Minerals are the spark of life, and without them we simply wouldn't function. Minerals are the basic components of all matter. They are built into key enzymes and hormones, and are part of cells, tissue, bone, blood and body fluids. They also assist in every aspect of life from the production of hormones and energy, digestion, nerve transmission and muscle contraction, to the regulation of pH, metabolism, cholesterol, and blood sugar. Our physical well-being is more directly dependent upon the minerals we take into our systems than upon calories or vitamins, or upon the precise proportion of starch, protein or carbohydrates we consume. Macro minerals and trace minerals supply neither energy nor fuel to the body but are instrumental in their production and use. All the vitamins in the world do us little good without minerals. Enzymes, which are composed of vitamins, minerals and proteins, also do us little good without adequate minerals.
There are more than 100 mineral elements found on earth. Four of these, oxygen, hydrogen, carbon and nitrogen, make up 96% of our body. The remaining 4% of our body is basically made up, in part, of the other minerals, which are available to us, and these may vary somewhat, depending on where we live. Our daily mineral intake is about 1.5 grams--our total intake of carbohydrates, proteins, and lipids are about 500 grams. Thus our mineral intake represents only about 0.3% of our total intake of nutrients, yet minerals are so potent and so important that without them we wouldn't be able to utilize the other 99.7% of foodstuffs and would quickly perish. There are seven major minerals. They are calcium, magnesium, potassium, phosphorus, sulfur, sodium and chlorine. Our bodies should contain significant amounts of each! Trace minerals, on the other hand, are present in the body in very small amounts. Each makes up less than one-hundredth of one percent of our body weight. Rocks are the parent material for soil which is the main source of nutrition for plants, animals and ultimately humans. The absorption of many minerals declines with old age. Stress and exposure to environmental pollution raise our requirements for minerals, especially zinc, calcium, and iron.
The health and survival of all plants, domestic or wild, depends on the health of the soil and its ability to provide a constant supply of minerals. According to science, millions of years ago the soil near the earth's surface, where our plants are grown, was saturated with dozens of minerals. At least 84 minerals were available nearly everywhere and some areas of the planet contained 100 minerals. When humans began to till the soil, wind and rain erosion began to take its toll along with continuous cropping, which gradually strip-mined the nutrients from the soil. Soil tests from all over the world have revealed that our soils are severely lacking in minerals, leaving us with mineral-deficient plants with very little food value. Most farmers never put back more than 6 minerals. Animals require at least 60 minerals, 12 essential amino acids, 16 vitamins, and 2 essential fatty acids. Soil depletion is the only reason today's plants contain no more than 16 minerals, on average, in most of the food available today, compared to more than 70 minerals millions of years ago. Man-made, chemical fertilizers, introduced in 1908, upset the delicate balance of minerals and organisms in humus-rich soil by killing off the beneficial bacteria. Lacking in the naturally occurring minerals, they are less available to plants. Farmers add 46 billion tons of synthetic fertilizer to their crops annually in an attempt to compensate for the useless soil. The more chemical fertilizers are used, the weaker the plants become, the more insects attack, and the more insecticides have to be used. Chemical fertilizers also saturate plant roots with too much of one nutrient, making it difficult for plants or crops to pick up and absorb other minerals they need so much.
We cheat ourselves of even more nutrients by eating refined foods. Food refining is the process of removing parts of a food. In the course of refining flour the grain is stripped of its bran and germ and virtually all that's left is starch. The body has a hard time processing starch without the trace mineral chromium, which affects the pancreas' handling of starch and throws the blood Sugar
out of balance. When removing the bran from grains, we lose trace minerals like silicon and zinc, by removing the germ we lose vital oils, zinc and vitamin E. We are left with high levels of the toxic trace element cadmium that accumulates in the starchy part of rice and wheat--the part we eat. Normally, the zinc would prevent the body from absorbing the cadmium, but zinc is taken out with the bran and germ. Eating refined Sugar
causes the body to use and lose more trace minerals than people realize. At every stage of Sugar
metabolism, minerals are withdrawn.
Scientists are aware that trace element deficiencies can affect both mind and body; in fact, every physical and mental process. Electrolytes are the sparks, which fire and fuel the neurotransmitters that enable us to think and process information. They are vital for good brain function and sanity.
In order for a body to grow and heal, it must have adequate, high quality, low stress protein, in an easily digested form. Specific trace minerals enable plants to produce protein. Legumes require molybdenum for it is an essential element for the growth of nitrogen-fixing bacteria on their roots. These bacteria convert atmospheric nitrogen to soluble nitrates
, which are absorbed by the plants to synthesize proteins. The protein content of food is high or low in about the same proportion as the minerals. This is because just about all the minerals are used in the amino acid enzymes which in turn are catalysts helping to make all the protein compounds.
Simple problems like muscle cramps and spasms have their origin in calcium, magnesium and electrolyte deficiency. Serious age-related disorders like deterioration of brain tissue, or senility are linked to electrolyte imbalance. Digestive enzyme production is impaired if minerals aren't available. Specific minerals create the starch digesting salivary enzyme amylase, which, if deficient, results in incomplete digestion of starches and intestinal fermentation. This limits the production of lactic acid, alters pH, and creates the kind of environment that putrefactive bacteria and candida love, and acidophilus bacteria struggle to survive in. As putrefaction takes place, food-decomposing bacteria produce toxins that are absorbed into the circulation. This condition adds to the risk of developing arteriosclerosis, kidney, gall bladder and liver disease. Cataracts, fungal infections, insomnia, glaucoma, allergies, digestive upsets, anorexia, immune disorders, fatigue, eczema, upsets, anorexia, immune disorders, fatigue, eczema, and psoriasis, are all involved with mineral depletion. In order for the body to effect rebalancing and regeneration it needs minerals and electrolytes in conjunction with any other treatment. They are the catalyst for healing. In the areas of the world where quality of life and longevity are legendary, there's high mineral content in soil, plants and water.
Most of the mineral supplement formulations available today contain no more than 10 to 15 minerals because most are derived from the earth, from ancient sea beds, clay or ground up rock and soil. This type of mineral is known as a metallic hydrophobic mineral! The type of mineral which comes from a plant has been assimilated or digested by the plant and is known as a water soluble, plant derived, hydrophilic mineral. No more than 5% to 8% of metallic minerals are actually assimilated by the human body. The hydrochloric acid in our stomach isn't strong enough to dissolve metals during the short 15 to 21 hour digestive cycle. The balance, or up to 92%, merely passes through the waste system without benefit. You could not live on soil or ground up rock, because it is not alive or enzymatically active like plant derived minerals from raw plants. Minerals create a healthy environment in which the body, using vitamins, proteins, carbohydrates and fats, can grow, function and heal itself.
A complete spectrum of minerals balances the pH level of bodily tissues. Most all microorganisms thrive in and prefer an environment of high pH or alkaline nature. A combination of many minerals lowers the pH of hydrochloric acid, thereby inhibiting microorganisms from gaining entrance to the digestive system and reproducing there. Both extra- and intra-cellular fluids function only because of a carefully maintained ratio of minerals, in conjunction with vitamins, in solution. The interaction of the two enables the body cells to take in nutrients and dispose of toxins, which are the by-products of that metabolism.
The human body is not designed to absorb or assimilate and use metallic or elemental minerals. Metallic minerals only have an 8% absorption. Chelated minerals were developed in the laboratory. This process involves wrapping amino acids or protein around metallic minerals to help the body metabolize them. But, this form of minerals has at best only a 40% assimilation. Chelated or not, they are still metallic minerals. If there is insufficient digestive acid in the stomach, minerals are poorly assimilated and deficiencies may develop quite rapidly. The aging process and stress both weaken digestion and stress itself is a major cause of mineral deficiency as it speeds up the body's use of these elements. It is best to add minerals to the soil, and eat the plants grown on it, rather than ingesting colloidal minerals in their "raw" state. Microorganisms act as an interface at the plant roots, ingesting minerals and altering them to a form that plants can use, then plants bio-transmute them to a form we can use.
The body is an electromagnetic organism. There is a vibrational emanation from every organ. These emanations have been tested with radionic instruments. Every organ has its own aura. It is the electromagnetic current that is received through the atmosphere that gives life to every plant, animal and human on Earth. Electrolytes are responsible for transferring energy and for the regeneration and rejuvenation of every cell. From the moment the sperm is attracted to the egg in the body of the mother, the electromagnetic forces of electrolytes are at work. Bodies cannot be built without electrolytes. Electrolytes are ionized salts (minerals) found in body fluids and the blood stream. In solution, or dissolved and transformed in water, the molecules split into electrically charged particles or ions. In this form, the ions then become capable of conducting an electric current. Electrolytes are essential to the production of enzymes, the function of cells, and in maintaining a normal pH balance in the body and digestive system. Electrolytes also maintain normal fluid balance including osmosis, and blood pressure. But they go one stage further--they bring a special aliveness to the body. All cellular structures become alive through electrolytic activity. Life begins with electrolytes. Trace minerals carry the life force in our bodies more than any other substance.
The whole body is a bioelectric organism and the nervous system and brain also operate on electrical energy. Electrolytes are both the switch and the energy source. When electrolytes are depleted, body systems become run down and sluggish, similar to weak batteries running a tape recorder that runs weaker and slower. Cells use fatty acids, water, and glucose. Each cell acts as a battery with a different electrical charge or voltage potential on the inside and the outside of its wall, and minerals act as positive and negative electrodes producing the voltage potential. The stimulation of a nerve cell sends a wave of depolarization down the nerve fiber, releasing potassium and moving sodium into the cell. As the current passes, the charge difference at the cell wall is re-established as potassium is pumped back inside the cell. This sets up an electromagnetic current which makes up our energy system. It is this subtle energy that produces life. As the magnetic iron in our red blood cells pass through capillaries, they pass through spirals of nerve cell fibers, acting like a coil of wire. When the iron passes through these spirals, a current of electricity is induced in them and this continuously keeps us "turned on"--as long as the blood is flowing freely and not anemic.
The balance of minerals is as important a consideration in health as their availability and assimilation. Minerals can compete with one another for absorption, especially if too much of one is available and not enough of others. For example, too much zinc can unbalance copper and iron levels in the body and large amounts of calcium reduce absorption of magnesium, zinc, phosphorus and manganese. A similar unbalancing of minerals can occur with excessive intake of single vitamins, either by producing a deficiency or increasing the retention of a particular mineral. The body can tolerate a deficiency of vitamins longer than it can a deficiency of minerals. Stress, pregnancy, growth, athletic training, sweating, illness, aging and drugs all increase normal electrolyte requirements. But most of us aren't even getting "normal" levels. Because of our diminishing mineral sources, anything that increases the body's need for them can send health into a tailspin and set the stage for degenerative disease later on.
We add insult to injury by taking drugs like corticosteroids and diuretics, which have a catastrophic effect on mineral and vitamin levels in the body. Potassium is only one of many minerals lost. Macro-minerals, including magnesium, are excreted in significant amounts, especially with thiazide diuretics; so too are vital trace elements including zinc. This loss, in the long-term, increases the chance of kidney and cardiovascular damage--precisely the organs that are malfunctioning when the physician prescribes diuretics for high blood pressure or edema. Because a loss of magnesium prevents the body from utilizing potassium properly, glucose tolerance is impaired. Drugs may deplete minerals by increasing their excretion, by interfering with mineral balance, or by antagonizing synergistic factors. Antacids, laxatives, anti-convulsants, corticosteroids and antibacterial agents exert a chelating action upon calcium and antagonize the metabolic effects of vitamin D, leading to rickets, osteomalacia and other calcium deficiency disorders. Antibiotics
block the absorption of macro- and trace-minerals, and minerals play an integral role in the health of the immune system. This includes zinc, which is important in the production and health of T-lymphocytes.
Plant minerals are different than metallic minerals. Their size and molecular weight is much smaller than metallic minerals and in most cases the plant minerals are attached to a different molecule even though they possess the same name. A plant mineral is several thousand, to as much as a hundred thousand times smaller than the smallest metallic mineral. A plant derived mineral is less than 0.00001 micron in size or 1/10,000th the size of a red blood cell. Their small size gives them an enormous surface area with an electrical charge. Plant minerals are much easier to assimilate or absorb than metallic minerals. Clay, silt and hydrophobic metallic minerals, on average, are considerably larger than hydrophilic acids or hydrophilic plant minerals. Pure plant minerals can be pumped through a pharmaceutical grade, .15-micron (absolute) filter. Most metallic minerals will not pass through this small membrane. Only the water passes through. A water molecule is only slightly smaller than hydrophilic complexes. Aluminum, arsenic, lead and nickel are minerals found in nearly all food we eat. As elemental minerals, if ingested in sufficient quantity they would be extremely toxic or fatal. But, these minerals found in foods are no longer the same as metallic minerals. Plant derived minerals are 100% absorbable. If you drank even 2 grains of free iodine, it would kill you. But, in its plant-derived form, Iodine
is not only harmless--it is beneficial.
Rocks provide the foundation for the creation of topsoil; living organisms slowly ingest them and release the minerals. Soil bacteria thrive when minerals are readily available, and their life cycle converts these raw elements into a smorgasbord of protoplasm and bioavailable minerals that are taken up by plant roots. The soil, micro-organisms, and plants have an intimate relationship. The plants rely on the presence of micro-organisms for their nourishment and immunity. The microorganisms act as an interface, converting the "raw" minerals in the soil into bioavailable minerals and nutrients for the plants. Like us, plants can build up their own autoimmune system and natural defenses as long as the nutrients are available to them. Earthworms are also important in nature's scheme of things--their burrowing aerates the land and breaks up hard soils. Their casts act in the creation of living soil because they contain ground minerals and microorganisms.
This is why any successful health-building program will include fresh, raw, organically grown fruit and vegetable juices. These foods contain the colloidal and crystalline form of minerals that have been through the microorganism and photosynthesis charging process. Also, Sea vegetables (sea weed) such as dulse, kelp, arame, hijiki, kombu, nori, alaria, etc. are a superior source of abundant minerals. All of the topsoil that was eroded from the land, ended up in the oceans. If you eat plants that grow in the ocean, then you can obtain these plant-derived minerals in a biologically utilizable form.
Sprouted seeds, especially alfalfa seeds, provide an abundance of minerals. The alfalfa plant has deep roots that reach up to 90 feet into the ground and pull in many rare trace elements. Raw spinach has an exceptional amount of minerals. All root vegetables have many minerals. Black-strap molasses can be used to add plant-based minerals that were removed during the refining of sugar cane or sugar beets. Another source of plant derived minerals is available from an area known as Emery County, Utah. Supposedly, a glacier or other cause of earth movement buried a large quantity of vegetative matter, which may have been a dense growth, or a washed-in bog of numerous plants, which is believed to have accumulated over a 600 year period. This material now exists as humic shale. On average, the humic shale is a 30 feet thick layer of prehistoric plant derivatives that was or still is under great pressure from the earth. All of the moisture has been compressed out of the humus. By submerging in pure, cold water, more than 70 plant minerals are leached from this humic shale. The mineral water is taken as a mineral supplement.
Thyroid and Adrenals
The thyroid gland and the adrenal glands are the main energy producing glands in the body, supplying the body with more than 98% of its energy. If you did not have these glands, you would not have enough energy to blink an eyelid. The thyroid gland, located right behind the Adam's apple in your neck, is about the size of a plum. The adrenal glands are much smaller and are located on top of each of your kidneys. Everyone has one thyroid gland (with two lobes) and two adrenal glands. These glands work very closely together. In non-technical terms, the adrenal glands "release" simple sugars in the body, which serve as the fuel for the thyroid gland. The thyroid gland then takes these sugars and ignites them into energy. The thyroid gland is like the spark plugs of your car in that it ignites the fuel and turns it into power. So it is these glands, working together, which produce the body's energy. To have maximum amounts of energy, these glands have to be functioning at peak capacity.
