1. Lose Weight
2. Get a Better Education
3. Get Fit
4. Eat Healthy Food
5. Manage Stress

Coming in to 2023, according to Statisa.com, America’s top New Year’s resolutions were¹:

What are your up coming New Year’s Resolutions going to be?

Lose Weight

Of course it’s easy to make resolutions, but hard to keep them. So what can you do to make it easier? While there is no substitute for willpower and commitment, this article will review some nutraceuticals which may actually help you be more effective at adhering to resolutions.

We all know that diet and exercise are necessary components for a successful weight loss program. In addition there are nutraceuticals which can also help. Two of these are L-carnitine and Garcinia cambogia.

L-carnitine
The amino acid L-carnitine plays an important role in energy production by chaperoning activated fatty acids into the mitochondrial matrix to be metabolized.² Unfortunately, research suggests that being overweight is associated with carnitine insufficiency, Studies have also shown that supplementation with L-carnitine is capable of promoting greater weight loss than with diet and exercise alone (500 mg-3 g/day),^4,5,6 and improving various measures of exercise performance and recovery (2 g/day).^{7,8,9,10,11,12,13,14}

Garcina cambogia
Garcina cambogia is a tropical plant that contains a compound known as (-)-hydroxycitric acid (HCA)—which has some interesting biological properties.¹⁵ Specifically, research indicates that HCA may help reduce the conversion of carbohydrates into fatty acids,^17,18 which could mean less fat stored in your fat cells. Also, research^{19,20,21,22,23,24} suggests that HCA may help reduce appetite and food intake. In one study with overweight men and women,²⁵ 300 mg HCA (as G. cambogia extract standardized for HCA), three times daily, 60 minutes before lunch and dinner, and 2 hours after dinner (to prevent snacking in the evening) resulted in 15–30 percent reduced calorie intake. Furthermore, human clinical research26 demonstrated that 440 mg HCA three times daily, 30 minutes prior to breakfast, lunch and dinner (as G. cambogia extract standardized for HCA) resulted in 14 lbs weight loss, compared to 8 lbs weight loss with diet and exercise alone (1200 calories/ day low fat diet, exercise 3 times/week). Other research has shown similar results.^27,28,29

GET A BETTER EDUCATION

Arguably, getting a better education will take more of a time commitment than any other resolution discussed in this article. Of course it’s also the resolution that is most likely to get you a better job and outlook for the future. Nevertheless, it will involve a great deal of reading and studying, which means that you need to have a good memory and good cognitive function. Phosphatidylserine (PS) may be able to help. PS is an integral component in the structure of the brain and spinal cord, and a significant amount of published clinical research has demonstrated that PS supplementation supports various cognitive parameters in adults and in children.³⁰ This is an important consideration if you’re a middle-aged adult going back to school, because that’s the time that age-related memory impairment can start to rear its ugly head. Luckily, research^31,32,33,34 has shown that 100–300 mg of PS daily has helped reduce memory complaints and improve memory difficulties (including learning and remembering written information) in age-related memory impairment. PS can also help young adult students. This was shown in a study³⁵ on 17–18 year old students who received 100 mg of PS daily. Supplementation with PS resulted in significant improvement in memory and improved cognitive performance in students.

GET FIT

Getting fit is primarily a function of a regular exercise program, as well as good nutrition. Naturally, anything that can help you achieve results more quickly or effectively is desirable— assuming that we’re talking about something healthy and legal. In this case, L-arginine, beta-alanine and branched-chain amino acids fit the bill exactly.

L-arginine
The amino acid L-arginine is a precursor to nitric oxide, a vasodilator produced by the body to facilitate circulation.³⁶ Consequently, supplementation with L-arginine has been shown to increase oxygen transport during exercise and improve aerobic exercise (6 g/day)^37,38 and increase circulating growth hormone levels in response to exercise (5–9 g/day, 30 minutes before exercise);³⁹ and growth hormone can help support the development of new muscle.

Beta-alanine
Research suggests that during high-intensity exercise and strength training, 2.4 grams to 6.4 grams daily of the amino acid beta-alanine improves some measures of physical performance (e.g. increases ventilatory threshold, time to onset of muscle fatigue, time to exhaustion, and total work). A meta-analysis of 15 studies demonstrated that beta-alanine significantly improved exercise measures compared to placebo.⁴⁰

Branched-chain amino acids
Leucine, isoleucine and valine are collectively referred to as the branched-chain amino acids (BCAAs). BCAAs have also been shown to significantly reduce the breakdown of skeletal muscle in normal and exercising Volunteers,^{41,42,43,45,46} decrease muscle soreness and muscle fatigue occurring for a few days after exercise,^47,48 and decrease lactic acid levels during exercise.^49,50,51,52 Doses of 1.3–5.7 g/day have been used.

EAT HEALTHY FOOD

If you think you need to eat a healthier diet, you’re in good company. According the USDA, only 10 percent of the American population eats a good diet.⁵³ So by all means, take every measure possible to eat healthier food. At the same time it’s important to realize that even when your diet improves, that doesn’t necessarily mean that you’ll be getting all of the vitamins and minerals you need. In fact, according to the goals of nutrient intake established by the USDA,⁵⁴ comparing the nutritional goals for Americans to the nutrient content of foods consumed in a 2000 calorie per day diet, there will be insufficient amounts of vitamin D, vitamin E, choline, magnesium (for men only) and potassium. So even if you follow dietary guidelines there is a good chance that you still won’t be reaching 100 percent of your nutrient intake goals.

This doesn’t mean that you shouldn’t bother eating a healthy diet; it just means that you need a nutrition insurance policy in the form of a good daily multivitamin. Not only will this help assure that you fill in the missing nutrient gaps,⁵⁵ but research suggests that a good daily multivitamin may offer other benefits as well, which include supporting better cardiovascular health,^{56,57,58,59,60,61} reducing the risk of certain types of cancer,⁶² improving stress and energy,^63,64,65 and maybe even help you live longer.⁶⁶

MANAGE STRESS

Given the many adverse effects that stress can have on our lives, it makes very good sense to try and manage it better. While this can and should include attempts to decrease external stressors, it can also include techniques like biofeedback to help you remain calmer in the face of stress. Another complementary approach is the use of L-theanine and lemon balm.
L-theanine
Asian cultures have often used teas for relaxation effects. The relaxing effect is, at least in part, caused by the presence of a neurologically active amino acid, L-theanine. In research, L-theanine was shown to significantly increase brain activity in the alpha frequency band (calming brain waves), and improve mental alertness while promoting relaxation,^67,68 L-theanine has also been shown to induce feelings of tranquility in subjects⁶⁹ and have a direct anti-stress effect via the inhibition of cortical neuron excitation (50–200 mg).⁷⁰

Lemon balm
The herb lemon balm is often used as a mild mood elevator and calming herb in people with anxiety. It has been shown to improve attention and calmness in healthy volunteers.⁷¹ In human clinical research,⁷² 600 mg lemon balm extract improved the negative mood effects of stress, with significantly increased self-ratings of calmness. Also, the European Scientific Cooperative on Phytotherapy (an umbrella organization representing national herbal medicine or phytotherapy [aka, herbal medicine] associations across Europe), lists tenseness, restlessness and irritability among the uses for lemon balm.⁷³ The use of lemon balm as a brewed herb offers the additional benefit of delivering the herb as a warm beverage, adding to its soothing qualities.

Conclusion
The use of the nutraceuticals discussed in this article won’t guarantee that you will stick to your New Year’s resolution. You still need willpower and commitment. That being said, these nutraceuticals will provide you with extra support, and they may help you be more effective at adhering to your resolutions.

