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Soda and Obesity

type 2 diabetes, obesityWhile a major study relating soda and obesity was done in California, the hypothesis, observations and outcomes are applicable to all the states of the Union.  More than half the adolescents in that state and almost a fourth of the adults treat themselves to at least one sweetened beverage every day.  One of the concerns expressed by UCLA researchers is that the serving size has grown from an average of 6.5 ounces and eighty-eight calories in the 1950’s to 20 ounces and two hundred sixty-six calories by the 2000’s.  In fast food restaurants in 2003, the average serving was 23 ounces (almost 300 calories).  These added caloric sweeteners, including high fructose corn syrup, are not only markers of a poor diet, but also are associated with overweight and obesity in all age groups.

CITATIONS FROM REPORT / ARTICLE
The UCLA Health Policy Research Brief from September, 2009, reports from its data that, “Adults who drink soda occasionally (not every day) are 15% more likely to be overweight or obese, and adults who drink one or more sodas per day are 27% more likely to be overweight or obese than adults who do not drink soda, even when adjusting for poverty status and race/ethnicity.”  Even though the prevalence of overweight in children is lower than in adults, the rates among children have increased more.  In fact, overweight has tripled in teenagers and quadrupled in those from six to eleven years old in the last three decades.  In California the cost of obesity approaches twenty-one billion dollars a year, burdening families, employers and the health care industry.  The study comments that, “California spends more public and private money on the health consequences of obesity than any other state.”  To compound the matter, the article admits that “…drinking soda is also associated with increased risk for type 2 diabetes.”

COMMENTARY
One third of American adults are obese. Their health care costs $1500 more a year than it does for an average-weight person.  The Center for Disease Control announced in July, 2011, that obesity in the entire United States costs $147 billion a year in direct medical costs.  Dr. Thomas R. Frieden, director of the CDC, said the problem is “getting worse rapidly.  The average American is now 23 pounds overweight.”  For Medicare, the cost of obesity is 72% greater just for prescription drugs.  The CDC says that one in three children born in 2000 will develop diabetes.  How did we get there?  Diet.  Does the rest of the world share the problem?  Yes.  Where does the blame go?  White flour, white sugar, high fructose corn syrup, soft drinks and fast food.

Whether it gets marketed as corn sugar or as high fructose corn syrup, which is what it is, this commodity is not equal to other sweeteners when it comes to weight gain.  HFCS costs less than table sugar because, being liquid, it’s easier to transport and blend.  It’s sweeter than sucrose (table sugar), so less is needed, and it’s cheaper because of a combination of corn subsidies and sugar tariffs and quotas.  Cheap corn, in fact, is the building block of the fast-food nation.  Cheap corn created the chubby 20-ounce bottle of soda we have today.

High fructose corn syrup commonly is 55% fructose and 45% glucose, somewhat different from the 50-50 mix in table sugar, where one fructose molecule is attached to one glucose molecule.  Some HFCS may be as high as 80% fructose.  Since all sugars contain four calories per gram, there must be something else about fructose that matters.  Fructose is metabolized more rapidly that glucose, flooding metabolic pathways and increasing triglyceride storage.   It doesn’t spur the production of insulin or leptin, the hormone that sequesters appetite.  The body then lacks satiety.  This elevates serum triglycerides and increases fat storage.  Since it may have less impact on appetite than glucose, fructose contributes to weight gain.  Ingesting lots of fructose may also reduce insulin sensitivity.  (Beck-Nielsen, 1980)

Soft drink consumption has more than doubled in the twenty years from 1977 to 1997.  Not surprisingly, obesity followed the same trend. Cause and effect? It’s been estimated that for each additional sweet drink consumed per day, the odds of obesity increase by sixty percent.  A study of more than fifty thousand nurses by Harvard compared time periods from 1991-1995 and 1995-1999, and found that women whose soda consumption increased had bigger rises in body-mass index than those who drank less or the same amounts of soda. Fast food seems to go well with it.  Unhealthy foods get along nicely with each other.

The debate between the soft drink industry and the health nuts is ongoing.  People who consume lots of fresh-squeezed juices, vegetables and fruits are not the same group that consumes soda and cold cut sandwiches.  The daily calories from soft drinks account for almost a fourth of the recommended daily intake for many Americans, who drink almost fifty-six gallons of soda a year.

In case you’re interested, more than 30% of Americans are obese. More than 24% of Mexicans, 23% of British, 22% of Slovakians, 22% of Greeks and Australians, 21% of New Zealanders, and 15% of Czechs, but only 3% of Japanese and Koreans. Go figure. Obesity, by the way, means being more than 20% above ideal weight for height.

References

UCLA Health Policy Research Brief
September 2009
Bubbling Over: Soda Consumption and Its Link to Obesity in California
Susan H. Babey, Malia Jones, Hongjian Yu and Harold Goldstein

In California, 62% of adolescents ages 12-17 and 41% of children ages 2-11 drink at least
one soda or other sweetened beverage every day. In addition, 24% of adults drink at least
one soda or other sweetened beverage on an average day. Adults who drink soda occasionally
(not every day) are 15% more likely to be overweight or obese, and adults who drink one or
more sodas per day are 27% more likely to be overweight or obese than adults who do not
drink soda, even when adjusting for poverty status and race/ethnicity.

The prevalence of overweight and obesity has increased dramatically in both adults
and children in the last three decades in the United States. In the 1970s, about 15% of
adults were obese and by 2004 the rate had climbed to 32%.1 Although the prevalence of
overweight among children is lower than among adults, the rates among children and
adolescents have increased considerably more. The prevalence of overweight and obesity
nearly tripled among 12-19 year olds and more than quadrupled among 6-11 year olds
in the last three decades.

In California, 21% of adults are currently obese and an additional 35% are overweight. Among adolescents, 14% are obese and another 16% are overweight.2 Similar to national trends, the trend in California is toward increasing weight in both adults and adolescents.3 Each year in California, overweight and obesity cost families, employers, the health care industry and the government $21 billion.4 California spends more public and private money on the health consequences of obesity than any other state.5

Overweight and obesity are associated with serious health risks. In children and adolescents, overweight and obesity are associated with increased risk for cardiovascular disease indicators including high total cholesterol, high blood pressure, and high fasting insulin, an early indicator of diabetes risk.6 In addition, overweight children and adolescents are more likely to be overweight or obese as adults.7 In adults, overweight and obesity are associated with increased risk for diabetes, heart disease, stroke, some types of cancer and premature death.1, 8, 9

Drinking sweetened beverages such as soda and fruit drinks that have added caloric sweeteners (e.g., sucrose, high fructose corn syrup) is one marker of a poor diet, and is
associated with overweight and obesity in people of all ages.10-13 A number of studies have found that greater consumption of sweetened beverages is associated with overweight and obesity among both adults and children.12-19 In addition, randomized controlled trials that examine the impact of reducing intake of sweetened beverages on weight indicate
that reducing consumption of soda and other sweetened drinks leads to reductions in
overweight and obesity.20, 21 Among adults, drinking soda is also associated with increased risk for type 2 diabetes.13 Moreover, drinking sweetened beverages has
increased, and it is now more common than ever, particularly among adolescents.22
Between 1977 and 2002 Americans increased their calorie intake from soft drinks by
228%.23 Portion sizes have also increased from an average serving size of 6.5 fl oz (88 calories) in the 1950s, to 12 fl oz (150 calories), 20 fl oz (266 calories), and even larger portion sizes common today.24-26 The average serving size of soft drinks in fast food restaurants in 2002 was 23 fl oz (299 calories), with some chains now commonly selling soft drinks in 32 to 64 fl oz portions (416 to 832 calories, respectively).27 Sweetened beverages are a significant contributor to total caloric intake, especially for children and adolescents, and they lack the nutrients our bodies need.24, 26, 28

Additionally, eating habits established in childhood are important determinants of
eating habits as adults.29, 30
http://www.healthpolicy.ucla.edu/pubs/files/Soda%20PB%20FINAL%203-23-09.pdf

SUPPORTING ABSTRACTS
Am J Clin Nutr February 1980 vol. 33 no. 2 273-278
Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects
H Beck-Nielsen, O Pedersen and HO Lindskov

We have studied whether the sucrose-induced reduction of insulin sensitivity and cellular insulin binding in normal man is related to the fructose or the glucose moiety. Seven young healthy subjects were fed their usual diets plus 1000 kcal extra glucose per day and eight young healthy subjects were fed their usual diets with addition of 1000 kcal extra fructose per day. The dietary regimens continued for 1 week. Before change of diet there were no statistically significant differences between body weight and fasting plasma concentrations of glucose, insulin, and ketone bodies in the two groups studied. High- glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding (P less than 0.05) and insulin sensitivity (P less than 0.05). The changes in insulin binding and insulin sensitivity correlated linearly (r = 0.52, P less than 0.01). We conclude that fructose seems to be responsible for the impaired insulin binding and insulin sensitivity induced by sucrose.

