Category: Health Concerns

PROSTATE CANCER (also see CANCER)


Natural Support Strategies for the most common male cancer in the U.S.

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). The incidence of disease increases with each decade of life over age 50. Prostate cancer rates have risen 108% since 1950, believed due in part to earlier detection. Death rates from the disease have increased 23% in spite of widespread use of surgery, radiation and chemotherapy.

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.

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. Herbal and nutritional treatment for cancer can be considered an adjuvant therapy in all cases of prostate carcinoma and the sole therapy in many cases. Even when conventional treatment is deemed advisable, non-traditional uses of conventional hormone-suppressive drugs (called “Androgen Deprivation Therapy” or ADT), may be safer and more advantageous than standard therapy alone. This is because, in it’s early stages, prostate cancer is highly controllable with hormone-blocking therapy.

Laboratory Evaluation of Prostate Cancer

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 reading could be clarified non-invasively with the additional use of the free-PSA test.

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.

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 therefore 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.

Specific Goals of Prostate Cancer Therapy

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

DIET AND LIFESTYLE RECOMMENDATIONS

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 anti-inflammatory.

A ketogenic (very low carbohydrate) diet such as The Super Fast Diet decreases 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 diet. In animal studies, even s 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 own hormone production. (Fat cells manufacture estrogen, a growth-promoting hormone).

Foods of Special Benefit

Garlic, lemon peel (the peel contains limonene), fish, flax seed, soy and soy products, fresh vegetables (especially non-starchy, dark leafy greens), 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, they do not need to be used at all until desired weight is achieved.

DIET AND LIFESTYLE RECOMMENDATIONS

  • A ketogenic diet such as The Super Fast Diet should be followed to lower insulin and glucose levels.
  • Achieve and maintain an optimal body weight and BMI. (BMI 18-22).
  • Exercise regularly to improve prostate circulation. Walking and running are the best for prostate circulation because they use the major leg muscles. Cycling restricts blood flow to the prostate and testicles and should not be used as the primary form of exercise for men.

PRIMARY SUPPORT

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of vitamin A, carotenes, C, D and selenium appear particularly important.
  • Omega 3 fatty acids:
    Flax seed meal, 2 teaspoons per day with food
    OR
    Max EPA (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day). (Or eat fish 3 times per week and use 2 teaspoons of ground flax seed per day added to food).
  • Vitamin D: 1,000-5,000IU per day based on blood test results
  • Bromelain: 1-2 caps, 3-4 times per day between meals.

  • Melatonin: 10-40mg before bed.

ADDITIONAL SUPPORT

(NOTE: These therapies should be undertaken with the guidance of a physician who can order laboratory tests to determine hormone levels and immune function, monitor the effectiveness of treatment, assess possible toxicity and prescribe drugs when advisable). Please strongly consider obtaining a consultation with Dr. Myatt.

To Decrease testosterone

  • Saw palmetto: Serenoa repens, S. serrulata (Palmaceae)
    Saw palmetto blocks the conversion of testosterone to
    dihydrotestosterone (DHT) and there is evidence that DHT may be five times as potent as testosterone in stimulating prostate cancer cell growth.
  • Chaste berry: Vitex agnus-castus, V. negundo (Verbenaceae)-
    Vitex spp. decreases testosterone production in vivo and inhibits prolactin synthesis and release in animal models. As the name “chaste tree” implies, this herb was traditionally used by monks to reduce libido.
  • Rx: Casodex, Flutamide, Lupron, Zoladex

To Decrease prolactin

  • Vitex spp.- Chaste tree
  • Vegetarian diet
  • Rx: Bromocriptine, Pergolide, Dostinex

Vitamin D3 (cholecalciferol): 1,000 I.U., 2-3 times per day with meals.
Vitamin D3 induces prostate cancer cell death (apoptosis) by apparent translocation of the cancer cell androgen receptor. This makes the cell less susceptible to testosterone-induced cell-growth stimulation. D3 encourages cancer cells to become more normal (induces differentiation), inhibits a cancer cell from developing it’s own blood supply (inhibits angiogenesis) and shows antitumor activity. Because vitamin D has the potential to cause toxicity, doses over 1,000 I.U. should be monitored by a physician. 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 decreased sunlight, increases of breast and colon cancer have been observed.

DR. MYATT’S COMMENTS

Prostate cancer, especially early and mid-stage cancers in older patients, respond favorably to natural remedies. Whether as an adjuvant to conventional therapy or as the sole therapy, such treatment strategies should be considered.

Cancer, including prostate cancer, behaves differently depending on the age of the patient, the extent of the disease, the patient’s basic level of health, hormone status, etc., etc. For this reason, cancer patients should seek qualified holistic medical help when designing a natural (adjuvant or primary) treatment protocol.

PHYSICIAN NOTE #1:
Digestive enzymes (multi 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, 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.

PHYSICIAN NOTE #2:
 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. In vitro, melatonin demonstrates anti-estrogen activity and immune stimulation. 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. Dosages used are much higher in cancer treatment than for insomnia or longevity protocols.

Prostate Cancer: Case Studies

The following case studies are meant to highlight for the reader or physician the effects of diet, hormone deprivation therapy, and adjuvant therapy on prostate cancer. Information about new prostate cancer blood tests, as well as new ways to interpret older tests, are also given. Anyone with a diagnosis of cancer should be working with a knowledgeable physician. Cancer can often be controlled through non-invasive measures but regular blood tests are important to verify the success of treatment. The interpretation of such tests is best done in conjunction with a physician. I am available for consultation.

Case # 1:

An otherwise healthy 65 year old male was found on routine physical exam to have a PSA of 19.7. Digital rectal exam (DRE) was unremarkable; Gleason score 2 + 3 on biopsy. Other relevant data: weight 208 pounds, height 5’11″, blood sugar 110, cholesterol 211, triglyceride 244.

The patient had originally declined conventional treatment offered him at the time of diagnosis. He began a self-prescribed regimen of CoQ10, vitamin A,C,E, N-acetyl cystein and MGN3 (mushroom preparation). In four months, his PSA was 14.0, other vitals remained relatively unchanged.

At this point, the patient consulted me. I performed a PAP which was 1.1, normal. I put the patient on a ketogenic diet, substituted Maxi Muli formula for his separate vitamins, added Maxi Greens and vitamin D3. One month later, his PSA was 10.2, weight 189, blood sugar 83, cholesterol 167 and triglycerides 43.

Dr. Myatt’s comments

PSA is an accurate marker of prostate cancer activity after the diagnosis of cancer has been established. Any significant decreases of PSA represent a slowing of the disease process, so this number can be used in early and mid-stage prostate cancer to assess efficacy of treatment. The patient’s initial decrease of PSA was due entirely to his supplement regimen since no diet changes were made at that time.

After beginning The Super Fast Diet, the patient had a further decline in PSA, accompanied by significant improvements in blood sugar, weight, cholesterol, and triglycerides. After two months and four months, the patient’s PSA’s remain at 10.2. A continuing decline is desirable, but this “holding pattern” is still good.

The ketogenic diet made the most dramatic improvement in this case. Not only did it result in further control of the cancer, but the patient is now at lower risk for cardiac and other weight-related problems as well. It is important to remember that a disease such as prostate cancer rarely appears in isolation. Overall improvement of the patient’s health is necessary to gain control of the disease and minimize risk of other diseases. What good is it to save a person from prostate cancer only to have them die of a heart attack?

Case # 2:

An obese (250 pounds+) 56 year old male with a history of asthma was found on routine physical exam to have a PSA of 4.4 and a free PSA of 5.9, suggesting cancer. Biopsy confirmed the diagnosis. During the first four weeks after diagnosis, the patient’s PSA rose from 4.4 to 6.2, a rapid increase suggesting a possibly aggressive cancer. The PAP was within normal limits, indicating no lymphatic or extra-capsular spread.

The patient was advised to follow a The Super Fast Diet (a ketogenic diet), which would be expected to benefit both the cancer and asthma. (Obesity is associated with an increased likelihood of asthma and contributes a large hormone burden to the body because fat cells manufacture estrogen. Estrogen is a growth factor for hormone-related cancers including prostate cancer). The patient has thus far failed to follow a ketogenic diet. Hormone deprivation therapy was initiated, and this dropped the PSA to less the 0.1 in one month, indicating current control of the disease. Since cancer cells eventually “escape” hormone suppression, this treatment will not be expected to work indefinitely. During this time, the patient will be encouraged to lose weight, preferably on a ketogenic diet. I will continue to encourage him to either have surgery or become more dedicated to a non-surgical cancer control program. Prostate cancer is one form of cancer that is highly amenable to diet and lifestyle modification if the individual is willing to make some modest positive changes.

This article is developed from the lecture notes for a lecture presented by Dr. Myatt in May of 2000 at the 2000 Pacific Northwest Herbal Symposium. A transcript of the original, fully annotated notes may be found at the link below:

Botanical and Nutritional Considerations in the
Treatment of Prostate Cancer
Dana Myatt, N.M.D.

References

Lab Evaluation and Incidence

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.

