ADHD and Magnesium

Magnesium deficiencyMagnesium deficiency has been reported in children with ADHD syndrome.  Signs of this malady include hyperactivity, hypermotivity with aggressiveness, and lack of attention, especially at school.  Biochemical and concurrent behavioral improvements have been realized by magnesium therapy in association with vitamin B6 supplementation.

An analysis of eighteen different study groups performed by Marianne Moussain-Bosc and her colleagues at a French institute for nervous system studies in 2006 indicated that ,”…B6/magnesium therapy benefits about half of autistic children,” but also noted that a related study showed benefits to those with ADHD, using the same doses of each supplement.  Children ranging from one to ten years of age “…received 0.6 milligrams per kilogram per day of vitamin B6 and 6 milligrams per kilogram per day of magnesium.  Treatment lasted an average of eight months.”  (Moussain-Bosc. 2006)   Both groups of children had significantly lower values of erythrocyte magnesium at the outset than the control group(s).  It was observed that after two months of the vitamin-mineral regimen there was a substantial change in clinical symptoms.

ADD and ADHD are on the upswing, and have been for some time.  Both conditions are hastily treated with drugs, often without a differential diagnosis, which is essentially a process of elimination.  Instead, the Diagnostic and Statistical Manual (DSM) of Mental Disorders criteria, and a series of observations and teacher questionnaires are employed.  (Pediatrics. 2000. No authors listed.)   Mineral and electrolyte imbalances are awfully hard to discover with that technique, don’t you think? Most parents wince at the thought of dosing their kids with “miracle” substances that have unknown long-term side effects. On the other hand, the clueless, self-centered, entitled faction applauds the quiet, calm, relatively immobile zombie of the house.

Although we live in plentiful times, where food, shelter, and clothing are accessible to all who earn them, there still exist children who are seriously shy of their required magnesium stores.  One reason is stress.  The number of stressors to which kids are exposed grows every year.  From sports practice, to violence in the streets and on television, to academic obligations, to peer pressure and self-image, and more, the kids are overloaded.  It’s the accompanying flood of adrenaline that siphons magnesium, since that hormone needs the mineral for its release.  Another reason is poor nutrition.  You know, processed foods, refined sugars, colorful and flavorful additives, artificial this and that…  This kind of diet is notoriously low in magnesium, which is calming to the nervous system.  The refined sugars and additives actually stress the body, especially the nervous system, as it tries to overcome the onslaught.  A double whammy.

In Poland, researchers studied ADHD children and assessed the value of magnesium supplementation on the DSM parameters, finding that six months of taking as little as 200 mg a day yielded a decrease in symptoms.  (Starobrat-Hermelin. 1997)  Later study performed by Moussain-Bosc saw a decrease in ADHD symptoms using a combined magnesium / B6 regimen in several dozens of children with low red blood cell magnesium stores.  (Moussain-Bosc. 2004)

Attention deficit hyperactivity disorder is a developmental perturbation characterized by attention problems and hyperactive behavior.  It’s the most commonly studied psychiatric disorder in children, affecting three to five percent of children worldwide.  Sadly, integrative therapies are spurned by traditional-minded doctors, so parents have taken it upon themselves to intervene, despite the lack of support from their physicians.

Bearing in mind that sugar has a nutrient-diluting effect might make a difference in ADHD management and magnesium stores in the body.  It’s normal to wonder where all the magnesium goes.  Doesn’t it stay still?  After all, it’s part of bone.  That’s true, but magnesium is also an electrolyte, helping to send calming electrical messages across the membrane of each cell, making it a natural calcium channel blocker.  It gets used up in the manufacture of more than three hundred enzymes the body needs, including those that make anti-inflammatory chemicals from fatty acids.  Situations and conditions within the body can push this mineral into the urine and then into the toilet.  Sugar intake, and even that of simple carbohydrates, increases the secretion of insulin by the pancreas.   Increased insulin, as might be found in insulin resistance, pushes magnesium out.  (Huerta. 2005)  The pancreas needs magnesium to make its other secretions, including those that break down proteins (trypsin and chymotripsin) and fats (lipase), as well as carbohydrates.  Carol Ballew and her colleagues found that carbonated beverages, namely soda, are negatively associated with magnesium levels This starts a vicious cycle because low magnesium is related to insulin resistance. (Ballew. 2000).