Medscape J Med. 2008;10(8):189. Epub 2008 Aug 12.
Soft drinks and weight gain: how strong is the link?
Wolff E, Dansinger ML.
Boston University School of Medicine, Boston, Massachusetts, USA. [email protected]

CONTEXT
Soft drink consumption in the United States has tripled in recent decades, paralleling the dramatic increases in obesity prevalence. The purpose of this clinical review is to evaluate the extent to which current scientific evidence supports a causal link between sugar-sweetened soft drink consumption and weight gain.

EVIDENCE ACQUISITION
MEDLINE search of articles published in all languages between 1966 and December 2006 containing key words or medical subheadings, such as “soft drinks” and “weight.” Additional articles were obtained by reviewing references of retrieved articles, including a recent systematic review. All reports with cross-sectional, prospective cohort, or clinical trial data in humans were considered.

EVIDENCE SYNTHESIS
Six of 15 cross-sectional and 6 of 10 prospective cohort studies identified statistically significant associations between soft drink consumption and increased body weight. There were 5 clinical trials; the two that involved adolescents indicated that efforts to reduce sugar-sweetened soft drinks slowed weight gain. In adults, 3 small experimental studies suggested that consumption of sugar-sweetened soft drinks caused weight gain; however, no trial in adults was longer than 10 weeks or included more than 41 participants. No trial reported the effects on lipids.

CONCLUSIONS
Although observational studies support the hypothesis that sugar-sweetened soft drinks cause weight gain, a paucity of hypothesis-confirming clinical trial data has left the issue open to debate. Given the magnitude of the public health concern, larger and longer intervention trials should be considered to clarify the specific effects of sugar-sweetened soft drinks on body weight and other cardiovascular risk factors.  PMID: 18924641

Diabetes Care. 2010 Nov;33(11):2477-83. Epub 2010 Aug 6.
Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis.
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB.

Department of Nutrition, Harvard School of Public Health, and Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA.

OBJECTIVE
Consumption of sugar-sweetened beverages (SSBs), which include soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks has risen across the globe. Regular consumption of SSBs has been associated with weight gain and risk of overweight and obesity, but the role of SSBs in the development of related chronic metabolic diseases, such as metabolic syndrome and type 2 diabetes, has not been quantitatively reviewed.

RESEARCH DESIGN AND METHODS
We searched the MEDLINE database up to May 2010 for prospective cohort studies of SSB intake and risk of metabolic syndrome and type 2 diabetes. We identified 11 studies (three for metabolic syndrome and eight for type 2 diabetes) for inclusion in a random-effects meta-analysis comparing SSB intake in the highest to lowest quantiles in relation to risk of metabolic syndrome and type 2 diabetes.

RESULTS
Based on data from these studies, including 310,819 participants and 15,043 cases of type 2 diabetes, individuals in the highest quantile of SSB intake (most often 1-2 servings/day) had a 26% greater risk of developing type 2 diabetes than those in the lowest quantile (none or <1 serving/month) (relative risk [RR] 1.26 [95% CI 1.12-1.41]). Among studies evaluating metabolic syndrome, including 19,431 participants and 5,803 cases, the pooled RR was 1.20 [1.02-1.42].

CONCLUSIONS
In addition to weight gain, higher consumption of SSBs is associated with development of metabolic syndrome and type 2 diabetes. These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases.

J Public Health Policy. 2004;25(3-4):353-66.
The obesity epidemic in the United States.
Morrill AC, Chinn CD.
Capacities Inc., Watertown, Massachusetts 02471, USA. [email protected]

We describe the epidemic of obesity in the United States: escalating rates of obesity in both adults and children, and why these qualify as an epidemic; disparities in overweight and obesity by race/ethnicity and sex, and the staggering health and economic consequences of obesity. Physical activity contributes to the epidemic as explained by new patterns of physical activity in adults and children. Changing patterns of food consumption, such as rising carbohydrate intake–particularly in the form of soda and other foods containing high fructose corn syrup–also contribute to obesity. We present as a central concept, the food environment–the contexts within which food choices are made–and its contribution to food consumption: the abundance and ubiquity of certain types of foods over others; limited food choices available in certain settings, such as schools; the market economy of the United States that exposes individuals to many marketing/advertising strategies. Advertising tailored to children plays an important role.  PMID: 15683071

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

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.

References

  • AUTISM RESEARCH REVIEW INTERNATIONAL Vol. 20, No.3, 2006
    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.

Food Safety: Packed Lunch

Food Safety and Packed LunchThe featured abstract, from the respected journal, Pediatrics, explores the condition of packed lunches at a pre-school.  There is no reason to think that other school environments are any different.  Despite a parent’s best efforts at keeping a child’s lunch from spoiling and causing food-related illnesses, such incidents still occur because of inattentive food handling at school.  Malevolence is not usually a factor.

The University of Texas initiated a study into the conditions at schools that can lead to food-borne pathogenic illnesses, and found that temperature control is the prime concern.  Ninety percent of kids’ packed lunches reach unsafe zones. Even with multiple ice packs, “…the majority of lunch items…were at unsafe temperatures.”  As is the case with all health-related measures, “Education of parents and the public must be focused on methods of packing lunches that allow the food to remain in the safe temperature zone to prevent foodborne illnesses.”
(Almansour. 2011)

The “danger zone” for foods lies between 40° F. and 140° F.  Therefore, foods kept outside the “zone” are subject to the growth of pathogenic micro-organisms, whether at school, on a picnic, in the backyard, or in the kitchen.  A mantra that has been embraced long ago is that food should not be kept out of refrigeration longer than two hours.  Luncheon meats, smoked meats, and other cured comestibles are not an exception.  If the ambient temperature is higher than 90° F., the limit is one hour.  Unless the classroom has a refrigerator, this is practically impossible to do at school.  Note that the insulated bags we use to pack our kids’ lunches can rebound inside a refrigerator and prevent the cold from getting to the food.

Of course, Mom or Dad has to start with clean ingredients prepared on a clean surface, using clean hands and clean implements.  The CDC holds that only 3% of food contamination can be attributed to the farm.  The other 97% occurs between there and the kitchen.  (Alliance for Food and Farmng.  2010)  Including an ice source is imperative if you know the lunch will be kept at room temperature, such as within a middle-school locker, where teachers have found last month’s French fries after the mephitis rendered the neighboring crowd semi-conscious.  If the timing can be figured out, it’s O.K. to freeze those items that can be frozen without compromising their sensory quality.  Dressings like mayonnaise, and delicate items like tomatoes, are not in this group.  Peanut butter and jelly, and whole fruits and vegetables need not be cold.

If salad ingredients are part of the repast, especially lettuce, it’s vital that they be kept below 39° F. or so, lest they start to show a significant decline in visual quality as well as in safety.  However, even if it looks good, lettuce can harbor and encourage proliferation of E. coli, a dastardly micro-organism with a reputation worse than Blackbeard’s. By the way, this bacterium can thrive even on the pre-washed, ready-to-eat greens you bring directly home from the supermarket.  (Luo. 2010)  Wash them anyway. Plain water works, but a 50-50 mix with hydrogen peroxide can set the mind at ease. Peroxide reverts to plain water after exposure to light and air. That’s why it comes in an opaque brown bottle.

Smaller amounts of food in shallow containers are easiest to handle. You really don’t want to be sorting leftovers after they’ve been on the bus ride home.  Getting the containers back is another story.

References

Pediatrics 2011; 128; peds.2010-2885
Published online August 8, 2011 (doi: 10.1542/peds.2010-2885)
Temperature of Foods Sent by Parents of Preschool-aged Children
Fawaz D. Almansour, MS, Sara J. Sweitzer, PhD, RD, LD, Allison A. Magness, BS, Eric E. Calloway, BS, Michael R. McAllaster, BS, Cynthia R. Roberts-Gray, PhD, Deanna M. Hoelscher, PhD, RD, LD, CNS, Margaret E. Briley, PhD, RD, LD

J Food Sci. 2010 Sep;75(7):M390-7.
Effect of storage temperature and duration on the behavior of Escherichia coli O157:H7 on packaged fresh-cut salad containing romaine and iceberg lettuce.
Luo Y, He Q, McEvoy JL.