Low Carbohydrate Diet

1.) Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB. Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate. 2008 Jan 1;68(1):11-9.
2.) Venkateswaran V, Haddad AQ, Fleshner NE, Fan R, Sugar LM, Nam R, Klotz LH, Pollak M. Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.J Natl Cancer Inst. 2007 Dec 5;99(23):1793-800. Epub 2007 Nov 27.
3.) Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.Nutr Metab (Lond). 2007 Feb 21;4:5.
4.) Borugian MJ, Sheps SB, Kim-Sing C, Van Patten C, Potter JD, Dunn B, Gallagher RP, Hislop TG. Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1163-72.
5.) Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P.: Role of glucose and ketone bodies in the metabolic control of experimental brain cancer.Br J Cancer. 2003 Oct 6;89(7):1375-82.
6.) Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schünemann HJ, Ram M, Freudenheim JL, Sieri S, Trevisan M, Berrino F. Fasting glucose is a risk factor for breast cancer: a prospective study. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1361-8.
7.) Meixensberger J, Herting B, Roggendorf W, Reichmann H: Metabolic patterns in malignant gliomas.J Neurooncol 1995, 24:153-161
8.) Fearon KC.: Nutritional pharmacology in the treatment of neoplastic disease.Baillieres Clin Gastroenterol. 1988 Oct;2(4):941-9.
9.) Pedersen PL: Tumor mitochondria and the bioenergetics of cancer cells. Prog Exp Tumor Res 1978, 22:190-274.

Foods of Special Benefit

Garlic

1.) Morioka, N., Morton, D.L., and Irie, R.F.: A protein fraction from aged garlic extract enhances cytotoxicity and proliferation of human lymphocytes mediated by interleukin-2 and conavalin. Proc Ann Meet Am Assoc Cancer 34:A3297, 1993.
2.) Legnani C., Frascaro M., Guazzaloca G., et al.: Effects of a dried garlic preparation on fibrinolysis and platelet aggragation in healthy subjects. Arzneim Forsch Drug Res 43:119-122, 1993.
3.) Kiesewetter H., et al.: effects of garlic coated tablets in peripheral arterial occlusive disease. Clin Investig 71:383-86, 1993.
4.) Lau, B.H., Yamasaki, T., and Gridley, D.S.: Garlic compounds modulate macrophage and T-lymphocyte function. Mol Biother 3:103-107, 1991.
5.) Dausch JG., Nixon DW.: Garlic: a review of its relationship to malignant disease. Prev Med 19:346-61, 1990.
6.) Kandil O.M., et al.: Garlic and the immune system in humans: its effect on natural killer cells. Fed Proc 46:441, 1987.
7.) Kandil, O.M. et. al.: Garlic and the immune system in humans: Its effect on natural killer cells. Fed Proc 46:441, 1987.
8.) Belman S.: Onion and garlic oils prohibit tumor promotion. Carcinogenesis 4(8):1063-5, 1983.
9.) Kroning, F.: Garlic as an inhibitor for spontaneous tumors in predisposed mice. Acta Unio Inter Contra Cancrum 20(3):855, 1964.

Super Foods

1.) Khan N, Afaq F, Mukhtar H. Cancer Chemoprevention Through Dietary Antioxidants: Progress and Promise. Antioxid Redox Signal. 2007 Dec 21 [Epub ahead of print].
2.) Moreno DA, López-Berenguer C, García-Viguera C. Effects of stir-fry cooking with different edible oils on the phytochemical composition of broccoli. J Food Sci. 2007 Jan;72(1):S064-8.
3.) Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst 2000;92(1):61–8.
4.) Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst 2000;92(1):61–8.
5.) Kune GA. Eating fish protects against some cancers: epidemiological and experimental evidence for a hypothesis. J Nutr Med 1990;1:139–44 [review].
6.) Rose DP, Connolley JM. Omega-3 fatty acids as cancer chemopreventive agents. Pharmacol Ther 1999;83:217–44.
7.) Demark-Wahnefried W, Price DT, Polascik TJ, et al. Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features. Urology2001;58:47–52.
8.) Davis JN, Singh B, Bhuiyan M, Sarkar FH. Genistein-induced upregulation of p21WAF1, downregulation of cyclin B, and induction of apoptosis in prostate cancer cells. Nutr Cancer 1998;32:123–31.
9.) Barnes S, Peterson TG, Coward L. Rationale for the use of genistein-containing soy matrices in chemoprevention trials for breast and prostate cancer. J Cell Biochem Suppl 1995;22:181–7.
10.) Jacobsen BK, Knutsen SF, Fraser GE. Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States). Cancer Causes Control 1998;9:553–7.
11.) Geller J, Sionit L, Partido C, et al. Genistein inhibits the growth of human-patient BPH and prostate cancer in histoculture. Prostate 1998;34:75–9.

Body Weight (BMI) and Prostate Cancer

1.) Talamini R, La Vecchia C, Decarli A, et al. Nutrition, social factors and prostatic cancer in a Northern Italian population. Br J Cancer 1986;53:817–21.
2.) Andersson S-O, Wolk A, Bergstrom R, et al. Body size and prostate cancer: a 20-year follow-up study among 135,006 Swedish construction workers. J Natl Cancer Inst 1997;89:385–9.

Exercise and Prostate Cancer

1.) Greenspan SL. Approach to the prostate cancer patient with bone disease. J Clin Endocrinol Metab. 2008 Jan;93(1):2-7.
2.) Barnard RJ, Leung PS, Aronson WJ, Cohen P, Golding LA.A mechanism to explain how regular exercise might reduce the risk for clinical prostate cancer. Eur J Cancer Prev. 2007 Oct;16(5):415-21.
3.) Darlington GA, Kreiger N, Lightfoot N, Purdham J, Sass-Kortsak A. Prostate cancer risk and diet, recreational physical activity and cigarette smoking. Chronic Dis Can. 2007;27(4):145-53.
4.) Farrell SW, Cortese GM, Lamonte MJ, Blair SN. Cardiorespiratory fitness, different measures of adiposity, and cancer mortality in men. Obesity (Silver Spring). 2007 Dec;15(12):3140-9.
5.) Galvão DA, Taaffe DR, Spry N, Newton RU. Exercise can prevent  and even reverse adverse effects of androgen suppression treatment in men with prostate cancer. Prostate Cancer Prostatic Dis. 2007;10(4):340-6. Epub 2007 May 8.
6.) Kruk J. Physical activity in the prevention of the most frequent chronic diseases: an analysis of the recent evidence. Asian Pac J Cancer Prev. 2007 Jul-Sep;8(3):325-38.
7.) Monga U, Garber SL, Thornby J, Vallbona C, Kerrigan AJ, Monga TN, Zimmermann KP. Exercise prevents fatigue and improves quality of life in prostate cancer patients undergoing radiotherapy. Arch Phys Med Rehabil. 2007 Nov;88(11):1416-22.
8.) Chang SC, Ziegler RG, Dunn B, Stolzenberg-Solomon R, Lacey JV Jr, Huang WY, Schatzkin A, Reding D, Hoover RN, Hartge P, Leitzmann MF. Association of energy intake and energy balance with postmenopausal breast cancer in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):334-41.

Multiple Vitamins and Cancer / Prostate Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
4.) Moyad MA. The use of complementary/preventive medicine to prevent prostate cancer recurrence/progression following definitive therapy. Part II–rapid review of dietary supplements. Curr Opin Urol. 2003 Mar;13(2):147-51.
5.) Kristal AR, Stanford JL, Cohen JH, Wicklund K, Patterson RE.Vitamin and mineral supplement use is associated with reduced risk of prostate cancer. Cancer Epidemiol Biomarkers Prev. 1999 Oct;8(10):887-92.

Antioxidants (General) and Prostate Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, Albanes D, Andriole GL, Urban DA, Peters U; PLCO Trial. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk.J Natl Cancer Inst. 2006 Feb 15;98(4):245-54.
4.) Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. 2005 Apr;24(2):172-83.
5.) Ferguson LR, Philpott M, Karunasinghe N. Dietary cancer and prevention using antimutagens. Toxicology. 2004 May 20;198(1-3):147-59.
6.) Borek C. Dietary antioxidants and human cancer.Integr Cancer Ther. 2004 Dec;3(4):333-41.
7.) Prasad KN. Multiple dietary antioxidants enhance the efficacy of standard and experimental cancer therapies and decrease their toxicity. Integr Cancer Ther. 2004 Dec;3(4):310-22.
8.) Heyland DK, Dhaliwal R, Suchner U, Berger MM. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 2005 Mar;31(3):327-37. Epub 2004 Dec 17.
9.) Drisko JA, Chapman J, Hunter VJ. The use of antioxidant therapies during chemotherapy. Gynecol Oncol. 2003 Mar;88(3):434-9.
10.) Prasad KN, Cole WC, Kumar B, Prasad KC. Scientific rationale for using high-dose multiple micronutrients as an adjunct to standard and experimental cancer therapies. J Am Coll Nutr. 2001 Oct;20(5Suppl):450S-463S; discussion 473S-475S.
11.) Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev. 1999 Oct;4(5):304-29.
12.) Prasad KN, Kumar A, Kochupillai V, Cole WC. High doses of multiple antioxidant vitamins: essential ingredients in improving the efficacy of standard cancer therapy. J Am Coll Nutr. 1999
Feb;18(1):13-25.
13.) Lupulescu A. The role of vitamins A, beta-carotene, E and C in cancer cell biology. Int J Vitam Nutr Res. 1994;64(1):3-14.
14.) Stähelin HB. Critical reappraisal of vitamins and trace minerals in nutritional support of cancer patients. Support Care Cancer. 1993 Nov;1(6):295-7.

