Posts

Flu and Vitamin D3

Flu and Vitamin DIn a sequestered environment such as a classroom or dormitory, influenza can evoke concerns that are more than just casual. It has been noted by scientists and physicians that seasonal variations in ultraviolet radiation from the sun parallel the outbreak of the flu. The more obvious the sun’s activity, the less pronounced are viral infections. The converse is also true. Places at high latitudes do not receive enough sunlight to help the body produce vitamin D, known for its ability to cause an immune response to pathogens.

Studies performed in Norway, at the Institute for Cancer Research at Oslo University Hospital, in 2010, stated definitively that, “Seasonal variations in ultraviolet B (UVB) radiation cause seasonal variations in vitamin D status.”  Immune response and seasonal influenza infection were directly related to vitamin D levels.  This conclusion was drawn from weekly records that monitored the number of influenza cases and flu-related deaths in Sweden, Norway, the United States, Singapore, and Japan in light of concomitant changes in UVB strength. Results of this study indicated that, “…influenzas mostly occur in the winter season in temperate regions,” adding that, “…at high latitudes very little, if any, vitamin D is produced in the skin during the winter.”  (Juzeniene. 2010)

Vitamin D deficiency is related to other matters besides the flu, including some cancers, heart disease, multiple sclerosis, diabetes, autism, and a host of others. (Cannell. 2008)  This pro-hormone has been produced by life forms since the Creation, and is vital to the growth and development of the organism, from gestation to the grave.  Of the common forms, D2 and D3, the latter is more biologically significant, since it is the one made by the skin in response to sunlight exposure.  The supplement is usually derived from either lanolin or cod liver oil.  This—D3— is the form that should be used to treat deficit.  The former, D2, comes from fungal sources by activating ergosterol with UV light, and is not naturally present in humans.  Synthetic, Rx forms are also available.

After being formed in the skin, vitamin D is converted into two different substances in the body. 25-hydroxyvitamin D (calcidiol) is the main storage form made by the liver.  1,25-dihydroxyvitamin D (calcitriol) is the most potent human steroid in the body, usually made in the kidneys. Calcitriol levels should not be used to determine vitamin D status.

Japanese research looked into seasonal flu among school children, from December 2008 to March 2009, and found that those who had not been taking vitamin D3 supplements were considerably more likely to get the flu than those who did supplement. Asthma sufferers experienced fewer exacerbations if they supplemented with the vitamin. (Urashima. 2010)

The sun has an eleven-year cycle during which its radiation level waxes or wanes.  Discovered in the 1840’s by Samuel Schwabe, the cycle can change the amount of UVB light reaching the earth by as much as 400%, more than enough to influence vitamin D stores.  The hypothesis that flu pandemics are associated with solar control of vitamin D levels has been developed and accepted. (Hayes. 2010)  Part of this is based on vitamin D’s ability to help the body make an innate antimicrobial peptide called cathelicidin, which depends upon vitamin D levels of 40 – 70 nanograms per milliliter.  (Cannell)  European researchers believe that the economic burden of the flu on that continent could be reduced by 187 billion euros a year by supplementing with 2000-3000 IU of vitamin D a day.  (Grant. 2009)  Food fortification, artificial UVB, and, of course, supplements are practical options when the sun is unable to do what we expect.

References

MAIN ABSTRACT
Int J Infect Dis. 2010 Dec;14(12):e1099-105. Epub 2010 Oct 29. The seasonality of pandemic and non-pandemic influenzas: the roles of solar radiation and vitamin D. Juzeniene A, Ma LW, Kwitniewski M, Polev GA, Lagunova Z, Dahlback A, Moan J.

Department of Radiation Biology, Institute for Cancer Research, the Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310 Oslo, Norway. [email protected]

SUPPORTING ABSTRACTS
Altern Med Rev. 2008 Mar;13(1):6-20.
Use of vitamin D in clinical practice.
Cannell JJ, Hollis BW.

Am J Clin Nutr. 2010 May;91(5):1255-60. Epub 2010 Mar 10.
Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren.
Urashima M, Segawa T, Okazaki M, Kurihara M, Wada Y, Ida H.

Medical Hypotheses. Volume 74, Issue 5, May 2010, Pages 831-834
Influenza pandemics, solar activity cycles, and vitamin D Daniel P. Hayes

Progress in Biophysics and Molecular Biology. 99(2-1); Feb-May 2009: 104-113
Estimated benefit of increased vitamin Dnext term status in reducing the economic burden of disease in western Europe William B. Grant, Heide S. Cross, Cedric F. Garland, et al

Journal of Clinical Virology Volume 50, Issue 3, March 2011, Pages 194-200
Vitamin D and the anti-viral state Jeremy A. Beard, Allison Bearden, and Rob Striker

Archives of Gerontology and Geriatrics
Article in Press, Corrected Proof – Received 15 October 2010; revised 25 February 2011; accepted 28 February 2011. Available online 1 April 2011.
Vitamin D: drug of the future. A new therapeutic approach N. Gueli, W. Verrusioa, A. Linguanti, F. Di Maio, A. Martinez, B. Marigliano and M. Cacciafesta

FASEB J. 2005 Jul;19(9):1067-77.
Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. Gombart AF, Borregaard N, Koeffler HP

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Sunflower Seeds Lower Cholesterol

plant sterols and stanolsSunflower seeds and pistachio nuts are top snacks for reducing cholesterol. Scientists have known for a long time that nuts and seeds are rich sources of phytosterols, plant compounds that are structurally related to cholesterol and may lower LDL levels. Keeping cholesterol in check may be your goal, but it’s not realistic to accomplish this without some work…as in exercise.

It’s been a few years since Science Daily first reported the news that chemists at Virginia Polytechnic Institute found the plant sterols in pistachios and sunflowers seeds to be valuable assets in the fight against rampant cholesterol numbers.  (ScienceDaily, 7 Dec. 2005. Web. 19 Aug. 2011.)  “Sesame seed and wheat germ had the highest total phytosterol content and Brazil nuts the lowest,” said scientists at VPI. (Phillips. 2005)  But these are not typically consumed as snack foods.  Sunflower seeds and pistachio nuts, on the other hand, are, and were found to be richest in these compounds.

Dietary phytosterols favorably alter cholesterol metabolism in a dose-dependent manner by reducing intestinal cholesterol absorption.  (Racette. 2010)  Even a moderate intake can be obtained from a healthy diet, without supplementation.  Of course, you have to eat the right foods.  Plants contain a large range of phytosterols, which are structural components of the cell wall.  (Plants have cell walls and cell membranes; animals just the membrane.)  What phytosterols do for plants, cholesterol does for animals.

As functional foods, plant sterols and stanols demonstrate a strong lipid-lowering effect. (Moore. 2011)  Including them as part of the diet may reduce risk for heart disease.  Studies at McGill University concentrated on patients with Type 2 diabetes and found that plant sterols had a significantly more profound effect on the cholesterol levels of Type 2 patients than on patients with high cholesterol without diabetes. (Lau. 2005)  LDL levels were lowered while the desirable HDL was relatively untouched.  Additional lipid study in Israel learned that consuming plant sterols also results in a drop in circulating insulin levels, pointing to their use as food enhancers that can reverse insulin resistance and hyperlipidemia, and possible help to control body weight.  (Ziv. 2009)

Controlling lipid levels with food or supplements is considerably more desirable than using drugs.  Suggested intake of two to three grams of these plant compounds a day, either from food, fortified foods, or supplements, can reduce lipids by almost ten percent.  (Baumgartner. 2011)  More than that affords no increased benefit.

Whether raw or roasted, sunflower seeds have a dedicated following.  Because they’re high in oil, the seeds are prone to rancidity, so refrigeration is a good idea.  They aren’t just for snacks, either.  They match pretty well with all the food groups and can really up the ante on nutrition.  Sauté them with vegetables, add them to your salads, fold them into meatloaf and mix them with baked goods and even eggs.  An ounce will give you two grams of fiber, almost half a day’s vitamin E, and a healthy ration of minerals.

References

American Chemical Society.
Sunflower Seeds, Pistachios Among Top Nuts For Lowering Cholesterol.
ScienceDaily, 7 Dec. 2005. Web. 19 Aug. 2011.

J. Agric. Food Chem., 2005, 53 (24), pp 9436–9445
Phytosterol Composition of Nuts and Seeds Commonly Consumed in the United States
Katherine M. Phillips, David M. Ruggio, and Mehdi Ashraf-Khorassani

Am J Clin Nutr January 2010 vol. 91 no. 1 32-38
Dose effects of dietary phytosterols on cholesterol metabolism: a controlled feeding study
Susan B Racette, Xiaobo Lin, Michael Lefevre, Catherine Anderson Spearie, Marlene M Most, Lina Ma, and Richard E Ostlund Jr

Curr Opin Endocrinol Diabetes Obes. 2011 Aug 11. [Epub ahead of print]
Functional foods and cardiovascular disease risk: building the evidence base.
Moore LL.

Am J Clin Nutr June 2005 vol. 81 no. 6 1351-1358
Plant sterols are efficacious in lowering plasma LDL and non-HDL cholesterol in hypercholesterolemic type 2 diabetic and nondiabetic persons
Vivian WY Lau, Mélanie Journoud and Peter JH Jones

Lipids Health Dis. 2009 Oct 12;8:42.
A high oleic sunflower oil fatty acid esters of plant sterols mixed with dietary diacylglycerol reduces plasma insulin and body fat accumulation in Psammomys obesus.
Ziv E, Patlas N, Kalman R, Pelled D, Herzog Y, Dror T, Cohen T.

Curr Pharm Des. 2011;17(9):922-32.
Plant sterols and stanols in the treatment of dyslipidemia: new insights into targets and mechanisms related to cardiovascular risk.
Baumgartner S, Mensink RP, Plat J.
Department of Human Biology, School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, The Netherlands.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

B Vitamins And Energy

happygirlA considerable fraction of the general population reports using one or more vitamin supplements. Reasons include fighting stress and tiredness, and improving mental function. Until recent decades, there was only modest support from the allopathic community that supplements could render any benefit.

