Vitamin K2: Building bones while beating back arterial calcification

Vitamin K2's time to shine has come—move over vitamin D! Once only known for its role as a "koagulation" factor in blood clotting, vitamin K2 is emerging as another fundamental anti-aging nutrient. While vitamins D and E have garnered the majority of interest in the last decade, the impact of vitamin K2 on aging bones and hearts demands that we give it equal attention.

Whereas most vitamin and mineral supplements use vitamin K in its form of K1 (phylloquinone sourced from plants) because it is easily available and cheap, it is the natural form of K2 (menaquinone sourced from friendly bacteria) that is the most biologically active and shown to enhance both bone formation and vascular health.

The full compilation of recent research underscores the idea that K1 and K2 should be appreciated as separate nutrients with distinct physiological actions and benefits. K1 is the more familiar vitamin known for its key role in directing blood-clotting in the body and the one given as a shot at birth (a common practice in many countries to curtail hemorrhage incidents in newborns.) The picture for K2 seems to be a bit more varied and is key in regulating calcium balance.

Vitamin K2 acts by activating the bone-building hormone (carboxylating osteocalcin) to clear calcium from the arteries and use it in bone mineralization. It effectively removes calcium that would otherwise end up deposited in arterial plaques. Since protecting arteries and soft tissues from calcification is one of the most important ways to stave off the ravages of aging on the body, consuming enough vitamin K2 daily is key for a long, healthy life.

Getting Enough K2

Because vitamin K2 is synthesized by friendly bacteria in the intestine, nutrition scientists have long assumed that that deficiencies were rare. However, new data are showing that intestinally synthesized vitamin K is not absorbed as easily as previously thought. Vitamin K also preferentially accumulates in the liver where it does have a clotting factor role.

In fact, once overlooked because "time to clot" was the test for vitamin K status, it is here where we are now seeing new signs of vitamin K deficiency previously only seen with vitamin D deficiency—fragile, brittle bones and increased fractures—even with adequate calcium and vitamin D.

Most people in North America should increase amounts consumed daily. The evidence finds that only with much higher intake do bone cells get their share and the same holds true for removal of calcium in arteries.

People can obtain enough vitamin K2 by eating plenty of fermented foods such as cheese, sauerkraut, and natto (a traditional Japanese soy-based food). Supplementation is another viable option as achieved with a quality multivitamin.

Regardless of how one gets it, it’s important not to underestimate value of this underdiscussed nutrient and to understand that most people are not getting enough. Consuming sufficient amounts of K2 along with a healthy diet will increase odds of a healthier life with clear arteries and stronger bones.

Sources

McCann and Ames. Vitamin K, an example of triage theory: is micronutrients inadequacy linked to diseases of aging?. Am J Clin Nutr 90:889-907, 2009.
Vitamin K2. Monograph. Alternative Medicine Review 14(3):284-293, 2009.
Koitaya. Et al. Effect of low dose vitamin K2 (MK-4) supplementation on bioindices in postmenopausal Japanese women. J Nutr Sci Vitaminol. 55:15-21, 2009.
Gast, et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovas Dis 19:504-510, 2009.
Shea, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 89: 1799-1807, 2009.
Shea MK, Booth SL Update on the role of vitamin K in skeletal health. Nutr Rev 66(10):549-57, 2008.

High doses of B vitamins may slow brain shrinkage and support memory

Unfortunately, getting older comes with a common consequence affecting up to 16 percent of elderly people – gradual reduction in brain size, which is associated with problems in learning and memory. However, a new study reports that daily supplementation with high doses of B vitamins may help slow the rate of brain degeneration.

Oxford researchers gave 168 individuals over the age of 70 supplements containing high doses of folic acid (0.8 milligrams per day), B6 (20 milligrams per day) and B12 (0.5 milligrams per day), or a placebo as part of a randomized, double-blind controlled trial. Then, following two years of the supplementation program, the participants’ brains were assessed using serial volumetric magnetic resonance imaging scans.

The researchers reported their results in the September issue of PLoS One: the rate of brain shrinkage, or atrophy, in the group taking the supplements was 53 percent lower in comparison to the group taking the placebo. Their conclusion was that the high doses of B vitamins slowed the rate of brain shrinkage in elderly with mild cognitive impairment.