Vitamin A , Carotenes and Prostate Cancer

1.)  Wu K, Erdman JW Jr, Schwartz SJ, Platz EA, Leitzmann M, Clinton SK, DeGroff V, Willett WC, Giovannucci E.Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study. Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):260-9.
2.) Gann PH, Ma J, Giovannucci E, Willett W, Sacks FM, Hennekens CH,Stampfer MJ. Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res. 1999 Mar 15;59(6):1225-30.
3.) Giovannucci E, Ascherio A, Rimm EB, Stampfer MJ, Colditz GA, Willett WC. ake of carotenoids and retinol in relation to risk of prostate cancer. J Natl Cancer Inst. 1995 Dec 6;87(23):1767-76.
4.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W.: Synergistic effect of retinoids and interferon alpha on tumor-induced angiogenesis: anti-angiogenic effect on HPV-harboring
tumor-cell lines.Int J Cancer. 1994 Apr 1;57(1):81-5.

Vitamin C and Cancer / Prostate cancer

1.) Hanck A. Vitamin C and cancer. Int J Vit Nutr Res 1983;(Suppl #24):87–104 [review].
2.) Murata A, Morishige F, Yamaguchi H. Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate. Int J Vit Nutr Res 1982;(Suppl #23):103–14.
3.)  Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1978;75:4538–42.
4.) Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1976;73:3685–9.

Vitamin D and Prostate Cancer

1.) Lappe J, Travers-Gustafson D, Davies K, Recker R, Heaney R. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. American Journal of Clinical Nutrition. Am J Clin Nutr. 2007 Jun;85(6):1586-91.
2.) Ma Y, et al. Study presented at the 2007 centennial meeting of the American Association for Cancer Research (AACR), April 14 to 18, 2007, Los Angeles.
3.) Holick MF.: Vitamin D: Its role in cancer prevention and treatment. Prog Biophys Mol Biol. 2006 Mar 10;
4.)Woo TCS, Choo R, Jamieson M, et al. Pilot study: potential role of vitamin D (cholecalciferol) in patients with PSA relapse after definitive therapy. Nutr Cancer 2005;51:32–6.
5.) Schwartz GG, Eads D, Rao A, Cramer SD, Willingham MC, Chen TC, Jamieson DP, Wang L, Burnstein KL, Holick MF, Koumenis C.:Pancreatic cancer cells express 25-hydroxyvitamin D-1 alpha-hydroxylase and their proliferation is inhibited by the prohormone 25-hydroxyvitamin D3.Carcinogenesis. 2004 Jun;25(6):1015-26. Epub 2004 Jan 23.
6.) Wietrzyk J, Pelczynska M, Madej J, Dzimira S, Kusnierczyk H, Kutner A, Szelejewski W, Opolski A.: Toxicity and antineoplastic effect of (24R)-1,24-dihydroxyvitamin D3 (PRI-2191).Steroids. 2004 Sep;69(10):629-35.
7.) Vegesna V, O’Kelly J, Said J, Uskokovic M, Binderup L, Koeffle HP.: Ability of potent vitamin D3 analogs to inhibit growth of prostate cancer cells in vivo. Anticancer Res. 2003 Jan-Feb;23(1A):283-9.
8.) Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.
9.) Majewski S, Skopinska M, Marczak M, Szmurlo A, Bollag W, Jablonska S.: Vitamin D3 is a potent inhibitor of tumor cell-induced angiogenesis. J Investig Dermatol Symp Proc. 1996 Apr;1(1):97-101.
10.) Schwartz GG, Hill CC, Oeler TA, Becich MJ, Bahnson RR.1,25-Dihydroxy-16-ene-23-yne-vitamin D3 and prostate cancer cell proliferation in vivo. Urology. 1995 Sep;46(3):365-9.
11.) 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.Cancer Lett. 1993 Nov 30;75(1):35-9.

Selenium and Cancer / Prostate Cancer

1.) Meyer F, Galan P, Douville P, et al. Antioxidant vitamin and mineral supplementation and prostate cancer prevention in the SU.VI.MAX trial. Int J Cancer 2005;116:182–6.
2.) Li H, Stampfer MJ, Giovannucci EL, Morris JS, Willett WC, Gaziano JM, Ma J.A prospective study of plasma selenium levels and prostate cancer risk. J Natl Cancer Inst. 2004 May 5;96(9):696-703.
3.)Clark LC, Combs GF Jr, Turnbull BW, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. JAMA 1996;276:1957–63.
4.)  Knekt P, Aromaa A, Maatela J, et al. Serum selenium and subsequent risk of cancer among Finnish men and women. J Natl Cancer Inst 1990;82:864–8.
5.) Fex G, Pettersson B, Akesson B. Low plasma selenium as a risk factor for cancer death in middle-aged men. Nutr Cancer 1987;10:221–9.
6.) Medina D. Mechanisms of selenium inhibition of tumorigenesis. Adv Exp Med Biol 1986;206:465–72.
7.) Willett WC, Polk BF, Morris JS, et al. Prediagnostic serum Selenium and risk of cancer. Lancet 1983;42:130–4.
8.) Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:417–68.
9.) Shamberger RJ, Rukoven E, Lonfield AK, et al. Antioxidants and cancer. Selenium in the blood of normals and cancer patients. J Natl Cancer Inst 1973;4:863–70.

Omega 3 Essential Fatty Acids and Prostate Cancer

1.) Ritch CR, Wan RL, Stephens LB, Taxy JB, Huo D, Gong EM, Zagaja GP, Brendler CB. Dietary fatty acids correlate with prostate cancer biopsy grade and volume in Jamaican men. J Urol. 2007 Jan;177(1):97-101; discussion 101.
2.) Hedelin M, Chang ET, Wiklund F, Bellocco R, Klint A, Adolfsson J, Shahedi K, Xu J, Adami HO, Grönberg H, Bälter KA. Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism. Int J Cancer. 2007 Jan 15;120(2):398-405.
3.) Kobayashi N, Barnard RJ, Henning SM, Elashoff D, Reddy ST, Cohen P, Leung P, Hong-Gonzalez J, Freedland SJ, Said J, Gui D, Seeram NP, Popoviciu LM, Bagga D, Heber D, Glaspy JA, Aronson WJ.Effect of altering dietary omega-6/omega-3 fatty acid ratios on prostate cancer membrane composition, cyclooxygenase-2, and prostaglandin E2. Clin Cancer Res. 2006 Aug 1;12(15):4662-70.
4.) Pilot study to explore effects of low-fat, flaxseed-supplemented diet on proliferation of benign prostatic epithelium and prostate-specific antigen. Urology. 2004 May;63(5):900-4.
5.) Augustsson K, Michaud DS, Rimm EB, Leitzmann MF, Stampfer MJ, Willett WC, Giovannucci E. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003 Jan;12(1):64-7.
6.) Dietary fat and cancer.Am J Med. 2002 Dec 30;113 Suppl 9B:63S-70S
7.) Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features. Urology. 2001 Jul;58(1):47-52.
8.) Comparison of fatty acid profiles in the serum of patients with prostate cancer and benign prostatic hyperplasia. Clinical Biochemistry, Vol. 32, August 1999, pp. 405-09.

Bromelain (anasas comosus) and Cancer

1.)Kalra N, Bhui K, Roy P, Srivastava S, George J, Prasad S, Shukla Y.Regulation of p53, nuclear factor kappaB and cyclooxygenase-2 expression by bromelain through targeting mitogen-activated protein kinase pathway in mouse skin.Toxicol Appl Pharmacol. 2008 Jan 1;226(1):30-7. Epub 2007 Aug 23.
2.) Báez R, Lopes MT, Salas CE, Hernández M. In vivo antitumoral activity of stem pineapple (Ananas comosus) bromelain. Planta Med. 2007 Oct;73(13):1377-83. Epub 2007 Sep 24.
3.) Beuth J, Braun JM. Modulation of murine tumor growth and colonization by bromelaine, an extract of the pineapple plant (Ananas comosum L.).In Vivo. 2005 Mar-Apr;19(2):483-5.
4.) Wallace JM. Nutritional and botanical modulation of the inflammatory cascade–eicosanoids, cyclooxygenases, and lipoxygenases–as an adjunct in cancer therapy. Integr Cancer Ther. 2002 Mar;1(1):7-37; discussion 37.
5.) Maurer HR.Bromelain: biochemistry, pharmacology and medical use. Cell Mol Life Sci. 2001 Aug;58(9):1234-45.
6.) Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S10-5.
7.) Hubarieva HO, Kindzel’s’kyĭ LP, Ponomar’ova OV, Udatova TV, Shpil’ova SI, Smolanka II, Korovin SI, Ivankin VS. Systemic enzymotherapy as a method of prophylaxis of postradiation complications in oncological patients] Lik Sprava. 2000 Oct-Dec;(7-8):94-100.
8.) Zavadova E, Desser L, Mohr T. Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation. Cancer Biother. 1995 Summer;10(2):147-52.
9.) Taussig SJ, Batkin S. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. 1988 Feb-Mar;22(2):191-203.
10.) Batkin S, Taussig SJ, Szekerezes J. Antimetastatic effect of bromelain with or without its proteolytic and anticoagulant activity. J Cancer Res Clin Oncol. 1988;114(5):507-8.

Melatonin and Cancer

1.) Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
2.) Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
3.) Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
4.) Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
5.) Lissoni P, Barni S, Cazzaniga M, Ardizzoia A, Rovelli F, Brivio F, Tancini G.: Efficacy of the concomitant administration of the pineal hormone melatonin in cancer immunotherapy with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 alone. Oncology. 1994 Jul-Aug;51(4):344-7.
6.) Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.

