Category: Immune Support

Vitamin D A Special HealthBeat News Report


Vitamin D – You have been reading about it in the news, and you have wondered what is real and what is hype.

Dr. Myatt and Nurse Mark have researched and prepared this special report for HealthBeat News Readers.

Vitamin D — The Short Course

1.) Vit D is produced in our bodies in response to sun exposure. Vit D is also available from food and supplements.

2.) Vit D is FAR more important to health than was previously realized. I’m talking FAR more important.

3.) Vit D deficiency is widespread, including North America, even in sunny climates like Arizona. Many people who think they are getting enough Vitamin D from sunlight are mistaken.

4.) How to Optimize Vit D Levels for Good Health:

I.)  Vit D test, supplement accordingly, re-test

II.) Supplement at 5,000IU for 3 months, then test your levels.

III.) Don’t test, run the risk of being deficient, but take at least 2,000IU total per day. (This is still an extremely conservative dose, but much higher than the RDA of 400IU which hasn’t been changed yet to reflect the newer findings about Vit D). 

5.) Natural ways to obtain Vit D: Foods, supplements and sun exposure.

Vitamin D — Nutrient of the Decade: Are You Getting Enough?

The Consequences of Low Vitamin D

Vitamin D is called “the sunshine Vitamin” because our bodies make it in response to sun exposure.

Vit D is necessary for normal bone formation in both children and adults. In children, deficiencies of Vit D lead to rickets. In adults, deficiencies are associated with osteoporosis and osteomalacia (soft bones), decreased muscle strength and increased risk of fall. (1,12,14,22,43-48)Until recently, the bone-protecting effect was  about all that Vit D was known for, but the past decade of medical research has changed all that.

The newly appreciated Vitamin D deficiency risks include:

1.) heart disease: myocardial infarction, high blood pressure, heart failure, myopathy, sudden cardiac death, stroke (11,13-26, 30, 49-50)

2.) blood sugar problems: glucose intolerance, diabetes mellitus, metabolic syndrome (13-14,19,23-24,27-29)

3.) cancer prevention and improved cancer survival rates (7,8,11,14,15,24,31-37)

4.) upper respiratory tract infections, influenza and tuberculosis (24,30,38)

5.) cognitive impairment and low mood (38-40)

6.) autoimmune disease (multiple sclerosis, RA, systemic lupus erythromatosis (SLE) (15,24,26,29,30,32,41,42)

7.) misc. diseases: psoriasis, polycystic ovarian syndrome, inflammatory bowel disease

8.) urinary incontinence (54)

9.) and all-cause mortality! (5,6,7,24,30,51)

How “significant” are these associations? Here are some of the conclusions of various studies and meta-analyses (lots of studies looked at together) concerning Vit D. Italics are mine for emphasis.

“Research strongly supports the view … Vitamin D status would have significant protective effects against the development of cancer …. cancers of the breast, colon, prostate, ovary, lungs, and pancreas…” (8)

“High levels of Vitamin D among middle-age and elderly populations are associated with a substantial decrease in cardiovascular disease, type 2 diabetes and metabolic syndrome.” (9)

“Low levels of [Vitamin D] are independently predictive for fatal strokes” (10)

“It is estimated that there is a 30 to 50% reduction in risk for developing colorectal, breast, and prostate cancer by either increasing Vitamin D intake or increasing sun exposure…” (11)

“Oral Vitamin D supplementation between 700 to 800 IU/d appears to reduce the risk of hip and any nonvertebral fractures in ambulatory or institutionalized elderly persons” (12)

” 28 studies including 99,745 participants … highest levels of serum [Vit D] were associated with a 43% reduction in cardiometabolic disorders (cardiovascular disease, diabetes and metabolic syndrome) …” (9)

Are Your Vitamin D Levels Optimal? (Vitamin D Deficiency is Widespread)

One billion people worldwide are estimated to be Vit D deficient, and the problem affects us here in the United States as well. (2) One study found that more than half of North American women receiving drugs for prevention or treatment of osteoporosis were Vitamin D deficient. (1) Another study found 48% of pre-adolescent girls to be Vit D deficient (3). Other studies have found that 40% to 100% of older men and women in both the United States and Europe are Vitamin D deficient.[2] Because of the importance of Vit D and how widespread Vit D deficiency is, an estimated $100 to $200 billion is spent (wasted) each year on diseases which may really just be Vitamin D deficiencies. [4]

Age, overweight, dark skin color, use of sunscreen, and overprotection from the sun’s rays are causes of decreased production of Vit D in response to sunlight. (52,52)

How Much Vitamin D Should You Take?

Ideally, you should take whatever amount of Vitamin D puts you in the “optimal” range. Since the amount will be highly variable depending on age, sex, race, weight, daily sun exposure and diet, there is no “one size fits all” answer. Instead, blood testing of Vitamin D levels and increasing intake until optimal levels are reached is the surest way to obtain optimal concentrations of Vitamin D in the body.

Deficiency Insufficiency Sufficiency * Optimal Excess (Toxicity) <20ng/ml 20-32ng/ml 32-100ng/ml 40-80ng/ml > 150ng/ml

* – conventional medicine says that 30 ng/ml is “sufficient.” Chart references (59-62)

At the wellness Club we believe the most accurate and effective way to embark on a program of Vit D supplementation is to perform a Vit D test, supplement Vit D in accordance with the results, and then re-test in 3 months at which time your daily doses of Vit D can be fine-tuned for maintenance. March (right now!) is the best time to test initially because Vit. D stores tend to be lowest in this month.

The Vitamin D Council, a non-profit group dedicated to Vitamin D research and education recommends people take 5,000 IU per day for 2-3 months, then perform a Vitamin D test. They then suggest adjusting the dosage so that blood levels are between 50-80 ng/mL (or 125-200 nM/L) year-round. (55)

Alternately, some people opt to supplement without knowing their initial Vit D levels. A dose of 2000IU is quite conservative but certainly safe for almost anyone. In cases of significant Vit D deficiency conservative dosing such as this may take considerable time to rebuild healthy stores of this important Vitamin.

For those who wish to calculate their own Vit D requirements, 100 IU of Vitamin D could be expected to raise blood level of 25(OH)D by 1 ng/ml. (11)

Can too much Vitamin D can be toxic? Research shows that massive doses may eventually cause toxicity. One source found that in adults a sustained intake of 50,000 IU daily could produce toxicity within a few months (58) and 40,000 IU per day in infants has been shown to produce toxicity within 1 to 4 months. (56) That is ten times the recommended dose for each of those age groups! Vitamin D testing is good insurance that will allow you to safely fine-tune your dosage to your actual needs. Be careful though, since not all testing is the same and lab references and standards vary – be sure that you are comparing “apples to apples” and obtaining useable results when you are tested.

The 25-hydroxyVitamin D blood test (25(OH)D blood test) is a test that measures the amount of calcidiol circulating in the blood. This is the most accurate measure of the amount of Vitamin D in the body. The Wellness Club offers Vitamin D testing – performed by a lab that adheres to standardized references and values so that you know what you are getting when you receive your results. This can is performed at home with a “spot” (finger stick) blood test. Other tests that require a blood draw are also available.

How to Get to Your Optimal Vitamin D Levels

Start Vitamin D supplementation eight to twelve weeks before testing. Dr. John Cannell of the Vitamin D Council suggests a starting dose of 1,000 IU per 25 pounds of body weight. For example, a 150 pound person would take 6,000 IU Vitamin D per day. (150 divided by 25 = 6; 1,000IU x 6 = 6,000). Maintain this dose for 8-12 weeks, then test.

This dose may or may not put you in the optimal target range, but it certainly won’t put you in any “toxic” range. Remember, most adults can safely take up to 10,000IU per day and still be far away from Vitamin D toxicity which typically appears at 40,000-50,000IU taken for several months.

Although this dose should theoretically put you in an optimal range, numerous personal variations alter Vitamin D requirements. Some people will need a higher dose than this calculation affords. However, taking the calculated dose should at least put you “in the ballpark” for optimal dosing.

When you test results come back, you can use the number to help you know whether or not you need to increase your Vit D dose and by how much. It is estimated that each 1,000 IU increase in supplemental Vitamin D will generally produce a 10 ng/ml increase in the Vitamin D blood level (8). If your test result shows that you are 10ng/ml below your target, increase daily Vit D intake by 1,000IU per day for a total of 7,000IU per day from the above example. Continue this dose and re-test in another 3 months to verify that you are now in your optimal range.

Congratulations! You have found your optimal daily Vitamin D intake needed to maintain optimal Vitamin D blood levels.

How to Obtain Vitamin D Naturally

Exposure to sun is the most natural way to boost Vit D levels. Medical scientists have found that the skin produces approximately 10,000 IU of Vitamin D in response to as little as 30 minutes of unprotected summer sun exposure. (57)

Vitamin D can be obtained from food too. Since rickets in children is such a crippling but preventable condition, governments have long encouraged the “fortification” of dairy products and breads and cereals with token amounts of Vitamin D. In the United States and Canada, for example, fortified milk typically provides 100 IU per glass.

It is difficult to obtain optimal levels of Vitamin D from food alone.

Food IUs per serving* Percent DV** Cod liver oil, 1 tablespoon 1,360 340 Salmon (sockeye), cooked, 3 ounces 794 199 Mushrooms that have been exposed to ultraviolet light to increase vitamin D, 3 ounces (not yet commonly available) 400 100 Mackerel, cooked, 3 ounces 388 97 Tuna fish, canned in water, drained, 3 ounces 154 39 Milk, nonfat, reduced fat, and whole, vitamin D-fortified, 1 cup 115-124 29-31 Orange juice fortified with vitamin D, 1 cup (check product labels, as amount of added vitamin D varies) 100 25 Yogurt, fortified with 20% of the DV for vitamin D, 6 ounces (more heavily fortified yogurts provide more of the DV) 80 20 Margarine, fortified, 1 tablespoon 60 15 Sardines, canned in oil, drained, 2 sardines 46 12 Liver, beef, cooked, 3.5 ounces 46 12 Ready-to-eat cereal, fortified with 10% of the DV for vitamin D, 0.75-1 cup (more heavily fortified cereals might provide more of the DV) 40 10 Egg, 1 whole (vitamin D is found in yolk) 25 6 Cheese, Swiss, 1 ounce 6 2 *IUs = International Units.

**DV = Daily Value. DVs were developed by the U.S. Food and Drug Administration to help consumers compare the nutrient contents of products within the context of a total diet. The DV for vitamin D is 400 IU for adults and children age 4 and older. Food labels, however, are not required to list vitamin D content unless a food has been fortified with this nutrient.

Table courtesy of the U.S. Government National Institutes of Health Office of Dietary Supplements

Although cod liver oil is high in Vitamin D, it is also high in Vitamin A which interferes with Vit D uptake, so cod liver oil is not the best supplemental form of Vit D. Keep daily intake of pre-formed Vitamin A to a maximum of 5,000IU per day so as not to interfere with Vitamin D absorption. Beta carotene does not appear to interfere with Vit. D uptake.

Vegetarians need to be sure they are getting plenty of sunshine, because other than tiny amounts that may be found in UV-irradiated mushrooms, there are no vegetable sources of Vitamin D.

The Bottom Line on Vitamin D

Achieving Optimal Vitamin D  levels appears to be one of the most important things we can do for our overall health and life expectancy.

Please click on the image below enjoy an interesting and instructive video which discusses the relationship between Vitamin D and Cancer.

