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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.

Diet Soda is Not A Free Ride

diet soda & weight gainThere is little doubt that obesity in America is on the upswing. Lots of people think that an artificially-sweetened beverage can offset the poor dietary decisions to which they have become accustomed. There has been established a relationship between non-sugar sweeteners and weight gain based on physiological responses to the message of satiety and the perceived need to consume more calories to achieve it. While the perception of sweet taste is supposed to satisfy appetite, the calculated deception to the body just might boomerang and call off all bets.

In the San Antonio Heart Study that ran from 1979 to 1988, researchers examined the association of artificially sweetened beverages with long-term weight gain, and found that, “A significant positive dose-response relationship emerged between baseline ASB (artificially sweetened beverage) consumption and all outcome measures…”  These outcome measures included overweight / obesity, weight gain, and changes in body mass index (BMI).  As with most nutrition research, considerations were made for demographics and behavioral characteristics.  Drinking more than twenty-one ASB’s a week had the most impact, with “…almost double risk of overweight / obesity among 1,250 baseline normal-weight individuals.”  For those with a body mass index already elevated, the changes were more pronounced.  This report concluded with, “These findings raise the question whether AS (artificial sweetener) use might be fueling—rather than fighting—our escalating obesity epidemic.”

That last sentence from the San Antonio Heart Study is quite the incrimination, would you say?
Diet soft drinks have long been thought to be healthier alternatives to their sugary counterparts, but reports like this one have linked increased incidence of weight gain, metabolic syndrome, and even diabetes to frequent intake of diet soft drinks.  Keep in mind, though, that all studies in all areas of health care are subject to scrutiny and critique.    Regardless of the topic, there are always two—or more—sides.  But here it may have been discovered that fooling the body is the instigator behind the concern.

When the body is told that something sweet has been ingested, it launches the production of insulin to carry the sweet to the cells to be burned for energy.  By the time the body finds out that there really is no sugar to be burned—in the form of glucose—the insulin has already been sent on its way to work.  Now the insulin has to find something to do, so it initiates a signal that says, “Feed me.  I need to carry glucose.”  That arouses hunger.  What do we grab for immediate satisfaction?  Carbohydrates, the simpler, the better.  Most of them spike glucose rapidly, which, if it fails to get burned for energy, is stored as fat.  It now appears that a lack of exercise becomes part of the equation.

There’s another tack to look at.  Some artificial sweeteners are alleged to block the brain’s production of serotonin, the neurotransmitter that controls mood, learning, sleep, and…appetite.  When the body experiences low levels of serotonin—and that can affect depressed mood—it seeks foods that can bring the levels back up.   Those foods happen to be the ones that will also bring the belt size up. Real sugar, of course, provides empty calories that can also cause weight gain as excessive energy intake.  But a weight conscious public does what it thinks is right.

Sweet taste enhances appetite.  Aspartame-sweetened water, for example, increased subjective hunger ratings when compared to glucose-sweetened water.  (Yang. 2010)  Other artificial sweeteners were associated with heightened motivation to eat, with more items selected on a food preference list. (Blundell. 1986)  This suggests that the calories in natural sweeteners trigger a response to keep overall energy intake constant, and that inconsistent coupling between sweet taste and actual caloric content can lead to compensatory overeating and consequential positive energy balance.  (This means that more energy came into the body than went out.)  People associate taste with calorie content.  You can tell that a crème brulee has more calories than the eggs from which it is made, but you’d probably eat more of it if made with artificial sweetener than with cane sugar.

Humans have a hedonic component.  We like those things that appeal to the senses and activate our food reward pathways.  That contributes to appetite increase.  But artificial sweeteners fail to provide completeness.  Unsweetening the American diet over the long haul, a little at a time, might just do the trick.  After all, it seems to work with salt.

References

MAIN ABSTRACT
Obesity (2008) 16(8), 1894–1900.
Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long-term Weight Gain Sharon P. Fowler, Ken Williams, Roy G. Resendez, Kelly J. Hunt, Helen P. Hazuda and Michael P. Stern

SUPPORTING ABSTRACTS
Diabetes Care. 2009 Apr;32(4):688-94. Epub 2009 Jan 16.
Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr.
SourceDivision of Epidemiology, University of Texas Health Sciences Center, Houston, Texas, USA. [email protected]

Physiol Behav. 2010 Apr 26;100(1):55-62. Epub 2010 Jan 6.
High-intensity sweeteners and energy balance.
Swithers SE, Martin AA, Davidson TL.