Saw Palmetto (Actions)

1.) Di Silverio F, Monti S, Sciarra A, et al. Effects of long-term treatment with Serenoa repens (Permixon®) on the concentrations and regional distribution of androgens and epidermal growth factor in benign prostatic hyperplasia. Prostate 1998;37:77–83.
2. Strauch G, Perles P, Vergult G, et al. Comparison of finasteride (Proscar®) and Serenoa repens (Permixon®) in the inhibition of 5-alpha reductase in healthy male volunteers. Eur Urol 1994;26:247–52.

Chaste Berry (Vitex) Actions

1.) Sliutz G, Speiser P, Schultz AM, et al. Agnus castus extracts inhibit prolactin secretion of rat pituitary cells. Horm Metab Res 1993;25:253–5.
2.) Böhnert KJ. The use of Vitex agnus castus for hyperprolactinemia. Quart Rev Nat Med 1997;Spring:19–21.

 

PSA CAPSULES (formerly called Prostate Support)


A PC-SPES-Like Herbal Formula for Prostate Cancer

Prostate Support – now called PSA Capsules – contains a combination of herbs that support the prostate gland and immune system in the presence of prostate cancer. This formula is similar to “PC-SPES” without the undisclosed drugs.

Suggested dose: 1-2 capsules, 3 times per day on an empty stomach.

Dr. Myatt’s comment: It is important to work with a skilled holistic physician when treating any form of cancer.

Each (two) capsules contain:
(Please Note: Due to variances in the processing of these herbs, actual mg amounts may vary slightly)

Reishi mushroom (Ganoderma lucidum)………..172 mg
Baikal skullcap root (Scutellaria baicalensis)…..146 mg
Rabdosia root (Rabdosia rubescens) …………….120 mg
San-Qi ginseng root (Panax notoginseng)……….112 mg
Ban Lan Gen root (AKA Dyer’s Woad root)
(Isatis indigotica)…………………………………………………94 mg
Mum flower (Dendranthema morifolium) …………..78 mg
Saw Palmetto berry (Serenoa repens)……………….70 mg
Licorice root (Glycyrrhiza glabra)…………………………70 mg

NOTE: This product is only available to Dr. Myatt’s private practice patients.

The Truth about PC-SPES

The product PC SPES worked well for many men. Unfortunately, it contained a number of undisclosed drugs which not only caused some undesirable side effects such as breast enlargement and tenderness, but also side effects that could be downright dangerous, even lethal. When tested, PC-SPES was found to contain diethylstilbesterol (DES), a synthetic form of the female hormone estrogen. This compound can cause a number of negative side effects, the most significant of which is blood clotting which can lead to cardiovascular events including heart attach and stroke, deep vein thrombosis (DVT) and pulmonary embolism (PE).

Another compound found in PC-SPES was Warfarin (aka “rat poison”) – a powerful blood thinner presumably included to counter the potential blood clotting effects of the DES. Finally, the drug Indomethacin (Indocid) – a non-steroidal anti-inflammatory (NSAID)- was found. This drug has the potential to cause severe gastrointestinal side effects such as GI bleeding, ulceration and blood clotting problems.

It is believed that the great success of PC Spes was due to the undisclosed DES (female hormone). As many have noted, men would vary the dose to achieve the best  effect – from one or two to as many as a dozen capsules per day. This exposed men to potentially very dangerous levels of the other undisclosed drugs in addition to high hormone levels.

I am including a link to a very informative paper on this subject, an essay by Subhuti Dharmananda, Ph.D., Director, Institute for Traditional Medicine, Portland, Oregon

ITM Online

Dr. Myatt’s product Prostate Support is the result of Dr. Myatt’s suspicions about the product PC Spes and her analysis of it which demonstrated the undisclosed drugs. She then formulated a replacement which contained the beneficial herbal components, without the potentially dangerous drugs. The drugs that were hidden in PC Spes are all easily available to a physician if they are needed, and Dr. Myatt felt that it was far safer and more effective to use carefully tailored separate doses of these drugs when necessary to achieve the desired effects.

This allowed Dr. Myatt to develop a very effective herbal formulation, without risking the potentially dangerous, even lethal side effects that could result from the hidden drugs. Her further observation regarding the PC Spes formula was that if the manufacturer was willing to hide drugs in it’s formula, what else was it willing to do? The drug were undisclosed – this means that the doses were also undisclosed and could be changed or even eliminated at any time.

As you will have seen from this website, we at The Wellness Club have no love for the FDA. In this instance, however, we believe that they did the right thing by removing PC Spes from the marketplace.

Dr. Myatt has a great deal of experience in treating prostate cancer. She also has a very personal interest – she has been treating her own father for prostate cancer for the two decades. His conventional physicians wanted to do the  “cut, burn, and poison” treatments when it was first discovered. Instead, Dr. Myatt pioneered a then-unconventional form of hormonal suppression therapy. This proved highly successful and she has used these techniques on hundreds of men since then with the same excellent results. Her techniques are now accepted and commonly used in conventional medicine.

Please visit our web pages where we discuss Cancer , Prostate Cancer , Prostate Enlargement , and Man Health & Fitness where Dr. Myatt discusses male hormones. There is information available on hormone testing on our Medical Tests page.

As I mentioned, my recommendation to any man who is dealing with prostate cancer – at any stage of development or treatment – is to run, not walk, to arrange a consultation with Dr. Myatt! Please see the information regarding her alternative medicine consultations  – a consultation with Dr. Myatt is an excellent investment in good health, and her patients find that the cost of her consultations is more than offset by the improved health and the money saved on both prescription drugs and treatments and on other non-prescription “treatments” of questionable value and safety.

Although different in every man who has it, prostate cancer is almost always a disease that can be managed as a chronic condition (like diabetes). Prostate cancer should certainly not be a death sentence when treated appropriately.

A transcript of the original, fully annotated notes for a lecture on Prostate Cancer presented by Dr. Myatt in May of 2000 at the 2000 Pacific Northwest Herbal Symposium may be found at the link below: Botanical and Nutritional Considerations in the Treatment of Prostate Cancer –
Dana Myatt, N.M.D.

 

Rate Your Plate – How Much Dietary Fiber Are You Getting Each Day?

Nutritional data taken from the USDA 2004 National Nutrient Database, Release 17

Daily menu:

Total grams of fiber:

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.

alt

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.

 

 

Vitamin-less Vegetables:


The New Nutrient Deficiency

Who Cares about Vegetables?

The National Academy of Sciences (NAS), the FDA and the USDA consider vegetables one of the primary dietary sources of vitamins, minerals and phytonutrients (non-vitamin, non-mineral nutrients derived from plants). Why? Because optimal levels of vitamins, minerals and phytonutrients are necessary to prevent cancer, heart disease, neurological disease, and diabetes to name only a few. In other words, those in science and medicine agree that humans need the nutrients contained in vegetables and some fruits for proper nutrition and good health. In fact, nutrient deficiencies are considered by many physicians and scientists to be one of the primary causes of disease today. Because of this, the current USDA recommendation is to eat 3-5 servings of vegetables and 2-4 servings of fruit per day.

The Sad News about Vegetables and Vitamins

YOU DO NOT EAT enough vegetables and high-nutrient fruits. How do I know this even if I don’t know you? Consider these facts:

I.) Most Americans do not achieve even the minimum 5 per day servings of produce. The current recommendations for veggie/fruit intake are 5-9 per day. A pickle, lettuce leaf, onion ring and ketchup on your burger DO NOT count as 4 servings of vegetables! Commercial fruit juice counts toward little but sugar intake because enzymes, fiber and vitamins are destroyed during processing. A side of french fries or onion rings with your burger don’t constitute a serving of nutrient-dense vegetable due to their high trans fat content and the fact that nutrients are destroyed during high-heat cooking. Further, for reason stated in #2 (below), even if you DO get 5-9 legitimate servings of vegetables per day, this current recommendation is almost surely NOT enough.

II.) Commercially grown vegetables and fruits today do not contain as many nutrients as before. According to Institute of Nutrition, recent studies of more than a dozen fruits and vegetables demonstrate a decrease in the nutrient value of most, and in some cases the drop is drastic. For instance, the Vitamin A content in apples has dropped from 90 mg to 53mg. Vitamin C in sweet peppers has decreased from 128mg to 89mg. This is why many at the NAS think the 5-9 servings recommendation should be doubled. (Math help: this updated recommendation would equal 10-18 servings per day of vegetables and fruits).

III.) Storing and/or cooking destroy many nutrients, rendering them “less” than a serving of the recommended daily dose.

Vitamins, minerals and phytonutrients (“plant nutrients” including bioflavonoids, carotenoids, proanthocyanidins, etc.) are crucial to good health, yet even a “good” Standard American Diet (SAD) does not contain enough of these nutrients to meet the proven standards that prevent disease. Further, surveys show that most Americans do not obtain the lower recommendation of 5 servings per day, let alone the upper recommendation of 9 servings per day. Nutritional Supplementation appears both valuable and necessary in achieving the proven health-protective doses of nutrients.

