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.
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These symptoms could be a sign that you are iron deficient. You may be surprised to learn that iron deficiency is the most common and widespread nutritional deficiency in the world. It is estimated that two billion people are anemic, many due to iron deficiency.

Who is at Risk?
Why is iron deficiency such a worldwide problem? As it turns out many health conditions can seriously deplete iron levels. Iron deficiency is especially prevalent amongst menstruating women or women who have excessive blood loss from heavy periods, pregnant and postpartum women, people with conditions that cause internal bleeding, vegans and vegetarians, children, athletes, and the elderly.

In addition, anyone having intestinal health issues such as leaky gut, ulcerative colitis, Irritable Bowel Syndrome, Celiac disease or ulcers are especially vulnerable to low iron levels because of a compromised ability to absorb adequate iron from their diet.

Rheumatoid arthritis and anemia are connected. RA can be associated with different types of anemia, including anemia of chronic inflammation and iron deficiency anemia. When you have an RA flare-up, the immune response causes inflammation in the joints and other tissues. Chronic inflammation can lower the production of red blood cells in your bone marrow. This can lead to the release of certain proteins that affect how the body uses iron.

What Causes Iron Deficiency?
Deficiency occurs when the body doesn’t have enough of these vital minerals. Iron is essential in order to make hemoglobin, which is a protein in your red blood cells that carries oxygen to your body’s organs and tissues and transports carbon dioxide from your organs and tissues back to your lungs.

When iron intake is chronically low, stores can become depleted, decreasing hemoglobin levels and leading to abnormally low levels of red blood cells. If your body doesn’t have enough hemoglobin, your tissues and muscles become starved of oxygen and are unable to function effectively.

There are two forms of dietary iron: heme iron and non-heme iron. Heme iron is the type of iron that comes from animal proteins such as red meat, pork, poultry and seafood. Non-heme iron, by contrast, is found in plant-based foods like grains, beans, dark green leafy vegetables, fruits, nuts, and seeds.

Heme iron is typically absorbed at a rate of 7-35 percent, while non-heme iron is typically absorbed at a rate of 2-20 percent. You can see that even though there is better overall absorption of heme iron, there is also a fairly large range of absorption regardless of the type of iron involved.

If the body requires the ability to make more blood or if there is an excessive loss of blood, then there is a greater demand for iron. In the case of intestinal disorders, there is an impaired ability to efficiently absorb nutrients, including iron from food as well as increased risk from gastrointestinal blood loss. Iron deficiency is always a concern for vegan and vegetarians because of their limited dietary choices and lack of heme-producing protein sources.

The Problem with Iron Supplements
If you are diagnosed with iron deficiency, it is usually recommended to take an iron supplement. Beware of taking the inorganic form of iron know as ferrous sulfate. Ferrous sulfate is also found in many multivitamins, including children’s multivitamins. It is a relatively toxic, inorganic metal that is difficult to absorb. In addition, it can lead to significant side effects which may include constipation, diarrhea, stomach pain, cramps, nausea, vomiting, heartburn, dizziness and fainting, fast heartbeat, and temporary staining of the teeth.

A New Approach to Safely and Efficiently Increase Iron Levels Naturally

Iron Catch, an all-natural supplement from Italy, is an exciting new product that has recently arrived on the scene. Instead of relying on an inorganic iron product to increase iron levels or trying to increase iron levels with other forms of iron supplementation, Iron Catch, provides a novel and effective way to significantly increase iron levels naturally, safely and quickly.

Iron Catch is the first iron-free solution for iron deficiency. It has been proven to rapidly produce significant results within as little as 30 days.¹ In fact, in as little as just one week, patients have improved their energy and vitality. This is great news especially for athletes taking part in endurance sport as well as vegetarians, who are known to be at risk from low iron levels.

Iron Catch is a food supplement with a patented formulation that elevates the iron levels by increasing the absorption of dietary iron by an amazing 3-5 times. Instead of supplementing with an iron pill, Iron Catch’s unique formula is an iron-free alternative that can profoundly increase iron absorption from everyday food consumption with no adverse reactions.

Unlike inorganic iron supplements, Iron Catch has no side effects and is safe for people of all ages. There is no risk of toxic iron overload, which can occur from taking many other kinds of iron supplements. Studies have shown impressive results in people who have iron deficiency and chronic anemia due to Inflammatory Bowel disease, Crohn’s disease, and ulcerative colitis.²

Iron Catch is the world’s first to solve the iron-deficiency problem by enhancing the absorption of iron from our heme and non-heme dietary choices.

