I Wish I Were Far From the Madding Crowd

May 5, 2010

PepsiCo CEO: “If all consumers exercised … obesity wouldn’t exist”

Pepsi CEO Indra Nooyi tells Fortune Magazine that obesity is all our fault

FORTUNE: You’ve said that Pepsi should be part of the solution, not the cause, of obesity. How are you and PepsiCo planning to go about that?

Nooyi: If all consumers exercised, did what they had to do, the problem of obesity wouldn’t exist….

(Thanks to Fooducate for finding that one!)

So there you have it.  It’s all our fault! (Since that’s the case, maybe we should just stop buying PepsiCo products.)

Based on the above, I would be willing to bet that Nooyi would disagree with the following article’s conclusions.  I would also be willing to bet that most major food and beverage companies spend a lot of money not just on advertising, but on marketing research, too.

Neurophysiological Pathways to Obesity: Below Awareness and Beyond Individual Control, Deborah A. Cohen, Diabetes July 2008 vol. 57 no. 7 1768-1773

doi: 10.2337/db08-0163

http://diabetes.diabetesjournals.org/content/57/7/1768.full

I think Cohen makes some very good arguments, but I would quibble with her on two points.

One, she says “the suppositions that a change in genetics and/or metabolism is responsible for the increase in obesity over the past three decades are implausible due to lack of evidence of mutations over this short period of time….” But if changes in metabolism are being caused epigenetically by exposure to chemicals in the environment, the rate of such changes could be much more accelerated than the rate of mutations one would expect from random mutations to people’s DNA.

Two, she says that arguments that it is totally the individuals’ fault that they are overweight or obese imply that 30 years ago people had more self-control.  Well, frankly, maybe they did!  That should not be discounted as a possibility.  But I would tend to go with the argument that most of the problem is caused by eating more and not being active enough.

Having said that,  I think her arguments about why people are eating more are quite valid and that food and beverage manufacturers are probably not going to make eating less any easier.

For the sake of argument let’s say that food and beverage manufacturers actually do want you to eat and drink less (well, at least as long as you keep eating and drinking their products).

So which companies are going to willingly cede market share to other companies?  Umm … none?  So what does that mean?  It means that they’re going to continue marketing their products as aggressively as they have in the past.  (It’s like a tragedy of the common food court!)  They’re just going to try to use different techniques to persuade people to but their products.  “Healthy. Organic. Natural.”  Most importantly, “Much better for you than that other company’s products….”

Or perhaps they figure that if their products are going to make us overweight or obese, then they’ll just sell us drugs to deal with metabolic syndrome and other health problems later.  (Huh, I wonder if any of the big food and beverage companies own any pharmaceutical firms.  Or have invested in them?)

Anyway, in the article Cohen identifies what she says are 10 neurophysiological pathways that can lead people to make food choices subconsciously or, in some cases, automatically.

These pathways include reflexive and uncontrollable neurohormonal responses to food images, cues, and smells; mirror neurons that cause people to imitate the eating behavior of others without awareness; and limited cognitive capacity to make informed decisions about food.

Given that people have limited ability to shape the food environment individually and no ability to control automatic responses to food-related cues that are unconsciously perceived, it is incumbent upon society as a whole to regulate the food environment, including the number and types of food-related cues, portion sizes, food availability, and food advertising.

There is a growing consensus that the global obesity epidemic is the result of increasing urbanization and globalization, coupled with significant changes in the food environment. Obesity was initially highest in developed countries, but developing countries are quickly catching up.

The dominant thinking about obesity is that prevention and treatment is a matter of self-control and individuals making wiser food choices.  However, if this is really the case, then it implies that 30 years ago, before obesity increased, the population had more self-control and made wiser choices, and since then, our collective capacity for self-control must have diminished. It also suggests that people who live in other countries with lower rates of obesity have more self-control than Americans.

Just as the suppositions that a change in genetics and/or metabolism is responsible for the increase in obesity over the past three decades are implausible due to lack of evidence of mutations over this short period of time, the idea that the levels of personal responsibility, knowledge, intelligence, or moral character of a majority of the population are rapidly declining is also not a credible explanation of this phenomenon. It is unlikely that the nature of people has changed so dramatically. What has changed dramatically, however, is the environment in which we now live.

