Antibiotics and their safe use

Antibiotics: Tips for Safe Use
A Primer on the Proper Use of Antibiotics
Aug. 8, 2007—

In the time since penicillin was discovered nearly 80 years ago, antibiotics have become one of the most important lifesaving weapons in doctors' arsenal against bacterial infection.

Now, the Lakeland, Fla.-based Publix grocery store chain is giving away seven of these drugs free of charge to those who have prescriptions for them.

Five of these -- amoxicillin, ampicillin, cephalexin, erythromycin and penicillin VK -- are commonly used by doctors to treat bacterial infections ranging from ear infections to gonorrhea.

But two of the drugs on the list -- ciprofloxacin and sulfamethoxazole/trimethoprim -- are high-grade antibiotics that doctors usually reserve for particularly serious infections.

While some hail the program as a godsend, others fear that the move could lead to overuse of the drugs.

This is because the use of antibiotics comes attached with important considerations. According to the American Academy of Family Physicians, there are certain situations in which antibiotics are helpful -- and many in which they can cause more harm than good.

Here are just a few tips that consumers can use to keep themselves safe when it comes to antibiotics:

Skip the antibiotics for the flu and the common cold. Antibiotics do not work against all infections. By their very nature, they are effective against only those caused by bacteria. This means that if you are suffering from a viral infection like the common cold or seasonal flu, they will likely do nothing to improve your health.

Never take antibiotics that have not been prescribed to you by a doctor. Taking these drugs inappropriately may not only bring no benefit but may also increase the chances that harmful bacteria present in your body could develop resistance to the drugs. The more resistant a bacteria is to treatment, the more dangerous it becomes.

Always finish the entire course of antibiotics you receive. Even if you start to feel better in the middle of the course of treatment, you must finish every pill that has been prescribed to you by a doctor. Failing to do so could increase the chances of developing bacterial resistance.

Keep careful track of any adverse reactions you experience when taking antibiotics. Many people experience adverse effects when taking certain antibiotics, whether they're allergic reactions or something else. It is important to make a note of these reactions so you can inform your doctor and lessen your chances of receiving the same drug again.

Vitamin B 6 deficiency

Vitamin B6 deficiency


Definition

Vitamin B6 is used by the body as a catalyst in reactions that involve amino acids. Vitamin B6 deficiency is rare, since most foods eaten contain the vitamin.

Description

Vitamin B6 is a water-soluble vitamin. The recommended dietary allowance (RDA) for vitamin B6 is 2.0 mg/day for the adult man and 1.6 mg/day for the adult woman. Vitamin B6 in the diet generally occurs as a form called pyridoxal phosphate. In this form, it cannot be absorbed by the body. During the process of digestion, the phosphate group is removed, and pyridoxal is produced. However, the body readily absorbs pyridoxal, and converts it back to the active form of the vitamin (pyridoxal phosphate).

Poultry, fish, liver, and eggs are good sources of vitamin B6, comprising about 3-4 mg vitamin/kg food; meat and milk contain lesser amounts of the vitamin. The vitamin also occurs, at about half this level, in a variety of plant foods, including beans, broccoli, cabbage, and peas. Vitamin B6 tends to be destroyed with prolonged cooking, with storage, or with exposure to light.

As mentioned, vitamin B6 takes various forms. One of these forms, called pyridoxine, is relatively stable. For this reason, pyridoxine is the form of vitamin B6 that is used in vitamin supplements, or when foods are fortified. Apples and other fruits are poor sources of the vitamin, containing only 0.2-0.6 mg vitamin/kg food.

Vitamin B6, used mainly in the body for the processing of amino acids, performs this task along with certain enzymes. The enzyme that participates in this type of complex is aminotransferase. Several types of aminotransferase exist. With vitamin B6 deficiency, while aminotransferase continues to occur in the various organs of the body, there is an abnormally low level of the active vitamin B6/aminotransferase complex present. Thus, this vitamin deficiency results in the impairment of a variety of activities in the body. With supplement correction of the vitamin B6 deficiency, the aminotransferase then readily forms the active complex, and normal metabolism is restored.

Vitamin B6 converts certain amino acids (glutamic acid, aspartic acid, glycine) to energy. This allows the body to process all dietary protein, even when the dietary protein is in excess of the body's needs. Vitamin B6 also allows the body to synthesize certain amino acids. For example, if the diet is deficient or low in certain amino acids, such as glycine or serine, vitamin B6 enables the body to make them from sugar. Vitamin B6 is used also for the synthesis of certain hormones, such as adrenaline.

Causes and symptoms

Vitamin B6 deficiency occurs rarely. When it does, it is usually associated with poor absorption of nutrients in the gastrointestinal tract (as in alcoholism, or with chronic diarrhea), the taking of certain drugs (as isoniazid, hydrolazine, penicillamine) that inactivate the vitamin, with genetic disorders that inhibit metabolism of the vitamin, or in cases of starvation.

The symptoms of vitamin B6 deficiency in adults are only vaguely defined. These include nervousness, irritability, insomnia, muscle weakness, and difficulty in walking. Vitamin B6 deficiency may produce fissures and cracking at the corners of the mouth. The deficiency occurred in infants fed early versions of commercial canned infant formula, when the vitamin had been inadvertently omitted from the formula. This error resulted in infants failing to grow, in irritability, and in seizures.

Diagnosis

Vitamin B6 status is measured by the transaminase stimulation test. This test requires extraction of red blood cells, and placement of the cells in two test tubes. Special chemicals (reagents) are added to both test tubes to allow for measurement of aminotransferase. This enzyme requires pyridoxal phosphate. A known quantity of pure pyridoxal phosphate is added to one of the test tubes. The activity level of the enzyme is measured, and compared, in both test tubes. If the added pyridoxal phosphate did not stimulate activity, the patient is considered not to be deficient in vitamin B6. Neither is the patient considered deficient if only slight stimulation occurred. But if a stimulation of four-fold or more occurred, a vitamin B6 deficiency is present.

Treatment

Vitamin B6 deficiency can be prevented or treated with consumption of the recommended dietary allowance, as supplied by food or by vitamin supplements.

Prognosis

The prognosis for correcting vitamin B6 deficiency is excellent.

Prevention

Vitamin B6 deficiency is not a major concern for most people. The deficiency can be prevented with consumption of a mixed diet that includes poultry, fish, eggs, meat, vegetables, and grains.

Key Terms

Amino acid
Amino acids are small molecules that are used as building blocks for all proteins. Some amino acids are also used in the body for the manufacture of hormones. There are about 20 nutritionally important amino acids, including glutamic acid, glycine, methionine, lysine, tryptophan, serine, and glycine.
Fat-soluble vitamins
Fat-soluble vitamins can be dissolved in oil or in melted fat.
Recommended Dietary Allowance (RDA)
The Recommended Dietary Allowances (RDAs) are quantities of nutrients in the diet that are required to maintain good health in people. RDAs are established by the Food and Nutrition Board of the National Academy of Sciences, and may be revised every few years. A separate RDA value exists for each nutrient. The RDA values refer to the amount of nutrient expected to maintain good health in people. The actual amounts of each nutrient required to maintain good health in specific individuals differ from person to person.
Water-soluble vitamins
Water-soluble vitamins can be dissolved in water or juice.
For Your Information

Resources

Books

Brody, T. Nutritional Biochemistry. San Diego: Academic Press, Inc., 1998.

Comparison of Iron Supplements

Comparison of Oral Iron Supplements

A new iron supplement product in the U.S. called Ferralet 90 is adding to the confusion surrounding the numerous oral iron supplements on the market. Ferralet 90 is a combination product containing carbonyl iron, B12, vitamin C, folic acid, and docusate and it is marketed as a prescription product. No oral iron dietary supplements are approved by the FDA, but manufacturers can choose to market their products as prescription only.8 There are two main iron salts forms (ferric and ferrous irons) and numerous formulations (e.g., amino-acid chelates, carbonyl iron, polysaccharide-iron complex, combination products, extended-release products, etc) available in the U.S. and Canada. All dietary iron has to be reduced to the ferrous form to enter the mucosal cells; therefore ferrous iron is absorbed three times more readily than the ferric form. Anecdotal claims that sustained-release iron preparations cause fewer gastrointestinal side effects have not been well substantiated.1,2 There is some evidence that controlled-release iron preparation causes less nausea and epigastric pain than conventional ferrous sulfate, but the discontinuation rates are similar.3 Theoretically, once-daily dosing can improve compliance. However, extended-release or enteric-coated formulations have been found to transport iron past the duodenum and proximal jejunum, thereby reducing the absorption of iron.1,2 Vitamin C is added to some products to enhance iron absorption. About 200 mg is needed to increase absorption of 30 mg of elemental iron.1 However, doses of 500 mg to 1000 mg only increase iron absorption by about 10%.2 Most iron preparations containing vitamin C don't have a sufficient amount of vitamin C to substantially affect iron absorption.1,2 In general, iron supplements should be taken on an empty stomach since food can decrease absorption by 40% to 50%. GI side effects such as nausea and abdominal pain occur more frequently as the quantity of soluble elemental iron in contact with the stomach and duodenum increases. Higher iron doses also increase the occurrence of constipation.1,10 Therefore, there should be no difference in GI tolerance when an equal quantity of elemental iron is administered regardless of the form of iron salt.2 A chart summarizing the differences among the various iron formulations is included.

There's confusion about the different oral iron products.

Many are promoted as better tolerated or absorbed...but not all of these claims can be substantiated.

Ferrous sulfate, ferrous gluconate, and ferrous fumarate contain different percentages of elemental iron. Efficacy and tolerability are similar for equal doses of elemental iron.

Carbonyl iron (Ferralet 90, Feosol Carbonyl Iron caplets, etc) is pure elemental iron that's absorbed slowly to reduce toxicity.
Prescribe these if you're concerned about accidental ingestion. Iron is still the #1 cause of pediatric fatalities due to toxicity.

Polysaccharide-iron complex (Niferex-150, etc) is iron bound to carbohydrates. It's promoted to improve tolerability, but there's no proof that there's a significant difference.

Heme iron polypeptide (Proferrin ES, etc) is derived from hemoglobin in animal red blood cells. It's better absorbed than the inorganic iron salts, especially when taken with food.

Use the inexpensive ferrous sulfate first-line...or carbonyl iron if toxicity is a concern.

Tell patients that GI tolerability is linked to the iron DOSE...not the salt. Enteric-coated and controlled-release preps might reduce nausea...but at the expense of lower absorption.

Vitamin C increases iron absorption, but most combo products don't contain enough. Over 200 mg is needed to increase absorption of 30 mg elemental iron.

Iron absorption

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Overview
Despite the fact that iron is the second most abundant metal in the earth's crust, iron
deficiency is the world's most common cause of anemia. When it comes to life, iron is more precious than
gold. The body hoards the element so effectively that over millions of years of evolution, humans have
developed no physiological means of iron excretion. Iron absorption is the sole mechanism by which iron
stores are physiologically manipulated.
The average adult stores about 1 to 3 grams of iron in his or her body. An exquisite balance between dietary
uptake and loss maintains this balance. About 1 mg of iron is lost each day through sloughing of cells from
skin and mucosal surfaces, including the lining of the gastrointestinal tract (Cook et al., 1986). Menstration
increases the average daily iron loss to about 2 mg per day in premenopausal female adults (Bothwell and
Charlton, 1982). No physiologic mechanism of iron excretion exists. Consequently, absorption alone
regulates body iron stores (McCance and Widdowson, 1938). The augmentation of body mass during
neonatal and childhood growth spurts transiently boosts iron requirements (Gibson et al., 1988).