This patented formula is made from oligosaccharides of specific hydrolyzed fish cartilage, which enhances rapid iron absorption. The formula also includes additional nutrients to support efficient iron absorption demonstrated by in-vitro studies on Caco-2 cells². They include vitamin C, zinc, copper, vitamin E, and folic acid.

It is recommended to take one tablet on an empty stomach before a main meal. For more rapid results, take two tablets on an empty stomach before a main meal daily for the first month and then one tablet daily for at least another two months before a main meal.

In a world where there are so many health issues that can lead to a serious loss of life-enhancing iron, it is exciting to know that there is an all-natural food supplement that offers a proven solution. The best news of all is that Iron Catch restores healthy levels of iron, rapidly, effectively, and safely.

Iron Catch truly earns its reputation as the first iron-free solution for iron deficiency!

References

1. Minerva Med. 2006 Oct;97(5):385-90. Rondanelli M, Opizzi A, Andreoni L, Trotti R. Effect of treatment with a food supplement (containing selected sea fish cartilage, vitamin C, vitamin E, folic acid, zinc, copper) in women with iron deficiency: double blind, randomized, placebo-controlled trial.
2. World J Gastroenterol 2007 March 14:13(10): 1575-1578 Andrea Belluzzi, Giulia Roda, Francesca Tonon, Antonio Soleti, Alessandra Caponi, Anna Tuci, Aldo Roda, Enrico Roda. (A new iron free treatment with oral fish cartilage polysaccharide for iron deficiency chronic anemia in inflammatory bowel disease: A pilot study

For more information or to purchase Iron Catch visit their website

The post Iron Catch: The First Iron-Free Solution for Iron Deficiency appeared first on Total Health Magazine.

There’s no question that CBD edibles have made self-administering CBD easier. Does the ease of self-administration with the edibles translate to faster absorption? Can CBD gummies get you instant relief?

How Does CBD Work?
Cannabidiol or CBD is one of the active compounds found in hemp, which is a strain of the cannabis sativa plant family. Although marijuana does contain trace amounts of CBD, this compound is most abundant in industrial hemp. Early research into CBD have suggested that it has various potential medical applications. Studies indicate that CBD may be a viable treatment and therapeutic option for a wide range of medical conditions including anxiety and sleep¹, chronic pain², and more.

Many have been using CBD for the treatment and management of various health issues. Despite this, however, data on the exact mechanism of action of CBD is limited. CBD belongs to a group of compounds called cannabinoids and such compounds trigger reactions in the body by attaching to receptors. The body itself produces its own cannabinoids, which can also attach to its cannabinoid receptors called CB1 and CB2 receptors³.

CB1 receptors, which are found mostly in the brain, are responsible for the body’s movement and coordination, for pain, mood, logical thinking and a number of other functions. The other cannabinoid receptor, CB2, regulates the body’s inflammatory and pain reactions. It was initially thought that CBD attaches to these two receptors to trigger positive responses. However, recent studies suggest that CBD actually encourages the body to produce its own cannabinoids and then attach to the CB1 and CB2 receptors.

Benefits of Supplementing with CBD

Once the body’s own cannabinoids are produced and subsequently attaches to the CB1 and CB2 receptors, it results in the following benefits.

Better circulation. Experts have observed that CBD has the ability to relax the veins in a phenomenon called vasodilation⁴. This allows the blood to circulate freely around the body, which in turn has a number of other health benefits. Vasodilation relieves some of the stress from the heart, thus may be effective in preventing certain heart conditions. The vasodilating properties of CBD may also help mitigate the effects of hypertension.

Pain management and anti-inflammatory properties. Many users of CBD swear by its ability to relieve chronic pain and relieve inflammation. Studies are still underway to fully understand how CBD does the job, but many are already enjoying its benefits, particularly those who would rather go with a natural product that does not cause stress the liver.

Mood regulation. Other users of CBD take regular doses to help mitigate and manage their anxiety and depression. Studies are also underway to determine the extent and long term effects of CBD’s anxiolytic properties.