Using questionnaires that tracked mood states, levels of perceived stress, and general health, researchers at the Brain Performance and Nutrition Center of Northumbria University, in the UK, discovered a relationship between vitamin supplement intake and overall performance as related to fatigue, mood, and feelings of well-being.  High-dose B-vitamin supplementation “…led to significant improvements in ratings…” in the vigor subscale of the subjective assessments.  (Kennedy. 2010)  Cognitive and executive function improved in parallel fashion as a result of physical reinvigoration.  The authors concluded that, “Healthy members of the general population may benefit from augmented levels of vitamins/minerals via direct dietary supplementation.”

When questioned about the rationale behind supplementation, the answer should list poor dietary choices, processed food, depleted soil, chemical fertilizers and biocides, synthetic additives, malabsorption, careless food preparation, haphazard storage and shipping, and the use of medications and alcohol.  Feel free to add a few.

Because the vitamin B complex is water-soluble and relatively delicate, it responds to whatever insults include boiling or steaming, heat, and prolonged exposure to light.  Not only that, but the complex is vulnerable to the aerosol pesticides used by the produce brokers who store foods prior to over-the-road shipping.

The B vitamins comprise a group that plays a vital role in cell metabolism.  They were once thought to be a single vitamin, but later were found to have distinct functions in the body, although they coexist in the same foods.  They received their numbers based on the order in which they were isolated.  In conjunction, the B complex is helpful to combat most symptoms and causes of conditions such as depression, stress, coronary heart disease and other cardiovascular concerns.  Working together, the B’s are able to support metabolic homeostasis, the immune system, and the nervous system, while simultaneously maintaining healthy skin, muscle tone, and promoting cell growth and division.  Neat, eh?

The water-solubility of B vitamins helps them disperse throughout the body, but also means that they need replacement every day.  Excess is excreted in urine, which explains the dark yellow-orange color that occurs after taking the supplement.  (That would be riboflavin, B2.)  One of the B group’s claims to fame is its role in the burning of carbohydrates for energy.  If this metabolic purpose is impaired, fatigue strikes, often with a vengeance.  Thiamine in particular, or one of its derivatives, is known to improve energy metabolism during physical fatigue (Nozaki.  2009), and is a reputed activator of carbohydrate processing (Masuda. 2010).

If taken as an isolated supplement, a singular B vitamin may act as a drug, even though there are few adverse reactions, with the possible exception of very high-dose pyridoxine (B6) being associated with sensory neuropathy.  (Scott. 2008)  Alcohol of any type, even the comparatively innocuous beer, will result in a net deficit of the B vitamins.

The stress that characterizes the Western lifestyle takes a physical, as well as psychological, toll.  The mood changes and testiness that follow physical exhaustion are shared with family and friends.  B-vitamin supplementation has shown itself to attenuate the causes and effects, either one at a time or together.  (Stough. 2011)  People with the lowest levels of the B vitamins in their diets usually have the poorest memories and cognitive abilities.  Those with gastric dysfunction, such as that characterized by low stomach acid or deficit of intrinsic factor, will absorb the least vitamin B12 from their foods, so are well-advised to supplement.

The interaction of the body’s chemistry is complex.  We need vitamin B2 to metabolize B6.  We need B6, B12, and folate to clear homocysteine, a marker for cardiac involvement.  But taking an isolated B vitamin without the rest of the family upsets the apple cart.  The RDA is a poor guide because it recommends only that dose of a nutrient that will prevent deficiency disease, such as beriberi or pellagra.  Meeting with a health care professional can help you to figure what’s what.

References

Kennedy DO, Veasey R, Watson A, Dodd F, Jones E, Maggini S, Haskell CF.
Effects of high-dose B vitamin complex with vitamin C and minerals on subjective mood and performance in healthy males.
Psychopharmacology (Berl). 2010 Jul;211(1):55-68.

SUPPORTING ABSTRACTS
Nozaki S, Mizuma H, Tanaka M, Jin G, Tahara T, Mizuno K, Yamato M, Okuyama K, Eguchi A, et al
Thiamine tetrahydrofurfuryl disulfide improves energy metabolism and physical performance during physical-fatigue loading in rats.
Nutr Res. 2009 Dec;29(12):867-72.

Masuda H, Matsumae H, Masuda T, Hatta H.
A thiamin derivative inhibits oxidation of exogenous glucose at rest, but not during exercise.
J Nutr Sci Vitaminol (Tokyo). 2010;56(1):9-12.

Scott K, Zeris S, Kothari MJ.
Elevated B6 levels and peripheral neuropathies.
Electromyogr Clin Neurophysiol. 2008 Jun-Jul;48(5):219-23.

Stough C, Scholey A, Lloyd J, Spong J, Myers S, Downey LA.
The effect of 90 day administration of a high dose vitamin B-complex on work stress.
Hum Psychopharmacol. 2011 Sep 8.

Bassett JK, Hodge AM, English DR, Baglietto L, Hopper JL, Giles GG, Severi G.
Dietary intake of B vitamins and methionine and risk of lung cancer.
Eur J Clin Nutr. 2011 Aug 31.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Thiamin—Vitamin B1

spinach-cauliflowerAbout half of thiamin is found in skeletal muscle. Beriberi, more common in the 19th century, is a thiamin deficiency disease caused by a diet of highly polished rice, where the thiamin-rich husk is removed.  Deficiency appears in alcoholics, those with malabsorption syndromes, and in long-term use of loop diuretics.

BENEFITS

  • Involved in metabolism of the branched-chain amino acids
  • Acts as an anti-oxidant and anti-atherosclerosis agent
  • Modulates mood and cognition
  • Protects kidneys and liver from lead-induced lipid peroxidation
  • Energy production
  • Carbohydrate and fatty acid metabolism

DEFICIENCY

  • Diseases of the nervous system
  • Weight loss
  • Emotional disorders
  • Weakness and pain in the limbs
  • Erratic heartbeat
  • Irreversible psychosis

SOURCES

  • Brewer’s yeast, wheat germ, oatmeal, while grains
  • Nuts, dried beans and peas
  • Spinach and cauliflower
  • Organ meats, pork, fish, poultry
  • Spinach and cauliflower

Subclinical thiamin deficiency may be more common than expected, and might appear as abnormal glucose tolerance.  Thiamin’s anti-oxidant properties have not been elucidated, but the brain damage associated with thiamin deficit indicates oxidative stress. Absorption of the nutrient is impeded by the tannins in coffee and tea, but may be offset by taking vitamin C. Some supplements used to treat osteoporosis, such as horsetail, can destroy thiamin in the stomach and lead to signs of thiamin deficiency, as can diseases such as Crohn’s, celiac, colitis, and diverticulitis.

 

B-Vitamins And Memory

confused-young-womanFrancis Bacon, who was a philosopher in the 16th century, said that, “Some books are to be tasted, others swallowed, and some few to be chewed and digested.” The same principle can apply to the written word of the present. If we took everything we read in magazines or over the internet as gospel, conflicting words and ideas would create such confusion that the truth would be more elusive than it has been for decades. While we are able to identify and to reject half-truths in the spoken word, we tend to give them credence if they appear in print. Such is the case with news and reports about the human body and its health and maintenance, and the things we can do and take to guarantee them.

Reports from Fox, Reuters and Medline, among other news services, have said that
B-vitamins can boost memory. Seeing that headline is all some folks need to draw a hasty conclusion, hoping that their loved ones with Alzheimer’s or some other neurological irregularity will be cured. At best, such a conclusion might be drawn following a syllogistic approach, a form of reasoning that relies on major and minor premises:  if this causes this, and if that causes that, then this causes that. Whether or not this is true depends on acceptance of the phrases, “some of the time” and “all of the time.”  Let’s see if we can make sense of the original proposition, that B-vitamins can boost memory.

The study cited by the news services was conducted by Dr. Janine Walker, a mental health researcher from the Australian National University, who reported in the American Journal of Clinical Nutrition that long-term supplementation with folic acid and vitamin B12 promotes improvement in cognitive functioning. (Walker, 2012)  What the headline doesn’t tell us is that the study lasted two years, and that physical exercise was part of the protocol. You have to read the small print, which means the details of the study need to be chewed and digested. The confounding factors and specific provisions must be considered.

Homocysteine (Hcy) is such a factor–and a provision if it’s measureable. Homocysteine is a homologue of the amino acid, cysteine, differing by an additional methylene group (CH2). It’s best known as a marker for inflammation associated with increased risk of cardiovascular disease. Whether or not lowering homocysteine will also lower CVD risk is still under examination, but it has been accepted that raised Hcy is associated with poor cognitive performance in the general population, not only in the elderly. Increases in serum folic acid levels are accompanied by decreases in Hcy levels. (Durga, 2007)  But this doesn’t mean that cognitive function will automatically improve. It takes time, another factor to be weighed. After three years of folic acid supplementation, Durga and his Dutch colleagues learned that the molecule, did, in fact, improve specific domains of cognitive function, particularly those that decline with age. What we are not told is that folic acid (vitamin B9) works best in the company of vitamins B12 and B6, where its role as a promoter of brain function can be fully realized.

If there is a pin to be put into this balloon, it comes courtesy of the Cochrane Database and its systematic reviews of primary research in health care and health policy. One of its 2008 reviews examined the effects of folic acid on demented people and their cognitive shortcomings, only to announce that no consistent evidence supports the use of folic acid—with or without vitamin B12—to effect improvement. They are carefully deliberate to add, however, that long-term use of folic acid (also known as folate in foods) does appear to improve the cognitive function of those individuals with elevated homocysteine levels. (Malouf, 2008)  Do you see the factor?  Long-term use.

Many elderly present with movement disorders to some degree. Swedish investigators looked at a population of community-dwelling septuagenarians who suffered both movement and cognitive disadvantages, treating them with vitamins B9, B6, and B12. More than 60% of the men and almost 50% of the women had high Hcy levels and high methylmalonic acid (MMA) concentrations, the latter indicating B12 deficiency. Vitamin therapy lowered both markers, but failed to mitigate both the movement and cognitive deficits. This does not mean the therapy is useless, though. The report allows that dosage could have been too low to prove effective, or that the physical and mental declines could have become irreversible. (Lewerin, 2005)  If such decline is recognized at all, could it / should it have been identified years—or even decades—sooner?   With all illness and debility, isn’t that ounce of prevention worth lots more than the pounds of cure?   To be considered also is that stores of nutrients decline sharply with age. For how long were they deficient?  How about the form of the nutrient?  Methylcobalamin is the much preferred form of vitamin B12, but the Swedish study used cyanocobalamin, a form that is unnatural to plants and animals. And, it contains an “insignificant” amount of cyanide that still must be eliminated from the body. Isn’t the mere four months duration of this study too little time to come to a righteous conclusion?  The factor?  Time.

