Wednesday, May 31, 2017

Colon Cancer may be preventable

50% of all colon cancer cases are preventable
By Erin Elizabeth - May 31, 2017

By Dr. Mercola
Colon cancer has been in the news as of late after the International Agency for Research on Cancer (IARC), which is part of the World Health Organization (WHO), concluded in late 2015 that processed meat can cause colorectal cancer in humans, classifying it as a Group 1 carcinogen.
Colorectal cancer, which includes both cancers of the colon and rectum, is the third most common cancer diagnosed in the U.S. (not including skin cancers). In 2016, it’s estimated there will be more than 95,000 new cases of colon cancer (and more than 39,000 cases of rectal cancer) diagnosed.
Your colon, also known as your large intestine, plays an incredibly important role in your health. As food passes through your colon, liquid and salt are removed to prepare it for elimination.
Aside from helping to form, store and eliminate waste, your colon contains billions of bacteria, a healthy balance of which is essential for optimal health.
Many Cases of Colon Cancer Are Preventable
Colorectal cancer is the second leading cause of cancer deaths in the U.S., but, like many types of cancer, it is often preventable.
Research published in Pharmaceutical Research suggested that only 5 percent to 10 percent of cancer cases are due to genetic defects, while the rest are linked to environment and lifestyle factors.
The researchers estimated that up to 35 percent of cancer-related deaths may be due to diet, another 30 percent due to tobacco, 20 percent due to infections and the rest due to other environmental factors including exposure to radiation, stress, physical activity levels and environmental pollution.
The American Institute for Cancer Research (AICR) also stated that about one-third of the most common U.S. cancer cases are preventable through a healthy diet, being physically active and maintaining a healthy weight.
In the case of colorectal cancer, the percentage that could be prevented via these lifestyle factors rises to 50 percent.
Top Tips to Prevent Colon Cancer
Today can be the day you start making healthy changes to lower your risk of this potentially deadly disease. Top steps include the following.
1.Eat More Vegetables and Some Fruits
Vegetables contain an array of antioxidants and other disease-fighting compounds that are very difficult to get anywhere else – like magnesium.
Results from one meta-analysis indicated that for every 100-milligram increase in magnesium intake, the risk of colorectal tumor decreased by 13 percent, while the risk of colorectal cancer was lowered by 12 percent.
The researchers noted magnesium’s anti-cancer effects may be related to its ability to reduce insulin resistance, which may positively affect the development of tumors.
Beyond magnesium, plant chemicals called phytochemicals can reduce inflammation and eliminate carcinogens, while others regulate the rate at which your cells reproduce, get rid of old cells and maintain DNA.
Vegetables are also one of the best forms of dietary fiber. Studies have repeatedly shown that people with higher vegetable intake have lower rates of cancer.
Cruciferous vegetables may be particularly beneficial due to the sulforaphane they contain. Sulforaphene, a naturally occurring derivative of sulforaphne, has been found to suppress growth of colon cancer-derived tumors, for example.
If you’re healthy, consuming some fruit in moderation may also be beneficial. According to one study, dried plums (i.e. prunes) may lower your risk of colon cancer by building your gut bacteria.
2.Eat More Fiber
Dietary fiber has been associated with a reduced risk of colorectal cancer, particularly incident colorectal adenoma and distal colon cancer. Further, for every 10 grams of fiber you add to your daily diet, your risk of colon cancer decreases by 10 percent.
A 2005 study similarly revealed that dried plums “favorably altered … colon cancer risk factors” in rats, possibly due to their high content of dietary fiber and polyphenolics.
Fortunately, if you follow the tip above and eat more vegetables, you’ll naturally be eating more fiber from the best possible source — vegetables. Psyllium seed husk, flax seeds, hemp seeds and chia seeds also provide valuable sources of soluble and insoluble fiber.
3.Optimize Your Vitamin D Levels
Vitamin D deficiency is a risk factor for colorectal cancer. In one study published in the journal Gut, people with higher blood levels of vitamin D were less likely to develop colorectal tumors.
This may be because vitamin D is beneficial for your immune system, which in turn may help to limit the growth of cancerous tumors. According to the researchers:
“Evidence suggests protective effects of vitamin D and antitumour immunity on colorectal cancer risk.
Immune cells in tumour microenvironment can convert 25-hydroxyvitamin D [25(OH)D] [vitamin D] to bioactive 1α,25-dihydroxyvitamin D3, which influences neoplastic and immune cells
… High plasma 25(OH)D level is associated with lower risk of colorectal cancer with intense immune reaction, supporting a role of vitamin D in cancer immunoprevention through tumour–host interaction.”
Regular sun exposure, use of a high-quality tanning bed and/or supplementation with a vitamin D3 supplement can get your vitamin D levels into the optimal range of 50-70 ng/ml. You’ll need to monitor your levels to be sure you stay within this target range.
4.Avoid Processed Meats
Processed meats are those preserved by smoking, curing, salting, or the addition of chemical preservatives.

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This includes bacon, ham, pastrami, salami, pepperoni, hot dogs, some sausages, and hamburgers (if they have been preserved with salt or chemical additives) and more. Particularly problematic are the nitrates that are added to these meats as a preservative, coloring, and flavoring.
The nitrates found in processed meats are frequently converted into nitrosamines, which are clearly associated with an increased risk of certain cancers. AICR warns that “there is no safe threshold” for eating processed meats.
5.Be Knowledgeable About Red Meat Consumption
Research suggests that people who eat the most red meat (in one study this was five ounces a day) have a 24 percent greater risk of colorectal cancer than those who eat the least.
Red meat is likely not the problem in and of itself, however, but the way it’s cooked, and the source it comes from, likely play a role. Grass-fed beef, for instance, contains cancer-fighting compounds.
On the other hand, it’s known that glyphosate, the active ingredient in Roundup herbicide, can have a detrimental impact on healthy gut bacteria and is carcinogenic. CAFO animals are typically fed grains contaminated with glyphosate.
Red meat cooked at high temperatures (such as barbecued or fried) may also contain carcinogenic cooking byproducts like heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs).
When it comes to meats, I recommend eating organically raised grass-fed meats only and cooking them only lightly (rare, not well-done). For the record, I believe most people need some animal protein to be optimally healthy, but most eat far more protein than is necessary (or healthy).
There is convincing evidence that regular exercise can significantly reduce your risk of colon cancer. One study revealed that physically active men and women have about a 30 percent to 40 percent reduction in the risk of developing colon cancer compared with inactive persons, for instance.
For starters, exercise drives your insulin levels down, and controlling insulin levels is one of the most powerful ways to reduce your cancer risk. It’s also been suggested that apoptosis (programmed cell death) is triggered by exercise, causing cancer cells to die.
Exercise also improves the circulation of immune cells in your blood. The job of these cells is to neutralize pathogens throughout your body, as well as destroy precancerous cells before they become cancerous. The better these cells circulate, the more efficient your immune system is at defending itself against infections and diseases like cancer.
7.Maintain a Healthy Weight and Control Belly Fat
A number of studies have linked obesity to an increased risk for about a dozen different cancers, including cancer of the colon. In a 2014 study that analyzed data from more than 5 million people over the age of 16, every 11-pound increase in body weight was associated with an increased risk for 10 types of cancer.
If you’re overweight or obese, even small amounts of weight loss can lead to significant benefits for your health. In terms of cancer prevention, losing excess belly fat is particularly important, as belly fat is linked to an increased risk of colon cancer regardless of your body weight.
8.Limit Your Alcohol Intake and Quit Smoking
Both excessive alcohol intake and smoking are associated with an increased risk of colorectal cancer. When it comes to alcohol, I generally define “moderate” alcohol intake (which is allowed in the beginner phase of my nutrition plan) as a 5-ounce glass of wine, a 12-ounce beer or 1 ounce of hard liquor, with a meal, per day.
As you progress further in the nutrition plan, I do recommend eliminating all forms of alcohol. If you’re a smoker, you can find tips for quitting here.
9.Eat Garlic
Garlic has been shown to kill cancer cells in laboratory studies, as well as shown promise when consumed via your diet. One study showed that women who regularly ate garlic (along with fruits and vegetables) had a 35 percent lower risk of colon cancer.
Those who consume high amounts of raw garlic also appear to have a lower risk of stomach and colorectal cancers. Furthermore, among people with inoperable forms of colorectal, liver, or pancreatic cancer, taking an extract of aged garlic for six months helped to improve immune function, which suggests it may be useful for helping your immune system during times of stress or illness.
When you add raw garlic in your diet the fresh clove must be crushed or chopped in order to stimulate the release of an enzyme called alliinase, which in turn catalyzes the formation of allicin.
Allicin, in turn, rapidly breaks down to form a number of different organosulfur compounds. So to “activate” garlic’s medicinal properties, compress a fresh clove with a spoon prior to swallowing it, chop it finely to add to a salad, or put it through your juicer to add to your vegetable juice.
Should You Have Routine Colonoscopies Starting at 50?
Men and women over the age of 50 at average risk of colorectal cancer are typically advised to get screened either by flexible sigmoidoscopy every five years, or by colonoscopy every 10 years. But are these screening tests safe and necessary? I’m over 60, and I’ve never had a colonoscopy and have no plans of ever getting one.
While I believe they can be valuable as a diagnostic tool, I feel confident that with my diet (which includes daily amounts of raw turmeric) and lifestyle it’s highly unlikely I would develop colon cancer.
But for many people who are at higher risk, colonoscopies may be an effective strategy. Colon cancer grows very slowly, and it’s one of the top leading cancers that kill people, so early detection is important. You could opt for an annual guaiac stool detection test — which checks for hidden blood in your stool — but this test produces many false positives, and the latest evidence suggests this test doesn’t work very well.
Another alternative is to get tested by flexible sigmoidoscopy every five years. It’s similar to a colonoscopy but uses a shorter and smaller scope, so it cannot see as far up into your colon. On the upside, it’s associated with fewer complications. Ultrasounds have also proven to be of value. Overall, visual inspection is the most reliable way to check for colon cancer, and this is what a colonoscopy allows your doctor to do.
If polyps are found in their early stages, your doctor can simply snip them off right then and there. So a colonoscopy is not only a diagnostic tool, it can also serve as a surgical intervention. They take a picture of the polyp, clip it, capture it, and send it to biopsy. It could save your life, and it’s definitely something to consider. However, be aware that about one in every 350 colonoscopies do serious harm. The death rate is about one for every 1,000 procedures.
Further, about 80 percent of endoscopes are cleaned using Cidex (glutaraldehyde), which does NOT properly sterilize these tools, potentially allowing for the transfer of material that could easily lead to infection. Asking what solution is used to clean the scope is a key question that could save your life. Make sure it’s been sterilized with peracetic acid to avoid potential transfer of infectious material from previous patients.
15 More Simple Cancer Prevention Tips
Cancer doesn’t typically develop overnight, which means you have a chance to make changes that can potentially prevent cancer from developing in the first place. Most of us actually carry around microscopic cancer cell clusters in our bodies all the time.
The reason why we all don’t develop cancer is because as long as your body has the ability to balance angiogenesis properly, it will prevent blood vessels from forming to feed these microscopic tumors. Trouble will only arise if, and when, the cancer cells manage to get their own blood supply, at which point they can transform from harmless to deadly. There are many steps you can take to lower your risk, including those that follow:
Stop drinking sugary drinks like soda and cut sugar from your diet
Sit less, move around more and try to take 10,000 steps a day
Drink green tea, an abundant source of epigallocatechin-3-gallate (EGCG), a cancer-fighting catechin polyphenol
Eat your broccoli steamed (broccoli cooked this way has more cancer-fighting glucosinolate than broccoli that’s boiled, fried or microwaved)
Eat Brazil nuts; they’re rich in selenium, a mineral that’s especially beneficial for reducing the risk of prostate, colorectal and lung cancers
Eat artichokes; they’re rich in silymarin, which is an antioxidant that may lower your risk of skin cancer
Get regular sun exposure, which will help you optimize your vitamin D levels, a key step to lowering your cancer risk
Marinate your meat with spices, beer or wine, which can lower the formation of cancer-causing substances when you cook it
Eat some “resistant starches” (such as green bananas), which act like fiber in your body.
They may help reduce the risk of colon cancer from a diet high in red meat.
Normalize your ratio of omega-3 to omega-6 fats by taking a high-quality krill oil and reducing your intake of processed vegetable oils, like corn, soy, and canola.
Sleep in complete darkness; light at night suppresses your body’s production of melatonin, which has anti-cancer effects
Eat onions, an excellent source of cancer-fighting quercetin; quercetin inhibits the growth of cancer cells from breast, colon, prostate, ovarian, endometrial and lung tumors
Avoid environmental toxins, including the cancer-causing dry cleaning chemical perc (perchloroethylene)
Avoid French fries and potato chips, which may contain high levels of cancer-causing acrylamide (a compound formed when foods are cooked at high temperatures)
Eat fermented vegetables; they’re beneficial for gut health and the fermentation process involved in creating sauerkraut produces cancer-fighting compounds such as isothiocyanates, indoles and sulforaphane

*Article originally appeared at Mercola.

