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Diabetes and Omega-3’s

Diabetes, Omega-3 fatty acids Super FoodsReading, interpreting and understanding scientific literature can be tedious because the authors often find that their previous paper on the subject missed its mark or was completely wrong. Easy to do when you are blazing new trails; however, the caution they go through to cover their tracks oftentimes makes for difficult reading. Luc Djousse and his colleagues at the U of Washington reported in the May 18, 2011 edition of the American Journal of Clinical Nutrition that, “With the use of objective biomarkers, long-chain omega 3 Fatty Acids (FAs) and Alpha-Linolenic Acid (ALA) were not associated with a higher incidence of diabetes. Individuals with the highest concentrations of both types of FAs had lower risk of diabetes.”

Speed reading is absolutely out of place. Omega-3 fatty acids in the body help to control the inflammation process, which is a benefit because the start of the healing process—initiated by the omega-6 arachidonic acid—also involves the possibility of getting carried away with the exercise. Say you have a cut or abrasion. The key activity that ensues is to stop the loss of fluids – save the blood.  It is that process which tells the body to start the healing by sending white blood cells and platelets to the site of the wound and to agglomerate and close the exit door by swelling the tissues, which is also another way of looking at inflammation. To inflame can be life saving. The omega-3’s are then involved in the work of modulating the activity helping to ease the inflammation that comes with the correction process.

Fatty acids, especially those that are long and highly unsaturated, increase cell membrane fluidity and functionality. Fatty acids are essential to membrane activity at the location of hormone receptors. Insulin resistance in adult-onset diabetes is directly associated with fewer membrane enhancing long-chain fatty acids, largely due to impaired function of desaturase and elongase enzymes needed for a healthy membrane. Ruiz-Gutierrez 1993, “We have studied the fatty acid composition of erythrocyte membrane phospholipids in nine Type 1 (insulin-dependent) diabetic patients and nine healthy control subjects. Cell membranes from the diabetic patients showed a marked decrease in the total amount of polyunsaturated fatty acids mainly at the expense of docosahexaenoic acid, DHA, and arachidonic acid C20:4n6”.

Cell membrane abnormalities in lipid content are found to be related to poor metabolic control, which is a characteristic of diabetes. Diet is a very important  factor, and interventions with dietary essential fatty acids (EFAs) in the correct ratio (found to be 4:1, omega-6:omega-3), can make a difference. Decsif  T., 2002, “Reduced availability of long-chain polyunsaturates in diabetic children suggests that an enhanced dietary supply of long-chain polyunsaturates may be beneficial”. Children with diabetes demonstrate a deficit of long-chain fatty acids, so incorporating them into a child’s diet is prudent. An unspoken benefit in the application of EFA’s to diabetes treatment is the decrease in triglyceride levels, themselves striking indicators of the potential for cardiovascular issues and very often appearing in persons with diabetes.

Herein resides the prolonged physiological support of the EFAs. For those who lack the efficient conversion of the omega-3 alpha linolenic acid from plant sources (notably flaxseeds and their oil) to EPA and DHA, fish oil may be a viable alternative. In fact the the FA conversion process with diabetes is almost non-existent, but also common with aging.

For quite some time the essential fatty acids have been misunderstood. Of the types of fatty acids, the omega-3’s have received the most publicity, having been applauded for positive health effects, principally, because over the last century the general population ate little fish and had little or no n-3s in the diet. Unless they were more or less health nuts, few did not have any exposure to omega 3s as in flax, and even if they did their ability to elevate up to EPA and DHA was minimal. Fish oil was the answer but the explosion that ensued caused over-consumption and still does.

Hence the comments of Djousse et al that n-3 FAs did not increase diabetes but if both the omega 6s and the 3 s were added together there was marked improvements. There is an inference that n-3s were of no benefit and needed the balance of both EFAs, which we applaud and so should you. Balance is paramount.

References

Djoussé L, Biggs ML, Lemaitre RN, King IB, Song X, Ix JH, Mukamal KJ, Siscovick DS, Mozaffarian D. Plasma omega-3 fatty acids and incident diabetes in older adults. Am J Clin Nutr. 2011 May 18.