According to the authors, however, it is still unclear which vitamin provided the greatest benefit for the brain. They found that the reduced rate of brain atrophy was a result of an increase in either vitamin B12 status or folic acid status, but could not conclude which of the two “vitamins is the most important.”

They added that vitamin B6 may be less important for brain health since there was a, “lack of association of atrophy with the change in cystathione levels, a marker of vitamin B6 status.”

Folic acid and vitamin B12 play a role in protecting the brain, most likely because their presence helps to lower the concentration of the amino acid homocysteine in plasma. Higher levels of homocysteine are a risk factor associated with smaller brain size as well as problems with learning and memory — as well as related to poor heart and cardiovascular health.

The study adds to emerging evidence that supplementation with B vitamins may be a convenient way for elderly to help support memory and learning.

Source: Smith AD, Smith SM, de Jager CA et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS One 2010;5:e12244.

Boron and Disease

Boron's ability to induce sex hormone levels give it a role preventing chronic disease. For example, adequate dietary boron may potentially reduce risk of lung cancer (1). The effects also explain why boron supplementation may support bone density guarding against osteoporosis (2).

However, caution should be exercised before supplementation with boron. Greater estrogen levels due to boron supplementation may potentially increase risk of breast cancer (1;2). Thus, boron should not be taken by women with high risk of breast cancer or who've had breast cancer.

Reference List

1. http://www.pccnaturalmarkets.com/health/2813008/
2. http://www.osteopenia3.com/Boron-Osteoporosis.html

Nickel toxicity

Nickel is a known carcinogen. When in the diet in toxic amounts it contributes to oxidative stress, just as mercury and cadmium do, by reducing glutathione thereby interfering with cell membrane integrity and increasing lipid peroxidation (1). The oxidative damage, like from free iron or copper, can cause DNA damage (2).

Reference List

1. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12:1161-208.

2. Tkeshelashvili LK, Reid TM, McBride TJ, Loeb LA. Nickel induces a signature mutation for oxygen free radical damage. Cancer Research; 53, 4172-4174, September 15, 1993.

Flouride and the World

As one travels around the world, especially in developing countries, the state of oral health stands out as an issue that needs attention. Fluoride treatment of drinking water can be an important step in improving oral health (1), but some populations may find it's not necessary because they may already be consuming adequate or even too much fluoride daily.
Careful review of fluoride exposure must be evaluated region by region before deciding to treat local water with fluoride (2). According to the World Health Organization (WHO), flouride intake can vary depending fluoride already in water, on diet and other variables such as local pollution (2).

Areas of greater volcanic activity, for example, tend have highest concentrations of fluoride in groundwater (2). The act of tea drinking can provide significant amounts of fluoride (1). In parts of China where high-fluoride coal is burned, the ash that pollutes crops may be providing fluoride (2). And in Tanzania, the use of contaminated trona to tenderize vegetables contributes fluoride can easily result in excess amounts of fluoride ingested daily (2).

Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.3.
2. World Health Organization. Fluoride in Drinking Water. Available at http://www.who.int/water_sanitation_health/publications/fluoride_drinking_water_full.pdf

Molybdenum and Gout

A young electrician with a painful gouty arthritis in 2005 became the first case observed of occupational exposure of toxic amounts of molybdenum (1). Molybdenum is an activator of xanthine oxidase, which oxidizes xanthine producing uric acid (2). Too much produced hyperuricemia (1). The electrician can be thankful that his doctors found the cause of the gout because of previous men afflicted with gout by having consumed 10 to 15 mg of molybdenum daily (3;4). Tolerable uptake limits are set at 2 mg (2).

Reference List
1. Selden AI, Berg NP, Soderbergh A, Bergstrom BE. Occupational molybdenum exposure and a gouty electrician. Occup Med (Lond) 2005;55:145-8.2. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.3. http://lpi.oregonstate.edu/infocenter/minerals/molybdenum/4. http://www.crnusa.org/safetypdfs/027CRNSafetyMolybdenum.pdf

Manganese as a Neurotoxin

Toxicity of manganese is more common than its deficiency (1), which unfortunately cause damage to the brain. Manganese appears to cause neurogeneration by activating microglia and causing them to release neurotoxins such as reactive oxygen and nitrogen species, which produce oxidative damage (2). The neurotoxins are also thought to possibly alter influence of neurotransmitters such as dopamine or gamma-aminobutyric acid (GABA) (1). According to a studies on non-human primates exposed to high doses of manganese, the mineral can lead to deficits in working memory performance and even induce an increase of beta-amyloid production linking manganese to Alzheimer's disease (3;4).