SourceDepartment of Psychological Sciences, Purdue University, 703 Third Street, West Lafayette, IN 47907, United States. [email protected]

Yale J Biol Med. 2010 June; 83(2): 101–108.
Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings
Neuroscience 2010
Qing Yang

The Lancet, Volume 327, Issue 8489, 10 May 1986, Pages 1092-1093
PARADOXICAL EFFECTS OF AN INTENSE SWEETENER (ASPARTAME) ON APPETITE J. E. Blundell, A. J. Hill

*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.

Is Sugar Affecting Your Immunity?

sweet-drinkThere is a metabolic difference between simple and complex carbohydrates.  The simple ones become glucose soon after they are eaten.  The complex ones take longer to turn into sugar and are less apt to spike insulin and cause energy crashes down the line.  But that isn’t the only difference between the two.

Almost forty years ago scientists had an interest in the relationship of diet to health, specifically of sugar intake to immunity.   But their curiosity went past simple sugar to include carbohydrates other than glucose.  The cells that are the backbone of the immune system are supposed to kill, swallow, and dispose of alien bodies, including bacteria, viruses and cancer cells.  Scientists at Loma Linda University in California examined the activity of neutrophilic phagocytes (cells that dissolve the enemy) after subjects ingested glucose, fructose, sucrose, honey, or orange juice and found that “…all significantly decreased the capacity of neutrophils to engulf bacteria…”  (Sanchez, Reeser, et al. 1973)  Looking more closely, the researchers also discovered that the greatest effects occurred within the first two hours after eating, but “…the effects last for at least 5 hours.”  (Ibid.)  If there is any promise, it’s that the effects can be undone by fasting from added sugars for the next two or three days.

At the start of the twentieth century, Americans consumed only about five pounds of sugar a year.  By the fifties, that had grown to almost 110 pounds a year, and to more than 152 by the year 2000.  Corn sweeteners account for 85 of those pounds.
(USDA Economic Research Service, http://www.usda.gov/factbook/chapter2.pdf )  America’s sweet tooth increased 39% between 1950 and 2000 as the use of corn sweetener octupled.

Although the cited study is decades old, its message is contemporary. HFCS began replacing sugar in soft drinks in the 1980’s, after it was portrayed by marketers as a healthful replacement for demon sugar.  It didn’t hurt the industry that it cost less, either.  The biological effects of sugar and HFCS are the same, however.  Neither has any food value—no vitamins, protein, minerals, antioxidants, or fiber—but they do displace the more nutritious elements of one’s diet, and we tend to consume more than we need to maintain our weight, so we gain.

Even though the number of calories from the glucose in a slice of bread or other starch is the same as that from table sugar (half fructose and half glucose), they are metabolized differently and have different effects on the body.  While fructose is metabolized by the liver, glucose is metabolized by every cell in the body.  When fructose reaches the liver, especially in liquid form (as in soda), it overwhelms the organ and is almost immediately converted to fat.  (Taubes. 2011)

Innate immunity is that which occurs as part of your natural makeup and defends you against infection by other organisms.  Short-term hyperglycemia, which might come from a pint of vanilla, has been found to affect all the major components of the innate immune system and to impair its ability to combat infection.  Reduced neutrophil activity, but not necessarily reduced neutrophil numbers, is one of several reactions to high sugar intake.  (Turina. 2005)  Way back in the early 1900’s, researchers noted a relationship between glucose levels and infection frequency among diabetes sufferers, but it wasn’t until the 1940’s that scientists found that diabetics’ white cells were sluggish. (Challem. 1997)  More recent study has corroborated the diabetes-infection connection, agreeing that neutrophil phagocytosis is impaired when glucose control is less than adequate.  (Lin. 2006)  Impaired immune activity is not limited to those with diabetes.  As soon as glucose goes up, immune function goes down.

Some folks think they’re doing themselves a favor by using artificial sweeteners.  Once the brain is fooled into thinking a sweet has been swallowed, it directs the pancreas to make insulin to carry the “sugar” to the cells for energy.  After the insulin finds out it’s been cheated of real sugar, it tells the body to eat in order to get some, and that creates artificial hunger, which causes weight increase from overeating.   Even environmental scientists have a concern with fake sweeteners in that they appear in the public’s drinking water after use.  You can guess how that works. (Mawhinney. 2011)

Mineral deficiencies, especially prevalent in a fast-food world, contribute to immune dysfunction by inhibiting all aspects of the system, from immune cell adherence to antibody activity.  Paramount among minerals is magnesium, which is part of both the innate and acquired immune responses.  (Tam. 2003)  Epidemiological studies have connected magnesium intake to decreased incidence of respiratory infections, and intravenous administration has shown effective in treating asthma. (PDR. 2000)  But sugar pushes magnesium—and other minerals—out of the body.  (Milne. 2000)  This will compromise not only immune function, but also bone integrity.  (Tjäderhane. 1998)