These are the glands that determine a person's rate of metabolism, the "oxidation type." If both the thyroid gland and the adrenal glands are overactive, a person will be known as a fast-oxidizer. In other words, he will have a very fast metabolism. These are the people who usually abound with energy. Now, if just one of these glands is overactive and one is underactive, a person will be a mixed-oxidizer. And if both of these glands are underactive, a person will be a slow-oxidizer. A slow oxidizer has a very slow rate of metabolism. These are the individuals who are usually lacking in energy. It is the adrenal glands which give a person extra energy when he needs it. Whenever a person faces an emergency, the adrenal glands release adrenalin, which gives the body the extra "boost" it needs.
There are four main minerals in the body, which help to regulate the thyroid and adrenal glands. These minerals are calcium (Ca), magnesium (Mg), sodium (Na), and potassium (K). These minerals could be called macro-minerals because they appear in larger proportions in the body than other minerals. If these four minerals are all at normal levels, the thyroid and adrenal glands will function at peak efficiency. However, if any one of these macro-minerals deviates much from normal range, this is when a person is going to have problems. Sometimes, even a relatively minor fluctuation in one of these minerals can cause either one of these glands to become underactive. A simple analogy, which further explains this principle, is to compare the mineral levels of the human body to a battery. Both the human body and a battery derive their energy from mineral electrolytes. When a battery has the perfect balance between certain minerals, it will be capable of producing its maximum energy potential. Likewise, when the human body has the perfect balance between certain minerals, it to will be capable of producing its maximum energy potential. However, when either the body or a battery has an imbalance in the minerals they contain, they lose their potential of carrying a charge. The minerals in your body determine the biochemical environment in which your organs must work. The more optimal is the mineral environment in your body, the better your organs will function, and the more energy you will have.
The real key to understanding health is the ratios between different minerals. The normal levels for each of these minerals are expressed in milligrams/percent. The normal level for calcium is 40, magnesium is 6, sodium is 25, and potassium is 10. If you add one zero to each of the numbers, you will get a figure representing parts per million. So the 40 for calcium represents a certain percentage of calcium which appears in the tissue cells of the body. The real key to understanding minerals and their effect on human health does not lie merely in evaluating individual mineral levels. Mineral levels can certainly help to give a tremendous amount of information about a person's energy levels. However, looking at individual levels can be deceiving if you look at them just by themselves.
Calcium and potassium ratios are called the thyroid ratio. Calcium and potassium are the two specific minerals that regulate the thyroid gland. Calcium slows down the thyroid and potassium speeds it up. In order for this gland to operate at its maximum capacity, there has to be just the right balance between these two minerals. If a person has too much calcium in his tissues (in proportion to potassium) he will have an underactive thyroid gland. If he has an excess of potassium in his tissues (in proportion to calcium) he will have an overactive thyroid gland. This is why once you know the ratio of calcium to potassium in the body you know immediately if this gland is too fast or too slow. And not only that, but you will know exactly how fast or slow it is. The normal value of the calcium to potassium ratio is 4. You get that by looking at the normal values for calcium and potassium, where calcium is 40 and potassium is 10. 40 divided by 10 is 4. If a person has a ratio of 4 to 1 between these two minerals, the thyroid gland will be functioning at peak capacity, assuming that the levels for these two minerals are also near normal. By comparing a person's actual ratio with the normal ratio, you can tell if the thyroid gland is underactive or overactive.
And once you know this, you will know approximately how much energy a person has. If a person has a thyroid ration (calcium to potassium ratio) which is greater than 4.7, his thyroid gland is underactive. The greater this ratio is between these two minerals, the weaker this gland will become and the less energy a person will have. It is impossible to have a poor thyroid ratio and still have an efficient thyroid gland. Even a 10% loss of efficiency can cause fatigue. Ten percent doesn't sound like a big number, but it is. If the average lifespan of 70 or so years were cut 10%, that would be a loss of 7 years. That's quite significant. If your average body temperature of 98.6 degrees were cut 10%, that would be a temperature of almost 9 degrees lower, which is a big difference. If the temperature went up 10%, that would be a temperature of almost 110 degrees, which for many people would mean death. So you can see that 10% in biological terms can be a pretty significant number. These mineral ratios are amazingly accurate. A person can have normal levels of thyroid hormone in his blood and still have a weak thyroid gland. The routine test for thyroid function is not very reliable. This test basically measures the levels of a number of thyroxin proteins in the blood. But many doctors fail to understand that a person can have normal levels of thyroxin (thyroid hormone) in the blood and still have a weak thyroid gland. Or, because of mineral imbalances the thyroxin may just be circulating around without being fully effective. So, in many cases, the doctor may be drawing false conclusions from the test. A hair analysis gives a more accurate measure of the function of the thyroid.
When you're talking about the adrenal gland, it is the sodium and magnesium which do the regulating. This could be called the adrenal ratio. When the ratio of these two minerals becomes unbalanced--even slightly, it can have a major impact on the adrenal gland. Too much magnesium, in relation to sodium, will slow down the adrenal gland. Just by looking at the ratio between these two minerals lets you know immediately how well this gland is performing. The normal level for the sodium to magnesium ratio is 4.17 to 1. You get this by dividing the normal levels for sodium (25) by the normal level for magnesium (6). So, if a person has an adrenal ratio of 4.17, the adrenal gland will be functioning at peak capacity, again assuming that the levels for these two minerals are also normal. The adrenal gland is underactive when the adrenal ratio (sodium to magnesium) is less than 3.2. Once you know a person's mineral ratios and fully understand them, you can determine the efficiency of major organs--without guessing. The normal sodium level in the body is 25. When the sodium level drops much below 20, a person's adrenal medulla will start to slow down. Many people have sodium levels that are lower than 15 and they usually have diminished levels of energy. Now, if your sodium level is very low, don't try to compensate by eating a lot of salt (sodium). If you do this, it won't help at all. It will probably only aggravate the problem.
You wouldn't expect this to happen, but it does. If you multiply the energy level of the thyroid gland times the energy level of the adrenal gland you get the total energy loss. If a person has a perfect ratio for the thyroid gland (100%), but has a 50% ratio for his adrenal gland, the person would have a total energy loss of approximately 50%. Multiply the energy level of the thyroid gland (100%) times the energy level of the adrenal gland (50%). This would be a bare minimum as far as a loss of energy is concerned. One strong gland will not usually make up for a weak gland. If someone else has a thyroid gland with a 50% energy loss and he also has adrenal glands with a 50% loss, that person would be operating on approximately 25% of his available energy. The main thing you should remember is that you have to take into consideration both glands when figuring a person's total energy loss. It gets a little more complicated when a person is a mixed oxidizer. Just remember that one strong gland will usually not make up for a weak gland. Most people are more fatigued than they would ever realize. They're so tired that they can't comprehend how exhausted they really are.
When we refer to various individuals as slow oxidizers or fast oxidizers, etc., this is just a way of classifying the rate at which the body is releasing energy from the foods a person eats. Some refer to this as a person's metabolism. There are four main classifications: slow oxidizer, fast oxidizer, mixed oxidizer and balanced oxidizer. The word oxidizer comes from the term oxidation. Oxidation comes from the word oxygen. Oxidation is the process by which certain elements in the body chemically combine with oxygen to release energy. Oxidation is the basic chemical process of burning. For example, when you burn a piece of wood, you are oxidizing the wood. You are causing the wood to combine rapidly with oxygen to cause a high-intensity energy release. Oxidation can occur at different speeds. It is not necessarily a fast process. It can occur quickly, as with burning wood, or it can occur slowly, as in the case of a rusting nail. When a nail is rusting, it is reacting with the oxygen in the air and being consumed. The rust you see is merely the evidence of incomplete combustion. All oxidation releases energy, whether you feel it or not. The reason you do not feel the heat from a rusty nail is because the oxidation process is occurring too slowly. Heat is being released, but it is dissipating as quickly as it is being released.
The human oxidation rate is the rate at which your cells are burning their fuel. When you hear that there are various types of oxidizers, it doesn't really mean that there are different kinds of oxidation. It means that people release energy from their foods at different rates. A slow oxidizer releases energy too slowly. He is like a wood stove whose fire is too small to heat the room. To help him, you must speed up his metabolic furnace or increase his oxidation rate. A fast oxidizer releases energy too quickly. He is like a wood stove with a fire of soft wood that is burning too fast, overheating the room (the body), and running out of fuel. His oxidation rate must be decreased. A mixed oxidizer has an erratic metabolism. Sometimes it is too fast. Other times it is too slow. To give a mixed oxidizer more energy, you must stabilize his oxidation rate. The balanced oxidizer has the most efficient metabolism. It is neither too slow nor too fast. His system produces the maximum amount of usable human energy. To bring a person into a state of balanced oxidation is the real goal of mineral rebalancing programs. Some rates of energy-release are more efficient than others. That's why some people are energetic and others are tired. It all has to do with oxidation rates. This is what the Science
of human energy is all about, the production of human energy. The more efficient a person's oxidation rate becomes the more energetic the person.
When your body is chronically fatigued, one of two things happens. You may burn up your minerals too quickly until you run out of minerals and die. This is what happens in fast oxidation. The second possibility is that you will be unable to utilize your minerals. They will deposit in your blood vessels and other tissues and choke your system. This is what happens in slow oxidation. Either route leads to premature death. Neither of these two possibilities needs to occur. By balancing the minerals, we can eliminate the fatigue. Then, the minerals will be used at a proper rate and in a proper way. This is what is meant by balanced oxidation, which is neither too fast nor too slow. Once we approach a state of balanced oxidation, premature aging will be prevented. Or, if it has already occurred, it will be reversed. It is the sodium and potassium from your adrenals and thyroid gland that keep your body pliable and flexible. Sodium and potassium are the great solvents in the body. They are the great dissolvers. They keep everything in solution that should be in solution. When you are chronically fatigued, your thyroid and adrenal glands become exhausted. When this occurs, your sodium and potassium can go either too low or too high. Too low is slow oxidation. Too high is fast oxidation. If your sodium and potassium levels go too low, it means there is not enough solvent left in your body. So your minerals begin to drop out of solution. They precipitate. They begin to pile up in your tissues, arteries, joints, your heart, your skin, etc. You become rigid and stiff. In other words, you age prematurely. The process is the same whether you are 20 years old and exhausted, or whether you are 65 years old and exhausted. Exhaustion is premature aging. There is no way around it.
You can compare slow oxidation to a woodstove that is not getting enough air. The fire is not hot enough. Combustion is not complete. Residues form, (clinkers) and these clog up the stove. Eventually, they clog it so much that the fire goes out. This is how slow oxidizers die; their bodies suffocate. The slow oxidizer is actually turning into stone. Fast oxidizers are just as tired as slow oxidizers. The only difference between fast and slow oxidizers is how they react to fatigue. The slow oxidizer slows down to conserve energy. The fast oxidizer speeds up to compensate for his underlying lack of energy. He burns out the little reserves he has, so that he does not have to slow down. The fast oxidizer appears to have more energy than the slow oxidizer, but he is just as tired. Fast oxidizers can be recognized as seeming to run on nervous energy, not calm energy. They are hyped-up. They have to be, to keep going. But there are consequences. When the thyroid and adrenals of the fast oxidizer become overactive, the sodium and potassium levels go too high. This causes too many minerals to go into solution. To keep going, the body starts cannibalizing tissues for minerals like you would strip down a car for parts.
A fast oxidizer can be compared to a fire that is getting too much air. The fire burns too hot. Everything burns completely with no residue. But the fire burns out quickly because it runs out of fuel. Either route is not good. The slow oxidizer dies from mineral accumulation, the fast oxidizer dies from mineral bankruptcy. Both of these conditions are the inevitable consequences of chronic fatigue. People are usually fast oxidizers early in life. If they lead a healthy life, they will become normal oxidizers for many of their years. Then as they become older, one gland will eventually weaken and slow down, and they will become mixed oxidizers. Then as they grow older still, both glands will weaken and they will become full-fledged slow oxidizers. Ninety-five percent of people die as slow oxidizers. Aging is just another word for chronic slow oxidation. The tragic thing about today's world is that many men and women have become chronic slow oxidizers while they are still in their teens. This alone explains why so many young people are tired.
Every single mineral in the body as an effect on every other mineral in the body. So if just one mineral is imbalanced in the body, this affects all minerals by starting a massive chain reaction of mineral imbalances. People say, "I'm just taking a little magnesium," or a little zinc or whatever it is. If people only knew the harm they could cause by taking even one mineral supplement they didn't need, or taking the right supplement in excessive quantities. For instance, consider iron. Thousands of people take iron tablets because they are tired. Unfortunately, if iron is not taken in the right ratio with other minerals, it will make you more tired. Everybody's mineral chart is different and the amount of iron, and other minerals, which you need for more energy may be completely different than for the person next to you. Here is what could happen to a person who takes an iron supplement.
1. Sodium goes up. This is the first thing that happens. The iron will cause sodium levels to rise as a consequence of stimulating the adrenal glands.
2. Magnesium goes down. Magnesium levels will go down because sodium lowers magnesium.
3. Calcium goes down. When magnesium goes down, calcium also goes down to try to maintain the same calcium/ magnesium ratio.
4. Potassium goes up. Calcium and potassium also move in opposite directions. So when calcium goes down, potassium moves up.
5. Nitrogen goes down. Since the person is going into fast oxidation, he is starting to cannibalize his own proteins, instead of building them. This lowers the nitrogen level.
6. Copper goes down. Since tissue respiration is speeding up, copper is being used more quickly. If the copper is already at low levels, or, if the person has a high zinc to copper ratio, then his copper availability could plunge to dangerously low levels. At levels below 1.0, the person moves into a cancer danger zone.
7. Zinc goes down. As copper goes down, zinc goes down to maintain the proper ratio with it. Since zinc is needed for proper functioning of the adrenal glands, the lowering of zinc will eventually exhaust the adrenals. This will make you more tired than before you started.
8. Manganese goes up. As zinc goes down, the manganese goes up, since they normally move n opposite directions. Eventually, manganese reserves will become depleted.
This is unfortunate, because manganese in combination with iron makes a person very powerful--physically and emotionally. As the manganese levels collapse the person becomes weak and indecisive (exhausted adrenals)--weaker than before he began taking the iron tablets. In other words, the taking of iron has made the anemia worse. All these mineral imbalances could easily be caused by just one mineral, which has become too high in relation to the others--in this case, iron. You can see now what can happen when you take "just a little iron" to get your energy up. So when a person has 21 minerals out of balance, just imagine how complicated it can get trying to balance them. Each mineral in the body has an effect on all the other minerals. No mineral works alone.
There is no way of telling what you are doing without the intelligent use of hair tests and kinesiologic testing. Feeling better is not really a criteria that a supplement is "working." It is possible to make a person temporarily feel better by making their condition worse. For instance, lets take a fast oxidizer who has a high level of sodium and potassium; this means his adrensals are overactive or overstressed. This person is already overstimulating himself to keep himself going. Now if he takes supplements like vitamin E and vitamin C, and a high B-complex stress vitamin, he might feel better. Yet he is really making his pattern worse. What happens is that the vitamin C, E, and B-complex raise the sodium and potassium even more. It is a drug-like effect, like taking a cup of coffee. The person notices a pick-up. What he will probably not be aware of is that by raising the sodium and potassium he has pushed himself closer to a heart attack. He will also not be aware that his calcium and magnesium levels are being lowerd at the same time. If he keeps doing this, long enough, the calcium and magnesium levels--and the ratios between them--can move into a cancer resonance range. Of course, if the person was diagnosed with cancer, he would never connect it to the supplements he was taking. He would probably tell himself, "If it weren't for the supplements, I probably would have goten cancer much sooner." the real truth is that WITHOUT the supplements, he may never have gotten cancer.
