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Soda and Obesity

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Diet Soda is Not A Free Ride

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

Calorie Restriction Extends Lifespan

calorie restrictionCalorie restriction (CR) in animals extends longevity by a considerable margin. Both primary and secondary aging processes are decelerated by limiting foods to those that are high in nutrients and relatively low in calories. Studies on humans are only now in progress, while those in animals have been unfolding for a few years. One of the boons of CR is a lowered core body temperature, which is that at which all physiological activity is most efficient. Not only this, but also fat reduction and consequent cardiac health can defer the foibles and imperfections of old age.

Studies at Washington University (St. Louis, MO) and the U. of California at San Francisco, sponsored in part by the Calorie Restriction Society, have found that” (calorie) restriction in animals seems to be the fountain of youth…” Studies on people may or may not yield the same results, primarily because free-living humans are not accepting of the same externally imposed restrictions as are endured by the animals. Human variables that need to be addressed include alterations in cognitions, behaviors, responses to stressors, and effects on other markers of health. However, humans have shown some of the same “…adaptations that are…involved in slowing primary aging in rats and mice.” Most notable here is a reduction in the inflammatory markers known as C-reactive protein and Tumor Necrosis Factor-alpha.

Primary aging is the gradual and inevitable process of physical deterioration that occurs throughout life.  You know, the aches and pains, the slowed movements, the loss of 20-20 vision, decreased resistance to infections, impaired hearing, and the rest of the baggage.  Secondary aging results from diseases and poor health practices (read lifestyle) that include smoking, torpor, booze and obesity, all of which can contribute to diseases in the first place.

Does CR work in people?  Yes, as long as it is reasonable…and that varies from person to person.  Decreasing calorie intake by only a few hundred can make a significant difference in health and longevity by reducing body fat, lowering blood pressure and cholesterol, and avoiding degenerative diseases, such as diabetes and heart disease.  Don’t forget about lowered body temperature, where the Washington University researchers learned that life expectancy was increased in animals. (Soare, 2011)  Of course, we can’t definitely tell how this affects people because we don’t know when each is programmed to die.  It is such, however, that family history of salubrious long life can be predictive of an individual’s longevity.

You might be interested to know that a nutritional supplement demonstrates an effect that mirrors calorie restriction.  We advise that you not yet jump for joy without the realization that this needs to be approached sensibly, which means being attentive to calorie intake. You can’t go wild on doughnuts, white flour bagels, ice cream and other culinary nonsense. You see, the mechanism behind calorie restriction’s success is not completely understood, but it is presumed that a protein called sirtuin is responsible for control of the aging process, and that CR directs the activity of sirtuin. Part of the aging procedure involves cellular stress, particularly in the mitochondria, the power plants of the cell that make energy. If we can slow down oxidation by ramping up the mitochondria’s defense mechanisms and simultaneously inhibiting the attack of reactive oxygen species, then we might be able to stave off the pangs of aging.  How do we do that without restriction of calories?  What supplement is held in such high regard? Resveratrol, the red wine polyphenol!

Independent of each other, Zoltan Ungvari (2009) and Thimmappa Anekonda (2006) discovered that resveratrol may have therapeutic value in the treatment of metabolic and neuronal diseases, based at least partially on the activity of sirtuin.  What is known about resveratrol’s mechanism of action is that it encourages the sirtuin homologue SIRT1 to ply its trade as a cellular regulator, where it slows down metabolism and any stimulatory reactions to environmental toxins, thus placing an organism into a defensive state so it can survive adverse circumstances.  Tobacco smoke-induced oxidative stress even becomes minimized.

We are individuals with different needs and responses to interventions, whether dietary or medical.  You will differ in your response to calorie restriction from your twin. You will differ in your response to resveratrol, if that is the route you choose.  But it seems more than likely you will experience a strengthened immune system, heightened energy, a healthier reproductive system, increased stamina…and looser trousers.

References

Exp Gerontol. 2007 Aug;42(8):709-12. Epub 2007 Mar 31.
Caloric restriction in humans.
Holloszy JO, Fontana L.

Toxicol Pathol. 2009;37(1):47-51. Epub 2008 Dec 15.
Caloric restriction and aging: studies in mice and monkeys.
Anderson RM, Shanmuganayagam D, Weindruch R.

Aging (Albany NY). 2011 Apr;3(4):374-9.
Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans.
Soare A, Cangemi R, Omodei D, Holloszy JO, Fontana L.