References
1. Popular New Year’s Resolutions.
2. Rebouche CJ. Carnitine. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern Nutrition in Health and Disease. 10th ed. Philadelphia: Lippincott, Williams & Wilkins; 2006:537-544.
3. Noland RC, Koves TR, Seiler SE, et al. Carnitine insufficiency caused by aging and over-nutrition compromises mitochondrial performance and metabolic control. J Biol Chem 2009;284(34):22840-52.
4. Sufeng, Z, Zhichian H, Jianping L, Hui S. L-Carnitine’s effect on comprehensive wight loss program in obese adolescents. Acta Nutr Sin 1997; 19(2):146-150.
5. Lurz R, Fischer R. Carnitine as supporting agent in weight loss in adiposity. Aerztezeitschrift für Naturheilverfahren 1998; 39(1):12-15.
6. Odo S, Tanabe K, Yamauchi M. A Pilot Clinical Trial on L-Carnitine Supplementation in Combination with Motivation Training: Effects on Weight Management in Healthy Volunteers. Food and Nutrition Sciences. 2013;(4)2:222-231.
7. Spiering BA, Kraemer WJ, Hatfield DL, Vingren JL, Fragala MS, Ho JY, Thomas GA, Häkkinen K, Volek JS. Effects of L-carnitine L-tartrate supplementation on muscle oxygenation responses to resistance exercise. J Strength Cond Res. 2008 Jul;22(4):1130-5.
8. Ho JY, Kraemer WJ, Volek JS, Fragala MS, Thomas GA, Dunn-Lewis C, Coday M, Häkkinen K, Maresh CM. l-Carnitine l-tartrate supplementation favorably affects biochemical markers of recovery from physical exertion in middle-aged men and women. Metabolism. 2010 Aug;59(8):1190-9.
9. Spiering BA, Kraemer WJ, Vingren JL, Hatfield DL, Fragala MS, Ho JY, Maresh CM, Anderson JM, Volek JS. Responses of criterion variables to different supplemental doses of L-carnitine L-tartrate. J Strength Cond Res. 2007 Feb;21(1):259-64.
10. Borghi-Silva A, Baldissera V, Sampaio LM, Pires-DiLorenzo VA, Jamami M, Demonte A, Marchini JS, Costa D. L-carnitine as an ergogenic aid for patients with chronic obstructive pulmonary disease submitted to whole-body and respiratory muscle training programs. Braz J Med Biol Res. 2006 Apr;39(4):465-74.
11. Kraemer WJ, Volek JS, French DN, Rubin MR, Sharman MJ, Gómez AL, Ratamess NA, Newton RU, Jemiolo B, Craig BW, Häkkinen K. The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery. J Strength Cond Res. 2003 Aug;17(3):455-62.
12. Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ, Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exerc. 2006 Jul;38(7):1288-96.
13. Volek JS, Kraemer WJ, Rubin MR, Gómez AL, Ratamess NA, Gaynor P. L-Carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E474-82.
14. Giamberardino MA, Dragani L, Valente R, Di Lisa F, Saggini R, Vecchiet L. Effects of prolonged L-carnitine administration on delayed muscle pain and CK release after eccentric effort. Int J Sports Med. 1996 Jul;17(5):320-4.
15. Jena BS, Jayaprakasha GK, Singh RP, Sakariah KK. Chemistry and biochemistry of (-)-hydroxycitric acid from Garcinia. Journal of agricultural and food chemistry. 2002;50(1):10-22.
16. Watson JA, Fang M, Lowenstein JM. Tricarballylate and hydroxycitrate: Substrate and inhibition of ATP:citrate oxaloacetatae lyase. Arch Biochem Biophys. 1969;135:209-217.
17. Hayamizu K, Ishii Y, Kaneko I, Shen M, Okuhara Y, Shigematsu N, Tomi H, Furuse M, Yoshino G, Shimasaki H. Effects of Garcinia cambogia (Hydroxycitric Acid) on Visceral Fat Accumulation: A Double-Blind, Randomized, Placebo-Controlled Trial. Current Therapeutic Research – Clinical and Experimental; 2003;64(8):551-567.
18. Jena BS, Jayaprakasha GK, Singh RP, Sakariah KK. Chemistry and biochemistry of (-)-hydroxycitric acid from Garcinia. Journal of agricultural and food chemistry. 2002;50(1):10-22.
19. Sullivan AC, Triscari J. Metabolic regulation as a control for lipid disorders, I. Influence of (-)-hydroxycitrate on experimentally induced obesity in the rodent. Am J Clin. Nutr. 1977;30:767-776.
20. Greenwood MR, Cleary MP, Gruen R, Blase´ D, Stern JS, Triscar J, Sullivan AC. ,1981. Effect of (-)-hydroxycitrate on development of obesity in the Zucker obese rat. Am J Physiol. 1981;240:E72-78.
21. Rao RN, Sakariah KK. Lipid-lowering and antiobesity effect of (-)-hydroxycitric acid. Nutr Res. 1988;8:209-212.
22. Sullivan AC, Triscari J, Hamilton JG, Miller ON, Wheatley VR. Effect of (-)-hydroxycitrate upon the accumulation of lipid in rat. I. Lipogenesis. Lipids. 1974;9:121-128.
23. Sullivan AC, Triscari J, Hamilton JG, Miller ON. Effect of (-)-hydroxycitrate upon the accumulation of lipid in the rat. II. Appetite. Lipids. 1974;9:129-134.
24. Panksepp J, Pollack A, Meeker RB, Sullivan AC. (-)-Hydroxycitrate and conditioned aversions. Pharmacol Biochem Behav. 1977;6:683-687.
25. Westerterp-Plantenga MS, Kovacs EMR. 2002. The effect of (-)-hydroxycitrate on energy intake and satiety in overweight humans. International Journal of Obesity. 2002;26:870-872.
26. Thom E. Hydroxycitrate (HCA) in the treatment of obesity. Int J Obes. 1996;20(supp4):48.
27. Mattes RD, Bormann L. Effects of (-)-hydroxycitric acid on appetitive variables. Physiology & Behavior. 2000;71(1-2):87-94.
28. Preuss HG, Bagchi D, Rao CVS, Echard BW, Satyanarayana S, Bagchi M. Effect of hydroxycitric acid on weight loss, Body Mass Index and plasma leptin levels in human subjects. FASEB Journal. 2002;16(5):pA. 1020.
29. Hayamizu K, Ishii Y, Kaneko I, Shen M, Okuhara Y, Shigematsu N, Tomi H, Furuse M, Yoshino G, Shimasaki H. Effects of Garcinia cambogia (Hydroxycitric Acid) on Visceral Fat Accumulation: A Double-Blind, Randomized, Placebo-Controlled Trial. Current Therapeutic Research – Clinical and Experimental; 2003;64(8):551-567.
30. Kidd, P.M. 1999, ‘A review of nutrients and botanicals in the integrative management of cognitive dysfunction’, Alternative Medicine Review, vol. 4, no. 3, pp. 144-61.
31. Kato-Kataoka, A., Sakai, M., Ebina, R., Nonaka, C., Asano, T. & Miyamori, T. 2010, ‘Soybean-Derived Phosphatidylserine Improves Memory Function of the Elderly Japanese Subjects with Memory Complaints’, J. Clin. Biochem. Nutr., vol. 47, pp. 246–255.
32. Gindin, J., Novikov, M., Dedar, D., Walter- Ginzburg, A., Naor, S., Levi, S. 2009, ‘The effect of plant phosphtidylserine on age-associated memory impairment and mood in the functioning elderly’, The Geriatric Institute for Education and Research, and Department of Geriatrics, Kaplan Hospital, Rehovot, Israel. Unpublished report.
33. Crook, T.H. 1998, “Treatment of Age-Related Cognitive Decline: Effects of Phosphatidylserine”, In Anti-Aging Medical Therapeutics, Vol II, edited by Klatz, R.M. Health Quest Publications, Chicago, pp. 20-29.
34. Cenacchi, T., Bertoldin, T., Farina, C., Fiori, M.G., Crepaldi, G., and participating investigators. 1993, ‘Cognitive decline in the elderly: A double-blind, placebo-controlled multicenter study on efficacy of phosphatidyiserine administration’, Aging Clin. Exp. Res., vol. 5, pp. 123-133.
35. Yong T, Qianyong Z, Mantian M, Gang H, Jing W. Research on human memory enhancement by phosphatidylserine fortified milk. Chongqing Medicine. 2011;30.003. doi: 10.3969.
36. Tapiero H, Mathe G, Couvreur P, et al. I. Arginine. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (France) 2002; 56(9):439-45.
37. Bailey SJ, Winyard PG, Vanhatalo A, Blackwell JR, DiMenna FJ, Wilkerson DP, Jones AM. Acute L-arginine supplementation reduces the O2 cost of moderate intensity exercise and enhances high-intensity exercise tolerance. J Appl Physiol. 2010 Nov;109(5):1394-403.
38. Koppo K, Taes YE, Pottier A, Boone J, Bouckaert J, Derave W. Dietary arginine supplementation speeds pulmonary VO2 kinetics during cycle exercise. Med Sci Sports Exerc. 2009 Aug;41(8):1626-32.
39. Collier SR, Casey DP, Kanaley JA. Growth hormone responses to varying doses of oral arginine. Growth Horm IGF Res. 2005 Apr;15(2):136-9.
40. Hobson RM, Saunders B, Ball G, et al. Effects of ß-alanine supplementation on exercise performance: a meta-analysis. Amino Acids 2012;43:25-37.
41. Louard RJ, Barrett EJ, Gelfand RA.Overnight branched-chain amino acid infusion causes sustained suppression of muscle proteolysis. Metabolism 1995;44(4):424-9.
42. MacLean DA, Graham TE, Saltin B. Branched-chain amino acids augment ammonia metabolism while attenuating protein breakdown during exercise. Am J Physiol 1994;267:E1010-22.
43. Greer BK, Woodard JL, White JP, Arguello EM, Haymes EM. Branched-chain amino acid supplementation and indicators of muscle damage after endurance exercise. Int J Sport Nutr Exerc Metab 2007;17(6):595-607.
44. Coombes JS, McNaughton LR. Effects of branched-chain amino acid supplementation on serum creatine kinase and lactate dehydrogenase after prolonged exercise. J Sports Med Phys Fitness 2000;40(3):240-6.
45. Shimomura Y, Murakami T, Nakai N, Nagasaki M, Harris RA. Exercise promotes BCAA catabolism: effects of BCAA supplementation on skeletal muscle during exercise. J Nutr 2004 Jun;134(6 Suppl):1583S-1587S.
46. Tang FC. Influence of branched-chain amino acid supplementation on urinary protein metabolite concentrations after swimming. J Am Coll Nutr 2006;25(3):188-94.
47. Shimomura Y, Murakami T, Nakai N, Nagasaki M, Harris RA. Exercise promotes BCAA catabolism: effects of BCAA supplementation on skeletal muscle during exercise. J Nutr 2004 Jun;134(6 Suppl):1583S-1587S.
48. Shimomura Y, Yamamoto Y, Bajotto G, Sato J, Murakami T, Shimomura N, Kobayashi H, Mawatari K. Nutraceutical effects of branched-chain amino acids on skeletal muscle. J Nutr 2006;136(2):529S-532S.
49. MacLean DA, Graham TE, Saltin B. Stimulation of muscle ammonia production during exercise following branched-chain amino acid supplementation in humans. J Physiol 1996;493(Pt 3):909-22.
50. De Palo EF, Gatti R, Cappellin E, Schiraldi C, De Palo CB, Spinella P. Plasma lactate, GH and GH-binding protein levels in exercise following BCAA supplementation in athletes. Amino Acids 2001;20(1):1-11.
51. Coombes JS, McNaughton LR. Effects of branched-chain amino acid supplementation on serum creatine kinase and lactate dehydrogenase after prolonged exercise. J Sports Med Phys Fitness 2000;40(3):240-6.
52. Koba T, Hamada K, Sakurai M, Matsumoto K, Hayase H, Imaizumi K, Tsujimoto H, Mitsuzono R. Branched-chain amino acids supplementation attenuates the accumulation of blood lactate dehydrogenase during distance running. J Sports Med Phys Fitness 2007;47(3):316-22.
53. Report Card on the Quality of Americans’ Diets. Nutrition Insights, INSIGHT 28. USDA Center for Nutrition Policy and Promotion. December 2002.
54. United States Department of Agriculture. Center for Nutrition Policy and Promotion/Comparison of Nutrient Content of each 2010 USDA Food Pattern to Nutritional Goals for that Pattern. Retrieved August 19, 2014 from http://www.cnpp.usda.gov/Publications/USDAFoodPatterns/
55. Fletcher RH, Fairfield KM. Vitamins for Chronic Disease Prevention in Adults. JAMA 2002; 287(23):3127-3129.
56. Earnest CP, Wood KA, Church TS. Complex Multivitamin Supplementation Improves Homocysteine and Resistance to LDL-C Oxidation. J Am Coll Nutr. 2003;22(5):400–407 .
57. 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.
58. Church TS, Earnest CP, Wood KA. James B. Kampert. Reduction of C-Reactive Protein Levels Through Use of a Multivitamin. Am J Med. 2003;115:702–707.
59. 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.
60. 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: 2650–2654.
61. 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.
62. 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.
63. 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.
64. 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.
65. Long SJ, Benton D. Effects of vitamin and mineral supplementation on stress, mild psychiatric symptoms, and mood in nonclinical samples: a meta-analysis. Psychosom Med. 2013 Feb;75(2):144-53.
66. Xu Q, Parks CG, DeRoo LA, Cawthon RM, Sandler DP, Chen H. Multivitamin use and telomere length in women. Am J Clin Nutr. 2009;89(6):1857-63.
67. Nobre AC, Rao A, Owen GN. L-theanine, a natural constituent in tea, and its effect on mental state. Asia Pac J Clin Nutr 2008;17 Suppl 1:167-8.
68. Mason,R. 200 mg of Zen. Alternative & Complementary Therapies 2001; 7(2):91-95.
69. Lu K, Gray MA, Oliver C, et al. The acute effects of L-theanine in comparison with alprazolam on anticipatory anxiety in humans. Hum Psychopharmacol Clin Exp 2004;19:457–65.
70. Kimura K, Ozeki M, Juneja LR, Ohira H. L-Theanine reduces psychological and physiological stress responses. Biol Psychol 2007;74(1):39-45
71. Abascal K, Yarnell E. Nervine herbs for treating anxiety Altern Compliment Ther. 2004 December:309-315.
72. Kennedy DO, Little W, Scholey AB. Attenuation of laboratory-induced stress in humans after acute administration of Melissa officinalis (Lemon Balm). Psychosom Med. 2004 Jul-Aug;66(4):607-13.
73. ESCOP. Melissae folium. Monographs on the Medicinal Uses of Plant Drugs. Exeter, U.K. European Scientific Cooperative on Phytotherapy; 1997.

The post Nutraceuticals to Help You Keep Your New Year’s Resolutions appeared first on Total Health Magazine.

The term essential fatty acid refers to a fatty acid, which the body cannot manufacture and must obtain from dietary sources. These essential fatty acids were originally designated as Vitamin F, until it was realized that they must be classified with the fats.³ There are two fatty acids designated as essential fatty acids: linoleic acid and alphalinolenic acid. This does not mean that the other 15 or so fatty acids found in the omega 3, 6 and 9 groups aren’t important, just that a healthy body can manufacture them as long as it gets enough linoleic acid and alpha-linolenic acid. Nevertheless, research demonstrates that there are health benefits to be had by obtaining some of the other non-essential fatty acids directly; more on this later. Now let’s discuss the roles of essential fatty acids (EFAs) in the body, as well as sources of EFAs.

Roles and sources of essential fatty acids
The body uses essential fatty acids (EFAs) 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, prostaglandins). These chemicals regulate numerous body functions including blood pressure, blood viscosity, vasoconstriction, immune and inflammatory responses.⁴

Dietary sources of the omega 6 fatty acids include some leafy vegetables, seeds nuts, grains, vegetable oils and meats. Dietary sources of the omega 3 fatty acids include some vegetable oils, nuts and seeds, shellfish and fish.⁵ Dietary supplement sources of essential fatty acids and nonessential fatty acids include Evening Primrose oil, Borage oil, Flax seed oil and Fish oils (marine lipid concentrate). Now let’s take a look at some of these individual dietary supplement sources of essential fatty acids, and the benefits they have to offer.