In tests done in the mid 90’s, it was discovered that elevated insulin levels result in increased magnesium excretion.  These researchers noted this as the explanation to the magnesium deficit that accompanies obesity, diabetes, and hypertension, as well as hyperinsulinemia.  (Djurhuus. 1995)  This same group later reported that high glucose levels, such as would come from a sugary breakfast or a plethora of sweet goodies, raise magnesium excretion by a factor greater than 2.0.  (Djurhuus. 2000)

The foods that once supplied dietary magnesium have become compromised by careless farming, harvesting, processing, storage, and handling practices.  We now get more calcium and less magnesium than ever in the history of mankind.  Sugar erases magnesium from the body’s slate. (Fuchs. 2002) (Tjaderhane. 1998) (Milne. 2000)  It’s time to put it back.  At 6.0 mg / kg / day, that equates to about 3.0 milligrams per pound of body weight…for all of us.


    Studies confirm benefits of vitamin B6/magnesium therapy for autism, PDD, and ADHD
    No Authors Cited


  • Magnes Res. 1997 Jun;10(2):143-8.
    Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD).
    Kozielec T, Starobrat-Hermelin B.


  • Pediatrics. 2000 May;105(5):1158-70
    Did not perform differentiated diagnosis
    Clinical practice guideline: diagnosis and evaluation of the child with attention-deficit/hyperactivity disorder. American Academy of Pediatrics.
    No authors listed


  • Magnes Res. 2006 Mar;19(1):53-62.
    Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6. II. Pervasive developmental disorder-autism.
    Mousain-Bosc M, Roche M, Polge A, Pradal-Prat D, Rapin J, Bali JP.


  • J Am Coll Nutr. 2004 Oct;23(5):545S-548S.
    Magnesium VitB6 intake reduces central nervous system hyperexcitability in children.
    Mousain-Bosc M, Roche M, Rapin J, Bali JP.


  • J Clin Invest. 1970 July; 49(7): 1458–1465.
    A comparison of the effects of glucose ingestion and NH4Cl acidosis on urinary calcium
    and magnesium excretion in man

    Edward J. Lennon and Walter F. Piering


  • J Abnorm Child Psychol. 1986 Dec;14(4):565-77.
    Behavioral effects of sucrose on preschool children.
    Goldman JA, Lerman RH, Contois JH, Udall JN Jr.


  • Arch Pediatr Adolesc Med. 2000;154:1148-1152
    Beverage Choices Affect Adequacy of Children’s Nutrient Intakes
    Carol Ballew, PhD; Sarah Kuester, MS, RD; Cathleen Gillespie


  • Diabetes Care. 2005 May;28(5):1175-81.
    Magnesium deficiency is associated with insulin resistance in obese children.
    Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, Patrie JT, Rogol AD, Nadler JL.
    SourceUniversity of Virginia, Department of Pediatrics, Box 800386, Charlottesville, VA 22908, USA. [email protected]


  • Diabetic Medicine.  Volume 12, Issue 8, pages 664–669, August 1995
    Insulin Increases Renal Magnesium Excretion: A Possible Cause of Magnesium
    Depletion in Hyperinsulinaemic States

    Dr. M.S. Djurhuus, P. Skøtt, O. Hother-Nielsen, N.A.H. Klitgaard, H. Beck-Nielsen


  • Scan Jou of Clin & Laboratory Investigation. 2000, Vol. 60, No. 5 , Pages 403-410
    Hyperglycaemia enhances renal magnesium excretion in Type 1 diabetic patients
    S. Djurhuus


  • J. Nutr. October 1, 1998 vol. 128 no. 10 1807-1810
    A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats
    Leo Tjäderhane, and Markku Larmas
    Institute of Dentistry, University of Oulu, 90220 Oulu, Finland


  • J Am Coll Nutr February 2000 vol. 19 no. 1 31-37
    The Interaction Between Dietary Fructose and Magnesium Adversely Affects
    Macromineral Homeostasis in Men

    David B. Milne, PhD and Forrest H. Nielsen, PhD

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

Kidney Stones: The Basics

green-healthy-foodUreterolithiasis, renal calculi, nephrolithiasis and kidney stone all mean the same thing:  agony.  The nurse told us the pain is equivalent to passing a five-pound canned ham through the southern end of the digestive system, with the lid opened.  If you’ve never experienced the long road to relief, thank the Creator for being excused.

