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No “Bones” About It…

Essential Fatty Acids and BonesEssential Fatty Acids may be a key ingredient in supporting bone health.

Essential fatty acids (EFAs) do not come to mind as the first thought in searching for nutritional answers regarding bone health.  “Recent evidence-based research, however, supports intervention with adequate amounts of specific nutrients including vitamin D, strontium, vitamin K, and essential fatty acids in the prevention and primary management of osteoporosis” (Genius, Clin Nutr. 2007).  Osteoporosis has become an epidemic in the Western World in recent years.  How do EFAs fit into this problem that plagues us especially as we get older?

When we think about osteoperosis, we think calcium.  Calcium and bone go together like salt and pepper.  Add in some vitamin D and that’s about it.  However, looking into it deeper we came up with a number of studies that say that EFAs should be right up front and strongly considered in our first line of bone defense.

Essential fatty acids are necessary to human survival, and are called essential because they must come from the diet; they cannot be made by the body.  The omega-6 and omega-3 fatty acids are the best known.  Learning that they are also important for bone health is something we need to know.

In vivo studies (that means in a living animal) have shown that supplementation with long chain n-6 poly-unsaturated fatty acids (PUFAs) in rats causes increases in intestinal Calcium absorption (Haag 2001).  Haag and his colleagues reported a higher total calcium balance and bone calcium content just by adding in either sunflower or safflower oil in their diet.

In another study pregnant female rats were made diabetic. They use a chemical called streptozotocin to duplicate the disorder in the animals.  They were then fed evening primrose oil (GLA) at 500 mg/kg/d throughout their pregnancy and found an almost complete restoration of bone ossification (process of laying down new bone) occurred just by adding in the primrose oils (Braddock, Pediatr Res. 2002).

Claassen et al, Prostaglandins 1995, found that the supplementation of essential fatty acids (EFAs) leads to increased intestinal calcium absorption and calcium balance. The main dietary EFAs they used were linoleic acid (LA) from sunflower oil and alpha-linolenic acid (ALA) from flax seed oil.  They were administered in a ratio of 3:1 which is very close to our 4:1 BodyBio Balanced oil.  The calcium balance (mg/24 h) and bone calcium (mg/g bone ash) increased significantly in the group that were on the EFAs as compared to the animals that were not given the oils.

Schlemmer et al, Prostaglandins 1999, found that if you make animal’s essential fatty acid deficient they flat out develop osteoporosis.  He then added in evening primrose oil (GLA) and completely reversed the loss of bone and reported positive effects on bone metabolism in both the growing male and female rat.

It certainly goes against what you might think.  Oils are thin, some of them even squishy, while bone is completely hard as a rock.  But leaning on our visual senses doesn’t work with body chemistry, obviously.

Bone remodeling is a life-long process where mature bone tissue is removed from the skeleton and is called resorption, while new bone tissue is formed.  It’s a process called ossification or new bone formation. These processes go on all the time and are managed by special cells that crawl along our bones and chew up excess bone growth, osteoclast.  There is another cell osteoblast, that busily does the opposite, laying down new growth where it’s needed.

In the first year of life, almost 100% of the skeleton is replaced.  In adults, remodeling proceeds at about 10% per year (Wheeless).  That means that in a span of 10 years our skeleton is brand new,  If the process is continuous those cells that do the work must be directly influenced by essential fatty acids, and if EFAs are needed to get the job done, well…

References

Genuis SJ, Schwalfenberg GK. Picking a bone with contemporary osteoporosis management: Nutrient strategies to enhance skeletal integrity. Clin Nutr. 2007 Apr;26(2):193-207

Haag M, Kearns SD, Magada ON, Mphata PR, Claassen N, Kruger MC. Effect of arachidonic acid on duodenal enterocyte ATPases. Prostaglandins Other Lipid Mediat. 2001 Aug;66(1):53-63

Braddock R, Siman CM, Hamilton K, Garland HO, Sibley CPGamma-linoleic acid and ascorbate improves skeletal ossification in offspring of diabetic rats. Pediatr Res. 2002 May;51(5):647-52.

Claassen N, Coetzer H, Steinmann CM, Kruger MC. The effect of different n-6/n-3 essential fatty acid ratios on calcium balance and bone in rats. Prostaglandins Leukot Essent Fatty Acids. 1995 Jul;53(1):13-9.

Schlemmer CK, Coetzer H, Claassen N, Kruger MC. Oestrogen and essential fatty acid supplementation corrects bone loss due to ovariectomy in the female Sprague Dawley rat. Prostaglandins Leukot Essent Fatty Acids. 1999 Dec;61(6):381-90

Wheeless Textbook of Orthopedics, Clifford R. Wheeless, III, MD.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Vitamins? Why?

vitaminsDo you take vitamins? Yes? Why? No? Why not?  Confusing, isn’t it? Can we ever get to the bottom of the yes-no controversy?

First of all, let’s find out what we’re talking about.

The word “vitamins” describes organic substances that are quite diverse in function and structure.  It was initially felt that these compounds could be obtained through a normal diet, and that they were capable of promoting growth and development, and of maintaining life.  The word itself was coined by a Polish biochemist named Casimir Funk, in 1911.  He deemed these substances to be chemical amines, thinking that all contained a nitrogen atom.  Since they were considered to be vital to existence (“vita” means “life” in Latin), they were called “vitamines.”  After it was discovered that they all did not have a nitrogen atom, and, therefore, were not amines, the terminal “e” was dropped.  Funk was working in London at the time, at the Lister Institute, where he isolated a substance without which chickens would suffer neurological inflammation.

The lettered names of the vitamins were ascribed to them in the order of their discovery.  Vitamin K, however, is the exception.  Its label was given by the Danish researcher Henrik Dam, from the word “koagulation.”

If a vitamin is improperly absorbed, or is absent from the diet, a deficiency exists and a specific disease may surface, such as Beriberi, which was noted by William Fletcher in 1905 when symptoms appeared in populations whose diet consisted mostly of polished rice, lacking the thiamine-rich husk.  Lack of thiamine, or vitamin B1, causes emotional disturbances, physical weakness, heart failure, impaired sensory perception, and, in severe circumstances, eventual death.

Scurvy, a deficiency of vitamin C, was once a common ailment of sailors and others who were out to sea for a longer time than their fruits and vegetables could remain edible.  The Latin name of this condition that caused bleeding from the mucus membranes and spongy gums is “scorbutus,” from which we get “ascorbic acid.”  James Lind, a surgeon in the Royal Navy, learned in the 1750s that scurvy could be treated with citrus fruits, and he wrote about his experiments in his 1753 book, “A Treatise of the Scurvy.”

If vitamins are so “vital,” what, exactly, are their roles in human health and well-being?  Vitamin A was first synthesized in 1947, though discovered around 1912 by researchers Elmer McCollum and M. Davis, and later isolated from butter by Yale scientists Thomas Osborne and Lafayette Mendel.  This nutrient contains carotene compounds that are responsible for transmitting light signals to the retina of the eye.  McCollum also uncovered the B vitamins, but later researchers isolated each of the individual factors.

We already know that a lack of B1 causes Beriberi, while a deficiency of B2 may lead to inflammation of the lining of the mouth.  Also called riboflavin, B2 is responsible for the reactions of enzymes, as is its partner, B3 (niacin).  In general, the gamut of B vitamins is involved in the same metabolic processes.  It was decided that a B vitamin must meet specific criteria:  it must be water-soluble, must be essential for all cells, and must function as a coenzyme.  B12 and folate have the added responsibility of being involved in the synthesis of nucleic acid.  Folate is the form of the nutrient naturally found in food, while folic acid is synthetic. Great excesses of one B vitamin can cause deficiencies of the others.  Therefore, if taken as supplements, it is recommended that they be taken together.

Besides preventing scurvy, as mentioned, vitamin C helps the body to make collagen, the protein that acts as the framework for the body.  Collagen is a major component of ligaments and cartilage, it strengthens blood vessels, and it is responsible for skin strength and elasticity.  Vitamin C was the first to be artificially made, in 1935.

Vitamin D is not actually a vitamin, but a prohormone, meaning that it is a precursor to a hormone, called 1,25-D, which helps the body to make its own steroids, such as cholesterol, a substance absolutely necessary to the integrity of each of our trillions of cells.  Vitamin D is needed to maintain correct calcium and phosphorus levels, to assure proper bone mineralization, and to support the immune system.  A severe deficiency leads to rickets, a softening of the bones—usually in children—that was studied in 1922 by Edward Mellanby.

Vitamin E is actually a group of isomers (like-structured molecules) that function as antioxidants.  Study of this fat-soluble nutrient has focused on its purported benefits to the cardiovascular system. University of California researchers discovered vitamin E while studying green, leafy vegetables, in the 1920s.

Another fat-soluble substance, vitamin K is used by the body to assist in the manufacture of bone, and in the manufacture of blood clotting proteins, without which serious bleeding episodes may occur.  This nutrient has been available from green leafy vegetables and from the brassica family, such as broccoli, cauliflower, and kale.

Now the question is, “Can we get all these nutrients from our food, or is supplementation necessary?”

Working at the University of Texas Biochemical Institute, Dr. Donald Davis led a crop-nutrient study in 2004.  He and his team found that the nutrient value of forty-three garden crops has declined considerably over the past fifty years.  As reported in the “Journal of the American College of Nutrition” in December of that year, the forty-three crops showed “statistically reliable declines” in protein, calcium, iron, phosphorus, riboflavin (vitamin B2), and ascorbic acid (vitamin C).  Some nutrients could not be compared because their values were not reported in the 1950s.  They include magnesium, zinc, vitamin B6, vitamin E, dietary fiber, and phytochemicals.

After accounting for possible confounders, the study concluded that the change in nutrient value could be ascribed to changes in cultivated varieties, in which there could have been a trade-off between crop yield and nutrient value.  Dr. Davis added that farmers are paid by the weight of a crop, not by its food value.

Some innovative farming techniques have given rise to faster-growing crops, which, by virtue of their seed-to-market time, do not have sufficient time to develop their nutrients.  They do not have the chance to absorb everything they need from the soil.

Crop rotation has fallen into disfavor by some farms because it requires more planning and management skills than are at hand, thus increasing the complexity of farming.  Rotation of crops helps to reduce insect and disease problems, improves soil fertility, reduces soil erosion, and limits biocide carryover.  If, however, a single crop is a big moneymaker for the farm, why should it bother even to try to grow something else?  Why bother to rotate crops when chemical fertilizers, herbicides, fungicides, and insecticides can help to guarantee a bumper crop?  Could nutrient value be affected by using these artificial chemicals?  Do these materials come into our bodies?  Do we have the proper kinds and amounts of nutrients to detoxify them?  Maybe we do; maybe not.

Nitrogen-fixing bacteria convert atmospheric nitrogen to organic nitrogen, thus contributing to the food value of the crop.  Certain crops, like the legumes, are better than others at replacing nitrogen lost from the soil.  Nitrogen is part of a protein molecule.  Without nitrogen there is no protein.  While it is beneficial to the food and the soil to plant a legume following the harvest of a more lucrative planting, it is not often done.

Therefore, the same plant in place continues to withdraw the same minerals repeatedly, year after year, with little chance for replenishment except by chemical means, if at all.  How many of us would prefer to get our dietary needs from unnatural sources, like iron from rusted nails, or zinc from galvanized wire?

In a study of peaches and pears published in the “Journal of Agriculture and Food Chemistry” in 2002, Marina Carbonaro, of the National Institute for Nutrition Studies, in Rome, reported a difference in the nutrition content of organic versus traditionally raised fruits.  Amounts of polyphenols, citric and ascorbic acids, and alpha-tocopherol were increased in the organically grown crops.  She and her colleagues concluded that the improved antioxidant defense of the plants developed as a result of organic cultivation methods.  Which do you think has more vitamin C?

