Nutrition

DIETARY INFLUENCES ON BEHAVIORAL PROBLEMS IN CHILDREN

James Greenblatt MD, Author of Finally Focused (www.finallyfocusedbook.com), Chief Medical Officer and Vice President of Medical Services at Walden Behavioral Care

It is well known that our food choices play a role in our long-term physical health. It is less recognized that nutrition can have profound effects on our mental health and our behavior. Overall, malnutrition in childhood can affect the brain throughout the lifespan, while specific food components can affect our short-term well-being. Sugar, wheat, and milk are among the most common dietary triggers for ADHD symptoms. Fluctuating blood sugar levels and partially-digested foods can also cause a wide range of symptoms from fatigue to hyperactivity. This article will discuss the dietary influences on behavioral problems in children, review how laboratory testing can be critical in identifying food sensitivities, and how to enhance digestion for maximum absorption of nutrients.

One of the most debated treatments for ADHD is the Feingold Diet, introduced in the early 1970’s by pediatrician and allergist Ben Feingold, MD. He initially suggested that children who are allergic to aspirin (which contains salicylates) may react to artificial food colors and naturally occurring salicylates. The Feingold Diet eliminates artificial food additives like flavorings, preservatives, sweeteners, and colors to reduce hyperactivity. The research over the years on the Feingold Diet has been mixed – some studies show no behavior change and some show increases in hyperactivity when children consume artificial ingredients. A landmark study conducted in the UK on three hundred 3-year-old and 8/9-year-old children in the general population found artificial colors or a sodium benzoate preservative (or both) in the diet resulted in increased hyperactivity (McCann et al., 2007). This study led the European Union to ask manufacturers to voluntarily remove several artificial food colors from foods and beverages or to add a warning label that the artificial food color “may have an adverse effect on activity and attention in children” (Arnold et al., 2012). Conversely, in the US, the FDA reviewed the study and determined that a causal relationship between consumption of color additives and hyperactivity in children could not be definitively established (Arnold et al., 2012).

Genetics often play a role in how a child’s ADHD symptoms are exacerbated. The children most likely to be affected by food additives have a genetic inability to metabolize the compounds. Genetic tests were conducted on the 300 UK children from the artificial food color study. Children with specific variations in the HNMT gene, which helps break down histamine in the body, had stronger behavioral reactions to artificial food colors than children without this variation (Stevenson et al., 2010). This means that in some children, food additives spur the release of histamine that in turn affect the brain.

The Barbados Nutrition Study was a longitudinal case-control study that began in the late 1960’s and investigated the physical, mental, and behavioral developmental effects of infant malnutrition. The 204 participants of this study experienced a single episode of moderate to severe malnutrition during their first year of life. Data was collected on these children through adulthood and compared to data from healthy children. By the end of puberty, all children completely caught up in their physical growth. However, cognitive and behavioral issues persisted into adulthood.

The consequences of malnutrition in infancy manifested in many ways. IQ scores of the children with a history of malnutrition at age 5-11 were significantly lower than those of the control children. 50% of the malnourished children had scores at or below 90 while only 17% of the control children had scores this low (Galler et al., 1983). According to teacher reports, attentional deficits, including shorter attention span, poorer memory, and more distractibility and restlessness, were found in 60% of the malnourished children compared to only 15% of the controls. They also had worse social skills, general health, sleepiness in the classroom, and emotional stability (Galler et al., 1983). When the children were reassessed on these measures at age 9-15, a history of early malnutrition was still associated with behavioral impairment at school, especially attention deficits (Galler & Ramsey, 1989).

Behavior problems reported by teachers when the participants were aged 5-11 significantly predicted conduct problems at age 11-17 (Galler et al., 2012). Age at 5-11, children malnourished as infants had lower performance on 8 out of 9 academic subject areas. 37 children (36 malnourished, 1 control) were below the expected grade for their age (Galler, Ramsey, & Solimano, 1984). Compared to control children, previously malnourished children at age 5-11 had significantly worse scores on parent-rated measures of good behavior (no antagonism between mother and child, obedience), social skills, mother-child relationship, frustration level, eating habits, sleeping habits, and school avoidance. Compared to their siblings, previously malnourished children had significantly worse scores on social skills, good behavior, helpfulness, mother-child interaction, eating habits, toilet training, and language (Galler, Ramsey, & Solimano, 1985). When the children were reassessed on these measures at age 9-15, the same results were seen, especially for aggression and distractibility (Galler & Ramsey, 1989). Problems with self-regulation, displayed as reduced executive functioning and aggression toward peers, persisted through adolescence (Galler et al., 2011).

Years later when the subjects were aged 37-43, attention problems were assessed using an adult ADHD scale and a computerized test of attention-related problems. There was a higher prevalence of attention deficits in the previously malnourished group relative to controls. 69% of the previously malnourished participants had at least one test score that fell within the clinical range for attention disorders (Galler et al., 2012). Previously malnourished participants also had worse educational attainment and income across the entire 40-year study (Galler et al., 2012).

Multiple connections have been made between sugar, hyperactivity, and the risk for ADHD. In group of almost 400 school-age children, researchers found that children with the greatest “sweet” dietary pattern had almost four times greater odds of having ADHD compared to those who ate sweets (ice cream, refined grains, sweet desserts, sugar, and soft drinks) less often (Azadbakht & Esmaillzadeh, 2012). In a similar study on 1,800 adolescents, having a “Western” dietary pattern (higher intakes of total fat, saturated fat, refined sugars, and sodium) more than doubled the odds of an ADHD diagnosis (Howard et al., 2011). Likewise, a study on 986 children, average age 9 years, found a high intake of sweetened desserts (ice cream, cake, soda) was significantly associated with worse inattention, hyperactivity-impulsivity, aggression, delinquency, and externalizing problems. In contrast, a high-protein diet was associated with better scores on these measures. A high level of sweetened dessert consumption was also associated with lower scores on tests of listening, thinking, reading, writing, spelling, and math (Park et al., 2012).