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

Technology And Children: A Negative Effect On Health?

Technology & ChildrenOne of the vagaries of parenthood is that we think we know more than our kids, enough to maintain a watchful eye over all they do and the places they go.  That might have been true before the advent of wireless technology and electronic media, but that’s an iffy proposition today.  Of course, the connected parent is concerned about his child’s safety and does all he can to ensure it.  But that idea transcends the physical, for the motivational, psychological and emotional dangers are ubiquitous.

Anything that has benefits, whether subjectively perceived or real, could be laden with risks.  Dr. Gwenn Schurgin O’Keeffe, detailing her research from a recent issue of Pediatrics and reporting to WebMD, feels that, “Some young people find the lure of social media difficult to resist, which can interfere with homework, sleep, and physical activity,” adding that, “Parents need to understand how their child is using social media so they can set appropriate limits.”   The element of internet risk is recognized by about half the parents interviewed, but only a fourth deems internet sites safe.  (WebMD. 3/28/11)

Concerning the children’s point of view, half admitted not to have spoken with their parents about their internet and social media activities.  Only four percent of parents realize that their kids log-on more than ten times a day, and twelve percent don’t even know their kids have a social account.  “Nurturing friendships and community engagement” are named as positive reasons to connect online, but the downsides of bullying and sexual inappropriateness receive equal attention.  Dr. O’Keeffe suggests that age thirteen is suitable for social interaction via the internet, agreeing with federal privacy rules outlined on some of the more popular networking sites, such as Facebook.  (O’Keeffe. 2011)

For years, health care professionals, teachers (especially PE teachers) and too few parents have been concerned with the amount of time their kids spend in front of the TV, which for many households had been an electronic babysitter from the get-go. While the Journal of Adolescence tells us that kids’ TV time hasn’t increased appreciably in the last fifty years (Marshall. 2006), their video game and social networking time has. Electronic sexual solicitation of underage youth is not as widespread as one would think from the reports (Ybarra. 2008), but that does not eliminate or reduce the risk.  Such solicitation is more likely to come through text messaging and in chat rooms, and harassment of one kind or another through instant messaging than through social networking sites (Ibid).

Nonetheless, kids spend more than seven hours a day, on average, in front of a screen.  Recent evidence raises concerns about media’s effects on aggression, sexual behavior, substance use, disordered eating, and academic difficulties.  Intense and regular parental involvement can increase the benefits and reduce the harm that media can have for a developing child and for adolescents.  (Strasburger. 2010)  Such anxieties are not limited to this side of the Atlantic or Pacific, either.  Online “addictions” were found to be related not only to aggression, but also to narcissistic personality traits and self-control, in studies conducted in Korea using international parameters.  (KIM. 2008)

The same kids who have problems with their peers at school or in the mall are likely to be the ones at risk for manipulation and targeting on the internet or smart phone.  Picking up signs of aberrant behavior are important, but we have to be vigilant.  Changes in behavior that include depression or aggression, delinquency or truancy, and becoming a loner or hanging with the wrong crowd are signals.  From the biomedical position, sedentary habits at a young age might just be able to predict health problems in adulthood.   Now, that’s another issue.  This topic should not entertain role reversal, even if your child is more adept at using the computer than you are.

References

http://www.webmd.com/parenting/news/20110328/social-networking-may-affect-kids-health
Social Networking May Affect Kids’ Health
Report Urges Parents to Communicate and Participate When Kids Socialize Online

Pediatrics Vol. 127 No. 4 April 1, 2011 pp. 800 -804
The Impact of Social Media on Children, Adolescents, and Families
Gwenn Schurgin O’Keeffe, MD, Kathleen Clarke-Pearson, MD,
Council on Communications and Media

J Adolesc. 2006 Jun;29(3):333-49. Epub 2005 Oct 21.
A descriptive epidemiology of screen-based media use in youth: a review and critique.
Marshall SJ, Gorely T, Biddle SJ.

Pediatrics Vol. 121 No. 2 February 1, 2008 pp. e350 -e357
How Risky Are Social Networking Sites? A Comparison of Places Online Where Youth Sexual Solicitation and Harassment Occurs
Michele L. Ybarra, MPH, PhD, Kimberly J. Mitchell, PhD

Pediatrics Vol. 125 No. 4 April 1, 2010 pp. 756 -767
Health Effects of Media on Children and Adolescents
Victor C. Strasburger, MDa, Amy B. Jordan, PhDb, Ed Donnerstein, PhDc

Eur Psychiatry. 2008 Apr;23(3):212-8. Epub 2007 Dec 31.
The relationship between online game addiction and aggression, self-control and narcissistic personality traits.
Kim EJ, Namkoong K, Ku T, Kim SJ.

Br J Sports Med. 2011 Sep;45(11):906-13.
Sedentary behaviour in youth.
Pate RR, Mitchell JA, Byun W, Dowda M.

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

Sleep and Kids

boy-watching-tv-with-remoteIt would be too easy if we put our kids to bed and they fell asleep in the average nine minutes it takes for an adult to drop into the arms of Morpheus. If your child struggles to fall asleep, know that this is not likely to resolve merely by moving from crib to bed. As he ages, there will fewer cries and screams, and more pleas and refusals. Could there be a reason behind this? Maybe television? Video games?

Each child is unique and has his own distinct needs for sleep.  Generally, a preschooler needs 10 to 12 hours a night, maybe with a nap during the day.  The surprise is that the school-age and preteen group benefit from the same, except for the nap.  But, “media use has been shown to negatively affect a child’s sleep,” according to researchers at Seattle’s Children’s Research Institute.  In their randomized controlled study of preschoolers, they found that the children had more than 70 minutes of screen time a day, with a fifth of that after 7 PM.  Almost 20% of the parents interviewed indicated at least one sleep problem with their preschooler.  Daytime TV showing violent behavior exacerbated problems.  (Garrison. 2011)  In a similar study a decade earlier, investigators at Brown University discovered that the sleep domains most affected by television were “bedtime resistance, sleep onset delay, and anxiety around sleep, followed by shortened sleep duration.”  (Owens. 1999)  In both studies—and in several between— it is agreed that a TV in the child’s bedroom compounds the matter and translates into less-than-stellar academic performance.

Recent assaults on Sponge Bob and his kin have raised the hackles of the entertainment industry.  But theirs is not righteous indignation, and transcends the humor of a “Who?  Me?” response.  It has been suspected for decades that the electronic babysitter would require a payback.  If a person believes that life is a series of trade-offs, here’s one of them, usually showing up during the school years, unknowingly invited earlier.

Children who watch fast-paced programs—even for as little as nine minutes — perform poorly in executive function tasks, those that control and regulate other behaviors and abilities, and are necessary for goal-directed activities.  These might include knowing when to start and stop behaviors and when to change them if the situation calls for it.  It also includes being able to plan ahead, to pay attention, and to fine tune memory and motor skills.  Although they are not easy to assess, their absence is noticeable.  (Lillard. 2011)  Teachers have lamented since the 1970’s that too many children start school with five-minute attention spans.

The U.S. is not the only nation facing this problem.  German researchers realized that 25% of their children do not get the ten hours of sleep they need.  They advise that parents and care givers limit TV time in order to prevent the negative consequences of sleep deprivation.  (Heins. 2007)  The Japanese learned that not only TV, but also after-school activities that last past 8 PM can interfere with sleep / wake patterns.  (Oka. 2008)

Other electronic entertainment, not only TV, plays a role in cerebral interference.  Electronics may induce the fight-or-flight state, increase blood pressure and pulse, and disrupt overall brain performance.  The unnatural brightness of the screen can interfere with production of melatonin, the signaling molecule that tells you to fall asleep.  Fast-moving and quick-changing scenes can interrupt the wiring of a young brain, possibly leading to bad dreams and restlessness.  Electromagnetic radiation is a by-product of anything electronic, affecting children more than adults, considering that their brain tissue is more conductive, radio frequency penetration is greater relative to head size, and children will have a longer lifetime exposure than adults.  (Kheifets. 2005)

Problems begin to manifest by age seven, the time when academic load may become a family affair.  When and if you help your child with his homework, you’re sure to notice what all this is about.  A two-hour delay between electronic stimulation and bedtime is not a bad idea.   Prior to that, naturally-paced shows, or even those seemingly in slow motion (Mr. Rogers), can offset, or even prevent, the surreal experiences that occur later. (Christakis. 2011)

References

Garrison MM, Liekweg K, Christakis DA.
Media use and child sleep: the impact of content, timing, and environment.
Pediatrics. 2011 Jul;128(1):29-35.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

Angeline S. Lillard, PhD,  Jennifer Peterson, BA
The Immediate Impact of Different Types of Television on Young Children’s Executive Function
Pediatrics. Published online September 12, 2011   (doi: 10.1542/peds.2010-1919)

Heins E, Seitz C, Schüz J, Toschke AM, Harth K, Letzel S, Böhler E.
Bedtime, television and computer habits of primary school children in Germany. [Article in German]
Gesundheitswesen. 2007 Mar;69(3):151-7.