In fact, if you change or rearrange a mineral pattern by 10-25%--in any direction--you can probably get relief from symptoms. You get short-term benefit by helping some parts of the mineral chart at the expense of others. Unfortunately, the damage you are doing does not show until later. It takes time to develop. So you never realize the harm you have done to yourself. Believe it or not, many times you have to make a person temporarily feel worse to get him better. Let's take the example of the fast oxidizer we were using before. The right way to help this person would be to lower his sodium and potassium levels. this would reduce the stress on his adrenal glands. It would slow down the person's metabolism and prevent him from burning out his mineral reserves and collapsing. You have to slow this kind of person down to save his life. But when you do it, he feels worse. He doesn't want to slow down. He wants to keep drivig himself. A person like this is won't voluntarily go into a healthfood store and buy supplements that will slow him down. No one would ever take supplements that would make him feel worse. If a person took something that made him feel worse, he would stop, and if it made him feel better, he would keep taking it. Now you can see some of the problems of randomly taking supplements without knowing what you are doing. So far, we've only mentioned four minerals, sodium, potassium, calcium and magnesium. You can imagine how complicated it can get when you consider the relationship between the other minerals, such as copper, zinc, manganese, chromium, phosphorus, iron, and so forth. The only way you can tell what supplements to take for your specific physical/emotional imbalances is to use the results of hair analysis or kinesiological muscle testing.
It is sad to see what goes on in the health field today. You could probably switch the labels on all the vitamins and minerals being sold and probably few people would physically notice the difference. Some people would even get better! That's how unscientific things are. People read in a magazine that zinc is good for them and they take some. They read that vitamin C is good for them and they take that too. They read that we are all deficient in magnesium, so they add some of that. If there is a special 20for-one sale on calcium tablets, they stock up on that. It is pathetic, but the way people go about choosing supplements, they could do almost as good using a roulette wheel. When you don't know what to take, you have to guess. Another thing you frequently find in the health field is the taking of a little of every mineral--"Just to be on the safe side." People believe that the body, with its infinite wisdom, knows exactly what to do with each and every mineral. They believe that whatever the body needs, it keeps; and whatever it doesn't need, it simply excretes in the urine, or through the proper body channels. If this were the case, then why do so many individuals have hair analyses which indicate that they have toxic amounts of copper, lead, cadmium, calcium, magnesium, iron, and zinc in their tissues? If all the minerals not needed by the body were excreted, and if all you had to do to correct "deficiencies" in the body was to give people the minerals they were low in, then it would be the easiest thing in the world to correct mineral imbalances. All you would need to do would be to give them a mineral supplement which contained all the essential minerals. If it were this easy, few people on mineral programs would ever remain ill.
But, of course, this is not the case. Many of the multiple supplements on the market today generally contain magnesium, zinc and copper along with Vitamin A and Vitamin B2. Unfortunately, a combination of these compounds will only serve to slow down an already slow metabolism. The idea behind taking a multiple mineral and vitamin supplement is logical. But you have to make sure that the multiple supplement is "balanced" for your particular metabolism. The whole philosophy of everyone taking the same kind of multiple supplement is just as absurd as everyone wearing the same shoe size. But, say that a balanced supplement has just the minerals which your body needs for your particular metabolism. The next question is, "Are all the minerals in the right ratios to one another?"
Sulfur & Mercury
Mercury, in its various forms, has a great affinity for certain minerals, and protein and nonprotein molecules in the body. Mercurials have a great attraction to the sulfhydryls, or thiols. The mercury atom or molecule will tend to bind withany molecule present that has sulfur or a sulfur-hydrogen combination in its structure. This process of combining with a metal to form a complex in which the metallic ion is sequestered and firmly bound is called chelation. A thiol is any organic compound containing a univalent radical called a sulfhydryl and identified by the symbol -SH (sulfur-hydrogen). A thiol can attract one atom of mercury in the ionized form and have it combine with itself. Because it is a radical, it can enter into or leave this combination without any change. Mercury and lead both have a great affinity for sulfur and sulfhydryls and are capable of affecting the transsulfuration pathways in the body. The primary sulfur-containing protein amino acids in the body are cystine, cyseteine, methionine, and taurine. There is also a sulfur-containing tripeptide (having three amino acids) called glutathione that is composed of glutamic acid, cysteine, and glycine. Sulfur exists in a reduced form (-SH) in cysteine and in an oxidized form (-S-S) as the double molecule, cystine. Whenever mercury binds to one of these sulfur-containing molecules, it reduces their availability for normal metabolic functions. Sulfur is present in all proteins, which makes it universally available throughout the body for binding with mercury. Some of the important biochemical sulfur-containing compounds of the body besides glutathione are insulin, prolactin, growth hormone, and vasopressin, and Science
has not yet investigated the effect of mercury upon them.
Mercury has a particularly high affinity for thiol groups and progressively less for other groups in the following sequence: Sulfur, amides, amines, carbon, and phosphate. Because of this capability, mercury has the potential of binding to proteins throughout the body. Mercury compounds are formed by the binding of mercury to the biological binders albumin or cysteine. The principal biological reaction fo mercury is with thiols to form mercury mercaptides. The sulfur groups are often referred to as mercaptans because of their marked affinity for mercury. Mercaptan is defined as any compound containing reduced sulfur bound to carbon. When a metal, such as mercury, replaces the hydrogen ion of the reduced sulfur, the resulting compound is called a mercaptide. Mercury can form at least three compounds with cysteine in which all or a part of the mercury is bound firmly as a mercaptide. Mercury may cause damage, especially to the placenta, by inactivation of sulfhydryl groups in cellular enzymes. Mercury interacts with sulfhydryl groups and disulfide bonds, as a result of which specific membrane transport is blocked and selective permeability of the membrane is altered. Mercury also combines readily with phosphate and heterocyclic base groups of DNA. It also combines with other ligands: amide, amine, carboxyl and phosphoryl groups.
Selenium closely resembles sulfur in its physical and chemical properties. The selenium concentration in the blood is 19-25 micrograms per 100 milliliters (U.S. population). It is found in the highest concentrations in the kidney, heart, spleen, and liver, and to some degree in all other tissues except fat. Selenium is an essential nutrient and deficiencies or low dietary intake has a bearing on mortality and morbidity associated with several major diseases. The mean blood selenium level of a cancer victim is significantly lower than the blood selenium level of individuals who do not get cancer. Significantly lower levels of selenium have been seen in patients with various types of cancer such as lymphocytic leukemia, breast, pulmonary, gastrointestinal, colon, genito-urinary, skin cancer, and Hodgkins's disease. Although selenium can be toxic by itself, it also prevents the toxicity of several other metals such as silver, mercury, cadmium, and lead. Mercury causes the loss of the needed metals copper and zinc, and selenium helps prevent that loss by binding the mercury. Contrary to accepted belief that the kidney is the prime accumulator of inorganic mercury, the thyroid and pituitary retain and accumulate more inorganic mercury than the kidney. Selenium deficiency is a common component of the malnutrition seen in AIDS patients. The mean blood platelet GSH-Px (glutathione peroxidase) activity of a coronary patient is significantly reduced. A low enzyme activity is a risk factor for the development of coronary artery disease. Mercury's ability to complex with selenium, increases its excretion, and reduces its bioavailability for primary metabolic functions.
It wasn't until 1974 that zinc was determined to be an essential element, but extensive research has associated zinc deficiency in humans with retarded growth, anorexia, hypogonadism, diminished sense of taste and/or smell, inadequate bodily development, dermatitis, dystrophy of the fingernails, and impaired wound healing. Zinc is an essential component of approximately 100 different enzymes. It is also involved in the synthesis of metallothionein, which is a complex involved in the storage or detoxification of cadmium, mercury, and copper. Zinc resembles cadmium and mercury in its ability to form complexes with thiols. Mercury can displace zinc in accordance with the binding affinities that metallothionein has for varioius metals. In order of attraction these are mercury, copper, cadmium adn zinc. Zinc-induced synthesis of metallothionein is perhaps the primary factor in reducing the toxicity of many heavy metals. Zinc also works together in the body with vitamin B6 (which increases B6 absorption) and vitamin E. Zinc deficiency may intensify vitamin E deficiency and thereby increase the requirement for vitamin E. The process of excreting zinc through the bile appears to be glutathione-dependent, with the glutathione molecule acting as a carrier. This might involve competition with other heavy metals such as copper, cadmium, and methylmercury, which also use glutathione as a carrier for biliary excretion and which ultimately can affect zinc balance in the body. Zinc can protect vertebrate embryo from the harmful effects produced by several different agents that cause birth defects. Patients with secondary immunodeficiency syndrome have low-serum zinc and elevated-serum copper levels. When given zinc supplements, the patients' condition improves. Zinc and copper balance are significantly altered in many immunodeficiency disorders and may be the cause of immunodeficiency.
Mild zinc deficiency is associated with and can play a role in the susceptibility of women to recurrent vaginal candidiasis. Mercury impairs zinc's biological functions. Current candida treatment protocols are not totally effective until mercury Amalgam
dental fillings are replaced. The most important aspect of mercury's biochemical effect on zinc is its inhibitory effect on zinc-responsive enzymes and coenzymes. Mercury inhibits the following zinc-involved enzymes or coenzymes: alcohol dehydrogenase, delta-aminolevulinic acid dehydrogenase, carbonic anhydrase, alkaline phosphatase, and aldolase. Chronic inhalation of mercury vapor from Amalgam
dental fillings increases the overall body burden of mercury enough to represent a significant metabolic factor in development of the imbalances of selenium, zinc, and copper.
One of the major effects of systemic exposure to mercury is neurological. Muscular function is controlled neurologically by the transmission of nerve impulses, which involve calcium and sodium, Mercury ions affect motor nerve terminals, causing irreversible depolarization, increased transmitter release, and subsequent irreversible block of transmitter release. The neurotoxic action of mercury is at an intracellular site and entry is gained through both sodium and calcium channels. Metals may inhibit transmitter release at either the calcium channel or at the release site, but irreversible toxicity is due to an intracellular action, possibly involving sulfhydryl groups.
Calcium is one of the great binders of nature: it causes cement to harden, blood to clot, bones to hold up. Every cell in the body uses it. It's needed for your nerves to fire, for your brain to function, and for your muscles to contract. Even your heart won't beat without calcium. Calcium maintains the organization of tissues. Coordination among the cells in a tissue is maintained mostly by bridges, known as tight junctions that bind the cells together physically and allow messages to be carried among them. The messages are carried by calcium atoms just like messages on a telephone line are carried by calcium atoms just like messages on a telephone line are carried by electrons. Tight junctions--and communication between cells--disappear when calcium in the fluid around the cells drops. The tissues become disorganized. Competition among the cells for food and oxygen replaces the usual cooperation, and a process of rapid evolution at the cell level begins. The result of this is that highly specialized, aggressive cells evolve that can command resources, invade other tissues, and kill other cells. This is called cancer.
The human body cannot manufacture calcium. We obtain calcium by eating or drinking foods that contain calcium. On a typical day, the average person takes in about one fortieth of an ounce of calcium, roughly the weight of a small feather (700 milligrams). Unfortunately, usually only 15-35 percent of the calcium we eat is absorbed by the body, depending upon a person's age, sex, vitamin D availability, and the presence of other foods that block calcium absorption. Your body will first allocate the calcium to your blood. If the calcium level in your blood is adequate, it will be shunted quickly to the extracellular fluid around your cells. The extracellular fluid surrounds each cell in your body and gives it the essentials that the cell needs for survival. Calcium from the extracellular fluid around the cells that make bone will be put to work. You are always making new bone. The process, called remodeling, allows the body to develop new and powerful bones throughout a person's lifetime. The ability to strengthen and develop new bone cells is particularly important for those who are physically active and during pregnancy. The typical adult woman consumes 490 milligrams of calcium per day and the typical adult man consumes 700 milligrams per day.
A 40-year-old man taking in an average amount of calcium for his age (700 milligrams) might absorb only 245 milligrams per day. At the same time, his body will lose 100 milligrams of the absorbed calcium in solid waste, 150 milligrams in urine, and 20 milligrams in sweat each day. He will have lost 270 milligrams, but only absorbed 245, leaving him with a daily loss of 25 milligrams. After a period ranging from minutes to hours, some of the calcium that is absorbed will be used to form a crystal called apatite in the bones throughout the body. It will move fastest to bones which specialize in storing calcium for fast access. These bones, called trabecular bones, are the body's equivalent of a 24-hour market, open day and night to meet unexpected needs. Some of the calcium that is absorbed goes to the kidneys, which excrete about 150 milligrams per day. The kidneys conserve calcium; only one one-hundredth of the amount of calcium that enters them is excreted under normal circumstances, although drinking lots of coffee, for example, can change this ratio, causing the kidneys to excrete much more calcium than they would normally. Calcium is used in two ways in your body. The first is for communication. The cells in your body talk constantly, using a special chemical code. They routinely communicate information necessary for you tissues to function properly. Calcium is vital to that communication between cells. Cells exchange information through tiny bridges between them, called calcium channels. Most calcium channels are located in structures called communicating junctions.
Cells transmit various kinds of messages, and we hypothesize that the most important of these is a "vote" to an adjacent cell on whether to divide. A normal cell in tissue called epithelium--the cells that make up the inside layer of your intestine, your skin, and which line the ducts of a woman's breast--decides whether to divide from adjacent cells using a calcium channel. Mercury blocks the calcium channel in cell membranes.
Your body can be seen as a giant cooperative venture with billions of cells working toward a common objective, your health. Many of the most important tissues in your body have an outermost layer that is only one cell thick. This is true of the cells lining the intestine, the cells in the lungs that exchange oxygen and carbon dioxide with the air we breathe, and the cells lining the inside of most of our internal organs. In the case of the small intestine, for example, a single layer of cells is devoted to absorbing nutrients. Cells exchange information or communicate by sending calcium ions from one cell to a neighboring cell via a communicating junction. When contact between cells is cut off for some reason, we cells interpret this as the loss of a neighboring cell. The apparent loss of nearby cells will stimulate the proliferation of cells that make new epithelium. Calcium carries a vital message between the cells that keeps them from dividing unnecessarily. When calcium in the fluid bathing the cells is very low, the communication system is disconnected. The cells can't receive signals from adjacent cells. And they don't have Cell Phone
s! If enough time passes without receiving signals from other cells, the cells that make new epithelium will divide. If the two cells produced do not receive signals from other cells, they too will divide, producing eight cells, and so on.
Before long, there will be several generations of new cells, each generation doubling the size of the previous generation. If these cells do not continue to receive growth-blocking signals via calcium channels from adjacent cells, they will continue to proliferate in a chain reaction. Soon this chaotic mitosis of cells will form a pileup, and take on peculiar shapes and sizes. When the pileup is large, the condition is called hyperplasia. Hyperplasia may be physical evidence of the breakdown in communication among cells. In the intestine, it appears long before cancer is present. The usual scenario of a breakdown in communication in the cells of the intestine may be for the cells to pile up until they form a polyp, which is an unusual extension of the lining of the intestine into the lumen, or opening, where the food passes through. Polyps seen under a microscope reveal that many are disorganized tissues. Most polyps don't start out as cancer, but rather seem to be a result of the body's attempt to deal with epithelial cells that are needlessly dividing due to a deficiency of calcium in the fluid bathing them.
Signals sent through a communicating junction to an adjacent cell inform it that another cell is nearby. Signals such as these sent from the surface of the cell are used by the cell nucleus, the specialized central command, to make a decision about the need to reproduce. If the signals coming to the cell membrane are constant, adjacent cells are considered to be present. If the signal from one surface of the cell stops coming in, it means that the adjacent cell is no longer present. Perhaps it had been washed away, as often happens in tissues such as the intestine. Or the cell might have died, shrinking slightly and leaving space. Cancer manifests in three phases: decoupling, initiation, and promotion. It is the first phase, decoupling, where calcium has the greatest effect. Decoupling is the process of cells splitting apart from one another. It happens when the amount of calcium in the extracellular fluid is low. It is due to loss of tight junctions that bind cells of the intestine, breast, and respiratory tissues together. When cell lose communication and begin to divide, the tissue becomes disorganized and the cells begin to pile up. The resulting mass of cells is called hyperplasia. If the cells are unusual shapes or are especially disorganized, it is called dysplasia. It isn't cancer, however--it often disappears spontaneously without a trace. Decoupling lays the groundwork for hyperplasia, which may precede the next stage in the formation of cancer, initiation.
