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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.

Medium-Chain Triglycerides Effect Weight Loss

less-weightMedium-chain triglycerides (MCT) are a unique kind of dietary fat that lend a wide range of positive health benefits, weight loss among them. MCT’s have a fatty acid chain length that varies between six and twelve carbon atoms, which is only one characteristic that distinguishes them from the more familiar long-chain fatty acids, such as the highly-celebrated fish oil. MCT’s are transported through the blood by the portal system, which bypasses the usual route of digestion and sends them directly to the liver.

Medium-chain triglycerides do not require the modifications of long-chain and very-long-chain fatty acids.  Neither do they require bile salts for digestion.  These qualities enable them to be less susceptible to hormone-sensitive lipase and to deposition into adipose (fat) tissue storage.  A study from England’s Oxford Brookes University in 2010 announced that, because of their particular character, “MCT’s have been researched for both benefits to exercise performance and health.”  In the former application, MCT’s may be “a means to maximizing an athlete’s ability to maintain their glycogen stores so they can be more competitive.”  From the health angle, these substances “increase fat oxidation and energy expenditure as well as reduce food intake and beneficially alter body composition.”  (Clegg. 2010)

If you watch the lose-weight ads on TV, you might be driven to buy one of the untested, unproven, and maybe even unsafe products that promise the physique of champions.  Read the small print to learn that exercise and diet are part of the program, and your dreams of Roman god-hood (or goddess) are shattered.  Back to the chips and dip, right?  There might be something that’s been tested, and found to be safe and effective for at least a little drop in weight.

Because MCT’s don’t need energy for absorption, utilization or storage, they’ve been used to treat malabsorption conditions.  But weight management has evoked more interest.  The milks from humans, dogs, and guinea pigs contain mostly long-chain fats.  Those from goats, cows, and sheep are primarily short-chain.  Horse milk has lots of medium-chain fatty acids.  Data suggest that the milk of all species depends on a partial resynthesis of pre-formed glycerides. (Breckenridge. 1967)  (Since horses run faster than cows, their milk is hard to bottle, and because they have only two spigots, it takes longer to get it.)

Decades ago, MCT’s had been studied for body fat management in obese persons without diabetes, but more recent work has focused on those with Type 2 diabetes.  The findings showed that a diet containing MCT’s at 18 grams a day (about 2/3 ounce) brought about a reduction in body weight and waist circumference, a decrease in insulin resistance, and a drop in serum cholesterol concentration.  (Han. 2007)  Compared to the subjects ingesting long-chain fatty acids, the results are significant.  The MCT users also enjoyed increased dietary satiety, meaning that they felt full sooner, so they ate less.  Still another welcome benefit was realized by a cohort in 2009, when Chinese investigators noted a significant decline in serum triglycerides and LDL-cholesterol, both markers for cardiovascular complications, in those ingesting 25-30 grams (there are 28 grams in an ounce) of MCT’s a day. (Zhang. 2009).  (Xue. 2009)

The fast rate of oxidation of medium-chain fatty acids leads to greater energy expenditure—almost without doing any hard work.  It’s impressive that such can be the case, especially where weight gain is reduced and the size of body fat deposits diminishes.  Note that fat cells are not normally lost once they appear; they merely shrink in size.  They are, however, prepared to expand again at the drop of a hat.  (Xue. 2009)

Since the 1960’s MCT’s have been advocated for use in weight control.  Back then the research entailed other factors as well, including  the balance of energy intake, the nature of the diet, the ratio of MCT to LCT (long-chain triglycerides), and duration of the protocol.  Nonetheless, the presence of MCT’s as part of the regimen made a difference.  Although the exact mechanism hasn’t been fingered, MCT’s are able to increase energy outgo, hasten satiety at the table, and facilitate weight control when consumed as a replacement for fats containing LCT’s.  ( St-Onge. 2002)  Increased heat production, known as thermogenesis, is one of the activities by which MCT’s burn fat. (Baba. 1982)

Palm oil and coconut oil are major food sources of medium-chain fats.  The fact that these are saturated fats means little because all sat fats are not created equal, displaying differing cholesterolemic effects.  Therefore, when you see them listed on an ingredient label, have no fear.  The less weight you need to lose, the faster you will see results, so it’ll pay to get started now. (St-Onge. 2003)

References

MAIN ABSTRACT
Clegg ME.
Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance.
Int J Food Sci Nutr. 2010 Nov;61(7):653-79.