What causes kidney stones?

There is no single cause, but a combination of factors.  The wrong balance of fluids, minerals and acids can put you on your knees faster than being knighted.  If urine has more crystal-making elements than the fluid can dilute, bingo, you have the makings of a stone…or stones.  In looking for a definitive cause, science has left no stone unturned.  No pun intended.  Beneath one of those stones is fluoride, having been fingered as causative a decade ago, but only in those with symptoms of skeletal fluorosis and the propensity to form stones in the first place (Singh, 2001).  That rules lots of us out.  Whether or not high doses of vitamin C are implicated in the formation of stones is debatable and based on the status of other nutrients.  By itself, vitamin C, chemically known as ascorbic acid, is able to be converted by the body into oxalates, which increases the likelihood of making oxalate stones among stone formers who take more than the recommended upper limit of 2000 mg of vitamin C a day (Massey, 2005). But you gotta be a stone former.  Is that like a mason?   Earlier research found that high intake of vitamin B6, pyridoxine, reduces the risk of stone formation from unrestricted doses of ascorbic acid (Curhan, 1999).   Up to 500 mg of pyridoxine a day was found to be useful in the control of elevated urinary oxalates (Mitwali, 1988).  In a study reported in the New England Journal of Medicine in the dark ages of the last century, the degree of oxaluria dictates the dosage of vitamin B6.  But the degree of supplementation depends on how much B6 comes from food (Yendt, 1985).

What are they made from?

Most stones (~80%) are calcium oxalate calculi, which crystallizes in a hurry.  It’s the stuff that forms a needle-like crust on the inside of a brewery container.  If you swallowed this material, you’d get really sick, and maybe die.  Calcium oxalate crystal formation is one of the effects of ingesting antifreeze.  A small dose of calcium oxalate will make your tongue burn and swell your throat shut.  This is what happens when the cat chews on a Dieffenbachia leaf in the living room window, and then requires a trip to the vet.

Some plants, including spinach, contain calcium oxalate in their leaves. If you’re a stone former, you might choose to avoid, or at least limit, raw spinach salads, although some researchers say it doesn’t matter, as long as you’re amply hydrated and your diet is sufficiently balanced to provide calcium and vitamin B6, both of which are found in spinach (Curhan, 1999).  A little baffling, huh?  After a stone passes through the urine and gets collected in that little strainer that painters use to get the globs out of a gallon of linen white, you’ll be asked to take that stone to the doctor so he can determine its makeup.  Then he’ll know what course of action to give you.

How do I prevent kidney stones?

If ever the proverbial ounce of prevention is worth a lot, this is the place.  Most experts agree that drinking fluids is the key.  Believe us when we say that a stone former is more than willing to increase his water intake, despite its lack of flavor.  If you need flavor, try lemon juice.  Counseling in this area is simple:  if you don’t drink enough water, you’ll experience this again.  That means you have to drink even when you’re not thirsty (McCauley, 2012).  Swapping soft drinks for water is prudent (Fink, 2009).

Increasing dietary calcium intake is inversely related to stone formation.  Supplemental calcium, on the other hand, may increase risk.  Dietary calcium blocks the amount of oxalates absorbed by the body, while supplements, especially if taken between meals, spill too much of the mineral into the urine.  If calcium supplementation is needed, take it with a meal to improve absorption.  We’re cautioned not to take more than 500 mg at a time, anyway.  It’s all about the timing (Curhan, 1997).

It’s believed that most stones form in the summer, when people are more likely to get dehydrated, so we’re admonished to drink ten to twelve glasses of water a day.  Other beverages, though, fare well in the prevention category.  Caffeinated and decaffeinated coffee, tea, and wine accounted for a decreased risk of stone formation, according to the Brigham and Women’s Hospital study of the 1990’s (Curhan, 1998).