Dr. Myatt’s Comment:

While the USDA, FDA and commercial agri-business assure us that vegetables and fruits are as healthy as ever, the USDA’s own records show a plummeting level of nutrients since the 1960’s. All the while, medical science keeps stacking up new studies that demonstrate the disease-preventing effects of optimal doses of vitamins, minerals and phytonutrients. Still, you’ll read propaganda that assures you that you don’t need supplements because you can obtain everything you need from “a good diet.” (And you probably could get everything you need from diet IF you ate 5-9 servings of produce that was home-grown and eaten fresh, meat that was grass-fed without antibiotics and hormones, and dairy from same). But that’s not the reality of the American diet. Perhaps that is why, in spite spending more money on healthcare than any country in the world, the US ranks only 24th in life expectancy.

All unsupported claims to the contrary, nutritional supplementation with vitamins, minerals and phytonutrients appears to be the safest, surest and least expensive way to stay healthy and reverse disease.

Here is what I personally take and recommend to others to help achieve optimal daily nutrition:

Maxi Multi multi vitamin, mineral and trace mineral supplement with optimal does of nutrients (the levels shown in studies to prevent disease), not minimal doses.
AND
Maxi Greens high potency multiple green food supplement in capsules
AND/OR
Greens First , a powdered, great-tasting green food supplement that has the equivalent of 10 servings of veggies in one refreshing drink. (The taste is so good you can even get kids to take it)!

And here’s a handy tip from Wellness Club member JoAnne, who dries out her empty water bottles, adds a serving of GreensFirst and takes the bottles to work. For a quick pick-me-up, she just adds water and shakes!

References

5-A-Day Guide^

USDA^

Veggies W/out Vitamins^

Drop in minerals concerns organic community^

Organic consumer association^

New Study Shows Decreasing Nutrient Value of Certain Fruits and Vegetables – An Increasing Need for Multivitamin and Mineral Complex Supplements^

Population Life Expectancy^

 

What’s Burning You?

The REAL Cause of Heartburn, Indigestion and GERD and “Sour Stomach”

Older people have considerably more digestive problems than younger folks, and this has typically but incorrectly been blamed on over-production of stomach acid. Not only have medical studies debunked excess stomach acid as the cause of indigestion, but common sense debunks the myth as well.

Why does this matter? Because the chronic use of antacids and acid-blocking drugs for indigestion has some dangerous and even deadly side-effects

The “Acid Over-Production” Myth Debunked

Do you really think that some bodily function starts working better with age? Hahahaha!

With age, nothing works as well as it did in earlier years. I hope I’m not popping anyone’s bubble here.

Come on – we don’t move as fast at age 57 as we did at 27. Vision and hearing are typically less acute in our 70s than they were in our 30s. Skin is less elastic at 69 than at 29. Production of hormones and body fluids decreases with age. Why would we think that our stomachs do the opposite of all other organs and become more active with age instead of less active? Only a drug salesman or a pill-pushing doctor would try to convince us of such foolishness.

The stomach’s primary job is to digest protein and emulsify fats, and it does this by making an extremely powerful acid called hydrochloric acid (HCL) and a protein-digesting enzyme called pepsin. The hydrochloric acid made by a healthy stomach is one million times stronger than the mild acidity of urine or saliva. A leather-like strip of jerky can be quickly turned into “beef soup” by the action of hydrochloric acid and pepsin in the stomach. That’s how normal digestion is supposed to work.

But just like the rest of an aging body, the stomach’s hydrochloric acid and pepsin production decreases over time. As a result, we do not digest food as well. The term “indigestion” implies lack of digestion, not over-digestion. This is why we can’t eat a whole pepperoni pizza washed down with a bottle of soda like we did when we were teenagers. Our aging stomachs don’t have the same digestive vigor – strong hydrochloric acid and pepsin – to digest food like youthful stomachs do.

Medical Science Verifies Low Acid Production

OK, that’s the common sense of it. Now here’s the science. Many older studies conducted on several thousand people in the 1930?s and 1940?s showed that half of all people by age 60 were functioning at only 50% gastric acid output. Numerous contemporary studies verify that that stomach acid production often declines with age.

The Bottom Line: when someone over age 40 has chronic or chronic / intermittent indigestion, that indigestion is almost certainly due to a weaker stomach with less acid and pepsin output, not a stronger stomach making more digestive juices.

“But My Symptoms Feel Like Too Much Acid…”

Strong stomach acid and pepsin quickly “emulsify” fats and proteins, making them ready for the next step of digestion, passage into the small intestine. When these digestive factors are weak, food remains in the stomach for longer and it begins to ferment. Gas pressure from the fermentation can cause bloating and discomfort and can can also cause the esophageal sphincter to open, allowing stomach contents to “backwash” into the esophagus.

Even though weak stomach acid is the central cause of this, even this weak stomach acid, which has no place in the esophagus, will “burn.” This burning sensation confuses many people, including doctors, who then “ASSuME” that excess acid is to blame. Too little acid, resulting in slowed digestion, and gas which creates back-pressure into the esophagus is the real cause of almost all “heartburn” and GERD.

Why People Take Acid-Blockers

Why in the world would anyone take antacids or acid blockers to correct a deficiency of stomach acid? In two words: symptom relief.

But if heartburn or gastro esophageal reflux disease (GERD) are caused by too little stomach acid, why does blocking more of the acid relieve the discomfort? And why isn’t that a good thing to do?

Remember, even weak stomach acid does not belong in the esophagus. When ALL acid production is blocked, the “backwash” of stomach contents into the esophagus will not burn. However, repeatedly using this “band-aid” method has some serious long-term consequences.

The Dangers of Antacids and Acid-Blocking Drugs

Our bodies need 60 or so essential nutrients. “Essential” means that the body MUST have this nutrient or death will eventually ensue, and the nutrient must be obtained from diet because the body cannot manufacture it. Many of these essential nutrients require stomach acid for their assimilation. When stomach acid production declines, nutrient deficiencies begin.

Calcium, for example, requires vigorous stomach acid in order to be assimilated. Interestingly, the rate of hip replacement surgery is much higher in people who routinely use antacids and acid-blocking drugs. We know that people who have “acid stomach” were already having trouble assimilating calcium from food and nutritional supplements due to lack of normal stomach acid production. When these symptoms are “band-aided” with drugs which decrease stomach acid even more, calcium assimilation can come to a near-halt. The result? Weak bones, hip fractures and joint complaints resulting in major surgery.

Jonathan Wright, M.D., well-known and respected holistic physician, states that:

“Although research in this area is entirely inadequate, its been my clinical observation that calcium, magnesium, iron, zinc, copper, chromium, selenium, manganese, vanadium, molybdenum, cobalt, and many other micro-trace elements are not nearly as well-absorbed in those with poor stomach acid as they are in those whose acid levels are normal. When we test plasma amino acid levels for those with poor stomach function, we frequently find lower than usual levels of one or more of the eight essential amino acids: isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine. Often there are functional insufficiencies of folic acid and/or vitamin B12.”

Remember, these are essential nutrients. Deficiencies of any single one of them can cause serious health problems over time. Weak bones, diminish immune function, failing memory, loss of eyesight and many other “diseases of aging” are often the result of decreased stomach function.

Ulcers can even be caused by too little acid. Surprised? We know today that most ulcers are caused by a bacterium called h. pylori. This little beastie is killed by strong stomach acid. But when stomach acid is weak, watch out! Weak stomach acid is how h. pylori gets a foot-hold. (People with active ulcers should not supplement hydrochloric acid until the ulcer has healed).

Diseases Associated with Low Gastric Function

Low stomach acid is associated with the following conditions:

  • Acne rosacea
  • Addison’s disease
  • Allergic reactions
  • Candidiasis (chronic)
  • Cardiac arrhythmias
  • Celiac disease
  • Childhood asthma
  • Chronic autoimmune hepatitis
  • Chronic cough
  • Dermatitis herpeteformis
  • Diabetes (type I)
  • Eczema
  • Gallbladder disease
  • GERD
  • Graves disease (hyperthyroid)
  • Iron deficiency anemia
  • Laryngitis (chronic)
  • Lupus erythromatosis
  • Macular degeneration
  • Multiple sclerosis
  • Muscle Cramps
  • Myasthenia gravis
  • Mycobacterium avium complex (MAC)
  • Osteoporosis
  • Pernicious anemia
  • Polymyalgia rheumatica
  • Reynaud’s syndrome
  • Rheumatoid arthritis
  • Scleroderma
  • Sjogren’s syndrome
  • Stomach cancer
  • Ulcerative colitis
  • Vitiligo

It also appears that many cases of depression, which appear related to too little neurotransmitters (which in turn are made from amino acids) may in fact be inability to absorb the necessary precursors due to – you guessed it – low stomach acid. I suspect there are a large number of other diseases that begin with a failing digestive system and that have not yet been recognized as such.

Even so, many people who have low stomach acid do not have symptoms of heartburn, “acid indigestion” or GERD.

The Gastric Acid Function Test

Here’s a simple question. Before your doctor diagnosed GERD from “too much stomach acid,” did he/she perform a stomach acid function test?

X-rays and gastroscopy do not evaluate stomach acid production. The medical test for stomach acid, called the Heidelberg test, requires swallowing a small capsule and then having it pulled back up on a “string.” You’d remember if you had this done. Interestingly, this test is ALMOST NEVER PERFORMED before excess stomach acid is diagnosed, hence the incorrect diagnosis!

Why The Blind Spot In Medicine?

From the 1800’s up until the 1950’s, hydrochloric acid (HCl) supplements (both with and without pepsin) were widely prescribed and used. Physicians simply considered replacement of digestive acid to be like replacement of thyroid hormone for a failing thyroid or hormone replacement for aging ovaries.

