Vaginal Pain

We are talking about the problem of vaginal dryness, also known as vaginal atrophy. This condition is accompanied by thinning of vaginal tissue and lack of lubrication.

Even though many women may be silent about vaginal dryness and vaginal atrophy, it is by no means a rare condition. As many as 14 million women over the age of 18 have experienced this problem. In fact, nearly half of all women over the age 40 have suffered from vaginal dryness at some point in their lives. And two-thirds of women over the age of 60, list vaginal dryness as one of the top two sexual health problems along with lack of libido.

Why is this a problem?
First, without adequate lubrication, sexual intercourse becomes uncomfortable and even painful. Because vaginal dryness is often accompanied by thinning of the vaginal tissue, it can result in lesions or tears of the vaginal wall. In addition, drying out of the mucosal membranes increases the risk of incontinence, bladder infections and urinary tract infections. Lack of vaginal lubrication can also make women vulnerable to contracting a vaginal infection called bacterial vaginosis.

The most common signs and symptoms of vaginal dryness include irritation and pain during sex, itching and stinging around the vaginal opening and in the lower third of the vagina and urinary tract infections. Another symptom is the occurrence of bleeding or spotting during sex or other times as a result of the thinning of vaginal tissue.

What is Going On?
Vaginal lubrication consists of clear fluid that seeps through the walls of the blood vessels encircling the vagina. When you’re sexually aroused, more blood flows to your pelvic organs, creating more lubricating vaginal fluid. But due to hormonal changes at perimenopause, menopause, childbirth, and even breast-feeding, this natural physiological process may be altered. Healthy vaginal walls are always coated in a thin layer of this moisture and mucus. Without adequate lubrication, vaginal tissues become dry, thin and prone to tearing.

Changes in vaginal moisture also occur in response to low estrogen levels. Estrogen is essential in keeping vaginal tissue supple and elastic. Adequate estrogen levels give the tissue its ability to produce slippery-smooth lubrication. Anytime a woman’s estrogen level is altered, for whatever reason including a hysterectomy or impaired ovarian function, vaginal thinning and dryness may occur.

Perimenopause and menopause are stages in a woman’s life cycle when estrogen levels may be fluctuating. Estrogen production can also be affected after childbirth and during breast-feeding.

There are many issues can alter the normal production of moisture. For instance, stressful situations, whether physical or emotional, constrict blood vessels that supply nutrients and oxygen to the vaginal tissue. Maintaining healthy vaginal secretions and vaginal elasticity requires adequate key nutrients such as essential fatty acids, vitamins A, C, and B.

Many medications have side effects that can directly alter vaginal secretions. They include steroid/cortisone drugs, cancer treatments, tamoxifen, aromatase-inhibitors, antihistamines, antidepressants, as well as ulcer and high blood pressure medications.

One little known side effect of oral contraceptives is reduced vaginal lubrication. The alteration of natural hormone production from taking the Pill has many consequences. Lack of healthy vaginal moisture can be one of them.

Commercial Lubricants-A Bad Idea
Many women turn to commercial lubricants when they become aware they are dealing with vaginal dryness. But beware! The chemicals used in them can irritate the delicate vagina tissue. Potential ingredients include fragrances, the antibacterial agent chlorhexidine, propylene glycol, glycerin, and a group of preservatives called parabens, (often listed as methyl-, butyl-, ethyl- and propyl-paraben). Some lubricants such as K-Y Jelly and Replens can alter the pH balance of the vagina, which would increase the risk of certain vaginal infections.

Beware of Vaginal Estrogen Creams
Since it is the hormone estrogen that causes the vagina to thicken and moisten, the medical approach is to prescribe an estrogen vaginal cream. However, when estrogen is applied in the vagina, it can be quickly absorbed into the blood stream and transported to other tissues. In fact, both vaginal applications of Premarin and Estrace raise your blood levels of estrogen much the same as estrogen pills.

Long-term exposure to high levels of estrogen can pose some risk to women diagnosed with breast cancer or at high risk of breast cancer by potentially elevating estrogen levels excessively. Doctors, therefore, discourage the use of these estrogens if a woman has a breast cancer risk.

Estriol is another form of estrogen that is often prescribed to women. While considered a safer form of estrogen, it still requires a doctor’s prescription and is expensive.

Hygeena – The Ultimate Vaginal Healing and Rejuvenation Formula

When it comes to healing delicate vaginal tissue and restoring healthy lubrication, it is vitally important to choose a natural, organic product. You especially want to use one that is specifically formulated to effectively and safely resolve the problem of dryness, thinning vaginal tissue, lack of lubrication, and risk of fungal or bacterial infections.

Hygeena, the first all-natural, hormone free and comprehensive formula, not only heals but also restores healthy vaginal tissues, lubrication, and imbalances. It is the best solution for providing overall vaginal rejuvenation.

Hygeena has been carefully formulated with a unique synergy of six all natural, organic and non-toxic ingredients that have been proven to heal, repair, lubricate and rejuvenate vaginal tissue as well as restore a healthy vaginal environment. And the best part is, it is easily administered as a vaginal suppository!

Pueraria Mirifica — Pueraria mirifica is a plant that grows in Thailand and other parts of Southeast Asia. For over 100 years, Pueraria mirifica have been used in traditional Thai medicine to promote youthfulness and rejuvenation in women. It has phytoestrogen benefits on vaginal tissue, including alleviating vaginal dryness and painful urination, improving vaginal atrophy, and restores thinning, drying and inflammation of the vaginal walls. Pueraria mirifia, as a phytoestrogen, promotes estrogenic effects but without any of the health risks associated with the prescribed estrogen hormone.

Hygeena is formulated with Puresterol®, a patented extract of Pueraria mirifica.¹

Hyaluronic Acid — Hyaluronic Acid (HA) is a natural compound produced in the body. It is a real superstar when it comes to rejuvenation. It has the unique ability to attract and retain more than 1000 times its weight in water. Thus, hyaluronic acid enables cells to retain moisture which keeps the tissues moist and hydrated.

As we age, HA levels diminish, and cells lose their ability to hold moisture. That translates into a loss of elasticity. HA is phenomenal at penetrating the skin’s layers where it affects tissue repair and protection while boosting elasticity and hydration. Another important feature of HA is its ability to transport nutrients from the blood directly to skin cells. All these benefits make hyaluronic acid a powerful ingredient in Hygeena to reverse vaginal dryness and revitalize vaginal tissue!

Omega 7’s (Sea Buckthorn oil) — Sea buckthorn oil has been used for thousands of years as a natural remedy against various ailments. It is extracted from the berries, leaves and seeds of the sea buckthorn plant (Hippophae rhamnoides), which is a small shrub that grows at high altitudes in the northwest Himalayan region.

Sea Buckthorn oil showed beneficial effects on vaginal health, helping to improve mucosal integrity and vaginal atrophy. A lack of essential fatty acids in the diet is a contributing factor to vaginal dryness. There is a very specific essential fatty acid derived from sea buckthorn oil that helps women to alleviate vaginal dryness.

Sea Buckthorn oil contains beta carotene, trace minerals, omega 3, 6 and 9 fatty acids and additionally is the richest source of omega 7 essential fats. Omega 7 essential fatty acids are important structural components of mucous membranes which form the protective lining of internal organs such as the vaginal, digestive and respiratory tracts, as well as the surface of the eyes and mouth. Sea Buckthorn oil not only promotes healthy regeneration of these membranes but also provides nutrients essential for the proper functioning of the membranes in the vaginal tract.

In a study conducted by The Department of Obstetrics and Gynecology in Finland, it was concluded that sea buckthorn oil was a natural and effective solution to contributing to the health of mucous membranes including vaginal dryness.²

Silver Biotics® — The patented Silver Biotics® with SilverSol Technology® is a unique and highly effective form of silver, known as nano-silver. Throughout the ages, silver has been renowned for its anti-microbial effects. SilverSol Nano-Silver Technology is the most effective form of silver ever created. It far surpasses either colloidal or ionic forms of silver for potency. It has been clinically tested and FDA approved demonstrating that it is totally safe and has no known side-effects.