“Over the short or medium term,” announces a Glasgow paper, cognitions did not improve with the vitamin cocktail. This study population, older than sixty-five and comparatively small at 185 participants, suffered ischemic vascular disease, that which decreases blood supply to an organ by constricting a blood vessel. Since all ischemia is not the same for all people, that condition might just confound the matter. This study lasted three months to one year. Here is a senior population with constrictive vascular disease, probably taking one or more medications, whose compliance is not monitored, with unknown dietary habits and unmentioned polypharmacy, and possibly experiencing other health issues. (MacDonald, 2005). Are we expected to accept the conclusion without question?

In ameliorative protocols where the patient is ambulatory, exercise is warranted, either as an isolated or as a supportive element. (Wen, 2010)  (Harkcom, 1085)  (Kirkcaldy, 1990)  Nonetheless, the administration of selected B-vitamins has an effect on the factors that interfere with brain function and memory, if only because they can mitigate the adverse effects of inflammation. Homocysteine is a documented CVD factor that is related to both vascular dementia and Alzheimer’s disease. (Stabler, 2003)  It appears that the attenuation of Hcy with folic acid, vitamin B6 and vitamin B12, accompanied by a modicum of exercise, and conducted over a reasonable period of time, can yield the desired result in cognitive change. IF homocysteine is related to cognitive decline, and IF a B-vitamin cocktail reduces homocysteine, THEN the cocktail may be able to reverse faulty cognition (in certain circumstances). Because these supplements are water-soluble, toxicity is of little concern regardless of the elevated dosage required.

References

Durga J, van Boxtel MP, Schouten EG, Kok FJ, Jolles J, Katan MB, Verhoef P.
Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial.
Lancet. 2007 Jan 20;369(9557):208-16.

Feng L, Ng TP, Chuah L, Niti M, Kua EH.
Homocysteine, folate, and vitamin B-12 and cognitive performance in older Chinese adults: findings from the Singapore Longitudinal Ageing Study.
Am J Clin Nutr. 2006 Dec;84(6):1506-12.

Ford AH, Flicker L, Alfonso H, Thomas J, Clarnette R, Martins R, Almeida OP.
Vitamins B(12), B(6), and folic acid for cognition in older men.
Neurology. 2010 Oct 26;75(17):1540-7.

Garcia A, Zanibbi K.
Homocysteine and cognitive function in elderly people.
CMAJ. 2004 Oct 12;171(8):897-904.

Thomas M. Harkcom MD, Richard M. Lampman PhD, Barbara Figley Banwell PT, C. William Castor MD
Therapeutic value of graded aerobic exercise training in rheumatoid arthritis
Arthritis & Rheumatism. Volume 28, Issue 1, pages 32–39, January 1985

Kirkcaldy, Bruce D.;Shephard, Roy J.
Therapeutic implications of exercise.
International Journal of Sport Psychology, Vol 21(3), Jul-Sep 1990, 165-184.

Lewerin C, Matousek M, Steen G, Johansson B, Steen B, Nilsson-Ehle H.
Significant correlations of plasma homocysteine and serum methylmalonic acid with movement and cognitive performance in elderly subjects but no improvement from short-term vitamin therapy: a placebo-controlled randomized study.
Am J Clin Nutr. 2005 May;81(5):1155-62.

Lonn E, Yusuf S, Arnold MJ, Sheridan P, Pogue J, Micks M, McQueen MJ, Probstfield J, Fodor G, Held C, Genest J Jr; Heart Outcomes Prevention Evaluation (HOPE) 2 Investigators.
Homocysteine lowering with folic acid and B vitamins in vascular disease.
N Engl J Med. 2006 Apr 13;354(15):1567-77.

Malouf R, Grimley Evans J.
Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people.
Cochrane Database Syst Rev. 2008 Oct 8;(4):CD004514.

McCaddon A, Hudson P, Davies G, Hughes A, Williams JH, Wilkinson C
Homocysteine and cognitive decline in healthy elderly.
Dement Geriatr Cogn Disord. 2001 Sep-Oct;12(5):309-13.

McCaddon, Andrew
Homocysteine and cognitive impairment; a case series in a General Practice setting
Nutrition Journal. 15 February 2006, 5:6

Oulhaj A, Refsum H, Beaumont H, Williams J, King E, Jacoby R, Smith AD.
Homocysteine as a predictor of cognitive decline in Alzheimer’s disease.
Int J Geriatr Psychiatry. 2010 Jan;25(1):82-90.

Sally P Stabler
Vitamins, homocysteine, and cognition
American Journal of Clinical Nutrition, Vol. 78, No. 3, 359-360, September 2003

A. David Smith, Stephen M. Smith, Celeste A. de Jager, Philippa Whitbread, Carole Johnston, Grzegorz Agacinski, Abderrahim Oulhaj, Kevin M. Bradley, Robin Jacoby, Helga Refsum
Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: A Randomized Controlled Trial
PLoS ONE. September 8, 2010; 5(9): e12244.

Stott DJ, MacIntosh G, Lowe GD, Rumley A, McMahon AD, Langhorne P, Tait RC, O’Reilly DS, Spilg EG, MacDonald JB, MacFarlane PW, Westendorp RG.
Randomized controlled trial of homocysteine-lowering vitamin treatment in elderly patients with vascular disease.
Am J Clin Nutr. 2005 Dec;82(6):1320-6.

van Uffelen JG, Chin A Paw MJ, Hopman-Rock M, van Mechelen W.
The effect of walking and vitamin B supplementation on quality of life in community-dwelling adults with mild cognitive impairment: a randomized, controlled trial.
Qual Life Res. 2007 Sep;16(7):1137-46.

van Uffelen JG, Chinapaw MJ, van Mechelen W, Hopman-Rock M.
Walking or vitamin B for cognition in older adults with mild cognitive impairment? A randomised controlled trial.
Br J Sports Med. 2008 May;42(5):344-51.

Walker JG, Batterham PJ, Mackinnon AJ, Jorm AF, Hickie I, Fenech M, Kljakovic M, Crisp D, Christensen H.
Oral folic acid and vitamin B-12 supplementation to prevent cognitive decline in community-dwelling older adults with depressive symptoms–the Beyond Ageing Project: a randomized controlled trial.
Am J Clin Nutr. 2012 Jan;95(1):194-203.

Wen D, Xu J, Xie X, Zhang J, Zhong Y, Sun Y, Duan Y.
Effect of physical exercise on the efficacy of mitoxantrone-loaded nanoparticles in treating early breast cancer.
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2010 Feb;27(1):109-12.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Special Vitamin K?

Eat Your GreensMany people think that vitamin K is used by the body only to clot blood after getting a cut.  That’s true, but this nutrient is much more complicated than that.  Because it’s fat-soluble, it requires fat to be absorbed, but unlike some other fat-soluble vitamins, it doesn’t get stored anywhere in large amounts.  Its name came from the German word koagulation in 1929, immediately after its newly discovered function.

Vitamin K is not a single substance, but a group of structurally similar vitamins that are necessary for the regulation of several proteins involved in metabolic pathways other than blood clotting, including bone and coronary health.  If all it did was to clot blood, vitamin K would be one of the more boring substances related to body function.  There are two natural forms of vitamin K—K1, also known as phylloquinone, and K2, also called menaquinone.   The former is made by plants; the latter, by animals, including humans.

The main dietary source of vitamin K as phylloquinone is plants, the bioavailability of which is questionable and lower than generally assumed.  The absorption of phylloquinone from plants is about one and a half times slower than the vitamin K from a supplement.  (Gijsbers, et al. 1996)  The liver absorbs it quickly and maintains the highest concentration, though significant amounts may be found in the heart.  Whether it is secreted by the liver and transported to other tissue is not known.  (Davidson. 1998)  Green leafy vegetables are rich in K1, and contribute almost half of the total dietary intake.

Vitamin K2, or menaquinone, is a collection of a few vitaminers, the most publicized of which are MK-4 and MK-7, although there are several other MK forms.  Found in egg yolks, butter, liver, certain cheeses and fermented soy products, K2 is also produced by bacteria that live in the gut.  The amount contributed by intestinal microflora is unclear, but dietary contribution of K2 is considerably less than that of K1.  The MK numeration refers to the number of side units that are attached to the main ring-like body of the molecule— MK-4 has four units; MK-7 has seven.  They range from one to ten.  These side chains are called isoprenoids, and are made from two or more hydrocarbons, each containing five carbon atoms.  MK-4 is not produced in significant amounts by bacteria, but appears to be made from phylloquinone.  There are at least three synthetic forms of vitamin K: K3, K4, and K5.  Vitamin K3, known as menadione and metabolized to vitamin K2, has demonstrated moderate toxicity, although it is being used in pet food.  Concentrations of menaquinones in tissue are higher than the phylloquinones, especially menaquinone-4 (MK-4), which is the major tissue-bound form.   Despite the difference, the origin of MK-4 is somewhat elusive.  Investigators in Japan determined that MK-4 is converted from phylloquinone by a metabolic removal of a side chain.  (Okano. 2008)

Deficiencies of vitamin K are uncommon, but are more likely to happen as a result of drug therapy or some diseases.  The most significant instances of deficiency manifest in newborns as an acquired disease, the hemorrhagic activity of which is quelled by oral and intramuscular administration of vitamin K at birth.  Efficiency of vitamin K absorption covers a wide range, from 10% to 80%.  The recommended allowances for this nutrient are set to forestall deficiency diseases, which concern themselves with blood clotting and little else.  The optimal amounts needed to address skeletal and arterial needs have been ignored.