Radiation or toxic chemicals can produce variation by attacking the DNA in the cells, causing mutations. Most of the mutated cells will die but a few will thrive. Those that thrive are better able to get food and oxygen than normal cells, and therefore better able to reproduce. If the generator of variation continues to act, more variation will occur. New mutations will arise in each generation of transformed cells. Again, most will die but those that survive will do so because they have an advantage in getting food and oxygen. These cells in turn will thrive and reproduce. Those that reproduce most rapidly are the most successful. If this process continues over many generations, a generation of highly aggressive, rapidly reproducing, mutated cells will come into being. These cells become potent competitors for food and oxygen at the expense of normal cells. In many cases they lose their fine structure and even some of their genes. These are cancer cells.
If the generator of variation is removed, the evolutionary process may be arrested before a new generation of cancer cells evolves. This is what happens when a person quits smoking. The predominant carcinogen in tobacco smoke is benzo-alpha-pyrene. Take it away and evolution of the cells toward cancer is usually arrested. If the cancer cells have evolved sufficiently already, then taking away the generator of variation will do little good. The die has been cast. This is why quitting smoking late in life doesn't always prevent cancer. The third stage of cancer is proliferation of the highly evolved cancer cells. A cancer can be promoted by a chemical that is not a cause of variation. There are many chemicals, such as the hormone estrogen, that do not appear to initiate cancer cells, but which can stimulate them to grow. The rate of spread of Breast Cancer
can be reduced dramatically in many women by eliminating the promoter estrogen (hormone replacement therapy, birth control pills, meat & poultry, etc). Without the promoter, the cancer tissue slows its rate of reproduction.
Calcium seems to prevent cancer in the decoupling phase of the disease. Cells can function normally without communication with other cells, at least for short periods of time. Eventually, though, in the absence of communication from other cells, the cells will divide. On the other hand, if calcium levels remain normal, cells will not divide unnecessarily, and the evolution will be slowed. A sufficient intake of calcium slows the evolution or normal cells toward cancer and can help to prevent it. The second major role of calcium inn the body is to provide structure. There are only a few elements in the world that are used routinely to provide structure for plants and animals. Almost all rigid structures of plants and animals contain calcium. Each cell in your body, with a few exceptions, has a skeleton, called a cytoskeleton that keeps the cell together. These cell skeletons differ in degrees of rigidity, but in places where they must be very rigid they include crystals of calcium. The reasons for this are that calcium is strong, easily dissolvable, and transportable. The disease osteoporosis occurs because calcium is easily dissolvable and transportable.
In the months preceding birth, collagen, a tough substance used by the body where flexible strength is needed, forms a net where bone will be created. Calcium in the fetus is then carried from the placenta to this net, where the calcium crystals are neatly caught from one edge of the developing bone to the other. In the months and years that follow, more calcium is added to the bone structure, giving the bone strength. Calcium is essential to the body at the cellular level, as a structural support and as a means of communication between cells, and in the formation and endurance of bones as well. A sufficient calcium intake is crucial to health and fitness.
Calcium tables and values printed on food packages and other calcium books have been based on crude laboratory methods. They show you how much calcium is present, but do not show you how much is usable. Many foods "steal" calcium. Such foods are "calcium robbers." They can steal the calcium you take in, as well as the calcium stored in reserve (teeth and bones). The molecules of calcium robbers bond extremely easily to calcium. They will readily abandon another element for calcium should they come into contact with calcium. Phytate, a molecule in certain nuts, seeds, and vegetables is a prime example. Phytate is usually bound to sodium or other elements. However, when it comes into contact with a calcium molecule, it will desert the other elements it is attached to and has a preference for and bonds with the calcium. The problem is that when calcium is bound to phytate, the body is usually unable to unbind the two molecules, and the calcium passes through the small intestine in an unusable form until it is excreted from the body. The calcium, for all the good it has done, might just as well not have been eaten. Similar to phytate is oxalate, another molecule that binds with calcium and makes it unusable. Many foods contain phytates and oxalates, and it is these foods that we term calcium robbers. Eating such foods with calcium-rich foods negates the potential benefits of a calcium-rich diet. The tendency of bran to bind calcium has long been known. Experimenters since the 1930s have fed bran-rich foods to animals to induce rickets.
Mercury blocks the enzyme in the cell membrane that actively passes calcium in and out of the muscle cells by attaching to the thiol part of the enzyme. Calcium is necessary for the proper function of heart muscle. High blood pressure is caused by mercury preventing the passage of calcium into the heart muscle cells, increasing the force of the heart muscle contraction. It takes time for chronic mercury exposure to cause enough damage to result in a clinically detectable dysfunction. This is a predominant characteristic of heart disease.
Fluorine (fluoride) is the most reactive element known to chemists and its greatest affinity is for calcium. Anyone with a calcium deficiency can experience muscle spasms and convulsions from fluoride ingestion. Fluorine interferes with the normal process of calcification of teeth during the process of their formation, so that affected teeth, in addition to being unusually discolored and ugly in appearance, are structurally weak and deteriorate early in life. Fluoride stimulates abnormal bone development. High dose fluoride treatment increases bone mass but the newly formed bone is structurally unsound. Thus, instead of reducing hip fracture, high doses of fluoride increase hip fracture.
High intake of protein will also cause you to lose calcium. If you eat more than 90 grams, or three ounces, of protein per day you begin to enter a dietary range where the protein will acidify the body and cause calcium loss, especially if organic sodium is not adequately supplied in the diet. You will lose 50 to 70 milligrams of calcium per day for each ounce of protein you eat above three ounces. This can make a big difference if you're an avid meat eater. Heavy intake of sugar will also acidify the body and cause you to lose calcium through excess excretion. If you eat more than two ounces
per day of sugar, honey, corn syrup, or other sugars in any form, you'll need to add calcium above the usual requirements to your diet. Coffee, tea, and alcohol also have an important effect on calcium absorption. The typical American drinks 24 ounces
of coffee and soft drinks every day. Coffee is brewed in 85% of American homes. Many people drink ten to twenty cups per day. Each cup of coffee causes you to lose about 10 milligrams of calcium. This may not seem like a lot, but the loss may mean trouble if your calcium intake is already low. Most people who take in less than 500 to 600 milligrams of calcium per day are losing calcium from their bodies. This amount just isn't sufficient to maintain a positive calcium balance according to sophisticated studies using a tracing method based on a calcium isotope.
People who drink a lot of alcohol tend to absorb vitamin D and calcium from their diet poorly. The result for those who drink a lot of alcohol is bone loss, even in young people. There are changes in the microscopic structure of the intestine of people who drink a lot of alcohol that make it hard for vitamin D to pass through the fine structures of the cells. The ultimate result is that the calcium is not absorbed, which causes an increase in the rate of cell division of the intestinal wall.
Some substances found in food act more as calcium transporters--gently carrying calcium molecules to the large intestine. Foremost of those transporters is pectin, a substance found in many fruits and vegetables, particularly in apples. Pectin refers to both pectin and its relatives, the polysaccharides, in fruits and vegetables that aren't derived from cellulose or its relatives or starch. The Latin root word polysaccharide means "many sugars." These sugars are bound together so they can't be absorbed by your body. Your body is able to absorb free sugars such as fructose (fruit sugar), sucrose (table sugar), maltose (honey sugar), lactose (milk sugar), and glucose (a sugar found in carrots and other vegetables), However, the body would need a special enzyme to break the polysaccharides into smaller free sugars, and our bodies don't have the enzyme to do it. But it doesn't leave your body, either. It does something even more important. Pectin is a faithful carrier of calcium to your large intestine. It does this with a molecular structure that looks and acts like an egg crate. It has a fascinating molecular structure that consists of a long chain of up to a thousand units of a simple plant acid. If you add calcium to pectin, a gel forms. One ounce of pectin gel contains 750 milligrams of calcium in its molecular egg crate. Because we don't have an enzyme in our bodies that will break down pectin in our stomach or small intestine, it passes through those organs intact to the large intestine.
After traveling through the small intestine, all that's left of the apple is three compounds: cellulose, lignin, and pectin. Cellulose and lignin are the compounds that make up the woody arts of the plant cell wall. They're unusable by the body and pass through untouched until they are eliminated. Pectin, however, is another matter. Pectin next enters the large intestine, where friendly bacteria take it apart and use it as a source of fuel for themselves. They are able to do this because they have an enzyme we don't. Although bacteria eat it, it has no caloric value to us. When pectin is digested by friendly bacteria that live in the large intestine, it releases calcium, where it can interact with potentially dangerous carcinogens, neutralizing to protect against intestinal cancer. The calcium is also slowly absorbed by the intestine while some of it reacts with fatty acids, bile salts, and other carcinogens in the intestine to form inert compounds called soaps. Calcium safely binds up the attackers, rendering them unable to harm the intestinal cells. Apples, oranges, lemons, limes, grapefruits, kiwi, and a wide range of other fruits, as well as most vegetables, contain substantial amounts of pectin.
Overview of Minerals and Their Function
Calcium is the most common mineral in the human body. About 99% of the calcium in the body is found in bones and teeth, while the other 1% is found in the blood and soft tissue. Calcium levels in the blood and fluid surrounding the cells (extracellular fluid) must be maintained within a very narrow concentration range for normal physiological functioning. The physiological functions of calcium are so vital to survival that the body will demineralize bone to maintain normal blood calcium levels when calcium intake is inadequate. Thus, adequate dietary calcium is a critical factor in maintaining a healthy skeleton.
Calcium is a major structural element in bones and teeth. The mineral component of bone consists mainly of hydroxyapatite crystals, which contain large amounts of calcium and phosphorus (about 40% calcium and 60% phosphorus). Bone is a dynamic tissue that is remodeled throughout life. Bone cells called osteoclasts begin the process of remodeling by dissolving or resorbing bone. Bone-forming cells called osteoblasts then synthesize new bone to replace the bone that was resorbed. During normal growth, bone formation exceeds bone resorption. Osteoporosis may result when bone resorption exceeds formation.
Calcium plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones, such as insulin. Excitable cells, such as skeletal muscle and nerve cells, contain voltage-dependent calcium channels in their cell membranes that allow for rapid changes in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions into the muscle cell. These calcium ions bind to activator proteins within the cell that release a flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein, troponin-c, initiates a series of steps that lead to muscle contraction. The binding of calcium to the protein, calmodulin, activates enzymes that breakdown muscle glycogen to provide energy for muscle contraction.
Cofactor for Enzymes and Proteins
Calcium is necessary to stabilize or allow for optimal activity of a number of proteins and enzymes. The binding of calcium ions is required for the activation of the seven "vitamin K-dependent" clotting factors in the coagulation cascade. The term, "coagulation cascade," refers to a series of events, each dependent on the other that stops bleeding through clot formation.
Regulation of Calcium Levels
Calcium concentrations in the blood and fluid that surrounds cells are tightly controlled in order to preserve normal physiological functioning. When blood calcium decreases (e.g., in the case of inadequate calcium intake), calcium-sensing proteins in the parathyroid glands send signals resulting in the secretion of parathyroid hormone (PTH). PTH stimulates the conversion of vitamin D to its active form, calcitriol, in the kidneys. Calcitriol increases the absorption of calcium from the small intestine. Together with PTH, calcitriol stimulates the release of calcium from bone by activating osteoclasts (bone resorbing cells), and decreases the urinary excretion of calcium by increasing its reabsorption in the kidneys. When blood calcium rises to normal levels, the parathyroid glands stop secreting PTH and the kidneys begin to excrete any excess calcium in the urine. Although this complex system allows for rapid and tight control of blood calcium levels, it does so at the expense of the skeleton.
A low blood calcium level usually implies abnormal parathyroid function, and is rarely due to low dietary calcium intake since the skeleton provides a large reserve of calcium for maintaining normal blood levels. Other causes of abnormally low blood calcium levels include chronic kidney failure, vitamin D deficiency, and low blood magnesium levels that occur mainly in cases of severe alcoholism. Magnesium deficiency results in a decrease in the responsiveness of osteoclasts to PTH. A chronically low calcium intake in growing individuals may prevent the attainment of optimal peak bone mass. Once peak bone mass is achieved, inadequate calcium intake may contribute to accelerated bone loss and ultimately the development of osteoporosis.
Vitamin D: Vitamin D is required for optimal calcium absorption. Several other nutrients (and non-nutrients) influence the retention of calcium by the body and may affect calcium nutritional status.
Sodium: Increased sodium intake results in increased loss of calcium in the urine, possibly due to competition between sodium and calcium for reabsorption in the kidney or by an effect of sodium on parathyroid hormone (PTH) secretion. Each 2.3-gram increment of sodium (6 grams of salt; NaCl) excreted by the kidney has been found to draw about 24-40 milligrams (mg) of calcium into the urine. Because urinary losses account for about half of the difference in calcium retention among individuals, dietary sodium has a large potential to influence bone loss. In adult women, each extra gram of sodium consumed per day is projected to produce an additional rate of bone loss of 1% per year if all of the calcium loss comes from the skeleton. Although animal studies have shown bone loss to be greater with high salt intakes, no controlled clinical trials have been conducted to confirm the relationship between salt intake and bone loss in humans. However, a 2-year study of postmenopausal women found increased urinary sodium excretion (an indicator of increased sodium intake) to be associated with decreased bone mineral density (BMD) at the hip.
Protein: As dietary protein intake increases, the urinary excretion of calcium also increases. Recommended calcium intakes for the U.S. population are higher than those for populations of less industrialized nations because protein intake in the U.S. is generally higher. The RDA for protein is 46 grams/day for adult women and 56 grams/day for adult men. However, the average intake of protein in the U.S. tends to be higher (65-70 grams/day in adult women and 90-110 grams per day in adult men). Weaver and colleagues have calculated that each additional gram of protein results in an additional loss of 1.75 mg of calcium/day. Because only 30% of dietary calcium is generally absorbed, each one-gram increase in protein intake/day would require an additional 5.8 mg of calcium/day to offset the calcium loss. At the other end of the spectrum of protein intake, the effect of dietary protein insufficiency on bone health has received much less attention. Inadequate protein intakes have been associated with poor recovery from osteoporotic fractures and serum albumin values (an indicator of protein nutritional status) have been found to be inversely related to hip fracture risk.
Phosphorus: Phosphorus, which is typically found in protein-rich foods, tends to decrease the excretion of calcium in the urine. However, phosphorus-rich foods also tend to increase the calcium content of digestive secretions, resulting in increased calcium loss in the feces. Thus, phosphorus does not offset the net loss of calcium associated with increased protein intake. Increasing intakes of phosphates from soft drinks and food additives
have caused concern among some researchers regarding the implications for bone health. Diets high in phosphorus and low in calcium have been found to increase parathyroid hormone (PTH) secretion, as have diets low in calcium. While the effect of high phosphorus intakes on calcium balance and bone health are presently unclear, the substitution of large quantities of soft drinks for milk or other sources of dietary calcium is cause for concern with respect to bone health in adolescents and adults.
Caffeine: Caffeine in large amounts increases urinary calcium content for a short time. However, caffeine intakes of 400 mg/day did not significantly change urinary calcium excretion over 24 hours in premenopausal women when compared to a placebo. Although one observational study found accelerated bone loss in postmenopausal women who consumed less than 744 mg of calcium/day and reported that they drank 2-3 cups of coffee/day, a more recent study that measured caffeine intake found no association between caffeine intake and bone loss in postmenopausal women. On average, one 8-ounce cup of coffee decreases calcium retention by only 2-3 mg.