Certain foods may not only influence behavioral and physical symptoms, but may also modify brain activity. When children aged 6-15 with food-induced ADHD consumed provocative foods, they showed an increase in beta activity in frontotemporal regions during EEG topographic mapping of brain electrical activity (Uhlig et al., 1997). Beta waves are involved in normal waking consciousness and tend to have a stimulating effect; while too much beta can lead to anxiety.

A food sensitivity to a protein found in milk or a protein found in wheat is a prevalent but neglected cause of ADHD. Milk and milk products like cheese and butter contain a protein called casein. Casein is different from lactose which is a milk sugar. Grains like wheat, rye, and barley contain a protein called gluten. During digestion, casein becomes casomorphin and gluten becomes gliadorphin. For most people, these proteins are further broken down into basic amino acids. For some with ADHD, they have inactive dipeptidyl peptidase IV, a zinc-dependent enzyme that breaks down both casein and gluten, leaving these opioid peptides substances to build up.

Children with ADHD who have high levels of casomorphin or gliadorphin often have severe, uncontrolled symptoms. Both casomorphin and gliadorphin are morphine-like compounds which attach to opiate receptors in the brain. These substances can act like an addicting drug in susceptible children and cause fatigue, irritability, and brain fog. A child with high levels of casomorphin may have strong cravings for milk products (ice cream, yogurt) and may become irritable when he or she doesn’t eat these types of foods. The Gluten/Casein Peptide Test is a simple urine test that can measure levels of casomorphin and gliadorphin. If a child has high levels of casomorphin or gliadorphin, they should try to eliminate casein or gluten. Supplementation with DPP-IV enzymes can also be beneficial and often required for clinical improvement.

Malnutrition can negatively affect behavior and cognition, but certain nutrients can have detrimental effects on children as well. Louise Goldberg, pediatric dietitian, put it succinctly: “Food allergies and sensitivities can come at children with a one-two punch - first making them agitated, and next robbing them of nutrients that might rein in their behavior” (Peachman, 2013). We are biochemically unique and have different physiological and psychological responses to different foods. The right food for one child may the wrong food for another. For instance, peanut butter on whole wheat toast may be a nutritionally-balanced, energy-boosting snack for one child, while this snack would be harmful to a child who cannot tolerate neither nuts nor wheat. Medical testing can clarify which nutrients a child is sensitive to. Fortunately, eliminating offending substances can rapidly improve physical and behavioral symptoms.

 

References:

Arnold, et al. (2012). Artificial food colors and attention-deficit/hyperactivity symptoms: Conclusions to dye for. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics, 9(3), 599-609.

Azadbakht & Esmaillzadeh. (2012). Dietary patterns and attention deficit hyperactivity disorder among Iranian children. Nutrition, 28(3), 242-249.

Galler et al. (1983). The influence of early malnutrition on subsequent behavioral development I. Degree of impairment in intellectual performance. Journal Of The American Academy Of Child And Adolescent Psychiatry, 22(1), 8-15.

Galler et al. (1983). The influence of early malnutrition on subsequent behavioral development II. Classroom behavior. Journal Of The American Academy Of Child And Adolescent Psychiatry, 22(1), 16-22.

Galler & Ramsey. (1989). A follow-up study of the influence of early malnutrition on development: Behavior at home and at school. Journal Of The American Academy Of Child And Adolescent Psychiatry, 28(2), 254-261.

Galler, Ramsey, & Solimano. (1984). The influence of early malnutrition on subsequent behavioral development III learning disabilities as a sequel to malnutrition. Pediatric Research, 18(4), 309-313.

Galler, Ramsey, & Solimano. (1985). Influence of early malnutrition on subsequent behavioral development: V. child’s behavior at home. Journal Of The American Academy Of Child Psychiatry, 24(1), 58-64.

Galler et al. (2011). Early malnutrition predicts parent reports of externalizing behaviors at ages 9-17. Nutritional Neuroscience, 14(4), 138-144.

Galler et al. (2012). Infant malnutrition predicts conduct problems in adolescents. Nutritional Neuroscience, 15(4), 186-192.

Galler et al. (2012). Infant malnutrition is associated with persisting attention deficits in middle adulthood. The Journal Of Nutrition, (4), 788.

Galler et al. (2012). Socioeconomic outcomes in adults malnourished in the first year of life: a 40-year study. Pediatrics, (1), 1.

Howard et al. (2011). ADHD Is Associated with a "Western" Dietary Pattern in Adolescents. Journal of Attention Disorders, 15(5), 403-411.

Lacy. (2004). Hyperactivity/ADHD-- new solutions. AuthorHouse.

Langseth & Dowd. (1978). Glucose tolerance and hyperkinesis. Food And Cosmetics Toxicology, 16(2), 129-133.

McCann et al. (2007). Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: A randomised, double-blinded, placebo-controlled trial. The Lancet, 370(9598), 1560-1567.

Niederhofer. (2011). Association of Attention-Deficit/Hyperactivity Disorder and Celiac Disease: A Brief Report. Primary Care Companion For CNS Disorders, 13(3), pii: PCC.10br01104.

Park et al. (2012). Association between dietary behaviors and attention-deficit/hyperactivity disorder and learning disabilities in school-aged children. Psychiatry Research, 198, 468-476.

Stevenson et al. (2010). The role of histamine degradation gene polymorphisms in moderating the effects of food additives on children's ADHD symptoms. The American Journal of Psychiatry, 167(9), 1108-15.

