Shop Vitamark Products

The February Health Show call hosted by Diamond Affiliate, Meme Groseth(MG) and Vitamark Vice President, Tom Mitcham(TM)is all about our wonderful Calcium product, Coral Calcium:

MG: Are you there Tommy?

TM: I sure am Meme, and I can't wait to give that free product. Tonight's free product is our Coral Calcium+ product--certainly a product that I hope everyone on this call is familiar with. Our Coral Calcium+ product contains 2 powerful, bioavailable forms of calcium: Coral Calcium and our special patented processed Amino Acid Chelate from eggshell calcium. It contains 2600 mgs of calcium raw materials to yield a full 1000mg of "elemental calcium"(this is the form in which the body uses calcium).* Calcium and Vit D3 are both elements found in Vitamark's Coral Calcium. Both Vit D3 andCalcium have been found in a four-year randomized study conducted by Creighton University School of Medicine to offer women taking them a "60% or greater reduction in cancer risk than women who did not get these two supplements ."* This based on tests conducted between 2000 and 2005 and reported in the June 8, 2007, online edition of the American Journal of Clinical Nutrition.

MG: I am really excited about this free product--as should everyone on
this call be-- especially if you are on the 100BP Autoship because the
Coral Calcium+ is the Feb free AutoShip product. This amazing product has many benefits from strong bones and teeth to alkalizing the body to assisting with immune function.* Research has shown calcium to be an effective tool in weight management,as well.* This powerful product includes magnesium, potassium, boron and Vit D3 to facilitate bioavailability and effectiveness!*

TM: Now to give that free product! Don't forget to call out your name before answering. Now for the first question from the current Vitamark E-News.

TM:
Q1: What group was the top Platinum group?
Ans: Jarvis Leadership Group
Winner:

Q2: Who had the top Personal Group?
Ans: Greg Leimbach
Winner:

Q3: Who recently sent a letter to David Bertrand and said, Im still amazed at the things that Vitamark does to help us succeed, to build our belief and help us to reach our dreams.?
Ans: 4 Star Platinum, Nicki Tompkins
Winner

Q4: Who was the young couple who qualified in June of 1977 for a trip to Paris?
Ans: David and Judy Bertrand
Winnner:

Q5: How can you go to Paris in Sept. of 2009?
Ans: Qualify for Vitamarks 2009 Leadership Trip.
Winner:

MG: Congratulations to all our winners-don't forget to call the home office to claim your free Coral Calcium+.

MG: Tommy, we are going talk about the coral calcium product tonight.

TM: Coral calcium is the hottest source for one of the minerals most critical to your bodys health. Vitamarks Coral Calcium+ combines 1 gram (1000 mg) of pure coral with amino acid chelated eggshell calcium, Vitamin D3, magnesium, potassium and boron per serving. The formulation is super-charged by the addition of EnZact 77k, Vitamarks exclusive enzymatic activation and delivery.
Why does coral have such a reputation as a health supplement able to deliver numerous health improvements?* Coral contains high amounts of calcium and virtually every mineral found in the human bodyand in similar proportions as those found in the human body, too. We cannot always get the minerals from our food source. In fact, much of the soil used in food production is mineral depleted. Coral minerals may be one of the most effective ways to put minerals into the blood because of the high absorbability of the minerals. Coral minerals are a full spectrum, organic, ionic, synergistic blend of seventy-four minerals.


MG: Our coral calcium is harvested from eco-friendly above sea sources in Okinawa. We archaeologically harvest only the pristine white coral heads in an ecologocially sound process that does not touch or alter the fragile state of the coral reefs and ocean environment. After it is collected, the coral is ground to a micron size to facilitate absorption and then purified.


TM: Our amino acid chelate calcium is processed from eggshell using a chemical-free, patented process that produces custom particle sizes for maximum absorption! The resulting amino acid chelate contains more than a dozen amino acids, including Glutamic Acid, Proline, Lysine, Valine, Threonine, Leucine, Isoleucine, Tyrosine, Aspartic Acid, Arginine and Alanine. In fact, the quality of our amino acid chelated eggshell calcium is so high that it meets the tough leadfree requirements of Californias Proposition 65.

TM: Calcium, the most abundant mineral in the human body, has several important functions. More than 99% of total body calcium is stored in the bones and teeth where it functions to support their structure [1]*. The remaining 1% is found throughout the body in blood, muscle, and the fluid between cells. Calcium is needed for muscle contraction, blood vessel contraction and expansion, the secretion of hormones and enzymes, and sending messages through the nervous system [2].* A constant level of calcium is maintained in body fluid and tissues so that these vital body processes function efficiently. *

MG: Calcium plays a role in a myriad of systems of the body like the skeletal system:*
Your bones are living tissues and continue to change throughout life. During childhood and adolescence, bones increase in size and mass. Bones continue to add more mass until around age 30, when peak bone mass is reached. Peak bone mass is the point when the maximum amount of bone is achieved. Because bone loss, like bone growth, is a gradual process, the stronger your bones are at age 30, the more your bone loss will be delayed as you age. Therefore, it is particularly important to consume adequate calcium and vitamin D throughout infancy, childhood, and adolescence.* It is also important to engage in weight-bearing exercise to maximize bone strength and bone density (amount of bone tissue in a certain volume of bone) to help prevent osteoporosis later in life. Weight bearing exercise is the type of exercise that causes your bones and muscles to work against gravity while they bear your weight. Resistance exercises such as weight training are also important because they help to improve muscle mass and bone strength.

Examples of weight bearing exercise
walking
running
dancing
aerobics
skating

Examples of NON-weight bearing exercise
swimming
bicycyling
water aerobics

(TM): Calcium is important in the treatment of osteopenia, osteoporosis, maintenance of normal blood pressure, colon cancer, kidney stones and weight management.*

Osteoporosis and osteopenia can result from dietary factors such as [11,24,25]:
chronically low calcium intake
low vitamin D intake
poor calcium absorption
excess calcium excretion*[all of the above]

When calcium intake is low or calcium is poorly absorbed, bone breakdown occurs because the body must use the calcium stored in bones to maintain normal biological functions such as nerve and muscle function. Bone loss also occurs as a part of the aging process. A prime example is the loss of bone mass observed in post-menopausal women because of decreased amounts of the hormone estrogen. Researchers have identified many factors that increase the risk for developing osteoporosis. These factors include being female, thin, inactive, of advanced age, cigarette smoking, excessive intake of alcohol, and having a family history of osteoporosis [26]. *[all above]

In 1993 the FDA authorized a health claim for food labels on calcium and osteoporosis in response to scientific evidence that an inadequate calcium intake is one factor that can lead to low peak bone mass and is considered a risk factor for osteoporosis [27]. The claim states that "adequate calcium intake throughout life is linked to reduced risk of osteoporosis through the mechanism of optimizing peak bone mass during adolescence and early adulthood and decreasing bone loss later in life".*[all above]

Various bone mineral density (BMD) tests, including those that measure your hip, spine, wrist, finger, shin bone, and heel, can help determine bone mass. These tests provide a T-score which is a measure of bone mineral density that compares an individual's BMD to an optimal BMD of a 30 year old healthy adult. See Figure 2 below. A T-Score of -1.0 and above indicates normal bone density. A T-score of -1.0 to -2.5 indicates that a person is considered to have low bone mass (osteopenia). A score below -2.5 indicates osteoporosis [28].

Figure 2: Interpreting Bone Mineral Density Scores*




Although osteoporosis affects people of different races, genders and ethnicities, women are at highest risk because their skeletons are smaller to start with and because of the accelerated bone loss that accompanies menopause. Adequate calcium and vitamin D intakes, as well as weight bearing exercise are critical to the development and maintenance of healthy bone throughout the lifecycle. Older adults should strive to maintain recommended daily calcium intakes as well as an adequate vitamin D intake. *[above]

Calcium and high blood pressure
Some observational studies (type of research study in which the treatment/intervention is observed and not controlled by the researchers) and experimental studies (type of research study in which the researchers control the treatments/interventions and that are assigned to participants) indicate that individuals who eat a vegetarian diet high in minerals (including calcium, magnesium and potassium) and fiber, and low in fat, tend to have reduced blood pressure [29-31].*

Findings from some clinical trials (a specific type of experimental study) used to evaluate the effects of one or more treatments/interventions in humans) indicate that an increased calcium intake lowers blood pressure and the risk of hypertension (high blood pressure) [32,33]. However, the results of some studies produced small and inconsistent reductions in blood pressure. One reason for these results is because these research studies tended to test the effect of single nutrients rather than foods on blood pressure. *

To help test the combined effect of nutrients including calcium from food on blood pressure, a study was conducted to investigate the impact of various dietary eating patterns on blood pressure. This study titled "Dietary Approaches to Stop Hypertension (DASH)" was reported in 1997 by the National, Heart, Lung and Blood Institute of the National Institutes of Health. It investigated the effect of various eating patterns on lowering blood pressure. The DASH study was a multi-center research trial where food was provided to over 450 adults. It examined the effects of three different diets on high blood pressure: a control, "typical American" diet and two modified diets (high fruits-and-vegetables and a combination "DASH" diet - high in fruits, vegetables, and low fat dairy). See Table 3 for a comparison of some of the components of the three diets.*


*


Of the three diets tested, the combination "DASH" diet resulted in the greatest decrease in blood pressure [34]. Thus, this finding from a large and carefully executed clinical trial helped demonstrate that the combination "DASH" diet, with increased calcium, decreased blood pressure [35]. A number of further studies have been done, all showing a similar relationship between increasing calcium intakes and decreased blood pressure [36]. A study conducted after the original "DASH" study, referred to as the "DASH-Sodium" study showed that the DASH diet without sodium restriction provided as much blood pressure reduction as did severe sodium restriction on the control diet (1500 mg sodium/day) [37]. Overall it appears that consuming an adequate intake of fruits and vegetables as well as calcium from low fat dairy products plays a significant role in controlling blood pressure. Additional information and sample DASH menu plans are available on the National Heart, Lung and Blood Institute's Web site (https://www.nhlbi.nih.gov/health/public/heart/hbp/dash/index.htm).*[above]

Calcium and cancer*[all statements that follow]
Colorectal cancer
The relationship between calcium intake and the risk of colon cancer has not been conclusively determined. Observational and experimental research studies investigating the role calcium plays in the prevention of colon cancer show mixed results. Some studies suggest that increased intakes of dietary (low fat dairy sources) and supplemental calcium are associated with a decreased risk of colon cancer [38-41]. Supplementation with calcium carbonate is reported to lead to reduced risk of adenomas (nonmalignant tumors) in the colon, a precursor to colon cancer, but it is not known if this will ultimately translate into reduced cancer risk [42]. Another study reported on the association between diet and colon cancer history in 135,000 men and women participating in two large health surveys, the Nurses' Health Study and the Physicians' Health Study. The authors found that those who consumed 700 to 800 mg calcium per day had a 40 to 50% lower risk of developing left side colon cancer [43]. However, a few other observational studies found inconclusive evidence regarding any association of calcium intake with colon cancer [44-46]. Although some research findings indicate a protective effect of calcium or low fat dairy foods against colon cancer, further studies are necessary to confirm this role for calcium.

Prostate cancer*[all]
There is some evidence to suggest that higher calcium (ranging from 600 mg to >2000 mg of calcium) and/or dairy intakes (>2.5 servings) may be associated with the development of prostate cancer [47-50]. However, these studies are observational in nature rather than clinical trials and cannot establish a definite causal relationship between calcium and prostate cancer. Other findings only show a weak relationship, no relationship at all or the opposite relationship between calcium and prostate cancer [51-54]. Thus, the relationship between calcium intake, dairy intake and prostate cancer risk remains unclear. At the present time, it is recommended that men ages 19 and over consume a "modest" intake of calcium ranging from 1000-1200 mg per day and maintain an intake below the upper tolerable limit (2500 mg) [1].

Calcium and kidney stones*[all]
Kidney stones are crystallized deposits of calcium and other minerals in the urinary tract. Calcium oxalate stones are the most common form of kidney stones in the US. High calcium intakes or high calcium absorption were previously thought to contribute to the development of kidney stones. However, more recent studies show that high dietary calcium intakes actually decrease the risk for kidney stones [55-57]. Other factors such as high oxalate intake and reduced fluid consumption appear to be more of a risk factor in the formation of kidney stones than calcium in most individuals [58].

Calcium and weight management*[all]
Several studies, primarily observational in nature, have linked higher calcium intakes to lower body weights or less weight gain over time [59-62]. Two explanations have been proposed for how calcium may help to regulate body weight. First, high-calcium intakes may reduce calcium concentrations in fat cells by lowering the production of two hormones (parathyroid hormone and an active form of vitamin D), which in turn increases fat breakdown in these cells and discourages its accumulation [61]. In addition, calcium from food or supplements may bind to small amounts of dietary fat in the digestive tract and prevent its absorption, carrying the fat (and the calories it would otherwise provide) out in the feces [61,63].

Dairy products in particular may contain additional components that have even greater effects on body weight than their calcium content alone would suggest [64-69]. Three small, recently published clinical trials show that calcium-rich dairy products may help obese individuals following reduced-calorie diets to lose some excess weight and fat [67-69]. In one trial, 32 obese adults were randomized to one of three groups: eating a standard diet providing 400-500 mg calcium, eating a standard diet supplemented with 800 mg calcium, and eating a diet with 3 servings/day of dairy products to provide 1,200-1,300 mg calcium [67]. The subjects ate 500 fewer calories a day over the 24 weeks of the study. All lost weight and body fat, but those taking the calcium supplements lost significantly more than subjects eating the unsupplemented standard diet, and those on the high-dairy diet lost by far the most. Dairy products also favorably affected body composition in a small group of obese African-American adults who followed a weight-maintenance program for 24 weeks [69]. Subjects who ate 3 servings/day of dairy products, which increased calcium intakes to 1,200 mg/day, lost significantly more fat (both total body and abdominal) and preserved lean body mass as compared to those who consumed less than one daily serving of these foods and 500 mg/day total calcium.*[all]

Despite the hopeful results of these studies, other recent clinical trials make it clear that the involvement of calcium and dairy products in weight regulation and body composition is complex, inconsistent, and not well understood [61,70]. For example, one study in young women of normal body weight found that higher intakes of dairy products had no effect on weight or fat mass over the course of one year [71]. Another study in which 100 overweight and obese pre- and post-menopausal women on reduced-calorie diets received either 1,000 mg/day calcium or a placebo for 25 weeks found no significant differences in weight or fat loss between the groups [72]. Similar results were obtained in a study of 1,471 postmenopausal women (somewhat overweight on average) who were randomly assigned to take 1,000 mg/day calcium or a placebo for 30 months, though there was a trend toward greater weight loss in those who took the calcium supplement and whose calcium intakes from food averaged less than 600 mg/day [73]. Clearly, larger clinical trials are needed to better assess the effects of calcium and dairy products on body weight, composition, and fat distribution [61,74].*[all]

Is there a health risk of too much calcium?
The Tolerable Upper Limit (UL) is the highest level of daily intake of calcium from food, water and supplements that is likely to pose no risks of adverse health effects to almost all individuals in the general population [2]. The UL for children and adults ages 1 year and older (including pregnant and lactating women) is 2500 mg/day. It was not possible to calculate an upper limit for infants 1 year and younger.