Oka Y, Suzuki S, Inoue Y.
Bedtime activities, sleep environment, and sleep/wake patterns of Japanese elementary school children.
Behav Sleep Med. 2008;6(4):220-33.

Leeka Kheifets, PhD, Michael Repacholi, PhD, Rick Saunders, PhD, Emilie van Deventer, PhD
The Sensitivity of Children to Electromagnetic Fields
Pediatrics Vol. 116 No. 2 August 1, 2005 pp. e303 -e313

Dimitri A. Christakis
The effects of Fast-Paced cartoons
Pediatrics. 2011; peds. 2011-2071;  Published Online, 12 Sept., 2011
http://pediatrics.aappublications.org/content/early/2011/09/08/peds.2011-2071.citation

Gröer M, Howell M.
Autonomic and cardiovascular responses of preschool children to television programs.
J Child Adolesc Psychiatr Ment Health Nurs. 1990 Oct-Dec;3(4):134-8.

Christakis DA, Zimmerman FJ, DiGiuseppe DL, McCarty CA.
Early television exposure and subsequent attentional problems in children.
Pediatrics. 2004 Apr;113(4):708-13.

Al-Khlaiwi T, Meo SA.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population.
Saudi Med J. 2004 Jun;25(6):732-6.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

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

Child Athletes Nutrition

children-sportsA child is not a miniature adult. His or her nutrition and hydration needs are not exactly the same, especially in sports participation.  With the growth and availability of sports opportunities, you’d think that related nutrition needs would be a concern. To the contrary, sports nutrition for youngsters receives less attention than it deserves.

“Most children and adolescents who are strongly committed to sports are not concerned about nutrition as it relates to energy balance and obesity,” states a report from a 2004 issue of Nutrition.  The interactions among nutrition, growth, and development deserve attention if a participant expects to achieve optimal performance and to avoid the injuries and problems that stem from nutritional deficiencies.   Daily fluid turnover in adult athletes has received intense study, but that for children and adolescents hasn’t.  That of adults may be two to three liters a day, but in youngsters has only been estimated at half that—and that has been based on sedentary youth.  Although “sweating capacity is typically reported to be lower in children,” there is an increase in sweat rate when adjusted for body surface area.  Besides the energy needed for normal growth and development, children athletes need to accommodate the greater expenditure from physical activity.  That can vary from one sport to another.  (Petrie. 2004).

Besides the fun, kids participate in sports to hone their skills, to experience the excitement of competition, to be part of a team, and to stay in shape, among other reasons.  But they pay little or no attention to fuel and hydration needs.  Parents and coaches, on the other hand, do.  At least they should.  Hectic schedules, availability of foods, limited time and extended days interfere with choices and timing.

Even though the number of kids playing organized sports is on the rise, fitness levels are on the decline, and are much lower than in previous decades.  This partially explains the spate of sports-related injuries.  (Cordelia. 2011).  Targeted intervention strategies include ample hydration and nutrition.  Because of maturation differences, kids need more protein to support growth, more calcium to support bone, and more attention to the prevention of hypohydration.  (Bar-Or. 2001).

Sweat helps to cool the body, and what comes out has to be replaced, otherwise performance suffers and health is at risk.  To prevent the dizziness, fatigue, nausea, and cramps that characterize dehydration, the young athlete should drink one or two cups of water or electrolyte within four hours of an event.  If no urine has been passed, or if urine is bright yellow and minimal, another 1 ½ cups is suggested within two hours of the game.  During the event, try to replace fluids as they are lost to sweat, about a cup every fifteen or twenty minutes if possible.  Plain water will do, but if the event is longer than an hour, use an electrolyte replacement.  Recovery is just as important to a preteen or teen as it is to an adult.  The best way to determine post-exercise hydration needs is to weigh the child to compute weight loss, and to replace fluid at one and a half times the volume lost to sweat.  One ounce of water (sweat) weighs one ounce, so the math is simple.  A kid’s thirst mechanism is not well-developed, so you’ll almost have to force him to drink…but do it.

The nutrients in which young athletes are most deficient include carbohydrates, calcium, vitamin B6, folate and iron, the last being especially important to girls.  Carbohydrate inadequacy leads to shortened glycogen stores and premature fatigue, especially if the game is sixty minutes or longer.  Once glycogen is gone, fat gets mobilized and the child will “bonk.”  The last thing you want is for the young athlete to burn protein for fuel. An active child will need as many as 500 to 1500 more calories a day than his inert peers.

Two to three hours before an event, give your athlete a light, carb-rich meal:  carrot sticks and a piece of cheese; a little pasta; a small sandwich.  Have him exert himself on a slightly empty stomach to avoid cramping, even fatigue.  Chips, cakes or cookies, and candy are out.  The protein your child needs will not build bulk.  That comes with age.  Normal muscle development will require as much as one and a half grams of protein for each kilogram of body weight, but need not be much more than fifteen to twenty percent of daily calorie intake.  Reduce that during the off season. Thirty percent fat in the daily intake will help to supply needed calories.  Reduce that off-season, too, lest you greet Tweedledee one morning.

The matter of iron deficiency is a particular concern for girls, especially after the onset of menarche, which can be a couple of years late for an iron-fisted ball player.  Iron-deficiency anemia is a real threat for female athletes.  Besides affecting performance and recovery, low iron stores impair immune function and may initiate other physiological problems.  Supplementation is not intended to replace food as a source of nutrients, but in the case of iron deficit, it may be recommended.  (Beard. 2000).  There’s no need for your daughter to join the 50% of the world population who are deficient in iron.  (Ahmadi. 2010).  Raw meat probably won’t help, but getting 15 mg a day from supervised supplementation will.

Youngsters are often grossly misinformed about what they need and don’t need.  Their peers and the internet are not always reliable sources of information.  Some young athletes need only a minor tweak to their diets; others need a complete overhaul.  If you feel inadequate, don’t be embarrassed.  There are dietitians and sports nutritionists who can help.

References

Petrie HJ, Stover EA, Horswill CA.
Nutritional concerns for the child and adolescent competitor.
Nutrition. 2004 Jul-Aug;20(7-8):620-31.

Cordelia W Carter, Lyle J Micheli
Training the child athlete: physical fitness, health and injury
Br J Sports Med 2011;45:880-885

Bar-Or O.
Nutritional considerations for the child athlete
Can J Appl Physiol. 2001;26 Suppl:S186-91.

Beard J, Tobin B.
Iron status and exercise.
Am J Clin Nutr. 2000 Aug;72(2 Suppl):594S-7S.

Ahmadi A, Enayatizadeh N, Akbarzadeh M, Asadi S, Tabatabaee SH.
Iron status in female athletes participating in team ball-sports.
Pak J Biol Sci. 2010 Jan 15;13(2):93-6.

Koehler K, Braun H, Achtzehn S, Hildebrand U, Predel HG, Mester J, Schänzer W.
Eur J Appl Physiol. 2011 May 19. [Epub ahead of print]
Iron status in elite young athletes: gender-dependent influences of diet and exercise.

Committee on Sports Medicine and Fitness
AMERICAN ACADEMY OF PEDIATRICS
Intensive Training and Sports Specialization in Young Athletes
Pediatrics Vol. 106 No. 1 July 1, 2000 : pp. 154 -157

Martinez LR, Haymes EM.
Substrate utilization during treadmill running in prepubertal girls and women.
Med Sci Sports Exerc. 1992 Sep;24(9):975-83.

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

Diabetes Prevention: Can We Stop Type 2 Before It Starts?

weigh-inPredictions for an increase in diabetes are dreadful. One in three children born in the United States in the year 2000 are apt to become diabetic unless they change the way they eat and start to move more. The implications of this epidemic are frightening because blindness, amputations, kidney failure and heart disease are in their futures. From the mid 60’s to the mid 90’s, the number of diagnosed diabetes cases has tripled. The type 2 diabetes that appeared at age forty is now showing up at age twelve. Almost all of those kids are overweight.