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References

1.) Holick MF, Siris ES, Binkley N, et al. Prevalence of Vitamin D inadequacy among postmenopausal North American women receiving osteoporosis therapy. J Clin Endocrinol Metab. 2005;90: 3215-3224.
2.) Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357:266-281.
3.) Sullivan SS, Rosen CJ, Halteman WA, Chen TC, Holick MF. Adolescent girls in Maine at risk for Vitamin D insufficiency. J Am Diet Assoc. 2005;105:971-974.
4.) GrassrootsHealth. The Vitamin D deficiency epidemic. A call to D*action. http://www.grassrootshealth.org/daction/epidemic.php. Accessed May 8, 2009.
5.) GrassrootsHealth. Disease incidence prevention by serum 25(OH)D level. http://www.grassrootshealth.org/_download/disease_incidence_prev_chart_101608.pdf. Accessed May 8, 2009.
6.) Autier P, Gandini S. Vitamin D supplementation and total mortality. Arch Intern Med. 2007;167(16):1730-1737.
7.) Thomas L. Lenz. Vitamin D Supplementation and Cancer Prevention. Am J Lifestyle Med. 2009;3(5):365-368.
8.) Ingraham BA, Bragdon B, Nohe A. Molecular basis of the potential of Vitamin D to prevent cancer. Curr Med Res Opin. 2008 Jan;24(1):139-49.
9.) Parker J, Hashmi O, Dutton D, Mavrodaris A, Stranges S, Kandala NB, Clarke A, Franco OH. Levels of Vitamin D and cardiometabolic disorders: systematic review and meta-analysis. Maturitas. 2010 Mar;65(3):225-36. Epub 2009 Dec 23.
10.) Pilz S, Dobnig H, Fischer JE, Wellnitz B, Seelhorst U, Boehm BO, März W. Low Vitamin d levels predict stroke in patients referred to coronary angiography. Stroke. 2008 Sep;39(9):2611-3. Epub 2008 Jul 17.
11.) Holick MF. Vitamin D and sunlight: strategies for cancer prevention and other health benefits. Clin J Am Soc Nephrol. 2008 Sep;3(5):1548-54. Epub 2008 Jun 11.
12.) Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with Vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA. 2005 May 11;293(18):2257-64.
13.) Anagnostis P, Athyros VG, Adamidou F, Florentin M, Karagiannis A. Vitamin D and Cardiovascular Disease: A Novel Agent for Reducing Cardiovascular Risk ? Curr Vasc Pharmacol. 2010 Feb 25. [Epub ahead of print]
14.) Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004 Mar;79(3):362-71.
15.) Holick MF. Vitamin D and sunlight: strategies for cancer prevention and other health benefits. Clin J Am Soc Nephrol. 2008 Sep;3(5):1548-54. Epub 2008 Jun 11.
16.) Judd SE, Tangpricha V. Vitamin D deficiency and risk for cardiovascular disease. Am J Med Sci. 2009 Jul;338(1):40-4.
17.) Kendrick J, Targher G, Smits G, Chonchol M.25-HydroxyVitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. Atherosclerosis. 2009 Jul;205(1):255-60. Epub 2008 Nov 11.
18.) Lee W, Kang PM. Vitamin D deficiency and cardiovascular disease: Is there a role for Vitamin D therapy in heart failure? Curr Opin Investig Drugs. 2010 Mar;11(3):309-14.
19.) Martins D, Wolf M, Pan D, Zadshir A, Tareen N, Thadhani R, Felsenfeld A, Levine B, Mehrotra R, Norris K. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyVitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2007 Jun 11;167(11):1159-65.
20.) McConnell JP, Foley KF, Vargas GM. HypoVitaminosis D: a new risk marker for cardiovascular disease. Clin Lab Sci. 2009 Fall;22(4):240-6.
21.) Mertens PR, Müller R. Vitamin D and cardiovascular risk. Int Urol Nephrol. 2009 Dec 29. [Epub ahead of print]
22.) Murlikiewicz K, Zawiasa A, Nowicki M. Vitamin D–a panacea in nephrology and beyond] Pol Merkur Lekarski. 2009 Nov;27(161):437-41.{article in Polish]
23.) Parker J, Hashmi O, Dutton D, Mavrodaris A, Stranges S, Kandala NB, Clarke A, Franco OH. Levels of Vitamin D and cardiometabolic disorders: systematic review and meta-analysis. Maturitas. 2010 Mar;65(3):225-36. Epub 2009 Dec 23.
24.) Pilz S, Dobnig H, Nijpels G, Heine RJ, Stehouwer CD, Snijder MB, van Dam RM, Dekker JM. Vitamin D and mortality in older men and women. Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18.
25.) Pilz S, März W, Wellnitz B, Seelhorst U, Fahrleitner-Pammer A, Dimai HP, Boehm BO, Dobnig H. Association of Vitamin D deficiency with heart failure and sudden cardiac death in a large cross-sectional study of patients referred for coronary angiography. J Clin Endocrinol Metab. 2008 Oct;93(10):3927-35. Epub 2008 Aug 5.
26.) Wu PW, Rhew EY, Dyer AR, Dunlop DD, Langman CB, Price H, Sutton-Tyrrell K, McPherson DD, Edmundowicz D, Kondos GT, Ramsey-Goldman R. 25-hydroxyVitamin D and cardiovascular risk factors in women with systemic lupus erythematosus. Arthritis Rheum. 2009 Oct 15;61(10):1387-95.
27.) Baz-Hecht M, Goldfine AB. The impact of Vitamin D deficiency on diabetes and cardiovascular risk. Curr Opin Endocrinol Diabetes Obes. 2010 Apr;17(2):113-9.
28.) Cheng S, Massaro JM, Fox CS, Larson MG, Keyes MJ, McCabe EL, Robins SJ, O’Donnell CJ, Hoffmann U, Jacques PF, Booth SL, Vasan RS, Wolf M, Wang TJ. Adiposity, cardiometabolic risk, and Vitamin D status: the Framingham Heart Study. Diabetes. 2010 Jan;59(1):242-8. Epub 2009 Oct 15.
29.) Holick MF. Sunlight and Vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr. 2004 Dec;80(6 Suppl):1678S-88S.
30.) Ginde AA, Scragg R, Schwartz RS, Camargo CA Jr. Prospective study of serum 25-hydroxyVitamin D level, cardiovascular disease mortality, and all-cause mortality in older U.S. adults. J Am Geriatr Soc. 2009 Sep;57(9):1595-603. Epub 2009 Jun 22.
31.) Grant WB. How strong is the evidence that solar ultraviolet B and Vitamin D reduce the risk of cancer?: An examination using Hill’s criteria for causality. Dermatoendocrinol. 2009 Jan;1(1):17-24.
32.) Holick MF, Chen TC. Vitamin D deficiency: a worldwide problem with health consequences. Am J Clin Nutr. 2008 Apr;87(4):1080S-6S.
33.) Holick MF. Vitamin D: its role in cancer prevention and treatment. Prog Biophys Mol Biol. 2006 Sep;92(1):49-59. Epub 2006 Mar 10.
34.) Ingraham BA, Bragdon B, Nohe A. Molecular basis of the potential of Vitamin D to prevent cancer. Curr Med Res Opin. 2008 Jan;24(1):139-49.
35.) Pilz S, Dobnig H, Winklhofer-Roob B, Riedmüller G, Fischer JE, Seelhorst U, Wellnitz B, Boehm BO, März W. Low serum levels of 25-hydroxyVitamin D predict fatal cancer in patients referred to coronary angiography. Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1228-33. Epub 2008 May 7.
36.) Pilz S, Tomaschitz A, Obermayer-Pietsch B, Dobnig H, Pieber TR. Epidemiology of Vitamin D insufficiency and cancer mortality. Anticancer Res. 2009 Sep;29(9):3699-704.
37.) Ginde AA, Mansbach JM, Camargo CA Jr. Association between serum 25-hydroxyVitamin D level and upper respiratory tract infection in the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2009 Feb 23;169(4):384-90.
38.) Annweiler C, Schott AM, Allali G, Bridenbaugh SA, Kressig RW, Allain P, Herrmann FR, Beauchet O. Association of Vitamin D deficiency with cognitive impairment in older women: cross-sectional study. Neurology. 2010 Jan 5;74(1):27-32. Epub 2009 Sep 30.
39.) Cherniack EP, Troen BR, Florez HJ, Roos BA, Levis S. Some new food for thought: the role of Vitamin D in the mental health of older adults. Curr Psychiatry Rep. 2009 Feb;11(1):12-9.
40.) Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40.
41.) Cutolo M, Otsa K. Review: Vitamin D, immunity and lupus. Lupus. 2008;17(1):6-10.
42.) Kamen DL, Cooper GS, Bouali H, Shaftman SR, Hollis BW, Gilkeson GS. Vitamin D deficiency in systemic lupus erythematosus. Autoimmun Rev. 2006 Feb;5(2):114-7. Epub 2005 Jun 21.
43.) Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with Vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA. 2005 May 11;293(18):2257-64.
44.) Bischoff HA, Stähelin HB, Tyndall A, Theiler R. Relationship between muscle strength and Vitamin D metabolites: are there therapeutic possibilities in the elderly? Z Rheumatol. 2000;59 Suppl 1:39-41.
45.) DIPART (Vitamin D Individual Patient Analysis of Randomized Trials) Group. Patient level pooled analysis of 68 500 patients from seven major Vitamin D fracture trials in US and Europe. BMJ. 2010 Jan 12;340:b5463. doi: 10.1136/bmj.b5463.
46.) Houston DK, Cesari M, Ferrucci L, Cherubini A, Maggio D, Bartali B, Johnson MA, Schwartz GG, Kritchevsky SB. Association between Vitamin D status and physical performance: the InCHIANTI study. J Gerontol A Biol Sci Med Sci. 2007 Apr;62(4):440-6.
47.) Kwon J, Suzuki T, Yoshida H, Kim H, Yoshida Y, Iwasa H. Concomitant lower serum albumin and Vitamin D levels are associated with decreased objective physical performance among Japanese community-dwelling elderly. Gerontology. 2007;53(5):322-8. Epub 2007 May 29.
48.) Pfeifer M, Begerow B, Minne HW. Vitamin D and muscle function. Osteoporos Int. 2002 Mar;13(3):187-94.
49.) Judd SE, Nanes MS, Ziegler TR, Wilson PW, Tangpricha V. Optimal Vitamin D status attenuates the age-associated increase in systolic blood pressure in white Americans: results from the third National Health and Nutrition Examination Survey. Am J Clin Nutr. 2008 Jan;87(1):136-41.
50.) Pilz S, Dobnig H, Fischer JE, Wellnitz B, Seelhorst U, Boehm BO, März W. Low Vitamin d levels predict stroke in patients referred to coronary angiography. Stroke. 2008 Sep;39(9):2611-3. Epub 2008 Jul 17.
51.) Melamed ML, Michos ED, Post W, Astor B.25-hydroxyVitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008 Aug 11;168(15):1629-37.
52.) Jacobs ET, Alberts DS, Foote JA, Green SB, Hollis BW, Yu Z, Martínez ME. Vitamin D insufficiency in southern Arizona. Am J Clin Nutr. 2008 Mar;87(3):608-13.
53.) Park S, Johnson MA. Living in low-latitude regions in the United States does not prevent poor Vitamin D status. Nutr Rev. 2005 Jun;63(6 Pt 1):203-9.
54.) Low Vitamin D Levels Tied to Incontinence. WebMD March 22, 2010 http://www.webmd.com/urinary-incontinence-oab/news/20100322/low-Vitamin-d-linked-incontinence.
55.) The Vitamin D Council. Vitamin D Council
56.) Wikipedia: Vitamin D. Wikipedia Vitamine D
57.) Holick MF. Environmental factors thatinfluence the cutaneous production of Vitamin D. Am J Clin Nutr. 1995 Mar;61(3 Suppl):638S-645S.
58.) Vieth R. Vitamin D supplementation, 25-hydroxyVitamin D concentrations, and safety. Am J Clin Nutr. 1999 May;69(5):842-56.
59.) Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357:266-281.
60.) GrassrootsHealth. Disease incidence prevention by serum 25(OH)D level.Grassroots Heaalth. Accessed May 8, 2009.
61.) Dall T, Anderson J. Vitamin D: merging research into clinical lipid practice. Lipid Spin. 2008;6(3):4-8.
62.) Heaney RP. What is a Vitamin D deficiency?Grassroots Health Vitamin D deficiency. Accessed May 8, 2009.

 

 

Potassium Iodide

Potassium Iodide (KI) Can Shield You From Thyroid Cancer

ARE YOU PREPARED FOR A RADIATION EMERGENCY?

With over 100 active commercial nuclear reactors in the United States, we live in constant threat of a nuclear emergency every day. A terrorist attack on any one of these facilities, or the release of a “dirty bomb” is also a possibility in today’s “highly charged” world. In fact, in an emergency, if you live within 200 miles of a nuclear reactor, you have a high risk of being exposed to significant doses of radioactive isotopes. In the event of a nuclear accident or attack radioactive materials can be released into the atmosphere, a high percentage of which is radioactive iodine. When a radioactive iodine cloud passes through a populated area, the radiation is concentrated into the thyroid gland of those exposed. The result is irreparable damage to the thyroid, which can lead to cancer. The 1986 Chernobyl accident in the Ukraine is a tragic example as is the Fukushima tragedy in Japan.

Even reactors in other countries can have adverse effects on people in the United States as prevailing winds can quickly spread the radioactive particulate matter from nuclear disasters.

The best protection against thyroid damage and thyroid cancer induced by radioactive iodine exposure is Potassium Iodide. This simple compound protects the thyroid by saturating all of the iodine binding sites in the gland, leaving no room for the binding of radioactive iodine. Potassium Iodide is a low-cost way to protect yourself and your family against the long-term consequences of exposure to radiation. When used correctly, potassium iodide tablets can prevent or reduce the amount of radioactive iodine taken up by the thyroid gland. Even the government and the military stocks up on potassium iodide in case of nuclear disaster.

The body can’t distinguish between radioactive and the benign version of iodine, which is necessary for thyroid function. Taking 130 mg of potassium iodide, the dosage widely recommended for the blocking of radioactive iodine in the event of a nuclear disaster, can quickly and completely protect the thyroid gland, which is one of the organs most commonly damaged by radioactive fallout.

It is important to remember that the precise dose of Potassium Iodide, whether it is 130mg or 125mg or 150mg (for a full-sized adult) is less critical than just simply offering the thyroid a good dose that will allow it to ignore the radioactive iodine that a person may have been exposed to.

Many Americans are cronically “undernourished” with iodine – iodine deficiency is common in North America. The FDA and CDC and other government agencies acknowledge this implicitly by recommending the use of Potassium Iodide in a radiation emergency since a thyroid gland that is not iodine deficient will not be prone to take up radioactive iodine.

Dr. Myatt’s Wellness Club offers a selection of supplements that contain potassium iodide.

Tablets are scored for easy breakage in the case of any need for exact or reduced dosages as recommended for children and pets.

How much do you need? The FDA recommends that you have one 130mg dose per person available for immediate use and up to 14 additional 130mg doses available for continuing use if needed.

Here is what the FDA recommends:

 What doses of potassium iodide (KI) should be taken for specific exposure levels?

Exposures greater than 5 cGy:
Birth through 1 mo.  – 16 mg.
1 mo. through 3 yrs.  – 32 mg.
3 yrs through 18 yrs.  – 65 mg. (Adolescents>150 pounds should take adult dose.)

Exposures greater than 10 cGy:
18 yrs through 40 yrs. – 130 mg

Exposures greater than 500 cGy:
Adults over 40 yrs – 130 mg.