Tm: Our Coral Calcium also contains Vitamin D3:
Vitamin D3 is one of the most useful nutritional tools we have at our disposal for improving overall health. This vitamin is unique because cholecalciferol (Vitamin D3) acquires hormone-like actions when cholecalciferol (Vitamin D3) is converted to 1,25-dihydroxy Vitamin D3 (Calcitriol) by the liver and kidneys. As a hormone, Calcitriol controls phosphorus, calcium, and bone metabolism and neuromuscular function. Vitamin D3 is the only vitamin the body can manufacture from sunlight (UVB). Yet, with todays indoor living and the extensive use of sunscreens due to concern about skin cancer, we are now a society with millions of individuals deficient in life-sustaining bone building and immune modulating 1,25-dihydroxy Vitamin D3.*[all]

For more than a century, scientists have recognized that Vitamin D3 is involved in bone health. Research has continued to accumulate, documenting Calcitriols role in the reduction of the risk of fractures to a significant degree. The latest research, however, shows that 1,25-dihyroxy Vitamin D3 deficiency is linked to a surprising number of other health conditions such as depression, back pain, cancer, both insulin resistance and pre-eclampsia during pregnancy, impaired immunity and macular degeneration.*[all]

As it becomes clear that Vitamin D3 plays a wide role in overall health, its becoming equally clear that a large percentage of individuals are deficient in this important nutrient, which has hormone-like activity. The fear of skin cancer has stopped many individuals from obtaining beneficial amounts of sunlight. The skin uses the energy of UVB to convert 7-dehydrocholesterol into Vitamin D3. Even individuals, who venture out into the sun often and use suntan lotion, may be deficient in Vitamin D3. Furthermore, as we age, we are less equipped to produce sufficient quantities of this vital nutrient. One study found that age-related declines in kidney function may require older people to ingest more Vitamin D3 to maintain the same blood levels as younger people.1*[all]

The Recommended Daily Intake (RDI) of Vitamin D3 is set so low those mature individuals who consume this small amount (400 to 600 International Unites (I.U.s)) are still likely to be deficient if they live north of the Tropic of Cancer or south of the Tropic of Capricorn. In fact, researchers have discovered that the RDI, which was considered adequate to prevent osteomalacia (a painful bone disease) or rickets, is not high enough to protect against the majority of diseases linked to 1,25-dihyroxy Vitamin D3 deficiency. For example, an analysis of the medical literature found that at least 1,000 to 2,000 IU of Vitamin D3 per day is necessary to reduce the risk of colorectal cancer and that lower doses of Vitamin D3 did not have the same protective effect.2*[all]

Researchers Call for Higher Doses*[All]

In an editorial in the March 2007 edition of the American Journal of Clinical Nutrition, a prominent group of researchers from leading institutions such as the University of Toronto, Brigham and Womens Hospital, Tufts University and University Hospital in Zurich, Switzerland, lashed out at the conventional media for its inaccurate reporting of Vitamin D supplementation.3

The researchers wrote, Almost every time the public media report that Vitamin D nutrition status is too low, or that higher Vitamin D intakes may improve measures of health, the advice that accompanies the report is outdated and thus misleading. Media reports to the public are typically accompanied by a paragraph that approximates the following: Current recommendations from the Institute of Medicine call for 200 IU/day from birth through age 50 years, 400 IU for those aged 5170 years, and 600 IU for those aged >70 years. Some experts say that optimal amounts are closer to 1,000 IU daily. Until more is known, it is wise not to overdo it. The only conclusion that the public can draw from this is to do nothing different from what they have done in the past.

The researchers point out that supplemental intake of 400 IU per day barely raises blood concentrations of 25(OH)D, which is the circulating Vitamin D metabolite that serves as the most frequently measured indicator of Vitamin D status. To raise 25(OH)D from 50 to 80 nmol/L requires an additional intake of 1,700 IU Vitamin D per day.

The researchers went on to write that, The balance of the evidence leads to the conclusion that the public health is best served by a recommendation of higher daily intakes of Vitamin D. Relatively simple and low-cost changes, such as increased food fortification or increasing the amount of Vitamin D in Vitamin supplement products, may very well bring about rapid and important reductions in the morbidity associated with low Vitamin D status.

One of the challenges is the outdated acceptable upper limit for Vitamin D3 consumption, which was set at 2,000 IU. However, researchers point out that more recent studies have shown that 10,000 IU is the safe upper limit.4

Dr. R. Vieth, one of the foremost authorities on Vitamin D3 supplementation, has extensively studied Vitamin D, and lamented the low requirements for Vitamin D3 in a recent issue of the Journal of Nutrition: Inappropriately low UL [upper limit] values, or guidance values, for Vitamin D have hindered objective clinical research on Vitamin D nutrition; they have hindered our understanding of its role in disease prevention, and restricted the amount of Vitamin D in multivitamins and foods to doses (that are) too low to benefit public health.5

MG: When examining the medical literature, it becomes clear that Vitamin D3 affects human health in an astonishing number of ways and that not obtaining enough of this important nutrient can leave the door open to developing a number of health conditions like depression, back pain, bone health, cognitive enhancement, cancer and immunity.6-14 Low levels of D3 are also related to high blood pressure, fibromyalgia, multiple sclerosis, rheumatoid arthritis, diabetes and the prevalence of early age related macular degeneration.11, 15-17 See more info in Janas Corner.*[all]

D3 effects the following areas of health:*[all]

Depression*

Vitamin D3 deficiency is common in older adults and has been implicated in psychiatric and neurologic disorders. For example, in one study of 80 older adults (40 with mild Alzheimers disease and 40 nondemented persons), Vitamin D3 deficiency was associated with low mood and with impairment on two of four measures of cognitive performance.6

Back Pain*

Musculoskeletal disorders have been linked to Vitamin D3 deficiency in a number of studies. One of the newest studies explored the role that low Vitamin D3 levels play in the development of chronic low back pain in women. Sixty female patients in Egypt complaining of low back pain lasting more than three months were studied. Researchers measured levels of Vitamin D3 in the women with low back pain and compared those levels to those of 20 matched healthy controls.

The study revealed that patients with low back pain had significantly lower Vitamin D3 levels than controls. Low Vitamin D3 levels (25 OHD < 40 ng/ml) were found in 49/60 patients (81 percent) and 12/20 (60 percent) of controls.7

Bone Health*

One of the best known and long-established benefits of Vitamin D3 is its ability to improve bone health and the health of the musculoskeletal system. It is well documented that Vitamin D3 deficiency causes osteopenia, precipitates and exacerbates osteoporosis, causes a painful bone disease known as osteomalacia, and exacerbates muscle weakness, which increases the risk of falls and fractures. Vitamin D3 insufficiency may alter the regulatory mechanisms of parathyroid hormone (PTH) and cause a secondary hyperparathyroidism that increases the risk of osteoporosis and fractures.8

Cognitive Enhancement*

Scientists are developing a greater appreciation for Vitamin D3s ability to improve cognition. In a recent study, Vitamin D3 deficient subjects scored worse on mental function tests compared to individuals who had higher levels of the Vitamin.9 The researchers wrote, In conclusion, the positive, significant correlation between serum 25(OH)D concentration and MMSE [mental state examination scores] in these patients suggests a potential role for Vitamin D in cognitive function of older adults.

Cancer*

One researcher first noted the connection between Vitamin D3 and protection from cancer in the 1940s, when he discovered that individuals at sunny latitudes had a reduced rate of deaths from cancer. He suggested that sunlight provided a relative cancer immunity.
Since then, a number of studies have strongly suggested that Vitamin D3 deficiency is associated with an increased risk of developing many forms of cancer including breast, ovarian, prostate and colon cancer.10 In one recent clinical trial, researchers studied 1,179 healthy, postmenopausal women (all 55 years or older and free of known cancers for at least 10 years prior to entering the study) who were taking large amounts of Vitamin D3 with calcium. The subjects were randomly assigned to take daily dosages of: (1) 1,400-1,500 mg supplemental calcium, (2) 1,400-1,500 mg supplemental calcium plus 1,100 IU of Vitamin D3, or (3) placebos. Over the four-year trial, women in the calcium/Vitamin D3 group experienced a 60 percent or greater reduced risk of cancer than their peers in the placebo group, who were not consuming these supplements.

Because there was the chance that some women may have had undiagnosed cancers at the studys start, the researchers threw out the first-year results and then analyzed the results from the last three years of the trial. These later years resulted in even more dramatic decrease, with the calcium/Vitamin D3 group experiencing a 77 percent reduction in cancer risk.

There was no statistically significant difference in cancer incidence between the participants taking placebos and subjects consuming only calcium supplements.11

Another interesting study demonstrated that in vitro Vitamin D3 may cause tumor cells to be more sensitive to chemotherapy drugs, increasing the efficacy of the cancer treatment.12

Immunity*

Scientists have linked various aspects of immune health to a Vitamin D3 deficiency. Vitamin D3 regulates T cells, which are important to the functioning of a strong immune system. Vitamin D3 acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the killing efficiency of macrophages. In addition, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in immune system cells such as neutrophils, monocytes, natural killer cells, and in cells lining the respiratory tract. These Vitamin-D3-stimulated peptides play a major role in protecting the lung from infection.13

In addition, Vitamin D3 deficiency may influence development and progression of various autoimmune diseases.14

Multi-Talented Nutrient*

Vitamin D3 deficiency has been linked to a host of other conditions such as high blood pressure, fibromyalgia, diabetes, multiple sclerosis, rheumatoid arthritis, and an increased risk of pre-eclampsia and insulin resistance during pregnancy.11,15-16 Most recently, low Vitamin D3 levels have been linked to an increased prevalence of early age-related macular degeneration.17

Proper Dosage*

In many of my patients, even after consuming 2,000 to 4,000 IU of Vitamin D3 per day, their test results indicate that their Vitamin D3 levels have not increased. These patients needed to consume 8,000 IU of Vitamin D3 per day to achieve proper blood levels of the Vitamin. Patients should, therefore, have their physicians test their serum 1,25-dihyroxy D3 levels to determine the proper level of supplementation required. Testing is very important due to the fact that, in a small number of patients, Vitamin D3 supplementation can raise calcium levels to an excessively high level. I have found this to be especially true in African American patients. Testing for 1,25-dihyroxy Vitamin D3, PTH and calcium blood levels should therefore become a part of every womans regular blood work.

Conclusion*

A growing number of researchers who have widely studied Vitamin D3 are almost begging the general public to consume more of this important nutrient. Due to Vitamin D3s high safety profile in doses up to 10,000 IU per day and because of the wide role it plays in our health, consuming 2,000 to 4,000 IU per day of this nutrient at times of the year when sunlight is scarce is a prudent way to improve overall health.

TM:Our Coral Calcium contains magnesium:

TM: Magnesium is the fourth most abundant mineral in the body and is essential to good health. Approximately 50% of total body magnesium is found in bone. The other half is found predominantly inside cells of body tissues and organs. Only 1% of magnesium is found in blood, but the body works very hard to keep blood levels of magnesium constant [1].*

TM: Magnesium is needed for more than 300 biochemical reactions in the body. It helps maintain normal muscle and nerve function, keeps heart rhythm steady, supports a healthy immune system, and keeps bones strong. Magnesium also helps regulate blood sugar levels, promotes normal blood pressure, and is known to be involved in energy metabolism and protein synthesis [2-3]. There is an increased interest in the role of magnesium in preventing and managing disorders such as hypertension, cardiovascular disease, and diabetes. More info in Janas Corner.*

*

*
*

Magnesium impacts:*[all]
Magnesium and blood pressure*
"Epidemiologic evidence suggests that magnesium may play an important role in regulating blood pressure [4]." Diets that provide plenty of fruits and vegetables, which are good sources of potassium and magnesium, are consistently associated with lower blood pressure [31-33]. The DASH study (Dietary Approaches to Stop Hypertension), a human clinical trial, suggested that high blood pressure could be significantly lowered by a diet that emphasizes fruits, vegetables, and low fat dairy foods. Such a diet will be high in magnesium, potassium, and calcium, and low in sodium and fat [34-36].

An observational study examined the effect of various nutritional factors on incidence of high blood pressure in over 30,000 US male health professionals. After four years of follow-up, it was found that a lower risk of hypertension was associated with dietary patterns that provided more magnesium, potassium, and dietary fiber [37]. For 6 years, the Atherosclerosis Risk in Communities (ARIC) Study followed approximately 8,000 men and women who were initially free of hypertension. In this study, the risk of developing hypertension decreased as dietary magnesium intake increased in women, but not in men [38].

Foods high in magnesium are frequently high in potassium and dietary fiber. This makes it difficult to evaluate the independent effect of magnesium on blood pressure. However, newer scientific evidence from DASH clinical trials is strong enough that the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that diets that provide plenty of magnesium are positive lifestyle modifications for individuals with hypertension. This group recommends the DASH diet as a beneficial eating plan for people with hypertension and for those with "prehypertension" who desire to prevent high blood pressure https://www.nhlbi.nih.gov/health/public/heart/hbp/dash/ [39-41].