The Department of Health and Exercise Science at Wake Forest University, in North Carolina, recently concluded a study of the Diabetes Prevention Program that focused on lifestyle influence on type 2 diabetes, and found that overweight and lack of exercise are still principal causes of the disease.  The study included more than three hundred volunteers with body mass indexes (BMI) between 25 and 40, some of whom served as controls, while the others received a diabetes education program that included dietary interventions.  By now, you already figured that the intervention group experienced significantly greater decrease in glucose, insulin, and insulin resistance.  Not only that, but also they lowered their BMI’s and lost about an inch from their waistlines.  (Katula. 2011)  Getting rid of that gut makes a ton of difference.  (Pun intended.)  Parallel studies at Indiana University Medical School yielded similar results, with the additional benefits of improved blood pressure and total cholesterol levels.  (Ackerman. 2011)

In type 1 diabetes, where insulin is required, science is trying to prevent the loss of beta cells, the ones in the pancreas that make insulin.  Examining genetic susceptibility to disease is one step in the process.  Family history is part of that.  Up to now, there are no known pre-diagnosis steps that can be taken to prevent the onset of type 1.  On the other hand, there are several possibilities for helping to save beta cells shortly after a diagnosis of diabetes.  (Wherrett. 2011)  Assiduous effort is put into this area, with the expectation that some factors known to trigger autoimmunity and the eventual destruction of beta cells can be controlled.  Early trials offer promise, but have not yet reached fruition.  (Thrower.  2009)

The list of diabetic complications is long and fearsome:  coronary artery disease, cerebrovascular disease, peripheral vascular disease, retinopathy, and neuropathy, to name a few.  Researchers are looking closely at plants that can offset the costs and side effects of pharmaceuticals, and even obviate their use, but admonish us that diet and lifestyle still need to be reined in.  (Haque. 2011)  Because soy foods are integral to Asian cuisine, it seems appropriate to look for components of soy chemistry that might affect blood glucose.  The soy phytoestrogen, genistein, was reported to protect against glucose-induce pancreas cell death in a study done in China.  (Zhong. 2011)  The applicability of this finding to either type 2 or type 1 diabetes, or both, is yet to be determined, but the prospects have merit.

Patients already diagnosed with type 2, or those who feel themselves candidates, may be comforted to know that alpha lipoic acid, a sulfur compound found in organ meats, spinach and broccoli, and also available as a supplement, prevents a rise in diabetes markers while improving the efficiency of glucose metabolism.  In German studies it was found that administration of alpha lipoic acid for ten days, either orally or intravenously, improves insulin sensitivity in both lean and obese individuals.  (Konrad. 1999)  (Jacob. 1999)  It would be imprudent, though, to expect supplemental alpha lipoic acid to do something we wouldn’t do for ourselves, such as lose weight and exercise.

Dietary fiber gets lots of attention, and is mostly associated with digestive health.  The soluble type is fermented in the gut and makes some physiologically active byproducts.  The insoluble type is comparatively inert and absorbs water to make elimination an efficient process.  Legumes, some cereals and fruits, psyllium, and tuberous vegetables provide soluble fiber.  Wheat and corn bran, whole grains, and nuts and seeds are sources of insoluble fiber.  Psyllium has received considerable interest as an ingredient in high-fiber breakfast cereals, where it’s been reputed to lower cholesterol and to reduce blood glucose response to a meal.  More than one study has reported psyllium to be effective for both.  As little as 5 grams of psyllium taken either with, or just before, a meal has effected improvement in lipid and glycemic control.  At the University of Virginia Diabetes Center, scientists noted a 14% reduction in postprandial glucose at breakfast, and a 20% reduction at dinner, compared to placebo, in people diagnosed with non-insulin-dependent type 2 diabetes.  (Pastors. 1991)  Analyses in Mexico and Texas arrived at the same conclusion, but recorded a pronounced positive effect on total cholesterol, LDL cholesterol and triglyceride levels.  (Rodriguez-Moran. 1998)  (Lee. 1994)

The United States is not alone in the quest to control the diabetes epidemic by recommending lifestyle changes.  The Japanese saw a risk reduction of more than 67% through weight loss, and the Finns realized risk reduction by controlling total and saturated fats and increasing dietary fiber, as well.  (Kosaka. 2005)  (Lindstron.  2006).   Globally, children do not eat enough vegetables.  Those who do, often limit their repertoire to only a few.  French fries don’t count.   What they are missing is magnesium, the prophylactic mineral that is able to improve glucose and insulin balance, especially in obesity.  (Song. 2004)  (Huerta. 2005)  (Lopez-Ridaura. 2004) This mineral is loaded with properties that boost health. The prevention of diabetes is as simple as exercising, losing a few pounds, getting ample fiber, and eating magnesium-rich produce.  Here, an ounce of prevention really is worth a few pounds of cure, not to mention getting stuck with a needle.

References

Katula JA, Vitolins MZ, Rosenberger EL, Blackwell CS, Morgan TM, Lawlor MS, Goff DC Jr.
One-year results of a community-based translation of the Diabetes Prevention Program: Healthy-Living Partnerships to Prevent Diabetes (HELP PD) Project.
Diabetes Care. 2011 Jul;34(7):1451-7.

Ackermann RT, Finch EA, Caffrey HM, Lipscomb ER, Hays LM, Saha C.
Long-term effects of a community-based lifestyle intervention to prevent type 2 diabetes: the DEPLOY extension pilot study.
Chronic Illn. 2011 Aug 12. [Epub ahead of print]

Wherrett DK, Daneman D.
Prevention of type 1 diabetes.
Pediatr Clin North Am. 2011 Oct;58(5):1257-70.

Thrower SL, Bingley PJ.
Strategies to prevent type 1 diabetes.
Diabetes Obes Metab. 2009 Oct;11(10):931-8.

Haque N, Salma U, Nurunnabi TR, Uddin MJ, Jahangir MF, Islam SM, Kamruzzaman M.
Management of type 2 diabetes mellitus by lifestyle, diet and medicinal plants.
Pak J Biol Sci. 2011 Jan 1;14(1):13-24.

Zhong WW, Liu Y, Li CL.
Mechanisms of genistein protection on pancreas cell damage in high glucose condition.
Intern Med. 2011;50(19):2129-34.

Konrad T, Vicini P, Kusterer K, Höflich A, Assadkhani A, Böhles HJ, Sewell A, Tritschler HJ, Cobelli C, Usadel KH.
Alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes.
Diabetes Care. 1999 Feb;22(2):280-7.

Jacob S, Henriksen EJ, Tritschler HJ, Augustin HJ, Dietze GJ.
Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid.
Exp Clin Endocrinol Diabetes. 1996;104(3):284-8.

Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, Dietze GJ.
Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid.
Arzneimittelforschung. 1995 Aug;45(8):872-4.

Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, Rett K.
Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial.
Free Radic Biol Med. 1999 Aug;27(3-4):309-14.

Pastors JG, Blaisdell PW, Balm TK, Asplin CM, Pohl SL.
Psyllium fiber reduces rise in postprandial glucose and insulin concentrations in patients with non-insulin-dependent diabetes.
Am J Clin Nutr. 1991 Jun;53(6):1431-5.

Rodríguez-Morán M, Guerrero-Romero F, Lazcano-Burciaga G.
Lipid- and glucose-lowering efficacy of Plantago Psyllium in type II diabetes.
J Diabetes Complications. 1998 Sep-Oct;12(5):273-8.

Lee NA, Reasner CA.
Beneficial effect of chromium supplementation on serum triglyceride levels in NIDDM.
Diabetes Care. 1994 Dec;17(12):1449-52.

Kosaka K, Noda M, Kuzuya T.
Prevention of type 2 diabetes by lifestyle intervention: a Japanese trial in IGT males.
Diabetes Res Clin Pract. 2005 Feb;67(2):152-62.

Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J; Finnish Diabetes Prevention Study Group
Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study.
Lancet. 2006 Nov 11;368(9548):1673-9.

Song Y, Manson JE, Buring JE, Liu S.
Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women.
Diabetes Care. 2004 Jan;27(1):59-65.

Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, Patrie JT, Rogol AD, Nadler JL.
Magnesium deficiency is associated with insulin resistance in obese children.
Diabetes Care. 2005 May;28(5):1175-81.

Lopez-Ridaura R, Willett WC, Rimm EB, Liu S, Stampfer MJ, Manson JE, Hu FB.
Magnesium intake and risk of type 2 diabetes in men and women.
Diabetes Care. 2004 Jan;27(1):134-40.

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

Cell Phone Radio Frequency And Child Behavior

Radiation-Cell-phoneUntil we’ve mastered the art of telepathy as a means of universal communication, we’re stuck with the cell phone and all that it brings to the table, some of which can be anticipated, like the bill at the end of the month, and some that can’t be expected, like the radio frequency radiation that is alleged to change your unborn child from Mother Teresa to Attila the Hun. Funny thing about science, there’s a study for everything, except for why the eye of a needle is not at the other end.