Zinc has been touted for its ability to shorten the duration of the common cold.  Like magnesium, zinc levels decrease with age, and even tiny deficiencies can have a large effect on immune health, particularly in the function of the thymus gland, which makes the T-cells of the immune system.  Zinc supplementation improves immune response in both the young and the old.  (Haase. 2009)  (Bogden. 2004)  (Bondestam. 1985)  All the microminerals, in fact, are needed in minute amounts for optimal growth and development…and physiology.  Low intakes suppress immune function by affecting T-cell and antibody response. Thus begins a cycle whereby infection prevents uptake of the minerals that could prevent infection in the first place.  Adequate intakes of selenium, zinc, copper, iron plus vitamins B6, folate, C, D, A, and E have been found to counteract potential damage by reactive oxygen species and to enhance immune function.  (Wintergest. 2007)

Who would have viewed something as sweet as sugar as being so hostile? It taste great to eat but has a nasty habit of pushing everything else out.

References

Albert Sanchez, J. L. Reeser, H. S. Lau, P. Y. Yahiku, et al
Role of sugars in human neutrophilic phagocytosis
American Journal of Clinical Nutrition, Nov 1973; Vol 26, 1180-1184

Profiling Food Consumption in America
USDA
http://www.usda.gov/factbook/chapter2.pdf

Taubes G.
“Is Sugar Toxic?”
in New York times Magazine, 13 April, 2011

Turina M, Fry DE, Polk HC Jr.
Acute hyperglycemia and the innate immune system: clinical, cellular, and molecular aspects.
Crit Care Med. 2005 Jul;33(7):1624-33.

Challem J and Heumer RP.
The Natural health Guide to Beating the Supergerms.
1997. Simon and Schuster Inc. New York.  Pp. 124-125

Lin JC, Siu LK, Fung CP, Tsou HH, Wang JJ, Chen CT, Wang SC, Chang FY.
Impaired phagocytosis of capsular serotypes K1 or K2 Klebsiella pneumoniae in type 2 diabetes mellitus patients with poor glycemic control.
J Clin Endocrinol Metab. 2006 Aug;91(8):3084-7.

Mawhinney DB, Young RB, Vanderford BJ, Borch T, Snyder SA.
Artificial sweetener sucralose in U.S. drinking water systems.
Environ Sci Technol. 2011 Oct 15;45(20):8716-22.

Tam M, Gómez S, González-Gross M, Marcos A.
Possible roles of magnesium on the immune system.
Eur J Clin Nutr. 2003 Oct;57(10):1193-7.

PDR:  Physicians’ Desk reference for Herbal Medicines.  Magnesium.  2nd edition.  Mintvale NJ: Medical Economics Company; 2000:  5340540

Milne David B, PhD and Forrest H. Nielsen, PhD
The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men
J Am Coll Nutr February 2000 vol. 19 no. 1 31-37

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

Fuchs, Nan Kathryn Ph.D.
Magnesium: A Key to Calcium Absorption
The Magnesium Web Site on November 22, 2002
http://www.mgwater.com/calmagab.shtml

Haase H, Rink L.
The immune system and the impact of zinc during aging.
Immun Ageing. 2009 Jun 12;6:9.

Bogden JD.
Influence of zinc on immunity in the elderly.
J Nutr Health Aging. 2004;8(1):48-54.

Bondestam M, Foucard T, Gebre-Medhin M.
Subclinical trace element deficiency in children with undue susceptibility to infections.
Acta Paediatr Scand. 1985 Jul;74(4):515-20.

Wintergerst ES, Maggini S, Hornig DH.
Contribution of selected vitamins and trace elements to immune function.
Ann Nutr Metab. 2007;51(4):301-23. Epub 2007 Aug 28.

Smolders I, Loo JV, Sarre S, Ebinger G, Michotte Y.
Effects of dietary sucrose on hippocampal serotonin release: a microdialysis study in the freely-moving rat.
Br J Nutr. 2001 Aug;86(2):151-5.

Jack Challem, Burton Berkson, M.D., Ph.D., Melissa Diane Smith
Glucose and Immunity
http://www.diabeteslibrary.org/View.aspx?url=Article638
Accessed 11/2011

Van Oss CJ.
Influence of glucose levels on the in vitro phagocytosis of bacteria by human neutrophils.
Infect Immun. 1971 Jul;4(1):54-9.