The most studied subtypes of vitamin K2 are MK-4 and MK-7.  MK-4 comes from K1, where its conversion may occur in the testes, pancreas, and arterial walls.  Because scientists have seen the conversion in germ-free mice (having no intestinal microflora), they concluded that bacterial activity is not necessary to make MK-4.  (Ronden. 1998)

Antibiotics are generally non-selective, and will kill the intestinal microflora upon which we depend to manufacture vitamin K from plants.  This can reduce vitamin K (menaquinone) production by more than 70% when compared to those who are not taking antibiotics.  (Conly. 1994)

Vitamin K helps to regulate calcium in both bone and the arteries, working by way of an amino acid called “Gla,” which stands for gamma-carboxyglutamic acid, or gamma-carboxyglutamyl.  Gla responds to changes in dietary intake, an age-dependent process, but several days are needed to observe any alterations.  (Ferland. 1993)   Vitamin K has a modulating effect on several proteins, where it performs an action called carboxylation.  This gives the proteins a kind of claw-like function that enables them to hold on to calcium and move it around.  Without enough vitamin K, the proteins lack their claws.  If this happens, calcium migrates away from bones and teeth, and degradation becomes an issue.  Of all the Gla proteins, osteocalcin (OC) is best known.  It’s synthesized by osteoblasts, the bone-forming cells.  Although everything about osteocalcin is not known, it is believed to be related to bone mineralization.  Osteocalcin that is under-carboxylated, labeled ucOC, is a marker for vitamin K status. High levels of ucOC are indicative of reduced bone mineral density (BMD) and increased risk for fractures.  Vitamin K intake of the general population may not be sufficient to guarantee the carboxylation needed to maintain osteocalcin activity.  (Bach. 1996)  The player in the background of all this activity is vitamin D, which regulates osteocalcin transcription.

(Lian.  1989)  Lian and his team found a large region of nucleotides directly upstream from the transcription start area that supports a ten-fold stimulation of transcription of the OC gene by 1,25-dihydroxy vitamin D.

The vitaminer MK-4 has demonstrated the capacity to reduce bone fracture risks, and even to reverse bone loss.  The synergy of vitamins K and D was recognized in studies performed by the University of California, where MK-4 received the nod as the leader of the pack.  (Kidd. 2010)  Japanese researchers who preceded that study reported that a dose of 45 mg a day of vitamin K, accompanied by calcium supplementation, would increase BMD and lead to the prevention of nonvertebral fractures. (Sato. 2005)  Additionally, K2 was found to reduce the incidence of vertebral fractures without having a substantial effect on BMD.  (Iwamoto. 2006)

Not to be outdone by its analog MK-4, MK-7, sourced from fermented soy, has been found to stimulate osteoblastic bone formation while inhibiting osteoclastic bone resorption, all the while limiting calcium depletion by modulating prostaglandin E2.
(Yamaguchi. 2006)   (Tsukamoto. 2004)

Some individuals with osteoporosis are likely to have an excess of calcium in their arteries.  Vascular calcification might even be viewed as vascular ossification—the formation of bone inside an artery.  The appearance of atherosclerotic plaques in arterial walls is a hallmark of cardiovascular disease (CVD).  The plaques cause decreased elasticity of the affected vessel and increased risk of clot formation.  In Dutch studies it was discovered that women with atherosclerotic calcifications have a lower bone mass, which, of course, puts them at greater risk for fractures.  Deficiency of vitamin K causes an increase of ucOC, leading to deposition of calcium in arteries, an activity that would be halted by carboxylated OC.  Menaquinone, including MK-4, but probably not phylloquinone, is associated with reduced coronary calcification.  (Beulens. 2009)  (Geleijnse. 2004)  These studies show that those who ingested the greatest amounts of vitamin K2 experienced a 57% reduction in cardiac fatalities.  No such relationship was found for K1.  In these studies, though, MK-4 and MK-7 were not separately analyzed, but were grouped together.  But in earlier studies it was learned that MK-4 has a distinct effect on plaque prevention in warfarin treatment, where MK-4 was three times more efficiently utilized in the aorta than vitamin K1, mostly by virtue of its bioavailability and use in carboxylation.  (Spronk. 2003)

Warfarin and other anticoagulants interfere with the activity of vitamin K.  Unfortunately, warfarin has the capacity to cause arterial calcification in the long run.  (Price. 1998)  (Danziger. 2008)   Generally, there are enough data to suggest that a constant dietary intake of 65-80 mcg of vitamin K a day during warfarin therapy is an acceptable practice, while avoiding fluctuations in vitamin K intake that would interfere with the activity of the drug.  (Booth. 1999)  It is strongly recommended that such patients work closely with their physicians to monitor prothrombin time, perhaps better known as INR.  It is accepted that vitamin K replacement is an important part of warfarin therapy. (Patriquin. 2011)  In some instances, aspirin may be the better choice.  (Chimowitz. 2005)

The activities of the special K vitamin extend beyond the scope of this newsletter.  Maybe that can be addressed another time.

References

Adams J, Pepping J.
Vitamin K in the treatment and prevention of osteoporosis and arterial calcification.
Am J Health Syst Pharm. 2005 Aug 1;62(15):1574-81.

Arunakul M, Niempoog S, Arunakul P, Bunyaratavej N.
Level of undercarboxylated osteocalcin in hip fracture Thai female patients.
J Med Assoc Thai. 2009 Sep;92 Suppl5:S7-11.

Bach AU, Anderson SA, Foley AL, Williams EC, Suttie JW.
Assessment of vitamin K status in human subjects administered “minidose” warfarin.
Am J Clin Nutr. 1996 Dec;64(6):894-902.

Berkner KL.
The vitamin K-dependent carboxylase.
J Nutr. 2000 Aug;130(8):1877-80.

Beulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, Witteman JC, Grobbee DE, van der Schouw YT.
High dietary menaquinone intake is associated with reduced coronary calcification.
Atherosclerosis. 2009 Apr;203(2):489-93. Epub 2008 Jul 19.

Booth SL, Centurelli MA
Vitamin K: a practical guide to the dietary management of patients on warfarin.
Nutr Rev. 1999 Sep;57(9 Pt 1):288-96.

Brody T. Nutritional Biochemistry. 2nd ed. San Diego: Academic Press; 1999.

Chatrou ML, Reutelingsperger CP, Schurgers LJ.
Role of vitamin K-dependent proteins in the arterial vessel wall.
Hamostaseologie. 2011 Nov;31(4):251-7.

Cheung AM, Tile L, Lee Y, Tomlinson G, Hawker G, Scher J, Hu H, Vieth R, Thompson L, Jamal S, Josse R.
Vitamin K supplementation in postmenopausal women with osteopenia (ECKO trial): a randomized controlled trial.
PLoS Med. 2008 Oct 14;5(10):e196.

Marc I. Chimowitz, M.B., Ch.B., Michael J. Lynn, M.S., Harriet Howlett-Smith, R.N., Barney J. Stern, M.D., Vicki S. Hertzberg, Ph.D., et al
Comparison of Warfarin and Aspirin for Symptomatic Intracranial Arterial Stenosis
N Engl J Med 2005; 352:1305-1316 March 31, 2005

Conly J, Stein K.
Reduction of vitamin K2 concentrations in human liver associated with the use of broad spectrum antimicrobials.
Clin Invest Med. 1994 Dec;17(6):531-9.

Danziger J.
Vitamin K-dependent proteins, warfarin, and vascular calcification.
Clin J Am Soc Nephrol. 2008 Sep;3(5):1504-10.

Davidson RT, Foley AL, Engelke JA, Suttie JW.
Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria.
J Nutr. 1998 Feb;128(2):220-3.

Ferland G, Sadowski JA, O’Brien ME.
Dietary induced subclinical vitamin K deficiency in normal human subjects.
J Clin Invest. 1993 Apr;91(4):1761-8.

Feskanich D, Weber P, Willett WC, Rockett H, Booth SL, Colditz GA.
Vitamin K intake and hip fractures in women: a prospective study.
Am J Clin Nutr. 1999 Jan;69(1):74-9.

Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, Hofman A, Witteman JC.
Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study.
J Nutr. 2004 Nov;134(11):3100-5.

Gijsbers BL, Jie KS, Vermeer C.
Effect of food composition on vitamin K absorption in human volunteers.
Br J Nutr. 1996 Aug;76(2):223-9.

Iwamoto J, Takeda T, Sato Y.
Menatetrenone (vitamin K2) and bone quality in the treatment of postmenopausal osteoporosis.
Nutr Rev. 2006 Dec;64(12):509-17.

Iwamoto J, Sato Y, Takeda T, Matsumoto H.
High-dose vitamin K supplementation reduces fracture incidence in postmenopausal women: a review of the literature.
Nutr Res. 2009 Apr;29(4):221-8.

Je SH, Joo NS, Choi BH, Kim KM, Kim BT, Park SB, Cho DY, Kim KN, Lee DJ.
Vitamin K supplement along with vitamin D and calcium reduced serum concentration of undercarboxylated osteocalcin while increasing bone mineral density in Korean postmenopausal women over sixty-years-old.
J Korean Med Sci. 2011 Aug;26(8):1093-8.

Jie KG, Bots ML, Vermeer C, Witteman JC, Grobbee DE.
Vitamin K status and bone mass in women with and without aortic atherosclerosis: a population-based study.
Calcif Tissue Int. 1996 Nov;59(5):352-6.

Jin DY, Tie JK, Stafford DW.
The conversion of vitamin K epoxide to vitamin K quinone and vitamin K quinone to vitamin K hydroquinone uses the same active site cysteines.
Biochemistry. 2007 Jun 19;46(24):7279-83.

Kanai T, Takagi T, Masuhiro K, Nakamura M, Iwata M, Saji F.
Serum vitamin K level and bone mineral density in post-menopausal women.
Int J Gynaecol Obstet. 1997 Jan;56(1):25-30.

Kidd PM.
Vitamins D and K as pleiotropic nutrients: clinical importance to the skeletal and cardiovascular systems and preliminary evidence for synergy.
Altern Med Rev. 2010 Sep;15(3):199-222.

Knapen MH, Schurgers LJ, Vermeer C.
Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women.
Osteoporos Int. 2007 Jul;18(7):963-72.

Lian J, Stewart C, Puchacz E, Mackowiak S, Shalhoub V, Collart D, Zambetti G, Stein G.
Structure of the rat osteocalcin gene and regulation of vitamin D-dependent expression.
Proc Natl Acad Sci U S A. 1989 Feb;86(4):1143-7.

Luo LZ, Xu L.
Vitamin K and osteoporosis.   [Article in Chinese]
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2003 Jun;25(3):346-9.

Patriquin C, Crowther M.
Treatment of warfarin-associated coagulopathy with vitamin K.
Expert Rev Hematol. 2011 Dec;4(6):657-67.

Price PA, Faus SA, Williamson MK.
Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves.
Arterioscler Thromb Vasc Biol. 1998 Sep;18(9):1400-7.