In the 1950’s, some badly designed and misinterpreted “research” was used to convince physicians that HCl and pepsin replacement therapy is unnecessary. Besides, the “replacement” therapy – HCL and pepsin – are natural substances that are difficult to patent. Instead, drug companies focused on patentable drugs to treat “hyperchlorhydria” (excess stomach acid), and the highly profitable prescription and OTC acid blocking drug industry was born.

Once again I ask: if a doctor diagnosed you with excess stomach acid, did he or she actually perform the Heidelberg test? If you diagnosed yourself, did you perform a gastric acid self-test? No? I rest my case.

The Gastric Acid Function Self-Test

Fortunately, the Heidelberg test is not required to arrive at a correct diagnosis of too little stomach acid. You can perform a gastric acid self-test at home using some betain HCL capsules taken with meals. If digestion improves – bingo! You’re hydrochloric acid deficient.

This issue of low stomach acid is central to so many diseases that I recommend a gastric acid self-test to EVERYONE over age 50 and anyone under age 50 who has any medical complaint related to nutrient deficiency.

I’ve put together an inexpensive yet highly effective “Gastric Acid Function Self Test Kit” that includes full instructions for testing your own stomach acid (it’s easy with the instructions) plus “test sizes” of the supplements – including hydrochloric acid and pepsin – needed for the test.

Testing your own digestive function is simple and easy, and it could save you much grief, sickness, and yes, heartburn.

References

1.) Gastric observations in achlorhydria. J Dig Dis. 1941, 8: 401-407.
2.) Gastrointestinal Tract Disorders in the Elderly, pp. 62-69. Edinburgh: Churchill Livingstone: 1984.
3.) Age related changes in gut physiology and nutritional status. Gut. 1996 Mar; 38(3):306-9.
4.) A retrospective study of the usefulness of acid secretory testing. Aliment Pharmacol Ther. 2000 Jan;14(1):103-11.
5.) Age related changes in gut physiology and nutritional status. Gut. 1996 Mar;38(3):306-9.
6.) Hypochlorhydria: a factor in nutrition. Annu Rev Nutr. 1989;9:271-85.
7.) Gastric hypochlorhydria and achlorhydria in older adults. JAMA. 1997 Nov 26;278(20):1659-60.
8.) The aging gut. Nutritional issues. Int J Nurs Pract. 2006 Apr;12(2):110-8. Summary: Aging is associated with decreased gastric output.
9.) The aging gut. Nutritional issues. Gastroenterol Clin North Am. 1998 Jun;27(2):309-24.
10.) Changes in gastrointestinal function attributed to aging. Am J Clin Nutr. 1992 Jun;55(6 Suppl):1203S-1207S.
11.) Digestive function and aging. Hum Nutr Clin Nutr. 1983 Mar;37(2):75-89.
12.) Symptomatic gastro-oesophageal reflux in a patient with achlorhydria. Gut. 2006 Jul;55(7):1054-5.
13.) Effects of aging process on digestive functions. Compr Ther. 1991 Aug;17(8):46-52.
14.) Fundic atrophic gastritis in an elderly population. Effect on hemoglobin and several serum nutritional indicators. J Am Geriatr Soc. 1986 Nov;34(11):800-6.
15.) Vitamin B12 (cobalamin) deficiency in elderly patients. CMAJ. 2004 Aug 3;171(3):251-9.
16.) Anemia caused by vitamin B 12 deficiency in subjects aged over 75 years: new hypotheses. A study of 20 cases. Rev Med Interne. 2000 Nov;21(11):946-54.
17.) Cobalamin, the stomach, and aging. Am J Clin Nutr. 1997 Oct;66(4):750-9.
18.) Age-related changes in cobalamin (vitamin B12) handling. Implications for therapy. Drugs Aging. 1998 Apr;12(4):277-92.
19.) Intestinal malabsorption in the elderly. Digestive Diseases. 2007;25(2):144-50.
20.) Gastric acid secretion in chronic iron-deficiency anaemia. Lancet. 1966 Jul 23;2(7456):190-2.
21.) Involvement of the corporal mucosa and related changes in gastric acid secretion characterize patients with iron deficiency anaemia associated with Helicobacter pylori infection. Aliment Pharmacol Ther. 2001 Nov;15(11):1753-61.
22.) The aging process as a modifier of metabolism. Am J Clin Nutr. 2000 Aug;72(2 Suppl):529S-32S.
23.) Low gastric hydrochloric acid secretion and mineral bioavailability. Adv Exp Med Biol. 1989;249:173-84.
24.) Effects of pH on mineral-phytate, protein-mineral-phytate, and mineral-fiber interactions. Possible consequences of atrophic gastritis on mineral bioavailability from high-fiber foods. J Am Coll Nutr. 1988 Dec;7(6):499-508.
25.) Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006 Dec 27;296(24):2947-53.
26.) Antral atrophy, Helicobacter pylori colonization, and gastric pH. Am J Clin Pathol. 1996 Jan;105(1):96-101.
27.) High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients. J Gastroenterol Hepatol. 1996 Jul;11(7):674-80.
28.) Rosacea keratitis and conditions with vascularization of the cornea treated with riboflavin. Arch Ophthamol 1940;23:899–907.
29.) Incidence of anti-Helicobacter pylori and anti-CagA antibodies in rosacea patients. Int J Dermatol. 2003 Aug;42(8):601-4.30.) Gastrointestinal findings in atopic children. Eur J Pediatr 1980;134:249–54.
31.) Suppression of gastric H2-receptor mediated function in patients with bronchial asthma and ragweed allergy.
Chest 1986;89:491–6.
32.) Allison JR. The relation of hydrochloric acid and vitamin B complex deficiency in certain sk
in diseases. South Med J 1945;38:235–41.
33.) Effect of hydrochloric acid on iron absorption. N Engl J Med 1968;279:672–4.
34.) The importance of gastric hydrochloric acid in the absorption of nonheme food iron. J Lab Clin Med 1978;92:108–16.
35.) Bray GW. The hypochlorhydria of asthma in childhood. Q J Med 1931;24:181–97.
36.) Candida overgrowth in gastric juice of peptic ulcer subjects on short- and long-term treatment with H2-receptor antagonists. Digestion.1983;28:158–63.
37.) Antibacterial activity of the pancreatic fluid. Gastroenterology 1985;88:927–32 [review].
38.) Non-immunological defense mechanisms of the gut. Gut 1990;33:1331–7 [review].
39.) Characterization of gastric mucosal lesions in patients with celiac disease: a prospective controlled study.Am J Gastroenterol. 1999 May;94(5):1313-9.
40.) Chronic cough due to gastroesophageal reflux disease: failure to resolve despite total/near-total elimination of esophageal acid. Chest. 2002 Apr;121(4):1132-40.
41.) Gastric lesion in dermatitis herpetiformis.Gut.1976 Mar;17(3):185-8.
42.) Auto-immune atrophic gastritis in patient with dermatitis herpetiformis. Acta Derm Venereol. 1976;56(2):111-3.
43.) Predictive value of gastric parietal cell autoantibodies as a marker for gastric and hematologic abnormalities associated with insulin-dependent diabetes. Diabetes. 1982 Dec;31(12):1051-5.
44.) Parietal cell antibodies and gastric secretion in children with diabetes mellitus. Acta Paediatr Scand. 1980 Jul;69(4):485-9.
45.) Oesophageal acid exposure and altered neurocardiac function in patients with GERD and idiopathic cardiac dysrhythmias. Aliment Pharmacol Ther. 2006 Jul 15;24(2):361-70.
46.) Capper WM, Butler TJ, Kilby JO, Gibson MJ. Gallstones, gastric secretion and flatulent dyspepsia. Lancet 1967;i:413–5.
47.) Gastric juice nitrite and vitamin C in patients with gastric cancer and atrophic gastritis: is low acidity solely responsible for cancer risk? Eur J Gastroenterol Hepatol. 2003 Sep;15(9):987-93.
48.) Correlation of ratio of serum pepsinogen I and II with prevalence of gastric cancer and adenoma in Japanese subjects. Am J Gastroenterol. 1998 Jul;93(7):1090-6.
49.) Atrophic body gastritis in patients with autoimmune thyroid disease: an underdiagnosed association. Arch Intern Med. 1999 Aug 9-23;159(15):1726-30.
50.) Early manifestations of gastric autoimmunity in patients with juvenile autoimmune thyroid diseases.J Clin Endocrinol Metab. 2004 Oct;89(10):4944-8.
51.) Review article: the role of pH monitoring in extraoesophageal gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2006 Mar; 23 Suppl 1:40-9. Summary: association with laryngitis, non-cardiac chest pain, etc.
52.) Age-Related Eye Disease Study Group. Risk factors associated with age-related macular degeneration. Opthamology.
53.) Altered gastric acidity in patients with multiple sclerosis. Cesk Gastroenterol Vyz. 1968 Dec;22(8):526-30.
54.) Gastroesophageal reflux disease, acid suppression, and Mycobacterium avium complex pulmonary disease. Chest. 2007 Apr;131(4):1166-72.
55.) Malabsorption of vitamin B12 in dermatitis herpetiformis and its association with pernicious anaemia. Acta Med Scand. 1986;220(3):261-8
56.) Small intestinal bacterial overgrowth in patients with rheumatoid arthritis. Ann Rheum Dis. 1993 Jul;52(7):503-10.
57.) Hartung EF, Steinbroker O. Gastric acidity in chronic arthritis. Ann Intern Med 1935;9:252.
58.) Hypochlorhydria and hypergastrinaemia in rheumatoid arthritis. Ann Rheum Dis. 1979 Feb;38(1):14-7
59.) Francis HW. Achlorhydria as an etiological factor in vitiligo, with report of four cases. Nebraska State Med J 1931;16(1):25–6.