7.  How long should potassium iodide (KI) be taken?

Since KI protects for approximately 24 hours, it should be dosed daily until the risk no longer exists.  Priority with regard to evacuation and sheltering should be given to pregnant females and neonates because of the potential for KI to suppress thyroid function in the fetus and neonate.  Unless other protective measures are not available, we do not recommend repeat dosing in pregnant females and neonates.

Remember that during an emergency, you may not be able to get to your home, thus it is recommended to have potassium iodide tablets stored in several places as well. Since the shelf life of this product is virtually unlimited, you should have to purchase your supply only once. Have this on hand for your family, and remember the children, pets, grandchildren, too!

Iodine for Radiation Protection

Iodoral – The Most Trusted Brand Of Natural Iodine

Iodoral (Iodine) For Healthy Thyroid FunctionIodoral® iodine tablets contain both iodine and iodide as the potassium salt. The preparation is absorbed into colloidal silica to prevent gastric irritation and specially coated with a thin film of pharmaceutical glaze to eliminate unpleasant taste.

Recommended Dose for daily use: 12.5 mg tablets – 1-2 tablets, 1-2 times per day as determined by iodine testing. A retest is suggested after 3 months. Best taken in the morning and afternoon to avoid nighttime stimulation.

Once whole body iodine sufficiency is achieved, Iodoral® maintenance dose is typically 1-4 tablets daily. People with thyroid disorders should work closely with their holistic physician or other health care professional.

NOTE: People with known iodine sensitivity should NOT use this product!

To make it easy to be prepared for a Radiation Emergency Dr. Myatt has Iodoral available:

Product # 309 Iodoral -90 tablets per bottle; 12.5mg iodine/iodide per tablet. $29.95

A More Convenient Product Is Also Available For Your Preparedness Kit:

Potassium Iodide Emergency Packs

Inexpensive protection – Click here to learn More.

Also Valuable for your Radiation Protection kit:

Modifilan (Laminaria japonica)

Thyroid and Immune Stimulant, Detoxification and Energizing Aid from the Sea

ModifilanThis “herb” (a variety of seaweed) might be the most important natural health discovery of the decade!

Modifilan was reportedly developed in Russia by scientists at the State Rehabilitation Institute, where victims of the Chernobyl nuclear catastrophe underwent treatment.

Hand-harvested from far Northern Pacific waters, Laminaria kelp has numerous health properties that set it apart from other species of seaweed.

Beneficial substances found in Modifilan include:

  • Organic iodine: Organic iodine feeds the thyroid gland, promoting normal metabolism and glandular function.
  • Fucoidan: a polysaccharide that promotes cancer cell death (apoptosis) and stimulates the immune system in animal studies. (1-4)
  • Laminarin: a polysaccharide that improves gut health in animal studies.(5)
  • Fucoxanthin: a natural pigment in the carotenoid family, is a potent antioxidant.(6-11)
  • Alginate: a natural polysaccharide that binds water and chelates radioactive toxins such as iodine-131 and strontium-90.(12-14)

Modifilan may be useful for:

  • Boosting the immune system with anti-viral and anti-cancer properties. (1-4, 15-21)
  • Helping lower blood sugar and cholesterol levels. (22-23)
  • Detoxifying the body from heavy metals, radioactive elements, free radicals and toxins.(12-14)
  • Aiding weight loss by improving thyroid, metabolism and GI-tract function.(24-25)
  • Helping smokers detoxify from heavy metals including strontium and cadmium.(12-14)

It takes 40 pounds or raw seaweed (conscientiously harvested to protect habitat) to make one pound of Modifilan.

Put some “pep in your step,” stimulate weight loss and energy while improving your immune system. This specially processed Laminaria is truly a unique gift from the sea.

Dr. Myatt’s Comment: Many of the “anti-cancer” and immune claims for Modifilan and other seaweed products have not yet been substantiated in humans. However, Modifilan is an excellent source of organic iodine and should be considered by anyone with low thyroid function.

Suggested dose:

For general health maintenance, 4-6 capsules per day.
For heavy metal chelation: 12 capsules per day.
For cancer: as directed by your physician (usually 6-12 capsules per day in divided doses).

#844 Modifilan (90 Caps) $29.97

Enter Quantity Desired and Click “Add To Cart” Button

References:

Potassium Iodide:

Food and Drug Administration (FDA) final Guidance on Potassium Iodide as a Thyroid Blocking Agent in Radiation Emergencies.

Food and Drug Administration (FDA) FAQ page on Potassium Iodide

Modifilan:

1.) Funahashi H, Imai T, Mase T, et al. Seaweed prevents breast cancer? Jpn J Cancer Res. 2001;92(5):483-487.
2.) Furusawa E, Furusawa S. Anticancer potential of Viva-Natural, a dietary seaweed extract, on Lewis lung carcinoma in comparison with chemical immunomodulators and on cyclosporine-accelerated AKR leukemia. Oncology. 1989;46(5):343-348.
3.) Itoh H, Noda H, Amano H, et al. Antitumor activity and immunological properties of marine algal polysaccharides, especially fucoidan, prepared from Sargassum thunbergii of Phaeophyceae. Anticancer Res. 1993;13(6A):2045-2052.
4.) Go H, Hwang HJ, Nam TJ. A glycoprotein from Laminaria japonica induces apoptosis in HT-29 colon cancer cells. Toxicol In Vitro. 2010 Sep;24(6):1546-53. Epub 2010 Jul 6.
5.) Lynch MB, Sweeney T, Callan JJ, O’Sullivan JT, O’Doherty JV. The effect of dietary Laminaria-derived laminarin and fucoidan on nutrient digestibility, nitrogen utilisation, intestinal microflora and volatile fatty acid concentration in pigs. J Sci Food Agric. 2010 Feb;90(3):430-7.
6.) Park PJ, Kim EK, Lee SJ, Park SY, Kang DS, Jung BM, Kim KS, Je JY, Ahn CB. Protective effects against H2O2-induced damage by enzymatic hydrolysates of an edible brown seaweed, sea tangle (Laminaria japonica). J Med Food. 2009 Feb;12(1):159-66.
7.) Wang J, Zhang Q, Zhang Z, Li Z. Antioxidant activity of sulfated polysaccharide fractions extracted from Laminaria japonica. Int J Biol Macromol. 2008 Mar 1;42(2):127-32. Epub 2007 Oct 9.
8.) Wang J, Wang F, Zhang Q, Zhang Z, Shi X, Li P. Synthesized different derivatives of low molecular fucoidan extracted from Laminaria japonica and their potential antioxidant activity in vitro. Int J Biol Macromol. 2009 Jun 1;44(5):379-84. Epub 2009 Feb 13.
9.) Wang J, Zhang Q, Zhang Z, Song H, Li P. Potential antioxidant and anticoagulant capacity of low molecular weight fucoidan fractions extracted from Laminaria japonica. Int J Biol Macromol. 2010 Jan 1;46(1):6-12. Epub 2009 Oct 31.
10.) Yan X, Chuda Y, Suzuki M, Nagata T. Fucoxanthin as the major antioxidant in Hijikia fusiformis, a common edible seaweed. Biosci Biotechnol Biochem 1999;63:605–7.
11.) Sachindra NM, Sato E, Maeda H, et al. Radical scavenging and singlet oxygen quenching activity of marine carotenoid fucoxanthin and its metabolites. J Agric Food Chem 2007;55:8516–22.
12.) Davis TA, Volesky B, Mucci A. A review of the biochemistry of heavy metal biosorption by brown algae. Water Res. 2003 Nov;37(18):4311-30.
13.) Sutton, A., Harrison, G. E., Carr, T. E., and Barltrop, D. Reduction in the absorption of dietary strontium in children by an alginate derivative. Br. J.Radiol. 44[523], 567. 1971.
14.) Sutton, A., Harrison, B. E., Carr, T. E., and Barltrop, D. Reduction in the absorption of dietary strontium in children by an alginate derivative. Int.J.Radiat.Biol.Relat Stud.Phys.Chem.Med. 19[1], 79-85. 1971
15.) [No authors listed][Production of cytokines by murine bone marrow dendritic cells in vitro mediated by sulfated polysaccharides obtained from sea brown algae].Zh Mikrobiol Epidemiol Immunobiol. 2010 Sep-Oct;(5):34-9. [Article in Russian]
16.) Damonte EB, Matulewicz MC, Cerezo AS. Sulfated seaweed polysaccharides as antiviral agents. Curr Med Chem. 2004 Sep;11(18):2399-419.
17.) Gerasimenko NI, Chaĭkina EL, Busarova NG, Anisimov MM. [Antimicrobic and hemolytic activity of low-molecular metabolits of brown seaweed Laminaria cichorioides Miyabe].Prikl Biokhim Mikrobiol. 2010 Jul-Aug;46(4):467-71. [Article in Russian]
18.) Ishikawa C, Tafuku S, Kadekaru T, Sawada S, Tomita M, Okudaira T, Nakazato T, Toda T, Uchihara JN, Taira N, Ohshiro K, Yasumoto T, Ohta T, Mori N. Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Int J Cancer. 2008 Dec 1;123(11):2702-12.
19.) Kim KN, Heo SJ, Kang SM, Ahn G, Jeon YJ. Fucoxanthin induces apoptosis in human leukemia HL-60 cells through a ROS-mediated Bcl-xL pathway. Toxicol In Vitro. 2010 Sep;24(6):1648-54. Epub 2010 Jun 8.
20.) Makarenkova ID, Deriabin PG, L’vov DK, Zviagintseva TN, Besednova NN. [Antiviral activity of sulfated polysaccharide from the brown algae Laminaria japonica against avian influenza A (H5N1) virus infection in the cultured cells]. Vopr Virusol. 2010 Jan-Feb;55(1):41-5. [Article in Russian].
21.) Yamamoto K, Ishikawa C, Katano H, Yasumoto T, Mori N. Fucoxanthin and its deacetylated product, fucoxanthinol, induce apoptosis of primary effusion lymphomas. Cancer Lett. 2010 Nov 13. [Epub ahead of print]
22.) Bu T, Liu M, Zheng L, Guo Y, Lin X. α-Glucosidase inhibition and the in vivo hypoglycemic effect of butyl-isobutyl-phthalate derived from the Laminaria japonica rhizoid. Phytother Res. 2010 Nov;24(11):1588-91. doi: 10.1002/ptr.3139.
23.) Woo MN, Jeon SM, Kim HJ, Lee MK, Shin SK, Shin YC, Park YB, Choi MS. Fucoxanthin supplementation improves plasma and hepatic lipid metabolism and blood glucose concentration in high-fat fed C57BL/6N mice. Chem Biol Interact. 2010 Aug 5;186(3):316-22. Epub 2010 May 16.
24.) Woo MN, Jeon SM, Shin YC, Lee MK, Kang MA, Choi MS. Anti-obese property of fucoxanthin is partly mediated by altering lipid-regulating enzymes and uncoupling proteins of visceral adipose tissue in mice. Mol Nutr Food Res. 2009 Dec;53(12):1603-11.
25.) You JS, Sung MJ, Chang KJ. Evaluation of 8-week body weight control program including sea tangle (Laminaria japonica) supplementation in Korean female college students. Nutr Res Pract. 2009 Winter;3(4):307-14. Epub 2009 Dec 31.

Prostate Cancer


:

Lecture Notes By Dr. Myatt

The text that follows is a transcript of the lecture notes for a lecture presented by Dr. Myatt in May of 2000 at the 2000 Pacific Northwest Herbal Symposium where Dr. Myatt was a featured lecturer speaking on several subjects. It is reproduced here in it’s entirety including annotations and references (as is expected of any lecture presented to a medical or scientific body) so that readers may verify the information for themselves and engage in further research. We hope that this will be information useful to persons with an interest in this disease.

Botanical and Nutritional Considerations in the Treatment of

Dana Myatt, N.M.D.

Abstract

Prostate carcinoma is a hormone-dependent cancer. Therefore, in addition to general immune enhancing and anti-cancer therapies, hormonal manipulation has a role to play in treatment of this disease.

Overview

Prostate carcinoma is the most common male cancer in the U.S. It accounts for an estimated 32% of all newly diagnosed cancers. (Other forms of prostate cancer, such as sarcoma, are rare and are not hormone-dependent). The incidence of disease increases with each decade of life over age 50. (1) Prostate cancer rates have risen 108% since 1950, believed due in part to earlier detection. Death rates from this disease have increased 23%. 
There is great debate in the medical community regarding the value of conventional treatment. Prostate cancer is, in most cases, slow-growing. Increased survival rates reported in some studies may be due to earlier detection, not treatment. Many newly diagnosed and early stage cancers in older men would never progress to morbidity or mortality. Considering the risk of impotence (50-60% with surgery), incontinence (from surgery or radiation) and other treatment side-effects, the value of conventional therapy must be questioned in all cases of cancer in older men.

Botanical and nutritional treatment for cancer can be considered an adjuvant therapy in all cases of prostate carcinoma and the sole therapy in many. Even when conventional treatment is deemed advisable, non-traditional uses of conventional drugs may be safer and more advantageous than standard therapy. This is because, in it’s early stages, prostate cancer is highly controllable with hormone-blocking therapy.

Laboratory Evaluation of

In additional to generalized immune testing and basic cancer workup (chemistry screen, CBC, TFT’s, etc.), several tests specific to prostate disease allow the clinician to track progression non-invasively and with greater accuracy. These tests include prostatic-specific antigen (PSA), free PSA, prostatic acid phosphatase (PAP), and prolactin. 