Uhlig et al. (1997). Topographic mapping of brain electrical activity in children with food-induced attention deficit hyperkinetic disorder. European Journal of Pediatrics, 156(7), 557-61.

The Green Smoothie Health Fad: This Road to Health Hell is Paved with Toxic Oxalate Crystals

William Shaw, PhD.

Recent internet news indicated the conviction of an oncologist who attempted to kill her boyfriend who was involved with another woman. The weapon of choice was ethylene glycol, popularly known as antifreeze, which had been placed in his coffee just after coitus. Although emergency measures saved the boyfriend's life, extensive deposits of oxalate crystals, the main toxic metabolite of ethylene glycol, had caused extensive kidney and liver damage, reducing the man's lifespan by about half.

Similar results in sabotaging your own health can occur through the regular consumption of a popular concoction called a "green smoothie". A recent Google search for "green smoothie" yielded 609,000 hits. In addition, a recent "improving your diet" seminar I attended promoted this same idea. Interestingly, on the same day, I reviewed test results of a urine organic acid test of a woman with oxalate values three times the upper limit of normal. A conversation with the patient indicated that she had recently turned to consuming daily "green smoothies" to "clean up her diet". The most common "green" components of the most popular green smoothies are spinach, kale, Swiss chard, and arugula. Each of these greens is loaded with oxalates. A typical internet recipe advises that two cups of packed raw spinach leaves is a good starting point for a good smoothie. In addition to the high oxalate greens added to the blender, green smoothie proponents frequently recommend adding a variety of berries or almonds, also containing high oxalate amounts. Similar high urine oxalate results were found in organic acid tests of a number of patients with kidney stones who had decided to eat large spinach salads daily as a "move to clean up my unhealthy diet". Unfortunately kidney stones are not the only health problems that people who regularly consume green smoothies and large spinach salads will experience with their new "clean" diet.

Seventy-five years ago, a food scientist of the Campbell Soup Company (1) reported: "Only a few foods, notably spinach, Swiss Chard, New Zealand spinach, beet tops, lamb's quarter, poke, purslane, and rhubarb have high oxalate content. In them, expressed as anhydrous oxalic acid, it is often considerably over 10% on a dry basis. In fifty-three samples, including practically all commercial and many experimental varieties grown in California and in Maryland as well as those shipped from Texas, Florida and Carolina, the average anhydrous oxalic acid content was 9.02% on the dry basis (maximum 12.6, minimum 4.5). Whereas spinach greatly increases the calcium content of the low calcium but well performing basal diet, it decidedly interferes with both growth and bone formation. If to a diet of meat, peas, carrots and sweet potatoes, relatively low in calcium but permitting good though not maximum growth and bone formation, spinach is added to the extent of about 8% to supply 60% of the calcium, a high percentage of deaths occurs among rats fed between the age of 21 and 90 days. Reproduction is impossible. The bones are extremely low in calcium, tooth structure is disorganized and dentine poorly calcified. Spinach not only supplies no available calcium but renders unavailable a considerable amount of the calcium in the other foods. Considerable amounts of the oxalate appear in the urine, much more in the feces."

The author also discovered that in addition to leading to excessive death and defective reproduction in the rats, high oxalate foods also cause soft and pliable bones and defective teeth.

Oxalate and its acid form oxalic acid are organic acids that come from three sources: the diet, fungus infections such as Aspergillus and Penicillium and possibly Candida (2-10), and also human metabolism (11).

Oxalic acid is the most acidic organic acid in body fluids and is used commercially to remove rust from car radiators. Antifreeze (ethylene glycol) is toxic primarily because it is converted to oxalate. Two different types of genetic diseases are known in which oxalates are high in the urine. The genetic types of hyperoxalurias (type I and type II) can be determined from the organic acid test done at The Great Plains Laboratory. Foods especially high in oxalates include spinach and similar leafy vegetables, beets, chocolate, soy, peanuts, wheat bran, tea, cashews, pecans, almonds, berries, and many others. Oxalates are not found in meat or fish at significant concentrations. Daily adult oxalate intake is usually 80-120 mg/d but it can range from 44-1000 mg/d in individuals who eat a typical Western diet. I estimate that the person who consumes a green smoothie with two cups (about 150 grams) of spinach leaves is consuming about 15 grams or 15,000 mg of oxalates or about 150 times the average daily oxalate intake. A complete list of high oxalate foods is available on the Internet at http://www.upmc.com/patients-visitors/education/nutrition/pages/low-oxalate-diet.aspx

High oxalate in urine and plasma was first found in people who were susceptible to kidney stones. Most kidney stones are composed of calcium oxalate. Stones can range in size from the diameter of a grain of rice to the width of a golf ball. It is estimated that 10% of males may have kidney stones some time in their lives. Because many kidney stones contain calcium, some people with kidney stones think they should avoid calcium supplements. However, the opposite is true. When calcium and magnesium are taken with foods that are high in oxalates, oxalic acid in the intestine combines with these minerals to form insoluble calcium and magnesium oxalate crystals that are eliminated in the stool. These forms of oxalate cannot be absorbed into the body. When calcium and/or magnesium are low in the diet, oxalic acid is soluble in the liquid portion of the contents of the intestine (called chyme) and is readily absorbed from the intestine into the bloodstream. If oxalic acid is very high in the blood being filtered by the kidney, it may combine with calcium and other metals, including heavy metals like lead and mercury to form crystals that may block urine flow, damage the kidney, and cause severe pain. These oxalate crystals can also form in the bones, skin, joints, eyes, thyroid gland, blood vessels, lungs, and even the brain (11-14). Oxalate crystals in the bone may crowd out the bone marrow cells, leading to anemia and immunosuppression (14). In addition to individuals with autism and kidney disease, individuals with fibromyalgia and women with vulvar pain (vulvodynia) may also suffer from the effects of excess oxalates (15-18).