Price PA, Faus SA, Williamson MK.
Warfarin-induced artery calcification is accelerated by growth and vitamin D.
Arterioscler Thromb Vasc Biol. 2000 Feb;20(2):317-27.

Ronden JE, Drittij-Reijnders MJ, Vermeer C, Thijssen HH.
Intestinal flora is not an intermediate in the phylloquinone-menaquinone-4 conversion in the rat.
Biochim Biophys Acta. 1998 Jan 8;1379(1):69-75.

Sato Y, Kanoko T, Satoh K, Iwamoto J.
Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer’s disease.
Bone. 2005 Jan;36(1):61-8. Epub 2004 Nov 24.

Shiomi S, Nishiguchi S, Kubo S, Tamori A, Habu D, Takeda T, Ochi H.
Vitamin K2 (menatetrenone) for bone loss in patients with cirrhosis of the liver.
Am J Gastroenterol. 2002 Apr;97(4):978-81.

Spronk HM, Soute BA, Schurgers LJ, Thijssen HH, De Mey JG, Vermeer C.
Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats.
J Vasc Res. 2003 Nov-Dec;40(6):531-7. Epub 2003 Dec 3.

Toshio Okano, Yuka Shimomura, Makiko Yamane, Yoshitomo Suhara, Maya Kamao, Makiko Sugiura and Kimie Nakagawa
Conversion of Phylloquinone (Vitamin K1) into Menaquinone-4 (Vitamin K2) in Mice
TWO POSSIBLE ROUTES FOR MENAQUINONE-4 ACCUMULATION IN CEREBRA OF MICE

The Journal of Biological Chemistry, April 25, 2008, 283, 11270-11279

Tsukamoto Y.
Studies on action of menaquinone-7 in regulation of bone metabolism and its preventive role of osteoporosis.
Biofactors. 2004;22(1-4):5-19.

Yamaguchi M.
Regulatory mechanism of food factors in bone metabolism and prevention of osteoporosis.
Yakugaku Zasshi. 2006 Nov;126(11):1117-37.

Vermeer C, Schurgers LJ.
A comprehensive review of vitamin K and vitamin K antagonists.
Hematol Oncol Clin North Am. 2000 Apr;14(2):339-53.

Wallin R, Schurgers L, Wajih N.
Effects of the blood coagulation vitamin K as an inhibitor of arterial calcification.
Thromb Res. 2008;122(3):411-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Blood Pressure and Vitamin C

healthy-fruitWhat Is High Blood Pressure?

Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps blood, and, if it stays elevated for a long time, can cause myriad health problems, including heart disease, stroke and kidney failure. Because it has no symptoms, it’s readily ignored. According to the CDC, about one third of Americans have elevated BP. If the first number is higher than 140 and the second is higher than 90, you have high blood pressure. If the first is 160 and the second is 100 or more, you are at stage 2 and really need intervention. It’s true that BP rises with age, but there still are things that can be, and should be, done about it.

There are factors you can control, and factors you can’t. Weight, too much salt, overdoing alcohol, insufficient potassium in the diet, sedentary lifestyle and smoking all are under your authority. Gender, race and family history aren’t. Despite the way it looks, stress can be managed, not always easily, but possible.

What Can I Do About It?

The DASH diet (Dietary Approaches to Stop Hypertension) focuses on very low sodium and high intake of fruits and vegetables, accompanied by a relatively low fat intake that includes lean meats, fish, and nuts and seeds. Being rich in fiber, nutrients and protein, the diet eliminates added sugars, added salt (you have to read labels), and sweets. Total salt consumption for the day shouldn’t exceed a teaspoonful. Because it’ll spike BP, alcohol is limited to two drinks a day for a man, one for a woman (McFarlane, 2007). Information about the DASH plan, either on paper or online, is available free at http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/index.htm.

We realize that the TV remote is a handy gadget. We also realize it put the kibosh on the last vestiges of physical activity for a slew of people. Before remotes were around, many of us used our kids to change channels. Not only high blood pressure, but also other health risks can be eliminated with a regimen of exercise. When you consider the options, exercise isn’t such a bad deal.

Most of us have a heart that is designed to pump blood a certain distance. Forcing it to pump harder and farther is akin to adding a hundred feet to the garden hose and watching it trickle for lack of water pressure. After a while, the heart gets tired of this slavery and goes on strike.  That’s when the trouble starts. Fat needs blood. Every extra pound of fat adds blood vessels.  The more than sixty thousand miles of tubes you already have doesn’t need to be enhanced by the extra miles that grow to feed fat. The bottom line? Lose weight and get your body mass index back where it belongs.

Inhaling a cigarette constricts blood vessels. That’s explains the light high that comes from the first smoke of the day. It reduces oxygen to the brain, just like booze, and you get a brief euphoria. But it can also make blood vessels stiff. Some say that smoking relieves stress.  Maybe so, but physical activity does the same thing and the effect lasts much longer. Plus, you can make new friends with exercise.

Do Supplements Help?

A recent report from Johns Hopkins University says that large doses of vitamin C can lower elevated blood pressure (Juraschek, 2012). The RDA for this vitamin is a mere 90 milligrams, barely enough to provide physiological benefit, but just enough to prevent scurvy. At 500 mg of vitamin C a day for at least eight weeks, subjects experienced a drop in systolic pressure of 3.8 mm Hg and a drop in diastolic pressure of 1.48 mm Hg. For those with existing high BP, the systolic drop was almost 5 mm Hg. Persons taking medication to control their BP could expect a 10 mm decrease. The lead author of this study, Edgar R. Miller, III, M.D., PhD, adds that, although the impact is moderate, it’s sufficient to decrease the number of stroke occurrences.  As is the case with any such investigation, additional study is warranted.

British scrutiny suggests that increased consumption of fruits and vegetables high in vitamin C is the way to go. This study indicated that people with high plasma values of the vitamin (from food) had lower clinical blood pressure. People who supplemented with vitamin C were excluded from this study, so one can only guess at the impact supplementation would have (Myint, 2011). Supplement users might be smiling at this point, or even smirking, but they need to know that combining vitamin C with certain other supplements might just undo what the vitamin can do. Lots of folks open several supplement bottles at one time without knowing of their interactions with each other, with foods, and with medications. This is not a prudent habit.  Many plant polyphenols are beneficial to human health. The timing of their ingestion is important. Australian researchers have found that combining vitamin C with grape seed polyphenols actually raises blood pressure. The hypothesis was that both substances, either alone or in combination, could lower elevated BP.  Vitamin C alone did. Polyphenols alone did not. The combo elevated BP by almost 5 points systolic and nearly 3 points diastolic (Ward, 2005). Need we advise caution and maybe a visit to a functional medicine dietitian or similarly-trained physician? Of course, this is only one study.

Beyond Vitamin C

Citrus fruits and their juices are among people’s favorites. A component of citrus called diosmin, also found in rosemary and used to address venous insufficiency, such as that in varicose veins and hemorrhoids, was found to be an anti-hypertensive agent in lab animals whose blood pressure was artificially elevated with a salt-laced compound. This flavonoid pigment was also found to rectify aberrant blood markers and to be protective of the heart and kidneys (Silambarasan, 2012).

Environmental Insults Raise Blood Pressure

Cadmium is one of the most important environmental pollutants that cause a number of adverse health effects. It’s a major component of tobacco smoke, emissions from steel and zinc production, waste incineration and coal combustion, and might be a fractional element of phosphate fertilizer manufacture (Hutton, 1983). Cadmium’s oxidative potential is witnessed in vascular dysfunction characterized by elevated arterial blood pressure and blunted response to vasoactive agents. Administration of ascorbic acid in a dose-dependent manner normalized blood pressure and improved vascular reactivity while suppressing the formation of oxidized substances (Donpunha, 2011). Lead exposure, whether chronic at low levels or acute at high levels, will elevate blood pressure in humans and animals. Like cadmium, it will generate free radicals and decrease available nitric oxide, the gas that relaxes blood vessels. Irani investigators found that vitamin C is able to prevent lead-induced hypertension (Mohammed, 2010).

Vitamins C is an anti-oxidant nutrient that seems to exert a healthful effect on blood pressure.  That does not leave room for self-treatment, however, because there is no definitive statement about eliminating the cause of hypertension or merely treating it as a symptom. Nonetheless, as adjunct to diet, exercise and lifestyle modification, it’s worth a try. But it isn’t without some pimples. It might reduce the response to warfarin and lower absorption, and might cause a false reading in some blood tests, as in a false increase in creatinine, a false increase in urinary calcium, and a false decrease in urinary sodium. Since vitamin C in large amounts is metabolized to oxalic acid, beware of kidney stones. On the other hand, if you smoke, you need high doses. In that case, get it from food.

References

Block G, Jensen CD, Norkus EP, Hudes M, Crawford PB.
Vitamin C in plasma is inversely related to blood pressure and change in blood pressure during the previous year in young Black and White women.
Nutr J. 2008 Dec 17;7:35

Chen J, He J, Hamm L, Batuman V, Whelton PK
Serum antioxidant vitamins and blood pressure in the United States population.
Hypertension. 2002 Dec;40(6):810-6.

Donpunha W, Kukongviriyapan U, Sompamit K, Pakdeechote P, Kukongviriyapan V, Pannangpetch P.
Protective effect of ascorbic acid on cadmium-induced hypertension and vascular dysfunction in mice.
Biometals. 2011 Feb;24(1):105-15.

Fernandes PR, Lira FA, Borba VV, Costa MJ, Trombeta IC, Santos Mdo S, Santos Ada C.
Vitamin C restores blood pressure and vasodilator response during mental stress in obese children.
[Article in English, Portuguese, Spanish]
Arq Bras Cardiol. 2011 Jun;96(6):490-7

He J, Wofford MR, Reynolds K, Chen J, Chen CS, Myers L, Minor DL, Elmer PJ, Jones DW, Whelton PK.
Effect of dietary protein supplementation on blood pressure: a randomized, controlled trial.
Circulation. 2011 Aug 2;124(5):589-95.

Hutton M.
Sources of cadmium in the environment.
Ecotoxicol Environ Saf. 1983 Feb;7(1):9-24.

Jalal DI, Smits G, Johnson RJ, Chonchol M
Increased fructose associates with elevated blood pressure.
J Am Soc Nephrol. 2010 Sep;21(9):1543-9.