Here is a sampling of how the nutrient content of broccoli and potatoes sold in Canada has changed from 1951 to 1999.  This information was compiled by Jeffrey Christian.

Broccoli, Raw, 3 spears, 93g. 100/93=1.08
Calcium (mg) Iron
(mg)
Vitamin A (I.U.) Vitamin C (mg) Thiamine (mg) Riboflavin (mg) Niacin (mg)
1951 130.00 1.30 3500 104.0 0.10 0.21 1.10
1972 87.78 0.78 2500 90.0 0.09 0.20 0.78
1999 48.30 0.86 1542 93.5 0.06 0.12 1.07
% Change -62.85 -33.85 -55.94 -10.10 -40.00 -42.86 -2.73
Potatoes, one potato, peeled before boiling, 136g. 100/136=.74
Calcium (mg) Iron
(mg)
Vitamin A (I.U.) Vitamin C (mg) Thiamine (mg) Riboflavin (mg) Niacin (mg)
1951 11.00 0.70 20.00 17.00 0.11 0.04 1.20
1972 5.74 0.49 0.00 16.39 0.09 0.03 1.15
1999 7.97 0.30 0.00 7.25 0.09 0.02 1.74

The USDA, in its statistical bulletin # 978, made public in June, 2002, titled “The Changing Landscape of U. S. Milk Production,” admitted that milk production has increased because of “advances in animal nutrition and health, improved artificial breeding techniques, and the recent addition of biotechnology, such as…rbST…”
rbST is a hormone that is administered to cows to increase milk production.  Take a look at how milk production has changed, and then decide if there might be implications that could involve humans.

In 1950, a single cow (I mean one cow, not an unmarried cow.) produced 5,314 pounds of milk.  By 1975, she increased her output to 10,360 pounds.  In 2000, that amount increased to 18,204 pounds.  The USDA admits that “…a 76-percent increase in milk per cow since 1975 is substantial.”  Substantial?  How about phenomenal, even miraculous?  Could a factory have increased its output by seventy-five percent in twenty-five years?  Could a weight lifter elevate that much of a weight increase in a military press as he did twenty-five years ago?  Could recombinant bovine somatotropin enter the milk supply and affect human growth and development, or even contribute to human misery?

Not only do modern agricultural techniques affect the quality of food, but also do the processes by which food is processed and packaged.  To prevent the growth of pathogenic bacteria, some canned foods are exposed to temperatures that compromise their nutritional value.  Acidic foods, like tomatoes, are excused from excessive heat because their nature does not support the growth of food poisoning bacteria.  Others are heated to temperatures high enough to destroy bacteria, yeasts, and molds that could cause foods to spoil.  Heating to 250 degrees Fahrenheit for three minutes not only kills pathogens, but also denigrates the potency of water-soluble vitamins.  If these foods are consumed without also consuming the water in which they are prepared, nutrition is sacrificed.

The USDA has a table of nutrient retention factors that compare the nutritional value of processed foods.  This table includes most nutrients from alpha-tocopherol to zinc.  It is noted that folate, for example, a nutrient easily lost in food preservation and preparation, is diminished by almost 50% in canned fruits as compared to fresh and frozen.  Additionally, canned foods are higher in sodium, and their texture is softer than either fresh or frozen.  The mineral and protein values of canned foods are usually undisturbed.  In rare instances, as with tomatoes and pumpkin, nutrient value is retained, or even increased, by canning.  We should note that canned fruits and vegetables are better than none at all.

Frozen foods, on the other hand, retain much of the nutrition they are destined to have.  The folate retention factor for frozen fruits is ninety-five, contrasted to fifty for canned.  There are some compromises, though, because frozen foods need to be blanched prior to being frozen.  Blanching, however, is no worse than what happens to foods during normal cooking activity.  This means that frozen vegetables provide levels of nutrition similar to fresh, provided they are stored and handled properly.  The “International Journal of Food Science and Technology,” reported in June of 2007 that the freezing process alone does not affect vitamin levels, but that the initial processing and later storage do.  About 25% of vitamin C and a higher percentage of folate are lost through the blanching process.  These numbers will vary according to the processing techniques.

An advantage to canned and frozen foods is that the foods themselves are harvested at their maximum stage of development, containing all the vitamins and minerals they could possibly extract from their environments.  What we call “fresh” vegetables are usually anything but.  They have been picked before their maximum ripeness so that they can be shipped across the country.  If not harvested locally, “fresh” vegetables are more accurately labeled as “raw,” or “unprocessed.”  Water-soluble vitamins, like the B complex and vitamin C, are affected by exposure to light and air.  Vitamin A is jeopardized by exposure to light, as well.  The amount of time that a raw vegetable spends in storage may take its toll on nutrient integrity, also.

Typical Maximum Nutrient Losses (as compared to raw food)
Vitamins Freeze Dry Cook Cook+Drain Reheat
Vitamin A 5% 50% 25% 35% 10%
  Retinol Activity Equivalent 5% 50% 25% 35% 10%
  Alpha Carotene 5% 50% 25% 35% 10%
  Beta Carotene 5% 50% 25% 35% 10%
  Beta Cryptoxanthin 5% 50% 25% 35% 10%
  Lycopene 5% 50% 25% 35% 10%
  Lutein+Zeaxanthin 5% 50% 25% 35% 10%
Vitamin C 30% 80% 50% 75% 50%
Thiamin 5% 30% 55% 70% 40%
Riboflavin 0% 10% 25% 45% 5%
Niacin 0% 10% 40% 55% 5%
Vitamin B6 0% 10% 50% 65% 45%
Folate 5% 50% 70% 75% 30%
  Food Folate 5% 50% 70% 75% 30%
  Folic Acid 5% 50% 70% 75% 30%
Vitamin B12 0% 0% 45% 50% 45%
Minerals Freeze Dry Cook Cook+Drain Reheat
Calcium 5% 0% 20% 25% 0%
Iron 0% 0% 35% 40% 0%
Magnesium 0% 0% 25% 40% 0%
Phosphorus 0% 0% 25% 35% 0%
Potassium 10% 0% 30% 70% 0%
Sodium 0% 0% 25% 55% 0%
Zinc 0% 0% 25% 25% 0%
Copper 10% 0% 40% 45% 0%

Can we get all the vitamins and minerals we need from food?  No.

Take a look at vitamin C, one of the most-studied nutrients.  Because of its fragile nature, vitamin C, a popular water-soluble supplement, needs special handling.  This characteristic may explain why it seems to have been a major focus of the food business for years.  It is extremely sensitive to heat, and slightly less so to light, and time.  Loss of vitamin C during processing ranges from about 10% in beets to almost 90% in carrots.  The amount of vitamin C at the start has no bearing on the outcome.  It’s the percentage that makes the matter a real concern.  Since this vitamin is easily oxidized, it is difficult to measure levels in drained liquids.  That goes for the cooking water, as well.  Canned foods are further insulted by cooking at high temperatures for a long time, without a lid.  It is nutritionally prudent to include the water from the can in the meal.  Otherwise, the ascorbic acid goes down the drain.  The table below demonstrates changes in vitamin C levels resulting from canning alone.

Ascorbic acid (g / kg−1 wet weight) in fresh and canned vegetables
Commodity Fresh Canned % Loss
Broccoli 1.12 0.18 84
Corn 0.042 0.032 0.25
Carrots 0.041 0.005 88
Green peas 0.40 0.096 73
Spinach 0.281 0.143 62
Green beans 0.163 0.048 63
Beets 0.148 0.132 10
J Sci Food Agric 87:930–944 (2007) Nutritional comparison of fresh, frozen and canned fruits and vegetables. Part 1. Vitamins C and B and phenolic compounds. Joy C Rickman, Diane M Barrett and Christine M Bruhn

 Freezing has less impact on nutrient levels than other types of processing. Because foods are harvested at their maximum maturity stage before freezing, they already contain the most nutritive value they can be expected to have. The table that follows shows losses of ascorbic acid (vitamin C) after periods of storage at various temperatures, starting at room temperature (20° C; 68° F), through the refrigerator crisper drawer (4° C; 39° F), to the freezer (-20° C; -4° F).

Losses of ascorbic acid (% dry weight) due to fresh and frozen storage
Commodity Fresh, 20 ◦C,
7 Days
Fresh, 4 ◦C,
7 Days
Frozen, −20 ◦C,
12 Months
Broccoli 56 0 10
Carrots 27 10
Green beans 55 77 20
Green peas 60 15 10
Spinach 100 75 30
J Sci Food Agric 87:930–944 (2007) Nutritional comparison of fresh, frozen and canned fruits and vegetables. Part 1. Vitamins C and B and phenolic compounds. Joy C Rickman, Diane M Barrett and Christine M Bruhn

Vitamin C does continue to degrade after long periods of freezing, but at a slower rate. What seems to be the main factor in this process is the moisture content of the food at the outset. Notice that refrigerating foods as soon as they come home from the market plays a serious role in maintaining nutritive value. The cook is the penultimate figure in the saga of a food’s life. The method of cooking can cause loss of ascorbic acid at the rate of 15% to 55%. Losses in canned products are probably minimal because the food already sits in water. Oddly, unheated canned products are occasionally comparable to that which is cooked fresh. But who has the wherewithal to determine that at home? Remember that, because vitamin C oxidizes in air, the value of frozen foods may be substantially higher than fresh foods that have been stored for a long time or under sub-optimal conditions. So…fresh (raw) may not always be the best. Whatever the case, additional research is expected to substantiate changes in vitamin C levels caused by cooking habits. Microwaving, for example, may have an unexpected influence, based on the solubility and diffusion of certain food solids, such as sugars that may diminish faster than ascorbic acid, leaving vitamin C behind.

It is necessary to realize that carrots are not exactly heralded for their vitamin C value in the first place, so losses are relatively insignificant. Also, note that sources of information may present nonconcurring results due to variations in measurement techniques, quality of raw ingredients, and other variables.

The water-soluble B vitamins (all are water-soluble) suffer a fate similar to that of ascorbic acid. Thiamin, the least stable of the vitamins to thermal indignity, is most sensitive to degradation caused by food processing. But, since fruits and vegetables are not exceptional sources of this nutrient, its retention or loss does not represent overall nutrient retention or loss of a particular food. Riboflavin is unstable in the presence of light. Processing and storage / display play a role in its stability. Clear glass containers can cause this vitamin to dwindle. Realization of this fact by the food industry is one reason that certain foods are now in opaque containers. The exception to the B-vitamin family is vitamin B12 because it is found mostly in animal products. The same considerations that apply to vitamin C are appropriate for the B vitamins.

The normal eating habits of Americans suggest that we are woefully inadequate in meeting dietary recommendations to achieve optimum well-being and health.  Most of us do not eat the recommended number of daily servings of fruits and vegetables.  For some nutrients, daily intake needs may be higher for some populations than for others, especially those in particularly vulnerable groups, such as those with gastrointestinal problems or poor absorption, those who are chronically ill, those who are alcohol or drug dependent, and the elderly.

The June 19, 2002 edition of the “Journal of the American Medical Association” recanted that august body’s negative position on vitamin supplements when it advised all adults to take at least one multivitamin tablet a day.  The article, “Vitamins for Chronic Disease Prevention in Adults,” authored by Robert H. Fletcher, MD, MSc, and others, agreed that suboptimal levels of folic acid and vitamins B6 and B12 are a risk factor for cardiovascular disease, neural tube defects, and colon and breast cancers.  It added that risks for other chronic diseases are increased by low levels of the antioxidant vitamins A, C, and E.