Bernstein J, Alpert S, et al
Depression of lymphocyte transformation following oral glucose ingestion
Am J Clin Nutr. 1977; 30: 613

Robert A. Good, Ellen Lorenz
Nutrition and cellular immunity
International Journal of Immunopharmacology. Vol 14, Iss 3, Apr 1992, Pp. 361-366

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

Fat Blocking Soda?

pepsi141112_insideNow we can eat all the fat we want in a meal and still lose weight. Forget that two cheeseburgers, fries and a soda, or fried onions rings/mushrooms and a juicy prime cut of beef with a gooey baked potato smothered in cheese sauce will render your blood as thick as petroleum jelly in a matter of minutes. The magic in this dining extravaganza is the soda, a new variety of cola that contains a fat blocker known as dextrin. But wait, first you have to travel to Japan to get this treat from Pepsi and its affiliate, Suntory, a company that distills booze “to bring happiness into the lives of our customers…in harmony with people and nature.” Yup, makes sense, eh?

Dextrin?
This is a group of carbohydrates that can be made by breaking down starch in the presence of water…hydrolysis. Dextrin also appears in the company of heat under acidic conditions, as happens to the crust on a loaf of bread, rendering flavor, color and crunch. Commercially, dextrins are used to make the glue on an envelope flap, the crispness enhancer in breaded frozen foods, and the cement that holds the pyrotechnics together in fireworks and sparklers. Because they are indigestible, dextrins are added to soluble fiber supplements, such as Benefiber. Whether they can help a person lose weight or not is another question; fiber’s claim to fame is increasing satiety and making you feel fuller faster. Fiber doesn’t actually push food through the system more quickly. Instead, it slows transit time through the stomach and small intestine, where digestion takes place. This is why fiber-rich foods keep you feeling full longer.  Once fiber gets to the large intestine, it keeps things in motion until they come out. It is true, though, that fiber can absorb some fat, but probably not enough to cause a significant weight loss in a short amount of time.

What About Fat?
Eliminating fat from the diet completely is not prudent. We need it to digest, absorb and transport vitamins A, D, E, and K, which are fat-soluble. The body demands the essential fatty acids, the omega-6’s and omega-3’s, to make substances that address inflammation, affect cell signaling, and add fluidity to the cell membrane. Furthermore, fat is an insulator and it provides a place for organs to attach while acting as a cushion, and it helps to keep the skin supple. If there is a problem with fat, it’s that one gram has 9 calories, contrasted to the 4 calories of carbohydrates and proteins. Fat gets broken down by enzymes, pancreatic lipase being the primary one. In the absence of this enzyme, fat molecules remain too large to be absorbed, so are excreted. The objective of the dextrins is to absorb some of this fat and usher it out the back door.

There are substances that do not absorb fats but prevent their breakdown, keeping their molecules too large to be metabolized so that they get eliminated quickly. One of the first of these was Orlistat, a prescription drug named Xenical that prevents the absorption of fat by inhibiting the enzymes that make the fat particles small enough to be metabolized.  But the side effects of drugs like this can be embarrassing, especially the urgent explosive diarrhea and gas, among a few other neat ones, like fainting or scratching yourself silly.  Alli is an over-the-counter version of Orlistat.

Does Dextrin Work?
According to the researchers at Japan’s NIH who studied this stuff, it works. The test animals were fed a high-cholesterol diet containing dextrin and a diglyceride, the latter molecule a fat used in foods to blend certain ingredients together, such as oil and water, which otherwise would not mix. Upon examination of the animals, the group found that serum triglycerides decreased and, strikingly, that the length of intestinal villi increased (Nagata, 2006).  Basically, less of the fat was absorbed. You can buy dextrin, either as Benefiber or Nutriose, and make your own soda or other high-fiber beverage (even one from Suntory).

What About The Vitamins?
Vitamin A, retinol, helps with night vision, bone growth, tooth development, reproduction, cell division and gene expression. It’s great for the skin and mucous membranes. It’s even recommended to treat acne. Vitamin D is needed to help the body to use calcium and phosphorus in the structure of bones. It supports the immune system and may help to prevent hypertension and common cancers. Vitamin E is an anti-oxidant that protects vitamins A and C, red blood cells and essential fatty acids from destruction via oxidative stress. Vitamin K is naturally produced by gut bacteria, but is also found in foods and as a supplement. It not only helps blood to clot normally, but also escorts calcium to bones where it can’t contribute to arterial plaque. There‘s more, but we don’t have the room for that right now. None of these can be utilized without fat in the diet, so if you choose to use dextrin to absorb fat from a meal, be deliberate, keep things in balance, and supplement.

References

Carter R, Mouralidarane A, Ray S, Soeda J, Oben J.
Recent advancements in drug treatment of obesity.
Clin Med. 2012 Oct;12(5):456-60.