Juraschek SP, Guallar E, Appel LJ, Miller ER 3rd.
Effects of vitamin C supplementation on blood pressure: a meta-analysis of randomized controlled trials.
Am J Clin Nutr. 2012 May;95(5):1079-88. Epub 2012 Apr 4.

McFarlane SI, von Gizycki H, Salifu M, Deshmukh M, Manieram M, Gebreegziabher Y, Gliwa AA, Bordia S, Shah S, Sowers JR.
Alcohol consumption and blood pressure in the adult US population: assessment of gender-related effects.
J Hypertens. 2007 May;25(5):965-70.

Mohammad A, Ali N, Reza B, Ali K.
Effect of ascorbic acid supplementation on nitric oxide metabolites and systolic blood pressure in rats exposed to lead.
Indian J Pharmacol. 2010 Apr;42(2):78-81.

Myint PK, Luben RN, Wareham NJ, Khaw KT.
Association between plasma vitamin C concentrations and blood pressure in the European prospective investigation into cancer-Norfolk population-based study.
Hypertension. 2011 Sep;58(3):372-9. Epub 2011 Jul 18.

Mullan BA, Young IS, Fee H, McCance DR.
Ascorbic acid reduces blood pressure and arterial stiffness in type 2 diabetes.
Hypertension. 2002 Dec;40(6):804-9.

Silambarasan T, Raja B.
Diosmin, a bioflavonoid reverses alterations in blood pressure, nitric oxide, lipid peroxides and antioxidant status in DOCA-salt induced hypertensive rats.
Eur J Pharmacol. 2012 Mar 15;679(1-3):81-9. Epub 2012 Jan 12.

Stamler J, Stamler R, Neaton JD.
Blood pressure, systolic and diastolic, and cardiovascular risks. US population data.
Arch Intern Med. 1993 Mar 8;153(5):598-615.

Teunissen-Beek KF, Dopheide J, Geleijnse JM, Bakker SJ, Brink EJ, de Leeuw PW, van Baak MA.
Protein supplementation lowers blood pressure in overweight adults: effect of dietary proteins on blood pressure (PROPRES), a randomized trial.
Am J Clin Nutr. 2012 Apr;95(4):966-71.

Vasdev S, Ford CA, Parai S, Longerich L, Gadag V.
Dietary vitamin C supplementation lowers blood pressure in spontaneously hypertensive rats.
Mol Cell Biochem. 2001 Feb;218(1-2):97-103.

Ward NC, Hodgson JM, Croft KD, Burke V, Beilin LJ, Puddey IB.
The combination of vitamin C and grape-seed polyphenols increases blood pressure: a randomized, double-blind, placebo-controlled trial.
J Hypertens. 2005 Feb;23(2):427-34.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Vitamin C For Bone Health?

skeleton-vitamin-cHow many bones are in the human skeleton? How come it’s on the inside? What does it do? Does anybody really care? Sometimes.

The human skeleton offers shape and protection to the body. It supplies a place for organs to attach or to be supported. It comprises 206 bones, the largest of which is the thigh (femur). It makes up about 15% of your body weight, part of which is water. This fifteen percent refers to ideal body weight, not to a 400-pound behemoth who is less than six feet tall. Infants have more than 206. The skull starts out with more than twenty bones, some of which fuse together during development. Besides helping you to move, bones make red and white blood cells in their marrow, and act as a storage house for minerals. It takes about twenty years to develop completely.

Bone is actually a type of connective tissue, obviously denser than cartilage, which is the flexible stuff at the flap of your ear (tragus) and the tip of your nose. Cartilage also makes the discs that separate your vertebrae from each other and the femur from the tibia at the knee. Bone tissue is heavily mineralized by a form of calcium called hydroxyapatite. Calcium is the mineral found in the greatest amount in the body, about ninety-nine percent of which is in bone. Phosphorus works with calcium to maintain bone health by combining to make hydroxyapatite. This aggregation helps bone to remodel—to break down and then to redeposit. Trace amounts of other minerals, including magnesium, boron, copper and zinc, stimulate bone growth. But there’s one element of bone health that is overlooked because it’s thought of as nothing more than an anti-oxidant—vitamin C, aka ascorbic acid.

In a study of prepubescent females done in Philadelphia, it was learned that specific bone parameters were positively affected by vitamin C, especially in combination with zinc. For every milligram a day of vitamin C intake, there was an increase in trabecular bone area (Laudermilk, 2012). That’s the porous part of a bone found in the center and at the end of a long bone, like the femur. It’s important to the manufacture of blood cells inside the red marrow. Because it’s porous, trabecular bone is not as strong as the harder cortical outer layer. As hormones change with development, bone requirements also change. This is why it’s necessary to lay down as much bone as possible in one’s early years. By the time a girl reaches thirty, she will have laid down all the bone she ever will, which is probably why a DXA scan compares/contrasts a patient’s bone density to that of a thirty-year-old. You can read about this at the NIH Osteoporosis and Related Bone Diseases National Resource Center website,
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp

If vitamin C intake promotes bone, then deficiency must degrade it. Too little vitamin C causes scurvy, the condition that once affected seamen who were deprived of fresh fruits and vegetables for prolonged periods. That doesn’t happen anymore; at least it shouldn’t. The sailors’ joints and muscles would hurt, they bruised easily, their gums would bleed, and their teeth would sometimes fall out. Since vitamin C is responsible for the formation of connective tissue, these occurrences seem relevant.  Spontaneous fractures caused by low bone mineral density, and considered to be induced by a failure of collagen synthesis, also characterize scurvy (Park, 2012). Deficiency of vitamin C is implicated in scurvy by the inhibition of osteoblast activity. You remember osteoblasts.  They’re the cells responsible for making new bone material.

Most animals do not require external sources of vitamin C because they can get it from glucose through their enzyme systems. Humans and other primates, guinea pigs, and fruit bats lack this ability, so they have to get it from their diets. Since fast foods have replaced fruits and vegetables, many of us may be vitamin C deficient in the absence of supplementation.  Lettuces, onions, apples and bananas don’t help. Citrus fruits, cruciferous vegetables and strawberries do. Besides diet, other lifestyle factors influence vitamin C status, especially smoking, a habit that seriously affects the neck of the femur (Sahni, 2008) unless ascorbic acid intake is considerably greater than the RDA. The dietary recommendation for vitamin C is that amount needed to prevent a condition caused by its lack, in this case, scurvy and its aftermath. Sixty milligrams a day is hardly enough to meet a human’s physiological and metabolic needs. The 400-pound gorilla at the zoo gets 4000 milligrams a day. Shouldn’t a 200-pound human get 2000, then?

Speaking of the femur…This is where the hip joint is, at the top of the thigh bone.  In a seventeen-year follow-up study conducted by Tufts University, those elderly (70-80 yrs.) in the highest third of vitamin C intake had significantly fewer hip and non-vertebral fractures than those in the bottom third, suggesting a protective effect of vitamin C on bone health (Sahni, 2009). It’s important to note that oral contraceptives may adversely affect vitamin C accumulation. Women who fail to supplement while taking hormones as oral contraceptives have lower plasma levels of vitamin C than those who do supplement (Kuo, 2002). This, however, would seem to be the case regardless of contraceptive use.  Concerning sex steroids, both estrogen and testosterone are important for developing peak bone mass (Riggs, 2002). In the case of hypogonadism, where sex glands produce little or no hormones, vitamin C stimulates bone formation (Zhu, 2012), allowing bone recovery in light of hormone deficit. This finding is particularly important to those at risk for osteoporosis, as may be such in developing countries, among the food insecure, and in men who have had certain treatments for prostate disease, including one called gonadotropin-releasing hormone, abbreviated GnRH  (Mittan, 2002).

Despite having lost the ability to synthesize vitamin C, humans can take supplements or increase dietary intake to avert the onset of osteoporosis, realizing that ascorbic acid can block osteoclast proliferation and bone loss while promoting osteoblast activity and bone remodeling.

References

Fain O.
Musculoskeletal manifestations of scurvy.
Joint Bone Spine. 2005 Mar;72(2):124-8.

Gabbay KH, Bohren KM, Morello R, Bertin T, Liu J, Vogel P.
Ascorbate synthesis pathway: dual role of ascorbate in bone homeostasis.
J Biol Chem. 2010 Jun 18;285(25):19510-20.

Kuo SM, Stout A, Wactawski-Wende J, Leppert PC.
Ascorbic acid status in postmenopausal women with hormone replacement therapy.
Maturitas. 2002 Jan 30;41(1):45-50.

Laudermilk MJ, Manore MM, Thomson CA, Houtkooper LB, Farr JN, Going SB.
Vitamin C and Zinc Intakes are Related to Bone Macroarchitectural Structure and Strength in Prepubescent Girls.
Calcif Tissue Int. 2012 Oct 18.

Lean JM, Davies JT, Fuller K, Jagger CJ, Kirstein B, Partington GA, Urry ZL, Chambers TJ.
A crucial role for thiol antioxidants in estrogen-deficiency bone loss.
J Clin Invest. 2003 Sep;112(6):915-23.

Mittan D, Lee S, Miller E, Perez RC, Basler JW, Bruder JM.
Bone loss following hypogonadism in men with prostate cancer treated with GnRH analogs.
J Clin Endocrinol Metab. 2002 Aug;87(8):3656-61.

NIH Osteoporosis and Related Bone Diseases National Resource Center
Bone Mass Measurement: What the Numbers Mean
January, 2012
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp

Park JK, Lee EM, Kim AY, Lee EJ, Min CW, Kang KK, Lee MM, Jeong KS.
Vitamin C deficiency accelerates bone loss inducing an increase in PPAR-γ expression in SMP30 knockout mice.
Int J Exp Pathol. 2012 Oct;93(5):332-40.

B. Lawrence Riggs, Sundeep Khosla and L. Joseph Melton II
Sex Steroids and the Construction and Conservation of the Adult Skeleton
Endocrine Reviews June 1, 2002 vol. 23 no. 3 279-302

Sahni S, Hannan MT, Gagnon D, Blumberg J, Cupples LA, Kiel DP, Tucker KL.
High vitamin C intake is associated with lower 4-year bone loss in elderly men.
J Nutr. 2008 Oct;138(10):1931-8.