Because it is accepted that high homocysteine levels are associated with increased risk of heart disease, the AMA’s recommendation for optimal levels of cardio-specific supplements are well founded.

Depending on a person’s physiological state, he or she may need more of a particular nutrient than is available from a multivitamin alone.  The bioavailability of a specific nutrient from a high quality supplement is close to one hundred percent, compared to a food whose life experiences might have been less than ideal.  In a society that falls short of consuming the five to nine servings of fruits and vegetables that are recommended, it would be inane to ask them to eat more fruits and vegetables to get the nutrients they lack.

This does not mean that a person should take a little of this and a little of that because he read about it somewhere.  On the contrary, supplementation with vitamins, minerals, and herbs is a scientific enterprise that entails one’s medical history, both distant and recent past, one’s current physiological state, and even one’s blood chemistry.

Do you take vitamins?

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

ADHD and Magnesium

Magnesium deficiencyMagnesium deficiency has been reported in children with ADHD syndrome.  Signs of this malady include hyperactivity, hypermotivity with aggressiveness, and lack of attention, especially at school.  Biochemical and concurrent behavioral improvements have been realized by magnesium therapy in association with vitamin B6 supplementation.

An analysis of eighteen different study groups performed by Marianne Moussain-Bosc and her colleagues at a French institute for nervous system studies in 2006 indicated that ,”…B6/magnesium therapy benefits about half of autistic children,” but also noted that a related study showed benefits to those with ADHD, using the same doses of each supplement.  Children ranging from one to ten years of age “…received 0.6 milligrams per kilogram per day of vitamin B6 and 6 milligrams per kilogram per day of magnesium.  Treatment lasted an average of eight months.”  (Moussain-Bosc. 2006)   Both groups of children had significantly lower values of erythrocyte magnesium at the outset than the control group(s).  It was observed that after two months of the vitamin-mineral regimen there was a substantial change in clinical symptoms.

ADD and ADHD are on the upswing, and have been for some time.  Both conditions are hastily treated with drugs, often without a differential diagnosis, which is essentially a process of elimination.  Instead, the Diagnostic and Statistical Manual (DSM) of Mental Disorders criteria, and a series of observations and teacher questionnaires are employed.  (Pediatrics. 2000. No authors listed.)   Mineral and electrolyte imbalances are awfully hard to discover with that technique, don’t you think? Most parents wince at the thought of dosing their kids with “miracle” substances that have unknown long-term side effects. On the other hand, the clueless, self-centered, entitled faction applauds the quiet, calm, relatively immobile zombie of the house.

Although we live in plentiful times, where food, shelter, and clothing are accessible to all who earn them, there still exist children who are seriously shy of their required magnesium stores.  One reason is stress.  The number of stressors to which kids are exposed grows every year.  From sports practice, to violence in the streets and on television, to academic obligations, to peer pressure and self-image, and more, the kids are overloaded.  It’s the accompanying flood of adrenaline that siphons magnesium, since that hormone needs the mineral for its release.  Another reason is poor nutrition.  You know, processed foods, refined sugars, colorful and flavorful additives, artificial this and that…  This kind of diet is notoriously low in magnesium, which is calming to the nervous system.  The refined sugars and additives actually stress the body, especially the nervous system, as it tries to overcome the onslaught.  A double whammy.

In Poland, researchers studied ADHD children and assessed the value of magnesium supplementation on the DSM parameters, finding that six months of taking as little as 200 mg a day yielded a decrease in symptoms.  (Starobrat-Hermelin. 1997)  Later study performed by Moussain-Bosc saw a decrease in ADHD symptoms using a combined magnesium / B6 regimen in several dozens of children with low red blood cell magnesium stores.  (Moussain-Bosc. 2004)

Attention deficit hyperactivity disorder is a developmental perturbation characterized by attention problems and hyperactive behavior.  It’s the most commonly studied psychiatric disorder in children, affecting three to five percent of children worldwide.  Sadly, integrative therapies are spurned by traditional-minded doctors, so parents have taken it upon themselves to intervene, despite the lack of support from their physicians.

Bearing in mind that sugar has a nutrient-diluting effect might make a difference in ADHD management and magnesium stores in the body.  It’s normal to wonder where all the magnesium goes.  Doesn’t it stay still?  After all, it’s part of bone.  That’s true, but magnesium is also an electrolyte, helping to send calming electrical messages across the membrane of each cell, making it a natural calcium channel blocker.  It gets used up in the manufacture of more than three hundred enzymes the body needs, including those that make anti-inflammatory chemicals from fatty acids.  Situations and conditions within the body can push this mineral into the urine and then into the toilet.  Sugar intake, and even that of simple carbohydrates, increases the secretion of insulin by the pancreas.   Increased insulin, as might be found in insulin resistance, pushes magnesium out.  (Huerta. 2005)  The pancreas needs magnesium to make its other secretions, including those that break down proteins (trypsin and chymotripsin) and fats (lipase), as well as carbohydrates.  Carol Ballew and her colleagues found that carbonated beverages, namely soda, are negatively associated with magnesium levels This starts a vicious cycle because low magnesium is related to insulin resistance. (Ballew. 2000).

In tests done in the mid 90’s, it was discovered that elevated insulin levels result in increased magnesium excretion.  These researchers noted this as the explanation to the magnesium deficit that accompanies obesity, diabetes, and hypertension, as well as hyperinsulinemia.  (Djurhuus. 1995)  This same group later reported that high glucose levels, such as would come from a sugary breakfast or a plethora of sweet goodies, raise magnesium excretion by a factor greater than 2.0.  (Djurhuus. 2000)

The foods that once supplied dietary magnesium have become compromised by careless farming, harvesting, processing, storage, and handling practices.  We now get more calcium and less magnesium than ever in the history of mankind.  Sugar erases magnesium from the body’s slate. (Fuchs. 2002) (Tjaderhane. 1998) (Milne. 2000)  It’s time to put it back.  At 6.0 mg / kg / day, that equates to about 3.0 milligrams per pound of body weight…for all of us.

References

  • AUTISM RESEARCH REVIEW INTERNATIONAL Vol. 20, No.3, 2006
    Studies confirm benefits of vitamin B6/magnesium therapy for autism, PDD, and ADHD
    No Authors Cited

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  • Magnes Res. 1997 Jun;10(2):143-8.
    Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD).
    Kozielec T, Starobrat-Hermelin B.

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  • Pediatrics. 2000 May;105(5):1158-70
    Did not perform differentiated diagnosis
    Clinical practice guideline: diagnosis and evaluation of the child with attention-deficit/hyperactivity disorder. American Academy of Pediatrics.
    No authors listed

    +

  • Magnes Res. 2006 Mar;19(1):53-62.
    Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6. II. Pervasive developmental disorder-autism.
    Mousain-Bosc M, Roche M, Polge A, Pradal-Prat D, Rapin J, Bali JP.

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  • J Am Coll Nutr. 2004 Oct;23(5):545S-548S.
    Magnesium VitB6 intake reduces central nervous system hyperexcitability in children.
    Mousain-Bosc M, Roche M, Rapin J, Bali JP.

    +

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    Edward J. Lennon and Walter F. Piering

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    Goldman JA, Lerman RH, Contois JH, Udall JN Jr.

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    Beverage Choices Affect Adequacy of Children’s Nutrient Intakes
    Carol Ballew, PhD; Sarah Kuester, MS, RD; Cathleen Gillespie

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    Magnesium deficiency is associated with insulin resistance in obese children.
    Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, Patrie JT, Rogol AD, Nadler JL.
    SourceUniversity of Virginia, Department of Pediatrics, Box 800386, Charlottesville, VA 22908, USA. [email protected]

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    Insulin Increases Renal Magnesium Excretion: A Possible Cause of Magnesium
    Depletion in Hyperinsulinaemic States

    Dr. M.S. Djurhuus, P. Skøtt, O. Hother-Nielsen, N.A.H. Klitgaard, H. Beck-Nielsen

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    Hyperglycaemia enhances renal magnesium excretion in Type 1 diabetic patients
    S. Djurhuus

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    A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats
    Leo Tjäderhane, and Markku Larmas
    Institute of Dentistry, University of Oulu, 90220 Oulu, Finland

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    The Interaction Between Dietary Fructose and Magnesium Adversely Affects
    Macromineral Homeostasis in Men

    David B. Milne, PhD and Forrest H. Nielsen, PhD

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Child Athletes Nutrition

children-sportsA child is not a miniature adult. His or her nutrition and hydration needs are not exactly the same, especially in sports participation.  With the growth and availability of sports opportunities, you’d think that related nutrition needs would be a concern. To the contrary, sports nutrition for youngsters receives less attention than it deserves.

“Most children and adolescents who are strongly committed to sports are not concerned about nutrition as it relates to energy balance and obesity,” states a report from a 2004 issue of Nutrition.  The interactions among nutrition, growth, and development deserve attention if a participant expects to achieve optimal performance and to avoid the injuries and problems that stem from nutritional deficiencies.   Daily fluid turnover in adult athletes has received intense study, but that for children and adolescents hasn’t.  That of adults may be two to three liters a day, but in youngsters has only been estimated at half that—and that has been based on sedentary youth.  Although “sweating capacity is typically reported to be lower in children,” there is an increase in sweat rate when adjusted for body surface area.  Besides the energy needed for normal growth and development, children athletes need to accommodate the greater expenditure from physical activity.  That can vary from one sport to another.  (Petrie. 2004).

Besides the fun, kids participate in sports to hone their skills, to experience the excitement of competition, to be part of a team, and to stay in shape, among other reasons.  But they pay little or no attention to fuel and hydration needs.  Parents and coaches, on the other hand, do.  At least they should.  Hectic schedules, availability of foods, limited time and extended days interfere with choices and timing.

Even though the number of kids playing organized sports is on the rise, fitness levels are on the decline, and are much lower than in previous decades.  This partially explains the spate of sports-related injuries.  (Cordelia. 2011).  Targeted intervention strategies include ample hydration and nutrition.  Because of maturation differences, kids need more protein to support growth, more calcium to support bone, and more attention to the prevention of hypohydration.  (Bar-Or. 2001).

Sweat helps to cool the body, and what comes out has to be replaced, otherwise performance suffers and health is at risk.  To prevent the dizziness, fatigue, nausea, and cramps that characterize dehydration, the young athlete should drink one or two cups of water or electrolyte within four hours of an event.  If no urine has been passed, or if urine is bright yellow and minimal, another 1 ½ cups is suggested within two hours of the game.  During the event, try to replace fluids as they are lost to sweat, about a cup every fifteen or twenty minutes if possible.  Plain water will do, but if the event is longer than an hour, use an electrolyte replacement.  Recovery is just as important to a preteen or teen as it is to an adult.  The best way to determine post-exercise hydration needs is to weigh the child to compute weight loss, and to replace fluid at one and a half times the volume lost to sweat.  One ounce of water (sweat) weighs one ounce, so the math is simple.  A kid’s thirst mechanism is not well-developed, so you’ll almost have to force him to drink…but do it.

The nutrients in which young athletes are most deficient include carbohydrates, calcium, vitamin B6, folate and iron, the last being especially important to girls.  Carbohydrate inadequacy leads to shortened glycogen stores and premature fatigue, especially if the game is sixty minutes or longer.  Once glycogen is gone, fat gets mobilized and the child will “bonk.”  The last thing you want is for the young athlete to burn protein for fuel. An active child will need as many as 500 to 1500 more calories a day than his inert peers.

Two to three hours before an event, give your athlete a light, carb-rich meal:  carrot sticks and a piece of cheese; a little pasta; a small sandwich.  Have him exert himself on a slightly empty stomach to avoid cramping, even fatigue.  Chips, cakes or cookies, and candy are out.  The protein your child needs will not build bulk.  That comes with age.  Normal muscle development will require as much as one and a half grams of protein for each kilogram of body weight, but need not be much more than fifteen to twenty percent of daily calorie intake.  Reduce that during the off season. Thirty percent fat in the daily intake will help to supply needed calories.  Reduce that off-season, too, lest you greet Tweedledee one morning.