Magnesium and diabetes*
Diabetes is a disease resulting in insufficient production and/or inefficient use of insulin. Insulin is a hormone made by the pancreas. Insulin helps convert sugar and starches in food into energy to sustain life. There are two types of diabetes: type 1 and type 2. Type 1 diabetes is most often diagnosed in children and adolescents, and results from the body's inability to make insulin. Type 2 diabetes, which is sometimes referred to as adult-onset diabetes, is the most common form of diabetes. It is usually seen in adults and is most often associated with an inability to use the insulin made by the pancreas. Obesity is a risk factor for developing type 2 diabetes. In recent years, rates of type 2 diabetes have increased along with the rising rates of obesity.

Magnesium plays an important role in carbohydrate metabolism. It may influence the release and activity of insulin, the hormone that helps control blood glucose (sugar) levels [13]. Low blood levels of magnesium (hypomagnesemia) are frequently seen in individuals with type 2 diabetes. Hypomagnesemia may worsen insulin resistance, a condition that often precedes diabetes, or may be a consequence of insulin resistance. Individuals with insulin resistance do not use insulin efficiently and require greater amounts of insulin to maintain blood sugar within normal levels. The kidneys possibly lose their ability to retain magnesium during periods of severe hyperglycemia (significantly elevated blood glucose). The increased loss of magnesium in urine may then result in lower blood levels of magnesium [4]. In older adults, correcting magnesium depletion may improve insulin response and action [42].

The Nurses' Health Study (NHS) and the Health Professionals' Follow-up Study (HFS) follow more than 170,000 health professionals through biennial questionnaires. Diet was first evaluated in 1980 in the NHS and in 1986 in the HFS, and dietary assessments have been completed every 2 to 4 years since. Information on the use of dietary supplements, including multivitamins, is also collected. As part of these studies, over 127,000 research subjects (85,060 women and 42,872 men) with no history of diabetes, cardiovascular disease, or cancer at baseline were followed to examine risk factors for developing type 2 diabetes. Women were followed for 18 years; men were followed for 12 years. Over time, the risk for developing type 2 diabetes was greater in men and women with a lower magnesium intake. This study supports the dietary recommendation to increase consumption of major food sources of magnesium, such as whole grains, nuts, and green leafy vegetables [43].

The Iowa Women's Health Study has followed a group of older women since 1986. Researchers from this study examined the association between women's risk of developing type 2 diabetes and intake of carbohydrates, dietary fiber, and dietary magnesium. Dietary intake was estimated by a food frequency questionnaire, and incidence of diabetes throughout 6 years of follow-up was determined by asking participants if they had been diagnosed by a doctor as having diabetes. Based on baseline dietary intake assessment only, researchers' findings suggested that a greater intake of whole grains, dietary fiber, and magnesium decreased the risk of developing diabetes in older women [44].

The Women's Health Study was originally designed to evaluate the benefits versus risks of low-dose aspirin and vitamin E supplementation in the primary prevention of cardiovascular disease and cancer in women 45 years of age and older. In an examination of almost 40,000 women participating in this study, researchers also examined the association between magnesium intake and incidence of type 2 diabetes over an average of 6 years. Among women who were overweight, the risk of developing type 2 diabetes was significantly greater among those with lower magnesium intake [45]. This study also supports the dietary recommendation to increase consumption of major food sources of magnesium, such as whole grains, nuts, and green leafy vegetables.

On the other hand, the Atherosclerosis Risk in Communities (ARIC) study did not find any association between dietary magnesium intake and the risk for type 2 diabetes. During 6 years of follow-up, ARIC researchers examined the risk for type 2 diabetes in over 12,000 middle-aged adults without diabetes at baseline examination. In this study, there was no statistical association between dietary magnesium intake and incidence of type 2 diabetes in either black or white research subjects [46]. It can be confusing to read about studies that examine the same issue but have different results. Before reaching a conclusion on a health issue, scientists conduct and evaluate many studies. Over time, they determine when results are consistent enough to suggest a conclusion. They want to be sure they are providing correct recommendations to the public.

Several clinical studies have examined the potential benefit of supplemental magnesium on metabolic control of type 2 diabetes. In one such study, 63 subjects with below normal serum magnesium levels received either 2.5 grams of oral magnesium chloride daily "in liquid form" (providing 300 mg elemental magnesium per day) or a placebo. At the end of the 16-week study period, those who received the magnesium supplement had higher blood levels of magnesium and improved metabolic control of diabetes, as suggested by lower Hemoglobin A1C levels, than those who received a placebo [47]. Hemoglobin A1C is a test that measures overall control of blood glucose over the previous 2 to 3 months, and is considered by many doctors to be the single most important blood test for diabetics.

In another study, 128 patients with poorly controlled type 2 diabetes were randomized to receive a placebo or a supplement with either 500 mg or 1000 mg of magnesium oxide (MgO) for 30 days. All patients were also treated with diet or diet plus oral medication to control blood glucose levels. Magnesium levels increased in the group receiving 1000 mg magnesium oxide per day (equal to 600 mg elemental magnesium per day) but did not significantly change in the placebo group or the group receiving 500 mg of magnesium oxide per day (equal to 300 mg elemental magnesium per day). However, neither level of magnesium supplementation significantly improved blood glucose control [48].

These studies provide intriguing results but also suggest that additional research is needed to better explain the association between blood magnesium levels, dietary magnesium intake, and type 2 diabetes. In 1999, the American Diabetes Association (ADA) issued nutrition recommendations for diabetics stating that "routine evaluation of blood magnesium level is recommended only in patients at high risk for magnesium deficiency. Levels of magnesium should be repleted (replaced) only if hypomagnesemia can be demonstrated" [21].

Magnesium and cardiovascular disease*
Magnesium metabolism is very important to insulin sensitivity and blood pressure regulation, and magnesium deficiency is common in individuals with diabetes. The observed associations between magnesium metabolism, diabetes, and high blood pressure increase the likelihood that magnesium metabolism may influence cardiovascular disease [49].

Some observational surveys have associated higher blood levels of magnesium with lower risk of coronary heart disease [50-51]. In addition, some dietary surveys have suggested that a higher magnesium intake may reduce the risk of having a stroke [52]. There is also evidence that low body stores of magnesium increase the risk of abnormal heart rhythms, which may increase the risk of complications after a heart attack [4]. These studies suggest that consuming recommended amounts of magnesium may be beneficial to the cardiovascular system. They have also prompted interest in clinical trials to determine the effect of magnesium supplements on cardiovascular disease.

Several small studies suggest that magnesium supplementation may improve clinical outcomes in individuals with coronary disease. In one of these studies, the effect of magnesium supplementation on exercise tolerance, exercise-induced chest pain, and quality of life was examined in 187 patients. Patients received either a placebo or a supplement providing 365 milligrams of magnesium citrate twice daily for 6 months. At the end of the study period researchers found that magnesium therapy significantly increased magnesium levels. Patients receiving magnesium had a 14 percent improvement in exercise duration as compared to no change in the placebo group. Those receiving magnesium were also less likely to experience exercise-induced chest pain [53].

In another study, 50 men and women with stable coronary disease were randomized to receive either a placebo or a magnesium supplement that provided 342 mg magnesium oxide twice daily. After 6 months, those who received the oral magnesium supplement were found to have improved exercise tolerance [54].

In a third study, researchers examined whether magnesium supplementation would add to the anti-thrombotic (anti-clotting) effects of aspirin in 42 coronary patients [55]. For three months, each patient received either a placebo or a supplement with 400 mg of magnesium oxide two to three times daily. After a four-week break without any treatment, treatment groups were reversed so that each person in the study then received the alternate treatment for three months. Researchers found that supplemental magnesium did provide an additional anti-thrombotic effect.

These studies are encouraging, but involved small numbers. Additional studies are needed to better understand the complex relationships between magnesium intake, indicators of magnesium status, and heart disease. Doctors can evaluate magnesium status when above-mentioned medical problems occur, and determine the need for magnesium supplementation.

Magnesium and osteoporosis*
Bone health is supported by many factors, most notably calcium and vitamin D. However, some evidence suggests that magnesium deficiency may be an additional risk factor for postmenopausal osteoporosis [4]. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium (20). Several human studies have suggested that magnesium supplementation may improve bone mineral density [4]. In a study of older adults, a greater magnesium intake maintained bone mineral density to a greater degree than a lower magnesium intake [56]. Diets that provide recommended levels of magnesium are beneficial for bone health, but further investigation on the role of magnesium in bone metabolism and osteoporosis is needed.

MG: Coral Calcium also contains Selenium:*
MG: Selenium is a trace mineral that is essential to good health but required only in small amounts [1,2]. Selenium is incorporated into proteins to make selenoproteins, which are important antioxidant enzymes. The antioxidant properties of selenoproteins help prevent cellular damage from free radicals. Free radicals are natural by-products of oxygen metabolism that may contribute to the development of chronic diseases such as cancer and heart disease [2,3]. Other selenoproteins help regulate thyroid function and play a role in the immune system [4-7].

MG: Selenium is involved in the remediation of cancer [34-45], heart disease[46-49], arthritis[50-55], and HIV[56-61] See studies in Janas Corner.
*

Selenium effects:*[all]

Selenium and cancer*
Observational studies indicate that death from cancer, including lung, colorectal, and prostate cancers, is lower among people with higher blood levels or intake of selenium [34-40]. In addition, the incidence of nonmelanoma skin cancer is significantly higher in areas of the United States with low soil selenium content [37]. The effect of selenium supplementation on the recurrence of different types of skin cancers was studied in seven dermatology clinics in the U.S. from 1983 through the early 1990s. Taking a daily supplement containing 200 ?g of selenium did not affect recurrence of skin cancer, but significantly reduced the occurrence and death from total cancers. The incidence of prostate cancer, colorectal cancer, and lung cancer was notably lower in the group given selenium supplements [41].

Research suggests that selenium affects cancer risk in two ways. As an anti-oxidant, selenium can help protect the body from damaging effects of free radicals. Selenium may also prevent or slow tumor growth. Certain breakdown products of selenium are believed to prevent tumor growth by enhancing immune cell activity and suppressing development of blood vessels to the tumor [42].

However, not all studies have shown a relationship between selenium status and cancer. In 1982, over 60,000 participants of the Nurse's Health Study with no history of cancer submitted toenail clippings for selenium analysis. Toenails are thought to reflect selenium status over the previous year. After three and a half years of data collection, researchers compared toenail selenium levels of nurses with and without cancer. Those nurses with higher levels of selenium in their toenails did not have a reduced risk of cancer [43].

Two important long-term studies, the SU.VI.MAX study in France and the Selenium and Vitamin E Cancer Prevention Trial (SELECT) study in the U.S., are now underway to further investigate the selenium/cancer prevention link.

The SU.VI.MAX Study is a prevention trial looking at the effects of antioxidant vitamins and minerals on chronic diseases such as cancer and cardiovascular disease. Doses of the nutrients provided in the study are one to three times higher than recommended intakes, including a daily supplement of 100 ?g selenium. The SU.VI.MAX study, which began in 1994, has followed more than 12,000 adult men and women. This study was designed to continue for eight years, and the research community is eagerly awaiting the results of this study [44].

The SELECT study, a long-term study sponsored by the NIH, is investigating whether supplemental selenium and/or vitamin E can decrease the risk of prostate cancer in healthy men. Past evidence as well as pre-clinical trials for the SELECT study suggests that these two nutrients may be effective in preventing prostate cancer. A daily supplement containing 200 ?g of selenium will be given to individuals in the selenium-only study group, while men in the combined-nutrients group will receive a daily supplement containing 200 ?g selenium and 400 mg vitamin E. The study, which will span from 2001 to 2013, will include 32,400 healthy adult men [45].

Selenium and heart disease*
Some population surveys have suggested an association between lower antioxidant intake and a greater incidence of heart disease [46]. Evidence also suggests that oxidative stress from free radicals, which are natural by-products of oxygen metabolism, may promote heart disease [47-49]. For example, it is the oxidized form of low-density lipoproteins (LDL, often called "bad" cholesterol) that promotes plaque build-up in coronary arteries [48]. Selenium is one of a group of antioxidants that may help limit the oxidation of LDL cholesterol and thereby help to prevent coronary artery disease [47-49]. Currently there is insufficient evidence available to recommend selenium supplements for the prevention of coronary heart disease; however, the SU.VI.MAX study mentioned earlier is looking at the effects of antioxidant nutrients such as selenium on heart disease.

Selenium and arthritis*
Surveys indicate that individuals with rheumatoid arthritis, a chronic disease that causes pain, stiffness, swelling, and loss of function in joints, have reduced selenium levels in their blood [50-51]. In addition, some individuals with arthritis have a low selenium intake [52].

The body's immune system naturally makes free radicals that can help destroy invading organisms and damaged tissue, but that can also harm healthy tissue [53]. Selenium, as an antioxidant, may help to relieve symptoms of arthritis by controlling levels of free radicals [54]. Current findings are considered preliminary, and further research is needed before selenium supplements can be recommended for individuals with arthritis.

Selenium and HIV*
HIV/AIDS malabsorption can deplete levels of many nutrients, including selenium. Selenium deficiency is associated with decreased immune cell counts, increased disease progression, and high risk of death in the HIV/AIDS population [55,56]. HIV/AIDS gradually destroys the immune system, and oxidative stress may contribute to further damage of immune cells. Antioxidant nutrients such as selenium help protect cells from oxidative stress, thus potentially slowing progression of the disease [57]. Selenium also may be needed for the replication of the HIV virus, which could further deplete levels of selenium [58].

An examination of 125 HIV-positive men and women linked selenium deficiency with a higher rate of death from HIV [59]. In a small study of 24 children with HIV who were observed for five years, those with low selenium levels died at a younger age, which may indicate faster disease progression [60]. Results of research studies have led experts to suggest that selenium status may be a significant predictor of survival for those infected with HIV [61].

Researchers continue to investigate the relationship between selenium and HIV/AIDS, including the effect of selenium levels on disease progression and mortality. There is insufficient evidence to routinely recommend selenium supplements for individuals with HIV/AIDS, but physicians may prescribe such supplements as part of an overall treatment plan. It is also important for HIV-positive individuals to consume recommended amounts of selenium in their diet.

TM: And lastly Coral Calcium contains Zinc:*

TM: Zinc is an essential mineral that is naturally present in some foods, added to others, and available as a dietary supplement. Zinc is also found in many cold lozenges and some over-the-counter drugs sold as cold remedies.