Evening Primrose & Borage Oils: Sources of GLA The oils from the Evening Primrose plant and Borage seed are rich in the omega 6 fatty acid, gamma linolenic acid (GLA); as well as EFAs. Although fatty acids are found in significant quantities in a variety of plants, GLA is only found in a few. GLA is a precursor to various natural chemicals found in the body. Among these are prostaglandins, a type of short-term hormone-like substances, which play a variety of roles in the body. Published research on these sources of GLA have demonstrated them to be useful in PMS^{6,7,8,9,10,11}, pregnancy and lactation^12,13, inflammatory conditions^14,15, rheumatoid arthritis^16,17,18, skin conditions^{19,20,21,22,23,24,25,26,27,28,29,20,32,32,33,34}, stress and performance^35,36, as well as migraine headaches.³⁷ Furthermore, the unique balance of GLA to EFAs in any one of these sources may have a distinct benefit over another source depending on the condition in question. For more detailed information on EPO and BO, read the Intelligent Supplementation article, “GLA: Gamma Linolenic Acid from Evening Primrose & Borage Oils.”

Fish Oils: Sources of EPA/DHA Omega 3 fatty acids
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega 3 fatty acids (O3FA). O3FA supplements are mostly derived from the oils of cold water species of fish like salmon, sardines, herring, and mackerel. There are many therapeutic applications for O3FA, primarily due to its cardiovascular-enhancing and anti-inflammatory benefits. Research has shown that O3FA cardiovascular benefits include reducing the risk of atherosclerosis^{38,39,40,41,42,43,44}, modifying cholesterol levels (i.e., increasing “good” HDL cholesterol, while decreasing “bad” LDL cholesterol) and decreasing triglycerides^{45,46,47,48,49}, and decreasing high blood pressure.60 O3FA have also been shown to block the production of certain inflammatory chemicals in our body. Consequently, studies have demonstrated the ability of O3FA to reduce inflammation in such disorders as rheumatoid arthritis^51,52,53,54, asthma^55,56,57,58, colitis^{59,60,61,62,63}, Crohn’s disease^64,65,66, and Lupus^67,68,69. In addition, O3FA have shown to reduce the symptoms of other disorders including angina^70,71, migraine headaches^72,73,74,75, psoriasis^{76,77,78,79,80}, and tinnitus.^81,82 For more detailed information on O3FA, read the Intelligent Supplementation article “Omega 3 Fatty Acids.”

Flax Seed Oils: Sources of Omega 3, 6 & 9 fatty acids

Flax seed naturally contain a complex of different categories of fatty acids, including alpha-linolenic acid (omega-3), linoleic acid (omega-6), and oleic acid (omega-9). Much of Flax seed’s benefits are a function of its alpha linolenic acid (ALA) content, and the fact that ALA can be converted by the body into EPA—the same omega-3 found in fish oil. As a matter of fact, research has found that supplementation with Flax seed oil can effectively increase EPA concentrations in tissues.⁸³ Lignans, also found in Flax seed, account for various benefits offered by this plant. Studies involving Flax seed have been conducted on its anti-inflammatory properties84, its antilupus properties⁸⁵, and its cardiovascular enhancing properties.^{86,87,88,89,90,91}

Just a quick note to mention that the omega 9 fatty acid, oleic acid, has been shown in research to lower heart attack risk and arteriosclerosis92, and aids in the prevention of breast cancer.⁹³

Conclusion
In addition to the two essential fatty acids, there are other fatty acids whose consumption may have benefits for human health. Both the essential and non-essential fatty acids can be obtained from dietary supplement sources including Evening Primrose oil, Borage oil, Flax seed oil and Fish oils (marine lipid concentrate). Each of these sources has their own potential advantages. Perhaps a combination of all of them may yield the broadest spectrum of both essential and nonessential fatty acids.

References:

1. Whitney EN, Cataldo CB, Rolfes SR. “Understanding Normal and Clinical Nutrition,” 5th ed. Belmont, CA:West/Wadsworth; 1998:141–75.
2. 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.
3. Answers to Frequently Asked Questions. USDA Nutrient Data Laboratory, Agricultural Research Service. Last modified July 22, 2005. Accessed on August 18, 2005
4. Davis B. Essential Fatty Acids in Vegetarian Nutrition. Andrews University Nutrition Department. Accessed August 18, 2005
5. Whitney EN, Cataldo CB, Rolfes SR. Understanding Normal and Clinical Nutrition, 5th ed. Belmont, CA:West/Wadsworth; 1998:141-175.
6. Horrobin DF, et al, J Nutr Med 1991; 2:259–64.
7. Puolakka J, et al, J Reprod Med 1985; 30:149–53.
8. Ockerman PA, et al, Rec Adv Clin Nutr 1986;2:404–5.
9. Massil H, O’Brien PMS, Brush MG. A double-blind trial of Efamol evening primrose oil in premenstrual syndrome (1987) September, 2nd International Symposium on PMS, Kiawah Island.
10. Casper R. A double-blind trial of evening primrose oil in premenstrual syndrome 1987; September, 2nd International Symposium on PMS, Kiawah Island.
11. McFayden IJ, et al, Br J Clin Pract 1992; 46:161–4.
12. D’Almeida A, et al, Women Health 1992; 19(2-3):117–31.
13. Cant A, Shay J, Horrobin DF, J Nutr Sci Vitaminol 1991; 37(6):573-9.
14. Chilton-Lopez; J Immunol 1996; 156(8):2941–7.
15. Ziboh VA, Fletcher MP, Am J Clin Nutr 1992; 55(1):39–45.
16. Vassilopoulos D, Clin Immunol Immunopathol 1997; 83(3):237–44.
17. Rothman D, DeLuca P, Zurier RB, Semin Arthritis Rheum 1995; 25(2):87–96.
18. Leventhal LJ, Boyce EG, Zurier RB, Ann Intern Med 1993; 119(9):867–73.
19. Tollesson A, Frithz A, Acta Derm Venereol 1993; 73(1):18–20.
20. Bahmer FA, Schafer J, Kinderarztl Prax 1992; 60(7):199–202.
21. Schafer L, Kragballe K, Lipids 1991; 26(7):557–60.
22. Kerscher MJ, Korting HC, Clin Investig 1992; 70(2):167–71.
23. Horrobin DF, Am J Clin Nutr 1993; 57(5 Suppl):732S–6S.
24. Manku MS, et al, Prostaglandins Leukot Med 1982; 9(6):615–28.
25. Lindskov R, Holmer G, Allergy 1992; 47(5):517–21.
26. Wright S, Bolton C, Br J Nutr 1989; 62(3):693–7.
27. Businco L, et al, J Allergy Clin Immunol 1993; 91(6):1134–9.
28. Morse PF, et al, Br J Dermatol 1989; 121(1):75–90.
29. Fiocchi A, et al, J Int Med Res 1994; 22(1):24–32.
30. Biagi PL, et al, Drugs Exp Clin Res 1988; 14(4):285–90.
31. Bordoni A, et al, Drugs Exp Clin Res 1988; 14(4):291–7.
32. Andreassi M, et al, J Int Med Res 1997; 25(5):266–74.
33. Borrek S, et al, Klin Padiatr 1997; 209(3):100–4.
34. Fiocchi A, et al, J Int Med Res 1994; 22(1):24–32.
35. Mills DE, et al, J Hum Hypertens 1989; 3(2):111–6.
36. Mills DE et al, Am J Physiol 1990; 259(6 Pt 2):R1164–71.
37. Wagner W, Nootbaar-Wagner U, Cephalalgia 1997; 17 (2):127–30.
38. Johansen O, et al, Arterioscler ThrombVasc Biol 1999; 19(7):1681–6.
39. Enikeeva NA, Kitaiskaia LS, Antoniuk MV, Klin Med 1999; 77(3):25–8.
40. von Schacky C, et al, Ann Intern Med 1999; 130(7):554–62.
41. Sucic M, Katica D, Kovacevic V, Coll Antropol 1998; 22(1):77–83.
42. Albert CM, Campos H, Stampfer MJ, Ridker PM, Manson JE, Willett WC, et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med 2002; 346:1113–8.
43. Hu FB, Bronner L, Willett WC, Stampfer MJ, Rexrode KM, Albert CM, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. JAMA 2002; 287:1815–21.
44. Seljeflot I, et al, Thromb Haemost 1999; 81(4):566–70.
45. Santos MJ, Lopez-Jurado M, Llopis J, et al. Influence of dietary supplementation with fish on plasma total cholesterol and lipoprotein cholesterol fractions in patients with coronary heart disease. J Nutr Med 1992; 3:107–15.
46. Kromhout D, Bosschieter EB, Coulander CdL, The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985; 312:1205–9.
47. Albert CM, Manson JE, O’Donnoell C, et al. Fish consumption and the risk of sudden death in the Physicians’ Health Study. Circulation 1996;94 (suppl 1): I–578 [abstract #3382].
48. Ibid.
49. Zak A, Zeman M, Tvrzicka E, Sb Lek 1997; 98(3):213–24.
50. Morris MC, Sacks F, Rosner B, Circulation 1993;88:523–33.
51. Alexander JW, Nutrition 1998; 14(7-8):627–33.
52. Ariza-Ariza R, Mestanza-Peralta M, Cardiel MH, Semin Arthritis Rheum 1998; 27(6):366–70.
53. de Deckere EA, et al, Eur J Clin Nutr 1998; 52(10):749–53.
54. Vargova V, et al, Cas Lek Cesk 1998; 137(21):651–3.
55. Villani F, et al, Respiration 1998; 65(4):265–9.
56. Broughton KS, et al, Am J Clin Nutr 1997; 65(4):1011-7.
57. Masuev KA, Ter Arkh 1997; 69(3):33–5.
58. Masuev KA, Ter Arkh 1997; 69(3):31–3.
59. Gramlich TL, Beeken W, Ann Intern Med 1992; 116(8):609–14.
60. Aslan A, Triadafilopoulos G, Am J Gastroenterol 1992; 87(4):432–7.
61. Almallah YZ, et al, Am J Gastroenterol 1998; 93(5):804–9.
62. Salomon P, Kornbluth AA, Janowitz HD, J Clin Gastroenterol 1990; 12(2):157–61.
63. McCall TB, et al, Aliment Pharmacol Ther 1989; 3(5):415–24.
64. Geerling BJ, et al, Am J Gastroenterol 1999; 94(2):410–7.
65. Kuroki F, et al, Dig Dis Sci 1997; 42(6):1137–41.
66. Vilaseca J, et al, Gut 1990; 31(5):539–44.
67. Kelley VE, et al, J Immunol 1985; 134:1914–19.
68. Walton AJE, et al, Ann Rheum Dis 1991; 50:463–66.
69. Westberg G, Tarkowski A, Scand J Rheumatology 1990; 19:137–43.
70. Saynor R, Verel D, Gillott T, Atheroscl 1984;50:3–10.
71. Mehta JL, et al, Am J Med 1988; 84:45–52.
72. McCarren T, et al, Am J Clin Nutr 1985;41(4):874 [abstr].
73. Glueck CJ, et al, Am J Clin Nutr 1986;43(4):710 [abstr].
74. Gibson RA, Australian and New Zealand Journal of Medicine 1988; 18(5):713–22.
75. McCarty MF, Medical hypotheses (1996) 47(6):461–6.
76. Bittiner SB, et al, Lancet 1988; i:378–80.
77. Kojima T, et al, Dermatologica 1991; 182:225–30.
78. Kojima T, et al, J Am Acad Dermatol 1989;21:150–51.
79. Dewsbury CE, Graham P, Darley CR, Br J Dermatol 1989; 120:581–84.
80. Ashley JM, et al, J Am Acad Dermatol 1988; 19:76–82.
81. Rudin, D., Med Hypotheses 1980; 6(4): 427–30.
82. Rudin, D., Biol Psychiatry 1981; 16(9): 837–50.
83. Mantzioris E, et al, Am J Clin Nutr 1994; 59(6):1304–9.
84. James MJ, Gibson RA, Cleland LG, Am J Clin Nutr 2000; 71(1Suppl):343S–8S.
85. Clark WF, et al, Kidney Int 1995; 48:475–80.
86. Bierenbaum ML, Reichstein R, Watkins TR, Journal of the American College of Nutrition 1993; 12(5):501–4.
87. Harris WS, Am J Clin Nutr 1997; 65(5 Suppl):1645S.
88. Cunnane SC, et al, Am J Clin Nutr 1995 ; 61(1):62–8.
89. Cunnane SC, et al, Br J Nutr 1993 ; 69(2):443–53.
90. Prasad K, Atherosclerosis 1997; 132(1):69–76.
91. Nestel PJ, et al, Arterioscler Thromb Vasc Biol 1997; 17(6):1163–70.
92. Rotella P. Healthy Fats–Essential Fatty Acids. Posted 13 April 2002, Last updated 22 October 2004. Accessed August 19, 2005 from http://goodfats.pamrotella.com.
93. Menendez JA, Vellon L, Colomer R, Lupu R. Annals of Oncology 2005; 16(3):359–71.