Free Radic Biol Med. 2011 Apr 22. [Epub ahead of print]
The controversial links among calorie restriction, SIRT1, and resveratrol.
Hu Y, Liu J, Wang J, Liu Q.

Am J Physiol Heart Circ Physiol. 2008 Jun;294(6):H2721-35. Epub 2008 Apr 18.
Vasoprotective effects of resveratrol and SIRT1: attenuation of cigarette smoke-induced oxidative stress and proinflammatory phenotypic alterations.
Csiszar A, Labinskyy N, Podlutsky A, Kaminski PM, Wolin MS, Zhang C, Mukhopadhyay P, Pacher P, Hu F, de Cabo R, Ballabh P, Ungvari Z.

Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1876-81. Epub 2009 Sep 11.
Resveratrol attenuates mitochondrial oxidative stress in coronary arterial endothelial cells.
Ungvari Z, Labinskyy N, Mukhopadhyay P, Pinto JT, Bagi Z, Ballabh P, Zhang C, Pacher P, Csiszar A.

Brain Res Rev. 2006 Sep;52(2):316-26.
Resveratrol–a boon for treating Alzheimer’s disease?
Anekonda TS.

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

MSG and Weight Gain

No MSGThe Body Mass Index (BMI) is a measure of the relative percentages of fat and muscle mass in the human body, based on a person’s weight and height, used to assess obesity. This barometer was used by researchers to determine the effect of the food additive, monosodium glutamate (MSG), on weight over a period of time. It was learned that those persons who consume MSG regularly experience changes in the part of the brain that controls appetite, thus having an influence on energy balance and consequent weight gain.

When researcher, Ka He, and his colleagues at the University of North Carolina began to look for a relationship between monosodium glutamate and weight gain, they hypothesized that it would be a positive one.  As a design element of the study, “…overweight was defined as a body mass index ≥ 25…based on World Health Organization recommendations for Asian populations.”  With an average MSG intake of 2.2 grams a day, and a five-year follow-up, the study population demonstrated that “MSG consumption was positively, longitudinally associated with overweight development…”

The better it tastes, the more we’ll eat.  That seems logical.  Most Americans eat so fast that their brains don’t have enough time to process the information that says they’re full.  Since that lag time is about twenty minutes, we should take at least that much time to eat.  But the school cafeteria, the incessant phone calls, the pressures of the job, and other lifestyle components disallow that.  Combine any of these facets of life with food additives that enhance flavor, and start looking for a longer belt.

Leptin is a hormone that plays an important role in energy intake and expenditure, and it tells us when to stop eating…if it works the right way.  It’s made by fat cells, oddly enough, but can also come from other parts of the body, such as the bones, stomach, and liver.  It acts on parts of the brain’s hypothalamus, where it inhibits appetite. If leptin is not appropriately received and taken up by the hypothalamus, appetite fails to shut off and food intake is uncontrolled.  Where does MSG fit into this picture?  It seems to be able to induce hypothalamic lesions and ensuing leptin resistance (He, et al. 2008).  The stage is now set for weight gain.

Glutamate is the major excitatory transmitter in the brain, meaning that it makes things happen, especially in cognition, memory and learning.  It also affects brain development, cellular survival and the manufacture of synapses.  Too much glutamate, though, can raise serious concerns because its excitatory nature becomes intensified by virtue of its accumulation, allowing excess calcium to enter a nerve cell and damage it beyond repair.  This is what happens in the hypothalamus.

Glutamate, sometimes as glutamic acid, is responsible for the tantalizing flavors of poultry, some fishes, and eggs, among other foods.  Its salt, MSG, was introduced to the United States after WW II as “Accent” flavor enhancer.  It can be made by the fermentation of beets, sugar cane, or molasses.  People began to experience adverse reactions to MSG after eating Chinese food prepared with it, thereby coining the expression “Chinese Restaurant Syndrome.”  Sensitivity to monosodium glutamate may present with headaches, asthmatic symptoms, hyperactivity (especially in children), and obesity.  Frequency of such responses is low, but if it happens in your family, it’s high enough to merit attention.

We all know that the world revolves around the dollar bill and the ball point pen, the latter often employed to guarantee the former.  As long as clandestine groups can get away with something, they’ll persist.  And so it is with MSG.  It has more disguises than Artemus Gordon and Sherlock Holmes combined.  Here are a couple handfuls of MSG aliases:  glutamic acid, monopotassium glutamate, magnesium, glutamate, monoammonium glutamate, yeast extract, hydrolyzed anything, calcium or sodium caseinate, yeast nutrient, gelatin, textured protein, soy protein isolate, soyprotein concentrate, whey protein, ajinomoto.