Reference List
1. Anderson JG, Fordahl SC, Cooney PT, Weaver TL, Colyer CL, Erikson KM. Manganese exposure alters extracellular GABA, GABA receptor and transporter protein and mRNA levels in the developing rat brain. Neurotoxicology 2008;29:1044-53.
2. Zhang P, Wong TA, Lokuta KM, Turner DE, Vujisic K, Liu B. Microglia enhance manganese chloride-induced dopaminergic neurodegeneration: role of free radical generation. Exp Neurol 2009;217:219-30.
3. Schneider JS, Decamp E, Clark K, Bouquio C, Syversen T, Guilarte TR. Effects of chronic manganese exposure on working memory in non-human primates. Brain Res 2009;1258:86-95.
4. Burton NC, Guilarte TR. Manganese neurotoxicity: lessons learned from longitudinal studies in nonhuman primates. Environ Health Perspect 2009;117:325-32.

Vanadium treatment of type 2 diabetes enhanced by organic ligands

Vanadyl ions can act in an insulin-like manner in the body. Thus, when taken orally they may potentiate insulin’s effects, which can potentially improve situations of type 2 diabetes (1).

Bioavailability of vanadyl compounds, however, can depend on whether of organic or inorganic nature (2). The organic bis-ligand oxovanadium appear to be far more bioavailable and efficacious than inorganic vanadyl sulfate (2).

According to a couple of trials performed earlier this year in Canada, the organic version taken in doses of 10-90mg has no adverse effects (2). Further, it was found to help reduce fasting blood glucose levels and improves glucose tolerance (2).

Reference List
1. Conconi MT, DeCarlo E, Vigolo S et al. Effects of some vanadyl coordination compounds on the in vitro insulin release from rat pancreatic islets. Horm Metab Res 2003;35:402-6. 2. Thompson KH, Lichter J, LeBel C, Scaife MC, McNeill JH, Orvig C. Vanadium treatment of type 2 diabetes: a view to the future. J Inorg Biochem 2009;103:554-8.

Life Depends on Arsenic?

As Gropper, Smitth and Groff tell it, arsenic "conjures an image of toxicity" unlike any other ultratrace mineral (1), but there are good things that come of arsenic and its story is worth discussion.

Without arsenic, DNA synthesis couldn't happen. This is because arsenic is needed for normal metabolism. Specifically, the mineral is required for forming and using methyl groups to S-adenosylmethionine (SAM) (1). SAM is used for methylation to form DNA compounds (1).

Arsenic, in fact, may have once been part of DNA itself. The mineral is very similar to phosphorus, which is currently the backbone of nucleic acids. Because this is is so it has been suggested that arsenic may have served as an alternate element early on, although not possible in modern biochemistry (3).

According to scientists Felisa Wolfe-Simon, Paul Davies and Ariel Anbar, there may even be possibility that organisms may still be using arsenic in their DNA today, but simply not yet found (3).

Reference List

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

2. Emsley J. Nature's Building Blocks: An A-Z Guide to the Elements. Oxford University Press, 2003.

3. Wolfe-Simon F, Davies PCW, Anbar A. Did nature also choose arsenic? Nature Precedings, Jan 2008.

Chromium and Glucose Tolerance

Because of chromium’s known ability to potentiate action of insulin, an adequate chromium status is important especially for people with diabetes, insulin resistance and hypoglycemia to maintain glycemic control (1;2).

According to an evaluation of 15 randomized clinical trials, amounts of about 200 mcg per day appear to improve use of glucose (3). In addition, a placebo-controlled trial of 180 Chinese patients found that doses at 200 mcg and as high as 1,000 mcg of chromium taken per day lowered blood glucose levels by 15-19% (3).

Dose may depend on form of chromium since one form may be more bioavailable than another. Chromium picolinate appears to be the most bioavailable and, thus, the most potent (3).

The amount of chromium taken, however, should not exceed 1,000 mcg per day due to potential toxicity (1). Chromium picolinate, in addition, should not be taken in amounts over 600 mcg because of association with renal failure and hepatic dysfunction (1).