Ruiz-Gutierrez V, Stiefel P, Villar J, García-Donas MA, Acosta D, Carneado J.  Cell membrane fatty acid composition in type 1 (insulin-dependent) diabetic patients: relationship with sodium transport abnormalities and metabolic control.  Diabetologia. 1993 Sep;36(9):850-6.

T. Decsif, H. Minda, R. Hermann, A. Kozári, É. Erhardt, I. Burus, Sz. Molnár and Gy. Soltész  Polyunsaturated fatty acids in plasma and erythrocyte membrane lipids of diabetic children  Prostaglandins, Leukotrienes and Essential Fatty Acids. 67(4); Oct 2002: 203-210

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

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.

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

Cancer And Sugar: How Sweet It Isn’t

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

What’s The Big Deal If My Insulin Spikes?

complex-carbsInsulin is the pancreatic hormone responsible for distributing the carbohydrates you eat in the form of glucose, whose job is to get inside each cell to provide the fuel you need for energy. If the glucose inside a cell is not burned because of inactivity, that which is floating around has no place to go, so it gets into trouble. If it then creates advanced glycation end products*, cells get crystallized like the topping of a crème brulee. That can make cell membranes brittle. If that happens, blood vessels and organs lose resilience and cause problems, such as high blood pressure. Even heart failure can result if the left ventricle stiffens. If carbs don’t get burned, they can get stored as fat because insulin likes to store things. Just like a squirrel, eh? The more insulin you have, the more storage goes on and the more fat builds up. After a while, cells get tired of being teased by insulin, expecting glucose to be escorted in, but frustrated in their anticipation because the old glucose still hasn’t been burned. Now the cells ignore the insulin and become resistant to its serenade. That is the start of type 2 diabetes. A big belly promises big problems. How do you feel about sticking yourself with a needle every day?

*Advanced glycation endproducts—AGE’s—are made when sugars react with proteins or amino acids, without the control of an enzyme, in a process called glycation. This is the equivalent of browning food in a sauté pan or in the oven, and is equally irreversible. When proteins accumulate AGE’s, they do, in fact, turn brown. Because they are cross-linked, the body cannot break them down. As a result, tissues lose tone and resiliency, and destruction begins.

How did this ever happen to me? Probably from simple carbohydrates. You know what they are—foods made from one or two sugars, having very little nutritional value. They’re digested faster than the blink of an eye, and demand immediate burning or they get stored as…well, you know. One-sugar carbs include fructose, galactose and glucose. Two-sugar carbs are lactose, maltose and sucrose (table sugar). Got white flour, honey, milk, candy, chocolate, fruit juice, fruit, jam/jelly, soda, packaged cereal, biscuits or molasses in the pantry?  You’ve got simple carbohydrates. That includes cakes, cookies, doughnuts, pies, and the Pillsbury Doughboy. The fibers, vitamins, minerals and phytonutrients in real, honest-to-goodness fruits bail them out…mostly. But the same can’t be said about juices, especially apple.

How about moderation? How about it? Try giving up wheat—that’s white flour—for a week and see what happens. Replacing white sugar with artificial sweeteners, by the way, might be upsetting the apple cart from another angle. If the brain is fooled into thinking something sweet has been eaten, it’ll still signal insulin to start flowing. At this point, insulin really has nothing to do, so it makes you hungry in order to get some glucose to carry. Now, what? You just took in more calories than you need. They get stored as…well, you know.

Carbohydrates include sugar, starch and fiber, the last not able to be broken apart into simple sugars, so it passes through without being digested. Fibers, both soluble and insoluble, provide no nourishment, but they do promote health. There isn’t much fiber in breads and sweets, but there is in vegetables, legumes and whole grains, the latter associated with increased insulin sensitivity (Liese, 2003) (de Munter, 2007). Restricting carbohydrates in favor of fats and proteins will not only help to control insulin spikes, but also to make your trousers bigger (Foster, 2003) (Samaha, 2003). If you’ve heard about drinking vinegar after a carb-studded repast, you might be interested to know that it seems to help control spikes (Ostman, 2005) (Leeman, 2005), but that’s a topic for another time.