The matter of iron deficiency is a particular concern for girls, especially after the onset of menarche, which can be a couple of years late for an iron-fisted ball player.  Iron-deficiency anemia is a real threat for female athletes.  Besides affecting performance and recovery, low iron stores impair immune function and may initiate other physiological problems.  Supplementation is not intended to replace food as a source of nutrients, but in the case of iron deficit, it may be recommended.  (Beard. 2000).  There’s no need for your daughter to join the 50% of the world population who are deficient in iron.  (Ahmadi. 2010).  Raw meat probably won’t help, but getting 15 mg a day from supervised supplementation will.

Youngsters are often grossly misinformed about what they need and don’t need.  Their peers and the internet are not always reliable sources of information.  Some young athletes need only a minor tweak to their diets; others need a complete overhaul.  If you feel inadequate, don’t be embarrassed.  There are dietitians and sports nutritionists who can help.

References

Petrie HJ, Stover EA, Horswill CA.
Nutritional concerns for the child and adolescent competitor.
Nutrition. 2004 Jul-Aug;20(7-8):620-31.

Cordelia W Carter, Lyle J Micheli
Training the child athlete: physical fitness, health and injury
Br J Sports Med 2011;45:880-885

Bar-Or O.
Nutritional considerations for the child athlete
Can J Appl Physiol. 2001;26 Suppl:S186-91.

Beard J, Tobin B.
Iron status and exercise.
Am J Clin Nutr. 2000 Aug;72(2 Suppl):594S-7S.

Ahmadi A, Enayatizadeh N, Akbarzadeh M, Asadi S, Tabatabaee SH.
Iron status in female athletes participating in team ball-sports.
Pak J Biol Sci. 2010 Jan 15;13(2):93-6.

Koehler K, Braun H, Achtzehn S, Hildebrand U, Predel HG, Mester J, Schänzer W.
Eur J Appl Physiol. 2011 May 19. [Epub ahead of print]
Iron status in elite young athletes: gender-dependent influences of diet and exercise.

Committee on Sports Medicine and Fitness
AMERICAN ACADEMY OF PEDIATRICS
Intensive Training and Sports Specialization in Young Athletes
Pediatrics Vol. 106 No. 1 July 1, 2000 : pp. 154 -157

Martinez LR, Haymes EM.
Substrate utilization during treadmill running in prepubertal girls and women.
Med Sci Sports Exerc. 1992 Sep;24(9):975-83.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Is Sugar Affecting Your Immunity?

sweet-drinkThere is a metabolic difference between simple and complex carbohydrates.  The simple ones become glucose soon after they are eaten.  The complex ones take longer to turn into sugar and are less apt to spike insulin and cause energy crashes down the line.  But that isn’t the only difference between the two.

Almost forty years ago scientists had an interest in the relationship of diet to health, specifically of sugar intake to immunity.   But their curiosity went past simple sugar to include carbohydrates other than glucose.  The cells that are the backbone of the immune system are supposed to kill, swallow, and dispose of alien bodies, including bacteria, viruses and cancer cells.  Scientists at Loma Linda University in California examined the activity of neutrophilic phagocytes (cells that dissolve the enemy) after subjects ingested glucose, fructose, sucrose, honey, or orange juice and found that “…all significantly decreased the capacity of neutrophils to engulf bacteria…”  (Sanchez, Reeser, et al. 1973)  Looking more closely, the researchers also discovered that the greatest effects occurred within the first two hours after eating, but “…the effects last for at least 5 hours.”  (Ibid.)  If there is any promise, it’s that the effects can be undone by fasting from added sugars for the next two or three days.

At the start of the twentieth century, Americans consumed only about five pounds of sugar a year.  By the fifties, that had grown to almost 110 pounds a year, and to more than 152 by the year 2000.  Corn sweeteners account for 85 of those pounds.
(USDA Economic Research Service, http://www.usda.gov/factbook/chapter2.pdf )  America’s sweet tooth increased 39% between 1950 and 2000 as the use of corn sweetener octupled.

Although the cited study is decades old, its message is contemporary. HFCS began replacing sugar in soft drinks in the 1980’s, after it was portrayed by marketers as a healthful replacement for demon sugar.  It didn’t hurt the industry that it cost less, either.  The biological effects of sugar and HFCS are the same, however.  Neither has any food value—no vitamins, protein, minerals, antioxidants, or fiber—but they do displace the more nutritious elements of one’s diet, and we tend to consume more than we need to maintain our weight, so we gain.

Even though the number of calories from the glucose in a slice of bread or other starch is the same as that from table sugar (half fructose and half glucose), they are metabolized differently and have different effects on the body.  While fructose is metabolized by the liver, glucose is metabolized by every cell in the body.  When fructose reaches the liver, especially in liquid form (as in soda), it overwhelms the organ and is almost immediately converted to fat.  (Taubes. 2011)

Innate immunity is that which occurs as part of your natural makeup and defends you against infection by other organisms.  Short-term hyperglycemia, which might come from a pint of vanilla, has been found to affect all the major components of the innate immune system and to impair its ability to combat infection.  Reduced neutrophil activity, but not necessarily reduced neutrophil numbers, is one of several reactions to high sugar intake.  (Turina. 2005)  Way back in the early 1900’s, researchers noted a relationship between glucose levels and infection frequency among diabetes sufferers, but it wasn’t until the 1940’s that scientists found that diabetics’ white cells were sluggish. (Challem. 1997)  More recent study has corroborated the diabetes-infection connection, agreeing that neutrophil phagocytosis is impaired when glucose control is less than adequate.  (Lin. 2006)  Impaired immune activity is not limited to those with diabetes.  As soon as glucose goes up, immune function goes down.

Some folks think they’re doing themselves a favor by using artificial sweeteners.  Once the brain is fooled into thinking a sweet has been swallowed, it directs the pancreas to make insulin to carry the “sugar” to the cells for energy.  After the insulin finds out it’s been cheated of real sugar, it tells the body to eat in order to get some, and that creates artificial hunger, which causes weight increase from overeating.   Even environmental scientists have a concern with fake sweeteners in that they appear in the public’s drinking water after use.  You can guess how that works. (Mawhinney. 2011)

Mineral deficiencies, especially prevalent in a fast-food world, contribute to immune dysfunction by inhibiting all aspects of the system, from immune cell adherence to antibody activity.  Paramount among minerals is magnesium, which is part of both the innate and acquired immune responses.  (Tam. 2003)  Epidemiological studies have connected magnesium intake to decreased incidence of respiratory infections, and intravenous administration has shown effective in treating asthma. (PDR. 2000)  But sugar pushes magnesium—and other minerals—out of the body.  (Milne. 2000)  This will compromise not only immune function, but also bone integrity.  (Tjäderhane. 1998)

Zinc has been touted for its ability to shorten the duration of the common cold.  Like magnesium, zinc levels decrease with age, and even tiny deficiencies can have a large effect on immune health, particularly in the function of the thymus gland, which makes the T-cells of the immune system.  Zinc supplementation improves immune response in both the young and the old.  (Haase. 2009)  (Bogden. 2004)  (Bondestam. 1985)  All the microminerals, in fact, are needed in minute amounts for optimal growth and development…and physiology.  Low intakes suppress immune function by affecting T-cell and antibody response. Thus begins a cycle whereby infection prevents uptake of the minerals that could prevent infection in the first place.  Adequate intakes of selenium, zinc, copper, iron plus vitamins B6, folate, C, D, A, and E have been found to counteract potential damage by reactive oxygen species and to enhance immune function.  (Wintergest. 2007)

Who would have viewed something as sweet as sugar as being so hostile? It taste great to eat but has a nasty habit of pushing everything else out.

References

Albert Sanchez, J. L. Reeser, H. S. Lau, P. Y. Yahiku, et al
Role of sugars in human neutrophilic phagocytosis
American Journal of Clinical Nutrition, Nov 1973; Vol 26, 1180-1184

Profiling Food Consumption in America
USDA
http://www.usda.gov/factbook/chapter2.pdf

Taubes G.
“Is Sugar Toxic?”
in New York times Magazine, 13 April, 2011

Turina M, Fry DE, Polk HC Jr.
Acute hyperglycemia and the innate immune system: clinical, cellular, and molecular aspects.
Crit Care Med. 2005 Jul;33(7):1624-33.

Challem J and Heumer RP.
The Natural health Guide to Beating the Supergerms.
1997. Simon and Schuster Inc. New York.  Pp. 124-125

Lin JC, Siu LK, Fung CP, Tsou HH, Wang JJ, Chen CT, Wang SC, Chang FY.
Impaired phagocytosis of capsular serotypes K1 or K2 Klebsiella pneumoniae in type 2 diabetes mellitus patients with poor glycemic control.
J Clin Endocrinol Metab. 2006 Aug;91(8):3084-7.

Mawhinney DB, Young RB, Vanderford BJ, Borch T, Snyder SA.
Artificial sweetener sucralose in U.S. drinking water systems.
Environ Sci Technol. 2011 Oct 15;45(20):8716-22.

Tam M, Gómez S, González-Gross M, Marcos A.
Possible roles of magnesium on the immune system.
Eur J Clin Nutr. 2003 Oct;57(10):1193-7.

PDR:  Physicians’ Desk reference for Herbal Medicines.  Magnesium.  2nd edition.  Mintvale NJ: Medical Economics Company; 2000:  5340540

Milne David B, PhD and Forrest H. Nielsen, PhD
The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men
J Am Coll Nutr February 2000 vol. 19 no. 1 31-37

Tjäderhane Leo, and Markku Larmas
A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats
J. Nutr. October 1, 1998 vol. 128 no. 10 1807-1810

Fuchs, Nan Kathryn Ph.D.
Magnesium: A Key to Calcium Absorption
The Magnesium Web Site on November 22, 2002
http://www.mgwater.com/calmagab.shtml

Haase H, Rink L.
The immune system and the impact of zinc during aging.
Immun Ageing. 2009 Jun 12;6:9.

Bogden JD.
Influence of zinc on immunity in the elderly.
J Nutr Health Aging. 2004;8(1):48-54.

Bondestam M, Foucard T, Gebre-Medhin M.
Subclinical trace element deficiency in children with undue susceptibility to infections.
Acta Paediatr Scand. 1985 Jul;74(4):515-20.

Wintergerst ES, Maggini S, Hornig DH.
Contribution of selected vitamins and trace elements to immune function.
Ann Nutr Metab. 2007;51(4):301-23. Epub 2007 Aug 28.

Smolders I, Loo JV, Sarre S, Ebinger G, Michotte Y.
Effects of dietary sucrose on hippocampal serotonin release: a microdialysis study in the freely-moving rat.
Br J Nutr. 2001 Aug;86(2):151-5.

Jack Challem, Burton Berkson, M.D., Ph.D., Melissa Diane Smith
Glucose and Immunity
http://www.diabeteslibrary.org/View.aspx?url=Article638
Accessed 11/2011

Van Oss CJ.
Influence of glucose levels on the in vitro phagocytosis of bacteria by human neutrophils.
Infect Immun. 1971 Jul;4(1):54-9.

Bernstein J, Alpert S, et al
Depression of lymphocyte transformation following oral glucose ingestion
Am J Clin Nutr. 1977; 30: 613

Robert A. Good, Ellen Lorenz
Nutrition and cellular immunity
International Journal of Immunopharmacology. Vol 14, Iss 3, Apr 1992, Pp. 361-366

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Kidney Stones: The Basics

green-healthy-foodUreterolithiasis, renal calculi, nephrolithiasis and kidney stone all mean the same thing:  agony.  The nurse told us the pain is equivalent to passing a five-pound canned ham through the southern end of the digestive system, with the lid opened.  If you’ve never experienced the long road to relief, thank the Creator for being excused.