Although trivalent chromium is recognized as a nutritionally essential mineral, scientists are not yet certain exactly how it functions in the body. The two most common forms of chromium are trivalent chromium (III) and hexavalent chromium (VI). Chromium (III) is the principal form in foods, as well as the form utilized by the body. Chromium (VI) is derived from chromium (III) by heating at alkaline pH and is used as a source of chromium for industrial purposes. It is a strong irritant and is recognized as a carcinogen when inhaled. At low levels, chromium (VI) is readily reduced to chromium (III) by reducing substances in foods and the acidic environment of the stomach, which serve to prevent the ingestion of chromium (VI).
A biologically active form of chromium participates in glucose metabolism by enhancing the effects of insulin. Insulin is secreted by specialized cells in the pancreas in response to increased blood glucose levels, for example, after a meal. Insulin binds to insulin receptors on the surface of cells, activating those receptors and stimulating glucose uptake by cells. Through its interaction with insulin receptors, insulin provides cells with glucose for energy and prevents blood glucose levels from becoming elevated. In addition to its effects on carbohydrate (glucose) metabolism, insulin also influences the metabolism of fat and protein. A decreased response to insulin or decreased insulin sensitivity may result in impaired glucose tolerance or type 2 diabetes, also known as non-insulin dependent diabetes mellitus (NIDDM). Type 2 diabetes is characterized by elevated blood glucose levels and insulin resistance.
The precise structure of the biologically active form of chromium is not known. Recent research suggests that a low-molecular-weight chromium-binding substance (LMWCr) may enhance the response of the insulin receptor to insulin. The following is a proposed model for the effect of chromium on insulin action. First, the inactive form of the insulin receptor is converted to the active form by binding insulin. The binding of insulin by the insulin receptor stimulates the movement of chromium into the cell and results in binding of chromium to apoLMWCr, a form of the LMWCr that lacks chromium. Once it binds chromium the LMWCr binds to the insulin receptor and enhances its activity. The ability of the LMWCr to activate the insulin receptor is dependent on its chromium content. When insulin levels drop due to normalization of blood glucose levels, the LMWCr may be released from the cell in order to terminate its effects.
Iron: Chromium competes for one of the binding sites on the iron transport protein, transferrin. However, supplementation of older men with 925 mcg of chromium/day for 12 weeks did not significantly affect measures of iron nutritional status. A study of younger men found an insignificant decrease in transferrin saturation with iron after supplementation of 200 mcg of chromium/day for 8 weeks, but no long-term studies have addressed this issue. Iron overload in hereditary hemochromatosis may interfere with chromium transport by competing for transferrin binding. This has led to the hypothesis that decreased chromium transport might contribute to the diabetes associated with hereditary hemochromatosis.
Vitamin C: Chromium uptake is enhanced in animals when given at the same time as vitamin C. In a study of three women, administration of 100 mg of vitamin C together with 1 mg of chromium resulted in higher plasma levels of chromium than 1 mg of chromium without vitamin C.
Carbohydrates: Diets high in simple sugars (e.g., sucrose), compared to diets high in complex carbohydrates (e.g., whole grains), increase urinary chromium excretion in adults. This effect may be related to increased insulin secretion in response to the consumption of simple sugars compared to complex carbohydrates.
Chromium deficiency was reported in patients on long-term intravenous feeding who did not receive supplemental chromium in their intravenous solutions. These patients developed evidence of abnormal glucose utilization and increased insulin requirements that responded to chromium supplementation. Additionally, impaired glucose tolerance in malnourished infants responded to an oral dose of chromium chloride. Because chromium appears to enhance the action of insulin and chromium deficiency has resulted in impaired glucose tolerance, chromium insufficiency has been hypothesized to be a contributing factor to the development of Type 2 diabetes.
Several studies of male runners indicated that urinary chromium loss was increased by endurance exercise, suggesting that chromium needs may be greater in individuals who exercise regularly. In a more recent study, resistive exercise (weight lifting) was found to increase urinary excretion of chromium in older men. However, chromium absorption was also increased, leading to little or no net loss of chromium as a result of resistive exercise.
At present, research on the effects of inadequate chromium intake and risk factors for chromium insufficiency are limited by the lack of sensitive and accurate tests for determining chromium nutritional status.
Copper (Cu) is an essential trace element for humans and animals. In the body, copper shifts between the cuprous (Cu1+) and the cupric (Cu2+) forms, though the majority of the body's copper is in the Cu2+ form. The ability of copper to easily accept and donate electrons explains its important role in oxidation-reduction (redox) reactions and the scavenging of free radicals. Although Hippocrates is said to have prescribed copper compounds to treat diseases as early as 400 B.C., scientists are still uncovering new information regarding the functions of copper in the human body.
Copper is a critical functional component of a number of essential enzymes, known as cuproenzymes. Some of the physiologic functions known to be copper-dependent are discussed below.
The copper-dependent enzyme, cytochrome c oxidase, plays a critical role in cellular energy production. By catalyzing the reduction of molecular oxygen (O2) to water (H2O), cytochrome c oxidase generates an electrical gradient used by the mitochondria to create the vital energy-storing molecule, ATP.
Connective Tissue Formation
Another cuproenzyme, lysyl oxidase, is required for the cross-linking of collagen and elastin, which are essential for the formation of strong and flexible connective tissue. The action of lysyl oxidase helps maintain the integrity of connective tissue in the heart and blood vessels and plays a role in bone formation.
Two copper-containing enzymes, ceruloplasmin (ferroxidase I) and ferroxidase II have the capacity to oxidize ferrous iron (Fe2+) to ferric iron (Fe3+), the form of iron that can be loaded onto the protein transferrin for transport to the site of red blood cell formation. Although the ferroxidase activity of these two cuproenzymes has not yet been proven to be physiologically significant, the fact that iron mobilization from storage sites is impaired in copper deficiency supports their role in iron metabolism.
Central Nervous System
A number of reactions essential to normal function of the brain and nervous system are catalyzed by cuproenzymes.
Neurotransmitter synthesis: Dopamine-b-monooxygenase catalyzes the conversion of dopamine to the neurotransmitter norepinephrine.
Metabolism of neurotransmitters: Monoamine oxidase (MAO) plays a role in the metabolism of the neurotransmitters norepinephrine, epinephrine, and dopamine. MAO also functions in the degradation of the neurotransmitter serotonin, which is the basis for the use of MAO inhibitors as antidepressants.
Formation and maintenance of myelin: The myelin sheath is made of phospholipids whose synthesis depends on cytochrome c oxidase activity.
The cuproenzyme, tyrosinase, is required for the formation of the pigment melanin. Melanin is formed in cells called melanocytes and plays a role in the pigmentation of the hair, skin, and eyes.
Superoxide dismutase: Superoxide dismutase (SOD) functions as an antioxidant by catalyzing the conversion of superoxide radicals (free radicals or ROS) to hydrogen peroxide, which can subsequently be reduced to water by other antioxidant enzymes. Two forms of SOD contain copper: 1) copper/zinc SOD is found within most cells of the body, including red blood cells, and 2) extracellular SOD is a copper containing enzyme found in high levels in the lungs and low levels in blood plasma.
Ceruloplasmin: Ceruloplasmin may function as an antioxidant in two different ways. Free copper and iron ions are powerful catalysts of free radical damage. By binding copper, ceruloplasmin prevents free copper ions from catalyzing oxidative damage. The ferroxidase activity of ceruloplasmin (oxidation of ferrous iron) facilitates iron loading onto its transport protein, transferrin, and may prevent free ferrous ions (Fe2+) from participating in harmful free radical generating reactions.
Regulation of Gene Expression
Copper-dependent transcription factors regulate transcription of specific genes. Thus, cellular copper levels may affect the synthesis of proteins by enhancing or inhibiting the transcription of specific genes. Genes regulated by copper-dependent transcription factors include genes for copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (another antioxidant enzyme), and proteins related to the cellular storage of copper.
Iron: Adequate copper nutritional status appears to be necessary for normal iron metabolism and red blood cell formation. Anemia is a clinical sign of copper deficiency, and iron has been found to accumulate in the livers of copper deficient animals, indicating that copper (probably in the form of ceruloplasmin) is required for iron transport to the bone marrow for red blood cell formation. Infants fed a high iron formula absorbed less copper than infants fed a low iron formula, suggesting that high iron intakes may interfere with copper absorption in infants.
Zinc: High supplemental zinc intakes of 50 mg/day or more for extended periods of time may result in copper deficiency. High dietary zinc increases the synthesis of an intestinal cell protein called metallothionein, which binds certain metals and prevents their absorption by trapping them in intestinal cells. Metallothionein has a stronger affinity for copper than zinc, so high levels of metallothionein induced by excess zinc cause a decrease in intestinal copper absorption. High copper intakes have not been found to affect zinc nutritional status.
Fructose: High fructose diets have exacerbated copper deficiency in rats, but not in pigs whose gastrointestinal systems are more like those of humans. Very high levels of dietary fructose (20% of total calories) did not result in copper depletion in humans, suggesting that fructose intake does not result in copper depletion at levels relevant to normal diets.
Vitamin C: Although vitamin C supplements have produced copper deficiency in laboratory animals, the effect of vitamin C supplements on copper nutritional status in humans is less clear. Two small studies in healthy young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C. In one study, vitamin C supplementation of 1,500 mg/day for 2 months resulted in a significant decline in ceruloplasmin oxidase activity. In the other study, supplements of 605 mg of vitamin C/day for 3 weeks resulted in decreased ceruloplasmin oxidase activity, although copper absorption did not decline. Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status.
Clinically evident or frank copper deficiency is relatively uncommon. Serum copper levels and ceruloplasmin levels may fall to 30% of normal in cases of severe copper deficiency. One of the most common clinical signs of copper deficiency is an anemia that is unresponsive to iron therapy but corrected by copper supplementation. The anemia is thought to result from defective iron mobilization due to decreased ceruloplasmin activity. Copper deficiency may also result in abnormally low numbers of white blood cells known as neutrophils (neutropenia), a condition that may be accompanied by increased susceptibility to infection. Osteoporosis and other abnormalities of bone development related to copper deficiency are most common in copper-deficient low-birth weight infants and young children. Less common features of copper deficiency may include loss of pigmentation, neurological symptoms, and impaired growth.
Individuals at Risk of Deficiency
Cow's milk is relatively low in copper, and cases of copper deficiency have been reported in high-risk infants and children fed only cow's milk formula. High-risk individuals include: premature infants, especially those with low-birth weight, infants with prolonged diarrhea, infants and children recovering from malnutrition, individuals with malabsorption syndromes, including celiac disease, sprue, and short bowel syndrome due to surgical removal of a large portion of the intestine. Individuals receiving intravenous total parenteral nutrition or other restricted diets may also require supplementation with copper and other trace elements. Recent research indicates that cystic fibrosis patients may also be at increased risk of copper insufficiency.
Iodine, a non-metallic trace element, is required by humans for the synthesis of thyroid hormones. Iodine
deficiency is an important health problem throughout much of the world. Most of the Earth's Iodine
is found in its oceans. In general, the older an exposed soil surface, the more likely the iodine has been leached away by erosion. Mountainous regions, such as the Himalayas, the Andes, and the Alps, and flooded river valleys, such as the Ganges , are among the most severely iodine deficient areas in the world.
Iodine is an essential component of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4) and is therefore, essential for normal thyroid function. To meet the body's demand for thyroid hormones, the thyroid gland traps iodine from the blood and converts it into thyroid hormones that are stored and released into the circulation when needed. In target tissues, such as the liver and the brain, T3, the physiologically active thyroid hormone, can bind to thyroid receptors in the nuclei of cells and regulate gene expression. T4, the most abundant circulating thyroid hormone, can be converted to T3 by enzymes known as deiodinases in target tissues. In this manner, thyroid hormones regulate a number of physiologic processes, including growth, development, metabolism, and reproductive function.
The regulation of thyroid function is a complex process that involves the brain (hypothalamus) and pituitary gland. In response to thyrotropin-releasing hormone (TRH) secretion by the hypothalamus, the pituitary gland secretes thyroid-stimulating hormone (TSH), which stimulates iodine trapping, thyroid hormone synthesis, and release of T3 and T4 by the thyroid gland. The presence of adequate circulating T4 decreases the sensitivity of the pituitary gland to TRH, limiting its secretion of TSH. When circulating T4 levels decrease, the pituitary increases its secretion of TSH, resulting in increased iodine trapping, as well as increased production and release of T3 and T4. Iodine deficiency results in inadequate production of T4. In response to decreased blood levels of T4, the pituitary gland increases its output of TSH. Persistently elevated TSH levels may lead to hypertrophy (enlargement) of the thyroid gland, also known as goiter.
Iodine deficiency is now accepted as the most common cause of preventable brain damage in the world. According to the World Health Organization (WHO), iodine deficiency disorders (IDD) affect 740 million people throughout the world, and nearly 50 million people suffer from some degree of IDD-related brain damage. The spectrum of IDD includes mental retardation, hypothyroidism, goiter, and varying degrees of other growth and developmental abnormalities. Nearly 2.2 million people throughout the world live in areas of iodine deficiency and risk its consequences. Major international efforts have produced dramatic improvements in the correction of iodine deficiency in the 1990's mainly through the use of iodized salt and iodized vegetable oil in iodine deficient countries. Thyroid enlargement, or goiter, is one of the earliest and most visible signs of iodine deficiency. The thyroid enlarges in response to persistent stimulation by TSH. In mild iodine deficiency, this adaptation response may be enough to provide the body with sufficient thyroid hormone. However, more severe cases of iodine deficiency result in hypothyroidism. Adequate iodine intake will generally reduce the size of goiters, but the reversibility of the effects of hypothyroidism depends on an individual's stage of development. Iodine deficiency has adverse effects in all stages of development, but is most damaging to the developing brain. In addition to regulating many aspects of growth and development, thyroid hormone is important for the myelination of the central nervous system, which is most active before and shortly after birth.
Effects of Iodine Deficiency by Developmental Stage
Prenatal development: Fetal iodine deficiency is caused by iodine deficiency in the mother. One of the most devastating effects of maternal iodine deficiency is congenital hypothyroidism, a condition that is sometimes referred to as cretinism and results in irreversible mental retardation. Congenital hypothyroidism occurs in two forms, although there is considerable overlap between them. The neurologic form is characterized by mental and physical retardation and deafness. It is the result of maternal iodine deficiency that affects the fetus before its own thyroid is functional. The myxedematous or hypothyroid form is characterized by short stature and mental retardation. In addition to iodine deficiency, the hypothyroid form has been associated with selenium deficiency and the presence of goitrogens in the diet that interfere with thyroid hormone production.
Newborns and infants: Infant mortality is increased in areas of iodine deficiency, and several studies have demonstrated an increase in childhood survival when iodine deficiency is corrected. Infancy is a period of rapid brain growth and development. Sufficient thyroid hormone, which depends on adequate iodine intake, is essential for normal brain development. Even in the absence of congenital hypothyroidism, iodine deficiency during infancy may result in abnormal brain development and, consequently, impaired intellectual development.
Children and adolescents: Iodine deficiency in children and adolescents is often associated with goiter. The incidence of goiter peaks in adolescence and is more common in girls. School children in iodine deficient areas show poorer school performance, lower IQs, and a higher incidence of learning disabilities than matched groups from iodine-sufficient areas. A recent meta-analysis of 18 studies concluded that iodine deficiency alone lowered mean IQ scores in children by 13.5 points.
Adults: Inadequate iodine intake may also result in goiter and hypothyroidism in adults. Although the effects of hypothyroidism are more subtle in the brains of adults than children, recent research suggests that hypothyroidism results in slower response times and impaired mental function.
Pregnancy and lactation: Iodine requirements are increased in pregnant and breastfeeding women. Iodine deficiency during pregnancy has been associated with increased incidence of miscarriage, stillbirth, and birth defects. Moreover, severe iodine deficiency during pregnancy may result in congenital hypothyroidism in the offspring. Iodine deficient women who are breastfeeding may not be able to provide sufficient iodine to their infants who are particularly vulnerable to the effects of iodine deficiency. A daily prenatal supplement providing 150 mcg of iodine will help to ensure that pregnant and breastfeeding women consume sufficient iodine during these critical periods.