SUPPORTING ABSTRACTS
W. C. Breckenridge and A. Kuksis
Molecular weight distributions of milk fat triglycerides from seven species
The Journal of Lipid Research. September 1967 (8): 473-478.

Han JR, Deng B, Sun J, Chen CG, Corkey BE, Kirkland JL, Ma J, Guo W.
Effects of dietary medium-chain triglyceride on weight loss and insulin sensitivity in a group of moderately overweight free-living type 2 diabetic Chinese subjects.
Metabolism. 2007 Jul;56(7):985-91.

Zhang YH, Liu YH, Zheng ZX, Wang J, Zhang Y, Zhang RX, Yu XM, Jing HJ, Xue CY, Wu J.
[Medium- and long-chain fatty acid triacylglycerol reduce body fat and serum triglyceride in overweight and hypertriglyceridemic subjects].    [Article in Chinese]
Zhonghua Yu Fang Yi Xue Za Zhi. 2009 Sep;43(9):765-71.

Xue C, Liu Y, Wang J, Zhang R, Zhang Y, Zhang J, Zhang Y, Zheng Z, Yu X, Jing H, Nosaka N, Arai C, Kasai M, Aoyama T, Wu J.
Consumption of medium- and long-chain triacylglycerols decreases body fat and blood triglyceride in Chinese hypertriglyceridemic subjects.
Eur J Clin Nutr. 2009 Jul;63(7):879-86.

Marie-Pierre St-Onge and Peter J. H. Jones
Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity1
J. Nutr. March 1, 2002; 132(3): 329-332

Baba N, Bracco EF, Hashim SA.
Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride
Am J Clin Nutr. 1982 Apr;35(4):678-82.

St-Onge MP, Jones PJ.
Greater rise in fat oxidation with medium-chain triglyceride consumption relative to long-chain triglyceride is associated with lower initial body weight and greater loss of subcutaneous adipose tissue.
Int J Obes Relat Metab Disord. 2003 Dec;27(12):1565-71.

Clegg ME.
Int J Food Sci Nutr. 2010 Nov;61(7):653-79.
Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance

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

USDA vs Healthy Eating

food-pyramid-on-plateThe food pyramids and plates conjured up by the USDA haven’t quite lived up to their expectations. In its attempts to get it right, this august, though somewhat misguided, body has delivered several versions, each one anticipated to be new and improved. So far, none has panned out.

The most visible sign of U.S. nutrition policy is the Food Pyramid, or lately, the Food Plate.  Recognizing that dietary quality plays a role in health and the prevention of chronic disease, the USDA issued a Pyramid revision in 2005 to address the shortcomings of the previous one.  Walter Willett, chair of Harvard’s nutrition department, comments, “…the previous pyramid was in substantial discordance with current scientific evidence.”   If such a guideline is out of harmony with what research concludes to be so, then a critical eye needs to be cast at the base of its formulation.  Willett adds that, “My Pyramid strays from much of the evidence generated through years of research and, in our opinion, fails to provide the public with clear information about healthy food choices.”  (Chiuve. 2007)

The older Food Pyramid had so many carbohydrates at its base that you could have made wallpaper paste for all your friends.  The bread, cereal, rice and pasta food group didn’t mention any difference between refined and whole grains.  Not that it makes much difference, since they’ll spike your insulin, anyhow, with high glycemic factors and initiate metabolic and hyperlipidemic aberrations, including insulin resistance, a precursor to Type 2 diabetes.  The newer 2005 Food Pyramid, with vertical lines instead of horizontal groups, is not only hard to fathom, but also vague.  However, it does mention whole grains.  In June, 2011, with lots of hoopla, the USDA replaced the much-maligned-but-deserving-of-it My Pyramid with a simpler icon, the fruit and vegetable-festooned My Plate.

It needs to be realized that the Department of Agriculture is not in the business of promoting health.  Its job is to promote farmers and foods.  Therefore, your hunt for sage dietary counsel has to travel another direction.  What’s good about the new My Plate is that the flawed My Pyramid has been dismantled.  What’s not so good about My Plate is its misplay in providing all the nutrition advice you need to choose the healthiest diet.  Picky?  Why not?  Who’s paying the freight?