What causes kidney stones?

There is no single cause, but a combination of factors.  The wrong balance of fluids, minerals and acids can put you on your knees faster than being knighted.  If urine has more crystal-making elements than the fluid can dilute, bingo, you have the makings of a stone…or stones.  In looking for a definitive cause, science has left no stone unturned.  No pun intended.  Beneath one of those stones is fluoride, having been fingered as causative a decade ago, but only in those with symptoms of skeletal fluorosis and the propensity to form stones in the first place (Singh, 2001).  That rules lots of us out.  Whether or not high doses of vitamin C are implicated in the formation of stones is debatable and based on the status of other nutrients.  By itself, vitamin C, chemically known as ascorbic acid, is able to be converted by the body into oxalates, which increases the likelihood of making oxalate stones among stone formers who take more than the recommended upper limit of 2000 mg of vitamin C a day (Massey, 2005). But you gotta be a stone former.  Is that like a mason?   Earlier research found that high intake of vitamin B6, pyridoxine, reduces the risk of stone formation from unrestricted doses of ascorbic acid (Curhan, 1999).   Up to 500 mg of pyridoxine a day was found to be useful in the control of elevated urinary oxalates (Mitwali, 1988).  In a study reported in the New England Journal of Medicine in the dark ages of the last century, the degree of oxaluria dictates the dosage of vitamin B6.  But the degree of supplementation depends on how much B6 comes from food (Yendt, 1985).

What are they made from?

Most stones (~80%) are calcium oxalate calculi, which crystallizes in a hurry.  It’s the stuff that forms a needle-like crust on the inside of a brewery container.  If you swallowed this material, you’d get really sick, and maybe die.  Calcium oxalate crystal formation is one of the effects of ingesting antifreeze.  A small dose of calcium oxalate will make your tongue burn and swell your throat shut.  This is what happens when the cat chews on a Dieffenbachia leaf in the living room window, and then requires a trip to the vet.

Some plants, including spinach, contain calcium oxalate in their leaves. If you’re a stone former, you might choose to avoid, or at least limit, raw spinach salads, although some researchers say it doesn’t matter, as long as you’re amply hydrated and your diet is sufficiently balanced to provide calcium and vitamin B6, both of which are found in spinach (Curhan, 1999).  A little baffling, huh?  After a stone passes through the urine and gets collected in that little strainer that painters use to get the globs out of a gallon of linen white, you’ll be asked to take that stone to the doctor so he can determine its makeup.  Then he’ll know what course of action to give you.

How do I prevent kidney stones?

If ever the proverbial ounce of prevention is worth a lot, this is the place.  Most experts agree that drinking fluids is the key.  Believe us when we say that a stone former is more than willing to increase his water intake, despite its lack of flavor.  If you need flavor, try lemon juice.  Counseling in this area is simple:  if you don’t drink enough water, you’ll experience this again.  That means you have to drink even when you’re not thirsty (McCauley, 2012).  Swapping soft drinks for water is prudent (Fink, 2009).

Increasing dietary calcium intake is inversely related to stone formation.  Supplemental calcium, on the other hand, may increase risk.  Dietary calcium blocks the amount of oxalates absorbed by the body, while supplements, especially if taken between meals, spill too much of the mineral into the urine.  If calcium supplementation is needed, take it with a meal to improve absorption.  We’re cautioned not to take more than 500 mg at a time, anyway.  It’s all about the timing (Curhan, 1997).

It’s believed that most stones form in the summer, when people are more likely to get dehydrated, so we’re admonished to drink ten to twelve glasses of water a day.  Other beverages, though, fare well in the prevention category.  Caffeinated and decaffeinated coffee, tea, and wine accounted for a decreased risk of stone formation, according to the Brigham and Women’s Hospital study of the 1990’s (Curhan, 1998).

Obesity increases the risk of kidney stones, but drastic weight loss measures that rely on high protein intake can stymie the good intentions.  So, too, can laxative abuse, rapid loss of lean tissue and, naturally, poor hydration.  A diet high in fruits and vegetables can alkalize urine enough to offset oxalate and uric acid stone formation ( Frassetto, 2011).  Produce is known for its magnesium content.  Intake of magnesium is related to reduced stone manufacture, and has been a recommendation since the 17th century.  Even without overt deficiency, magnesium intake, at 500 mg a day in the form of magnesium hydroxide, was shown to decrease stone formation, and it has no adverse side effects as long as it’s not overzealously done (Johansson, 1980 and 1982).  Too much magnesium may induce laxation.  That’s an individual response.   Later study learned that magnesium combined with vitamin B6 offered a substantial decline in the risk for oxalate stones (Rattan, 1994)

Kale, turnip greens, radishes, chard and other leafy greens, broccoli, Brussels sprouts, and cabbage are good sources of dietary calcium.  Almonds and cashews, pumpkin seeds, barley, quinoa, leafy greens, white and black beans are a few good sources of magnesium.  Since calcium and magnesium compete for occupancy in the body, with calcium the winner, magnesium supplementation is a good idea.  An Epsom salts bath allows magnesium levels to increase transdermally…and it’ll help you fall asleep.  Drink water.  Prevent stones.

References

Conte A, Pizá P, García-Raja A.
Urinary lithogen risk test: usefulness in the evaluation of renal lithiasis treatment using crystallization inhibitors (citrate and phytate).
Arch Esp Urol. 1999 Jan-Feb;52(1):94-9.

Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ.
Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.
Ann Intern Med. 1997 Apr 1;126(7):497-504.

Curhan GC, Willett WC, Speizer FE, Stampfer MJ.
Beverage use and risk for kidney stones in women.
Ann Intern Med. 1998 Apr 1;128(7):534-40

Curhan GC, Willett WC, Speizer FE, Stampfer MJ.
Intake of vitamins B6 and C and the risk of kidney stones in women.
J Am Soc Nephrol. 1999 Apr;10(4):840-5.

Curhan GC.
Epidemiologic evidence for the role of oxalate in idiopathic nephrolithiasis.
J Endourol. 1999 Nov;13(9):629-31.

Fink HA, Akornor JW, Garimella PS, MacDonald R, Cutting A, Rutks IR, Monga M, Wilt TJ.
Diet, fluid, or supplements for secondary prevention of nephrolithiasis: a systematic review and meta-analysis of randomized trials.
Eur Urol. 2009 Jul;56(1):72-80. Epub 2009 Mar 13.

Frassetto L, Kohlstadt I.
Treatment and prevention of kidney stones: an update.
Am Fam Physician. 2011 Dec 1;84(11):1234-42.

Gill HS, Rose GA.
Mild metabolic hyperoxaluria and its response to pyridoxine.
Urol Int. 1986;41(5):393-6.

Grases F, Costa-Bauzá A.
Phytate (IP6) is a powerful agent for preventing calcifications in biological fluids: usefulness in renal lithiasis treatment.
Anticancer Res. 1999 Sep-Oct;19(5A):3717-22.

Habbig S, Beck BB, Hoppe B.
Nephrocalcinosis and urolithiasis in children.
Kidney Int. 2011 Dec;80(12):1278-91. doi: 10.1038/ki.2011.336. Epub 2011 Sep 28.

Johansson G, Backman U, Danielson BG, Fellström B, Ljunghall S, Wikström B.
Biochemical and clinical effects of the prophylactic treatment of renal calcium stones with magnesium hydroxide.
J Urol. 1980 Dec;124(6):770-4.

Johansson G, Backman U, Danielson BG, Fellström B, Ljunghall S, Wikström B.
Effects of magnesium hydroxide in renal stone disease.
J Am Coll Nutr. 1982;1(2):179-85.

Massey LK, Liebman M, Kynast-Gales SA.
Ascorbate increases human oxaluria and kidney stone risk.
J Nutr. 2005 Jul;135(7):1673-7.

McCauley LR, Dyer AJ, Stern K, Hicks T, Nguyen MM.
Factors influencing fluid intake behavior among kidney stone formers.
J Urol. 2012 Apr;187(4):1282-6. Epub 2012 Feb 15.

Miggiano GA, Migneco MG.
[Diet and nutrition in nephrolitiasis].   [Article in Italian]
Clin Ter. 2007 Jan-Feb;158(1):49-54.

Mitwalli A, Ayiomamitis A, Grass L, Oreopoulos DG.
Control of hyperoxaluria with large doses of pyridoxine in patients with kidney stones.
Int Urol Nephrol. 1988;20(4):353-9.

Moyad MA.
Calcium oxalate kidney stones: another reason to encourage moderate calcium intakes and other dietary changes.
Urol Nurs. 2003 Aug;23(4):310-3.

Rattan V, Sidhu H, Vaidyanathan S, Thind SK, Nath R.
Effect of combined supplementation of magnesium oxide and pyridoxine in calcium-oxalate stone formers.
Urol Res. 1994;22(3):161-5.

Saxena A, Sharma RK.
Nutritional aspect of nephrolithiasis.
Indian J Urol. 2010 Oct;26(4):523-30.

Singh PP, Barjatiya MK, Dhing S, Bhatnagar R, Kothari S, Dhar V.
Evidence suggesting that high intake of fluoride provokes nephrolithiasis in tribal populations.
Urol Res. 2001 Aug;29(4):238-44.

Yendt ER, Cohanim M.
Response to a physiologic dose of pyridoxine in type I primary hyperoxaluria.
N Engl J Med. 1985 Apr 11;312(15):953-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Vitamin C For Bone Health?

skeleton-vitamin-cHow many bones are in the human skeleton? How come it’s on the inside? What does it do? Does anybody really care? Sometimes.

The human skeleton offers shape and protection to the body. It supplies a place for organs to attach or to be supported. It comprises 206 bones, the largest of which is the thigh (femur). It makes up about 15% of your body weight, part of which is water. This fifteen percent refers to ideal body weight, not to a 400-pound behemoth who is less than six feet tall. Infants have more than 206. The skull starts out with more than twenty bones, some of which fuse together during development. Besides helping you to move, bones make red and white blood cells in their marrow, and act as a storage house for minerals. It takes about twenty years to develop completely.

Bone is actually a type of connective tissue, obviously denser than cartilage, which is the flexible stuff at the flap of your ear (tragus) and the tip of your nose. Cartilage also makes the discs that separate your vertebrae from each other and the femur from the tibia at the knee. Bone tissue is heavily mineralized by a form of calcium called hydroxyapatite. Calcium is the mineral found in the greatest amount in the body, about ninety-nine percent of which is in bone. Phosphorus works with calcium to maintain bone health by combining to make hydroxyapatite. This aggregation helps bone to remodel—to break down and then to redeposit. Trace amounts of other minerals, including magnesium, boron, copper and zinc, stimulate bone growth. But there’s one element of bone health that is overlooked because it’s thought of as nothing more than an anti-oxidant—vitamin C, aka ascorbic acid.