The post Essential & Nonessential Fatty Acids appeared first on Total Health Magazine.

Calcium and Vitamin D
Calcium’s role in supporting the maintenance and repair of healthy bone is well established and does not require further elucidation here. Likewise, vitamin D has a long-established role in facilitating calcium absorption; and research indicates that vitamin D supplementation can help to prevent bone loss^1,2.

SierraSil^TM
SierraSil is a naturally-occurring mineral composite found only in the high Sierra Mountains. Research has demonstrated that SierraSil suppresses cartilage degradation and inflammation.³ In an unpublished double-blind, placebo-controlled study SierraSil was evaluated in patients with osteoarthritis. Results indicated that with doses of 2000 or 3000 mg, SierraSil improved joint flexibility and quality of life.⁴ A previous unpublished pilot study on SierraSil in osteoarthritis patients demonstrated similar results.⁵ SierraSil has a patent pending for supporting joint mobility, flexibility and active lifestyles.

Paractin^TM
Spasov et al⁶ has reported that standardized extracts of Andrographis paniculata have been investigated in a number of studies, showing significant reduction of major symptoms of common cold and other upper respiratory tract infections. Paractin^TM is a patented, standardized extract of Andrographis paniculata which has been shown in preliminary research to stimulate immune response at low doses and to reduce inflammation high doses.^7,8,9 It does this by invigorating the activation of Peroxisome Proliferator-Activated Receptor gamma (PPARΥ), which in turn inhibits inflammatory chemicals in the body such as NF kappa B interferon gamma (IFNΥ), and Interleukin 2 (IL-2). By supplementing the body’s ability to naturally activate PPARΥ, Paractin^TM helps promote healthy inflammation response while maintaining normal cellular structure and activity in the joints, bones, and throughout the body.

Glucosamine Sulfate
According to the book, The Arthritis Cure, there are three requirements to keep cartilage healthy: water for lubrication and nourishment, proteoglycans to attract and hold the water, and collagen to keep the proteoglycans in place. Proteoglycans are large molecules made of protein and sugar. They trap water like a sponge and make cartilage resilient.¹⁰ Glucosamine sulfate figures into healthy cartilage since it is a major building block of the water-loving proteoglycans. In addition, glucosamine sulfate’s very presence stimulates the production of more proteoglycans. The fact that glucosamine sulfate increases the synthesis of these key elements of cartilage means that it actually helps repair damaged or eroded cartilage.¹¹ In fact, for many years glucosamine sulfate has been successfully used in the therapy of osteoarthritis, and has met all standards of an efficient and well tolerated drug (albeit a natural drug). This has been demonstrated by experimental as well as clinical studies, in which glucosamine sulfate led to long-lasting pain reduction and functional improvement.¹²

Chondroitin Sulfate
Chondroitin sulfate is the perfect complement to glucosamine sulfate since chondroitin acts like a liquid magnet, attracting fluid into the proteoglycans. This fluid acts as a shock absorber and also brings nutrients with it into the cartilage. Perhaps of greater significance than its fluid-enhancing properties, chondroitin sulfate protects existing cartilage from premature breakdown by inhibiting certain cartilage-chewing enzymes. Furthermore, like glucosamine, chondroitin stimulates the production of proteoglycans and collagen that are needed for healthy new cartilage. As a matter of fact, chondroitin works synergistically with glucosamine.

Plant Based Enzymes
Research has shown that certain plant-based (fungal) enzymes were shown to have powerful effects on protein digestion at the University of Rhode Island. Specifically, 300 to 500 mg of these fungal enzymes successfully released 62,000 mg of free form amino acids from protein (in the form of beef steak) that’s 42 percent more amino acids than stomach acid and enzymes alone, without fungal enzymes. Furthermore, in the laboratory fungal enzymes release branched chain amino acids from beef steak at up to 200 percent the rate of stomach acid and enzymes alone. This is particularly important since branched chain amino acids (BCAA) make up at least 35 percent of key muscle proteins. The results of this research clearly demonstrate that these enzymes cause amino acids in protein to become more bioavailable. This can help to rebuild and repair muscle tissue.

References:

1. Dawson-Hughes B, et al. Ann Intern Med 1991;115:505–12.
2. Dawson-Hughes B, et al. Am J Clin Nutr 1995; 61:1140–45.
3. Miller MJS, Ahmed S, Bobrowski P, Haqqi TM. Suppression of Human Cartilage Degradation and Chondrocyte Activation by a Unique Mineral Supplement (SierraSil™) and a Cat’s Claw Etract, Vincaria®. JANA 2004; 7(2):32–39.
4. Raut V, Gala J, Dhumale R. A double-blind randomized placebo-controlled study to compare two doses of a mineral supplement and a herbo-mineral combination in alleviating the symptoms of osteoarthritis of the knee. (unpublished)
5. A pilot study to test the safety and efficacy of the mineral supplement SierraSil™ in osteoarthritis of the knee. (unpublished)
6. Spasov AA, Ostrovskij OV, Chernikov MV, Wikman G. Comparative Controlled Study of Andrographis paniculata Fixed Combination, Kan Jang® and an Echinacea Preparation as Adjuvant, in the Treatment of Uncomplicated Respiratory Disease in Children. Phytother Res 2004; 18:47–53.
7. Paractin useful for the treatment of autoimmune diseases, and alzeimer disease by activation of PPAR- Receptor. Juan L. Hancke. Instituto de Farmacologia, Universidad Austral de Chile, Valdivia Chile. Paractin interferes with T cell activation and reduces Experimental Autoimmune Encephalomyelitis in the Mouse. Iruretagoyena MI, Tobar JA, Gonzalez PA, Sepulveda SE, Figueroa CA, Burgos RA, Hancke JL, Kalergis AM. Uniersidad Austral de Chile. Journal of Pharmacology & Exp Therapeutics, August 26 2004.
8. Paractin interferes DNA binding of NF-kB in HL-60/Neutrophils cells. María A. Hidalgo, Alex Romero, Jaime Figueroa, Patricia Cortés, Ilona I. Concha, Juan L. Hancke, & Rafael A. Burgos. Uniersidad Austral de Chile.
9. Theodosakis, J., et al, The Arthritis Cure, (1997) St. Martin’s Press: New York, 203 pgs.
10. Theodosakis, J., ibid.
11. Anonymous, Fortschr Med Suppl (1998) 183:1–12.
12. Theodosakis, J., ibid.

The post Athletic Recovery: Too Much Pain, No Gain appeared first on Total Health Magazine.

Echinacea
Echinaceais an herb best known for its benefits in the treatment of the common cold, although it has other benefits as well. First of all, there are three species of Echinacea commonly used in herbal medicine: Echinacea purpurea, E. angustifolia, and E. pallida (of these, the first two are most popular). The aerial (above ground) parts of the herb and the root contain the medicinal components. These include phenolics, caffeic acid esters (e.g., echinacosides), flavonoids, alkylamides, volatile oils, polysaccharides, polyacetylenes.¹

Echinacea is an immune stimulant/supporter. It is excellent in helping to prevent and treat colds and influenza. Research reveals that Echinacea supports the immune system by activating white blood cells (lymphocytes and macrophages).² Echinacea also increases the production of interferon, an immune component, which is important in responding to viral infections.³

Several double-blind, clinical studies have confirmed Echinacea‘s effectiveness in treating colds and flu.^4,5,6,7 However, some research suggests that Echinacea may be more effective if used at the onset of these conditions.^8,9 One study involving 238 subjects confirmed that Echinacea was safe and effective in producing a rapid improvement of cold symptoms. In the subgroup of patients who started therapy at an early phase of their cold, the effectiveness of Echinacea was most prominent.¹⁰ In a similar study, 246 subjects with a cold were treated with Echinacea preparations or a placebo. Those treated with the Echinacea preparations experienced a reduction of symptoms, significantly more effective than the placebo. The researchers concluded that the Echinacea preparations “represent a low risk and effective alternative to the standard symptomatic medicines in the acute treatment of common cold.”¹¹

In a meta-analysis of 14 studies¹², researchers found that taking Echinacea cut the risk of catching the common cold by 58 percent, and if subjects already had a cold it decreased the duration by 1.4 days. In one of the studies, Echinacea taken in combination with vitamin C reduced cold incidence by 86 percent, and when the herbal was used alone the incidence of cold was reduced by 65 percent. The bottom line is that when used appropriately, Echinacea is effective in preventing and treating the common cold.

Besides colds and flu, Germany’s Commission E Monographs (an internationally authoritative source of credible information on the use of herbs for various disorders) indicates that among Echinacea’s uses, this herb can be used to treat chronic infections of the respiratory tract.¹³ Other current and evidence based uses of Echinacea include, but are not limited to: Vaginal candidiasis, ear, urinary and sinus infections, allergies, herpes, cystitis, bronchitis, prostatitis, tonsillitis, and laryngitis.¹⁴

A good dosage range for Echinacea extract is 200-400 mg with 4 percent total phenolics (including cichoric acid, chlorogenic acid, captaric acid) and/or 4 percent echinacoside, three to five times daily for acute infection.¹⁵ Some sources have suggested that Echinacea should not be used with drugs intended to suppress the immune system, but such suggestions are speculative and lack clinical documentation.¹⁶

Shiitake & AHCC

For thousands of years, mushrooms have been used as both food and medicine in various cultures. One of those mushrooms, Shiitake (Lentinula edodes)¹⁷, is currently used for promoting healthy immune function¹⁸, healthy liver function¹⁹ and modulating the unwanted growth of mutated stomach²⁰ and pancreas cells21, and has been validated in scientific literature for these purposes.

