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American Sugar: The Untold Story.

There 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. America’s sweet tooth increased 39% between 1950 and 2000 as the use of corn sweetener octupled.

Although the statistics above are decades old, its message is contemporary. High-fructose corn syrup has become the bad boy of the anti-sugar crusade. 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 people 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 (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). Mix a sweet alcohol cocktail and find the whammy doubled. (Fuchs. 2002).

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 to its host? It likes to let itself in, but has the nasty character of pushing everything else out.

Reference

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

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.

Maple Syrup – M’m! M’m! GOOD!

anti-diabetes maple-syrupAstounding as it may seem, maple syrup—real maple syrup—has been found to have anti-cancer and anti-diabetes properties. Plant researchers at the University of Rhode Island have isolated compounds from maple tree sap that are strikingly beneficial to human health. What’s more, some of these compounds are brand new, and surface only after the sap is processed into syrup.

A Science Daily report from March, 2011, announces that the University of Rhode Island medicinal plant researcher, Navindra Seeram, has discovered thirty-four new beneficial compounds in pure maple syrup to be added to the twenty he found the year before, “…five of which have never been seen in nature.” The researcher is quoted, “It’s important to note that in our laboratory research we found that several of these compounds possess anti-oxidant and anti-inflammatory properties, which have been shown to fight cancer, diabetes and bacterial illnesses.” Seeram applauds Mother Nature as the best chemist, commenting that, “…maple syrup is becoming a champion food when it comes to the number and variety of beneficial compounds found in it.” (Science Daily; Mar. 30, 2011) Seeram’s team acknowledges that inflammation is at the center of several nefarious disease, including heart disease, diabetes, certain cancers, and neurodegenerative diseases such as Alzheimer’s. The maple syrup compounds may show medicinal promise, but the scientists suggest that consumers not consume large quantities of the syrup, but to use it instead of artificial products found in the marketplace.

The scientific names of the compounds derived from maple syrup are enough to scare you away.  With thirty or more letters and numbers, these unpronounceable words sound serious.  And they are.  Among them are phenolic compounds and plant lignans, the former having anti-oxidant properties and the latter having hormonal properties.  Of these two major constituents, the phenolics are more active (Li and Seeram. 2010), and were found to be comparable to vitamin C (Li and Seeram. 2011).

Plants make certain chemicals for themselves, often to remain protected from predation or environmental damage, as may occur from heavy metal exposure via exhaust from the electric company’s smokestack, which often contains mercury.  These beneficial chemicals transfer to us when we eat those plants, where they may act as chelators besides anti-oxidants.  The more a plant is stressed, the more it produces phenolic anti-oxidants, the bioflavonoids being the best-known among them.

Real maple syrup demonstrates quite a nutritional profile compared to the fake stuff, which is primarily high-fructose corn syrup (HFCS) flavored with a synthetic ingredient.  Ounce for ounce, maple syrup has slightly fewer calories and carbohydrates than HFCS, eleven times the calcium, and more magnesium and zinc.  Plus, it tastes a whole lot better.

Two phenols in maple syrup, ethyl acetate and butanol, are able to inhibit enzymes that are relevant to Type 2 diabetes (Apostolidis. 2011), with butanol being more active.  Additionally, butanol converts to butyric acid, which plays a role in DNA transcription.  Real maple syrup is allowed to be labeled as such.  In Quebec, the largest producer of real maple syrup, the locals refer to imitation syrup as “pole syrup,” implying that it has been tapped from telephone poles.  That’s not too outlandish a comment.   In fact, a brand new compound that forms only during the processing of the sap has been named quebecol, in honor of the Province.  (Li and Seeram. J Func Food. 2011)  It is not uncommon for heat (in this case, sap boiling) to separate chemical components and then rearrange them to form something else, all mass being retained.

It had already been established that anti-oxidants reside in the leaves, bark and twigs of the maple tree, so examining the sap is a logical step.  Exposure to direct sunlight appears to enhance anti-oxidant production.  Besides Seeram, other research teams, especially from Canada, have hopped onto the maple syrup train.  Because all these scientists are headed in the same direction, why not?