It has been assumed that using a cell phone in front of your unborn child will render cerebral changes in him/her that will eventuate into attention deficit and hyperactivity. Such is the conclusion of a group of Yale School of Medicine researchers who worked with mice. The authors of this study noted an increase of neurobehavioral disorders in children and decided to look for a cause. To be fair to researchers, mice are used in the laboratory because some of their metabolic characteristics parallel those of humans, and because they mature quickly enough to track their development in a reasonable time span. They also share 99% of their genes with humans.

In this experiment, pregnant mice were exposed to an activated, but muted, cell phone suspended above their cage, while a pregnant control group was exposed to a deactivated phone. As adults, those mice subjected to cell phone radiation as fetuses tended to be more hyperactive and had reduced memory capacity compared to the controls. The outcome was attributed to dose-responsive impaired glutamatergic synaptic transmission onto layer V pyramidal neurons of the prefrontal cortex. Got it?  Not exactly a topic at your next cocktail party, this scientific crooning means that the neurological wires in the front part of the brain don’t develop the right way. This is the section of the brain in charge of complex cognitive behaviors, personality expression, decision making and social behavior.  Like other pronouncements in the research world, “further experiments are needed…to determine the risk of exposure during pregnancy.”  (Aldad, 2012)

Rodent pregnancies typically last fewer than three weeks, and the brains of newborn mice are far less developed than those of human babies. Despite the findings, potential risks in humans might not be similar. However, in human studies done in Germany, scientists found that about 6% of children who were exposed to radio-frequency electromagnetic fields at any time in their existence exhibited “abnormal mental behavior.”  Here, too, “more studies…are warranted…”  (Thomas, 2010)

If a definitive case can be made for the hazard of cell phone radiation, it’ll certainly be a major public health concern. But a trend in this direction might have been established in a Danish study that recruited the cell-phone-using mothers of more than 13,000 children. The mothers were enrolled early in their pregnancies, and seven years later were asked to submit a subjective questionnaire regarding the current health and behavior status of their school-aged children. Those children who had prenatal or postnatal exposure to cell phone use demonstrated greater association with behavioral difficulties and hyperactivity. (Divan, 2008)  Other, confounding, factors may have come into play, though, including diet, lifestyle and permissiveness, exposure to environmental contaminants such as heavy metals, and genetics. Cognitive and language development seem not to be affected by cell phones, as evidenced in a subsequent study by the same research team. (Divan, 2011)

Repeatability is characteristic of a well-constructed study. To ascertain the results of their 2008 report, Divan and colleagues duplicated that work, but with more than twice the number of subjects and the consideration of the confounders. The findings were the same:  prenatal and postnatal cell phone use is associated with behavior problems in school-aged children. (Divan, 2010)  To confuse the issue, Spanish researchers found little evidence of abnormal neurodevelopment in a prenatal group exposed to cell phone radiation when tested at 14-months of age and compared to a group of nonusers. (Vrijheid, 2010)  What seems to be needed is a longitudinal study, one that tracks the development of, and tests, the same group of users and nonusers over a period of time, maybe ten or more years.

If the results of a ten-year study were absolutely definitive of cell phone culpability, it’s unlikely that patterns of cell phone use would change, despite a risk of uncomfortable child behavior. Returning to the dark ages of landlines is unthinkable. Besides, in a few years the problem will belong to somebody else. What self-respecting parent would sacrifice immediate convenience for the future?

References

Divan HA, Kheifets L, Obel C, Olsen J.
Prenatal and postnatal exposure to cell phone use and behavioral problems in children.
Epidemiology. 2008 Jul;19(4):523-9.

Divan HA, Kheifets L, Obel C, Olsen J.
Cell phone use and behavioural problems in young children.
J Epidemiol Community Health. 2010 Dec 7. [Epub ahead of print]

Divan HA, Kheifets L, Olsen J.
Prenatal cell phone use and developmental milestone delays among infants.
Scand J Work Environ Health. 2011 Jul;37(4):341-8. doi: 10.5271/sjweh.3157. Epub 2011 Mar 14.

Tamir S. Aldad, Geliang Gan, Xiao-Bing Gao, & Hugh S. Taylor
Fetal Radiofrequency Radiation Exposure From 800-1900 Mhz-Rated Cellular Telephones Affects Neurodevelopment and Behavior in Mice
Scientific Reports. Volume:2 ,Article number:312  doi:10.1038/srep00312  15 March 2012

Thomas S, Heinrich S, von Kries R, Radon K.
Exposure to radio-frequency electromagnetic fields and behavioural problems in Bavarian children and adolescents.
Eur J Epidemiol. 2010 Feb;25(2):135-41. Epub 2009 Dec 4.

Vrijheid M, Martinez D, Forns J, Guxens M, Julvez J, Ferrer M, Sunyer J.
Prenatal exposure to cell phone use and neurodevelopment at 14 months.
Epidemiology. 2010 Mar;21(2):259-62.

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

Milk – It Does A Body Something, For Sure

milk-carton-glassMost advertisements try to float the reader / viewer to the side of the river that hosts the heralded product. You’ll unlikely see a car salesman tell you there’s a better deal across the street.  If you know someone who tells the doctor what medications to Rx based on TV blurbs, you know the story.  It’s all in the power of the ad, truth or not.  You probably don’t know that the dairy industry has a champion called the International Dairy Journal, a highly-respected periodical that doesn’t exactly promote good old dihydrogen oxide, the most abundant molecule on the planet.  In January of 2012 there appeared in this publication a piece that addressed dairy foods and cognitive decline, commonly known as dementia, declaring that study participants who consumed dairy products at least once a day performed better on measures of cognitive function than those who rarely or never consumed dairy.  (Crichton, 2012)  What?  Did you expect something less stellar?  At least, the study candidly admits that the causal mechanisms “are still to be determined.”  Maybe there’s more to dairy than we know about if something needs to be determined.

Two years prior to this study, the same authors told us that drinking low-fat milk improves social functioning, stress and memory.  Maybe this proclamation means that low-fat milk can make you a better dancer and that you won’t worry about it if you think you are, but really aren’t, whether you forget or not.  Funny thing, whole milk has no such benefit.  (Crichton, 2010)  Yet, there’s the admission that the jury is still out.  Neither report had a definitive conclusion.  Both of these studies took place in Australia, but that shouldn’t make any difference because Australian and American cows speak the same language, except the Aussies add “mate” after “moo.”

Not to pop the milk drinkers’ balloon, despite the pleasure it might bring, but an in-between 2011 investigation performed by the Agricultural Research Service section of the USDA found that milk was less effective than meat for improving cognitive function and physical activity, but this time in a child population.  (Allen, 2011)  What this boils down to is that the stuff in meat is the same as the stuff in milk, but there’s more of it.  That would be iron, zinc, riboflavin, vitamin B12, and the rest of the nutrients for which animal products are hailed.

There is, however, another side to this coin. (Maybe “dodecahedron” would be a better metaphor because there are a few sides.)  That milk contains about four hundred different fatty acids makes it the most complex of all natural fats.  These fats come from one of two sources—the feed or the microbial happenings in the cow’s rumen.  In the olden days, back in the 1940s and early 50s, these fats floated on top of the milk because homogenization either wasn’t used or didn’t work as planned.  The kid who was the first to rise in the morning could retrieve the glass container from the front steps and eat the cream from the top of the bottle, leaving the low-fat remainder for the rest of the family.  Little did he or she realize that the goodness of butyric acid, a salutary short-chain fatty acid, was accompanied by the not-so-goodness of saturated fat and a little trans fat.  A small fraction of the beneficent essential fatty acids is in the mix, but hardly enough to make much difference.  However, there are other things in milk.  Among them are somatic cells, which some people equate with pus.  Aww, they wouldn’t allow that, would they?  Note that the job of the USDA is to promote agricultural interests, not yours.  In fact, clever inventors have devised ways to measure the somatic cells in your milk bottle with amazing precision (Tsenkova, 2001), with each state in the nation setting its own allowable levels based on regional variables.  (http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5089395.) and
(http://aipl.arsusda.gov/publish/dhi/dhi11/sccrpt.htm)

Where does this stuff come from? The milking machine.  A cow’s udder is treated with iodine prior to being sucked dry, and both the iodine and a few of the cow’s body cells end up in the milk.  Doesn’t pasteurization kill germs?  Some.  But the dead cells are still in the milk, and besides, pasteurization is not sterilization.  The latter is intended to kill everything.  The former is intended to achieve a reduction in the number of viable organisms, reducing their number so they are unlikely to cause disease.  Milk can be pasteurized by heating to 145° F for half an hour or to 163° F for fifteen seconds.  The thermoduric bacteria that survive are held in check by refrigeration. To add insult to injury, the iodine may induce thyroid or dermatological issues over time.  That’s another story, though.

