Weight...or height?

Is trying to control our country's height just as plausible as trying to control our country's weight? Maybe so.

Economists estimate that excess weight accounts for 9% of the U.S.'s medical spending. And while there's no similar figure for height, it is clear that both obesity and short stature cause similar economic strain [1].

Whatever the reason as to why, higher weight and lower height are associated with chronic disease, low wages, and poor educational attainment. In the US, the shorter you are the higher risk you're at for developing coronary heart disease, diabetes, and stroke. Women weighing more than 212 pounds at 5'4" tall are paid up to 9% less for their work, for example. According to survey data collected from over 450,000 adults suggests that male college graduates are, on average, more than an inch taller than men who never finished high school [1].

Is the reshaping of America both a war against fatness and shortness? How can one increase stature?

Height is not only genetic, but nurture and nature-related. Exposure to malnutrition, infectious disease, chronic stress, and poverty can abbreviate children's proper growth and height. Promoting foods which are low in calories and high in micronutrients, such as fruits and vegetables, is one feasible option. Increasing and improving education as a means of decreasing poverty and environmental stress is another. And of course, access to quality health care providers to improve prenatal and postnatal care is imperative [1].

This information is simply food for thought...and a topic that peeked my interest. Or maybe we should just throw everyone on growth hormone and run a blow-out sale on bariatric surgery!!

Kidding.

Yesterday checked out like so...

Breakfast:
1 cup steel cut oats, prepared (2 carbs)
1 Tbsp pumpkin butter (1 carb)
1/2 tsp turbinado (0 carbs)
     Total: 3 carbs

Lunch:
1 slice Buffalo Chicken Lasagna (2 1/2 carbs)
1 2% string cheese (0 carbs)
apple (1 carb)

     Total: 3 1/2 carbs

Snack:
6 ounces fat-free yogurt (1 1/2 carbs)

Dinner:
1 serving Chicken Tamale Casserole (2 1/2 carbs)

     Total: 2 1/2 carbs (low)

Snack:
4 peanut butter crackers (1 carb)

10 more days of being a diabetic...I can DO IT!!!!! Though, I am yet to look up the carbohydrate content of the INCREDIBLE pumpkin spice cappuccino I mixed with Dark Roast coffee this morning. It was worth the splurge though, I swear!!

Gina, CandidRD, is having a great give away on her site. Go here for more information!

[1]. Engber, Daniel. The Fat and Short of It. The New York Times. October 15, 2009.

Fat Gene

In 2007, UK researchers discovered a gene variant that may help to explain the variation in weight status among humans. It is noted, however, that this gene is unlikely to be the cause of the global obesity epidemic. The gene, called "FTO", helps to regulate the amount of fat in the body and thus, is a strong indicator in predicting BMI. The FTO gene is known to play a role with the hypothalamus, which regulates appetite in the brain. The strength of the relationship between the gene and weight status depends on whether or not an individual has inherited one of two copies of the FTO gene variant. For an individual with two copies of FTO, their weight is an average of 6.6 pounds more than an individual without the variant. For an individual with one copy of the FTO variant, their weight is approximately 2.6 pounds more than an individual without the variant. It was estimated that 16% of Europeans have two copies of the variant with half of the population containing at least one copy of the variant [1].

The FTO gene aforementioned is not to be confused with the estimated genetic predisposition to "severe" obesity, which is estimated at 1 on 10,000. The UK research team confirms a genetic link to obesity, but reminds that while genetics have not changed, environment and eating patterns have changed [1].

Emily Sonestedt, author and member of the research group at Lund University Diabetes Centre, says that in the case of FTO, the critical determinant of obesity of what you eat. The September 14, 2009 article by Science Daily states, "The risk of becoming obese is 2.5 times higher for those who have double copies of the best known risk gene for overweight and obesity [FTO]." The article goes on to explain that a low-fat diet "neutralizes" the harmful effects of the FTO gene [2].

While exercise has been studied in relation to the FTO gene, Sonestedt's research is the first study where the effect of the gene is being studied in relation to food. After extensive questionnaires and interviews, as well as food diaries kept by study participants, a clear pattern between fat consumption and obesity risk emerged -- the risk of obesity was dramatically increased only in the case of high fat consumption [2].

Sonestedt's research shows that the harmful effects of the gene can be canceled by improving diet and mapping the effects of other obesity genes, allowing professionals to better individualize nutrition counseling for those that want to avoid gaining weight. She also states, "This shows that we are not slaves to our genes. Even if we are born with an inherited predisposition to obesity, life style is important" [2].

To all the people of the world wanting to lose weight: YOU CAN DO IT!

[1]. Paddock, Catherine. Obesity Gene Discovered. Medical News Today. April 13, 2007.
[2]. Obesity Risk Gene. ScienceDaily. September 14, 2009.