Obesity increases the risk of kidney stones, but drastic weight loss measures that rely on high protein intake can stymie the good intentions.  So, too, can laxative abuse, rapid loss of lean tissue and, naturally, poor hydration.  A diet high in fruits and vegetables can alkalize urine enough to offset oxalate and uric acid stone formation ( Frassetto, 2011).  Produce is known for its magnesium content.  Intake of magnesium is related to reduced stone manufacture, and has been a recommendation since the 17th century.  Even without overt deficiency, magnesium intake, at 500 mg a day in the form of magnesium hydroxide, was shown to decrease stone formation, and it has no adverse side effects as long as it’s not overzealously done (Johansson, 1980 and 1982).  Too much magnesium may induce laxation.  That’s an individual response.   Later study learned that magnesium combined with vitamin B6 offered a substantial decline in the risk for oxalate stones (Rattan, 1994)

Kale, turnip greens, radishes, chard and other leafy greens, broccoli, Brussels sprouts, and cabbage are good sources of dietary calcium.  Almonds and cashews, pumpkin seeds, barley, quinoa, leafy greens, white and black beans are a few good sources of magnesium.  Since calcium and magnesium compete for occupancy in the body, with calcium the winner, magnesium supplementation is a good idea.  An Epsom salts bath allows magnesium levels to increase transdermally…and it’ll help you fall asleep.  Drink water.  Prevent stones.


Conte A, Pizá P, García-Raja A.
Urinary lithogen risk test: usefulness in the evaluation of renal lithiasis treatment using crystallization inhibitors (citrate and phytate).
Arch Esp Urol. 1999 Jan-Feb;52(1):94-9.

Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ.
Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.
Ann Intern Med. 1997 Apr 1;126(7):497-504.

Curhan GC, Willett WC, Speizer FE, Stampfer MJ.
Beverage use and risk for kidney stones in women.
Ann Intern Med. 1998 Apr 1;128(7):534-40

Curhan GC, Willett WC, Speizer FE, Stampfer MJ.
Intake of vitamins B6 and C and the risk of kidney stones in women.
J Am Soc Nephrol. 1999 Apr;10(4):840-5.

Curhan GC.
Epidemiologic evidence for the role of oxalate in idiopathic nephrolithiasis.
J Endourol. 1999 Nov;13(9):629-31.

Fink HA, Akornor JW, Garimella PS, MacDonald R, Cutting A, Rutks IR, Monga M, Wilt TJ.
Diet, fluid, or supplements for secondary prevention of nephrolithiasis: a systematic review and meta-analysis of randomized trials.
Eur Urol. 2009 Jul;56(1):72-80. Epub 2009 Mar 13.

Frassetto L, Kohlstadt I.
Treatment and prevention of kidney stones: an update.
Am Fam Physician. 2011 Dec 1;84(11):1234-42.

Gill HS, Rose GA.
Mild metabolic hyperoxaluria and its response to pyridoxine.
Urol Int. 1986;41(5):393-6.

Grases F, Costa-Bauzá A.
Phytate (IP6) is a powerful agent for preventing calcifications in biological fluids: usefulness in renal lithiasis treatment.
Anticancer Res. 1999 Sep-Oct;19(5A):3717-22.

Habbig S, Beck BB, Hoppe B.
Nephrocalcinosis and urolithiasis in children.
Kidney Int. 2011 Dec;80(12):1278-91. doi: 10.1038/ki.2011.336. Epub 2011 Sep 28.

Johansson G, Backman U, Danielson BG, Fellström B, Ljunghall S, Wikström B.
Biochemical and clinical effects of the prophylactic treatment of renal calcium stones with magnesium hydroxide.
J Urol. 1980 Dec;124(6):770-4.

Johansson G, Backman U, Danielson BG, Fellström B, Ljunghall S, Wikström B.
Effects of magnesium hydroxide in renal stone disease.
J Am Coll Nutr. 1982;1(2):179-85.

Massey LK, Liebman M, Kynast-Gales SA.
Ascorbate increases human oxaluria and kidney stone risk.
J Nutr. 2005 Jul;135(7):1673-7.

McCauley LR, Dyer AJ, Stern K, Hicks T, Nguyen MM.
Factors influencing fluid intake behavior among kidney stone formers.
J Urol. 2012 Apr;187(4):1282-6. Epub 2012 Feb 15.

