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Top Fertility Tests for Women: An Integrative Medicine Perspective

Posted By Administration, Monday, August 30, 2010
Updated: Friday, April 18, 2014

by Fiona McCulloch, ND

Top Fertility tests :  A Quick Reference for Women from an Integrative Medicine PerspectiveLab Testing for Infertility

FSH – Follicle Stimulating Hormone

Day 3 FSH can indicate how hard the pituitary is working to stimulate the ovaries.  Though traditionally a higher FSH is given a poor prognosis, I don’t always see it this way clinically.  The FSH can very much change depending on the quality of the antral follicles, which depends on ovarian health over the previous months as well as ovarian reserve.  The poorer the quality of the eggs, the more free radical damage they have accumulated and the poorer ovarian blood flow is, the more FSH the pituitary will have to put out in order to stimulate the antral follicles.  Healthy follicles are responsive to lower amounts of FSH.  If treatments are started to enhance ovarian health over 120 days of folliculogenesis prior to ovulation, the lowered FSH that can result can indeed indicate that the quality of the eggs in the ovaries has increased.  Please keep in mind that I have seen many women with high FSH become pregnant when egg quality and ovarian health is worked on so having a high FSH is not untreatable.

FSH Levels (Day 3)
Excellent less than 6 mIU/mL
Good 6-9 mIU/mL
Low 10-13 mIU/mL
Very Low above 13 mIU/mL

LH – Luteinizing Hormone

This is a test which is often done on day 3 of the cycle.  If higher than the FSH, especially if higher than a 2:1 ratio, it can indicate polycystic ovarian syndrome.  Having a high LH level will result in increased ovarian testosterone production,  altered estrogen production, and abnormalities with ovulation.  Normal day 3 range : <7 mIU/mL

Estradiol

Measured on day 3 of the cycle.  If elevated, estradiol can lower the fsh, thereby masking elevated fsh levels.  This can happen in cases of low ovarian reserve or functional cysts.  Estradiol can be low in conditions of low ovarian reserve.   Women who have estradiol over 294 pmol/L (or 80 pg/ml) have a lower chance of success with an IVF cycle since they will not respond to stimulation as well.

Progesterone

This is often measured on day 21.  This is used to determine whether ovulation has occurred as a healthy corpus luteum produces progesterone.  It is important to measure progesterone 7 days after your ovulation, measuring on day 21 only applies to women who ovulate on day 14.  Levels higher than 16 nmol/L strongly suggest an ovulatory cycle.


Cortisol

Often measured in the morning can indicate the impact of stress on the reproductive system.  Elevated cortisol can affect ovarian circulation and function.  Normal levels :  250 – 850 nmol/L taken between 6-8am.  Low cortisol can be found in congenital adrenal hyperplasia. Normal levels for am cortisol 101-536 nmol/L

Testosterone

The total level of testosterone in the system.  If elevated this can indicate polycystic ovarian syndrome.  High testosterone can interfere with normal ovulation often causing delayed ovulation or anovulation.   Levels can also be low around which can negatively affect ovarian function.  Normal levels for females 0.3- 4.0 nmol/L

Free testosterone

The amount of testosterone that is not bound to carriers and is available to stimulate tissues.  The higher this is, the more androgenic effect on the tissues.  This can be elevated in PCOS and specific adrenal conditions such as non-classical congenital adrenal hyperplasia (non classical CAH).  Normal levels for females 0.1-8.9 pmol/L

Prolactin

A hormone normally elevated in nursing and pregnancy.  If elevated in other situations it can interfere with ovulation and fertility.  It can be elevated due to stress, medications such as antidepressants or painkillers, thyroid disease, or pituitary conditions such as microadenomas.  normal levels in women 3.3 – 26.7 ug/l.

DHT – Dihydrotestosterone

A form of testosterone which is very potent.  DHT Can be elevated in pcos or enzyme conversion disorders resulting in androgen excess signs and symptoms.  Serum testing for DHT is often unreliable.

Sex hormone binding globulin
Can be low in patients with androgen excess conditions such as pcos or in hypothyroidism. Can be high in non classical CAH, hyperthyroidism.  Normal levels :  Follicular phase 24 – 200 nmol/L, Luteal phase 48 – 185 nmol/L

HbA1C

A long termarker of insulin resistance and blood glucose control. Can be elevated in pcos.  Marks the previous 3 months of blood glucose control.  Normal levels 0.040 – 0.060

DHEA – S
A precursor to hormones, most especially androgens.  DHEA is made by the adrenal gland.  Levels tend to reduce with age and can be reduced in low ovarian reserve.  Levels can be elevated in PCOS.    Normal range for women 0-11 µmol/liter

Ferritin
A marker for stored iron.  Levels can be low in patients with infertility.   I recommend patients to achieve ferritin levels of above 50.

TSH -  thyroid stimulating hormone

I like to achieve levels of approximately 2 – 2.5.  Levels above this can put the patient at risk for early miscarriage.  Normal Ranges are :  0.4 – 4 mIU/L.   If levels are above 3, and especially if thyroid antibodies such as antithyroglobulin and anti-thyroid peroxidase are present with signs and symptoms of hypothyroidism, this and may present risks for fertility.

Vitamin D
Important for overall health, hormone balance, and stress levels.  Normal levels of 1, 25 Hydroxy Vitamin D 40 -150 pmol/L

Homocysteine

A marker of inflammation and circulatory health.  This test is only recently being found to be important for ovarian health.  Elevated levels can be found in autoimmune conditions, ovarian aging and endometriosis.  Normal range : 4.7 – 14.1 umol/L

INR
A measure of blood clotting.  Blood which clots excessively may interfere with implantation. Can also elevated in endometriosis or fibroids.  Normal value for INR 0.9 – 1.2

Anti sperm antibodies

The presence of anti- sperm antibodies in women can destroy or damage the sperm before they have the chance to fertilize the egg.  Around 5% of infertile women have these antibodies in their bloodstreams.
Anti thyroid antibodies

These include antithyroid peroxidase and antithyroglobulin.  These antibodies, if present will reduce fertility by 13%, even if thyroid function is normal.   These antibodies can cause alterations in thyroid function and also can be cross reactive with ovarian tissue.  Women with PCOS who don’t respond to clomid have a higher liklihood of having antithyroid antibodies.

Anti nuclear antibodies

These antibodies are present in autoimmune disease such as Lupus and Sjogrens syndrome.

Special Ovarian Reserve Markers:

Amh
Antimullerian hormone is produced by growing follicles and prevents premature recruitment of primordial follicles.  This value generally correlates with the number of functional primordial and antral follicles remaining in the ovary.  Generally, the higher the AMH,  the more healthy follicles are in the ovary.  Antimullerian hormone can predict the age of onset of menopause with some degree of accuracy.   Low AMH often does not give a good prognosis for IVF because IVF is based on the stimulation of multiple follicles – women with lower AMH tend to get fewer follicles during IVF stimulation.  However, even if AMH is low, conception is possible.  Even if there are not many follicles remaining in the ovary, their quality can be improved with treatments including antioxidants and circulatory enhancing therapies.  Natural conception with low AMH can and does happen.    Normal ranges :

AMH Levels
Optimal Fertility: 28.6 pmol/L – 48.5 pmol/L  or over 1.0 ng/ml
Satisfactory Fertility: 15.7 pmol/L – 28.6 pmol/L  or  over 1.0 ng/ml
Low Fertility: 2.2 pmol/L – 15.7 pmol/L or  0.3 – 0.9 ng/ml
Very Low/Undetectable: 0.0 pmol/L – 2.2 pmol/L or less than 0.3 ng/ml
High Level found in PCOS > 48.5 pmol/L or over 3 ng/ml

Inhibin b
A marker of ovarian function and reserve, this protein is secreted by small developing follicles and works to inhibit FSH levels, hence the name inhibin.  This test is completed on day 3 of the cycle.  As inhibin is secreted by the follicles, it can indicate the number of and function of the remaining folliciles. This test is not widely available.  Normal = above 45 pg/ml Low = below 45 pg/mL  Inhibin B is a spectrum however, and this line is a general guideline not a strict cutoff.  Like with AMH even if inhibin B is low, conception is possible if the health of the remaining follicles is enhanced.

References

Mosby’s Manual of Diagnostic and Laboratory Tests.  4th Ed. 2010

Speroff, Clinical Gynecologic Endocrinology and Infertility.  7th Edition 2005.

Tags:  fertility  Infertility 

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Vitamin C and Cancer Revisited

Posted By Administration, Friday, August 27, 2010
Updated: Friday, April 18, 2014

3237070041_a872337c89_oIn the issue of Proceedings of the National Academy of Sciences of the United States of America (PNAS), Chen et al. (1) it shows that i.p. injection of “pharmacologic doses” of vitamin C decreases the growth and weight of human, rat, and murine tumor xenografts in athymic, nude mice. This work follows a number of articles by the same group, led by Mark Levine at the National Institute of Diabetes and Digestive and Kidney Diseases, showing that millimolar concentrations of extracellular vitamin C kill cancer cells but not normal cells in a hydrogen peroxide (H2O2)-dependent manner (1–3). Such millimolar concentrations of vitamin C can be achieved in humans by i.v. infusion but not by diet or supplements (4). Hence, vitamin C is postulated to exert local pro-oxidant effects in the interstitial fluid surrounding tumor cells, killing them or inhibiting their growth, while leaving normal cells intact (1–3). 

It is well known that vitamin C, or ascorbic acid, is an effective biologic antioxidant and does not act as a pro-oxidant under normal conditions (5) because it does not readily autoxidize, i.e., react with oxygen (O2) to produce reactive oxygen species, such as superoxide radicals (O2•−) or H2O2. However, ascorbate readily donates an electron to redox-active transition metal ions, such as cupric (Cu2+) or ferric (Fe3+) ions, reducing them to cuprous (Cu+) and ferrous (Fe2+) ions, respectively (Reaction 1). In fact, reduction of copper or iron in the catalytic site of certain enzymes underlies ascorbate's well known biologic function as a co-substrate in procollagen, carnitine, and catecholamine biosynthesis (6). Reduced transition metal ions, in contrast to ascorbic acid, readily react with O2, reducing it to superoxide radicals (Reaction 2), which in turn dismutate to form H2O2 and O2 (Reaction 3): 

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The H2O2 produced this way (Reactions 1–3) seems to be key to ascorbate's antitumor effect because H2O2 causes cancer cells to undergo apoptosis, pyknosis, and necrosis (2). In contrast, normal cells are considerably less vulnerable to H2O2. The reason for the increased sensitivity of tumor cells to H2O2 is not clear but may be due to lower antioxidant defenses (7). In fact, a lower capacity to destroy H2O2—e.g., by catalase, peroxiredoxins, and GSH peroxidases—may cause tumor cells to grow and proliferate more rapidly than normal cells in response to low concentrations of H2O2. It is well known that H2O2 exerts dose-dependent effects on cell function, from growth stimulation at very low concentrations to growth arrest, apoptosis, and eventually necrosis as H2O2 concentrations increase (8). This dose-dependency may be shifted to the left in tumor cells, making them more sensitive to both the growth stimulatory and cytotoxic effects of H2O2. Whatever the exact mechanism, the increased sensitivity of tumor cells to killing by H2O2 may provide the specificity and “therapeutic window” for the antitumor effect of extracellular ascorbate (1, 2). 

 


Millimolar concentrations of extracellular vitamin C kill cancer cells but not normal cells. 

The chemical reactions linking ascorbate to H2O2, as explained above (Reactions 1–3), require a redox-active transition metal—without it, ascorbate cannot exert pro-oxidant effects. Chen et al. (2) speculate that there is an extracellular “metalloprotein catalyst” of between 10 and 30 kDa in size that interacts with ascorbate. Identification of this metal-containing protein will be critical because it seems to be the cause for millimolar concentrations of ascorbate to act as a pro-oxidant in interstitial fluid. In contrast, the protein must be absent or inactive in blood, otherwise ascorbate would become oxidized to the ascorbyl radical or be unstable, which is not observed (1). If this putative metalloprotein can be identified and characterized, it may serve as an additional target for anticancer therapy. For example, other naturally occurring reducing agents, such as certain flavonoids or thiol compounds, may be particularly effective in reducing the protein's metal center, or drugs may be developed specifically targeting this center. 

Although Chen et al. (1) provide no direct evidence for the existence of the metalloprotein or the formation of reduced transition metal ions by extracellular ascorbate, they measure the other reaction product formed between ascorbate and the putative metal center, i.e., the ascorbyl radical (Reaction 1). They show formation of this radical in a time-dependent and ascorbate-dose-dependent manner in interstitial fluid of tissues, including tumor xenografts, but not in blood (1, 3). They also show that the concentration of the ascorbyl radical correlates with the concentration of H2O2 in interstitial fluid, whereas no H2O2 can be detected in blood or plasma (3, 9). These observations, combined with the inhibitory effect on xenograft growth, provide the proof of concept that millimolar concentrations of extracellular ascorbate, achievable by i.p. injection or i.v. infusion in experimental animals and humans, respectively, exert pro-oxidant, antitumor effects in vivo

PERSPECTIVE 

Why is it important to understand how vitamin C can produce H2O2 and kill cancer cells but not normal cells? Because without this detailed knowledge, we do not have a scientific rationale to revisit the question of whether i.v. infusion of vitamin C may have value in treating cancer patients. The potential cancer-therapeutic activity of vitamin C has a long and controversial history. In 1973, Linus Pauling and Ewan Cameron (10) postulated that vitamin C inhibits tumor growth by enhancing immune response and stabilizing glycosaminoglycans of the extracellular matrix by inhibiting hyaluronidase. Cameron and Campbell (11) reported on the response of 50 consecutive patients with advanced cancer to continuous i.v. infusions (5–45 g/d) and/or oral doses (5–20 g/d) of vitamin C. No or minimal response was observed in 27 patients; 19 patients exhibited tumor retardation, cytostasis, or regression; and 4 patients experienced tumor hemorrhage and necrosis. The first clinical study by Cameron and Pauling (12) compared survival times between 100 patients with terminal cancer treated with i.v. and oral vitamin C, usually 10 g/d, and 1,000 comparable patients not given vitamin C. Patients treated with vitamin C survived approximately four times longer than controls, with a high degree of statistical significance (P < 0.0001). A follow-up study reported that patients given vitamin C had a mean survival time almost 1 year longer than matched controls (13). Overall, 22% of vitamin C-treated patients but only 0.4% of controls survived for more than 1 year. 

The National Cancer Institute sponsored two randomized, placebo-controlled, double-blind trials of vitamin C and advanced cancer at the Mayo Clinic (14, 15). In both trials, patients were given 10 g/d vitamin C or placebo. Survival rates were essentially the same for all groups. Plasma concentrations of vitamin C were not measured in either study, and vitamin C was given only orally. In retrospect, the Mayo Clinic trials may have failed to properly evaluate the clinical efficacy of vitamin C in cancer because of insufficient plasma concentrations of vitamin C attained with oral supplementation (4). 

Pauling and colleagues (16) emphasized host resistance to cancer but recognized the anticancer role of redox chemistry, especially reactive oxygen species formed from the reaction of vitamin C with copper. When mice were inoculated with Ehrlich tumor cells and injected i.p. with the copper-containing tripeptide copper:glycylglycylhistidine (Cu:GGH) and vitamin C, 40% survived 60 days, whereas no controls survived for longer than 30 days. The combination of Cu:GGH and vitamin C was also toxic to Ehrlich tumor cells in vitro, but the cytotoxicity was abrogated by catalase, suggesting that H2O2 was the cytotoxic species. The work of Chen et al. (1–3) also strongly suggests that H2O2 is responsible for the anticancer activity of vitamin C. 

Interestingly, Chen et al. (1) noted that metastases were present in ≈30% of athymic mice grafted with glioblastoma tumors, whereas no metastases were detected in similar mice injected i.p. with ascorbate. This observation warrants further investigation because metastases account for a substantial percentage of cancer mortality.   

RECENT CLINICAL STUDIES 

Two Phase 1 clinical trials of cancer and vitamin C have recently been published that demonstrated remarkable tolerance and safety for high-dose (up to 1.5 g/kg) i.v. vitamin C in patients screened to eliminate hyperoxaluria, glucose-6-phosphate dehydrogenase deficiency, and other medical conditions (17, 18). Additionally, a series of case reports indicated that high-dose i.v. vitamin C was associated with long-term tumor regression in three patients with advanced renal cell carcinoma, bladder carcinoma, or B-cell lymphoma (19). Clinical plausibility has been repeatedly suggested, and Chen et al. (1–3) now have convincingly demonstrated biologic plausibility and are poised to explore the potential value of “pharmacologic ascorbate in cancer treatment” in humans. 

FOOTNOTES 

The authors declare no conflict of interest. See companion article on page 11105. 

REFERENCES 

1. Chen Q, et al. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Proc Natl Acad Sci USA. 2008;105:11105–11109. [PMC free article] [PubMed] 

2. Chen Q, et al. Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a pro-drug to deliver hydrogen peroxide to tissues. Proc Natl Acad Sci USA. 2005;102:13604–13609. [PMC free article] [PubMed] 

3. Chen Q, et al. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. Proc Natl Acad Sci USA. 2007;104:8749–8754. [PMC free article] [PubMed] 

4. Padayatty SJ, et al. Vitamin C pharmacokinetics: Implications for oral and intravenous use. Ann Intern Med. 2004;140:533–537. [PubMed] 

5. Carr A, Frei B. Does vitamin C act as a pro-oxidant under physiological conditions? FASEB J. 1999;13:1007–1024. [PubMed] 

6. Englard S, Seifter S. The biochemical functions of ascorbic acid. Annu Rev Nutr. 1986;6:365–406. [PubMed] 

7. Oberley TD, Oberley LW. Antioxidant enzyme levels in cancer. Histol Histopathol. 1997;12:525–535. [PubMed] 

8. Davies KJ. The broad spectrum of responses to oxidants in proliferating cells: A new paradigm for oxidative stress. IUBMB Life. 1999;48:41–47. [PubMed] 

9. Frei B, Yamamoto Y, Niclas D, Ames BN. Evaluation of an isoluminol chemiluminescence assay for the detection of hydroperoxides in human blood plasma. Anal Biochem. 1988;175:120–130. [PubMed] 

10. Cameron E, Pauling L. Ascorbic acid and the glycosaminoglycans. Oncology. 1973;27:181–192. [PubMed] 

11. Cameron E, Campbell A. The orthomolecular treatment of cancer. II. Clinical trial of high-dose ascorbic acid supplements in advanced human cancer. Chem-Biol Interact. 1974;9:285–315. [PubMed] 

12. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA. 1976;73:3685–3689. [PMC free article] [PubMed] 

13. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA. 1978;75:4538–4542. [PMC free article] [PubMed] 

14. Creagan ET, et al. Failure of high-dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer. A controlled trial. N Engl J Med. 1979;301:687–690. [PubMed] 

15. Moertel CG, et al. High-dose vitamin C versus placebo in the treatment of patients with advanced cancer who have had no prior chemotherapy: A randomized double-blind comparison. N Engl J Med. 1985;312:137–141. [PubMed] 

16. Kimoto E, Tanaka H, Gyotoku J, Morishige F, Pauling L. Enhancement of antitumor activity of ascorbate against Ehrlich ascites tumor cells by the copper:glycylglycylhistidine complex. Cancer Res. 1983;43:824–828. [PubMed] 

17. Riordan HD, et al. A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR Health Sci J. 2005;24:269–276. 

18. Hoffer LJ, et al. Phase I clinical trial of i.v. ascorbic acid in advanced malignancy. Ann Oncol. 2008 doi: 10.1093/annonc/mdn 377. [Cross Ref] 

19. Padayatty SJ, et al. Intravenously administered vitamin C as cancer therapy: Three cases. Can Med Assoc J. 2006;174:937–942. [PMC free article] [PubMed]

Source: Frei, Balz. Lawson, Stephen. Linus Pauling Institute, Oregon State University, Corvallis, OR 97331. Proc Natl Acad Sci U S A. 2008 August 12; 105(32): 11037–11038. Published online 2008 August 5. doi: 10.1073/pnas.0806433105. 

Tags:  cancer  vitamin C 

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Tumeric and Alzheimer's Disease

Posted By Administration, Monday, August 23, 2010
Updated: Friday, April 18, 2014

by Holly Lucille, ND, RN 1481271856_d1046f2f35_b  

In India, Alzheimer's disease is relatively uncommon. People over the age of 65 living in certain rural areas of India have a less than 1 percent (0.84%) chance of developing the disease. In the larger cities and rural areas of India, the risk is just 2.4 percent.(1,2)

Compare these findings to people over the age of 65 living in the United States. Again, depending on where we are living, our chances of developing Alzheimer's disease range from a little under 5 percent to an astonishing 17 percent.(3,4)

So what are people who are living in India doing that we aren't doing here in the US to account for these dramatic differences? The answer seems to be curry, that zesty spice and staple of Indian foods. Research has shown that a compound in curry not only prevents changes in the brain that lead to Alzheimer's disease, it actually reverses some of the damage already present.(5)

  • How can curry prevent these changes in the brain? Isn't that a lot to expect from a spice?
Evidently, it's not too much to expect from this spice. Curry comes from the turmeric plant - Curcuma longa is the plant's official name. Curcumin, a plant compound in turmeric, is the source of curry's instantly recognizable bright yellow pigment. When it comes to the scientific research of Curcuma longa, the terms curcumin and turmeric are both used. Both refer to the same thing - turmeric extract.(6)

There have been more than 1300 studies on turmeric and its health benefits for humans. Research has shown turmeric is able to help the body get rid of cancer-causing toxins. Turmeric also blocks estrogen receptors and enzymes that promote cancer. And it's been found to stop the growth of new blood vessels in cancerous tumors - an important factor in keeping cancer from getting larger and spreading throughout the body.(7-9)

But one of turmeric's most exciting health benefits is its ability to reduce, prevent, and stop inflammation. While inflammation is a normal and needed response to injury or disease, chronic inflammation can cause damage to tissues. And researchers are now finding inflammation plays a huge role in Alzheimer's disease.