The sections of My Plate don’t give us all the dope we need to make good food choices.  For one thing, it forgets to tell the shopper that whole grains are better for health, since refined grains can contribute to weight gain and elevated triglycerides.
(Hudgins. 2000)  (Parks.  2001)  It also fails to say that all proteins are not created equal.  Some are better for us than others because they have less saturated fat and, like fish, more polyunsaturated essential fats.  Processed meats are harmful to health.  That includes the ubiquitous hot dog.  How about beans and nuts as protein sources?  Good choices.  A hot dog or hamburger on a white-bread bun with fries and a shake can be part of the My Plate cuisine…despite the fact that high red meat and processed meat intake can increase risk for disease.  (Pan. 2011)  (Bernstein. 2010)

My Plate doesn’t distinguish between potatoes and other vegetables.  Potatoes are loaded with rapidly digested starch, having the same effect on blood sugar as refined grains and sweets.  (Hu. 2009)  Sadly, My Plate is silent about fats—the healthy fats, the essential fats.  The good fats can keep cholesterol under control…and the rest of the lipid panel, for that matter.  (Bester. 2010)

The topic of dairy can polarize a community.  Even though it contains a foreign protein, is a poor distributor of calcium, and is allowed to carry a percentage of bovine somatic cells, dairy has its following.  In fact, there is little solid evidence that high dairy intake prevents osteoporosis, but to the contrary, that the countries consuming the most dairy have the highest rates.  (Feskanich. 1997)  (Cumming. 1994)  My Plate recommends dairy at every meal.  It includes nothing about sugary drinks and fiberless juices.

What to do?  For starters, Dr. Willett relates, “If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks, we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases.”  His colleague, Dr. Frank Hu, admits that, “The country’s big low-fat message backfired.  The overemphasis on reducing fat caused the consumption of carbohydrates and sugars to soar.  The shift may be linked to the biggest health problems in America today.”  (LA Times. 2010)  For a better food plate, check out Harvard School of Public Health, at http://www.hsph.harvard.edu/nutritionsource/  Then swap carbohydrate and fat percentages in your daily intake.

References

Chiuve SE, Willett WC. The 2005
Food Guide Pyramid: an opportunity lost?
Nat Clin Pract Cardiovasc Med. 2007 Nov;4(11):610-20.

Hudgins LC.
Effect of high-carbohydrate feeding on triglyceride and saturated fatty acid synthesis.
Proc Soc Exp Biol Med. 2000 Dec;225(3):178-83.

Parks EJ.
Effect of dietary carbohydrate on triglyceride metabolism in humans.
J Nutr. 2001 Oct;131(10):2772S-2774S.

Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Willett WC, Hu FB.
Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis
Am J Clin Nutr. 2011 Aug 10.

Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC.
Major dietary protein sources and risk of coronary heart disease in women.
Circulation. 2010 Aug 31;122(9):876-83.

Hu Y, Block G, Sternfeld B, Sowers M.
Dietary glycemic load, glycemic index, and associated factors in a multiethnic cohort of midlife women.
J Am Coll Nutr. 2009 Dec;28(6):636-47.

Bester D, Esterhuyse AJ, Truter EJ, van Rooyen J.
Cardiovascular effects of edible oils: a comparison between four popular edible oils.
Nutr Res Rev. 2010 Dec;23(2):334-48.

Feskanich D, Willett WC, Stampfer MJ, Colditz GA.
Milk, dietary calcium, and bone fractures in women: a 12-year prospective study.
Am J Public Health. 1997 Jun;87(6):992-7.

Cumming RG, Klineberg RJ.
Case-control study of risk factors for hip fractures in the elderly.
Am J Epidemiol. 1994 Mar 1;139(5):493-503.