Recent evidence also points to the involvement of oxalates in stroke, atherosclerosis, and in endothelial cell dysfunction (19-21). High amounts of oxalates were found concentrated in atherosclerotic lesions of the aortas and coronary arteries of a number of individuals at autopsy. These individuals did not have oxalate deposits in the kidney but did have oxalate deposits in other organs such as the thyroid gland and testis. Since the stains used by most pathologists examining atherosclerotic lesions cannot readily determine the presence of oxalates in diseased arteries, it seems possible that this cause of atherosclerosis may be much more common than previously realized. I suspect that oxalates are a much more common cause of atherosclerosis than high cholesterol. Furthermore, since ethylenediaminetetraacetic acid (EDTA) is effective in the removal of oxalate crystals deposited in the tissues (22,23), the benefits of intravenous EDTA in the treatment of cardiovascular disease may be mediated largely by the removal of oxalate crystals and their associated heavy metals from the tissues in which they are deposited.

Oxalate crystals may cause damage to various tissues due to their sharp physical structure and they may increase inflammation. Iron oxalate crystals may also cause significant oxidative damage and diminish iron stores needed for red blood cell formation (11). Oxalates may also function as chelating agents and may chelate many toxic metals such as mercury and lead. However, unlike common chelating agents like EDTA and DMSA that cause metals to be excreted, a reaction of oxalate with heavy metals like mercury and lead leads to the precipitation of the heavy metal oxalate complex in the tissues, increasing the toxicity of heavy metals by delaying their excretion (24).

What steps can be taken to control excessive oxalates?

  • Use antifungal drugs to reduce yeast and fungi that may be causing high oxalates. Children with autism frequently require years of antifungal treatment. I have noticed that arabinose, a marker indicating yeast/fungal overgrowth on the organic acid test at The Great Plains Laboratory, is correlated with high amounts of oxalates (Figure 1). Candida albicans produces high amounts of the enzyme collagenase (25), which breaks down collagen in the gastrointestinal tract to form the amino acid hydroxyproline, which in a series of reactions is converted to oxalates, especially in people with low vitamin B6. Candida organisms have also been found surrounding oxalate stones in the kidney (10).
  • Give supplements of calcium citrate and magnesium citrate to reduce oxalate absorption from the intestine. Citrate is the preferred calcium form to reduce oxalate because citrate also inhibits oxalate absorption from the intestinal tract. The best way to administer calcium citrate would be to give it with each meal. Children over the age of 2 need about 1000 mg of calcium per day. Of course, calcium supplementation may need to be increased if the child is on a milk-free diet. The most serious error in adopting the gluten-free, casein-free diet is the failure to adequately supplement with calcium.
  • Give chondroitin sulfate to prevent the formation of calcium oxalate crystals (26).
  • Vitamin B6 is a cofactor for one of the enzymes that degrades oxalate in the body and has been shown to reduce oxalate production (27).
  • Consume a low-oxalate diet, avoiding high-oxalate foods such as leafy greens, beans, berries, nuts, tea, chocolate, wheat germ, and soy. Dr. Clare Morrison, a general practitioner from the U.K. who has fibromyalgia found relief from symptoms after changing to a low-oxalate diet. In a 2012 article in the Daily Mail, she said, "I cut these out of my diet and overnight my symptoms disappeared — the disabling muscle pains, tingling legs, fatigue and inability to concentrate all went" (28).
  • Increase water intake to help eliminate oxalates.

Measuring oxalate toxicity

The organic acid test (Table 1) is one of the best measures for determination of both genetic and nutritional factors that lead to toxic oxalates. The organic acid test includes two additional markers, glycolic and glyceric acids, that are markedly elevated in genetic causes of excessive oxalate, the hyperoxalurias I and II. In addition, the organic acid test includes factors such as high fungal and Candida markers that make oxalate (fungus) or their precursors (Candida). Finally, although vitamin C poses little risk of excess oxalates at doses up to 2000 mg per day, I have measured marked increases in oxalates (more than ten times the upper limit of normal) in a child with impaired kidney function after a 50,000 mg intravenous vitamin C megadose. The organic acid test also includes the main vitamin B6 metabolite pyridoxic acid that diminishes the body's own production of oxalates.

Clinical References:

  • Kohmani EF. Oxalic acid in foods and its behavior and fate in the diet. Journal of Nutrition. (1939) 18(3):233-246,1939
  • Tsao G. Production of oxalic acid by a wood-rotting fungus. Appl Microbiol. (1963) May; 11(3): 249-254.
  • Takeuchi H, Konishi T, Tomoyoshi T. Observation on fungi within urinary stones. Hinyokika Kiyo. (1987) May;33(5):658-61.
  • Lee SH, Barnes WG, Schaetzel WP. Pulmonary aspergillosis and the importance of oxalate crystal recognition in cytology specimens. Arch Pathol Lab Med. (1986) Dec;110(12):1176-9.
  • Muntz FH. Oxalate-producing pulmonary aspergillosis in an alpaca. Vet Pathol. (1999) Nov;36(6):631-2.
  • Loewus FA, Saito K, Suto RK, Maring E. Conversion of D-arabinose to D-erythroascorbic acid and oxalic acid in Sclerotinia sclerotiorum. Biochem Biophys Res Commun. (1995) Jul 6;212(1):196-203.
  • Fomina M, Hillier S, Charnock JM, Melville K, Alexander IJ, Gadd GM. Role of oxalic acid overexcretion in transformations of toxic metal minerals by Beauveria caledonica. Appl Environ Microbiol. (2005) Jan;71(1):371-81.
  • Ruijter GJG, van de Vondervoort PJI, Visser J. Oxalic acid production by Aspergillus niger: an oxalate-non-producing mutant produces citric acid at pH 5 and in the presence of manganese. Microbiology (1999) 145, 2569–2576.
  • Ghio AJ, Peterseim DS, Roggli VL, Piantadosi CA. Pulmonary oxalate deposition associated with Aspergillus niger infection. An oxidant hypothesis of toxicity. Am Rev Respir Dis. (1992) Jun;145(6):1499-502.
  • Takeuchi H, Konishi T, Tomoyoshi T. Detection by light microscopy of Candida in thin sections of bladder stone. Urology. (1989) Dec;34(6):385-7.
  • Ghio AJ, Roggli VL, Kennedy TP, Piantadosi CA. Calcium oxalate and iron accumulation in sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis. (2000) Jun;17(2):140-50.
  • Ott SM, Andress DL, Sherrard DJ. Bone oxalate in a long-term hemodialysis patient who ingested high doses of vitamin C. Am J Kidney Dis. (1986) Dec;8(6):450-4.
  • Hall BM, Walsh JC, Horvath JS, Lytton DG. Peripheral neuropathy complicating primary hyperoxaluria. J Neurol Sci. (1976) Oct;29(2-4):343-9.
  • Sahin G, Acikalin MF, Yalcin AU. Erythropoietin resistance as a result of oxalosis in bone marrow. Clin Nephrol. (2005) May;63(5):402-4.
  • Sarma AV, Foxman B, Bayirli B, Haefner H, Sobel JD. Epidemiology of vulvar vestibulitis syndrome: an exploratory case-control study. Sex Transm Infect. (1999) Oct;75(5):320-6.
  • http://wisewitch.blogspot.com/2006/07/guaifenesinfibromyalgia-and-oxalates.html
  • http://www.diagnoseme.com/cond/C510175.html
  • http://www.vulvarpainfoundation.org/Lowoxalatetreatment.htm
  • Fishbein GA, Micheletti RG, Currier JS, Singer E, Fishbein MC. Atherosclerotic oxalosis in coronary arteries. Cardiovasc Pathol. (2008) ; 17(2): 117–123.
  • Levin RI, PW Kantoff, EA Jaffe. Uremic levels of oxalic acid suppress replication and migration of human endothelial cells. Arterioscler Thromb Vasc Biol (1990), 10:198-207
  • Di Pasquale G, Ribani M, Andreoli A, Angelo Zampa G, Pinelli G. Cardioembolic stroke in primary oxalosis with cardiac involvement. Stroke (1989), 20:1403-1406.
  • Ziolkowski F, Perrin DD. Dissolution of urinary stones by calcium-chelating agents: A study using a model system. Invest Urol. (1977) Nov;15(3):208-11.
  • Burns JR, Cargill JG 3rd. Kinetics of dissolution of calcium oxalate calculi with calcium-chelating irrigating solutions. J Urol. (1987) Mar;137(3):530-3.
  • http://www.greatplainslaboratory.com/home/eng/oxalates.asp
  • Kaminishi H, Hagihara Y, Hayashi S, Cho T. Isolation and characteristics of collagenolytic enzyme produced by Candida albicans. Infect Immun. (1986) August; 53(2): 312–316.
  • Shirane Y, Kurokawa Y, Miyashita S, Komatsu H, Kagawa S. Study of inhibition mechanisms of glycosaminoglycans on calcium oxalate monohydrate crystals by atomic force microscopy. Urol Res. (1999) Dec; 27(6):426-31.
  • Chetyrkin SV, Kim D, Belmont JM, Scheinman JI, Hudson BG, Voziyan PA. Pyridoxamine lowers kidney crystals in experimental hyperoxaluria: a potential therapy for primary hyperoxaluria. Kidney Int. (2005) Jan;67(1):53-60.
  • Morrison C. Ditch healthy berries to beat muscle pain: The eating plan that helped me cure my aches and pains. The Daily Mail Online. August 13, 2012. http://www.dailymail.co.uk/health/article-2187890/Ditch-healthy-berries-beat-muscle-pain-The-eating-plan-helped-cure-aches-pains.html. (Accessed November 21, 2014)

    The Role of Diet and the Gut in Mental Health

    Terri Hirning

    While the traditional mental health model focuses on brain function, neurotransmitters and potentially pharmaceutical medications, the ever burgeoning integrative mental health field understands there is more to it than that. Even mainstream media is starting to get the hint. Our gut influences our mind, emotions, cognition and mental health more than we've given it credit for in recent history. Whether we want to focus on the role food allergies play on mental health (1), (2) or how the gut-brain axis impacts our mental health (3), or even how the microbiome shapes our mental functioning (4) we can see the trend in research confirming what many integrative physicians and clinicians know: the gut matters

    When we talk about the gut, we must cover diet. Some literature even suggests that a debilitating mental health disorder like Alzheimer's now be called "Type 3 Diabetes" (5) because of its links to certain kinds of foods and a generally poor diet. What is causing the alarming trend of food allergies, food sensitivities and the increase in auto-immune conditions? Is it GMO's? Is it Glyphosate (the herbicide used in products like Monsanto's Roundup)? Is it the prevalence of processed grains in our diets now? It may be all of thesethings, or none of these things, but as physicians and clinicians, the data suggests we take a closer look at our patients' diets and here are some things to consider:

    Is there an underlying food allergy or multiple allergies? This can be an easy and yet very powerful place to start. Research shows that food allergies can indeed cause manifestations of mental health disorders. Running a simple IgG food allergy test from the Great Plains Laboratory, which also includes markers for Candida (harmful fungus in the gut) can be a great first step. More mainstream information on the treatment of Celiac disease can be also helpful in finding its connections to many mental health disorders like dementia, seizures, schizophrenia, etc.(6), and one does not have to be diagnosed with Celiac disease to be sensitive and reactive to gluten.