These ingredients often contain glutamic acid:  carrageenan, bouillon, stock, maltodextrin, barley malt, protease, malt extract, soy sauce, and any protein that is fortified or fermented.  Additionally, these work with MSG to further enhance flavor:  Disodium 5’-guanylate; Disodium 5’-inositate; and Disodium 5’-ribonucleotides.  Wherever these three abide, it’s almost guaranteed that MSG is a companion.

Individual amino acids are not generally listed on the ingredients labels of food or health care products.  Binders and fillers may or may not contain MSG.  Believe it or not, MSG may also appear in cosmetics, including shampoos, soaps and hair conditioners.  If the words “hydrolyzed,” “amino acids,” or “protein” appear on the label, MSG could be in it.  Live virus vaccines may also have it.  Even though reactions to MSG are dose-dependent, you could react to a very small amount all of a sudden, when you never did so before.  Yes, MSG is natural, but so is arsenic.  To most of us, MSG does not cause problems.  MSG might make you want to eat more.  It might affect the state of your hypothalamus.  On the other hand, it’s not likely to make you wash your hair more often.  Is it?

Referneces

Am J Clin Nutr. 2011 Jun;93(6):1328-36. Epub 2011 Apr 6.
Consumption of monosodium glutamate in relation to incidence of overweight in Chinese adults: China Health and Nutrition Survey (CHNS).
He K, Du S, Xun P, Sharma S, Wang H, Zhai F, Popkin B
Departments of Nutrition and Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC.

Acta Physiol Hung. 2011 Jun;98(2):177-88.
Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring.
Afifi MM, Abbas AM.
Department of Biochemistry, Zagazig University, Zagazig, Egypt.
Abstract

Am J Clin Nutr. 2011 Jun;93(6):1328-36. Epub 2011 Apr 6.
Consumption of monosodium glutamate in relation to incidence of overweight in Chinese adults: China Health and Nutrition Survey (CHNS).
He K, Du S, Xun P, Sharma S, Wang H, Zhai F, Popkin B.

Nutrition. 2005 Jun;21(6):749-55.
Monosodium glutamate in standard and high-fiber diets: metabolic syndrome and oxidative stress in rats.
Diniz YS, Faine LA, Galhardi CM, Rodrigues HG, Ebaid GX, Burneiko RC, Cicogna AC, Novelli EL.
Department of Clinical Cardiology, Faculty of Medicine, University of São Paulo State, Botucatu, Brazil.

Mol Pharmacol. 1989 Jul;36(1):106-12.
Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death.
Manev H, Favaron M, Guidotti A, Costa E.
Fidia-Georgetown Institute for the Neurosciences, Georgetown 4niversity, Washington, DC 20007.

Cell Calcium. 2003 Feb;33(2):69-81.
Calcium influx constitutes the ionic basis for the maintenance of glutamate-induced extended neuronal depolarization associated with hippocampal neuronal death.
Limbrick DD Jr, Sombati S, DeLorenzo RJ.

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

Sleep and Weight

sleeping-manAhh, yes, that state of rest for body and soul.  It’s the time when will power and consciousness are suspended, and when body functions are mostly in neutral. Most sleep scientists agree that sleep has considerable value as a recuperative and adaptive function in humans.   Because it takes work for the body to maintain a constant temperature in an environment with temperature ranges, the eight-hour respite affords a chance to reconstitute cells and tissues.  While the body slows down, the brain, on the other hand, revs up its metabolic activity during the REM phase of sleep to get ready for the input of the next day.  Complicated stuff, for sure.

The negative consequences of too little sleep can rattle your chain with fanfare.  Falling asleep at the wheel is scary.  Falling off the pew in church is embarrassing.  Dozing during a business call gets expensive.  And being cranky all day gets you no favors.  But guess what.  Lack of sleep can make you fat, too.  Try to figure that out, since nobody eats when they’re asleep.  Do they?