Harvard School of Public Health
The Nutrition Source
http://www.hsph.harvard.edu/nutritionsource/

Marni Jameson
A reversal on carbs: Fat was once the devil. Now more nutritionists are pointing accusingly at sugar and refined grains.
Los Angeles Times.  December 20, 2010
http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220

Dina Fitzsimons
Why Milk Won’t Prevent Osteoporosis-And The Protein Myth-
https://www.msu.edu/~corcora5/food/vegan/osteo.html

Harvard School of Public Health
The Nutrition Source
Calcium and Milk: What’s Best for Your Bones and Health?
http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/calcium-full-story/

Belin RJ, Greenland P, Allison M, Martin L, et al
Diet quality and the risk of cardiovascular disease: the Women’s Health Initiative (WHI).
Am J Clin Nutr. 2011 Jul;94(1):49-57.

Am J Clin Nutr. 2011 Jul;94(1):247-53. Epub 2011 May 25.
Alternative Healthy Eating Index and mortality over 18 y of follow-up: results from the Whitehall II cohort.
Akbaraly TN, Ferrie JE, Berr C, Brunner EJ, Head J, Marmot MG, et al

Willett WC, McCullough ML.
Dietary pattern analysis for the evaluation of dietary guidelines.
Asia Pac J Clin Nutr. 2008;17 Suppl 1:75-8.

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

Shift Work and Your Health

overworked-workerRotating shifts causes difficulties because it works in opposition to the body’s normal circadian rhythms, the most influential being the sleep/wake cycle.  There is also the matter of social isolation that comes from working when everybody else is asleep, and vice-versa.  One of the complications of changing shifts is the incidence of gastrointestinal upset.  Shift workers have a notoriously high occurrence of ulcers, based partly on disruption of sleep patterns and partly on the activation of H. pylori infection if it is at all present and waiting for the opportunity to strike.  (Pietroiusti, 2006)  (Segawa, 1987)  Chronic fatigue, untimely sleepiness, and even failure to fall asleep are some other physical interruptions caused by shift work.  Among the worst social perturbations is divorce, an element that hits some jobs more than others, law enforcement being a prime example.

Canada’s Institute for Work and Health delved into this topic and found that night work is associated with an increase in breast cancer among women who work rotating shifts for long durations.  (IWH, 2010)  The etiology of breast cancer is mostly uncertain, but about one fourth its incidences can be attributed to genetic factors.  At least a little blame has been put on light at night and its effect on melatonin, the hormone produced by the pineal gland that communicates information about light to different parts of the body in order to regulate biologic rhythms.  When the eye’s pupil detects changes in brightness—night—it sends the sleep message to the brain by way of melatonin.  When this activity gets stymied, melatonin is not able to exert its anti-cancer character, and the risk of breast cancer is elevated after a prolonged time. (Schernhammer, 2001)   (Hansen, 2001)   Melatonin is a popular sleep aid, especially for those experiencing jet lag, but few have associated it with anti-cancer function.  (Knower, 2012)  An interesting realization in this circumstance is the body’s inability to manufacture vitamin D from exposure to natural light, raising the question of the appropriateness of supplementation.  (Shao, 2012)  Among researchers’ quests is the determination of the actual concentrations of vitamin D in women who have survived breast cancer and whether or not insufficiency is prevalent among sufferers, survivors, and healthy controls.  (Trukova, 2012)  (Blask, 2009)

Little is known about sleep taken at night, and even less about sleep taken during the day, when years of natural law dictate otherwise.  Nobody really knows how much sleep is necessary for optimal health.  But there is evidence that long sleepers and very short sleepers have increased mortality.  (Ferrie, 2007)  The first part of sleep lasts about fifteen minutes, and is labeled as Stage 1.  If you are awakened from this stage, you may even deny having been asleep.  Stage 2 occupies about half of sleep time, yet is the least understood part.  Being deprived of this stage results in almost total sleep loss because this is the part from which other stages develop.  This, by the way, is the stage affected by medications and sleep aids.  Stages 3 and 4 are combined into the slow-wave-sleep stage, differing only by the number of delta waves measureable by an EEG.  Contrasted to Stage 2, this is the one common to most persons, and is the one compensated after long periods of sleep deprivation.  This is the one needed for body repair and the activity of growth hormone(s).  Rapid eye movement (REM) sleep is the best known stage and throughout its duration the body is virtually paralyzed and loses its ability to regulate heat.  Dreams, which are deemed necessary to psychological well-being, occur here.  REM, dominating the late stages of sleep episodes, is strongly influenced by circadian rhythm.   Daytime sleep is normally one or two hours shorter than night time sleep.  REM, therefore, is shortened.  This adds to the alertness problems of the night shift.