Can CBD Gummies Give You Quick Relief?
The simple answer is yes however people will react differently. CBD has been observed to be highly bioavailable and that it crosses the blood-barrier easily. Some studies are being conducted to see if it is possible for CBD to serve as transport for certain drugs to be absorbed into the system faster and more efficiently. Once you pop a CBD gummy into your mouth, your saliva and chewing action will start breaking it down. While chewing, some of the CBD will be instantly absorbed via the mucous membranes inside the mouth. More of the CBD in the gummies will be absorbed quickly once it hits the intestines as the stomach enzymes further breaks down the gummies.

Consuming CBD in general, whether in the form of tinctures or edibles, can give you quick results. The real question should be, what is the right CBD dose for your needs and how often should you self-administer throughout the day. This is of course, a subject for another discussion.

References:

1. Scott Shannon, MD,corresponding author Nicole Lewis, ND, Heather Lee, PA-C, and Shannon Hughes, PhD. Cannabidiol in Anxiety and Sleep: A Large Case Series Perm J. 2019; 23: 18-041. Published online 2019 Jan 7. doi: 10.7812/TPP/18-041
2. Jan M Schilling, Chloe G Hughes, Mark S Wallace, Michelle Sexton, Miroslav Backonja, and Tobias Moeller-Bertram Cannabidiol as a Treatment for Chronic Pain: A Survey of Patients’ Perspectives and Attitudes J Pain Res. 2021; 14: 1241–1250. Published online 2021 May 5. doi: 10.2147/JPR.S278718
3. K Mackie Mechanisms of CB1 receptor signaling: endocannabinoid modulation of synaptic strength Int J Obes 30 (Suppl 1), S19–S23 (2006). https://doi.org/10.1038/sj.ijo.0803273
5. P. Pacher, S. Bátkai, and G. Kunos Cardiovascular Pharmacology of Cannabinoids Handb Exp Pharmacol. 2005; (168): 599–625. doi: 10.1007/3-540-26573-2_20

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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.

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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.

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.
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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.

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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.

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Resveratrol Background
Before jumping into a discussion about the fascinating human research, however, let’s take a moment to review just what resveratrol is, in case you’re unfamiliar with it. Resveratrol is a type of natural phenol by several plants in response to injury or attack by pathogens.^3,4 These plants include grapes, peanuts⁵ and Japanese Knotweed (Polygonum cuspidatum).⁶ Resveratrol helps provide protection to the plants, at least in part, due to its demonstrated antioxidant properties.⁷ These antioxidant properties benefit humans too, as shown in research where resveratrol provided a direct antioxidant effect against free radicals, and facilitated an increase in vitamin E⁸—another powerful antioxidant.

There are two primary isomers (i.e. two forms) of resveratrol, trans- and cis-. To be clear, trans-resveratrol has been unequivocally shown to have much greater activity than cis-resveratrol.⁹ Consequently, when purchasing a resveratrol product, make sure to check the supplement facts panel to verify that the product contains trans-resveratrol. If just”resveratrol” is listed, without the trans-designation, or if cis-resveratrol is listed, you would be better off choosing a different product that lists trans-resveratrol. In any case, for ease of reading, I will drop references to trans– in the rest of this article, although it can be assumed that any mention of resveratrol will actually refer to trans-resveratrol.

Cardiovascular Health
As its first claim to fame, resveratrol has been found to have activity that may have protective effects on the cardiovascular system. In both test-tube and animal research, resveratrol has been shown to inhibit platelet aggregation (i.e. the clumping together of blood platelets). This has value since excessive or inappropriate aggregation of platelets can lead to formation of blood clots and subsequent blockages in blood vessels that result in insufficient blood flow, heart attack or stroke.¹⁰ Resveratrol can also promote vasodilation (a relaxed and expanded state of the artery that accommodates increased blood flow) by enhancing the production of a naturally occurring substance in the body called nitric oxide.¹¹

More importantly, human clinical research¹² has demonstrated that 100 mg/day of resveratrol significantly reduced arterial stiffness (a major indicator of atherosclerosis) compared to placebo, and also lowered systolic blood pressure by 5.5 points in patients with type 2 diabetes. Another human study,¹³ which used a much higher dose (2.3 g) in older adults, found that resveratrol not only improved vascular function more than placebo, but also increased the number of mitochondria.those parts of the cells that help to generate energy for our body! Another interesting cardiovascular benefit is resveratrol’s effect on Apolipoprotein B (ApoB), a primary component of many lipoproteins such as LDL (the gbad cholesterolh) that are involved in atherosclerosis and cardiovascular disease. In human clinical research¹⁴ on overweight or obese individuals with mild hypertriglyceridemia, 1000 mg/day of resveratrol for one week followed by 2000 mg/day for two weeks reduced ApoB production rate by an impressive 22 percent. In addition, flow-mediated dilatation (a measure of arterial circulation and endothelial function) was increased in human studies^15,16,17 where 10 mg to 270 mg/day of resveratrol was given. In one of the studies,¹⁸ LDL cholesterol levels were also significantly decreased.