Iron Absorption
Iron absorption occurs predominantly in the duodenum and
upper jejunum ( Muir and Hopfer, 1985) (Figure 1). The
mechanism of iron transport from the gut into the blood
stream remains a mystery despite intensive investigation
and a few tantalizing hits (see below). A feedback
mechanism exists that enhances iron absorption in people
who are iron deficient. In contrast, people with iron
overload dampen iron absorption.
The physical state of iron entering the duodenum greatly
influences its absorption however. At physiological pH,
ferrous iron (Fe2+) is rapidly oxidized to the insoluble ferric
(Fe3+) form. Gastric acid lowers the pH in the proximal
duodenum, enhancing the solubility and uptake of ferric
iron (Table 1). When gastric acid production is impaired
(for instance by acid pump inhibitors such as the drug,
prilosec), iron absorption is reduced substantially.
Heme is absorbed by machinery completely different to that
of inorganic iron. The process is more efficient and is
independent of duodenal pH . Consequently meats are
excellent nutrient sources of iron. In fact, blockade of heme
catabolism in the intestine by a heme oxygenase inhibitor

The iron is coupled to transferrin (Tf) in the
circulation which delivers it to the cells of the
body. Phytates, tannins and antacids block
iron absorption.

Table 1. Factors That Influence Iron Absorption
Physical State (bioavailability) heme > Fe2+ > Fe3+
Inhibitors phytates, tannins, soil clay, laundry starch, iron overload, antacids
Competitors lead, cobalt, strontium, manganese, zinc
Facilitators ascorbate, citrate, amino acids, iron deficiency
can produce iron deficiency (Kappas et al., 1993). The
paucity of meats in the diets of many of the people in the
world adds to the burden of iron deficiency.

A number of dietary factors influence iron absorption. Ascorbate and citrate increase iron uptake in part by
acting as weak chelators to help to solubilize the metal in the duodenum (Table 1) (Conrad and Umbreit,
1993). Iron is readily transferred from these compounds into the mucosal lining cells. Conversely, iron
absorption is inhibited by plant phytates and tannins. These compounds also chelate iron, but prevent its
uptake by the absorption machinery (see below). Phytates are prominent in wheat and some other cereals,
while tannins are prevalent in (non-herbal) teas.
Lead is a particularly pernicious element to iron metabolism (Goya, 1993). Lead is taken up by the iron
absorption machinery, and secondarily blocks iron through competitive inhibition. Further, lead interferes
with a number of important iron-dependent metabolic steps such as heme biosynthesis. This multifacted
attack has particularly dire consequences in children, were lead not only produces anemia, but can impair
cognitive development. Lead exists naturally at high levels in ground water and soil in some regions, and
can clandestinely attack children's health. For this reason, most pediatricians in the U.S. routinely test for
lead at an early age through a simple blood test.
Immaturity of the gastrointestinal tract can exacerbate iron deficiency in newborns. The gastrointestinal tract
does not achieve competency for iron absorption for several weeks after birth. The problem is even more
severe for premature infants, who tend to be anemic for a variety of reasons. A substantial portion of iron
stores in newborns are transferred from the mother late in pregnancy. Prematurity shortcircuits this process.
Parenteral iron replacement is possible, but not often used because of the often delicate health of premature
infants. Transfusion becomes the default option in this circumstance.

The mechanism by which iron enters the mucosal cells lining the upper gastrointestinal tract is unknown. Most
cells in the rest of the body are believed to acquire iron from plasma transferrin (an iron-protein chelate),
via specific transferrin receptors and receptor-mediated endocytosis (Klausner, et al, 1983). The hypothesis
that apotransferrin (or an equivalent molecule) secreted by intestinal cells or present in bile chelates
intestinal iron and facilitates its absorption(Huebers et al., 1983) is unsubstantiated. The transferrin gene is
not expressed in intestinal cells. Later work indicated that transferrin found in the intestinal lumen is derived
from plasma (Idzerda et al., 1986). Plasma transferrin entering bile is fully saturated with iron, obviating
any intraluminal chelating function (Schumann et al., 1986). Furthermore, hypoxia, which greatly increases
iron absorption, has no effect on intestinal transferrin levels (Simpson et al., 1986). Exogenous transferrin
cannot donate iron to intestinal mucosal cells (Bezwoda et al., 1986), and the brush boarder membrance
lacks transferrin receptors (Parmley et al., 1985) (although they are present on the basolateral surface of
intestinal epithelial cells (Levin et al., 1984); (Banerjee et al., 1986). Lastly and perhaps most compellingly,
humans and mice with hypotransferrinemia paradoxically absorb more dietary iron than normal. Although
the erythron is iron deficient, these individuals develop hepatic iron overload (Heilmeyer et al., 1961);
(Craven et al., 1987).


Mechanism of Iron Absorption
In searching for molecules involved in intestinal iron transport, Conrad and co-workers took the approach of
characterizing proteins that bind iron [summarized in (Conrad and Umbreit, 1993)]. Their hypothesis of iron
transport is based on identification of iron binding proteins at several key sites. They propose that mucins
bind iron in the acid environment of the stomach, thereby maintaining it in solution for later uptake in the
alkaline duodenum. According to their model, mucin-bound iron subsequently crosses the mucosal cell
membrane in association with integrins. Once inside the cell, a cytoplasmic iron-binding protein, dubbed
"mobilferrin", accepts the element, and shuttles it to the basolateral surface of the cell, where it is delivered
to plasma. In this model mobilferrin could serve as a rheostat sensitive to plasma iron concentrations. Fully
occupied mobilferrin would dampen mucosal iron uptake, and while the process would be enhanced by
unsaturated mobilferrin (Conrad and Umbreit, 1993). This model has not gained universal acceptance
however.
A very different scheme of iron uptake has been proposed by investigators studying iron transport in yeast.
Yeast face the problem of taking in iron from the environment, a process similar to that of intestinal
mucosal cells. Dancis et al. used genetic selection to isolate Sacchromyces cerevisiae mutants with defective
iron transport (Dancis et al., 1994); (Stearman et al., 1996). They constructed an expression plasmid in
which an enzyme necessary for histidine biosynthesis was under the control of an iron-repressible promoter.
The plasmid was introduced into a yeast histidine auxotroph (i.e. a strain of yeast that requires histidine to
survive). Mutants were selected in the absence of histidine, in the presence of high levels of iron. Among
the mutats they isolated, were cells with defective iron uptake. They discovered that membrane iron
transport depends absolutely upon copper transport. In this model, ferric iron in yeast culture medium is
reduced to its ferrous form by an externally oriented reductase (FRE1). The element is shuttled rapidly into
the cell by a ferrous transporter, which appears to be coupled to an externally oriented copper-dependent
oxidase (FET3) embedded in the cell membrane (De Silva et al., 1995); (Stearman et al., 1996). FET3 is
strikingly homologous to the mammalian copper oxidase ceruloplasmin. The re-oxidation of ferrous to ferric
iron is apparently an obligatory step in the transport mechanism, although the coupling mechanism of
oxidation and membrane transport is unclear. (De Silva et al., 1995); (Stearman et al., 1996); (Yuan et al.,
1995). Although the genetic evidence for this scheme is compelling, the central component, the ferrous
transporter itself, remains elusive. These investigators speculate that mammalian intestinal iron transport is
analogous to the yeast iron uptake process (Harford et al., 1994). This assertion is supported by studies of
copper-deficient swine, which show co-existing iron deficiency unresponsive to iron therapy (Lahey et al.,
1952); (Gubler et al., 1952); (Cartwright et al., 1956).

Genetic Insights into Mammalian Iron Absorption
Mouse genetics provides a different perspective on mammalian intestinal iron transport. Mouse breeders
readily recognize pale animals, and have developed anemic stocks with various mutations. Intestinal
mucosal iron transport is defective in two mutant strains. Microcytic (mk) mice and sex-linked anemia (sla)
mice have severe iron deficiency due apparently to defects in iron uptake and release, respectively, from the
intestinal cell (reviewed in [Bannerman, 1976].) Mice with the homozygous autosomal recessive mk
mutation absorb iron poorly, have low serum iron levels, and lack stainable iron in intestinal mucosal cells.
These findings are consistent with a defect in an apical iron transport molecule. Intriguingly, mk/mk mice
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are not rescued by parenteral iron replacement. Anemia develops in normal mice tranplanted with mk bone
marrow, indicating that mk erythroid precursor cells also have a defect in red cell iron uptake. A common
component to iron transport may therefore exist in intestinal cells and red cell precursors (Andrews, et al,
2000).
ÝMice that are homozygous or heterozygous for the sla mutation (sla/sla or sla/y) also have low serum iron
levels. In contrast to mk mice, they have abnormal iron deposits within intestinal mucosal cells, suggesting
that this X-linked defect impairs intracellular iron trafficking or basolateral export of iron to the plasma. The
sla animals differ further from the mk mice by correction of anemia by parenteral iron. Based on studies of
these mutants, distinct apical and basolateral iron transport systems possibly exist that function coordinately
to transfer iron from intestinal lumen to plasma.
ÝWhatever the mechanism of iron uptake, normally only about 10% of the elemental iron entering the
duodenum is absorbed. However, this value increases markedly with iron deficiency (Finch, 1994). In
contrast, iron overload reduces but does not eliminate absorption, reaffirming the fact that absorption is
regulated by body iron stores. In addition, both anemia and hypoxia boost iron absorption. A portion of the
iron that enters the mucosal cells is retained sequestered within ferritin. Intracellular intestinal iron is lost
when epithelial cells are sloughed from the lining of the gastrointestinal tract. The remaining iron traverses
the mucosal cells, to be coupled to transferrin for transport through the circulation.
Erythropoiesis and Iron Absorption
ÝApproximately 80% of total body iron is ultimately incorporated into red cell hemoglobin. An average
adult produces 2 x 1011 red cells daily, for a red cell renewal rate of 0.8 percent per day. Each red cell
contains more than a billion atoms of iron, and each ml of red cells contains 1 mg of iron. To meet this
daily need for 2 x 1020 atoms (or 20 mg) of elemental iron, the body has developed regulatory mechanisms
whereby erythropoiesis profoundly influences iron absorption. Plasma iron turnover (PIT) represents the
mass turnover of transferrin-bound iron in the circulation, expressed as mg/kg/day (Huff et al., 1950).
Accelerated erythropoiesis increases plasma iron turnover, which is associated with enhanced iron uptake
from the gastrointestinal tract (Weintraub et al., 1965). The mechanism by which PIT alters iron absorption
is unknown.
ÝA circulating factor related to erythropoiesis that modulates iron absorption has been hypothesized, but not
identified (Beutler and Buttenweiser, 1960); (Finch, 1994). Several candidate factors have been excluded,
including transferrin (Aron et al., 1985) and erythropoietin (Raja et al., 1986). Clinical manifestations of this
apparent communication between the marrow and the intestine includes iron overload that develops in
patients with severe thalassemia in the absence of transfusion. The accelerated (but ineffective)
erythropoiesis in this condition substantially boosts iron absorption. In some cases, the coupling of increased
PIT and increased gastrointestinal iron absorption is beneficial. In pregnancy, placental removal of iron
raises the PIT. This process enhances gastrointestinal iron absorption thereby increasing the availability of
the element to meet the needs of the growing and developing fetus.
ÝCompetition studies suggest that several other heavy metals share the iron intestinal absorption pathway.
These include lead, manganese, cobalt and zinc (Table 1). Enhanced iron absorption induced by iron
deficiency also augments the uptake of these elements. As iron deficiency often coexists with lead
intoxication, this interaction can produce particularly serious medical complications in children (Piomelli et
al., 1987). Interestingly, copper absorption and metabolism appear to be handled mechanisms different to
those of iron.