Because iodine deficiency results in increased iodine trapping by the thyroid, iodine deficient individuals of all ages are more susceptible to radiation-induced thyroid cancer as well as to iodine-induced hyperthyroidism.
Selenium deficiency can exacerbate the effects of iodine deficiency. Iodine is essential for the synthesis of thyroid hormone, but selenium-dependent enzymes (iodothyronine deiodinases) are also required for the conversion of thyroxine (T4) to the biologically active thyroid hormone, triiodothyronine (T3). Deficiencies of vitamin A or iron may also exacerbate the effects of iodine deficiency.
Some foods contain substances that interfere with iodine utilization or thyroid hormone production, known as goitrogens. The occurrence of goiter in the Democratic Republic of Congo has been related to the consumption of casava, which contains a compound that is metabolized to thiocyanate and blocks thyroidal uptake of iodine. Some species of millet and cruciferous vegetables (for example, cabbage, broccoli, cauliflower, and Brussel sprouts) also contain goitrogens. The soybean isoflavones, genistein and daidzein, have also been found to inhibit thyroid hormone synthesis. Most of these goitrogens are not of clinical importance unless they are consumed in large amounts or there is coexisting iodine deficiency. Recent findings also indicate that tobacco smoking may be associated with an increased risk of goiter in iodine deficient areas.
Individuals at Risk of Iodine Deficiency
While the risk of iodine deficiency for populations living in iodine-deficient areas without adequate iodine fortification programs is well recognized, concerns have been raised that certain subpopulations may not consume adequate iodine in countries considered iodine-sufficient. Vegetarian and nonvegetarian diets that exclude iodized salt, fish, and seaweed have been found to contain very little iodine. Urinary iodine excretion studies suggest that iodine intakes are declining in Switzerland , New Zealand , and the U.S. , possibly due to increased adherence to dietary recommendations to reduce salt intake. Although iodine intake in the U.S. remains sufficient, further monitoring of iodine intake has been recommended.
Iron has the longest and best described history among all the micronutrients. It is a key element in the metabolism of almost all living organisms. In humans, iron is an essential component of hundreds of proteins and enzymes.
Oxygen Transport and Storage
Heme is an iron-containing compound found in a number of biologically important molecules. Hemoglobin and myoglobin are heme-containing proteins that are involved in the transport and storage of oxygen. Hemoglobin is the primary protein found in red blood cells and represents about two thirds of the body's iron. The vital role of hemoglobin in transporting oxygen from the lungs to the rest of the body is derived from its unique ability to acquire oxygen rapidly during the short time it spends in contact with the lungs and to release oxygen as needed during its circulation through the tissues. Myoglobin functions in the transport and short-term storage of oxygen in muscle cells, helping to match the supply of oxygen to the demand of working muscles.
Electron Transport and Energy Metabolism
Cytochromes are heme-containing compounds that are critical to cellular energy production and therefore, life, through their roles in mitochondrial electron transport. They serve as electron carriers during the synthesis of ATP, the primary energy-storage compound in cells. Cytochrome P450 is a family of enzymes that functions in the metabolism of a number of important biological molecules, as well as the detoxification and metabolism of drugs and pollutants. Nonheme iron-containing enzymes, such as NADH dehydrogenase and succinate dehydrogenase, are also critical to energy metabolism.
Antioxidant and Beneficial Pro-oxidant Functions
Catalase and peroxidases are heme-containing enzymes that protect cells against the accumulation of hydrogen peroxide, a potentially damaging reactive oxygen species (ROS), by catalyzing a reaction that converts hydrogen peroxide to water and oxygen. As part of the immune response, some white blood cells engulf bacteria and expose them to ROS in order to kill them. The synthesis of one such ROS, hypochlorous acid, by neutrophils is catalyzed by the heme-containing enzyme myeloperoxidase.
Inadequate oxygen (hypoxia), such as that experienced by those who live at high altitudes or those with chronic lung disease, induces compensatory physiologic responses, including increased red blood cell formation, increased blood vessel growth (angiogenesis) and increased production of enzymes utilized in anaerobic metabolism. Under hypoxic conditions transcription factors, known as hypoxia inducible factors (HIF), bind to response elements in genes that encode various proteins involved in compensatory responses to hypoxia and increase their synthesis. Recent research indicates that an iron-dependent prolyl hydroxylase enzyme plays a critical role in regulating HIF and consequently, physiologic responses to hypoxia. When cellular oxygen tension is adequate, newly synthesized HIFa subunits are modified by a prolyl hydroxylase enzyme in an iron-dependent process that targets HIFa for rapid degradation. When cellular oxygen tension drops below a critical threshold, prolyl hydroxylase can no longer target HIFa for degradation, allowing HIFa to bind to HIFb and form an active transcription factor that is able to enter the nucleus and bind to specific response elements on genes.
Ribonucleotide reductase is an iron-dependent enzyme that is required for DNA synthesis. Thus, iron is required for a number of vital functions, including growth, reproduction, healing, and immune function.
Regulation of Intracellular Iron
Iron response elements are short sequences of nucleotides found in the messenger RNA (mRNA) that codes for key proteins in the regulation of iron storage and metabolism. Iron regulatory proteins (IRP) can bind to iron response elements and affect mRNA translation, thereby regulating the synthesis of specific proteins. It has been proposed that when the iron supply is high, more iron binds to IRPs and prevents them from binding to iron response elements on mRNA. When the iron supply is low, less iron binds to IRPs, allowing increased binding of iron response elements. Thus, when less iron is available, translation of mRNA that codes for the iron storage protein, ferritin, is reduced because iron is not available for storage. Translation of mRNA that codes for the key regulatory enzyme of heme synthesis in immature red blood cells is also reduced to conserve iron. In contrast, IRP binding to iron response elements in mRNA that codes for transferrin receptors inhibits mRNA degradation, resulting in increased synthesis of transferrin receptors and increased iron transport to cells.
Vitamin A: Vitamin A deficiency may exacerbate iron deficiency anemia. Vitamin A supplementation has been shown to have beneficial effects on iron deficiency anemia and improve iron status among children and pregnant women. The combination of vitamin A and iron seems to ameliorate anemia more effectively than either iron or vitamin A alone.
Copper: Adequate copper nutritional status appears to be necessary for normal iron metabolism and red blood cell formation. Anemia is a clinical sign of copper deficiency. Animal studies demonstrate a role for copper in iron absorption, and iron has been found to accumulate in the livers of copper deficient animals, indicating that copper is required for iron transport to the bone marrow for red blood cell formation.
Zinc: High doses of iron supplements taken together with zinc supplements on an empty stomach can inhibit the absorption of zinc. When taken with food, supplemental iron does not appear to inhibit zinc absorption. Iron-fortified foods have no effect on zinc absorption.
Calcium: When consumed together in a single meal, calcium has been found to decrease the absorption of iron. However, little effect has been observed on serum ferritin levels (iron stores) with calcium supplement levels ranging from 1,000 to 1,500 mg/day.
Iron deficiency is the most common nutrient deficiency in the U.S. and the world. Three levels of iron deficiency are generally identified and are listed below from least to most severe:
Storage iron depletion: Iron stores are depleted, but the functional iron supply is not limited.
Early functional iron deficiency: The supply of functional iron is low enough to impair red blood cell formation, but not low enough to cause measurable anemia.
Iron deficiency anemia: There is inadequate iron to support normal red blood cell formation, resulting in anemia. The anemia of iron deficiency is characterized as microcytic and hypochromic, meaning red blood cells are measurably smaller than normal and their hemoglobin content is decreased. At this stage of iron deficiency, symptoms may be a result of inadequate oxygen delivery due to anemia and/or sub-optimal function of iron-dependent enzymes. It is important to remember that iron deficiency is not the only cause of anemia, and that the diagnosis or treatment of iron deficiency solely on the basis of anemia may lead to misdiagnosis or inappropriate treatment of the underlying cause (12). Folic acid and Vitamin B12 can be involved in nutritional causes of anemia.
Symptoms of Iron Deficiency
Most of the symptoms of iron deficiency are a result of the associated anemia, and may include fatigue, rapid heart rate, palpitations, and rapid breathing on exertion. Iron deficiency impairs athletic performance and physical work capacity in several ways. In iron deficiency anemia, the reduced hemoglobin content of red blood cells results in decreased oxygen delivery to active tissues. Decreased myoglobin levels in muscle cells limit the amount of oxygen that can be delivered to mitochondria for oxidative metabolism. Iron depletion also decreases the oxidative capacity of muscle by diminishing the mitochondrial content of cytochromes and other iron-dependent enzymes required for electron transport and ATP synthesis. Lactic acid production is also increased in iron deficiency. The ability to maintain a normal body temperature on exposure to cold is also impaired in iron-deficient individuals. Severe iron deficiency anemia may result in brittle and spoon-shaped nails, sores at the corners of the mouth, taste bud atrophy, and a sore tongue. In some cases, advanced iron-deficiency anemia may cause difficulty in swallowing due to the formation of webs of tissue in the throat and esophagus. The development of esophageal webs, also known as Plummer-Vinson syndrome, may require a genetic predisposition in addition to iron deficiency. Pica, a behavioral disturbance characterized by the consumption of non-food items, may be a symptom and a cause of iron deficiency.
Individuals at Increased Risk of Iron Deficiency
Infants and children between the ages of 6 months and 4 years: A full-term infant's iron stores are usually sufficient to last for 6 months. High iron requirements are due to the rapid growth rates sustained during this period.
Adolescents: Early adolescence is another period of rapid growth. In females, the blood loss that occurs with menstruation adds to the increased iron requirement of adolescence.
Pregnant women: Increased iron utilization by the developing fetus and placenta, as well as blood volume expansion significantly, increase the iron requirement during pregnancy.
Individuals with chronic blood loss: Chronic bleeding or acute blood loss may result in iron deficiency. One milliliter (ml) of blood with a hemoglobin concentration of 150 grams/liter contains 0.5 mg of iron. Thus, chronic loss of very small amounts of blood may result in iron deficiency. A common cause of chronic blood loss and iron deficiency in developing countries is intestinal parasitic infection. Individuals who donate blood frequently, especially menstruating women, may need to increase their iron intake to prevent deficiency because each 500 ml of blood donated contains between 200 and 250 mg of iron.
Individuals with helicobacter pylori infection: H. pylori infection is associated with iron deficiency anemia, especially in children, even in the absence of gastrointestinal bleeding.
Vegetarians: Because iron from plant sources is less efficiently absorbed than that from animal sources, the U.S. Food and Nutrition Board (FNB) has estimated that the bioavailability of iron from a vegetarian diet is only 10%, while it is 18% from a mixed diet. Therefore, the recommended dietary allowance (RDA) for iron from a completely vegetarian diet should be adjusted as follows: 14 mg/day for adult men and postmenopausal women, 33 mg/day for premenopausal women, and 26 mg/day for adolescent girls.
Individuals who engage in regular, intense exercise: Daily iron losses have been found to be greater in athletes involved in intense endurance training. This may be due to increased microscopic bleeding from the gastrointestinal tract or increased fragility and hemolysis of red blood cells. The FNB estimates that the average requirement for iron may be 30% higher for those who engage in regular intense exercise.
Magnesium plays important roles in the structure and the function of the human body. The adult human body contains about 25 grams of magnesium. Over 60% of all the magnesium in the body is found in the skeleton, about 27% is found in muscle, while 6 to 7% is found in other cells, and less than 1% is found outside of cells.
Magnesium is involved in more than 300 essential metabolic reactions, some of which are discussed below.
The metabolism of carbohydrates and fats to produce energy requires numerous magnesium-dependent chemical reactions. Magnesium is required by the adenosine triphosphate (ATP) synthesizing protein in mitochondria. ATP, the molecule that provides energy for almost all metabolic processes, exists primarily as a complex with magnesium (MgATP).
Synthesis of Essential Molecules
Magnesium is required at a number of steps during the synthesis of nucleic acids (DNA and RNA) and proteins. A number of enzymes participating in the synthesis of carbohydrates and lipids require magnesium for their activity. Glutathione, an important antioxidant, requires magnesium for its synthesis.
Magnesium plays a structural role in bone, cell membranes, and chromosomes.
Ion Transport Across Cell Membranes
Magnesium is required for the active transport of ions like potassium and calcium across cell membranes. Through its role in ion transport systems, magnesium affects the conduction of nerve impulses, muscle contraction, and the normal rhythm of the heart.
Cell signaling requires MgATP for the phosphorylation of proteins and the formation of the cell signaling molecule, cyclic adenosine monophosphate (cAMP). cAMP is involved in many processes, including the secretion of parathyroid hormone (PTH) from the parathyroid glands.
Calcium and magnesium levels in the fluid surrounding cells affect the migration of a number of different cell types. Such affects on cell migration may be important in wound healing.
Zinc: High doses of zinc in supplement form appear to interfere with the absorption of magnesium. A zinc supplement of 142 mg/day in healthy adult males significantly decreased magnesium absorption and magnesium balance (the difference between magnesium intake and magnesium loss).
Fiber: Large increases in the intake of dietary fiber have been found to decrease magnesium utilization in experimental studies. However, the extent to which dietary fiber affects magnesium nutritional status in individuals with a varied diet outside the laboratory is not clear.
Protein: Dietary protein may affect magnesium absorption. One study found that magnesium absorption was lower when protein intake was less than 30 grams/day, and higher protein intakes (93 grams/day vs. 42 grams/day) were associated with improved magnesium absorption in adolescents.
Vitamin D and calcium: The active form of vitamin D (calcitriol) may increase the intestinal absorption of magnesium to a small extent. However, magnesium absorption does not seem to be calcitriol-dependent as is the absorption of calcium and phosphate. High calcium intake has not been found to affect magnesium balance in most studies. Inadequate blood magnesium levels are known to result in low blood calcium levels, resistance to parathyroid hormone (PTH), and resistance to some of the effects of vitamin D.
Magnesium deficiency in healthy individuals who are consuming a balanced diet is quite rare because magnesium is abundant in both plant and animal foods and because the kidneys are able to limit urinary excretion of magnesium when intake is low. The following conditions increase the risk of magnesium deficiency.
Gastrointestinal disorders: Prolonged diarrhea, Crohn's disease, malabsorption syndromes, surgical removal of a portion of the intestine, and intestinal inflammation due to radiation may all lead to magnesium depletion.
Renal disorders (magnesium wasting): Diabetes mellitus and long-term use of certain diuretics may result in increased urinary loss of magnesium.
Chronic alcoholism: Poor dietary intake, gastrointestinal problems, and increased urinary loss of magnesium may all contribute to magnesium depletion, which is frequently encountered in alcoholics.
Age: Several studies have found that elderly people have relatively low dietary intakes of magnesium. Because intestinal magnesium absorption tends to decrease and urinary magnesium excretion tends to increase in older individuals, suboptimal dietary magnesium intake may increase the risk of magnesium depletion in the elderly.
Although severe magnesium deficiency is uncommon, it has been induced experimentally. When magnesium deficiency was induced in humans, the earliest sign was decreased serum magesium levels (hypomagnesemia). Over time serum calcium levels also began to decrease (hypocalcemia) despite adequate dietary calcium. Hypocalcemia persisted despite increased parathyroid hormone (PTH) secretion. Usually, increased PTH secretion quickly results in the mobilization of calcium from bone and normalization of blood calcium levels. As the magnesium depletion progressed, PTH secretion diminished to low levels. Along with hypomagnesemia, signs of severe magnesium deficiency included hypocalcemia, low serum potassium levels (hypokalemia), retention of sodium, low circulating levels of PTH, neurological and muscular symptoms (tremor, muscle spasms, tetany), loss of appetite, nausea, vomiting, and personality changes.
Manganese is a mineral element that is both nutritionally essential and potentially toxic. The derivation of its name from the Greek word for magic remains appropriate because scientists are still working to understand the diverse effects of manganese deficiency and manganese toxicity in living organisms.
