drug were invented that yielded such preventive results!
Again, you might ask about skin cancer rates. Wouldn’t they rise in response to increased sun exposure? Approximately 500 women a year die from nonmelanoma skin cancer. Given that the above statistics show that 27,500 women die prematurely because of underexposure to sunlight, it becomes evident that 55 women die prematurely because of underexposure to sunlight for every 1 who dies prematurely from overexposure to sunlight.
Hang tight: I’ll be answering all your questions about sunlight and skin cancer
in chapter 8. For now, let’s keep the focus on the types of cancer that kill more people and don’t cry mercy too often when diagnosed and treated.
Prostate Cancer
Only heart attacks and lung cancer kill more men than cancer of the prostate, which every year claims more than fifty thousand lives in the United States alone. Prostate cancer kills one in four men who get this disease, making it one of the most deadly forms of cancer. About forty thousand American men die every year from prostate cancer—more than ten times as many as are killed by melanomas.
Cancer of the prostate is especially feared by men because surgical treatment for this form of cancer frequently results in impotence. A study in the August 2001 issue of the Lancet proves that the risk of developing prostate cancer is directly related to sunlight exposure. The study divided people into four groups according to how much sunlight they had been exposed to. The lowest quarter, or quartile, of the study participants were three times more likely to develop prostate cancer than those in the highest quartile of sun exposure. The results show that those in the highest quartile reduced their risk of developing prostate cancer by 66 percent. Those in the second and third quartiles also had a significantly lower chance of getting prostate cancer compared with those in the lowest quartile, who received the least sun exposure. Another study took a long look, over almost two years, at men with prostate cancer who received 2,000 IU of vitamin D a day and found that overall the men had a 50 percent reduction in the rise of their levels of prostate-specific antigen (PSA), which is an indicator of prostate cancer activity.
Only about six hundred men die prematurely each year from nonmelanoma skin cancer, but thirty-seven thousand men die prematurely each year from prostate cancer. It’s possible to conclude that fifty-five men die prematurely from underexposure to sunlight for every one who dies prematurely due to overexposure. Even when you include melanoma—for which excessive sunshine is only one of several risk factors—the numbers are still lopsided: about ten to one.
Colon Cancer
Cancer of the colon and its neighboring area, known sometimes as colorectal cancer, affects both men and women. Like breast cancer and prostate cancer, colorectal cancer is seen much more frequently than skin cancers and is much more deadly. About 150,000 Americans are told each year that they have colon cancer, and about 35 percent of these will die of it. There are many contributing factors in why someone gets colon cancer, but the most commonly acknowledged one is diet. Diets high in fat and nonorganic non-grass-fed red meat are especially dangerous. Other diets, such as diets high in fruits, vegetables, and other natural raw and organic foods, help prevent colon cancer.
A study published in the Journal of Clinical Oncology in 2008, conducted by lead researcher Dr. Kimmie Ng of the Dana-Farber Cancer Institute in Boston found that high blood levels of 25-vitamin D increased colon cancer patients’
survival rate by 48 percent. In this study, Dr. Ng and her team collected data on 304 patients who had been diagnosed with colon cancer between 1991 and 2002.
Everyone in the study had had their 25-vitamin D blood levels measured a minimum of two years before being diagnosed with the disease. The patients were tracked until they died or until the study ended in 2005; 123 patients died, 96 of them from colon or rectal cancer during the follow-up period. Dr. Ng and her team found that the patients with the highest 25-vitamin D levels were 39 percent less likely to die from colorectal cancer than the patients who had the lowest levels.
These findings are consistent with dozens and dozens of other observations that have been made in the past decade, including those by Dr. Cedric Garland.
His lab reports that you are three times less likely to die from colon cancer if you have healthy levels of 25-vitamin D in your bloodstream.
How Vitamin D Takes the Life out of Cancer
The link between vitamin D and cancer may have gained a strong foothold just recently within the medical community at large, but the research started long ago. Toward the end of the 1980s, I was part of a small but growing movement of medical scientists who believed that the active form of vitamin D that I had discovered a decade earlier had benefits well beyond bone health. We theorized that people who lived in sunnier climates had lower rates of cancer and heart disease because the vitamin D produced by their exposure to the sun was somehow benefiting cells throughout the body. A few studies backed this up at
the time, but what exactly was causing this?
My fellow researchers had successfully proved the relationship between sunlight and cellular health, but I believed their conclusion as to why sunlight and increased vitamin D production benefited cellular health was incorrect. They thought that vitamin D benefited cells throughout the body in the same way we understood it benefited bone health. That is, the more sunshine you get, the more 25-vitamin D there is circulating in your bloodstream that can be converted by the kidneys into activated vitamin D. According to this theory, this activated vitamin D would then be sent by the kidneys to different parts of the body, where it would benefit different cell groups by regulating their growth and preventing them from becoming malignant. This theory assumes that the more vitamin D you get from the sun and your diet, the more activated vitamin D your kidneys will make.
I believed something quite different. At the time, my theory was considered heretical, and it probably still would be if my colleagues and I hadn’t proved it.
We understood that activated vitamin D is one of the most potent inhibitors of abnormal cell growth, but we knew that no matter how much you increased the supply of 25-vitamin D in a person’s body through sunlight and diet, you couldn’t get the kidneys to make any additional activated vitamin D. I didn’t think the very limited amount of activated vitamin D the kidneys are able to produce could be responsible for all the cellular benefits that we had identified.