Carvalho MA, Zecchin KG, Seguin F, Bastos DC, Agostini M, Rangel AL, Veiga SS, Raposo HF, Oliveira HC, Loda M, Coletta RD, Graner E.
Fatty acid synthase inhibition with Orlistat promotes apoptosis and reduces cell growth and lymph node metastasis in a mouse melanoma model.
Int J Cancer. 2008 Dec 1;123(11):2557-65.

Kimura Y, Nagata Y, Buddington RK.
Some dietary fibers increase elimination of orally administered polychlorinated biphenyls but not that of retinol in mice.
J Nutr. 2004 Jan;134(1):135-42.

Lefranc-Millot C, Guérin-Deremaux L, Wils D, Neut C, Miller LE, Saniez-Degrave MH.
Impact of a resistant dextrin on intestinal ecology: how altering the digestive ecosystem with NUTRIOSE®, a soluble fibre with prebiotic properties, may be beneficial for health.
J Int Med Res. 2012;40(1):211-24.

Nagata J, Saito M.
Effects of simultaneous intakes of indigestible dextrin and diacylglycerol on lipid profiles in rats fed cholesterol diets.
Nutrition. 2006 Apr;22(4):395-400. Epub 2006 Feb 2.

Sheikh-Taha M, Ghosn S, Zeitoun A.
Oral aphthous ulcers associated with orlistat.
Am J Health Syst Pharm. 2012 Sep 1;69(17):1462, 1464. doi: 10.2146/ajhp120073.

Seguin F, Carvalho MA, Bastos DC, Agostini M, Zecchin KG, Alvarez-Flores MP, Chudzinski-Tavassi AM, Coletta RD, Graner E.
The fatty acid synthase inhibitor orlistat reduces experimental metastases and angiogenesis in B16-F10 melanomas.
Br J Cancer. 2012 Sep 4;107(6):977-87. doi: 10.1038/bjc.2012.355. Epub 2012 Aug 14.

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

Cancer And Sugar: How Sweet It Isn’t

sugar-cubes-smTalk about linking sugar to cancer can be confusing. The “facts” are often presented in a misleading manner that can cause anxiety in those who have the disease. Yet, learning about the science behind the connection can help us make educated decisions about nutrition choices for better health. Sugar, or rather glucose, feeds every cell in the body. We need it to produce energy. Even if we eliminate sugar from our diets, our bodies will still make glucose from other sources, including proteins and fats. It’s a little more complicated than meets the eye. Eating lots of sugar forces the body to make more insulin, one of whose properties is to tell cells to grow. For healthy cells, this is good because all cells grow, divide, die and get replaced by new ones. However, cancer cells can be told to grow, too, when the body makes too much insulin (Goodwin, 2002) (Duggan, 2013). So, yes, there can be too much of a good thing. Knowing from the start that sugar in itself is not evil, we can proceed to the science.

A recent study at the University Rey Carlos in Madrid found a mechanism that links obesity and diabetes with cancer, based on gene activity that promotes the manufacture of insulin. Once sugar reaches the intestine a hormone called GIP is secreted. This enhances insulin release by the pancreas. GIP is controlled by a protein known as β-catenin, a suspected oncogene whose activity depends on sugar levels. Oncogenes are those that transform normal cells into cancerous ones, and mutations of the β-catenin gene are implicated in the incidence of colon and ovarian cancers, among others. Normal sugar levels do not induce accumulation of this protein in the nucleus, but diabetes and its characteristic elevated blood glucose levels does, and is associated with increased cancer risk (Chocarro-Calvo, 2012). The suspicion of a sugar-cancer link was investigated in Korea more than half a decade earlier, when physicians closed a ten-year study in which was recorded health parameters from the biennial physical exams of people receiving national health insurance. Adjusting for smoking and alcohol use, investigators found that those with the highest glucose levels had higher death rates from all cancers combined (Jee, 2005). Associations of sugar to cancer were strongest in pancreatic cancer for both genders. This was followed by esophagus, liver and colon cancers for men and by liver and cervix cancers for women. The bottom line is that cancer risk is elevated with increased fasting serum glucose (Ibid.).

For the last twenty years, diabetes rates have grown. Almost twenty-six million Americans are so diagnosed, but another seven million remain undiagnosed. The disease has been around since the Egyptians, whose ancient writings mention frequent urination as a disturbing problem. Not to be left out of the medical world, the Greeks coined the word diabetes two hundred years before Christ, and Indian physicians noted that diabetic urine would attract ants. In Type II diabetes, insulin resistance is the underlying pathology, accounting for most diagnoses.