TM: Zinc is involved in numerous aspects of cellular metabolism. It is required for the catalytic activity of approximately 100 enzymes [1,2] and it plays a role in immune function [3,4], protein synthesis [4], wound healing [5], DNA synthesis [2,4], diarrhea[56-60], the common cold[61-66], age-related macular degeneration[67-70]and cell division [4]. Zinc also supports normal growth and development during pregnancy, childhood, and adolescence [68] and is required for proper sense of taste and smell [9]. A daily intake of zinc is required to maintain a steady state because the body has no specialized zinc storage system [10].

TM: With stars like calcium, D3, magnesium, selenium and zinc; its no wonder that the response to our Coral Calcium product is so great.*

MG: Tom its time to say goodnight.

TM: Does anyone have a closing testimonial that they would like to give before we say goodnight.

TESTIMONIALS

TM: Thank You and remember this is the day the Lord has made let us rejoice and be glad in it!

Zinc impacts:*

Immune function *
Severe zinc deficiency depresses immune function [44], and even mild to moderate degrees of zinc deficiency can impair macrophage and neutrophil functions, natural killer cell activity, and complement activity [45]. The body requires zinc to develop and activate T-lymphocytes [2,46]. Individuals with low zinc levels have shown reduced lymphocyte proliferation response to mitogens and other adverse alterations in immunity that can be corrected by zinc supplementation [45,47]. These alterations in immune function might explain why low zinc status has been associated with increased susceptibility to pneumonia and other infections in children in developing countries and the elderly [4851].

Wound healing*
Zinc helps maintain the integrity of skin and mucosal membranes [45]. Patients with chronic leg ulcers have abnormal zinc metabolism and low serum zinc levels [52], and clinicians frequently treat skin ulcers with zinc supplements [53]. The authors of a systematic review concluded that zinc sulfate might be effective for treating leg ulcers in some patients who have low serum zinc levels [54,55]. However, research has not shown that the general use of zinc sulfate in patients with chronic leg ulcers or arterial or venous ulcers is effective [54,55].

Diarrhea*
Acute diarrhea is associated with high rates of mortality among children in developing countries [56]. Zinc deficiency causes alterations in immune response that probably contribute to increased susceptibility to infections, such as those that cause diarrhea, especially in children [45].

Studies show that poor, malnourished children in India, Africa, South America, and Southeast Asia experience shorter courses of infectious diarrhea after taking zinc supplements [57]. The children in these studies received 440 mg of zinc a day in the form of zinc acetate, zinc gluconate, or zinc sulfate [57].

In addition, results from a pooled analysis of randomized controlled trials of zinc supplementation in developing countries suggest that zinc helps reduce the duration and severity of diarrhea in malnourished or zinc-deficient children [58]. Similar findings were reported in a meta-analysis published in 2008 and a 2007 review of zinc supplementation for preventing and treating diarrhea [59,60]. The effects of zinc supplementation on diarrhea in children with adequate zinc status, such as most children in the United States, are not clear.

The World Health Organization and UNICEF now recommend short-term zinc supplementation (20 mg of zinc per day, or 10 mg for infants under 6 months, for 1014 days) to treat acute childhood diarrhea [56].

The common cold*
The effect of zinc treatment on the severity or duration of cold symptoms is controversial. Researchers have hypothesized that zinc directly inhibits rhinovirus binding and replication in the nasal mucosa and suppresses inflammation [61,62]. However, no data are available to support this hypothesis [62].

In a randomized, double-blind, placebo-controlled clinical trial, 50 subjects (within 24 hours of developing the common cold) took a zinc acetate lozenge (13.3 mg zinc) or placebo every 23 wakeful hours. Compared with placebo, the zinc lozenges significantly reduced the duration of cold symptoms (cough, nasal discharge, and muscle aches) [63].

In another clinical trial involving 273 participants with experimentally induced colds, zinc gluconate lozenges (providing 13.3 mg zinc) significantly reduced the duration of illness compared with placebo but had no effect on symptom severity [64]. However, treatment with zinc acetate lozenges (providing 5 or 11.5 mg zinc) had no effect on either cold duration or severity. Neither zinc gluconate nor zinc acetate lozenges affected the duration or severity of cold symptoms in 281 subjects with natural (not experimentally induced) colds in another trial [64].

In 77 participants with natural colds, a combination of zinc gluconate nasal spray and zinc orotate lozenges (37 mg zinc every 23 wakeful hours) was also found to have no effect on the number of asymptomatic patients after 7 days of treatment [65].

In September of 2007, Caruso and colleagues published a structured review of the effects of zinc lozenges, nasal sprays, and nasal gels on the common cold [62]. Of the 14 randomized, placebo-controlled studies included, 7 (5 using zinc lozenges, 2 using a nasal gel) showed that the zinc treatment had a beneficial effect and 7 (5 using zinc lozenges, 1 using a nasal spray, and 1 using lozenges and a nasal spray) showed no effect. A Cochrane review of the effects of zinc lozenges on cold symptoms also reported inconclusive findings [66], although the author of another review concluded that zinc can reduce the duration and severity of cold symptoms [61].

The available data are therefore inconclusive regarding the use of zinc lozenges, nasal gels, and sprays to treat the common cold.

As previously noted, the safety of intranasal zinc has been called into question due to several reports of anosmia (permanent loss of smell) from the use of zinc-containing nasal gels or sprays [14,15]. These safety concerns do not apply to cold lozenges containing zinc.

Age-related macular degeneration*
Researchers have suggested that both zinc and antioxidants delay the progression of age-related macular degeneration (AMD) and vision loss, possibly by preventing cellular damage in the retina [67,68]. In a population-based cohort study in the Netherlands, high dietary intake of zinc as well as beta carotene, vitamin C, and vitamin E was associated with reduced risk of AMD in elderly subjects [69]. However, the authors of a systematic review and meta-analysis published in 2007 concluded that zinc is not effective for the primary prevention of early AMD [70], although zinc might reduce the risk of progression to advanced AMD.

The Age-Related Eye Disease Study (AREDS), a large, randomized, placebo-controlled, clinical trial (n = 3,597), evaluated the effect of high doses of selected antioxidants (500 mg vitamin C, 400 IU vitamin E, and 15 mg beta-carotene) with or without zinc (80 mg as zinc oxide) on the development of advanced AMD in older individuals with varying degrees of AMD [68]. Participants also received 2 mg copper to prevent the copper deficiency associated with high zinc intakes. After an average follow-up period of 6.3 years, supplementation with antioxidants plus zinc (but not antioxidants alone) significantly reduced the risk of developing advanced AMD and reduced visual acuity loss. Zinc supplementation alone significantly reduced the risk of developing advanced AMD in subjects at higher risk but not in the total study population. Visual acuity loss was not significantly affected by zinc supplementation alone.

Two other small clinical trials evaluated the effects of supplementation with 200 mg zinc sulfate (providing 45 mg zinc) for 2 years in subjects with drusen or macular degeneration. Zinc supplementation significantly reduced visual acuity loss in one of the studies [71] but had no effect in the other [72].

A Cochrane review concluded that the evidence supporting the use of antioxidant vitamins and zinc for AMD comes primarily from the AREDS study [67]. Further research is required before public health recommendations can be made, but individuals who have or are developing AMD might wish to talk to their physician about using dietary supplements.

Interactions with iron and copper*
Iron-deficiency anemia is a serious world-wide public health problem. Iron fortification programs have been credited with improving the iron status of millions of women, infants, and children. Fortification of foods with iron does not significantly affect zinc absorption. However, large amounts of supplemental iron (greater than 25 mg) might decrease zinc absorption [2,73]. Taking iron supplements between meals helps decrease its effect on zinc absorption [73].

High zinc intakes can inhibit copper absorption, sometimes producing copper deficiency and associated anemia [74,75].