Silver Biotics® liquid has been scientifically proven to quickly kill harmful bacteria, viruses, and fungus. The good news is that it will not cause antibiotic resistance or alteration of healthy vaginal microflora. In addition to its lubricating and anti-microbial effects, it is also able to quickly reduce inflammation, itching, pain and burning while at the same time accelerating tissue repair and healing. Studies have demonstrated that in just 10 minutes, it successfully killed Candida!

The broad-spectrum nature of Silver Biotics® also helps to prevent urinary tract infections that are caused by vaginal bacteria by stopping the migration into the urinary tract.

Natural Vitamin E (alpha-tocopherol) — Vitamin E oil has proven effective in relieving symptoms of combat dryness, vaginal atrophy and soothes irritation. Research suggests that the topical form of this vitamin helps skin hold on to water, a key factor not only in softness but in healthy, resilient skin.

Aloe Vera — Aloe Vera is used in the place of water as base for hydration and as an anti-inflammatory star. Its benefits are due to a combination of a very wide range of ingredients including Vitamins A and B, proteins, amino acids, good fatty acids and triglycerides. Its medicinal properties fight off bacteria, help dilate capillaries and increase blood flow, as well as helping to relieve pain and itching.

The Natural Solution for Vaginal Healing, Restoration and Rejuvenation

The healing power of nature is profound. As women journey through the many stages of life, nature has provided the solutions to support health, vitality and healing. This is also true for the changes that cause hormones to fluctuate. Vaginal dryness and tissue atrophy can occur during many stages of life, either as a transitory problem or as symptom of deeper hormonal shifts.

Hygeena truly is an elixir for vaginal health. Hygeena’s unique formula incorporating Pueraria mirifica, Hyaluronic Acid, Silver Biotics®, Sea Buckthorn Oil, Natural Vitamin E and Cocoa butter has provided some of Nature’s most healing gifts to support women to be healed, revitalized and rejuvenated throughout their lifetime.

References:

1. Manonai J1, Chittacharoen A, Theppisai U, Theppisai H., Effect of Pueraria mirifica on vaginal health Menopause. 2007 Sep-Oct;14(5):919-24. DOI: 10.1097/gme.0b013e3180399486
2. Larmo PS1, Yang B2, Hyssälä J3, Kallio HP2, Erkkola R4., Effects of sea buckthorn oil intake on vaginal atrophy in postmenopausal women: a randomized, double-blind, placebo-controlled study. Maturitas. 2014 Nov;79(3):316-21. DOI: 10.1016/j.maturitas.2014.07.010

The post Hygeena – The Ultimate Vaginal Healing and Rejuvenation Solution appeared first on Total Health Magazine.

7-keto DHEA is a metabolite of DHEA and may prove to be a safer alternative. Unlike DHEA, 7-keto-DHEA is not converted to androgens and estrogens.^9,10,11 Oral or topical administration of 7-keto-DHEA does not affect plasma levels of steroid hormones.^12,13 Similarly to DHEA, 7-keto-DHEA is rapidly converted to the sulfated form, known as 7-keto-DHEAS¹⁴.

Areas Of Benefit
Clinical studies have been conducted on supplementation with both DHEA and 7-keto-DHEA. Based upon that research, DHEA offers potential benefits for adrenal support, youthful skin, sexual support, bone mineral density, mood support/ mental function, healthy inflammatory response in body tissues, fatigue reduction, menopause, weight loss, and insulin sensitivity. Clinical studies on 7-keto DHEA have identified three major areas of potential benefit, including weight loss, cognitive function, and immune function. Following is an overview of the research on each of these dietary supplement ingredients.

DHEA: Adrenal Support
In individuals with suboptimal adrenal function, daily supplementation with 20–50 mg DHEA seems to improve feelings of well-being, skin and hair, and sexuality responsiveness.^15,16 DHEA also helps support healthy maturation of the adrenal glands in children with sub-optimal adrenal function.¹⁷

DHEA: Youthful Skin
As previously discussed. DHEA levels decline with age. In research with individuals 60–79 years old, taking 50 mg DHEA daily helped reverse certain parameters of aging skin. Subjects experienced an increase in epidermal thickness, sebum production, skin hydration, and decrease facial skin pigmentation.¹⁸

DHEA: Sexual Support
Aging males supplemented with 50 mg DHEA daily for six months experienced improvements in parameters of male performance, including erection, orgasmic function, sexual desire, and overall sexual satisfaction. DHEA helped improve male performance in men with sub-optimal blood pressure balance or whose performance was sub-optimal for unknown reasons, but did not improve performance in individuals with diabetes or neurological disorders.^19,20

In postmenopausal women, clinical evidence has demonstrated that a single 300 mg dose of DHEA improved sexual response, including significantly greater mental and physical sexual arousal.²¹ Furthermore, vaginal application of DHEA was found to be effective in reducing vaginal atrophy in elderly postmenopausal women.₂₂

DHEA: Bone Mineral Density
Loss of bone mineral density (BMD) is common with aging. Daily supplementation with 50–100 mg DHEA has been shown to improve BMD in older women and men with sub-optimal BMD._23,24 It also helps improve BMD in younger women with eating disorders.²⁵

DHEA: Mood Support / Mental Function
Experiencing moodiness or “the blues” is common during the lifecycle but can increase with age.²⁶ Some clinical research suggests that taking DHEA orally might improve symptoms of moodiness in elderly subjects.^27,28,29 Taking DHEA orally seems to improve healthy mental function in individuals with sub-optimal perception or expression of reality.³⁰

DHEA: Healthy Inflammatory Response In Body Tissues
Some individuals experience acute and chronic inflammation of various tissues of the body resulting from an attack by their body’s own immune system. Taking DHEA orally in conjunction with conventional treatment may help support a healthy inflammatory response in various tissues.^{31,32,33,34,35,36,37} It may also help promote the normalization of symptoms such as muscle ache.38 In addition, DHEA also seems to improve bone mineral density in such individuals whose conventional medications adversely affect bone mineral density.^39,40,41

DHEA: Fatigue Reduction
Some individuals, who experience a period of high physical and/or emotional stress, also experience the onset of fatigue of a chronic nature. DHEA may be able to help. In a clinical study, supplementation with DHEA led to a significant reduction in associated pain, fatigue, limitations in activities of daily living, helplessness, anxiety, difficulty thinking, poor memory, and sexual problems over the period of the study.⁴²

DHEA: Menopause
In a clinical study, 25 mg of DHEA daily increased the levels of all the hormones that derive from DHEA metabolism. It also increased neurosteroids and endorphin levels. The results were an improvement of vasomotor symptoms such as hot flashes, as well as psychological symptoms throughout 12 months of therapy.⁴³

DHEA: Weight Loss & Insulin Sensitivity
In a randomized, double-blind, placebo-controlled study, 56 elderly subjects took 50 mg DHEA daily for six months. Subjects taking the DHEA experienced a significant decrease in abdominal fat, and improvements in insulin sensitivity compared to those using the placebo.⁴⁴

7-keto: Weight Loss
7-keto-DHEA is thought to be beneficial in weight loss by increasing metabolism and thermogenesis. Early evidence in animals suggests 7-keto-DHEA can increase thermogenesis, possibly by stimulation of thermogenic enzymes in the liver⁴⁵ ; however this effect has not yet been reported in humans. Clinical evidence suggests 7-keto-DHEA might increase basal metabolism.

In obese patients, 7-keto-DHEA can significantly increase the thyroid hormone triiodothyronine (T3) when used over four weeks.⁴⁶ This effect on thyroid function may positively influence metabolism⁴⁷, helping patients reduce body weight and body fat. In fact, one clinical study seems to support the hypothesis that the supplement can enhance weight loss.