A modern concern about shift work is increased risk of type 2 diabetes and the metabolic syndrome, compounded by the possible elevation of cardiovascular jeopardy.  This affects women more than men, but the combination of obesity, high triglycerides, and low HDL cholesterol is common to both.  (Karlsson, 2001)  Years of rotating night shift work are associated with weight gain that comes from failed attempts to eat right and from limited time for exercise.  And to think that all this is precipitated by disturbed circadian periodicity.  Eating on the run and mindless snacking are more common among night workers than their daytime counterparts.  Even if day and night workers had the same major CVD factors, the night workers admit to increased job strain and greater at-work physical exertion, both of which contribute to the altered parameters that incite metabolic syndrome.  (Esquirol, 2009)  In Japan, where the work ethic is ubiquitously strong, different work schedules have been associated with a rise in the incidence of diabetes.  (Morikawa, 2005)  (Suwazono, 2006)  Over the long term, changes are evident not only in daily glucose levels, but also in glycosylated hemoglobin (HbA1c), which measures glucose over an extended time.  (Suwazono, 2009)

Workplace cafeterias commonly close at night.  Workers are then left to their own culinary devices, and that often translates to unhealthy eating habits by virtue of convenience and time constraints.  A healthy work force is a boon to productivity and accident prevention, areas in which companies can demonstrate an interest that supersedes complaining about the opposite.  If a company is reactive, it can get you to the First-Aid station or to the HR person for failure to perform.  By being proactive, it can prevent both while saving money on bandages and the expense of training a replacement.

If there is a best-case scenario for shift work, scheduling a rotation that lasts at least six weeks seems to work by affording enough time to adapt one’s circadian dance to the situation.  There are those who prefer steady nights, but that breed is rare.  If we think adapting to factory work schedules is tough, we should look at those who work in the emergency room.  At least some of us have a scapegoat for tight trousers.

References

Blask DE.
Melatonin, sleep disturbance and cancer risk.
Sleep Med Rev. 2009 Aug;13(4):257-64. Epub 2008 Dec 17.

Costa G.
Shift work and breast cancer. 
G Ital Med Lav Ergon. 2010 Oct-Dec;32(4):454-7.

Esquirol Y, Bongard V, Mabile L, Jonnier B, Soulat JM, Perret B.
Shift work and metabolic syndrome: respective impacts of job strain, physical activity, and dietary rhythms.
Chronobiol Int. 2009 Apr;26(3):544-59.

Ferrie JE, Shipley MJ, Cappuccio FP, Brunner E, Miller MA, Kumari M, Marmot MG.
A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort.
Sleep. 2007 Dec;30(12):1659-66.

Ha M, Park J.
Shiftwork and metabolic risk factors of cardiovascular disease.
J Occup Health. 2005 Mar;47(2):89-95.

Hansen J.
Light at night, shiftwork, and breast cancer risk.
J Natl Cancer Inst. 2001 Oct 17;93(20):1513-5.

Institute for Work and Health (IWH)
Scientific Symposium, Toronto, 12 April, 2010
Scientific Symposium on the Health Effects of Shift Work
http://www.iwh.on.ca/shift-work-symposium

Karlsson B, Knutsson A, Lindahl B.
Is there an association between shift work and having a metabolic syndrome? Results from a population based study of 27,485 people.
Occup Environ Med. 2001 Nov;58(11):747-52.

Knower KC, To SQ, Takagi K, Miki Y, Sasano H, Simpson ER, Clyne CD.
Melatonin suppresses aromatase expression and activity in breast cancer associated fibroblasts.
Breast Cancer Res Treat. 2012 Jan 12.

Kroenke CH, Spiegelman D, Manson J, Schernhammer ES, Colditz GA, Kawachi I.
Work characteristics and incidence of type 2 diabetes in women.
Am J Epidemiol. 2007 Jan 15;165(2):175-83.

Morikawa Y, Nakagawa H, Miura K, Soyama Y, Ishizaki M, Kido T, Naruse Y, Suwazono Y, Nogawa K
Shift work and the risk of diabetes mellitus among Japanese male factory workers.
Scand J Work Environ Health. 2005 Jun;31(3):179-83.