Manganese (Mn) plays an important role in a number of physiologic processes as a constituent of some enzymes and an activator of other enzymes.
Manganese superoxide dismutase (MnSOD) is the principal antioxidant enzyme of mitochondria. Because mitochondria consume over 90% of the oxygen used by cells, they are especially vulnerable to oxidative stress. The superoxide radical is one of the reactive oxygen species produced in mitochondria during ATP synthesis. MnSOD catalyzes the conversion of superoxide radicals to hydrogen peroxide, which can be reduced to water by other antioxidant enzymes.
A number of manganese-activated enzymes play important roles in the metabolism of carbohydrates, amino acids, and cholesterol. Pyruvate carboxylase, a manganese-containing enzyme, and phosphoenolpyruvate carboxykinase (PEPCK), a manganese-activated enzyme, play critical roles in gluconeogenesis— the production of glucose from non-carbohydrate precursors. Arginase, another manganese-containing enzyme, is required by the liver for the urea cycle, a process that detoxifies ammonia generated during amino acid metabolism.
Manganese deficiency results in abnormal skeletal development in a number of animal species. Manganese is the preferred cofactor of enzymes called glycosyltransferases, which are required for the synthesis of proteoglycans that are needed for the formation of healthy cartilage and bone.
Wound healing is a complex process that requires increased production of collagen. Manganese is required for the activation of prolidase, an enzyme that functions to provide the amino acid, proline, for collagen formation in human skin cells. A genetic disorder known as prolidase deficiency results in abnormal wound healing among other problems, and is characterized by abnormal manganese metabolism. Glycosaminoglycan synthesis, which requires manganese-activated glycosyltranserases, may also play an important role in wound healing.
Iron: Although the specific mechanisms for manganese absorption and transport have not been determined, some evidence suggests that iron and manganese can share common absorption and transport pathways. Absorption of manganese from a meal is reduced as the meal's iron content is increased. Iron supplementation (60 mg/day for 4 months) was associated with decreased blood manganese levels and decreased MnSOD activity in white blood cells, indicating a reduction in manganese nutritional status. An individual's iron status can affect manganese bioavailability. Intestinal absorption of manganese is increased during iron deficiency, and increased iron stores (ferritin levels) are associated with decreased manganese absorption. The finding that men generally absorb less manganese than women may be related to the fact that men usually have higher iron stores than women.
Magnesium: Supplemental magnesium (200 mg/day) decreased manganese bioavailability slightly, either by decreasing manganese absorption or by increasing its loss in healthy adults.
Calcium: In one set of studies, supplemental calcium (500 mg/day) resulted in slightly lower manganese bioavailability in healthy adults. As a source of calcium, milk had the least effect, while calcium carbonate and calcium phosphate had the greatest effect. Several others studies have found the effect of supplemental calcium on manganese metabolism to be minimal.
Manganese deficiency has been observed in a number of animal species. Signs of manganese deficiency include impaired growth, impaired reproductive function, skeletal abnormalities, impaired glucose tolerance, and altered carbohydrate and lipid metabolism. In humans, demonstration of a manganese deficiency syndrome has been less clear. A child on long-term total parenteral nutrition (TPN) that lacked manganese developed bone demineralization and impaired growth that were corrected by manganese supplementation. Young men who were fed a low-manganese diet developed decreased serum cholesterol levels and a transient skin rash. Blood calcium, phosphorus, and alkaline phosphatase levels were also elevated, which may indicate increased bone remodeling as a consequence of insufficient dietary manganese. Young women fed a manganese-poor diet developed mildly abnormal glucose tolerance in response to an intravenous (IV) infusion of glucose.
Molybdenum is an essential trace element for virtually all life forms. It functions as a cofactor for a number of enzymes that catalyze important chemical transformations in the global carbon, nitrogen, and sulfur cycles. Thus, molybdenum-dependent enzymes are not only required for the health of the Earth's people, but for the health of its ecosystems as well.
The biological form of molybdenum present in almost all molybdenum-containing enzymes (molybdoenzymes) is an organic molecule known as the molybdenum cofactor. In humans, molybdenum is known to function as a cofactor for three enzymes. Sulfite oxidase catalyzes the transformation of sulfite to sulfate, a reaction that is necessary for the metabolism of sulfur-containing amino acids, such as cysteine. Xanthine oxidase and aldehyde oxidase catalyze hydroxylation reactions involving a number of different molecules with similar structures. Xanthine oxidase catalyzes the breakdown of nucleotides (precursors to DNA and RNA) to form uric acid, which contributes to the antioxidant capacity of the blood. Xanthine oxidase and aldehyde oxidase also play a role in the metabolism of drugs and toxins. Of these three enzymes, only sulfite oxidase is known to be crucial for human health.
Copper: Excess dietary molybdenum has been found to result in copper deficiency in grazing animals (ruminants). In ruminants, the formation of compounds containing sulfur and molybdenum, known as thiomolybdates, appears to prevent the absorption of copper. This interaction between thiomolybdates and copper does not occur to a significant degree in humans. One early study reported that molybdenum intakes of 500 and 1,500 mcg/day from sorghum increased urinary copper excretion. However, the results of a more recent and well-controlled study of molybdenum intake and copper metabolism in 8 healthy young men indicated that very high dietary molybdenum intakes (up to 1,500 mcg/day) did not adversely affect copper nutritional status.
Dietary molybdenum deficiency has never been observed in healthy people. The only documented case of acquired molybdenum deficiency occurred in a patient with Crohn's disease on long-term total parenteral nutrition (TPN) without molybdenum added to the TPN solution. The patient developed rapid heart and respiratory rates, headache, night blindness, and ultimately became comatose. He also demonstrated biochemical signs of molybdenum deficiency, including low plasma uric acid levels, decreased urinary excretion of uric acid and sulfate, and increased urinary excretion of sulfite. The symptoms disappeared when the administration of amino acid solutions was discontinued. Molybdenum supplementation (160 mcg/day) reversed the amino acid intolerance and improved his clinical condition.
Current understanding of the essentiality of molybdenum in humans is based largely on the study of individuals with very rare inborn errors of metabolism that result in a deficiency of the molybdoenzyme, sulfite oxidase. Two forms of sulfite oxidase deficiency have been identified: 1) isolated sulfite oxidase deficiency, in which only sulfite oxidase activity is affected and 2) molybdenum cofactor deficiency, in which the activity of all three molybdoenzymes is affected. Because molybdenum functions only in the form of the molybdenum cofactor in humans, any disturbance of molybdenum cofactor metabolism can disrupt the function of all molybdoenzymes. Together, molybdenum cofactor deficiency and isolated sulfite oxidase deficiency have been diagnosed in more than 100 individuals worldwide. Both disorders result from recessive traits, meaning that only individuals who inherit two copies of the abnormal gene (one from each parent) develop the disease. Individuals who inherit only one copy of the abnormal gene are known as carriers of the trait but do not exhibit any symptoms. The symptoms of isolated sulfite oxidase deficiency and molybdenum cofactor deficiency are identical and usually include severe brain damage, which appears to be due to the loss of sulfite oxidase activity. At present, it is not clear whether the neurologic effects are a result of the accumulation of a toxic metabolite, such as sulfite, or inadequate sulfate production. Isolated sulfite oxidase deficiency and molybdenum cofactor deficiency can be diagnosed relatively early in pregnancy (10-14 weeks of gestation) through chorionic villus sampling, and in some cases, carriers of molybdenum cofactor deficiency can be identified through genetic testing. No cure is presently available for either disorder, although anti-seizure medications and dietary restriction of sulfur-containing amino acids may be beneficial in some cases.
Phosphorus is an essential mineral that is required by every cell in the body for normal function. The majority of the phosphorus in the body is found as phosphate (PO4). Approximately 85% of the body's phosphorus is found in bone.
Phosphorus is a major structural component of bone in the form of a calcium phosphate salt called hydroxyapatite. Phospholipids (e.g., phosphatidylcholine) are major structural components of cell membranes. All energy production and storage are dependent on phosphorylated compounds, such as adenosine triphosphate (ATP) and creatine phosphate. Nucleic acids (DNA and RNA), responsible for the storage and transmission of genetic information, are long chains of phosphate-containing molecules. A number of enzymes, hormones, and cell signaling molecules depend on phosphorylation for their activation. Phosphorus also helps to maintain normal acid-base balance (pH) in its role as one of the body's most important buffers. The phosphorus-containing molecule 2,3-diphosphoglycerate (2,3-DPG) binds to hemoglobin in red blood cells and affects oxygen delivery to the tissues of the body.
Fructose: A recent study of 11 adult men found that a diet high in fructose (20% of total calories) resulted in increased urinary loss of phosphorus and a negative phosphorus balance (i.e., daily loss of phosphorus was higher than daily intake). This effect was more pronounced if the diet was also low in magnesium. A potential mechanism for this effect is the lack of feedback inhibition of the conversion of fructose to fructose-1-phosphate in the liver. In other words, increased accumulation of fructose-1-phosphate in the cell does not inhibit the enzyme that phosphorylates fructose, using up large amounts of phosphate. This phenomenon is known as phosphate trapping. This finding is relevant because fructose consumption in the U.S. has been increasing rapidly since the introduction of high fructose corn syrup in 1970, while magnesium intake has decreased over the past century.
Calcium and Vitamin D: Dietary phosphorus is readily absorbed in the small intestine, and any excess phosphorus absorbed is excreted by the kidneys. The regulation of blood calcium and phosphorus levels is interrelated through the actions of parathyroid hormone (PTH) and vitamin D.A slight drop in blood calcium levels (e.g., in the case of inadequate calcium intake) is sensed by the parathyroid glands resulting in their increased secretion of PTH. PTH stimulates increased conversion of vitamin D to its active form (calcitriol) in the kidneys. Increased calcitriol levels result in increased intestinal absorption of both calcium and phosphorus. Both PTH and vitamin D stimulate bone resorption, resulting in the release of bone mineral (calcium and phosphate) into the blood. Although PTH stimulation results in decreased urinary excretion of calcium, it results in increased urinary excretion of phosphorus. The increased urinary excretion of phosphorus is advantageous in bringing blood calcium levels up to normal because high blood levels of phosphate suppress the conversion of vitamin D to its active form in the kidneys.
Is high phosphorus intake detrimental to bone health? Some investigators are concerned about the increasing amounts of phosphates in the diet which can be attributed to phosphoric acid in soft drinks and phosphate additives
in a number of commercially prepared foods. Because phosphorus is not as tightly regulated by the body as calcium, serum phosphate levels can rise slightly with a high phosphorous diet, especially after meals. High blood phosphate levels reduce the formation of the active form of vitamin D (calcitriol) in the kidneys, reduce blood calcium, and lead to increased PTH release by the parathyroid glands. However, high serum phosphorus levels also lead to decreased urinary calcium excretion. If sustained, elevated PTH levels could have an adverse effect on bone mineral content, but this effect has only been observed in humans on diets that were high in phosphorus and low in calcium. Moreover, similarly elevated PTH levels have been reported in diets that were low in calcium without being high in phosphorus. Recently, a controlled trial in young women found no adverse effects of a phosphorus-rich diet (3,000 mg/day) on bone-related hormones and biochemical markers of bone resorption when dietary calcium intakes were maintained at almost 2,000 mg/day. At present there is no convincing evidence that the dietary phosphorus levels experienced in the U.S. adversely affect bone mineral density in humans. However, the substitution of phosphate containing soft drinks and snack foods for milk and other calcium rich foods does represent a serious risk to bone health.
Inadequate phosphorus intake results in abnormally low serum phosphate levels (hypophosphatemia). The effects of hypophosphatemia may include loss of appetite, anemia, muscle weakness, bone pain, rickets (in children), osteomalacia (in adults), increased susceptibility to infection, numbness and tingling of the extremities, and difficulty walking. Severe hypophosphatemia may result in death. Because phosphorus is so widespread in food, dietary phosphorus deficiency is usually seen only in cases of near total starvation. Other individuals at risk of hypophosphatemia include alcoholics, diabetics recovering from an episode of diabetic ketoacidosis, and starving or anorexic patients on refeeding regimens that are high in calories but too low in phosphorus.
Potassium is an essential dietary mineral that is also known as an electrolyte. The term electrolyte refers to a substance that dissociates into ions (charged particles) in solution making it capable of conducting electricity. The normal functioning of our bodies depends on the tight regulation of potassium concentrations both inside and outside of cells.
Maintenance of Membrane Potential
Potassium is the principal positively charged ion (cation) in the fluid inside of cells, while sodium is the principal cation in the fluid outside of cells. Potassium concentrations are about 30 times higher inside than outside cells, while sodium concentrations are more than 10 times lower inside than outside cells. The concentration differences between potassium and sodium across cell membranes create an electrochemical gradient known as the membrane potential. A cell's membrane potential is maintained by ion pumps in the cell membrane, especially the sodium, potassium-ATPase pumps. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium. Their activity has been estimated to account for 20%-40% of the resting energy expenditure in a typical adult. The large proportion of energy dedicated to maintaining sodium/potassium concentration gradients emphasizes the importance of this function in sustaining life. Tight control of cell membrane potential is critical for nerve impulse transmission, muscle contraction, and heart function.
Cofactor for Enzymes
A limited number of enzymes require the presence of potassium for their activity. The activation of sodium, potassium-ATPase requires the presence of sodium and potassium. The presence of potassium is also required for the activity of pyruvate kinase, an important enzyme in carbohydrate metabolism.
An abnormally low plasma potassium concentration is referred to as hypokalemia. Hypokalemia is most commonly a result of excessive loss of potassium, e.g., from prolonged vomiting, the use of some diuretics, some forms of kidney disease, or disturbances of metabolism. The symptoms of hypokalemia are related to alterations in membrane potential and cellular metabolism. They include fatigue, muscle weakness and cramps, and intestinal paralysis, which may lead to bloating, constipation, and abdominal pain. Severe hypokalemia may result in muscular paralysis or abnormal heart rhythms (cardiac arrhythmias) that can be fatal.
Conditions that increase the Risk of Hypokalemia
The use of potassium-wasting diuretics (e.g., thiazide diuretics or furosemide)
Severe vomiting or diarrhea
Overuse or abuse of laxatives
Anorexia nervosa or bulimia
Congestive heart failure (CHF)
In rare cases, habitual consumption of large amounts of black licorice has resulted in hypokalemia. Licorice contains a compound (glycyrrhizic acid) with similar physiologic effects to those of aldosterone, a hormone that increases urinary excretion of potassium. Low dietary intakes of potassium do not generally result in hypokalemia. However, recent research indicates that insufficient dietary potassium increases the risk of a number of chronic diseases.
Selenium is a trace element that is essential in small amounts, but can be toxic in larger amounts. Humans and animals require selenium for the function of a number of selenium-dependent enzymes, also known as selenoproteins. During selenoprotein synthesis, selenocysteine is incorporated into a very specific location in the amino acid sequence in order to form a functional protein. Unlike animals, plants do not appear to require selenium for survival. However, when selenium is present in the soil, plants incorporate it non-specifically into compounds that usually contain sulfur.
At least 11 selenoproteins have been characterized, and there is evidence that additional selenoproteins exist.
Four selenium-containing glutathione peroxidases (GPx) have been identified: cellular or classical GPx, plasma or extracellular GPx, phospholipid hydroperoxide GPx, and gastrointestinal GPx. Although each GPx is a distinct selenoprotein, they are all antioxidant enzymes that reduce potentially damaging reactive oxygen species (ROS), such as hydrogen peroxide and lipid hydroperoxides, to harmless products like water and alcohols by coupling their reduction with the oxidation of glutathione. Sperm mitochondrial capsule selenoprotein, an antioxidant enzyme that protects developing sperm from oxidative damage and later forms a structural protein required by mature sperm, was once thought to be a distinct selenoprotein, but now appears to be phospholipid hydroperoxide GPx.