The casein in milk protein yields peptides called casomorphins, with different breeds of cattle offering different peptides, totaling about thirteen variants, each of which is divided into categories known as A1 and A2.  A1 caseins contain the amino acid histidine, essential for the growth and repair of tissue, but also responsible for manufacturing histamine, the stuff that makes your nose runny in an allergic reaction or that makes you itch after a mosquito attack. Although concentration-dependent, this state of affairs is uncomfortable at best, and is blamed specifically on beta-casomorphine-7, “…a naturally occurring product of cow’s milk with opiate-like activity…” (Kurek, 1992).  A2 caseins contain proline, a non-essential amino acid that is a component of cartilage.  That casomorphins have opioid activity matters little in light of the discovery that particular A1 casein can become glycated and promote adverse immune effects (Elliott, 2006), among them diabetes.

So, what is glycation?  It’s the result of a sugar bonding to a protein or a fat without the watchful eye of an enzyme, such as might happen in a frying pan or even in the body after ingesting a sugar, resulting in a haphazard process that impairs cellular function.  This is not to be confused with glycosylation, an enzyme-controlled process aimed at a specific molecule to enable its particular function.  Glycation forms advanced-glycation-end products, or AGE’s that are implicated in neurodegenerative diseases (Li, 2012) and mitochondrial dysfunction (Hashimoto, 2003).

About 8% of infants under age one are allergic to cow’s milk (Constantinide, 2011).  This might account for the crankiness of the child who is unable to define the earache or the gastric distress that cause discomfort and pain.  Yes, a child may outgrow milk allergy, only to be bombarded with symptoms decades later, most of which arise from reactions to the foreign protein that is casein, a material once used to make paint.  Casomorphin from type A1 is believed to play a role in ischemic heart disease, while that from type A2 encourages neither heart disease nor diabetes (Kaminski, 2007).  Are you expected to test your milk to find whether it’s higher in one or the other variant?  Type A1 Beta-casomorphin-7 is implicated in several human miseries, and is especially hazardous to those with leaky gut syndrome, to this day a questionable diagnosis to the traditional medical community.  Nonetheless, BCM-7 affects GI motility and mucosal immune function (Elitsur & Luk, 1991).  Now that it’s been established that type A1 is the bad casein, here’s the list of cattle ranked according to A1 casein content, from bad to good:  Holstein (much more A1 than A2); Jersey, Ayrshire and Milking Shorthorn (these three have almost equal levels);  Brown Swiss (more A2 than A1), and Guernsey (almost a 100 x A2 than A1).  The next time you get milk from the supermarket, the neighborhood convenience store or the gas station around the corner, be sure to ask the dairy manager/clerk from which breed of cow the milk was pumped.

There is much more to deny a cow its center stage, ranging from mineral imbalances to disease promotion via shared hormones with humans, items to be addressed another time.  But if there’s cognitive benefit to be derived from milk, it comes from phospholipids (Schubert, 2011) (Lopez, 2008), the structural and functional cellular components that are better obtained, without unwanted tag-a-longs, from non-dairy sources.  Milk phospholipid and fat content depends on what the cow is fed.  Cattle feed high in flaxseed, for example, will produce milk higher in polyunsaturated fats and lower in saturated ones (Lopez, 2008).  Regardless, only about 1% of milk lipids are phospholipids.  Even if there were a higher percentage, the heat of pasteurization that destroys enzymes (It takes only 120° F to deactivate an enzyme.) also would oxidize the phospholipids to uselessness.

Cow’s milk does a body good if you’re a calf.  The ideal for humans is, well, breast milk.  If breast feeding is out of the question, there are alternatives that supply the fats an infant needs for development.  Hemp milk is one of these, but it’s expensive.  It’s loaded with omega-3 fatty acids and potassium, and enough vitamins to meet the need.  Omega-6 fats can be fortified with sunflower, safflower or evening primrose oils, and phospholipid needs can be more than satisfied with real, honest-to-goodness phosphatidylcholine.  After age four, a tot can switch to alternative milk, but the supplementary essential fats and phosphatidylcholine should stay because they definitely do a body good…all the way into old age.  It is not common for animals to drink the milk of another species.  Who chose cattle to be the source of beverage,  cavemen?  “Hey, Charlie, let’s yank on that thing hangin’ down under that animal and drink what comes out.”  One more thing:  what milk does to a prostate gland shouldn’t happen to anyone (Schmitz-Dräger, 2011)  (Tate, 2011)  (Torfadottir, 2012).

References

Allen LH, Dror DK.
Effects of animal source foods, with emphasis on milk, in the diet of children in low-income countries.
Nestle Nutr Workshop Ser Pediatr Program. 2011;67:113-30

Cie Li Ska A, Kostyra EB, Kostyra H, Ole Ski K, Fiedorowicz E, Kami Ski SA.
Milk from cows of different ?-casein genotypes as a source of ?-casomorphin-7.
Int J Food Sci Nutr. 2011 Nov 14.

Clemens RA.
Milk A1 and A2 peptides and diabetes.
Nestle Nutr Workshop Ser Pediatr Program. 2011;67:187-95. Epub 2011 Feb 16.

Constantinide P, Trandafir LM, Burlea M.
The role of specific IgE to evolution and prognosis of cow’s milk protein allergies in child. 
Rev Med Chir Soc Med Nat Iasi. 2011 Oct-Dec;115(4):1012-7.

Crichton GE, Murphy KJ, Bryan J.
Dairy intake and cognitive health in middle-aged South Australians.
Asia Pac J Clin Nutr. 2010;19(2):161-71

Crichton GE,  M.F. Eliasb, G.A. Dore, M.A. Robbins
Relation between dairy food intake and cognitive function: The Maine-Syracuse Longitudinal Study
International Dairy Journal. Volume 22, Issue 1, January 2012, Pages 15–23

Elitsur Y, Luk GD.
Beta-casomorphin (BCM) and human colonic lamina propria lymphocyte proliferation.
Clin Exp Immunol. 1991 Sep;85(3):493-7.

Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE.
Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption.
Diabetologia. 1999 Mar;42(3):292-6.

Elliott RB.
Diabetes–a man made disease.
Med Hypotheses. 2006;67(2):388-91.

Federal Milk Order Marketing Area, 2011
Somatic cell count of producer milk
http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5089395

Hashimoto M, Rockenstein E, Crews L, Masliah E.
Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimer’s and Parkinson’s diseases.
Neuromolecular Med. 2003;4(1-2):21-36.

Høst A, Halken S, Jacobsen HP, Christensen AE, Herskind AM, Plesner K.
Clinical course of cow’s milk protein allergy/intolerance and atopic diseases in childhood.
Pediatr Allergy Immunol. 2002;13 Suppl 15:23-8.

Kamiński S, Cieslińska A, Kostyra E.
Polymorphism of bovine beta-casein and its potential effect on human health.
J Appl Genet. 2007;48(3):189-98.

Kurek M, Przybilla B, Hermann K, Ring J.
A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man.
Int Arch Allergy Immunol. 1992;97(2):115-20.

Kurek M, Czerwionka-Szaflarska M, Doroszewska G.
Pseudoallergic skin reactions to opiate sequences of bovine casein in healthy children.
Rocz Akad Med Bialymst. 1995;40(3):480-5.

Li J, Liu D, Sun L, Lu Y, Zhang Z.
Advanced glycation end products and neurodegenerative diseases: Mechanisms and perspective.
J Neurol Sci. 2012 Mar 11.

Christelle Lopez, Valerie Briard-Bion, Olivia Menard, Florence Rousseau, Philippe Pradel and Jean-Michel Besle
Phospholipid, Sphingolipid, and Fatty Acid Compositions of the Milk Fat Globule Membrane are Modified by Diet
J. Agric. Food Chem., 2008, 56 (13), pp 5226–5236

Månsson, Helena Lindmark
Fatty acids in bovine milk fat
Food Nutr Res. 2008; 52: 10

H.D. Norman, T.A. Cooper, and F.A. Ross, Jr.
Somatic cell counts of milk from Dairy Herd Improvement herds during 2010
Animal Improvement Programs Laboratory, Agricultural Research Service, USDA, Beltsville, Md
20705   http://aipl.arsusda.gov/publish/dhi/dhi11/sccrpt.htm

Schubert M, Contreras C, Franz N, Hellhammer J.
Milk-based phospholipids increase morning cortisol availability and improve memory in chronically stressed men.
Nutr Res. 2011 Jun;31(6):413-20.