Thirty overweight adults were randomized into a prospective, double-blind, placebo controlled eight-week study.⁴⁸ Fifteen subjects received 100 mg 7-Keto DHEA twice per day whereas the other 15 subjects received a matching placebo. All subjects exercised three times per week, 60 minutes per session of cross-training (aerobic and anaerobic) under the supervision of an exercise physiologist. The exercise plus 7-Keto DHEA group lost a significant amount of body weight as compared with the exercise plus placebo group.

When analyzed per a four-week interval, the 7-Keto DHEA group lost 3.17 lbs per interval, whereas placebo lost 1.09 lbs. In terms of actual body composition changes, the exercise plus 7-Keto DHEA group lost 1.8 percent body fat as compared to 0.57 percent for the placebo group. When viewed as a change in body fat per four-week interval, the 7-Keto DHEA group lost 0.89 percent body fat per interval as compared to 0.29 percent for the placebo.

In a later randomized, double-blind, placebo-controlled, crossover trial⁴⁹, 7-Keto DHEA was tested in overweight adults maintained on a calorie-restricted diet to determine efficacy in increasing the resting metabolic rate (RMR). The results were that RMR increased significantly by 1.4 percent in the 7-Keto DHEA group, whereas RMR decreased by 3.9 percent in the placebo group. In this study, 7-Keto reversed the decrease in RMR normally associated with dieting and was generally well tolerated with no serious adverse events.

7-Keto: Cognitive Function
Research has indicated that that DHEA administration might be beneficial in terms of neuroprotection against age-related loss of brain functions like learning and memory.⁵⁰ Furthermore, DHEA showed insignificant effects on both learning/memory ability in aging rats.⁵¹ Higher DHEA-S levels are also independently and favorably associated with executive function, concentration, and working memory in humans.⁵² In addition, other research suggests that 7-keto-DHEA improves chemically-induced and age-related memory impairment.⁵³

7-Keto: Immune Function
7-keto DHEA has also been studied for its potential immune-boosting properties. This includes immunomodulatory effects by stimulating interleukin-2 production by human lymphocytes in-vitro.⁵⁴ Researchers think that it may also stimulate the activity and effectiveness of T-lymphocytes. These T-lymphocytes may in turn stimulate additional immune system functions.⁵⁵ Studies based on these observations suggest that 7-keto DHEA may have a future as an important immune system enhancer.^56,57 Thus, 7-keto DHEA could prove to be therapeutically useful in a wide range of conditions. Studies suggest that DHEA may reduce the replication of certain types of viruses.⁵⁸