In conjunction with the compound thioredoxin, thioredoxin reductase participates in the regeneration of several antioxidant systems, possibly including vitamin C. Maintenance of thioredoxin in a reduced form by thioredoxin reductase is important for regulating cell growth and viability.
Iodothyronine deiodinases (thyroid hormone deiodinases)
The thyroid gland releases very small amounts of biologically active thyroid hormone (triiodothyronine or T3) and larger amounts of an inactive form of thyroid hormone (thyroxine or T4) into the circulation. Most of the biologically active T3 in the circulation and inside cells is created by the removal of one iodine atom from T4 in a reaction catalyzed by selenium-dependent iodothyronine deiodinase enzymes. Through their actions on T3, T4, and other thyroid hormone metabolites, three different selenium-dependent iodothyronine deiodinases (types I, II, and III) can both activate and inactivate thyroid hormone, making selenium an essential element for normal development, growth, and metabolism through the regulation of thyroid hormones.
Selenoprotein P is found in plasma and also associated with vascular endothelial cells (cells that line the inner walls of blood vessels). Although the function of selenoprotein P has not been clearly delineated, it has been suggested to function as a transport protein, as well as an antioxidant capable of protecting endothelial cells from damage by a reactive nitrogen species (RNS) called peroxynitrite.
Selenoprotein W is found in muscle. Although its function is presently unknown, it is thought to play a role in muscle metabolism.
Incorporation of selenocysteine into selenoproteins is directed by the genetic code and requires the enzyme selenophosphate synthetase. A selenoprotein itself, selenophosphate synthetase catalyzes the synthesis of monoselenium phosphate, a precursor of selenocysteine which is required for the synthesis of selenoproteins.
As an integral part of the glutathione peroxidases and thioredoxin reductase, selenium probably interacts with every nutrient that affects the pro-oxidant/antioxidant balance of the cell. Other minerals that are critical components of antioxidant enzymes include copper, zinc (as superoxide dismutase), and iron (as catalase). Selenium as gluthathione peroxidase also appears to support the activity of vitamin E (a-tocopherol) in limiting the oxidation of lipids. Animal studies indicate that selenium and vitamin E tend to spare one another and that selenium can prevent some of the damage resulting from vitamin E deficiency in models of oxidative stress. Thioredoxin reductase also maintains the antioxidant function of vitamin C by catalyzing its regeneration.
Selenium deficiency may exacerbate the effects of iodine deficiency. Iodine is essential for the synthesis of thyroid hormone, but the selenoenzymes, iodothyronine deiodinases, are also required for the conversion of thyroxine (T4) to the biologically active thyroid hormone triiodothyronine (T3). Selenium supplementation in a small group of elderly individuals decreased plasma T4, indicating increased deiodinase activity with increased conversion to T3.
Insufficient selenium intake results in decreased activity of the glutathione peroxidases. Even when severe, isolated selenium deficiency does not usually result in obvious clinical illness. However, selenium deficient individuals appear to be more susceptible to additional physiological stresses.
Individuals at Increased Risk of Selenium Deficiency
Clinical selenium deficiency has been observed in chronically ill patients who were receiving total parenteral nutrition (TPN) without added selenium for prolonged periods of time. Muscular weakness, muscle wasting, and cardiomyopathy (inflammation and damage to the heart muscle) have been observed in these patients. TPN solutions are now supplemented with selenium to prevent such problems. People who have had a large portion of the small intestine surgically removed or those with severe gastrointestinal problems, such as Crohn's disease, are also at risk for selenium deficiency due to impaired absorption. Specialized medical diets used to treat metabolic disorders, such as phenylketonuria (PKU), are often low in selenium. Specialized diets that will be used exclusively over long periods of time should have their selenium content assessed to determine the need for selenium supplementation.
Keshan disease is a cardiomyopathy that affects young women and children in a selenium deficient region of China . The acute form of the disease is characterized by the sudden onset of cardiac insufficiency, while the chronic form results in moderate to severe heart enlargement with varying degrees of cardiac insufficiency. The incidence of Keshan disease is closely associated with very low dietary intakes of selenium and poor selenium nutritional status. Selenium supplementation has been found to protect people from developing Keshan disease but cannot reverse heart muscle damage once it occurs. Despite the strong evidence that selenium deficiency is a fundamental factor in the etiology of Keshan's disease, the seasonal and annual variation in its occurrence suggests that an infectious agent is involved in addition to selenium deficiency. Coxsackievirus is one of the viruses that has been isolated from Keshan patients, and this virus has been found to be capable of causing an inflammation of the heart called myocarditis in selenium deficient mice. Studies in mice indicate that oxidative stress induced by selenium deficiency results in changes in the viral genome capable of converting a relatively harmless viral strain to a myocarditis-causing strain. Though not proven in Keshan disease, selenium deficiency may result in a more virulent strain of virus with the potential to invade and damage the heart muscle.
Kashin-Beck disease is characterized by the degeneration of the articular cartilage between joints (osteoarthritis) and is associated with poor selenium status in areas of northern China , North Korea , and eastern Siberia . The disease affects children between the ages 5 and 13 years. Severe forms of the disease may result in joint deformities and dwarfism, due to degeneration of cartilage forming cells. Unlike Keshan disease, there is little evidence that improving selenium nutritional status prevents Kashin-Beck disease. Thus, the role of selenium deficiency in the etiology of Kashin-Beck disease is less certain. A number of other causative factors have been suggested for Kashin-Beck disease, including fungal toxins in grain, iodine deficiency, and contaminated drinking water.
Salt (sodium chloride) is essential for life. The tight regulation of the body's sodium and chloride concentrations is so important that multiple mechanisms work in concert to control them. Although scientists agree that a minimal amount of salt is required for survival, the health implications of excess salt intake represent an area of considerable controversy among scientists, clinicians, and public health experts.
Sodium (Na+) and chloride (Cl-) are the principal ions in the fluid outside of cells (extracellular fluid), which includes blood plasma. As such, they play critical roles in a number of life-sustaining processes.
Maintenance of Membrane Potential
Sodium and chloride are electrolytes that contribute to the maintenance of concentration and charge differences across cell membranes. Potassium is the principal positively charged ion (cation) inside of cells, while sodium is the principal cation in extracellular fluid. Potassium concentrations are about 30 times higher inside than outside cells, while sodium concentrations are more than 10 times lower inside than outside cells. The concentration differences between potassium and sodium across cell membranes create an electrochemical gradient known as the membrane potential. A cell's membrane potential is maintained by ion pumps in the cell membrane, especially the sodium, potassium-ATPase pumps. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium. Their activity has been estimated to account for 20%-40% of the resting energy expenditure in a typical adult. The large proportion of energy dedicated to maintaining sodium/potassium concentration gradients emphasizes the importance of this function in sustaining life. Tight control of cell membrane potential is critical for nerve impulse transmission, muscle contraction, and cardiac function.
Nutrient Absorption and Transport
Absorption of sodium in the small intestine plays an important role in the absorption of chloride, amino acids, glucose, and water. Similar mechanisms are involved in the reabsorption of these nutrients after they have been filtered from the blood by the kidneys. Chloride, in the form of hydrochloric acid (HCl), is also an important component of gastric juice, which aids the digestion and absorption of many nutrients.
Maintenance of Blood Volume and Blood Pressure
Because sodium is the primary determinant of extracellular fluid volume, including blood volume, a number of physiological mechanisms that regulate blood volume and blood pressure work by adjusting the body's sodium content. In the circulatory system, pressure receptors (baroreceptors) sense changes in blood pressure and send excitatory or inhibitory signals to the nervous system and/or endocrine glands to affect sodium regulation by the kidneys. In general, sodium retention results in water retention and sodium loss results in water loss. Below are descriptions of two of the many systems that affect blood volume and blood pressure through sodium regulation.
Renin angiotensin-aldosterone-system: In response to a significant decrease in blood volume or pressure (e.g, serious blood loss or dehydration), the kidneys release renin into the circulation. Renin is an enzyme that splits a small peptide (Angiotensin I) from a larger protein (angiotensinogen) produced by the liver. Angiotensin I is split into a smaller peptide (angiotensin II) by angiotensin converting enzyme (ACE), an enzyme present on the inner surface of blood vessels, and in the lungs, liver, and kidneys. Angiotensin II stimulates the constriction of small arteries, resulting in increased blood pressure. Angiotensin II is also a potent stimulator of aldosterone synthesis by the adrenal glands. Aldosterone is a steroid hormone that acts on the kidneys to increase the reabsorption of sodium and the excretion of potassium. Retention of sodium by the kidneys increases the retention of water, resulting in increased blood volume and blood pressure.
Anti-diuretic hormone (ADH): Secretion of ADH by the posterior pituitary gland is stimulated by a significant decrease in blood volume or pressure. ADH acts on the kidney to increase the reabsorption of water.
Sodium (and chloride) deficiency does not generally result from inadequate dietary intake, even in those on very low-salt diets.
Hyponatremia is defined as a serum sodium concentration of less than 136 mmol/liter, and may result from increased fluid retention (dilutional hyponatremia) or increased sodium loss. Dilutional hyponatremia may be due to inappropriate anti-diuretic hormone (ADH) secretion, which is associated with disorders affecting the central nervous system and a number of drugs. In some cases, excessive water intake may also lead to dilutional hyponatremia. Conditions that increase the loss of sodium and chloride include severe or prolonged vomiting or diarrhea, excessive and persistent sweating, the use of some diuretics, and some forms of kidney disease. Symptoms of hyponatremia include headache, nausea, vomiting, muscle cramps, fatigue, disorientation, and fainting. Complications of severe and rapidly developing hyponatremia may include cerebral edema (swelling of the brain), seizures, coma, and brain damage. Acute or severe hyponatremia may be fatal without prompt and appropriate medical treatment.
Prolonged Endurance Exercise and Hyponatremia
Hyponatremia has recently been recognized as a potential problem in individuals competing in very long endurance exercise events, such as marathons, ultramarathons, and Ironman triathlons. In 1997, 25 out of 650 participants in an Ironman triathlon (almost 4%) received medical attention for hyponatremia. Participants who developed hyponatremia during an Ironman triathlon had evidence of fluid overload despite relatively modest fluid intakes, suggesting that fluid excretion was inadequate and/or the fluid needs of these ultradistance athletes may be less than currently recommended. It has been speculated that the use of non-steroidal anti-inflammatory drugs (NSAIDs) may increase the risk of exercise-related hyponatremia by impairing water excretion, but firm evidence is presently lacking.
Zinc is an essential trace element for all forms of life. The significance of zinc in human nutrition and public health was recognized relatively recently. Clinical zinc deficiency in humans was first described in 1961, when the consumption of diets with low zinc bioavailability due to high phytic acid content was associated with "adolescent nutritional dwarfism" in the Middle East . Since then, zinc insufficiency has been recognized by a number of experts as an important public health issue, especially in developing countries.
Numerous aspects of cellular metabolism are zinc-dependent. Zinc plays important roles in growth and development, the immune response, neurological function, and reproduction. On the cellular level, the function of zinc can be divided into three categories: 1) catalytic, 2) structural, and 3) regulatory.
Nearly 100 different enzymes depend on zinc for their ability to catalyze vital chemical reactions. Zinc-dependent enzymes can be found in all known classes of enzymes.
Zinc plays an important role in the structure of proteins and cell membranes. A finger-like structure, known as a zinc finger motif, stabilizes the structure of a number of proteins. For example, copper provides the catalytic activity for the antioxidant enzyme copper-zinc superoxide dismutase (CuZnSOD), while zinc plays a critical structural role. The structure and function of cell membranes are also affected by zinc. Loss of zinc from biological membranes increases their susceptibility to oxidative damage and impairs their function.
Zinc finger proteins have been found to regulate gene expression by acting as transcription factors (binding to DNA and influencing the transcription of specific genes). Zinc also plays a role in cell signaling and has been found to influence hormone release and nerve impulse transmission. Recently zinc has been found to play a role in apoptosis (gene-directed cell death), a critical cellular regulatory process with implications for growth and development, as well as a number of chronic diseases.
Taking large quantities of zinc (50 mg/day or more) over a period of weeks can interfere with copper bioavailability. High intake of zinc induces the intestinal synthesis of a copper-binding protein called metallothionein. Metallothionein traps copper within intestinal cells and prevents its systemic absorption. More typical intakes of zinc do not affect copper absorption and high copper intakes do not affect zinc absorption.
Supplemental (38-65 mg/day of elemental iron) but not dietary levels of iron may decrease zinc absorption. This interaction is of concern in the management of iron supplementation during pregnancy and lactation and has led some experts to recommend zinc supplementation for pregnant and lactating women taking more than 60 mg/day of elemental iron.
High levels of dietary calcium impair zinc absorption in animals, but it is uncertain whether this occurs in humans. Increasing the calcium intake of postmenopausal women by 890 mg/day in the form of milk or calcium phosphate (total calcium intake 1,360 mg/day) reduced zinc absorption and zinc balance in postmenopausal women, but increasing the calcium intake of adolescent girls by 1,000 mg/day in the form of calcium citrate malate (total calcium intake 1,667 mg/day) did not affect zinc absorption or balance. Calcium in combination with phytic acid reduces zinc absorption. This effect is particularly relevant to individuals consuming a diet that is highly dependent on tortillas made with lime (calcium oxide). For more information on phytic acid.
The bioavailability of dietary folate is increased by the action of a zinc-dependent enzyme, suggesting a possible interaction between zinc and folic acid. In the past, some studies found low zinc intake to decrease folate absorption, while other studies found folic acid supplementation to impair zinc utilization in individuals with marginal zinc status. However, a more recent study found that supplementation with a relatively high dose of folic acid (800 mcg/day) for 25 days did not alter zinc status in a group of students being fed low-zinc diets (3.5 mg/day), nor did zinc intake impair folate utilization.
Severe zinc deficiency
Much of what is known about severe zinc deficiency was derived from the study of individuals born with acrodermatitis enteropathica, a genetic disorder resulting from the impaired uptake and transport of zinc. The symptoms of severe zinc deficiency include the slowing or cessation of growth and development, delayed sexual maturation, characteristic skin rashes, chronic and severe diarrhea, immune system deficiencies, impaired wound healing, diminished appetite, impaired taste sensation, night blindness, swelling and clouding of the corneas, and behavioral disturbances. Before the cause of acrodermatitis enteropathica was known, patients typically died in infancy. Oral zinc therapy results in the complete remission of symptoms, though it must be maintained indefinitely in individuals with the genetic disorder. Although dietary zinc deficiency is unlikely to cause severe zinc deficiency in individuals without a genetic disorder, zinc malabsorption or conditions of increased zinc loss, such as severe burns or prolonged diarrhea, may also result in severe zinc deficiency.
Mild zinc deficiency
More recently, it has become apparent that milder zinc deficiency contributes to a number of health problems, especially common in children who live in developing countries. The lack of a sensitive indicator of mild zinc deficiency hinders the scientific study of its health implications. However, controlled trials of moderate zinc supplementation have demonstrated that mild zinc deficiency contributes to impaired physical and neuropsychological development, and increased susceptibility to life-threatening infections in young children. For a more detailed discussion of the relationship of zinc deficiency to health problems.
Individuals at risk of zinc deficiency
Infants and children
Pregnant and lactating (breastfeeding) women, especially teenagers
Patients receiving total parenteral nutrition (intravenous feedings)
Malnourished individuals, including those with protein-energy malnutrition and anorexia nervosa
Individuals with severe or persistent diarrhea
Individuals with malabsorption syndromes, including sprue and short bowel syndrome
Individuals with inflammatory bowel disease, including Crohn's disease and ulcerative colitis
Individuals with alcoholic liver disease have increased urinary zinc excretion and low liver zinc levels
Individuals with sickle cell anemia
Older adults (65 years and older)
Strict vegetarians: The requirement for dietary zinc may be as much as fifty percent greater for strict vegetarians whose major food staples are grains and legumes because high levels of phytic acid in these foods reduce the absorption of zinc.