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Weintraub, L. R., Conrad, M. E., and Crosby, W. H. (1965). Regulation of the intestinal absorption of
iron by the rate of erythropoiesis. British Journal of Hematology 2, 432.
Yuan, D. S., Stearman, R., Dancis, A., Dunn, T., Beeler, T., and Klausner, R. D. (1995). The
Menkes/Wilson disease gene homologue in yeast provides copper to a ceruloplasmin-like oxidase
required for iron uptake. Proceedings of the National Academy of Sciences (USA) 92, 2632-2636.

Shingles vaccine .. Pros and Cons

Maybe you haven't heard anything about the shingles vaccine. Or maybe you have, but decided against getting it for any of a number of reasons like these:

- Although it has been approved by the U.S. Food and Drug Administration and by the European Commission for people 60 and older, you are only 45.

- It protects just half of those vaccinated, and you would just as soon take your chances.

- No one yet knows how long the benefits will last.

- No one yet knows about delayed side effects.

- You do not know anything about shingles, so how common or bad can it be?

- Your insurance does not cover it.

Before dismissing the vaccine entirely, you may want to consider Merritt ClappSmith's recent encounter with shingles. Although at 39 she is much younger than the typical shingles patient, her experience with confusing symptoms and a twice-missed diagnosis occurs at all ages. This is her story:

"My shingles case began with the periodic sensation that bugs were crawling in my hair. Three weeks later, I developed a headache that was one-sided but unlike a migraine. The pain was so bad I couldn't go to work. That evening, I discovered a raised and very tender ridge on my scalp.

"Unable to sleep and in terrible pain, I went to the local emergency room. The doctor there gave me an intravenous painkiller, tested me for meningitis or encephalitis, and concluded that I had a migraine and infected hair follicle.

"The terrible head pain grew, as did the sensitivity of the rash, and at 3 a.m. the next day, my husband drove me to a major hospital. The doctor cursorily looked at the blistering rash and treated me for a migraine. He had no explanation for the rash.

"After another horrible night and day of pain and a growing rash, my husband drove me to Urgent Care, where a nurse immediately suspected shingles, and the doctor concluded 'shingles' in 30 seconds. I got acyclovir for the virus and Vicodin for pain. I slept a lot, and my eye swelled. When the blisters scabbed over, I returned to work, but I was so tired and my eye was so sensitive to light that I had to cut short my workdays."

ClappSmith, an urban planner from St. Paul, Minnesota, said that after her experience she encouraged her mother, who is 71, to get the shingles vaccine. But that decision is not always simple.

Shingles, or herpes zoster, can afflict anyone who has had chickenpox. Both are caused by the varicella zoster virus. It is not known whether shingles can develop in people who received the chickenpox vaccine, which contains a live attenuated form of the virus.

This virus never leaves the body. It lies dormant for years in nerve roots near the spinal cord and can be reactivated as a shingles infection at any time, especially in people whose immune system is weakened by advanced age, extreme stress, a disease like cancer or AIDS or medications like chemotherapy, steroids and drugs used to prevent organ rejection. Sometimes, a physical stress like cold or sunburn can bring on an attack.

Reactivated, the virus migrates down the nerve until it reaches the skin, where it causes vague symptoms of irritation, pain, numbness, itching or tingling, followed in two or three days by a painful, blistering rash on one side of the face, head or body. Untreated, the rash lasts two to four weeks.

The pain can be severe and may be accompanied by headache, fever, chills and an upset stomach. In rare cases, it can lead to pneumonia, hearing loss, blindness, encephalitis and, rarer still, death.

After the rash clears, about one patient in five develops post-herpetic neuralgia, or PHN, a debilitating pain that does not always respond to treatment and can be devastating to ordinary life for months or even years.

Treatment with the antiviral drug acyclovir is best administered as early as possible, preferably within 72 hours of the first sign of a rash, to shorten the course of the disease and prevent the severe symptoms that ClappSmith experienced. Anti-viral drugs, if taken early, can reduce the severity of subsequent post-herpetic neuralgia, but starting anti-virals after PHN develops is of no help.

About one million cases of shingles a year occur in the United States, and the risk of it and of PHN increases with age. Half of 85-year-olds will have had shingles and, as people age, shingles-associated nerve pain increases in frequency and severity.

Debilitating nerve pain occurs in nearly a third of people with shingles who are 60 or older, and about 12 percent of older people who have shingles have pain that lasts three months or longer. The pain of PHN, which is difficult to treat, has been described as burning, throbbing, aching, stabbing or shooting. Even clothing touching the skin or a cool breeze can cause excruciating pain.

The shingles vaccine, Zostavax by Merck, was licensed in May 2006 in the United States after a study of more than 38,500 men and women 60 and older showed that it prevented about half of cases of shingles and reduced the risk of PHN by two-thirds.

"Among vaccine recipients who did get shingles, the episodes generally were far milder than they otherwise would have been," said Dr. Stephen Straus, an infectious disease specialist at the National Institute of Allergy and Infectious Diseases.

The vaccine, given in a single dose by injection, contains the same attenuated virus as the chickenpox vaccine, but is 14 times as potent.

The side effects have been minimal, usually redness, soreness, swelling or itching at the injection site and, rarely, headaches.

Based on the study, the researchers estimated that the vaccine could prevent 250,000 cases of shingles a year in the United States and significantly reduce its severity and complications in another 250,000 people. The vaccine is most effective in people 60 to 69, and less so with advancing age.

The vaccine is approved for use in people 60 and older who have had chickenpox. The Advisory Committee on Immunization Practices for the Centers for Disease Control and Prevention recommended that it be given to people who have had shingles, though the chances of another attack are low. The manufacturer's price for the vaccine is about $150. The patients' cost in the United States is often $300.

Because people in their 50s account for one in every seven cases of shingles, some physicians administer the vaccine "off label" to those younger than 60, even though its safety and effectiveness in younger people are not known. Also unknown is whether the vaccine is safe to administer to people whose immune systems are already weakened.

Follow-up studies are under way to determine how long the vaccine remains effective. If immunity wanes, a booster shot may be necessary.

Until the unknowns are resolved, the vaccine is not recommended for those with immune systems weakened by disease or drug treatment, women who are pregnant or might be pregnant and people with active untreated tuberculosis. Nor should the vaccine be given to anyone who has had a life-threatening allergic reaction to gelatin or the antibiotic neomycin.

Hepatitis C - The Facts

What is hepatitis C?
Hepatitis C is a disease caused by the hepatitis C virus which results in infection of the liver. Hepatitis C is the most common (but not the only) cause of post-transfusion hepatitis in the United States.

Who gets hepatitis C?
Anyone can get hepatitis C, but IV drug users, transfusion recipients, and dialysis patients are at high risk of getting the infection. Health care workers who have frequent contact with blood have also been shown to be at risk.

How is the virus spread?
The hepatitis C virus is spread by contact with contaminated blood or plasma. Contaminated needles and syringes are a source of spread among IV drug users. The role of person-to-person contact and sexual activity in the spread of this disease is unclear. While spread may occur by these routes, it is less frequent than with the hepatitis B virus.
Hepatitis C virus is NOT spread through casual contact or in typical school, office, or food service settings. It is NOT spread by coughing, sneezing, or drinking out of the same glass.

What are the symptoms?
Symptoms develop slowly and may include loss of appetite, stomach pain, nausea, vomiting. Jaundice (yellowing of the skin or whites of the eyes) does not occur as commonly with hepatitis C as it does with hepatitis B. The severity of the illness can range from no symptoms to fatal cases (rare). Long-term infection is common. Liver disease may result from long-term infection, but the illness more often improves after two to three years. People who have a long term infection may or may not have symptoms. People who do not have symptoms can spread disease.

How soon do the symptoms appear?
Symptoms commonly appear within six to nine weeks. However, they can occur as soon as two weeks and as long as six months after infection.

How long can an infected person spread the virus?
Infected people may spread the virus indefinitely.

How is hepatitis C diagnosed?
A positive blood test for hepatitis C virus antibody can mean any of the following:
Current or acute infection - This diagnosis is usually made if a person has signs and symptoms of liver disease, blood tests showing abnormal liver function, and negative tests for hepatitis A and B.
Chronic carrier - A chronic carrier is a person who was infected more than 6 months prior to the positive antibody blood test. The carrier does not have signs or symptoms of liver disease although there may be abnormal liver function tests. The carrier can transmit the virus to others. Over time the virus may cause liver damage, carriers should be followed closely by a physician. If there is evidence of progressive liver damage, the patient should be referred to a doctor specializing in the treatment of liver disease.
Immunity - The person was infected with hepatitis C in the past but has cleared the virus from their body. The person has a positive hepatitis C antibody test, no signs or symptoms of liver disease, and normal liver function tests. The immune person cannot spread hepatitis C to anyone else, and the antibodies protect them from infection in the future.
False Positive Test - The blood test is not 100% accurate. Rarely, the test is positive even though the person has never been infected with hepatitis C. There is no evidence of liver disease. Repeat hepatitis C antibody tests may be negative.

How good is the blood test?
The hepatitis C test used by blood donation centers is only a screening test to eliminate hepatitis C virus from the nation’s blood and plasma supply. Individuals who test positive on the hepatitis C virus antibody test should be retested using the RIBA hepatitis C test or testing for hepatitis C virus using PCR technology. These tests cannot determine whether the disease is acute or chronic.

How can hepatitis C be prevented?
Syringes, tattooing, and acupuncture needles should not be reused. Control measures against hepatitis B infection also apply. Blood banks should properly discard units of blood that are positive for the hepatitis C virus.

UTAH DEPARTMENT OF HEALTH
BUREAU OF EPIDEMIOLOGY
August 2001

Traveling to Costa Rica - be prepared

Travel to Costa Rica has increased remarkably lately so I thought that I would post the recommended vaccinations so you can be prepared for travel.

Malaria: Prophylaxis with chloroquine is recommended for the provinces of Alajuela, Limon (except for Limon City), Guanacaste, and Heredia.