Inflammation
In addition to showing anti-inflammatory effects in in-vitro and animal studies, resveratrol has also been shown to comprehensively suppress oxidative and inflammatory stress with as little as 40 mg/day in normal human subjects.¹⁹ This included the reduction of inflammatory markers such as TNF-alpha, IL-6, and C-reactive protein, with no changes in the placebo group. Similarly, in postmenopausal women with osteoarthritis pain, 75 mg of resveratrol twice daily significantly reduced pain and improved total well-being.²⁰

Ulcerative colitis (UC), a chronic inflammatory bowel disease, has also responded to treatment with resveratrol. In one study²¹ with 56 UC patients, those receiving 500 mg/day of resveratrol had significant symptom improvement, reduced malondialdehyde (a highly reactive oxidative stress compound), and increased superoxide dismutase (SOD), and total antioxidant capacity. In another human study²² with 50 UC patients, 500 mg/day of resveratrol also reduced the activity of inflammatory compounds, including TNF-α, hs-CRP, and activity of NF-κB. Furthermore, in a study²³ of firefighters, supplementation with 100 mg/day resveratrol for 90 days, plasma biomarkers of inflammation were reduced after a physical fitness test, including IL-6 and TNF-α. This adds further credence to resveratrol’s anti-inflammatory effects.

Immune Health/Breast Cancer Prevention
Resveratrol’s effect on immune health can be as fundamental as increasing certain circulating immune cells, or as profound at reducing the risk of breast cancer. For example, human research²⁴ was conducted to assess the effects of repeated doses of resveratrol (1000 mg/day for 28 days) on circulating immune cells in healthy individuals. The results were that resveratrol was safe and well tolerated and was associated with significant increases in the numbers of circulating gamma delta T cells (functioning as a first line of defense and a bridge between innate and adaptive responses) and regulatory T cells—demonstrating that resveratrol has clear biological effects on human circulating immune cells.

With regard to breast cancer prevention, resveratrol may help in a couple of ways. First, resveratrol has been shown to have a dose-dependent effect on reducing the formation of mammary tumors in-vitro as a result of down-regulating DNA methyltransferases. To see if it had a similar effect in humans, a study²⁵ was conducted in which 39 adult women at increased breast cancer risk received a placebo, 5 or 50 mg of resveratrol twice daily for 12 weeks. Results were that there was indeed decrease in methylation of the tumor suppressor gene with increasing levels of resveratrol (P = .047).

In another study²⁶ of 34 overweight, postmenopausal women (BMI ≥ 25 kg/m2), the clinical effect of resveratrol on systemic sex steroid hormones were investigated, since high estrogen levels may contribute to breast cancer. The subjects received 1 g of resveratrol daily for 12 weeks. The results were that resveratrol supplementation led to an average of 73 percent increase in urinary 2-hydroxyestrone (the “good estrogen”) levels leading to a favorable change in estrogen ratios that are less conducive to the development of breast cancer. This research demonstrated that among overweight and obese postmenopausal women, a daily 1 g dose of resveratrol has favorable effects on estrogen metabolism.

Muscle Health
In a 12-week study,²⁷ older men and women (aged 65.80 years) exercised and took either a placebo or 500 mg/day of resveratrol to determine if resveratrol would have additive effects to those of exercise. Results showed that exercise added to resveratrol treatment increased the number of mitochondria, and improved muscle fatigue resistance more than placebo and exercise treatments. In addition, subjects treated with resveratrol had an increase in muscular torque and power after training, whereas exercise did not increase these parameters in the placebo-treated older subjects. Furthermore, exercise combined with resveratrol significantly improved muscle fiber. Together, these data suggest that resveratrol combined with exercise might provide a better approach for reversing sarcopenia than exercise alone.