Active Hexose Correlated Compound (AHCC) is an extract derived from Shiitake, as well as other species of Basidiomycete family of mushrooms. AHCC is a mixture of polysaccharides, amino acids, lipids, and minerals. Oligosaccharides make up about 74 percent of AHCC.²² Like its predecessor, AHCC has antioxidant effects, and is thought to act as a biological response modifier. It seems to promote the activity of natural killer (NK) cells in patients with unwanted growth of mutated cells. In animal models, it also seems to protect against carbon tetrachloride-induced liver damage, promote healthy blood glucose levels within a normal range, and decrease apoptosis (i.e., programmed cell death) of the thymus.²³

AHCC demonstrated early clinical promise in promoting healthy immune response.²⁴ This was shown in animal research where AHCC helped restore immune response that had been negatively affected by trauma, infection, and food deprivation.²⁵ In humans, the effect of AHCC on immune response was investigated by measuring the number and function of circulating dendritic cells (DCs), a type of immune cell, in healthy volunteers. Twenty-one healthy volunteers were randomized to receive placebo or AHCC for four weeks. The results were that the AHCC group had a significantly higher number of total DCs compared to when they first started the study, and compared to the control subjects. Other types of immune cells were also significantly increased in the AHCC group compared to controls.²⁶

The effects of AHCC in a clinical setting were examined in patients who had surgery for the undesirable growth of mutated liver cells. A total of 269 patients participated in the study, with 113 receiving AHCC. The results were that the AHCC group had a significantly longer period of no recurrence of mutated liver cells, and an increased overall survival rate when compared to the control group.²⁷

A prospective cohort study was performed with 44 patients with undesirable growth of mutated liver cells. All of the patients underwent supportive care. Survival time, quality of life, clinical and immunological parameters related to liver function, cellular immunity, and patient status were determined. Of the 44 patients, 34 and 10 received AHCC and placebo (control) orally, respectively. Patients in the AHCC treated-group had a significantly prolonged survival when compared to the control group, and quality of life in terms of mental stability, general physical health status, and ability to have normal activities were significantly improved after three months of AHCC treatment.²⁸

In a safety study, high doses (9 grams) of AHCC were given to healthy subjects in a liquid form. The results were that AHCC caused no significant abnormality in laboratory parameters, and the adverse effects were minimal with the high dose being tolerated by 85 percent of the subjects.²⁹ Research has not demonstrated adverse effects at the lower doses typically used.

In a study AHCC was examined for potential drug interactions with chemotherapy agents. The results were that AHCC does have the potential for drug-drug interactions involving chemotherapy agents such as doxorubicin or ondansetron, which are metabolized by the liver enzyme CYP450 2D6. However, the overall data suggest that AHCC would be safe to administer with most other chemotherapy agents that are not metabolized via the CYP450 2D6 pathway.³⁰

References:

1. Blumenthal M, Hall T, Goldberg A, Kunz T, Dinda K (eds.). The ABC Clinical Guide to Herbs. Austin TX: American Botanical Council; 2003:88-96.
2. See DM, Broumand N, Sahl L, Tilles JG. In vitro effects of Echinacea and ginseng on natural killer and antibody-dependent cell cytotoxicity in healthy subjects and chronic fatigue syndrome or acquired immunodeficiency syndrome patients. Immunpharmacol 1997;35:229-35.
3. Leuttig B, Steinmuller C, Gifford GE, et al. Macrophage activation by the polysaccharide arabinogalactan isolated from plant cell cultures of Echinacea purpurea. J Natl Cancer Inst 1989;81:669-75.
4. Melchart D, Linde K, Worku F, et al. Immunomodulation with Echinacea-a systematic review of controlled clinical trials. Phytomedicine 1994;1:245-54.
5. Dorn M, Knick E, Lewith G. Placebo-controlled, double-blind study of Echinacea pallida redix in upper respiratory tract infections. Comp Ther Med 1997;5:40-2.
6. Blumenthal M, Hall T, Goldberg A, Kunz T, Dinda K (eds.). The ABC Clinical Guide to Herbs. Austin TX: American Botanical Council; 2003:88-96.
7. Brinkeborn RM, Shah DV, Degenring FH. Echinaforce and other Echinacea fresh plant preparations in the treatment of the common cold. A randomized, placebo controlled, double-blind clinical trial. Phytomedicine 1999; 6(1):1 6.
8. Melchart D, Walther E, Linde K, et al. Echinacea root extracts for the prevention of upper respiratory tract infections: A double-blind, placebo-controlled randomized trial. Arch Fam Med 1998;7:541-5.
9. Grimm W, Müller HH. A randomized controlled trial of the effect of fluid extract of Echinacea purpurea on the incidence and severity of colds and respiratory tract infections. Am J Med 1999;106:138-43.
10. Henneicke von Zepelin H, Hentschel C, Schnitker J, et al. Efficacy and safety of a fixed combination phytomedicine in the treatment of the common cold (acute viral respiratory tract infection): results of a randomised, double blind, placebo controlled, multicentre study. Curr Med Res Opin 1999; 15(3):214 27.
11. Brinkeborn RM, Shah DV, Degenring FH. Echinaforce and other Echinacea fresh plant preparations in the treatment of the common cold. A randomized, placebo controlled, double blind clinical trial. Phytomedicine 1999; 6(1):1 6.
12. Shah SA, Sander S, White CM, Rinaldi M, Coleman CI. Evaluation of Echinacea for the prevention and treatment of the common cold: a meta-analysis. The Lancet Infectious Diseases 2007; (7)7:473-480.
13. Blumenthal M (ed), et al. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines / CD version. Austin, Texas:American Botanical Council; 1998.
14. Mills S, Bone K. Principles and Practice of Phytotherapy. Edinburgh;Churchill Livingstone; 2000.
15. Blumenthal M, Hall T, Goldberg A, Kunz T, Dinda K (eds.). The ABC Clinical Guide to Herbs. Austin TX: American Botanical Council; 2003:88-96.
16. Blumenthal M, Hall T, Goldberg A, Kunz T, Dinda K (eds.). The ABC Clinical Guide to Herbs. Austin TX: American Botanical Council; 2003:88-96.
17. Jones K. Shiitake: The Healing Mushroom. Rochester, VT: Healing Arts Press, 1995.
18. Chang R. Functional properties of edible mushrooms. Nutr Rev 1996;54(11 Pt 2):S91-3.
19. Jones K. Shiitake” A major medicinal mushroom. Alt Compl Ther 1998;4:53-9.
20. Taguchi I. Clinical efficacy of lentinan on patients with stomach cancer: End point results of a four-year follow-up survey. Cancer Detect Prevent Suppl 1987;1:333-49.
21. Matsuoka H, Seo Y, Wakasugi H, et al. Lentinan potentiates immunity and prolongs survival time of some patients. Anticancer Res 1997;17:2751-6.
22. Ye SF, Ichimura K, Wakame K, Ohe M. Suppressive effects of Active Hexose Correlated Compound on the increased activity of hepatic and renal ornithine decarboxylase induced by oxidative stress. Life Sci 2003;74:593-602.
23. Ye SF, Ichimura K, Wakame K, Ohe M. Suppressive effects of Active Hexose Correlated Compound on the increased activity of hepatic and renal ornithine decarboxylase induced by oxidative stress. Life Sci 2003;74:593-602.
24. Kidd PM. The use of mushroom glucans and proteoglycans in cancer treatment. Altern Med Rev 2000;5(1):4-27.
25. Aviles H, O’Donnell P, Sun B, Sonnenfeld G. Active hexose correlated compound (AHCC) enhances resistance to infection in a mouse model of surgical wound infection. Surg Infect (Larchmt) 2006;7(6):527-35.
26. Terakawa N, Matsui Y, Satoi S, et al. Immunological effect of active hexose correlated compound (AHCC) in healthy volunteers: a double-blind, placebo-controlled trial. Nutr Cancer 2008;60(5):643-51.
27. Matsui Y, Uhara J, Satoi S, et al. Improved prognosis of postoperative hepatocellular carcinoma patients when treated with functional foods: a prospective cohort study. J Hepatol 2002;37(1):78-86.
28. Cowawintaweewat S, Manoromana S, Sriplung H, Khuhaprema T, Tongtawe P, Tapchaisri P, Chaicumpa W. Prognostic improvement of patients with advanced liver cancer after active hexose correlated compound (AHCC) treatment. Asian Pac J Allergy Immunol 2006;24(1):33-45.
29. Spierings EL, Fujii H, Sun B, Walshe T. A Phase I study of the safety of the nutritional supplement, active hexose correlated compound, AHCC, in healthy volunteers. J Nutr Sci Vitaminol (Tokyo) 2007;53(6):536-9.
30. Mach CM, Fugii H, Wakame K, Smith J. Evaluation of active hexose correlated compound hepatic metabolism and potential for drug interactions with chemotherapy agents. J Soc Integr Oncol 2008;6(3):105-9.

The post Echinacea & Shiitake for Immune Health appeared first on Total Health Magazine.

Glutathione absorption
As a dietary supplement, glutathione has had a rocky beginning due to perceived bioavailability problems. The reason for this is that, in the 1990s, some researchers pointed out that despite being present in fruits, vegetables, and meats, the levels of glutathione in the body do not seem to correlate to dietary intake; this suggested that oral GSH might be inactivated by peptidases in the gut.⁹ Also in the 1990s, one small study¹⁰ showed that there was no increase in blood GHS levels when seven healthy people were given a single application of up to 3,000 mg of glutathione. Consequently, other strategies were used to increase GSH levels, such as supplementation.

Fast forward to 2014. A new study¹¹ was published in the Journal of Agricultural and Food Chemistry, which helped put a new light on the old research. The new study demonstrated that intact GSH could be rapidly transported across intestinal epithelial cells. Then, the GSH was rapidly converted into oxidized glutathione (GSSG) and accumulated in red blood cells and the liver but was little present in plasma. So, to reiterate, the GSH was definitely absorbed (in fact very quickly) but didn’t show up in blood plasma since it was converted to GSSG and then stored in red blood cells and the liver. The take home message from this research is that supplementation with GSH is an effective way to increase GSH levels in the body.

Reasons to supplement with GSH
Now that you know that it is bioavailable, let’s talk about the reasons you may want to consider supplementing with GSH. Aside from the general functions of GSH listed in the first paragraph, there are studies demonstrating some specific beneficial effects of GSH supplementation. This includes its effectiveness as:

• part of the liver’s natural detoxification process,
• an agent to reduce UV-induced skin spots,
• a treatment for nonalcoholic fatty liver disease,
• a means of preventing muscle fatigue.

Detoxification
Liver cells have sophisticated mechanisms to break down potentially toxic substances, including both internal and external compounds. Every drug, chemical, pesticide, and hormone is broken down via two detoxification stages in your liver, which are known as phase I and phase II. During phase II, the toxin is attached or conjugated to a water-soluble substance. This attachment makes the toxic molecule more water-soluble, less harmful, and easier to get rid of via the urine or bile. Glutathione conjugation produces water-soluble mercaptates, which are excreted via the kidneys, and effectively detoxifies acetaminophen and nicotine. The elimination of fat-soluble compounds, especially heavy metals like mercury and lead, is dependent upon adequate levels of glutathione.¹² Likewise, GSH is used as a cofactor by multiple peroxidase enzymes, to detoxify peroxides generated from oxygen radical attack on biological molecules, and by transhydrogenase enzymes to reduce oxidized centers on DNA, proteins, and other biomolecules.¹³

UV-induced skin spots
UV-induced skin spots (aka, age spots or liver spots) are small dark areas on the skin, varying in size and usually appearing on the face, hands, shoulders and arms-areas most exposed to the sun and its UV rays. They’re caused by overactive pigment cells. Ultraviolet (UV) light accelerates the production of melanin. On the areas of skin that have had years of frequent and prolonged sun exposure, age spots appear when melanin becomes “clumped” or is produced in high concentrations.¹⁴ To determine whether supplementing with 500 mg of glutathione daily for four weeks, affects the skin melanin index compared with placebo, a randomized, double-blind, two-arm, placebo-controlled study¹⁵ was conducted with 60 otherwise healthy medical students. Melanin indices were measured at six different sites on the body. Results were that, at four weeks, melanin indices decreased consistently at all six sites in subjects who received glutathione. The reductions were statistically significantly greater than those receiving placebo at two sites, namely the right side of the face and the sun-exposed left forearm (p = 0.021 and 0.036, respectively). This was similarly reflected in the changes in the number of UV spots. Both glutathione and placebo were very well tolerated. In conclusion, oral glutathione administration results in a lightening of skin color in the subjects tested.