References

http://www.sciencedaily.com/releases/2011/03/110330131316.htm
54 Beneficial Compounds Discovered in Pure Maple Syrup
Science Daily (Mar. 30, 2011)

J. Agric. Food Chem., 2010, 58 (22), pp 11673–11679
Maple Syrup Phytochemicals Include Lignans, Coumarins, a Stilbene, and Other Previously Unreported Antioxidant Phenolic Compounds
Liya Li and Navindra P. Seeram

J. Agric. Food Chem., 2011, 59 (14), pp 7708–7716
Further Investigation into Maple Syrup Yields 3 New Lignans, a New Phenylpropanoid, and 26 Other Phytochemicals
Liya Li and Navindra P. Seeram

Journal of Functional Foods. Volume 3, Issue 2, April 2011, Pages 100-106
In vitro evaluation of phenolic-enriched maple syrup extracts for inhibition of carbohydrate hydrolyzing enzymes relevant to type 2 diabetes management
Emmanouil Apostolidis, Liya Li, Chong Lee and Navindra P. Seeram

Journal of Functional Foods. Volume 3, Issue 2, April 2011, Pages 125-128
Quebecol, a novel phenolic compound isolated from Canadian maple syrup
Liya Lia and Navindra P. Seeram

*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.

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.

Coconut Water: Is It What It’s Cracked Up To Be?

fresh-coconutWhether or not Robinson Crusoe was sustained by it, coconut water—not coconut milk—has gathered a following among those fitness fans looking for an all-natural alternative to sports drinks. However, it just might not be good enough for all athletes.  The liquid endosperm of young coconuts, coconut water is considered one of the world’s most versatile natural products. To enhance that image, science has found evidence to support the role of coconut water in health and medicinal applications. One of the traditional uses of coconut water is as a growth supplement in plant tissue propagation and culture, but a wider application can be justified by its unique chemical composition of sugars, vitamins, minerals, amino acids and phytohormones. The last category holds a few welcome surprises, since soy genistein has hogged the spotlight for years.

What’s The Big Deal?
Coconut water is the liquid endosperm and is served directly as a beverage to quench thirst, while coconut milk is the product obtained by grating the solid endosperm with or without additional water to get a food ingredient useful in traditional recipes. Coconut water is more than 90% water; the milk about 50% water, but also containing fat and protein (Seow, 1997). Coconut water is a clear isotonic solution plentiful in young coconuts. (Isotonic means that the tonicity, or tension, of a solution is similar to that of a body fluid and exerts basically the same pressure on both sides of a membrane.) As the coconut matures, its chemical composition and liquid volume change. The liquid may exceed half a liter at nine month’s maturity (Jackson, 2004).

Coconut water is touted as being high in potassium, one of the electrolytes essential to muscle function as the body’s predominant intracellular cation. One cup of coconut water (240 gm) carries about 600 mg of potassium, which is a fraction of the Institute of Medicine’s recommended 4700 mg (http://www.iom.edu/Reports/2004/Dietary-Reference-Intakes-Water-Potassium-Sodium-Chloride-and-Sulfate.aspx). Of course, 8 glasses will put you over the top. The concern is that potassium needs to be balanced with sodium, the electrolyte first lost to heavy sweating. This is where coconut water falls short as a sports beverage. Sodium content of one cup of coconut water is about 250 mg, not enough to aid recovery after a hard workout that spent eighteen times that by sweating more than a day’s worth of suggested intake. There’s more sodium in a glass of vegetable juice. If you have an interest in electrolytes’ role in human health — and you should, really — check out this site for a cogent explanation:  http://crampnomore.com/sportshealth/electrolytes-101.html.

What Good Is It, Then?
In an era of anti-aging curiosity, coconut water seems to be able to hold its own.  The vitamin content of coconut water is insignificant, although considerably better than the zero of plain water, but its phytonutrients, cytokinin and its analog kinetin, have demonstrated appreciable impact as anti-senescent agents. Isolated more than half a century ago, cytokinin has a potent biological effect on plant cells and tissues that influence gene expression, cell cycle, chloroplast development and biosynthesis, stimulation of vascular architecture, and delay of senescence. This characteristic was extrapolated to humans and cell membrane lipid peroxidation (Mik, 2011). Against placebo, in a randomized, double-blind, controlled study, a combination of topical cosmetic ingredients that featured kinetin and niacinamide was found to induce a reduction in spots, pores, and wrinkles and to re-establish evenness after eight weeks (Chiu, 2007). Additionally, age-related changes attributed to lipofuscin, an indicator of damage represented as brown pigmentations from oxidized fats, were delayed (Rattan, 1994).