Paul A. Schulte, PhD, Gregory R. Wagner, MD, Aleck Ostry, PhD, et al
Work, Obesity, and Occupational Safety and Health
American Journal of Public Health. Mar 2007; 97:3, 428-436

Pietroiusti A, Forlini A, Magrini A, Galante A, Coppeta L, Gemma G, Romeo E, Bergamaschi A.
Shift work increases the frequency of duodenal ulcer in H pylori infected workers.
Occup Environ Med. 2006 Nov;63(11):773-5.

Prasai MJ, George JT, Scott EM.
Molecular clocks, type 2 diabetes and cardiovascular disease.
Diab Vasc Dis Res. 2008 Jun;5(2):89-95.

Schernhammer ES, Laden F, Speizer FE, Willett WC, Hunter DJ, Kawachi I, Colditz GA.
Rotating night shifts and risk of breast cancer in women participating in the nurses’ health study.
J Natl Cancer Inst. 2001 Oct 17;93(20):1563-8.

Scott AJ.
Shift work and health.
Prim Care. 2000 Dec;27(4):1057-79.

Segawa K, Nakazawa S, Tsukamoto Y, Kurita Y, Goto H, Fukui A, Takano K.
Peptic ulcer is prevalent among shift workers.
Dig Dis Sci. 1987 May;32(5):449-53.

Shao T, Klein P, Grossbard ML.
Vitamin D and Breast Cancer.
Oncologist. 2012 Jan 10.

Suwazono Y, Sakata K, Okubo Y, Harada H, Oishi M, Kobayashi E, Uetani M, Kido T, Nogawa K.
Long-term longitudinal study on the relationship between alternating shift work and the onset of diabetes mellitus in male Japanese workers.
J Occup Environ Med. 2006 May;48(5):455-61.

Suwazono Y, Dochi M, Oishi M, Tanaka K, Kobayashi E, Sakata K.
Shiftwork and impaired glucose metabolism: a 14-year cohort study on 7104 male workers.
Chronobiol Int. 2009 Jul;26(5):926-41.

Trukova KP, Grutsch J, Lammersfeld C, Liepa G.
Prevalence of Vitamin D Insufficiency Among Breast Cancer Survivors.
Nutr Clin Pract. 2012 Jan 6.

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

BHT In My Cereal?

cereal-bagCan there be too much of a good thing? Drinking too much water can dilute the electrolytes in the body and short circuit the wiring.  It’s called water intoxication, and can lead to death.  Though eating too much candy might not cause a person to die, the resultant stomach distress might bring on the wish to expire early.  If there can be too much of a good thing, can there also be too little of a bad thing, meaning how much of a toxin can I consume before the symptoms show up or I keel over? Such is the case with some food additives. If enough people pronounce a falsehood as fact, does that make it true merely by the sheer number of proponents? Let’s talk about BHT and you decide whether it’s good or bad.

Butylated Hydroxytoluene is a horrendous sounding name.  Its presence lets us to keep a box of cereal in the cabinet for weeks at a time, and allows the product to withstand its protracted journey from maker to kitchen.  Its absence, on the other hand, yields a noxious aroma akin to a week-old dishrag that really needs a bath.  The culprit?  Rancid fats.  But what does BHT do to people?

BHT and its relative, BHA, have been used extensively as antioxidants for decades.  BHT was patented in 1947.  Since then it has become the most prevalent and approved antioxidant in the world.  The FDA, disbelieved by many consumers, approved BHT as an additive to foods and food packaging in 1954.  BHT is a phenol derivative that slows the rate of oxidation.  Oxygen prefers BHT to the fats in our foods.  The public gets upset when it learns that a material used to make non-foods appears in their victuals.  Yes, it is true that BHT is used in the manufacture of tires, some plastics and diesel fuel.   But it does what it is supposed to do without adverse effects.  It’s even been certified Kosher by the Union of Orthodox Jewish Congregations of America, and also certified Halal by the Islamic Food Nutrition Council of America.

Toxicology studies that added BHT to animal feed found that adverse effects were dose-dependent.  Amounts of BHT in excess of 526 mg/kg/day resulted in pleural and peritoneal hemorrhage in laboratory rats. (Takahashi.  1978) A human consumes in the neighborhood of 0.1 mg/kg/day of BHT.  Research shows that 500 times this amount yields no injurious effects.  (Branen.  1975)  This study added that 7 ounces of BHT per pound of body weight would result in pathological, enzyme, and lipid alterations that may be causative of certain cancers.  (Ibid.)