Just because body functions slow down, it doesn’t mean they stop.  Hormones and other body chemicals are still at work.  Two of those, ghrelin and leptin, are responsible for turning appetite on and off, respectively.  Sleep deprivation seems to crank up the ghrelin and stimulate appetite.  When that happens, you crave more food while losing the sensitivity—or even the common sense—to know when to stop eating.  This problem could well be a circuitous matter:  does fatness cause lack of sleep or is it the other way around, or do they share a common factor?  Hmm.  Michael Breus, sleep researcher extraordinaire, addresses this conundrum in his recently published, “The Sleep Doctor’s Diet Plan:  Lose Weight Through Better Sleep” (Rodale, 2011).  And Dr. Marie-Pierre St-Onge, researcher at the New York Obesity Nutrition Research Center at St. Luke’s-Roosevelt Hospital, adds her expertise by pointing out that sleep-deprived people burn the same number of calories during the day as sound sleepers, but, she adds, eat about three hundred more calories a day.  Since there are 3500 calories in a pound, a person will add that pound to his repertoire in a little less than two weeks (St-Onge, 2011)

The interest in the association of lousy sleep to weight problems is international.  Even in Japan, there’s a St. Luke’s Hospital.  Here, doctors checked out more than 21,000 middle-aged guys’ sleep habits and compared them to individual body mass index, finding that the variability of sleep duration is related to weight gain.  And these participants thought that 6 hours’ sleep was enough (Kobayashi, 2012).  Guess they were wrong.  A year earlier, the same docs at the same hospital compared ~7-hour sleepers to ≤5-hour sleepers, and found weight gain and obesity in the deprived group.  It was interesting to note that there was little difference between the 7-hour and 8-hour subjects (Kobayashi, 2011).  The kicker in the 2011 study is that the investigators also found metabolic syndrome to be related to poor sleep (Kobayashi, Takahashi, et al 2011).

In experimentally-induced sleep loss, insulin sensitivity decreases without compensation in beta-cell function, resulting in impaired glucose tolerance and increased risk for diabetes.  Sleep loss down-regulates leptin function, lowers satiety, and up-regulates the appetite enhancing ghrelin.  Increased appetite = increased food intake=weight gain  (Morselli, 2010) (Chamorro, 2011).  Sleep fragmentation—waking every couple hours—causes daytime sleepiness (Mavanji, 2012). We need a study to show that?   In the valiant effort to revitalize, we turn to sugary foods in the hope they’ll provide bursts of energy lasting long enough to get us through the rest of the day.  Empty calories here.  And the energy high is soon followed by an almost audible crash.

With all the studies being performed in this area, you’d think somebody would be working on a remedy.  Maybe we already have one, but don’t know it.  Have you spoken to your doctor about poor sleep?  If you’d rather do it alone, consider a few simple steps.  Go to bed at the same time every night.  The body needs to know when to go to sleep.  Exercise a little bit every day.  That’ll reduce anxiety, one of the biggest reasons for poor sleep.  But don’t do it just before bed.  Do it a few hours beforehand.  If you’re a worrier, keep a journal.  That helps to identify things that aren’t likely to happen, anyway, so you don’t have to worry about them in the first place.  Try not to delay what needs to be done to prepare for the next day.  You’ll only add to the worry list.  Coffee will try to keep you awake for several hours after the last cup in the afternoon, so don’t drink any after, say, 2 or 3 o’clock.  Alcohol will not improve sleep.  It might make you fall asleep faster, but almost certainly will interrupt restorative sleep.  In the AM, drink water before anything else, and get fifteen minutes of sunlight to help reset your circadian clock.

Although the link between sleep loss and weight gain is convincing, the exact science behind the connection is to be determined.  You can always stay up all night and try to catch the leather fairy cutting your belt a little shorter.  Or you can try an alternative sleep aid, such as valerian, melatonin, or a hops sachet under your pillow.  But check with a healthcare professional before you embark.

References

Chamorro RA, Durán SA, Reyes SC, Ponce R, Algarín CR, Peirano PD.
[Sleep deprivation as a risk factor for obesity].  [Article in Spanish]
Rev Med Chil. 2011 Jul;139(7):932-40.

Knutson KL.
Does inadequate sleep play a role in vulnerability to obesity?
Am J Hum Biol. 2012 Jan 24. doi: 10.1002/ajhb.22219. [Epub ahead of print]

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Relation between metabolic syndrome and sleep duration in Japan: a large scale cross-sectional study.
Intern Med. 2011;50(2):103-7. Epub 2011 Jan 15.