Cytokinin and its analogs were found to induce cell death and to inhibit cell proliferation in diverse cancer cell lines (Vermeulen, 2002), where researchers were surprised to find anti-cancer effects that extended beyond the original discoveries (Voller, 2010). An item of interest is that these studies were conducted outside the United States, but not necessarily where coconuts are native. There is a modicum of protein in a cup of coconut water (less than 2.0 grams), but when part of a more voluminous coconut protein product, it is sufficiently influential to contribute to an increase and a strengthening of the immune cells that are born in bone marrow (Vigila, 2008). All the while, non-malignant cells are left alone, as cytokinin and kinetin are selective in their inhibition of cell proliferation (Dudzik, 2011).

To Use Or Not To Use?
Though not quite as balanced as serious electrolyte replacement beverages, coconut water has a place in health promotion and disease prevention. To some, it is the darling of India’s Ayurvedic medical practice, where the coconut palm is labeled “Kalpavriksha,” the all-giving tree that provides antibacterial, antifungal, antiparasitic, hypoglycemic, immunostimulant and hepatoprotective properties (DebMandal, 2011) (Preetha, 2012).   To overcome coconut water’s sodium shortfall, some formulators add salt and other enhancements to their drink and then market it as a complete sports beverage. There’s a lot more to learn about what’s in the marketplace, since adulteration is common and can ramp up calories from the basic 46 per cup.

Oral rehydration using coconut water following bouts of diarrhea, especially in children, can forestall the need for intravenous therapy in those who are amply nourished prior to the onset of the infirmity. It is contraindicated in cases of dehydration for lack of electrolyte balance (Adams, 1992). The absorption of coconut water is far superior to that of soft drinks, too, which are often used as fluid replacements by those who are unaware of the options (Chavalittamrong, 1982). The problem with this application, however, is the variability of sodium and glucose content of the coconut fluid at various stages in its development (Fagundes, 1993). A legitimate coconut water purveyor will have analyzed his product before packaging, and will put that data on the label.  Coconut water costs about fifteen cents an ounce. A quality electrolyte replacement concentrate, making four gallons of sports beverage, costs about four cents an ounce…and has the right balance of potassium and sodium, the two important players in muscle contraction and relaxation.

References

Adams W, Bratt DE.
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Adolf K Awua, Edna D Doe and Rebecca Agyare
Exploring the influence of sterilisation and storage on some physicochemical properties of coconut (Cocos nucifera L.) water
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Casati S, Ottria R, Baldoli E, Lopez E, Maier JA, Ciuffreda P.
Effects of cytokinins, cytokinin ribosides and their analogs on the viability of normal and neoplastic human cells.
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Chavalittamrong B, Pidatcha P, Thavisri U.
Electrolytes, sugar, calories, osmolarity and pH of beverages and coconut water.
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Chee C. Seow, Choon N. Gwee
Coconut milk: chemistry and technology
International Journal of Food Science & Technology. May 1997; 32(3):  189-201


Chiu PC, Chan CC, Lin HM, Chiu HC.
The clinical anti-aging effects of topical kinetin and niacinamide in Asians: a randomized, double-blind, placebo-controlled, split-face comparative trial.
J Cosmet Dermatol. 2007 Dec;6(4):243-9.


DebMandal M, Mandal S.
Coconut (Cocos nucifera L.: Arecaceae): in health promotion and disease prevention.
Asian Pac J Trop Med. 2011 Mar;4(3):241-7. Epub 2011 Apr 12.


Dudzik P, Dulińska-Litewka J, Wyszko E, Jędrychowska P, Opałka M, Barciszewski J, Laidler P
Effects of kinetin riboside on proliferation and proapoptotic activities in human normal and cancer cell lines.
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Fagundes Neto U, Franco L, Tabacow K, Machado NL.
Negative findings for use of coconut water as an oral rehydration solution in childhood diarrhea.
J Am Coll Nutr. 1993 Apr;12(2):190-3.