Sahni S, Hannan MT, Gagnon D, Blumberg J, Cupples LA, Kiel DP, Tucker KL.
Protective effect of total and supplemental vitamin C intake on the risk of hip fracture–a 17-year follow-up from the Framingham Osteoporosis Study.
Osteoporos Int. 2009 Nov;20(11):1853-61.

Markus J. Seibel, Colin R. Dunstan, Hong Zhou, Charles M. Allan and David J. Handelsman
Sex Steroids, Not FSH, Influence Bone Mass
Cell. 2006 Dec 15;127(6):1079

Simon JA, Hudes ES.
Relation of ascorbic acid to bone mineral density and self-reported fractures among US adults.
Am J Epidemiol. 2001 Sep 1;154(5):427-33.

Zhu L-L, Cao J, Sun M, Yuen T, Zhou R, Mne Zaidi, et al.
Vitamin C Prevents Hypogonadal Bone Loss.
PLoS ONE (2012); 7(10): e47058.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Mineral Balance: Sodium-Potassium

sodium-potassium-scaleLike children on a see-saw, some minerals work to balance each other in the body. Almost everything in nature is about balance. In humans and animals it’s called homeostasis, which is the property of the body to maintain its internal environment in a stable, constant condition. Occasionally, mainstream medicine overlooks the balance aspect and tends to look at isolated parts and actions of the body. One of these oversights involves sodium and its relationship with potassium, working together as the sodium-potassium pump, which is the mechanism of active transport by which sodium and potassium ions are moved across the cell membrane, into and out of the cell. With the help of ATP as the source of energy, sodium is extruded from the cell and potassium is invited in. This energetic display is necessary for protein biosynthesis, maintenance of osmotic equilibrium, initiation of nerve impulses and transport of some other molecules, such as glucose, across the membrane. To clarify, ATP is a high-energy phosphate compound used by the body to get things done, including muscle contractions and enzyme metabolism, among others.

Sodium (Na) and potassium (K) are essential minerals and electrolytes. As the latter, they dissociate into ions (charged particles), allowing them to conduct electricity. In order for the body to function the right way, they need to be regulated on both sides of the cell membrane. The recommended intake of sodium had been 2300 milligrams a day, but is now 1500 mg/d; that for potassium being unchanged at 4700 mg/day. The sodium:potassium ratio, therefore, has moved from 1:2 to almost 1:3, which is closer to what is believed to be the body’s ideal. In plants, of which humans eat too few, the natural ratio of Na to K is about 1:10.

Sodium is the chief ion outside the cell, potassium inside. Inside the cell, sodium concentrations are ten times lower than outside. Potassium concentration inside are about thirty times higher than outside. The difference across the membrane creates an electrochemical gradient known as membrane potential, which uses a lot of the body’s energy to maintain itself. Without this tight control, muscles would suffer, especially the heart. In the typical American diet, intake of sodium (as sodium chloride) is three times higher than potassium, just the opposite of what it should be. The dietary guidelines for sodium consumption are currently being met by only a tiny percent of the population (Drewnowski, 2012)

Table salt is about 39% sodium. A simple explanation is that one teaspoon of salt, which has a mass about 6200 mg, contains approximately 2400 mg of sodium.

The National Health and Nutrition Examination Survey (NHANES), first conducted in the early 70’s, reported in 2012 that more than 90% of adults consumed more than 2300 mg/d of sodium a day, and less than 2%–that’s two percent—met the recommendation for potassium (Cogswell, 2012). It’s no small surprise that high blood pressure is rampant (Wenberger, 1986) (Elliot, 1991, 1996) (Dyer, 1995) (He, 2004) (Levings, 2012)  Of course, you could argue that the relationship of sodium intake to hypertension is a genetic matter, but do you know your genes?

Increasing potassium and reducing sodium intake will help to reduce blood pressure. But be careful not to overdo it by using supplements without strict supervision, since potassium overload is almost as bad as potassium deficiency. After all, potassium is used to stop the heart in lethal injections. Aiming for the recommended 4700 mg a day means that vegetables and fruit intake needs to go up, while intake of cakes, cookies and prepared foods needs to go down. Overdosing potassium from foods is almost impossible…you can’t eat that much food.

If less than 2% of Americans get the recommended amount of potassium, how much do we get?  From data collected in 2009-2010, women get about 50% of the RDI, men about 81% (USDA, 2012). Besides supporting coronary health, potassium seems to lower the risk of stroke (Ascherio, 1998) (Larsson, 2011). If you’ve got abnormally high urinary calcium levels, you might be looking at kidney stones in your future, something we wouldn’t wish on anyone.  Increasing dietary potassium levels by increasing fruit and vegetable intake has been found to decrease urinary calcium excretion. Taking a supplement under supervision will do the same thing. It has been found that getting more than 4000 mg of potassium a day reduces risk of kidney stones (Curhan, 2004).

Diuretics may lower potassium levels, but not all do, so check with your doctor to find out if your diuretic is potassium-sparing or not. Laxatives, caffeine, tobacco and lots of sugar may also compromise potassium stores. Physical and mental stress interferes with potassium metabolism. If you haven’t already, try to increase potassium foods, including sweet potatoes, bananas, tomatoes, oranges, beans, squashes, nuts and seeds, green foods, avocados, garlic and a host of other produce. Look here for a list:
http://www.health.gov/dietaryguidelines/dga2005/document/html/appendixb.htm.

Look at both sodium and potassium in the context of what you eat every day and try to balance foods before you consider a potassium supplement. You know where most of the salt comes from (processed foods and the salt shaker), but you’ll have to read labels to find the rest. If you can maintain a ratio of one to one, you’ll be better off than most, but trying to get two to one, potassium to sodium, is preferred. Limiting sodium to about 500 mg in a meal is a virtuous endeavor. Look at some soup cans and you’ll see more than that in a tiny serving’s worth.  Even certain “light” soups have 650 mg of sodium in a 1-cup serving. Potassium values of these products are half that, which is the opposite of what it should be.  If the whole can is consumed, sodium-potassium balance needs to be addressed at other meals. Seeing kids unbalanced on a see-saw can be amusing. Viewing sodium-potassium balance from a gurney is not.

References

Arcand J, Steckham K, Tzianetas R, L’Abbe MR, Newton GE.
Evaluation of Sodium Levels in Hospital Patient Menus
Arch Intern Med. 2012;172(16):1261-1262.

Ascherio A, Rimm EB, Hernán MA, Giovannucci EL, Kawachi I, Stampfer MJ, Willett WC.
Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men.
Circulation. 1998 Sep 22;98(12):1198-204.

Barri YM, Wingo CS.
The effects of potassium depletion and supplementation on blood pressure: a clinical review.
Am J Med Sci. 1997 Jul;314(1):37-40.

Centers for Disease Control and Prevention (CDC).
Usual sodium intakes compared with current dietary guidelines — United States, 2005-2008.
MMWR Morb Mortal Wkly Rep. 2011 Oct 21;60(41):1413-7.

Cogswell ME, Zhang Z, Carriquiry AL, Gunn JP, Kuklina EV, Saydah SH, Yang Q, Moshfegh AJ.
Sodium and potassium intakes among US adults: NHANES 2003-2008.
Am J Clin Nutr. 2012 Sep;96(3):647-57.

Curhan GC, Willett WC, Knight EL, Stampfer MJ.
Dietary factors and the risk of incident kidney stones in younger women: Nurses’ Health Study II.
Arch Intern Med. 2004 Apr 26;164(8):885-91.

Denton D, Weisinger R, Mundy NI, Wickings EJ, Dixson A, Moisson P, Pingard AM, Shade R, Carey D, Ardaillou R, et al.
The effect of increased salt intake on blood pressure of chimpanzees.
Nat Med. 1995 Oct;1(10):1009-16.

Drewnowski A, Maillot M, Rehm C.
Reducing the sodium-potassium ratio in the US diet: a challenge for public health.
Am J Clin Nutr. 2012 Aug;96(2):439-44.

Dyer AR, Stamler R, Elliott P, Stamler J.
Dietary salt and blood pressure.
Nat Med. 1995 Oct;1(10):994-6.

Elliott P
Observational studies of salt and blood pressure.
Hypertension. 1991 Jan;17(1 Suppl):I3-8.

Elliott P, Stamler J, Nichols R, Dyer AR, Stamler R, Kesteloot H, Marmot M.
Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. Intersalt Cooperative Research Group.
BMJ. 1996 May 18;312(7041):1249-53.

He FJ, MacGregor GA.
Effect of longer-term modest salt reduction on blood pressure.
Cochrane Database Syst Rev. 2004;(3):CD004937

Hoorn EJ, Betjes MG, Weigel J, Zietse R.
Hypernatraemia in critically ill patients: too little wat
er and too much salt.

Nephrol Dial Transplant. 2008 May;23(5):1562-8.

Krishna GG, Chusid P, Hoeldtke RD.
Mild potassium depletion provokes renal sodium retention.
J Lab Clin Med. 1987 Jun;109(6):724-30.

Krishna GG.
Role of potassium in the pathogenesis of hypertension.
Am J Med Sci. 1994 Feb;307 Suppl 1:S21-5.

Larsson SC, Virtamo J, Wolk A.
Potassium, calcium, and magnesium intakes and risk of stroke in women.
Am J Epidemiol. 2011 Jul 1;174(1):35-43.

Levings J, Cogswell M, Curtis CJ, Gunn J, Neiman A, Angell SY.
Progress toward sodium reduction in the United States.
Rev Panam Salud Publica. 2012 Oct;32(4):301-6.

National Institute of Health
Jan. 26, 2009
Sodium/Potassium Ratio Linked to Cardiovascular Disease Risk
http://www.nih.gov/researchmatters/january2009/01262009hypertension.htm

Akira Okayama; Katsuyuki Miura; Tomonori Okamura; Nagako Okuda; Shigeyuki Saitoh; et al
Abstract MP077: Dietary Sodium Potassium Ratio as a Risk Factor for Stroke, Cardiovascular Diseases and All-cause Death Among Japanese: Nippondata80.
Circulation. 2012; 125: AMP077

Quanhe Yang, PhD; Tiebin Liu, MSPH; Elena V. Kuklina, MD, PhD; et al.
Sodium and Potassium Intake and Mortality Among US AdultsProspective Data From the Third National Health and Nutrition Examination Survey FREE
Arch Intern Med. 2011;171(13):1183-1191.