Vaccinations:
Hepatitis A Recommended for all travelers
Typhoid Recommended for all travelers
Hepatitis B For travelers who may have intimate contact with local residents, especially if visiting for more than 6 months
Yellow fever Required for travelers arriving from a yellow-fever-infected country in Africa or the Americas
Measles, mumps, rubella (MMR) Two doses recommended for all travelers born after 1956, if not previously given
Tetanus-diphtheria Revaccination recommended every 10 years

Antibiotics and dental work

The American Heart Association has come out with new guidelines regarding the need for antibiotics and dental procedures to protect heart valves. They are based on clinical opinion (experts) but there is very little clinical evidence to show that antibiotics really do help. Are you surprised?
To be sure, the efficacy of antibiotics and the cost effectiveness of the antibiotics have never been proven. In only 4-7.5 % of cases, can we even site sequential relationships between the dental procedure and valve infections.
The infection that we are trying to prevent is called infective endocarditis. It is an infection on the heart valve that can be life threatening. There are about 10-20 thousand new cases of infective endocarditis every year and the mortality is 20-30%, making it a very serious infection.
In order for there to be an infection, the valve must have been the “victim” of an injury. Then, following the injury, bacteria must come along (from the blood) to seed the area.
Bacteria in the blood (bacteremia) is quite common. We “throw” bacteria into the blood when we do something as simple as brushing our teeth. It is thought to be more common when we have dental work. We are not sure how much bacteremia is necessary (how many bacteria need to be exposed to the damaged valve) in order to seed the valve and set the stage for the infection to propagate.

Here are the current recommendations (as of 2007).
Patients to consider for antibiotics should include:
1) A patient with a prosthetic valve (a valve replacement)
2) A patient with a previous history of endocarditis
3) Patients with specific congenital heart disease (ask me the specifics)
4) A patient who is has had a valvulopathy after cardiac transplantation.

The following are the recommendations for use:
1) Amoxicillin 2 grams in adults taken orally
2) Allergy to Penicillin - Clindamycin 600 mg or Azithromycin 50 mg also taken orally

If a patient cannot take oral medication, there are intramuscular or intravenous substitutes.
The bottom line here is those patients with a murmur DO NOT NEED any antibiotic. This is fabulous news but will undoubtedly stir the pot and many of the local dentists will have a tizzy. Have them call me. Those patients belonging to Choice Care can save themselves tons of trouble and time by just referring your dentist to our website or to my phone or email. As usual, we are happy to oblige.

Bisphosphonates, The risks and benefits

Much has been written about the bisphosphonates (Fosamex, Actonel, Boniva) mostly in the lay press about the potential for osteonecrosis or bone death. Bisphosphonates are used as preventives against osteoporosis, or a loss of bone density. Osteoporosis has been linked to fracture and it is a condition that increases with age.
The incidence of osteonecrosis appears to be about 2-4% and occurs mostly in those treated with intravenous bisphosphonate. Further, it seems to occur more often in those treated with higher doses, patients, often with cancer. Those who have been on steroid drugs, are immunosuppressed, long time smokers and those with poor oral hygiene also seem to be at increased risk when taking the oral version of the drugs.
The bottom line: it is clear that there is minimal risk. Brushing your teeth, getting lots of weight bearing exercise, and taking your medications correctly (including calcium) seem to be the best means of minimizing your risk of both osteoporosis and the rare event of osteonecrosis secondary to bisphosphonate use either oral or intravenous.

Nutrition after Gastric Bypass

Anemia and a variety of other nutrition issues are very common after gastric bypass surgery. Here are some tips.
Deficiencies in fat soluble vitamins are common after bypass surgery. The fat soluble vitamins are Vitamins A, D, E and K. Calcium and iron absorption are also problematic. That leaves bariatric patients with an increased risk of anemia and osteoporosis.
The surgery results in a reduction in the acid that is most prevalent in the stomach, hydrochloric acid. That makes it very difficult to absorb calcium as calcium carbonate. Calcium citrate is much more available for absorption and is the preferred form of calcium in bariatric patients.
Iron is also not absorbed very well because the duodenum is bypassed and that is where iron is absorbed. If patients consume calcium with vitamin C (ascorbic acid), there is a greater chance that the iron will be absorbed in the stomach.
There are also some medications that might be a problem in bypass patients. For instance, there may be a delay in the effectiveness after taking ambien, a sleeping pill that usually works immediately. It may take a little longer to get those eyes closed for the night but the problem can be minimized if the ambien is taken on an empty stomach.
Zocor is another medication that may be problematic. Another statin may have to be used.
Niacin should be taken with a low-fat snack.
Ramipril and enalapril, common blood pressure medications may not be as effective as other angiotensin converting enzyme inhibitors and they may need to be substituted.
Metformin is also not absorbed well and glucose should probably be followed closely.
Finally, metoprolol is absorbed very quickly in the stomach and duodenum generally but given the weight loss that occurs with the bypass may mean that fewer blood pressure medications will be necessary.
B12 should be taken in sublingual forms, eliminating the problem of Vitamin B12 deficiency.
While we don’t need a mega-doses of Vitamins, bypass patients should definitely take a multi-vitamin every day in order to be sure that they don’t be come deficient.

New recommendations for PPD

There are new recommendations for those patients who turn PPD positive in their adult life and have a normal CXR. This is now called “latent tuberculosis.”

The recommendation is as follows:
1) All patients regardless of age should be treated with Isoniazid (INH) for 9 months.
2) Precautions should be taken regarding liver dysfunction and liver enzymes should be followed monthly.
3) Patients should be monitored carefully if they are on Coumadin or other drugs metabolized in the liver.
Dosing for INH is as follows [5 mg/kg PO/IM qd x6-9mo]
Max: 300 mg/day; Alt: 15 mg/kg PO/IM 2x/wk if therapy directly observed, max 900 mg/dose;
Info: to prevent progression in PPD-positive pts; give on empty stomach

Tetanus - Do you need the vaccine? Why?

What causes tetanus?
Tetanus is caused by a toxin (poison) produced by
a bacterium, Clostridium tetani. The C. tetani bacteria
cannot grow in the presence of oxygen. They
produce spores that are very difficult to kill as they
are resistant to heat and many chemical agents.
How does tetanus spread?
C. tetani spores can be found in the soil and in the
intestines and feces of many household and farm
animals and humans. The bacteria usually enter the
human body through a puncture (in the presence of
anaerobic [low oxygen] conditions, the spores will
germinate).
Tetanus is not spread from person to person.
How long does it take to show signs of tetanus after
being exposed?
The incubation period varies from 3-21 days, with
an average of eight days. The further the injury site
is from the central nervous system, the longer the
incubation period. The shorter the incubation period,
the higher the risk of death.
What are the symptoms of tetanus?
The symptoms of tetanus are caused by the tetanus
toxin acting on the central nervous system. In the
most common form of tetanus, the first sign is spasm
of the jaw muscles, followed by stiffness of the neck,
difficulty in swallowing, and stiffness of the abdominal
muscles.
Other signs include fever, sweating, elevated blood
pressure, and rapid heart rate. Spasms often occur,
which may last for several minutes and continue for
3-4 weeks. Complete recovery, if it occurs, may take
months.
How serious is tetanus?
Tetanus has a high fatality rate; during 1998-2000,
the case-fatality rate for reported tetanus in the
United States was 18%.
What are possible complications from tetanus?
Laryngospasm (spasm of the vocal cords) is a complication
that can lead to interference with breathing.
Patients can also break their spine or long bones
from convulsions. Other possible complications include
hypertension, abnormal heart rhythm, and
secondary infections, which are common because of
prolonged hospital stays.
Obviously, the high possibility of death is a major
complication.
How is tetanus diagnosed?
The diagnosis of tetanus is based on the clinical signs
and symptoms only. Laboratory diagnosis is not useful
as the C. tetani bacteria often cannot be recovered
from the wound of an individual who has tetanus,
and conversely, can be isolated from the skin of
an individual who does not have tetanus.
What kind of injuries might allow tetanus to enter
the body?
Tetanus bacilli live in the soil, so the most dangerous
kind of injury involves possible contamination
with dirt, animal feces, and manure. Although we
have traditionally worried about deep puncture
wounds, in reality many types of injuries can allow
tetanus bacilli to enter the body. In recent years, a
higher proportion of cases had minor wounds than
had major ones, probably because severe wounds
were more likely to be properly managed. People
have become infected with tetanus following surgery,
burns, lacerations, abrasions, crush wounds,
ear infections, dental infections, animal bites, abortion,
pregnancy, body piercing and tattooing, and
injection drug use. People can also get tetanus from
splinters.
I stepped on a nail in our yard. What should I do?
Any wound that may involve contamination with
tetanus bacilli should be attended to as soon as possible.
Treatment depends on your vaccination status
and the nature of the wound. In all cases, the wound
should be cleaned. Seek treatment immediately and
bring your immunization record with you.
With wounds that involve the possibility of tetanus
contamination, a patient with an unknown or incomplete
history of tetanus vaccination needs a tetanus-
and diphtheria-containing shot (Td or Tdap)
and a dose of tetanus immune globulin (TIG) as
soon as possible.
A person with a documented series of three tetanusand
diphtheria-containing shots (Td or Tdap) who
has received a booster dose within the last ten years
should be protected. However, to ensure adequate
protection, a booster dose of vaccine may still be
given if it has been more than five years since the
last dose and the wound is other than clean and
minor.
Is there a treatment for tetanus?
There is no “cure” for tetanus once a person develops
symptoms, just supportive treatment and management
of complications. The best “treatment” is
prevention through immunization.
How common is tetanus in the United States?
Tetanus first became a reportable disease in the late
1940s. At that time, there were 500-600 cases reported
per year. After the introduction of the tetanus
vaccine in the mid-1940s, reported cases of tetanus
dropped steadily.
During 1990-2001, a total of 534 cases of tetanus
were reported. Most (56%) of these cases occurred
among adults age 19-64 years and 38% were among
persons age 65 years or older.
Almost all cases of tetanus are in persons who have
never been vaccinated, or who completed their
childhood series, but did not have a booster dose in
the preceding 10 years.
What is neonatal tetanus?
Neonatal tetanus is a form of tetanus that occurs in
newborn infants, most often through the use of an
unsterile cutting instrument on the unhealed umbilical
stump. These babies usually have no temporary
immunity passed on from their mother because their
mother hasn’t been vaccinated and therefore has no
immunity.
Neonatal tetanus is very rare in the United States
(three cases reported during 1990-2004), but is
common in some developing countries. It causes
more than 215,000 deaths worldwide per year.
Can you get tetanus more than once?
Yes! Tetanus disease does not cause immunity because
so little of the potent toxin is required to cause
the disease. Persons recovering from tetanus should
begin or complete the vaccination series.
When did tetanus vaccine become available?
The first tetanus toxoid (inactivated toxin) was produced
in 1924 and was used successfully to prevent
tetanus in the armed services during World War II.
In the mid-1940s, tetanus vaccine was combined
with diphtheria toxoid and inactivated pertussis
bacteria to make the combination DTP vaccine for
routine childhood immunization.
In 1991, DTaP vaccine was licensed in the United
States. The pertussis component of this vaccine is a
more purified “acellular” version, which produces
fewer side effects.
In 2005, two new tetanus toxoid-diphtheria-acellular
pertussis (Tdap) vaccines were licensed. These
vaccines are the first pertussis-containing vaccines
that can be given to persons older than 7 years.
What kind of vaccine is the tetanus toxoid?
The tetanus vaccine is an inactivated toxin (poison)
called a toxoid. It is made by growing the bacteria
in a liquid medium and purifying and inactivating
the toxin. Because it is not a live vaccine, a person’s
immunity tends to decline with time, which is why
booster doses are recommended.
What’s the difference between all the vaccines containing
tetanus toxoid?
It’s like alphabet soup!
Tetanus toxoid is available as a single shot (TT) but
it rarely is given that way as it’s best to also provide
needed protection against other diseases at the same
time.
Children younger than age seven years receive DTaP
(tetanus, diphtheria, and acellular pertussis). If they
cannot receive the pertussis component of the combined
vaccine, they can receive DT (diphtheria and
tetanus toxoids for pediatric use). DTaP also can be
given as part of two different combination vaccines;
one includes DTaP, inactivated polio vaccine, and
hepatitis B vaccine, and another contains DTaP and
Hib vaccine.
Children ages seven years and older and adults
should be given a different formulation (i.e., Td or
Tdap).
How is this vaccine given?
The DTaP, DT, Td, and Tdap preparations are all
given as an injection in the muscle.
Who should get this vaccine?
Infants should receive DTaP vaccine (or DT-pediatric
if they cannot receive the pertussis component)
as part of their routine immunization. Adults should
be given a routine booster dose of Td every 10 years.
Adults without documentation of ever receiving the
basic series of tetanus and diphtheria toxoids should
first receive a primary series of three doses, properly
spaced. A single dose of Tdap is recommended for
persons age 11 years and older in place of one of the
Td doses, preferably the first one.
How many doses of DTaP vaccine are needed?
The usual schedule for infants is a series of four
doses given at two, four, six, and 15-18 months of
age. A fifth shot, or booster dose, is recommended
at 4-6 years of age, unless the fourth dose was given
late (after the fourth birthday).
When should adolescents and adults get vaccinated
against tetanus? Should they get vaccinated with Td
or Tdap?
Immunization experts recommend that the first dose
of Tdap be given at age 11-12 as a booster during
the routine adolescent immunization visit if the adolescent
has finished the childhood DTaP schedule
and has not already received a dose of Td or Tdap.
Adults should continue to receive a booster dose of
Td every ten years. Adults age 19-64 years who have
never received Tdap should receive a single dose of
Tdap to replace a single dose of Td so they can boost
their resistance to pertussis as well.
If someone experiences a deep or puncture wound,
or a wound contaminated with dirt, an additional
booster dose may be given if the last dose was more
than five years ago. It is important to keep an up-todate
record of all immunizations so that repeat
doses don’t become necessary. Although it is vital to
be adequately protected against tetanus, receiving
more doses than recommended can lead to increased
local reactions, such as painful swelling of
the arm.
Who recommends this vaccine?
The Centers for Disease Control and Prevention
(CDC), the American Academy of Pediatrics (AAP),
the American Academy of Family Physicians (AAFP),
and the American College of Physicians (ACP) all
recommend this vaccine.
How safe is this vaccine?
Most children have no serious reactions from the
combined DTaP vaccine. The most common reactions
are local reactions at the injection site, such as
soreness, redness, and swelling, especially after the
fifth dose. Other possible reactions may include
fussiness, fever, loss of appetite, tiredness, and vomiting.
The use of the more purified DTaP instead of
DTP has decreased these reactions substantially.
For adults receiving Td vaccine, localized non-serious
side effects are common (redness, soreness, etc.)
but are generally self-limiting and require no treatment.
What side effects have been reported with this vaccine?
Moderate to serious reactions are uncommon with
DTaP vaccine. Such reactions include crying for
three hours or more (up to about one child out of
1,000) and high fever (about one child out of
16,000). Most of these side effects are believed to be
due to the pertussis component of the vaccine, and
a child experiencing such a reaction may still be able
to be protected against tetanus and diphtheria with
the DT vaccine. More serious reactions, such as seizures,
are so rare that it is hard to tell if they are
caused by the vaccine.
As mentioned above, adults who received more than
the recommended doses of Td vaccine can experience
increased local reactions, such as painful swelling
of the arm. This is due to the high levels of tetanus
antibody in their blood.
The most frequently reported side effects following
vaccination with Tdap were headache, generalized
body aches, and tiredness.
Some of my patients describe having had a severe
reaction to something they were given for tetanus
many years ago. What could this be?
The allergic reactions these people experienced may
have actually been serum sickness, a reaction to
equine antitoxin. Equine antitoxin was the only
product available for the prevention of tetanus prior
to the mid 1940s. It was used for postexposure prophylaxis
until the late 1950s, when tetanus immune
globulin was introduced. Tetanus toxoid has never
contained any horse protein.
How effective is tetanus-diphtheria toxoid (Td)?
Td is close to 100% effective for persons receiving
the correct primary series (as a child or adult) and
a routine booster dose every ten years. It is felt that
Tdap vaccine will provide the same level of protection.
Who should NOT receive tetanus toxoid?
People who had a serious allergic reaction to one
dose of tetanus toxoid should not receive another.
Persons with a moderate or severe acute illness
should postpone receiving the vaccine until they are
improved. Most reactions to the combined DTaP
vaccine are due to the pertussis component. Please
see the “Pertussis” section for more information on
possible precautions to the use of this vaccine.
Can the vaccine cause tetanus?
No.