Reference List

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Pohl M, Mayr P, Mertl-Roetzer M et al. Glycemic control in patients with type 2 diabetes mellitus with a disease-specific enteral formula: stage II of a randomized, controlled multicenter trial. JPEN J Parenter Enteral Nutr 2009;33:37-49.
3. Linus Pauling Institute. Chromium. Micronutrient Information Center. Available at: http://lpi.oregonstate.edu/infocenter/minerals/chromium/.

Chromium nicotinate, but not picolinate may improve body composition

Advertisements that suggest chromium picolinate may help consumers lose fat or gain muscle mass are largely overstated.

A double-blind, randomized, placebo-controlled 12-week trial in 2001 found that chromium picolinate offered moderately obese women participating in an exercise program no significant changes to body composition, resting metabolic rate, plasma glucose, serum insulin, plasma glucagon, serum C-peptide or serum lipid concentrations (1).

The 2001 study’s results supported at least three previous studies of which had also shown that chromium picolinate had been ineffective in changing body composition in obese women, in military personnel and in weight-lifting football players (2-4).

A 12-week randomized, placebo-controlled trial in 2008 combined chromium picolinate with conjugated linoleic acid and evaluated effects on body composition changes of young, overweight women for 12 weeks (5).; still, no significant changes were found (5).

Lastly, because of chromium’s known effects on enhancing insulin signaling and glucose uptake, a randomized, placebo-controlled clinical trial in 2006 investigated effects of chromium picolinate on glycogen synthesis on overweight men after intense exercise (cycling) and high-carbohydrate feeding (6). Chromium picolinate did not appear to augment glycogen synthesis, but did appear to lower activity of phosphoinositol-3-kinase, an enzyme involved in regulating glucose uptake (6).

Chromium nicotinate, however, does appear to have effects on body composition.

One study on young, obese women who were given either chromium picolinate or chromium nicotinate found that chromium picolinate while "resulted" in weight gain for subjects, it also found that chromium nicotinate, when combined with exercise, did produce weight loss and lower insulin response (2).

Another randomized, double-blinded, placebo-controlled, crossover study on African American women gave 200mcg chromium nicotinate for over 2 months (2). The study did find significant fat loss and "sparing of muscle" in the women taking chromium nicotinate when combined with moderate exercise (7).

Reference List

1. Volpe SL, Huang HW, Larpadisorn K, Lesser II. Effect of chromium supplementation and exercise on body composition, resting metabolic rate and selected biochemical parameters in moderately obese women following an exercise program. J Am Coll Nutr 2001;20:293-306.
2. Grant KE, Chandler RM, Castle AL, Ivy JL. Chromium and exercise training: effect on obese women. Med Sci Sports Exerc 1997;29:992-8.
3. Trent LK, Thieding-Cancel D. Effects of chromium picolinate on body composition. J Sports Med Phys Fitness 1995;35:273-80.
4. Clancy SP, Clarkson PM, DeCheke ME et al. Effects of chromium picolinate supplementation on body composition, strength, and urinary chromium loss in football players. Int J Sport Nutr 1994;4:142-53.
5. Diaz ML, Watkins BA, Li Y, Anderson RA, Campbell WW. Chromium picolinate and conjugated linoleic acid do not synergistically influence diet- and exercise-induced changes in body composition and health indexes in overweight women. J Nutr Biochem 2008;19:61-8.
6. Volek JS, Silvestre R, Kirwan JP et al. Effects of chromium supplementation on glycogen synthesis after high-intensity exercise. Med Sci Sports Exerc 2006;38:2102-9.
7. Crawford V, Scheckenbach R, Preuss HG. Effects of niacin-bound chromium supplementation on body composition in overweight African-American women. Diabetes Obes Metab 1999;1:331-7.

Selenium and Prostate Cancer

Prostate cancer has been associated with low serum selenium concentration. To investigate the mechanisms by which selenium affects gene expression prostate tissue, researchers set out to measure activity of glutathione peroxidase in men with relatively high serum selenium concentration (1).

The researchers measured serum selenium concentration in 98 men using atomic absorption spectrometry. Afterward, 12 men were selected for having the highest serum selenium concentration and another 12 were identified as having the lowest serum selenium concentration. Fresh prostate tissue samples were taken of the selected men to measure selenium concentration and glutathione peroxidase activity.