The availability and affordability of food has increased, due to a combination of technological advances in food preservation and packaging, increased food production and crop yields, and decreases in food costs relative to total income. In many parts of the world, food is available to all socioeconomic classes 24 h/day, 7 days a week. Moreover, while food advertising is not new, greater sophistication in marketing—including the development of branding, expanded use of vending machines and other mechanisms for self-service, technologies like eye movement tracking, and the application of social psychology — are all widely used to increase impulse buying and sales of highly processed foods. The techniques are increasingly more sophisticated, customized, and targeted to increase their efficacy. (Emphasis added.)

Could the increases in food availability, food salience, and the sophistication of modern marketing explain the obesity epidemic? If so, there must be neurophysiological pathways within humans that facilitate consumption of readily available food. Further, these mechanisms should affect all population groups similarly, regardless of income or level of education.

Although individuals with a higher level of education have lower rates, the prevalence of overweight and obesity is increasing in well-educated individuals at roughly the same rate as in less educated individuals. It is not unusual to see doctors, nurses, and dietitians possessing expert knowledge about nutrition and weight control who are themselves overweight or obese. Thus, it is likely that the mechanisms affecting food intake are not a matter of conscious decision making based on knowledge but are operating below the level of individual awareness and beyond individual control.

This article will review the interaction between the food environment and human neurophysiology to provide some initial evidence that, to a large extent, obesity is the consequence of automatic and largely uncontrollable responses to an environment with excessive food availability and aggressive and unrelenting cues that cause people to eat too much. Ten possible neurophysiological pathways are proposed that, in conjunction with unprecedented increases in food availability and food marketing, might explain how and why people consume more calories than they expend, especially without their full awareness or control of their behavior. The mechanisms include 1) physiological reflexive response to food and images of food; 2) inborn preferences for sugar and fat; 3) hardwired survival strategies, including foraging behaviors in response to food variety and novelty, also without awareness; 4) inability to judge volume or calories either through visual perception or internal signals of satiety; 5) natural tendency to conserve energy; 6) mirror neurons that lead people to mimic the behavior of other humans, often without awareness; 7) automatic stereotype activation; 8) conditioned responses that result in desire for food when confronted with food-related cues; 9) automatic responses to priming; and 10) limited cognitive capacity and self-regulatory control. In addition, speculations on specific mechanisms that deserve further study and direction for obesity control are discussed.

April 18, 2010

Sugar is sugar … or not?

If you’ve followed any of the discussion about high fructose corn syrup (HFCS) vs. sucrose, you’ve probably heard representatives of the soft drink industry and HFCS refiners repeatedly say that fructose is no different than sucrose and that they’re metabolized the same (which, according to more and more research, is debatable).  I’ll get to that a little further on.

How much sugar we’re consuming

Amber Waves article “Behind the Data: Estimating Consumption of Caloric Sweeteners.” (April 2003)

Amount of HFCS and refined sugar delivered to food and beverage manufacturers in 2001

Intake levels represent the difference between total deliveries of calorie sweeteners for food and beverage use and estimated losses
Graphics from http://www.ers.usda.gov/AmberWaves/April03/Indicators/behinddata.htm

Make note of that 31.1 teaspoons per day figure for 2001.  (Daily intake in teaspoons = average annual intake in pounds / 365 days per year x 16 ounces per pound x 28.3495 grams per ounce / 4.2 grams per teaspoon.)

Think about the last item in that formula.  If the label on a box of cereal says 9 g of sugars, that means that a single serving contains 2 tsps of sugar.  A 12 oz. soda containing 39 g of sugars contains more than NINE teaspoons of sugar.  You get the idea.

According to Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005 (see references), for 2005 it was down to 30 teaspoons per day.

What does this tell us?

Several points, one, representatives of the Corn Refiners Association and beverage manufacturers are right when they say that whether it’s fructose or sucrose doesn’t really matter.  If you’re consuming almost 4 times the amount of added sugars you should be, you are going to have problems!

Two, sucrose contained in beverages begins to undergo hydrolysis once it’s bottled and separates into its component parts (that is, fructose and glucose).  So in many cases when you’re drinking a sugar-sweetened soda you’re not drinking sucrose in solution, but sucrose, fructose, and glucose.  If enough time goes by most of the sucrose turns into free fructose and glucose.