Nonalcoholic fatty liver disease
Nonalcoholic fatty liver disease (NAFLD) refers to the accumulation of fat in the liver of people who drink little or no alcohol. Unfortunately, NAFLD is common-with easily one-third of all American adults being affected¹⁶-and often causes no signs and symptoms, and sometimes no complications. In more serious cases, however, the fat that accumulates in NAFLD can cause liver inflammation and scarring.¹⁷ In addition, NAFLD is usually associated with insulin resistance, central obesity, reduced glucose tolerance, type-2 diabetes and high triglyceride levels. Given the crucial roles of GSH in phase 2 liver detoxification, an open label, single arm, multicenter, pilot trial¹⁸ was conducted to examine the therapeutic effects of GSH supplementation (300 mg/day) in 29 patients with NAFLD. Clinical parameters were evaluated before and after GSH supplementation. Liver fat and fibrosis were also quantified. The primary outcome of the study was the change in alanine aminotransferase (ALT) levels. Results were that ALT levels significantly decreased. Triglycerides, non-esterified fatty acids, and ferritin levels also decreased. This pilot study demonstrates the potential therapeutic effects of oral administration of glutathione in practical dose for patients with NAFLD. Large-scale clinical trials are needed to verify its efficacy.

Muscle fatigue
A study¹⁹ in mice and humans investigated the effect of GSH intake on muscle metabolism and fatigue induced by exercise. In the mouse experiment, mice were divided into four different groups: sedentary, sedentary treated with GSH, exercise, and exercise treated with GSH. After two weeks of treatment, results showed that GSH improved fat metabolism and reduced acidification in the muscles during exercise. Of particular importance is that mitochondria DNA significantly increased. Mitochondria are the “energy factories” in cells that produce ATP, the muscles energy molecule. This indicates that GSH stimulated the production of new mitochondria. In the double-blind, crossover human study, eight healthy men supplemented with 1,000 mg GSH or placebo for two weeks, and then performed cycling ergometer for 60 minutes. Psychological tests and blood biochemical parameters were examined after exercise. Results were that blood lactic acid levels were suppressed by GSH, and psychological factors related to fatigue were significantly decreased with GSH compared with placebo. These results suggest that GSH improved fat metabolism and acidification in muscle during exercise, which leads to the decrease of muscle fatigue.

Conclusion
GSH is a tripeptide of paramount importance for a wide variety of functions in the body. Despite previous misconceptions to the contrary, it is now understood that supplemental GSH is bioavailable and will increase GSH levels in the body. Research has demonstrated the effectiveness of GSH as a part of the liver’s natural detoxification process, an agent to reduce UV-induced skin spots, a treatment for nonalcoholic fatty liver disease, and a means of preventing muscle fatigue.

References

1. Franco R, Schoneveld OJ, Pappa A, Panayiotidis MI. The central role of glutathione in the pathophysiology of human diseases. Arch Physiol Biochem. 2007 Oct-Dec;113(4-5):234-58.
2. Forman HJ, Zhang H, Rinna A. Glutathione: overview of its protective roles, measurement, and biosynthesis. Mol Aspects Med. 2009 Feb-Apr;30(1-2):1-12.
3. Anderson ME. Glutathione: an overview of biosynthesis and modulation. Chem Biol Interact 1998;24;111-112:1-14.
4. Lu SC. Regulation of hepatic glutathione synthesis: current concepts and controversies. FASEB J 1999;13:1169-83.
5. Lomaestro BM, Malone M. Glutathione in health and disease: pharmacotherapeutic issues. Ann Pharmacother 1995;29:1263-73.
6. Powers SK, Hamilton K. Antioxidants and exercise. Clin Sports Med 1999;18:525-36.
7. Hong SY, Gil HW, Yang JO, Lee EY, Kim HK, Kim SH, Chung YH, Hwang SK, Lee ZW. Pharmacokinetics of glutathione and its metabolites in normal subjects. J Korean Med Sci. 2005 Oct;20(5):721-6.
8. Glutathione, Reduced (GSH) Monograph. Altern Med Review. 2001;6(6):601-7.
9. Lomaestro BM, Malone M. Glutathione in health and disease: pharmacotherapeutic issues. Ann Pharmacother 1995;29:1263-73.
10. Witschi A, Reddy S, Stofer B, Lauterburg BH. The systemic availability of oral glutathione. Eur J Clin Pharmacol 1992;43:667-9.
11. Kovacs-Nolan J, Rupa P, Matsui T, Tanaka M, Konishi T, Sauchi Y, Sato K, Ono S, Mine Y. In vitro and ex vivo uptake of glutathione (GSH) across the intestinal epithelium and fate of oral GSH after in vivo supplementation. J Agric Food Chem. 2014 Oct 1;62(39):9499-506.
12. Liska D, Lynon M, Jones DS. Detoxification and Biotransformational Imbalances. In: Jones DS, Ed. Textbook of Functional Medicine. Gig Harbor, WA: Institute for Functional Medicine; 2006:275-298.
13. Glutathione, Reduced (GSH) Monograph. Altern Med Review. 2001;6(6):601-7.
14. May Clinic Staff.Age spots (liver spots). May Clinic. March 6, 2018. Retrieved September 24, 2019.
15. Arjinpathana N, Asawanonda P. Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study. J Dermatolog Treat. 2012 Apr;23(2):97-102.
16. Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, Grundy SM, Hobbs HH. Prevalence of hepatic steatosis in an urban population in the United States: Impact of ethnicity. Hepatology 2004;40(6):1387-1395.
17. Sanyal AJ. American Gastroenterological Association: AGA technical review on nonalcoholic fatty liver disease (national guidelines). Gastroenterology 2002; 123:1705-1725.
18. Honda Y, Kessoku T, Sumida Y, et al. Efficacy of glutathione for the treatment of nonalcoholic fatty liver disease: an open-label, single-arm, multicenter, pilot study. BMC Gastroenterol. 2017 Aug 8;17(1):96.
19. Aoi W, Ogaya Y, Takami M, Konishi T, Sauchi Y, Park EY, Wada S, Sato K, Higashi A. Glutathione supplementation suppresses muscle fatigue induced by prolonged exercise via improved aerobic metabolism. J Int Soc Sports Nutr. 2015 Feb 6;12:7.

The post Glutathione: A Tripeptide of Paramount Importance 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.

The post Understanding DHEA and 7-Keto DHEA appeared first on Total Health Magazine.

Children’s exposure to blue light
More than 70 percent of American adults report their children receive more than two hours of screen time per day-and among the most popular activities children engage in are playing on a digital device (23.1 percent) and watching TV (20.1 percent). Not surprisingly, American adults report their children experience the following after being exposed to two or more hours of screen time:²¹

• Headaches (8.8%)
• Neck/shoulder pain (5%)
• Eye strain, dry or irritated eyes (9.1%)
• Reduced attention span (15.2%)
• Poor behavior (13.3%)
• Irritability (13.5%)

Now consider that personal electronic devices are able to stimulate blue-light-sensitive ganglion cell photoreceptors that regulate circadian rhythms.²² As a result, cellular telephone, tablet and personal computer use before bedtime can delay sleep onset, degrade sleep quality and impair alertness the following day.²³ Extended use of these devices has also been shown to cause symptoms of dry eyes, blurred vision and headaches.²⁴ Limitation of personal electronic device use before bedtime is recommended to be the most effective method for reducing light-induced sleep disruption in children.

The importance of lutein and zeaxanthin isomers
So besides restricting digital device us, what can concerned parents do to help protect their children’s eyes from damaging blue light? Enter lutein and zeaxanthin isomers (rr- and rs-(meso)-zeaxanthin). These carotenoids (related to beta-carotene and lycopene) are found in high concentrations in the part of the retina where they play a critical role in protecting against blue light.²⁵ Furthermore, supplementation with lutein and zeaxanthin isomers can provide substantial protection against blue light damage.

Of all the carotenoids, only lutein and zeaxanthin isomers are located in the eye, and make up the macular pigment. As a result of these carotenoids being yellow, they selectively absorb blue light, which protects the retina from associated damage. In short, they act as primary filters of blue light.

However, the average daily intake of lutein and zeaxanthin in the U.S. is less than 2 mg and less than 0.5 mg, respectively-which is far below the 10-20 mg of lutein and 2-4 mg of zeaxanthin shown in research to be beneficial. That’s why supplementation with these carotenoids is so important.

Eye strain, eye fatigue, headache and visual performance

A study conducted at the University of Georgia showed a relationship between exposure to blue light from digital devices and visual performance. They found that supplementing with lutein and zeaxanthin isomers (as Lutemax® 2020 from OmniActive Health Technologies) reduced headaches, eye fatigue, and eye strain. Another double-blind, placebo-controlled, 12-month trial^26,27,28 examined the effects of lutein and zeaxanthin isomers (as Lutemax® 2020) versus placebo. Two levels of daily lutein supplementation were used: 10 mg (2 mg Z), and 20 mg (4 mg Z). The results were that both doses significantly improved contrast sensitivity (CS), glare performance, and photo stress recovery (i.e. a clinical procedure measuring the amount of time required for the macula to return to its normal level of function after being exposed to a bright light source). In addition, lutein/zeaxanthin improved levels of BDNF, a neurotrophin that is particularly active in hippocampus, cortex, and basal forebrain-areas that are involved in learning, memory, and higher cognitive processes.²⁹

Stress and health
Another 12-week, double-blind, placebo-controlled trial30 was conducted at the University of Georgia in 28 healthy subjects using three different daily dosage levels of lutein and zeaxanthin isomers (as Lutemax® 2020) versus placebo. The three doses of lutein were 6 mg (1.5 mg Z), 10 mg (2 mg Z), and 20 mg (4 mg Z), versus placebo. The results were that supplementation with lutein/zeaxanthin isomers increased the amount of optical pigment density (greater increase with higher doses), which helped subjects maintain a lower psychological stress profile (p = 0.0087). After 12 weeks of lutein supplementation, psychological stress levels were found to be reduced significantly. The placebo group did not change in this regard. Furthermore, those with higher optical pigment density tended to have fewer health-related problems, such as being sick less often and suffering less from allergies (p = 0.002). After 12 weeks of lutein supplementation, each group exhibited a significant reduction in health-related problems (6 mg: p = 0.041; 10 mg: p = 0.029; 20 mg: p = 0.047).

Quality of sleep
The primary function of melatonin, a hormone, secreted by the pineal gland,³¹ is regulation of the body’s circadian rhythm, and sleep patterns.^32,33 However, too much light exposure, particularly at night, can inhibit melatonin secretion and interfere with sleep.^34,35 Even blue light from smart phones can negatively impact sleep with nighttime exposure.³⁶ But lutein and zeaxanthin isomers can help. A 3-month, double-blind, placebo-controlled trial with 45 healthy individuals (the first of a two-part study³⁷) found that 20 mg lutein and 4 mg zeaxanthin isomers daily (as Lutemax® 2020) significantly improved overall sleep quality (p = 0.0063), with no changes in the placebo group. The second 6-month, double-blind, placebo-controlled trial in 34 healthy individuals found similar results.

Delivery forms
Generally, lutein/zeaxanthin isomers are readily available as capsule or tablet supplements for adults. Children, however, cannot easily swallow capsules or tablets. Consequently, chewable tablets or gummies are preferable lutein/zeaxanthin isomer delivery forms for children. Gummies, in particular, are likely the best choice as children tend to see gummies as a treat, rather than treatment-so to speak.

Conclusion
Blue light, especially from digital devices, has the potential to damage retinal tissue and cause a variety of eye-related problems, including eye strain, eye fatigue, headache, visual impairment, psychological stress, and poor sleep quality. This is particularly true in children since their eyes absorb more blue light than adults. The good news is that daily supplementation with lutein (10-20 mg) and zeaxanthin isomers (2-4 mg)-most likely in a gummy supplement-can help reduce these risks and support eye health.