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

Saturated Fats and The Big Fat Lie 


“For every complicated problem there is a solution that is simple, direct, understandable, and wrong.” — H.L. Mencken

 Everybody knows that saturated fats are unhealthy, just like everybody knew once upon a time that the earth was flat. The saturated fat myth has seriously compromised the heart-health of Americans, and it’s all based on a Big Fat Lie. Here’s how this fairy tale came to be….

How Bad Science (And Urban Health Legends) Get Started

Once upon a time, not so very long ago in a place called Nebraska (where the corn grows as high as an elephant’s eye) there lived a handsome young man who was very wealthy and powerful and kept himself very fit. This young man worked hard making millions of dollars in the construction industry and he loved to eat hamburgers. Though he was a very happy young man with a fine family and a successful business, all was not well. One day the young man became very sick. He suffered a heart attack, and almost died.

The young man’s doctors were very skilled and they saved the his life, but this turn of events frightened the young man very much and he set out to discover why such a dreadful thing happened to him. He found out that his blood cholesterol was high and his doctors told him that this was the cause of his heart attack. Without questioning whether this was true or not, the young man made up his mind to ensure that this would never happen again. He set out to learn as much as he could about heart disease and cholesterol, and quickly decided that the foods he was eating were to blame for his troubles. You see, the experts at that time believed that certain kinds of fats called saturated fats would cause high blood cholesterol and dangerous buildups of a substance called plaque in peoples blood vessels. The young man listened carefully to these “experts,” and being a fine young man who wished to help others avoid the troubles that he had experienced, he decided that he would do everything in his power to make sure that saturated fats never ever harmed anyone again.

The young man wrote many letters and spent much of his own money to take out big newspaper ads telling people how they were being poisoned by saturated fats. He made a lot of people believe in the same things that he believed – that is, that saturated fats were bad and would make them sick and had no place in a healthy diet. The young man’s efforts were quite successful and many big companies were forced to change the way they cooked their foods. They stopped using the saturated fats, and began to use fats that were created especially for them by big industries in big factories. They said that these fats were healthier, and the young man was pleased.

The young man became very popular, and dedicated the rest of his life to his mission of spreading the word about “bad saturated fats” and cholesterol to all who would listen. He didn’t live happily ever after, but he did live a long life, and became known as “America’s Number One Cholesterol Fighter” before he became sick with heart failure and passed away just a few years ago.

While this sounds like a fairy tale, it really isn’t. Philip Sokolof was a handsome and wealthy young man who suffered a heart attack that was blamed on high cholesterol and who dedicated himself and his millions to becoming a self-described “amateur cardiologist” and championing the cause of removing the saturated fats that he believed caused elevated blood cholesterol levels from the American diet. While his intentions were good, his science was shaky (he was a high school graduate, not a biochemist or a doctor – much less a cardiologist) and his misguided campaign resulted in the replacement of stable, healthy saturated fats with artificially created trans fatty acids that we now know as extremely dangerous “trans fats.”

Big Business (Can You Say “Proctor and Gamble”?) Helps Promote the Sat Fat Myth

While Sokolof was largely responsible for the vilification of saturated fats in America, he was not alone. The campaign against saturated fats actually began many years earlier, and Sokolof’s efforts were going on at the same time as the efforts from other political organizations were gathering momentum. A few years prior to Sokolof’s efforts, in 1986, the American Soybean Association began a campaign protesting the importation of competing palm and coconut oils. Two years later the “watchdog” organization, the Center for Science in the Public Interest, took up the cry against saturated fats with the publication of a booklet that was later found to contain mistakes, errors of biochemistry, and erroneous statements about the fat composition of foods. This concerted campaign against saturated tropical oils paid off, and ” fats” have been considered poison ever since by mainstream medicine and nutrition “experts.”

To discover why saturated fats have been given such a bad rap we need to go a little further back into history – perhaps as far back as the riverboat days of Mark Twain, but at least to the Second World War, when Japanese forces occupied much of the south Pacific and supplies of most of the tropical oils in the US were cut off for a number of years. Americans turned to home-grown substitutes: polyunsaturated oils such as corn, peanut, cottonseed, and a product of the aforementioned American Soybean Association, soy oil. As the use of these oils grew the growers and industries involved in their production became more powerful and eager to protect their market at any cost.

At this same time, in the early 1950′s, America began to notice a sharp increase in rates of cardiovascular disease and researchers were looking for answers. A study conducted by a Russian researcher found that rabbits, fed with animal fats (cholesterol) added to their feed developed fatty deposits in their skin and other tissues, including their blood vessels. (I’ll bet those normally vegetarian bunnies wondered what they were being fed!) Another sensational study relied on autopsies of American soldiers that had died in the Korean conflict and found that many of those examined had buildups of arterial plaque – atherosclerosis. (Which surely couldn’t have had anything to do with the military diet of the day, right? Or with the popularity of cigarette smoking?) This study, which made major news at the time, overshadowed other studies of the period which showed similar degrees of atherosclerosis in populations which had less mortality from heart disease despite high fat and high meat diets, or that ate far more vegetarian diets and suffered similar degrees of atherosclerosis, and generally indicated that the thickening of the arterial walls is a natural and unavoidable process. The press took the headline-grabbing autopsy results and ran with them using their usual logic of “the rooster crows every morning, and then the sun rises: therefore, the crowing of the rooster is what makes sunrise happen!”

During the 1960′s the attack on saturated fats continued with unabated vigor: despite scientific studies showing a decided lack of benefits companies such as Mazola and Proctor and Gamble promoted their vegetable oil creations as being especially healthy, and medical journals of the day promoted Fleischman’s unsalted margarine as being especially good for patients with high blood pressure. The American Medical Association was initially skeptical of all this hype but after the American Heart Association published its dietary guidelines damning animal fats and praising vegetable oils the AMA quickly fell into line. In 1966 a little self-help book called “Your Heart Has Nine Lives” advocated the substitution of vegetable oils for butter and other so-called “artery clogging” saturated fats. This book was sponsored by makers of Mazola Corn Oil and Mazola Margarine – no surprise – and was widely and freely circulated.

And that brings us to the handsome young man with his clogged arteries. Despite volumes of evidence to the contrary, saturated fats have been the “fall guy” for coronary artery disease since the 1950′s when in fact, as early as 1956 one researcher had suggested that the increasing use of hydrogenated vegetable oils might be the underlying cause of the CAD epidemic. Unwilling to stand idly by and let profits be imperiled by such things as health or humanitarian concerns, the massive and powerful edible oil industry in the United States has obfuscated, bullied, manipulated, and outright lied to protect it’s burgeoning market share. Supporting the flawed science of Philip Sokolof and pressuring legislators to adopt the anti-saturated fat / tropical oils legislation that he promoted was just good business.

Setting the Record Straight about Sat Fats

So, just what are these so-called saturated fats, where do they come from, and what are they used for? Well, the answers to these questions might be a surprise – sat fats are not what we have been led to believe. The most exact answers to the question “what is a saturated fat?” require some tedious and complicated science, and there are varying degrees of saturation. It is easier to simply think of the properties of “hardness” of fats.

A fat that is fully “saturated” would be as hard as wax, and quite indigestible. Fats that are almost totally “unsaturated” are very liquid, easily absorbed, and not at all common in the natural food supply. This “hardness” of fats is also dependant upon temperature. Many fats are liquid when warm, and solid when cold. Butter, for example, is quite hard when refrigerated, but soft at room temperature. Animal fats such as beef fat, lard, or chicken fat, while usually called “saturated fats” are actually not so: they are mixtures of naturally occurring fats and are actually less than half “saturated.” So-called “saturated fats” include things such as cocoa butter, dairy fats (milk fats and butter for example), palm oil, and tallow. Even breast milk is high in saturated fats! Monounsaturated fats include most animal fats, olive oil, canola oil, and peanut oil. Polyunsaturated fats include corn, cotton, and soybean oils, borage and primrose oil, flax seed oil, and fish oil.

Then there are the “modified” oils: oils that have been altered through a process called “hydrogenation” to make them more useful for certain applications. Margarine is a perfect example of hydrogenation: liquid oil such as cottonseed oil or corn oil, something that humans would never eat in nature, is altered to make it more solid and hard at room temperature. Crisco is another example – the name stands for CRyStalized Cottonseed Oil. The degree of hydrogenation is varied according to the desired use of the oil. Heavily hydrogenated oils might become stick margarine, while less hydrogenated or “partially hydrogenated” oils would become “spreads” or other “food products.”

Then there are the “trans fats” that have been in the news lately. These are fats that have had their molecular geometry altered, either on purpose or accidentally, and they are with very few and minor exceptions, not found in nature. Trans fats, when eaten by humans, tend to have some very bad effects on our bodies as they enter our cells and change how the cell walls function. Effects of trans fats in humans (and animals too) range from unfavorable changes in cholesterol levels to causing blood to become more “sticky”, to reduced ability to utilize insulin and increased blood sugar levels and increased weight, to alterations in hormone balances, and more. Trans fats are really only a very small step away from polyunsaturated fats – many polyunsaturated fats can be turned “trans” simply by heating them too much in cooking!