References

1. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci U S A 1995;92:6617–9.
2. Moffat SD, Zonderman AB, Harman M, et al. The relationship between longitudinal declines in dehydroepiandrosterone sulfate concentrations and cognitive performance in older men. Arch Int Med 2000;160:2193–8.
3. Pepping J. DHEA: dehydroepiandrosterone. Am J Health Syst Pharm 2000;57:2048-50, 2053– 4, 2056.
4. Oelkers W. Dehydroepiandosterone for adrenal insufficiency (editorial). N Engl J Med 1999;341:1073– 4.
5. van Vollenhoven RF. Dehydroepiandrosterone in systemic lupus erythematosus. Rheum Dis Clin North Am 2000;26:349- 62.
6. Tchernof A, Labrie F. Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies. Eur J Endocrinol 2004;151:1– 14.
7. Mortola J, Yen SSC. The Effects of Oral Dehydroepiandrosterone on Endocrine-Metabolic Parameters in Postmenopausal Women. J Clin Endocrin 1990;71(3): 696–704.
8. Morales AJ, Nolan JJ, Nelson JC, Yen SS. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrin 1994;78(6):1360– 7.
9. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci U S A 1995;92:6617–9.
10. Davidson MH, Weeks C, Lardy H, et al. Clinical Safety and Endocrine Effects of 7-KETO-DHEA. Abstract presented at: Experimental Biology 98, April 19-22, 1998, San Francisco, CA. Abstract obtained from Humanetics Corporation website.
11. Colker CM, Torina GC, Swain MA, Kalman DS. Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxodehydroepiandrosterone on Body Composition and the Endocrine System in Overweight Adults. Journal of Exercise Physiology Online 1999;2(4):Abstract #30.
12. Davidson M, Marwah A, Sawchuk RJ, et al. Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers. Clin Invest Med 2000;23:300–10.
13. Sulcova J, Hill M, Masek Z, et al. Effects of transdermal application of 7-oxo-DHEA on the levels of steroid hormones, gonadotropins and lipids in healthy men. Physiol Res 2001;50:9– 18.
14. Davidson M, Marwah A, Sawchuk RJ, et al. Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers. Clin Invest Med 2000;23:300–10.
15. Arlt W, Callies F, van Vlijmen JC, et al. Dehydroepiandosterone replacement in women with adrenal insufficiency. N Engl J Med 1999;341:1013–20.
16. Johannsson G, Burman P, Wiren L, et al. Low dose dehydroepiandrosterone affects behavior in hypopituitary androgen-deficient women: a placebo-controlled trial. J Clin Endocrinol Metab 2002;87:2046– 52.
17. Kim SS, Brody KH. Dehydroepiandrosterone replacement in Addison’s disease. Eur J Obstet Gynecol Reprod Biol 2001;97:96– 7.
18. Baulieu EE, Thomas G, Legrain S, et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging. Contribution of the DHEAge study to a sociobiomedical issue. Proc Natl Acad Sci U S A 2000;97:4279- 84.
19. Reiter WJ, Pycha A, Schatzl G, et al. Dehydroepiandosterone in the treatment of erectile dysfunction: A prospective, double-blind, randomized, placebo-controlled study. Urol 1999;53:590– 5.
20. Reiter WJ, Schatzl G, Mark I, et al. Dehydroepiandrosterone in the treatment of erectile dysfunction in patients with different organic etiologies. Urol Res 2001;29:278–81.
21. Hackbert L, Heiman JR. Acute dehydroepiandrosterone (DHEA) effects on sexual arousal in postmenopausal women. J Womens Health Gend Based Med 2002;11:155– 62.
22. Labrie F, Diamond P, Cusan L, et al. Effect of 12 month dehydroepiandrosterone replacement therapy on bone, vagina, and endometrium in postmenopausal women. J Clin Endocrinol Metab 1997;82:3498–505.
23. Sun Y, Mao M, Sun L, et al. Treatment of osteoporosis in men using dehydroepiandrosterone sulfate. Chin Med J (Engl) 2002;115:402–4.
24. Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf) 2000;53:561– 8.
25. Gordon CM, Grace E, Emans SJ, et al. Effects of oral dehydroepiandrosterone on bone density in young women with anorexia nervosa: a randomized trial. J Clin Endocrinol Metab 2002;87:4935– 41.
26. Hybels CF and Blazer DG. Epidemiology of late-life mental disorders. Clinics in Geriatric Medicine 2003; 19:663– 696.
27. Wolkowitz OM, Reus VI, Keebler A, et al. Double-blind treatment of major depression with dehydroepiandosterone. Am J Psychiatry 1999;156:646–9.
28. Bloch M, Schmidt PJ, Danaceau MA, et al. Dehydroepiandrosterone treatment of midlife dysthymia. Biol Psychiatry 1999;45:1533–41.
29. Wolkowitz OM, Reus VI, Manfredi F, et al. Dehydroepiandrosterone (DHEA) treatment of depression. [Abstract] Biol Psychiatry 1997;41:311–8.
30. Strous RD, Maayan R, Lapidus R, et al. Dehydroepiandrosterone augmentation in the management of negative, depressive, and anxiety symptoms in schizophrenia. Arch Gen Psychiatry 2003;60:133– 41.
31. van Vollenhoven RF, Morabito LM, Engleman EG, et al. Treatment of systemic lupus erythematosus with dehydroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285– 9.
32. van Vollenhoven RF, Engleman EG, McGurie JL. Dehydroepiandrosterone in Systemic Lupus Erythematosus. Arth Rheum 1995;38:1826– 31.
33. van Vollenhoven RF, Engleman EG, McGuire JL. Dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheum 1994;37:1305–10.
34. an Vollenhoven RF, Park JL, Genovese MC, et al. A double-blind, placebo-controlled, clinical trial of dehydroepiandrosterone in severe lupus erythematosus. Lupus 1999;8:181–7.
35. Mease PJ, Merrill JT, Lahita RG, et al. GL701 (prasterone, dehydroepiandrosterone) improves systemic lupus erythematosus. 2000 American College of Rheumatology Meeting. Philadelphia, PA. October 29–November 2. Abstract 1230.
36. Petri MA, Mease PJ, Merrill JT, et al. Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum 2004;50:2858–68.
37. Petri MA, Lahita RG, Van Vollenhoven RF, et al. Effects of prasterone on corticosteroid requirements of women with systemic lupus erythematosus: a double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2002;46:1820–9.
38. Petri MA, Mease PJ, Merrill JT, et al. Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum 2004;50:2858–68.
39. Mease PJ, Merrill JT, Lahita RG, et al. GL701 (prasterone, dehydroepiandrosterone) improves systemic lupus erythematosus. 2000 American College of Rheumatology Meeting. Philadelphia, PA. October 29-November 2. Abstract 1230.
40. Mease PJ, Ginzler EM, Gluck OS, et al. Improvement in bone mineral density in steroid-treated SLE patients during treatment with GL701 (prasterone, dehydroepiandrosterone). 2000 American College of Rheumatology Meeting. Philadelphia, PA. October 29-November 2. abstract 835.
41. van Vollenhoven RF, Park JL, Genovese MC, et al. A double-blind, placebo-controlled, clinical trial of dehydroepiandrosterone in severe lupus erythematosus. Lupus 1999;8:181–7. 42. Himmel PB, Seligman TM. A Pilot Study Employing Dehydroepiandrosterone (DHEA) in the Treatment of Chronic Fatigue Syndrome. [Abstract] J Clin Rheumatol 1999:5:56–9.
42. Genazzani AD, Stomati M, Bernardi F, et al. Long-term low-dose dehydroepiandrosterone oral supplementation in early and late postmenopausal women modulates endocrine parameters and synthesis of neuroactive steroids. Fertil Steril 2003;80:1495–501.
43. Villareal DT, Holloszy JO. Effect of DHEA on abdominal fat and insulin action in elderly women and men. JAMA 2004;292:2243–8.
44. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci U S A 1995;92:6617–9.
45. Colker CM, Torina GC, Swain MA, Kalman DS. Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxodehydroepiandrosterone on Body Composition and the Endocrine System in Overweight Adults. Journal of Exercise Physiology Online 1999;2(4):Abstract #30.
46. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci USA 1995;92(14):6617–9.
47. Colker CM, Torina GC, Swain MA, Kalman DS. Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxodehydroepiandrosterone on Body Composition and the Endocrine System in Overweight Adults. Journal of Exercise Physiology Online 1999;2(4):Abstract #30.
48. Zenk JL, Frestedt JL, Kuskowski MA. HUM5007, a novel combination of thermogenic compounds, and 3-acetyl-7-oxodehydroepiandrosterone: each increases the resting metabolic rate of overweight adults. J Nutr Biochem. 2007;18(9):629–34.
49. Taha A, Mishra M, Baquer NZ, Sharma D. Na+ K(+)-ATPase activity in response to exogenous dehydroepiandrosterone administration in aging rat brain. Indian J Exp Biol. 2008;46(12):852–4.
50. Chen C, Lang S, Zuo P, Yang N, Wang X. Treatment with dehydroepiandrosterone increases peripheral benzodiazepine receptors of mitochondria from cerebral cortex in D-galactose-induced aged rats. Basic Clin Pharmacol Toxicol 2008;103(6):493–501.
51. Davis SR, Shah SM, McKenzie DP, Kulkarni J, Davison SL, Bell RJ. Dehydroepiandrosterone sulfate levels are associated with more favorable cognitive function in women. J Clin Endocrinol Metab 2008;93(3):801–8.
52. Shi J, Schulze S, Lardy HA. The effect of 7-oxo-DHEA acetate on memory in young and old C57BL/6 mice. Steroids 2000;65:124–9.
53. Nelson R, Herron M, Weeks C, Lardy H. Dehydroepiandrosterone and 7-KETO-DHEA augment Interleukin 2 (IL2) Production by Human Lymphocytes In Vitro. Abstract presented at: The 5th Conference on Retroviruses and Opportunistic Infections, February 1–5, 1998, Chicago, IL. Abstract obtained from Humanetics Corporation.
54. Whittington R, Faulds D. Interleukin-2. A review of its pharmacological properties and therapeutic use in patients with cancer. Drugs 1993;46(3):446–514.
55. Nelson R, Herron M, Weeks C, Lardy H. Dehydroepiandrosterone and 7-keto DHEA Augment Interleukin 2 (IL2) Production by Human Lymphocytes in Vitro. The 5th Conference on Retroviruses and Opportunistic Infections. Chicago, IL. Feb 1998;598:49.
56. Hampl R. 7-Hydroxydehydroepiandrosterone–a natural antiglucocorticoid and a candidate for steroid replacement therapy? Physiol Res 2000;49 Suppl 1:S107–12.
57. Henderson E, Yang JY, Schwartz A. Dehydroepiandrosterone (DHEA) and synthetic DHEA analogs are modest inhibitors of HIV-1 IIIB replication. AIDS Res Hum Retroviruses 1992;8(5):625–31.

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MULTIVITAMINS

There is a good case for the daily use of a multivitamin, as a nutrition insurance policy that helps to fill in the gaps for those nutrients people may not be getting in their diet. Furthermore, in a study¹ of 90,771 men and women, the regular use of a multivitamin was found to significantly improve adequate intake of nutrients compared to non-users. Also, research² found that multivitamin supplements are generally well tolerated, do not increase the risk of mortality, cerebrovascular disease, or heart failure, and their use likely outweighs any risk in the general population (and may be particularly beneficial for older people). So, the bottom line is that multivitamins really do work as a nutrition insurance policy.

Other multivitamin benefits
In addition to functioning as a nutrition insurance policy, the daily use of a multivitamin may offer other benefits as well.

Cardiovascular Disease
A 12-week, randomized, placebo-controlled study³ of 182 men and women (24 to 79 years) found that a multivitamin was able to lower homocysteine levels and the oxidation of LDLcholesterol—both of which are highly beneficial in reducing the risk for cardiovascular disease. Other multivitamin research⁴ has also demonstrated effectiveness in lowering homocysteine levels.

A 6-month, randomized, double-blind, placebo-controlled study⁵ of 87 men and women (30 to 70 years) found that multivitamin use was associated with lower levels of C-reactive protein, a measurement of inflammation associated with cardiovascular disease and other degenerative diseases. Other multivitamin research⁶ in women has shown similar results.

A Swedish, population-based, case-control study⁷ of 1296 men and women (45 to 70 years) who previously had a heart attack and 1685 healthy men and women as controls, found those using a multivitamin were less likely to have a heart attack. Other multivitamin research⁸ in Swedish women has shown similar results.

Cancer:
A large-scale, randomized, double-blind, placebo-controlled study⁹ was conducted with 14,641 male U.S. physicians initially 50 years or older, including 1312 men with a history of cancer, to determine the long-term effects of multivitamin supplementation on the incidence of various types of cancers. Results showed that during a median follow-up of 11.2 years, men with a history of cancer who took a daily multivitamin had a statistically significant reduction in the incidence of total cancer compared to those taking a placebo.