A number of studies have shown that fructose is metabolized differently than glucose, but other studies seem to indicate that’s not as much of a concern, except possibly in two cases: one, when the ratio of fructose to glucose consumption is high, or in cases of high consumption of calories.  I would say that we have a combination of those, a relatively high ratio of fructose to glucose consumption (look at the relative amounts of HFCS to refined sugars used by beverage manufacturers!) together with consuming too many calories from sugar.  (And remember, that’s just the average amount.  Some people are consuming even larger amounts of sugar.)

Background on high fructose syrups

I recently came across a very interesting article, coauthored by John S. White, who is, or at least has been, a consultant to the Corn Refiners Association.

“Manufacturing, composition, and applications of fructose.”  L. Mark Hanover and John S. White.  American Journal of Clinical Nutrition, 1993, v.58(suppl.), 724S-732S.
http://www.ajcn.org/cgi/content/abstract/58/5/724S

The article describes the manufacturing and refining process of HFCS (or, as the authors call it, HFS), the composition of various grades of HFCS (as well as crystalline fructose and crystalline fructose syrup), functional properties and uses, and regulatory status.

What I found so fascinating about this particular article though, were these bits of information scattered throughout it.  According to the authors , HFS-42 (that is, HFCS that is 42% fructose) was the “first generation syrup of commerce.”  (p.726S)

They go on to note that :

Japanese and US manufacturers were producing HFS containing 55% fructose by the late 1970s.  HFS-55 was adopted by the carbonated-beverage industry and became the predominant sweetener in colas by late 1984. (p.726S)

On p. 727S, a table showing the typical composition of the various grades of fructose (ranging from 42% all the way up to 80% and 95%).

  • HFS-42 is 42% fructose, 53% dextrose (i.e. glucose), and 5% oligosaccharides
  • HFS-55 is 55% fructose, 42% glucose, and 3% oligosaccharides
  • HFS-80 is 80% fructose, 18% glucose, and 2% oligosaccharides
  • HFS-95 is 95% fructose, 4% glucose, and 1% oligosaccharides

One of the minor differences between HFS-80 and HFS-95 is that they, unlike the other two, contain less sulfated ash and no sulfur dioxide.  (Okay, the HFS-42 and -55 contain only 2 parts per million.)

The crystalline fructose and crystalline fructose syrup are both 99.5% or greater fructose.

What is interesting is that the authors note, p. 731S, that HFS-55 was being used in colas by late 1984, but that in 1988 the FDA had “proposed to recognize the long history of safety for fructose and reaffirm the GRAS status of HFS as a direct human food ingredient.” (FDA, 1992, 21 CFR 182.1866)  GRAS = “Generally Recognized As Safe” (for particular uses of a substance), CFR = Code of Federal Regulations

They go on to note: “The petition is specific for HFS-42, but may include HFS-55 on review of its additional processing steps.”

I’m not a lawyer, but to me that sounds like HFS-55 had not actually been approved for use as a direct human food ingredient at the time that cola manufacturers were starting to use it.  (I guess they must have just done that after the fact.)

HFS-55 vs. HFS-42

“The carbonated beverage industry is the largest user of HFS-42 and -55.” (p. 729S)  HFS-42 is primarily used in non-colas and HFS-55 in many colas, though colas can also be made using more HFS-42.  (See the graphic above about the use of sugar vs. HFCS by food vs. beverage manufacturers.)

In 1993 more than than 90% of energy-containing carbonated beverages produced in the U.S. were sweetened with HFS.

If I understand Hannover and White correctly, before 1984 most colas apparently were sweetened with HFS-42 and after 1984 with HFS-55.  In other words, the HFCS had approximately a 13% increase in the amount of fructose in it after the switch.

More importantly, the ratio of fructose to glucose changed from 42:53 to 55:42.  Why is that important?

Fructose malabsorption

Too much fructose in the diet can cause irritable bowel syndrome and other gastrointestinal problems.  However, studies have found that the problems are reduced when fructose is consumed with glucose.  (A certain percentage of the population is more prone to this, but it doesn’t seem to be an issue for most people.)