References

Jeroen S L de Munter, Frank B Hu, Donna Spiegelman, Mary Franz, Rob M van Dam
Whole Grain, Bran, and Germ Intake and Risk of Type 2 Diabetes: A Prospective Cohort Study and Systematic Review
PLoS Med 4(8): e261. 2007

Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S.
A randomized trial of a low-carbohydrate diet for obesity.
N Engl J Med. 2003 May 22;348(21):2082-90.

Foster-Powell K, Holt SH, Brand-Miller JC.
International table of glycemic index and glycemic load values: 2002.
Am J Clin Nutr. 2002 Jul;76(1):5-56.

Halton TL, Willett WC, Liu S, Manson JE, Albert CM, Rexrode K, Hu FB.
Low-carbohydrate-diet score and the risk of coronary heart disease in women.
N Engl J Med. 2006 Nov 9;355(19):1991-2002.

Johnson LW, Weinstock RS.
The metabolic syndrome: concepts and controversy.
Mayo Clin Proc. 2006 Dec;81(12):1615-20.

Leeman M, Ostman E, Björck I.
Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects.
Eur J Clin Nutr. 2005 Nov;59(11):1266-71.

Liese AD, Roach AK, Sparks KC, Marquart L, D’Agostino RB Jr, Mayer-Davis EJ.
Whole-grain intake and insulin sensitivity: the Insulin Resistance Atherosclerosis Study.
Am J Clin Nutr. 2003 Nov;78(5):965-71.

Maki KC, Rains TM, Kaden VN, Raneri KR, Davidson MH.
Effects of a reduced-glycemic-load diet on body weight, body composition, and cardiovascular disease risk markers in overweight and obese adults.
Am J Clin Nutr. 2007 Mar;85(3):724-34.

Ostman E, Granfeldt Y, Persson L, Björck I.
Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects.
Eur J Clin Nutr. 2005 Sep;59(9):983-8.

Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L.
A low-carbohydrate as compared with a low-fat diet in severe obesity.
N Engl J Med. 2003 May 22;348(21):2074-81.

*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]
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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.
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Blundell JE, Hill AJ.
Paradoxical effects of an intense sweetener (aspartame) on appetite.
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Brown RJ, de Banate MA, Rother KI.
Artificial sweeteners: a systematic review of metabolic effects in youth.
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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.
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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.
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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.
Appetite. 2012 Apr;58(2):504-7.

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.
Am J Clin Nutr. 2005 Nov;82(5):1011-6.

Stellman SD, Garfinkel L.
Artificial sweetener use and one-year weight change among women.
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Swithers SE, Martin AA, Davidson TL.
High-intensity sweeteners and energy balance.
Physiol Behav. 2010 Apr 26;100(1):55-62. Epub 2010 Jan 6.

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

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

Diabetes Management: Dietary Interventions

diabetes-mangmntDiabetes, the word, is loosely derived from a Greek translation of “one that straddles,” probably referring to a person who urinates frequently. You already know this is considered a metabolic disease of several types, marked by frequent urine discharge, persistent thirst, and the inability to process sugars in the diet due to a decrease in, or absence of, insulin production. There also may be target tissue insulin resistance. Type 1 diabetes mellitus is one of the two major types. Here, the symptoms arise abruptly, often in early adolescence, and the person relies on exogenous insulin to sustain life. Onset may occur at any age, though. Among other miseries, type 1 affects blood vessel health (especially the tiny ones), and manifests in the retina, kidneys, and the underlying connective layer of arterioles. Type 2 diabetes often strikes between ages thirty and forty, with gradual onset that shows few symptoms of metabolic disturbance, at least not right away. With good fortune and careful management, there may be no need for exogenous insulin; diet and perhaps oral hypoglycemic medications can do the trick. Insulin response in type 2 is delayed or reduced, but insulin secretion is not necessarily absent. In this disorder blood vessels of various sizes are affected, particularly the large ones. This can lead to premature atherosclerosis, sometimes followed by myocardial infarction and stroke. Neither of these types of diabetes is to be taken lightly. There is also a third type of diabetes, diabetes insipidus, usually caused by hormone or kidney anomalies.