PSA is now used as the preferred screening test for both benign prostatic hypertrophy (BPH) and prostate cancer. Because PSA may be elevated in both benign and cancerous prostate disease, the test is not specific for prostate cancer. Values in the “indeterminate” range (4-12) present a special diagnostic dilemma. It is further estimated that 25% of men with prostate cancer will have PSA’s less than 4. Taken together, the PSA test poses a significant number of both false-negative and false-positive results. The PSA is an accurate measure of cancer cell activity once the diagnosis has been established.

Free-PSA is a more recent marker that has not yet been universally embraced by conventional medicine. Current research suggests that the free-PSA is a useful “next step” for evaluating elevated PSA’s. In men with PSA’s ranging from 4.1-10, higher levels of free-PSA (18.9 median value) correlated with benign disease while lower levels of free-PSA (10.1 median) correlated with cancer. It is estimated that 95% of “indeterminate” PSA readings could be clarified non-invasively with the additional use of the free-PSA test. (3)

Prostatic acid phosphatase (PAP) was the prostate cancer screening test that preceded use of the PSA. An elevated PAP in a patient with known prostate cancer is indicative of lymphatic spread of the disease. (4)

Prolactin hormone is an additional growth factor to the prostate gland, and rising prolactin levels correlate with progression in advanced prostate cancer cases. Prolactin receptors are found on prostate cancer cells, and it is postulated that these receptors may facilitate the entry of testosterone into the cell. Even with hormone ablation therapy, detectable androgen remains in the blood from adrenal sources. Blocking prolactin secretion may there fore be another method for slowing progression of the disease. It is recommended that prolactin levels be kept below 3 in all patients with hormone-responsive cancers. (5)

Specific Goals of Therapy

Testosterone, prolactin, cortisol, insulin, and arachidonic acid-derived prostaglandins (especially PGE2) act as growth factors for prostate cancer. Cyclooxygenase is the enzyme that catalyzes the conversion of arachidonic acid to prostaglandins. Decreasing circulating levels of these hormones and blocking inflammatory pathways should be undertaken in addition to non-specific cancer therapies such as immune enhancement.

References

1.) Beers, Mark M.D., Berkow, Robert M.D. , editors, The Merck Manual of Diagnosis and Therapy, Merck research Laboratories, 1999, p. 1918.
2.) Boik, John, Cancer and Natural Medicine, Oregon Medical Press, 1996, p. 87
3.) Faloon, William, Disease Prevention and Treatment Protocols, Life Extension foundation, Hollywood, FL, 1998, p. 192.
4.) Murphy, Gerald M.D., Lawrence, Walter Jr. M.D., Lenhard, Raymond M.D., Clinical Oncology, American Cancer Society, Atlanta, 1995, p. 315. [copies of this textbook may be obtained by calling your local branch of the American Cancer Society or call 1-800-ACS-2345].
5.) European Journal of Cancer, Vol 31A, No. 6, 1995.

Materia Medica classified by action

Reduce sex hormone bioavailability

Glycine max -soy
Linum ussatatissimum -flax
Arctium lappa -burdock
low dietary saturated fat
high dietary fiber

Decrease testosterone

Cannabis sativa- marijuana
Serenoa Spp.- Saw palmetto
Vitex spp
Rx: Casodex, flutamide, Lupron, Zoladex

Decrease prolactin

Vitex spp.
vegetarian diet
Rx: Bromocriptine, Pergolide, Dostinex

Botanical Materia Medica

Arctium lappa (Compositae)- Burdock

Burdock reduces sex hormone bioavailability, perhaps due to its lignan content.(1) In vitro, it induces differentiation and inhibits tumor cell proliferation. (2) Burdock is considered highly in both Western and Chinese medicine as a detoxifier and it is an ingredient in the Hoxey formula. it is thought to stimulate the removal of excess metabolic acids. (3)

Linum ussitatissimum (Linacea)- Linseed, flax seed

Flax seed is much higher in lignans than other plants. Lignans inhibit sex hormone availability. Antiinflammatory effects are attributed to the high omega-3 fatty acid content of the seed oil.

Glycine max (Leguminosae)-Soy

Soy beans contain protease inhibitors, fixed oils, coumestrol, isoflavones including daidzein and genistein, lecithin, protein, vitamins and minerals. Soy foods reduce hormone bioavailability and cholesterol levels through several possible mechanisms, including weak estrogenic effects of the phytoestrogenic isoflavones and fiber content. Genistein is cytotoxic, induces apoptosis and differentiation, inhibits angiogenesis and metastasis (4), and blocks protein kinase which is a cancer growth factor (11) . The isoflavones in soy are both antioxidant and antimutagenic.(5)

One study of 8,000 Japanese living in Hawaii found that men who had the highest intake of soy had the lowest incidence of prostate cancer. Soy-eaters diagnosed with prostate cancer nevertheless have the lowest death rate in the world from the disease.(6)

Cannabis sativa (Cannabinaceae)- Marijuana

Marijuana contains flavonoids, volatile oils, alkaloids and over 60 different cannabinoids including THC.(7) Smoking the herb reduced testosterone levels or inhibited testosterone receptors in both animals and humans. It is known that marijuana smoking decreases male fertility. (8,9,10)

Serenoa repens, S. serrulata (Palmaceae)- Saw palmetto

Saw palmetto blocks the conversion of testosterone to dihydrotestosterone (DHT) (11) and there is evidence that DHT may be five times as potent as testosterone in stimulating prostate cancer cell growth. (12)

Vitex agnus-castus, V. negundo (Verbenaceae)- Chaste berry

Vitex spp. decreases testosterone production in vivo (13) and inhibits prolactin synthesis and release in animal models (14). As the name “chaste tree” implies, this herb was traditionally used by monks to reduce libido.

PC-SPEC

PC-SPEC is a new and novel Chinese herb formula used in the treatment of prostate cancer. “Spec” is Latin for hope, and the formula is reported to be effective in extending quality and length of life even in advanced, hormone-refractory cancers. The formula is cytostatic and cytotoxic, and regulates apoptosis (1). It may stimulate T4 (helper) cells and macrophages (2) and lower PSA levels (3). The popularity of the formula was enhanced by a recent mention in the New England Journal of Medicine which reported that:

“We found PC-Spec…. has potent estrogenic activity in yeast, mice, and humans. In patients with prostate cancer, it causes clinically significant reductions in serum testosterone concentrations, decreases PSA, and with side effects similar to those of pharmacologic doses of estrogen….. PC-SPEC may prove useful in the treatment of hormonally sensitive prostate cancer…..”(3).

The formula contains herbs which may address prostate cancer on a number of levels. According to the book New Guidelines for Surviving (4), the herbs and actions of PC-SPEC include:

1.) Isatis indigotica (da qing ye) contains beta sitosterol, a phytosterol which lowers the bioavailability of estrogen and reduces tumor yield in animals.
2.) Glycyrrhiza spp. (gan cao) stimulates the immune system and possesses in vitro antitumor activity. It also helps lower testosterone levels.
3.) Panax pseudo-ginseng (san qi) stimulates NK cell activity.
4.) Ganoderma lucidum (ling zi) contain polysaccharides that inhibit cancer cells and extend the lifespan of test animal with lung cancer up to 195%.
5.) Scutellaria baicalensis (huang qin) promotes apoptosis, stimulates the immune system and inhibits tumor-cell proliferation.
6.) Dendranthema morifolium Tzvel (Chu-hua) is a lesser-known Chinese herb with reported antiviral and detoxifying properties.
7.) Rabdosia rubescens (don ling cau) is a pain-relieving herb with multiple antitumor effects. Increased survival rates have been noted in patients with esophageal cancer.
8.) Serenoa repens or S. serrulata (Saw palmetto) decreases the bioavailability of testosterone and is widely used in the treatment of BPH.

The recommended dose is 6-12 capsules per day depending on the stage of the disease. This puts the cost of the formula at $300-$600 per month. (CHT averages $800 per month to give some perspective). Since the formula is a non-FDA approved herbal combination, it is available without a prescription.

Dr. Myatt’s comment: This formula has gotten a lot of good press lately. I’d like to see if the results will meet the hype. Unfortunately, since the formula is a non-FDA approved herbal remedy, I have found it challenging to get patients to take it with consistency in the doses recommended. I have yet to see results in two patients who have used it with regularity. PC-SPEC may indeed represent a breakthrough in the treatment of cancer. It could also be that some herbal product manufacturers are getting as clever as the drug companies in creating “buzz,” and getting journal space, about new products. How many “breakthrough” drugs have come and gone? Let’s hope PC-SPEC fares better than the current conventional treatments for prostate cancer.

References

1.) Halicka HD et al.: Apoptosis and cell cycle effects induced by extracts of the Chinese herbal preparation PC-SPEC. Intl J Oncology, 1997;11:437-448.
2.) Whittaker J: The Art of Alternative Medicine. ACAM Conference Proceedings Notes, Nov. 1998.
3.) DiPaola RS et al.: Clinical and biologic activity of an estrogenic herbal combination (PC-SPEC) in prostate cancer. New Engl J Med, Sept. 17, 1998;339(12);785-791.
4.) Lewis, James Jr.: New Guidelines for Surviving , Westbury, NY: Health Education Library Publisher, 1998.

Nutritional Materia Medica

Vitamin D3 (cholecalciferol)

Vitamin D3 induces prostate cancer cell apoptosis by apparent translocation of the cancer cell androgen receptor. This makes the cell less susceptible to testosterone-induced proliferation (15). D3 induces differentiation, inhibits angiogenesis and shows antitumor activity. It may also upregulate vitamin A receptors. (16)

Because vitamin D has the potential to cause toxicity, doses over 1,000mg should be carefully monitored. Increased blood calcium levels can result from toxicity. In clinical practice, D3 appears to benefit metastatic bone disease in higher doses, perhaps because this vitamin is needed for normal calcification of bone matrix.

Food sources of vitamin D include cold water fish (salmon, mackerel, herring), butter, egg yolks and dark green leafy vegetables. Sunlight acting on the skin will also create vitamin D. In areas of decrease sunlight, increases of breast and colon cancer have been observed. (17)

Melatonin

Melatonin is a hormone produced by the pituitary gland. It regulates circadian rhythms and plays a role in sleep regulation. It is also a more potent antioxidant than glutathione or vitamin E (19). In vitro, melatonin demonstrates antiestrogen activity and immune stimulation (18). Recent research shows that melatonin inhibits cell proliferation profoundly in vivo but only weakly in vitro. It is synergistic with IL-2 and increases the effectiveness of IL-2 treatment. (20)
 

CoQ10 (ubiquinone)

CoQ10 is a vitamin-like substance that is involved in mitochondrial energy production. The heart is a high user of CoQ10, and many chemotherapeutic drugs deplete body stores of this nutrient. CoQ10 has been used successfully to reduce chemotherapy-induced cardiotoxicity.
In breast cancer patients, a dose of 90mg daily increase late-stage survival dramatically. Three cases of complete remission have been documented at higher doses (300-400mg) per day. (21)

Enzymes (multi enzymes)

Digestive enzymes, whether from animal sources (pancreatin, etc.) or botanical (bromelain, papain), have been shown to increase survival time, inhibit metastasis, and stimulate immune cells. Enzymes induce differentiation and inhibit angiogenesis (22), possibly through antifibrinolytic mechanisms. It has also been postulated that enzymes may help unmask tumor cells and make them more accessible to the immune system.

Dietary Guidelines

Low saturated fat diets decrease the body’s endogenous and exogenous hormone production. Conversely, diets high in saturated fats decrease NK cell activity and increase arachidonic acid, an inflammatory precursor. Rates of breast, colon, prostate, uterine, ovarian and testicular cancers are significantly higher in countries with high saturated fat intakes.

Saturated fats promote inflammatory prostaglandin synthesis while omega-3 fatty acids are antiinflammatory.

Low carbohydrate diets decrease the availability of glucose and insulin. Insulin is a growth factor for cancer and the primary metabolic pathway of cancer cells is anaerobic glycolysis, meaning that cancer cells thrive with a high glucose environment. In animal studies, even slight change toward metabolic acidosis resulted in tumor regression. A low carbohydrate diet which induces ketosis (metabolic acidosis) may duplicate this effect. Overweight patients can afford to lose weight on such a diet, to further reduce their endogenous hormone production. (Fat cells manufacture estrogen).
 