Some scientific research deals with topics and events that are way out there, seeming to have no bearing on real health issues.  (Gee, if I swallow a handful of number eight woodscrews and drink a cup of WD-40, will the screws still rust?)  There’s a similarly inane study in which lab animals were given more than four ounces of BHT per pound of body weight a day for three days, combined with a healthy dose of E.coli bacteria to learn of adverse effects on the liver.  What do you think happened?  The conclusion was that there is risk of liver damage with high-dose BHT in the presence of pathogenic bacteria.  (Engin. 2011)  This makes you wonder whose dime is in the phone booth.

The World Health Organization (WHO) asked its expert committee on food additives to evaluate the intake of BHT in ten participating countries in 1999.  After identifying certain foods as major contributors to overall intake, the committee agreed that 0.3 mg/kg of body weight a day is tolerable. (WHO, Geneva. 1999)  It is interesting to note that more BHT is allowable in the United States than in the other countries.  This might be explained by the fact that packaging materials are also treated with BHT, and that these plastics and waxed papers may carry as much as 7.8 mg/kg.  (Xiong. 2011)

That BHT has antioxidant properties was acknowledged by Korean researchers when they determined that, according to the National Health and Nutrition Survey, first conducted in 1971 and regularly afterward, one hundred thirty-three foods in twelve categories actually held significantly less BHT than the maximum limits. (Suh. 2005)  For most of these foods, less than 0.008 mg/kg was consumed.  Not to be outdone, Dutch scientists sought a connection between BHT intake and gastric cancers, studying a group of more than 120 thousand individuals, starting in 1986.  This longitudinal study examined BHT foods that included mayonnaise, cooking fats and oils, creamy salad dressings, and dried soups.  Via food frequency questionnaire, it was ascertained that the average intake of BHT was 351 micrograms a day total, not per pound or kilogram.  No association with gastric cancer was observed.  Oddly, an inverse association was found.  (Botterweck. 2000)

Around the time Christopher Columbus was floating in the Atlantic and Caribbean, a Swiss physician named Paracelsus, the first guy to call zinc, zinc, who is also known as the father of toxicology, was attributed with the dictum, “The dose makes the poison.”  His intended meaning was that a substance considered toxic may be harmless in small doses and that, conversely, an ordinarily harmless substance may be toxic in large doses—like water.  Such may be the case with BHT.

BHT was lauded as being protective against atherosclerosis in work performed in Sweden in the early 1990’s, where BHT was added to a 1% cholesterol diet in rabbits, whose digestive prowess parallels humans’.  Although lipid profiles were elevated, atherosclerotic involvement was considerably lower in the BHT rabbits than in those not receiving the substance in the same diet.  These investigators concluded that the antioxidant character of BHT prevented unwelcomed cardiac influences, although modulation of monocyte adhesion may be a factor.  (Björkhem. 1991)  Further study along this line, using a similar dietary protocol, discovered that LDL from other BHT-fed rabbits was less sensitive to oxidation than LDL from rabbits whose diets lacked BHT.
(Freyschuss. 2001)  It is accepted that oxidized LDL is the cause of ischemic heart disease.

What about cancer?  Pathologists at New York Medical College assessed BHT as a food additive in meta-analyses that inferred no cancer hazard at levels commonly used in food processing and manufacturing.  (Williams. 1999)  Laboratory animals that were purposely exposed to carcinogenic substances, notably aflatoxins that cause liver cancer, were spared from disease when administered BHT at doses of 1.5 mg/kg total over a period of twenty weeks (about 25 micrograms/kg, 3 x a week).  (Williams. 1986)  Other substances used to model liver carcinogenesis were almost completely neutralized in the presence of BHT, as reported in a study performed more than three decades ago.  (Ulland. 1973)

The dermatological use of BHT, as in cosmetics and other topically administered products, tells a somewhat different story in laboratory animals, since BHT is absorbed through the skin.  Stomach acid and digestive fluids appear to attenuate any pathogenic activity of the chemical.  Although the mechanism has not been completely explained, acute doses of BHT, as much as 1.0 g/kg, have caused some renal and hepatic damage in lab rats.  That is not to say that the same thing will happen to a human, since people are not likely to have exposure to such concentrated amounts.  (Lanigan. 2002)

For the time being, it looks like your cereal is off the hook.  There is one lingering question, though.  If natural vitamin E, as d-alpha-tocopherol, can do the same thing as BHT, why isn’t it being used?  It must be the money.