 


  • I've always heard that Alzheimer's disease was caused by complex growths in the brain called plaques and tangles. How can simple inflammation cause such a devastating disease?

You are right. Plaques and tangles are indeed the hallmarks of Alzheimer's disease. But researchers looking at the brain damage caused by Alzheimer's have always noted the presence of inflammation wherever plaques and tangles form.(10) In the past, this inflammation was thought to be simply a consequence of Alzheimer's disease. Now scientists believe the inflammation itself starts a chain reaction ultimately contributing to the development of Alzheimer's disease.(11)

When cells in the brain are disrupted by inflammation, amyloid, a protein normally found in the brain, begins to act chaotically. This chaos results in the creation of beta-amyloid, a protein that is toxic to cells in the brain. Sticky deposits of beta-amyloid build up and collect around the cells, making dense clumps or plaques. Because the brain can't break the plaques down or get rid of them, they stay right where they are and slowly accumulate.(10,12,13)

Tangles result when long protein fibers that act like scaffolding for brain cells begin to twist and tangle. The cell is damaged and eventually dies. But the tangled proteins remain in the brain even after the dead neuron has been cleared away.(10,14) And inflammation might be the culprit causing the long protein fibers to start tangling.(15)

The consequence of these abnormalities of protein in the brain is more than the cell death they cause. They also act as roadblocks, interfering with electrochemcial messengers being shot from cell to cell. Therefore, the remaining healthy cells’ activity is diminished as well.

Research of identical twins has repeatedly shown that if one twin has Alzheimer's disease, the other has a 60% chance of developing the disease, too. Scientists from the Karolinska Institute in Stockholm, Sweden, looked at information from 20,000 twins collected in the 1960s and found 109 pairs of siblings where only one twin had been diagnosed with Alzheimer's. When the Swedish researchers analyzed data about the twins' health, they found the twin with Alzheimer's disease almost always had chronic gum disease. While bleeding gums are definitely not the cause of Alzheimer's disease, the inflammation that plays a large part of chronic gum disease may signal an inflammatory process stuck in overdrive.(16)

In fact, the inflammatory process might occur years before the onset of Alzheimer's, and be the result of any number of infections people can contract. That's why current research is searching for ways to protect brain cells from inflammation. And why some countries have low rates of Alzheimer's disease, like India.

  • Why curry? Couldn't other lifestyle differences account for the low rates of Alzheimer's disease in India?

That's a good question. When researchers begin studying a disease, like Alzheimer's, they look for trends to help them determine how and why the disease occurs. For example, we all now know the connection between cigarette smoking and lung cancer. But, it wasn't until the 1930's that doctors noticed the trend for cigarette smokers to have more lung cancer than people who didn't smoke.(17)

So it has been with researchers studying Alzheimer's disease. They know Alzheimer's disease has an important connection to inflammation. They also know turmeric reduces inflammation. And when researchers noticed these trends - that people in India eat high amounts of curry from turmeric and have very little Alzheimer's disease - they began to theorize that turmeric might be able to prevent or even treat the illness. And the research they designed around these trends has unequivocally found turmeric to be one common denominator.(18-21)

  • What have the turmeric studies shown so far?

Simply amazing findings are coming from curry research. Not only does turmeric slow down cancer growth, it's also been found to correct the cystic fibrosis defect in mice, help prevent the onset of alcoholic liver disease, and may slow down other serious brain diseases like multiple sclerosis.(22)

Researchers from the University of California Los Angeles (UCLA) studying turmeric have found it to be more effective than the drugs currently being investigated for Alzheimer's disease treatment and prevention. The researchers have discovered the actual structure and shape of turmeric allows it to penetrate the blood-brain barrier effectively and bind to beta amyloid.(23) Other research findings shows turmeric helps remove beta-amyloid that's already built up in the neurons.(24) Turmeric helps maintain healthy brain cellular metabolism, helps the cells repair themselves, and keeps the cells connected to each other.(25,26) In other words, turmeric helps brain cells stay healthy.

And now the UCLA Alzheimer's Disease Research Center (ADRC) is using turmeric in clinical trials and studying the effect of this powerful spice in patients diagnosed with this devastating disease. Clinical trials are the gold standard of medical research. But it's rare in Alzheimer's disease. And it's even more rare when all-natural herbs and spices like turmeric are used in hopes that positive benefits will be discovered. The head of UCLA's research team was recently interviewed and stated that setting out to hopefully prove turmeric's ability to prevent and treat Alzheimer's disease was “tremendously exciting.”(27)

  • I recently read that one of the nonsteroidal anti-inflammatory drugs (NSAID) was found to prevent Alzheimer's disease. Is this true?
Scientists recently studied ibuprofen, one of the NSAIDs investigated for Alzheimer's Disease Prevention.(28) Ibuprofen belongs to a family of drugs that includes naproxen, indomethacin, nabumetone, and several others. These drugs are used most often to get rid of headaches, mild arthritis, and other kinds of pain and inflammation.(29) In the studies, the average dose of ibuprofen was 800mg a day. Patients took the product for two years. While the results suggested that ibuprofen might reduce the risk of developing Alzheimer's, ibuprofen's side effects are too harmful to be a valid lifelong prevention aid treatment.(28) Ibuprofen, like other NSAIDs, can cause gastrointestinal bleeding when used at high dosages over a long period of time. Long term use of ibuprofen can also lead to analgesic nephropathy, a kind of kidney damage caused by NSAIDs.(29)

As we discussed earlier, turmeric appears to block and break up brain plaques that cause the disease and helps reverse some of the damage already present.(19,21,26) Ibuprofen does not provide any protection against free radical damage. No anti-inflammatory medicine can do this.(29)

  • If I eat curry will I be protected against Alzheimer's disease? There aren't many foods or recipes I make that require curry, do I need to eat it every day? And how much do I need?

If you enjoy Indian cuisine, by all means, enjoy these delicious foods. You'll benefit your brain and your appetite. But you make a good point, American meals rarely contain curry. That's why supplements that contain extracts are suddenly quite popular. In fact, there are numerous turmeric/curcumin supplements on the market today.

But like all nutritional supplements, some turmeric supplements are superior to others. You need to read their labels to make sure the turmeric extract you are buying will provide the protection you need. Look for high-potency turmeric extract from turmeric (Curcuma longa) rhizome. And make sure the extract is standardized to contain 90% curcuminoids, the active ingredient in turmeric responsible for the positive research findings.

Conclusion

Researchers once thought that preventing for Alzheimer's disease would elude them for decades. In fact, several scientists privately speculated the disease might never be ameliorated. They thought the origin of the disease was too complex and the symptoms of the disease were too profound. That's why the ongoing research on turmeric is so exciting. A safe, natural, and effective way to protect against Alzheimer's disease almost seems too good to be true. But, the nation of India and its low incidence of Alzheimer's disease are proof these are not just fluke findings - making turmeric extract a supplement to remember.

References

1. Jha S, Patel R. Some observations on the spectrum of dementia. Neurol India. 2004;52:213-4.

2. Vas CJ, Pinto C, Panikker D, et al. Prevalence of dementia in an urban Indian population. Int Psychogeriatr. 2001;13:439-50.

3. The Alzheimer's Disease Fact Sheet. Alzheimer's Disease Education & Referral Center. A service of the National Institute of Aging. Accessed on September 8, 2005. Available at: http://www.alzheimers.org/pubs/adfact.ht ml#Contents.

4. Chandra V, Pandav R, Dodge HH, et al. Incidence of Alzheimer's disease in a rural community in India: the Indo-US study. Neurology. 2001;57:985-9. 5. Ringman JM, Frautschy SA, Cole GM, Masterman DL, Cummings JL. A potential role of the curry spice curcumin in Alzheimer's disease. Curr Alzheimer Res. 2005;2:131-6.

6. Curcuma longa (turmeric). Monograph. Altern Med Rev. 2001;6 Suppl:S62-6.

7. Sharma RA, Gescher AJ, Steward WP.Curcumin: The story so far. Eur J Cancer. 2005;41:1955-68.

8. Weber WM, Hunsaker LA, Abcouwer SF, Deck LM, Vander Jagt DL. Anti-oxidant activities of curcumin and related enones.Bioorg Med Chem. 2005;13:3811-20.

9. Karunagaran D, Rashmi R, Kumar TR. Induction of apoptosis by curcumin and its implications for cancer therapy. Curr Cancer Drug Targets. 2005;5:117-

10. Curtis SM, Porth CM. Alzheimer's disease. In: Porth CM. Pathophysiology: Concepts of Altered Health States. 5th ed. Philadelphia, Pa: Lippincott; 2002: 914- 917.

11. Fryer JD, Holtzman DM. The bad seed in Alzheimer's disease. Neuron. 2005;47:167-8.

12. Kranenburg O, Bouma B, Gent YY, et al. Beta-amyloid (Abeta) causes detachment of N1E-115 neuroblastoma cells by acting as a scaffold for cell-associated plasminogen activation. Mol Cell Neurosci. 2005;28:496-508.

13. Morgan C, Colombres M, Nunez MT, Inestrosa NC. Structure and function of amyloid in Alzheimer's disease. Prog Neurobiol. 2004;74:323-49.

14. Liazoghli D, Perreault S, Micheva KD, Desjardins M, Leclerc N. Fragmentation of the Golgi apparatus induced by the overexpression of wild-type and mutant human tau forms in neurons. Am J Pathol. 2005;166:1499-514.

15. Minghetti L. Role of inflammation in neurodegenerative diseases. Curr Opin Neurol. 2005;18:315-21.

16. Andel R, Crowe M, Pedersen NL, Mortimer J, Crimmins E, Johansson B, Gatz M. Complexity of work and risk of Alzheimer's disease: a population-based study of Swedish twins. J Gerontol B Psychol Sci Soc Sci. 2005;60:P251-8.

17. Heady JA, Kennaway EL. The increase in deaths attributed to cancer of the lung. Br J Cancer. 1949;3:311-20.

18. Park SY, Kim DS. Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult: a drug discovery effort against Alzheimer's disease. J Nat Prod. 2002;65:1227-31.

19. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem. 2005;280:5892-901.

20. Ono K, Hirohata M, Yamada M. Ferulic acid destabilizes preformed beta-amyloid fibrils in vitro. Biochem Biophys Res Commun. 2005;336:444-449.

21. Ono K, Hasegawa K, Naiki H, Yamada M. Curcumin has potent anti-amyloidogenic effects for Alzheimer's beta-amyloid fibrils in vitro. J Neurosci Res. 2004;75:742-50.

22. Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 2004;1030:434-41.

23. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem. 2005;280:5892-901.

24. Giri RK, Rajagopal V, Kalra VK. Curcumin, the active constituent of turmeric, inhibits amyloid peptide-induced cytochemokine gene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor. J Neurochem. 2004;91:1199-210.

25. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci. 2001;21:8370-7.

26. Cole GM, Morihara T, Lim GP, Yang F, Begum A, Frautschy SA. NSAID and Antioxidant Prevention of Alzheimer's Disease: Lessons from In Vitro and Animal Models. Ann N Y Acad Sci. 2004;1035:68-84.

27. The Univerity of California at Los Angeles (UCLA) Alzheimer's Disease Research Center (ADRC) Current studies: Mild to Moderate Alzheimer's Disease and Curcumin. Information available at the ADRC Website: http://www.npistat.com/adrc/Treatment. asp.

28. Pasinetti GM. From epidemiology to therapeutic trials with anti-inflammatory drugs in Alzheimer's disease: the role of NSAIDs and cyclooxygenase in betaamyloidosis and clinical dementia. J Alzheimers Dis. 2002;4:435-45.

29. What You Need to Know About Nonsteroidal Anti-Inflammatory Medications (NSAIDs). The Cleveland Clinic Health Information Center. Accessed on September 8, 2005. Available at: http://www.clevelandclinic.org/health/h ealthinfo/ docs/0700/0714.asp?index=4901.

Tags:  alzheimer's  tumeric 

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Is Your Medication Robbing You of Nutrients?

Posted By Administration, Friday, August 20, 2010
Updated: Friday, April 18, 2014

by Hyla Cass, MD 3308079338_c8c107bc7f_b   

 

A little known but potentially life-saving fact is that common medications deplete vital nutrients essential to your health. Here's a practical guide to avoid drug-induced nutrient depletion, and even replace your medications with natural supplements.

 

We have been called a pill-popping society, and statistics bear this out. Nearly 50 percent of American adults take at least one prescription drug, and 20 percent take three or more. In a survey(1), more than half of those over 65 and 30 percent of people 45 to 65 used at least three prescription drugs in a one-month period. With our increasing reliance on medications comes nutrient depletion, a problem we can't ignore. Every medication, including over-the-counter drugs, will drain the body of specific nutrients. On top of this, most Americans are already suffering from nutrient depletion. In fact, many of the conditions we see in everyday practice may actually be related to this deficiency.

The good news is that with the right supplements, you can avoid depletion side effects, and even better, you may be able to control and prevent chronic diseases, such as diabetes, cardiovascular disease and osteoporosis.

 


A Common Scenario

I have seen case after case of patients who have experienced nutrient loss from taking prescribed medications. Too often, neither the patients nor their doctors were aware that the cause of symptoms was the medications themselves.

For example, a 57-year-old retired schoolteacher, Kathy, was being treated by her internist with three medications: the thiazide diuretic, Diuril, for high blood pressure; Fosamax for osteoporosis; and the beta-blocker, Tenormin, for heart palpitations.

She was referred to me, an integrative psychiatrist, because she suffered from fatigue, anxiety, depression and insomnia. I couldn't find an obvious psychological explanation for these symptoms, except perhaps for the stress of her physical illnesses.

The likeliest cause of her symptoms was the drugs themselves. So, rather than adding an antidepressant, an anti-anxiety pill or sleeping agent, I checked the known nutrient depletions associated with these medications. Lab results confirmed that Kathy was deficient in three essential minerals: magnesium, potassium and zinc.

Any one of her three medications could deplete potassium and magnesium, causing arrhythmias, hypertension, fatigue and depression. The diuretic also could be depleting zinc. Her internist agreed that he would continue to oversee her medications while I supervised her nutritional regimen.

Daily doses of magnesium, zinc and potassium, in addition to a high-potency multivitamin, resolved Kathy's "psychiatric" symptoms. Once her mineral levels were restored, her energy and mood were back to normal. She was not only spared the burden of an additional medication, but was able to lower the doses of the three she was taking.

I see cases similar to Kathy's more frequently than I'd like. Physicians will often tell these patients that their symptoms are "part of the illness" or "just signs that they're getting older." They then prescribe an additional drug or two for the side effects, further compounding the problem.

To understand the role of medications in nutrient depletion, we must first understand the variety of nutrient-depleting mechanisms in pharmacy.

Many drugs, such as the stimulants Ritalin (methylphenidate) and Adderall, are prescribed for attention deficit disorder. These can reduce appetite. This, in turn, decreases the intake of beneficial nutrients. Some antidepressants also tend to have this appetite-reducing effect.

On the flip side, a drug can reduce nutritional status by increasing the desire for unhealthy foods, such as refined carbohydrates. Many of the neuroleptics (antipsychotic drugs) and some antidepressants cause insulin resistance or metabolic syndrome, with resulting blood sugar swings. Patients then crave simple carbohydrates, such as sugar, bread and pasta. Steroid drugs, including those given by an inhaler, can create similar issues as well.

Certain medications reduce the absorption of nutrients. In passing through the gastrointestinal tract, drugs often bind to specific nutrients before they're absorbed into the bloodstream. The antibiotic, tetracycline, for example, can block absorption by binding with minerals such as calcium, magnesium, iron and zinc in the GI tract.

Weight loss drugs and cholesterol lowering medicines similarly bind to fats, preventing them from being absorbed. Drugs that treat acid reflux or heartburn raise the pH environment of the upper GI tract, which reduces absorption of needed vitamins and minerals. This is especially problematic among the elderly, who often are already low in stomach acid.

Nutrients are essential to the metabolic activities of every cell in the body. They're used up in the process and need to be replaced by new nutrients in food or supplements. Some drugs deplete nutrients by speeding up this metabolic rate. These drugs include antibiotics (including penicillin and gentamicin) and steroids, such as prednisone and the gout medication, colchicine.

Other drugs block the nutrients' effects or production at the cellular level. In addition to the intended effect on enzymes or receptors, medications can influence enzymes or receptors that help process essential nutrients. For example, widely prescribed statin drugs block the activity of HMG-CoA, an enzyme that's required to manufacture cholesterol in the body. This action also depletes the body of coenzyme Q10, which requires HMG-CoA for its production. This has a serious negative impact on muscle and heart health.

Drugs also can increase the loss of nutrients through the urinary system. Any drug that does this can drain the body's levels of water-soluble nutrients, including B vitamins and minerals, such as magnesium and potassium. The major offenders are medications to treat hypertension, particularly the diuretics that reduce blood pressure by increasing the volume of water flushed out of the body.

Drug-induced nutrient depletion is far more common than we think. In evaluating patients' symptoms, doctors must assess whether symptoms are due to the illness, to side effects of the drugs or to drug-induced nutrient depletion. Considering the inadequate nutrition of most people, we must remember that the illness itself may be due, in part, to nutrient deficiency. To cover all bases, it is easiest to provide baseline coverage: a daily high potency multivitamin mineral formula, CoQ10 (200 mg), omega-3 fatty acids (2 grams) and additional vitamin D and probiotics, especially if you've taken antibiotics.

The bottom line: As physicians, we must look more deeply and determine underlying causes to determine whether drugs are harming patients, and what we can do to reverse these effects. As a consumer, be aware of these drug-nutrient depletions, and do what you can to avoid taking medications whenever you can, using natural products instead.

1. Centers for Disease Control and Statistics. Health United States 2006. Accessed via www.cdc.gov/nchs/data/hus/hus06.pdf#093.

Tags:  side effects 

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Was Your Child Mislabed with ADHD?

Posted By Administration, Wednesday, August 18, 2010
Updated: Friday, April 18, 2014

by Gina Nick, NMD, PhD

4355506063_4105c0c877_oA new study released by Michigan State University found that nearly 1 million children have been misdiagnosed with attention deficit hyperactivity disorder (ADHD).  The reason, the study found, was that kids who are youngest in their grades have a 60% greater chance of being diagnosed with ADHD. Nothing to do with brain chemistry, or the genuine need for medications.  Simply due to their age. The details of this study were just published in USA Today.

 

There are beneficial naturopathic treatments for those labeled with ADHD. The beauty of Naturopathic Medicine is that doctors are treating the individual. Even if your child was diagnosed with ADHD,  a licensed Naturopathic Medical Doctor will work on the underlying cause of the behavioral challenges and not simply treat the label your child was given by writing a script for Ritalin or other popular ADHD medication.  This individualized treatment helps to prevent misdiagnosis and unnecessary treatments with unknown long-term effects to a child’s developing brain and nervous system. Let’s focus on what is in the best interest of the children, now and in the future.  Finding a doctor who takes the time to get to know your child, run appropriate lab tests to pinpoint the imbalances, and is focused on addressing the underlying cause of your child’s behavioral challenges is a reasonable place to start.

Tags:  ADD/ADHD  ADHD/ADD 

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Hair Supply - Here Today, Gone Tomorrow

Posted By Administration, Friday, August 13, 2010
Updated: Friday, April 18, 2014

by Joel Lopez, MD, CNS 4336272863_3653acf839_b  

Why is it that we’re seeing younger people getting hair loss at such an early age? Is it just a genetic issue or does it have to do with environmental factors as well? I believe that it’s due to both. Genetic causes of chronic degenerative disease is only about 3-4%, compared to greater than 90% due to environmental causes.

There’s a lot we can do to prevent or even reverse hair loss. We have to know the factors that lead to this condition. One, there’s the issue of poor circulation. Our hair needs to be nourished. Poor circulation means less nutrients going to the hair follicles. What causes poor circulation? Dietary factors such as intake of trans-fats or hydrogenated oils as well as calcium build-up along the arterial lining can do that. Poor nutrition also leads to hair loss. Where do you think our hair comes from? It comes from our food. Hair is primarily protein. Therefore, an adequate intake of amino acids should lead to a full head of hair. But, it’s not just that. An adequate amount of certain vitamins, minerals and glycosaminoglycans are also needed for healthy hair. Nutritious food should contain adequate nutrients. However, this is not always true because certain produce, esp. ones that are produced through commercial, chemical farming are nutritionally deficient. Produce farmed bio-dynamically and not just organically, should contain adequate amounts of nutrients to help our body renew itself (and that includes the hair).

What about personal products that damage the hair or hair follicles? There’s a substance in hair gels or products that could actually clog the hair follicles and cause them to ultimately die. The one implicated the most is a chemical called PVP coplymer, a petrochemical product. Avoid this at all costs. There are other chemicals that could cause damage to cells in general such as pthalates and sodium lauryl/laureth sulfate. Just notice how more companies are touting that they don’t contain these products.

