Is spinach a good source of magnesium?

Japanese researchers evaluated spinach’s magnesium bioavailability in rats in a study published in 1995 (1). Their conclusions were that spinach was a "one of the most promising" sources of magnesium and that oxalic acid in spinach after cooking (boil or fried) would not affect magnesium bioavailability.

Looking at their data, though, cooking did affect calcium absorption and, of course, oxalic acid had additional effects.

The researchers had divided rats into six groups, which led to this data:

• Mg-deficient diet
  o Serum magnesium decrease
  o Ca absorption 87.0%
  o Increase of calcium and phosphorus in liver and kidneys
  o Especially large calcium accumulation in kidneys
• Mg-deficient diet supplemented with raw powdered spinach
  o Mg absorption 88.9%
  o Ca absorption 84.1%
  o Large calcium accumulation in kidneys
  o Significantly higher liver and kidney Mg and phosphorus
• Mg-deficient diet with boiled powdered spinach
  o Mg absorption 88.4%
  o Ca absorption 57.3%
  o Large calcium accumulation in kidneys
  o Significantly higher liver and kidney Mg and phosphorus
• Mg-deficient diet with powdered fried spinach
  o Mg absorption 90.4%
  o Ca absorption 66.2%
  o Large calcium accumulation in kidneys
  o Significantly higher liver and kidney Mg and phosphorus
• Control diet with supplemented oxalic acid
  o Mg absorption 88.1%
  o Ca absorption 53.3%
  o Large calcium accumulation in kidneys
  o Significant decrease in weight
• Control diet
  o Mg absorption 87.7%
  o Ca absorption 83.5%o
  o Significant increase in weight gain in comparison to other groups
  

Reference List

1. Kikunaga S, Ishii H, Takahashi M. The bioavailability of magnesium in spinach and the effect of oxalic acid on magnesium utilization examined in diets of magnesium-deficient rats. J Nutr Sci Vitaminol (Tokyo) 1995;41:671-85.

Which exercise should I do to improve calcium status?

We’ve known for awhile that exercise improves bone health, but unsure what effects it has on calcium absorption and loss. There have been recent studies trying to find out more.

Just last April, researchers from San Diego State published a study in which they had investigated urinary calcium excretion in two groups of men—one sedentary and the other on a “high-impact and resistance-exercise program”—in a randomized crossover study of three weeks (1). The active men were found to have “significantly less” urinary calcium loss in comparison to week of restricted activity (1).

But, we should note, an earlier study in 2007 reported that exercise actually increased calcium losses through sweating (2). Quite different than the other study, this one which was evaluating effects of calcium supplementation, came to the conclusion that supplementation should be used to correct the negative calcium balance from dermal loss from exercise (2).

What’s the deal?

While the 2009 study used exercise that was high in impact and resistance, the type of exercise in the 2007 study was cycling, an aerobic exercise not high in impact or high in resistance. One could infer that the type of exercise could have much to do with the type of results researchers get. Could it also be that resistance training has a role in improving calcium absorption and reducing calcium excretion?

Reference List
1. Nemoseck T, Kern M. The effects of high-impact and resistance exercise on urinary calcium excretion. Int J Sport Nutr Exerc Metab 2009;19:162-71. 2. Martin BR, Davis S, Campbell WW, Weaver CM. Exercise and calcium supplementation: effects on calcium homeostasis in sportswomen. Med Sci Sports Exerc 2007;39:1481-6.

“No Single Universal Calcium Requirement”

In 2000, with a bit of an incendiary tone, professor Christopher Nordin of Australia called for a rational position on calcium requirements based on individual variances and culture. The matter was one of controversy, lacking human studies because of their difficulty, but despite plenty of evidence that low calcium causes osteoporosis in animals.

Modern human studies in which researchers deprive subjects of calcium for long periods would be immoral, Nordin points out, although there have been at least a couple in the past. One in particular was performed 50 years ago on Norwegian prisoners that showed deprivation led to negative calcium balance, which would result in osteoporosis.

We also know that diet higher in animal protein and sodium increase urinary calcium; thus, the implication would be that populations of the developed world would need more calcium intake. And status of vitamin D influences calcium absorption; thus, living at a higher latitude, darker skin color, and less exposure to sunlight should never be ignored.

Of course, periods of hormonal changes deserves special attention. According to Nordin in a 2001 interview, “very little work” had been done to determine calcium requirements in postmenopausal state despite that the lacking estrogen effects on the bone are profound.