Institute of Medicine of the National Academies
Dietary Reference Intakes: Water, Potassium, Sodium, Chloride, and Sulfate
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Jose C. Jackson, Andre Gordon, Gavin Wizzard, Kayanne McCook and Rosa Rolle
Changes in chemical composition of coconut (Cocos nucifera) water during maturation of the fruit
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Kende H, Zeevaart J.
The Five “Classical” Plant Hormones.
Plant Cell. 1997 Jul;9(7):1197-1210.


Mik V, Szüčová L, Smehilová M, Zatloukal M, Doležal K, Nisler J, Grúz J, Galuszka P, Strnad M, Spíchal L.
N9-substituted derivatives of kinetin: effective anti-senescence agents.
Phytochemistry. 2011 Jun;72(8):821-31. Epub 2011 Feb 25.


Eze K. Nwangwa and Chukwuemeka P. Aloamaka
Regenerative Effects of Coconut Water and Coconut Milk on the Pancreatic β–Cells and
Cyto Architecture in Alloxan Induced Diabetic Wistar Albino Rats

American Journal of Tropical Medicine & Public Health. 2011; 1(3): 137-146


Preetha PP, Devi VG, Rajamohan T.
Hypoglycemic and antioxidant potential of coconut water in experimental diabetes.
Food Funct. 2012 Jul;3(7):753-7. Epub 2012 Jun 27.


Rattan SI, Clark BF.
Kinetin delays the onset of ageing characteristics in human fibroblasts.
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Sandhya VG, Rajamohan T.
Beneficial effects of coconut water feeding on lipid metabolism in cholesterol-fed rats.
J Med Food. 2006 Fall;9(3):400-7.


Vermeulen K, Strnad M, Krystof V, Havlícek L, Van der Aa A, Lenjou M, Nijs G, Rodrigus I, Stockman B, van Onckelen H, Van Bockstaele DR, Berneman ZN.
Antiproliferative effect of plant cytokinin analogues with an inhibitory activity on cyclin-dependent kinases.
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A. Geo Vigila and X. Baskaran
Immunomodulatory Effect of Coconut Protein on Cyclophosphamide Induced Immune Suppressed Swiss Albino Mice
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Vigliar R, Sdepanian VL, Fagundes-Neto U.
Biochemical profile of coconut water from coconut palms planted in an inland region.
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Voller J, Zatloukal M, Lenobel R, Dolezal K, Béres T, Krystof V, Spíchal L, Niemann P, Dzubák P, Hajdúch M, Strnad M.
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Phytochemistry. 2010 Aug;71(11-12):1350-9. Epub 2010 Jun 1.


tJean W. H. Yong, Liya Ge, Yan Fei Ng and Swee Ngin Tan
The Chemical Composition and Biological Properties of Coconut (Cocos nucifera L.) Water
Molecules. 2009, 14, 5144-5164

*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.
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Airley RE, Mobasheri A.
Hypoxic regulation of glucose transport, anaerobic metabolism and angiogenesis in cancer: novel pathways and targets for anticancer therapeutics.
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Baron JA, Weiderpass E, Newcomb PA, Stampfer M, Titus-Ernstoff L, Egan KM, Greenberg ER.
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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
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Jóźwiak P, Lipińska A.
The role of glucose transporter 1 (GLUT1) in the diagnosis and therapy of tumors
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La Vecchia C.
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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.
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Moerman CJ, Bueno de Mesquita HB, Runia S.
Dietary sugar intake in the aetiology of biliary tract cancer.
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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.

Sweet And Large

sweetnersA corned beef special with extra Russian dressing, a side of cole slaw, and a hunk of New York cheese cake for dessert, chased with a Diet Coke. This was pretty common lunchtime fare for a raft of patrons at a local eatery. Were they looking to cut calories? Or was diet soda merely the rage? If these folks were trying to fight the Battle of the Bulge, they chose the losing faction. If marketing diet soft drinks, they joined the pack.