Foods of Special Benefit

garlic
lemon zest (the peel contains limonene)
fish
flax seed
soy and soy products
fresh vegetables (especially non-starchy, dark leafy greens)
olive oil
blueberries and other berries (high in flavonoids and low in sugars)
grains (whole grain only, to reduce insulin response and increase fiber content. Grains should be used sparingly. In patients with more than twenty pounds to lose, gains need not be used at all until desired weight is achieved)

Materia Medica References

1.) Boik, John: Cancer and Natural Medicine, Oregon Medical Press, 1995, p. 159
2.) Ibid., p. 177
3.) Tilgner, Sharol N.D.: Medicines from the Earth, Wise Acres Press, 1999, p. 44.
4.) Ibid, Boik, p. 184.
5.) Editors of time-Life Books: The Drug and Natural Medicine Advisor, time-Life Books, Alexandria, VA. 1997, p.704.
6.) Yeager, Selene, editor: Food Remedies., Prevention Health Books, Rodale Press, 1998, p. 494.
7.) Chevallier, Andrew: Encyclopedia of Medicinal Plants. DK Publishing, London, 1996, p.180.
8.) Barnett G.,Chaing CW, Licko V: Effects of Marijuana on testosterone in male subjects. J Theor Biol 1983 Oct 21; …104(4):685-92
9.) Fujimoto GI, Morrill GA, O’Connell ME, Kostello AB: Effects of cannabinoids given orally and reduced appetite on the male rat reproductive system. Pharmagology 1982;24(5):303-13.
10.) Purohoit V, Ahluwahlia BS, Vigersky RA: Marijuana inhibits dihydrotestosterone binding to the androgen receptor. Endocrinology, 1980 Sep; 107(3):848-50.
11.) Sultan C, Terraza A, Devillier C, Carilla E, et al.: Inhibition of androgen metabolism and binding by a liposteric extract of Serenoa repens B in human forskin fibroblasts. J Steroid Biochem 1984 Jan; 20(1):515-9.
12.) The effects of Flutamide on total DHT and nuclear DHT levles in the human prostate. Prostate, 1981, 2/3: 309-314.
13.) Bhargava SK: Antiandrogenic effects of a flavonoid-rich fraction of Vitex negundo seeds: a histological and biochemical study in dogs. J Ethnopharmacol 1989 Dec; 27(3):327-39.
14.) Bohnert KJ: The use of Vitex agnus castus for Hyperprolactinemia. Quarterly Review of Nat Med Spring 1997;19-20.
15.) Vitamin D and : 1,25 Dihydroxyvitamin D3 receptors and actions in human prostate cancer cell lines. Endocrin 1993;132(5):1952-60.
16.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W: Inhibition of tumor-cell induced angiogenesis by retinoids, 1,25-dihydroxyvitamin D3 and their combination. Canceer Lett 1993 Nov 30; 75(1):35-9.
17.) Murray M: Encyclopedia of Nutritional Supplements. Prima Publishing, 1996: p.40.
18.) reiter RJ, Melchiorri D, Swewerynek E, Poeggeler B, et al.: A review of the evidence supporting melatonin’s role as an antioxidant. J Pineal Res 1995; 57:125-28.
19.) Hill SM, Spriggs LL, Simon MA: The growth inhibitory action of melatonin on human breast cancer cells is linked to the estrogen response system. Cancer Lett 1992 Jul 10;64(3):249-56.
20.) Lissoni P, Barni S, Cazzaniga M, et al.: Efficacy of the concommitant administration of the pineal hormone melatonin in cancer immunotherpay with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 therpay alone. Oncology 1994b Jul-Aug; 51(4):344-7.
21.) Boik, John: Cancer and Natural Medicine, Oregon Medical Press, 1995, p. 71.
22.) 22.) Ibid., p.184.

 

Turmeric:


Powerful Cancer-fighting Herb
that drug companies are rushing to imitate.

An ever-growing body of scientific evidence demonstrates that turmeric — the bright yellow spice herb used in East Indian cooking — has potent anti-cancer properties. According to Bharat Aggarwal, chief of cytokine research at the University of Texas M.D. Anderson Cancer Center, the research to date shows that turmeric’s anti-cancer “promise is enormous.” This evidence and opinion was reported at the recent Society for Integrative Oncology conference and is also posted on the American Cancer Society’s website (www.cancer.org).

Turmeric, and it’s primary active ingredient curcumin, is the main ingredient in curry and a member of the ginger family. In addition to it’s anti-cancer properties, turmeric is a potent antioxidant, anti-inflammatory and liver-protecting herb. Expect to see and read a lot more about this herb in the future, although Wellness Club members have known about the benefits of turmeric for over a decade!

You can learn more about turmeric and find one of the most potent turmeric supplements available on The Wellness Club website by visiting Turmeric: Antioxidant, Anti-inflammatory and Anti-Cancer Herb.

References

1.) Curcumin inhibits the mammalian target of rapamycin-mediated signaling pathways in cancer cells. Beevers,Li,Liu,Huang. Int J Cancer. 2006 Mar 20
2.) Antitumor action of curcumin in human papillomavirus associated cells involves downregulation of viral oncogenes, prevention of NFkB and AP-1 translocation, and modulation of apoptosis. Divya CS, Pillai MR. Mol Carcinog. 2006 May;45(5):320-32.
3.) Curcumin mediates ceramide generation via the de novo pathway in colon cancer cells. Moussavi M, Assi K, Gomez-Munoz A, Salh B. Carcinogenesis. 2006 Feb 25; [Epub ahead of print]
4.) Overexpression of p65/RelA potentiates curcumin-induced apoptosis in HCT116 human colon cancer cells. Collett GP, Campbell FC. Carcinogenesis. 2006 Feb 23; [Epub ahead of print]
5.) Induction of G2/M arrest and inhibition of cyclooxygenase-2 activity by curcumin in human bladder cancer T24 cells. Park C, Kim GY, Kim GD, Choi BT, Park YM, Choi YH. Oncol Rep. 2006 May;15(5):1225-31.
6.) Molecular targets of dietary agents for prevention and therapy of cancer. Aggarwal BB, Shishodia S. Biochem Pharmacol. 2006 Feb 23; [Epub ahead of print]
7.) Inhibition of telomerase activity and induction of apoptosis by curcumin in K-562 cells. Chakraborty S, Ghosh U, Bhattacharyya NP, Bhattacharya RK, Roy M. Mutat Res. 2006 Jan 27; [Epub ahead of print]
8.) Curcumin differentially sensitizes malignant glioma cells to TRAIL/Apo2L-mediated apoptosis through activation of procaspases and release of cytochrome c from mitochondria. Gao X, Deeb D, Jiang H, Liu YB, Dulchavsky SA, Gautam SC. J Exp Ther Oncol. 2005;5(1):39-48.
9.) Multiple biological activities of curcumin: a short review. Maheshwari RK, Singh AK, Gaddipati J, Srimal RC. Life Sci. 2006 Mar 27;78(18):2081-7. Epub 2006 Jan 18.
10.) Curcumin, an atoxic antioxidant and natural NFkappaB, cyclooxygenase-2, lipooxygenase, and inducible nitric oxide synthase inhibitor: a shield against acute and chronic diseases. Bengmark S. JPEN J Parenter Enteral Nutr. 2006 Jan-Feb;30(1):45-51.
11.) Antiproliferation and apoptosis induced by curcumin in human ovarian cancer cells. Shi M, Cai Q, Yao L, Mao Y, Ming Y, Ouyang G. Cell Biol Int. 2006 Mar;30(3):221-6. Epub 2005 Dec 22.
12.) Synergistic inhibitory effects of curcumin and 5-fluorouracil on the growth of the human colon cancer cell line HT-29. Du B, Jiang L, Xia Q, Zhong L. Chemotherapy. 2006;52(1):23-8. Epub 2005 Dec 9.
13.) Curcumin induces human HT-29 colon adenocarcinoma cell apoptosis by activating p53 and regulating apoptosis-related protein expression. Song G, Mao YB, Cai QF, Yao LM, Ouyang GL, Bao SD. Braz J Med Biol Res. 2005 Dec;38(12):1791-8. Epub 2005 Nov 9.
14.) Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines. Nagai S, Kurimoto M, Washiyama K, Hirashima Y, Kumanishi T, Endo S. J Neurooncol. 2005 Sep;74(2):105-11.
15.) Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Chen A, Xu J, Johnson AC. Oncogene. 2006 Jan 12;25(2):278-87.

 

 

Psoriasis


Do You Suffer “The Heartbreak Of Psoriasis”?

Once thought to be little more than an annoying and unsightly skin condition, research now shows psoriasis to be a symptom of much more serious problems.

What is Psoriasis?

Psoriasis is an autoimmune disease with abnormally fast production of skin cells (up to 1,000 times normal) accompanied by inflammation.

Rapidly-multiplying skin cells pile up, creating a silvery scale. Skin underneath this scale is typically inflamed, itchy and painful. The condition is not contagious.

Psoriasis, once considered a “skin disease,”  is now recognized as a systemic (body-wide) autoimmune condition highly associated with:

  • Cardiovascular disease, high blood pressure and stroke (1-14)
  • Diabetes and metabolic syndrome (7-15)

Other conditions associated with psoriasis include depression, insomnia/sleep difficulties, COPD, GERD and arthritis.

What Causes Psoriasis?

The precise cause of psoriasis is not known but a number of factors and have been identified:

  • Genetic.  About one-third of people with psoriasis have a family member who also has the disease, suggesting a genetic component in some sufferers.
  • High cGMP to cAMP ratios
  • Excess inflammation
  • High inflammatory cytokines (immune-regulating communication molecules)
  • Auto-immune

In holistic medicine we also consider:

  • Incomplete digestion (especially protein digestion).
  • Bbowel dysbiosis
  • Impaired liver function
  • Food allergies
  • Nutritional deficiencies
  • Stress appears to worsen the condition, and stress-reducing practices have shown to be helpful in these cases.

Each individual case of psoriasis should be considered as some combination  of these factors.

Conventional medical treatment:

Topical treatments such as steroid cream can greatly help or even “cure” psoriasis. Unfortunately, steroid cream can cause skin atrophy, stretch marks, spider veins and easy bruising when used long-term. The effects can also become systemic and disrupt hormone levels, contributing to osteoporosis and even psychosis.

Steroid creams don’t work for everyone, and there is often a decreasing effect of treatment with continual use. There can also be serious rebound effects with sudden discontinuance.

Immune-suppressive drugs such as cyclosporin and methotrexate are used, but liver, kidney and blood values must be monitored regularly because of the toxicity of these drugs.

Dr. Myatt’s Holistic Self-Help Recommendations

Diet and Lifestyle

Primary Support

  • Maxi Multi: 3 caps, 3 times per day with meals. Maxi Multi contains optimal (not minimal) doses of all essential vitamins, minerals, and trace minerals, including those often deficient in psoriasis.  The most important deficiencies in psoriasis are:
    vitamin A, vitamin E, chromium, selenium, zinc, and vitamin D.
  • Omega 3 fatty acids: especially EPA and DHA as found in fish oil. Target dose is 1.8grams EPA and 1.2 grams DHA. This can be obtained from:
    Max EPA    : 10 caps per day with meals
    OR
    Maxi Marine O-3: 4 caps per day with meals
  • Maxi-Flavone: 1-2 caps per day with meals. This ultra-potent formula contains herbs which decrease inflammatory cytokines.
  • Vitamin D: additional vitamin D as needed to obtain optimal blood levels. Learn about vitamin D testing here. Optimal vitamin D levels are very important for psoriasis success.

Additional Support

  • Forskolin: 1 cap, 2 times per day. This herb help normalize
    the cAMP /cGMP ratio which is imbalanced in psoriasis.
  • Treat GI Dysbiosis if present (highly likely), best done with the results of a Comprehensive GI Health Profile. Treatment may include goldenseal (hydrastis), milk thistle, probiotics, and other gut treatments.

Lifestyle / Topical Treatments

  • Sunlight. UVB exposure has long been known to aid psoriasis  This could be due to increased vitamin D production.
    Newer prescription creams for psoriasis include synthetic vitamin D, further showing the importance of vitamin D for psoriasis.
  • Topicals (how to wash and protect psoriatic skin).
    Wash – Use mild, chemical-free soaps and cosmetics. Harsh alkaline soaps can cause further irritation.
    Moisturize – Chemical-free, gentle moisturizers should be applied after every shower or bath.
    Bathe – baths with baking soda, oatmeal or bentonite clay can be very soothing and detoxifying. Soak for 15-20 minutes in warm water. Do NOT use a bath for cleansing, only for soaking. Be sure that you are using pure, uncontaminated water! Be sure that you are using pure, uncontaminated water! If you are unsure about your water quality you may need to consider adding a water filter to your home.
    Shower     – for actual skin cleansing, take a shower. Use chemical-free oatmeal soap, other mild soap or Dove brand bar soap. But please remember, when you’re hot (and your skin’s pores are wide-open), you can absorb toxins from the water. Shower-head filters are inexpensive and reliable.
  • DON’T pick or scratch skin! Psoriatic lesions tend to grow at the site of skin injury. If itching is uncontrollable, use a skin brush to gently exfoliate without causing dermal injury.
  • Drink pure water – A Good Water Filter is a Cheap Investment in Your Health. A reliable, highly-effective under-sink water filter is an excellent health investment, especially when you consider how important water is to health. The human body is about 60% water. That means we can have 60% of our total body weight contaminated with a variety of toxins if we drink lousy water.

    The highest-rated water filters cost about the same as the cheap junk. Aquasana Water Purifiers  makes some of the highest-rated filters at the best prices

Tests

Dr. Myatt’s Comments

  • Diet and balanced digestion / gut function are primary
  • Correcting nutrient deficiencies with supplementation and ensuring optimal vitamin D levels are also very important

ALL psoriasis patients, whether symptomatic or not, should pay special attention to cardiovascular and metabolic risks. I recommend looking at cardio risk factors including the “other” risk factors at a regular interval.

Psoriasis can be challenging, but starting with the basics (good gut, adequate nutrients) often corrects or at least greatly improves symptoms. When natural, corrective treatment is used, improvement in skin lesions can be expected to include improvement associated risks such as heart disease and diabetes.

Topical treatments alone, even when they decrease skin lesions, do not correct systemic risks. Psoriasis should therefore be treated as a systemic disease, not a skin disease.