Lynn D. Silver, MD, MPH; Thomas A. Farley, MD, MPH
Sodium and Potassium Intake: Mortality Effects and Policy ImplicationsComment on “Sodium and Potassium Intake and Mortality Among US Adults”
Arch Intern Med. 2011;171(13):1191-1192.

Stofan JR, Zachwieja JJ, Horswill CA, Murray R, Anderson SA, Eichner E
Sweat and sodium losses in NCAA football players: a precursor to heat cramps?
Int J Sport Nutr Exerc Metab. 2005 Dec;15(6):641-52.

U.S. Department of Agriculture, Agricultural Research Service. 2012.
Total Nutrient Intakes: Percent Reporting and Mean Amounts of Selected Vitamins and Minerals from Food and Dietary
Supplements, by Family Income (as ! of Federal Poverty Threshold) and Age, What We Eat in America, NHANES 2009-2010. Available: www.ars.usda.gov/ba/bhnrc/fsrg.
USDA, Agricultural Research Services

USDA
Dietary Guidelines for Americans 2005
Appendix B-1. Food Sources of Potassium
http://www.health.gov/dietaryguidelines/dga2005/document/html/appendixb.htm

USDA. Downloadable pdf Tables.
What We Eat in America, 2009-2010.
http://www.ars.usda.gov/Services/docs.htm?docid=18349

Weinberger MH, Miller JZ, Luft FC, Grim CE, Fineberg NS.
Definitions and characteristics of sodium sensitivity and blood pressure resistance.
Hypertension. 1986 Jun;8(6 Pt 2):II127-34.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Mineral Balance: Copper-Zinc

copper-zinc-scaleThe last mineral topic we covered dealt with sodium and potassium. Important stuff, this mineral balance. Recall that the amounts of minerals needed by the body are not an indication of their importance, and that we probably can’t get all that we need from our foods because of untrustworthy practices from seed to table. Remember, too, that kids, especially, need to eat the plants to get the minerals. The recommended number of servings of fruits and vegetables is now nine to thirteen, up from five to nine. Either way, how many people do you know who eat that much?

Copper and zinc are antagonists, and the balance between them is an example of biological dualism. This does that, and that does this, and they often fight with each other. Kind of a simple explanation, but maybe you get it. Yes, it’s possible for there to be zinc toxicity and copper toxicity. In the past, it’s been copper toxicity and zinc deficiency. Today it might be just the reverse, considering that people take supplements without the faithful reading of labels. Both minerals play important roles in the body.

Copper is necessary for blood vessel formation, a strong heart and for stabilizing collagen. You know what collagen is…the glue that holds us together. We need copper for brain development and for communication between nerve cells in the brain. Copper is essential to a number of enzymes involved in energy production by the mitochondria.  It helps to make superoxide dismutase to get rid of reactive oxygen species (free radicals). Because it’s found in a number of foods, copper deficiency is not common. Meats, shellfish, nuts, and seeds are premier sources, followed by mushrooms, lentils, shredded wheat and chocolate. Daily intake by adults normally is a little more than a milligram, which is only a bit higher than the RDA of 0.9 mg. The tolerable upper limit for adults is 10 mg, while most supplements contain 2 mg. Infants fed a cow’s milk diet are the ones most likely deficient because milk has little copper, but people with malabsorption disorders are close behind. Anemia and low white blood cell count are signs of deficit. Take care to note that very high doses of vitamin C might interfere with copper-related enzyme efficiency (Finley, 1983). But that’s not written in stone. Zinc overdose, however, might be a legitimate cause of copper deprivation.

Now, here’s the rub with zinc. Concerns arise when you take several supplements that each contain zinc. The tolerable upper limit, the dose above which there may be adverse reactions, is 40 milligrams for an adult. Let’s see, Hmm, prostate formula contains 15 mg; cold/flu formula contains 15 mg; daily multi-vitamin contains 15 mg; nasal spray contains 5 mg; other zinc complexes aimed at myriad conditions contain more…  Can you see where we’re going?  Copper deficiency now becomes a possibility. The need for zinc hovers around 11 mg for a guy, about 8 mg for a non-pregnant female.

Zinc is needed for steroid hormone synthesis, being a well-known catalyst for testosterone manufacture as well as luteinizing hormone, the one that stimulates ovulation. Of all the body parts, the prostate contains the highest concentrations. More than a hundred different enzymes rely on zinc for their ability to catalyze chemical reactions in the body. It plays a structural role in the superoxide dismutase mentioned in the earlier paragraph and in the integrity of the cell membrane. In fact, the loss of zinc from biological membranes increases their susceptibility to oxidative damage (O’Dell, 2000). Then, we have these nifty little things called zinc fingers, which are transcription factors that bind to DNA and influence specific genes, which are stabilized by the presence of zinc. Taking too much zinc over a period of a few weeks will upset copper bioavailability, possibly resulting in hematology issues down the line. Meanwhile, the bioavailability of folate/folic acid/folinic acid is enhanced by zinc.

Zinc deficiency usually follows genetic disorders and is identified as such. Immune deficiencies, impaired healing, diminished sense of taste (and perhaps smell), night blindness, opacity of the cornea, behavioral disturbances, and delayed maturation are common signs of low zinc values. Deficiency in children is dramatic in that neuropsychological development is impeded and susceptibility to life-threatening infections is increased (Hambidge, 2000).

Do those zinc lozenges advertisements have any immune system merit? We know that zinc deficiency causes immune dysfunction, but there is mixed commentary on the efficacy of zinc mega-doses for colds and other viral infections in people with ample zinc stores (Baum, 2000) (Salqueiro, 2000) (Fraker, 2000). The immune system relies on more than just zinc for its competence. Essential amino and fatty acids, selenium and iron, folic acid and vitamins B6 and B12, and vitamins E, A and C have a say in the immune system’s function. Consider, too, that a deficiency in one of these is likely to follow a deficiency in one or more of the others. Intakes of nutrients in excess of the recommendations do not necessarily translate to a boost in all immune activity unless a deficiency has been identified. Even then, despite the disparity in research conclusions, mega-doses of one mineral can knock another one out of the ring. On the other hand, using zinc lozenges as soon as cold symptoms appear seems to reduce severity and duration, depending on the formulation (Singh, 2011).

Balancing copper and zinc, though vitally important, may not be as easy as expected. Exposure to other metals, especially to lead that may originate from ancient water pipes, contaminated ground water, the shooting sports, some toys and paints,and fishing sinkers, can push zinc out. Iron, particularly from a supplement, may inhibit intestinal absorption of both zinc and copper through competition for transport molecules located in the gut. Wilson’s disease, the inability to metabolize copper out of the body, requires a dietary change that precludes mushrooms, nuts, chocolate, shellfish and dried fruits, and includes zinc therapy (Chasapis, 2012). The testing for zinc and copper values is not completely established because reference ranges are based on statistical averages, not on optimum functional levels. As with other nutrients, availability from foods is too often questionable, but supplementation should to be considered under the guidance of a knowledgeablenutrition professional, such as a credentialed nutritionist or dietitian. A caveat: Don’t even think about drinking water from a galvanized container. There are reports of a family that had collected its drinking water from a brand new refuse container and suffered from zinc overdose. Some denture adhesives contain zinc. Be careful. Read labels.

References

Baum MK, Shor-Posner G, Campa A.
Zinc status in human immunodeficiency virus infection.
J Nutr. 2000 May;130(5S Suppl):1421S-3S.

Brewer GJ, Yuzbasiyan-Gurkan V, Lee DY.
Use of zinc-copper metabolic interactions in the treatment of Wilson’s disease.
J Am Coll Nutr. 1990 Oct;9(5):487-91.

Calder PC, Kew S.
The immune system: a target for functional foods?
Br J Nutr. 2002 Nov;88 Suppl 2:S165-77.

Chan S, Gerson B, Subramaniam S.
The role of copper, molybdenum, selenium, and zinc in nutrition and health.
Clin Lab Med. 1998 Dec;18(4):673-85.

Chasapis CT, Loutsidou AC, Spiliopoulou CA, Stefanidou ME.
Zinc and human health: an update.
Arch Toxicol. 2012 Apr;86(4):521-34.

Finley EB, Cerklewski FL.
Influence of ascorbic acid supplementation on copper status in young adult men.
Am J Clin Nutr. 1983 Apr;37(4):553-6.

Fraker PJ, King LE, Laakko T, Vollmer TL.
The dynamic link between the integrity of the immune system and zinc status.
J Nutr. 2000 May;130(5S Suppl):1399S-406S.

Hambidge M.
Human zinc deficiency.
J Nutr. 2000 May;130(5S Suppl):1344S-9S.

Hulisz D.
Efficacy of zinc against common cold viruses: an overview.
J Am Pharm Assoc (2003). 2004 Sep-Oct;44(5):594-603.

Jackson JL, Lesho E, Peterson C.
Zinc and the common cold: a meta-analysis revisited.
J Nutr. 2000 May;130(5S Suppl):1512S-5S.

McElroy BH, Miller SP.
Effectiveness of zinc gluconate glycine lozenges (Cold-Eeze) against the common cold in school-aged subjects: a retrospective chart review.
Am J Ther. 2002 Nov-Dec;9(6):472-5.

Milne DB, Davis CD, Nielsen F
Low dietary zinc alters indices of copper function and status in postmenopausal women.
Nutrition. 2001 Sep;17(9):701-8.

O’Dell BL.
Role of zinc in plasma membrane function.
J Nutr. 2000 May;130(5S Suppl):1432S-6S.

Perrone L, Di Palma L, Di Toro R, Gialanella G, Moro R.
Interaction of trace elements in a longitudinal study of human milk from full-term and preterm mothers.
Biol Trace Elem Res. 1994 Jun;41(3):321-30.

Salgueiro MJ, Zubillaga M, Lysionek A, Cremaschi G, Goldman CG, Caro R, De Paoli T, Hager A, Weill R, Boccio J.
Zinc status and immune system relationship: a review.
Biol Trace Elem Res. 2000 Sep;76(3):193-205.

Singh M, Das RR.
Zinc for the common cold.
Cochrane Database Syst Rev. 2011 Feb 16;(2):CD001364.

Turnlund J, Costa F, Margen S.
Zinc, copper, and iron balance in elderly men.
Am J Clin Nutr. 1981 Dec;34(12):2641-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.