Stress/Energy:
A human clinical study¹⁰ with 96 healthy men (18 to 46 years) examined the effect of multivitamin supplementation in relation to plasma interleukin-6 (IL-6, a pro-inflammatory chemical produced by the body) and anger, hostility, and severity of depressive symptoms. The results showed that plasma IL-6 was associated with anger, hostility, and severity of depressive symptoms, and that multivitamin use was associated with lower plasma IL-6 levels.

A review¹¹ of the scientific literature indicated that patients complaining of fatigue, tiredness, and low energy levels may have low levels of vitamins and minerals. Certain risk groups like the elderly and pregnant women were identified, as was the role of B-vitamins in energy metabolism. Results found that supplementation with nutrients including B-vitamins (e.g., a multivitamin) can alleviate deficiencies, but supplements must be taken for an adequate period of time.

A meta-analysis¹² of eight randomized and placebo-controlled studies evaluated the influence of diet supplementation on stress and mood. Results showed that supplementation reduced the levels of perceived stress, mild psychiatric symptoms, anxiety, fatigue, and confusion. Supplements containing high doses of B-vitamins (e.g., multivitamins) may be more effective in improving mood states.

Aging:
At the ends of our chromosomes are stretches of DNA called telomeres. These telomeres protect our genetic data, making it possible for cells to divide. Each time a cell divides, telomeres get shorter. When they get too short, the cell can no longer divide and becomes inactive or “senescent” or dies. This process is associated with aging. In a cross-sectional analysis of data from 586 women (35 to 74 years), multivitamin use was assessed, and relative telomere length was measured. The results were that multivitamin use was significantly associated with longer telomeres. Compared with nonusers, the relative telomere length was on average 5.1 percent longer among daily multivitamin users. It is possible, therefore, that multivitamins may help us live longer.

VITAMIN D

Vitamin D is the “sunshine vitamin,” so coined because exposure to the sun’s ultraviolet light will convert a form of cholesterol under the skin into vitamin D. This nutrient is best known for its role in helping to facilitate the absorption of calcium and phosphorus (as well as magnesium), and so helping to promote bone health.¹³ Over the past decade, however, research on vitamin D has identified numerous other roles it plays in human health and wellness, which includes:

• Inhibiting the uncontrolled proliferation of cells (as in the case of cancer) and stimulating the differentiation of cells (specialization of cells for specific functions).¹⁴
• Helping prevent cancers of the prostate and colon.^15,16
• Functioning as a potent immune system modulator.^17,18
• Helping prevent autoimmune reactions.^19,20,21
• Helping improve insulin secretion.^22,23,24
• Decreasing the risk of high blood pressure via the reninangiotensin system’s regulation of blood pressure.²⁵
• Reducing osteoporotic fractures.^26,27,28
• Reducing the incidence of falls in older adults.^29,30
• Reducing the risk of developing premenstrual syndrome (PMS).³¹
• Reducing the prevalence of depression, especially in the elderly.³²
• Reducing the prevalence of urinary infections and lower urinary tract symptoms (e.g., benign prostatic hyperplasia or BPH).³³

Vitamin D deficiency and insufficiency
Outright vitamin D deficiency is present in 41.6 percent of the U.S. population,³⁴ while vitamin D insufficiency (i.e., lacking sufficient vitamin D) is present in 77 percent of the world’s population.³⁵ If you are deficient in vitamin D you will not be able to absorb enough calcium to satisfy your body’s calcium needs.³⁶ It has long been known that severe vitamin D deficiency has serious consequences for bone health, but other research indicates that lesser degrees of vitamin D deficiency are common and increase the risk of osteoporosis and other health problems.^37,38

Vitamin D sufficiency is measured by serum 25-hydroxyvitamin D levels in the body.³⁹ Laboratory reference ranges for serum 25-hydroxyvitamin D levels are based upon average values from healthy populations. However, recent research examining the prevention of secondary hyperparathyroidism and bone loss suggest that the range for healthy 25-hydroxyvitamin D levels should be considerably higher. Based upon the most current research, here are the ranges for serum 25-hydroxyvitamin D values:

• Less than 20–25 nmol/L: Indicates severe deficiency associated with rickets and osteomalacia.^40,41
• 50–80 nmol/L: Previously suggested as normal range.⁴²
• 75–125 nmol/L: More recent research suggests that parathyroid hormone^43,44 and calcium absorption⁴⁵ are optimized at this level; this is a healthy range.⁴⁶

Based upon the 75–125 nmol/L range, it is estimated that one billion people in the world are currently vitamin D deficient.⁴⁷ Furthermore, research indicates that supplementation with at least 800–1,000 IU daily are required to achieve serum 25-hydroxyvitamin D levels of at least 80 nmol/L.^48,49 Furthermore, there are many groups of individuals who currently are at risk for vitamin D deficiency. These include:

• Exclusively breast-fed infants: Especially if they do not receive vitamin D supplementation and if they have dark skin and/or receive little sun exposure.⁵⁰
• Dark skin: People with dark-colored skin synthesize less vitamin D from sunlight than those with light-colored skin.⁵¹ In a U.S. study, 42 percent of African American women were vitamin D deficient compared to four percent of white women.⁵²
• The Elderly: When exposed to sunlight have reduced capacity to synthesize vitamin D.⁵³
• Those using sunscreen: Applying sunscreen with an SPF factor of eight reduces production of vitamin D by 95 percent.⁵⁴
• Those with fat malabsorption syndromes: The absorption of dietary vitamin D is reduced in Cystic fibrosis and cholestatic liver disease.⁵⁵
• Those with inflammatory bowel disease: An increased risk of vitamin D deficiency occurs in those with inflammatory bowel disease like Crohn’s disease.⁵⁶
• Obese individuals: Obesity increases the risk of vitamin D deficiency.⁵⁷

Vitamin D2 and D3
There are two forms of vitamin D available as a dietary supplement: cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2). Cholecalciferol is the form made in the human body, and it is more active than ergocalciferol. In fact, Vitamin D2 potency is less than one third that of vitamin D3.⁵⁸

Commercially, ergocalciferol is derived from yeast, and so is considered vegetarian, while cholecalciferol is commonly derived from lanolin (from sheep) or fish oil—although a vegetarian D3 derived from lichen is available.

Ideal dosing for vitamin D
The Linus Pauling Institute recommends that generally healthy adults take 2,000 IU of supplemental vitamin D daily.⁵⁹ The Vitamin D Council states that if well adults and adolescents regularly avoid sunlight exposure, then it is necessary to supplement with at least 5,000 IU of vitamin D daily.⁶⁰ The Council for Responsible Nutrition recommends 2,000 IU daily for adults.⁶¹ Taking a conservative position, at least 2,000 IU of vitamin makes sense for adults.

OMEGA-3 FATTY ACIDS
Chemically, a fatty acid is an organic acid that has an acid group at one end of its molecule, and a methyl group at the other end.⁶² Fatty acids are typically categorized in the omega groups 3, 6 and 9 according to the location of their first double bond (there’s also an omega 7 group, but these are less important to human health).⁶³ The body uses fatty acids for the formation of healthy cell membranes, the proper development and functioning of the brain and nervous system, and for the production of hormone-like substances called eicosanoids (thromboxanes, leukotrienes, and prostaglandins). These chemicals regulate numerous body functions including blood pressure, blood viscosity, vasoconstriction, immune and inflammatory responses.⁶⁴

Deficiency of omega-3 fatty acids
While omega-3, 6 and 9 fatty acids are all important for different reasons, it is the omega-3 fatty acids (O3FA) that are currently particularly critical—and specifically the O3FA known as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The reason for this current importance is that Western diets are deficient in O3FA, and have excessive amounts of omega-6 fatty acids. While human beings evolved on a diet with approximately a 1:1 ratio of omega-6 to omega-3 fatty acids (EFA), the current Western diet provides about a 16:1 ratio.⁶⁵ As a matter of fact, a recent Harvard School of Public Health study indicates that Omega-3 deficiency causes 96,000 U.S. deaths per year.⁶⁶ Other research has clearly shown that excessive amounts of omega-6 fatty acids and a very high omega-6 to omega-3 ratio, as is found in today’s Western diets, promote many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 (a low omega-6 to omega-3 ratio) exert protective effects.⁶⁷