Schmitz-Dräger BJ, Lümmen G, Bismarck E, Fischer C; Mitglieder des Arbeitskreises Prävention, Umwelt und Komplementärmedizin.
Primary prevention of urologic tumors: prostate cancer.
Urologe A. 2011 Oct;50(10):1271-2, 1274-5.

Tate PL, Bibb R, Larcom LL.
Milk stimulates growth of prostate cancer cells in culture.
Nutr Cancer. 2011 Nov;63(8):1361-6. Epub 2011 Nov 1.

Torfadottir JE, Steingrimsdottir L, Mucci L, Aspelund T, Kasperzyk JL, Olafsson O, Fall K, Tryggvadottir L, Harris TB, Launer L, Jonsson E, Tulinius H, Stampfer M, Adami HO, Gudnason V, Valdimarsdottir UA.
Milk intake in early life and risk of advanced prostate cancer.
Am J Epidemiol. 2012 Jan 15;175(2):144-53. Epub 2011 Dec 20.

Tsenkova R, Atanassova S, Kawano S, Toyoda K
Somatic cell count determination in cow’s milk by near infra-red spectroscopy: a new diagnostic tool
J Anim Sci. 2001; 79: 2550-2557

University at Buffalo.
Acne, Milk And The Iodine Connection.
ScienceDaily, 7 Dec. 2005.
http://www.sciencedaily.com/releases/2005/12/051207181144.htm

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

Food Coloring And Behavior

food-coloringListen to a lie long enough and you’ll start to accept it as the truth. Didn’t the tobacco industry use images of physicians and athletes to sell cigarettes back in the last century? Babe Ruth hawked White Owl cigars and Raleigh cigarettes. William Bendix sold Chesterfield. The highly-trusted and unquestionably credible FDA had a meeting last March to discuss the properties of artificial food colorings and evaluate their relationship to hyperactivity in children. Based on their review of the published data, “FDA concludes that a causal relationship between exposure to color additives and hyperactivity in children in the general population has not been established.” For certain susceptible children, however, they admit their condition “may be exacerbated by exposure to a number of substances in food, including, but not limited to, synthetic color additives.”

The toxicity potential of synthetic food additives is hard to pin down. Just because a single substance demonstrates no harmful effects doesn’t explain what happens when it’s combined with another “harmless” substance.  Many foods contain more than one colorant. An example of single-substance safety is ammonia. Used with adequate ventilation it’s a relatively harmless cleaner unless abused.  The same for chlorine bleach.  But mix the two and you get a toxic gas, hydrazine, used to make rocket fuel.  That’ll clean the scum off the shower walls!   With the amount of adverse publicity about artificial colorings, you’d think the makers would look for something more natural, like beets.

Companies use artificial colors to make their products look pretty.  Foods with vibrant, saturated colors are more appealing than those without.  Hot dogs are naturally gray.  When’s the last time you saw one?  The color of a food tells us that it has value.  Red apples are more valued than green ones.  The natural medicines in foods are colorful.  Beta-carotene is associated with yellow and orange; anthocyanins with red and purple.  Even purple cabbage has its fans.  Some oranges don’t turn that color unless growing conditions are perfect: cool nights, warm days.  Many folks won’t buy green oranges from Florida, so what’s the broker to do?  Spray ‘em orange.  Now the mind is fooled into thinking this orange is healthier than the blotchy one next to it.

Most studies on food additives last for too short a time to render meaningful results.  A comet assay is a sensitive but uncomplicated testing procedure that detects DNA damage at the level of the cell.  Using this procedure, scientists at Japan’s Laboratory of Genotoxicity at Hachinohe National College found that, of the types of food additives, dyes are most genotoxic.  Dose-related DNA damage from commonly-used food dyes was found in the stomach, colon, and bladder of test animals, with colon damage appearing at doses close to the acceptable daily intake.  (Sasaki. 2002) (Tsuda. 2001)

Coal tar and petrochemicals are the main sources of the artificial colors that go into our foods, and these are ultimately dangerous to our health.  It makes little sense to put these into our food supply if we’re not designed to ingest them in the first place.  But selling products and making money are the bottom line.  Without at least a little prior knowledge, the unsuspecting consumer would never know that yellow #5 is cleverly disguised by its chemical name, tartrazine, sometimes called E102.  If mixed with blue #1, called E133, it makes green. Blue #1 may contain aluminum, although potassium and calcium salts are more common.  Most of E133 ends up in the feces, which could be green.  Tartrazine has provoked allergic reactions in sensitive persons, but you never know who that is until it happens, and most of us never make a connection.  (Kashanian. 2011)  To its credit, the FDA will seize products that do not declare the presence of tartrazine, which also is alleged to exacerbate asthma symptoms.  There is a blue #2, but it’s seldom used in foods because it fades at alkali pH.  Its use in snacks and candies may evoke a hyperactivity reaction.

Red #40 is an azo dye, meaning that it contains two nitrogens.  It’s also known as allura red or E129.  Originally made from coal tar, red #40 is now made from petroleum.  Isn’t that a comfort?  Contrary to popular misconception, it is not made from insects.  Carmine is, made from the female cochineal insect, whose body is dried and pulverized or otherwise processed.  From intensive European studies it was concluded that behavioral anomalies in children arise especially when the blues and the reds are combined with benzoate preservatives.  (McCann. 2007)  Red #3 is called erythrosine, E127, and is not that common in the U.S., having been replaced by #40.  Number 3 was found to be a potent inhibitor of a substance that blocks and destroys cancer cells, named tumor necrosis factor.  So, while some research says it may not directly cause cancer, red #3 interferes with the body’s protection against it, while simultaneously showing cytotoxicity, particularly to breast tissue.  (Ganesan. 2011) (Dees. 1997)

Why take the chance when there are natural colorants?  Read the labels.  Sweets and sports drinks, blueberry muffins and cereals with “fruits,” yogurt and canned icing could give you more than you bargained for.  Caramel coloring from sugar, annatto red-orange from achiote, chlorophyll green, turmeric yellow, paprika red, elderberry purple, butterfly pea blue, beet red, and blue from red cabbage are real.

References

http://www.ift.org/knowledge-center/focus-areas/product-development-and-ingredient-innovations/~/media/Knowledge%20Center/Focus%20Areas/ProductDev/ArtificialColors.pdf
Olsson Frank Weeda Terman Bode Matz PC;  Attorneys at Law;  Suite 400; 1400 Sixteenth Street, NW; Washington, D.C. 20036  www.ofwlaw.com

Sasaki YF, Kawaguchi S, Kamaya A, Ohshita M, Kabasawa K, Iwama K, Taniguchi K, Tsuda S
The comet assay with 8 mouse organs: results with 39 currently used food additives.
Mutat Res. 2002 Aug 26;519(1-2):103-19.

Tsuda S, Murakami M, Matsusaka N, Kano K, Taniguchi K, Sasaki YF.
DNA damage induced by red food dyes orally administered to pregnant and male mice.
Toxicol Sci. 2001 May;61(1):92-9.

Kashanian S, Zeidali SH.
DNA binding studies of tartrazine food additive.
DNA Cell Biol. 2011 Jul;30(7):499-505.

McCann D, Barrett A, Cooper A, Crumpler D, Dalen L, Grimshaw K, Kitchin E, Lok K, Porteous L, Prince E, Sonuga-Barke E, Warner JO, Stevenson J.
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.
Lancet. 2007 Nov 3;370(9598):1560-7.

Ganesan L, Margolles-Clark E, Song Y, Buchwald P.
The food colorant erythrosine is a promiscuous protein-protein interaction inhibitor.
Biochem Pharmacol. 2011 Mar 15;81(6):810-8.

Dees C, Askari M, Garrett S, Gehrs K, Henley D, Ardies CM.
Estrogenic and DNA-damaging activity of Red No. 3 in human breast cancer cells.
Environ Health Perspect. 1997 Apr;105 Suppl 3:625-32.

Shimada C, Kano K, Sasaki YF, Sato I, Tsudua S.
Differential colon DNA damage induced by azo food additives between rats and mice.
J Toxicol Sci. 2010 Aug;35(4):547-54.

Shaw DW.
Allergic contact dermatitis from carmine.
Dermatitis. 2009 Oct;20(5):292-5.

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