Miggiano GA, Migneco MG.
[Diet and nutrition in nephrolitiasis].   [Article in Italian]
Clin Ter. 2007 Jan-Feb;158(1):49-54.

Mitwalli A, Ayiomamitis A, Grass L, Oreopoulos DG.
Control of hyperoxaluria with large doses of pyridoxine in patients with kidney stones.
Int Urol Nephrol. 1988;20(4):353-9.

Moyad MA.
Calcium oxalate kidney stones: another reason to encourage moderate calcium intakes and other dietary changes.
Urol Nurs. 2003 Aug;23(4):310-3.

Rattan V, Sidhu H, Vaidyanathan S, Thind SK, Nath R.
Effect of combined supplementation of magnesium oxide and pyridoxine in calcium-oxalate stone formers.
Urol Res. 1994;22(3):161-5.

Saxena A, Sharma RK.
Nutritional aspect of nephrolithiasis.
Indian J Urol. 2010 Oct;26(4):523-30.

Singh PP, Barjatiya MK, Dhing S, Bhatnagar R, Kothari S, Dhar V.
Evidence suggesting that high intake of fluoride provokes nephrolithiasis in tribal populations.
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Yendt ER, Cohanim M.
Response to a physiologic dose of pyridoxine in type I primary hyperoxaluria.
N Engl J Med. 1985 Apr 11;312(15):953-7.

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

Truth About Magnesium Stearate

mag-glassWe’ve all seen pitchmen, the medium-pressure peddlers who unashamedly try to lure us to their side of the street with great deals on auto insurance or oxygenated household cleaners. Forceful voices and rapid chatter are attention grabbers. But it needn’t be fast talk and loud volume that get our attention. It can be capital letters, bold print, fancy fonts, or any combination of these on the internet that tries to persuade or dissuade us from buying, doing, ingesting or using a tangible or intangible thing.

Recent internet talk, some by celebrity physicians, has focused on—and maligned—magnesium stearate, an innocuous substance used in the pharmaceutical and supplement industries as an excipient. Yes, it does have lubricative properties that prevent adhesion of a material to the tumbling and pressing surfaces of a tablet forming machine, but more importantly, it helps to ensure consistency and homogeneity of the finished product. It guarantees even distribution of the active ingredients in a tablet or capsule, so that each is identical to the last and the next. Acting as a flow agent, magnesium stearate lowers manufacturing costs, as well. Were this not the case, consumer dander would rise to greet the consequent price increase. If the active ingredient of a medication or supplement did cling to machine surfaces, dosages would be hit or miss. The average amount of magnesium stearate in a tablet or capsule is far less than 1.0% of the total weight, with many supplement makers using fractional amounts, down to thousandths of a percent.

Pharmaceutical and supplement companies are not deaf to consumers’ interests. They add only that amount of magnesium stearate necessary to the desired outcome, changing according to a specific blend. The variables involved in drug or nutrient manufacturing are numerous. Particle size of the main ingredient, moisture content, chemical nature, solubility, cohesive properties, mixing order of the components, electrostatic forces that cause factory explosions, mixing time, hydrophobicity, dissolution expectations, and factors herein unknown contribute to the complexity of the process. Each step is carefully monitored as part of a fail-safe system employed by responsible, accountable, cGMP-compliant companies. Sadly, there are those businesses that perpetrate fraud against consumers knowingly. It is these who market supplements for a buck ninety-nine. It is these whose cut-rate pharmaceuticals yield undesirable effects.

What started all the hoopla about magnesium sulfate is a 1990 report whose conclusions were never put to use. This was a preliminary cell study that sought an immunosuppressive drug for people with organ transplants and autoimmune diseases.  In the experiments, T cells and B cells were exposed to a concoction that mixed stearic acid with diatomaceous earth and bovine albumin—a little different from magnesium stearate. The intent of the study was to injure T cells with the brew after they were exposed to a toxic challenge, meaning that exposure to the cocktail had to be adequate to damage them. Any association with pharmaceuticals or supplement manufacture escapes even a casual reader.  What is particularly bothersome is the faulty conclusion that stearic acid destroys T cells and is, therefore, immune toxic. The study’s title is incriminating to stearic acid:  “Molecular basis for the immunosuppressive action of stearic acid on T cells,” having appeared in the journal Immunology in July, 1990. B cells in this test were unscathed, while T cells lost membrane integrity to stearic acid influx, which increased membrane rigidity. Only stearic acid, the 18.0 saturated fat common to chocolate and lean beef, was implicated. The roles of diatomaceous earth and bovine albumin remain a mystery. The former is an industrial filtering component and filler for paints and abrasives. The latter is a protein concentration standard used in cell cultures and immunohistochemistry because it has no effect on enzymes that do not need it for stabilization, and it takes part in very few biochemical reactions. Bovine albumin is inexpensive, too.