This is where you run into the problems of fructose metabolic products related to metabolic syndrome.   (The results of some studies also suggested that fructose malabsorption and metabolism problems were more likely to be associated with copper deficiency.)

Is HFCS the biggest problem?

I was going to say that HFCS is not the innocent player some portray it to be, then I realized that’s not really accurate.  The use of HFCS is not in and of itself the problem; the problem is food and beverage manufacturers putting it in almost every food and beverage they can.  It’s cheaper than refined sugar.  And most fast food places and restaurants reportedly make a higher profit margin off of soft drinks.  Once HFCS was introduced soft drink ingredients became so inexpensive that a lot of places started offering free refills.  I’m sure someone has brought that up before, but perhaps free refills are one of the main contributing factors to the increase in obesity (!?).   When people had to pay for a second glass of soda, they drank less.  Sorry, I don’t have a citation for that, but that seems obvious.  (Okay, I had to check.  I did a search on Google Scholar on +”obesity epidemic” +”free refills” and got 21 hits.   Google Scholar searches the scientific literature and books, as opposed to the entire Web.)

One example (with excerpt containing search terms):

Fructose, insulin resistance, and metabolic dyslipidemia

H Basciano, L Federico, K Adeli – Nutrition & Metabolism, 2005 – biomedcentral.com
in humans and animals, but the emphasis on fat reductions has had no significant benefits relative to the obesity epidemic. bombarded by huge million-dollar advertising campaigns for soft drinks, offered extra-extra-large serving sizes with free refills.

Apparently this is known as “portion distortion.”

Put that together with chronic overconsumption of sugar (regardless of whether they’re fructose or sucrose), unbalanced diets (deficiencies in vitamin D?), and not as much exercise as we should be getting.

Then throw in genetics, add a good dose of epigenetics in the form of gene-environment interactions, and you have all the conditions for development of metabolic syndrome and an obesity epidemic.

More on this in another post.

References

Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005, by Hodan Farah Wells and Jean C. Buzby, Economic Information Bulletin No. (EIB-33) 27 pp, March 2008, http://www.ers.usda.gov/Publications/EIB33/

April 5, 2010

Busyness and fast food

How timely, given my recent post on busyness (which this nicely ties together with fast food).

A paper, “You Are How You Eat: Fast Food and Impatience,” to be published in Psychological Science., discusses how fast food (and even symbols of fast food) can cause increased impatience.  Okay, I don’t know if I buy that, but if the literature they cite is accurate, that could help explain Kabat-Zinn’s observations about how we feel more rushed today even though we have more “time-saving” devices at our disposal.

Zhong and DeVoe, researchers at the University of Toronto, note:

From the selection of ingredients to preparation of food and to consuming the end products, the goal of fast food is to save time. Fast food allows people to fill their stomach as quickly as possible and move on to other things. It represents a culture that emphasizes time efficiency and immediate gratification.

Based on recent advancements in the behavioral priming literature, we suggest that exposure to fast food concepts can automatically induce time-saving behaviors.

They note that the effects of that are probably mixed.

Although fast food has certainly contributed to a culture of time efficiency, the exposure to fast food might have also promoted haste and impatience.

They point out that it’s impossible to know whether fast food in part caused the value for time efficiency in our culture or is merely a consequence of it—but, according to the press release, “it’s clear from their findings that exposure to fast food reinforces an emphasis on impatience and instant gratification.”

And while they say that everyone is affected by this to some degree, I can see how especially with respect to eating it could (has?) become a vicious cycle.  You’re too busy too cook, so you grab some fast food.  Which is self-reinforcing so that after a while you’re too impatient to make your own meals.  (And that’s even truer when what you’re eating lights up the reward centers in your brain.)

And thus, Sandra Boynton can write songs like “BusyBusyBusy” that describe all too well our haste and impatience.)

———-

Originally seen in Nutrition Updates from Stone Hearth Newsletters: Exposure to fast food, and its symbols, can make us impatient: study

The update was originally posted on EurekAlert as a press release: Rotman paper finds exposure to fast food can make us impatient

April 3, 2010

Obesity, HFCS, and fatty liver disease in children (as well as increased heart disease risk)

I personally am very interested in this topic because just over three years ago I had gone in to see my doctor because of abdominal pain.  My triglycerides and LDL were high.  He thought it might be my gallbladder so I went in for an ultrasound, which revealed that I had a fatty liver.