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Association between weight gain, obesity, and sleep duration: a large-scale 3-year cohort study.
Sleep Breath. 2011 Sep 3. [Epub ahead of print]

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Association between weight gain, obesity, and sleep duration: a large-scale 3-year cohort study.
Sleep Breath. 2011 Sep 3. [Epub ahead of print]

Kobayashi D, Takahashi O, Shimbo T, Okubo T, Arioka H, Fukui T.
High sleep duration variability is an independent risk factor for weight gain.
Sleep Breath. 2012 Feb 22. [Epub ahead of print]

Mavanji V, Billington CJ, Kotz CM, Teske JA.
Sleep and obesity: a focus on animal models.
Neurosci Biobehav Rev. 2012 Mar;36(3):1015-29. Epub 2012 Jan 16.

Morselli L, Leproult R, Balbo M, Spiegel K
Role of sleep duration in the regulation of glucose metabolism and appetite.
Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):687-702.

Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.
Insufficient sleep undermines dietary efforts to reduce adiposity.
Ann Intern Med. 2010 Oct 5;153(7):435-41.

Patel SR, Malhotra A, White DP, Gottlieb DJ, Hu FB.
Association between reduced sleep and weight gain in women.
Am J Epidemiol. 2006 Nov 15;164(10):947-54. Epub 2006 Aug 16.

St-Onge MP, Roberts AL, Chen J, Kelleman M, O’Keeffe M, RoyChoudhury A, Jones PJ.
Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals.
Am J Clin Nutr. 2011 Aug;94(2):410-6.

St-Onge MP, McReynolds A, Trivedi ZB, Roberts AL, Sy M, Hirsch J.
Sleep restriction leads to increased activation of brain regions sensitive to food stimuli.
Am J Clin Nutr. 2012 Apr;95(4):818-24.

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

Fat Blocking Soda?

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

Reduce Inflammation through Weight Loss

acute-pain-in-a-woman-kneeSome of us know inflammation too well. When getting out of bed in the morning becomes an auditory event in your joints that rivals a flamenco dancer’s castanets, you know inflammation. What you may not know, or at least not realize, is that your weight has something to do with it. For many of us, the seeds of inflammation were planted years ago. Our genes, body weight, diet, lifestyle and fitness determine our states of wellness and non-wellness, some of which we cannot sense. Silent inflammation is probably worse than that we can feel from getting cut or hit by a baseball. If it hurts or is uncomfortable, we’ll take care of it right away. If it’s not noticeable, it can smolder for years, eventually exploding into a chronic illness.

Inflammation is the response of tissue to injury or insult, occasionally caused by an invading pathogen. Characteristics, which you can sense, include increased blood flow to the injured area, elevated temperature, redness, swelling and pain. Inflammatory responses to what should have been a harmless agent include allergies and autoimmune diseases, states where the response is either out of proportion to the threat it faces or is directed against an inappropriate target, such as self. In these cases, the response is worse than anything the agent itself could have generated, and is often insensate. The cascade of cellular and molecular signals that accompany inflammation can perpetuate it and make it chronic, in which case monocytes and macrophages take over the management. This may sound cool, but the chemicals they create inside the tissues wreak havoc. Macrophages begin to swallow everything that appears derelict, including senescent cells and whatever is deemed a pathogen, whether it truly is or not.

At some point in this chronology, chemical mediators are released, including things like Interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-a) and prostaglandins that keep the ball rolling…on and on. When the body tries to control all this nefarious activity it replaces damaged tissue with replacement cells of the same type, but occasionally fails and results in diseased states, such as asthma, rheumatoid arthritis, tendonitis, celiac and inflammatory bowel diseases.

Inflammation is recognized as causal to several chronic diseases and all-cause mortality, and is prevalent among those who have a body mass index above 30.0.  Biomarkers of inflammation are used to examine the relationship of inflammation to chronicity, with C-reactive protein (CRP), IL-6, TNF-a, and IL-8 as indicators. CRP probably is the first one your doctor will interpret, since it’s a prime marker of inflammation. It just doesn’t pinpoint the location. CRP is a native protein made by the liver in response to factors released by fat cells. In acute inflammation, such as from an infection, levels can rise in less than six hours and be hundreds of times higher than normal, which is lower than 10 mg per liter. With a severe bacterial infection, it can reach 200 or more. The absolutely perfect reading is 1.0. Levels above 2.4 are supposed to be associated with increased risk of cardiovascular events, but that’s debatable because the studies were done with people who had unstable angina (Pepys, 2003).