    What about healthy gut function and microbiome population? Our microbiome is sensitive to our diets, and quickly reactive to changes. Looking at potential gut dysbiosis and the levels of beneficial flora in the gut is very important. An organic acids test will show you a wide range of metabolic markers, including several for bacteria (like Clostridia) and fungus (like Candida albicans) in the gut. If a patient has high levels of these, a course of treatment can be started to rid them of these invaders, possibly including dietary restrictions (like a low sugar, low carb diet) and adding helpful antibacterial or antifungal supplements. Then, to assess the beneficial bacteria in the gut, you may want to run a comprehensive stool analysis. This will help determine whether a patient needs to add a high-quality probiotic supplement to their diet and possibly increase his/her intake of probiotic-rich and fermented foods like kefir and sauerkraut.

    Today's mental health disorders are very complex. Their treatment requires a well-rounded look at the many factors impacting the body and brain, including diet, lifestyle, the microbiome, and more. When an integrative approach is used and these many factors considered when creating a treatment plan, time and time again we see improvements in functioning and a reduction in clinical symptoms.

    Clinical References:

    • Jackson J1, Eaton W2, Cascella N3, Fasano A4, Santora D5, Sullivan K6, Feldman S6, Raley H7, McMahon RP6, Carpenter WT Jr6, Demyanovich H6, Kelly DL8.Gluten sensitivity and relationship to psychiatric symptoms in people with schizophrenia Schizophr Res. (2014) Oct 10. pii: S0920-9964(14)00511-8. doi: 10.1016/j.schres.2014.09.023.
    • Genuis SJ1, Lobo RA2. Gluten sensitivity presenting as a neuropsychiatric disorder . Gastroenterol Res Pract. (2014);2014:293206. doi: 10.1155/2014/293206.
    • Nemani K1, Hosseini Ghomi R2, McCormick B3, Fan X3. Schizophrenia and the gut-brain axis. Prog Neuropsychopharmacol Biol Psychiatry. (2014) Sep 19;56C:155-160. doi: 10.1016/j.pnpbp.2014.08.018.
    • Severance EG1, Yolken RH2, Eaton WW3. Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling. Schizophr Res. (2014) Jul 14. pii: S0920-9964(14)00319-3. doi: 10.1016/j.schres.2014.06.027.
    • De la Monte S, Wands J. Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed. J Diabetes Sci Technol. (2008) 2(6): 1101–1113.
    • Velasquez-Manoff Moises (2014 October 12). Can Celiac Disease Affect the Brain? The New York Times. Retrieved from:http://www.nytimes.com/2014/10/12/opinion/sunday/can-celiac-disease-affect-the-brain.html?smid=tw-share&_r=0

    The Role of Vitamins, Antioxidants, and Anti-Inflammatories in Breast Cancer Prevention and Treatment

    Terri Hirning

    October is Breast Cancer Awareness Month. As such, we would like to take a moment to focus on how nutritional and supplement therapy can play a role in the prevention and treatment of cancer. When we look at how antioxidants impact cancer, we can see that there is scientific documentation of reduced development of breast cancer in those with high dietary intake of antioxidants. One study in late 2014 titled The Rotterdam Study provides this information: "These results suggest that high overall dietary antioxidant capacity are associated with a lower risk of breast cancer."1 Women who had higher rates of antioxidant intake via diet were less likely to develop breast cancer. What about those who already had breast cancer? Could it help with treatment? A March 2014 issue of Anticancer Research featured a study showing the use of lycopene and beta-carotene in cell death of human breast cancer cell lines. "Our findings show the capacity of lycopene and beta-carotene to inhibit cell proliferation, arrest the cell cycle in different phases, and increase apoptosis."2 Vitamin C has also been studied in terms of its potential impact on breast cancer deaths and has been shown to have a positive effect on mortality rates. "Dietary vitamin C intake was also statistically significantly associated with a reduced risk of total mortality and breast cancer-specific mortality."3

    If we can look at the data and determine that higher intake of antioxidants and nutrients can not only reduce development of breast cancer but can also positively impact the mortality rates of cancer, the question then becomes how do we encourage our patients and clients to incorporate these into their diets with higher frequency? We must educate them on the role antioxidants play and the resources available to obtain them, whether from foods or supplements. For example, lycopene is a nutrient that is highlighted for its anticancer properties, specifically in reference to breast cancer. Lycopene is a carotenoid that gives many fruits and vegetables their red color. Unlike other carotenes, lycopene does not get converted into vitamin A. The top 10 sources of dietary lycopene are:

    • Guava
    • Watermelon
    • Tomatoes (cooked)
    • Papaya
    • Grapefruit
    • Sweet Red Peppers (cooked)
    • Asparagus (cooked)
    • Red (purple) cabbage
    • Mango
    • Carrots

    Continued from BioMed Today:

    Encouraging patients to incorporate more foods with lycopene, like those listed above, into their diets is one component. Supplements can also be suggested as a potential option. This is especially true in the case of vitamin D, for which there are many studies showing its role in the prevention of cancers. Adequate vitamin D is being revealed as a critical factor for preventing many diseases, including breast cancer, today.8 "Case-control studies and laboratory tests have consistently demonstrated that vitamin D plays an important role in the prevention of breast cancer."9 Unfortunately due to a variety of reasons, many people are deficient in vitamin D which then can then compromise optimal health. Testing for vitamin D levels, ideally twice a year, is a great way to monitor this critical nutrient and help your patients optimize their health and wellness. Supplementation can then also be recommended to optimize levels. Another promising resource for warding off disease and cancer is curcumin, the extract of the turmeric root. Because of its potent antioxidant and antimicrobial properties, it is being studied extensively for its potential in cancer treatment. The American Cancer Society's website has this to say about it: "Curcumin can kill cancer cells in laboratory dishes and also slows the growth of the surviving cells. Curcumin has been found to reduce development of several forms of cancer in lab animals and to shrink animal tumors."4 The typical therapeutic dose, between 3 and 10 grams per day, exceeds what is normally used in cooking and obtained through dietary consumption so a supplement would be most effective.