Still, nine years later and despite the data, many doctors and nutritionists in the U.S.A. and other countries are recommending calcium in general terms of simply meeting RDA. Or, those who understand that certain individuals need more or less calcium, may not be educating patients on facts relating to animal protein, sodium and vitamin D.

A complete, holistic view of each individual patient is necessary and national guidelines should be more forthright in making this assertion. As Nordin states, there is “no single universal calcium requirement” and we need to make sure that our patients know the facts.

Allosteric enzymes

Allosteric enzymes are those that are controlled by the binding of an allosteric effector. The effector may be positive or negative in activating or inactivating the enzyme, respectively, and creates a conformational change of the enzyme. The product may be the allosteric effector in itself producing feedback or feedforward control.

There are two classes of allosteric enzymes based on the effect of the effector on Km and Vmax. If the effector alters Km it is in K class and if the effector alters Vmax it is in V class. There are also enzymes that have both Km and Vmax affected.
K class allosteric enzymes are affected by negative effector binding because it affects the affinity of the binding site for the substrate. V class allosteric enzymes are affective positively or negatively by effectors that increase or decrease rate of enzyme-substrate complex breakdown to products.

Given the conformational change and resulting activation and inactivation of an enzyme, catalysis of reactions would be unidirectional. Examples are hexokinase (or glucokinase), phosphofructokinase, and pyruvate kinase in the regulation of glycolysis. Glucokinase is activated by fructose-6-phosphate and inhibited by fructose-1-phosphate. Phosphofructokinase is activated by fructose 2,6 biphosphate and inhibited by ATP. Pyruvate kinase is activated by fructose-1-6-biphosphate (feedforward) and inhibited by ATP and alanine.

Reference List

1. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002, pp893-4. p401-4; 587-89; 863-5
2. Stanford. Regulation of glycolysis. Available at: http://cmgm.stanford.edu/biochem200/regulation/

Why So Many Hormones?

Hormones are any substance in the body that carries a signal to regulate growth, differentiation and function of a variety of cells. The more signals needed, the more hormones in an organism. The big-brained human body is no different. In higher animals signal pathways of many hormonal systems originate in the brain. Because hormones are so specific in communicating between cells, we can expect yet more discovery of hormones in the future to add to the large number already found.

Their are major categories of hormones: peptide and protein, thyroid, catecholamine and steroid. The hormones are specific in targeting cognate receptors that are expressed for specific hormones (1). For example, catecholamine hormones epinephrine and norepinephrine as well as peptide hormones target specific cell surface receptors while steroid hormones target intracellular receptors.

Endocrine hormones are those synthesized in a gland and travels to reach distant target cells. Paracrine hormones are secreted by a cell and travel a short distance to reach a neighboring cell's receptors. Autocrine hormones are produced in a cell that functions as a target for the paracrine hormones.

Hormonal cascade systems may involve a number of hormones. A system may operate through a releasing hormone, anterioir pituitary tropic (or posteror pituitary) hormones and ultimate hormones (1). The posterior pituitary system branches off the right of the hypothalamus and is the system involving oxytocin and vasopressin.

A signal is generally transmitted first through the central nervous system, then innervate the hypothalamus secreting a releasing hormone and it begins the amplified cascade. Generally there is a feedback loop (ultra-short, short, or long) and a final hormone binds a cognate receptor to stop secretion or synthesis of releasing hormone.

If a hormone is not systemic, acting in an anatomically restricted site, it is said to be a local hormone. A hormone that functions locally as an autocrine and paracrine hormone is the neurotransmitter acetylcholine. Acetylcholine in neuron-neuron interaction acts as an excitatory transmitter. It is released after stimulation of a neuron, travels across the synapse and binds to specific nicotinic-acetylcholine receptor.

Reference List

1. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002, pp893-4.

Can vitamin D prevent autoimmune diseases?

Vitamin D, apart from its role in calcium nutrition, has been recently studied for its surprising immunomodulation effects, which could have far implications (1). Not only does the hormone-like vitamin acts on vitamin D receptors, which are present on immune cells such as dentritic cells, but it has also been discovered that activated dentritic cells appear to produce vitamin D (2;3).

Because autoimmune diseases such as systemic lupus erythematosus, multiple sclerosis and rheumatoid arthritis have each been linked to low vitamin D status, vitamin D supplementation is thought to have potential use as a treatment (3-5). Its use for HIV infection and cancer are also being studied (6;7).