Tuesday, May 30, 2017

Robert David Steele Explains We The People - Unity for Integrity

200 Evidence-Based Reasons Not to Vaccinate Free Research PDF Download

200 Evidence-Based Reasons NOT To Vaccinate - FREE Research PDF Download!

Posted on: Sunday, February 22nd 2015 at 1:45 pm
This article is copyrighted by GreenMedInfo LLC, 2017

(Please read the description for context of what you are getting, and what to do with it.)
The media, your pediatrician, politicians and health authorities like the CDC and FDA claim that vaccines are safe and effective. So why do hundreds of peer-reviewed studies indicate the opposite is true? Read, download, and share this document widely to provide the necessary evidence-based counterbalance to the pro-vaccination propaganda that has globally infected popular consciousness and discussion like an intractable disease. 
It is abundantly clear that if the present-day vaccine climate, namely, that everyone must comply with the CDC's one-size-fits-all vaccination schedule or be labeled a health risk to society at large, is to succumb to open and balanced discussion, it is the peer-reviewed biomedical evidence itself that is going to pave the way towards making rational debate on the subject happen.
With this aim in mind, has painstakingly collected over 300 pages of study abstracts culled directly from the National Library of Medicine's bibliographic database on the wide-ranging adverse health effects linked to vaccines in the today's schedule (over 200 distinct adverse effects, including death), as well as numerous studies related to vaccine contamination, and vaccine failure in highly vaccine compliant populations.
This is the literature that the media, politicians and governmental health organizations like the CDC, pretend with abject dishonesty does not exist – as if vaccine injury did not happen, despite the over 3 billion dollars our government has paid out to vaccine injured through the National Vaccine Injury Compensation Fund since it was inaugurated in 1986.

We have written extensively about this research previously, highlighting different studies, focusing on translating their implications to the lay persons (view our vaccine article section here), but we believe that collecting and condensing solely the primary literature itself makes a much more powerful statement.
This document is being made free to download to the world at large in order to encourage the lay public, health professionals, activists, and elected officials alike to read, acknowledge and share the voluminous literature with their family, friends, colleagues and related stakeholders. You will find this research undermines the national and global agenda to continue to expand the vaccine schedule (on behalf of a vaccine industry that is indemnified against lawsuit for defective or harmful products), with increasing legislative pressure to remove exemptions and mandate them against the evidence of harm and at best equivocal effectiveness as a preventive health measure.
If the vaccination arm of modern medicine today is to continue to promote itself as a science- and evidence-based practice, it must acknowledge and incorporate the implications of the research we are releasing here, or lose any pretense at credibility. Failing to do so will reveal that the widespread push to remove your choice in the matter is agenda and not evidence driven, and due to the fact that vaccines all  carry the risk of irreversible harm and even death (any vaccine insert proves this), it clearly violates the Nuremberg code of medical ethics to promote them as a priori safe and effectiveness. 

Please don't forget to share this document and/or link far and wide. Thank you! 

The GMI Research Group (GMIRG) is dedicated to investigating the most important health and environmental issues of the day.  Special emphasis will be placed on environmental health.  Our focused and deep research will explore the many ways in which the present condition of the human body directly reflects the true state of the ambient environment.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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Monday, May 29, 2017

Portland killer and fake news

SALT Dr. Joe Mercola

Surprise! Everything You've Been Told About Salt Is Wrong
  • May 29, 2017

  • Eating lots of salt will not make you thirsty or cause greater urine output. A study involving Russian cosmonauts reveal eating more salt actually lowered their thirst — yet increased hunger
  • As your salt intake increases, your glucocorticoid hormone level rises, causing greater water availability (hence lower thirst) and increased fat and muscle breakdown — an energy-intensive process resulting in increased hunger
  • A high-salt diet will not increase your risk of heart disease. Having the correct potassium to sodium balance influences your risk for high blood pressure and heart disease to a far greater extent than high sodium alone

By Dr. Mercola
Do you believe high amounts of salt provoke thirst and contribute to high blood pressure and heart disease? If so, you're likely wrong. Studies have consistently failed to support either of these notions, showing the converse is actually true. Here's a summary of findings that may surprise you:
• Eating large amounts of salt will not make you thirsty or cause greater urine output (which could lead to dehydration). A study1 involving Russian cosmonauts reveal eating more salt actually lowered their thirst — yet increased hunger.2,3 Recent animal research4 support these results, showing a high-salt diet resulted in increased metabolism, forcing the animals to eat 25 percent more calories just to maintain weight. This suggests salt may have a surprising influence on your weight
• Evidence shows having the correct potassium to sodium balance influences your risk for high blood pressure and heart disease to a far greater extent than high sodium alone, and processed foods are typically low in potassium and high in sodium
• Studies suggest a low-salt diet can actually worsen cardiovascular disease and raise rather than lower the risk for early death among patients at high risk of heart disease5
• The vast majority, approximately 71 percent, of your salt intake comes from processed food.6 Hence, if you avoid processed foods, you have virtually no risk of consuming too much salt.7 Eating a whole food diet will also ensure a more appropriate sodium-to-potassium ratio
• When lowering salt in processed foods, many manufacturers started adding monosodium glutamate (MSG) instead — a flavor enhancer associated with obesity, headaches, eye damage,8 fatigue and depression. Due to its ability to overexcite neurons, MSG may even raise your risk for neurological disorders such as Alzheimer's, Parkinson's and Lou Gehrig's disease
Counterintuitive Results Show How Poor Our Understanding of Salt Is
It's pretty bizarre that our understanding about salt is this poor, yet that's what can happen when you assume the science is settled and you've got it all figured out. As reported by The New York Times:9
"If you eat a lot of salt — sodium chloride — you will become thirsty and drink water, diluting your blood enough to maintain the proper concentration of sodium. Ultimately you will excrete much of the excess salt and water in urine. The theory is intuitive and simple. And it may be completely wrong … [Recent research] contradicts much of the conventional wisdom about how the body handles salt and suggests that high levels may play a role in weight loss."
The research is the culmination of a quest by Dr. Jens Titze, a kidney specialist at Vanderbilt University Medical Center, who in 1991 became puzzled by the discovery that astronauts' urine output followed a seven-day cycle. There seemed to be no rhyme or reason for why their urine output would increase and decrease in this cyclical manner.
Your Body Maintains a Constant Sodium Balance Regardless of Salt Intake
Then, in 1994, Titze studied the urine output patterns of a crew on the Mir station, discovering a 28-day rhythm in sodium retention — and that the amount of sodium in the astronauts' bodies was completely unrelated to their urine output. This was a truly puzzling finding. As noted in the featured article:10
"The sodium levels should have been rising and falling with the volume of urine. Although the study wasn't perfect — the crew members' sodium intake was not precisely calibrated — Dr. Titze was convinced something other than fluid intake was influencing sodium stores in the crew's bodies. The conclusion, he realized, 'was heresy' …
When the crew ate more salt, they excreted more salt; the amount of sodium in their blood remained constant, and their urine volume increased. 'But then we had a look at fluid intake, and were more than surprised,' he said.
Instead of drinking more, the crew were drinking less … when getting more salt. So where was the excreted water coming from? 'There was only one way to explain this phenomenon,' Dr. Titze said. 'The body most likely had generated or produced water when salt intake was high.'"
Salt Has Surprising Metabolic Effects
The other puzzling finding was that the astronauts complained of being constantly hungry when given higher amounts of salt. Interestingly, urine tests revealed they were producing higher amounts of glucocorticoid hormones, which affect both your metabolism and immune function.
Follow-up animal testing confirmed the results, showing the more salt the mice were given, the less water they drank and the more food they required to avoid weight loss. The reason why then became apparent. As the salt intake increased, the animals produced higher amounts of glucocorticoid hormones, causing increased fat and muscle breakdown.
These broken-down muscle proteins are then converted into urea, which is known to help your body excrete waste via urine. Through some still-unknown mechanism, this urea also helps your body retain water. In other words, a side effect of higher salt consumption is that it frees up water for your body to use.
However, this process is energy-intensive, which is why the animals required more food when on a high-salt diet and why the astronauts complained of hunger. Titze believes the increase in glucocorticoid hormones are also somehow responsible for the bizarre cyclical fluctuations in urine output.
"Scientists knew that a starving body will burn its own fat and muscle for sustenance. But the realization that something similar happens on a salty diet has come as a revelation," The New York Times reports.11
"People do what camels do, noted Dr. Mark Zeidel, a nephrologist at Harvard Medical School who wrote an editorial accompanying Dr. Titze's studies. A camel traveling through the desert that has no water to drink gets water instead by breaking down the fat in its hump.
One of the many implications of this finding is that salt may be involved in weight loss. Generally, scientists have assumed that a high-salt diet encourages a greater intake of fluids, which increases weight. But if balancing a higher salt intake requires the body to break down tissue, it may also increase energy expenditure."
As noted by Dr. Melanie Hoenig, nephrologist and assistant professor of medicine at Harvard Medical School, "The work suggests that we really do not understand the effect of sodium chloride on the body."12
Sodium/Potassium Ratio Is Key to Normalize Your Blood Pressure
While salt has gotten a bad rap, suspected of increasing your risk for high blood pressure and heart disease, research shows the real key to relaxing your arteries and reducing your blood pressure is actually the ratio of sodium to potassium you have — not your sodium intake alone.13
Potassium is a naturally occurring mineral your body uses as an electrolyte (substance in solution that conducts electricity), and it is vital for optimal health and normal functioning. Most of your potassium resides inside your cells, unlike sodium, which resides outside your cells.
Potassium works in your body to relax the walls of your arteries, keep your muscles from cramping and lower your blood pressure.14 The reduction in blood pressure with added potassium has also been associated in studies with a reduced risk of stroke.15
Recent research16 found that women without high blood pressure who consumed the most potassium (nearly 3,200 milligrams per day) had a 21 percent reduced risk of stroke. Women who consumed the most potassium were also 12 percent less likely to die during the study period than those who consumed the least.
A meta-analysis published in 1997, which analyzed 29 trials, also found that low levels of potassium resulted in higher systolic blood pressure readings.17 Subsequent studies have found similar results.18,19
How's Your Sodium/Potassium Balance?
It's generally recommended that you consume five times more potassium than sodium, but most Americans eat twice as much sodium as potassium. If you're eating mostly processed foods and few fresh vegetables, your sodium-to-potassium balance is virtually guaranteed to be inversed. Imbalance in this ratio not only can lead to high blood pressure but also contribute to a number of other health problems, including:
Kidney stones
Memory decline
Erectile dysfunction
Stomach ulcers
Stomach cancer

One simple way to check your ratio is to use my customized version of the free nutrient tracker,, which will calculate your sodium-to-potassium ratio automatically based on the foods you enter.
A great deal of good could come from revising public health recommendations to focus on a high-quality diet rich in potassium rather than sodium reduction, as potassium helps offset the hypertensive effects of sodium. Potassium also has other important health benefits.
Other Health Benefits of Potassium
Adequate amounts of potassium are associated with quicker recovery from exercise and improved muscle strength.20,21 As an electrolyte, potassium helps to regulate the fluid balance in your cells and throughout your body.22 This fluid balance is essential to maintaining life, preventing dehydration at the cellular level and maintaining brain function.23
For example, potassium is important in the transmission of nerve impulses in your brain, spinal cord and peripheral nervous system.24 Nerve impulses transmitting information from one nerve to the next happens as the result of electrical activity. This activity is what an electrocardiogram measures as it tracks heart activity.
Low levels of potassium have also been linked with high levels of insulin and glucose, which are aassociated with metabolic syndrome and type 2 diabetes.25 These results have been found in several studies,26 leading researchers to recommend dietary choices that boost potassium levels.
Your KEY Strategy — Eat Real Food
Getting nutrients from your food instead of supplements is preferable as your food contains more than a single nutrient and in different forms. For instance, potassium found in fruits and vegetables is potassium citrate or potassium malate, while supplements are often potassium chloride.
Green vegetable juicing is an excellent way to ensure you're getting enough nutrients for optimal health, including potassium. Particularly potassium-rich foods include:
Swiss chard, 1 cup = 1 gram potassium
Lima beans, 1 cup = 1 gram 
Avocado, 1/2 Florida variety = 0.8 gram
Dried apricots, 1/2 cup = 0.9 gram
Baked potato, 1 large = 0.9 gram
Winter squash, 1 cup = 0.9 gram
Cooked spinach, 1 cup = 0.8 gram
Beets, 1 cup = 0.4 gram
The citrate and malate forms help produce alkali, which may promote bone health27 and preserve lean muscle mass as you age.28 Bone loss may lead to brittle bones or even osteoporosis. While potassium in fruits and vegetables may help build bone health, potassium chloride may not. As researcher Dr. Bess Dawson-Hughes from Tufts University explains:29
"If you don't have adequate alkali to balance the acid load from the grains and protein in a typical American diet, you lose calcium in the urine and you have bone loss … When the body has more acid than it is easily able to excrete, bone cells get a signal that the body needs to neutralize the acid with alkali … And bone is a big alkali reservoir, so the body breaks down some bone to add alkali to the system."
Research by Dawson-Hughes found that people who were in the neutral range for net acid excretion, meaning they had a fairly healthy balance for bone and muscle health, were eating just over eight servings of fruits and vegetables per day along with 5.5 servings of grains. When they rounded this out, it came to about half as many grains as fruits and vegetables.
For many Americans, a simple recommendation to increase your alkali (and potassium) while reducing acid is to eat more vegetables and fewer grains and processed foods in general.30 When cooking from scratch, you have complete control over how much salt you add.
Healthy Versus Unhealthy Salt
When you do use salt, make sure its unrefined and minimally processed. My personal favorite is Himalayan pink salt, rich in naturally-occurring trace minerals needed for healthy bones, fluid balance and overall health. The same cannot be said for modern table salt.
Salt is a nutritional goldmine provided you consume the right kind. Salt provides two elements — sodium and chloride — that are essential for life. Your body cannot make these elements on its own, so you must get them from your diet. Some of the many biological processes for which natural salt is crucial include:
Being a major component of your blood plasma, lymphatic fluid, extracellular fluid and even amniotic fluid
Carrying nutrients into and out of your cells and helping maintain your acid-base balance
Increasing the glial cells in your brain, responsible for creative thinking and long-term planning.
Both sodium and chloride are also necessary for the firing of neurons
Maintaining and regulating blood pressure
Helping your brain communicate with your muscles so that you can move on demand via sodium-potassium ion exchange
Supporting the function of your adrenal glands, which produce dozens of vital hormones
Natural salt typically contains 84 percent sodium chloride and 16 percent naturally-occurring trace minerals, including silicon, phosphorous and vanadium. Processed (table) salt, on the other hand, contains over 97 percent sodium chloride; the rest is man-made chemicals such as moisture absorbents and flow agents. A small amount of iodine may also be added.
Some European countries, where water fluoridation is not practiced, also add fluoride to their salt.31 In France for example, 35 percent of table salt sold contains either sodium fluoride or potassium fluoride, and use of fluoridated salt is widespread in South America.