REFERENCES
CALCIUM REFERENCES

1. Shils ME. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins, 1999.
2. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. Washington DC: The National Academies Press, 1997.
3. U.S. Department of Agriculture. Results from the United States Department of Agriculture's 1994-96 Continuing Survey of Food Intakes by Individuals/Diet and Health Knowledge Survey. 1994-96.
4. Subar AF, Krebs-Smith SM, Cook A, Kahle LL. Dietary sources of nutrients among US adults. J Am Diet Assoc 1998;98:537-47.
5. Weaver CM, Proulx WR, Heaney RP. Choices for achieving adequate dietary calcium with a vegetarian diet. Am J Clin Nutr 1999;70:543S-8S.
6. U.S. Department of Agriculture ARS. USDA Nutrient Database for Standard Reference Release 16. Nutrient Data Laboratory Home Page. 2003. https://www.nal.usda.gov/fnic/foodcomp.
7. Pennington J, Bowes A, Church H. Bowes & Church's Food Values of Portions Commonly Used. 17th ed: Lippincott Williams & Wilkins Publishers, 1998.
8. Heaney RP, Dowell MS, Rafferty K, Bierman J. Bioavailability of the calcium in fortified soy imitation milk, with some observations on method. Am J Clin Nutr 2000;71:1166-69.
9. United States Department of Agriculture (USDA), United States Department of Health and Human Services (DHHS). Nutrition and Your Health: Dietary Guidelines for Americans. Home and Garden Bulletin No. 232. 2000.
10. United States Department of Agriculture (USDA), Center for Nutrition Policy and Promotion. Food Guide Pyramid. 1992 (slightly revised 1996). https://www.nal.usda.gov/fnic/Fpyr/pyramid.html.
11. NIH. National Institutes of Health consensus statement: Optimal calcium intake. 1994;12:1-31.
12. Heaney RP, Recker RR, Stegman MR, Moy AJ. Calcium absorption in women: Relationships to calcium intake, estrogen status, and age. J Bone Miner Res 1989;4:469-75.
13. Heaney RP, Weaver CM, Fitzsimmons ML. Soybean phytate content: Effect on calcium absorption. Am J Clin Nutr 1991;53:745-47.
14. Heaney RP. Bone mass, nutrition, and other lifestyle factors. Nutr Rev 1996;54:S3-S10.
15. Sellmeyer DE, Schloetter M, Sebastian A. Potassium citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet. J Clin Endocrinol Metab 2002;87:2008-12.
16. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington DC: The National Academies Press, 2004.
17. Barrett-Connor E, Chang JC, Edelstein SL. Coffee-associated osteoporosis offset by daily milk consumption. JAMA 1994;271:280-83.
18. Massey LK, Whiting SJ. Caffeine, urinary calcium, calcium metabolism, and bone. J Nutr 1993;123:1611-14.
19. Calvo MS. Dietary phosphorus, calcium metabolism and bone. J Nutr 1993;123:1627-1633.
20. Heaney RP, Rafferty K. Carbonated beverages and urinary calcium excretion. Am J Clin Nutr 2001;74:343-47.
21. Hirsch PE, Peng TC. Effects of alcohol on calcium homeostasis and bone. In: Anderson J, Garner S, eds. Calcium and Phosphorus in Health and Disease. Boca Raton, FL: CRC Press, 1996:289-300.
22. NIH. Osteoporosis prevention, diagnosis, and therapy. NIH Consensus Statement Online 2000 March 27-29, 2000:1-36.
23. Riggs BL, Melton L. The worldwide problem of osteoporosis: Insights afforded by epidemiology. Bone 1995;17:505S-511S.
24. National Research Council. Recommended Dietary Allowances: 10th Edition. Washington, DC: National Academy Press 1989;Report of the subcommittee on the tenth edition of the RDAs, Food and Nutrition Board, and the Commission on Life Sciences.
25. Department of Health and Human Services. Healthy People 2000: National Health Promotion and Disease Prevention Objectives. Washington, DC: US Government Printing Office 1990;DHHS Publ. No (PHS) 91-50212:466-67.
26. National Osteoporosis Foundation. NOF osteoporosis prevention - risk factors for osteoporosis. 2003. https://www.nof.org/prevention/risk.htm.
27. Food and Drug Administration. Health Claims: calcium and osteoporosis. 1993. https://www.cfsan.fda.gov/~lrd/cf101-72.html.
28. National Osteoporosis Foundation. Bone mineral density testing: What the numbers mean. NOF, Bone Health Updates. 2001. https://www.nof.org/osteoporosis/bmdtest.htm.
29. Rouse IL, Beilin LJ, Armstrong BK, Vandongen R. Blood-pressure-lowering effect of a vegetarian diet: controlled trial in normotensive subjects. Lancet 1983;1:5-10.
30. Margetts BM, Beilin L, Armstrong BK, Vandongen R. Vegetarian diet in the treatment of mild hypertension: a randomized controlled trial. J Hypertens 1985:S429-31.
31. Beilin LJ, Armstrong BK, Margetts BM, Rouse IL, Vandongen R. Vegetarian diet and blood pressure. Nephron 1987;47:37-41.
32. Allender PS, Cutler JA, Follmann D, Cappuccio FP, Pryer J, Elliott P. Dietary calcium and blood pressure. Ann Intern Med 1996;124:825-831.
33. Bucher HC, Cook RJ, Guyatt GH, et al. Effects of dietary calcium supplementation on blood pressure. JAMA 1996;275:1016-1022.
34. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;336:1117-24.
35. Miller GD, DiRienzo DD, Reusser M, McCarron D. Benefits of dairy product consumption on blood pressure in humans:A summary of the biomedical literature. J Am Coll Nutr 2000;19:147S-164S.
36. McCarron D, Reusser M. Finding consensus in the dietary calcium-blood pressure debate. J Am Coll Nutr 1999;18:398S-405S.
37. Vollmer W, Sacks FM, Ard J, et al. Effect of diet and sodium intake on blood pressure: subgroup analysis of the DASH-Sodium trial. Ann Intern Med 2001;135:1019-28.
38. Slattery M, Edwards S, Boucher K, Anderson K, Caan B. Lifestyle and colon cancer: An Assessment of Factors Associated with Risk. Am J Epidemiol 1999;150:869-77.
39. Kampman E, Slattery M, Bette C, Potter J. Calcium, vitamin D, sunshine exposure, dairy products, and colon cancer risk. Cancer Causes Control 2000;11:459-66.
40. Holt P, Atillasoy E, Gilman J, et al. Modulation of abnormal colonic epithelial cell proliferation and differentiation by low-fat dairy foods. JAMA 1998;280:1074-79.
41. Biasco G, Paganelli M. European trials on dietary supplementation for cancer prevention. Ann N Y Acad Sci 1999;889:152-156.
42. Baron JA, Beach M, Mandel JS, et al. Calcium supplements for the prevention of colorectal adenomas. N Engl J Med 1999;340:101-7.
43. Wu K, Willett WC, Fuchs CS, Colditz GA, Giovannucci EL. Calcium intake and risk of colon cancer in women and men. J Natl Cancer Inst 2002;94:437-46.
44. Bergsma-Kadijk JA, van't Veer P, Kampman E, Burema J. Calcium does not protect against colorectal neoplasia. Epidemiology 1996;7:590-597.
45. Cascinu S, Del Ferro E, Cioccolini P. Effects of calcium and vitamin supplementation on colon cancer cell proliferation in colorectal cancer. Cancer Invest 2000;18:411-416.
46. Martinez ME, Willett WC. Calcium, vitamin D, and colorectal cancer: A review of epidemiologic evidence. Cancer Epidemiol Biomarkers Prev 1998;7:163-68.
47. Chan JM, Stampfer MJ, Gann PH, Gaziano JM, Giovannucci EL. Dairy products, calcium, and prostate cancer risk in the Physicians Health Study. Am J Clin Nutr 2001;74:549-54.
48. Giovannucci EL, Rimm EB, Wolk A, et al. Calcium and fructose intake in relation to risk of prostate cancer. Cancer Res 1998;58:442-447.
49. Chan JM, Giovannucci E, Andersson SO, Yuen J, Adami HO, Wok A. Dairy products, calcium, phosphorous, vitamin D, and risk of prostate cancer (Sweden). Cancer Causes Control 1998;9:559-566.
50. Chan JM, Giovannucci EL. Dairy products, calcium, and vitamin D and risk of prostate cancer. Epidemiol Rev 2001;23:87-92.
51. Chan JM, Pietinen P, Virtanen M, et al. Diet and prostate cancer risk in a cohort of smokers, with a specific focus on calcium and phosphorus (Finland). Cancer Causes Control 2000;11:859-67.
52. Schuurman AG, Van den Brandt PA, Dorant E, Goldbohm RA. Animal products, calcium and protein and prostate cancer risk in the Netherlands Cohort Study. Br J Cancer 1999;80:1107-13.
53. Kristal AR, Stanford JL, Cohen JH, Wicklund K, Patterson RE. Vitamin and mineral supplement use is associated with reduced risk of prostate cancer. Cancer Epidemiol Biomarkers Prev 1999;8:887-92.
54. Vlajinac HD, Marinkovic JM, Ilic MD, Kocev NI. Diet and prostate cancer: a case-control study. Eur J Cancer 1997;33:101-7.
55. Curhan G, Willett WC, Rimm E, Stampher MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993;328:833-8.
56. Bihl G, Meyers A. Recurrent renal stone disease-advances in pathogenesis and clinical management. Lancet 2001;358:651-56.
57. Hall WD, Pettinger M, Oberman A, et al. Risk factors for kidney stones in older women in the Southern United States. Am J Med Sci 2001;322:12-18.
58. Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med 2002;346:77-84.
59. Davies KM, Heaney RP, Recker RR, Lappe JM, Barger-Lux MJ, Rafferty K, Hinders S. Calcium intake and body weight. J. Clin Endocrinol Metab 2000;85:4635-8.
60. Heaney RP. Normalizing calcium intake: projected population effects for body weight. J Nutr 2003;133:268S-70S.
61. Parikh SJ, Yanovski JA. Calcium intake and adiposity. Am J Clin Nutr 2003;77:281-7.
62. Zemel MB. Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications. J Am Coll Nutr 2002;21:146S-51S.
63. Jacobsen R, Lorenzen JK, Toubro S, Krog-Mikkelsen I, Astrup A. Effect of short-term high dietary calcium intake on 24-h energy expenditure, fat oxidation, and fecal fat excretion. Int J Obes 2005;29:292-301.
64. Heaney RP. Calcium and weight: clinical studies. J Am Coll Nutr 2002;21:152S-5S.
65. Shi H, DiRienzo DD, Zemel MB. Effects of dietary calcium on adipocyte lipid metabolism and body weight regulation in energy-restricted aP2-agouti transgenic mice. FASEB J 2001;15:291-3.
66. Zemel MB, Shi H, Greer B, DiRienzo D, Zemel P. Regulation of adiposity by dietary calcium. FASEB J 2000;14:1132-8.
67. Zemel MB, Thompson W, Milstead A, Morris K, Campbell P. Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults. Obes Res 2004;12:582-90.
68. Zemel MB, Richards J, Mathis S, Milstead A, Gebhardt L, Silva E. Dairy augmentation of total and central fat loss in obese subjects. Int J Obes 2005;29:391-7.(a)
69. Zemel MB, Richards J, Milstead A, Campbell P. Effects of calcium and dairy loss on body composition and weight loss in African-American adults. Obes Res 2005;13:1-8. (b)
70. Barr SI. Increased dairy product or calcium intake: is body weight or composition affected in humans? J Nutr 2003;133:245S-8S.
71. Gunther CW, Legowski PA, Lyle RM, McCabe GP, Eagan MS, Peacock M, Teegarden D. Dairy products do not lead to alterations in body weight or fat mass in young women in a 1-y intervention. Am J Clin Nutr 2005;81:751-6.
72. Shapses SA, Heshka S, Heymsfield SB. Effect of calcium supplementation on weight and fat loss in women. J Clin Endocrinol Metab 2004;89:632-7.
73. Reid IR, Horne A, Mason B, Ames R, Bava U, Gamble GD. Effects of calcium supplementation on body weight and blood pressure in normal older women: a randomized controlled trial. J Clin Endocrinol Metab 2005;90:3824-9.
74. Sakhaee K, Maalouf NM. Editorial: dietary calcium, obesity and hypertensionthe end of the road? J Clin Endocrinol Metab 2005;90:4411-3.
75. Gallagher JC, Goldgar D, Moy A. Total bone calcium in women: Effect of age and menopause status. J Bone Min Res 1987;2:491-96.
76. Breslau NA. Calcium, estrogen, and progestin in the treatment of osteoporosis. Rheum Dis Clin North Am 1994;20:691-716.
77. Gallagher JC, Riggs BL, Deluca HF. Effect of estrogen on calcium absorption and serum vitamin D metabolites in postmenopausal osteoporosis. J Clin Endocrinol Metab 1980;51:1359-64.
78. Daniels CE. Estrogen therapy for osteoporosis prevention in postmenopausal women. Pharmacy Update-NIH 2001;March/April.
79. Dawson-Hughes B, Dallal GE, Krall EA, Sadowski L, Sahyoun N, Tannenbaum S. A controlled trial of the effect of calcium supplementation on bone density in postmenopausal women. N Engl J Med 1990;323:878-83.
80. Elders PJ, Lips P, Netelenbos JC, et al. Long-term effect of calcium supplementation on bone loss in perimenopausal women. J Bone Min Res 1994;9:963-70.
81. Menopausal hormone therapy: Summary of a scientific workshop. Ann Intern Med 2003;138:361-364.
82. American College of Obstetricians and Gynecologists. Questions and answers on hormone therapy. American College of Obstetricians and Gynecologists Web site response to the WHI study results on estrogen and progestin hormone therapy. 2002.
83. The North American Menopause Society. Position Statement: Role of progestrogen in hormone therapy for postmenopausal women: position statement of The North American Menopause Society. Menopause 2003;10:113-132.
84. American College of Sports Medicine. Menstrual cycle dysfunction. Current comment from the American College of Sports Medicine, October 2000.
85. Abrams SA, Silber TJ, Esteban NV, et al. Mineral balance and bone turnover in adolescents with anorexia nervosa. J Pediatr 1993;123:326-331.
86. Drinkwater B, Bruemner B, Chesnut C. Menstrual history as a determinant of current bone density in young athletes. JAMA 1990;263:545-48.
87. Marcus R, Cann C, Madvig P, et al. Menstrual function and bone mass in elite women distance runners: Endocrine and metabolic features. Ann Intern Med 1985;102:158-63.
88. Nattiv A. Stress fractures and bone health in track and field athletes. J Sci Med Sport 2000;3:268-79.
89. Subcommittee on Body Composition and Nutrition and Health of Military Women, Committee on Military Nutrition Research, Food and Nutrition Board, Institute of Medicine. Reducing Stress Fracture in Physically Active Military Women. Washington, DC: National Academy Press, 1998.
90. Johnson AO, Semenya JG, Buchowski MS, Enwonwu CO, Scrimshaw NS. Correlation of lactose maldigestion, lactose intolerance, and milk intolerance. Am J Clin Nutr 1993;57:399-401.
91. Nose O, Iida Y, Kai H, Harada T, Ogawa M, Yabuuchi H. Breath hydrogen test for detecting lactose malabsorption in infants and children: Prevalence of lactose malabsorption in Japanese children and adults. Arch Dis Child 1979;54:436-40.
92. Rao DR, Bello H, Warren AP, Brown GE. Prevalence of lactose maldigestion: Influence and interaction of age, race, and sex. Dig Dis Sci 1994;39:1519-24.
93. Coffin B, Azpiroz F, Guarner F, Mlagelada JR. Selective gastric hypersensitivity and reflex hyporeactivity in functional dyspepsia. Gastroenterology 1994;107:1345-51.
94. Horowitz M, Wishart J, Mundy L, Nordin BEC. Lactose and calcium absorption in postmenopausal osteoporosis. Arch Intern Med 1987;147:534-36.
95. Tremaine WJ, Newcomer AD, Riggs BL, McGill DB. Calcium absorption from milk in lactase-deficient and lactase-sufficient adults. Dig Dis Sci 1986;31:376-78.
96. Suarez FL, Savaiano DA, Arbisi P, Levitt MD. Tolerance to the daily ingestion of two cups of milk by individuals claiming lactose intolerance. Am J Clin Nutr 1997;65:1502-06.
97. Suarez FL, Savaiano DA, Levitt MD. A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance. N Engl J Med 1995;333:1-4.
98. Johnson AO, Semenya JG, Buchowski MS, Enwonwu CO, Scrimshaw NS. Adaptation of lactose maldigester to continued milk intakes. Am J Clin Nutr 1993;58:879-81.
99. Hertzler SR, Huynh B, Savaiano DA. How much lactose is "low lactose". J Am Diet Assoc 1996;96:243-46.
100. Hertzler SR, Savaiano DA. Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. Am J Clin Nutr 1996;64:1232-36.
101. Hertzler SR, Savaiano DA, Levitt MD. Fecal hydrogen production and consumption measurements: Response to daily lactose ingestion by lactose maldigesters. Dig Dis Sci 1997;42:348-53.
102. Martini MC, Savaiano DA. Reduced intolerance symptoms from lactose consumed during a meal. Am J Clin Nutr 1988;47:57-60.
103. Pribila BA, Hertzler SR, Martin BR, Weaver CM, Savaiano DA. Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet. J Am Diet Assoc 2000;100:524-528.
104. Marsh AG, Sanchez TV, Midkelsen O, Keiser J, Mayor G. Cortical bone density of adult lacto-ovo-vegetarian and omnivorous women. J Am Diet Assoc 1980;76:148-51.
105. Reed JA, Anderson JJ, Tylavsky FA, Gallagher JCJ. Comparative changes in radial-bone density of elderly female lacto-ovo-vegetarians and omnivores. Am J Clin Nutr 1994;59:1197S-1202S.
106. Janelle KC, Barr SI. Nutrient intakes and eating behavior scores of vegetarian and non-vegetarian women. J Am Diet Assoc 1995;95:180-86.
107. Burckhardt P, Dawson-Hughes B, Heaney RP. Nutritional aspects of osteoporosis. Academic Press 2001.
108. Spencer H, Menczel J, Lewin I, Samachson J. Effect of high phosphorus intake on calcium and phosphorus metabolism in man. J Nutr 1965;86:125-32.
109. Schiller L, Santa Ana C, Sheikh M, Emmett M, Fordtran J. Effect of the time of administration of calcium acetate on phosphorus binding. N Engl J Med 1989;320:1110-13.
110. Hallberg L, Rossander-Hulten L, Brune M, Gleerup A. Calcium and iron absorption: Mechanism of action and nutritional importance. Eur J Clin Nutr 1992;46:317-27.
111. Clarkson EM, Warren RL, McDonald SJ, de Wardener HE. The effect of a high intake of calcium on magnesium metabolism in normal subjects and patients with chronic renal failure. Clin Sci 1967;32:11-18.
112. Shannon MT, Wilson BA, Stang CL. Health Professionals Drug Guide. Stamford, CT: Appleton and Lange, 2000.
113. Jellin JM, Gregory P, Batz F, Hitchens K. Pharmacist's Letter/Prescriber's Letter Natural Medicines Comprehensive Database. 3rd edition ed. Stockton, CA: Therapeutic Research Facility, 2000.
114. Department of Health and Human Services. Nutrition and Your Health: Dietary Guidelines for Americans. Home and Garden Bulletin No. 232 2000;Fifth Edition.
115. Nutrition Business Journal. NBJ's supplement business report 2003. US consumer sales in $mil. San Diego, 2002:6.22.
116. Andon MB, Peacock M, Kanerva RL, De Castro JAS. Calcium absorption from apple and orange juice fortified with calcium citrate malate (CCM). J Am Coll Nutr 1996;15:313-16.
117. Heaney RP, Saville PD, Recker RR. Calcium absorption as a function of calcium intake. J Lab Clin Med 1975;85:881-90.
118. Heaney RP, Recker RR, Hinders SM. Variability of calcium absorption. Am J Clin Nutr 1988;47:262-64.
Levenson D, Bockman R. A review of calcium preparations. Nutr Rev 1994;52:221-32.