References

1. Nakashima Y, Ohta S1, Wolf AM2. Blue light-induced oxidative stress in live skin. Free Radic Biol Med. 2017 Mar 15. pii: S0891-5849(17)30134-X.
2. Tosini G, Ferguson I, Tsubota K. Effects of blue light on the circadian system and eye physiology. Mol Vis. 2016 Jan 24;22:61-72.
3. The Vision Council. Eyes Overexposed: The Digital Device Dilemma. 2016 Digital Eye Strain Report. Thevisioncouncil.org.
4. The Vision Council. Hindsight is 20/20/20: Protect your eyes from digital devices. 2015 Digital Eye Strain Report. Thevisioncouncil.org.
5. Smick K, et al. Blue Light Hazard: New Knowledge, New Approaches to Maintaining Ocular Health. Report of a Roundtable: March 16, 2013, New York City, NY, USA. Essilor of America.
6. Kuse Y, Ogawa K, Tsruma K, Shimazawa M, Hara H. Damage of photoreceptor-derived cells in culture induced by light emitting diode-derived blue light. Sci Rep. 2014 Jun 9;4:5223.
7. Tosini G, Ferguson I, Tsubota K. Effects of blue light on the circadian system and eye physiology. Mol Vis. 2016 Jan 24;22:61-72.
8. Wu J, Seregard S, Algvere PV. Photochemical damage of the retina. Surv Ophthalmol. 2006 Sep-Oct;51(5):461-81.
9. Algvere PV, Marshall J, Seregard S. Age-related maculopathy and the impact of blue light hazard. Acta Ophthalmol Scand. 2006 Feb;84(1):4-15.
10. Scientific Committee on Emerging and Newly Identified Health Risks (SCENIHR). 2012. Health Effects of Artificial Light. Accessed from http://ec.europa.eu/health/scientific_committees/emerging/docs/scenihr_o_035.pdf.
11. Cruickshanks KJ, Klein R, Klein BEK. Sunlight and age-related macular degeneration-the Beaver Dam Eye Study. Arch Ophthalmol. 1993;111:514-8.
12. Klein R, Klein BEK, Jensen SC, Cruickshanks KJ. The relationship of ocular factors to the incidence and progression of age-related maculopathy. Arch Ophthalmol. 1998;116:506-13.
13. Algvere PV, Marshall J, Seregard S. Age-related maculopathy and the impact of blue light hazard. Acta Ophthalmol Scand. 2006;84:4-15.
14. Taylor HR, Muñoz B, West S, Bressler NM, Bressler SB, Rosenthal FS. Visible light and risk of age-related macular degeneration. Trans Am Ophthalmol Soc. 1990;88:163-73.
15. Kowalska M, Zejda JE, Bugajska J, Braczkowska B, Brozek G, Mali?ska M. [Eye symptoms in office employees working at computer stations]. [Article in Polish] Med Pr. 2011;62(1):1-8.
16. Tomany SC, Cruickshanks KJ, Klein R, Klein BE, Knudtson MD. Sunlight and the 10-year incidence of age-related maculopathy: the Beaver Dam Eye Study. Arch Ophthalmol. 2004;122:750-7.
17. Cruickshanks KJ, Klein R, Klein BE, Nondahl DM. Sunlight and the 5-year incidence of early age-related maculopathy: the beaver dam eye study. Arch Ophthalmol. 2001;119:246-50.
18. Akinbinu TR, Mashalla YJ. Impact of computer technology on health: Computer Vision Syndrome (CVS). Medical Practice and Review. 2014;5(3):20-30.
19. Boettner EA, Wolter JR. Transmission of the Ocular Media. Investigative Ophthalmology 1962;1:776-83.
20. Behar-Cohen F, Martinsons C, Viénot F, Zissis G, Barlier-Salsi A, Cesarini JP, Enouf O, Garcia M, Picaud S, Attia D. Light-emitting diodes (LED) for domestic lighting: any risks for the eye? Prog Retin Eye Res. 2011 Jul;30(4):239-57.
21. Digital Eye Strain. The Vision Council. Retrieved February 19, 2019 from https://www.thevisioncouncil.org/content/digital-eye-strain.
22. Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science 2002;295:1070-3.
23. Chang AM, Aeschbach D, Duffy JF, Czeisler CA. Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proc Natl Acad Sci U S A 2015;112:1232-7.
24. Klamm J, Tarnow KG. Computer Vision Syndrome: A Review of Literature. Medsurg Nurs 2015;24:89-93.
25. Bone RA. Landrum JT. Distribution of macular pigment components, zeaxanthin and lutein, in human retina. Methods Enzymol 1992:213:360-6.
26. Stringham JM, O’Brien KJ, Stringham NT. Macular carotenoid supplementation improves disability glare performance and dynamics of photo stress recovery. Eye Vis (Lond). 2016 Nov 11;3:30.
27. Stringham NT, Holmes PV, Stringham JM. Supplementation with macular carotenoids reduces psychological stress, serum cortisol, and sub-optimal symptoms of physical and emotional health in young adults. Nutr Neurosci. 2017 Feb 15:1-11.
28. Contrast sensitivity – Accepted (IOVS) in press.
29. Stringham NT et al. Macular Carotenoid Supplementation Increases Serum BDNF in Healthy Young Adults. EB Abstract 2016.
30. Stringham J. Effects of three levels of lutein supplementation on macular pigment optical density, psychological stress levels, and overall health. Nutritional Neuroscience Laboratory, University of Georgia. Unpublished. 2016:17 pgs.
31. Nurnberger JI Jr, Adkins S, Lahiri DK, et al. Melatonin suppression by light in euthymic bipolar and unipolar patients. Arch Gen Psychiatr 2000;57:572-9.
32. Brzezinski A. Melatonin in humans. N Engl J Med 1997;336:186-95.
33. Lissoni P, Barni S, Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854-6.
34. Brzezinski A. Melatonin in humans. N Engl J Med 1997;336:186-95.
35. Daneault V, Dumont M, Massé É, Vandewalle G, Carrier J. Light-sensitive brain pathways and aging. J Physiol Anthropol. 2016 Mar 15;35:9.
36. Yoshimura M, Kitazawa M, Maeda Y, Mimura M, Tsubota K, Kishimoto T. Smartphone viewing distance and sleep: an experimental study utilizing motion capture technology. Nat Sci Sleep. 2017 Mar 8;9:59-65.
37. Stringham JM et al. Short-term macular carotenois supplementation improves overall sleep quality. ARVO 2016 Annual Meeting Abstracts.

The post Lutein & Zeaxanthin: Eye Health Protectors for Your Children appeared first on Total Health Magazine.

WHAT IS IT?
Vitamin C, also known as ascorbic acid, is a water-soluble micro-nutrient. Human beings cannot manufacture their own vitamin C and must rely on outside sources, including food and supplements, to obtain it. Other forms of vitamin C, which may be found in supplements include, ascorbyl palmitate (a fat-soluble form) and mineral ascorbates such as calcium ascorbate.

Vitamin C is found in different fruits and vegetables. Although the vitamin C content varies depending upon the produce,¹ about five servings (2½ cups) of fruits and vegetables should average out to about 200 mg of vitamin C. Rich sources of vitamin C include sweet red peppers, strawberries, orange juice, grapefruit juice, oranges, and broccoli. Other good sources include grapefruit, tomatoes and potato.

WHAT DOES IT DO?
Vitamin C is best known for its role in the synthesis of collagen, a connective tissue protein used as a structural component of blood vessels, tendons, ligaments, and bone. A deficiency of vitamin C leads to the deficiency disease “scurvy,” characterized by insufficient collagen production. This water-soluble vitamin is also needed for the synthesis of: 1) the neurotransmitter norepinephrine, which performs critical brain function including an effect on mood, and 2) the amino acid carnitine, which is essential for the transport of fat into cellular mitochondria, where the fat is converted to energy or ATP.² Vitamin C may also be involved in the metabolism of cholesterol to bile acids, which may be important for blood cholesterol levels and the incidence of gallstones.³

Another significant function of vitamin C is the important role it plays as an antioxidant, protecting vital molecules in the body from damage by free radicals and reactive oxygen species. These molecules include proteins, lipids (fats), carbohydrates, and nucleic acids (DNA and RNA). Vitamin C also plays a complementary role with other antioxidants, such as vitamin E, helping to regenerate them from their oxidized form back into their reduced (active) form.^4,5

Vitamin C also plays a profound role in the health of the immune system, stimulating the production and function of white blood cells, including leukocytes, neutrophils, lymphocytes and phagocytes.^{6,7,8,9,10,11,12} In addition, research has demonstrated that supplemental vitamin C increases serum levels of antibodies^13,14 and C1q complement proteins.^15,16,17 Also, vitamin C has been shown to increase interferon levels in vitro,¹⁸ and research on supplemental vitamin C and the common cold suggests that it promotes an antiviral effect in humans.¹⁹

WHO SHOULD USE IT?
Given that humans do not make any vitamin C themselves, everyone would do well to supplement with vitamin C. This is especially true during times when additional immune support is desirable—such as during cold and flu season.

DOSAGE/TIMING
The RDA for vitamin C is 90 mg for men and 75 mg for women. The RDA for men and women smokers is 125 mg and 110 mg, respectively. However, studies conducted at the National Institutes of Health indicated that plasma and circulating cells in healthy subjects attain near-maximal concentrations of vitamin C at a dose of about 400 mg/day—a dose much higher than the current RDA.²⁰ This suggests that a daily intake of 400 mg is advisable.

Vitamin C can be taken with or without food, so the timing is not critical.

ADVERSE REACTIONS/ INTERACTIONS
An adult dose of up to 10 grams of vitamin C daily has not been found to be toxic or detrimental to health. High dose of vitamin C, however, may induce diarrhea. The concept of “bowel tolerance” describes utilizing vitamin C in amounts just short of the doses, which produce diarrhea.²¹ The Food and Nutrition Board recommends an upper limit of 2,000 mg daily in order to prevent most adults from experiencing diarrhea and gastrointestinal disturbances.²²

There is some controversial evidence that high doses of vitamin C (16 grams/day) reduced the response to warfarin in two people,^23,24 possibly by causing diarrhea and reducing warfarin absorption.²⁵ To be safe, individuals on anticoagulants should limit their vitamin C intake to 1 gram/day.

CONCLUSION
In conclusion, vitamin C performs several important roles in the body. It is necessary for the synthesis of the structural protein collagen, needed for blood vessels, tendons, ligaments, and bone, as well as for the synthesis of the neurotransmitter norepinephrine, which affects mood. Vitamin C is also necessary for the synthesis of the amino acid carnitine, which is essential for fat transport and energy production. This critical nutrient may be involved in the metabolism of cholesterol to bile acids and provides significant antioxidant protection against free radicals. Finally, vitamin C plays a profound role in the health of the immune system, stimulating the production and function of white blood cells.