The grading of obesity according to body mass index (BMI) aligns with disease specificity. The BMI of healthy people is 18.5-24.9. Between 25.0 and 29.9, a person is overweight. Grade I obesity runs from 30.0-34.0; Grade II from 35.0-39.9; and Grade III above 40.0. The sixty-six inch person who weighs four hundred pounds is off the charts. You can compute your BMI by multiplying your weight by 703, dividing by your height in inches, and then dividing by your height in inches once more.  A recent issue of the Journal of the AMA announced that obesity Grades II and III are associated with significantly higher all-cause mortality, and that simple overweight is associated with significantly lower all-cause death (Flegal, 2013). Imagine what a person with a BMI of 64.6 has to anticipate!

Of the cancer-awareness organizations, breast cancer support groups receive much attention, and rightly so because of this cancer’s ubiquity and horrid nature. It was realized years ago that a relationship between breast cancer and sugar intake exists, where insulin carries the onus of induction. Elevated sugar intake causes a rise in insulin. If the body’s regulatory mechanism is overtaxed, insulin levels get out of hand. Those with diabetes are especially susceptible (Seely, 1983). Just being overweight, in the absence of diabetes, is also a risk factor for breast disease (Lof, 2009). Men are not excused from soft tissue disease just by virtue of their gender. Dietary sugars, notably sucrose (table sugar), may present an ill-defined risk in males, but a risk nonetheless for pancreas, prostate, testis and even lung cancers (Burley, 1998) (DeStefani, 1998).

The glycemic index (GI) is a measure of the effects of carbohydrates on blood glucose levels. Foods that break down quickly and release glucose rapidly have a high GI; those that break down slowly and release glucose gradually have a lower GI. Glucose is used as the reference point. In light of this, scrutiny has been given to an association of high-GI foods to colon cancer. Although no definitive conclusions were reached, there is enough evidence to suggest avoiding foods that are more energy-dense (read sugars and simple carbs) than nutrient-dense to prevent colon and other gastric disease (Galeone, 2012) (Tuyns, 1992) (Moerman, 1993).

Cancer cells thrive on sugar (Dell’Antone, 2012) (Sandulache, 2011), and glucose transport is misregulated in active disease.  Tumor cells have shown increased levels of glucose uptake, as seen in diagnostic images that use radio-labeled glucose analogs as identifiers (Adekola, 2012) (Jóźwiak, 2012). To compound the disorder, sugar increases angiogenesis, which is the growth of new blood vessels. That’s the last thing we want for a tumor—a feeding tube. Yes, angiogenesis is required for growth and development of an organism and for the healing of wounds, but it needs to stop there. Anti-angiogenic protocols are being studied as novel therapies (Merchan, 2010) (Brown, 1998) (Airley, 2007).

All sugars and carbohydrates need not be avoided. The healthy carbohydrates include vegetables, fruits, whole grains and legumes. There is debate about the value of grains in the diet, but we have to admit they are sources of fiber, phytochemicals, vitamins and minerals, and compounds yet to be identified. To keep insulin levels at bay, be sure to eat protein, fat and fiber. These work even in the presence of simpler carbs and sugars. Compared to the whole fruit with its fiber, fruit juices don’t make the cut. Limit desserts to a few times a week, dump sodas and other concentrated sugars, and focus on whole foods.

References

Adekola K, Rosen ST, Shanmugam M.
Glucose transporters in cancer metabolism.
Curr Opin Oncol. 2012 Nov;24(6):650-4.

Airley RE, Mobasheri A.
Hypoxic regulation of glucose transport, anaerobic metabolism and angiogenesis in cancer: novel pathways and targets for anticancer therapeutics.
Chemotherapy. 2007;53(4):233-56.

Baron JA, Weiderpass E, Newcomb PA, Stampfer M, Titus-Ernstoff L, Egan KM, Greenberg ER.
Metabolic disorders and breast cancer risk (United States).
Cancer Causes Control. 2001 Dec;12(10):875-80.

Brown NS, Bicknell R.
Thymidine phosphorylase, 2-deoxy-D-ribose and angiogenesis.
Biochem J. 1998 Aug 15;334 ( Pt 1):1-8.

Burley VJ.
Sugar consumption and human cancer in sites other than the digestive tract.
Eur J Cancer Prev. 1998 Aug;7(4):253-77.

Chocarro-Calvo A, García-Martínez JM, Ardila-González S, De la Vieja A, García-Jiménez C.
Glucose-Induced β-Catenin Acetylation Enhances Wnt Signaling in Cancer.
Mol Cell. 2012 Dec 26. pii: S1097-2765(12)00979-3.