Besides these basic differences in nutritional content, the processing also radically alters the chemical structure of the salt. So, while you definitely need salt for optimal health, not just any salt will do. What your body needs is natural, unprocessed salt, without added chemicals.

The Most Deadly Water Purification Mistakes

The Most Deadly Water Purification Mistakes

Water. Water is the key to survival. If the grid goes down or the dollar crashes or, well, you just get hung out in a bad hiking situation, you might need to figure out your water situation in fast order. And for many folks, that’s a complicated matter. Many people think they are filtering when in fact, they are leaving themselves open to getting themselves and their families sick.

Often times, water appears to be a clear source for drinking; but looks can most certainly be deceiving. Water can be deadly even when it looks quenching and blissful. Filtration is a huge necessity to water purification.
The issue with skipping the filtration process in a survival scenario is that your water is often left with what is known as, micro waterborne cysts. While that name alone should terrify you, I will extend upon my point here for those who still aren’t freaked out. These cysts really are not visible in water. It isn’t as if we see them floating about and can allow ourselves a common sense warning system. Instead, they are too small to be visible. They also reside in a tough shell casing that allows them to avoid the destruction of boiling water (purification processes). You know where that shell breaks down? In your digestive system. And then the cysts are able to do their damage.
You never saw them. You never FILTERED them.

So, my fellow survivalists, let’s get practical here. Filtration doesn’t have to be super complicated, but it does need to be accomplished if you want to keep you and your family as safe as possible. You can filter using charcoal or coffee filters. You could use cotton balls plugging the top of a bottle. There is a grip of ways, the idea is that you need to filter out particles like the evil cysts we just discussed.
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If you are in a dire situation with no practical filtering applications (as mentioned above), you could just pour the water in a glass and allow it to sit and then scoop the water off the top. In this case, you are hoping that bacteria have settled at the bottom. Following this, you purify the water via chemical or boil. Certainly, this isn’t the safest way, but if your option is this or severe dehydration, then I suppose you have your answer.
The concept is that you want to filter the water down into a container whereas you can then treat the water. You could use some purification tablets. I recommend that everyone have purification tablets on hand, these are essential survivalist product.
Now, sans the tablets, you could use bleach. Here’s a chart. Graph via Clorox Company.

Prep For That TIP: You can destroy bacteria if you boil water for one minute at 212 degrees Fahrenheit. The same is true for 145 degrees Fahrenheit for one hour. Higher elevations can and do effect this chemistry.
Here’s a cool way with a survival water bottle that can go inside of your bug out bag. This is called a Berkey Sport Bottle for Purification.

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Here’s a cheap DIY filter bottle.

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Keep surviving my friends.

Sunday, May 28, 2017

The Risks and Benefits of Sun Exposure 2016

Dermatoendocrinol. 2016 Jan-Dec; 8(1): e1248325.
Published online 2016 Oct 19. doi:  10.1080/19381980.2016.1248325
PMCID: PMC5129901
The risks and benefits of sun exposure 2016
Author information ► Article notes ► Copyright and License information ►

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Public health authorities in the United States are recommending that men, women and children reduce their exposure to sunlight, based on concerns that this exposure will promote skin cancer. On the other hand, data show that increasing numbers of Americans suffer from vitamin D deficiencies and serious health problems caused by insufficient sun exposure. The body of science concerning the benefits of moderate sun exposure is growing rapidly, and is causing a different perception of sun/UV as it relates to human health. Melanoma and its relationship to sun exposure and sunburn is not adequately addressed in most of the scientific literature. Reports of favorable health outcomes related to adequate serum 25(OH)D concentration or vitamin D supplementation have been inappropriately merged, so that benefits of sun exposure other than production of vitamin D are not adequately described. This review of recent studies and their analyses consider the risks and benefits of sun exposure which indicate that insufficient sun exposure is an emerging public health problem. This review considers the studies that have shown a wide range health benefits from sun/UV exposure. These benefits include among others various types of cancer, cardiovascular disease, Alzheimer disease/dementia, myopia and macular degeneration, diabetes and multiple sclerosis. The message of sun avoidance must be changed to acceptance of non-burning sun exposure sufficient to achieve serum 25(OH)D concentration of 30 ng/mL or higher in the sunny season and the general benefits of UV exposure beyond those of vitamin D.
KEYWORDS: cancer, cardiovascular disease, melanoma, ultraviolet radiation, vitamin D, 25-hydroxyvitamin D
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Public health authorities in the United States are currently advising that human sun exposure be reduced.1 At the same time, NHANES data show that 32% of Americans suffer from vitamin D insufficiency.a
In this paper we review the current state of the science of the risks and benefits of sun exposure and suggest that public health advice be changed to recommend that all men, women and children accumulate sufficient non-burning sun exposure to maintain their serum 25hydroxyvitaminD [25(OH)D] levels at 30 ng/mL or more year-round.
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The first scientifically-established health benefit of sun exposure was the discovery in 1919 that sunlight cured rickets.4-5 This was followed in 1924 up by the discovery that an inactive lipid in the diet and skin could be converted by UV light into an antirachitic substance.6 The identification of vitamin D occurred in 1931.7 The association between sun exposure and reduced cancer mortality in North America was identified in the 1960s. In the 1980s, it was hypothesized that vitamin D was the protective factor. For most of the intervening years, instead of pursuing further benefits of sun exposure, scientific inquiry focused on the health risks of sun exposure, especially melanoma and other types of skin cancer.8 Chemical sunscreens were developed in 1928.9 Avoidance of intentional sun exposure and use of chemical sunscreens persisted as the standard advice of physicians and public health authorities for reducing the risk of melanoma and other forms of skin cancer.1,8 The risks of inadequate sun exposure have been largely ignored. Recently, however, scientific inquiry has increasingly turned to the benefits of moderate sun exposure and the public health risks of inadequate sun exposure.10
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Risks of sun exposure
The mechanism of melanoma is unknown, but is believed to be linked to genetic factors.11 The principal identified non-genetic risk factor is ultraviolet radiation (UVR) exposure, and the relationship between melanoma and UVR is 2-sided: non-burning sun exposure is associated with a reduced risk of melanoma, while sunburns are associated with a doubling of the risk of melanoma.12 It has long been observed that outdoor workers have a lower incidence of melanoma than indoor workers.13-19 A 1997 meta-analysis found an OR of 0.86 (95% CI: 0.77–0.96) for occupational sun exposure.18
Biologically, UVB is known to induce DNA damage through the creation of pyrimidine dimers while UVA does so at orders of magnitude less efficiently.20 Oxidative damage through the creation of free radicals (singlet oxygen and hydrogen peroxide) occurs at all UVR frequencies.20 However, the human body has many defenses against such damage including DNA repair mechanisms, cell cycle and growth inhibitions, reduced proliferation, enhanced sensitivity to apoptosis, enhancement of cellular differentiation and anti-inflammatory effects; many of which are related to vitamin D produced by exposure to UVB.21-25
With respect to sunburns, melanocytes are not replicating cells, so once DNA damage has occurred, it is necessary for cellular replication to take place for the possibility of unrepaired or mis-repaired melanocytes to develop into malignant melanoma.20 Sunburns correspond with rare occasions of cell divisions and ensuing vulnerability to mutations in otherwise indolent melanocytes.20 With respect to chronic non-burning sun exposure, it is thought that protection against sunburn and development of melanoma derives from photo-adaptation (increased melanisation and epidermal thickening) or from the induction of higher levels of vitamin D, or possibly both.12,25-28 Vitamin D produced by UVB exposure is converted to the active form of vitamin D by its sequential metabolism in the liver to form the major circulating form of vitamin D, 25-hydroxyvitamin D [25(OH)D] which is then converted in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D]. Evidence suggests that vitamin D that is produced in the skin can also be converted in the skin to its active form 1,25(OH)2D25, thereby enhancing DNA repair29 and lowering cancer risk.
The incidence of melanoma in the United States has increased dramatically from 1 per 100,000 people per year in 1935 to 23 per 100,000 per year in 2012. Various explanations for this phenomenon have been suggested, including diagnostic drift,30 depletion of the ozone layer,31 the widespread use of artificial UVR devices,32 and the proliferation of large windows in office buildings.15 None of these explanations is particularly satisfactory for the reason that none explains the steady increase in melanoma incidence since 1935. While sunburns have been associated with a doubling of melanoma risk,12 chronic non-burning sun exposure and outdoor occupations have been associated with reduced risk of melanoma.12-19 Indoor occupations such as professional, managerial, clerical, sales and service workers grew from 25% to 75% of total employment between 1910 and 2000.33 25% of Americans lived on farms in 1930 whereas only 2% do so today.34 Indoor attractions such as air conditioning, television, computers and the internet probably have led to Americans spending more of their leisure time indoors, the prevalence of sunburns is high and has been increasingb , and serum 25(OH)D levels of the American public, a likely marker for sun exposure, are low and have been declining.c A more plausible explanation for the rise in melanoma incidence since 1935 may be the continually-increasing insufficient non-burning sun exposure and related increasing vitamin D deficiency/insufficiency, and the increasing sunburn prevalence experienced by the American public over the same time periodd . Furthermore, epidemiological studies do not indicate any difference in melanoma risk based on the age at which UVR exposure occurs.12,17,18 Sunburns appear to be equally risky at any age.17 The public health messages of the past 50 y to avoid sun exposure and to use chemical sunscreens may have contributed to the rise in melanoma incidence.
We can find no consistent evidence that use of chemical sunscreens reduces the risk of melanoma. Green et al. 2011,42 found in a prospective study that there may be an association between sunscreen use and reduced risk of melanoma. However, since the participants were told they were participants in a skin cancer prevention trial and were questioned periodically during the trial on their use of sunscreen, the likelihood that they were significantly more diligent in applying sunscreen in accordance with manufacturers' instructions than ordinary users of sunscreen cannot be discounted.e In addition, this study took place in a tropical environment, differing significantly from the environments of North America and Europe. Use of a placebo sunscreen was barred by ethical concerns.
Sunscreens do, however, reduce acclimatization to UVR and vitamin D production in the skin.46 Since public health authorities recommend liberal use of sunscreens for good health, the labeling of sunscreens should contain a statement about the possibility of vitamin D deficiency that may result from excessive use of sunscreens. Labeling should also state that sunscreens have not been shown to be effective in reducing the risk of melanoma. Sunscreens have been shown in one study to be effective in reducing the risk of squamous cell, but not basal cell, skin cancer.47
Nonmelanoma skin cancer (NMSC)
There are no official registries for basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), and estimates of the prevalence of these carcinomas vary widely. One group of investigators examined Medicare fee-for-service data, extrapolated to the entire United States population, and estimated that 2,152,500 persons were treated for 3,507,693 NMSCs in 2006.48 Several of the same investigators estimated that 3,315,554 persons were treated for 5,434,193 NMSCs in 2012 and revised the 2006 estimates to 2,463,567 persons and 4,013,890 NMSCs.49 These latter estimates indicated a 14% increase in Medicare NMSCs over the 6-year period 2006–2012 and a 54% increase in non-Medicare NMSCs over the 6-year period. It is not clear in this analysis that all treatments for NMSCs were in fact treatments for malignancies rather than for non-cancerous lesions, and these investigators found the ratio of BCC to SCC to be 1 to 1 instead of the expected 4 to 1. Another recent study50 which histologically confirmed all cases but studied only BCCs, calculated based on an analysis of a Kaiser Permanente BCC registry that approximately 2 million BCCs are treated annually in the United States in an undisclosed number of persons. Assuming a 4 to 1 ratio of BCC to SCC, this would indicate that 2.5 million NMSCs are treated annually. This study found that the incidence of BCC increased 17% during the 15-year period from 1998 to 2012.
As with melanoma, sunburns are associated with increased risk of SCC and BCC.16,17,51 Cumulative sun exposure, which is associated with decreased risk of melanoma, is apparently associated with increased risk of SCC and BCC, although the relationship between cumulative sun exposure and NMSC is not entirely clear. Armstrong and Kricker 200117 found that only SCC, not BCC, is related to total sun exposure, and Rosso et al. 199852 found no association between cumulative lifetime sun exposure and BCC. Kennedy et al. 200316 found a positive association between increasing lifetime sun exposure and the development of SCC and BCC but statistical significance was not always reached after age adjustment. English et al. 199853 found that total time spent outdoors was only weakly associated with SCC. Gallagher et al. 1995a,b54,55 found no association between cumulative lifetime sun exposure and risk of SCC or BCC, but Gallagher et al. 1995b55 found that occupational sun exposure in the 10 y prior to diagnosis was associated with increased risk of SCC. Many studies have found increased risk of SCC and to a lesser extent BCC from occupational sun exposure.17,51,56,57 Alam et al. 200158 found that the risk of SCC, but not BCC, is directly related to cumulative total dose of ionizing radiation from x-rays, that SCC may develop on sun-exposed areas in people with certain genodermatoses, such as oculocutaneous albinism, that chemical agents such as soot, arsenic and polycyclic hydrocarbons have historically been a major cause of SCC, and that human papillomavirus infection has been associated with SCC. The US. Preventive Services Task Force, in its May 2012 Final Recommendation Statement on skin cancer counseling,59,60 stated that studies that measured long-term or total sun exposure had found no association between cumulative sun exposure and either SCC or BCC.
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Benefits of sun exposure; Risks of inadequate sun exposure
Scientific inquiry into the benefits of sun exposure languished for many decades following the observation in the 1920s that farmers in Europe developed non-melanoma skin cancer on their most sun-exposed areas - their ears, face, nose and backs of their hands.61 Research on the benefits of sun exposure has accelerated in the past 15 y and particularly in the past 5 y.62
Vitamin D