In a study of prepubescent females done in Philadelphia, it was learned that specific bone parameters were positively affected by vitamin C, especially in combination with zinc. For every milligram a day of vitamin C intake, there was an increase in trabecular bone area (Laudermilk, 2012). That’s the porous part of a bone found in the center and at the end of a long bone, like the femur. It’s important to the manufacture of blood cells inside the red marrow. Because it’s porous, trabecular bone is not as strong as the harder cortical outer layer. As hormones change with development, bone requirements also change. This is why it’s necessary to lay down as much bone as possible in one’s early years. By the time a girl reaches thirty, she will have laid down all the bone she ever will, which is probably why a DXA scan compares/contrasts a patient’s bone density to that of a thirty-year-old. You can read about this at the NIH Osteoporosis and Related Bone Diseases National Resource Center website,
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp

If vitamin C intake promotes bone, then deficiency must degrade it. Too little vitamin C causes scurvy, the condition that once affected seamen who were deprived of fresh fruits and vegetables for prolonged periods. That doesn’t happen anymore; at least it shouldn’t. The sailors’ joints and muscles would hurt, they bruised easily, their gums would bleed, and their teeth would sometimes fall out. Since vitamin C is responsible for the formation of connective tissue, these occurrences seem relevant.  Spontaneous fractures caused by low bone mineral density, and considered to be induced by a failure of collagen synthesis, also characterize scurvy (Park, 2012). Deficiency of vitamin C is implicated in scurvy by the inhibition of osteoblast activity. You remember osteoblasts.  They’re the cells responsible for making new bone material.

Most animals do not require external sources of vitamin C because they can get it from glucose through their enzyme systems. Humans and other primates, guinea pigs, and fruit bats lack this ability, so they have to get it from their diets. Since fast foods have replaced fruits and vegetables, many of us may be vitamin C deficient in the absence of supplementation.  Lettuces, onions, apples and bananas don’t help. Citrus fruits, cruciferous vegetables and strawberries do. Besides diet, other lifestyle factors influence vitamin C status, especially smoking, a habit that seriously affects the neck of the femur (Sahni, 2008) unless ascorbic acid intake is considerably greater than the RDA. The dietary recommendation for vitamin C is that amount needed to prevent a condition caused by its lack, in this case, scurvy and its aftermath. Sixty milligrams a day is hardly enough to meet a human’s physiological and metabolic needs. The 400-pound gorilla at the zoo gets 4000 milligrams a day. Shouldn’t a 200-pound human get 2000, then?

Speaking of the femur…This is where the hip joint is, at the top of the thigh bone.  In a seventeen-year follow-up study conducted by Tufts University, those elderly (70-80 yrs.) in the highest third of vitamin C intake had significantly fewer hip and non-vertebral fractures than those in the bottom third, suggesting a protective effect of vitamin C on bone health (Sahni, 2009). It’s important to note that oral contraceptives may adversely affect vitamin C accumulation. Women who fail to supplement while taking hormones as oral contraceptives have lower plasma levels of vitamin C than those who do supplement (Kuo, 2002). This, however, would seem to be the case regardless of contraceptive use.  Concerning sex steroids, both estrogen and testosterone are important for developing peak bone mass (Riggs, 2002). In the case of hypogonadism, where sex glands produce little or no hormones, vitamin C stimulates bone formation (Zhu, 2012), allowing bone recovery in light of hormone deficit. This finding is particularly important to those at risk for osteoporosis, as may be such in developing countries, among the food insecure, and in men who have had certain treatments for prostate disease, including one called gonadotropin-releasing hormone, abbreviated GnRH  (Mittan, 2002).

Despite having lost the ability to synthesize vitamin C, humans can take supplements or increase dietary intake to avert the onset of osteoporosis, realizing that ascorbic acid can block osteoclast proliferation and bone loss while promoting osteoblast activity and bone remodeling.

References

Fain O.
Musculoskeletal manifestations of scurvy.
Joint Bone Spine. 2005 Mar;72(2):124-8.

Gabbay KH, Bohren KM, Morello R, Bertin T, Liu J, Vogel P.
Ascorbate synthesis pathway: dual role of ascorbate in bone homeostasis.
J Biol Chem. 2010 Jun 18;285(25):19510-20.

Kuo SM, Stout A, Wactawski-Wende J, Leppert PC.
Ascorbic acid status in postmenopausal women with hormone replacement therapy.
Maturitas. 2002 Jan 30;41(1):45-50.

Laudermilk MJ, Manore MM, Thomson CA, Houtkooper LB, Farr JN, Going SB.
Vitamin C and Zinc Intakes are Related to Bone Macroarchitectural Structure and Strength in Prepubescent Girls.
Calcif Tissue Int. 2012 Oct 18.

Lean JM, Davies JT, Fuller K, Jagger CJ, Kirstein B, Partington GA, Urry ZL, Chambers TJ.
A crucial role for thiol antioxidants in estrogen-deficiency bone loss.
J Clin Invest. 2003 Sep;112(6):915-23.

Mittan D, Lee S, Miller E, Perez RC, Basler JW, Bruder JM.
Bone loss following hypogonadism in men with prostate cancer treated with GnRH analogs.
J Clin Endocrinol Metab. 2002 Aug;87(8):3656-61.

NIH Osteoporosis and Related Bone Diseases National Resource Center
Bone Mass Measurement: What the Numbers Mean
January, 2012
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp

Park JK, Lee EM, Kim AY, Lee EJ, Min CW, Kang KK, Lee MM, Jeong KS.
Vitamin C deficiency accelerates bone loss inducing an increase in PPAR-γ expression in SMP30 knockout mice.
Int J Exp Pathol. 2012 Oct;93(5):332-40.

B. Lawrence Riggs, Sundeep Khosla and L. Joseph Melton II
Sex Steroids and the Construction and Conservation of the Adult Skeleton
Endocrine Reviews June 1, 2002 vol. 23 no. 3 279-302

Sahni S, Hannan MT, Gagnon D, Blumberg J, Cupples LA, Kiel DP, Tucker KL.
High vitamin C intake is associated with lower 4-year bone loss in elderly men.
J Nutr. 2008 Oct;138(10):1931-8.

Sahni S, Hannan MT, Gagnon D, Blumberg J, Cupples LA, Kiel DP, Tucker KL.
Protective effect of total and supplemental vitamin C intake on the risk of hip fracture–a 17-year follow-up from the Framingham Osteoporosis Study.
Osteoporos Int. 2009 Nov;20(11):1853-61.

Markus J. Seibel, Colin R. Dunstan, Hong Zhou, Charles M. Allan and David J. Handelsman
Sex Steroids, Not FSH, Influence Bone Mass
Cell. 2006 Dec 15;127(6):1079

Simon JA, Hudes ES.
Relation of ascorbic acid to bone mineral density and self-reported fractures among US adults.
Am J Epidemiol. 2001 Sep 1;154(5):427-33.

Zhu L-L, Cao J, Sun M, Yuen T, Zhou R, Mne Zaidi, et al.
Vitamin C Prevents Hypogonadal Bone Loss.
PLoS ONE (2012); 7(10): e47058.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Calcium and CVD, Is There a Connection?

dairy-productsIs there a difference between, “I have blue paint in my bedroom,” and “My bedroom walls are painted blue?”  A gallon of paint in the closet or on the floor in your bedroom verifies the first quote. An empty can and blue walls verify the second. Maybe this isn’t the best analogy, but you can apply it to the calcium in your body, which is either part of your bones or used as an electrolyte, or not. It’s either where it belongs, or not. The body has a remarkable system for keeping the concentrations of calcium in the blood and tissues just right, for ensuring that calcium is where it belongs. If the balance gets upset, certain organs will suffer. You see, besides bones and teeth, calcium helps muscles by keeping nerve impulses firing properly; otherwise the muscles can twitch and cramp. This is the last thing we want to happen to the heart muscle. If necessary, calcium is drawn from bone, where ninety-nine percent is stored, to maintain body pH in times of calcium deficiency. The protein-bound calcium of the blood is a secondary reservoir of calcium, usually becoming available locally to meet needs, as in clotting after getting cut. In the electrophysiology of the heart, calcium works with sodium to enable a heartbeat.

Research on calcium in the last ten years, particularly on supplements, has raised eyebrows about calcium intake and the form in which it is taken. Whether inadvertently or by design, co-factors that enhance calcium bioavailability and absorption from supplements were overlooked by some researchers and the supplements were accused of causing heart attacks. One study, published in the British Medical Journal in 2008, decided that adverse cardiac events were attributable to calcium supplements. The study included almost fifteen hundred women over seventy years old, and reported that those who used calcium supplements experienced more heart problems than those who did not (Bolland, 2008). Neither health conditions, smoking habits, environmental and lifestyle status, prior illnesses, family history, dietary regimens, type of supplement used (carbonate, malate, citrate, etc.), nor other influences were scrutinized. Later study by the same group added vitamin D to the equation and arrived at the same conclusion, that calcium supplements with or without vitamin D modestly increased the risk of cardiovascular episodes, but only in women who did not take calcium supplements regularly and scrupulously prior to the study. It seems, then, that the sudden onrush of calcium nutrition was too much for the body of a geriatric subject, who might even have suffered a different pathology, to handle at one time, and that instead of moving to bone, the mineral clogged up the works (Bolland, 2011). These papers recommended that the role of calcium supplementation in the management of osteoporosis be reassessed. But it doesn’t stop here.

Critics of these studies question the accuracy of the conclusions by closely examining coronary artery calcification, wondering how the calcium got there in the first place, when it’s supposed to make bone, not arterial plaques. When comparing / contrasting dietary calcium and supplemental calcium, the results were similar:  there is no support for the hypothesis that high calcium intake increases risk for coronary artery calcification, held to be a definitive measure of atherosclerosis burden (Samelson, 2012) (Prince, 2011).

We know that vitamin D is necessary for the absorption of calcium and that its insufficiency is common in the northern latitudes. Oddly, insufficiency also occurs in the sub-tropical areas of the planet, partly because of sun avoidance and partly because of sunscreen use, though other factors weigh in, such as cloud cover, altitude and air pollution. Vitamin D is supposed to regulate serum calcium and phosphorus concentrations. In the absence of vitamin D, only about 10% of calcium is absorbed. Maybe the rest goes to places where it doesn’t belong, like your arteries. But you have to get enough vitamin D to make a difference.  The 400 IU used in the study (Bolland, 2011) is barely enough to prevent outright deficiency.

An inflammatory model of CVD has challenged the cholesterol model, and vitamin D plays a role in sequestering the cascade of activities that lead to cardiac episodes. When monocytes rush to the site of inflammation they become macrophages that swallow oxidized LDL and then provide the basis for plaque formation, part of which is trapped calcium. Because vitamin D can suppress macrophage cholesterol uptake, it can interrupt the foam cell cycle and subsequent plaques (Oh, 2009), thereby disrupting the cardiac incident. That’s cool. Hold on, there’s more…vitamin K. Most of us consider blood clotting and vitamin K in the same thought. While that’s true, this compound, associated with green leafy vegetables, does a few more things. There is evidence that low vitamin K levels are associated with reduced bone mineral density and increased arterial calcification (Jie, 1996). Concurrent work shows that vitamin K is able to escort calcium to the place where it belongs—bone. Although deficiency of this vitamin is infrequent, insufficiency is common, and that almost certainly would account for the presence of calcium where it isn’t supposed to be (Vermeer, 2000). Proteins that rely on vitamin K for their activity have shown the ability to inhibit vascular calcification. Even accounting for smoking, diabetes, age, dietary habits and other factors, it was found that subjects with the highest vitamin K levels in the menaquinone form (vitamin K2) experienced fewer incidents of all-cause mortality (Geleijnse, 2004), especially coronary heart disease (Beulens, 2009).

Humans can absorb only about 500 mg of supplemental calcium at a time, with the citrate form having better assimilation than the carbonate. Taking it with food, which encourages stomach acid formation to aid mineral metabolism, practically evens the field (Heaney, 2001, 1999). Considering that calcium is essential to human health, that dairy is not a significant player in most adult diets, that some vegetables high in calcium are also high in oxalates that bind the calcium,  that produce with available calcium contains only small amounts, and that too many of us shun beans for social reasons, supplementation remains the option. Get a dietitian to look at your diet and determine your calcium sources and values. Then take a supplement to bring daily intake up to about a thousand milligrams.  By monitoring vitamins D and K, too, vascular calcification becomes a relative non-issue. An important matter, though, remains for those taking warfarin. It might thin your blood and prevent a clot, but it also interferes with the activity of the proteins supported by menaquinone, and replaces the clot with a plaque.