Benefits of omega-3 fatty acids

O3FA offer a broad range of benefits in human health. These benefits are listed below categorically:

Cardiovascular Health
In several studies O3FA have been shown to help lower triglyceride levels.⁶⁸ In fact, the FDA has even approved an O3FA product for this purpose.⁶⁹ Individually, EPA and DHA also have triglyceride-lowering properties. Consuming 1 gram/day of fish oils from fish (about 3 ounces of fatty fish such as salmon) or fish oil supplements has a cardioprotective effect.⁷⁰

Evidence suggests increased consumption of O3FA from fish or fish-oil supplements, but not of alpha-linolenic acid, reduces the rates of all-cause mortality, cardiac and sudden death, and possibly stroke.⁷¹ Higher consumption of fish and O3FA has been associated with a lower risk of coronary heart disease.^72,73 Clinical research shows that DHA supplementation helps increase HDL cholesterol levels (the “good cholesterol”).^74,75 Supplementation with fish oil produces modest, but significant reductions in systolic and diastolic blood pressure in patients with mild hypertension.^76,77,78

Inflammation
O3FA have been shown to help relieve inflammation caused by a variety of factors.^79,80

Arthritis

Research⁸¹ has demonstrated that fish oil supplementation is effective in the treatment of rheumatoid arthritis.

Menopause
Clinical research shows that taking supplements with 500 mg EPA, three times daily, modestly but significantly reduces the frequency of hot flashes compared to placebo in menopausal women.⁸²

ADHD
Research has shown children with attention deficit/hyperactive disorder (ADHD) may have low plasma levels of EPA and DHA.^83,84 Clinical research suggests that supplementation with DHA might improve aggression and social relationships in ADHD children.⁸⁵

Macular degeneration
Increased dietary consumption of DHA is associated with reducing the risk of macular degeneration.⁸⁶

Alzheimer’s Disease
Participants who consumed fish once per week or more had 60 percent less risk of Alzheimer’s disease compared with those who rarely or never ate fish, and this was attributed to the DHA content of the fish.⁸⁷

The sources of omega-3 fatty acids

To begin with, the overwhelming majority of research on the health benefits of supplementation with O3FA has been conducted using fish oil products. Consequently, a strong argument can be made that fish oil supplements are the preferred source of O3FA. Amongst these, the primary fish used commercially as the source from which O3FA are derived include mackerel, herring, tuna, halibut, salmon and cod liver.⁸⁸ Although some fish are touted as superior over others as sources for supplemental fish oil, it is the opinion of this author that they all provide acceptable sources of omega-3s. Still, there are other sources of O3FA besides fish oil. This includes squid, krill, flax seed oil and algae oil.

Squid
Squid-derived O3FA are derived from by-products of squid that are usually discarded when squid are commercially fished, and provides a much higher concentration of DHA (up to 50 percent) than do fish oil. However, there is a lack of human clinical data on squid-source O3FA, although they likely will have similar effects as fish oil.

Krill
Krill oil derived from the shrimp-like crustacean know as krill contain significant amounts of the EPA and DHA omega-3 fatty acids, as well as phospholipids (e.g., phosphatidylcholine),⁸⁹ vitamin A, vitamin E and astaxanthin, a powerful carotenoid antioxidant.^90,91 Human clinical research⁹² has shown that krill oil has greater absorption than fish oil—although krill provides significantly less EPA/DHA per gram than fish oil.

Flaxseed
Flaxseed oil contains about 52–55 percent omega-3s, but as alpha-linolenic acid (ALA), not EPA/DHA.⁹³ This is significant since ALA has to be converted to EPA and DHA before it will provide the much-touted health benefits attributed to O3FA. This is problematic since studies indicate that in men approximately eight percent of ALA is converted to EPA and 0–4 percent is converted to DHA.⁹⁴ In women, approximately 21 percent of dietary ALA is converted to EPA and nine percent is converted to DHA.⁹⁵ This is not to say that flaxseed oil has no value. It does, but just not as significant a value as fish oil.

Algae oil
Certain algae extracts provide a vegetarian source of O3FA—but in this case the O3FA are EPA and DHA, not ALA. Consequently, for vegetarians, algae oil is a viable substitute for fish oil. That being said, human clinical research on algae oil sources of O3FA is limited, and the cost is far more than fish oil.

References:

1. Murphy SP, White KK, Park SY, Sharma S. Multivitamin-multimineral supplements’ effect on total nutrient intake. Am J Clin Nutr. 2007 Jan;85 (1):280S–4S.
2. Ward E. Addressing nutritional gaps with multivitamin and mineral supplements. Nutr J. 2014 Jul 15;13(1):72. 43 Earnest CP, Wood KA, Church TS.
3. Complex Multivitamin Supplementation Improves Homocysteine and Resistance to LDL-C Oxidation. J Am Coll Nutr. 2003;22(5):400–7.
4. den Heijer M, Brouwer IA, Bos GM, et al. Vitamin supplementation reduces blood homocysteine levels: a controlled trial in patients with venous thrombosis and healthy volunteers. Arterioscler Thromb Vasc Biol. 1998 Mar;18(3):356–61.
5. Church TS, Earnest CP, Wood KA. James B. Kampert. Reduction of C-Reactive Protein Levels Through Use of a Multivitamin. Am J Med. 2003;115:702–7.
6. Wang C, Li Y, Zhu K, Dong YM, Sun CH. Effects of supplementation with multivitamin and mineral on blood pressure and C-reactive protein in obese Chinese women with increased cardiovascular disease risk. Asia Pac J Clin Nutr. 2009;18(1):121–30.
7. Holmquist C, Larsson S, Wolk A, de Faire U. Multivitamin Supplements Are Inversely Associated with Risk of Myocardial Infarction in Men and Women— Stockholm Heart. Epidemiology Program (SHEEP). J Nutr. 2003;133: 2650–4.
8. Rautiainen S, Akesson A, Levitan EB, Morgenstern R, Mittleman MA, Wolk A. Multivitamin use and the risk of myocardial infarction: a population-based cohort of Swedish women. Am J Clin Nutr. 2010 Nov;92(5):1251–6.
9. Gaziano JM, Sesso HD, Christen WG, Bubes V, Smith JP, MacFadyen J, Schvartz M, Manson JE, Glynn RJ, Buring JE. Multivitamins in the prevention of cancer in men: the Physicians’ Health Study II randomized controlled trial. JAMA. 2012 Nov 14;308(18):1871–80.
10. Suarez EC. Plasma interleukin-6 is associated with psychological coronary risk factors: moderation by use of multivitamin supplements. Brain Behav Immun. 2003 Aug;17(4):296–303.
11. Huskisson E, Maggini S, Ruf M. The role of vitamins and minerals in energy metabolism and well-being. J Int Med Res. 2007 May–Jun;35(3):277–89.
12. Long SJ, Benton D. Effects of vitamin and mineral supplementation on stress, mild psychiatric symptoms, and mood in nonclinical samples: a metaanalysis. Psychosom Med. 2013 Feb;75(2):144–53.
13. Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004;79(3):362–71.
14. Ibid.
15. Lin R, White JH. The pleiotropic actions of vitamin D. Bioessays. 2004; 26(1):21–8.
16. Gorham ED, Garland CF, Garland FC, et al. Vitamin D and prevention of colorectal cancer. J Steroid Biochem Mol Biol. 2005;97(1-2):179–94.
17. Griffin MD, Xing N, Kumar R. Vitamin D and its analogs as regulators of immune activation and antigen presentation. Annu Rev Nutr. 2003;23:117–45.
18. Hayes CE, Nashold FE, Spach KM, Pedersen LB. The immunological functions of the vitamin D endocrine system. Cell Mol Biol. 2003;49(2):277–300.
19. Ibid.
20. Munger KL, Zhang SM, O’Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology 2004;62:60–5.
21. Merlino LA, Curtis J, Mikuls TR, et al. Vitamin D intake is inversely associated with rheumatoid arthritis. Arthritis Rheum 2004;50:72–7.
22. Zeitz U, Weber K, Soegiarto DW, Wolf E, Balling R, Erben RG. Impaired insulin secretory capacity in mice lacking a functional vitamin D receptor. FASEB J. 2003;17(3):509–11.
23. Borissova AM, Tankova T, Kirilov G, Dakovska L, Kovacheva R. The effect of vitamin D3 on insulin secretion and peripheral insulin sensitivity in type 2 diabetic patients. Int J Clin Pract. 2003;57(4):258–61.
24. Inomata S, Kadowaki S, Yamatani T, Fukase M, Fujita T. Effect of 1 alpha (OH)-vitamin D3 on insulin secretion in diabetes mellitus. Bone Miner. 1986;1(3):187–192.
25. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest. 2002;110(2):229–38.
26. Feskanich D, Willett WC, Colditz GA. Calcium, vitamin D, milk consumption, and hip fractures: a prospective study among postmenopausal women. Am J Clin Nutr. 2003;77(2):504–511.
27. 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;293(18):2257–64.
28. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84(1):18–28.
29. Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, et al. Effect of Vitamin D on falls: a meta-analysis. JAMA 2004;291:1999–2006.
30. Bischoff HA, Stahelin HB, Dick W, et al. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res 2003;18:343–51.
31. Bertone-Johnson ER, Hankinson SE, Bendich A, et al. Calcium and vitamin D intake and risk of incident premenstrual syndrome. Arch Intern Med 2005;165:1246–52.
32. Hoogendijk WJG, Lips P, Dik MG, Deeg DJH, Beekman ATF, Penninx BWJH. Depression Is Associated With Decreased 25-Hydroxyvitamin D and Increased Parathyroid Hormone Levels in Older Adults. Archives of General Psychiatry 2008; 65(5):495.
33. Vaughan CP, Johnson TM 2nd, Goode PS, Redden DT, Burgio KL, Markland AD. Vitamin D and lower urinary tract symptoms among US men: results from the 2005–2006 National Health and Nutrition Examination Survey. Urology. 2011 Dec;78(6):1292–7.
34. Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31(1):48–54.
35. Ginde AA, Liu MC, Camargo CA Jr. Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med. 2009;169:626–32.
36. Holick MF. Vitamin D: A millenium perspective. J Cell Biochem. 2003;88(2):296–307.
37. Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003;78(5):912–9.
38. Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence? Br J Nutr. 2003;89(5):552–72.
39. Wharton B, Bishop N. Rickets. Lancet. 2003;362(9393):1389–1400. 40 Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003;78(5):912–919.
40. Ibid. 79
41. Malabanan A, Veronikis IE, Holick MF. Redefining vitamin D insufficiency. Lancet. 1998;351(9105):805–6.
42. Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int. 1997;7(5):439–43.
43. Thomas MK, Lloyd-Jones DM, Thadhani RI, et al. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338(12):777–83.
44. Heaney RP, Dowell MS, Hale CA, Bendich A. Calcium absorption varies within the reference range for serum 25-hydroxyvitamin D. J Am Coll Nutr. 2003;22(2):142–6.
45. Holick MF. Vitamin D deficiency: what a pain it is. Mayo Clin Proc. 2003;78(12):1457–9.
46. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266–281.
47. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr. 1999;69(5):842–56.
48. Tangpricha V, Koutkia P, Rieke SM, Chen TC, Perez AA, Holick MF. Fortification of orange juice with vitamin D: a novel approach for enhancing vitamin D nutritional health. Am J Clin Nutr. 2003;77(6):1478–83.
49. Wagner CL, Greer FR, and the Section on Breastfeeding and Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. American Academy of Pediatrics. 2008;122(5):1142–52.
50. Ibid. 53
51. Nesby-O’Dell S, Scanlon KS, Cogswell ME, et al. Hypovitaminosis D prevalence and determinants among African American and white women of reproductive age: third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin Nutr. 2002;76(1):187–92.
52. Harris SS, Soteriades E, Coolidge JA, Mudgal S, Dawson-Hughes B. Vitamin D insufficiency and hyperparathyroidism in a low income, multiracial, elderly population. J Clin Endocrinol Metab. 2000;85(11):4125–30.
53. Ibid. 53
54. Food and Nutrition Board, Institute of Medicine. Vitamin D. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington D.C.: National Academies Press; 1999:250–87.
55. Jahnsen J, Falch JA, Mowinckel P, Aadland E. Vitamin D status, parathyroid hormone and bone mineral density in patients with inflammatory bowel disease. Scand J Gastroenterol. 2002;37(2):192–9.
56. Arunabh S, Pollack S, Yeh J, Aloia JF. Body fat content and 25-hydroxyvitamin D levels in healthy women. J Clin Endocrinol Metab. 2003;88(1):157–161.
57. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387–91.
58. Higdon J, Drake VJ, DeLuca HF.Vitamin D. The Linus Pauling Institute Micronutrient Information Center 2000–2010; Last updated 11/30/10. Retrieved December 6, 2010 from http://lpi.oregonstate.edu/infocenter/vitamins/vitaminD/.
59. Understanding Vitamin D Cholecalciferol. The Vitamin D Council, n.d., Retrieved December 6, 2010 from http://www.vitamindcouncil.org/.
60. CRN Reacts to Institute of Medicine DRI Recommendations for Vitamin D. November 30, 2010. Retrieved December 6, 2010 from https://www.crnusa.org/CRNPR10_CRNVitDDRIresp113010.html.
61. Whitney EN, Cataldo CB, Rolfes SR. Understanding Normal and Clinical Nutrition, 5th ed. Belmont, CA:West/Wadsworth; 1998:141–75.
62. Jones PJH, Papamandjaris AA. “Chapter 10 – Lipids: Cellular Metabolism” IN Present Knowledge in Nutrition, 8th ed. Bowman BA, Russell RM (eds). Washington, DC: ILSI Press; 2001:104–14
63. Davis B. Essential Fatty Acids in Vegetarian Nutrition. Andrews University Nutrition Department. Accessed August 18, 2005 from http://www.andrews.edu/NUFS/essentialfat.htm.
64. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002;56(8):365–79.
65. Danaei G, Ding EL, Mozaffarian D, et al. The Preventable Causes of Death in the United States: Comparative Risk Assessment of Dietary, Lifestyle, and Metabolic Risk Factors. PLoS Med. 2009 Apr 28;6(4):e1000058.
66. Ibid. 105
67. Harris WS. n-3 fatty acids and serum lipoproteins: human studies. Am J Clin Nutr. 1997;65(5 Suppl):1645S–54S.
68. Lovaza: Omega-3 Acid Ethyl Esters. Retrieved August 6, 2009 from http://www.lovaza.com/index.html?banner_s=208381923&rotation_s=30492788.
69. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106(21):2747–57.
70. Wang C, Harris WS, Chung M, et al. n-3 Fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review. Am J Clin Nutr. 2006;84(1):5–17.
71. Hu FB, Bronner L, Willett WC, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. JAMA. 2002;287(14):1815–21.
72. Jarvinen R, Knekt P, Rissanen H, Reunanen A. Intake of fish and long-chain n-3 fatty acids and the risk of coronary heart mortality in men and women. Br J Nutr. 2006;95(4):824–9.
73. Agren JJ, Hanninen O, Julkunen A, et al. Fish diet, fish oil and docosahexaenoic acid rich oil lower fasting and postprandial plasma lipid levels. Eur J Clin Nutr 1996;50:765–71.
74. Mori TA, Burke V, Puddey IB, et al. Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men. Am J Clin Nutr 2000;71:1085–94.
75. Prisco D, Paniccia R, Bandinelli B, et al. Effect of medium-term supplementation with a moderate dose of n-3 polyunsaturated fatty acids on blood pressure in mild hypertensive patients. Thromb Res 1998;1:105–12.
76. Toft I, Bonaa KH, Ingebretsen OC, et al. Effects of n-3 polyunsaturated fatty acids on glucose homeostasis and blood pressure in essential hypertension. A randomized, controlled trial. Ann Intern Med 1995;123:911–8.
77. Yosefy C, Viskoper JR, Laszt A, et al. The effect of fish oil on hypertension, plasma lipids and hemostasis in hypertensive, obese, dyslipidemic patients with and without diabetes mellitus. Prostaglandins Leukot Essent Fatty Acids 1999;61:83–7.
78. Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280–9.
79. Calder PC. n-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. Am J Clin Nutr. 2006;83:1505S–19S.
80. Fortin PR, Lew RA, Liang MH, et al. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. J Clin Epidemiol. 1995;48(11):1379–90.
81. Lucas M, Asselin G, Merette C, et al. Effects of ethyl-eicosapentaenoic acid omega-3 fatty acid supplementation on hot flashes and quality of life among middle-aged women: a double-blind, placebo-controlled, randomized clinical trial. Menopause. 2009;16:357–66.
82. Stevens LJ, Zentall SS, Deck JL, et al. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. Am J Clin Nutr. 1995;62:761–8.
83. Voigt RG, Llorente AM, Jensen CL, et al. A randomized, double-blind, placebo-controlled trial of docosahexaenoic acid supplementation in children with attention-deficit/hyperactivity disorder. J Pediatr. 2001;139:189–6.
84. Hamazaki T, Hirayama S. The effect of docosahexaenoic acid-containing food administration on symptoms of attention-deficit/hyperactivity disorder-a placebo-controlled double-blind study. Eur J Clin Nutr. 2004;58:838.
85. Cho E, Hung S, Willet W, et al. Prospective study of dietary fat and the risk of age-related macular degeneration. Am J Clin Nutr. 2001;73:209–18.
86. Morris MC, Evans DA, Bienias JL, et al. Consumption of fish and n-3 fatty acids and risk of incident Alzheimer disease. Arch Neurol. 2003;60:940–6.
87. MedlinePlus. Fish Oil. U.S. National Library of Medicine. Last reviewed–12/10/2011.
88. Bottino NR. Lipid composition of two species of Antarctic krill: Euphausia superba and E. crystallorophias. Comp Biochem Physiol B 1975;50:479–84.
89. Ibid.
90. Dunlap WC, Fujisawa A, Yamamoto Y, et al. Notothenioid fish, krill and phytoplankton from Antarctica contain a vitamin E constituent (alphatocomonoenol) functionally associated with cold-water adaptation. Comp Biochem Physiol B Biochem Mol Biol 2002;133:299–305.
91. Ulven SM, Kirkhus B, Lamglait A, Basu S, Elind E, Haider T, Berge K, Vik H, Pedersen JI. Metabolic effects of krill oil are essentially similar to those of fish oil but at lower dose of EPA and DHA, in healthy volunteers. Lipids 2011;46(1):37–46.
92. Vereshagin AG and Novitskaya GV. The triglyceride composition of linseed oil. Journal of the American Oil Chemists’ Society 1965;42:970–4.
93. Burdge GC, Jones AE, Wootton SA. Eicosapentaenoic and docosapentaenoic acids are the principal products of alpha-linolenic acid metabolism in young men. Br J Nutr. 2002;88(4):355–64.
94. Burdge GC, Wootton SA. Conversion of alpha-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. 2002;88(4):411–20.