References:

  1. Abou-Raya A, Abou-Raya S. Inflammation: a pivotal link between autoimmune diseases and atherosclerosis. Autoimmun Rev. 2006 May;5(5):331-7. Epub 2006 Feb 3.
  2. Boehncke WH, Boehncke S. Research in practice: the systemic aspects of psoriasis. J Dtsch Dermatol Ges. 2008 Aug;6(8):622-5. Epub 2008 Jun 16.
  3. Gottlieb AB, Chao C, Dann F. Psoriasis comorbidities.J Dermatolog Treat. 2008;19(1):5-21.
  4. Kaplan MJ. Cardiometabolic risk in psoriasis: differential effects of biologic agents. Vasc Health Risk Manag. 2008;4(6):1229-35.
  5. Ludwig RJ, Herzog C, Rostock A, Ochsendorf FR, Zollner TM, Thaci D, Kaufmann R, Vogl TJ, Boehncke WH.Psoriasis: a possible risk factor for development of coronary artery calcification. Br J Dermatol. 2007 Feb;156(2):271-6.
  6. Wakkee M, Thio HB, Prens EP, Sijbrands EJ, Neumann HA. Unfavorable cardiovascular risk profiles in untreated and treated psoriasis patients. Atherosclerosis. 2007 Jan;190(1):1-9. Epub 2006 Aug 30.
  7. Wu Y, Mills D, Bala M. Psoriasis: cardiovascular risk factors and other disease comorbidities.J Drugs Dermatol. 2008 Apr;7(4):373-7.
  8. Kourosh AS, Miner A, Menter A. Psoriasis as the marker of underlying systemic disease. Skin Therapy Lett. 2008 Feb;13(1):1-5.
  9. Gottlieb AB, Dann F, Menter A. Psoriasis and the metabolic syndrome. J Drugs Dermatol. 2008 Jun;7(6):563-72.
  10. Sommer DM, Jenisch S, Suchan M, Christophers E, Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis. Arch Dermatol Res. 2006 Dec;298(7):321-8. Epub 2006 Sep 22.
  11. Puig-Sanz L. [Psoriasis, a systemic disease?] Actas Dermosifiliogr. 2007 Jul-Aug;98(6):396-402. [article in Spanish]
  12. Azfar RS, Gelfand JM. Psoriasis and metabolic disease: epidemiology and pathophysiology. Curr Opin Rheumatol. 2008 Jul;20(4):416-22.
  13. Gisondi P, Girolomoni G. Psoriasis and atherothrombotic diseases: disease-specific and non-disease-specific risk factors. Semin Thromb Hemost. 2009 Apr;35(3):313-24. Epub 2009 May 18.
  14. Shapiro J, Cohen AD, David M, Hodak E, Chodik G, Viner A, Kremer E, Heymann A. The association between psoriasis, diabetes mellitus, and atherosclerosis in Israel: a case-control study.J Am Acad Dermatol. 2007 Apr;56(4):629-34. Epub 2006 Dec 8.
  15. Cohen AD, Sherf M, Vidavsky L, Vardy DA, Shapiro J, Meyerovitch J. Association between psoriasis and the metabolic syndrome. A cross-sectional study. Dermatology. 2008;216(2):152-5. Epub 2008 Jan 23.

 

Rosacea

A Challenging Condition That Can Respond Well To Natural Treatment Approaches

There are four main subtypes of rosacea:

Ocular rosacea leaves sufferers with red, dry and irritated eyes and eyelids and symptoms including  itching and burning and feelings of having dust or grit or a foreign body in the eye.

Erythematotelangiectatic rosacea causes a permanent redness of the skin with a tendency to blush or flush easily and frequently small blood vessels are visible near the surface of the skin.

Papulopustular rosacea can cause some permanent redness with red bumps and / or pus-filled bumps or lesions which usually last for 1 to 4 days – this can be easily mistaken for acne.

Phymatous rosacea is most commonly associated with rhinophyma, an enlargement of the nose. Symptoms include thickening of the skin, irregular surface nodules or bumps, and enlargement. Phymatous rosacea can also affect the chin, forehead, cheeks, eyelids, and ears. As with Erythematotelangiectatic rosacea small blood vessels visible near the surface of the skin (known as telangiectasias) may be present.

So, what causes rosacea and what can be done for it?

Conventional Medicine does not recognize any one specific cause for rosacea – but has several theories which involve things such as Cathelicidins, elevated levels of stratum corneum tryptic enzymes (SCTEs), overgrowth of intestinal bacteria, Demodex mites (which may be increased in steroid-induced rosacea), stress, sunburn, temperature extremes, alcohol, caffiene, histamine intolerance, drugs, and steroids – which are often prescribed to treat other skin conditions. Unfortunately for Conventional Medicine there is no one simple test to diagnose rosacea – leaving Conventional Doctors in the difficult position of having to “do it the old way” – by actually examining and listening to their patient!

The response to rosacea by Conventional Medicine is equally predictable – for it involves throwing a variety of patented Big Pharma drug offerings at the problem in the hopes that something will work and provide relief. Antibiotics are ever-popular as is clonidine (an antihypertensive drug that is also used to help addicts withdraw from opiates!) and other antihypertensive drugs. Of course, if all else fails (or even before all else fails) some Conventional Doctors may fall back to their old faithful, steroids – despite the fact that steroids can actually cause rosacea symptoms for many people.

Some more natural approaches to rosacea include:

Methylsulfonylmethane (MSM) and Silymarin – which have been clinically examined and found to be of benefit. MSM, a biologically active form of sulfur has a long history of benefit to the skin and silymarin – a flavonoid found in Milk Thistle is a powerful antioxidant with a special affinity for the liver.

High potency fish oil has a valuable place in the treatment of rosacea, for the powerful antiinflammatory effects of Omega-3 fatty acids EPA and DHA.

Antiinflammatory flavonoids such as are found in Dr. Myatt’s Maxi Flavone could be expected to reduce inflammation since Maxi Flavone contains contains optimal doses of the flavonoid herbs which quench Radical Oxygen Species (ROS), lower TNF alpha and NK cell activity and decrease excess inflammation. Maxi Flavone is a potent formula providing support for immune function, circulatory health, liver detoxification mechanisms, and antioxidant pathways.

High dose Folic Acid and Vitamin C have been investigated and found helpful in some cases of rosacea.

Vitamin D is becoming increasingly recognized for it’s relationship to overall health and skin health – and many Americans are deficient in this important vitamin. Fortunately, Vitamin D testing is easy and accurate, and supplementation is safe and effective in restoring Vitamin D to healthy levels. A warning though: vitamin D and retinoic acid may promote expression of cathelicidin, which has been implicated as a causitive factor for some rosacea sufferers. Other researchers take an opposing view, feeling that Vitamin D may play an important role in treatment because of the cathelicidins.

There are many other herbs that have been tried in the treatment of rosacea, with varying degrees of success. What seems to work for one sufferer often shows little benefit for another – underscoring the importance of an individualized and holistic approach to each individual.

Finally, digestive factors appear to be very important in almost all cases of rosacea that we have treated here at The Wellness Club. Many sufferers are found to be deficient in hydrochloric acid – a problem which initiates a whole cascade of other digestion-related problems. Fortunately, Gastric Acid Function Self Testing is quick and easy and gives a very clear indication of a person’s gastric acid function. For those deficient in stomach acid, Betaine Hydrochloride can provide what may seem like a “miracle cure” to symptoms of rosacea.

Food allergies have also been implicated in rosacea – and many sufferers are well aware of certain foods that exacerbate their symptoms. For others, the allergens may not be so obvious, and Food Intolerance Testing may be indicated. In difficult cases further digestive system testing such as Gastro-Intestinal (GI) Health Profile with Parasitology to rule out bacterial and parasitic infections (remember, even Conventional Medicine is now grudgingly accepting that bacterial overgrowth may be a causative factor in rosacea) and Intestinal Permeability testing because of the relationship between intestinal permeability (AKA “Leaky Gut Syndrome”) and generalized inflammation and toxicity may be needed.

So there you have it: Rosacea can be an embarassing condition and difficult to treat – but a good holistic doctor who is willing to take the time and make the effort to work with a sufferer can usually work wonders!

References:

Berardesca E, Cameli N, Cavallotti C, Levy JL, Piérard GE, de Paoli Ambrosi G (2008). “Combined effects of silymarin and methylsulfonylmethane in the management of rosacea: clinical and instrumental evaluation”. J Cosmet Dermatol 7 (1): 8–14.

Yamasaki, Kenshi; Di Nardo, Anna; Bardan, Antonella; Murakami, Masamoto; Ohtake, Takaaki; Coda, Alvin; Dorschner, Robert A.; Bonnart, Chrystelle; Descargues, Pascal; Hovnanian, Alain; Morhenn, Vera B.; Gallo, Richard L. (2007)     Increased serine protease activity and  cathelicidin  promotes skin inflammation in rosacea Nature Medicine 13(8),  975-980.

Journal of Investigative Dermatology (2008) 128, 773–775. doi:10.1038/jid.2008.35 Vitamin D Regulation of Cathelicidin in the Skin: Toward a Renaissance of Vitamin D in Dermatology? Siegfried Segaert

Prostate Cancer, PSA, and Biopsies – A Critical Look

By Nurse Mark

Cancer is a terrifying word. It generates mental images of pain and suffering and disfigurement and disability. It seems almost everyone knows of someone who has died a hideous death from cancer. We instinctively recoil from cancer as we might from a venomous reptile or insect. We react with revulsion. The “ick factor.”

For this reason the word “cancer” can be used by doctors to justify almost anything – no matter how risky, unproven, or nonsensical, if something is presented as being necessary to “fight this thing” or “catch it early” most people will meekly agree in order to purge themselves of the “ick factor” that the thought of cancer brings.

Prostate cancer is especially troublesome for men, because it hits us “where it hurts” – like a “kick in the…” – well, you know what I mean… It conjures up visions of emasculation, incontinence, and unpleasant medical and surgical procedures performed on our most sensitive parts.

But is prostate cancer really all that it is made up to be? Is it really a dread disease that strikes down virile men in their prime, killing all it touches? Or is that the “marketing angle” used to sell expensive tests, surgeries, drugs, and treatments?

Let’s look at the whole issue a little more deeply.

Normal Prostate AnatomyWhat the heck is this prostate thing anyway?

In men the prostate is a walnut-sized lump of tissue that surrounds the urethra – the tube that carries urine out of the bladder – just below the urinary bladder. It normally weighs around 11 grams (just over 1/3 of an ounce) but can range from 7 to 11 grams and be considered normal. Its main purpose is to produce a fluid that aids in reproduction, transporting and protecting the sperm during the reproductive act.

Women have a similar organ, and female paraurethral glands called Skene’s glands were officially renamed the female prostate by the Federative International Committee on Anatomical Terminology in 2002. But that is a whole different story, since the female prostate doesn’t seem to encounter the same troubles as the male prostate does…

So what’s the big deal about it?

For men, there are a couple of potential problems with the prostate.

First, and most commonly, like ears and noses the prostate just doesn’t seem to know when to stop growing. In older men this leads to a condition known as Benign Prostatic Hypertrophy (or BPH) and can cause problems with urination since while it grows in size outwardly it also tends to tighten down on the urethra as it gets larger – with predictable results. Difficulty starting urination and difficulty emptying the bladder fully lead to a condition known as Urinary Frequency. This usually results in multiple trips to the bathroom through the day and more significantly through the night.Normal and Enlarged Prostate

It is believed that this unnecessary growth of the prostate begins at around age 30 and that by age 50 at least 50% of men will have evidence of BPH. This number increases to include 75% of men who reach the age of 80, and some 40% to 50% of those men will experience symptoms from this otherwise benign growth.

The second and more serious problem occurs when some of those ever-increasing numbers of prostate cells become cancerous.

Most prostate cancers are what considered “indolent” (that’s right – indolent means lazy, lethargic or idle) and more men than you might imagine actually have cancerous cells in their prostate but never, ever know it. One autopsy study of men who died of other causes found prostate cancer in 30% of men in their 50s, and in 80% of men in their 70s. It seems that any man who lives long enough will have prostate cancer eventually.

A few of those cancers however are of a more aggressive nature and can grow quickly, escaping the confines of the prostate gland and affecting other areas of the body in a process known as metastasis. These prostate cancers tend not to be without symptoms however, and are usually easy for an observant doctor to detect – a simple Digital Rectal Exam (the “dreaded DRE”) where the doctor inserts a finger into the rectum and simply feels the surface of the prostate gland will quickly reveal any lumps or bumps or hardness that could indicate a cancer.

Well, how can a fellow know?

Good question – since most men go through life with nary an untoward symptom from their prostate.

Even though they may actually have an “enlarged” prostate, or even a cancerous prostate, chances are very good that most men will never know it and will go on to die from some other cause – things like a heart attack or stroke, an infection like pneumonia, an accident, old age, or even (as the joke goes) “shot by a jealous husband” are a far more likely end for most men.

When they do occur, symptoms of BPH that might send a man to his doctor include urinary hesitancy, frequent urination, urinary tract infections, urinary retention, or insomnia caused by frequent awakening to urinate through the night.

Cancer in the prostate, as mentioned, is often quite asymptomatic (without symptoms or complaints) for most men since it is usually “indolent” – slow growing and not aggressive. When the cancer is an aggressive kind the symptoms will often be fairly obvious: as in BPH they include frequent urination, nocturia (increased urination at night), and difficulty starting and maintaining a steady stream of urine.

Because the cancerous cells are abnormal additional symptoms can include hematuria (blood in the urine), and dysuria (painful urination). Problems with sexual function and performance like difficulty achieving an erection or painful ejaculation can occur. And, should the cancer escape the prostate other areas of the body can be affected – the bone is a common site for these metastasis, with bone pain and weakness being common symptoms.