In the study, stearic acid was likened to the anti-rejection drug, cyclosporine, which suppresses the immune system following allograft. This drug is also selectively used to treat severe cases of psoriasis, rheumatoid arthritis, atopic dermatitis, and even dry eyes as an ophthalmic emulsion. But its adverse effects are numerous and intense, and it is suspected of carcinogenicity. If stearic acid, with zero side effects, could replace cyclosporine, it would be a welcome alternative. However, doses would have to exceed the no-effect level of magnesium stearate’s 2500 mg/kg of bodyweight/day (Søndergaard, 1980). That equates to 6 ounces of magnesium stearate for a 150-pound person each day.

Magnesium stearate is a compound of magnesium and solid organic acids, containing two equivalents of stearate and one of magnesium. The magnesium moiety is used to address conditions besides hypomagnesemia. Laxation aside, this mineral has been applied to respiratory and cardiovascular needs, aberrant lipid profiles, neuromuscular and neuroskeletal diseases, ADD/ADHD and other behavior disorders, restless leg syndrome, migraine headaches, and prevention of hearing loss, among others. Being the second most plentiful cation in the human body, magnesium is involved in more than three hundred enzyme systems and is divided almost equally between bone and soft tissue.  A fraction of magnesium sits on the surface of bone, acting as a reservoir to maintain the extracellular magnesium concentration.  Fifty-five percent of plasma magnesium is free; about thirty percent is bound to proteins.  The rest is complexed to anions.

Absorption of supplemental magnesium, probably occurring in distal duodenum, is inversely proportional to the amount ingested.  Even dietary (from foods) mineral enjoys only about one-third absorption, depending on body stores and physiological/metabolic needs.  In supplements, magnesium oxide is the least bioavailable; citrate and glycinate among the more available.  Enteric coating reduces absorption.

Magnesium deficit is associated with cardiac arrhythmia, cessation of bone growth (activity of osteoclasts and osteoblasts), muscle spasticity, anorexia, seizures, confusion, muscle cramping and hypertension, among other disorders.  Such deficiency is common in diabetes, malabsorption syndromes, alcohol abuse, and in extended use of thiazide and loop diuretics.  Magnesium is intimately linked to calcium in the manufacture of adenosine triphosphate (ATP).  On the other hand, they antagonize each other in the synthesis of nucleic acids and proteins.  In some ways, magnesium is nature’s calcium channel blocker because it regulates the intracellular flow of calcium ions.  The virtues of magnesium extend beyond the scope of this newsletter, but it is worth noting that foods high in fiber are usually good sources of magnesium.

Stearic acid is one of the most common long-chain fatty acids, found in both animal and vegetable fats, appearing in foods in amounts far greater than in any supplement.  This fatty acid is the immediate precursor to oleic acid, an important fatty acid in olive oil.  Studies in humans have determined that stearic acid, desaturated to oleic acid by the liver, is less apt to elevate cholesterol than other saturated fatty acids, possibly due to absorption vagaries.  Nonetheless, the rapid conversion of stearic to oleic acid suggests that stearic acid is as effective as oleic acid in lowering plasma cholesterol when it replaces palmitic acid in the diet (Bonanome, 1988).  But more dramatic is the finding that stearic acid may be toxic to cancer cells.  Decreased cell membrane rigidity is a characteristic of malignant cells, partly because of the desaturation of stearic acid.  British tests that examined a chemically-induced murine mammary carcinoma line discovered that subcutaneous administration of stearic acid at weekly intervals prevented tumor development (Habib, 1987).  Later study found that stearic acid inhibited colony forming abilities of several human cancer cell lines (Fermor, 1992).  The innocuous nature of stearic acid had been established well before it was maligned as being part of a “persona non grata” molecule.