The study, which was published in July 2007, reported a positive correlation found between a higher serum selenium concentration and a prostate tissue concentration. However, there was no significant increase of glutathione peroxidase activity associated with the higher concentration of selenium concentration.

Discussion: Because the subjects of this study were already were identified as having high serum selenium concentrations, the results indicate simply that glutathione peroxidase activity is not increased by greater concentration of selenium beyond a certain requirement. The data suggest selenium dietary intake exceeding established amounts to correct deficiency do not present any additional benefit in prevention of prostate cancer.

Reference List

1. Takata Y, Morris JS, King IB, Kristal AR, Lin DW, Peters U. Correlation between selenium concentrations and glutathione peroxidase activity in serum and human prostate tissue. Prostate 2009.

Iron in Summary

Humans contain about 2-4g iron of which most is in hemoglobin and to a lesser extent myoglobin. Iron from diet is found in heme (animal foods) and nonheme (plant foods) forms. The heme iron needs to be hydrolyzed where as the nonheme is enzymatically freed.

Heme iron is absorbed intact accross the brushborder of the enterocyte whereas nonheme iron is released as ferric in the stomach, which may be reduced to ferrous. The ferric is absorbed across brush border by binding to transporters and the ferrous facilitated by chelators and membrane proteins.Chelators inhibit or enhance absorption of iron. Absorption is also regulated by hepcidin and ferroportin. Other iron-absorption enhancers are sugars, acids, animal meat, and mucin. Other inhibitors are polyphenols, oxalates, phytates, phosvitin and some minerals.Iron is stored in the liver, bone marrow and spleen. Uptake into tissues depends on transferrin.

Iron needs depend on its loss such as through menstrual losses and dietary intake. Deficiency mainly can affect infants and children, teenagers, menstruating females and pregnant women (whose iron needs expand due to increased blood volume). Iron deficiency can develop gradually into anemia. Toxicity may occur due to taking too much iron in supplements or if one has a genetic disorder called hemochromatosis. In the case of hemochromatosis, which is most prevalent among caucasian males, a diet with limited meat intake may be necessary.

Copper-zinc

A mineral supplement I've taken in the past includes 10mg zinc and 1mg of copper. Thus, the amount of zinc is not at the "higher than 50mg" level that can cause a copper deficiency because of interference with bioavailability (1). This is exactly the 10:1 ratio as suggested to avoid any copper deficiency (2). Someone did his/her homework.

1. http://lpi.oregonstate.edu/infocenter/minerals/zinc/
2. http://www.pccnaturalmarkets.com/health/2934002/

Top zinc-rich foods I eat frequently

1 chicken drumstick, broilers or fryers, meat and skin, cooked, roasted = 2.98mg
3 Eggs, whole, cooked, scrambled = 1.83mg
1 burrito, bean and cheese, microwaved = 1.33mg
1 cup milk, whole, 3.25% milkfat = .98mg
1 fish fillet, trout, rainbow, farmed = .32mg

Data found at: http://www.nal.usda.gov/fnic/foodcomp/

Zinc and copper not effective for acute diarrhea

Purpose of study: Zinc and copper are lost in significant amounts in acute diarrhea and zinc has been suggested as a therapy for its possible facilitation of water and electrolyte transport across intestinal mucosa to prevent villous atrophy and modulate immune response. This study evaluated whether or not zinc and copper supplementation had any beneficial effect on acute watery or bloody diarrhea when given with standard treatment.

Type of study: Randomized, double-blinded placebo-controlled trial

Method used to conduct study: Children ages 6-59 months with acute diarrhea were given standard treatment and randomized to placebo, zinc only (Zn 20mg/5ml elemental zinc), or zinc and copper (2mg/5ml of elemental copper) together via syrup. There were 808 children chosen for the study out of 1,200 screened over the period of Aug 2003 and Oct 2006. Each provided more than three stool samples in prior 24 hours, who had duration of diarrhea for up to 72 hours and who were able to orally accept fluid or food. Exclusions were those with positive HIV, kwashiorkor or participating in another study.

Summary: There was no observed impact on duration or total stool output in acute diarrhea found between the groups supplemented with zinc only, zinc and copper, or placebo. No serious adverse events were associated with the three syrups. Critique: Measures were taken in this study to ensure quality control and appropriate data analysis and interpretation. The quality of the study make its results valid given the amount of subjects and assessment of the data.