The post The 3 Dietary Supplements Everyone Should Be Taking appeared first on Total Health Magazine.

We know the main risk factors that promote abnormal cervical cells include using the birth control pill, increasing age, infection with the Human Papilloma Virus—HPV (the virus that also causes warts), smoking, and nutritional deficiencies of folic acid, vitamin A and vitamin C.

We definitely do not want to ignore abnormal PAP test results. In North America, we grade our PAP tests based on this scale: a CINI, CINII, CINIII, or a CINIV. A CINIV is cancer. Most women are not treated until they have an invasive CINIII. Always ask what grade your test is. Too many women are advised that they have an abnormal test result, told to come back in six months for another test, but not given any suggestions for how to get their cervical cells to return to normal. Yes, sometimes abnormal cells return to normal with no treatment, but what if simply taking a nutritional supplement could ensure a normal PAP?

We know that HPV is implicated in a large majority of cervical dysplasia and cervical cancer cases. New research has shown that a nutrient called Indole-3-carbinol (I3C) can reverse abnormal cervical lesions before they have a chance to develop into cancer. In one of many studies 30 women with CINII and CINIII cervical lesions took 200mg of I3C daily for six months. Fifty percent in the treatment group had complete regression of their lesions, while none in the placebo group experienced any change in their lesions.

There are other nutrients that also help balance female hormones, protect us from abnormal cell growth and reduce our risk of breast cancer that I believe we should be taking everyday. These include:

• Indole-3-carbinol (I3C) not only keeps our PAP smears normal but it also helps to break down cancer-causing estrogens to non-toxic forms. I3C is the most heavily researched nutrient shown to inhibit breast cancer tumors. We should call this the “breast cancer prevention nutrient.”
• Calcium D-glucarate is a powerful detoxifier of excess and toxic estrogens from the liver. D-glucarate is very important as it ensures that toxins are excreted and not released elsewhere in the body. If you think about toxins as being wrapped up and packaged for removal from the body then D-glucarate ensures that somewhere along the way the package does not open and the toxic contents spill out. It is most often used in combination with I3C.
• Green Tea Extract contains polyphenols, catechins and flavonoids shown to be protective against estrogen-dominant breast cancers. Research used the standardized extracts. Daily consumption of green tea is also cancer protective.
• Curcumin is the yellow pigment of turmeric. Research using it in capsules found it be a powerful anti-inflammatory agent and to inhibit all steps of cancer formation: initiation, promotion, and progression. Curcumin also protects against inflammatory calcium loss from our bones.
• Milk Thistle enhances detoxification from the liver, inhibits breast cancer cells from replicating and reduces the toxic effects of chemotherapy. Our hormones are processed and packaged in the liver, and a healthy liver is essential to healthy hormones.
• Rosemary Extract, a potent antioxidant, inhibits breast cancer development, and it helps to detoxify carcinogenic estrogens.
• Lycopene was recently shown to reduce a women’s risk of breast cancer by 36 percent when those women took 6.5 mg per day.
• Sulfurophane, from broccoli sprout extract, has been shown to stimulate the body’s production of detoxification enzymes that eliminate xenoestrogens. Recent research points to this nutrient as a powerful anti-breast cancer agent. A modified sulfurophane is slated to be the next hot cancer drug.
• Lignans found in flaxseed have been found to reduce the growth of breast cancer tumors, increase the excretion of toxic estrogens and inhibit hormone dominant cancers. Researchers at the University of Toronto believe that daily consumption of lignans can prevent breast cancer.
• Omega 3s from fish oil, when taken in 3 gram per day doses, were found to improve the fatty acid composition of women’s breast tissue, thereby lowering breast cancer risk.

Cervical dysplasia and cervical cancer can be prevented. Have your annual PAP smear and make sure your mom has hers as well. Too many women after menopause are not having annual tests. PAP tests save lives! Smart women also take their multivitamin with minerals everyday and include Indole-3carbinol and the nutrients mentioned above to reduce their risk of cancer and hormonal problems.

The post This Test Could Save Lives – 30 Percent of Women Have Not Had It. appeared first on Total Health Magazine.