References

Bo Abrahamsen, Opinder Sahota
Do calcium plus vitamin D supplements increase cardiovascular risk?
BMJ 2011; 342; (19 April 2011): d2080

Beulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, Witteman JC, Grobbee DE, van der Schouw YT.
High dietary menaquinone intake is associated with reduced coronary calcification.
Atherosclerosis. 2009 Apr;203(2):489-93. Epub 2008 Jul 19.

Mark J Bolland, P Alan Barber, Robert N Doughty,  Barbara Mason,  Anne Horne,  Ruth Ames, Gregory D Gamble, Andrew Grey,  Ian R Reid
Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial
BMJ. 31 Jan 2008; 336:262

Bolland MJ, Avenell A, Baron JA, Grey A, MacLennan GS, Gamble GD, Reid IR.
Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis.
BMJ. 2010 Jul 29;341:c3691. doi: 10.1136/bmj.c3691.

Bolland MJ, Grey A, Avenell A, Gamble GD, Reid IR.
Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis.
BMJ. 2011 Apr 19;342:d2040. doi: 10.1136/bmj.d2040.

Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, Hofman A, Witteman JC.
Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study.
J Nutr. 2004 Nov;134(11):3100-5.

Heaney RP, Dowell MS, Barger-Lux MJ.
Absorption of calcium as the carbonate and citrate salts, with some observations on method.
Osteoporos Int. 1999;9(1):19-23.

Heaney RP, Dowell MS, Bierman J, Hale CA, Bendich A.
Absorbability and cost effectiveness in calcium supplementation.
J Am Coll Nutr. 2001 Jun;20(3):239-46.

Heller HJ, Greer LG, Haynes SD, Poindexter JR, Pak CY.
Pharmacokinetic and pharmacodynamic comparison of two calcium supplements in postmenopausal women.
J Clin Pharmacol. 2000 Nov;40(11):1237-44.

Jie KG, Bots ML, Vermeer C, Witteman JC, Grobbee DE.
Vitamin K status and bone mass in women with and without aortic atherosclerosis: a population-based study.
Calcif Tissue Int. 1996 Nov;59(5):352-6.

Khurana C, Rosenbaum CG, Howard BV, Adams-Campbell LL, Detrano RC, Klouj A, Hsia J.
Coronary artery calcification in black women and white women.
Am Heart J. 2003 Apr;145(4):724-9.

Li K, Kaaks R, Linseisen J, Rohrmann S.
Associations of dietary calcium intake and calcium supplementation with myocardial infarction and stroke risk and overall cardiovascular mortality in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition study (EPIC-Heidelberg).
Heart. 2012 Jun;98(12):920-5.

Oh J, Weng S, Felton SK, Bhandare S, Riek A, Butler B, Proctor BM, Petty M, Chen Z, Schechtman KB, Bernal-Mizrachi L, Bernal-Mizrachi C.
1,25(OH)2 vitamin d inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus.
Circulation. 2009 Aug 25;120(8):687-98. Epub 2009 Aug 10.

Richard L Prince,  Kun Zhu,  Joshua R Lewis
Calcium, vitamin D, and risk: Evidence of harm is unconvincing
BMJ. 7 Jun 2011; 342:  d3541 

Elizabeth J Samelson, Sarah L Booth, Caroline S Fox, Katherine L Tucker, Thomas J Wang, Udo Hoffmann, L Adrienne Cupples, Christopher J O’Donnell, and Douglas P Kiel
Calcium intake is not associated with increased coronary artery calcification: the Framingham Study
Am J Clin Nutr December 2012 vol. 96 no. 6 1274-1280

Vermeer C, Schurgers LJ.
A comprehensive review of vitamin K and vitamin K antagonists.
Hematol Oncol Clin North Am. 2000 Apr;14(2):339-53.

Weber P.
Vitamin K and bone health.
Nutrition. 2001 Oct;17(10):880-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Healthy Smile And Nutrition

white-teethGot teeth? Wanna keep ‘em? Brush the ones you want to keep. The others? Might as well brush them while you’re at it. How come? Because we said so? We can do better than that. Since prevention is truly worth more than the cure, give it a go to keep periodontal disease, like gingivitis, at bay. Though the two terms are often interchanged, they are actually different conditions in the spectrum of periodontal (which means “surrounding the tooth”) disease. Gingivitis refers to inflammation of the gums from excess plaque on the teeth, often resulting in redness and swelling, and bleeding when you brush your teeth. In contrast, periodontitis is more severe and the gums pull away from the teeth to form pockets where bacteria can set up house and cause an infection. If it hurts when you chew, if your teeth are getting crooked, if they’re getting loose or overly sensitive, it’s time to see the tooth doctor. Periodontitis is rare in kids; gingivitis is not. Diligent oral hygiene that entails flossing as well as brushing, and regular professional cleaning, go the distance in the prevention of gum disease and the inflammation that comes with it. Free radicals, reactive oxygen species (ROS), and pathogenic micro-organisms can cause collagen and periodontal cell degradation. It’s been found that oral ROS can be scavenged by specific anti-oxidants, thereby reducing collagen abasement (Prakash, 2010). This doesn’t mean that a person can pop pills and forget the paste and brush, but it does allow at least one adjunctive measure to enhance their efficacy. The one we have in mind is also the one with the best reputation and subsequent publicity—Co-Enzyme Q 10, sometimes called ubiquinol, ubiquinone, or CoQ10. CoQ10 belongs to a family of substances that are fat-soluble and participate in the electron transport chain, a pathway that produces energy in the form of adenosine triphosphate (ATP), which is the stuff that fuels our cells.

For the record, number 10 is not the only coenzyme Q. This digital appellation is based on the number of isoprenoids units in the “tail” of the molecule. Isoprenoids, also called terpenoids, are generally the most common hydrocarbons in the human body. In fact, we make them at a rate of about seventeen milligrams a day, to be used in the manufacture of cholesterol and other endogenous steroids, such as the sex hormones and vitamin D. Isoprenes are found in foods. Carotenes, such as beta-carotene, lycopene and lutein are relatives. The coenzymes Q number from 1 to 12.

An enzyme is not the same thing as a coenzyme. Enzymes are proteins (usually) that increase the speed of a chemical reaction without being used up by the reaction; coenzymes are non-proteins (usually) that carry chemicals between enzymes and are continuously recycled. Levels of Co-Enzyme Q10 are depleted by the statin drugs prescribed to reduce cholesterol. This occurs because CoQ10 and cholesterol share a common pathway. When CoQ10 values are diminished, a cell’s mitochondria cannot convert food to usable energy.   What compounds the matter is that CoQ10 levels decline with age, which often is the time of life when cholesterol is mistakenly treated as an agent of disease. In some countries outside the U.S., statins are combined with CoQ10 to buffer the drugs’ side effects, namely the myopathies (Zlatohlavek, 2012) (DiNicolantonio, 2012) (Willis, 1990).

Intake of supplemental CoQ10 has benefits beyond statin amelioration. As an anti-oxidant, CoQ10 prevents damage by ROS and increases efficiency of mitochondrial energy production (Saini, 2011). That it has other significant roles in human health is secondary to the aim of this newsletter, however.  Persons with active gingival disease have been found to be deficient in Co-enzyme Q10 (Littaru, 1971) as determined by gingival biopsies (Nakamura, 1974). Because these tissue samples exhibit persistent oxidative stress, researchers inferred that CoQ10 could reverse it (Battino, 2005). Investigating leukocytes from gum tissue deficient in CoQ10, scientists found that such a coenzyme deficit could predispose this tissue to periodontitis, and that periodontitis exacerbates CoQ10 deficit (Hansen, 1976), leading to the suggestion that adjunctive use of CoQ10 will improve outcome.

Dry mouth from reduced saliva secretion, often connected to aging, was assuaged in sixty-six patients given oral doses of either ubiquinone or ubiquinol at 100 mg/day (Ryo, 2011). Is this a factor in periodontitis? Yes. Xerostomia is associated with an increase in cavities, gingival disease, and even Candida (Ram, 2011). Prevention of periodontal disease may even be accomplished with xylitol-laced chewing gum (Feio, 2005) (Curro, 2008) because of increased saliva production. Treatment with CoQ10 reduces the likelihood of long-term tooth loss, too, with the promise of reversal of symptoms. If nicotine, especially, is one’s toxin of choice, CoQ10 supplementation is indicated. Spanish investigators discovered that CoQ10 stimulated the pathway of biological mechanisms that promote bone health and growth by exciting the synthesis of powerful hormones dedicated to bone formation (Figuero, 2006). Nicotine is a catabolic oxidative agent—it breaks things down. CoQ10 intervenes.

Good nutrition is related to periodontal health. Several supplements promote the biochemistry of teeth and related bone (Folkers, 1977). For example, zinc and copper enhance immunity; vitamin C helps to prevent bleeding gums; calcium and magnesium help to prevent bone loss; and chamomile tea, though not a supplement, may sooth gum tissue. Control of plaque, therefore, is not the only step to oral health. Diet counts, as well. Topical use of CoQ10 can improve the clinical parameters in periodontal assessment and treatment can heal in a fashion labeled as “extraordinarily effective” (Wilkinson, 1975).  If topical sources interest you, there are mouthwashes and toothpastes available made with CoQ10.

Oral supplements of CoQ10 are well-tolerated. Doses of more than 100 mg a day should be separated if mild gastric effects arise. Since most of us don’t eat mammal organ meats regularly, capsules might be the most convenient form, although sardines and mackerel count as decent food sources. Vegetables have only moderate amounts of CoQ10, with spinach, broccoli and sweet potatoes leading the pack. Cooking reduces levels in all food sources. If you opt to take CoQ10 for dental health, you’ll be glad to realize the benefits we didn’t have room to mention.

References

Battino M, Bompadre S, Politi A, Fioroni M, Rubini C, Bullon P.
Antioxidant status (CoQ10 and Vit. E levels) and immunohistochemical analysis of soft tissues in periodontal diseases.
Biofactors. 2005;25(1-4):213-7.

Curro FA.
Gum chewing as an adjunct to use of medications.
J Am Dent Assoc. 2008 May;139 Suppl:6S-8S.

DiNicolantonio JJ.
CoQ10 and L-carnitine for statin myalgia?
Expert Rev Cardiovasc Ther. 2012 Oct;10(10):1329-33.

Feio M, Sapeta P.
Xerostomia in palliative care.
Acta Med Port. 2005 Nov-Dec;18(6):459-65. Epub 2006 Mar 6.

Figuero E, Soory M, Cerero R, Bascones A.
Oxidant/antioxidant interactions of nicotine, Coenzyme Q10, Pycnogenol and phytoestrogens in oral periosteal fibroblasts and MG63 osteoblasts.
Steroids. 2006 Dec;71(13-14):1062-72. Epub 2006 Oct 11.

Folkers K, Watanabe T.
Bioenergetics in clinical medicine-X. Survey of the adjunctive use of coenzyme Q with oral therapy in treating periodontal disease.
J Med. 1977;8(5):333-48.

Hanioka T, Tanaka M, Ojima M, Shizukuishi S, Folkers K.
Effect of topical application of coenzyme Q10 on adult periodontitis.
Mol Aspects Med. 1994;15 Suppl:s241-8.

Mayank Hans, Shobha Prakash, and Subhash Gupta
Clinical evaluation of topical application of perio-Q gel (Coenzyme Q10) in chronic periodontitis patients
J Indian Soc Periodontol. 2012 Apr-Jun; 16(2): 193–199.