Another cause of hair loss is hormonal imbalance. Undiagnosed thyroid issues could cause hair loss. A testosterone metabolite called DHT could cause hair loss, thus the popularity of synthetic DHT blockers such as Propecia or Avodart. A more natural way to influence testosterone metabolism is through the use of zinc supplements (which by the way is a very common nutritional deficiency). Other natural DHT blockers include saw palmetto, lycopene (from tomatoes), pygeum and stinging nettle. Low testosterone levels in men as well as low estrogen levels in women could also lead to hair loss. Isolated HGH deficiency could cause regeneration and repair to slow down as we age. That means, less production of new tissue, including our hair.

What do you do to improve HGH levels? Besides exercise, there are amino acids that stimulate HGH release from the pituitary. The most effective one for people over the age of 40 is L-glutamine. Goji berries has been used in Traditional Chinese Medicine to stimulate HGH release from the pituitary. Otherwise, a peptide called HGHRH (analogue) could also be used. I found this as effective as HGH, with less side effects.

What are other natural remedies that could stimulate hair growth? An Ayurvedic treatment includes the use of neem hair oil. Traditional Chinese medicine may recommend fo-ti pr he she wou. Essential oils that stimulate hair growth include therapeutic-grade peppermint, cedarwood, rosemary, lavender, thyme and sandalwood. Minoxidil works for some people but it does work better combined with substances such as retin-A, aldactone, progesterone, azelaic acid, copper peptides, SOD, and copper-zinc binding peptides.

Procedures one should consider before the last resort (hair transplant) include the use of low level laser therapy and the use of a micro-dermaroller. Consult with your holistic health care practitioner before incorporating any of the above suggestions.

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Resveratrol for Polycystic Ovarian Syndrome

Posted By Administration, Thursday, August 12, 2010
Updated: Friday, April 18, 2014

by Fiona McCulloch, ND 

3944981634_216f370e16Polycystic ovarian syndrome is a complex condition involving multiple hormonal components.  Treatment of this disease therefore must be multifold:   low glycemic index diets, exercise, therapies to reduce excessive tissue androgens and estrogens, enhancement of insulin resistance and antioxidant status, and improvement of luteal phase health and progesterone balance. In this article I will discuss one newly studied therapy for PCOS : resveratrol.  It can greatly effect the health of the ovary in PCOS and can be an excellent addition to an overall protocol for the treatment of this condition.

Different women will present with different symptoms, degrees, and signs of PCOS, and each woman will require very customized treatment.  In women with PCOS  and especially in those who have enlarged ovaries or multiple cysts in the ovaries, the theca-interstitial cells of the ovary are especially prone to growing excessively.   These cells do not undergo the normal cycle which allows the cells to die off and get replaced by new cells (known as apoptosis) .

The theca interstitial cells of the ovary are responsible for producing male hormones which are normally required for healthy ovarian function.  However in PCOS , the large amount of these cells causes a large amount of male hormones to be produced,  causing problems with normal ovulation.  This often results in delays in ovulation (and therefore in menstruation)  or lack of ovulatory cycling altogether in more severe cases.   These hormonal changes also greatly reduce egg quality and health.

There are two causes for the excessive overgrowth of these theca interstitial cells of the ovary  1) high levels of oxidative stress and 2) high levels of insulin in the local tissues. Both of these factors play a great role in the pathology of polycystic ovarian syndrome.

A new study just released in April 2010 indicates that resveratrol (a antioxidant compound found in grapes) has powerful benefits in this type of condition.  Although other forms of grape antioxidants have long been used to treat infertility, it is the oligomeric proanthocyanadin (also known as OPC) component that has been traditionally used.  The effect of resveratrol however is different from the effects of OPCs, which are both antioxidants and pro circulatory compounds.   Resveratrol does reduce oxidative stress like many other types of antioxidants,  but importantly, it is also an antiproliferative compound which is well known to reduce growth of and  induce cell death in cancer cells (another form of cell which proliferates excessively and out of bounds of healthy control).

This study, completed by the University of California School of Medicine, Department of Gynecology and Obstetrics, investigated the effect of resveratrol on the theca interstitial ovarian cells of rats.    The cells were cultured with and without resveratrol and/or insulin.  This was done in order to gauge the effect of resveratrol on these abnormally growing cells without other factors, and also in the presence of insulin, a factor which is high in patients with PCOS and which is known to further stimulate unhealthy cellular growth.

The results showed that the ovarian cells cultured in resveratrol alone showed a potent, concentration dependent decrease in the abnormal growth of cells.  In the ovarian cells cultured with both resveratrol and insulin (mimicking the common conditions of PCOS) it was found that the resveratrol was able to counter the negative effects of the insulin on the ovarian cells and allow them to undergo the normal cell death process required for healthy ovarian function.

This versatile and powerful compound found in grapes may be a promising new treatment for PCOS (this disease coincidentally, often causes a ” bunch of grapes ” appearance of the ovaries when examined by ultrasound, due to the large number of cysts or accumulated follicles).  Resveratrol may prove to be a very effective part of multi faceted protocols to enhance ovarian health and restore normal ovarian hormone production for the millions of women worldwide with PCOS.

References

Effects of resveratrol on proliferation and apoptosis in rat ovarian theca-interstitial cells.
Wong DH, Villanueva JA, Cress AB, Duleba AJ.
Mol Hum Reprod. 2010 Apr;16(4):251-9.

 

Effects of insulin and insulin-like growth factors on proliferation of rat ovarian theca-interstitial cells.
Duleba AJ, Spaczynski RZ, Olive DL, Behrman HR.
Biol Reprod. 1997 Apr;56(4):891-7.

Cytotoxic Effect of Wine Polyphenolic Extracts and Resveratrol Against Human Carcinoma Cells and Normal Peripheral Blood Mononuclear Cells.
Matić I, Zižak Z, Simonović M, Simonović B, Gođevac D, Savikin K, Juranić Z.
J Med Food. 2010 May 18.

Proliferation of ovarian theca-interstitial cells is modulated by antioxidants and oxidative stress.
Duleba AJ, Foyouzi N, Karaca M, Pehlivan T, Kwintkiewicz J, Behrman HR. Hum Reprod. 2004 Jul;19(7):1519-24.

Tags:  polycystic ovarian syndrome  resveratrol 

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Staying Ahead of the Curve on Parkinson's Disease

Posted By Administration, Monday, August 9, 2010
Updated: Friday, April 18, 2014

by Zina Kroner, DO 4090198486_ef681509fb_o   

More recently, doctors are being urged to treat dementia more aggressively in Parkinson's patients, as it would optimize quality of life for the patients and their caregivers. It is established that one third of patients with Parkinson’s disease experience dementia. Cognitive impairments are the hallmark features, including decreased attention span, executive functioning and memory deficits. Obtaining a legitimate diagnosis of dementia can be quite tricky in that symptoms may widely fluctuate and therefore the diagnostic instruments that physicians use to diagnose Parkinson’s dementia may not always give reliable results.  Research is conflicting at this point as to which is the best medical agent to use in this population. 

 

Optimize Diet 

There are multiple safe nutritionally oriented treatments that patients may engage in to help prevent early onset dementia as it is related to Parkinson’s disease.  First and foremost, optimization of diet is critical. There is much research to suggest that a diet that is high on the glycemic index scale can exacerbate dementia.  Insulin resistance, associated with a diet that is chronically high on the glycemic index, has been associated with Alzheimer’s disease. The connection has been labeled type 3 diabetes by some. (See my published article under the References section of my website on this topic).

Low Glycemic Index, No Pesticides, No MSG 3013741860_ab25d8ce03_z  

Eating organic, MSG and pesticide free foods that can exacerbate both Parkinson’s as well as dementia is important.  Remember that MSG can trigger glutamate receptors in Parkinson’s and non-Parkinson’s patients alike.  Following a Mediterranean style diet that is high in unheated extra virgin olive oil, fish and poultry, nuts, vegetables, low glycemic index fruits, whole grains that are gluten free and unprocessed foods is key.   

Just Do It

 

3218300813_2a10d6453c_bAdding a daily exercise component is imperative. Exercise can trigger dopamine levels to rise, help with coordination, drive down cortisol, improve insulin resistance, and help with mental acuity. These are all essential when hoping to help prevent dementia and improve Parkinson’s symptoms. Exercise should include weight bearing exercise as well as core bodywork.

 

DHEA 

The adrenal hormone DHEA has been shown to boost dopamine levels. There is also a significant amount of research pointing to DHEA helping with improvement in memory in dementia patients. DHEA is ever present in brain tissue and helps to offset the negative effects of cortisol.  It is, however, a precursor to many of the other hormones and needs to be used judiciously and under medical supervision. 

Follow an Anti-Inflammatory Program

Low grade chronic inflammation may be a precursor to neurodegenerative disease. An excellent anti-inflammatory program, including diet and supplements may help to quiet the inflammation down. 

Polyphenols, excellent antioxidants found in green tea, have recently been studied to see if they modify the course of Parkinson’s.  The Chinese study enrolled 410 untreated people with Parkinson’s disease and were randomized to receive 0.4g, 0.8g, or 1.2 g of green tea polyphenols daily. As a reference, 2 cups of green tea contain approximately 300mg of polyphenols.  At 6 months a significant improvement was noted in each dosage category based on the Unified Parkinson's Disease Rating Scale. At 12 months, however, unexplainably, the scores did not differ from placebo. Improvements were more profound for those with a greater severity of disease.  There were no notable side effects except for insomnia for those not accustomed to green tea intake. 

The reduction of oxidative stress on neurologic tissue in Parkinson’s as well as dementia patients is important.  Utilization of polyphenols, vitamin C, tocotrienols, bioflavanoids, proanthocyandins from grape seed extract, coenzymeQ10, and curcumin may have a beneficial effect.   

Tags:  parkinson's disease 

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Statins' Laundry List

Posted By Administration, Sunday, August 8, 2010
Updated: Friday, April 18, 2014

by Zina Kroner, DO

4700292186_7114d6584f_o (1)According to a recent study not funded by a pharmaceutical company, in the journal Lancet, use of statins (Lipitor, zocor, etc) is associated with a small risk of developing diabetes.  When looking at 90,000 subjects in this meta-analysis, it was found that there was a 9% increase in diabetes risk as compared to controls. This association was of greater significance with increasing age. 

How does this affect you, statistically speaking?  

Well, for every 255 patients treated with a statin medication for four years, there is the potential, according to the authors of this study, to produce one additional case of diabetes.

Add it to the Laundry List

This is yet another adverse effect added to statins’ already long list of side-effects.  It means that physicians as well as patients have to be cognizant of this fact and monitor for signs and symptoms of glucose imbalance on a regular basis.  

Remember that statin drugs are effective at reducing overall cardiovascular risk, so cardiologists will argue that the benefits of statins far outweigh the risks.  From a conventional standpoint, it is, therefore, not recommended to change the existing indications for statin therapy in the setting of cardiovascular risk prevention.  

Tags:  statin 

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Overcoming Pre-Menstrual Syndrome Naturally

Posted By Administration, Tuesday, July 27, 2010
Updated: Friday, April 18, 2014

3631665064_c3604847b5_oby Hyla Cass, MD

 

Our mothers once called them "women's problems." Now we know that these mood swings and physical changes, from PMS to menopause, are all part of a delicate balance among our various hormones. In my years of practicing integrative medicine, I have helped hundreds of women overcome PMS and menopausal symptoms naturally, and here's how.

Let's start by defining hormones. They are chemical messengers secreted by any one of the body's endocrine (ductless) glands. They travel through the bloodstream, telling various systems what to do. Besides reproductive functions, hormones affect virtually every body system from digestion to metabolism to hair growth.

All women have the same hormones but in varying quantities, making your own hormonal profile as unique as your fingerprint. When your hormones are in harmony, you will have predictable menstrual cycles --and moods. When out of balance, you will have irregular cycles and a host of symptoms, from bloating, cramps, weight gain and acne to food cravings, irritability and depression. Perimenopause, the transition to menopause, which can start as early as your late 30's, often causes an increase in PMS. In fact, many women report experiencing PMS for the first time at that point. Also common in peri-menopausal women, is a loss of libido, due to a dip in testosterone which governs sexual desire, and of course, those hot flashes and night sweats, which make sex the last thing on your mind!

Medical Management

For a full picture of your hormonal status, we need to check levels of estrogen, progesterone, DHEA-S and testosterone in blood, saliva, or urine, taken on day 19-21 of the cycle. For perimenopausal women, I also order FSH (follicule stimulating hormone) and LH (luteinizing hormone) blood tests to assess ovarian function. I will check cortisol levels (saliva test) and thyroid hormones (blood test), too, since they are a part of the overall hormone symphony.

You can find home testing kits online. Take these tests on days 19-21 of your cycle, with day one being the first day of your period. If you are post-menopausal, it won't matter when you take the tests. If you're irregular, do your best to estimate the appropriate date.

Hormone Therapy

If testing reveals that your hormone levels to be below the normal range, it may be due to perimenopause or other physiological factors. Faced with fluctuating hormones, doctors have traditionally prescribed synthetic hormone replacement therapy (HRT), such as Premarin (from pregnant mares' urine) and Prempro (Premarin plus synthetic progesterone), to correct imbalances. The recent Women's Health Initiative study showed that women taking this form of HRT had 27 percent more heart attacks, a higher rate of breast cancer, 38 percent more strokes and double the number of blood clots. There are safer ways to balance hormones successfully, ranging from supplements and herbs to bio-identical hormone therapy.


Natural Ways to Balance Sex Hormones

The first step to balancing your hormones is a clean diet:

• Eat fewer animal products, with lots of vegetables, including raw broccoli and other 
cruciferous veggies 
• Reduce or eliminate caffeine, alcohol, nicotine and sugar. 
• Reduce or eliminate high-fat dairy products. 
• Eliminate as much processed food as possible
• Reduce salt intake. 
• Eat small, regular meals.

Yoga and meditation are helpful for PMS sufferers because they work on the nervous system to help balance hormones.

 


Supplements for PMS:

I give my patients magnesium (100 mg two to three times daily) and vitamin B6 (25-100 mg) to relieve irritability and tight muscles as well as premenstrual water retention.

Another important nutrient is GLA, an omega-6 fatty acid which also helps reduce the water retention, breast tenderness and moodiness associated with PMS, likely by it's action on the hormone prolactin. GLA is found in borage oil (1500 mg of borage twice daily), black currant seed or evening primrose oils.

The herb, Chasteberry (Vitus Agnus Castus), helps to balance the hormone, progesterone, relieving symptoms of PMS and heavy or irregular periods as well. Dose is 50-200 mg daily depending on symptoms.
 Do not take if you're pregnant.

The herb, Dong Quai, helps to balance the hormone estrogen. Like Vitex, the dose is 50-200 mg daily depending on symptoms and also do not take if you're pregnant.

Another useful nutrient is the amino acid, 5-HTP (5-hydroxytryptophan) 500-200 mg daily, depending on your individual needs. It helps to raise levels of the feel-good and calming brain chemical, serotonin, which is often low in PMS sufferers.

These nutrients plus wild yam a source of natural hormone production, can all be found in the formulation, PMS Balance. I have had many women report almost immediate relief upon taking this or a similar formula. Others may take a month or two to feel the full effects.

With menopausal symptoms, I may also add black cohosh and red clover extract. While there was a recent study that claimed that black cohosh didn't work, it was in fact, flawed, and contradicted numerous well-done studies that found it to be very effective. I have also discovered a remarkable new product called FemmePhase. Even the majority of my hard-core hot flashers have found relief with it.


Bio-identical Hormones

When the nutrients aren't quite doing the job, you can add over-the-counter natural progesterone cream (up to 30 mg daily) for one week prior to your period. This is a maximum of 3 percent progesterone, or 30 mg per 1 gram dose.

I may also prescribe higher dose bio-identical hormones for my patients. The progesterone is often 10 percent, which is three times as strong as the over-the counter dose. Made from highly purified derivatives of soy and wild yams, these formulas are carbon copies of your own natural hormones. Prescription strength bio-identical hormones are available only from compounding pharmacies, and are prescribed by your doctor. Doses are based on your individual hormonal needs as determined by your lab tests.

As I say repeatedly - "you don't have to live with PMS/peri-menopausal symptoms." This applies to both the woman herself and her long-suffering loved ones. This information should help you take care of most cases of PMS and peri-menopausal symptoms. I have many grateful women, and their partners, for whom PMS has truly become a thing of the past.

Tags:  fertility  Infertility  menstrual 

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Best Alternatives to Statins for Treating Hyperlipidemia

Posted By Administration, Friday, July 23, 2010
Updated: Friday, April 18, 2014

Clinical Question

When statin therapy is not tolerated, what are the best alternative treatments for patients with hyperlipidemia?

Evidence-Based Answer

Most alternatives to statin therapy reduce cholesterol levels but do not consistently demonstrate a reduction in cardiac-related and all-cause mortality in patients with or without coronary heart disease (CHD). Fibrates and niacin decrease the risk of major coronary events; however, no statistically significant reductions in mortality have been shown. (Strength of Recommendation [SOR]: A, based on systematic review of randomized controlled trials [RCTs]).

Resins decrease cardiovascular mortality but not total mortality. (SOR: A, based on review of RCTs).

The effects of ezetimibe (Zetia) on cardiovascular outcomes and mortality are unknown. (SOR: C, based on a single RCT with disease-oriented evidence).

Omega-3 fatty acid supplementation does not clearly demonstrate reductions in mortality. (SOR: A, based on two meta-analyses of RCTs).

There is insufficient evidence to recommend the use of herbal therapy for the treatment of hyperlipidemia. (SOR: A, based on a systematic review of RCTs).

Evidence Summary

A literature search found one systematic review that included 97 RCTs comparing different classes of antilipidemic therapies.1 Other studies focused on specific therapies and included one high-quality systematic review of 12 RCTs, 22 prospective cohort studies, four case reports, and one cross-sectional study evaluating cardiovascular outcomes for omega-3 fatty acid supplementation; one systematic review of 27 RCTs on garlic; and one systematic review of 25 limited-quality RCTs of 11 herbal products.24 Additional studies included a systematic review of 48 RCTs and 41 cohort studies evaluating the effect of omega-3 fatty acid supplementation on mortality, cardiovascular disease, and cancer; a subsequent Cochrane review that addressed omega-3 fatty acid supplementation for the prevention and treatment of cardiovascular disease; and a meta-analysis of 53 RCTs evaluating fibrates and 30 RCTs evaluating niacin therapy.57

FIBRATES

A meta-analysis of medications that increase high-density lipoprotein (HDL) cholesterol levels included eight RCTs evaluating the long-term clinical end points of fibrates.7 Pooled results of these studies indicate a clinically significant reduction in coronary events (number needed to treat = 33 for four years). Reductions in cardiac-related and all-cause mortality were not significant, and noncardiovascular mortality was similar in the treatment and placebo groups (relative risk [RR] = 1.10; 95% confidence interval [CI], 0.96 to 1.26). An earlier systematic review, which included the World Health Organization Cooperative Trial on primary prevention with clofibrate (not available in the United States), showed that fibrates were associated with a small but statistically significant increase in mortality (RR = 1.13; 95% CI, 1.01 to 1.27).1

NIACIN AND RESINS

Based on a meta-analysis that included a single long-term outcome study of 2,248 men treated with immediate-release niacin, cardiovascular events were reduced by 27 percent at 10-year follow-up compared with placebo; however, it should be noted that this study had a more than 70 percent drop-out rate.7

A systematic review that included two RCTs of 3,107 patients with CHD did not demonstrate a clinically significant reduction in cardiovascular mortality in those treated with niacin (RR = 0.95; 95% CI, 0.82 to 1.10).1 In this same systematic review, which included eight RCTs of resins, chole-styramine (Questran) and colestipol (Coles-tid) demonstrated significant reductions in cardiovascular death in the treatment groups (RR = 0.70; 95% CI, 0.5 to 0.99) but no significant reductions in overall mortality.1


OMEGA-3 FATTY ACIDS

A systematic review of 14 RCTs reported that omega-3 fatty acid supplementation resulted in a clinically significant reduction in overall mortality in patients with pre-existing CHD (RR = 0.77; 95% CI, 0.63 to 0.94).1 This review, however, excluded one RCT of 3,114 male patients with angina in the data synthesis. When this study was included, reduction in mortality was not statistically significant and had a wide confidence interval (RR = 0.84; 95% CI, 0.66 to 1.06). Based on a pooled estimate from a subsequent review that included this RCT, there was no significant reduction in cardiovascular events or mortality with omega-3 fatty acid treatment.5Another concern noted in this review and an associated Cochrane review was that relative risk of mortality seemed to increase with duration of treatment.5,6 Trials subgrouped by duration revealed a protective effect, with decreased deaths in trials lasting 24 to 47 months (RR = 0.84; 95% CI, 0.75 to 0.93) but a significant harmful effect in those lasting longer than 48 months (RR = 1.31; 95% CI, 1.07 to 1.59).5 This harmful effect was based on a single RCT.