In other words, the kidneys could not be the sole ruler in the vitamin D land. I believed that there had to be another source of activated vitamin D.
What my colleagues and I proposed was that cells throughout the body don’t have to rely on the meager supply of activated vitamin D from the kidneys because each group of cells has its own enzymatic machinery to convert 25-vitamin D into activated 25-vitamin D. In other words, cells can make their own activated vitamin D on the spot without having to rely on activated vitamin D sent from the distant kidneys. (If this story sounds familiar, that’s because I told it earlier from a slightly different angle and in broader strokes.)
We proved this theory in a study published in 1998 that involved collaboration with Dr. Gary Schwartz and my colleague Dr. Tai Chen. Our findings completely changed the way medical science perceives the relationship between vitamin D and cellular and organ health. In this study we exposed normal prostate cells to 25-vitamin D to see what would happen. The cells converted 25-vitamin D to activated vitamin D (1,25-vitamin D). We then exposed prostate cancer cells to 25-vitamin D. In cancerous fashion, these cells were reproducing out of control.
When we exposed these prostate cancer cells to 25-vitamin D, they converted that substance into activated vitamin D and stopped their chaotic reproduction.
What we had actually proved was that, just like the kidney, normal prostate cells and prostate cancer cells could make activated vitamin D. But unlike the activated vitamin D made by the kidneys, which regulates calcium metabolism and promotes bone health, the activated vitamin D created within the prostate has the job of ensuring healthy cell growth. Not only was this confirmed in subsequent studies, but similar studies by my research group and other researchers found that the same enzymatic machinery to activate vitamin D also exists in the cells of the colon, breast, lung, and brain.
This finding helped make more sense out of other mysteries about the body’s use of vitamin D. The vitamin D activated in the kidneys specifically travels to the intestine and bone to regulate calcium metabolism. So if your kidneys were to make a lot more active vitamin D, there would be negative health consequences, such as hypercalcemia (high blood calcium) and hypercalciuria (high urine calcium). What the body cleverly does instead is allow other tissues and cells in your body to activate vitamin D. If you have a patient who has no kidneys, he has no circulating blood levels of activated vitamin D. Therefore, it used to be assumed that only the kidneys made activated vitamin D. What was shown by my lab and others was that the body was smarter and could activate vitamin D locally in the prostate, colon, and breast.
Activated vitamin D, locally produced, can regulate up to two thousand different genes that control cell growth and other cellular functions, produce insulin in the pancreas, and regulate production of the hormone renin in the kidneys. Once it carries out these functions, activated vitamin D triggers the expression of 25-vitamin D-24-hydroxylase, which is an enzyme that rapidly destroys activated vitamin D. Activated vitamin D never leaves the cell, and therefore its signature is never picked up in the bloodstream. It’s a silent soldier that essentially commits suicide once its task is finished on site. Another brilliant example of how the body self-regulates.
The consequences of this discovery are mind-boggling. We had discovered the likely reason why sun exposure has such a profound effect on cancer rates.
When you are exposed to more sunlight and make more vitamin D, it can be converted by the liver into 25-vitamin D, which can be activated by the prostate, colon, ovaries, breast, pancreas, brain, and probably most other tissues to prevent unhealthy cell growth. The more 25-vitamin D you make, the healthier these disease-prone tissues will be. Because we don’t have to rely on a supply of
activated vitamin D from our kidneys, there is an enormous capacity to prevent cancer just by having ample supplies of 25-vitamin D around that originate either from the sunlight’s action in the skin or from supplementation of vitamin D2 or D3. Powerful new synthetic forms of activated vitamin D also are being studied to see how they could hinder cancer growth.
While the potential for activated vitamin D to be used as a treatment for cancer seems logical given vitamin D’s preventive actions on cells, there’s more to the cancer story that bears understanding. For one thing, cancer cells are clever. Once a malignancy takes hold, those cancerous cells begin to make more of a protein that controls the expression of genes, called a transcription factor.
And one of those transcription factors, called Snail, binds to the vitamin D receptor and renders it dysfunctional. Once that happens, activated vitamin D can no longer regulate gene expression and thus can no longer work on cells to protect them. It’s like a switch that’s been flipped off. The cancerous cells essentially become closed for business with activated vitamin D and, left to their own devices, continue to grow and inflict harm on nearby tissues.
A New Model for Cancer?
Though it’s a stretch to say vitamin D can totally prevent and cure cancer, some scientists have been bold enough to suggest a whole new theory about cancer.
Just last year, the Garland brothers raised the possibility that there’s another story behind cancer’s genesis in the body. The current scientific model assumes that a genetic mutation is cancer’s point of origin. But what if that assumption is wrong? What if there is another way to explain how cancer develops? Those are the questions the Garlands put forth, which were published in the Annals of Epidemiology and immediately picked up by the media.
First, Dr. Cedric Garland and his team pointed to a host of research that suggests cancer develops when cells lose the ability to stick together in a healthy, normal way. He went on to argue that the key factor in this initial triggering of a malignancy could well be a lack of vitamin D. According to Dr. Garland, researchers have documented that with enough activated vitamin D present, cells adhere to one another in tissue and act as normal, mature cells. But if there is a deficiency of activated vitamin D, cells can lose this stick-to-each-other quality, as well as their identity as differentiated cells. The result? They may revert to a