Vitamin D... an excellent review

This is an excellent review of Vitamin D and how it works. It is written by an endocrinologist.

Vitamin D Deficiency and Thyroid Disease
Theodore C. Friedman, M.D., Ph.D.

Vitamin D deficiency and thyroid diseases
Vitamin D is an important vitamin that not only regulates calcium, but also has many other
beneficial actions. Not many endocrinologists realize this, but several articles published
over 20 years ago showed that patients with hypothyroidism have low levels of vitamin D.
This may lead to some of the bone problems related to hypothyroidism. It was thought that
one of two mechanisms may explain the low levels of vitamin D in patients with
hypothyroidism, 1) the low levels of vitamin D may be due to poor absorption of vitamin D
from the intestine or 2) the body may not activate vitamin D properly. Other articles have
demonstrated that patients with Graves disease also have low levels of Vitamin D.
Importantly, both vitamin D and thyroid hormone bind to similar receptors called steroid
hormone receptors. A different gene in the Vitamin D receptor was shown to predispose
people to autoimmune thyroid disease including Graves’ disease and Hashimoto’s
thyroiditis. For these reasons, it is important for patients with thyroid problems to
understand how the vitamin D system works.

Sources of Vitamin D
Vitamin D is really two different compounds, cholecalciferol (vitamin D2), found mainly in
plants and ergocalciferol (vitamin D3), found mainly in animals. Both of these hormones
are collectively referred to as vitamin D, and they can either be obtained in two ways. One
is by exposure of the skin to the ultraviolet (UV) rays of sunlight or also from dietary intake.
Vitamin D is found naturally in fish (such as salmon and sardines) and fish oils, eggs and
cod liver oil. However most Vitamin D is obtained from foods fortified with Vitamin D,
especially milk and orange juice. Interestingly, as breast feeding has become more popular,
the incidence of Vitamin D deficiency has increased as less fortified milk is consumed.
Vitamin D deficiency may also occur in patients with malabsorption from their intestine,
such as in the autoimmune disease called Celiac Disease, which occurs frequently in
patients with thyroid problems. Multivitamins also contain Vitamin D, as does some
calcium supplements like Oscal-D and Citracal plus D..

Different Forms of Vitamin D and How To Diagnose Vitamin D
Vitamin D itself is inactive and needs to get converted in the liver to 25-hydroxy vitamin D
(25-OH vitamin D) and then in the kidney to 1, 25-hydroxy vitamin D. It is only the 1, 25-
OH vitamin D which is biologically active. This form of vitamin D acts to allow for
absorption of calcium from the intestinal tract. Therefore, patients with low vitamin D
levels will have low calcium and in severe cases get rickets (in children) or osteomalacia (in
adults) which is when the bone bows out and is poorly formed. In mild cases of vitamin D
deficiency, osteoporosis occurs.
The conversion from the 25-OH vitamin D to the 1, 25-OH vitamin D that occurs in the
kidney is catalyzed by parathyroid hormone, also called PTH. Therefore, patients with low
vitamin D levels will have relatively high PTH levels along with low calcium levels. This is
similar to patients with primary hypothyroidism having elevated TSH levels while having
normal thyroid hormone levels. Additionally, the 25-OH vitamin D form which is the
storage form and is much more abundant that the 1, 25-OH vitamin D form which, although
is active, is less abundant. Therefore, in states of vitamin D deficiency, low levels of 25-OH
vitamin D are found, but the 1, 25-OH vitamin D levels are either normal or actually slightly
high. They are slightly high because the excess PTH that is stimulated by the low 25-OH
vitamin D levels stimulates the conversion up to 25-OH vitamin D to the 1, 25-OH vitamin
D. Thus, patients that are vitamin D deficient usually have a low 25-OH vitamin D level, a
high PTH level, a low normal calcium, and a normal or an elevated 1, 25-OH vitamin D
level.
Dr. Friedman usually recommends measuring PTH, calcium, and 25-OH vitamin D to
determine if a patient does have vitamin D deficiency. The 25-OH vitamin D assay has a
normal range of approximately 20-60 ng/dL. However, this range may be too low for many
patients. Additionally, the assay may not be that good at measuring the low levels of
vitamin D. In general, Dr. Friedman would recommend treatment of patients that have a 25-
OH vitamin D of less than 30 ng/dL, but these patients should have a PTH in the high
normal range. Optimal levels of 25-OH Vitamin D for patients with thyroid diseases are
probably 35-60 ng/dL It is unclear what to do with a patient with a PTH in the high normal
range and a completely normal 25-OH vitamin D level or the other way around for patients
with a low 25-OH vitamin D level but a completely normal PTH level.

Treatment of Vitamin D Deficiency
There are several ways to correct for the depletion of vitamin D, and these would involve
either increasing sunlight exposure or increasing dietary intake. In general, Dr. Friedman
feels there is an ongoing battle between endocrinologists and dermatologists about sunlight
exposure, and mild sunlight exposure probably does not have that much of an increased risk
of skin cancer yet would be helpful to prevent vitamin D deficiency. Because of our busy
schedule, many of us do not go outside during the day much and our sunlight exposure is
minimal. Blacks and other dark skinned patients absorb less Vitamin D and need more
sunlight exposure. Dr. Friedman recommends a patient to be exposed to the sun for 15-30
minutes a day, especially in the morning, to correct for vitamin D deficiency. However, in
northern latitudes, little light of the proper wavelength goes through the atmosphere in the
winter, so this exposure needs to occur in the spring and summer at which time stores of
vitamin D are built up. The body has mechanisms so that too much vitamin D can not be
synthesized by prolonged sun exposure. An alternative is to go to a tanning salon for
approximately three times. Another alternative for replacing mild vitamin D deficiency is to
take two multivitamins a day. Each multivitamin contains 400 international units of vitamin
D so a total of 800 international units of vitamin D will correct mild cases of low vitamin D
levels. For more severe levels, the patient can take 50,000 international units of vitamin D
orally once or twice a week. This needs to be given by a prescription. If this treatment
regimen is used, the patient needs to be monitored carefully with calcium and 25-OH
vitamin D levels to make sure the patient is not over replaced with vitamin D. The patient
may need this level of treatment for approximately three months and should be checked
monthly. The main side effect of vitamin D therapy is overtreatment leading to
hypercalcemia.
Patients with kidney problems cannot convert vitamin D to the active 1, 25-OH vitamin D
levels and need to take calcitriol which is 1, 25-OH vitamin D. Additionally, patients with
hypoparathyroidism are usually placed on the calcitriol as well.