The street vendors have declared magnesium stearate as causative of intestinal biofilms that interfere with absorption of nutrients and foods.  Yet, no proof is offered.  To the contrary, the molecules used by micro-organisms to make biofilms are inhibited by stearic and several other saturated fatty acids (Soni, 2008).  Since most people have never heard of biofilms, mentioning them as ominous factors is an effective marketing tool.  The bacteria that form biofilms to protect themselves use polyunsaturated fats to flourish by injecting a fat with an oxygen molecule in order to form an oxylipin, which is a pro-inflammatory eicosanoid.  It is not likely that a saturated fat has room to accept another atom, much less a molecule.

Even though FDA credibility has raised a few eyebrows in recent years, it is generally accepted that its revised 2006 Code of Federal Regulations is reliable. Title 21, Volume 3 of that tome allows that stearic acid is a GRAS substance that can be used according to Good Manufacturing Practices (GMP’s).

The science agrees that magnesium stearate is a safe analog of stearic acid.   Red meats, chocolate products and Brazil nuts are ordinary sources of stearic acid.  Despite its fat content, chocolate does not have any adverse effect on plasma lipids, not even milk chocolate.  Stearic acid deserves not to be spoken in the same sentence with other saturated fats (Kris-Etherton, 1994).  In fact, stearic acid has shown itself to increase excretion of endogenous cholesterol (Schneider, 2000) and even to lower LDL’s compared with other fatty acids (Mensink, 2005).  If at fault, the worst that magnesium stearate does is to prolong dissolution of the main ingredient.  Does it matter whether it comes from animal or vegetable sources?  Concerning dissolution and safety, no.  Concerning the force needed to eject a tablet from its mold, the animal-derived product has stronger adhesion properties (Hamad, 2008).  Paracelsus, the Renaissance physician held to be the father of toxicology, pointed out that the dose makes the poison.  In that matter, water can be a lethal substance.  Beware of misleading and inaccurate information.


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GRAS Substances (SCOGS) Database
Select Committee on GRAS Substances (SCOGS) Opinion: Stearic acid (packaging)
Stearic acid (packaging)
SCOGS-Report Number: 54*
Type Of Conclusion: 1
ID Code: 57-11-4
Year: 1975
21 CFR Section: 184.1090

Habib NA, Hershman MJ, Salem R, Barker W, Apostolov K, Wood CB.
Increased erythrocyte stearic acid desaturation in rats with chemically induced colorectal carcinomas.
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N. A. Habib, C. B. Wood, K. Apostolov, W. Barker, M. J. Hershman, M. Aslam, D. Heinemann, B. Fermor, R. C. Williamson, W. E. Jenkins
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Hamad ML, Gupta A, Shah RB, Lyon RC, Sayeed VA, Khan MA.
Functionality of magnesium stearate derived from bovine and vegetable sources: dry granulated tablets.
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M.S.H. Hussain, P. York, P. Timmins
Effect of commercial and high purity magnesiumstearates on in-vitro dissolution of paracetamol DC tablets
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Khalil MH, Marcelletti JF, Katz LR, Katz DH, Pope LE.
Topical application of docosanol- or stearic acid-containing creams reduces severity of phenol burn wounds in mice.
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Kris-Etherton PM, Mustad VA.
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Stress and Childhood Obesity

weigh-inBeing a kid doesn’t necessarily mean having a carefree life, yet that’s how most adults view childhood. Because kids don’t have jobs, bills to pay, and children to raise what could they possibly have to worry about? More than we realize. Even the very young among us have stressors, slight though they may be. Stress is a function of the demands we face and our ability to handle them. Often it comes from outside sources. You know—family, job, friends, school, and expectations. Sometimes stress comes from inside, related to what we think we should do compared to what we actually do, say or think.