Biological plausibility
Vitamin D is a hormone and most cells and organs in the human body have a vitamin D receptor, which explains the wide variety of diseases and disorders that have been linked to vitamin D insufficiency in epidemiological studies.63 The production of vitamin D by UV B radiation, the availability of vitamin D in food and supplements, and the biological plausibility of vitamin D as a mediator for a large variety of favorable health outcomes are well described in the literature.22-25,63-65

Recommended vitamin D status
There is considerable controversy within the scientific community regarding optimum 25(OH)D levels for human health. In 2010, the Institute of Medicine defined vitamin D deficiency as 25(OH)D of less than 12 ng/mL and vitamin D insufficiency as 25(OH)D of less than 20 ng/mL.2 In 2011, The Endocrine Society defined vitamin D deficiency as 25(OH)D below 20 ng/mL and vitamin D insufficiency as 25(OH)D of 21–29 ng/mL.66 Others have suggested even higher levels.22,67-69 A letter signed by many respected vitamin D scientists and physicians recommends 40–60 ng/mL70 which is in line with what the Endocrine Society recommended as the preferred range for health – i.e, a 25(OH)D of 40–60 ng/mL.66 Most reference laboratories have raised the lower boundary of the normal range to 30 ng/mL.68

Prevalence of vitamin D deficiency/insufficiency
Ginde et al. 200938 reported that NHANES data on serum 25(OH)D levels show that the prevalence of 25(OH)D of less than 10 ng/mL increased from 2% of the US population in NHANES III (1988–1994) to 6% in NHANES 2001–2004, and that over the same period the prevalence of 25(OH)D of less than 20 ng/mL increased from 22% of the US population to 36%.f The IOM report did not offer a solution to this problem since that was not its purpose; the IOM was charged with determining the DRI of vitamin D supplements and found that there was insufficient scientific evidence on the benefits of vitamin D supplementation to support raising the DRI of vitamin D supplements to more than 600 International Units (IUs) per day.g Using the Endocrine Society's definition of vitamin D sufficiency of 30 ng/mL, the level of vitamin D insufficiency increased from 55% of the US population in NHANES III to 77% in NHANES 2001–2004,38 which indicates that the vast majority of Americans have an insufficient vitamin D status.
Mediators other than vitamin D
Several studies, discussed below, have found that mediators other than vitamin D are or may be involved in the beneficial effects of adequate sun exposure.
Benefits of vitamin D/sun exposure; Risks of vitamin D insufficiency/inadequate sun exposure
We next examined the health benefits associated with increasing levels of sun exposure and/or circulating serum 25(OH)D and the health risks associated with inadequate sun exposure and/or inadequate serum 25(OH)D, with particular emphasis on studies published since the 2010 IOM report.
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All-cause mortality
Chowdhury et al. 201472 performed a meta-analysis of data from 73 cohort studies with 849,000 participants and 22 randomized controlled trials with 31,000 participants. This study found an inverse association of circulating 25(OH)D with risks of death due to cardiovascular diseases, cancer and other causes (RR 1.35, 95% CI 1.22–1.49 for all cause mortality, comparing the bottom third versus top 2-thirds of baseline circulating 25(OH)D distribution), but found that, with respect to possible benefits of vitamin D supplementation, further investigation is required before any widespread supplementation occurs. The prevalence of vitamin D insufficiency (defined as 25(OH)D less than 30 ng/mL) was found to be 69.5% for the United States and 86.4% for Europe. The authors further estimate that 9.4% of all deaths in Europe and 12.8% in the United States could be attributable to vitamin D insufficiency. Other meta analyses include Garland et al. 201473 who pooled the data from 32 studies (30 cohort studies and 2 nested case-control studies) that examined age-adjusted all-cause mortality and serum 25(OH)D levels and found that the overall age-adjusted hazard ratio for all-cause mortality comparing the lowest (0–9 ng/mL) group to the highest (greater than 50 ng/mL) was 1.9 (95% CI 1.6–2.2), indicating that individuals in the lowest group had nearly twice the age-adjusted death rate as those in the highest quantile. Schottker et al. 201474 conducted a meta-analysis of 8 cohort studies with 26,000 participants and found a 1.6-fold higher all-cause mortality in the bottom quintile (25(OH )D approximately <12 approximately="" compared="" ml="" nbsp="" ng="" quintile="" the="" top="" with=""> 24 ng/mL) (RR 1.57, 95% CI 1.36–1.81).
Lindqvist et al. 201475 assessed the avoidance of sun exposure as a risk factor for all-cause mortality for 29,518 Swedish women in a prospective 20-year follow-up of the Melanoma In Southern Sweden cohort and found that the population attributable risk for all-cause mortality for those habitually avoiding sun exposure was 3%. As compared to the highest sun exposure group, the all-cause mortality rate was doubled (RR 2.0, 95% CI 1.6–2.5) among avoiders of sun exposure and increased by 40% (RR 1.4, 95% CI 1.1–1.7) in those with moderate exposure. The authors noted that Sweden has national guidelines providing restrictive advice on sun exposure habits in order to lower the risk of skin cancer, and stated that these guidelines may be harmful in terms of overall health of the population. Lindqvist et al. 201676 found that women with active sun exposure habits were mainly at lower risk of cardiovascular disease mortality and other non-cancer mortality, and noted that avoidance of sun exposure is a risk factor for death of a similar magnitude as smoking. “Our finding that avoidance of sun exposure was a risk factor for all-cause death of the same magnitude as smoking is novel.”
Afzal et al. 201477 conducted a Mendelian randomization analysis showing that genetically low 25(OH)D levels were associated with increased all-cause mortality, but not with cardiovascular mortality. These results confirm that the measured low 25(OH)D levels in the general population associated with increased mortality as indicated in the above meta-analyses are related to vitamin D rather than simply a consequence of poor health or sequestration of vitamin D in adipose tissue, but indicate that some mediator other than vitamin D may be involved in cardiovascular mortality. Afzal et al. 201477 was the first study with sufficient sample size to investigate the association of genetically low 25(OH)D levels with increased mortality.
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Colorectal cancer
Rebel et al. 201478 showed for the first time the causality of the relationship between moderate UVR exposure and primary intestinal tumors in mice. The UVR-induced reduction in intestinal cancer in mice could at least in part be attributed to vitamin D. However, the investigators also found a reduced progression to malignancy as a result of UVR exposure which appeared not to be attributable to vitamin D. Three groups of hairless mice were compared: one on a low-vitamin D diet without vitamin D supplementation or UVR exposure, one on a low-vitamin D diet with vitamin D supplementation but without UVR exposure, and one on a low-vitamin D diet without vitamin D supplementation but with moderate UVR exposure. This permitted the comparison of effects of dietary vitamin D supplementation and UVR exposure. The tumor load (area) was similarly and significantly reduced in both the vitamin D supplementation group and the UVR exposure group, but only the UVR exposure group had a lower percentage of malignant adenocarcinomas. Thus the study provided the first experimental evidence that physiologically relevant, moderate UVR exposure can reduce the load of primary intestinal tumors, which reduction can at least in part be explained by an increase in vitamin D status as a comparable reduction in tumor load was observed in the vitamin D supplementation group that had a similar increase in vitamin D status. However, a reduction in malignant progression and growth of adenocarcinomas could not be attributed to vitamin D as these effects were only observed with moderate UVR exposure and not with dietary vitamin D supplementation. Rebel et al. 201478 noted that prior studies had long shown that low exposure to solar UVR is significantly associated with increased risk of colon cancer, and that several recent studies showed that increased risk of colon cancer was significantly associated with prediagnostic low vitamin D status. The 2010 IOM report64 acknowledged that epidemiological studies examining associations between vitamin D status and colorectal cancer incidence generally supported an inverse association, but declined to base vitamin D DRI's on colon cancer outcomes because of the paucity and conflicting findings of prospective randomized controlled trials involving vitamin D supplementation. Notably, the most recent, and only observational, study reviewed in the IOM report found no association of vitamin D supplementation with colon cancer risk, but found that patients in the highest quintile of prediagnostic circulating 25(OH)D concentration (more than 40 ng/mL) had a 42% reduced risk of colon cancer as compared to patients with the lowest quintile (less than 10 ng/mL).79
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Breast cancer incidence and mortality
Mohr et al. 201480 conducted a meta-analysis of data from 5 studies on the relationship between serum 25(OH)D levels at time of breast cancer diagnosis and breast cancer mortality which found that patients in the highest quintile of 25(OH)D (more than 32 ng/mL) had approximately half the death rate from breast cancer as those in the lowest quintile (less than 14 ng/mL) (HR 0.56; 95% CI: 0.4–0.7). The authors recommended that serum 25(OH)D levels in all breast cancer patients should be restored to the normal range, which the authors defined as 30–80 ng/mL.
Engel et al. 201081 found a 27% reduced risk of breast cancer incidence in women in the highest tertile of 25(OH)D (greater than 27ng/mL) as compared to the lowest tertile (less than 19.8 ng/mL) in a nested case-control study (OR 0.73; 95% CI: 0.55–0.96). The authors noted that all 6 previous case-control studies on the subject have reported a significant inverse association between serum 25(OH)D levels and breast cancer and that an inverse effect between sun exposure and breast cancer has previously been observed. John et al. 199982 found that women with higher solar UVB exposure in NHANES III had only about half the incidence of breast cancer as those with lower solar exposure (RR 0.50; 95% CI: 0.33–0.80) and Knight et al 200783 found that increasing sun exposure from ages 10 to 19 reduced breast cancer risk by 35% (OR 0.65, 95% CI 0.50–0.85 for the highest quartile of outdoor activities vs. the lowest).
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Non-hodgkins lymphoma, colorectal, prostate and breast cancer, and multiple sclerosis
Van der Rhee et al. 201384 noted that the association between solar radiation and reduced cancer mortality in North America was identified more than 60 y ago85 and that in 1980 it was hypothesized that vitamin D was the protective factor.40 The authors conducted a systematic review to verify if epidemiological evidence is in line with the hypothesis that the possible preventive effect of sunlight on cancer is more than just the effect of vitamin D. Vitamin D intake studies were excluded from the review and the authors stated that their review presented the sum of epidemiological knowledge on the influence of sun exposure and circulating 25(OH)D levels on the risk of colorectal cancer, prostate cancer, breast cancer and non-Hodgkin's lymphoma (NHL). They concluded that: 1) there is an inverse association between sun exposure and both colorectal cancer risk and colorectal cancer mortality; 2) there is an inverse association between vitamin D status and both colorectal cancer risk and colorectal cancer mortality; 3) there is a negative association between sun exposure and prostate cancer risk and prostate cancer mortality but not between vitamin D status and prostate cancer risk or mortality; 4) there is an inverse correlation between sun exposure and breast cancer risk and breast cancer mortality, and possibly between 25(OH)D and breast cancer mortality, but studies on the association between 25(OH)D and breast cancer risk are inconclusive; 5) there is a negative association between sun exposure and NHL risk and NHL mortality but not between vitamin D status and NHL risk or mortality; 6) there is a negative association between sun exposure and lymphoma risk, but no association between lymphoma risk and vitamin D intake or 25(OH)D levels; and, 7) for multiple sclerosis, both experimental and epidemiological studies show that the preventative role of sun exposure is independent of vitamin D production. The authors concluded that for colorectal cancer and breast cancer the benefit of sun exposure is mediated by high vitamin D levels produced by sun exposure, whereas for prostate cancer, NHL and multiple sclerosis the benefit of sun exposure is independent of vitamin D.84