An Agency for Healthcare Research and Quality (AHRQ) evidence report based on a comprehensive systematic review indicated that although some studies did show benefit with omega-3 fatty acid, there was an imbalance in the design of the studies, and data on women and the specific effects of different CHD outcomes are uncertain.2

EZETIMIBE

One RCT found that treatment with ezeti-mibe (a cholesterol absorption inhibitor) resulted in an average low-density lipoprotein (LDL) cholesterol level reduction of about 18 percent; however, its effect on important patient health outcomes (e.g., mortality) is unknown.8

GARLIC AND HERBAL MEDICATIONS

A high-quality systematic review on the effects of garlic on cardiovascular disease, which was conducted for an AHRQ evidence report, evaluted 37 studies.3 Although some modest short-term improvements in lipid measures were found, effects on cardiovascular outcomes were either not measured or not found. Thus, there is insufficient evidence to recommend use of garlic for the treatment of hyperlipidemia.3 Based on a systematic review of 25 RCTs, various herbal medications (guggul, fenugreek, red yeast rice, artichoke) may lower average total cholesterol by 10 to 33 percent; however, these studies are of poor quality overall, and an impact on mortality has not been established.4

Recommendations from Others

National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP-III) guidelines outline treatment goals in the management of hyperlipidemia with LDL cholesterol goals based on 10-year risk of CHD.9 Statins are the preferred treatment, and resins and niacin are options for add-on therapy or for treatment in patients with modest elevations of LDL cholesterol level. Fibrates have a higher risk profile and should be reserved for use in combination with statins or in patients with moderate or severe hypertriglyceridemia (triglyceride level higher than 500 mg per dL [5.65 mmol per L]). A scientific statement from the American Heart Association recommends that patients with known CHD should consume 1 g of omega-3 fatty acids containing eicosapentaenoic acid plus docosahexaenoic acid per day, preferably from oily fish.10

Clinical Commentary

Reducing morbidity and mortality is the objective of treating hyperlipidemia, and statins are the drugs that have been best proven to accomplish this. Lowering LDL cholesterol level by any other means is widely accepted as the “logical” alternative for patients who cannot tolerate statins. This approach is recommended by the NCEP ATP-III guidelines; however, the effect of this practice on mortality has not been demonstrated. Pharmaceutical companies certainly benefit from physicians' enthusiasm for “treating the numbers,” but this review should be a reminder that patients might not. It will be interesting to see if the Improved Reduction of Outcomes: Vytorin Efficacy International Trial or other trials now under way show the newest and most expensive nonstatin LDL-lowering drug to be any more beneficial than its predecessors.

When faced with a patient with hyper-lipidemia who cannot tolerate statins, it is important to take another look at the overall risk of cardiovascular disease and to inform the patient of the data (or lack thereof) regarding the expected benefits and risks of alternative treatments. The informed patient who previously decided to take statins based on the explanation of proven risk reduction may choose not to consent to take a medication with less certain benefit.

 

REFERENCES

 

 

1. Studer M, Briel M, Leimenstoll B, Glass TR, Bucher HC. Effect of different antilipidemic agents and diets on mortality: a systematic review. Arch Intern Med. 2005;165:725–30. 

2. Balk E, Chung E, Lichtenstein A, Chew P, Kupelnick B, Lawrence A, et al. Effects of omega-3 fatty acids on cardiovascular risk factors and intermediate markers of cardiovascular disease. Evid Rep Technol Assess (Summ). 2004:1–6. 

3. Mulrow C, Lawrence V, Ackerman R, Gilbert Ramirez G, Morbidoni L, Aguilar C, et al. Garlic: effects on cardiovascular risks and disease, protective effects against cancer, and clinical adverse effects. Evid Rep Technol Assess (Summ). 2000:1–4. 

4. Thompson Coon JS, Ernst E. Herbs for serum cholesterol reduction: a systematic review. J Fam Pract. 2003;52:468–78. 

5. Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ. 2006;332:752–60. 

6. Hooper L, Thompson RL, Harrison RA, Summerbell CD, Moore H, Worthington HV, et al. Omega 3 fatty acids for prevention and treatment of cardiovascular disease. Cochrane Database Syst Rev. 2004;(4):CD003177. 

7. Birjmohun RS, Hutten BA, Kastelein JJ, Stroes ES. Efficacy and safety of high-density lipoprotein cholesterol-increasing compounds: a meta-analysis of randomized controlled trials. J Am Coll Cardiol. 2005;45:185–97. 

8. Brown WV. Cholesterol absorption inhibitors: defining new options in lipid management. Clin Cardiol. 2003;26:259–64. 

9. Expert Panal on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285:2486–97. 

10. Kris-Etheron PM, Harris WS, Appel LJ, for the American Heart Association Nutrition Committee. Fish Consumption, fish oil, omega-3 fatty acids and cardiovascular disease [published correction appears in Circulation 2003;107:512]. Circulation. 2002;106:2747–57.

Source: Bouknight, Patricia, Mackler, Leslie, Heffington, Mark. Am Fam Physician. 2007 Oct 1;76(7):1027-1029.

Tags:  hyperlipidemia  statin 

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Medication Side Effects and How to Prevent Them

Posted By Administration, Thursday, July 22, 2010
Updated: Friday, April 18, 2014

227906487_17d94931a3_oby Joel Lopez, MD, CNS

Medications are essential for certain acute conditions. There are people who take medications for chronic symptoms, however. It’s all fine and well until side effects happen. That’s why, a person’s biochemical individuality should always be taken into account when a person has to take medications long-term. A regular review of your medications should be in order, taking into account that there’s less metabolism or excretion of medications as we age.

Fortunately, there are genomic tests available that could tell you instantly and reliably on the kind of pharmacological substances which are most suitable for you. It furthermore advises you which dose grants you optimized therapeutic success.

One such lab is called Genosense in Vienna, Austria. They have a genomic test called Pharmacosensor. This test examines carefully selected polymorphisms which lead to structural changes in proteins that strongly influence the speed of metabolism in a series of pharmacological substances and also account for the accelerated or reduced transformation of harmless precursors of given medication into highly efficient substances.

If a person is unable to do this test, then at least they should be aware of possible nutritional deficiencies their medications could cause and make sure to replenish them.

One such class of medications are the antacid or ulcer medications. Nutrient deficiencies in Vitamins B12, folic acid, Calcium, Iron and Zinc could occur with the following potential health problems: anemia,depression, birth defects, increased cardiovascular risk, cervical dysplasia, heart disease, cancer risk, osteoporosis, muscle weakness, hearing loss, tooth decay, hair loss, brittle nails, loss of sense of taste or smell, and sexual dysfunction.

Another class of meds are the cholesterol-lowering agents called “statins”. They deplete the body of Coenzyme Q10. When this happens, various cardiovascular problems, a weakened immune system and low energy could occur.

Anticonvulsants could deplete the body of Vitamins D, B1, B2, B3, B6, B12, C, Magnesium, Selenium and Zinc. Potential health issues could include osteoporosis, muscle weakness, hearing loss, tooth decay, heart and blood pressure irregularities, cervical dysplasia, anemia, hair loss, depression, dermatitis, fatigue, reduced antioxidant protection, poor wound healing and skeletal problems.

My purpose is not to alarm people who take these medications but to make them aware that an integrative approach to any medical condition yields better results. It’s a good thing that we can now check for nutritional deficiencies. One such functional test is done through Spectracell. It checks for 33 nutrient deficiencies. I love this test because it takes the guesswork out of supplementation. Better yet, most PPO’s and Medicare cover for this test.

Tags:  side effects 

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Sunburn Savvy

Posted By Administration, Friday, July 16, 2010
Updated: Friday, April 18, 2014

by Andrea Purcell, ND 3792695572_9f7455f59e_b  

Summer is finally here and so are those warm healing rays. Even on the hazy days I had multiple reports of sunburn because the direct effects of the sun are less obvious. It can be deceiving but even though we can’t see the sun the Ultraviolet light still gets through. It’s important to practice safe sun to get the Vitamin D we need without the effects of sun overdose. However if you will be out too long here are some helpful tips in choosing a safe sunscreen:

Choose ingredients such as Zinc oxide or Titanium oxide. For an entire breakdown of safe sunscreens please visit www.ewg.org, 2010 sunscreen guide.

As with everything in life moderation is essential. In case you were fooled into thinking that you could garden all day in a tank top here are a few natural health tips to make soothing the burn a little easier.

My favorite natural tools in treating sunburn involve 3 topical remedies and 3 homeopathic remedies.

In choosing a topical remedy you can select from one of the following, as it would do no good to use all three together.

1) Calendula Cream – made from an infusion of calendula flowers, it is well known for healing scrapes, repairing burned skin, and promoting healing.

2) Aloe Vera – the fresh gel from the plant or in a bottle from the health food store. Cooling & soothing to burned skin.

3) Liquid Minerals from Trace Minerals research – Apply the liquid minerals to your palm rub your palms together and rub repeatedly and deeply into the burned area. The trace minerals have a way of balancing and re-hydrating the areas of damaged skin. This can initially generate more heat and feel sharp and tingly on the skin.

The top three homeopathic remedies for burned skin are:

1) Calendula 30c – Soothing the burn and helping heal the damaged skin.

2) Cantharis 30c –Itching, burned skin, with small vesicles, scalding pain, & restlessness.

3) Apis 30c - Swollen skin, worse with hot applications, better with cold.

Dosing: 2 pellets dissolved on tongue every 2 hours over 36 hrs or until burn subsides or patient falls asleep.

My personal story: The first time I traveled to Ecuador, I was deceived by the notion that I could sit under an umbrella all day with SPF 15 and practice safe sun. Well by the time I had returned to my lodging that night I was as red as a lobster! Initially I couldn’t understand what had happened since I was technically in the shade all day but then it hit me, the Ultraviolet rays had passed right through the umbrella and had been cooking me slowly for hours. After all I was on the Equator. I promptly got out my first aid bag of natural remedies and selected Cantharis, and Apis. I promptly twisted two pellets of each out of the caps and dissolved them on my tongue, which I did every two hours until night fall. I slathered trace minerals all over the burned areas and rubbed them in deeply. Then I dressed in loose clothing and went to dinner. The next day I was still burned, less red and my skin was tight but no blisters. I continued my dosing of the remedies and the minerals for an additional 24 hours. By the third day the burn had turned into a deep tan, and I was without discomfort. Two weeks after I returned home the top layer of my skin peeled and that was it! I attribute the remedies in my kit to saving me from 2nd degree burns & blistered skin.

Tags:  skin  sun 

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Natural Solutions to Sleep Deprivation

Posted By Administration, Thursday, July 15, 2010
Updated: Friday, April 18, 2014

by Hyla Cass, MD   4521897133_8536c3ea22_b  

I'm seeing increasing numbers of patients with sleep problems, ranging from difficulty in falling asleep, to being unable to sleep soundly through the night. Rather than waking up in the morning restored and rejuvenated, they are dragging themselves out of bed, facing another day feeling drained and exhausted. (1)

As you know, disrupted sleep can exert a severe toll on your emotional and physical health, interfering with mental abilities, productivity and performance - leaving you feeling stressed, cranky, depressed and drowsy. (2) Poor sleep patterns are linked to a growing list of serious health conditions, including obesity, heart disease, Type two diabetes, and even, premature deaths in older adults.

Sleep Problems Begin in Middle Age

Sleep researchers at the University of Pittsburgh have recently shown that alterations in normal sleep patterns actually begin in middle age. (3) Studying 110 volunteers between 20 to 59 years of age, they discovered that the quality and duration of sleep changed dramatically between the mid-20s and the mid-50s, with subjects going to bed and waking up earlier. The subjects also slept less, woke up more often during the night, and experienced fewer stages of deep sleep. (4)

According to study author, Dr. Julie Carrier, "Middle age is a turning point for sleep. Some sleep patterns have already changed significantly by the time an average adult reaches age 30." Dr. Carrier observed that these changes are most likely tied to gradual age-related changes in features of the biological clock. "We need to learn where the system breaks down. If we are able to find out what is causing the biological clock to change with age, we may be able to discover ways to overcome these changes and help get these people back on track."

Restoring Natural Sleep Cycles

Given the scope of the problem it's little wonder that the number of prescriptions for sleep aids has increased dramatically. According to data from IMS Health, 56,287,000 prescriptions were written last year for sleep medications like Ambien® and Lunesta®, a seven percent rise since 2007. My choice is to avoid prescribing fast-acting sleeping pills that tend to knock patients out and leave them with a hangover in the morning. I prefer, instead, to work with natural supplements combining nutrients that work together to gently promote a state of calm, initiate and support the natural process of falling asleep, and improve the overall quality of sleep to allow you to wake up feeling refreshed, energized and restored.

I most often recommend starting with two well-established supplements -- the neurohormone, melatonin, that is commonly used to treat jet lag and aid shift workers (e.g. police officers and nurses), and the amino acid, 5-HTP, which promotes serotonin production. More details on these in Natural Highs. I then add, if needed, a selection of traditional plant extracts, such as passionflower and valerian, that promote deep, restful sleep. Another favorite of mine is L-theanine, an amino acid derived from green tea that has been shown to aid in relaxing the mind and promoting a sense of calm.

Most recently I've been very impressed with a newly available version of a traditional Chinese herbal compound, Wulinshen, available in an aptly named formula, SleepCycle, along with the above-mentioned natural sleep enhancers. Wulinshen is known to help to re-synchronize the body's biological clock and sleep rhythms. It is rich in unique "deep-sleep" nutrients that help to relax the brain and promote a sense of calm to restore restful, recuperative sleep without next-day brain fog. It also reduces the time needed to fall to sleep, and, especially after seven to eight days of use, helps you to stay asleep longer. Wulinshen contains glutamic acid, gamma-aminobutyric acid (GABA, a calming amino acid, as well as a relaxing neurotransmitter) and glutamate decarboxylase, all of which are natural tranquilizers.

Many of my patients come to me after trying all the typical prescription and natural sleep products. They report that SleepCycle works even better than expected: they now just go to bed, fall asleep, and wake up feeling refreshed. It seems to gradually and steadily restore an optimal state of balance, promoting deep, restorative, recuperative sleep cycles over time.

In summary, rather than introducing foreign chemicals that can cause a host of their own problems, my preference is always to go for the natural products that work with the body's own chemistry.

 

References

1.Stoller, MK. Economic effects of insomnia. Clin Ther . 1994;16:873-97. Development Program. State-of-the-Science Conference.

2. Knipling R, Wang J. Revised estimates of the U.S. drowsy driver crash problem size based on general estimates system case reviews. Thirty-Ninth Annual Proceedings of the Association for the Advancement of Automotive Medicine . Des Plaines, IL: Association for the Advancement of Automotive Medicine; 1995:415-466.

3. E. J. W. Van Someren. "Circadian and sleep disturbances in the elderly." Experimental Gerontology, Volume 35, Issues 9-10, December 2000, Pages 1229-1237.


4. University Of Pittsburgh Medical Center. "Deterioration Of Sleep During Middle Age Related To Changes In The Biological Clock." ScienceDaily 25 June 1998.

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Vitamin C: Intravenous Use by Complementary and Alternative Medicine Practitioners and Adverse Effects

Posted By Administration, Monday, July 12, 2010
Updated: Friday, April 18, 2014

Abstract 

Background: Anecdotal information and case reports suggest that intravenously administered vitamin C is used by Complementary and Alternate Medicine (CAM) practitioners. The scale of such use in the U.S. and associated side effects are unknown. 

Methods and Findings: We surveyed attendees at annual CAM Conferences in 2006 and 2008, and determined sales of intravenous vitamin C by major U.S. manufacturers/distributors. We also queried practitioners for side effects, compiled published cases, and analyzed FDA’s Adverse Events Database. Of 199 survey respondents (out of 550), 172 practitioners administered IV vitamin C to 11,233 patients in 2006 and 8876 patients in 2008. Average dose was 28 grams every 4 days, with 22 total treatments per patient. Estimated yearly doses used (as 25g/50ml vials) were 318,539 in 2006 and 354,647 in 2008. Manufacturers’ yearly sales were 750,000 and 855,000 vials, respectively. Common reasons for treatment included infection, cancer, and fatigue. Of 9,328 patients for whom data is available, 101 had side effects, mostly minor, including lethargy/fatigue in 59 patients, change in mental status in 21 patients and vein irritation/phlebitis in 6 patients. Publications documented serious adverse events, including 2 deaths in patients known to be at risk for IV vitamin C. Due to confounding causes, the FDA Adverse Events Database was uninformative. Total numbers of patients treated in the US with high dose vitamin C cannot be accurately estimated from this study. 

Conclusions: High dose IV vitamin C is in unexpectedly wide use by CAM practitioners. Other than the known complications of IV vitamin C in those with renal impairment or glucose 6 phosphate dehydrogenase deficiency, high dose intravenous vitamin C appears to be remarkably safe. Physicians should inquire about IV vitamin C use in patients with cancer, chronic, untreatable, or intractable conditions and be observant of unexpected harm, drug interactions,orbenefit.

 

Introduction 

Among the most enduring of alternative medical treatments, vitamin C (ascorbic acid, ascorbate) is also one of the most popular. In 2007, it was the most widely sold single vitamin, with sales of 884 million dollars in the US1 [1]. Independent of its use to treat the deficiency disease scurvy, vitamin C has been used by non- mainstream physicians orally and parenterally for more than 60 years as a therapeutic agent [2–7]. Oral vitamin C is widely used by the public to prevent or treat infections, especially the common cold [8]. In one of its more controversial applications, gram doses of vitamin C were promoted by the two-time Nobel Laureate Linus Pauling as a cancer treatment agent [9,10]. Anecdotal evidence led us to posit that intravenous (IV) vitamin C is still used by Complementary and Alternative Medicine (CAM) practitioners to treat diverse conditions including infections, autoimmune diseases, cancer and illnesses of uncertain origin [11–13]. 

Despite its purported popularity, the extent of use of IV vitamin C is unknown. Its use in CAM has not been well publicized by practitioners and their patients, and is likely to be unrecognized by mainstream physicians. Benefits if any and especially side effects of such use may be unreported or under-reported. It is useful to know if high dose IV vitamin C therapy is widely used, and if so how and for what, so that conventional physicians can improve patient care by identifying any ill effects or drug interactions, and reporting benefit if any. 

New knowledge has elucidated possible mechanisms of action of IV vitamin C and for the first time made therapeutic effects biologically plausible [14]. It is now known that IV but not oral administration of vitamin C produces pharmacologic plasma concentrations of the vitamin [15,16]. Past studies used oral and/ or IV routes inconsistently, making such studies, in retrospect, flawed and difficult to interpret [17]. Recent in vitro experiments indicated that vitamin C only in pharmacologic concentrations killed cancer cells but not normal cells, and that the mechanism was via hydrogen peroxide formation [18]. In vivo animal data indicated that hydrogen peroxide was produced selectively in extracellular fluid around normal and tumor tissues by pharma- cologic vitamin C concentrations [19,20]. At these concentrations, vitamin C slowed tumor growth [20,21]. Pharmacologic vitamin C concentrations produced in animals by parenteral administration were reproduced in patients in a recent phase I clinical trial [16]. 

Because of the new interest in IV vitamin C, coupled to need to characterize use and uncover side effects, we surveyed CAM practitioners anonymously. We also searched for side effects of IV vitamin C administration in the published medical literature and in the Food and Drug Administration (FDA) adverse events database, and estimated sales volumes of IV vitamin C preparations. 

Our study obtained quantitative information that substantiated previous anecdotal reports. Despite unexpected wide use, we found side effects of vitamin C were surprisingly few when patients were properly screened. The findings in this paper will alert conventional practitioners about unrecognized wide use of IV vitamin C, will remind them to query patients about such use, and may help to uncover either unexpected adverse events or benefit and spur further research in this area. 

 


Methods 

Survey Methods 

The study was reviewed by the Human Subjects Committee/ Institutional Review Board at the University of Kansas Medical Center. The survey was categorized as an exempt study. It contained no personal identifiers; therefore informed consent was not necessary under exempt status and was not obtained. Survey forms were distributed to practitioners attending a conference on CAM in 2006 and 2008. Participants were requested to return completed survey forms before the end of each conference. Participants were asked whether they used high dose IV vitamin C during the preceding 12 months, and if so, to detail its use by answering specific questions in the survey form (see Survey S1 for the survey form used). It was not possible to identify the respondent from the survey form or survey data. The same form was used in both years, with an additional line on the 2008 form inquiring whether the respondent had also responded in 2006 (See Survey S1). 

Vitamin C doses sold 

The major manufacturers/importers in the US of vitamin C preparations that can be administered IV were contacted by telephone. Data on annual sales of vitamin C in the US were obtained with the understanding that the names and sales figures of individual companies would not be linked nor made public. 

Side effects of high dose IV vitamin C

We searched the Adverse Events Reporting System, a database of drug side effects maintained by the Food and Drug Administration (FDA). Data from 20 consecutive quarters available from 2004–2008 were queried. We also searched for side effects in publications on therapeutic use of high dose IV vitamin C. We searched Medline, Web of Science (ISI Thompson) and Scopus databases for papers in English that reported IV vitamin C administration in humans. Several different search terms and possible variants of each search term were used to capture the maximum number of papers. Papers reporting oral vitamin C treatment only, or those using IV doses of 1g or less, were excluded. Because vitamin C is sometimes administered IV in patients undergoing hemodialysis, there are many published studies in this area. A separate search was conducted for papers reporting these to ensure that these were excluded from our analysis. IV administered vitamin C is also used to study the acute effects of antioxidants or of vitamin C itself on metabolism and physiology, particularly on cardiovascular and endothelial reac- tivity. This does not constitute a therapeutic use of vitamin C. Hence publications reporting these were identified and removed from the search results. Separately, we searched the same databases for specific reports of side effects of IV administered vitamin C and followed up references and cited papers. From papers so collected, we manually eliminated duplicate citations and those that did not meet the above criteria. From the remaining reports, adverse reactions attributable to IV adminis- tered vitamin C were noted. 