Fatty liver disease has not been considered a children’s disease, so it’s disturbing to read that children and adolescents are developing it, especially since there are usually few symptoms until the disease has progressed to a more advanced stage of steatohepatitis (aka hepatosteatosis) and scarring has already occurred.

According to the American Heart Association, more than 6 million children in the United States are affected.

High Fructose Corn Syrup Linked to Liver Scarring (HealthDay, March 19, 2010)

Reports on a study, “Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease,” which found that increased consumption of HFCS led to increased fibrosis (scarring) in patients suffering from NAFLD.

Fatty Liver Disease May Raise Heart Disease Risk in Overweight, Obese Kids (American Heart Association, April 3, 2010)

A fatty liver disease that is not well-known in overweight and obese children may be a precursor of cardiovascular disease, researchers reported in Circulation: Journal of the American Heart Association.

The overweight children with NAFLD had significant cardiovascular risk including higher levels of fasting glucose, insulin, total cholesterol, low-density lipoprotein (LDL, “bad” cholesterol), triglycerides and higher systolic and diastolic blood pressure than the control group.

NAFLD is the most common cause of liver disease in children and is associated with metabolic syndrome, a clustering of risk factors for the development of cardiovascular disease and type 2 diabetes. NAFLD is characterized by the presence of oily droplets of triglycerides in liver cells. More than 6 million children in the United States are affected.

NAFLD in overweight children is strongly associated with metabolic syndrome. The association is independent of both body mass index and insulin sensitivity.

Fatty liver disease often has no outward symptoms, which contributes to it going undetected. Although some children will have symptoms such as abdominal pain or fatigue, the majority remain symptom-free until the disease is in very advanced stages.

American Heart Association Scientific Statement on Metabolic Syndrome in Children and Adolescents (2009)

Since 2003, substantial new information has emerged in children on the clustering of obesity, insulin resistance, inflammation, and other risk factors and their collective role in conveying heightened risk for cardiovascular disease and type 2 diabetes. A constellation of these interrelated cardiovascular risk factors in adults has come to be known as the metabolic syndrome.

The scientific statement covers the following topics:

Selected References

Steinberger J, Daniels SR. Obesity, insulin resistance, diabetes and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Circulation. 2003; 107: 1448–1453.[Free Full Text]

Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement [published corrections appear in Circulation. 2005;112:e297 and 2005;112:e298]. Circulation. 2005; 112: 2735–2752.[Free Full Text]

Non-alcoholic fatty liver disease (NAFLD)

Once considered an illness of adults over 40, more and more children are being diagnosed with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH).  NAFLD can be a precursor to NASH, which can progress to cirrhosis.

According to Children’s Memorial Hospital in 2005 an estimated 1.6 million children were affected with fatty liver disease

But the American Heart Association now says that 6 million children have NAFLD (see above).

Note: The Children’s Memorial Hospital’s NASH program is a member of the NASH clinical research network.  In 2005, the NASH clinical research network launched a trial for treatment of liver disease in children. The NASH CRN website contains links to related information for patients.  Most of the website, however, is technical and requires an account to access.)

When complications such as cirrhosis cannot be controlled with treatment or when the liver becomes so damaged from scarring that it completely stops functioning, a liver transplant is necessary.

Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans with obesity. In the past 10 years, the rate of obesity has doubled in adults and tripled in children. Obesity also contributes to diabetes and high blood cholesterol, which can further complicate the health of someone with NASH.  (From the NASH page on the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) website.)

From “Fatty Liver Disease is Common in the US

Source: Spare the exercise, spoil the liver

More information about fatty liver can be found on the American Liver Foundation’s Fatty Liver page and in their Fatty Liver Brochure.

In case you’re wondering what I did after my diagnosis…

At the ultrasound the technician had said, “Your gallbladder is fine, but you have a fatty liver.”  The way she said it made it sound like it was more than just a casual observation, so when I got home I did a quick search on the National Library of Medicine’s website, where I found a lot of information about NAFLD.  (I’m not a teetotaler, but I don’t drink much.)