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Bladder cancer
Zhao et al. 201686 found a 30% reduced risk of bladder cancer associated with 25(OH)D concentrations above 30 ng/mL compared to less than 15 ng/mL.
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Cardiovascular disease (CVD)
Liu et al. 201487 found that hypertension is reduced by UVR-induced nitric oxide independent of vitamin D. They showed that stores of nitrogen oxides in the human skin are mobilized to the systemic circulation by exposure of the body to UVA radiation, causing arterial vasodilation and a resultant decrease in blood pressure independent of vitamin D, confirming the hypothesis of Feelisch et al. 2010.88 These results correlate with the findings of Afzal et al. 201477 that genetically low 25(OH)D levels were associated with increased all-cause mortality but not with cardiovascular mortality, indicating that a mediator other than vitamin D may be involved in cardiovascular mortality, and with the results of Tunstall-Pedoe et al. 201589 challenging vitamin D's alleged role in cardiovascular disease.
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Metabolic syndrome (MetS) and type 2 diabetes
Vitezova et al. 201590 found that higher 25(OH)D levels were associated with lower prevalence of metabolic syndrome (OR 0.61, 95% CI 0.49–0.77 for more than 30 ng/mL versus less than 20 ng/mL) in the elderly in an analysis of data from 3240 people (median age 71.2 years) imbedded in the Rotterdam Study, a prospective population-based cohort study of middle-aged and elderly adults. Importantly, after adjustment for body mass index (BMI), higher 25(OH)D levels were still significantly associated with lower odds of MetS. Almost concurrent with Vitezova et al. 2015, Clemente-Postigo et al. 201591 showed that low 25(OH)D levels are associated with type 2 diabetes independently of BMI. These findings are important in light of the 2010 IOM report's discounting of the association studies linking low 25(OH)D levels to increased risk of type 2 diabetes on the ground that they may be confounded by obesity, which not only predispose individuals to type 2 diabetes but may also cause lower 25(OH)D levels as a result of sequestration of vitamin D in adipose tissue and possibly other mechanisms. Vitezova et al. 2015 noted that other recent studies had found an inverse association between vitamin D status and MetS in younger populations, but only one other study of older persons had found the association while another study of older persons had not. Neither Vitezova et al. 2015,125 nor Clemente-Postigo et al. 201591 cited Geldenhuys et al. 2014,92 which found that UVR exposure levels, not vitamin D supplements or 25(OH)D levels, reduced the risk of obesity and type 2 diabetes, indicating that 25(OH) levels may be to some extent a marker for UVR exposure in this regard.
Afzal et al. 201393 measured 25(OH)D levels in 9841 persons of whom 810 developed type 2 diabetes during 29 y of follow-up. The investigators observed an association of low 25(OH)D with increased risk of type 2 diabetes (HR 1.35, 95% CI 1.09–1.66 for lowest (less than 5 ng.mL) vs. highest (more than 20 ng/mL) quartile of 25(OH)D. This finding was substantiated by the authors' meta-analysis of 14 studies representing 16 cohorts with a total of 72,204 participants and 4,877 type 2 diabetes events (HR 1.50, 95% CI 1.33–1.70 for the bottom vs. top quartile of 25(OH)D). A prior 2011 meta-analysis [134 Mitri 201194] had shown that individuals with 25(OH)D levels above 25 ng/mL had a 43% lower risk of developing type 2 diabetes (95% CI, 2457%–) compared with individuals with 25(OH)D levels below 14 ng/mL, and that vitamin D supplementation had no effect.
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Alzheimer disease and cognitive decline
Littlejohns et al. 201495 [135] studied a group of 1,658 Americans age 65 and older who were able to walk unaided and who were free of dementia. The participants were followed for 6 y to investigate who went on to develop Alzheimer disease and other forms of dementia. The investigators found that participants with serum 25(OH)D levels below 10 ng/mL were more than twice as likely to develop Alzheimer disease than participants with serum 25(OH)D levels greater than 20 ng/mL (HR 2.22, 95% CI 1.02–4.83) and participants with serum 25(OH)D levels of 10 ng/mL to 20 ng/mL were 69% more likely to develop Alzheimer disease than participants with serum 25(OH)D levels greater than 20 ng/mL (HR 1.69, 95% CI 1.06–2.69). Similar results were obtained for all-cause dementia. According to the authors, this was the first large, prospective, population-based study incorporating a comprehensive adjudicated assessment of dementia and Alzheimer to examine their relationship with vitamin D concentrations. This study confirms other recent studies linking low vitamin D levels with cognitive decline.96-102
Keeney et al. 201396 manipulated vitamin D status in middle-age to old-age rats by dietary supplementation with low, moderate and high levels of vitamin D. The results suggested that dietary vitamin D deficiency contributes to significant nitrosative stress in the brain and may promote cognitive decline in middle-age and elderly humans.
Annweiler et al. 201397 was a systematic review and meta-analysis finding that 25(OH)D levels were lower in Alzheimer cases than in controls (summary random effect size 1.40, 95% CI 0.26–2.54), which means that the probability is about 140% that an individual without Alzheimer would have a higher 25(OH)D level than an individual with Alzheimer if both individuals were chosen at random from a population.
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Multiple sclerosis (MS), type 1 diabetes, rheumatoid arthritis
Wang et al. 2014103 found that UVR suppressed experimental autoimmune encephalomyelitis (EAE - an animal model of MS), independent of vitamin D production, confirming the conclusions of van der Rhee et al. 201384 and the findings of Becklund et al. 2010.104 The investigators showed that UVB irradiation did not suppress immune response in the periphery, but suppressed EAE by blocking selectively the infiltration and binding of inflammatory cells into the central nervous system. These findings support the long-held view that the incidence of MS is inversely related to UVR exposure.105-109
Baarnhielm et al. 2012110 was an association study finding that persons with low UVR exposure had a significantly increased risk of MS compared with those who reported the highest exposure (OR 2.2, 95% CI 1.5–3.3), and that this association persisted after adjustment for vitamin D status. Wang et al. 2014103 and Baarnhielm et al. 2012110 confirmed the conclusions of van der Rhee et al. 201383 that sun exposure reduces the risk of MS through pathways independent of vitamin D.
Ponsonby et al. 2005108 stated that genetic factors appear to be involved in MS, but the low concordance among identical twins for MS111 and trends of increasing incidence of MS over time112 suggest environmental factors are also important determinants, and that UVR exposure may be one factor that can attenuate MS through several mechanisms and that some the pathways are independent of vitamin D. Similar conclusions were made about 2 other autoimmune diseases, type 1 diabetes and rheumatoid arthritis. The authors concluded that it was critical to consider the benefits of sun exposure as well as the risks, and to provide information to the public on the minimum sun exposure required for beneficial health effects as well as the maximal sun exposure to avoid the adverse health effects associated with excessive sun exposure. Mokry et al. 2015113 was a Mendelian randomization analysis showing that genetically low 25(OH)D levels were associated with increased risk of MS. Jalkanen et al. 2015114 found a high level of vitamin D deficiency during pregnancy in MS patients.
Jacobsen et al. 2015115 found that more sun exposure in the third gestational trimester was associated with lower risk of type 1 diabetes in male children. Sawah et al. 2016116 found a high prevalence of vitamin D deficiency (25(OH)D levels less than 20 ng/mL) in children and adolescents with type 1 diabetes. Kostoglou-Athanassiou et al. 2012117 found a high prevalence vitamin D deficiency in patients with rheumatoid arthritis.
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Gisondi et al. 2012118 found that the prevalence of 25(OH)D of less than 20 ng/mL was 57.8% in patients with psoriasis vs. 29.7% in healthy controls, and that in a logistic regression analysis, vitamin D deficiency was associated with psoriasis independently of other factors (OR 2.50, 95% CI 1.18–4.89). The investigators noted that topical vitamin D derivatives and UVB radiation are used in the treatment of psoriasis. Vitamin D status was found to be unrelated to levels of self-reported sun exposure, but the measure used for sun exposure, which was minutes per day of sun exposure from March to September, may not have been appropriate for vitamin D production since it apparently did not include the time of day or the area of skin exposed.
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Liver disease
Gorman et al. 2015119 in a review stated that a large number of studies in recent Years92,120,121 have shown that exposure to UVR has the potential to curtail the development of non-alcoholic fatty liver disease (NAFLD) through vitamin D dependent and vitamin D independent mechanisms. The authors noted that most observational studies support an inverse association between serum 25(OH)D levels and NAFLD, but that vitamin D supplementation did not produce the same results. The authors further stated that circulating vitamin D levels may represent a proxy for bodily exposure to sunlight122 explaining the observation that mediators induced by sun exposure other than vitamin D may play important roles in curtailing NAFLD.
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Statin intolerance and muscle pain, weakness
Khayznikov et al. 201567 found that statin intolerance because of myalgia, myositis, myopathy, or myonecrosis associated with serum 25(OH)D less than 23 ng/mL can be resolved with vitamin D supplementation raising serum 25(OH)D to 53 ng/mL. Aleksic et al. 2015123 found that low vitamin D levels are a potentially significant and correctible risk factor for statin-related myopathy, especially in African-Americans.
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Macular degeneration
Millen et al. 2015124 observed a 6.7-fold increased risk of age-related macular degeneration (AMD) among women with serum 25(OH)D levels less than 12 ng/mL who also had genetic risk for AMD, and noted that previous studies had found that decreased odds of AMD are associated with high compared to low concentrations of 25(OH)D.
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Dental caries in infants
Schroth et al. 2014125 found that low prenatal 25(OH)D concenratations were associated with increased risk of dental caries among offspring in the first year of life.
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Reverse causation
Autier et al. 2014126 suggested that low serum 25(OH)D levels may be the result rather than the cause of diseases associated with low serum 25(OH)D levels in observational studies (reverse causation). The authors offer little evidence to support such a hypothesis, and it is contraindicated by the prospective nature of many of the studies linking serum 25(OH)D levels with health outcomes, by Mendelian randomization studies77,113 and by the body of knowledge concerning the bioactivity of vitamin D, particularly its cancer-inhibiting properties.
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Geldenhuys et al. 201492 suggests that UVR exposure may be an effective means of suppressing the development of obesity and metabolic syndrome through mechanisms that are independent of vitamin D but dependent on other UVR-induced mediators such as nitric oxide. This study investigated whether UVR and/or vitamin D supplementation had an effect on the development of obesity and type 2 diabetes in mice fed a high-fat diet, and found that UVR significantly suppressed weight gain but vitamin D supplementation did not. These results indicate that low vitamin D status in obese persons may only be a marker for low UVR exposure or a result of sequestration of vitamin D in adipose tissue, and provide a new view of previous studies showing a consistent association between increasing body mass index and lower serum 25(OH)D levels.127