Cognitive Health
Research suggests that resveratrol may have cognitive health benefits in people with and without dementia. For example, the ongoing dysfunction of small blood vessels in patients with type 2 diabetes mellitus (T2DM) may impair the ability of cerebral vessels to supply blood to various brain regions, thereby increasing risks of dementia. To determine if resveratrol could benefit cerebral circulation, a study²⁸ was conducted in which 36 dementia-free, non-insulin dependent T2DM older adults (49–78 years old) consumed single doses of resveratrol (0, 75, 150, and 300 mg) at weekly intervals. Results were that 75–300 mg of resveratrol enhanced vasodilator responsiveness in cerebral vessels.

In another study,²⁹ 80 post-menopausal women aged 45–85 years received resveratrol or placebo for 14 weeks to examine the effect on cognitive performance and other parameters. Results were that compared to placebo, significant improvements were observed in the performance of cognitive tasks in the domain of verbal memory (p = 0.041) and in overall cognitive performance (p = 0.020). Mood also tended to improve in multiple measures. These results indicate that regular consumption of a modest dose of resveratrol can enhance both cerebrovascular function and cognition in post-menopausal women, potentially reducing their heightened risk of accelerated cognitive decline and offering a promising therapeutic treatment for menopause-related cognitive decline.

To test³⁰ whether supplementation of resveratrol (200 mg/ day for 26 weeks) would enhance memory performance in older adults, 23 healthy overweight older individuals were pairwise matched to 23 participants that received placebo (total n = 46, 18 females, 50–75 years). Results showed a significant effect of resveratrol on retention of words over 30 min compared with placebo (p = 0.038), significant increases in hippocampal functional connectivity, decreases in glycated hemoglobin (HbA1c) and body fat, and increases in leptin compared with placebo (all p < 0.05). This study provides initial evidence that supplementary resveratrol improves memory performance in association with improved glucose metabolism in older adults, providing a basis for helping to maintain brain health during aging.

To determine the effects of oral resveratrol on localized cerebral blood flow, a study³¹ was conducted with which 22 healthy human adults received placebo and two doses (250 and 500 mg) of resveratrol in counterbalanced order on separate days. After a 45-min resting absorption period, the participants performed a selection of cognitive tasks. Resveratrol administration resulted in dose-dependent increases in cerebral blood flow during task performance, and enhanced oxygen extraction. These results showed that single doses of orally administered resveratrol can modulate cerebral blood flow variables.

Finally, a clinical study³² was conducted to determine if up to 1 g of resveratrol twice daily could benefit Alzheimer’s disease (AD) patients. The results demonstrated that resveratrol decreased CSF MMP9 (a biomarker for confirmed AD), modulates neuro-inflammation, and induces adaptive immunity— suggesting that resveratrol may be a viable target for treatment or prevention of neurodegenerative disorders.

Weight Loss
One of the reasons that resveratrol has received widespread interest is because of its ability to mimic effects of calorie restriction. To gain more insight into this effect on adipose tissue, a study³³ was conducted in which healthy obese subjects were supplemented with 150 mg/day of resveratrol or placebo for 30 days. Results showed that resveratrol significantly decreased the size of adipocytes (fat cells), with a shift toward reducing the proportion of large and very-large adipocytes and an increase in small adipocytes. Furthermore, lysosomal/phagosomal pathway and transcription factor EB were up-regulated reflecting an alternative pathway of lipid breakdown by autophagy.

Similarly,³⁴ T2DM patients received 3 g resveratrol or placebo daily for 12 weeks. Results were that there was a significant increase in both SIRT1 expression and resting metabolic rate compared with the placebo group. In patients with T2DM, treatment with resveratrol helped regulate energy expenditure, suggesting that resveratrol may have beneficial exercise-mimetic effects.

Again,³⁵ healthy, obese subjects were treated with placebo and 150 mg/day resveratrol for 30 days. The results were that resveratrol increased SIRT1 and improved the muscle’s use of fatty acids as an energy fuel, demonstrating that 30 days of resveratrol supplementation induces metabolic changes in obese humans, mimicking the effects of calorie restriction. Given these results, one might think that resveratrol may aid in weight loss—and indeed this has been shown to be the case in clinical research.

Orlistat is an over-the-counter drug (also known as Alli®) designed to treat obesity by reducing the absorption of fats from the human diet. A study³⁶ was conducted to evaluate the efficacy of combining orlistat with resveratrol in 84 obese subjects over a 6-month period. The subjects consumed a diet with 500 fewer calories than their usual diet for two weeks, and were randomly assigned to four groups, placebo, resveratrol, orlistat, or the O-R combination, and they consumed the energy-reduced diet for 6-months. Results were significant weight loss of 15 lbs in the O-R group compared with 7.7 lbs in the placebo group. Significant decreases in BMI, waist circumference, fat mass, triglycerides, leptin, and leptin/adiponectin ratio were observed with the O-R combination, indicating that it was the most effective weight loss treatment.