Kathleen A. Cooney, MD; Stephen B. Gruber, MD, PhD, MPH
Hyperglycemia, Obesity, and Cancer Risks on the Horizon
JAMA. 2005;293(2):235-236.

Dell’ Antone P.
Energy metabolism in cancer cells: how to explain the Warburg and Crabtree effects?
Med Hypotheses. 2012 Sep;79(3):388-92.

De Stefani E, Deneo-Pellegrini H, Mendilaharsu M, Ronco A, Carzoglio JC.
Dietary sugar and lung cancer: a case-control study in Uruguay.
Nutr Cancer. 1998;31(2):132-7.

Duggan C, Wang CY, Neuhouser ML, Xiao L, Smith AW, Reding KW, Baumgartner RN, Baumgartner KB, Bernstein L, Ballard-Barbash R, McTiernan A.
Associations of insulin-like growth factor and insulin-like growth factor binding protein-3 with mortality in women with breast cancer.
Int J Cancer. 2013 Mar 1;132(5):1191-200.

Katherine M. Flegal, PhD; Brian K. Kit, MD; Heather Orpana, PhD; Barry I. Graubard, PhD
Association of All-Cause Mortality With Overweight and Obesity Using Standard Body Mass Index CategoriesA Systematic Review and Meta-analysis
JAMA. 2013;309(1):71-82.

Galeone C, Pelucchi C, La Vecchia C.
Added sugar, glycemic index and load in colon cancer risk.
Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):368-73.

Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J, Madarnas Y, Hartwick W, Hoffman B, Hood N.
Fasting insulin and outcome in early-stage breast cancer: results of a prospective cohort study.
J Clin Oncol. 2002 Jan 1;20(1):42-51.

Sun Ha Jee, PhD, MHS; Heechoul Ohrr, MD, PhD; Jae Woong Sull, PhD, MHS; Ji Eun Yun, MPH; Min Ji, MPH; Jonathan M. Samet, MD, MS
Fasting Serum Glucose Level and Cancer Risk in Korean Men and Women
JAMA. 2005;293(2):194-202.

Jóźwiak P, Lipińska A.
The role of glucose transporter 1 (GLUT1) in the diagnosis and therapy of tumors
Postepy Hig Med Dosw (Online). 2012 Jan 4;66:165-74.

La Vecchia C.
Mediterranean diet and cancer.
Public Health Nutr. 2004 Oct;7(7):965-8.

Lof M, Weiderpass E
Impact of diet on breast cancer risk.
Curr Opin Obstet Gynecol. 2009 Feb;21(1):80-5.

Merchan JR, Kovács K, Railsback JW, Kurtoglu M, Jing Y, Piña Y, Gao N, Murray TG, Lehrman MA, Lampidis TJ.
Antiangiogenic activity of 2-deoxy-D-glucose.
PLoS One. 2010 Oct 27;5(10):e13699.

Moerman CJ, Bueno de Mesquita HB, Runia S.
Dietary sugar intake in the aetiology of biliary tract cancer.
Int J Epidemiol. 1993 Apr;22(2):207-14.

Sakanaka C, Sun TQ, Williams LT.
New steps in the Wnt/beta-catenin signal transduction pathway.
Recent Prog Horm Res. 2000;55:225-36.

Sandulache VC, Ow TJ, Pickering CR, Frederick MJ, Zhou G, Fokt I, Davis-Malesevich M, Priebe W, Myers JN.
Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells.
Cancer. 2011 Jul 1;117(13):2926-38.

Schernhammer ES, Hu FB, Giovannucci E, Michaud DS, Colditz GA, Stampfer MJ, Fuchs CS.
Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts.
Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2098-105.

Seely S, Horrobin DF.
Diet and breast cancer: the possible connection with sugar consumption.
Med Hypotheses. 1983 Jul;11(3):319-27.

Tuyns AJ, Kaaks R, Haelterman M, Riboli E.
Diet and gastric cancer. A case-control study in Belgium.
Int J Cancer. 1992 Apr 22;51(1):1-6.

Wang X, Goode EL, Fredericksen ZS, Vierkant RA, Pankratz VS, Liu-Mares W, Rider DN, Vachon CM, Cerhan JR, Olson JE, Couch FJ.
Association of genetic variation in genes implicated in the beta-catenin destruction complex with risk of breast cancer.

Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):2101-8.

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

Soda And Heart Risk: And We Thought It Was Only Teeth We Had To Worry About

soda-glassDid your mother ever say, “If you know what’s good for you, you’ll…?” Know what the matter is?  Even as adults who know what’s good for us, we drop the ball as if we didn’t know what’s good for us. Some of us even put the ball down on purpose from time to time. Hey, if we don’t know what’s good for us, how are we supposed to know what’s bad for us?