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French et al. 2015128 was a review stating that recent epidemiological evidence suggests that children who spend more time outdoors are less likely to be or to become myopic, irrespective of how much near work they do or whether their parents are myopic. The likely mechanism for this protective effect is visible light stimulating release of dopamine from the retina, which inhibits increased axial elongation, the structural basis of myopia. The authors describe the effect of time outdoors on the risk of myopia as robust. The prevalence of myopia in the US in persons 12 to 54 y old increased 66% between 1971–1972 and 1999–2004, from 25.0% to 41.6%, according to the National Eye Institute of the National Institutes of Health.129,130 For African Americans, the increase was 157.7%.130 This high prevalence of myopia presents a major public health problem since, in addition to requiring corrective lenses, myopia poses substantially increased risk of retinal detachment, glaucoma, macular degeneration, amblyopia and cataracts.131,132
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Other benefits of sun exposure
Lambert et al. 2002133 suggested that the prevailing amount of sunlight affects brain serotonergic activity. Deficiencies in serotonin and brain serotonergic activity have been linked to sudden infant death syndrome,134 seasonal affective disorder,133 depression,135 schizophrenia,136 Alzheimer disease,137 and migraine headaches.138 Beta-endorphin, a neuorohormone that acts as an analgesic, has been known for many years to be released in the human body by exercise,139 producing a feeling of wellbeing similar to the feeling of wellbeing induced by sun exposure. A recent study showed that UVR exposure significantly raised circulating plasma β-endorphin levels in a UV-exposure mouse model, leading to suggestions that UVR exposure is addictive.140 Alternatively, the release of β-endorphins by sun exposure could be a natural reward mechanism encouraging sun exposure.
The benefits of serotonin and β-endorphin, as well as the effects of sun exposure on melatonin, photodegradation of folic acid, immunumodulation, photoadaptation, and circadian clocks, are reviewed in van der Rhee et al. 2016.10
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Vitamin D supplements vs. sun exposure
In light of the studies discussed in this review that found health outcomes related to sun exposure independent of vitamin D, health outcomes dependent on serum 25(OH)D levels but not vitamin D supplementation, and health outcomes dependent on mediators other than vitamin D, it is apparent that vitamin D supplements are not an effective substitute for adequate sun exposure.
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Balancing the risks of moderate non-burning sun exposure against the risks of inadequate sun exposure
The only identified risk associated with the amount of non-burning sun exposure needed to achieve serum 25(OH)D levels of 30 ng/mL is some possible increased risk of nonmelanoma skin cancer. The amount of sun exposure required to produce this level of vitamin D varies among individuals and according to time of year, time of day and latitude. White people with Type II skinsh at 40 degrees latitude can obtain their annual requirements of vitamin D by spending about 15 minutes in the sun with face, arms and legs exposed (half that time if in a bathing suit) 2 to 3 times a week between 11 a.m. and 3 p.m. during the months of May through October.141 In comparison, nonmelanoma skin cancer is associated with many thousands or tens of thousands of cumulated hours of lifetime sun exposure.16,52,53 Moreover, inadequate acclimatization to UVR in daily life carries the risk of sunburn and corresponding increased risk of both nonmelanoma skin cancer and melanoma.
The risks of inadequate non-burning sun exposure include increased risks of all-cause mortality, colorectal cancer, breast cancer, non-Hodgkins lymphoma, prostate cancer, pancreatic cancer, hypertension, cardiovascular disease, metabolic syndrome, type 2 diabetes, obesity, Alzheimer disease, multiple sclerosis, type 1 diabetes, rheumatoid arthritis, psoriasis, non-alcoholic fatty liver disease, statin intolerance, macular degeneration and myopia.
People with darker skins require more time in the sun to produce their requirements of vitamin D but also have lower risks of nonmelanoma skin cancer, and people with Type I skins, who are unable to tan, require less time in the sun but have higher risks of nonmelanoma skin cancer. All persons should avoid sunburns, which are associated with substantial increased risk of melanoma and nonmelanoma skin cancer.
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Insufficient sun exposure has become a major public health problem, demanding an immediate change in the current sun-avoidance public health advice. The degree of change needed is small but critically important. The public must be advised to obtain enough sun exposure and vitamin D supplementation to maintain a serum 25(OH)D level of at least 30 ng/mL. The skin has a large capacity to produce vitamin D and a single whole body exposure to an amount of sunlight that is equal to 1 minimal erythemal dose is equivalent to ingesting approximately 15,000–20,000 IUs of vitamin D. Therefore to produce an equivalent of 4000 IUs of vitamin D a day would require that 50% of the body surface be exposed to 0.5 MEDs. To achieve a blood level of at least 30 ng/ML would require ingesting 2000 IUs of vitamin D daily which would be equivalent to 25% of the body surface exposed to 0.5 MEDs 2–3 times a week.24 The amount of sun exposure required to achieve an MED depends on skin pigmentation, latitude, time of day and time of year. Warnings on the dangers of sunburn at any age should be emphasized. Periodic testing of serum 25(OH)D levels is also reasonable especially at the end of the summer which is when the blood level of 25(OH)D is at its highest level.141
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aThe 2010 Institute of Medicine vitamin D report defined vitamin D deficiency as serum 25(OH)D levels of less than 12ng/mL and vitamin D insufficiency as serum 25(OH)D levels of less than 20 ng/mL.2 NHANES data for 2001–2006 show that 8% of Americans had 25(OH)D below 12 ng/mL and 32% had 25(OH)D below 20 ng/mL.3
bAccording to the Centers for Disease Control and Prevention, the prevalence of sunburns increased from 32% of all adults in 1999 to 34% in 200435 and up to 50% in 2012.36 Among adolescents aged 12–18 in 1999, 83% reported at least one sunburn in the previous summer and 36% reported three or more sunburns in the previous summer.37
cData on temporal trends in vitamin D levels are contained in study by Ginde et al. 200938 who reported that NHANES data on serum 25(OH)D levels show that the prevalence of 25(OH)D of less than 10 ng/mL increased from 2% in 1988–1994 to 6% in 2001–2004 while over the same time period the prevalence of 25(OH)D of less than 20 ng/mL increased from 22% to 36%, and for 25(OH)D of less than 30 ng/mL increased from 55% to 77%.
dSuch an explanation is not new. White et al. 198839 (published as Garland et al. 199040) proposed that low levels of vitamin D (either locally available in skin or circulating in plasma) allow melanomas which were previously initiated by sunlight exposure to develop into clinically apparent disease in continually sunlight deprived individuals. This proposal was apparently ignored as precautions against melanoma focused on sun avoidance and liberal use of chemical sunscreens, with inadequate attention paid to the role of sunburns in melanomagenesis and to the role of vitamin D in inhibiting cancer. The first cancer cell line shown in 1980 to be inhibited in growth by 1,25(OH)2D was in fact a melanoma cell line. In 1989 Gallagher et al.41 suggested that part of the increased incidence in melanoma could be attributed to the decline in outdoor workers.
eSunscreens are intended to prevent sunburn when used in thickness and frequency recommended by manufacturers or used in setting SPFs. However, studies have shown that the incidence of sunburn is higher or the same in people who almost always use sunscreens compared with those who rarely use sunscreens.43-45
fThe differences between NHANES III and NHANES 2001- 2004 may be attenuated by approximately 4 ng/mL after adjustment for improvements in the serum 25(OH)D assay performance from NHANES III to NHANES 2001-2004.71
gThe Endocrine Society's 2012 review of the nonskeletal effects of vitamin D also found there was insufficient evidence to support a role of vitamin D supplementation in correcting vitamin D insufficiency.66
hThere are 6 categories of skin on the Fitzpatrick Scale: Type I Very Fair White - always burns, never tans;Type II Fair White - usually burns, tans minimally; Type III Cream White – sometimes mild burn, gradually tans; Type IV Brown – rarely burns, tans with ease; Type V Dark Brown – very rarely burns, tans very easily; Type VI Black – never burns, tans very easily.
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5(OH)D25-hydroxyvitamin DBCCbasil cell carcinomaCIconfidence intervalCVDcardiovascular diseaseHRhazard ratioIUinternational unitsMSmultiple sclerosisNMSCnon-melanoma skin cancerng/mLnanograms per milliliterNHLnon-Hodgkins lymphomaORodds ratioRRrelative riskSCCsquamous cell carcinomaUVRUltraviolet Radiation (290–400 nm)UVAUltraviolet-A (316–400 nm)UVBUltraviolet-B (290–315 nm)
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Disclosure of potential conflicts of interest
No potential conflicts of interest were disclosed.
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[1] The Surgeon General's Call to Action to Prevent Skin Cancer, U.S. Department of Health and Human Resources, Office of the Surgeon General, Washington, D.C; 2014.; Sun Exposure, Centers for Disease Control and Prevention; Guidelines for School Programs to Prevent Skin Cancer, Centers for Disease Control and Prevention _ doing/guidelines.htm; How Can I Protect My Children from the Sun?, Centers for Disease Control and Prevention,; What Can I Do to Reduce My Risk of Skin Cancer?, Centers for Disease Control and Prevention
[2] Institute of Medicine Dietary Reference Intakes for Calcium and Vitamin D, pages S-11 and 8–7. National Academies Press; 2010.
[3] Looker AC, Johnson CL, Lacher DA, Pfeiffer CM, Schleicher RL, Sempos CT. Vitamin D Status: United States, 2001–2006. NCHS Data Brief, No. 59, March 2011.
[4] Huldshinsky K. Heilung von rachitis durch kunstlich hohen-sonne. Deut Med Wochenscher 1919; 45:712-3; [Cross Ref]Huldshinsky K. The ultra-violet light treatment of rickets. Alpine Press New Jersey, USA 1928, 3-19.
[5] Hess AF, Unger LL. The cure of infantile rickets by sunlight. JAMA 1921; 77:39-41.
[6] Steenbock H, Black A. Fat-soluble vitamins XXIII. The induction of growth-promoting and calcifying properties in fats and their unsaponifiable constituents by exposure to light. J Biol Chem 1925; 64:263-98.
[7] Askew FA, Bourdillon RB, Bruce HM, Jenkins RGC, Webster TA. The distillation of vitamin D. Proc R Soc 1931; B107:76-90.
[8] Albert MR, Ostheimer KG.. The evolution of current medical and popular attitudes toward ultraviolet light exposure: part 3. J Am Acad Dermatol 2003; 49:1096-106; PMID:14639391; [PubMed] [Cross Ref]
[9] Shaath NA. Evolution of modern sunscreen chemicals. In:Lowe NJ, Shaath NA, editors. Sunscreens: development, evaluation and regulatory aspects. New York: M. Dekker. 1990:3-35.
[10] van der Rhee H, de Vries E, Coomans C, van de Velde P, Coebergh JW. Sunlight: For better or for worse? A review of positive and negative effects of sun exposure. Cancer Res Front 2016: 2:156-83; [Cross Ref]
[11] Nelson AA, Tsao H. Melanoma and genetics. Clinics in Dermatol 2009; 27:46-52; [PubMed] [Cross Ref]
[12] Gandini S, Sera F, Cattaruzza MS, Pasquini P, Abeni D, Boyle P, Melchi CF.. Meta-analysis of risk factors for cutaneous melanoma: II. Sun exposure. Eur J Cancer 2005; 41:45-60; PMID:15617990; [PubMed] [Cross Ref]
[13] Vuong K, McGeechan K, Armstrong BK, AMFS Investigators, GEM Investigators, Cust AE.. Occupational sun exposure and risk of melanoma according to anatomical site. Int J Cancer 2014; 134:2735-41; PMID:24288300; [PMC free article] [PubMed] [Cross Ref]
[14] Moan J, Porojnicu AC, DAhlback A, Setlow RB.. Addressing the health benefits and risks, involving vitamin D or skin cancer, of increased sun exposure. PNAS 2008; 105:668-73; PMID:18180454; [PMC free article] [PubMed] [Cross Ref]
[15] Godar DE, Landry RJ, Lucas AD. Increased UVA exposures and decreased cutaneous Vitamin D3 levels may be responsible for the increasing incidence of melanoma. Med Hypoth 2009; 72:434-43; [PubMed] [Cross Ref]
[16] Kennedy C, Bajdik CD, Willemze R, de Gruijl FR, Bavinck JNB.. The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi, and skin cancer. J Invest Dermatol 2003; 120:1087-93; PMID:12787139; [PubMed] [Cross Ref]
[17] Armstrong BK, Kricker A. The epidemiology of UV induced skin cancer. J Photochem Photobiol 2001; 63:8-18; [PubMed] [Cross Ref]