Not too long ago scientists re-examined the effects of artificial sweeteners on human physiology, prompted, it seems, by the obesity epidemic that is sweeping the country and a considerable part of the Western World. It is presumed that eliminating the cause will also eliminate the effect. The cause in this case has multiple personalities, starting with saccharin, the oldest fake sugar, discovered at Johns Hopkins in the late 1870’s…from coal tar. Sounds yummy, right? Yep, a little waterproofing/shampoo in your coffee gets the day off to a running start, and it’ll even treat dandruff and kill lice. In its infancy, saccharin was featured on drug store shelves as a sugar replacement for people with diabetes. It was put into soda in the 1940’s for those who wanted to limit sugar intake, which was ironic because sugar was limited during World War II anyway. Saccharin is 300 times sweeter than table sugar and has a bitter aftertaste. Cyclamate came out in the 30’s, and was blended with saccharin to improve the flavor. Both were GRAS—generally recognized as safe—at first, in the late 50’s. In the late 60’s, however, cyclamate was abandoned by the U.S. as a carcinogen, and saccharin was viewed with suspicion. Other countries allow cyclamates to this day. Saccharin had received a warning label, but that was removed in 2000 by the Sweetness Act. How adorable! In 2010, the EPA took saccharin off its hazardous chemical list. Did you know this stuff is made from toluene, which has limited carcinogenic potential but still is paint thinner?

Aspartame was stumbled upon when Big Pharma was looking to make a new ulcer drug in the mid 1960’s. A combination of the amino acids phenylalanine and aspartic acid linked to a methanol backbone, aspartame is supposed to be avoided by those with phenylketonuria, a rare inherited metabolic disorder that fails to process phenylalanine, leading to mental retardation and other serious problems. Popular reports cite aspartame as causative of seizures and mood changes, an allegation that is still hotly debated (Magnuson, 2007) (Pediatrics, 1997). Its sweetness parallels that of saccharin.

Neotame, a product of Monsanto’s NutraSweet, is 7,000 times sweeter than sugar. That was approved in 2002. It’s the sweetest child on the block. Acesulfame potassium (K) hit the streets in dry foods in the 80’s and as a general sweetener in ’03. But the hot one these days is sucralose–Splenda®. It’s the most popular artificial sweetener, used mostly in soft drinks, but also in some baby foods (Why?).

What’s this got to do with obesity? For starters, the brain doesn’t appreciate being fooled. As soon as it gets the message that something sweet is eaten it initiates the secretion of insulin by the pancreas to start metabolizing glucose. When there is no nutritive entity to provide glucose, the brain makes you hungry enough to get some. You then eat.

Dr. Yanina Pepino and her team of researchers at Washington University School of Medicine found that sucralose is not an inert ingredient, but one that has a definite effect on blood sugar peaks. When subjects drank a sucralose beverage prior to drinking a glucose beverage, their sugar levels rose 20 percent higher than when they drank plain water before the glucose drink. The analysts related this to enhanced insulin and glucose responses caused by the artificial sweetener (Pepino, 2013), possibly leading to insulin resistance. True sweet taste cues serve to regulate energy balance, while non-nutritive sweeteners may promote increased food intake and consequent weight gain (Swithers, 2010).

Sucralose has chlorine groups replacing hydroxide groups in a glucose molecule, making it an organochloride that is related to some pesticides and plastics. It has the capability of lowering intestinal pH, making it acidic and hostile to beneficent colonic bacteria. Even after stopping sucralose, the changed pH may persist (Abou-Donia, 2008). Isn’t chlorine used in swimming pool and bathroom cleaners to kill bacteria?

Before sucralose hit the market, similar investigations focused on then-current artificial sweeteners, aspartame paramount among them. Where a 1986 project found ambiguity concerning appetite signals (Blundell, 1986), later study found that aspartame-sweetened carbonated water increased appetite in the short term (Black, 1993), implying a subsequent intake of excess energy. While the cheesecake crowd was enjoying its low-cal sodas, scientists were already looking at weight management in a highly homogeneous group of middle-aged women, learning that heavier gals were more likely to use non-nutritive sweeteners than their normal weight counterparts, but that, in the long term, artificial sweeteners were not able to prevent weight gain or help weight loss (Stellman, 1986). As with much of what we ingest, dose makes the difference. Those imbibing up to three artificially-sweetened drinks a day appear more likely to risk overweight and obesity than those who consume none (Fowler, 2008). For those who exercise, the difference is insignificant.

