Obese or Not to Be?

Right mouse: You wanna go to da club tonight?

Left mouse: Yeah, I wanna club sandwich.

Right mouse: No, no, never mind...

The scoop: The mouse on the left is unable to produce leptin, an adipokine (hormone secreted by your fat cells (adipocytes)) that signals the changing level of fat storage in the body and modulates long-term appetite control and body weight management: less fat = eat more, store fat / more fat = eat less, burn fat. Two possibilities for obesity development, among many others, are: 1) a leptin deficiency or 2) leptin resistance. Leptin deficiency can be curbed by leptin therapy; but for those who are leptin resistant, leptin is already present in high levels in the blood; it just doesn't stimulate the metabolic system anymore because the body has gotten used to the stimulation, in a sense (either the leptin receptors on target cells have lessened in number in response due to over-stimulation by leptin, or they have diminished in sensitivity, yet overall the end result is the same).

If one is consuming more calories than what you're burning, the energy is stored in the body first in the liver as glycogen, a branched polymer made of individual glucose molecules, and then as fat (adipose tissue) when no more glycogen can be made. So, with the leptin targets overwhelmed and unable to keep up with the over-signaling --> the body's signal (leptin) for telling your brain (hypothalamus) that you have too much fat already can't keep up with how much fat is being made --> therefore, the amount of fat burned will less than the amount of fat being laid down in your body's architecture --> this cycle continues until one becomes obese and then it is very difficult to break the cycle, physiologically and psychologically.

There might be ways to rebound from leptin resistance. Both of the ones I will mention involve losing weight, so don't get too excited. For one, losing the amount of fat in your body will directly lessen the level of leptin in your system (remember, fat cells produce leptin, so the less fat cells you have = the less leptin); this will reduce the amount of leptin overwhelming your system and allow the body to catch up to its fat-burning potential. Also, losing fat will increase the amount of another adipokine, adiponectin, which similar to leptin serves to lessen appetite and stimulate the metabolic catabolism of fat, yet it has not been correlated to the same decrease in sensitivity in obese people that accompanies leptin. (Got it? Less fat = More adiponectin).

In the absence of food, adiponectin helps muscle cells (myocytes) take up more blood glucose, stimulates the breakdown of fat (fatty acid catabolism) for use as fuel in our muscles, decreases inflammation, stops generation of new glucose (gluconeogenesis) in the liver while also decreasing the deposition of fat in the liver , . However, it seems that the overweight and obese can often have deficiencies of this hormone which would curb their bodies' ability to lessen appetite and metabolize fat as well as the rest of us. And since adiponectin seems to be a mediator for decreasing the risk of developing Type II diabetes, then it would partially explain why overweight and obese citizens have a greater risk of developing this disease.

Dr. Philipp Scherer at UT Southwestern Medical Center, who discovered adiponectin in 1994, also performed a study in 2007 that showed high levels of adiponectin protected severely obese mice, which were also genetically altered to be leptin-deficient, from developing symptoms of Type II diabetes. This was contrary to the other group of leptin-defincient mice who ALL developed such symptoms. To me, that's sounds like a pretty good case, especially when they showed that the location of fat in adiponectin-heavy mice was most, if not all, subcutaneous rather than visceral, which means that it lies under the skin instead of around your vital organs (e.g. liver, heart).

Now onto foods: The Mediterranean diet, according to a 2006 study in The American Journal of Clinical Nutrition, is positively correlated to a higher observance of adiponectin in the plasma: women who closely adhered to the diet showed a 23% higher plasma adiponectin concentration than women who loosely adhered to the diet. An example of the Mediterranean food pyramid is shown below.

 

In particular, alcohol, fruits, nuts and whole grains showed statistically significant, positive associations to adiponectin concentrations (More eaten = Higher adiponectin levels). The authors of the study admit that the associations were modest, however it does support what decades of research and nutrition education has told us all along. Well, maybe except for the alcohol part...


Places to find out about leptin, adiponectin, the Mediterranean diet and their effects: Wikipedia (Obesity, Leptin, Adiponectin), Fat Resistance Diet, MedPageToday.com, Adipocyte.co.uk, Science and Reason, The American Journal of Clinical Nutrition, WebMD.com, and The Mayo Clinic.

Lunch Much?

The City Critic on School Lunches

A step in the right direction, even before the rest of the country had put on their sneakers. Thanks to NYC for having their finger on the pulse of what needs to be done to help kids learn and keep healthy appetites.

The scoop: Someone who's also making waves in New York cafeterias...Plattsburgh, New York that is...is Professor Brian Wansink of Cornell University. An expert in human eating behavior, an application of the studies of consumer behavior and behavioral economics, his strategy for getting kids to eat more fresh fruit is to "trick" them. Basically, to make the consumer (the child) choose the desired behavior (taking fresh fruit and vegetables) by strategically placing the product (fruits & veggies) in locations (by the cash register) or in attractive packaging that will end in seamless incorporation of the product into the consumer's cart. Has it worked? Yes, it most definitely has (phew!)

In January 2010, the school lunch manager instituted Dr. Wansink's plan and witnessed a surprising 4-fold increase in fruit sales by March! Even better news came from parents who reported their children talking about the fruit in the cafeteria. Did we just enter the twilight zone?

No, snap out of it, it actually happened. These cheap and simple changes are based on Wansink's theory of behavioral engineering. To avoid resistance, he believes (and, as far as I'm concerned, has proven) that making a consumer feel as though they have chosen the behavior/product themselves is crucial to curbing consumer behavior to the outcome you want. Big Brother anyone? At least he's using his powers for good and not evil. The author of best-selling book Mindless Eating believes people make about 250 eating decisions a day and that most of those are "'mindless' decisions triggered by his or her environment." Therefore, changing the environment can encourage people to change their eating behavior and this success of this centers on 4 concepts: 1) placement (e.g. broccoli at the beginning of the line, 2) marketing/advertisement (e.g. attractive packaging of veggie snacks or verbally offering salad to children), 3) convenience (e.g. putting chocolate milk behind the plain milk), and 4) visual cues (e.g. keeping ice cream in opaque freezers. 

Now housed in the just 1-year-old Cornell Center for Behavioral Economics in Child Nutrition Programs, the prospects of healthy changes in the lunchroom are looking good thanks to the team led by Prof. Brian Wansink.

So the next time you buy strawberries because you want them, think again, you might have just been hoodwinked!

The original article entitled "Meal Plan" that discusses Prof. Wansink's work was written by Edward Lewine and can be found in the March 2011 Hemispheres Inflight Magazine by Continental Airlines.