Human adipose tissue expresses and releases the pro-inflammatory artifacts, inducing low-grade systemic inflammation in people with too much body fat. Pediatricians in the Netherlands looked at overweight children in their country and saw higher levels of CRP than in normal-weight children (Visser, 2001), accompanied by higher white cell counts. In 2007, the Archives of Internal Medicine published an analysis of more than thirty separate studies, concluding that weight loss is a major factor in the reduction of CRP, adding that a loss of one kilogram (2.2 lbs) equates to a 0.13 mg/L drop in CRP (Selvin, 2007).

Many parents think that their kids will outgrow the chubby stage. Sometimes, yes; often, no. We now see 400-pound 20-year-olds who were obese at age eight, whose parents ignored admonitions to address the foreboded tragedy at the early age. That collection of fat that hangs over the belt, sometimes reaching the thighs, is called a panniculus, and is more than just a dormant spare tire. It secretes adipokines, or chemical signals, to other parts of the body, increasing risk of serious disease through disrupted homeostasis (Rosenow, 2010). If this describes someone you know, eventually you’ll likely see diabetes, heart disease, and maybe even some form of cancer (Ibid).

There are plenty of overweight seniors, some of whom achieve that senior designation at age 40, others above 70. Just by virtue of their age, they’re more likely to report joint pain, but obesity at any age is a predictor of low-grade chronic inflammatory state.  Whether by diet or exercise, or both, weight loss is extremely vital to maintaining one’s health. In comparisons, the low-carb folks lost more weight than the low-fat. Think about this.  The knee pain in the 50-year-old guy is so bad he can’t walk behind his lawnmower. The problem is that he’s carrying 375 pounds on a frame designed to carry 150-180, and his femur is squeezing the cushions at the tibia. Yes, it’s distinctly possible that thyroid issues are causative of the extra weight. There may be other factors that include lack of sleep, too much stress, certain medications, uncontrolled cortisol (kinda rare), and menopause in women. Some of these can be managed and can be worked out with the family physician and maybe a visit to a dietitian. However, looking more closely at his eating habits, we see carbohydrates as the main source of gustatory input, with beneficial fats and lean protein given the back seat. Self-inflicted obesity has no excuse. Inflammatory biomarkers can be attenuated with even a small reduction in weight (Miller, 2008) (You, 2006).  Now, get this. The physical movement required to mow the lawn might be just enough to reduce inflammation, despite the immediate discomfort, which will eventually taper off. (Ford, 2002) (Miller, 2008).

Obesity is a problem of epidemic proportions. Certain people are perceived as anathema, bête noir, pariah, and may pay for self-destructive behavior. If cigarette cessation clears the lungs, could weight reduction clear the blood? Yep. Dietary interventions will help both, but sticking a finger into the dike doesn’t quite do it.

References

Clément K, Viguerie N, Poitou C, Carette C, Pelloux V, Curat CA, Sicard A, Rome S, Benis A, Zucker JD, Vidal H, Laville M, Barsh GS, Basdevant A, Stich V, Cancello R, Langin D.
Weight loss regulates inflammation-related genes in white adipose tissue of obese subjects.
FASEB J. 2004 Nov;18(14):1657-69.

Mary Elizabeth Dallas
Losing Weight May Lower Cardiac Risks
Study finds both low-carb and low-fat diets help overweight people reduce inflammation
NIH, 5 Nov, 2012
MedlinePlus Trusted Health Information for You A service of the U.S. National Library of Medicine
From the National Institutes of HealthNational Institutes of Health
http://www.nlm.nih.gov/medlineplus/news/fullstory_131011.html

Esposito K, Pontillo A, Di Palo C, Giugliano G, Masella M, Marfella R, Giugliano D.
Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial.
JAMA. 2003 Apr 9;289(14):1799-804.

Ford, Earl S.
Does Exercise Reduce Inflammation? Physical Activity and C-Reactive Protein Among U.S. Adults
Epidemiology:. September 2002 – Volume 13 – Issue 5 – pp 561-568

Gilbert CA, Slingerland JM.
Cytokines, Obesity, and Cancer: New Insights on Mechanisms Linking Obesity to Cancer Risk and Progression.
Annu Rev Med. 2012 Oct 26. [Epub ahead of print]

Kawasaki N, Asada R, Saito A, Kanemoto S, Imaizumi K.
Obesity-induced endoplasmic reticulum stress causes chronic inflammation in adipose tissue.
Sci Rep. 2012;2:799. Epub 2012 Nov 12.