Nutritional implications and implications of future study: The researchers offered that the lack of effect would not have been due to low dose, poor adherence to treatment or failure to replenish zinc loss. They did offer that extent of zinc deficiency in study populations could be why other studies showed therapeutic benefits from zinc, but that not all therapeutic studies reported benefits of zinc in children with deficiency. Therapeutic supplementation with zinc may, in fact, depend on diarrhea etiology at different ages in populations. There may also have been interaction with zinc and the standard treatment, which included a multivitamin with vitamin A and B vitamins. Future study may need to evaluate zinc supplementation with different etiologies for diarrhea and separately with regards to multivitamin interaction.

Reference: Patel A, Dibley MJ, Mamtani M, Badhoniya N, Kulkarni H. Zinc and copper supplementation in acute diarrhea in children: a double-blind randomized controlled trial. BMC Med 2009;7:22. Available at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19416499

Iron Deficiency Symptoms

As iron deficiency develops gradually without anemia, symptoms can appear that can include pallor and problems of behavior, cognition, learning and attention span. These can particularly manifest themselves in children. Adults may witness problems related to work performance and productivity.

The effects may be related to impairment of the neurotransmitter gamma-aminobutyric acid (GABA) used to inhibit dopamine production in the brain and/or immune system impairment leading to more susceptibility to infection and inability to keep a normal body temperature.

The first stages of iron deficiency result in diminished liver, spleen and bone marrow iron stores and decreased plasma ferritin. Second stages begin when stores are low and iron transport decreases. Transferrin saturation decreases, which increases total iron-binding capacity, and there is limited iron for function in hemoglobin. This leads to a rise in protoporphyrin, the precursor to heme in hemoglobin. Finally, the anemia occurs.

Reference

Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009, pp. 485-87.

Hemochromatosis a Neolithic adaptation?

Hemochromatosis is a genetic disorder caused by one of several mutations related to double-than-normal iron absorption, which increases susceptibility to iron overload (1). Although the disorder affects about one in 200 in the U.S., it’s still largely unrecognized and can lead to deposits in organs—such as the liver—leading to organ damage and failure if not treated early enough (2-4).

Because the disorder is most prevalent in males of Northern European ancestry, particularly Celtic (5), it was hypothesized as recently as 2007 to be a possible Neolithic adaptation (6). The Neolithic period marked an early European dietary transition from high intake of meat to cereal grains (6).

Whether or not this hypothesis is correct, the state of the disorder suggests potential dietary management through eating primarily vegetarian foods such as the one eaten during the time of these early ancestors—cereal grains, little red meat, and limited vitamin C intake. This low-iron diet to prevent to iron overload, according to the Hemochromatosis Management Working Group, can help to “decrease the frequency and severity of iron overload,” thereby preventing many of the detrimental effects of the disorder (4).

Reference List

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Borgaonkar MR. Hemochromatosis. More common than you think. Can Fam Physician 2003;49:36-43.
3. Dolbey CH. Hemochromatosis: a review. Clin J Oncol Nurs 2001;5:257-60.
4. Barton JC, McDonnell SM, Adams PC et al. Management of hemochromatosis. Hemochromatosis Management Working Group. Ann Intern Med 1998;129:932-9.
5. Pozzato G, Zorat F, Nascimben F et al. Haemochromatosis gene mutations in a clustered Italian population: evidence of high prevalence in people of Celtic ancestry. Eur J Hum Genet 2001;9:445-51.
6. Naugler C. Hemochromatosis: a Neolithic adaptation to cereal grain diets. Med Hypotheses 2008;70:691-2.

Potassium Guards Against Sodium-induced Bone Loss

Reference: Sellmeyer DE, Schloetter M, Sebastian A. Potassium citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet. J Clin Endocrinol Metab 2002;87:2008-12. Available at: http://jcem.endojournals.org/cgi/content/full/87/5/2008?ijkey=b46c2855f83d19e380eb6674c66c94e884ed56a0

Purpose of study: To study effects of dietary potassium citrate added to diets high in sodium, as commonly found in industrialized nations, in postmenopausal women. Postmenopausal women are at higher risk of osteoporosis, especially if consuming a high-sodium diet.