The progression from NAFLD to NASH to cirrhosis to needing a liver transplant or you die got my attention. Even before I got the formal diagnosis from my doctor I changed my diet (I started eating fish, raisins, and nuts, as well as more fruit, nuts, raisins, whole grains, leafy green vegetables, and fiber (even tried quinoa); and fewer sugar-sweetened drinks) and lots more exercise.  I dropped about twenty pounds in four months and, more importantly, my triglyceride level dropped a lot.

I had relapsed a bit since then, but after viewing Dr. Lustig’s presentation on the effects of fructose (and having done some follow up reading on the topic) I have once again cut back on sugar consumption and have started working out more regularly once more.

If you’re been sort of blasé about fructose you might find yourself changing your mind if you look at the slides on the “Detrimental Effects of Fructose” from a presentation he gave at the National Institute of Environmental Health Sciences (NIEHS) (pp. 15-27, with final slides on p. 27 showing the end result) and look at how fructose metabolized by the liver ultimately results in the creation of lipid droplets (these are what create a “fatty liver”), FFA (free fatty acids) (which help trigger insulin resistance), and triglycerides (TG), resulting in higher blood pressure and inflammation (among other things).

March 21, 2010

U.S. Task Force on Childhood Obesity looking for ideas

We’ll see whether this has any impact, given some of the recent discoveries about the role of fructose in the obesity epidemic.

Task Force asks public for ideas on how to solve the obesity challenge (March 17, 2010, press release)

Federal Register request for input, March 16, 2010:

[Text version] [PDF version]

On Feb. 9, 2010, President Obama created the first-ever federal task force to enhance coordination between private sector companies, not-for-profits, agencies within the government and other organizations to address the problem of childhood obesity. The Presidential Memo that established the Task Force directed senior officials from executive agencies and the White House to develop a comprehensive interagency action plan that details a coordinated strategy, identifies key benchmarks and goals, describes research gaps and needs, and assists in the development of legislative, budgetary, and policy proposals that can improve the health and well-being of children, their families, and communities.

Now, Dr. Robert Lustig spoke about the basic problem with FDA and USDA on this issue in a lecture (see “The toxic effects of … sugar“).  He said that the biggest problem is not lack of exercise, but ingesting too much fructose.  (If lack of exercise is the reason, explain why there’s an epidemic of obese six-month-olds.)

Lustig says that the studies linking fat consumption and heart disease did not control for sugar consumption.  He pointed out that in Western societies high-fat diets are high-sugar diets.   And he said that FDA won’t regulate fructose because it’s not an acute toxin, but a chronic toxin leading to metabolic syndrome (plus, the FDA considers it “natural”—which Dr. Lustig notes is true only on the technicality that HFCS is made from a natural product—HFCS is highly processed and refined).  And the USDA, which controls the food pyramid, won’t touch high fructose corn syrup because it’s made from corn.  (See also “Junk food turns rats into addicts. Bacon, cheesecake, Ho Hos alter brain’s pleasures centers.”)

The Federal Register notice points people to First Lady Michelle Obama’s “Let’s Move” initiative – http://www.letsmove.gov/.  I certainly support this, but I think they need to go further and start looking at the connection between fructose and obesity.  The site has links to all sorts of useful information, including a link to the Food Environment Atlas from USDA which shows consumption of various foods around the U.S., as well as maps showing diabetes and obesity rates (under “Health”).

While there’s no acknowledgement that the type of sugar we’re consuming has an effect, I did notice that there are signs that someone in the government is paying attention.  Water is recommended as the main drink.  Fruit juices are discouraged, as are “added sugars.”  But they don’t appear to have made the leap yet to the connection between fructose and the metabolic syndrome, which appears to be even more important than the number of calories consumed or burned.

Related posts:

Update on fructose – Dr. Lustig on Nightline” and “Fructose overdose

See also:

Laura Sanders.  “Junk food turns rats into addicts. Bacon, cheesecake, Ho Hos alter brain’s pleasures centers.” Science News.  November 21, 2009.

Paul Johnson and Paul Kenny. “Society of Neuroscience Program.”  ‘Neuroscience 2009′ Conference. October 17-21, 2009.  Chicago.

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