Prevention of autoimmune diseases are also associated with immunomodulation from vitamin D. A higher levels of vitamin D is associated with lower risk of multiple sclerosis (8) and with lower risk of type 1 diabetes mellitus (9;10). Vitamin D’s action for preventing type 1 diabetes and other autoimmune diseases is thought to be modulation of dentritic action and modifying T-cell differentiation (10).

Animal studies make the research more exciting. In an older study on mice, vitamin D was able to completely prevent the mouse model of multiple sclerosis (11). Others have also suggested use in preventing encephalomyelitis, rheumatoid arthritis, and systemic lupus erythematosus (12). It should be noted that, in each case, a high-calcium diet was required (12).

Reference List

1. Adams JS, Hewison M. Unexpected actions of vitamin D: new perspectives on the regulation of innate and adaptive immunity. Nat Clin Pract Endocrinol Metab 2008;4:80-90.
2. Adorini L, Penna G. Dendritic cell tolerogenicity: a key mechanism in immunomodulation by vitamin D receptor agonists. Hum Immunol 2009;70:345-52.
3. Cutolo M, Otsa K. Review: vitamin D, immunity and lupus. Lupus 2008;17:6-10.
4. Do JE, Kwon SY, Park S, Lee ES. Effects of vitamin D on expression of Toll-like receptors of monocytes from patients with Behcet's disease. Rheumatology (Oxford) 2008;47:840-8.
5. Vojinovic S, Vojinovic J, Cosic V, Savic V. [Effects of alfacalcidol therapy on serum cytokine levels in patients with multiple sclerosis]. Srp Arh Celok Lek 2005;133 Suppl 2:124-8.
6. Adorini L, Daniel KC, Penna G. Vitamin D receptor agonists, cancer and the immune system: an intricate relationship. Curr Top Med Chem 2006;6:1297-301.
7. Villamor E. A potential role for vitamin D on HIV infection? Nutr Rev 2006;64:226-33.
8. Correale J, Ysrraelit MC, Gaitan MI. Immunomodulatory effects of Vitamin D in multiple sclerosis. Brain 2009;132:1146-60.
9. Arnson Y, Amital H, Shoenfeld Y. Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Ann Rheum Dis 2007;66:1137-42.
10. Mathieu C, Badenhoop K. Vitamin D and type 1 diabetes mellitus: state of the art. Trends Endocrinol Metab 2005;16:261-6.
11. Hayes CE, Cantorna MT, Deluca HF. Vitamin D and multiple sclerosis. Proc Soc Exp Biol Med 1997;216:21-7.
12. Deluca HF, Cantorna MT. Vitamin D: its role and uses in immunology. FASEB J 2001;15:2579-85.

Which Vitamin K for Heart Disease?

The most meaningful (and exciting) new data on vitamin K is on it’s relationship with coronary heart disease (CHD), but it’s a bit confusing.

A cross-sectional study published in Atherosclerosis in 2009 indicated menaquinone reduced coronary calcification, but maybe not phylloquinone (1). This supported a hypothesis made earlier that menaquinone, but not phylloquinone reduced risk of cardiovascular disease (2).

However, an intention-to-treat analysis in Am J Clin Nutr also published this year found phylloquinone supplementation appeared to slow coronary artery calcification (3). This study was performed on older adults with preexisting calcification (3).

One more piece of the puzzle is another not-yet-published September cohort study from Nutr Metab Cardiovasc Dis (4). The study followed 16,057 women ages 49-79 who did not have CHD at baseline (4). Questionnaires were used to determine estimation of vitamin K intake and multivariates were reduced as needed (4). According to its conclusions, menaquinones may have preventative effects against CHD, but not phylloquinone (4).

Eventually more studies will be needed to shed more light on the roles of both phylloquinone and menaquinone and, ultimately, the research will reveal best intake levels for CHD prevention.

Reference List

1. Beulens JW, Bots ML, Atsma F et al. High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis 2009;203:489-93.
2. Erkkila AT, Booth SL. Vitamin K intake and atherosclerosis. Curr Opin Lipidol 2008;19:39-42.
3. Shea MK, O'Donnell CJ, Hoffmann U et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 2009;89:1799-807.
4. Gast GC, de Roos NM, Sluijs I et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovasc Dis 2009;19:504-10.