Catch this newsy tidbit. A lady in Monaco (you know, the place where Grace Kelly used to hang out) made her way to the ER with a palpitating heart that played syncopated rhythms. Intermittent fainting spells were included…free. After all was said and done, it turned out that the only thing she drank for the previous sixteen years was soda—a half-gallon a day, cola at that. If you’re thinking she got her 8 x 8 (eight, 8-ounce glasses of fluids a day), she really got more than she bargained for. The water part of soda is good; the other part isn’t so good.

Ingredients in soda are basically useless. The caramel color comes from heating corn or cane sugar until it reaches the desired color. Desired? By whom? The amount of sugar in a can of regular, non-diet, soda can reach twelve teaspoons. Would you let your child eat even ten spoons of sugar right from the bowl? If a person opts for diet soda, aspartame or some other fake sweetener is in the mix. That earns a chapter of its own. Phosphoric acid adds tang and tartness, but the label doesn’t say it also erodes tooth enamel (Brown, 2007), borrows calcium from bones, and is associated with kidney problems. “Natural flavors” don’t turn soda into health food. Caffeine, we are told, is added to enhance flavor, even to non-colas. Funny thing…a panel of trained tasters couldn’t tell the difference between caffeinated and non-caffeinated colas (Keast, 2007). It adds a slight bitterness and, of course, acts as a stimulant. Soda does, however, contain less caffeine than a cup of coffee.

Caffeine is a diuretic. You well know that a cup of coffee after, say 7 PM, is gonna make you get out of bed at three in the morning. A cola nightcap might do the same thing. Excess urine production—and maybe even diarrhea—will flush potassium from the body. That’s what seems to have happened to the Monaco Miss—potassium deficit. Well, now, does that make any difference? Let’s see what potassium is all about. It’s the number one positively charged ion in the fluid inside a cell, having a sodium counterpart on the other side of the membrane. Their concentration differences create an electrochemical gradient known as membrane potential, which allows a cell to work like a battery to provide power for its function. Simply, sodium tells your fingers to pick up a pencil; potassium says to let it go. Sodium contracts, potassium relaxes. If potassium is in short supply, muscle—including the heart—keeps trying to contract without being relaxed. Not good, right? Right. It’s bad enough that most of us are potassium shy because we fail to get the 4700 milligrams a day that we need, but it’s worse that soda can dissolve what’s left. Potassium helps the heart maintain a regular beat; deficiencies cause irregularities (Poole-Wilson, 1984).

Additional concerns about caffeine intake involve weight loss “miracles” that propose to suppress appetite and increase energy. Most of us are unaware that supplements can contain caffeine without it being listed on the label. A Brazilian tea that is marketed as an energy enhancing beverage, guarana, actually has twice the caffeine of coffee. While that can zoom you up, it can also induce seizures and blurred vision (Pendleton, 2012). O.K., so caffeine keeps you awake, that is, if you’re not accustomed to it. But it is related to sleep-disordered breathing if it comes from soda, though not coffee or tea (Aurora, 2012).

Through a process called osmotic diuresis, glucose and water are eliminated in urine. The kidneys normally reabsorb water and glucose, but excess sugar interferes with normal kidney function. The extra sugar attracts water, which has to go somewhere…the drain…and it takes potassium with it (Packer, 2008) (Sharma, 2013). And then there’s the likelihood that fructose will elevate uric acid levels and cause gout (Choi, 2008). Gosh, heart trouble or arthritic agony?  Choices, choices.

If you’ve been a heavy soda drinker for years, it only takes a week to set things straight. The CDC says that fewer than two percent of us get enough potassium (Cogswell, 2012). Potassium-rich foods aren’t that hard to find. Sweet and white potatoes, beet greens, tomatoes, bananas, orange, prune and tomato juices, spinach, sunflower seeds and molasses are some of the foods to consider. Keeping soda to less than a pint a day could keep you out of the ER. There are some places you really don’t need to be.

References

Aurora RN, Crainiceanu C, Caffo B, Punjabi NM.
Sleep-disordered breathing and caffeine consumption: results of a community-based study.
Chest. 2012 Sep;142(3):631-8.

Barri YM, Wingo CS.
The effects of potassium depletion and supplementation on blood pressure: a clinical review.
Am J Med Sci. 1997 Jul;314(1):37-40.

Brown CJ, Smith G, Shaw L, Parry J, Smith AJ
The erosive potential of flavoured sparkling water drinks.
Int J Paediatr Dent. 2007 Mar;17(2):86-91.

Brown CM, Dulloo AG, Montani JP.
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