Results 

Survey response 

We distributed 300 survey forms in 2006 to attendees at their annual CAM conference. 106 forms were returned, a response rate of 35%. In 2008, 250 survey forms were distributed and 93 completed forms were returned, a response rate of 37%. Of the 2008 respondents, 22 (24%) had previously responded in 2006. An unknown number of conference attendees were not practitioners but spouses, researchers or industry representatives who did not return survey forms, reducing response rates. 

Vitamin C usage 

Of 199 total respondents for 2006 and 2008: 172 practitioners administered vitamin C; 27 did not use IV Vitamin C; 48 practitioners treated more than 100 patients each per year; and 5 treated more than 1000 patients each per year (Figure 1A, B). 11,233 patients received IV vitamin C in 2006 and 8876 in 2008 (figure 1A, B). On average, each patient received 22 treatments (Table 1). Treatments occurred at a mean of once every 4 days, each at a mean dose of 28 grams (Table 1). Doses used were as low as 1gram or as high as 200grams, with a similar wide range for each of the parameters queried. Based on dosing vials of 25g/ 50ml, estimated total yearly dosing vials administered were 318,539 in 2006 and 354,647 in 2008. Estimated total number of dosing vials sold was independently obtained from the major manufacturers of vitamin C in the U.S. Total dosing vials of IV vitamin C sold in the United States were approximately 750,000 in 2006 and 855,000 in 2008 (Table 1). 

Seventy seven percent of respondents reported the numbers of patients treated for broad indications, labeled as infection (44%), cancer (19%) or other conditions (37%) (Table 2). Numbers of practitioners who listed specific indications for treatment are shown in figure 2. Practitioners listed fatigue as the most common specific single indication for treatment in 2006, and breast cancer in 2008. There were a large number of indications for which less than four practitioners used high dose IV vitamin C (Table S1). 

Adverse effects 

Adverse events reported by survey respondents were minor (Table 3). No side effects were reported for 9227 patients while 59 were reported to have lethargy or fatigue. A single practitioner listed change in mental status in 10% of his patients (20 patients) but provided no details. One patient with pre existing renal impairment and cancer metastases to kidneys was reported to have developed unconfirmed renal failure. Some practitioners reported side effects without reporting patient numbers. The most common of these side effects were lethargy or fatigue (reported by 27 practitioners), vein irritation (by 9 practitioners), and nausea and vomiting (by 9 practitioners). Other reported side effects are listed in table 3. Less commonly reported adverse effects are listed in Table S2. 

Data obtained from the FDA Adverse Events Reporting System database for 20 consecutive quarters indicated that 77 patients treated with 0.2–1.0 gram doses of IV vitamin C had reported adverse events (Table 4). However, all patients either had serious or life-threatening systemic illnesses, and/or were receiving many potentially toxic drugs (i.e. cancer therapeutics) in addition to IV vitamin C (for details, see Table S3). Some individual patients appear to have been reported multiple times (see Table S3). In comparison to CAM practitioners, the dose of vitamin C administered was very low (1 gram or less). In no case could we exclude multiple confounding factors as the cause of the reported adverse effects (Table 4). Whether vitamin C caused or contributed to these side effects cannot be determined from the available data. 

Through searching published literature (see methods for details), 187 papers were found on the use of high dose IV vitamin C, including papers that reported side effects. There were three cases of renal failure, all in patients with pre existing renal impairment [22,23], [24]. Two patients with glucose 6 phosphate dehydroge- nase deficiency developed hemolysis [25,26] (Table 5). 

Practitioner Demographics 

86% of practitioners were physicians (Table 6) and most patients were treated at for-profit centers. Some practitioners did not provide requested demographics data. Therefore, the numbers given in this table do not tally with the total number of survey respondents. (For detailed demographic information, see Table S4).

Table 1. Details of high dose IV vitamin C use by survey respondents for the years 2006 and 2008. 

2006

 

                                                                                                                      Mean Median Range

Dose (g/treatment)                                                                 28    31       1-200

Number of treatments per patient                                                19    16       1-80

Number treated by one practitioner                                              121    40       1-1150

Duration of treatments (min)                                                      105    90       2-1440

Frequency of treatments (once every so many days)                           4     3.5       1-7

Lowest dose (g/treatment)                                                         12    9       1-60

Highest dose (g/treatment)                                                         79    75       5-200

Infusion rate (g/min)                                                                0.89    0.5     0.03-25

Total number of vials of vitamin C used (25g/50ml) (Calculated from survey data)       318,539

Total number of vials of vitamin C sold by companies in the US (25g/50 ml)               750,000

2008

                                                                                                                         Mean Median Range

 

Dose (g/treatment)                                                                                          28    50       1-200

Number of treatments per patient                                       24    16       1-80                

Number treated by one practitioner                                                               112    40       1-3000

Duration of treatments (min)                                                                         81    90       1-900

Frequency of treatments (once every so many days)                                      4      2       1-7

Lowest dose (g/treatment)                                                                             17    15       1-75

 

Highest dose (g/treatment)                                                                            87    95       20-200

Infusion rate (g/min)                                                                                      0.525  0.5    0.028-2.5        

Total number of vials of vitamin C used (25g/50ml) (Calculated from survey data)     354,647 

Total number of vials of vitamin C sold by companies in the US (25g/50 ml)          855,000 

Vitamin C is supplied in 50 ml bottles containing 25 grams. Estimated total number of doses (bottles) used each year was calculated as the cumulative sum of each practitioners’ number of patients that practitioners’ average dose in bottles that practitioner’s average number of doses per patient. doi:10.1371/journal.pone.0011414.t001

 

 

Table 2.Indications for treatment with high dose IV vitamin C. 

 

 

 

 

Year                                                                                                        2006     2008

Total number of patients treated                                                          11233    8876

 

Number of patients with data available                             9481      5928

Number of patients with          Infection                                  4587      2264

                              Cancer                              1379     1509

                              Other Conditions                   3515     2155

 

 

 

 

 

Some respondents did not list the number of patients treated for each of the 

 

 

 

conditions for which they used intravenous vitamin C treatment. Therefore, the 

 

 

 

data do not provide indications for treatment for all patients who received IV 

 

 

 

vitamin C. 

 

 

 

doi:10.1371/journal.pone.0011414.t002

 

 

Discussion 

The data here show that 11,233 and 8876 patients received IV vitamin C over two periods of one year each, with a mean number of infusions per patient of 19–24 and a mean dose of approximately 28 grams per patient. We estimate that survey respondents used approximately 318,539 and 354,647 dosing units of vitamin C each year. These numbers account for less than half of the doses of vitamin C doses sold within the United States for the matching year. Considered together, these data indicate that use of IV vitamin C was both substantial and probably underestimated. This is one of the first papers to document previously unrecognized and widespread use of a CAM agent administered IV. To our knowledge, only two other CAM therapies are used IV. The first, chelation therapy, is also used in standard medical practice [27]. The second, an IV vitamin and mineral mixture termed the Myer’s cocktail, has variable components, has had little formal investigation, and contains less than 5 grams of vitamin C [28,29]. Further, there have been few surveys of CAM practitioners, as opposed to surveys of patients. There were minimal adverse effects reported, which was also the case in the published literature. Exceptions were for patients with pre-existing renal insufficiency/failure or glucose 6-phosphate dehydrogenase (G6PD) deficiency, both known to predispose to vitamin C toxicity [30]. Adverse events reported to the FDA could not be interpreted due to confounding factors. 

Table 3. Adverse events reported with IV vitamin C use in the survey for the years 2006 and 2008.

                                                                                                              # of Patients

 

Complication                                                                                         2006   2008 

None Described                                                   5349   3878 

Lethargy/Fatigue                                                 10       49 

Local Vein Irritation                                                3        - 

Phlebitis                                                           3        - 

Kidney Stone (oxalate)                                             -         1 

Kidney Stone (urate)                                               -         1 

Kidney Stone (unspecified)                                         2         - 

Hemolysis                                                         2         - 

Elevated Blood Glucose                                            2         - 

Muscle Cramps                                                                 1         - 

Headache                                                         1        - 

Change in Mental Status                                           1       20 

Nausea/Vomiting                                                  1       - 

Flu Like Syndrome                                                 1        - 

Renal Failure                                                                   -         1* 

Syncope                                                                         -         1 

Pain at Tumor                                                     -         1 

No Data                                                                        5857      4924 

Data included in the table represent only those practitioners who reported exact patient numbers. *Described as ‘‘not confirmed (possible). Patient had partial renal failure and cancer metastases to kidneys.’’ Data on practitioners who reported adverse events but did not report the number of patients affected are detailed below as: side effect (with the number of practitioners who reported each side effect in parenthesis). For the year 2006: lethargy/fatigue (9), local vein irritation (3), nausea/vomiting (2), hypoglycemia (2), allergy (2), phlebitis (1), cellulitis (1), hematuria (1), dry mouth (1), Herxheimer reaction (1), localized thrombosis (1), and syncope (1). For the year 2008: lethargy/fatigue (9), nausea/vomiting (6), local vein irritation (4), headache (3), phlebitis (3), heartburn (1), dizziness (1), venosclerosis (1), mild palpitation (1), and cold (1), dizziness (1), ‘‘initiation of mem occasionally’’ (1), and other (1). doi:10.1371/journal.pone.0011414.t003

Soon after its discovery and synthesis in 1932, parenteral vitamin C was shown to significantly decrease polio virus infections in primates [31,32]. Although these findings were not repeatable [33,34], one practitioner treated thousands of patients with parenteral vitamin C, primarily for infections, and popular- ized its use [2,3,5]. Such reports probably were a basis for continued use of parenteral vitamin C by other CAM practitioners [6,7,35]. Independently, others postulated that vitamin C could be useful in cancer treatment by enhancing or strengthening collagen and intercellular matrix synthesis and thereby decreasing metas- tases [36,37]. Ewan Cameron, joined by Nobelist Linus Pauling, reported in retrospective case series that oral and IV vitamin C might benefit patients with advanced cancers [9,10]. Placebo- controlled double blinded clinical trials at the Mayo Clinic showed no efficacy [38–40] but CAM practitioners continued to use IV vitamin C [11,13,35], consistent with our survey results. Pharmacokinetics evidence [15,41,42] now reveals that the exclusively oral vitamin C doses used in the Mayo studies would have produced peak plasma concentrations of approximately 0.2 mM, while the same dose given IV would produce peak plasma concentrations approximately 25 fold higher [15].  

Table 4.Adverse effects reported to the Food and Drug Administration (FDA) in patients treated with IV vitamin C. 

 

Year      Number of Cases reported        Dose Range(g/day)        Can confounders be eliminated? 

2004       15                                              0.5–1                               No 

2005       7                                                0.25–1                             No 

2006      11                                               0.2–1                               No 

2007      11                                              Not Given                         No 

2008      33                                               0.5–1                               No 

 

When the vitamin C dose was provided as ml, the dose was converted to mg on the basis that vitamin C is supplied as 0.5gram/ml solution. Some practitioners did not mention the dose of vitamin C used. The format of the FDA adverse events database did not permit identification of specific patients, so that the same patient may have been reported multiple times in the same quarter or in several quarters, inflating the number of patients with adverse events. doi:10.1371/journal.pone.0011414.t004 

 

 

Pharmacologic doses of vitamin C given IV may produce drug effects in many body tissues, mediated by hydrogen peroxide formation in extracellular fluid but not blood [18–20]. Emerging clinical data are consistent with plausibility [43] and safety [16], but whether there is benefit or harm in humans can only be addressed by rigorous clinical trials. 

IV vitamin C administered in gram doses can cause serious side effects in some patients. A metabolic end-product of vitamin C metabolism is oxalate, and oxalate nephropathy has been reported in patients with renal impairment given gram doses of IV vitamin C [22–24]. Prolonged treatment with vitamin C increases plasma oxalate concentrations in patients with renal failure [44] and results in increased urinary oxalate in patients receiving total parenteral nutrition [45], although in these patient groups the consequences of hyperoxalemia are unknown. Patients with glucose 6-phosphate dehydrogenase deficiency can develop intravascular hemolysis when gram doses of vitamin C are given IV [25,26]. Vitamin C, even with oral dosing, might induce hemolysis in patients with Paroxysmal Nocturnal Hemoglobinuria [46,47]. A recent phase one study of high dose IV vitamin C in patients with advanced cancer did not find any serious side effects [16]. Exclusion criteria for the phase I study included renal failure and glucose-6-phosphate dehydrogenase deficiency. Recently, a study in mice reported decreased efficacy of cancer chemother- apeutic agents with parenteral dehydroascorbic acid, a metabolite of vitamin C [48]. Dehydroascorbic acid cannot be detected in human blood or tissues, is not commercially available for parenteral use nor used by CAM practitioners, is toxic at high concentrations [49,50], and should not be administered parenterally in humans. 

No definitive serious adverse events were reported by survey respondents. Despite the anonymity of the survey, practitioners may have been reluctant to describe adverse events. Whether IV vitamin C is safe for general use remains to be determined. Because of the possibility of unrecognized side effects or of drug interactions, practitioners should enquire whether their patients, especially those with chronic, intractable or difficult to treat conditions, are receiving high dose IV vitamin C treatment elsewhere. Physicians should be alert to potential interactions of high dose vitamin C not only with conventional medicines but also with CAM treatments. An example is the case of exacerbated, severe cyanide poisoning in a patient on concurrent treatment with high dose oral vitamin C and Amygdalin (laetrile, a metabolic product of which is cyanide) [51]. 

Our study has limitations that, when considered together, may underestimate use of IV vitamin C. Because our survey was distributed to participants in a CAM conference, the survey excluded the vast majority of CAM practitioners. Respondents who filled in the survey form did so from memory without access to records, so that the information obtained can only be considered approximate. The format of the survey questions may have inadvertently resulted in underestimating vitamin C use, because the survey questions used ranges, for simplicity. For example, the highest value listed for numbers of patients treated in a calendar year was ‘‘>40’’. If practitioners did not specify precise numbers as requested in subsequent questions, 40 was used as the number of patients treated, although the true number may have been higher. That there was only 24% overlap between survey respondents in 2006 and 2008 provides additional evidence that community use of IV vitamin C was underestimated. Data concerning industry sales of IV ascorbate only give approxima- tions of use. On one hand, because not all units sold would have been used, use may be overestimated. Conversely, other smaller companies and compounding pharmacies may supply parenteral vitamin C but were not included in the survey. Therefore, the total number of vials sold may also be underestimated. The exact number of doses of parenteral vitamin C used in the US per year remains unknown. The survey response rate of approx 35% suggests we underestimated use, and perhaps adverse events. A reduced response rate may have occurred because some conference attendees were not practitioners and therefore did not return survey forms. Because of these uncertainties, the number of US patients treated with IV vitamin C cannot be accurately estimated from survey data. Since a primary aim of the survey was to determine if IV administered vitamin C is in use, and not a census of patients treated, the response rate does not detract from the value of the data. 

Data obtained on adverse effects from PUBMED and the FDA also have limitations. Physicians may have not reported compli- cations because they were not recognized, or were delayed, or were not attributed to vitamin C. Most practitioners do not report or publish adverse events. There may be as yet unknown adverse effects or interactions of IV ascorbate with other drugs. Side effects reported to FDA are difficult to interpret because of confounding factors. All reported patients received other potentially toxic drugs and/or had other diagnoses that may have been responsible for the reported adverse effects (see Table S3). Because of the FDA adverse events format, the same patient was likely to have been reported multiple times. Because of the low doses of IV vitamin C in the FDA dataset, it is highly unlikely that any of the reported adverse effects were due to the vitamin. Despite this, and because the information available in the FDA database is limited, it is not possible to accurately determine whether vitamin C caused or contributed to the reported side effects. 

IV vitamin C is already in wide use, and physicians should know that their patients may seek IV vitamin C treatment in addition to conventional therapies. Beneficial effects of intravenous vitamin C on the disease conditions for which it is used are unproven, but side effects appear to be minor. Physicians should be cognizant of potential adverse or other unexpected effects, and of unrecognized interactions with drugs used in conventional and alternative medicine. CAM practitioners have an obligation to screen patients and should not administer high dose IV vitamin C to patients with pre existing renal disease, renal insufficiency or renal failure; glucose 6-phosphate dehydrogenase deficiency; a history of oxalate nephrolithiasis; or paroxysmal nocturnal hemoglobinuria. Based on emerging evidence, vitamin C in pharmacologic concentrations appears to be a pro-drug for delivery of hydrogen peroxide to the extravascular space. High dose IV vitamin C appears to have a positive safety profile, favorable pharmacology, evidence for mechanism of action, some anti-cancer effects in vitro and in animals, and widespread use outside conventional medicine with minimal harm, but without any proven clinical benefit. 

Supporting Information 

Table S1 

Found at: doi:10.1371/journal.pone.0011414.s001 (0.18 MB DOC) 

Table S2 

Found at: doi:10.1371/journal.pone.0011414.s002 (0.05 MB DOC) 

Table S3 

Found at: doi:10.1371/journal.pone.0011414.s003 (0.17 MB DOC) 

Table S4 

Found at: doi:10.1371/journal.pone.0011414.s004 (0.04 MB DOC) 

Survey S1 Survey Form 

Found at: doi:10.1371/journal.pone.0011414.s005 (0.05 MB DOC) 

Acknowledgments 

We thank CAM practitioners for their cooperation in completing the surveys, and Dr. Jill Norris, University of Colorado Health Sciences Center, for advice on preparing the survey. 

Author Contributions 

Conceived and designed the experiments: SJP AYS QC MGE JD ML. Performed the experiments: SJP AYS QC MGE JD ML. Analyzed the data: SJP AYS QC MGE JD ML. Contributed reagents/materials/analysis tools: SJP AYS QC MGE JD ML. Wrote the paper: SJP AYS QC MGE JD ML.

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Source: Padayatty SJ, Sun AY, Chen Q, Espey MG, Drisko J, et al. (2010) Vitamin C: Intravenous Use by Complementary and Alternative Medicine Practitioners and Adverse Effects. PLoS ONE 5(7): e11414. doi:10.1371/journal.pone.0011414. Editor:Joel Joseph Gagnier, University of Michigan, Canada. ReceivedFebruary 23, 2010;AcceptedMay 30, 2010;PublishedJuly 7, 2010. 

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Coenzyme Q10 and the Heart

Posted By Administration, Wednesday, July 7, 2010
Updated: Friday, April 18, 2014

 

Zinaby Zina Kroner, DO

CoQ10 has been considered for prevention and treatment of cardiovascular disease related to atherosclerosis, hypertension, diabetes and other common risk factors. LDL (“bad cholesterol”) in the walls of arteries can be oxidatively damaged and that may be an initiating event leading to atherosclerosis. In these cases, the antioxidant function of CoQ10 might be beneficial. There are other properties of CoQ10 that are of interest, such as its ability to decrease the amount of a specific substance on the surface of cells that can collect on the blood vessel walls (1).

An analysis of available research in 2003 found conflicting results. Some improvement in cardiac function was observed in some studies, but not confirmed in others (4). 

CoQ10 is considered as a possible treatment for cardiomyopathy, which is an abnormality or disease of the cardiac muscle. Improvements in cardiac output have been found in some small studies. It has also been shown to help congestive heart failure as the result of coronary heart disease in other small studies. Again, there is a need for more large-scale clinical trials (1, 3).

Levels of CoQ10 have been considered as an independent predictor for outcome in patients with chronic heart failure. Those with lower levels have a higher risk of death. In one recent study, the correlation was strong enough for investigators to call for more interventional studies using CoQ10 to treat heart failure (4). 

This same pattern repeats for almost all types of cardiovascular disease and treatment. From the treatment of angina (lack of blood supply to the heart muscle), to high blood pressure and damage of the lining of the blood vessels, there is some evidence of benefit from CoQ10 and a need for more studies (1).  

I make sure that my patients' coq10 levels are assessed and they are treated accordingly.

 

Citations:

1. Higdon, J. Coenzyme Q10. Micronutrient Information Center. Linus Pauling Institute. 2/2003. Updated 2/2007. lpi.oregonstate.edu/infocenter/othernuts/coq10/#deficiency (Accessed 5/27/2010)

2. Shekelle P, Morton S, Hardy M. Effect of Supplemental Antioxidants Vitamin C, Vitamin E, and Coenzyme Q10 for the Prevention and Treatment of Cardiovascular Disease. Summary, Evidence Report/Technology Assessment: Number 83. AHRQ Publication Number 03-E042, June 2003. Agency for Healthcare Research and Quality, Rockville, MD. www.ahrq.gov/clinic/epcsums/antioxsum.htm.

3. Dallner, G, Stocker, R. Coenzyme Q10. Encyclopedia of dietary supplements, ed Paul M. Coates.  Marcel Dekker, New York. 2005.

4. Molyneux, SL, Florkowski, CM, George, PM, et al. Coenzyme Q10: An Independent Predictor of Mortality in Chronic Heart Failure. J. Am. Coll. Cardiol. 2008;52;1435-1441.

Tags:  coenzyme Q10  heart 

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Acupuncture for Ovulation Disorders and PCOS

Posted By Administration, Friday, July 2, 2010
Updated: Friday, April 18, 2014

 

by Fiona McCulloch, ND

 

Polycystic ovarian syndrome is the number one reproductive disease in women.   This disease disrupts normal ovulatory cycles which can result in heartbreaking infertility for millions of women.  Known hormonal changes in PCOS include excess androgens (ie: testosterone), and insulin resistance.  Most thought now is leaning towards insulin resistance being the primary cause of PCOS, with genetic factors playing a role, but once the cycle of anovulation begins it feeds back on itself, causing the condition to remain in a vicious cycle.  Women with PCOS have not only insulin resistance, but also have neuroendocrine imbalances, resulting in elevated LH (lutenizing hormone) levels.  Having a high LH to FSH ratio is one of the hallmarks of polycystic ovarian syndrome or persistent anovulation.  In response to a combination of high LH and insulin resistance, the follicles in the ovary will begin to secrete too many male hormones (androgens) which then inhibit the hormonal pathways that are needed to stimulate ovulation.