    Could another reason for the efficacy of curcumin on cancer cell death be its potent anti-inflammatory properties? Curcumin has been studied widely for both its safety and anti-inflammatory potential.5,6 "The laboratory studies have identified a number of different molecules involved in inflammation that are inhibited by curcumin including phospholipase, lipooxygenase, cyclooxygenase 2, leukotrienes, thromboxane, prostaglandins, nitric oxide, collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1 (MCP-1), interferon-inducible protein, tumor necrosis factor (TNF), and interleukin-12 (IL-12)."7 We see science validating the role our lifestyle has in development of cancer. Diet, exercise, supplementation, our stress level, and other factors all contribute to the whether or not we develop disease and also to our ability to reverse it. It is important to find ways to offer a variety of prevention and treatment options that work with our patients' lifestyles.

    Clinical References:

    • Pantavos A, Ruiter R, Feskens E, E deKeyser C, Hofman A, H Stricker B, H Franco O, C Kiefte-deJong J (2014). Total dietary antioxidant capacity, individual antioxidant intake and breast cancer risk: The rotterdam study, International Journal of Cancer. 2014 Oct 4. doi: 10.1002/ijc.29249. [Epub ahead of print]
    • Gloria NF, Soares N, Brand C, Oliveira FL, Borojevic R, Teodoro AJ (2014).Lycopene and beta-carotene induce cell-cycle arrest and apoptosis in human breast cancer cell lines, Anticancer Research. 2014 Mar;34(3):1377-86.
    • Harris HR, Orsini N, Wolk A (2014). Vitamin C and survival among women with breast cancer: a meta-analysis,European Journal ofCancer. 2014 May;50(7):1223-31. doi: 10.1016/j.ejca.2014.02.013. Epub 2014 Mar 7.
    • Turmeric (2012). Retrieved on October 5, 2014 from Link
    • Chainani-Wu NJ (2003). Safety and anti-inflammatory activity of curcumin: a component of tumeric (Curcuma longa), Journal of Alternative and Complementary Medicine. 2003 Feb; 9(1):161-8.
    • Jurenka, JS (2009). Anti-inflammatory Properties of Curcumin, a Major Constituent of Curcuma longa: A Review of Preclinical and Clinical Research, Alternative Medicine Review. Volume 14, Number 2, 2009.
    • Nita Chainani-Wu (2003). The Journal of Alternative and Complementary Medicine. February 2003, 9(1): 161-168. doi:10.1089/107555303321223035.
    • Vitamin D and Cancer Prevention (2013). Retrieved on October 5, 2014 from http://www.cancer.gov/cancertopics/factsheet/prevention/vitamin-D
    • Walentowicz-Sadłecka M, Sadłecki P, Walentowicz P, Grabiec M (2013). The role of vitamin D in the carcinogenesis of breast and ovarian cancer, Ginekologia Polska. 2013 Apr;84(4):305-8.

    The SCD, GAPS, and Paleo Diets: How They Compare and How They May Help Your Patients

    Terri Hirning

    Special diets have become increasingly common and more popular in recent years. Reports from both physicians and patients, many with laboratory tests confirming, say they can be helpful for a variety of diseases including autism, ADHD, multiple sclerosis, auto-immunity, rheumatoid arthritis, bowel conditions, and many more. Three diets in particular appear to help address gut dysbiosis, the overgrowth of microbes such as yeast and bacteria, which can be problematic for many individuals. Research shows that more than 70% of children with an Autism Spectrum Disorder (ASD) report a history of GI complaints.1 "Leaky Gut", or intestinal permeability, results from larger than normal spaces between the cells of the gut wall. These spaces allow undigested food and toxins to enter the blood stream. When this happens, the immune system can mount an attack against the foreign particles which may result in food sensitivities and/or allergies. When the offending foods are eaten again, the release of antibodies triggers inflammation. This chronic inflammation further exacerbates the cycle by lowering Immunoglobulin A (IgA) levels. Adequate IgA levels are required to protect the intestinal tract from the gut pathogens such as clostridia and yeast. This continuous cycle can increase gut dysbiosis and negatively impact the overall health of your patients. All three of these special diets – SCD, GAPS, and Paleo may help address these issues by reducing the amount of undigested and allergenic foods being consumed and healing both the gut and brain.

    Understanding how the SCD, GAPS, and Paleo diets may help the gut and brain, as well as the major differences between the three diets, can help you provide guidance to your patients when addressing food allergies, autoimmunity, and gut dysbiosis. All three diets share the basic foundations of reducing carbohydrates, avoiding grains (including those that are gluten-free) avoiding refined sugar, avoiding packaged/processed foods, focusing on nutrient-dense foods, and emphasizing the importance of eating a variety of vegetables. Each diet also has its own unique elements, and here is how they compare:

    SCD – Specific Carbohydrate Diet:

    • This diet was pioneered by Dr. Sidney V. Haas.
    • Patients are encouraged to follow the program in the book Breaking the Vicious Cycle by Elaine Gottschall.
    • Carbohydrates allowed on this diet are classified by their molecular structure.
    • Allowed carbohydrates are monosaccharides and have a single molecule structure that allow them to be easily absorbed by the intestine wall.
    • Disaccharides (double molecules) and polysaccharides (chain molecules) are not allowed.
    • Some dried beans and legumes can be added in after symptoms resolve and in accordance with the soaking and preparing instructions from the book.
    • This diet does allow some dairy (fermented/cultured).
    • Results of a Rush University SCD study show the diet leads to better microbial gut diversity.2
    • This diet focuses on reduction of pathogenic organisms in the gut rather than introducing beneficial bacteria.
    • Website: http://www.breakingtheviciouscycle.info/home/