Endnotes

1. U.S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Release 22. 2009. Available at: http://www.nal.usda.gov/fnic/foodcomp/search/.
2. Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Am J Clin Nutr. 1999;69(6):1086–107.
3. Simon JA, Hudes ES. Serum ascorbic acid and gallbladder disease prevalence among US adults: the Third National Health and Nutrition Examination Survey (NHANES III). Arch Intern Med. 2000;160(7):931–6.
4. See note 2 above.
5. Bruno RS, Leonard SW, Atkinson J, et al. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radic Biol Med. 2006;40(4):689–97.
6. Prinz W, Bortz R, Bregin B, Hersch M. The effect of ascorbic acid supplementation on some parameters of the human immunological defense system. Int J Vitam Nutr Res. 1977;47(3):248–57.
7. Vallance S. Relationships between ascorbic acid and serum proteins of the immune system. Br Med J. 1977;2(6084):437–438.
8. Kennes B, Dumont I, Brohee D, Hubert C, Neve P. Effect of vitamin C supplements on cell-mediated immunity in old people. Gerontology. 1983;29(5):305–10.
9. Panush RS, Delafuente JC, Katz P, Johnson J. Modulation of certain immunologic responses by vitamin C. III. Potentiation of in vitro and in vivo lymphocyte responses. Int J Vitam Nutr Res Suppl. 1982;23:35–47.
10. Jariwalla RJ, Harakeh S. Antiviral and immunomodulatory activities of ascorbic acid. In: Harris JR (ed). Subcellular Biochemistry. Vol. 25. Ascorbic Acid: Biochemistry and Biomedical Cell Biology. New York: Plenum Press; 1996:215–31.
11. Levy R, Shriker O, Porath A, Riesenberg K, Schlaeffer F. Vitamin C for the treatment of recurrent furunculosis in patients with impaired neutrophil functions. J Infect Dis. 1996;173(6):1502–5.
12. Anderson R, Oosthuizen R, Maritz R, Theron A, Van Rensburg AJ. The effects of increasing weekly doses of ascorbate on certain cellular and humoral immune functions in normal volunteers. Am J Clin Nutr. 1980;33(1):71–6.
13. Prinz W, Bloch J, Gilich G, Mitchell G. A systematic study of the effect of vitamin C supplementation on the humoral immune response in ascorbate-dependent mammals. I. The antibody response to sheep red blood cells (a T-dependent antigen) in guinea pigs. Int J Vitam Nutr Res. 1980;50(3):294–300.
14. Feigen GA, Smith BH, Dix CE, et al. Enhancement of antibody production and protection against systemic anaphylaxis by large doses of vitamin C. Res Commun Chem Pathol Pharmacol. 1982;38(2):313–33.
15. Haskell BE, Johnston CS. Complement component C1q activity and ascorbic acid nutriture in guinea pigs. Am J Clin Nutr. 1991;54(6 Suppl):1228S–30S.
16. Johnston CS, Cartee GD, Haskell BE. Effect of ascorbic acid nutriture on protein-bound hydroxyproline in guinea pig plasma. J Nutr. 1985;115(8):1089–93.
17. Johnston CS, Kolb WP, Haskell BE. The effect of vitamin C nutriture on complement component C1q concentrations in guinea pig plasma. J Nutr. 1987;117(4):764–8.
18. Dahl H, Degre M. The effect of ascorbic acid on production of human interferon and the antiviral activity in vitro. Acta Pathol Microbiol Scand B. 1976;84B(5):280–4.
19. Sasazuki S, Sasaki S, Tsubono Y, Okubo S, Hayashi M, Tsugane S. Effect of vitamin C on common cold: randomized controlled trial. Eur J Clin Nutr. 2006;60(1):9–17.
20. Higdon J, Drake VJ. Vitamin C. Linus Pauling Institute, Oregon State University. 2006-2009. Retrieved June 15, 2011 from http://lpi.oregonstate.edu/infocenter/vitamins/vitaminC/index.html#lpi_recommend.
21. Cathcart RF. Vitamin C, titrating to bowel tolerance, anascorbemia, and acute induced scurvy. Med Hypotheses. 1981;7(11):1359–76.
22. Food and Nutrition Board, Institute of Medicine. Vitamin C. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington D.C.: National Academy Press; 2000:95–185.
23. Rosenthal G. Interaction of ascorbic acid and warfarin. JAMA 1971;215:1671.
24. Smith EC, Skalski RJ, Johnson GC, Rossi GV. Interaction of ascorbic acid and warfarin. JAMA 1972;221:1166.
25. Feetam CL, Leach RH, Meynell MJ. Lack of a clinically important interaction between warfarin and ascorbic acid. Toxicol Appl Pharmacol 1975;31:544–7.

The post An Overview Of Vitamin C appeared first on Total Health Magazine.

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.

About Inflammation

Let’s start with a brief review about inflammation, a useful natural reaction that the body has in response to injury and certain other conditions. Chronic inflammation, however, can be more destructive than beneficial and is a major component in many human diseases. Furthermore, it must be understood that chronic inflammation isn’t just associated with disease states. In fact, higher intakes of red and processed meats, sweets, desserts, French fries, and refined grains are associated with experiencing more inflammation,¹ as is exposure to colder temperatures (i.e. colder climates).²

Since prolonged inflammation is detrimental to the host, higher organisms have evolved protective mechanisms to ensure resolution of the inflammatory response in a limited and specific time-and space-manner. Once thought as a mere passive process of dilution of inflammation, resolution is today envisioned as a highly orchestrated process coordinated by a complex regulatory network of cells and mediators.³

Pro-resolving Mediators
Among the molecules that facilitate resolution of inflammation, resolvins, protectins, and maresins produced from O3FA are the lipid mediators which are particularly important. These internally produced anti-inflammatory and pro-resolving mediators counteract the effects of proinflammatory signaling systems and act as “braking signals” of the persistent vicious cycle leading to unremitting inflammation.

In fact, the same pro-inflammatory factors that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of pro-resolving mediators. Resolvins, protectins and maresins and have been shown to reduce airway inflammation, dermal inflammation colitis, arthritis, and postoperative pain. Studies have shown that these mediators increase with time during the inflammatory process.^4,5,6

DHA The most well-known O3FA are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). While these two O3FA can be used to generate resolvins, there is another O3FA called docosapentaenoic acid (DPA), which is a particularly effective precursor to different resolvins.⁷ DPA is an intermediate in the biosynthesis of DHA from EPA. In any case, DPA is not always seen in omega-3 fatty acid products. It can, however, be found in some cod liver oil products.

Cod Liver Oil And Inflammation

It should be noted that cod liver oil is a natural source of vitamins A and D, in addition to O3FA. This is significant since maintaining healthy vitamin D levels is necessary for supporting cardiovascular health,^8,9,10,11 and vitamin D plays an important role in healthy skin and in regulating a healthy immune system.¹² Furthermore, some cod liver oil products are a direct source of pro-resolving mediators. Not surprisingly, cod liver oil has shown value for its anti-inflammatory effects.

A study¹³ was conducted to compare the effects of supplementation with either sunflower oil (source of omega-6) or cod liver oil (source of omega-3) oil, in rates with inflammatory colitis. Inflammatory markers increased in rats fed sunflower oil but was blunted in rats fed cod liver oil. In fed cod liver oil group, the damage score was markedly reduced by day 30, and inflammation and ulceration were almost absent by day 50.

A 9-month, double-blind, placebo-controlled, randomized human study¹⁴ was conducted in 58 patients with rheumatoid arthritis (RA) to determine whether cod liver oil supplementation would help reduce daily NSAID (pain medication) requirement. Patients took either 10 g of cod liver oil containing or identical placebo capsules. Documentation of NSAID daily requirement, clinical and laboratory parameters of RA disease activity, and safety checks were done at 0, 4, 12, 24 and 36 weeks. At 12 weeks, patients were instructed to gradually reduce, and if possible, stop their NSAID intake. Results were that 39 percent of patients in the cod liver oil group and 10 percent of patients in the placebo group were able to reduce their daily NSAID requirement by more than 30 percent. Researchers concluded that cod liver oil supplements containing n-3 fatty acids can be used as NSAID-sparing agents in RA.

Cod Liver Oil and Beauty
In addition to inflammation, cod liver oil may also have a “beauty from within” application. Here’s the rationale. O3FA have been shown to help reduce the visible signs of aging, and support cell rejuvenation. In one study, a diet providing as little as 295 mg/day of EPA was shown to decrease the risk in photoaging (i.e. more rapidly aged skin due to sun exposure) in women.¹⁵ In addition, vitamin D has been shown to play an important role in maintaining healthy hair due to its relationship with vitamin D receptors in hair follicles.^16,17,18 Given that cod liver oil is a natural source of both O3FA and vitamin D, it may serve as an ideal supplement for the skin and hair.

Conclusion
Due to its naturally occurring EPA, DHA, DPA, and pro-resolving mediators, cod liver oil is an ideal supplement for helping to reduce inflammation. Furthermore, it is a natural source of vitamins A and D; and may also have “beauty from within” applications. That being said, if you’re going to use a cod liver oil supplement, it is important to use a clean product. I suggest looking for supplements from cod from Alaskan waters (a more pristine area) that are line-caught and flash-frozen to preserve freshness.

References:

1. Lopez-Garcia E, Schulze MB, Fung TT, Meigs JB, Rifai N, Manson JE, Hu FB. Major dietary patterns are related to plasma concentrations of markers of inflammation and endothelial dysfunction. Am J Clin Nutr. 2004 Oct;80(4):1029–35.
2. Halonen JI, Zanobetti A, Sparrow D, Vokonas PS, Schwartz J. Associations between outdoor temperature and markers of inflammation: a cohort study. Environ Health. 2010 Jul 23;9:42.
3. Clària J. Resolution of Acute Inflammation and the Role of Lipid Mediators. Scientific World Journal. 2010; 10:1553–5.
4. Recchiuti A, Serhan CN. Pro-resolving lipid mediators (SPMs) and their actions in regulating miRNA in novel resolution circuits in inflammation. Front Immunol. 2012 Oct 22;3:298.
5. Serhan CN. Novel Pro-Resolving Lipid Mediators in Inflammation Are Leads for Resolution Physiology. Nature. 2014 Jun 5; 510(7503): 92–101.
6. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 November 12; 107(10): 1170–84.
7. Primdahl KG, Aursnes M, Walker ME, Colas RA, Serhan CN, Dalli J, Hansen TV, Vik A. Synthesis of 13(R)-Hydroxy- 7Z,10Z,13R,14E,16Z,19Z Docosapentaenoic Acid (13R-HDPA) and Its Biosynthetic Conversion to the 13-Series Resolvins. J Nat Prod. 2016 Oct 28;79(10):2693–2702.
8. Wang TJ, Pencina MJ, Booth SL, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008;117;503–11.
9. Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels with all-cause and cardiovascular mortality. Arch Intern Med 2008;168:1340–49.
10. Giovannucci E, Liu Y, Hollis BW, Rimm EB. 25-hydroxyvitamin D and risk of myocardial infarction in men. Arch Intern Med 2008;168:1174–80.
11. Martins D, Wolf M, Pan D, et al. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin D in the United States. Arch Intern Med 2007;167:1159–65.
12. Institute of Medicine. Food and Nutrition Board. Vitamin A. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC; 2001:82–161.
13. Vilaseca J, Salas A, Guarner F, Rodríguez R, Martínez M, Malagelada JR. Dietary fish oil reduces progression of chronic inflammatory lesions in a rat model of granulomatous colitis. Gut. 1990 May;31(5):539–44.
14. Galarraga B, Ho M, Youssef HM, Hill A, McMahon H, Hall C, Ogston S, Nuki G, Belch JJ. Cod liver oil (n-3 fatty acids) as an nonsteroidal anti-inflammatory drug-sparing agent in rheumatoid arthritis. Rheumatology (Oxford). 2008 May;47(5):665–9.
15. Latreille J, Kesse-Guyot E, Malvy D, Andreeva V, Galan P, Tschachler E, Hercberg S, Guinot C, Ezzedine K. Association between dietary intake of n-3 polyunsaturated fatty acids and severity of skin photoaging in a middle-aged Caucasian population. J Dermatol Sci. 2013 Dec;72(3):233–9.
16. Daroach M1, Narang T, Saikia UN, Sachdeva N, Sendhil Kumaran M. Correlation of vitamin D and vitamin D receptor expression in patients with alopecia areata: a clinical paradigm. Int J Dermatol. 2018 Feb;57(2):217–222.
17. Gerkowicz A, Chyl-Surdacka K, Krasowska D, Chodorowska G. The Role of Vitamin D in Non- Scarring Alopecia. Int J Mol Sci. 2017 Dec 7;18(12).
18. Cheung EJ, Sink JR, English Iii JC. Vitamin and Mineral Deficiencies in Patients With Telogen Effluvium: A Retrospective Cross-Sectional Study. J Drugs Dermatol. 2016 Oct 1;15(10):1235–37.

The post Cod Liver Oil – The Inflammation And Beauty Connection appeared first on Total Health Magazine.