So, now, what’s the worry, insulin resistance or weight gain? Being a little overweight doesn’t automatically translate to type 2 diabetes, but it is one of the risk factors. Daily consumption of diet soda was associated with a 36% greater relative risk of metabolic syndrome and a 67% greater risk of incident type 2 diabetes, compared to non-consumption, in a 2009 report from the U of TX (Nettleton, 2009). Whatever the concern might be, fake sugars stir the soup and promote insulin release (Malaisse, 1998). One of the mechanisms involves faking out the brain, not only with renegade appetite signals, but also with altered reward processing of the sweet sensation that rightfully belongs outside the sphere of artificial sweeteners (Green, 2012). As with all heath topics, the debate goes on because some people remain completely unaffected. And we thought that only Superman was bulletproof. The bottom line is that artificial sweeteners do not activate the food reward pathways in the same fashion as natural ones (Smeets, 2005).

References

[No authors listed]
“Inactive” ingredients in pharmaceutical products: update (subject review). American Academy of Pediatrics Committee on Drugs.
Pediatrics. 1997 Feb;99(2):268-78.

Abou-Donia MB, El-Masry EM, Abdel-Rahman AA, McLendon RE, Schiffman SS.
Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats.
J Toxicol Environ Health A. 2008;71(21):1415-29.

Stephen D. Anton, Corby K. Martin, Hongmei Han, Sandra Coulon, William T. Cefalu, Paula Geiselman, Donald A. Williamson
Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels
Appetite 55(1); Aug 2010: 37-43

Black RM, Leiter LA, Anderson GH.
Consuming aspartame with and without taste: differential effects on appetite and food intake of young adult males.
Physiol Behav. 1993 Mar;53(3):459-66.

Blundell JE, Hill AJ.
Paradoxical effects of an intense sweetener (aspartame) on appetite.
Lancet. 1986 May 10;1(8489):1092-3.

Brown RJ, de Banate MA, Rother KI.
Artificial sweeteners: a systematic review of metabolic effects in youth.
Int J Pediatr Obes. 2010 Aug;5(4):305-12.

Brusick D, Borzelleca JF, Gallo M, Williams G, Kille J, Wallace Hayes A, Xavier Pi-Sunyer F, Williams C, Burks W.
Expert panel report on a study of Splenda in male rats.
Regul Toxicol Pharmacol. 2009 Oct;55(1):6-12.

Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP.
Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain.
Obesity (Silver Spring). 2008 Aug;16(8):1894-900.

Green E, Murphy C.
Altered processing of sweet taste in the brain of diet soda drinkers.
Physiol Behav. 2012 Nov 5;107(4):560-7.

Magnuson BA, Burdock GA, Doull J, Kroes RM, Marsh GM, Pariza MW, Spencer PS, Waddell WJ, Walker R, Williams GM.
Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies.
Crit Rev Toxicol. 2007;37(8):629-727.

Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F.
Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets.
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Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr.
Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA).
Diabetes Care. 2009 Apr;32(4):688-94

Pepino MY, Tiemann CD, Patterson BW, Wice BM, Klein S.
Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load.
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Rogers PJ, Carlyle JA, Hill AJ, Blundell JE.
Uncoupling sweet taste and calories: comparison of the effects of glucose and three intense sweeteners on hunger and food intake.
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Rudenga KJ, Small DM.
Amygdala response to sucrose consumption is inversely related to artificial sweetener use.
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Smeets PA, de Graaf C, Stafleu A, van Osch MJ, van der Grond J.
Functional magnetic resonance imaging of human hypothalamic responses to sweet taste and calories.
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Stellman SD, Garfinkel L.
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Qing Yang
Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings:Neuroscience 2010
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Electrolytes and Sugar(s): Stuff You Need To Know

sports-drinkAlthough we are admonished not to mix electrolytes with sugars, we do it anyway. Most of the time it’s isn’t “we”, the consumer; it’s “we”, the marketer. The soda industry wouldn’t sell much product if it weren’t sweet. Plain carbonated lemon juice, cola syrup or turkey gravy just wouldn’t cut it. Even Ragu contains sugar, but thank goodness it isn’t fizzy. Sugar has no place in an electrolyte replacement beverage.