    GAPS – Gut and Psychology Syndrome Diet:

    • Dr. Natasha Campbell-McBride expanded on the principles of GAPS in her book The Gut and Psychology Syndrome.
    • GAPS is very similar to SCD except for that it adds many probiotic-rich, cultured foods.These foods may help recolonize good bacteria and counteract bad bacteria.
    • This diet has more phases and may be seen as more rigorous than SCD.
    • GAPS emphasizes addressing brain health over gut health, but should certainly assist with both.
    • Website: http://www.gapsdiet.com/Home_Page.html

    Paleo Diet:

    • This diet is based upon the concept that the optimal diet is the one to which we are genetically adapted. It recommends modern, everyday foods that mimic the food groups of our pre-agricultural, hunter-gatherer ancestors
    • Paelo allows some starches that the other diets do not allow.
    • It does not allow dairy products.
    • It does not allow legumes or beans.
    • This diet may be seen as the least restrictive of the three diets.
    • Website: http://thepaleodiet.com/

    How to know when to suggest a diet like SCD, GAPS or Paleo for your patients: Have clinical tests like our Organic Acids Test or Microbial Organic Acids Test indicated yeast and/or bacterial overgrowth? Have repeated courses of antibiotics and/or antifungals failed to resolve these often chronic disorders? Have you tried multiple probiotics which have failed to repopulate the gut with good bacteria and yeast? Has IgG food allergy testing shown continued food allergies despite removal of the common allergens like wheat, dairy, and soy? Has your patient developed new or increasing food allergies despite being on an "allergy-friendly" diet? If you answered yes to any of these questions, considering a more specific and restrictive diet beyond GFCF (Gluten Free, Casein Free) could be the next step in healing for your patients.

    Diet can be a very effective way to reduce harmful gut pathogens by removing their food supply and decreasing the inflammation they cause. Diligence, dedication, and strict adherence is required from your patients to see the full benefits of these special diets. In cases where antibiotics, antifungals, supplements, and probiotics have not been successful, these diets may help reverse the gut dysbiosis, after which reintegrating various supplements and probiotics may be effective . For newly diagnosed patients, implementing one of these diets may be a good way to begin their healing process quickly and effectively. As Ann Wigmore, health practitioner, nutritionist, and whole foods advocate said, "The food you eat can be either the safest and most powerful form of medicine or the slowest form of poison".

    Clinical References

    Vitamins E, C and Age‐Related Diseases

    Matt Pratt‐Hyatt, Ph.D.

    Age‐related diseases are becoming more commonplace as the population's average age increases. These age‐related diseases include macular degeneration (AMD), hearing loss, and dementia. Many people believe that development of these diseases is inevitable, and that nothing can be done to control their occurrence; however studies have shown that treatment with antioxidant vitamins prevents and sometimes reverses the onset of these age‐related diseases.

    As our population's average age increases, the incidence of dementia as well as hearing and vision loss has also increased. The Eye Diseases Prevalence Research Group projects that the rate of age‐related macular degeneration (AMD) in the United States would double from 2004 to 2020. The Better Hearing Institute reports that 3 in 10 people over the age of 60 have hearing loss. The development of vision and hearing loss can be a very stressful situation for patients. Difficulty with hearing can cause stress in social situations due to the production of muffled sounds, required frequent repetition of others speaking, and ringing in the ears. Loss of vision can also create its own difficulties such as struggles with reading and the decreased ability to drive over time.

    Recent studies have found that antioxidant intake can have beneficial effects in the alleviation of these age‐related diseases. In 2001 the National Institutes of Health published a report in the Journal of the American Medical Association Ophthalmology of a study with 3,640 participants that indicated that supplementation with vitamins C and E, beta carotene, and zinc decreased AMD and vision loss. In 2013 a joint study between the University of Michigan, University of Toronto, and Seoul National University of Medicine found that patients that took supplements of vitamin C and magnesium had significantly better hearing at high frequencies. Finally a 2010 study of 5,395 participants who were 55 years and older found that patients that took vitamin E supplements were 25% less likely to develop dementia. This study collaborates an earlier longitudinal study in 2000 of 3,385 men that suggested that vitamin E and C supplements may protect against dementia.

    These studies raises the question of how much vitamin E and C someone worried about age‐related disease should be taking. The consensus of these studies is that 500 mg of vitamin C and 400 international units (I.U.) of Vitamin E were sufficient to obtain these results. However, patients should consult with their medical practitioner before starting a vitamin regiment.

    Clinical References:

    • 1. Kochkin S. (2001). MarkeTrak VI: The VA and direct mail sales spark growth in hearing aid market. The Hearing Review, 8 (12): 16‐24,63‐65.
    • 2. Age‐Related Eye Disease Study Research Group. (2001) A Randomized, Placebo‐Controlled, Clinical Trial of High‐Dose Supplementation With Vitamins C and E, Beta Carotene, and Zinc for Age‐Related Macular Degeneration and Vision Loss: AREDS Report No. 8. Arch Ophthalmol. 2001;119(10):1417‐1436.
    • 3. Choi Y et al. (2014) Antioxidant vitamins and magnesium and the risk of hearing loss in the US general population. Am J Clin Nutr. 99 (1) 148‐55.
    • 4. Devore EE et al. (2010) Dietary antioxidants and long‐term risk of dementia. Arch Neurol. 67 (7) 819‐825.
    • 5. Masaki KH et al. (2000) Association of Vitamin E and C supplement use with cognitive function and dementia in elderly men. Neurology 54 (6): 1265‐72.