You might have heard people refer to themselves as having “a touch of diabetes.”  That’s the equivalent of being a little bit pregnant. Either you are, or you aren’t. Maybe you’ll hear folks say their sugar is “a little high.”  Either expression hints that diabetes is not a serious matter. That is wrong. Managing diabetes may not be the easiest thing in the world, but it certainly is achievable, and in the long run it’s well worth the effort. When your blood sugar is normal, you feel better—you have more energy, are less tired and thirsty, have fewer skin or bladder infections, you heal faster, and you have fewer problems with your vision, teeth and feet. Taking care of yourself will avoid heart attack and stroke, the possibility of blindness, nerve damage that causes tingling and numbness in hands and feet, kidney disease that may kill you, and gum disease that causes tooth loss. Hmm, this is serious business.

Unfortunately, the body is not modular in that an organ can be removed and replaced when the warranty is near expiration. It’s not like rotating tires. Even artificial joints don’t come with grease fittings. We have to make parts last as long as possible, despite that some can be replaced…an uncomfortable though to many of us. Prevention is still the best cure. Diabetes can lead to cardiovascular damage. Yes, eyesight and nerves can be damaged, too, but space restricts us to one topic at a time. Changes in the body don’t necessarily happen independently. The cycle of progressive vascular damage from diabetes affects the heart. Changing how we eat can manage glucose levels and prevent heart disease.  One dietary technique follows the glycemic index (GI), which is a measure of how fast blood sugar rises in response to a certain food.  The index estimates how much a gram of carbohydrate elevates blood sugar after consumption, relative to consumption of pure glucose, which is given an index value of 100. Subjects with diabetes managed only by a diet focusing on optimal glycemic control were found to have reduced postprandial glucose levels, accompanied by lower markers of inflammation, notably C-reactive protein (CRP), and improved lipid panels (Wolever, 2008). From time to time, meta-analyses are employed to examine relationships among disease-causing variables. Scrutinizing the GI relationship to CVD, Australian scientists, whose colleagues are credited with designing the GI, discovered a reduction in the risk for cardiovascular disease among diabetes patients who complied with the low GI regimen (Barclay, 2008). The low GI has such potential in the management of chronic disease that those who are morbidly obese may find heart-healthy value in following the plan (Ebbeling, 2005). Even in cases where diabetes is poorly controlled, adhering to the low GI diet has merit when combined with reduced carbohydrate intake in modulating CVD risk factors, including glycated hemoglobin, called HbA1c ( Afaghi, 2012) (Eskesen, 2013) (Zhang, 2012).  Glycated hemoglobin is formed through a non-enzyme pathway when hemoglobin is exposed to high plasma levels of glucose. Glycation forms end products that cause extreme oxidative stress on the body, affecting nearly every cell and molecule. The advanced glycation end products, termed AGE’s, increase vascular permeability, inhibit vascular dilation (and elevate blood pressure), interfere with nitric oxide production (which allows blood vessels to dilate), oxidize LDL, and excite excretion of cytokines. These pathological states invite cardiac entanglement, but can be managed successfully through dietary modification.

The Mediterranean Diet has been touted for its cardiovascular benefits, but little attention has been paid to its effect on diabetes issues.  This diet is a relative newcomer to us, although it’s been a way of life in the Mediterranean for years, generally in the less opulent areas of southern Italy, parts of Greece and a few islands. Despite being called such, this diet is not typical of the entire area. For instance, wine is avoided by the Muslims of the region, and butter, lard and other animal fats comprise part of the cuisine of various indigenous groups. One thing that is easily identifiable about this regional lifestyle is ambulation—everybody walks everywhere. You know very well that accounts for a lot. The diet is abundant in plant foods. Fruit is dessert, as opposed to the sugary stuff Americans eat. The main fat is olive oil; cheese and yogurt are the chief dairy products; red meat is more an accoutrement than a feature. Legumes, unrefined non-GMO cereals, huge amounts of fruits and vegetables, moderate consumption of fish and poultry, and little saturated fat are the norm.