A few electrolyte drinks aimed at professional athletes contain some kind of sugar. The only purpose served by the sweetener is to add palatability. It does absolutely nothing—nada, zilch, zero—for bioavailability and efficacy of the electrolyte minerals. But it sure turns the coach into fly food after a win.

Tests at the University of Nebraska found that fructose increases fecal excretion of minerals, mostly iron and magnesium, but other electrolyte balances are likewise negatively affected (Ivatur, 1986). Sucrose is not without guilt. Well, now, magnesium is an electrolyte, which is supposed to be accompanied by sodium, potassium, chloride and calcium, all of them working to initiate and to inhibit a muscle contraction. In the absence of such contractions you couldn’t pick up the ten dollars your brother owes you. Even more dramatic, your heart might not run on all its cylinders.

Calling sugar a carbohydrate on a food ingredient label is misleading, so labeling guidelines now call it what it is…sugar. Itself, sugar arrests the secretion of stomach acid so that processing of nutrients, including the electrolyte minerals, is stymied. Creating acid in the intestine, however, sugar can lower pH by as much as one or two units, and being logarithmic, represent a tenfold or twentyfold difference in acidity (Rosen, 1965) (Stephan, 1943). Sugar even increases the acidity that tumors find so hospitable to their growth and development (DiPette, 1986).

Many of us are deficient in magnesium, partly because of sugar consumption. Beverage choices are paramount in this affliction (Ballew, 2000), and sports drinks containing sugar elevate insulin as part of the metabolic process, thus increasing the renal excretion of magnesium (Djurhuus, 1995, 2000) and calcium (Hodgkinson, 1965).

Mineral absorption occurs at the juncture of the duodenum and the jejunum. Sugar increases an acidic environment at that point, where it interferes with the alkalinity that minerals enjoy for absorption. The acidity might help the utilization of sugar, but does little for the electrolytes (Daniel, 1986). Major uptake of potassium and sodium occurs at pH of 8.0, with the others close behind. Electrolytes quite possibly are still absorbed at less-than-ideal pH, but why take a chance?

References

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

J A Blair, M L Lucas, and A J Matty
Acidification in the rat proximal jejunum.
J Physiol. 1975 February; 245(2): 333–350.

Daniel H, Rehner G.
Effect of metabolizable sugars on the mucosal surface pH of rat intestine.
J Nutr. 1986 May;116(5):768-77.

Donald J. DiPette, Kimberly A. Ward-Hartley, and Rakesh K. Jain
Effect of Glucose on Systemic Hemodynamics and Blood Flow Rate in Normal and
Tumor Tissues in Rats

CANCER RESEARCH 46, 6299-6304, December 1986

Dr. M.S. Djurhuus, P. Skøtt, O. Hother-Nielsen, N.A.H. Klitgaard, H. Beck-Nielsen
Insulin Increases Renal Magnesium Excretion: A Possible Cause of Magnesium Depletion in Hyperinsulinaemic States
Diabetic Medicine. Volume 12, Issue 8, pages 664–669, August 1995

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

Hodgkinson, A and Heaton FW
The effect of food ingestion on the urinary excretion of calcium and magnesium
Clinica Chimica Acta. Volume 11, Issue 4, April 1965, Pages 354-362

Holbrook JT, Smith JC Jr, Reiser S.
Dietary fructose or starch: effects on copper, zinc, iron, manganese, calcium, and magnesium balances in humans.
Am J Clin Nutr. 1989 Jun;49(6):1290-4.

Rao Venkata Krishna Ivatur
Mineral bioutilization as affected by sugars
ETD collection for University of Nebraska – Lincoln.(January 1, 1986). Paper AAI862953

Ivaturi R, Kies C.
Mineral balances in humans as affected by fructose, high fructose corn syrup and sucrose.
Plant Foods Hum Nutr. 1992 Apr;42(2):143-51.

Rosen S, Weisenstein PR.
The effect of sugar solutions on pH of dental plaques from caries-susceptible and caries-free individuals.
J Dent Res. 1965 Sep-Oct;44(5):845-9.

Stephan RM, Miller BF.
A quantitative method for evaluating physical and chemical agents which modify production of acids in bacterial plaques on human teeth.
J Dent Res. 1943;22;45-51.

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