Stephen P Messier, Claudine Legault, Shannon Mihalko, Gary D Miller, Richard F Loeser, Paul DeVita, Mary Lyles, Felix Eckstein, David J Hunter, Jeff D Williamson and Barbara J Nicklas
The Intensive Diet and Exercise for Arthritis (IDEA) trial: design and rationale
BMC Musculoskeletal Disorders 2009, 10:93

Miller GD, Nicklas BJ, Loeser RF.
Inflammatory biomarkers and physical function in older, obese adults with knee pain and self-reported osteoarthritis after intensive weight-loss therapy.
J Am Geriatr Soc. 2008 Apr;56(4):644-51. Epub 2008 Feb 28.

Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS, Klein S, Coppack SW.
Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo.
J Clin Endocrinol Metab. 1997 Dec;82(12):4196-200.
Navarro SL, Brasky TM, Schwarz Y, Song X, Wang CY, Kristal AR, Kratz M, White E, Lampe JW.
Reliability of serum biomarkers of inflammation from repeated measures in healthy individuals.
Cancer Epidemiol Biomarkers Prev. 2012 Jul;21(7):1167-70. Epub 2012 May 7.

Nicklas BJ, Ambrosius W, Messier SP, Miller GD, Penninx BW, Loeser RF, Palla S, Bleecker E, Pahor M.
Diet-induced weight loss, exercise, and chronic inflammation in older, obese adults: a randomized controlled clinical trial.
Am J Clin Nutr. 2004 Apr;79(4):544-51.

Pepys MB, Hirschfield GM.
C-reactive protein: a critical update.
J Clin Invest. 2003 Jun;111(12):1805-12.

Anja Rosenow, Tabiwang N. Arrey, Freek G. Bouwman, Jean-Paul Noben, Martin Wabitsch, Edwin C.M. Mariman, Michael Karas, and Johan Renes
Identification of Novel Human Adipocyte Secreted Proteins by Using SGBS Cells
J. Proteome Res., 2010, 9 (10), pp 5389–5401

Roth CL, Kratz M, Ralston MM, Reinehr T.
Changes in adipose-derived inflammatory cytokines and chemokines after successful lifestyle intervention in obese children.
Metabolism. 2011 Apr;60(4):445-52. Epub 2010 May 24.

Elizabeth Selvin, PhD, MPH; Nina P. Paynter, MHS; Thomas P. Erlinger, MD, MPH
The Effect of Weight Loss on C-Reactive ProteinA Systematic Review
Arch Intern Med. 2007;167(1):31-39

Tam CS, Clément K, Baur LA, Tordjman J.
Obesity and low-grade inflammation: a paediatric perspective.
Obes Rev. 2010 Feb;11(2):118-26. Epub 2009 Oct 21.

André Tchernof, PhD; Amy Nolan, RD; Cynthia K. Sites, MD; Philip A. Ades, MD; Eric T. Poehlman, PhD
Weight Loss Reduces C-Reactive Protein Levels in Obese Postmenopausal Women
Circulation. 2002; 105: 564-569

You T, Nicklas BJ
Chronic inflammation: role of adipose tissue and modulation by weight loss.
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Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB.
Elevated C-reactive protein levels in overweight and obese adults.
JAMA. 1999 Dec 8;282(22):2131-5.

Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB.
Low-grade systemic inflammation in overweight children.
Pediatrics. 2001 Jan;107(1):E13.

Viviane Zorzanelli Rocha, M.D., Eduardo J. Folco, PhD, Galina Sukhova, PhD, Koichi Shimizu, M.D., Israel Gotsman, M.D., Ashley H. Vernon, M.D., and Peter Libby, M.D.
Interferon-gamma, a Th1 Cytokine, Regulates Fat Inflammation A Role for Adaptive Immunity in Obesity
Circ Res. 2008 August 29; 103(5): 467–476.

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

Stress and Childhood Obesity

weigh-inBeing a kid doesn’t necessarily mean having a carefree life, yet that’s how most adults view childhood. Because kids don’t have jobs, bills to pay, and children to raise what could they possibly have to worry about? More than we realize. Even the very young among us have stressors, slight though they may be. Stress is a function of the demands we face and our ability to handle them. Often it comes from outside sources. You know—family, job, friends, school, and expectations. Sometimes stress comes from inside, related to what we think we should do compared to what we actually do, say or think.

Today, kids have to learn scores of times more information than their parents did at the same age. That we can blame on an electronic era. And they have to learn these things in the same allotted time. Preschoolers get stressed when their moms leave them at daycare. As they get older, kids are pressured by academics and social position. After all, they need to fit in. Their lives get so hectic they seldom have time for themselves, for creative play, or even for relaxation. They are overscheduled with activities that would tax even the adult mind. Disturbing images on TV, news of wars, terrorism and natural disasters, and concerns for personal and family safety add to the burden. Illness, death and divorce don’t help.