A cohort of more than thirteen thousand Spanish university graduates was followed for four years to assess an association of diet and diabetes. Participants who followed the Mediterranean protocol had a lower risk of disease (Martinez-Gonzalez, 2008) (Dominguez, 2012). There was no beating about the bush in this report. The conclusion was stated with conviction. At the same time, it was noted that seduction by the typical Western diet of fast and prepared foods leads to increases in cardiovascular and metabolic complications (Tarabusi, 2010).

In all the controlled trials reviewed in recent years, those that featured low GI, low carbohydrate and Mediterranean diets all led to greater improvement in glycemic control, with the Mediterranean having the most profound influence on both glucose control and weight loss, enhanced by increases in HDL (Ajala, 2013). Reduction in markers of inflammation and decreases in AGE’s are among the goals in the management of blood glucose and coronary health. AGE’s affect the physiological profiles of proteins by creating cross-links, and they induce vascular dysfunction by stiffening blood vessels and myocardial tissue. Keeping HbA1c where your doctor wants it will keep you alive long enough to be chastised for decades.

References

Abiemo EE, Alonso A, Nettleton JA, Steffen LM, Bertoni AG, Jain A, Lutsey PL.
Relationships of the Mediterranean dietary pattern with insulin resistance and diabetes incidence in the Multi-Ethnic Study of Atherosclerosis (MESA).
Br J Nutr. 2012 Aug 30:1-8.

Afaghi A, Ziaee A, Afaghi M.
Effect of low-glycemic load diet on changes in cardiovascular risk factors in poorly controlled diabetic patients.
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Ajala O, English P, Pinkney J.
Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes.
Am J Clin Nutr. 2013 Mar;97(3):505-16.

Anastasios S Dontas, Nicholas S Zerefos, Demosthenes B Panagiotakos, and Dimitrios A Valis
Mediterranean diet and prevention of coronary heart disease in the elderly
Clin Interv Aging. 2007 March; 2(1): 109–115.

Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, Brand-Miller JC.
Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies.
Am J Clin Nutr. 2008 Mar;87(3):627-37.

Bédard A, Riverin M, Dodin S, Corneau L, Lemieux S.
Sex differences in the impact of the Mediterranean diet on cardiovascular risk profile.
Br J Nutr. 2012 Oct 28;108(8):1428-34.

Chiu CJ, Liu S, Willett WC, Wolever TM, Brand-Miller JC, Barclay AW, Taylor A.
Informing food choices and health outcomes by use of the dietary glycemic index.
Nutr Rev. 2011 Apr;69(4):231-42.

Domínguez LJ, Bes-Rastrollo M, de la Fuente-Arrillaga C, Toledo E, Beunza JJ, Barbagallo M, Martínez-González MA.
Similar prediction of decreased total mortality, diabetes incidence or cardiovascular events using relative- and absolute-component Mediterranean diet score: The SUN cohort.
Nutr Metab Cardiovasc Dis. 2012 Mar 6.

Due A, Larsen TM, Mu H, Hermansen K, Stender S, Astrup A.
Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial.
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Ebbeling CB, Leidig MM, Sinclair KB, Seger-Shippee LG, Feldman HA, Ludwig DS.
Effects of an ad libitum low-glycemic load diet on cardiovascular disease risk factors in obese young adults.
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K. Eskesen, M. T. Jensen, S. Galatius, H. Vestergaard, P. Hildebrandt, J. L. Marott,
J. S. Jensen
Glycated haemoglobin and the risk of cardiovascular disease, diabetes and all-cause mortality in the Copenhagen City Heart Study
Journal of Internal Medicine. Vol 273, Iss 1, pp 94–101, January 2013