In another study,³⁷ 24 patients with metabolic syndrome received resveratrol (500 mg) three times per day before meals for 90 days. Resveratrol administration resulted in significant differences in total weight (P=0.007), body mass index (BMI) (P=0.006), fat mass (P=0.001), and waist circumference (P=0.004). In conclusion, administration of resveratrol significantly decreased weight, BMI, and fat mass.

Blood Sugar/Insulin Resistance
A study³⁸ was conducted using 480 mg/day of resveratrol or placebo for four weeks on 43 patients with diabetes who also had chronic periodontitis (i.e. gum disease). Results were that serum levels of fasting insulin and insulin resistance were significantly lower in the resveratrol group compared with control group. With regard to periodontal disease, there was also a significant difference in the gum pocket depth between intervention and control groups with resveratrol. The researchers recommended that resveratrol supplementation might be beneficial as adjuvant therapy along with non-surgical periodontal treatment in insulin resistance and improving periodontal status among patients with diabetes with periodontal disease.

Another human clinical trial³⁹ was conducted in 32 over-weight, older adults (average age: 73 years). Participants received placebo, 300 mg/day of resveratrol, or 1000 mg/day of resveratrol for 90 days. Results were that, compared to placebo, glucose levels were significantly lower at after treatment among participants receiving either dose of resveratrol (P<0.05), and were well tolerated.

In this study,⁴⁰ 62 patients with T2DM received either an oral hypoglycemic medication, or an oral hypoglycemic medication along with 250 mg/day of resveratrol. Results were that supplementation with resveratrol for three months significantly improved the mean hemoglobin A1c (P<0.05), a measure of long-term glucose control, systolic blood pressure (P<0.05), total cholesterol (P<0.05), and total protein (P<0.05) in T2DM. The researchers concluded that oral supplementation with resveratrol was effective in improving glycemic control and may be a potential adjuvant for the treatment and management of diabetes.

In a pilot study,⁴¹ subjects with impaired glucose tolerance (aged 72 ± 3 years) received 1, 1.5, or 2 g/day of resveratrol for four weeks. After four weeks of resveratrol supplementation, results showed that post-meal (P=0.003) and 3-hour glucose levels (P=0.001) declined. Researchers concluded that, at doses between 1 and 2 g/day, resveratrol improves insulin sensitivity and post-meal plasma glucose in subjects with impaired glucose tolerance. Likewise, in a 4-week study,⁴² T2DM patients received 10 mg/day resveratrol or a placebo. Results showed that, after the fourth week, resveratrol significantly improved insulin sensitivity, which might be due to a resveratrol-induced decrease in oxidative stress that leads to a more efficient insulin-signaling pathway.

Non-Alcoholic 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 affected⁴³—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.⁴⁴ In addition, NAFLD is usually associated with insulin resistance, central obesity, reduced glucose tolerance, T2DM and high triglyceride levels.

In a clinical study,⁴⁵ 50 NAFLD patients received either a 500 mg/day of resveratrol or a placebo for 12 weeks. Both groups were advised to follow an energy-balanced diet and physical activity recommendations. Results were that resveratrol supplementation reduced alanine aminotransferase (a marker for NAFLD) and hepatic steatosis (fatty liver) significantly more than placebo (P<0E05).

In another study,⁴⁶ 60 NAFLD patients received two 150 mg resveratrol capsules twice daily for three months. Results were that, compared with the placebo group, resveratrol significantly decreased aspartate aminotransferase, glucose and low-density lipoprotein cholesterol (P.0.001) alanine aminotransferase, total cholesterol (P=0.002), and insulin resistance (P=0.016). The researchers concluded that resveratrol supplementation might benefit patients with NAFLD.

Other Resveratrol Benefits
In addition to the aforementioned applications for resveratrol, there are additional benefits for this nutraceutical as well. Two such benefits are related to bone health, and for those who are smokers.