[18] Elwood JM, Jopson J.. Melanoma and sun exposure: An overview of published studies. Int J Cancer 1997; 73:198-203; PMID:9335442;;2-R [PubMed] [Cross Ref]
[19] Green AC, O'Rourke MGE.. Cutaneous malignant melanoma in association with other skin cancers. JNCI 1985; 74:977-80; PMID:3858585 [PubMed]
[20] van Schanke A, Jongsma MJ, Bisschop R, van Venrooij GMCAL, Rebel H, de Gruijl FR.. Single UVB overexposure stimulates melanocyte proliferation in murine skin, in contrast to fractionated or UVA-1 exposure. J Invest Dermatol 2005; 124:241-7; PMID:15654980; [PubMed] [Cross Ref]
[21] Institute of Medicine Dietary Reference Intakes for Calcium and Vitamin D, Chapter 3. National Academies Press; 2010:91-92.
[22] Holick MF. Vitamin D Physiology, Molecular Biology, and Clinical Applications, Second Ed. Humana Press; 2010.
[23] Rosen CJ, Adams JS, Bikle DD, Black DM, Demay MB, Manson JE, Murad MH, Kovacs CS.. The nonskeletal effects of vitamin D: An endocrine society scientific statement. Endocrine Reviews 2012; 33:456-92; PMID:22596255; [PMC free article] [PubMed] [Cross Ref]
[24] Wacker M, Holick MF. Sunlight and vitamin D: A global perspective for health. Dermato-Endocrinol 2013; 5:51-108; [PMC free article] [PubMed] [Cross Ref]
[25] Bikle DD. The Vitamin D Receptor: A Tumor Suppressor in Skin Sunlight, Vitamin D and Skin Cancer, Chapter 16, Second Edition. Reichrath Jorg, editor. Landes Bioscience and Springer Science+Business Media. 2014:282-302
[26] Newton-Bishop JA, Chang Y, Elliott F, Chan M, Leake S, Karpavicius B, Haynes S, Fitzgibbon E, Kukalizch K, Randerson-Moor J, et al. Relationship between sun exposure and melanoma risk for tumours in different body sites in a large case-control study in a temperate climate. Eur J Cancer 2011; 47:732-741; PMID:21084183; [PMC free article] [PubMed] [Cross Ref]
[27] Reichrath J, Reichrath S.. The relevance of the vitamin D endocrine system (“VDES) for tumorigenesis, prevention, and treatment of non-melanoma skin cancer (NMSC): Present concepts and future perspectives. Dermato-Endocrinology 2013; 5:38-50; PMID:24494041; [PMC free article] [PubMed] [Cross Ref]
[28] Dixon KM, Norman AW, Sequeira VB, Mohan R, Rybchyn MS, Reeve VE, Halliday GM, Mason RS. 1a, 25(OH)2-vitamin D and a nongenomic vitamin D analogue inhibit ultraviolet radiation-induced skin carcinogenesis. Cancer Prev Res 2011; 4:1485-94; [PubMed] [Cross Ref]
[29] Gordon-Thomson C, Tongkao-on W, Song EJ, Carter SE, Dixon KM, Mason RS.. Protection from ultraviolet damage and photocarcinogenesis by vitamin D compounds. Adv Exp Med Biol 2014; 810:303-28; PMID:25207373 [PubMed]
[30] Levell JN, Beattie CC, Shuster S, Greenberg DC.. Melanoma epidemic: a midsummer night's dream? Br J Dermatol 2009; 161:630-4; PMID:19519827; [PubMed] [Cross Ref]
[31] Schaart FM, Garbe C, Orfanos CE.. Disappearance of the ozone layer and skin cancer; attempt at risk assessment. Hautarzt 1993; 44:63-8; PMID:8449695 [PubMed]
[32] Lazovich D, Vogel RI, Berwick M, Weinstock MA, Anderson KE, Warshaw EM.. Indoor tanning and risk of melanoma: a case-control study in a highly exposed populations. Cancer Epidemiol Biomarkers Prev 2010;19:1557-68; PMID:20507845; [PMC free article] [PubMed] [Cross Ref]
[33] Ian D. Wyatt and Daniel E. Hecker, Occupational changes in the 20th century. Monthly Labor Review, March 2006. pp 35-57: Office of Occupational Statistics and Employment Projections, Bureau of Labor Statistics.
[35] MMWR Weekly Report June 1, 2007. / 56(21);524-528;Table 1. [PubMed]
[36] MMWR Weekly Report May 11, 2012. / 61(18);317-322. [PubMed]
[37] Geller AC, Colditz G, Oliveria S, Emmons K, Jorgensen C, Aweh GN, Frazier AL.. Use of sunscreen, sunburning rates, and tanning bed use among more than 10,000 US children and adolescents. Pediatrics 2002; 109:1009-14; PMID:12042536; [PubMed] [Cross Ref]
[38] Ginde AA, Liu MC, Camargo CA.. Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med 2009; 169:626-32; PMID:19307527; [PMC free article] [PubMed] [Cross Ref]
[39] White MR, Garland FC, Garland CF, Shaw E, Gorham ED. Malignant melanoma in US Navy personnel. Report No. 88-27 Naval Medical Research and Development Command 1988.
[40] Garland CF, Garland FC.. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol 1980; 9:227-31; PMID:7440046; [PubMed] [Cross Ref]
[41] Gallagher RP, Elwood JM, Yang CP.. Is chronic sunlight exposure important in accounting for increases in melanoma incidence? Int J Cancer 1989; 44:813-5; PMID:2583861; [PubMed] [Cross Ref]
[42] Green AC, Williams GM, Logan V, Strutton GM.. Reduced melanoma after regular sunscreen use: Randomized trial follow-up. J Clin Oncol 2011; 29:257-63; PMID:21135266; [PubMed] [Cross Ref]
[43] Neale R, Williams G, Green A.. Application patterns among participants randomized to daily sunscreen use in a skin cancer prevention trial. Arch Dermatol 2002; 138:1319-25; PMID:12374537; [PubMed] [Cross Ref]
[44] Dobbinson S, Borland R. Reaction to the 1996/1997 SunSmart Campaign: Results from a Representative Household Survey of Victorians. Melbourne, Australia Anti-Cancer Council of Victoria 1999; SunSmart Evaluation Studies No. 6.
[45] Morris J, McGee R, Bandaranayake M. Sun protection berhaviours and the predictors of sunburn in young children. J Paediatr Child Health 1998; 34:557-62. [PubMed]
[47] van der Pols JC, Williams GM, Pandeya N, Logan V, Green AC. Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer Epidemiol Bio Prev 2006; 15:2546-8; [PubMed] [Cross Ref]
[48] Rogers HW, Weinstock MA, Harris AR, Hinckley MR, Feldman SR, Fleischer AB, Coldiron BM.. Incidence estimate of non-melanoma skin cancer in the United States, 2006. Arch Dermatol 2010; 146:283-7; PMID:20231499; [PubMed] [Cross Ref]
[49] Rogers HW, Weinstock MA, Feldman SR, Coldiron BM.. Incidence estimate of non-melanoma skin cancer (keratinocyte carcinomas) in the US Population, 2012. JAMA Dermatol 2015; 151:1081-6; PMID:25928283; [PubMed] [Cross Ref]
[50] Asgari MM, Moffet HH, Ray GT, Quesenberry CP.. Trends in Basal Cell Carcinoma Incidence and Identification of High-Risk Subgroups, 1998-2012. JAMA Dermatol 2015; 151:976-81; PMID:26039887; [PubMed] [Cross Ref]
[51] de Vries E, Arnold M, Altsitsiadis E, Trakatelli M, Hinrichs B, Stockfleth E.. Coebergh J on behalf of the EPIDERM Group. Potential impact of interventions resulting in reduced exposure to ultraviolet (UV) radiation (UVA and UVB) on skin cancer incidence in four European countries, 2010–2050. Brit J Derm 2012; 167(Suppl. 2):53-62; PMID:22881588; [PubMed] [Cross Ref]
[52] Rosso S, Zanetti R, Martinez C, Tormo MJ, Schraub S, Sancho-Garnier H, Franceschi S, Gafà L, Perea E, Navarro C, et al. The multicentre south European study ‘Helios’ II: different sun exposure patterns in the aetiology of basal cell and squamous dell carcinomas of the skin. Br J Cancer 1996; 73:1447-54; PMID:8645596; [PMC free article] [PubMed] [Cross Ref]
[53] English DR, Armstrong BK, Kricker A, Winter MG, Heenan PJ, Randell PL.. Case-control study of sun exposure and squamous cell carcinoma of the skin. Int J Cancer 1998; 77:347-53; PMID:9663594;;2-O [PubMed] [Cross Ref]
[54] Gallagher RP, Hill GB, Bajdik CD, Fincham S, Coldman AJ, McLean DI, Threlfall WJ.. Sunlight exposure, pigmentary factors, and risk of nonmelanocytic skin cancer. I. Basal cell carcinoma. Arch Dermatol 1995; 131:157-63; PMID:7857111; [PubMed] [Cross Ref]
[55] Gallagher RP, Hill GB, Bajdik CD, Coldman AJ, Fincham S, McLean DI, Threlfall WJ.. Sunlight exposure, pigmentary factors, and risk of nonmelanocytic skin cancer. II. Squamous cell carcinoma. Arch Dermatol 1995; 131:164-9; PMID:7857112; [PubMed] [Cross Ref]
[56] Schmitt J, Seidler A, Diepgen TL, Bauer A.. Occupational ultraviolet light exposure increases the risk of the development of cutaneous squamous cell carcinoma: a systematic review and meta-analysis. Br J Dermatol 2011; 164:291-307; PMID:21054335; [PubMed] [Cross Ref]
[57] Bauer A, Diepgen TL, Schmitt J.. Is occupational solar ultraviolet irradiation a relevant risk factor for basal cell carcinoma? A systematic review and meta-analysis of the epidemiological literature. Br J Dermatol 2011; 165:612-25; PMID:21605109 [PubMed]
[58] Alam M, Ratner D.. Cutaneous squamous-cell carcinoma. N Engl J Med 2001; 344:975-83; PMID:11274625; [PubMed] [Cross Ref]
[59] Final Recommendation Statement: Skin Cancer Counseling U.S. Preventive Services Task Force. May 2012.
[60] Lin JS, Eder M, Weinmann S.. Behavioral counseling to prevent skin cancer: A systematic review for the U.S. Preventative Services Task Force. Ann Intern Med 2011; 154:190-201; PMID:21282699; [PubMed] [Cross Ref]
[61] Holick MF. The UV Advantage, iBooks 2003.
[62] Holick MF. Biologic effects of sunlight, ultraviolet radiation, visible light, infrared, and vitamin D for health. Anticancer 2016; 36:1345-56. [PubMed]
[63] Hossain-nezhad A, Holick MF. Vitamin D for health: A global perspective. Mayo Clinic Proc 2013; 88:720-55; [PMC free article] [PubMed] [Cross Ref]
[64] Institute of Medicine Dietary Reference Intakes for Calcium and Vitamin D. Chatper 4. National Academies Press; 2010:142-5.
[65] Holick MF, Chen TC, Lu Z, Sauter E. Vitamin D and skin physiology: A D-Lightful story. J Bone Mineral Res 2007; 22:V28-33; [PubMed] [Cross Ref]
[66] Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, Weaver CM.. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011; 96:1911-30; PMID:21646368; [PubMed] [Cross Ref]
[67] Khayznikov M, Hemachrandra Pandit R, Kumar A, Wang P, Glueck CJ.. Statin intolerance because of myalgia, myositis, mypathy, or myonecrosis can in most cases be safely resolved by vitamin D supplementation. N Am J \Med Sci 2015; 7:86-91; PMID:25838999; [PMC free article] [PubMed] [Cross Ref]
[68] Rosen CJ. Vitamin D insufficiency. N Eng J Med 2011; 364:248-54; [PubMed] [Cross Ref]
[69] Holick MF. Cancer, sunlight and vitamin D. J Clin Transl Endocrinol 2014; 1:179-86; [Cross Ref]
[70] Garland CF, Gorham ED, Mohr SB, Garland FC.. Vitamin D for cancer prevention: Global perspective. Ann Epidemiol 2009; 19:468-83; PMID:19523595; [PubMed] [Cross Ref]
[71] Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA.. Serum 25-hydroxyvitamin D status of the US population: 1988-1994 versus 200-2004. Am J Clin Nutr 2008; 88:1519-27; PMID:19064511; [PMC free article] [PubMed] [Cross Ref]
[72] Chowdury R, Kunutsor S, Vitezova A, Oliver-Williams C, Chowdhury S, Kiefte-de-Jong JC, Khan H, Baena CP, Prabhakaran D, Hoshen MB, et al. Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies. BMJ 2014; 348:g1903; PMID:24690623; [PMC free article] [PubMed] [Cross Ref]
[73] Garland CF, Kim JJ, Mohr SB, Gorham ED, Grant WB, Giovannucci EL, Baggerly L, Hofflich H, Ramsdell JW, Zeng K, et al. Meta-Analysis of all-cause mortality according to serum 25-hydroxyvitamin D. Am J Pub Health 2014; 104:e43-50; [PMC free article] [PubMed] [Cross Ref]
[74] Schottker B, Peasey A, Thorand B, Jansen EHJM, de Groot L, Streppel M, Gardiner J, Ordonez-Mena JM, Perna L, Wilsgaard T, et al. Vitamin D and mortality: meta-analysis of individual participant data from a large consortium of cohort studies from Europe and the United States. BMJ 2014; 348:g3656; PMID:24938302; [PMC free article] [PubMed] [Cross Ref]
[75] Lindqvist PG, Epstein E, Landin-Olsson M, Ingvar C, Nielsen K, Stenbeck M, Olsson H.. Avoidance of sun exposure is a risk factor for all-cause mortality: results from the melanoma in Southern Sweden cohort. J Intern Med 2014; 276:77-86; PMID:24697969; [PubMed] [Cross Ref]
[76] Lindqvist PG, Epstein E, Nielsen K, Landin-Olsson M, Ingvar C, Olsson H. Avoidance of sun exposure as a risk factor for major causes of death: A competing risk analysis of the melanoma in a southern Sweden cohort. J Int Med 2016; 280:375-87; [PubMed] [Cross Ref]
[77] Afzal S, Brondum-Jacobsen P, Bojesen SE, Nordestgaard BG.. Genetically low vitamin D concentrations and increased mortality: Mendelian randomisation analysis in three large cohorts. BMJ 2014; 349:G6330; PMID:25406188; [PMC free article] [PubMed] [Cross Ref]
[78] Rebel H, der Spek CD, Salvatori D, van Leeuwen JP, Robanus-Maanday EC, de Gruijl FR.. UV exposure inhibits intestinal tumor growth and progression to malignancy in intestine-specific Apc mutant mice kept on low vitamin D diet. Int J Cancer 2014; 136:271-7; PMID:24890436; [PubMed] [Cross Ref]
[79] Jenab M, Bueno-de-Mesquita HB, Ferrari P, van Duijnhoven FJ, Norat T, Pischon T, Jansen EH, Slimani N, Byrnes G, Rinaldi S, et al. Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations: a nested case-control study. BMJ 2010; 340:b5500; PMID:20093284; [PMC free article] [PubMed] [Cross Ref]
[80] Mohr SB, Gorham ED, Kim J, Hofflich H, Garland CF.. Meta-analysis of vitamin D sufficiency for improving survival of patients with breast cancer. Anticancer Res 2014; 34:1163-6; PMID:24596354 [PubMed]
[81] Engel P, Fagherazzi G, Boutten A, Dupre T, Mesrine S, Boutron-Rualt MC, Clavel-Chapelon F. Serum 25(OH)D vitamin D and risk of breast cancer: A nested case-control study from the French E3N Cohort. Cancer Epidemiol Bio Prev 2010; 19:2341-50; [PubMed] [Cross Ref]