Conclusion
Vitamin D appears to have many effects besides being related to calcium and bone health.
Some patients with low vitamin D levels have fatigue and bone pain, which is easily
reversible with proper replacement of vitamin D. Vitamin D may protect against heart
disease and some types of cancer. Vitamin D may also have some role in regulating the
immune system and also reducing blood sugar levels in patients with diabetes. Proper
vitamin D levels are needed to prevent osteoporosis. In conclusion, proper vitamin D levels
are essential for one’s health, especially if you have thyroid problems. Unless a patient is
exposed to sunlight or foods containing vitamin D, screening for Vitamin D deficiency is
recommended for all thyroid patients.
This article is not intended to offer medical advice and is offered for information purposes
only. Do not act or rely upon information from this article without seeking professional
medical advice. For more information about Dr. Friedman or to schedule an appointment,
please go to goodhormonehealth.com

The Best Living Will

I, , being of sound mind and body, do not wish to be kept alive indefinitely by artificial means. Under no circumstances should my fate be put in the hands of pinhead politicians who couldn't pass ninth-grade biology if their lives depended on it, or lawyers / doctors interested in simply running up the bills. If a reasonable amount of time passes and I fail to ask for at least one of the following:

Glass of wine
chocolate
Margarita
chocolate
sex
Cold Beer
chocolate
Chicken fried steak
cream gravy
chocolate
Mexican food
chocolate
sex
chocolate
Pizza
chocolate
ice cream
sex
chocolate
sex
Chocolate
Sex
Chocolate

It should be presumed that I won't ever get better. When such a determination is reached, I hereby instruct my appointed person and attending physicians to pull the plug, reel in the tubes, let the 'fat lady sing,' and call it a day!

The Miracle of Vitamin D

By Krispin Sullivan, CN
In April of 2000 a clinical observation published in Archives of Internal Medicine caught my attention. Dr. Anu Prabhala and his colleagues reported on the treatment of five patients confined to wheelchairs with severe weakness and fatigue. Blood tests revealed that all suffered from severe vitamin D deficiency. The patients received 50,000 IU vitamin D per week and all became mobile within six weeks.1
Dr. Prabhala’s research sparked my interest and led to a search for current information on vitamin D, how it works, how much we really need and how we get it. The following is a small part of the important information that I found.
Any discussion of vitamin D must begin with the discoveries of the Canadian-born dentist Weston A. Price. In his masterpiece Nutrition and Physical Degeneration, Dr. Price noted that the diet of isolated, so-called “primitive” peoples contained “at least ten times” the amount of “fat-soluble vitamins” as the standard American diet of his day.2 Dr. Price determined that it was the presence of plentiful amounts of fat-soluble vitamins A and D in the diet, along with calcium, phosphorus and other minerals, that conferred such high immunity to tooth decay and resistance to disease in nonindustrialized population groups.
Today another Canadian researcher, Dr. Reinhold Vieth, argues convincingly that current vitamin D recommendations are woefully inadequate. The recommended dose of 200-400 international units (IU) will prevent rickets in children but does not come close to the optimum amount necessary for vibrant health.3 According to Dr. Vieth, the minimal daily requirement of vitamin D should be in the range of 4,000 IU from all sources, rather than the 200-400 currently suggested, or ten times the Recommended Daily Allowance (RDA). Dr. Vieth’s research perfectly matches Dr. Price’s observations of sixty years ago!

Vitamin D From Sunlight
Pick up any popular book on vitamins and you will read that ten minutes of daily exposure of the arms and legs to sunlight will supply us with all the vitamin D that we need. Humans do indeed manufacture vitamin D from cholesterol by the action of sunlight on the skin but it is actually very difficult to obtain even a minimal amount of vitamin D with a brief foray into the sunlight.4,5
Ultraviolet (UV) light is divided into 3 bands or wavelength ranges, which are referred to as UV-C, UV-B and UV-A.6 UV-C is the most energetic and shortest of the UV bands. It will burn human skin rapidly in extremely small doses. Fortunately, it is completely absorbed by the ozone layer. However, UV-C is present in some lights. For this reason, fluorescent and halogen and other specialty lights may contribute to skin cancer.
UV-A, known as the “tanning ray,” is primarily responsible for darkening the pigment in our skin. Most tanning bulbs have a high UV-A output, with a small percentage of UV-B. UV-A is less energetic than UV-B, so exposure to UV-A will not result in a burn, unless the skin is photosensitive or excessive doses are used. UV-A penetrates more deeply into the skin than UV-B, due to its longer wavelength. Until recently, UV-A was not blocked by sunscreens. It is now considered to be a major contributor to the high incidence of non-melanoma skin cancers.7 Seventy-eight percent of UV-A penetrates glass so windows do not offer protection.
The ultraviolet wavelength that stimulates our bodies to produce vitamin D is UV-B. It is sometimes called the “burning ray” because it is the primary cause of sunburn (erythema). However, UV-B initiates beneficial responses, stimulating the production of vitamin D that the body uses in many important processes. Although UV-B causes sunburn, it also causes special skin cells called melanocytes to produce melanin, which is protective. UV-B also stimulates the production of Melanocyte Stimulating Hormone (MSH), an important hormone in weight loss and energy production.8
The reason it is difficult to get adequate vitamin D from sunlight is that while UV-A is present throughout the day, the amount of UV-B present has to do with the angle of the sun’s rays. Thus, UV-B is present only during midday hours at higher latitudes, and only with significant intensity in temperate or tropical latitudes. Only 5 percent of the UV-B light range goes through glass and it does not penetrate clouds, smog or fog.
Sun exposure at higher latitudes before 10 am or after 2 pm will cause burning from UV-A before it will supply adequate vitamin D from UV-B. This finding may surprise you, as it did the researchers. It means that sunning must occur between the hours we have been told to avoid. Only sunning between 10 am and 2 pm during summer months (or winter months in southern latitudes) for 20-120 minutes, depending on skin type and color, will form adequate vitamin D before burning occurs.9
It takes about 24 hours for UV-B-stimulated vitamin D to show up as maximum levels of vitamin D in the blood. Cholesterol-containing body oils are critical to this absorption process.10 Because the body needs 30-60 minutes to absorb these vitamin-D-containing oils, it is best to delay showering or bathing for one hour after exposure. The skin oils in which vitamin D is produced can also be removed by chlorine in swimming pools.
The current suggested exposure of hands, face and arms for 10-20 minutes, three times a week, provides only 200-400 IU of vitamin D each time or an average of 100-200 IU per day during the summer months. In order to achieve optimal levels of vitamin D, 85 percent of body surface needs exposure to prime midday sun. (About 100-200 IU of vitamin D is produced for each 5 percent of body surface exposed, we want 4,000 iu.) Light skinned people need 10-20 minutes of exposure while dark skinned people need 90-120 minutes.11
Latitude and altitude determine the intensity of UV light. UV-B is stronger at higher altitudes. Latitudes higher than 30° (both north and south) have insufficient UV-B sunlight two to six months of the year, even at midday.12 Latitudes higher than 40° have insufficient sunlight to achieve optimum levels of D during six to eight months of the year. In much of the US, which is between 30° and 45° latitude, six months or more during each year have insufficient UV-B sunlight to produce optimal D levels. In far northern or southern locations, latitudes 45° and higher, even summer sun is too weak to provide optimum levels of vitamin D.13-15 A simple meter is available to determine UV-B levels where you live.
Vitamin D From Food
What the research on vitamin D tells us is that unless you are a fisherman, farmer, or otherwise outdoors and exposed regularly to sunlight, living in your ancestral latitude (more on this later), you are unlikely to obtain adequate amounts of vitamin D from the sun. Historically the balance of one’s daily need was provided by food. Primitive peoples instinctively chose vitamin-D-rich foods including the intestines, organ meats, skin and fat from certain land animals, as well as shellfish, oily fish and insects. Many of these foods are unacceptable to the modern palate.
For food sources to provide us with D the source must be sunlight exposed. With exposure to UV-B sunlight, vitamin D is produced from fat in the fur, feathers, and skin of animals, birds and reptiles. Carnivores get additional D from the tissues and organs of their prey. Lichen contains vitamin D and may provide a source of vitamin D in the UV-B sunlight-poor northern latitudes.16 Vitamin D content will vary in the organs and tissues of animals, pigs, cows, and sheep, depending on the amount of time spent in UV-B containing sunlight and/or how much D is given as a supplement. Poultry and eggs contain varying amounts of vitamin D obtained from insects, fishmeal, and sunlight containing UV-B or supplements. Fish, unlike mammals, birds and reptiles, do not respond to sunlight and rely on vitamin D found in phytoplankton and other fish. Salmon must feed on phytoplankton and fish in order to obtain and store significant vitamin D in their fat, flesh, skin, and organs. Thus, modern farm-raised salmon, unless artificially supplemented, may be a poor source of this essential nutrient.
Modern diets usually do not provide adequate amounts of vitamin D;17 partly because of the trend to low fat foods and partly because we no longer eat vitamin-D-rich foods like naturally reared poultry and fatty fish such as kippers, and herring. Often we are advised to consume the egg white while the D is in the yolk or we eat the flesh of the fish avoiding the D containing skin, organs and fat. Sun avoidance combined with reduction in food sources contribute to escalating D deficiencies. Vegetarian and vegan diets are exceptionally poor or completely lacking in vitamin D predisposing to an absolute need for UV-B sunlight. Using food as one’s primary source of D is difficult to impossible.

Vitamin D Miracles
Sunlight and vitamin D are critical to all life forms. Standard textbooks state that the principal function of vitamin D is to promote calcium absorption in the gut and calcium transfer across cell membranes, thus contributing to strong bones and a calm, contented nervous system. It is also well recognized that vitamin D aids in the absorption of magnesium, iron and zinc, as well as calcium.
Actually, vitamin D does not in itself promote healthy bone. Vitamin D controls the levels of calcium in the blood. If there is not enough calcium in the diet, then it will be drawn from the bone. High levels of vitamin D (from the diet or from sunlight) will actually demineralize bone if sufficient calcium is not present.
Vitamin D will also enhance the uptake of toxic metals like lead, cadmium, aluminum and strontium if calcium, magnesium and phosphorus are not present in adequate amounts.18 Vitamin D supplementation should never be suggested unless calcium intake is sufficient or supplemented at the same time.
Receptors for vitamin D are found in most of the cells in the body and research during the 1980s suggested that vitamin D contributed to a healthy immune system, promoted muscle strength, regulated the maturation process and contributed to hormone production.
During the last ten years, researchers have made a number of exciting discoveries about vitamin D. They have ascertained, for example, that vitamin D is an antioxidant that is a more effective antioxidant than vitamin E in reducing lipid peroxidation and increasing enzymes that protect against oxidation.19;20
Vitamin D deficiency decreases biosynthesis and release of insulin.21 Glucose intolerance has been inversely associated with the concentration of vitamin D in the blood. Thus, vitamin D may protect against both Type I and Type II diabetes.22
The risk of senile cataract is reduced in persons with optimal levels of D and carotenoids.23
PCOS (Polycystic Ovarian Syndrome) has been corrected by supplementation of D and calcium.24
Vitamin D plays a role in regulation of both the “infectious” immune system and the “inflammatory” immune system.25
Low vitamin D is associated with several autoimmune diseases including multiple sclerosis, Sjogren’s Syndrome, rheumatoid arthritis, thyroiditis and Crohn’s disease.26;27
Osteoporosis is strongly associated with low vitamin D. Postmenopausal women with osteoporosis respond favorably (and rapidly) to higher levels of D plus calcium and magnesium.28
D deficiency has been mistaken for fibromyalgia, chronic fatigue or peripheral neuropathy.1;28-30
Infertility is associated with low vitamin D.31 Vitamin D supports production of estrogen in men and women.32 PMS has been completely reversed by addition of calcium, magnesium and vitamin D.33 Menstrual migraine is associated with low levels of vitamin D and calcium.81
Breast, prostate, skin and colon cancer have a strong association with low levels of D and lack of sunlight.34-38
Activated vitamin D in the adrenal gland regulates tyrosine hydroxylase, the rate limiting enzyme necessary for the production of dopamine, epinephrine and norepinephrine. Low D may contribute to chronic fatigue and depression.39
Seasonal Affective Disorder has been treated successfully with vitamin D. In a recent study covering 30 days of treatment comparing vitamin D supplementation with two-hour daily use of light boxes, depression completely resolved in the D group but not in the light box group.40
High stress may increase the need for vitamin D or UV-B sunlight and calcium.41
People with Parkinsons and Alzheimers have been found to have lower levels of vitamin D.42;43
Low levels of D, and perhaps calcium, in a pregnant mother and later in the child may be the contributing cause of “crooked teeth” and myopia. When these conditions are found in succeeding generations it means the genetics require higher levels of one or both nutrients to optimize health.44-47
Behavior and learning disorders respond well to D and/or calcium combined with an adequate diet and trace minerals.48;49