In a clinical study,⁴⁷ 66 middle-aged, obese subjects with metabolic syndrome (average age: 49.3 } 6.3 years) received oral treatment with 1,000 mg or 150 mg of resveratrol, or a placebo daily for 16 weeks to assess changes in the bone turnover marker bone alkaline phosphatase (BAP), and bone mineral density (BMD). Results were that BAP increased dose dependently with resveratrol (P<0.001), compared with placebo. Lumbar spine trabecular volumetric bone mineral density also increased dose dependently with resveratrol (P=0.036), with a significant increase of 2.6 percent in the 1,000 mg resveratrol group compared with placebo (P=0.043). In addition, changes in BAP and bone mineral density were positively correlated (P=0.027).

Smokers typically experience a state of low-grade systemic inflammation and oxidant-antioxidant imbalance. To determine whether resveratrol has beneficial effects on markers of inflammation and oxidative stress, a study⁴⁸ was conducted with 50 healthy adult smokers who alternatively were given 500 mg/ day of resveratrol and placebo. Results were that resveratrol significantly reduced the inflammatory marker C-reactive protein (CRP), triglyceride concentrations, and increased Total Antioxidant Status (TAS) values. The researchers concluded that, because resveratrol has anti-inflammatory, anti-oxidant, and hypotriglyceridemic effects, its supplementation might beneficially affect the increased cardiovascular risk of healthy smokers.

Improving The Bioavailability And Efficacy Of Resveratrol

Now that we’ve reviewed some of the many benefits associated with resveratrol supplementation, let’s briefly consider ways to improve the bioavailability and efficacy of this valuable nutraceutical. First, take resveratrol on an empty stomach. The reason for this recommendation is a study showing that the absorption rate of resveratrol following an oral 400 mg single dose was significantly delayed by the presence of food.⁴⁹

Second, resveratrol may work better when taken together with pterostilbene (a related antioxidant) and quercetin (a flavonoid). In this study,⁵⁰ the antioxidant activities of resveratrol, pterostilbene and quercetin, and the effect of their combination were investigated in human blood cells in-vitro. When used together, the combination protected the blood cells against destruction and against depletion of the important antioxidant, glutathione. Also, the combination of resveratrol with quercetin or pterostilbene synergistically inhibited oxidative injury of membrane lipids. These protective effects may partially explain the health benefit of these bioactive micro-components when together in the diet.

Conclusion
The value of supplementation with resveratrol has moved beyond the “French paradox” and the activation of the SIRT 1 gene, associated with longevity. Human clinical research has demonstrated efficacy of resveratrol for inflammation, immune health/breast cancer prevention, muscle health, cognitive health, weight loss, blood sugar/insulin resistance, non-alcoholic fatty liver disease, and more.

Endnotes

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The post Resveratrol: A Research Review appeared first on Total Health Magazine.

1. Statin drugs—Depletes Beta Carotene, vitamin E and Co-enzyme Q10, which can cause heart failure with long-term use.
2. Anti-acids (aluminum)—Depletes vitamin A, folic acid, vitamin D, calcium, chromium, iron, magnesium, phosphorous and zinc. Too much acid does not cause most acid reflux cases; they are actually caused by too little acid.
3. Ciprofloxacin—Depletes biotin, inositol, thiamin, niacin, riboflavin, vitamin B6, vitamin B12, vitamin K, zinc and intestinal bacteria. Long-term use of anti-bacterials, such as ciprofloxacin, can contribute to the development of drug resistant strains of bacteria.
4. Glyburide plus Metformin (Glucovance)—Depletes folic acid, vitamin B12, sodium and coenzyme Q10. In most cases, diabetes drugs can be avoided with better diet and exercise. An NIH study proved this with a group of pre-diabetics who did nearly 100 percent better with diet and exercise improvements to avoid advancing to full diabetes, then they did on Metformin.
5. Prednisone —Depletes vitamin A, vitamin B6, folic acid, vitamin C, vitamin D, vitamin K, calcium, magnesium, potassium, selenium and zinc. Natural treatments for respiratory and gastrointestinal problems often work much better without side effects.
6. The Sartan class of drugs (Micardes HCT, Diovan HCT)—Depletes magnesium, phosphorus, potassium, sodium, zinc and CoQ10. These blood pressure medications treat the symptoms of high blood pressure and lower it in some cases. In most patients, changes in diet will resolve the problem. This was proven in a book called the “DASH Diet.”

These are just a few examples of the nutrient depletions caused by prescription medications. For more on this topic please see articles from the Life Extension Foundation.

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