So, what does all this mean in more practical terms? It means that we must choose our fats carefully, and use them wisely. It means that we must cautiously weigh the claimed benefits of the vegetable-based hydrogenated “designer fats” that are so very commonplace in our modern “fast foods / prepared foods” diet against the known benefits of those traditional and natural fats that have been a part of mankind’s diet for millions of years.

We humans have evolved over the millennia as creatures that are well-adapted to, and in fact require, animal fats and proteins in our diets for optimal health – the claims of the vegetarian and vegan folks notwithstanding. Indeed, our very first meal, at our mother’s breast, supplied us with a high energy drink that gave our tiny bodies the cholesterol needed for development, and a special fat called Lauric Acid. This Lauric Acid, which is also found in the now-vilified tropical oils coconut oil and palm kernel oil has very strong antifungal and antibacterial properties and helps our tiny infant bodies develop strong immune systems. We are very well equipped to utilize fatty acids in the form of saturated fats such as dairy fats, and monounsaturated fats such as animal fats and olive oil. It is only with the advent of modern industrial processes that polyunsaturated fats such as corn and soybean oils have been available for our consumption – though fish oils (a form of polyunsaturated animal fat) have historically been considered to be healthy.

Why You Should Eat Butter and Lard

Butter, as another example, has a far healthier composition as a saturated fat than the synthesized creations that are the various margarines. Being a combination of saturated, monounsaturated, and polyunsaturated fats it is not as “stable” as margarine – that is, it will turn rancid (a form of turning “trans”) if not refrigerated. But then, who would eat rancid butter? It also contains a variety of health-giving vitamins, minerals, and other nutrients.

Does anyone remember the jar of bacon grease that was a fixture in every kitchen before the days of “spray-on” cooking oils, non-stick fry pans and fat-phobia? My mother carefully saved the grease from the morning bacon, and it was used to cook all sorts of wonderful things, from our morning eggs to delectable entrees and even desserts. We keep a jar of bacon grease in our own kitchen – it is far healthier than the canola oil and soy lecithin and “propellants” (your guess?) that are in our can of “no stick cooking spray.”

Then there is our obsession with “vegetable oils” as found in the aforementioned Crisco shortening. It is interesting to note that Proctor and Gamble, perhaps seeing the writing on the wall, or perhaps in a belated fit of conscience, has sold off the Crisco name and product. This “all vegetable oil” creation, once made from cottonseed oil, is now made from canola oil which must be hydrogenated (as was the cottonseed oil) to make it semi-solid. Smuckers, the new owners of Crisco, claims “Our entire line of Crisco Shortening products have been reformulated to contain zero grams trans fat per serving”. Can anyone reading this remember the days when lard was used? All-natural, no-trans-fat lard that made such wonderfully fluffy pastries and flaky pie crusts? Do we really think that humans are well-equipped to consume the kinds of oils that require bushels of rape seed or corn or soybeans per gallon to produce? Any more than we might be equipped to consume petroleum oils – no matter how they are “modified”?

Just like our handsome young man who made it his life’s mission to vilify healthful fats, we live in a fairy-tale world where we are led to believe that with a little help from chemistry and science we can fool mother nature into allowing us to consume “food products” that our bodies were never intended to have to deal with. Unfortunately, life in that fairy tale world is having very real and very serious consequences for Americans and people around the world who are buying into the anti-sat-fat fantasy being promoted by the vegetable oils industry. We are gambling our health and our lives and our future on a grand industrial experiment, and it is paying off with increasing rates of heart disease, cancer, diabetes, obesity, and more.

At the beginning of the last century, most of the fats in our forefathers diet were either saturated or monounsaturated, mostly from butter, lard, tallow, coconut oil and small amounts of olive oil. Today most of the fats in our diet are polyunsaturated from vegetable oils mostly from soy, as well as from corn, safflower and canola. Before 1920 coronary heart disease was a rarity in America, causing no more than 10% of all deaths. Today heart disease accounts for at least 40% of all deaths. Is there a connection? We believe there is, and a growing body of scientists, researchers, and health care professionals is beginning to stand up to the politically correct diet dogma that is dictating low fat diets and vegetable fats instead of animal or tropical fats. For a historically interesting end to this article we go back to 1956 when Dr. Dudley White, in a television interview, noted that heart disease in the form of myocardial infarction (heart attack) was almost nonexistent in 1900 when egg consumption was three times what it was in 1956 and when corn oil was unavailable. When pressed to support the low-fat, vegetable oil based “Prudent Diet”, Dr. White replied: “See here, I began my practice as a cardiologist in 1921 and I never saw an MI patent until 1928. Back in the MI free days before 1920, the fats were butter and lard and I think that we would all benefit from the kind of diet that we had at a time when no one had ever heard the word corn oil.”

Former surgeon general Dr. C. Everett Koop even said, during congressional hearings in 1988: “the coconut scare is foolishness. . . To get the word to commercial interests terrorizing the public about nothing is another matter.” Could it be that it is time to turn away from the dangerous designer oils and fats of Big Industry and return to the animal and tropical fats that served our ancestors so well? We think it is!

Finally, let’s look briefly at this current medical fad that demands that we reduce cholesterol levels in our bloodstream to the lowest possible levels. Remember, cholesterol is essential to life; so essential that your liver will make it “de novo” – from new – if your body senses that it doesn’t have enough of this precious material. Even conventional medicine, in the form of The Framingham Report – the oldest, longest, and biggest study into heart disease in history – determined that when total serum cholesterol is reduced below 160 the risk of heart disease actually increases. Even more interestingly, the Director of The Framingham Study, Dr. William Castelli said in the July 1992 issue of the Archives of Internal Medicine “At Framingham, we found that the people who ate the most saturated fat, the most cholesterol and the most calories weighed the least, were more physically active and had the lowest serum cholesterol levels.” We can only imagine the dismay that this information must have cause for Philip Sokolof; he must have been aware of it as it was published over a decade before his death. Nevertheless, Sokolof persisted in his efforts to vilify saturated fats and remove cholesterol from the American diet and we can only guess as to why he would continue these efforts in the face of research showing them to be wrong, even harmful. Was he simply too stubborn to accept the facts that proved him wrong, or was he too fully caught up in the whirlwind of Big Politics, Big Industry, Big Agriculture, and Big Pharmacy to be able to change? We’ll never know…

References
1.) Sokolof article http://www.cbsnews.com/stories/2003/11/26/health/main585849.shtml
2.) Sokolof death http://www.blogofdeath.com/archives/000902.html
3.) D Groom, “Population Studies of Atherosclerosis,” Annals of Int Med , July 1961, 55:1:51-62; W F Enos, et al, “Pathogenesis of Coronary Disease in American Soldiers Killed in Korea,” JAMA , 1955, 158:912
4.) “Hydrogenated vegetable oils might be the underlying cause of the CAD epidemic”
A Keys, “Diet and Development of Coronary Heart Disease,” J Chron Dis, Oct 1956, 4(4):364-380
5.) Excerpt from “The Coconut Diet: The Secret Ingredient That Helps You Lose Weight While You Eat Your Favorite Foods” by Cherie Calbom http://www.enotalone.com/article/3242.html
6.) http://easydiagnosis.com/articles/oiling.html “The Oiling of America” by Enig and Fallon – many rerferences following this 4 part series.
7.) http://www.westonaprice.org/knowyourfats/skinny.html#lipid
The Weston A Price Society Enig & Fallon article “The Skinny on Fats”
8.) Framingham Study reports re: total cholesterol <160:
“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years” (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). Anderson KM JAMA 1987
9.) The Honolulu Heart Study:
“Our data accord with previous findings of increased mortality in elderly people with low serum cholesterol, and show that long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier that patients start to have lower cholesterol concentrations, the greater the risk of death.” Lancet Aug 2001.

 

Senior Health


Good Health for the Golden Years

Healthy, Active SeniorsAs I wrote in one HealthBeat article, “The ‘golden years’ can kiss my grits.” What I meant was that “The Golden Years” — that time in life when the family is raised and we are “hopefully” financially secure enough to stop working full time, and to travel or work at our favorite hobbies if we so choose — are often tarnished by failing health. I think that’s a pity, but it doesn’t have to be that way.

If you read the discussion on aging at the Anti-Aging Health Solution Center, you know that the human life expectancy should be on the order of 120 years. I’m not talking about just living long, either. I’m talking about spending those years in good health. Many people start crawling toward the grave from young or middle adulthood, plagued with aches, pains and illnesses. That’s not the way it is in many cultures.

By following some Basic Rules of Good Health and choosing natural, corrective measures over often-dangerous drugs and surgical “band aids,” a longer, healthier life is certainly possible.

Please visit these various areas of our site to find out how to be healthy and happy well into old age.

The Health Solutions Center at Left is a Great Place to Begin Your Search for Better Health.

Here are some additional articles for past HealthBeat News that you may find of benefit:

Neurological Disease: What You’re NOT Going to Hear From Your Conventional Doctor

Rejuvenate Your Heart in 9 Simple Steps

5 Proven Ways to Slow Dementia and Alzheimer’s

7 Ways to Decrease Your Cancer Risk

Stay informed! Claim your own  FREE subscription to HealthBeat News here: HealthBeat News