Vitamin D and Heart Disease
Research suggests that low levels of vitamin D may contribute to or be a cause of syndrome X with associated hypertension, obesity, diabetes and heart disease.50 Vitamin D regulates vitamin-D-binding proteins and some calcium-binding proteins, which are responsible for carrying calcium to the “right location” and protecting cells from damage by free calcium.51 Thus, high dietary levels of calcium, when D is insufficient, may contribute to calcification of the arteries, joints, kidney and perhaps even the brain.52-54
Many researchers have postulated that vitamin D deficiency leads to the deposition of calcium in the arteries and hence atherosclerosis, noting that northern countries have higher levels of cardiovascular disease and that more heart attacks occur in winter months.55-56
Scottish researchers found that calcium levels in the hair inversely correlated with arterial calcium—the more calcium or plaque in the arteries, the less calcium in the hair. Ninety percent of men experiencing myocardial infarction had low hair calcium. When vitamin D was administered, the amount of calcium in the beard went up and this rise continued as long as vitamin D was consumed. Almost immediately after stopping supplementation, however, beard calcium fell to pre-supplement levels.27
Administration of dietary vitamin D or UV-B treatment has been shown to lower blood pressure, restore insulin sensitivity and lower cholesterol.58-60

The Battle of the Bulge
Did you ever wonder why some people can eat all they want and not get fat, while others are constantly battling extra pounds? The answer may have to do with vitamin D and calcium status. Sunlight, UV-B, and vitamin D normalize food intake and normalize blood sugar. Weight normalization is associated with higher levels of vitamin D and adequate calcium.61 Obesity is associated with vitamin-D deficiency.62-64 In fact, obese persons have impaired production of UV-B-stimulated D and impaired absorption of food source and supplemental D.65
When the diet lacks calcium, whether from D or calcium deficiency, there is an increase in fatty acid synthase, an enzyme that converts calories into fat. Higher levels of calcium with adequate vitamin D inhibit fatty acid synthase while diets low in calcium increase fatty acid synthase by as much as five-fold. In one study, genetically obese rats lost 60 percent of their body fat in six weeks on a diet that had moderate calorie reduction but was high in calcium. All rats supplemented with calcium showed increased body temperature indicating a shift from calorie storage to calorie burning (thermogenesis).61

The Right Fats
The assimilation and utilization of vitamin D is influenced by the kinds of fats we consume. Increasing levels of both polyunsaturated and monounsaturated fatty acids in the diet decrease the binding of vitamin D to D-binding proteins. Saturated fats, the kind found in butter, tallow and coconut oil, do not have this effect. Nor do the omega-3 fats.66 D-binding proteins are key to local and peripheral actions of vitamin D. This is an important consideration as Americans have dramatically increased their intake of polyunsaturated oils (from commercial vegetable oils) and monounsaturated oils (from olive oil and canola oil) and decreased their intake of saturated fats over the past 100 years.
In traditional diets, saturated fats supplied varying amounts of vitamin D. Thus, both reduction of saturated fats and increase of polyunsaturated and monounsaturated fats contribute to the current widespread D deficiency.
Trans fatty acids, found in margarine and shortenings used in most commercial baked goods, should always be avoided. There is evidence that these fats can interfere with the enzyme systems the body uses to convert vitamin D in the liver.80

Vitamin D Therapy
In my clinical practice, I test for vitamin-D status first. If D is needed, I try to combine sunlight exposure with vitamin D and mineral supplements.
Single, infrequent, intense, skin exposure to UV-B light not only causes sunburn but also suppresses the immune system. On the other hand, frequent low-level exposure normalizes immune function, enhancing NK-cell and T-cell production, reducing abnormal inflammatory responses typical of autoimmune disorders, and reducing occurrences of infectious disease.26;67;68-71 Thus it is important to sunbathe frequently for short periods of time, when UV-B is present, rather than spend long hours in the sun at infrequent intervals. Adequate UV-B exposure and vitamin-D production can be achieved in less time than it takes to cause any redness in the skin. It is never necessary to burn or tan to obtain sufficient vitamin D.
If sunlight is not available in your area because of latitude or season, sunlamps made by Sperti can be used to provide a natural balance of UV-B and UV-A. Used according to instructions, these lamps provide a safe equivalent of sunlight and will not cause burning or even heavy tanning. Tanning beds, on the other hand, are not acceptable as a means of getting your daily dose of vitamin D because they provide high levels of UV-A and very little UV-B.
If you have symptoms of vitamin-D insufficiency or are unable to spend time in the sun, due to season or lifestyle or prior skin cancer, consider adding a supplement of 1,000 IU daily. Higher levels may be needed but should be recommended and monitored by your health care practitioner after testing serum 25(OH)D. 1,000 iu can be obtained from a concentrated supplement or from 2 teaspoons of high quality cod liver oil. Both Carlson Labs and Solgar make a 1,000 IU vitamin-D supplement naturally derived from fish oil. (Do not attempt to obtain large amounts of vitamin D from cod liver oil alone, as this would supply vitamin A in excessive and possibly toxic amounts.)
Supplementation is safe as long as sarcoidosis, liver or kidney disease is not present and the diet contains adequate calcium, magnesium and other minerals.
Adequate calcium and magnesium, as well as other minerals, are critical parts of vitamin D therapy. Without calcium and magnesium in sufficient quantities, vitamin-D supplementation will withdraw calcium from the bone and will allow the uptake of toxic minerals. Do not supplement vitamin D and do not sunbathe unless you are sure you have sufficient calcium and magnesium to meet your daily needs. Weston Price suggested a minimum of 1,200-2,400 mg of calcium daily. Research suggests that 1,200-1,500 mg is adequate as a supplement for most adults, both men and women. (Magnesium intake should be half that of calcium.)
Two excellent sources of calcium in the human diet are dairy products and bone broths.2 If the diet does not contain sufficient amounts, you will need to add supplements. Bone meal, dolomite powder or calcium and magnesium tablets (Solgar or Kal), or calcium carbonate or lactate (Solgar, Kal, Now or Twinlab) are good calcium sources, inexpensive and safe.74 All of these brands have been tested and found to be free of lead and other heavy metals.
In my experience, the forms of calcium given in supplements should be equivalent to those found in food—bone meal as in the broth, calcium lactate as in milk products and dolomite as in lime used to process cornmeal products. These forms work most efficiently and with the least cost for bone repletion and general repletion of serum calcium status.75 If your diet is high in protein, calcium lactate or carbonate is probably a better source of calcium.
Read the label carefully to see how much elemental calcium is contained in each dose or tablet and make sure to take the right amount. If the label says a serving size is three tablets and contains 1,000 mg of calcium, you must take the full serving size to get that amount.
Higher amounts of calcium are important for anyone diagnosed with bone loss. Total daily calcium as a supplement may range from 1,500 mg to 2,000 mg depending on current bone status and your body size. Make the effort to split up your daily dose. Do not take all your calcium and magnesium once a day. A higher percentage of the calcium dose is absorbed if delivered in smaller, more frequent amounts.82
Expensive “chelated” calciums are not necessary if vitamin-D status is adequate. Taking calcium without sufficient D may cause other problems. Vitamin D controls the production of some calcium binding proteins, which are critical to normal calcium utilization.
Patients on vitamin-D therapy report a wide range of beneficial results including increased energy and strength, resolution of hormonal problems, weight loss, an end to sugar cravings, blood sugar normalization and improvement of nervous system disorders.
A paradoxical transient and non-complicating hypercalciuria (more calcium in the urine) may occur when the program is first initiated. This resolves quickly when adequate calcium and other minerals are consumed. Two other temporary side effects may occur during the first several months of treatment. One is daytime sleepiness after calcium is taken. This usually resolves itself after about one week. The other condition is the reappearance of pain and discomfort at the site of old injuries, a sign of injury remodeling or proper healing, which may take some time to clear up.

Toxicity Issues
Vitamin programs usually omit vitamin D because of concerns about toxicity. These concerns are valid because vitamin D in all forms can be toxic in pharmacological (drug-like) doses. The dangers of toxicity have not been exaggerated, but the doses needed to result in toxicity have been ill defined with the unfortunate result that many people currently suffer from vitamin-D deficiency or insufficiency.
Abnormally high levels of vitamin D are indicated by blood levels exceeding 65 ng/ml or 162 nmol/l for extended periods of time and may be associated with chronic toxicity. Levels of 200-300 nmol/l or higher have been seen in several studies using supplementation and quickly resolve when supplementation is stopped. In such cases no long-term problems have been found. Long-term supplementation, without monitoring, may have serious consequences.
Before 1993, there was no affordable and available blood test for vitamin D. Now there is. To avoid problems, anyone engaging in levels of vitamin-D supplementation above 1,000 iu daily should have periodic blood tests. Don’t forget to calculate your total vitamin-D intake from all sources—sunlight, food (including vitamin D in milk) and supplements, including cod liver oil.
Dr. Vieth suggests that critical toxicity may occur at doses of 20,000 IU daily and that the Upper Limit (UL) of safety be set at 10,000 IU, rather than the current 2,000 IU. While this may or may not be the definitive marker for safety in healthy persons with no active liver or kidney disease, there is no clinical evidence that long-term supplementation needs to be greater than 4,000 IU for optimal daily maintenance. This level would be somewhat lower when combined with exposure to UV-B.3;76
Doses used in clinical studies range from as little as 400 IU daily to 10,000-500,000 IU, given either as a single onetime dose or daily, weekly or monthly. Such large doses are given either as a prophylactic or because compliance is considered a problem. There seems to be some evidence that vitamin D works better, without toxicity, when given in lower, more physiologic doses of 2,000-4,000 IU daily rather than as 100,000 IU once a month. However, a single monthly dose of 100,000 IU did replete low levels of vitamin D in adolescents during winter.77
In my experience and that of other researchers, high, infrequent dosing can lead to problems. In one recent study, blood levels rose from low to extremely high, (more than 300 nmol/l) 2 to 4 hours after a 50,000 IU oral dose,65 and then slowly returned to pretreatment suboptimal levels. Clearly this must disrupt normal feedback mechanisms in D and calcium regulation.
Vitamin A can be administered in large, infrequent doses from consumption of animal or fish liver (or injections, used in third world countries to prevent blindness) because we have storage capacity for vitamin A in our livers. Vitamin D is different. It has only a small storage pool in the liver and peripheral fat. Our ancestors most definitely did not get vitamin D in large, infrequent doses. While vitamin D is stored in body fat, storage is not sufficient to maintain optimum blood levels during winter months.78 A single exposure to UV-B light will raise levels of vitamin D over the next 24 hours and then return to baseline or slightly higher within 7 days. Historically our requirements for D were satisfied by daily exposure to sunlight and/or daily intake from food. Lowfat diets and lack of seafood in the diet further contribute to the current worldwide insufficiency of vitamin D.