Type of study: Randomized, double-blinded placebo-controlled trial

Method used to conduct study: After three weeks in which 60 post-menopausal women adhered to a low-salt diet, they were provided sodium chloride pills, salt packets (for sprinking on food) and one cup of bouillon per day. They were randomized and either take potassium citrate (90 mmol/d) or placebo. Twenty-four-hour urine samples were analyzed to determine compliance after 12 days. When compliance was compromised, subjects were contacted to enforce regimen. After four weeks, urine samples and fasting blood samples were collected. Fifty two of the women completed seven-week study of which 26 had taken placebo and 26 potassium citrate. Exclusions at the beginning of the study included women who were less than 2 years past menopause, on bone metabolism medications or who had past history of bone disease.

Summary: Calcium excretion increased by 42+-12 mg/d (33%) from low-salt to high-salt diet in the women on placebo. Calcium excretion decreased by 8+- 14mg (4%) in women on potassium citrate. The results suggest that potassium citrate prevented bone resorption in response to salt increase in the diet.

The method is thought to be the natriuretic and chloruretic effects of potassium alkaline salts. These potentially reduce extracellular volume expansion associated with higher salt intake. The alkaline salts also reduce endogenous acid, increase blood pH and bicarbonate. Calcium excretion in the urine can change depending on acid production.

Critique: Examining effects of potassium through a placebo-controlled trial goes far to point out the intracellular cations biological effects on calcium excretion. The results are significant. The researchers took appropriate measures in assuring that the postmenopausal women were compliant in their diets. A seven-week study, however, may not be long enough to determine whether or not potassium citrate will make a significant difference in reducing risk of bone loss and hip fracture.

Nutritional implications and implications of future study: Post-menopausal women at risk for osteoporosis, especially who eat a high-sodium diet, should consider increases of dietary sources of potassium, which are mainly fruits and vegetables. For the benefit of post-menopausal women who may dislike fruits and vegetables and eat mainly processed foods, it may be wise to add potassium to these processed foods. Similar trials should be conducted to determine effects of potassium-added, high-sodium processed foods.

Why Gatorade May Not Rehydrate You Any Faster Than Water

Research Summary Critique

Reference: Jeukendrup AE, Currell K, Clarke J, Cole J, Blannin AK. Effect of beverage glucose and sodium content on fluid delivery. Nutr Metab (Lond) 2009;6:9. Available at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19232115

Purpose of study: The objective of many oral rehydration drinks is rapid fluid delivery to correct fluid balance in sports. This study investigated carbohydrate (CHO) and sodium (Na) effects on fluid delivery with a deuterium oxide (D20) tracer.

Previous research suggests Na concentration may increase delivery, but that CHO content is more important factor.

Type of study: Equivalence trial of eight different solutions.

Method used to conduct study: Two groups of 10 male subjects (ages 20 +- 1 y, weight: 81.2 +-7.5kg) were split into a CHO or NA group. The CHO group ingested four drinks, each with 20 mmol/L sodium, and with a stepped increase of 3% glucose from 0-9%. The Na group ingested four drinks, each with 6% glucose, with a stepped increase of 20 mmol/L from 0 mmol/L to 60 mmol/L. All drinks contained 3g of D20.

Each trial was performed in laboratory after overnight fast (7-9a.m.) and emptying of bladder. After ingesting drink, blood was taken every five minutes in the first hour and every 10 minutes in the second hour. Plasma D20 was analysed using isotope ratio mass spectrometry.

Summary: CHO concentration at 3% increased fluid delivery in comparison to 0%. Concentration above 6% led to fluid delivery that was slower than 0% and 3%. Sodium concentration in any amount did not show any increase in intestinal water absorption.

Critique: The researchers acknowledge that the investigation, which used the “triple lumen technique”, takes into account a section of the small intestine, but not gastric emptying. It may not represent total fluid availability in the body. However, D20 is useful to provide an integrative measure of gastric emptying and intestinal fluid absorption.

Nutritional implications and implications of future study: Because the study’s findings are that added sodium to oral rehydration drinks (sport drinks) has no effect on fluid delivery, it may change the way consumers choose these beverages. Sodium addition may not be preferred or it may still be for other reasons unrelated to fluid delivery such as for possible electrolyte replacement.