D3 References
1. Vieth R, Ladak Y, Walfish PG. Age-related changes in the 25-hydroxyVitamin D versus parathyroid hormone relationship suggest a different reason why older adults require more Vitamin D. J Clin Endocrinol Metab. 2003 Jan;88(1):185-91.
2. Gorham ED, Garland CF, Garland FC, Grant WB, Mohr SB, Lipkin M, Newmark HL, Giovannucci E, Wei M, Holick MF. Optimal Vitamin D status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 2007 Mar;32(3):210-6.
3. Vieth R, Bischoff-Ferrari H, Boucher BJ, Dawson-Hughes B, Garland CF, Heaney RP, Holick MF, Hollis BW, Lamberg-Allardt C, McGrath JJ, Norman AW, Scragg R, Whiting SJ, Willett WC, Zittermann A. The urgent need to recommend an intake of Vitamin D that is effective. American Journal of Clinical Nutrition. March 2007;85(3):649-650.
4. Hathcock JN, Shao A, Vieth R, Heaney R. Risk assessment for Vitamin D. Am J Clin Nutr. 2007 Jan;85(1):6-18.
5. Vieth R. Critique of the considerations for establishing the tolerable upper intake level for Vitamin D: critical need for revision upwards. J Nutr. 2006 Apr;136(4):1117-22.
6. Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40.
7. Lotfi A, Abdel-Nasser AM, Hamdy A, Omran AA, El-Rehany MA. HypoVitaminosis D in female patients with chronic low back pain. Clin Rheumatol. 2007 Mar 22; [Epub ahead of print].
8. Perez-Lopez FR. Vitamin D and its implications for musculoskeletal health in women: An update. Maturitas. 2007 Jun 28; [Epub ahead of print].
9. Przybelski RJ, Binkley NC. Is Vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyVitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Apr 15;460(2):202-5.
10. Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.
11. Lappe J, Travers-Gustafson D, Davies K, Recker R, Heaney R. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. American Journal of Clinical Nutrition. June 8;85(6):1586-1591.
12. Ma Y, et al. Study presented at the 2007 centennial meeting of the American Association for Cancer Research (AACR), April 14 to 18, 2007, Los Angeles.
13. Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E. Epidemic influenza and Vitamin D. Epidemiol Infect. 2006 Dec;134(6):1129-40.
14. KuryAowicz A, Bednarczuk T, Nauman J. [The influence of Vitamin D deficiency on cancers and autoimmune diseases development.] [Article in Polish] Endokrynol Pol. 2007;58(2):140-152.
15. Bodnar LM, Catov JM, Simhan HN, Holick MF, Powers RW, Roberts JM. Maternal Vitamin D deficiency increases the risk of preeclampsia. J Clin Endocrinol Metab. 2007 May 29; [Epub ahead of print].
16. Maghbooli Z, Hossein-Nezhad A, Karimi F, Shafaei AR, Larijani B. Correlation between Vitamin D(3) deficiency and insulin resistance in pregnancy. Diabetes Metab Res Rev. 2007 Jul 2; [Epub ahead of print].
17. Parekh N, Chappell RJ, Millen AE, Albert DM, Mares JA. Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994. Arch Ophthalmol. May 2007;125: 661-669.

Magnesium References
1. Rude RK. Magnesium deficiency: A cause of heterogeneous disease in humans. J Bone Miner Res 1998;13:749-58. [PubMed abstract]
2. Wester PO. Magnesium. Am J Clin Nutr 1987;45:1305-12. [PubMed abstract]
3. Saris NE, Mervaala E, Karppanen H, Khawaja JA, Lewenstam A. Magnesium: an update on physiological, clinical, and analytical aspects. Clinica Chimica Acta 2000;294:1-26.
4. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. National Academy Press. Washington, DC, 1999.
5. U.S. Department of Agriculture, Agricultural Research Service. 2003. USDA National Nutrient Database for Standard Reference, Release 16. Nutrient Data Laboratory Home Page, https://www.nal.usda.gov/fnic/foodcomp.
6. Ford ES and Mokdad AH. Dietary magnesium intake in a national sample of U.S. adults. J Nutr. 2003;133:2879-82.
7. Vormann J. Magnesium: nutrition and metabolism. Molecular Aspects of Medicine 2003:24:27-37.
8. Feillet-Coudray C, Coudray C, Tressol JC, Pepin D, Mazur A, Abrams SA. Exchangeable magnesium pool masses in healthy women: effects of magnesium supplementation. Am J Clin Nutr 2002;75:72-8.
9. Ladefoged K, Hessov I, Jarnum S. Nutrition in short-bowel syndrome. Scand J Gastroenterol Suppl 1996;216:122-31. [PubMed abstract]
10. Rude KR. Magnesium metabolism and deficiency. Endocrinol Metab Clin North Am 1993;22:377-95.
11. Kelepouris E and Agus ZS. Hypomagnesemia: Renal magnesium handling. Semin Nephrol 1998;18:58-73. [PubMed abstract]
12. Ramsay LE, Yeo WW, Jackson PR. Metabolic effects of diuretics. Cardiology 1994;84 Suppl 2:48-56. [PubMed abstract]
13. Kobrin SM and Goldfarb S. Magnesium Deficiency. Semin Nephrol 1990;10:525-35. [PubMed abstract]
14. Lajer H and Daugaard G. Cisplatin and hypomagnesemia. Ca Treat Rev 1999;25:47-58. [PubMed abstract]
15. Tosiello L. Hypomagnesemia and diabetes mellitus. A review of clinical implications. Arch Intern Med 1996;156:1143-8. [PubMed abstract]
16. Paolisso G, Scheen A, D'Onofrio F, Lefebvre P. Magnesium and glucose homeostasis. Diabetologia 1990;33:511-4. [PubMed abstract]
17. Elisaf M, Bairaktari E, Kalaitzidis R, Siamopoulos K. Hypomagnesemia in alcoholic patients. Alcohol Clin Exp Res 1998;22:244-6. [PubMed abstract]
18. Abbott L, Nadler J, Rude RK. Magnesium deficiency in alcoholism: Possible contribution to osteoporosis and cardiovascular disease in alcoholics. Alcohol Clin Exp Res 1994;18:1076-82. [PubMed abstract]
19. Shils ME. Magnesium. In Modern Nutrition in Health and Disease, 9th Edition. (edited by Shils, ME, Olson, JA, Shike, M, and Ross, AC.) New York: Lippincott Williams and Wilkins, 1999, p. 169-92.
20. Elisaf M, Milionis H, Siamopoulos K. Hypomagnesemic hypokalemia and hypocalcemia: Clinical and laboratory characteristics. Mineral Electrolyte Metab 1997;23:105-12. [PubMed abstract]
21. American Diabetes Association. Nutrition recommendations and principles for people with diabetes mellitus. Diabetes Care 1999;22:542-5. [PubMed abstract]
22. Rude RK and Olerich M. Magnesium deficiency: Possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int 1996;6:453-61. [PubMed abstract]
23. Bialostosky K, Wright JD, Kennedy-Stephenson J, McDowell M, Johnson CL. Dietary intake of macronutrients, micronutrients and other dietary constituents: United States 1988-94. Vital Heath Stat. 11(245) ed: National Center for Health Statistics, 2002:168.
24. Takahashi M, Degenkolb J, Hillen W. Determination of the equilibrium association constant between Tet repressor and tetracycline at limiting Mg2+ concentrations: a generally applicable method for effector-dependent high-affinity complexes. Anal Biochem 1991;199:197-202.
25. Xing JH and Soffer EE. Adverse effects of laxatives. Dis Colon Rectum 2001;44:1201-9.
26. Qureshi T and Melonakos TK. Acute hypermagnesemia after laxative use. Ann Emerg Med 1996;28:552-5. [PubMed abstract]
27. DePalma J. Magnesium Replacement Therapy. Am Fam Phys 1990;42:173-6.
28. Klasco RK (Ed): USP DI Drug Information for the Healthcare Professional. Thomson MICROMEDEX, Greenwood Village, Colorado 2003.
29. Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Intestinal absorption of magnesium from food and supplements. J Clin Invest 1991;88:296-402.
30. Firoz M and Graber M. Bioavailaility of US commercial magnesium preparation. Magnes Res 2001;14:257-62.
31. Appel LJ. Nonpharmacologic therapies that reduce blood pressure: A fresh perspective. Clin Cardiol 1999;22:1111-5. [PubMed abstract]
32. Simopoulos AP. The nutritional aspects of hypertension. Compr Ther 1999;25:95-100. [PubMed abstract]
33. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;336:1117-24. [PubMed abstract]
34. Sacks FM, Obarzanek E, Windhauser MM, Svetkey LP, Vommer WM, McCullough M, Karanja N, Lin PH, Steele P, Praschen MA, Evans M, Appel LJ, Bray GA, Vogt T, Moore MD for the DASH investigators. Rationale and design of the Dietary Approaches to Stop Hypertension trial (DASH). A multicenter controlled-feeding study of dietary patterns to lower blood pressure. Ann Epidemiol 1995;5:108-18. [PubMed abstract]
35. Sacks FM, Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A dietary approach to prevent hypertension: A review of the Dietary Approaches to Stop Hypertension (DASH) Study. Clin Cardiol 1999;22:6-10. [PubMed abstract]
36. Svetkey LP, Simons-Morton D, Vollmer WM, Appel LJ, Conlin PR, Ryan DH, Ard J, Kennedy BM. Effects of dietary patterns on blood pressure: Subgroup analysis of the Dietary Approaches to Stop Hypertension (DASH) randomized clinical trial. Arch Intern Med 1999;159:285-93. [PubMed abstract]
37. Ascherio A, Rimm EB, Giovannucci EL, Colditz GA, Rosner B, Willett WC, Sacks FM, Stampfer MJ. A prospective study of nutritional factors and hypertension among US men. Circulation 1992;86:1475-84. [PubMed abstract]
38. Peacock JM, Folsom AR, Arnett DK, Eckfeldt JH, Szklo M. Relationship of serum and dietary magnesium to incident hypertension: the Atherosclerosis Risk in Communities (ARIC) Study. Annals of Epidemiology 1999;9:159-65.
39. National Heart, Lung, and Blood Institute. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157:2413-46. [PubMed abstract]
40. Schwartz GL and Sheps SG. A review of the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Curr Opin Cardiol 1999;14:161-8. [PubMed abstract]
41. Kaplan NM. Treatment of hypertension: Insights from the JNC-VI report. Am Fam Physician 1998;58:1323-30. [PubMed abstract]
42. Paolisso G, Sgambato S, Gambardella A, Pizza G, Tesauro P, Varricchio H, D'Onofrio F. Daily magnesium supplements improve glucose handling in elderly subjects. Am J Clin Nutr 1992;55:1161-7. [PubMed abstract]
43. Lopez-Ridaura R, Willett WC, Rimm EB, Liu S, Stampfer MJ, Manson JE, Hu FB. Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care 2004;27:134-40.
44. Meyer KA, Kishi LH, Jacobs DR Jr., Slavin J, Sellers TA, Folsom AR. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Am J Clin Nutr 1999;71:921-30.
45. Song V, Manson JE, Buring JE, Liu S. Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women. Diabetes Care 2003;27:59-65.
46. Kao WHL, Folsom AR, Nieto FJ, MO JP, Watson RL, Brancati FL. Serum and dietary magnesium and the risk for type 2 diabetes: The Atherosclerosis Risk in Communities Study. Arch Intern Med 1999;159:2151-59.
47. Rodriguez-Moran M and Guerrero-Romero F. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects. Diabetes Care 2003;26:1147-52.
48. De Lourdes Lima, M, Cruz T, Pousada JC, Rodrigues LE, Barbosa K, Canguco V. The effect of magnesium supplementation in increasing doses on the control of type 2 diabetes. Diabetes Care 1998;21:682-86.
49. Altura BM and Altura BT. Magnesium and cardiovascular biology: An important link between cardiovascular risk factors and atherogenesis. Cell Mol Biol Res 1995;41:347-59. [PubMed abstract]
50. Ford ES. Serum magnesium and ischaemic heart disease: Findings from a national sample of US adults. Intl J of Epidem 1999;28:645-51. [PubMed abstract]
51. Liao F, Folsom A, Brancati F. Is low magnesium concentration a risk factor for coronary heart disease? The Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J 1998;136:480-90. [PubMed abstract]
52. Ascherio A, Rimm EB, Hernan MA, Giovannucci EL, Kawachi I, Stampfer MJ, Willett WC. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation 1998;98:1198-204. [PubMed abstract]
53. Shechter M, Bairey Merz CN, Stuehlinger HG, Slany J, Pachinger O, Rabinowitz B. Effects of oral magnesium therapy on exercise tolerance, exercise-induced chest pain, and quality of life in patients with coronary artery disease. Am J Cardiol 2003;91:517-21.
54. Shechter M, Sharir M, Labrador MJ, Forrester J, Silver B, Bairey Merz CN. Oral magnesium therapy improves endothelial function in patients with coronary artery disease. Circulation 2000;102:2353-58.
55. Shechter M, Merz CN, Paul-Labrador M, Meisel SR, Rude RK, Molloy MD, Dwyer JH, Shah PK, Kaul S. Oral magnesium supplementation inhibits platelet-dependent thrombosis in patients with coronary artery disease. American Journal of Cardiology 1999;84:152-6.
56. Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PW, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69(4):727-36.
57. Jaing T-H, Hung I-H, Chung H-T, Lai C-H, Liu W-M, Chang K-W. Acute hypermagnesemia: a rare complication of antacid administration after bone marrow transplantation. Clinica Chimica Acta 2002;326:201-3.
58. Whang R. Clinical disorders of magnesium metabolism. Compr Ther 1997;23:168-73. [PubMed abstract]
59. Ho J, Moyer TP, Phillips S. Chronic diarrhea: The role of magnesium. Mayo Clin Proc 1995;70:1091-2. [PubMed abstract]
60. Nordt S, Williams SR, Turchen S, Manoguerra A, Smith D, Clark R. Hypermagnesemia following an acute ingestion of Epsom salt in a patient with normal renal function. J Toxicol Clin Toxicol 1996;34:735-9. [PubMed abstract]
61. Dietary Guidelines Advisory Committee, Agricultural Research Service, United States Department of Agriculture (USDA). HG Bulletin No. 232, 2000. https://www.usda.gov/cnpp/DietGd.pdf.
Center for Nutrition Policy and Promotion, United Stated Department of Agriculture. Food Guide Pyramid, 1992 (slightly revised 1996). https://www.nal.usda.gov/fnic/Fpyr/pyramid.html.