Hartog JW, Voors AA, Bakker SJ, Smit AJ, van Veldhuisen DJ.
Advanced glycation end-products (AGEs) and heart failure: pathophysiology and clinical implications.
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Konstantinidou V, Covas MI, Sola R, Fitó M.
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Kuhlmann M., Levin N.
Interaction between Nutrition and Inflammation in Hemodialysis Patients. in “Cardiovascular Disorders in Hemodialysis”
Ronco C. Vicenza and Brendolan A. Vicenza, editors. Basel, Karger, 2005, vol 149, pp 200-207

Lagiou P, Sandin S, Weiderpass E, Lagiou A, Mucci L, Trichopoulos D, Adami HO.
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Lagiou P, Sandin S, Lof M, Trichopoulos D, Adami HO, Weiderpass E.
Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study.
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Lajous M, Boutron-Ruault MC, Fabre A, Clavel-Chapelon F, Romieu I.
Carbohydrate intake, glycemic index, glycemic load, and risk of postmenopausal breast cancer in a prospective study of French women.
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Talya Lavi, RD, Avraham Karasik, MD, Nira Koren-Morag, PHD, Hannah Kanety, PHD,
Micha S. Feinberg, MD, Michael Shechter, MD, MA
The Acute Effect of Various Glycemic Index Dietary Carbohydrates on Endothelial Function in Nondiabetic Overweight and Obese Subjects
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Martínez-González MA, de la Fuente-Arrillaga C, Nunez-Cordoba JM, Basterra-Gortari FJ, Beunza JJ, Vazquez Z, Benito S, Tortosa A, Bes-Rastrollo M.
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Martínez-González MA, García-López M, Bes-Rastrollo M, Toledo E, Martínez-Lapiscina EH, Delgado-Rodriguez M, Vazquez Z, Benito S, Beunza JJ.
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Massaro M, Carluccio MA, De Caterina R.
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Peppa M, Raptis SA.
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Rose Marie Robertson, MD; Lynn Smaha, MD, PhD
Can a Mediterranean-Style Diet Reduce Heart Disease?
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Valeria Tarabusi, Carla Cavazza, Francesca Pasqui, Alessandra Gambineri, Renato Pasquali
Quality of diet, screened by the Mediterranean diet quality index and the evaluation of the content of advanced glycation endproducts, in a population of high school students from Emilia Romagna
Mediterranean J Nutrition and Metabolism. Sep 2010, Vol 3, Iss 2, pp 153-157

Temelkova-Kurktschiev TS, Koehler C, Henkel E, Leonhardt W, Fuecker K, Hanefeld M.
Postchallenge plasma glucose and glycemic spikes are more strongly associated with atherosclerosis than fasting glucose or HbA1c level.
Diabetes Care. 2000 Dec;23(12):1830-4.

Uchiki T, Weikel KA, Jiao W, Shang F, Caceres A, Pawlak D, Handa JT, Brownlee M, Nagaraj R, Taylor A.
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Wolever TM, Gibbs AL, Mehling C, Chiasson JL, Connelly PW, Josse RG, Leiter LA, Maheux P, Rabasa-Lhoret R, Rodger NW, Ryan EA.
The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein.
Am J Clin Nutr. 2008 Jan;87(1):114-25.

Yurong Zhang, Gang Hu, Zuyi Yuan, Liwei Chen
Glycosylated Hemoglobin in Relationship to Cardiovascular Outcomes and Death in Patients with Type 2 Diabetes: A Systematic Review and Meta-Analysis
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Ziaee A, Afaghi A, Sarreshtehdari M.
Effect of low glycemic load diet on glycated hemoglobin (HbA1c) in poorly-controlled diabetes patients.
Glob J Health Sci. 2011 Dec 29;4(1):211-6.

*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.
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Daniel H, Rehner G.
Effect of metabolizable sugars on the mucosal surface pH of rat intestine.
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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
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Hodgkinson, A and Heaton FW
The effect of food ingestion on the urinary excretion of calcium and magnesium
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Holbrook JT, Smith JC Jr, Reiser S.
Dietary fructose or starch: effects on copper, zinc, iron, manganese, calcium, and magnesium balances in humans.
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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.
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Stephan RM, Miller BF.
A quantitative method for evaluating physical and chemical agents which modify production of acids in bacterial plaques on human teeth.
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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.