Hansen IL, Iwamoto Y, Kishi T, Folkers K, Thompson LE.
Bioenergetics in clinical medicine. IX. Gingival and leucocytic deficiencies of coenzyme Q10 in patients with periodontal disease.
Res Commun Chem Pathol Pharmacol. 1976 Aug;14(4):729-38.

Gian Paolo Littarru, Ryo Nakamura, Lester Ho, Karl Folkers, and William C. Kuzell
Deficiency of Coenzyme Q10 in Gingival Tissue from Patients with Periodontal Disease
Proc Natl Acad Sci U S A. 1971 October; 68(10): 2332–2335.

Littarru GP, Langsjoen P.
Coenzyme Q10 and statins: biochemical and clinical implications.
Mitochondrion. 2007 Jun;7 Suppl:S168-74. Epub 2007 Mar 27.

Mabuchi H, Higashikata T, Kawashiri M, Katsuda S, Mizuno M, Nohara A, Inazu A, Koizumi J, Kobayashi J.
Reduction of serum ubiquinol-10 and ubiquinone-10 levels by atorvastatin in hypercholesterolemic patients.
J Atheroscler Thromb. 2005;12(2):111-9.

Marcoff L, Thompson PD.
The role of coenzyme Q10 in statin-associated myopathy: a systematic review.
J Am Coll Cardiol. 2007 Jun 12;49(23):2231-7.

Matsumura T, Saji S, Nakamura R, Folkers K.
Evidence for enhanced treatment of periodontal disease by therapy with coenzyme Q.
Int J Vitam Nutr Res. 1973 Apr;43(4):537-48.

Ryo Nakamura, Gian Paolo Littarru, Karl Folkers, and Edward G. Wilkinson
Study of CoQ10-Enzymes in Gingiva from Patients with Periodontal Disease and Evidence for a Deficiency of Coenzyme Q10
Proc Natl Acad Sci U S A. 1974 April; 71(4): 1456–1460.

Päivä H, Thelen KM, Van Coster R, Smet J, De Paepe B, Mattila KM, Laakso J, Lehtimäki T, von Bergmann K, Lütjohann D, Laaksonen R.
High-dose statins and skeletal muscle metabolism in humans: a randomized, controlled trial.
Clin Pharmacol Ther. 2005 Jul;78(1):60-8.

Ram S, Kumar S, Navazesh M.
Management of xerostomia and salivary gland hypofunction.
J Calif Dent Assoc. 2011 Sep;39(9):656-9.

Shobha Prakash, J. Sunitha, and Mayank Hans
Role of coenzyme Q10 as an antioxidant and bioenergizer in periodontal diseases
Indian J Pharmacol. 2010 December; 42(6): 334–337.

Ryo K, Ito A, Takatori R, Tai Y, Arikawa K, Seido T, Yamada T, Shinpo K, Tamaki Y, Fujii K, Yamamoto Y, Saito I.
Effects of coenzyme Q10 on salivary secretion.
Clin Biochem. 2011 Jun;44(8-9):669-74.

Rajiv Saini
Coenzyme Q10: The essential nutrient
J Pharm Bioallied Sci. 2011 Jul-Sep; 3(3): 466–467.

Vervelle A, Mouhyi J, Del Corso M, Hippolyte MP, Sammartino G, Dohan Ehrenfest DM.
Mouthwash solutions with microencapsuled natural extracts: Efficiency for dental plaque and gingivitis.
Rev Stomatol Chir Maxillofac. 2010 Jun;111(3):148-51.

Wilkinson EG, Arnold RM, Folkers K, Hansen I, Kishi H.
Bioenergetics in clinical medicine. II. Adjunctive treatment with coenzyme Q in periodontal therapy.
Res Commun Chem Pathol Pharmacol. 1975 Sep;12(1):111-23.

R A Willis, K Folkers, J L Tucker, C Q Ye, L J Xia, and H Tamagawa
Lovastatin decreases coenzyme Q levels in rats.
Proc Natl Acad Sci U S A. 1990 November; 87(22): 8928–8930.

 Zlatohlavek L, Vrablik M, Grauova B, Motykova E, Ceska R.
The effect of coenzyme Q10 in statin myopathy.
Neuro Endocrinol Lett. 2012 Nov 28;33(Suppl2):98-101. [Epub ahead of print]

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Is It The Time To Take Your Vitamins?

supplement-timeLots of people take vitamins and minerals without knowing the reason. It might be that a friend recommended them or because “everybody takes vitamins.” Occasionally, a doctor or other credentialed health care practitioner might suggest them. But what is the basis for such a recommendation? One reason is that the food supply is terribly deficient in nutrient content. Vegetables that are picked before reaching maturity so they don’t spoil in storage and shipping offer us only a fraction of what they did a few decades ago. Petroleum-based fertilizers and biocides upset the balance of minerals that we have trusted soil to provide. Another reason for using supplements is that we don’t always eat three squares a day and, even if we think we do, can’t guarantee their squareness. Those of us who live alone often fail to eat anything that even resembles a meal unless we spend time with friends and family, either at their tables or at some eating establishment. Still others of us may be harboring a medical condition or may be taking medications that interfere with nutrient absorption and metabolism. Whatever the case might be, including having more than a few drinks a day, there are legitimate reasons to use vitamin and mineral—and other—supplements.

Vitamins are simply organic compounds needed in small amounts to provide a biological activity that would be missing or haphazard in their absence or deficiency. They are not foods and cannot stand alone as food substitutes. They can, however, help us to get from our food all that the food has to offer by acting as catalysts and co-factors. Many of the health claims for vitamin effectiveness in addressing a particular concern can be proven. Those not substantiated by science should be discounted. Taking a quality multivitamin supplement to prevent or to overcome deficit has been supported by the AMA (Fairfield, 2002), who admonishes, though, to be prudent about taking too much of a good thing.

Minerals, unlike vitamins, play a structural role as well as a functional role in the body. Calcium, magnesium and phosphorus make bone, for example, but they also control electrical circuits and enzyme functions. Magnesium alone is part of more than three hundred enzymes. All these micro-nutrients act like spark plugs to initiate or to facilitate metabolic and physiologic processes, such as releasing energy from carbohydrates and fats. Some minerals are not found in supplement form, like sulfur, which is part of the proteins that make the skin, hair, liver and pancreas. Instead, they exist in amino acids.

Other things you might swallow from a bottle include the essential fatty acids and the phytonutrients found in plants. Common to these are fish oil, flavonoids and other organic compounds that afford physiologic activity. Most of us ignore an important consideration in the supplement regimen—timing. Popping too many tablets or capsules can backfire sooner or later and even present as a condition they’re trying to prevent, but so can taking them at the wrong time of day or in the wrong combination.

Since micro-nutrients work together with the macro-nutrients (proteins, carbs and fats), and since they appear together in foods (when they can), it might just be prudent to take supplements with meals, either during or after. If nothing else, it’ll prevent a belly ache and the exciting laxation that can follow essential fatty acids taken on an empty stomach. Besides, taking any supplement without something in the stomach hastens transit time, which impairs absorption and utilization. Additionally, food stimulates the production of stomach acid, which improves the benefits of the supplements (Mulligan, 2010) (Heaney, 1989) (Kelly, 1984).

Taken with breakfast, multivitamins can spend their time being amply assimilated, but this meal needs to be more substantial than a doughnut and a cup of coffee. Minerals are a bit fussier. Some forms of calcium should be taken with food because a rock-hard mineral refuses to dissolve without stomach acid. The citrate form, though, differs because of the citric acid to which the calcium is tied. Iron absorption peaks in the the presence of vitamin C, which also enhances calcium uptake. Be aware that calcium supplements tend to interfere with assimilation of other minerals, especially iron, magnesium and zinc, even in food. For that reason, taking calcium away from foods might be a prudent move, knowing that the citrate form of calcium will dissolve without stomach acid. Since we can absorb only about 500 milligrams of calcium at a time, spacing intake is important.

In the United States, about a third of prescription drug users also take at least one supplement. This opens the door to possible interactions. Admittedly, most of the allopathic medical community know little or next to nothing about nutrition and the use of supplements. Instead of taking the time and effort to learn about those topics, many practitioners take the easy way out and tell their clientele that supplements are useless. Nonetheless, we need to let our medical people know about supplement intake. If the doctor doesn’t know about drug-supplement interactions, the pharmacist might, the dietitian could, and the integrative/functional dietitian-nutritionist most likely will.

Drug-supplement interaction is a two-way street. A medication may inhibit or enhance the activity of a nutrient, and a nutrient may do the same to a drug. You do not take vitamin A with a tetracycline antibiotic or vitamin C with a blood thinner. Vitamin B1 has the potential to dilate blood vessels, so you might want to keep it away from your blood pressure pills. Supplement-supplement interactions also require attention. Taking vitamin C with grape seed extract may affect blood pressure. You don’t take fish oil with warfarin. Allowing at least a two-hour window between a drug and a supplement is a good idea. With some, four hours is better.

Yes, vitamin, mineral, and herbal supplements have a rightful place in our daily regimens; and yes, herbals could be taken on an empty stomach; and yes, each can support everything the body does and is. If separating doses is a bother, at least take supplements with a meal because fat-soluble vitamins require fat to be assimilated, most need stomach acid to dissolve, and all will be less likely to talk back to you.

References

Ranjit Kumar Chandraa
Nutrition, immunity, and outcome; Past, present, and future. 11th Gopalan Gold Medal Oration
Nutrition Research. Volume 8, Issue 3, March 1988, Pages 225–237

Domrongkitchaiporn S, Sopassathit W, Stitchantrakul W, Prapaipanich S, Ingsathit A, Rajatanavin R.
Schedule of taking calcium supplement and the risk of nephrolithiasis.
Kidney Int. 2004 May;65(5):1835-41.

Kathleen M. Fairfield, MD, DrPH; Robert H. Fletcher, MD, MSc
Vitamins for Chronic Disease Prevention in Adults
JAMA. 2002;287(23):3116-3126.

Heaney RP, Smith KT, Recker RR, Hinders SM.
Meal effects on calcium absorption.
Am J Clin Nutr. 1989 Feb;49(2):372-6.

Kelly SE, Chawla-Singh K, Sellin JH, Yasillo NJ, Rosenberg IH.
Effect of meal composition on calcium absorption: enhancing effect of carbohydrate polymers.
Gastroenterology. 1984 Sep;87(3):596-600.

Lonn EM, Yusuf S.
Is there a role for antioxidant vitamins in the prevention of cardiovascular diseases? An update on epidemiological and clinical trials data.
Can J Cardiol. 1997 Oct;13(10):957-65.

Mulligan GB, Licata A.
Taking vitamin D with the largest meal improves absorption and results in higher serum levels of 25-hydroxyvitamin D.
J Bone Miner Res. 2010 Apr;25(4):928-30

Prasad KN, Hernandez C, Edwards-Prasad J, Nelson J, Borus T, Robinson WA.
Modification of the effect of tamoxifen, cis-platin, DTIC, and interferon-alpha 2b on human melanoma cells in culture by a mixture of vitamins.
Nutr Cancer. 1994;22(3):233-45.

Prasad KN, Cole WC, Kumar B, Prasad KC.
Scientific rationale for using high-dose multiple micronutrients as an adjunct to standard and experimental cancer therapies.
J Am Coll Nutr. 2001 Oct;20(5 Suppl):450S-463S; discussion 473S-475S.

David L. Watts, D.C., Ph.D., F.A.C.E.P.
Nutrient Interrelationships: Minerals — Vitamins — Endocrines
J of Orthomolecular Med. Vol. 5; 1st Quarter: 1990

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.