Selenium References

1. Thomson CD. Assessment of requirements for selenium and adequacy of selenium status: a review. Eur J Clin Nutr 2004;58:391-402.
2. Goldhaber SB. Trace element risk assessment: essentiality vs. toxicity. Regulatory Toxicology and Pharmacology. 2003;38:232-42.
3. Combs GF, Jr and Gray WP. Chemopreventive agents: Selenium. Pharmacol Ther 1998; 79:179-92.
4. McKenzie RC, Rafferty TS, Beckett GJ. Selenium: an essential element for immune function. Immunol Today 1998;19:342-5.
5. Levander OA. Nutrition and newly emerging viral diseases: An overview. J Nutr 1997;127: 948S-50S. [PubMed abstract]
6. Arthur JR. The role of selenium in thyroid hormone metabolism. Can J Physiol Pharmacol 1991;69:1648-52. [PubMed abstract]
7. Corvilain B, Contempre B, Longombe AO, Goyens P, Gervy-Decoster C, Lamy F, Vanderpas JB, Dumont JE. Selenium and the thyroid: How the relationship was established. Am J Clin Nutr 1993;57 (2 Suppl):244S-8S. [PubMed abstract]
8. Longnecker MP, Taylor PR, Levander OA, Howe M, Veillon C, McAdam PA, Patterson KY, Holden JM, Stampfer MJ, Morris JS, Willett WC. Selenium in diet, blood, and toenails in relation to human health in a seleniferous area. Am J Clin Nutr 1991;53:1288-94. [PubMed abstract]
9. Pennington JA and Schoen SA. Contributions of food groups to estimated intakes of nutritional elements: Results from the FDA total diet studies, 1982-91. Int J Vitam Nutr Res 1996;66:342-9. [PubMed abstract]
10. Pennington JA and Young BE. Total diet study nutritional elements. J Am Diet Assoc 1991;91:179-83. [PubMed abstract]
11. U.S. Department of Agriculture, Agricultural Research Service. 2003. USDA National Nutrient Database for Standard Reference, Release 16. Nutrient Data Laboratory Home Page, https://www.nal.usda.gov/fnic/foodcomp.
12. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academy Press, Washington, DC, 2000.
13. Bialostosky K, Wright JD, Kennedy-Stephenson J, McDowell M, Johnson CL. Dietary intake of macronutrients, micronutrients and other dietary constituents: United States 1988-94. Vital Heath Stat. 11(245) ed: National Center for Health Statistics, 2002.
14. Zhou BF, Stamler J, Dennis B, Moag-Stahlberg A, Okuda N, Robertson C, Zhao L, Chan Q, Elliott P for the INTERMAP Research Group. Nutrient intakes of middle-aged men and women in China, Japan, United Kingdom, and United States in the alte 1990s: The INTERMAP Study. J of Human Hypertension. 2003;17:623-30.
15. Ellis DR and Salt DE. Plants, selenium and human health. Curr Opin Plant Biol 2003;6:273-9.
16. Combs GF. Food system-based approaches to improving micronutrient nutrition: the case for selenium. Biofactors 2000;12:39-43.
17. Zimmerman MB and Kohrle J. The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid 2002;12:867-78.
18. Beck MA, Levander O, Handy J. Selenium deficiency and viral infection. J of Nutr 2003;133:1463S-67S.
19. Levander OA and Beck MA. Interacting nutritional and infectious etiologies of Keshan disease. Insights from coxsackie virus B-induced myocarditis in mice deficient in selenium or vitamin E. Biol Trace Elem Res 1997;56:5-21. [PubMed abstract]
20. Levander OA. Scientific rationale for the 1989 recommended dietary allowance for selenium. J Am Diet Assoc 1991;91:1572-6. [PubMed abstract]
21. Gramm HJ, Kopf A, Bratter P. The necessity of selenium substitution in total parenteral nutrition and artificial alimentation. J Trace Elem Med Biol 1995;9:1-12. [PubMed abstract]
22. Abrams CK, Siram SM, Galsim C, Johnson-Hamilton H, Munford FL, Mezghebe H. Selenium deficiency in long-term total parenteral nutrition. Nutr Clin Pract 1992;7:175-8. [PubMed abstract]
23. Rannem T, Ladefoged K, Hylander E, Hegnhoj J, Staun M. Selenium depletion in patients with gastrointestinal diseases: Are there any predictive factors? Scand J Gastroenterol 1998;33:1057-61. [PubMed abstract]
24. Kuroki F, Matsumoto T, Lida M. Selenium is depleted in Crohn's disease on enteral nutrition. Digestive Diseases 2003;21:266-70.
25. Rannem T, Ladefoged K, Hylander E, Hegnhoj J, Jarnum S. Selenium status in patients with Crohn's disease. Am J Clin Nutr 1992;56:933-7. [PubMed abstract]
26. Bjerre B, von Schenck H, Sorbo B. Hyposelaemia: Patients with gastrointestinal diseases are at risk. J Intern Med 1989;225:85-8. [PubMed abstract]
27. Gartner R, Albrich W, Angstwurm MW. The effect of a selenium supplementation on the outcome of patients with severe systemic inflammation, burn, and trauma. BioFactors 14 2001; 199-204.
28. Berdanier, CD. Advanced Nutrition: Micronutrients. CRC Press 1998; 208-11.
29. Derumeaux H, Valeix P, Castetbon K, Bensimon M, Boutron-Ruault MC, Arnaud J, Hercberg S. Association of selenium with thyroid volume and echostructure in 35- to 60-year-old French adults. Eur J Endocrinol 2003;148(3):309-15.
30. Schrauzer GN. Commentary: Nutrition selenium supplements: Product types, quality, and safety. J Am College of Nutr 2001;20:1-4.
31. Schrauzer GN. The nutritional significance, metabolism and toxicology of selenomethionine. Adv Food Nutr Res 2003:47:73-112.
32. Clark LC, Combs Jr GF, Turnbull BW, Slate EH, Chalker D, Chow J, Davis LS, Glover RA, Graham GF, Gross EG, Krongrad A, Lesher JL, Park HK, Sanders BB, Smith CL, Taylor JR. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. J Am Med Assoc 1996;276:1957-63.
33. Neve J. Human selenium supplementation as assessed by changes in blood selenium concentration and glutathione peroxidase activity. J Trace Elem Med Biol 1995;9:65-73.
34. Russo MW, Murray SC, Wurzelmann JI, Woosley JT, Sandler RS. Plasma selenium levels and the risk of colorectal adenomas. Nutr Cancer 1997;28:125-9. [PubMed abstract]
35. Patterson BH and Levander OA. Naturally occurring selenium compounds in cancer chemoprevention trials: A workshop summary. Cancer Epidemiol Biomarkers Prev 1997;6:63-9. [PubMed abstract]
36. Knekt P, Marniemi J, Teppo L, Heliovaara M, Aromaa A. Is low selenium status a risk factor for lung cancer? Am J Epidemiol 1998;148:975-82. [PubMed abstract]
37. Fleet JC. Dietary selenium repletion may reduce cancer incidence in people at high risk who live in areas with low soil selenium. Nutr Rev 1997;55:277-9. [PubMed abstract]
38. Shamberger RJ. The genotoxicity of selenium. Mutat Res 1985;154:29-48. [PubMed abstract]
39. Young KL and Lee PN. Intervention studies on cancer. Eur J Cancer Prev 1999;8:91-103. [PubMed abstract]
40. Burguera JL, Burguera M, Gallignani M, Alarcon OM, Burgueera JA. Blood serum selenium in the province of Merida, Venezuela, related to sex, cancer incidence and soil selenium content. J Trace Elem Electrolytes Health Dis 1990;4:73-7. [PubMed abstract]
41. Combs GF, Jr., Clark LC, Turnbull BW. Reduction of cancer risk with an oral supplement of selenium. Biomed Environ Sci 1997;10:227-34. [PubMed abstract]
42. Combs GF, Clark LC, Turnbull BW. An analysis of cancer prevention by selenium. BioFactors 14 2001; 153-9.
43. Garland M, Morris JS, Stampfer MJ, Colditz GA, Spate VL, Baskett CK, Rosner B, Speier FE, Willett WC, Hunter DJ. Prospective study of toenail selenium levels and cancer among women. J Natl Cancer Inst 1995;87:497- 505. [PubMed abstract]
44. Hercberg S, Galan P, Preziosi P, Roussel AM, Arnaud J, Richard MJ, Malvy D, Paul-Dauphin A, Briancon S, Favier A. Background and rationale behind the SU.VI.MAX Study, a prevention trial using nutritional doses of a combination of antioxidant vitamins and minerals to reduce cardiovascular diseases and cancers. Supplementation en VItamines et Mineraux AntiXydants Study. Int J Vitam Nutr Res 1998;68:3-20. [PubMed abstract]
45. Klein EA, Thompson IM, Lippman SM, Goodman PJ, Albanes D, Taylor PR, Coltman C. SELECT: the next prostate cancer prevention trial. Selenium and Vitamin E Cancer Prevention Trial. Journal of Urology 2001;166(4):1311-5.
46. Gey KF. Vitamins E plus C and interacting conutrients required for optimal health. A critical and constructive review of epidemiology and supplementation data regarding cardiovascular disease and cancer. Biofactors 1998;7:113-74. [PubMed abstract]
47. Ozer NK, Boscoboinik D, Azzi A. New roles of low density lipoproteins and vitamin E in the pathogenesis of atherosclerosis. Biochem Mol Biol Int 1995;35:117-24. [PubMed abstract]
48. Lapenna D, de Gioia S, Ciofani G, Mezzetti A, Ucchino S, Calafiore AM, Napolitano AM, Di Ilio C, Cuccurulo F. Glutathione-related antioxidant defenses in human atherosclerotic plaques. Circulation 1998;97:1930-4. [PubMed abstract]
49. Neve J. Selenium as a risk factor for cardiovascular diseases. J Cardiovasc Risk 1996;3:42-7. [PubMed abstract]
50. Kose K, Dogan P, Kardas Y, Saraymen R. Plasma selenium levels in rheumatoid arthritis. Biol Trace Elem Res 1996;53:51-6. [PubMed abstract]
51. Heliovaara M, Knekt P, Aho K, Aaran RK, Alfthan G, Aromaa A. Serum antioxidants and risk of rheumatoid arthritis. Ann Rheum Dis 1994;53:51-3. [PubMed abstract]
52. Stone J, Doube A, Dudson D, Wallace J. Inadequate calcium, folic acid, vitamin E, zinc, and selenium intake in rheumatoid arthritis patients: Results of a dietary survey. Semin Arthritis Rheum 1997;27:180-5. [PubMed abstract]
53. Grimble RF. Nutritional antioxidants and the modulation of inflammation: Theory and practice. New Horizons 1994;2:175-85. [PubMed abstract]
54. Aaseth J, Haugen M, Forre O. Rheumatoid arthritis and metal compounds- perspectives on the role of oxygen radical detoxification. Analyst 1998;123:3- 6. [PubMed abstract]
55. Look MP, Rockstroh JK, Rao GS, Kreuzer KA, Spengler U, Sauerbruch T. Serum selenium versus lymphocyte subsets and markers of disease progression and inflammatory response in human immunodeficiency virus-1 infection. Biol Trace Elem Res 1997;56(1):31-41.
56. Singhal N and Austin J. A clinical review of micronutrients in HIV infection. J Int Assoc Physicians AIDS Care 2002;1:63-75.
57. Romero-Alvira D and Roche E. The keys of oxidative stress in acquired immune deficiency syndrome apoptosis. Medical Hypotheses 1998;51(2):169-73.
58. Patrick L. Nutrients and HIV; Part One - Beta carotene and selenium. Altern Med Rev 1999;4:403-13. [PubMed abstract]
59. Baum MK, Shor-Posner G, Lai S, Zhang G, Lai H, Fletcher MA, Sauberlich H, Page JB. High risk of HIV-related mortality is associated with selenium deficiency. J Acquir Immune Defic Syndr Hum Retrovirol 1997;15:370-4. [PubMed abstract]
60. Campa A, Shor-Posner G, Indacoche F, Zhang G, Lai H, Asthana D, Scott GB, Baum MK. Mortality risk in selenium-deficient HIV-positive children. J Acquir Immune Defic Syndr Hum Retrovirol 1999;15:508-13. [PubMed abstract]
61. Baum MK and Shor-Posner G. Micronutrient status in relationship to mortality in HIV-1 disease. Nutr Rev 1998;56:S135-9. [PubMed abstract]
62. Koller LD and Exon JH. The two faces of selenium-deficiency and toxicity are similar in animals and man. Can J Vet Res 1986;50:297-306. [PubMed abstract]
63. Hathcock J. Vitamins and minerals: Efficacy and safety. Am J Clin Nutr 1997;66:427-37. [PubMed abstract]
64. Raisbeck MF, Dahl ER, Sanchez DA, Belden EL, O'Toole D. Naturally occurring selenosis in Wyoming. J Vet Diagn Invest 1993;5:84-7. [PubMed abstract]
65. Dietary Guidelines Advisory Committee, Agricultural Research Service, United States Department of Agriculture (USDA). HG Bulletin No. 232, 2000. https://www.usda.gov/cnpp/DietGd.pdf.
Center for Nutrition Policy and Promotion, United Stated Department of Agriculture. Food Guide Pyramid, 1992 (slightly revised 1996). https://www.nal.usda.gov/fnic/Fpyr/pyramid.html.