 

Various medications are traditionally used to induce ovulation in women with PCOS.  A growing body of evidence now exists indicating that low-frequency electroacupuncture is as effective as commonly used medications in inducing ovulation.  Furthermore, this form of acupuncture can benefit many of the hormonal imbalances seen in polycystic ovarian syndrome.  Thousands of women worldwide use acupuncture therapy for PCOS and so I’d like to discuss how it works, and why it is so beneficial to induce ovulation.

General principles of how electroacupuncture stimulates the ovaries through the nervous system

Electroacupuncture has been found to profoundly effect the reproductive organs, through mechanisms in the sympathetic nervous system, endocrine system, and neuroendocrine system.  When needles are inserted into certain points and stimulated in a specific manner, this produces a neurological reflex transmitted to the organ correlated with that nerve pathway.  For example, needles inserted into the leg muscles below the knee, lower back, or abdomen in specific regions cause a response which measurably affects the ovary.  In addition, the nervous system will transmit a signal to the brain, and the brain then emits a response which affects the organ from a central mechanism.  These effects have been investigated through measurements of hormones, neuropeptides, and circulatory changes on both animals and humans receiving this specific type of electroacupuncture.

Nervous system alterations in PCOS

Evidence indicates that women with pcos have abnormal circulating levels of a neurohormone called β-endorphin.  β-endorphin is known to increase insulin production and reduce insulin excretion by the liver, which is very much implicated in PCOS.   It has also been found that women with PCOS have unusually high amounts of sympathetic nerve fibres in their ovaries.  These nerve fibres cause unusual stimulation of the ovary by the sympathetic nervous system (the part of the nervous system associated with “flight or fight” responses in the body, among other processes).  Stimulation of these nerve fibres can cause the ovaries to produce androgens, which then impair normal ovulation.  Women with PCOS have also been found to have high amounts of nerve growth factors in their ovaries, something which is associated with high levels of sympathetic nervous system activity.   Disturbances in central and peripheral β-endorphin release, high androgens, insulin resistance, abdominal obesity, and cardiovascular disease are associated with increased sympathetic nervous system activity, and all of these are also associated with the pathology of PCOS.  In a recent study by Elizabet Stener-Vitorin in Sweden, direct intraneural testing found a strong correlation between levels of sympathetic nervous system activity and testosterone levels in women with PCOS.  Those who had the highest amounts of sympathetic nervous system activity were found to have the highest testosterone levels and the most severe PCOS conditions.

What evidence exists for acupuncture inducing ovulation?

Several studies exist on low frequency electroacupuncture and ovulation induction.  In one trial, the effect of a series of 14 electroacupuncture treatments on 24 anovulatory women with pcos was investigated.  In 38% of these women, regular ovulation was induced.   Three months after the last treatment, LH/FSH ratios and testosterone levels were significantly decreased, a sign of improvement in PCOS pathology.   In another study done on a group of women given human menopausal gonadotrophin (a commonly used drug in the treatment of infertility), acupuncture was compared to hCG injections in order to assess its effect on ovulation.  Traditionally hCG is given to stimulate ovulation during medicated cycles at fertility clinics.  It was found that a single acupuncture treatment induced ovulation as effectively as the as the hCG injection and reduced the incidence of ovarian hyperstimulation syndrome, a painful side effect of medicated cycles.  Other studies have also indicated enhanced ovarian response when acupuncture is added to medicated cycles.  Female rats with PCOS induced by chronic exposure to DHT (a form of testosterone) were given low frequency electroacupuncture and physical exercise.  The treatment increased the amount of healthy follicles in the ovaries,  and significantly normalized cycles.

Effects of electroacupuncture on nervous system changes in PCOS

It has also been found that electro-acupuncture can regulate parts of the central nervous system related to dysfunction in PCOS.  Specifically, beneficial effects on neurohormones such as GnRH(Gonadotropin releasing hormone) and androgen receptor proteins, indicate that electro-acupuncture significantly benefits the hypothalamic-pituitary-ovarian axis and through this can help to restore normal cycling.  Electroacupuncture was also found in 3 recent studies to increase ovarian blood flow through effects on sympathetic nervous system pathways.  In addition, it has been found in two studies to reduce high peripheral circulating β-endorphins in women with PCOS, and thereby improve insulin resistance.   As sympathetic nerve activity appears to contribute to the development and maintenance of PCOS, the beneficial effects of electroacupuncture, and also exercise, may be mediated by nervous system modulation to the ovaries.

Electro-acupuncture appears to work through multiple pathways to disrupt the “vicious cycle” of PCOS.  Even though much more research needs to be done to determine all of the mechanisms involved, its safety and low incidence of side effects makes it an excellent therapy to stimulate ovulation naturally for the many women who suffer with this disease.

References

Andersson, S., Lundeberg, T., 1995. Acupuncture — from empiricism to science:functional background to acupuncture effects in pain and disease. Med. Hypotheses 45, 271–281.

 

Cai, X., 1997. Substitution of acupuncture for HCG in ovulation induction. J. Tradit. Chin. Med. 17, 119–121.

Carmina, E., Ditkoff, E.C., Malizia, G., Vijod, A.G., Janni, A., Lobo, R.A., 1992. Increased circulating levels of immunoreactive beta-endorphin in polycystic ovary syndrome is not caused by increased pituitary secretion. Am. J. Obstet. Gynecol. 167,

Chen, B.Y., Yu, J., 1991. Relationship between blood radioimmunoreactive beta-endorphin and hand skin temperature during the electro-acupuncture induction of ovulation. Acupunct. Electrother.

Lobo, R.A., Granger, L. R., Paul, W.L., Goebelsmann, U., Mishell Jr., D.R., 1983. Psychological stress and increases in urinary norepinephrine metabolites, platelet serotonin, and adrenal androgens in women with polycystic ovary syndrome. Am. J. Obstet. Gynecol. 145, 496–503.

Feng, Y., Johansson, J., Shao, R., Manneras, L., Fernandez-Rodriguez, J., Billig, H., Stener-Victorin, E., 2009. Hypothalamic neuroendocrine functions in rats with dihydrotestosterone-induced polycystic ovary syndrome: effects of low-frequency electroacupuncture. PLoS ONE 4, e6638. produces skeletal muscle vasodilation following antidromic stimulation of unmyelinated afferents in the dorsal root in rats. Neurosci. Lett. 283, 137–140.

Jin, C.L., Tohya, K., Kuribayashi, K., Kimura, M., Hirao, Y.H., 2009. Increased oocyte production after acupuncture treatment during superovulation process in mice. J. of Reprod. & Conception 20, 35–44.

Manneras, L., Cajander, S., Lonn, M., Stener-Victorin, E., 2009. Acupuncture and exercise restore adipose tissue expression of sympathetic markers and improve ovarian morphology in rats with dihydrotestosterone-induced PCOS. Am. J. Physiol. Regul. Integr. Comp. Physiol. 296, R1124–R1131.

Stener-Victorin, E., Wu, X., Effects and mechanisms of acupuncture in the reproductive system, Auton. Neurosci.(2010)

Stener-Victorin, E., Lindholm, C., 2004. Immunity and beta-endorphin concentrations in hypothalamus and plasma in rats with steroid-induced polycystic ovaries: effect of low-frequency electroacupuncture. Biol. Reprod. 70, 329–333.

Stener-Victorin, E., Waldenstrom, U., Tagnfors, U., Lundeberg, T., Lindstedt, G., Janson, P.O., 2006. Effects of electro-acupuncture on anovulation in women with polycystic ovary syndrome. Acta Obstet. Gynecol. Scand.

Stener-Victorin, E., Lundeberg, T., Waldenstrom, U., Manni, L., Aloe, L., Gunnarsson, S., Janson, P.O., 2000a. Effects of electro-acupuncture on nerve growth factor and ovarian morphology in rats with experimentally induced polycystic ovaries. Biol. Reprod. 63, 1497–1503.

Stener-Victorin, E., Lundeberg, T., Waldenstrom, U., Bileviciute-Ljungar, I., Janson, P.O., 2001. Effects of electro-acupuncture on corticotropin-releasing factor in rats with experimentally-induced polycystic ovaries. Neuropeptides 35, 227–231.

Stener-Victorin, E., Kobayashi, R., Kurosawa, M., 2003a. Ovarian blood flow responses to electro-acupuncture stimulation at different frequencies and intensities in anaesthetized rats. Auton. Neurosci.: Basic and Clin. 108, 50–56.

Stener-Victorin, E., Lundeberg, T., Cajander, S., Aloe, L., Manni, L., Waldenstrom, U., Janson, P.O., 2003b. Steroid-induced polycystic ovaries in rats: effect of electro- acupuncture on concentrations of endothelin-1 and nerve growth factor (NGF), and expression of NGF mRNA in the ovaries, the adrenal glands, and the central nervous system. Reprod. Biol. Endocrinol. 1, 33.

Stener-Victorin, E., Fujisawa, S., Kurosawa, M., 2006. Ovarian blood flow responses to electroacupuncture stimulation depend on estrous cycle and on site and frequency of stimulation in anesthetized rats. J. Appl. Physiol. 101, 84–91.

Stener-Victorin, E., Jedel, E., Manneras, L., 2008. Acupuncture in polycystic ovary syndrome: current experimental and clinical evidence. J. Neuroendocrinol. 20, 290–298.

Stener-Victorin, E., Jedel, E., Janson, P.O., Sverrisdottir, Y.B., 2009. Low-frequency electro-acupuncture and physical exercise decrease high muscle sympathetic nerve activity in polycystic ovary syndrome. Am.J.Physiol.Regul.Integr.Comp.Physiol. 297 (2), R387R395.

Zhao, H., Tian, Z.Z., Chen, B.Y., 2003a. An important role of corticotropin-releasing hormone in electroacupuncture normalizing the subnormal function of hypothalamus–pituitary–ovary axis in ovariectomized rats. Neurosci. Lett. 349, 25–28.

Tags:  acupuncture  fertility  Infertility 

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Rhythm is the Answer

Posted By Administration, Thursday, July 1, 2010
Updated: Friday, April 18, 2014

by Joel Lopez, MD, CNS

411913693_09923741a9_zThere is a rhythm in life. You see it everywhere in nature. Moon cycles, seasonal changes, circadian rhythms, migratory patterns, growth spurts, planting/harvesting times, etc. There is nothing static in nature. Everything is in a constant flux. The only thing that’s static is death. At least, that’s what we know for now. If there are rhythmic patterns in our bodies, doesn’t it make sense to give hormones (if a person’s symptomatic, deficient or has sub-optimal numbers) in a rhythmic pattern as well? This idea was actually brought forth by a person named TS Wiley. She’s trained as an anthropologist and unfortunately (or fortunately?) is not an MD. Otherwise, a lot of doctors, especially in the anti-aging community would have jumped onto the bandwagon of prescribing bioidentical hormones in a rhythmic manner. That is, changing the dose every so often, to mimic nature. Doctors, just like every one else, are creatures of habit. Nobody wants to mess with the status quo. A German philosopher named Arthur Schopenhauer put it succinctly, “All truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident.” Anyway, hormonal imbalance is just one of the causes of accelerated, symptomatic aging. Other factors such as nutritional deficiencies, chronic inflammatory processes, toxicities, oxidative stress and mitochondrial dysfunction need to be addressed as well if a person wants to age well.

Tags:  rhythm 

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Do You Have a Toxic Workplace?

Posted By Administration, Tuesday, June 29, 2010
Updated: Friday, April 18, 2014

by, Holly Lucille, ND, RN

74046939_7b6c18ce63_bI am not talking about the "toxic workplace" often reported when a work environment is full of backstabbing, gossiping co-workers, a controlling boss or demanding clients. I am talking about toxic substances in your workplace that might be making you physically sick.

It is bad enough that we live in a society that is extremely dependent on harmful chemicals. We are exposed to these ubiquitous and devious substances everyday, hiding in plastics, pesticides, car exhaust, soaps, emulsifiers, health and beauty aids, household cleaning products and a number of other places. They are in the food we eat, the water we drink and the air that we breathe. However, depending on where you work, your exposure to toxic substances could be intensified, contributing significantly to your health issues.

Occupational allergies are becoming an extremely common concern with cases increasing in numbers and severity in recent years. There have been countless articles written on both "Sick Building Syndrome" and "Occupational Asthma." Under these two modern diagnoses, people have complained of a variety of symptoms including watery eyes, runny nose, headaches, dizziness, nausea and tightening sensation in the chest. The curious thing about most of these symptoms is that they have a distinct pattern of getting worse while in the work environment and significantly better over vacations or weekends.

If you work in an enclosed office space, you might feel falsely safe and protected from environmental allergens at work. Modern office buildings are not only being built with toxic chemicals but, in order to conserve energy, they are also built tight as a drum with poor ventilation, leaving allergens and irritants with no place to go. Common sources, such as malfunctioning or inappropriate, inefficient use of heating devices, can produce irritating pollutants such as carbon monoxide, nitrogen dioxide and sulfur dioxide at harmful levels. Formaldehyde exposure is widespread and found in resins in finishes, plywood, paneling, fiberboard and particleboard, and in some backings and adhesives for carpets. Biological air pollutants like dander, molds, and dust mites are carried by animals and people into and throughout buildings.

Scents and hairsprays, construction products such as finishes, heavy duty cleaners, paints, thinners, dry cleaning fluids, some copiers and printers, some glues and adhesives, markers, and photo solutions are among some of the common office products that emit harmful volatile organic compounds (VOC). New installations, carpet, wall coverings, paint or construction can all heighten problems with VOCs. If that isn’t enough to worry about, almost everyone has heard of the dangers of toxic mold thriving in cool, damp, dark places behind walls and under carpeting.

Some occupations that are even higher risk for exposure include: industrial workers handling paints, chemicals, solvents, and plastics; beauticians who work daily with hair dyes, perms, and nail polish/removers; people who are in the farming industry dealing with fertilizers and pesticides; photocopier technicians and dry cleaning merchants working with machines emitting potentially harmful gases.

If you feel that your workplace is making you sick, there are things you can do, short of quitting your job. Reducing exposure is important but it is also important to remember that having an allergic response to something often has less to do with the trigger and more to do with our body’s inability to respond to it appropriately. Make sure you are protecting your immune system by choosing healthy, organic foods in your diet for adequate nutrients and fiber, drink plenty of filtered water, exercise regularly, choose non-toxic products for your home and consider partnering with a qualified healthcare practitioner to partake in a comprehensive body detoxification. Enzymatic Therapy’s (www.enzy.com) Whole Body Cleanse is a very effective and easy cleanse that you can get at a health food store near you.

In your workplace, consider talking with both your supervisor and your OSHA or union representative regarding the air exchange system in your building. Interior landscaping can help absorb some of the off-gassing from VOC and formaldehyde. Buying plants like a Dwarf date palm, Bamboo palm or Janet Craig is an inexpensive, efficient method of cleansing the air. Keep your work area free of clutter, dust regularly and use a HEPA-type table top air purifier. Even though we cannot completely escape the toxins that surround us, we can make a difference for us as individuals and, little by little, the environment as a whole!

Tags:  toxins  work 

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Insights into Vegetarianism

Posted By Administration, Wednesday, June 23, 2010
Updated: Friday, April 18, 2014

 

2085739779_b0dc7d4d28_bby Andrea Purcell, ND

Patients come to vegetarianism for a variety of reasons.

The three most common reasons I hear are:

I heard it was better for my health.

It’s a religious or customary choice.

It’s less cruel to animals and our planet.

The food choices I most commonly see among the vegetarian patient base are nothing close to vegetarianism as defined by the term.

So to clarify, the word vegetable is contained within the word vegetarian. In order to be a vegetarian you must eat vegetables, which means that you must buy, prepare, occasionally cook and chew them on a regular basis.

The type of vegetarianism I commonly find in my patients who come to the office and say that they are vegetarian, are really carbo-vegetarians. This means that they consume easy to prepare, on the run processed food forms of carbohydrates that are animal free.

These include, rice, pasta, breads, cakes, cookies, frozen yogurt, bean burritos in white flour tortillas, pancakes, bagels, waffles, fruit, veggie sandwiches, pizza, vegetable dumplings, vegetable lasagna, chips and salsa, hummus with carrots. All of the vegetarian options in this example are simple carbohydrates. They have been processed and refined, meaning that they have been bleached of their nutrients, and stripped of their fiber. Simple carbohydrates are exactly what they say, simple. Not the nutrient and fiber dense food, of what they once were, or of how nature intended it be delivered to us.

Being a healthy vegetarian means being a responsible vegetarian. This means that vegetarians need to work very hard to get enough fat and protein in their diets in order to maintain the level of health that famous vegetarians brag about.

Responsible vegetarianism includes a balance of fat, protein, complex carbohydrates, and of course vegetables at every meal and snack.

Eating fruit in place of vegetables would technically make a person a fruitarian, which is not the topic of this blog.

Complex Carbohydrates include: Whole grains such as brown rice, quinoa, amaranth, and millet. Whole beans, black, lentil, red, white, mung, garbanzo and vegetables in every color.

Protein sources include: Nuts, beans, seeds, tofu, tempeh, possibly eggs or dairy depending on the type of vegetarian, certain vegetables (avocado, spinach, broccoli).

Fat sources include: Nuts, seeds, avocado, coconut milk & meat, oils in many forms.

To Drink: Juiced Vegetables! Try my favorite mixture: Celery, cucumber, spinach, Swiss chard, ½ apple.

Be a responsible vegetarian, your body will thank you for it!

Tags:  food and drink  vegetarianism 

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Heavy Metals Increase Risk of Depression and Panic Disorder

Posted By Administration, Tuesday, June 22, 2010
Updated: Friday, April 18, 2014

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by Gina Nick, NMD, PhD

Even at low levels generally considered to pose little or no risk, exposure to environmental lead might increase – by as much as 2.3 times – the risk of depression and panic disorder but not of generalized anxiety disorder. That was the suggestion of a Canadian study appearing in the December, 2009 issue of the Archives of General Psychiatry. Gender and ethnicity were also factors and the researchers stressed that lead exposure cannot be determined to be a cause of these psychological problems.

One of the main, and often overlooked, sources of heavy metals, including lead, is our water supply-both drinking water and shower water.   I recommend investing in a quality water filtration and ionization system to all of our patients.  The link between heavy metal exposure and mental illness suggested in this study and proven in many others (including practical, real life studies completed with patients at LTP Medical) is one of the reasons why we always test patients with mental health challenges for exposure to environmental toxins including heavy metals and treat them using the LTP Medical Custom Purification Program to remove the toxins from their systems.  This is one of the simplest and most effective ways to see immediate benefit in patients suffering needlessly with these challenges. Other treatments include custom amino acid therapy, fatty acid therapy, orthomolecular therapy, hormone therapy and food allergy testing and treatment.

Tags:  anxiety  depression  heavy metal  panic disorder 

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Curbing Inflammation May Reduce Heart Disease Risk

Posted By Administration, Monday, June 21, 2010
Updated: Friday, April 18, 2014

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by Zina Kroner, DO

It has been established in prior studies that if one has an inflammatory condition such as psoriasis, for example, the risk of heart disease increases substantially.  A pro-inflammatory agent called tumor necrosis factor (TNF) tends to be elevated in patients with many  inflammatory conditions such as psoriasis and rheumatoid arthritis.  Prior studies have shown us that when patients took medication that act again TNF, the risk of heart disease decreased (J Am Acad Dermatol 2005; 52:262).

A recent study in Norway looked at patients with 3 different inflammatory conditions: rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis.  Patients were treated with TNF antagonists and aortic stiffness was assessed as a marker of heart disease.  It was found that those receiving anti-TNF agents as compared to placebo had statistically significant decreases in aortic stiffness and C-reactive protein levels (a marker for heart diseaes).  Although the study was of small sample size and of short duration, it can be concluded that TNF-antagonists may potentially decrease heart disease risk. 

Medications that are TNF antagonists have a wide and potentially detrimental side effect profile and need to be prescribed judiciously. There are an array of natural treatments that can be catered to one's condition that can potentially lower TNF and cardio-CRP levels as well. 

This is an important study in that it substantiates the fact that decreasing inflammation in our bodies will help reduce cardiovascular risk.  This can be done via a number of fronts depending on one's unique inflammatory condition. 


Source: Angel K et al. Tumor necrosis factor-{alpha} antagonists improve aortic stiffness in patient with inflammatory arthropathies: A controlled study. Hypertension 2010 Feb; 55:333.

Tags:  heart disease  inflammation 

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Glutathione and Parkinson's Disease

Posted By Administration, Wednesday, June 16, 2010
Updated: Friday, April 18, 2014

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by Zina Kroner, DO

Glutathione has been used to help alleviate some of the symptoms of Parkinson's disease.  Glutathione is a small peptide made up of three amino acids – glutamic acid, cysteine and glycine.  The active group of this peptide is the sulfhydryl or thiol (SH) group, a bond formed between the amine (NH2) group of cysteine and carboxyl group (COOH) of glutamic acid.  

In the human body, glutathione occurs in two forms:

1. the majority of glutathione is present in the reduced form (GSH) 

2. and a small percentage of it is present in the oxidized form (GSSG or glutathione disulphide).  