But my doctor – can he know?

Digital Rectal Exam of the Prostate GlandSure – if you help. Your doctor will do a number of things – but the most important thing will be to sit and talk with you. He (or she) will start out by just talking – asking about your family history, any symptoms you may be experiencing, your recent and past medical history, and so on. He will do a physical examination with DRE, and may order some lab tests – more on that in a moment.

For most men that’s as far as it needs to go – if you are not having any symptoms and the doctor doesn’t find anything on physical exam that rings his alarm bells then you can relax until next year’s annual physical exam when he should be doing the same thing all over again for you.

Well, what about the PSA test – isn’t that the best way to know?

Maybe, and no. There is a lot of controversy surrounding the PSA test and it’s promoted use as a “screening tool” for prostate cancer. While the drug companies, laboratories, and urologists continue to support PSA testing as a universal screening tool for all men, most of the rest of conventional medicine is quietly turning away from the test except in specific circumstances.

Even the discoverer of PSA, researcher Richard J Ablin – whose father died of prostate cancer – concluded in a 2010 OpEd article in The New York Times:

“I never dreamed that my discovery four decades ago would lead to such a profit-driven public health disaster. The medical community must confront reality and stop the inappropriate use of P.S.A. screening. Doing so would save billions of dollars and rescue millions of men from unnecessary, debilitating treatments.”

He says in his letter:

“American men have a 16 percent lifetime chance of receiving a diagnosis of prostate cancer, but only a 3 percent chance of dying from it. That’s because the majority of prostate cancers grow slowly. In other words, men lucky enough to reach old age are much more likely to die with prostate cancer than to die of it.”

And he continued:

“Even then, the [PSA] test is hardly more effective than a coin toss. As I’ve been trying to make clear for many years now, P.S.A. testing can’t detect prostate cancer and, more important, it can’t distinguish between the two types of prostate cancer — the one that will kill you and the one that won’t.”

More and more conventional medical governing bodies are moving away from PSA testing:

The American College of Preventive Medicine conducted a study that found:

“…no convincing evidence that early screening, detection, and treatment improves mortality. Limitations of prostate cancer screening include potential adverse health effects associated with false-positive and negative results, and treatment side effects.”

They issued a statement to say that

“there is insufficient evidence to recommend routine population screening with DRE or PSA.”

The American College of Physicians has taken a similar cautionary stance:

“…PSA is not just a blood test. It can open the door to more testing and treatment that a man may not want or that may harm him. Because chances of being harmed are greater than chances of benefiting, each man should have the opportunity to decide for himself whether to be screened.”

The American Society of Clinical Oncology and the American College of Physicians together concluded that based on recent research:

“…it is uncertain whether the benefits associated with PSA testing for prostate cancer screening are worth the harms associated with screening and subsequent unnecessary treatment.”

The U.S. Preventive Services Task Force says in their recommendation against the use of PSA testing:

“…many men are harmed as a result of prostate cancer screening and few, if any, benefit.”

Even The American Urological Association – whose members obviously stand to profit handsomely from all things associated with the prostate – has issued a guideline that makes the following statements:

  • PSA screening in men under age 40 years is not recommended.
  • Routine screening in men between ages 40 to 54 years at average risk is not recommended.
  • For men ages 55 to 69 years, the decision to undergo PSA screening involves weighing the benefits of preventing prostate cancer mortality in 1 man for every 1,000 men screened over a decade against the known potential harms associated with screening and treatment. For this reason, shared decision-making is recommended for men age 55 to 69 years that are considering PSA screening, and proceeding based on patients’ values and preferences.
  • To reduce the harms of screening, a routine screening interval of two years or more may be preferred over annual screening in those men who have participated in shared decision-making and decided on screening. As compared to annual screening, it is expected that screening intervals of two years preserve the majority of the benefits and reduce over diagnosis and false positives.
  • Routine PSA screening is not recommended in men over age 70 or any man with less than a 10-15 year life expectancy.

Now, to be fair, there a number of medical experts (besides the drug and laboratory industry) that are still actively, even enthusiastically promoting universal PSA screening for men – the British Journal of Urology published a “consensus statement” created by a group of self-described “leading prostate cancer experts from around the world” who met at the 2013 Prostate Cancer World Congress in Melbourne, Australia and presented their recommendations for PSA testing.

Here are some highlights of their statement called The Melbourne Consensus Statement on Prostate Cancer Testing:

First, the authors emphasize that:

“For men aged 50–69, level 1 evidence demonstrates that PSA testing reduces prostate cancer-specific mortality and the incidence of metastatic prostate cancer.”

BUT they go on to say…

“…the degree of over-diagnosis and over-treatment reduces considerably with longer follow-up.
While routine population-based screening is not recommended, healthy, well-informed men in this age group should be fully counseled about the positive and negative aspects of PSA testing to reduce their risk of metastases and death. This should be part of a shared decision-making process.”

AND…

“Although screening is essential to diagnose high-risk cases within the window of curability, it is clear that many men with low-risk prostate cancer do not need aggressive treatment.
While it is accepted that active surveillance does not address the issue of over-diagnosis, it does provide a vehicle to avoid excessive intervention.”

AND…

“PSA testing should not be considered on its own, but rather as part of a multivariable approach to early prostate cancer detection. PSA is a weak predictor of current risk and additional variables such as digital rectal examination, prostate volume, family history, ethnicity, risk prediction models, and new tools such as the phi test, can help to better risk stratify men.”

AND FINALLY…

“…a man in his 70s who has had a stable PSA at or below the median for a number of years previously is at low risk of developing a threatening prostate cancer and regular PSA screening should be discouraged.”

In other words: With regular PSA testing a very narrowly defined group of men in a narrow age range might have an aggressive, treatable cancer detected but routine screening of all men is not recommended. They recognize that PSA testing frequently leads to over-diagnosis and over-treatment and that for many men there is no need for aggressive treatment. And finally, they admit that PSA testing “is a weak predictor of current risk” and should be considered only one part of an overall approach to men’s prostate health.

But I did get tested, and my PSA is going up. The doctor said stuff like “PSA Velocity” and scared the heck out of me!

PSA Velocity is a fancy way of saying how quickly (or not) a PSA level has increased over a given amount of time. It’s a fiddly, complicated mathematical exercise that looks really impressive to laypeople, but is being discredited by many authorities

In an article in the National Cancer Institute Cancer Bulletin we can find the following statement:

“A rapid increase in prostate-specific antigen (PSA) levels is not grounds for automatically recommending a prostate biopsy, according to a study published online February 24, 2011, in the Journal of the National Cancer Institute.”

The study looked at over 5500 men to determine if using the “PSA Velocity” calculations could help doctors detect more prostate cancers. Here is what they found:

“Adding PSA velocity to the model would have identified 115 additional cancers (although not necessarily fatal cancers) but also resulted in 433 “unnecessary biopsies” that would have shown no cancer.”

In other words, they might have found a few more cancers, but they would have had to do a lot of unnecessary biopsies to do it.

The researchers at the Memorial Sloan-Kettering Cancer Center in New York conclude:

“We found no evidence to support the recommendation that men with high PSA velocity should be biopsied in the absence of other indications; this measure should not be included in practice guidelines.”

Well, my urologist says that the biopsy is “No Big Deal” and I shouldn’t worry about it…

Again, conventional medical authorities are turning against that old party line, and so they should – because evidence of the dangers of prostate biopsies just keeps piling up.

A recent Bloomberg.com news article went into great detail on the risks, starting out with this statement:

“Doctors are changing their approach to prostate biopsies as evidence mounts that the danger of complications from the procedure may outweigh its usefulness identifying some cancers.

An increasing incidence of potentially lethal, difficult- to-treat bloodstream infections tied to prostate biopsies has become so serious that urologists are reassessing when, how and even if they do the procedure.”

Prostate BiopsyThe problem is in the geographical location of the prostate in the body. It lives just under the bladder, and is most easily accessible to a doctor by way of the rectum – which is why the Digital Rectal Exam or DRE is such a convenient tool for your doctor.

Biopsies of the prostate are performed by stabbing a special needle into the prostate gland in a half-dozen or more places to pull out bits of tissue for the pathologist to inspect for cancerous cells

The most common way to get at the prostate for these needle pokes is, like the finger exam, up the rectum.

Since the lower bowel and rectum are a region of our body that is rich in bacteria and almost impossible to “sterilize” or even thoroughly clean, you can imagine the risks!

Just one errant bacterium dragged from the rectum into the prostate or bloodstream as the needle penetrates can result in potentially life-threatening sepsis or even septicemia (aka “blood poisoning”). Since we have been using antibiotics with such wild abandon over the past few decades and have created “superbugs”, many of those bacteria are now antibiotic resistant and virtually untreatable.

But my urologist says he’ll use a different procedure that avoids the rectum – that will be safer, right?

Your urologist is talking about using a trans-perineal approach and may even boast that it will allow him to access more of the prostate gland and take even more biopsy samples.

It is also a much bigger money-maker for your urologist – here is what that Bloomberg article had to say about it:

“The perineum, the skin between the bottom of the scrotum and the anus, is a safer entry point because it can be cleaned with antiseptic, unlike the rectum, said Lindsay Grayson, Austin Hospital’s head of infectious diseases.

The lower risk of infections means urologists can take more core samples of the prostate, especially of the part of the gland that’s difficult to reach from the rectum, Frydenberg said.

On the downside, the procedure takes at least twice as long to perform, requires heavier patient sedation, six people in an operating theater, and equipment costing about $100,000, he said.”

And still not without risk…

Though the transperineal approach may carry less risk of infection, it still exposes men to the same risk as the rectal approach – the risk of spreading an indolent cancer from inside the confines of the prostate where it was sleeping peacefully to the blood and other areas of the body as those cells are dragged out through the surrounding tissues.

In an article in Medical News Today titled Prostate Biopsy Spreads Prostate Cancer Cells, the Diagnostic Center For Disease in Sarasota Florida discussed the phenomenon called “tracking” that occurs:

“A more important issue that is often not discussed between physician and patient involves the possibility of “needle tracking”, the very real possibility of spreading cancer cells beyond the prostate when a biopsy is performed. An extensive review of the literature confirms that once a needle penetrates the capsule of an organ, a phenomenon called “needle tracking” takes place. When the needle is withdrawn from the targeted organ, the chance of spreading cancer cells (when encountered) establishes itself, and every puncture of the prostate adds to this risk.

Despite the significance of this risk to the patient, physicians generally fail to acknowledge a process that allows cells to lie dormant or incubate for up to 10 years or more regardless of the treatment rendered. In a 2 billion dollar prostate biopsy industry, the phenomenon of “needle tracking” takes place approximately 20-30 percent of the time.”

This same article also discusses some of the other risks of prostate biopsy:

“…all men suffer the potential risk for bleeding, scarring, infection or sepsis and needless intrusion that has reportedly resulted in impotency and/or incontinence in some patients.”

But, my PSA is up and my doctor says he’s worried…

There are more reasons than just prostate cancer that might account for a rising PSA – and most of those reasons are quite benign.

Once again let’s see what the discoverer of PSA, Richard J Ablin, has to say:

“Even then, the test is hardly more effective than a coin toss. As I’ve been trying to make clear for many years now, P.S.A. testing can’t detect prostate cancer and, more important, it can’t distinguish between the two types of prostate cancer — the one that will kill you and the one that won’t.

Instead, the test simply reveals how much of the prostate antigen a man has in his blood. Infections, over-the-counter drugs like ibuprofen, and benign swelling of the prostate can all elevate a man’s P.S.A. levels, but none of these factors signals cancer.”

PSA naturally rises as a man ages and the prostate continues growing, but that’s not all:

  • A urinary tract infection or prostatitis can elevate PSA.
  • A healthy activity like a vigorous bicycle (or horseback) ride can elevate PSA.
  • PSA can also be falsely and transiently elevated from something as innocent as having sex with your wife within a day or two of the test.
  • Even the DRE that the doctor performed can cause an elevation of the PSA.

Yes that’s right; an unscrupulous doctor could conceivably perform a “vigorous” or “thorough” DRE “prostate exam” knowing that an elevated PSA would be the result and then use that PSA result to sell his patient a completely unnecessary biopsy procedure!

So, it looks like the PSA is a Bust and shouldn’t ever be used?

Not at all! There are some specific situations where the PSA is a useful tool for the wise doctor to have at his disposal. The following are some of those men who may be wise to follow their PSA:

  • Men with a family history of aggressive prostate cancer, early onset prostate cancer, or death from prostate cancer.
  • Men, especially younger men, (under age 50 or so) who have symptoms of prostate enlargement or disease or unusual findings on DRE.
  • Men of African ethnicity, who tend to develop more aggressive prostate cancers, earlier in life.
  • Men who have been treated for prostate cancer or who has had a prostatectomy performed.

And those biopsies – are there any alternatives?

There may be times when you and your doctor just really need to know – because of symptoms, an unusual finding on DRE, or a rapidly rising PSA over several tests… but biopsy may not be the only option.

Recently, an imaging technology called a “3.0 Tesla Magnetic Resonance Imaging Spectroscopy” scan (MRI -S) is being used to predict and confirm the presence of prostate cancer. This technology is claimed to be the most sensitive and specific diagnostic tool for prostate evaluation in the world, and is said to be able to replace less accurate scanning procedures like the PET scan, CAT scan and Prostascint scans. This is certainly something to discuss with your urologist.

Ultrasound, while not as accurate, may also be employed and is frequently used to guide needle biopsy procedures, either by itself or in combination with MRI imaging.