[82] John E, Schwartz G, Dreon D, Koo J. Vitamin D and breast cancer risk: The NHANES I epidemiologic follow-up study, 1971-75 to 1992. Cancer Epidemiol Bio Prev 1999; 8:399-406. [PubMed]
[83] Knight JA, Lesosky M, Barnett H, Raboud JM, Vieth R. Vitamin D and reduced risk of breast cancer: a population-based case-control study. Cancer Epidemiol Bio Prev 2007; 16: 422-9; [PubMed] [Cross Ref]
[84] van der Rhee H, Coebergh JW, de Vries E.. Is prevention of cancer by sun exposure more than just the effect of vitamin D? A systematic review of epidemiological studies. Eur J Cancer. 2013; 49:1422-36; PMID:23237739; [PubMed] [Cross Ref]
[85] Apperly FL. The relation of solar radiation to cancer mortality in North America. Cancer Res 1941; 1:191-5.
[86] Zhao Y, Chen C, Pan W, Gao M, He W, Mao R, Lin T, Huang J.. Comparative efficacy of vitamin D status in reducing the risk of bladder cancer: A systematic review and network meta-analysis. Nutrition 2016; 32:515-23; PMID:26822497; [PubMed] [Cross Ref]
[87] Liu D, Fernandez BO, Hamilton A, Lang NN, Gallagher JMC, Newby DE, Feelisch M, Weller RB.. UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase. J Invest Dermatol 2014; 134:1839-46; PMID:24445737; [PubMed] [Cross Ref]
[88] Feelisch M, Kolb-Bachofen V, Liu D, Lundberg JO, Revelo LP, Suschek CV, Weller RB.. Is sunlight good for our heart? Eur Heart J 2010; 31: 1041-5; PMID:20215123; [PubMed] [Cross Ref]
[89] Tunstall-Pedoe H, Woodward M, Hughes M, Anderson A, Kennedy G, Balch J, Kuulasmaa K.. Prime Mover or fellow treaveller: 25-hydroxy vitamin D's seasonal variation, cardiovascular disease and death in the Scottish Heart Health Extended Cohort (SHHEC). Int J Epidemiol 2015; 1602-12; PMID:26095374; [PMC free article] [PubMed] [Cross Ref]
[90] Vitezova A, Zillikens MC, van Herpt TTW, Sijbrands EJG, Hofman A, Uitterlinden AG, Franco OH, Kiefte-de Jong JC. Vitamin D status and metabolic syndrome in the elderly: the Rotterdam Study. Eur J Endocrin 2015; 172:327-35; [PubMed] [Cross Ref]
[91] Clemente-Postigo M, Munoz-Garach A, Serrano M, Garrido-Sanchez L, Bernal-Lopez MR, Fernandez-Garcia D, Moreno-Santos I, Garriga N, Castellano-Castillo D, Camargo A, et al. Serum 25-hydroxyvitamin D and adipose tissue vitamin D receptor gene expression: relationship with obesity and type 2 diabetes. J Clin Endocrinol Metab 2015; 100:E591-5; PMID:25706239; [PubMed] [Cross Ref]
[92] Geldenhuys S, Hart PH, Endersby R, Jacoby P, Feelisch M, Weller RB, Matthews V, Gorman S.. Ultraviolet radiation suppresses obesity and symptoms of metabolic syndrome independently of vitamin D in mice fed a high-fat diet. Diabetes 2014; 63:3759-69; PMID:25342734; [PubMed] [Cross Ref]
[93] Afzal S, Bojesen SE, Nordestgaard BG.. Low 25-hydroxyvitamin D and risk of Type 2 diabetes: A prospective cohort study and metaanalysis. Clin Chem 2013; 59:381-91; PMID:23232064; [PubMed] [Cross Ref]
[94] Mitri J, Muraru MD, Pittas AG.. Vitamin D and type 2 diabetes: a systematic review. Eur J Clin Nutr 2011; 65:1005-15; PMID:21731035; [PMC free article] [PubMed] [Cross Ref]
[95] Littlejohns TJ, Henley WE, Lang IA, Annweiler C, Beauchet O, Chaves PHM, Fried L, Kestenbaum GR, Kuller LH, Langa KM, et al. Vitamin D the risk of dementia and Alzheimer disease. Neurology 2014; 83:920-8; PMID:25098535; [PMC free article] [PubMed] [Cross Ref]
[96] Keeney JTR, Förster S, Sultana R, Brewer LD, Latimer CS, Cai J, Klein JB, Porter NM, Butterfield BA.. Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine nitration and proteomics changes in levels of key proteins in brain: Implications for low vitamin D-dependent age-related cognitive decline. Free Radic Biol Med 2013; 65:324-34; PMID:23872023; [PMC free article] [PubMed] [Cross Ref]
[97] Annweiler C, Montero-Odasso M, Llewellyn DJ, Richard-Devantoy S, Duque G, Beauchet O.. Meta-analysis of memory and executive dysfunctions in relation to vitamin D. J Alzheimers Dis 2013; 37:147-71; PMID:23948884 [PubMed]
[98] Balion C, Griffith LE, Strifler L.. Vitamin D, cognition, and dementia: a systematic review and meta-analysis. Neurology 2012; 79:1397-405; PMID:23008220; [PMC free article] [PubMed] [Cross Ref]
[99] Slinen Y, Paudel M, Taylor BC, Ishani A, Rossom R, Yaffe K, Blackwell T, Lui L-Y, Hochberg M, Ensrud KE, for the Study of Osteoporotic Fractures Research Group .. Association between serum 25(OH)Vitamin D and the risk of cognitive decline in older women. J Gerontol A Biol Sci Med Sci 2012; 67:1092-8; PMID:22454371; [PMC free article] [PubMed] [Cross Ref]
[100] Llewellyn DJ, Lang IA, Langa KM, Melzer D.. Vitamin D and cognitive impairment in the elderly US population. J Gerontol A Biol Sci Med Sci 2011; 66:59-65; PMID:21041201; [PMC free article] [PubMed] [Cross Ref]
[101] Dickens AP, Lang IA, Langa KM, Kos K, Llewellyn DJ. Vitamin D, cognitive dysfunction and dementia in older adults. CNS Drugs 2011; 24:629-39; [PMC free article] [PubMed] [Cross Ref]
[102] Llewellyn DJ, Lang IA, Langa KM, Muniz-Terrera G, Phillips CL, Cherubuni A, Ferrucci L, Melzer D.. Vitamin D and risk of cognitive decline in elderly persons. Arch Intern Med 2010; 170:1135-41; PMID:20625021; [PMC free article] [PubMed] [Cross Ref]
[103] Wang Y, Marling SJ, Beaver EF, Severson KS, Deluca HF. UV light selectively inhibits spinal cord inflammation and demyelination in experimental autoimmune encephalomyelitis. Arch Biochem Biophys 2015; 587:75-82; [PubMed] [Cross Ref]
[104] Becklund BR, Severson KS, Vang SV, DeLuca HF. UV radiation suppresses experimental encephalomyelitis independent of vitamin D production. Proc Natl Acad Sci USA 2010; 197:6418-23; [PMC free article] [PubMed] [Cross Ref]
[105] Knippenberg S, Damoiseaux J, Bol Y, Hupperts R, Taylor BV, Ponsonby A-L, Dwyer T, Simpson T, van der Mei IAF.. Higher levels of reported sun exposure, and not vitamin D status, are associated with less depressive symptoms and fatigue in multiple sclerosis. Acta Neurol Scand 2014; 129:123-31; PMID:23763464; [PubMed] [Cross Ref]
[106] Correale J, Farez MF.. Modulation of multiple sclerosis by sunlight exposure: role of cis-urocanic acid. J Neuroimmunol 2013; 261:134-40; PMID:23800457; [PubMed] [Cross Ref]
[107] Simpson S Jr, Blizzard L, Otahal P, Van der Mei I, Taylor B.. Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis. J Neurol Neurosurg Psychiatry. 2011; 82:1132-41; PMID:21478203; [PubMed] [Cross Ref]
[108] Ponsonby AL, Lucas RM, van der Mei IAF.. UVR, vitamin D and three autoimmune diseases-multiple sclerosis, type 1 diabetes, rheumatoid arthritis. Photochem Photobiol. 2005; 81:1267-75; PMID:15971932; [PubMed] [Cross Ref]
[109] Acheson ED, Bachrach CA, Wright FM.. Some comments on the relationship of the distribution of multiple sclerosis to latitude, solar radiation, and other variables. Acta Psychiatr Scand Suppl 1960; 35:132-47; PMID:13681205; [PubMed] [Cross Ref]
[110] Baarnhielm M, Hedstrom AK, Kockum I, Sundqvist E, Gustafsson SA, Hillert J, Olsson T, Alfredsson L. Sunlight is associated with decreased multiple sclerosis risk: no interaction with human leukocyte antigen-DRB1*15. Eur J Neuro 2012; 19:955-62; [PubMed] [Cross Ref]
[111] Hogancamp WE, Rodriguez M, Weinshenker BG.. The epidemiology of multiple sclerosis. Mayo Clin Proc 1997; 72:871-8; PMID:9294536; [PubMed] [Cross Ref]
[112] Bach J-F. The effect of infections on susceptibility to autoimmune and allergic diseases. N Eng J Med 2002; 347:911-20; [PubMed] [Cross Ref]
[113] Mokry LE, Ross S, Ahmad OS, Forgetta V, Smith GD, Leong A, Greenwood CMT, Thanassoulis G, Richards JB.. Vitamin D and risk of multiple sclerosis: A Mendelian randomization study. PLOS Med 2015; 12(8):e1001866; PMID:26305103; [PMC free article] [PubMed] [Cross Ref]
[114] Jalkanen A, Kauko T, Turpeinen U, Hamalainen E, Airas L.. Multiple sclerosis and vitamin D during pregnancy and lactation. Acta Neurol Scand 2015: 131:64-7; PMID:25216350; [PubMed] [Cross Ref]
[115] Jacobsen R, Frederiksen P, Heitmann BL. Exposure to sunshine early in life prevented development of type 1 diabetes in Danish boys. J Pediatr Endocrinol Metab 2016; 19:417-24. [PubMed]
[116] Sawah SA, Compher CW, Hanlon AL, Lipman TH. 25-Hydroxyvitamin D and glycemic control: a cross-sectional study of children and adolescents with type 1 diabetes. Diabetes Res Clin Prac 2016; 115:54-9; [PubMed] [Cross Ref]
[117] Kostoglou-Athanassiou I, Athanassiou P, Lyraki A, Raftakis I, Antoniadis C.. Vitamin D and rheumatoid arthritis. Ther Adv Endocrinol Metab 2012; 3:181-7; PMID:23323190; [PMC free article] [PubMed] [Cross Ref]
[118] Gisondi P, Rossini M, De Cesare A, Idolazzi L, Farini S, Beltrami G, Peris K, Girolomini G.. Vitamin D status in patients with chronic plaque psoriasis. Br J Dermatol 2012; 166:505-10; PMID:22013980; [PubMed] [Cross Ref]
[119] Gorman S, Black LJ, Feelisch M, Hart PH, Weller R.. Can Skin Exposure to Sunlight Prevent Liver Inflammation? Nutrients 2015; 7:3219-39; PMID:25951129; [PMC free article] [PubMed] [Cross Ref]
[120] Gorman S, Scott NM, Tan DH, Weeden CD, Tuckey RC, Bisley JL, Grimbaldeston MA, Hart PH.. Acute erythemal ultraviolet radiation causes systemic immunsuppression in the absence of increased 25-hydroxyvitamin D levels in male mice. PLoS ONE 2012; 7:e46006; PMID:23049920; [PMC free article] [PubMed] [Cross Ref]
[121] Nakano T, Cheng YF, Lai CY, Hsu LW, Chang YC, Deng JY, Huang YZ, Honda H, Chan KD, Wang CC, et al. Impact of artificial sunlight therapy on the progress of non-alcoholic fatty liver disease in rats. J Hepatol 2011; 55:415-25; PMID:21184788; [PubMed] [Cross Ref]
[122] Feelisch M, Gorman S, Weller RB. Vitamin D status and ill health. Lancet Diab Endocrin 2014; 2:e8; [PubMed] [Cross Ref]
[123] Aleksic S, et al. Abstract 404 Presented at AACE 24th Annual Scientific & Clinical Congress, May 13-17, 2015, Nashville, TN.
[124] Millen AE, Meyers KJ, Liu Z, Engelman CD, Wallace RB, LeBlanc ES, Tinker LF, Lyengar SK, Robinson JG, Sarto GE, et al. Association between vitamin D status and age-related macular degeneration by genetic risk. JAMA Ophthalmol 2015; 133:1171-9; published online August27, 2015; PMID:26312598; [PMC free article] [PubMed] [Cross Ref]
[125] Schroth RJ, Lavelle C, Tate R, Bruce S, Billings RJ, Moffatt MEK.. Prenatal vitamin D and dental caries in infants. Pediatrics 2014; 133:e1277-84; PMID:24753535; [PubMed] [Cross Ref]
[126] Autier P, Boniol M, Pizot C, Mullie P.. Vitamin D status and ill health: a systematic review. Lancet Diabetes Endocrinol 2014; 2:76-89; PMID:24622671; [PubMed] [Cross Ref]
[127] Vanlint S. Vitamin D and Obesity. Nutrients 2013; 5:949-56; PMID:23519290; [PMC free article] [PubMed] [Cross Ref]
[128] French AN, Ashby RS, Morgan IG, Rose KA.. Time outdoors and the prevention of myopia. Exp Eye Res 2013; 114:58-68; PMID:23644222; [PubMed] [Cross Ref]
[130] Vitale S, Sperduto RD, Ferris FL III.. Increased Prevalence of Myopia in the U.S. between 1971-1972 and 1999-2004. Arch Ophthalmol 2009; 127:1632-9; PMID:20008719; [PubMed] [Cross Ref]
[131] Saw S-M, Gazzard G, Shih-Yen EC, Chua W-H. Myopia and associated pathological complications. Ophthal Physiol Opt 2005; 25:381-91; [PubMed] [Cross Ref]
[132] Chen S-J, Lu P, Zhang W-F, Lu J-H.. High myopia as a risk factor in primary open angle glaucoma. Int J Ophthalmol 2012; 5:750-3; PMID:23275912 [PMC free article] [PubMed]
[133] Lambert GW, Reid C, Kaye DM, Jennings GL, Esler MD.. Effect of sunlight and season on serotonin turnover in the brain. Lancet 2002; 360:1840-2; PMID:12480364; [PubMed] [Cross Ref]
[134] Duncan JR, Paterson DS, Hoffman JM, Mokler DJ, Borenstein NS, Belliveau RA, Krous HF, Haas EA, Stanley C, et al. Brainstem Serotonergic Deficiency in Sudden Infant Death Syndrome. JAMA 2010; 303:430-7; PMID:20124538; [PMC free article] [PubMed] [Cross Ref]
[135] Svenningsson P, Chergui K, Rachleff I, Flajolet M, Zhang X, El Yacoubi M, Vaugeois JM, Nomikos GG, Greengard P.. Alterations in 5-HT1B receptor function by p11 in depression-like states. Science 2006; 311:77-80; PMID:16400147; [PubMed] [Cross Ref]
[136] Abi-Dargham A, Laruelle M, Aghajanian GK, Charney D, Krystal J. The role of serotonin in the pathophysiology and treatment of schizophrenia. J Neuropsychiat 1997; 9:1-17; [PubMed] [Cross Ref]
[137] Cross AJ. Serotonin in Alzheimer-type dementia and other dementing illness. Ann NY Acad Sci 1990; 600:405-17; PMID:1701291; [PubMed] [Cross Ref]
[138] Hamel E. Serotonin and migraine: biology and clinical implications. Cephalalgia 2007; 27:1295-300; [PubMed] [Cross Ref]
[139] Goldfarb AH, Jamurtas AZ.. Beta-endorphin response to exercise. An update. Sports Med 1997; 24:8-16; PMID:9257407; [PubMed] [Cross Ref]
[140] Fell GL, Robinson KC, Mao J, Woolf CJ, Fisher DE.. Skin Beta-Endorphin Mediates Addiction UV Light. Cell 2014; 157:1527-34; PMID:24949966; [PMC free article] [PubMed] [Cross Ref]
[141] Kroll MH, Bi C, Garber CC, Kaufman HW, Liu D, Caston-Balderrama A, Zhang K, Clarke N, Xie M, Reitz RE, et al. Temporal relationship between vitamin D status and parathyroid hormone in the United States. PLoS One 2015; 10(3):e0118108; PMID:25738588; [PMC free article] [PubMed] [Cross Ref]

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