All stressors are not created equal, and all people do not respond to stress the same way. Children often learn to handle stress from their parents. Sometimes that’s good; sometimes not. The idea that, “If it doesn’t kill me, it’ll make me stronger,” doesn’t apply to youngsters who’ve not yet developed a coping mechanism. What does this have to do with obesity, a childhood plague that’s more than doubled in the last few decades?  Lots.

A person’s reaction to stress will likely invoke the fight-or-flight (-or freeze) response as the primary means of dealing with a novel situation perceived as threatening. Children who overreact to stress will manufacture more cortisol than the body can dump, and that’s where the problem begins—emotional eating (Michels, 2012). Cortisol is a steroid hormone made by the adrenal glands, released in response to stress. Its main job is to increase blood sugar to power the fight-flight machinery. Cortisol counteracts insulin and contributes to insulin resistance (Goran, 2010) by lowering glucose transport to the cell membrane. Small increases in cortisol can provide a quick burst of energy in an emergency. At the same time it can heighten memory, briefly but powerfully enhance immunity and lower sensitivity to pain. But the return to normal is needed lest the body idle at high rpm’s. With our high-stress culture that has become the norm…chronic stress. That eventually induces impairment of cognitive function, suppresses thyroid activity, throws blood sugar out of whack, menaces bone density, elevates blood pressure, and actually lowers immune responses. And it increases deposition of abdominal fat, setting the stage for metabolic syndrome, depressed affect (Endocrine Society, 2009) (Dockray, 2009) and cardiovascular entanglement, even at a young age.

Children’s biological response to stressors was examined recently by researchers from Penn State and Johns Hopkins Universities.  A group of pre-teens was assigned public speaking and mathematical tasks with little preparation time allowed for either. Cortisol content of their saliva was measured before and after. Following the assignment, the children were offered an array of snack foods regardless of their hunger status. The amount of calories they consumed varied, but those with the highest body mass indexes, who also had the highest cortisol levels, consumed more calories, even in the absence of hunger, than did those with lower cortisol levels. The outcome suggests that children with poor response to stress are at risk for becoming overweight or obese (Francis, 2013). Other factors that contribute to eating in the absence of hunger include poverty, living in a violent environment and food insecurity.

The determination of childhood obesity needs to be made on an individual basis, not from a chart developed by an insurance company that focuses on only one ethnicity or population. Anthropometric measurements and family history need to be included in an evaluation. Pathologies need to be ruled out, genetics must be considered, and psychosocial factors scrutinized. The comorbidities of obesity are varied and many, and their prophylaxis calls for early intervention, some of which transcends diet. Overweight children face the same health conditions as their parents, with hypertension, discordant lipid panels, abnormal glucose levels, and elevated inflammation markers among them. Lifestyle changes, where parents are the managers, may be all that is needed. This may include dietary interventions that eliminate simple carbohydrates, especially sugars and refined starches common to the foods kids like the most. These foods will spike insulin, which will spike cortisol, which will encourage eating, which will add pounds. Avoiding pharmaceutical anorectic agents is strongly encouraged.

Mental stress is associated with emotional eating, which typically ignores healthy dietary patterns (Michels, 2013). Cortisol levels peak in the morning, but can remain elevated in stressful surroundings. Admittedly, some of those surroundings are beyond a parent’s control, so coping mechanisms are helpful. Without being a helicopter parent, it’s possible to create a comfortable atmosphere for a child, even when he is away from you. Teaching coping skills by example starts early. Believe it or not, kids watch, listen and emulate. There are three-year-olds with vocabularies that would make you wince. If kids can learn to be tense and confrontational, they can also learn to relax and to take things in stride.

Limiting cortisol manufacture might be as easy as increasing magnesium in thediet. How?  Vegetables. Essential fatty acids, music therapy and phospholipids,and even vitamin C and tea have been shown to curtail cortisol release (Rains,2011) (Arent, 2010) (Peters, 2001).

References

Adam TC, Hasson RE, Ventura EE, Toledo-Corral C, Le KA, Mahurkar S, Lane CJ, Weigensberg MJ, Goran MI.
Cortisol is negatively associated with insulin sensitivity in overweight Latino youth.
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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.

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

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

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

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

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

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

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

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

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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.