So, what’s the bottom line?

  • Most men as they age will have an increase in the size of their prostate. This is normal.
  • Most men as they age will have increased PSA levels. This is normal.
  • Most men, if they live long enough, will have cancer in their prostate.
  • Most prostate cancers are very slow growing and cause no problems.
  • Most men with prostate cancer will never know it and will die from something else.
  • PSA testing by itself cannot detect cancer.
  • PSA testing is unreliable in many cases and often leads to unnecessary biopsies and treatments.
  • Prostate biopsy procedures are risky for many reasons.
  • Treatments for prostate cancer can cause more harm than good in many cases.

It is clear that for every aggressive prostate cancer found, treated, and “life saved”, there are many more lives made into a misery of impotence and incontinence through aggressive and unnecessary diagnostics and treatments.

We must do better.

References and Resources:

Epidemiology of BPH: http://emedicine.medscape.com/article/1950546-overview#aw2aab6b5

Latent carcinoma of prostate at autopsy in seven areas. Collaborative study organized by the International Agency for Research on Cancer, Lyons, France: http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910200506/abstract

Richard J Ablin – The Great Prostate Mistake: Published: March 9, 2010 New York Times – http://www.nytimes.com/2010/03/10/opinion/10Ablin.html?_r=0

Screening for prostate cancer in U.S. men ACPM position statement on preventive practice.: http://www.ncbi.nlm.nih.gov/pubmed/18201648

Screening for Prostate Cancer: A Guidance Statement From the Clinical Guidelines Committee of the American College of Physicians: http://annals.org/article.aspx?articleid=1676184

The USPSTF recommends against PSA-based screening for prostate cancer.: http://www.uspreventiveservicestaskforce.org/prostatecancerscreening.htm

AUA RELEASES NEW CLINICAL GUIDELINE ON PROSTATE CANCER SCREENING – http://www.auanet.org/advnews/press_releases/article.cfm?articleNo=290

PSA Screening Does More Harm Than Good, Says New Analysis: http://www.medscape.com/viewarticle/811846

The Melbourne Consensus Statement on Prostate Cancer Testing: http://www.bjuinternational.com/bjui-blog/the-melbourne-consensus-statement-on-prostate-cancer-testing/

PSA Velocity Does Not Improve Prostate Cancer Detection: http://www.cancer.gov/clinicaltrials/results/summary/2011/psa-velocity2011

An empirical evaluation of guidelines on prostate-specific antigen velocity in prostate cancer detection.: http://www.ncbi.nlm.nih.gov/pubmed/21350221

Prostate Cancer Test Causing Sepsis Spurs Biopsy Concerns. Bloomberg, Apr 24, 2013: http://www.bloomberg.com/news/2013-04-24/prostate-cancer-test-causing-sepsis-spurs-biopsy-concerns.html

The Impact of Repeat Biopsies on Infectious Complications in Men with Prostate Cancer on Active Surveillance.: http://www.ncbi.nlm.nih.gov/pubmed/24018237

Diagnostic Center For Disease: Prostate Biopsy Spreads Prostate Cancer Cells – http://www.medicalnewstoday.com/releases/97872.php

Mortality Results from a Randomized Prostate-Cancer Screening Trial: http://www.nejm.org/doi/full/10.1056/NEJMoa0810696

Screening and Prostate-Cancer Mortality in a Randomized European Study: http://www.nejm.org/doi/full/10.1056/NEJMoa0810084

Harvard School of Public Health – Men with prostate cancer more likely to die from other causes: http://ki.se/ki/jsp/polopoly.jsp?d=130&a=146954&l=en&newsdep=130

Accurate Use of Prostate-specific Antigen in Determining Risk of Prostate Cancer: http://www.medscape.com/viewarticle/718972_1

ECC 2013 Press Release: Organised Screening for Prostate Cancer using the Prostate-Specific Antigen Test, Does more Harm than Good – Prostate cancer screening using the prostate-specific antigen (PSA) test is widely used in France despite a lack of evidence showing that it reduces cancer deaths.: http://www.esmo.org/Conferences/European-Cancer-Congress-2013/News/ECC-2013-Press-Release-Organised-Screening-for-Prostate-Cancer-using-the-Prostate-Specific-Antigen-Test-Does-more-Harm-than-Good

 

Muscular Soreness and Pain


Natural Strategies and Support

Muscular and joint pain is a very common and vexing problem that interferes with the enjoyment of life’s pleasures for most of us at some time or other. There are some excellent natural solutions to this problem – read on:

Dr. Myatt received this letter recently:

Hi!
I am a friend of a patient of yours and he mentioned that you could probably suggest a vitamin/mineral that might help my muscle soreness. Have been to a Dr. who ruled out Fibromyalgia. I am very active with work, motorcycles and horses. Have any suggestions?
Thank You, Tanya N.

Hi Tanya,

Thank you for your question. Muscle soreness can result from many things, and combinations of things. The very best way to sort this out would be to arrange an alternative medicine consultation with Dr. Myatt – this will save you time, money, and uncertainty, and provide you with a very definitive plan for better health.

Here are some general suggestions:

An optimal dose multiple vitamin / mineral / micronutrient formula such as Maxi-Multi is a cornerstone for anyone’s good health. Without optimal nutrition, the cells of your body (including your muscles) cannot function properly.

CoEnzyme Q 10 (CoQ10) is an important energy molecule for the mitochondria (the energy units) of our body’s cells. The body produces CoQ10 naturally, but many people are deficient for a number of reasons, including prescription medication use – particularly the use of cholesterol-lowering drugs. Without adequate energy supplies your muscles cannot function at their best and may feel tired and achy. CoQ10 is also a powerful antioxidant.

Omega-3 fatty acids are essential to many processes in the body. They are anti-inflammatory. Deficiencies in Omega-3 fatty acids can contribute to a subtle body-wide inflammatory state. The Standard American Diet is woefully deficient in Omega-3 fatty acids. An excellent source is Max EPA .

Bromelain is nature’s premier anti-Inflammatory herb, useful for all types of infection, injuries, inflammation, sinusitis, cardiovascular disease, rheumatic disease, autoimmune disease, and cancer. It is very effective at reducing swelling and inflammation, thereby reducing pain and discomfort of muscle soreness.

Cox-2 Support is a new product that many of Dr. Myatt’s patients and Wellness Club members have reported excellent results with. This herbal blend was created to help support normal healthy Cox-2 levels. You are no doubt familiar with the Cox-2 inhibitor drugs such as Vioxx and Bextra and others which have earned a reputation for being  dangerous. Cox-2 support was formulated to give similar pain relief by helping the body to produce normal, healthy levels of Cox-2 compounds instead of creating artificially high levels of these compounds in the body by preventing their normal metabolism as the discredited Cox-2 inhibitor drugs are designed to do. It is well worth a try for relieving all kinds of muscular and joint discomfort.

Hope this helps,

Cheers,
Nurse Mark

 

Neuro Restore

NEURO-RESTORE 

Natural Solutions for Neurotransmitter Disorders

Neurotransmitter Restoration:
Key to Depression, Anxiety and
Other Neurotransmitter-Related Disorders

A deficiency of neurotransmitters (also called “NT’s or “brain hormones”) causes or contributes to a wide variety
of diseases including depression, anxiety, and
overweight / obesity.

Low Levels of Neurotransmitters in the Body Can
Cause or Contribute to the Following Disorders:

  • Attention Deficit Disorder (ADD / ADHD)
  • Adrenal Fatigue / Burnout
  • Addictions / addiction withdrawal
  • Aggression (inappropriate)
  • Alzheimer’s Disease
  • Anger (inappropriate)
  • Anorexia
  • Anxiety
  • Bulimia
  • Chronic Fatigue Syndrome
  • Cognitive Impairment / Mild Cognitive Impairment
  • Crohn’s Disease
  • Dementia
  • Depression
  • Eating Disorders
  • Fibromyalgia
  • Hormone Dysfunction
  • Hyperactivity
  • Impulsivity
  • Insomnia / Sleep Disorders
  • Irritable Bowel Syndrome (IBS)
  • Irritability
  • Menopausal Symptoms
  • Migraine Headaches
  • Mood Disorder (anger, anxiety, depression)
  • Nocturnal Myoclonus
  • Obesity / Overweight / Eating Disorders
  • Obsessive-Compulsive Disorder (OCD)
  • Pain (chronic)
  • Panic Attacks
  • Pre-Menstrual Syndrome (PMS)
  • Psychosis / Psychotic Disorder
  • Restless Legs Syndrome
  • Tension Headaches
  • Tempero-Mandibular Joint Dysfunction (TMJ)

What Causes Low Neurotransmitters?

I.) Decreased production of neurotransmitters due to:

  • A deficiency of NT precursors (not enough “raw materials” in the body to correctly manufacture NT’s)
  • Inborn errors of metabolism (an individual may have a genetic need for more of the “raw materials” used to build neurotransmitters)
  • Toxic damage to portions of the brain or peripheral nervous system that produce NT’s

II.) Increased need for neurotransmitters due to:

  • Toxic damage to or destruction of the nerve cells the respond to NT input

  • Excess degradation of existing NeuroTransmitters due to reuptake inhibiting drugs or recreational drugs

Diseases Related to Neurotransmitter (NT) Deficiencies

What Causes Low Neurotransmitters?

Butterbur (MigraMAXX)


Natural Support For Migraine Headache and Hay Fever

ButterburrButterbur (Petasites hybridus) contains petasin, a substance which relaxes blood vessels and certain smooth muscles and is anti-inflammatory. Studies have shown that butterbur is useful for:

  • hay fever
  • migraine headaches

Butterbur and Hay Fever

Butterbur has been shown in studies to be as effective as drugs at relieving hay fever symptoms but without adverse side effects

One study compared Butterbur to the drug cetirizine (Zyrtec) and found that both relieved symptoms equally well. However, the drug was associated with a higher rate of adverse side effects including drowsiness.

A second study compared butterbur extract with fexofenadine (Allegra). Butterbur was just as effective as fexofenadine at relieving symptoms.

Butterbur and Migraine Headache

Studies have shown that Butterbur reduces the frequency of migraine headaches. The amount of Butterbur needed to be effective was 75mg of a standardized 15% petasin extract taken at least twice per day. Smaller doses were not effective in reducing migraine frequency.

Butterbur may contain pyrrolizidine alkaloids which can cause liver damage, use only extracts which have the pyrrolizidine alkaloids removed. This will be stated on the label.

References

1.) Wang GJ, Shum AY, Lin YL, et al. Calcium channel blockade in vascular smooth muscle cells: Major hypotensive mechanism of S-petasin, a hypotensive sesquiterpene from Petasites formosanus. J Pharmacol Exp Ther 2001;297:240–6.
2.) Thomet OA, Schapowal A, Heinisch IV, et al. Anti-inflammatory activity of an extract of Petasites hybridus in allergic rhinitis. Int Immunopharmacol 2002;2:997–1006.
3.) Lipton RB, Gobel H, Einhaupl KM, et al. Petasites hybridus root (butterbur) is an effective preventive treatment for migraine. Neurology 2004;63:2240–4.
4.) Lee DK, Haggart K, Robb FM, Lipworth BJ. Butterbur, a herbal remedy, confers complementary anti-inflammatory activity in asthmatic patients receiving inhaled corticosteroids. Clin Exp Allergy 2004; 34:110–4.
5.) Ziolo G, Samochewiec L. Study on clinical properties and mechanism of action of petasites in bronchial asthma and chronic obstructive bronchitis. Pharm Acta Helv 1998;72:378–80.
6.) Schapowal A, Petasites Study Group. Randomised controlled trial of butterbur and cetirizine for treating seasonal allergic rhinitis. BMJ 2002;324:144–6.
7.) Lee DK, Gray RD, Robb FM, et al. A placebo-controlled evaluation of butterbur and fexofenadine on objective and subjective outcomes in perennial allergic rhinitis. Clin Exp Allergy 2004;34:646–9.
8.) Schapowal A; Petasites Study Group. Butterbur Ze339 for the treatment of intermittent allergic rhinitis: dose-dependent efficacy in a prospective, randomized, double-blind, placebo-controlled study. Arch Otolaryngol Head Neck Surg. 2004 Dec;130(12):1381-6.
9.) Lee DK, Carstairs IJ, Haggart K, Jackson CM, Currie GP, Lipworth BJ. Butterbur, a herbal remedy, attenuates adenosine monophosphate induced nasal responsiveness in seasonal allergic rhinitis. Clin Exp Allergy. 2003 Jul;33(7):882-6.
10.) Käufeler R, Polasek W, Brattström A, Koetter U. Efficacy and safety of butterbur herbal extract Ze 339 in seasonal allergic rhinitis: postmarketing surveillance study.Adv Ther. 2006 Mar-Apr;23(2):373-84.
11.) Diener HC, Rahlfs VW. Danesch U. The first placebo-controlled trial of a special butterbur extract for the prevention of migraine: reanalysis of efficacy criteria. Eur Neurol 2004;51:89–97.
12.) Grossmann M, Schmidramsl H. An extract of Petasites hybridus is effective in the prophylaxis of migraine. Int J Clin Pharmacol Ther 2000;38:430–5.
13.) Pothmann R, Danesch U. Migraine prevention in children and adolescents: results of an open study with a special butterbur root extract. Headache 2005;45:196–203.
14.) Lipton RB, Gobel H, Einhaupl KM, et al. Petasites hybridus root (butterbur) is an effective preventive treatment for migraine. Neurology 2004;63:2240–4.