Sunlight on the Inside
If any nutrient incorporates the properties of sunlight, it is vitamin D. The healthy “primitive” peoples that Dr. Price observed not only had broad, round, “sunny” faces, they also had sunny dispositions and optimistic attitudes towards life in spite of many hardships. Typical food intakes for peoples who have not been “civilized” range from 3,000 IU-6,000 IU. Modern intakes are paltry in comparison. The standard American diet provides vitamin D only in very low quantities.
The first step towards redressing some of the ills of civilized life—from depression to road rage, from cavities to osteoporosis—would be to get more light, inside or outside. Vitamin D adds sunlight to life from childhood through the golden years. In nonagenarians and centagenarians high levels of vitamin D in the blood and normal thyroid function were the strongest markers of health and longevity.79
Whether in the form of sunlight or dietary vitamin D from food and fish oils, optimal levels of the sunshine vitamin allow your body and mind to thrive, even during periods of stress.

About the Author
Krispin Sullivan, CN is a researcher and clinical nutritionist in practice in Woodacre, California. She is currently working on a book, Naked at Noon: The Importance of Sunlight and Vitamin D, to be published in 2001.
Instructions for physician monitoring of vitamin D, calcium and magnesium repletion are available from www.sunlightandvitamind.com or by contacting Krispin at krispin@krispin.com or 1-415-488-9636.

References
Sidebar Articles

Food Sources of Vitamin D
USDA databases compiled in the 1980s list the following foods as rich in vitamin D. The amounts given are for 100 grams or about 3 1/2 ounces. These figures demonstrate the difficulty in obtaining 4,000 IU vitamin D per day from ordinary foods in the American diet. Three servings of herring, oysters, catfish, mackerel or sardines plus generous amounts of butter, egg yolk, lard or bacon fat and 2 teaspoons cod liver oil (500 iu per teaspoon) yield about 4,000 IU vitamin D—a very rich diet indeed!

Cod Liver Oil 10,000 IU
Lard (Pork Fat) 2,800 IU
Atlantic Herring (Pickled) 680 IU
Eastern Oysters (Steamed) 642 IU
Catfish (Steamed/Poached) 500 IU
Skinless Sardines (Water Packed) 480 IU
Mackerel (Canned/Drained) 450 IU
Smoked Chinook Salmon 320 IU
Sturgeon Roe 232 IU
Shrimp (Canned/Drained) 172 IU
Egg Yolk (Fresh) 148 IU
(One yolk contains about 24 IU)
Butter 56 IU
Lamb Liver (Braised) 20 IU
Beef Tallow 19 IU
Pork Liver (Braised) 12 IU
Beef Liver (Fried) 12 IU
Beef Tripe (Raw) 12 IU
Beef Kidney (Simmered) 12 IU
Chicken Livers (Simmered) 12IU
Small Clams (Steamed/Cooked Moist) 8 IU
Blue Crab (Steamed) 4 IU
Crayfish/Crawdads (Steamed) 4 IU
Northern Lobster (Steamed) 4 IU

The Many Forms of Vitamin D
There are two types of vitamin D found in nature. Vitamin D2 is formed by the action of UV-B on the plant precursor ergosterol. It is found in plants and in was formerly added to irradiated cows milk. Most milk today contains D3. Vitamin D3 or cholecalciferol is found in animal foods. Both forms of vitamin D have been used successfully to treat rickets and other diseases related to vitamin D insufficiency.
Many consider D3 the preferred vitamin, having more biologic activity. Vitamin D3 as found in food or in human skin always comes with various metabolites or isomers that may have biological benefit. Dr. Price believed that there were as many as 12 metabolites or isomers in the vitamin D found in animal foods. When vitamin D is taken in the form of fish oil, or eaten in foods such as eggs or fish, these metabolites will be present. Both D2 and D3 can be toxic when taken inappropriately in large amounts.
When humans take in vitamin D from food or sunlight, it is converted first in the liver to the form 25(OH)D and then in the kidney to 1,25(OH)D. These active forms of vitamin D are available by prescription and are given to patients with liver or kidney failure or those with an hereditary metabolic defect in vitamin-D conversion.
Assessing Vitamin D Status
Blood Testing: Currently there are two tests available for physicians to assess vitamin-D status. One is for the somewhat biologically active precursor 25(OH)D and another for 1,25(OH)D, the most active form, which is converted in the kidney and other organs. The latter is often normal in the blood even when the precursor 25(OH)D is low or deficient. The precursor is a better marker of vitamin-D status (or reserves) than the most active 1,25(OH)D form. It is the optimum level of 25(OH)D that is most strongly associated with general good health. (The test values given in this article are for 25(OH)D.) For many years the acceptable level of 25(OH)D has been at least 9 ng/ml (23 nmol/l). Some researchers believe that 20 ng/ml (50 nmol/l) should be the lower acceptable limit72 but Dr. Vieth presents a large amount of data to support his claim that this is far from optimal.3 Optimal levels are certainly at least 32 ng/ml (80 nmol/l) and preferably closer to 40 ng/ml (100 nmol/l).
Salivary pH Testing for calcium sufficiency: A method of assessing ionized calcium levels has been used by Weston Price, DDS and Carl Reich, MD and has confirmation in current research.73 After determining your serum-D status (testing) and undertaking a program of supplementation with vitamin D, calcium and magnesium, morning salivary pH should read 6.8-7.2. Lower values may indicate insufficient vitamin D (retest), or low levels of calcium in the diet. Look for pH paper with a range of 5.5-8.0 and increments of 0.2. PH papers with 0.5-degree increments are not sensitive enough to monitor progress. (Note: Do not take more than 1,000 IU of vitamin D without testing and supervision by a knowledgeable healthcare practitioner. Calcium can be adjusted within the ranges suggested. Several months of supplementation may be required to show positive results if the deficiency is severe and prolonged.)

Sources
UV-B Meter: Sunsor, Inc. (800) 492-9815 Sunsor
pH Testing Papers: Pike Agri-Lab Supplies (207) 684-5131 or info@pikeagri.com
Carlson Labs Vitamin D: (888) 880-3055 www.vitaminshoppe.com
Solgar Vitamin D: L & H Vitamins (800) 221-1152
Sperti Sunlamps: (800) 544-3757 www.sperti.com

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Vitamin D Update, Winter 2000
by Krispin Sullivan, CN

Note: This update appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Winter 2000.

Since the publication of “The Miracle of Vitamin D” in the last issue of Wise Traditions, some clarification is necessary. The action of vitamin D, whether from food, supplements or sunlight conversion, is that of a “pro-hormone,” rather than of a vitamin.
According to the dictionaries, a hormone is a substance, usually a peptide or steroid, produced by one tissue and conveyed by the bloodstream to another. Hormones affect physiological activity, such as growth or metabolism. More generally, a hormone is one of various similar substances found in plants and insects that regulate development. By contrast, vitamins are various fat-soluble or water-soluble organic substances essential in minute amounts for normal growth and activity of the body. They are obtained naturally from plant and animal foods.
Hormones are powerful regulators that can have both good and bad effects. With progesterone, DHEA, estrogen, thyroid or any other hormone, including vitamin D, there can be a profound cellular response when levels are altered by supplementation. Vitamins and minerals are elements used by the body to make enzymes, bone, immune fractions and other substances in the human body, but they are not regulators.
As a pro-hormone, vitamin D can be dangerous because too much has the potential for great harm as does too little. That is why testing is important for those on vitamin-D therapy. When you take thyroid hormones, you are instructed to test first and retest to make sure the amount you are taking is correct. So, too, with vitamin D. The rule is test, treat (if necessary) and retest until you find the right amount to meet your daily need. According to our current levels of knowledge, there are no obvious symptoms of vitamin D overdose until the overdose is nonreversible. Testing can alert us not only to deficiency but also toxicity. Fortunately, we now have tests for vitamin D status that are not expensive.
In my practice, I am discovering that some people may need upwards of 4,000 IU daily to maintain optimal blood levels. Others may find that anything over 200-400 IU puts them in a situation of overdose. This is a problem of genetics. Some people utilize vitamin D better than others. Before the days of travel and great population migrations, the process of natural selection created population groups that best responded to the levels of vitamin D available through exposure to sunlight and in the diet. Migration, immigration and intermarriage make it impossible to determine needs without testing.
Once you test and determine the level of D from sunlight, food and supplements that maintains optimum levels of vitamin D in your blood, then you know the “dose” that you will need as long as you live at that altitude and latitude. You should test twice a year as in many locations the need for D may vary greatly from summer to winter.
For detailed information visit my website sunlightandvitamind.com

VITAMIN D UPDATE-A WARNING, Fall 2002
By Krispin Sullivan, CN
I have reported in this magazine on the substantial benefits that can be gained from vitamin D therapy (Wise Traditions, Fall 2000). However, my own clinical experience and the research of others is clearly showing chronic subclinical vitamin D toxicity is possible, from both supplements or tropical sunlight. Elevated levels of serum vitamin D can cause significant bone loss and calcification of soft tissues.
If you are using supplements of vitamin D (natural or synthetic) or are light skinned and have had significant sun exposure in tropical or subtropical areas and haven’t done so before, it is very important to test your blood levels of D.
Optimal values of 25(OH)D are 40-50 ng/ml
Acceptable values of 25(OH)D are 35-55 ng/ml
Levels above 55 ng/ml will be toxic for some individuals.
There is no good reason to maintain levels of D in this higher range and strong evidence showing potential harm.
You need to TEST. The correct test to order is 25(OH)D, also called 25-hydroxyvitamin D. Make sure this is the test you get. Labs often give the test for 1,25-dihydroxyvitamin D, the active hormone. This test is the wrong test as it offers no meaningful data regarding D status.
Lab One offers the least expensive testing I have found nationwide and is available in most states. Your physician can reach them at 1-800-646-7788. The test is 25-hydroxyvitamin D. The Lab One test number, just to be sure you get the right test, is #3247. Rarely does insurance cover the cost for this test, which is about $60 including lab fees. Other labs I have queried charge $100-180 for the same test.
The important thing to remember if you are doing vitamin D therapy, or spending lots of time in the sun, is to TEST!
The original article with sidebars and references appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Fall 2000. Updates appeared in the journal in the Winter 2000 issue and the Fall 2002 issue.
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This page was first posted on 31 DEC 2000, with updates 30 MAR 2001 and 31 DEC 2002.