The reduced form of glutathione is the active form, and it donates its electrons to highly reactive molecules like free radicals, peroxides and superoxides to stabilize them.  The process is called neutralizing the free radicals.  During this process, glutathione is oxidized and the harmful free radicals are reduced and neutralized.  

The free radicals, peroxides and superoxides are unstable and highly reactive molecules formed as part of normal metabolic processes.  These can literally snatch electrons from the surrounding molecules (like DNA, cell membrane and other cell organelles) to stabilize themselves, making the other molecules unstable, that repeats the process, setting off a chain reaction producing more unstable molecules, which can easily result in the collapse of the cell membrane and the membranes of other cell organelles.  

Glutathione is synthesized internally in the liver and does not need to be supplied in the diet.  A balanced diet has all the necessary precursors for the internal synthesis of glutathione. The ability of glutathione to neutralize these harmful free radicals makes it a major powerful intracellular antioxidant.  For glutathione to be active, it needs to be kept in the reduced form in the blood.  The oxidized glutathione is immediately recycled back to its reduced form by an enzyme called glutathione reductase, and glutathione is again ready to donate electrons to free radicals.  The reduced and oxidized forms of glutathione together are called a redox couple.  

Glutathione preserves the integrity and fluidity of the cell membrane.  It is available in the cells in relatively high concentrations in the reduced form.  Depletion of glutathione levels in the cells leads to excessive formation of reactive oxygen species which puts more stress on the cells.  This is called oxidative stress.  This increased oxidative stress causes the cell organelles to burn out gradually and lead to eventual cell death.  Increased oxidative stress plays a major role in increasing the risk for a variety of cancers, inflammatory and degenerative diseases.  

Glutathione and Parkinson’s disease

Glutathione has been extensively studied for its role as an antioxidant in Parkinson’s disease, an adult-onset progressive neurodegenerative disorder.  In Parkinson’s disease, there is a selective degeneration of dopaminergic neurons in the substantia nigra of midbrain.  Substantia nigra is the part of the brain responsible for physical movement (like walking, moving hands and legs, etc).  Hence, degeneration of dopaminergic neurons in substantia nigra causes physical symptoms like tremors, bradykinesia (slow movements), muscle stiffness and loss of automatic movements in Parkinson’s disease. 

Progressive degeneration of dopaminergic neurons in substantia nigra is caused by:

1. Excessive formation of reactive oxygen species (ROS)

2. Increased oxidative stress accumulation of abnormal proteins in the cells

3. Drastic depletion of glutathione (GSH) levels 

Dopaminergic neurons are more prone to oxidation due to a combination of factors like the metabolism of dopamines, auto-oxidation, increase in iron levels, decrease in glutathione levels and excessive formation of ROS. Oxidative stress needs to be reduced to slow down the progression of symptoms of Parkinson’s disease. Research suggests that oxidative stress can be effectively reduced by increasing the glutathione levels or slowing its degradation in the substantia nigra.

In the body, glutathione is synthesized from 3 amino acids – glutamic acid, cysteine and glycine.  The availability of cysteine is the deciding factor (or rate limiting factor) in the synthesis of glutathione.   


Dr. Perlmutter’s Research

Dr. David Perlmutter, a board certified neurologist from Naples, Florida, started using intravenous glutathione in 1998 for his Parkinson's patients after he did extensive research on Parkinson’s disease and effects of supplemental glutathione on improving the symptoms of Parkinson’s disease.  He is the pioneer in using intravenous glutathione in the treatment of Parkinson’s disease.  His research opened new doors in the treatment of Parkinson’s disease and other neurodegenerative diseases.  Dr. Perlmutter has successfully used intravenous glutathione in patients with significant improvement in the symptoms.  Although glutathione treatment cannot prevent the occurrence of symptoms, it significantly slows down the occurrence of symptoms with improvement in the existing symptoms.

Glutathione supplements do not directly raise the dopamine levels in the brain, instead they improve the efficiency of dopamine in the brain and also increase the sensitivity to dopamine and serotonin.

Glutathione Treatment

Glutathione supplements are available in oral, intramuscular, and intravenous forms.

Oral – Glutathione is available in capsule form and also precursors of glutathione are available in powder form to be used as oral supplements.  However, recent research suggests that glutathione is digested in the gastrointestinal tract and broken down to its constituents even before it enters the blood.  So, oral glutathione supplements are not effective.  I prefer to give the natural precursors to glutathione to my patients.  

Intramuscular – Glutathione injections are also given intramuscularly.  These are mildly effective according to anectodal data.

Intravenous – Glutathione injections given intravenously are the best and most effective form of supplementation. Not only does it reach the brain and potentially improves Parkinson’s symptoms, it also reaches the liver and helps in a variety of functions like neutralization of free radicals via detox pathways.  Standard dosage for glutathione supplements is 1400 milligrams mixed with saline, given intravenously for ten minutes three times a week.  

Contraindications and Safety:

Glutathione is in the GRAS (generally regarded as safe) category, according to the FDA.  However, if you are taking other prescription medicines, glutathione supplements may reduce the efficacy of these medicines.  This is because glutathione plays a role in the detoxification function in the liver, removing foreign substances from the body.  Prescription medicines may therefore be removed from the system, thus reducing their efficacy

 

Sources:

1.Hauser, RA, Lyons, KE, McClain, T, et al. Randomized, Double-Blind, Pilot Evaluation of Intravenous Glutathione in Parkinson’s Disease. Movement Disorders. 2009;24(7): 979–983.

2.Sechi, G, Deledda, MG, Bua, G, et al. Reduced intravenous glutathione in the treatment of early Parkinson's disease. Prog Neuropsychopharmacol Biol Psychiatry. 1996;20(7):1159-70. 

3.Perlmutter, D. “New Advances in Parkinson’s Disease.” From BrainRecovery.com. Last updated 2004, currently unavailable. Chapter found at www.inutritionals.com/healthy-living/neurodegenerative-conditions/parkinsonsdisease/glutathione/glutathione-8

4. Bharath S, Hsu M, Kaur D, Rajagopalan S, Andersen JK, Glutathione, iron and Parkinson's disease. Biochem Pharmacol. 2002 Sep;64(5-6):1037-48.

5. Martin HL, Teismann P. Glutathione--a review on its role and significance in Parkinson's disease. FASEB J. 2009 Oct;23(10):3263-72. Epub 2009 Jun 19.

6. Chinta SJ, Andersen JK. Redox imbalance in Parkinson's disease. Biochim Biophys Acta. 2008 Nov;1780(11):1362-7. Epub 2008 Mar 4.

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The Diagnosis and Treatment of Hypothyroidism

Posted By Administration, Monday, June 14, 2010
Updated: Friday, April 18, 2014

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by Michael Schachter, MD, CNS

Hypothyroidism, or an underactive thyroid system, is one of the most underdiagnosed and important conditions in the United States. It has been called the "unsuspected illness" and accounts for a great number of complaints in children, adolescents and adults.

What kinds of complaints characterize an underactive thyroid system? Low energy and fatigue or tiredness, especially in the morning are frequent in these patients. Difficulty losing weight, a sensation of coldness--especially of the hands and feet, depression, slowness of thought processes, headaches, swelling of the face or fluid retention in general, dry coarse skin, brittle nails, chronic constipation, menstrual problems-such as PMS and menstrual irregularities including heavy periods, fertility problems, stiffness of joints, muscular cramps, shortness of breath on exertion and chest pain are some of the symptoms that can be seen in people with underactive thyroid systems. Be aware that a person with a low functioning thyroid doesn't have to have all of these symptoms, he may have only a few.

Function of the Thyroid Gland
Where is the thyroid located in the body and what does it do? The thyroid gland consists of two small lobes connected together. It is located in the front of the neck, just below the voice box. The thyroid gland is responsible for the speed of metabolic processes in the body and therefore affects every organ and organ system. It is the metabolic stimulator, analogous to the accelerator of a car. Normal growth requires normal thyroid functioning. When the thyroid is not functioning properly, organs become infiltrated with metabolic wastes and all functions become sluggish.

When the thyroid gland is working properly, it uses the amino acid tyrosine and iodine to make the thyroid hormone called thyroxine or T4. Thyroxine is called T4 because it contains four iodine atoms. If a person is deprived of iodine in his diet, he develops an enlarged thyroid gland, called a goiter and symptoms of an underactive thyroid or hypothyroidism.

The other important thyroid hormone is triiodothyronine or T3, which has three iodine atoms. T3 is actually the major active thyroid hormone, being much more active than T4. T4 is produced within the thyroid gland and is later converted to the active T3 outside the thyroid gland in peripheral tissues. Under certain conditions, such as stress, the thyroid gland may produce sufficient amounts of T4 to obtain normal thyroid blood tests, but its conversion to T3 may be inhibited, causing a relative insufficiency of active T3. Under this circumstance, the patient will have hypothyroid symptoms in spite of normal thyroid blood tests. As you will see, this fact results in many missed diagnoses of an underactive thyroid system.

The production and release of T4 from the thyroid gland is controlled by a hormone from the pituitary gland, which is located at the base of the brain. This hormone is called thyroid stimulating hormone or TSH. When the level of T4 in the bloodstream is low, the pituitary increases TSH production and release, which in turn stimulates the thyroid gland to produce and release more T4. The T4 then feeds back to the pituitary, reducing the secretion of TSH in a negative feedback loop. When a person has trouble making T4 due to iodine deficiency or for some other reason, one would expect to find an elevated TSH. The pituitary's TSH is trying to get the thyroid gland to produce more T4. If both T4 and TSH are low, this may indicate a pituitary problem with a low TSH secretion resulting in the low production and secretion of T4.

Diagnosis of Hypothyroidism
So, how is hypothyroidism diagnosed today by conventional medicine? Unfortunately, the diagnosis by conventional physicians, including thyroid specialists called endocrinologists, is made almost exclusively from blood tests. Generally, T4 and TSH are measured in the bloodstream. Additionally, a protein that binds T4 is also measured. From this protein and T4, the free T4 is calculated. If a patient has a normal TSH and a normal free T4, he is told by the conventional physician that he does not have hypothyroidism, no matter how many symptoms or signs of hypothyroidism he has. This is the fatal error because these tests only pick up the most severe cases of hypothyroidism and miss virtually all of the milder cases that would respond favorably to thyroid hormone treatment.

If most hypothyroid cases cannot be diagnosed by the usual blood tests, how can they be diagnosed? Prior to the extensive use of blood tests, hypothyroid states were diagnosed by astute clinicians, who obtained careful medical histories, including family histories from the patient, and who performed a complete physical examination. Later basal metabolic rates were measured using special equipment. Then came the blood tests--the protein bound iodine or PBI, T4, TSH and even T3 by special radioactive studies. Instead of using the blood tests as adjuncts to diagnosis, they were soon relied upon exclusively. To properly diagnose hypothyroidism, the clinician must go back to the careful medical history, physical examination and measurement of the basal temperature of the body. I'll discuss important aspects of the medical history and physical examination relevant to the diagnosis of hypothyroidism.

 


Medical History
What in the medical history suggests the likelihood of hypothyroidism? With regard to infancy and childhood, a high birth weight of over 8 lbs. suggests low thyroid. During childhood, early or late teething, late walking or late talking suggests a low functioning thyroid in the child. Also, frequent ear infections, colds, pneumonia, bronchitis or other infections; problems in school including difficulty concentrating, abnormal fatigue--especially having difficulty getting up in the morning and poor athletic ability all suggest a low thyroid. Keep in mind that a person with low thyroid functioning may have only a few of these characteristics. You don't have to find all of them to suspect a low thyroid.

During puberty, we see the same types of problems in school and with fatigue, which is worse in the morning and gets a little better later in the day. Often, adolescent girls suffer from menstrual irregularity, premenstrual syndrome and painful periods. Drug and alcohol abuse are common.

Throughout life, disorders associated with hypothyroidism include headaches, migraines, sinus infections, post-nasal drip, visual disturbances, frequent respiratory infections, difficulty swallowing, heart palpitations, indigestion, gas, flatulence, constipation, diarrhea, frequent bladder infections, infertility, reduced libido and sleep disturbances, with the person requiring 12 or more hours of sleep at times. Other conditions include intolerance to cold and/or heat, poor circulation, Raynaud's Syndrome, which involves the hands and feet turning white in response to cold, allergies, asthma, heart problems, benign and malignant tumors, cystic breasts and ovaries, fibroids, dry skin, acne, fluid retention, loss of memory, depression, mood swings, fears, and joint and muscle pain.

With regard to the family history, all of the above disorders can be checked in family members. Particular emphasis should be placed on hypothyroid conditions in parents or siblings. Also, a family history of Tuberculosis suggests the possibility of low thyroid.

Physical Examination
The physical examination often reveals the hair to be dry, brittle and thinning. The outer third of the eyebrows is often missing. One often finds swelling under the eyes. The tongue is often thick and swollen. The skin may be rough, dry and flaky and show evidence of acne. The skin may also have a yellowish tinge due to high carotene in it. Nails tend to be brittle and break easily. The thyroid gland may be enlarged. The patient is more often overweight, but may also be underweight. Hands and feet are frequently cold to the touch. Reflexes are either slow or absent. The pulse rate is often slow even though the patient is not a well trained athlete.

Measuring Basal Body Temperature
Instructions for taking basal body temperatures are relatively easy. Use an oral glass thermometer. Shake the thermometer down before going to bed, and leave it on the bedside table within easy reach. Immediately upon awakening, and with as little movement as possible, place the thermometer firmly in the armpit next to the skin, and leave it in place for 10 minutes. Record the readings for three consecutive days. Menstruating women must only take the basal temperature test for thyroid function on the 1st, 2nd, 3rd or 4th day of menses(preferably beginning on the 2nd day). Males, pre-pubertal girls, and post-menopausal or non-menstruating women may take basal temperatures any day of the month. Women taking progesterone should not take it the day before and the days that the basal temperatures are taken.

Most of the information on the manifestations of hypothyroidism, its diagnosis, including the technique for measuring and interpreting basal temperatures, and the treatment to be discussed was compiled and described by the late Dr. Broda O. Barnes. He is the author of the book Hypothyroidism: the Unsuspected Illness. His work is disseminated to physicians and the public by the foundation bearing his name, which is located in Trumbull, Connecticut.

How does one interpret the results of the basal body axillary temperature test? If the average temperature is below 97.8 Fahrenheit, then the diagnosis of a low functioning thyroid system is likely. An average temperature between 97.8 and 98.2 is considered normal. An average temperature above 98.2 is considered high and might reflect an infection or a hyperthyroid condition.

Treatment of Hypothyroidism
Once a pattern of hypothyroid symptoms is established and the basal body temperatures are found to be low, the next step is a therapeutic trial of thyroid hormone. Dr. Barnes, his physician followers and many patients have found that the most effective thyroid medication is Armour Desiccated Thyroid Hormone. This medication is derived from the thyroid gland of the pig. It most closely resembles the human thyroid gland. It is dried or desiccated and processed into small tablets. In contrast, most conventional physicians prefer to use the synthetically produced thyroxine or T4. In my experience and the experience of many other physicians using Dr. Barnes' protocol, the synthetic T4 is not as effective as the desiccated thyroid.

How can we monitor the results of treatment if the blood tests are inadequate to the job? We do this by how the person feels, whether or not the thyroid symptoms and signs have improved or disappeared, whether or not symptoms of an overactive thyroid gland have developed, and by monitoring the basal body temperature.

Generally, the dosage of Armour thyroid is best started at a low dose, with a gradual increase every week or two, until the optimal therapeutic dosage is reached. It may take four to six weeks at the optimal dosage to feel the full therapeutic benefits. In my practice, I generally start the patient on 1/4 grain or 15 milligrams daily. Every week or two, I increase the dosage by 1/4 grain per day until 1 to 2 grains daily are reached. Usually, the optimal dosage is in this range, provided that the patient is doing the other adjunctive necessary things, which I will discuss in a moment. Occasionally, the dosage may need to be 2 and a half grains daily or more. Full therapeutic benefits many not be fully realized for months and the basal temperatures may not come up to normal for a year or more. The dosage for infants is usually 1/8 to 1/4 grain daily and from one to six years old, the dosage is usually 1/4 grain. From 7 years to puberty, 1/2 grain is usually used, but it may need to be increased.

Special Cases: Recent Heart Attacks and Weak Adrenal Function
There are a few special cases that needs to be discussed in the context of this treatment. If a person has recently had a heart attack, treatment should not begin for at least two months following the heart attack. After that, the protocol discussed above can be used.

If a person has evidence of weak adrenal function, the adrenal gland problem must be treated first or simultaneous to the thyroid treatment. The reason for this is that hydrocortisone is necessary for the conversion of T4 to the active T3. If the weak adrenal is not addressed, the patient may actually feel worse and/or develop symptoms of an overactive thyroid gland, such as palpitations, a rapid heart beat and increased sweating. Clues to low adrenal functioning include a low blood pressure (less than 120/80), allergies, asthma, breathing difficulties, skin problems (such as acne, eczema, psoriasis, lupus, dry flaky skin), joint or muscle pains, as in arthritis, and emotional problems, such as mood swings, weeping, fears and phobias. Using low physiologic doses of hydrocortisone along with Armour Thyroid, when the patient shows evidence of both low adrenal and low thyroid function, will help to assure the desired results.

Problems in Converting T4 to the T3 Hormone
The conversion of the relatively inactive T4 to the active T3 thyroid hormone is an important process. As mentioned previously, frequently low thyroid function is not due to the low production of thyroxine, T4, by the thyroid, but due to the failure of conversion of T4 to T3 by peripheral tissues. What nutrients are necessary to help with this conversion? In addition to sufficient quantities of cortisol, iron, zinc, copper and selenium are necessary for this conversion. Deficiencies of any of these minerals can prevent the conversion T4 to T3 and should be corrected if present. Sufficient protein and especially the amino acid, tyrosine, and iodine are necessary to make T4 in the thyroid gland.

Another approach to the problem of conversion failure of T4 to T3 has been proposed by a young physician, Dennis Wilson. He has found that the body often adapts to various stressful situations by switching to a conservative mode in order to preserve energy. For example, when a famine occurs, an excellent adaptive change that the body can make in order to use less energy because food calories are unavailable, is to stop converting T4 to T3. However, this response appears to occur to a wide variety of stressors and sometimes this mode is not reversed, even after the stress is removed. This can lead to all of the symptoms and signs of a low thyroid that I have been discussing.

He has suggested the use of a special long acting T3 preparation to reset the conversion of T4 to T3 process. Dosages of T3 are given exactly every 12 hours in increasing amounts with close monitoring of oral temperatures during the day. High doses of T3 may be given and in order to normalize the oral temperature to 98.6 F. After the optimal temperature is reached and maintained for approximately three weeks or if the patient develops an intolerance to the particular dosage of long-acting T3, the dosage is tapered down to zero.

When the treatment is successful, the temperature will remain optimal with the loss of hypothyroid symptoms, even after the medication is tapered to zero. In other words, the thyroid system is reset at a higher temperature. This process may take several cycles of going up and down on the T3. This treatment requires a lot of discipline from the patient and often leads to symptoms during the treatment. However, it does seem to be useful in some patients. If the patient is stressed significantly and again enters the low thyroid system mode, the entire process can be repeated again. Usually, the treatment is easier at each subsequent episode.

Nevertheless, for most patients, especially if there are adrenal problems or other medical complications, the use of Armour desiccated thyroid on a continuous basis is probably easier and preferable.

Recent studies indicate that patients who have been treated with excessive doses of thyroid hormone over long periods of time may be at increased risk for developing osteoporosis. This may be due not only to too much thyroid, but also to an imbalance between the anabolic and catabolic endocrine hormones. The catabolic hormones are those that help to break down dead tissues and rid the body of metabolic waste. These would include thyroid hormone and hydrocortisone. The anabolic hormones are those that help to rebuild the body and would include DHEA, estrogens, progesterone and the male hormone, testosterone. A physician who is trying to balance a person's thyroid system must also look at all of the other hormones and also all aspects of the person's lifestyle, including diet, nutritional supplements, exercise patterns and stress coping mechanisms. The nutrients that are especially important to a proper functioning thyroid system are iodine and the amino acid tyrosine to make thyroid hormone in the thyroid gland and the minerals iron, selenium, zinc and copper to convert the inactive T4 to the active T3.

How Long Should Patients Take Thyroid Hormone?
When using the desiccated thyroid protocol, patients often remain on the thyroid for life. However, there may be times when the patient can be weaned off the thyroid as all other functions improve, as long as the patient is carefully monitored for the development of low thyroid symptoms and signs and low basal temperatures. When a person's basal temperatures are low, many of the enzymes of the body function in a suboptimal way, which leads to all of the problems we have discussed.

On the other hand, well treated hypothyroid patients should enjoy a vibrant life with lowered risks of all of the degenerative diseases including arthritis, cancer and heart disease. I personally have seen a number of patients whose arthritis pains have completely cleared when treated with proper doses of thyroid. With regard to cancer, the well known alternative cancer treatment developed by Max Gerson, involves the use of Armour Desiccated Thyroid in virtually all of his cancer patients. High serum cholesterol and the development of atherosclerosis are well known effects of hypothyroidism. Therefore, all patients with coronary artery disease and other atherosclerotic conditions should be checked carefully for evidence of a low functioning thyroid condition and treated cautiously and appropriately if a low thyroid condition is found. Psychiatrists have found that the addition of thyroid hormone to patients suffering from refractory depression often is helpful, even when the blood tests are normal.