Zinc References

1. Sandstead HH. Understanding zinc: recent observations and interpretations. J Lab Clin Med 1994;124:322-7. [PubMed abstract]
2. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: NationalAcademy Press, 2001.
3. Solomons NW. Mild human zinc deficiency produces an imbalance between cell-mediated and humoral immunity. Nutr Rev 1998;56:27-8. [PubMed abstract]
4. Prasad AS. Zinc: an overview. Nutrition 1995;11:93-9. [PubMed abstract]
5. Heyneman CA. Zinc deficiency and taste disorders. Ann Pharmacother 1996;30:186-7. [PubMed abstract]
6. Simmer K, Thompson RP. Zinc in the fetus and newborn. Acta Paediatr Scand Suppl 1985;319:158-63. [PubMed abstract]
7. Fabris N, Mocchegiani E. Zinc, human diseases and aging. Aging (Milano) 1995;7:77-93. [PubMed abstract]
8. Maret W, Sandstead HH. Zinc requirements and the risks and benefits of zinc supplementation. J Trace Elem Med Biol 2006;20:3-18. [PubMed abstract]
9. Prasad AS, Beck FW, Grabowski SM, Kaplan J, Mathog RH. Zinc deficiency: changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and in noncancer subjects. Proc Assoc Am Physicians 1997;109:68-77. [PubMed abstract]
10. Rink L, Gabriel P. Zinc and the immune system. Proc Nutr Soc 2000;59:541-52. [PubMed abstract]
11. U.S. Department of Agriculture, Agricultural Research Service. USDA Nutrient Database for Standard Reference, Release 14. [https://www.nal.usda.gov/fnic/foodcomp/search/]
12. Sandstrom B. Bioavailability of zinc. Eur J Clin Nutr 1997;51 (1 Suppl):S17-9. [PubMed abstract]
13. Wise A. Phytate and zinc bioavailability. Int J Food Sci Nutr 1995;46:53-63. [PubMed abstract]
14. Jafek BW, Linschoten MR, Murrow BW. Anosmia after intranasal zinc gluconate use. Am J Rhinol 2004;18:137-41. [PubMed abstract]
15. Alexander TH, Davidson TM. Intranasal zinc and anosmia: the zinc-induced anosmia syndrome. Laryngoscope 2006;116:217-20. [PubMed abstract]
16. Alaimo K, McDowell MA, Briefel RR, Bischlf AM, Caughman CR, Loria CM, et al. Dietary Intake of Vitamins, Minerals, and Fiber of Persons Ages 2 Months and Over in the United States: Third National Health and Nutrition Examination Survey, Phase 1, 1988-91. Hyattsville, MD: Centers for Disease Control and Prevention, National Center for Health Statistics, 1994:1-28.
17. Interagency Board for Nutrition Monitoring and Related Research. Third Report on Nutrition Monitoring in the United States. Washington, DC: U.S. Government Printing Office, 1995.
18. Ervin RB, Kennedy-Stephenson J. Mineral intakes of elderly adult supplement and non-supplement users in the third national health and nutrition examination survey. J Nutr 2002;132:3422-7. [PubMed abstract]
19. Ribar DS, Hamrick KS. Dynamics of Poverty and Food Sufficiency. Food Assistance and Nutrition Report Number 36, 2003. Washington, DC: U.S. Department of Agriculture, Economic Research Service. [https://www.ers.usda.gov/publications/fanrr36/fanrr36.pdf]
20. Dixon LB, Winkleby MA, Radimer KL. Dietary intakes and serum nutrients differ between adults from food-insufficient and food-sufficient families: Third National Health and Nutrition Examination Survey, 1988-1994. J Nutr 2001;131:1232-46. [PubMed abstract]
21. Prasad AS. Zinc deficiency: its characterization and treatment. Met Ions Biol Syst 2004;41:103-37. [PubMed abstract]
22. Wang LC, Busbey S. Images in clinical medicine. Acquired acrodermatitis enteropathica. N Engl J Med 2005;352:1121. [PubMed abstract]
23. Hambidge KM, Mild zinc deficiency in human subjects. In: Mills CF, ed. Zinc in Human Biology. New York, NY: Springer-Verlag, 1989:281-96.
24. King JC, Cousins RJ. Zinc. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins, RJ, eds. Modern Nutrition in Health and Disease, 10th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2005:271-85.
25. Krasovec M, Frenk E. Acrodermatitis enteropathica secondary to Crohn's disease. Dermatology 1996;193:361-3. [PubMed abstract]
26. Ploysangam A, Falciglia GA, Brehm BJ. Effect of marginal zinc deficiency on human growth and development. J Trop Pediatr 1997;43:192-8. [PubMed abstract]
27. Nishi Y. Zinc and growth. J Am Coll Nutr 1996;15:340-4. [PubMed abstract]
28. Hunt JR. Bioavailability of iron, zinc, and other trace minerals from vegetarian diets. Am J Clin Nutr 2003;78 (3 Suppl):633S-9S. [PubMed abstract]
29. Van Wouwe JP. Clinical and laboratory assessment of zinc deficiency in Dutch children. A review. Biol Trace Elem Res 1995;49:211-25. [PubMed abstract]
30. Hambidge KM, Krebs NF. Zinc deficiency: a special challenge. J Nutr 2007;137:1101-5. [PubMed abstract]
31. Prasad AS. Zinc deficiency in women, infants and children. J Am Coll Nutr 1996;15:113-20. [PubMed abstract]
32. Naber TH, van den Hamer CJ, Baadenhuysen H, Jansen JB. The value of methods to determine zinc deficiency in patients with Crohn's disease. Scand J Gastroenterol 1998;33:514-23. [PubMed abstract]
33. Prasad AS. Zinc deficiency. BMJ 2003;326:409-10. [PubMed abstract]
34. American Dietetic Association, Dietitians of Canada. Position of the American Dietetic Association and Dietitians of Canada: vegetarian diets. J Am Diet Assoc 2003;103:748-65. [PubMed abstract]
35. Caulfield LE, Zavaleta N, Shankar AH, Merialdi M. Potential contribution of maternal zinc supplementation during pregnancy to maternal and child survival. Am J Clin Nutr 1998;68 (2 Suppl):499S-508S. [PubMed abstract]
36. Krebs NF. Zinc supplementation during lactation. Am J Clin Nutr 1998;68 (2 Suppl):509S -12S. [PubMed abstract]
37. Brown KH, Allen LH, Peerson J. Zinc supplementation and children's growth: a meta-analysis of intervention trials. Bibl Nutr Dieta 1998;54:73-6.
38. Leonard MB, Zemel BS, Kawchak DA, Ohene-Frempong K, Stallings VA. Plasma zinc status, growth, and maturation in children with sickle cell disease. J Pediatr 1998;132:467-71. [PubMed abstract]
39. Zemel BS, Kawchak DA, Fung EB, Ohene-Frempong K, Stallings VA. Effect of zinc supplementation on growth and body composition in children with sickle cell disease. Am J Clin Nutr 2002;75:300-7. [PubMed abstract]
40. Prasad AS. Zinc deficiency in patients with sickle cell disease. Am J Clin Nutr 2002;75:181-2. [PubMed abstract]
41. Kang YJ, Zhou Z. Zinc prevention and treatment of alcoholic liver disease. Mol Aspects Med 2005;26:391-404. [PubMed abstract]
42. Menzano E, Carlen PL. Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunctiona review. Alcohol Clin Exp Res 1994;18:895-901. [PubMed abstract]
43. Navarro S, Valderrama R, To-Figueras J, Gimenez A, Lopez JM, Campo E, et al. Role of zinc in the process of pancreatic fibrosis in chronic alcoholic pancreatitis. Pancreas 1994;9:270-4. [PubMed abstract]
44. Shankar AH, Prasad AS. Zinc and immune function: the biological basis of altered resistance to infection. Am J Clin Nutr 1998;68:447S-63S. [PubMed abstract]
45. Wintergerst ES, Maggini S, Hornig DH. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab 2007;51:301-23. [PubMed abstract]
46. Beck FW, Prasad AS, Kaplan J, Fitzgerald JT, Brewer GJ. Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. Am J Physiol 1997;272:E1002-7. [PubMed abstract]
47. Prasad AS. Effects of zinc deficiency on Th1 and Th2 cytokine shifts. J Infect Dis 2000;182 (Suppl):S62-8. [PubMed abstract]
48. Bahl R, Bhandari N, Hambidge KM, Bhan MK. Plasma zinc as a predictor of diarrheal and respiratory morbidity in children in an urban slum setting. Am J Clin Nutr 1998;68 (2 Suppl):414S-7S. [PubMed abstract]
49. Brooks WA, Santosham M, Naheed A, Goswami D, Wahed MA, Diener-West M, et al. Effect of weekly zinc supplements on incidence of pneumonia and diarrhoea in children younger than 2 years in an urban, low-income population in Bangladesh: randomised controlled trial. Lancet 2005;366:999-1004. [PubMed abstract]
50. Meydani SN, Barnett JB, Dallal GE, Fine BC, Jacques PF, Leka LS, et al. Serum zinc and pneumonia in nursing home elderly. Am J Clin Nutr 2007;86:1167-73. [PubMed abstract]
51. Black RE. Zinc deficiency, infectious disease and mortality in the developing world. J Nutr 2003;133:1485S-9S. [PubMed abstract]
52. Lansdown AB, Mirastschijski U, Stubbs N, Scanlon E, Agren MS. Zinc in wound healing: theoretical, experimental, and clinical aspects. Wound Repair Regen 2007;15:2-16. [PubMed abstract]
53. Anderson I. Zinc as an aid to healing. Nurs Times 1995;91:68, 70. [PubMed abstract]
54. Wilkinson EA, Hawke CI. Does oral zinc aid the healing of chronic leg ulcers? A systematic literature review. Arch Dermatol 1998;134:1556-60. [PubMed abstract]
55. Wilkinson EA, Hawke CI. Oral zinc for arterial and venous leg ulcers. Cochrane Database Syst Rev 2000;(2):CD001273. [PubMed abstract]
56. World Health Organization and United Nations Children Fund. Clinical management of acute diarrhoea. WHO/UNICEF Joint Statement, August, 2004.[ https://www.unicef.org/nutrition/files/ENAcute_Diarrhoea_reprint.pdf]
57. Black RE. Therapeutic and preventive effects of zinc on serious childhood infectious diseases in developing countries. Am J Clin Nutr 1998;68:476S-9S. [PubMed abstract]
58. Bhutta ZA, Bird SM, Black RE, Brown KH, Gardner JM, Hidayat A, et al. Therapeutic effects of oral zinc in acute and persistent diarrhea in children in developing countries: pooled analysis of randomized controlled trials. Am J Clin Nutr 2000;72:1516-22. [PubMed abstract]
59. Lukacik M, Thomas RL, Aranda JV. A meta-analysis of the effects of oral zinc in the treatment of acute and persistent diarrhea. Pediatrics 2008;121:326-36. [PubMed abstract]
60. Fischer Walker CL, Black RE. Micronutrients and diarrheal disease. Clin Infect Dis 2007;45 (1 Suppl):S73-7. [PubMed abstract]
61. Hulisz D. Efficacy of zinc against common cold viruses: an overview. J Am Pharm Assoc (2003) 2004;44:594-603. [PubMed abstract]
62. Caruso TJ, Prober CG, Gwaltney JM Jr. Treatment of naturally acquired common colds with zinc: a structured review. Clin Infect Dis 2007;45:569-74. [PubMed abstract]
63. Prasad AS, Beck FW, Bao B, Snell D, Fitzgerald JT. Duration and severity of symptoms and levels of plasma interleukin-1 receptor antagonist, soluble tumor necrosis factor receptor, and adhesion molecules in patients with common cold treated with zinc acetate. J Infect Dis 2008 ;197:795-802. [PubMed abstract]
64. Turner RB, Cetnarowski WE. Effect of treatment with zinc gluconate or zinc acetate on experimental and natural colds. Clin Infect Dis 2000;31:1202-8. [PubMed abstract]
65. Eby GA, Halcomb WW. Ineffectiveness of zinc gluconate nasal spray and zinc orotate lozenges in common-cold treatment: a double-blind, placebo-controlled clinical trial. Altern Ther Health Med 2006;12:34-8. [PubMed abstract]
66. Marshall I. Zinc for the common cold. Cochrane Database Syst Rev 2000;(2):CD001364. [PubMed abstract]
67. Evans JR. Antioxidant vitamin and mineral supplements for slowing the progression of age-related macular degeneration. Cochrane Database Syst Rev 2006;(2):CD000254. [PubMed abstract]
68. Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol 2001;119:1417-36. [PubMed abstract]
69. van Leeuwen R, Boekhoorn S, Vingerling JR, Witteman JC, Klaver CC, Hofman A, et al. Dietary intake of antioxidants and risk of age-related macular degeneration. JAMA 2005;294:3101-7. [PubMed abstract]
70. Chong EW, Wong TY, Kreis AJ, Simpson JA, Guymer RH. Dietary antioxidants and primary prevention of age related macular degeneration: systematic review and meta-analysis. BMJ 2007;335:755. [PubMed abstract]
71. Newsome DA, Swartz M, Leone NC, Elston RC, Miller E. Oral zinc in macular degeneration. Arch Ophthalmol 1988;106:192-8. [PubMed abstract]
72. Stur M, Tittl M, Reitner A, Meisinger V. Oral zinc and the second eye in age-related macular degeneration. Invest Ophthalmol Vis Sci 1996;37:1225-35. [PubMed abstract]
73. Whittaker P. Iron and zinc interactions in humans. Am J Clin Nutr 1998;68:442S-6S. [PubMed abstract]
74. Broun ER, Greist A, Tricot G, Hoffman R. Excessive zinc ingestion. A reversible cause of sideroblastic anemia and bone marrow depression. JAMA 1990;264:1441-3. [PubMed abstract]
75. Willis MS, Monaghan SA, Miller ML, McKenna RW, Perkins WD, Levinson BS, et al. Zinc-induced copper deficiency: a report of three cases initially recognized on bone marrow examination. Am J Clin Pathol 2005;123:125-31. [PubMed abstract]
76. Lewis MR, Kokan L. Zinc gluconate: acute ingestion. J Toxicol Clin Toxicol 1998;36:99-101. [PubMed abstract]
77. Hooper PL, Visconti L, Garry PJ, Johnson GE. Zinc lowers high-density lipoprotein-cholesterol levels. J Am Med Assoc 1980;244:1960-1. [PubMed abstract]
78. Johnson AR, Munoz A, Gottlieb JL, Jarrard DF. High dose zinc increases hospital admissions due to genitourinary complications. J Urol 2007;177:639-43. [PubMed abstract]
79. Lomaestro BM, Bailie GR. Absorption interactions with fluoroquinolones. 1995 update. Drug Saf 1995;12:314-33. [PubMed abstract]
80. Penttila O, Hurme H, Neuvonen PJ. Effect of zinc sulphate on the absorption of tetracycline and doxycycline in man. Eur J Clin Pharmacol 1975;9:131-4. [PubMed abstract]
81. Natural Medicines Comprehensive Database. Zinc. [https://www.NaturalDatabase.com]
82. Brewer GJ, Yuzbasiyan-Gurkan V, Johnson V, Dick RD, Wang Y. Treatment of Wilson's disease with zinc: XI. Interaction with other anticopper agents. J Am Coll Nutr 1993;12:26-30. [PubMed abstract]
83. Wester PO. Urinary zinc excretion during treatment with different diuretics. Acta Med Scand 1980;208:209-12. [PubMed abstract]

*These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any diseases.