References

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    O. Takahashi, K. Hiraga
    Dose-response study of hemorrhagic death by dietary butylated hydroxytoluene (BHT) in male rats
    Toxicology and Applied Pharmacology.  Volume 43, Issue 2, February 1978, Pages 399-406

    A.L. Branen
    Toxicology and biochemistry of Butylated Hydroxyanisole and  Butylated Hydroxytoluene
    J Am Oil Chem Soc. 1975, Feb.; 52(2): 59-63

    Engin AB, Bukan N, Kurukahvecioglu O, Memis L, Engin A.
    Effect of butylated hydroxytoluene (E321) pretreatment versus l-arginine on liver injury after sub-lethal dose of endotoxin administration.
    Environ Toxicol Pharmacol. 2011 Nov;32(3):457-64. Epub 2011 Sep 10.

    WORLD HEALTH ORGANIZATION
    INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

    World Health Organization, Geneva, 1999
    IPCS - International Programme on Chemical Safety
    EVALUATION OF NATIONAL INTAKE ASSESSMENTS OF
     BUTYLATED HYDROXYTOLUENE (BHT)
    http://www.inchem.org/documents/jecfa/jecmono/v042je24.htm 
      Xiong Z, Wang L, Li N, Yu Y, Jia X
    Determination of antioxidant residues in polymer food package using gas chromatography.
    Se Pu. 2011 Mar;29(3):273-6.

    Suh HJ, Chung MS, Cho YH, Kim JW, Kim DH, Han KW, Kim CJ.
    Estimated daily intakes of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT) and tert-butyl hydroquinone (TBHQ) antioxidants in Korea.
    Food Addit Contam. 2005 Dec;22(12):1176-88

    Botterweck AA, Verhagen H, Goldbohm RA, Kleinjans J, van den Brandt PA.
    Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study.
    Food Chem Toxicol. 2000 Jul;38(7):599-605.

    Björkhem I, Henriksson-Freyschuss A, Breuer O, Diczfalusy U, Berglund L, Henriksson P.
    The antioxidant butylated hydroxytoluene protects against atherosclerosis.
    Arterioscler Thromb. 1991 Jan-Feb;11(1):15-22.

    Freyschuss A, Al-Schurbaji A, Björkhem I, Babiker A, Diczfalusy U, Berglund L, Henriksson P.
    On the anti-atherogenic effect of the antioxidant BHT in cholesterol-fed rabbits: inverse relation between serum triglycerides and atheromatous lesions.
    Biochim Biophys Acta. 2001 Dec 30;1534(2-3):129-38.

    G.M Williams, M.J Iatropoulos, J Whysner
    Safety Assessment of Butylated Hydroxyanisole and Butylated Hydroxytoluene as Antioxidant Food Additives
    Food and Chemical Toxicology.  Vol 37, Iss 9-10, Sep-Oct 1999, Pages 1027-1038

    Williams GM, Tanaka T, Maeura Y.
    Dose-related inhibition of aflatoxin B1 induced hepatocarcinogenesis by the phenolic antioxidants, butylated hydroxyanisole and butylated hydroxytoluene.
    Carcinogenesis. 1986 Jul;7(7):1043-50.

    B.M. Ulland, J.H. Weisburger†, R.S. Yamamoto, Elizabeth K. Weisburger
    Antioxidants and carcinogenesis: butylated hydroxytoluene, but not diphenyl-p-phenylenediamine, inhibits cancer induction by N-2-fluorenylacetamide and by N-hydroxy-N-2-fluorenylacetamide in rats*
    Food and Cosmetics Toxicology.  Volume 11, Issue 2, 1973, Pages 199-207

    Lanigan RS, Yamarik TA.
    Int J Toxicol. 2002;21 Suppl 2:19-94.
    Final report on the safety assessment of BHT(1).

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