The proper appreciation of low thyroid conditions and their subsequent treatment should aid greatly in reducing the morbidity and premature mortality of virtually all degenerative diseases.


Schachter Director of the Schachter Center for Complementary Medicine, Michael B. Schachter, M.D., is a 1965 graduate of Columbia College of Physicians & Surgeons. He is board certified in Psychiatry, a Certified Nutrition Specialist, and has obtained proficiency in Chelation Therapy from the American College for Advancement in Medicine (ACAM). Dr. Schachter has more than 30 years experience in complementary and alternative medicine. Our talented staff of trained professionals work together to evaluate and treat patients who have a wide variety of medical complaints as well as those who simply wish to optimize their health. Sophisticated biochemical testing is available.

Using the latest advances, our clinical staff strives to uncover the underlying causes of disease and to change the physical and emotional terrain to establish an environment that supports the body's natural ability to heal itself. You can also see their website at http://www.mbschachter.com/

Source: healthy.net. The Diagnosis And Treatment of Hypothyroidism. Schachter, Michael.

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What Lies Behind the Vitamin D Revolution?

Posted By Administration, Friday, June 11, 2010
Updated: Friday, April 18, 2014

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by Ronald Hoffman, MD

Generations of medical professionals have been taught to approach vitamin D supplementation with great caution and trepidation. As a fat-soluble vitamin known to enhance calcium absorption, vitamin D taken in excessive amounts was thought to raise the specter of hypercalcemia with its attendant risks of nephrolithiasis and even metastatic calcification. Our understanding of vitamin D's health benefits was limited to its familiar role in maintaining bone strength by means of regulating calcium uptake. But thanks to an explosion in vitamin D research, a broader perspective is rapidly evolving.


Powered by its pervasive influence on myriad physiological processes, vitamin D is staking its claim as "Nutrient of the Decade." We now recognize that vitamin D transcends the definition of a mere vitamin: It is actually a prohormone, and vitamin D receptors are expressed by cells in most organs, including the brain, heart, skin, gonads, prostate gland, and mammary glands. In the digestive tract and parathyroid glands, active vitamin D metabolites are responsible for calcium uptake. Vitamin D receptors are also involved in immune regulation and mediate response to infection and inflammatory processes. Additionally, the nutrient is associated with cell proliferation and differentiation.


Fracture prevention


Vitamin D's traditionally acknowledged role is in bone metabolism. The pathognomonic vitamin D deficiency disease is rickets, but less overt prolonged insufficiency results in osteomalacia. This condition is characterized by softening of the bones and musculoskeletal pain, the result of periosteal traction. Not surprisingly, an association between vitamin D repletion and relief of unexplained body aches has been observed in some studies. 


Chronic vitamin D deficiency can result in secondary hyperparathyroidism with consequent osteoporosis. Vitamin D deficiency in childhood and adolescence impairs attainment of optimal bone mass. Frequently, clinicians neglect to assess vitamin D status and don't consider the treatment option of aggressive repletion when using drugs to manage osteopenia or osteoporosis. A new minimum threshold for vitamin D of 50-75 nmol/L (20-30 ng/mL) was recently proposed to prevent osteoporosis. However, vitamin D receptor polymorphisms modulate skeletal response to vitamin D supplementation even in healthy girls, and individual requirements for bone optimization may vary. A minimal threshold of 40 ng/mL for healthy bone metabolism has also been proposed.


The ultimate goal of osteoporosis treatment is fracture prevention. Considerable evidence suggests vitamin D can support muscle strength and thereby reduce the incidence of falls, particularly in elderly, at-risk patients. In addition, vitamin D arguably has an indirect role in staving off fractures: As a nondrug treatment for osteoporosis, the use of vitamin D reduces polypharmacy with various cardiovascular, anti-inflammatory, and psychiatric medications that can induce nutrient depletions and impair balance in frail seniors. 


Cardiovascular disease


Vitamin D deficiency is associated with increased risk for cardiovascular events and mortality. In the Multi-Ethnic Study of Atherosclerosis, 25-hydroxyvitamin D (25[OH]D)levels were inversely associated with the risk of coronary artery calcification, a measure of coronary atherosclerosis.


Cardiovascular disease (CVD) represents the culmination of an array of predisposing influences, and vitamin D may intervene beneficially in several ways. Studies confirm an association between obesity and vitamin D deficiency, and low vitamin D status is predictive of insulin resistance. Overweight women replete with vitamin D shed pounds more successfully. Moreover, studies have found correlation between suboptimal vitamin D status and both hypertension and diabetes.


In renal disease, characterized by problematic vitamin D metabolism, CVD is rampant—but cardiovascular risk is known to be attenuated by vitamin D administration.


Evidence also indicates that vitamin D deficiency—common in elderly, debilitated patients—plays a role in congestive heart failure, which is mediated by the nutrient's effect on myocyte contractility.



Cancer


Sun exposure is clearly required for vitamin D sufficiency. However, latitude, season, time of day, weather conditions, shade, skin pigmentation, air pollution, clothing, use of sunscreen, and age impact cutaneous vitamin D activation. Below 32º latitude (corresponding to a line stretching from Los Angeles to Columbia, S.C.), sunlight exposure can activate vitamin D year-round. But above 44º north latitude (which extends from the northern tip of California to Boston), no cutaneous activation is possible from November through February.


It has long been noted that colon cancer rates increase with higher geographic latitude. This epidemiologic correlation was initially attributed to Western diet and lifestyle, but subsequent studies controlled for extraneous factors and confirmed the protective role of sunlight. Scientists were then able to establish the biological plausibility for the impact of vitamin D in cancer prevention, recognizing the vitamin's effects on cell proliferation, oncogenesis, and apoptosis. Since then, investigators have explored a putative involvement of vitamin D in both primary and secondary prevention of prostate cancer and breast cancer as well as non-Hodgkin's lymphoma, melanoma, and other malignancies.


Immunity


Cells involved in innate and adaptive immune responses —including macrophages, dendritic cells, T cells, and B cells—express the vitamin D receptor. In the 19th century, before the advent of antibiotics, caregivers recognized that individuals with TB could benefit from sunlight and fresh air during their stays in mountain sanitoria. Research has confirmed that host response to TB is partially mediated by vitamin D, and that vitamin D deficiency is associated with dysregulation of macrophage response. 


The observed seasonal correlation between sunlight exposure and the incidence of viral upper respiratory infections has prompted speculation about the role played by vitamin D. Research confirms that vitamin D dramatically stimulates the expression of potent antimicrobial peptides. These compounds exist in neutrophils, monocytes, natural killer cells, and epithelial cells lining the respiratory tract, where they play a major role in protecting the lung from infection. The action of vitamin D serves as a key link between Toll-like receptor activation and antibacterial responses in innate immunity. An association between vitamin D insufficiency (25[OH]D <40 nmol/L) and acute respiratory tract infection was recently confirmed. As yet, prospective intervention studies are few and small in scale.


Autoimmunity


The incidence of certain autoimmune diseases correlates positively with latitude from the equator, as reflected by the epidemiology of rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, and multiple sclerosis (MS). Studies confirm that patients suffering from autoimmune disease have vitamin D levels below the international norm. There is substantial biological rationale for vitamin D as a cytokine modulator. 


Animal models of autoimmune disease suggest a response effect with vitamin D administration; large human therapeutic trials using vitamin D are still lacking, but the first results of phase I/II studies are promising. Meanwhile, it is now acknowledged that administering vitamin D in patients with autoimmune diseases is justifiable. 


Other conditions


Perhaps the most persuasive rationale for considering vitamin D optimization comes from a study of 3,400 French men, age 50 years and older, correlating vitamin D status with all-cause mortality. Men in the lowest quartile of 25(OH)D levels had a 44% higher death rate. The authors qualified their findings by stating that although the study controlled for lifestyle variables and comorbidities, a possibility exists that low levels of vitamin D are merely reflective, and not causative, of poor health status.


Because of the ubiquity of the nutrient's impact on physiologic processes, some researchers have proposed associations between vitamin D status and incidence of autism, allergic diseases, depression, schizophrenia, cognitive impairment, pre-eclampsia, fibromyalgia, Parkinson disease, polycystic ovary syndrome, and benign prostatic hyperplasia. Athletic trainers, cognizant of research suggesting that vitamin D may augment muscle strength, are increasingly embracing oral supplementation and UV-light exposure for purposes of performance enhancement. 


Of course, a long-observed relationship between sunlight exposure and severity of psoriasis suggests mediation by vitamin D; topical calcipotriene (Dovonex), a synthetic vitamin D analogue, is a standard dermatologic treatment for the condition.


Vitamin D has received renewed interest for its role in pregnancy. Studies suggest that higher levels of vitamin D supplementation than are currently recommended for pregnant women may safeguard offspring from the risks of low birth weight, autism, juvenile diabetes, asthma and allergic rhinitis, and infectious diseases. The Canadian Pediatric Society recently recommended that pregnant women increase their intake of vitamin D to 2,000 IU/day.


 

Pervasiveness of deficiency and risk factors


A number of health authorities now acknowledge that vitamin D deficiency is a pervasive problem in the United States and the developed world. Sun deprivation, already a problem for inhabitants of temperate latitudes, is exacerbated by indoor occupations and recreation and is further encouraged by warnings against sun exposure to prevent skin cancer.


Although overt vitamin D deficiency is no longer common in U.S. children, lesser degrees of vitamin D insufficiency are widespread. Groups at heightened risk for vitamin D deficiency include: the homebound elderly; older individuals overall (due to the declining potential for vitamin D production as the skin ages); darker-skinned individuals (melanin in skin protects the skin from UV radiation but increases the exposure time required for photoactivation of pre-vitamin D in the skin); and members of communities that require their constituents to cover up. Obesity also is associated with vitamin D deficiency, and some evidence indicates that adipose tissue is involved in sequestration of the nutrient.


Conditions that predispose a person to vitamin D deficiency include liver disease, which interferes with the 25 hydroxylation of vitamin D; chronic renal failure, which interferes with 1 hydroxylation; and malabsorption syndromes, which are either iatrogenic (e.g., status after bariatric surgery or in users of fat-sequestering medications such as cholestyramine) or the result of biliary tract disease, cystic fibrosis, celiac disease, inflammatory bowel disease, or similar conditions. Certain drugs, including anti-epileptic medications, deplete vitamin D. To complicate matters, research points to vitamin D receptor polymorphisms, which attenuate end-organ response to circulating levels of vitamin D. 


Routine, modest supplementation is not a reliable bulwark against vitamin D deficiency. Researchers were recently surprised to note the high prevalence of vitamin D deficiency in pregnant women—the very group most likely to be shielded from this problem because of high compliance with prenatal-vitamin regimens. Additionally, living in the sunny, warm regions of the country may raise a person's chances of achieving vitamin D sufficiency, but a recent study of Hispanics in Arizona uncovered a high rate of vitamin D inadequacy.


Dietary sources of vitamin D are limited (Table 1). Milk, which is the only dairy product routinely fortified with the nutrient, supplies a mere 100 IU/cup, which represents only a quarter of the minimal requirement for adults. Human breast milk delivers only 25 IU/L on average. Herring, tuna, eel, and mackerel are all good sources of vitamin D, but many people avoid these foods because they do not like the taste. 


Measurement


The two forms of vitamin D most commonly measured by clinical laboratories are 25(OH)D (calcidiol) and 1,25 hydroxyvitamin D (1,25[OH]2D) (calcitriol). Until recently, health-care providers predominantly relied on the latter for vitamin D assessment, but new findings suggest that its utility is limited (except in renal disease, in which 1 hydroxylation is an issue). Not infrequently, 1,25(OH)2D levels are found to be sufficient or even supra-normal while 25(OH)D levels remain suboptimal. 


Because of its greater reliability, a 25(OH)D level is now favored as the accepted method for determining vitamin D nutritional status. The optimal level of serum 25(OH)D is 35-55 ng/mL (90-140 nmol/L), with some medical scientists advocating for the slightly higher value.


Many reference labs have adopted a classification system that stratifies vitamin D levels as follows (to convert conventional [ng/mL] units to SI [nmol/L] units, multiply by 2.5):


0-14.9 ng/mL = Severely deficient 


15.0-31.9 ng/mL = Mildly deficient 


32.0-100.0 ng/mL = Optimal 


>100.0 ng/mL = Toxicity possible 


Findings of elevated bone isoforms of alkaline phosphorous, elevated parathyroid hormone, or urinary N-telopeptide should prompt suspicion of vitamin D deficiency (to be confirmed by serum measurement of 25[OH]D).


Toxicity


The threshold for vitamin D toxicity is currently being re-evaluated, with most experts now agreeing that previous benchmarks have been unduly conservative (Table 2). This change in thinking stems partially from the realization that a single, minimal erythemal dose of sun exposure promotes synthesis of 10,000 IU of vitamin D. Early reports of vitamin D toxicity with doses as low as 3,600 IU/day have been challenged due to methodologic flaws. It has been reported that human toxicity likely begins to occur after chronic daily vitamin D consumption of approximately 40,000 IU/day. 


A theoretical risk of vitamin D toxicity exists when prolonged sunlight exposure is combined with aggressive supplementation, but feedback inhibition occurs with UV-light activation of vitamin D in the dermis, rendering this possibility less likely.


Clinicians must administer vitamin D cautiously in patients with certain medical conditions. For example, individuals with primary hyperparathyroidism are at risk for hypercalcemia, which might be exacerbated by additional vitamin D. (Conversely, in secondary hyperparathyroidism, correction of the underlying vitamin D deficiency helps normalize elevated calcium).


In sarcoidosis and such malignancies as oat-cell cancer and non-Hodgkin's lymphoma, aberrant conversion of 25(OH)D to calcitriol results in hypercalcemia, offering a relative contraindication to vitamin D administration.


The main symptoms associated with vitamin D toxicity result from hypercalcemia. Anorexia, nausea, and vomiting can develop, followed in some cases by renal failure. The diagnosis can be confirmed through measurement of serum 25(OH)D (typically >140 ng/mL) in the presence of elevated serum calcium.


Treatment involves stopping vitamin D intake. If necessary, the clinician can hydrate the patient with IV normal saline and administer corticosteroids or bisphosphonates (which inhibit bone resorption) to reduce blood calcium levels.


Recommendations for supplementation 


The longtime government recommendation for vitamin D intake in adults and older children was set rather arbitrarily at 400 IU/day. This is thought to derive from the historical precedent that a teaspoon of cod liver oil, a traditional source of supplementation, delivers approximately 400 IU of vitamin D.


For infants younger than age 4 years, the Daily Value (developed by the FDA to help consumers compare the nutrient contents of products within the context of a total diet) is just 200 IU, but in 2008 the American Academy of Pediatrics took the lead in advancing the threshold to 400 IU in light of evidence of the safety and benefits of vitamin D.


The Food and Nutrition Board of the Institute of Medicine is currently re-examining Daily Values for vitamin D and calcium and plans to issue revised guidelines this year. Most nutrition scientists are expecting upward revisions.


Controversy now rages over what constitutes "deficiency" versus "sufficiency." Alternatively, optimal therapeutic levels may be appropriate for various health conditions. Guidelines for prevention of rickets, for example, may be inadequate for prevention or reversal of osteoporosis. Some argue that nutritional support for such autoimmune diseases as MS might call for pharmacologic doses of vitamin D. In a recent study, 16% of 25 MS patients who were given an average of 14,000 IU/day of vitamin D for one year suffered relapses. In contrast, close to 40% of 24 MS patients who took an average of 1,000 IU/day—the stepped-up supplementation belatedly acknowledged to be necessary by many MS specialists—relapsed. 


A clue to the amount of vitamin D needed to optimize serum levels of 25(OH)D in seniors comes from a study of men and women older than age 64 years. The intakes required to maintain serum 25(OH)D concentrations of >15 ng/mL, >20 ng/mL, and >32 ng/mL in 97.5% of the sample were 688 IU/day, 988 IU/day, and 1,548 IU/day, respectively. Note that these levels of supplementation are well above the current Daily Values yet do not even attain what some consider being optimal thresholds for vitamin D.


Vitamin D supplements are available in two forms, D2 (ergocalciferol) and D3 (cholecalciferol). High-dose prescription vitamin D 50,000 IU (Drisdol, Calderol, Calciferol), commonly prescribed for rapid remediation of vitamin D deficiency, is vitamin D2. Vitamin D2 is manufactured by the UV irradiation of ergosterol in yeast, and vitamin D3 is manufactured by the irradiation of 7-dehydrocholesterol from lanolin and the chemical conversion of cholesterol.


Some argue that vitamin D3 could be more than three times as effective as vitamin D2 in raising serum 25(OH)D concentrations and maintaining those levels for a longer time, and that its metabolites have superior affinity for vitamin D-binding proteins in plasma. Further research is required to compare the clinical efficacy of the two forms.


Most supplements available from health-food stores are vitamin D3. Commonly available doses range from 400 to 5,000 IU, variously delivered in tablet, capsule, and liquid forms. Parenteral forms of vitamin D are also available but are seldom needed to reach target levels outside the settings of chronic renal failure and dialysis.


Suggested treatment of vitamin D deficiency 


Vitamin D deficiency (25[OH]D level <20 ng/mL): Vitamin D 50,000 IU once a week for three months; repeat 25(OH)D level.


If >20 ng/mL but <30ng/mL, change the vitamin D supplement to 5,000 IU/day until levels of 40-50 ng/mL are attained.


If still <20 ng/mL, advance vitamin D to 50,000 IU twice a week, or consider giving it more frequently. (In certain clinical situations, especially those involving malabsorption syndromes, up to 50,000 IU three times a week may be needed.) 


Vitamin D insufficiency (25[OH]D level 20-30 ng/mL): Administer vitamin D 5,000 IU daily for three months, repeat 25(OH)D level.


If <30 ng/mL, advance vitamin D to 50,000 IU once a week or more frequently if needed.


Once 25(OH)D levels are restored to >40 ng/mL, administer maintenance supplementation of 2,000-5,000 IU/day. 


For reasons that are not yet completely clear, considerable variability in response to vitamin D supplementation exists among patients. Clinicians should monitor a patient's 25(OH)D levels frequently to assess reaction to therapy until stable levels are achieved, subject to seasonal variations and changes in health status.


- Ronald Hoffman, MD

Dr. Hoffman is founder and Medical Director of the Hoffman Center in New York City. The author has no relationships to disclose relating to the content of this article.


Read on


  • Arabi A, Zahed L, Mahfoud Z, et al. Vitamin D receptor gene polymorphisms modulate the skeletal response to vitamin D supplementation in healthy girls. Bone. 2009;45:1091-1097.

  • Lips P, Bouillon R, van Schoor NM, et al. Reducing fracture risk with calcium and vitamin D. Clin Endocrinol (Oxf). 2009; September 10 (published online ahead of print).

  • Stechschulte SA, Kirsner RS, Federman DG. Vitamin D: bone and beyond, rationale and recommendations for supplementation. Am J Med. 2009;122:793-802. 

  • Janssens W, Lehouck A, Carremans C, et al. Vitamin D beyond bones in chronic obstructive pulmonary disease: time to act. Am J Respir Crit Care Med. 2009;179:630-636.

  • Holick MF. The vitamin D deficiency pandemic and consequences for nonskeletal health: mechanisms of action. Mol Aspects Med. 2008;29:361-368.

  • Rovner AJ, O'Brien KO. Hypovitaminosis D among healthy children in the United States: a review of the current evidence. Arch Pediatr Adolesc Med. 2008;162:513-519. 
  • Cannell JJ, Hollis BW. Use of vitamin D in clinical practice. Altern Med Rev. 2008;1:6-20.

  • Autier P, Gandini S. Vitamin D supplementation and total mortality: 
a meta-analysis of randomized controlled trials. Arch Intern Med. 2007;10:167:1730-1737. 
  • Arnson Y, Amital H, Shoenfeld Y. Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Ann Rheum Dis. 2007;66:1137-1142.

  • Holick MF. Medical Progress: vitamin D deficiency. N Engl J Med. 2007;357:266-281. 
  • Niino M, Fukazawa T, Kikuchi S, Sasaki H. Therapeutic potential of vitamin D for multiple sclerosis. Curr Med Chem. 2008;15:499-505.

  • Garland CF, Gorham ED, Mohr SB, Garland FC. Vitamin D for cancer prevention: global perspective. Ann Epidemiol. 2009;19:468-483.

  • de Boer IH, Kestenbaum B, Shoben AB, et al. 25-hydroxyvitamin D levels inversely associate with risk for developing coronary artery calcification. J Am Soc Nephrol. 2009;20:1805-1812. 

  • Cannell JJ, Zasloff M, Garland CF, et al. On the epidemiology of influenza. Virol J. 2008;5:29.
  • Laaksi I, Ruohola J-P, Tuohimaa P, et al. An association of serum vitamin D concentrations <40 nmol/L with acute respiratory tract infection in young Finnish men. Am J Clin Nutr. 2007;86:714-717. 
  • Szulc P, Claustrat B, Delmas PD. Serum concentrations of 17beta-E2 and 25-hydroxycholecalciferol (25[OH]D) in relation to all-cause mortality in older men—the MINOS study. Clin Endocrinol (Oxf). 2009;71:594-602.

  • Cashman, KD, Wallace J MW, Horigan G, et al. Estimation of the dietary requirement for vitamin D in free-living adults >64 y of age. Am J Clin Nutr. 2009;89:1366-1374.


All electronic documents accessed February 10, 2010.


Published March 1, 2010. The Clinical Advisor. What Lies Behind the Vitamin D Revolution. By Ronald Hoffman, MD.

Tags:  vitamin D 

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