Today, kids have to learn scores of times more information than their parents did at the same age. That we can blame on an electronic era. And they have to learn these things in the same allotted time. Preschoolers get stressed when their moms leave them at daycare. As they get older, kids are pressured by academics and social position. After all, they need to fit in. Their lives get so hectic they seldom have time for themselves, for creative play, or even for relaxation. They are overscheduled with activities that would tax even the adult mind. Disturbing images on TV, news of wars, terrorism and natural disasters, and concerns for personal and family safety add to the burden. Illness, death and divorce don’t help.

All stressors are not created equal, and all people do not respond to stress the same way. Children often learn to handle stress from their parents. Sometimes that’s good; sometimes not. The idea that, “If it doesn’t kill me, it’ll make me stronger,” doesn’t apply to youngsters who’ve not yet developed a coping mechanism. What does this have to do with obesity, a childhood plague that’s more than doubled in the last few decades?  Lots.

A person’s reaction to stress will likely invoke the fight-or-flight (-or freeze) response as the primary means of dealing with a novel situation perceived as threatening. Children who overreact to stress will manufacture more cortisol than the body can dump, and that’s where the problem begins—emotional eating (Michels, 2012). Cortisol is a steroid hormone made by the adrenal glands, released in response to stress. Its main job is to increase blood sugar to power the fight-flight machinery. Cortisol counteracts insulin and contributes to insulin resistance (Goran, 2010) by lowering glucose transport to the cell membrane. Small increases in cortisol can provide a quick burst of energy in an emergency. At the same time it can heighten memory, briefly but powerfully enhance immunity and lower sensitivity to pain. But the return to normal is needed lest the body idle at high rpm’s. With our high-stress culture that has become the norm…chronic stress. That eventually induces impairment of cognitive function, suppresses thyroid activity, throws blood sugar out of whack, menaces bone density, elevates blood pressure, and actually lowers immune responses. And it increases deposition of abdominal fat, setting the stage for metabolic syndrome, depressed affect (Endocrine Society, 2009) (Dockray, 2009) and cardiovascular entanglement, even at a young age.

Children’s biological response to stressors was examined recently by researchers from Penn State and Johns Hopkins Universities.  A group of pre-teens was assigned public speaking and mathematical tasks with little preparation time allowed for either. Cortisol content of their saliva was measured before and after. Following the assignment, the children were offered an array of snack foods regardless of their hunger status. The amount of calories they consumed varied, but those with the highest body mass indexes, who also had the highest cortisol levels, consumed more calories, even in the absence of hunger, than did those with lower cortisol levels. The outcome suggests that children with poor response to stress are at risk for becoming overweight or obese (Francis, 2013). Other factors that contribute to eating in the absence of hunger include poverty, living in a violent environment and food insecurity.

The determination of childhood obesity needs to be made on an individual basis, not from a chart developed by an insurance company that focuses on only one ethnicity or population. Anthropometric measurements and family history need to be included in an evaluation. Pathologies need to be ruled out, genetics must be considered, and psychosocial factors scrutinized. The comorbidities of obesity are varied and many, and their prophylaxis calls for early intervention, some of which transcends diet. Overweight children face the same health conditions as their parents, with hypertension, discordant lipid panels, abnormal glucose levels, and elevated inflammation markers among them. Lifestyle changes, where parents are the managers, may be all that is needed. This may include dietary interventions that eliminate simple carbohydrates, especially sugars and refined starches common to the foods kids like the most. These foods will spike insulin, which will spike cortisol, which will encourage eating, which will add pounds. Avoiding pharmaceutical anorectic agents is strongly encouraged.

Mental stress is associated with emotional eating, which typically ignores healthy dietary patterns (Michels, 2013). Cortisol levels peak in the morning, but can remain elevated in stressful surroundings. Admittedly, some of those surroundings are beyond a parent’s control, so coping mechanisms are helpful. Without being a helicopter parent, it’s possible to create a comfortable atmosphere for a child, even when he is away from you. Teaching coping skills by example starts early. Believe it or not, kids watch, listen and emulate. There are three-year-olds with vocabularies that would make you wince. If kids can learn to be tense and confrontational, they can also learn to relax and to take things in stride.

Limiting cortisol manufacture might be as easy as increasing magnesium in thediet. How?  Vegetables. Essential fatty acids, music therapy and phospholipids,and even vitamin C and tea have been shown to curtail cortisol release (Rains,2011) (Arent, 2010) (Peters, 2001).


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