Archive for the ‘obesity’ Category

The evidence keeps accumulating that obesity in children, even infants, has long-term consequences for the overall health of these individuals as they reach adulthood.  The latest studies, especially a new Dutch study, center around diabetes and heart disease.

Previous research has linked being overweight in childhood with a higher risk of these chronic diseases in adulthood, but the new study is the first to identify the ages between 2 and 6 years as the most important in predicting later risk of metabolic syndrome, says the study’s lead author, physician Marlou de Kroon of VU University Medical Center in Amsterdam. The condition is associated with increased risk of type 2 diabetes and cardiovascular diseases.

The new work “is very interesting,” says cardiologist Gerald Berenson, because it reveals the earliest and most critical age for predicting adult weight problems and risk of serious chronic disease. Berenson, who was not involved in the new study, is director of Tulane University’s Center for Cardiovascular Health in New Orleans.

In the face of a growing epidemic of childhood obesity, these data are very disturbing, Berenson says. People often disregard children’s weight problems, rationalizing “that kids will grow out of it during puberty,” he says.   Adults even joke about “baby fat.”

To explore the relationship between early weight gain and later disease risk, researchers repeatedly measured the height and weight of 642 Dutch children born between 1977 and 1986 in Terneuzen, the Netherlands. From these measurements, scientists calculated the youngsters’ body-mass index — or BMI, which is a measure of heaviness that accounts for height — at least once a year from birth through age 18. Then they plotted how BMI changed over time. Later, as young adults aged 18 to 28, the participants returned for follow-up measurements of waist circumference, fat under the skin and blood tests.

Increasing BMI between the ages of 2 and 6 more than tripled the risk that a young adult would exhibit signs of metabolic syndrome, de Kroon and her colleagues report. BMI increases between the ages of 10 and 18 also posed a substantial — albeit lower — link to metabolic syndrome. The analyses indicated less than a 5 percent likelihood these associations were due to chance.

Metabolic syndrome is a constellation of symptoms that occur together and tend to include elevated blood pressure, elevated triglycerides (fat in the blood), elevated C-reactive protein (a marker of chronic, systemic inflammation) and diminished high density lipoprotein cholesterol, also known as good cholesterol. Until recently, metabolic syndrome was rarely observed before middle age.

Earlier this year, de Kroon’s team also reported that BMI gains between the ages of 2 and 6 were most predictive that a young adult would be overweight.

Although increasing BMI was a strong risk factor for adult disease, being a big baby with an unvarying but high BMI was also associated with higher risk of metabolic syndrome in adulthood, de Kroon says. Weighing too much appears to be bad for adult health, whether a child starts big or merely gets that way during childhood. Moreover, she points out, “if a very thin child is becoming heavier, it may still have a very high risk [of adult disease] even if it never seems too fat.” So even parents of slim kids should watch that children don’t exceed the normal growth curve, she says.

As director of the Bogalusa Heart Study in Louisiana, Berenson and his colleagues tracked weight changes in children from 8 to 17 and showed that a high BMI in childhood was a strong predictor that metabolic syndrome and prediabetes would emerge in adulthood.

Are the new data strong enough for pediatricians to begin cautioning all parents to avoid weight gain in children? “Oh gosh, you know they are,” Berenson says. But, he notes, “We’ve been riding like the dickens to get even cardiologists interested in primordial prevention” — taking action to prevent the development of heart and diabetes risks in apparently healthy individuals. And that should definitely start with addressing the growing number of pudgy children, he says.

Megan Moriarty-Kelsey and Stephen R. Daniels of the University of Colorado School of Medicine in Aurora agree. “Not only is obesity associated with higher rates of cardiovascular risk factors in childhood, but there is emerging evidence that obese children have increased risk for cardiac events and early mortality as adults,” they write in the October issue of Childhood Obesity. In fact, they argue, the impact could be “that life expectancy could be reduced for the first time” and there could be “potentially dramatic increases in health care costs.”

  • J.M. Kindblom, et al. BMI changes during childhood and adolescence as predictors of amount of adult subcutaneous and visceral tissue in men: The GOOD study. Diabetes, Vol. 58, April 2009, p. 8
  • S.R. Srinivasan, L. Myers and G.S. Berenson. Predictability of childhood adiposity and insulin for developing insulin resistance syndrome (Syndrome X) in young adulthood: The Bogalusa Heart Study. Diabetes, Vol. 51, January 2002, p. 204.
  • C.H.D. Fall, et al. Adult metabolic syndrome and impaired glucose tolerance are associated with different patterns of BMI gain during infancy. Diabetes Care, Vol. 31, December 2008, p. 2349.
  • J. Raloff. Don’t push babies’ growth. Science News, Vol. 172, Feb. 15, 2007.
  • J. Raloff. When it’s no longer baby fat. Science News, Vol. 165, April 15, 2004.
  • M.L.A. de Kroon, et al. The Terneuzen birth cohort: BMI changes between 2 and 6 years correlate strongest with adult overweight. PloS One, Vol. 5, February 11, 2010, p. e9155.
  • M.L.A. de Kroon, et al. The Terneuzen birth cohort: BMI change between 2 and 6 years is most predictive of adult cardiometabolic risk. PloS One, Vol. 5, November 12, 2010, p. e13966.

The difference between being thin or fat may come down to genetic differences in dopamine receptors in the brain.

Dopamine is an amazing chemical.  It is the feel good chemical of the brain.  When we do something that is good or satisfying it typically involves dopamine.  All the dopamine in the world, however, will not give you the desired response if you do not have adequate dopamine receptors in your brain.  The number of dopamine brain receptors is  under genetic control and that is why different individuals require different amounts of a drug or activity to get the same amount of “reward”.

For years, evidence has shown that obese individuals have fewer dopamine (D2) receptors in the brain relative to lean individuals and the suggestion has always been that obese individuals overeat to compensate for this reward deficit. It turns out to be a little more interesting than that.

In a bid to uncover why obese people tend to overeat, researchers have found evidence of the vicious cycle created when an obese individual overeats to compensate for reduced pleasure from food. (1)

The study confirmed that obese individuals have fewer pleasure receptors and overeat to compensate.  Furthermore, the evidence shows that the very act of overeating further weakens the responsiveness of the pleasure (dopamine) receptors, further diminishing the rewards gained from overeating.  The result is a runaway feedback system.  The more you eat, the less you are gratified by the food, so you eat still more, further diminishing the reward, and so on.  It is a vicious cycle.

“Although recent findings suggested that obese individuals may experience less pleasure when eating, and therefore eat more to compensate, this is the first prospective evidence to show that the overeating itself further blunts the award circuitry,” says Stice, a senior scientist at Oregon Research Institute, a non-profit, independent behavioral research center. “The weakened responsivity of the reward circuitry increases the risk for future weight gain in a feed-forward manner. This may explain why obesity typically shows a chronic course and is resistant to treatment.”

Using Functional Magnetic Resonance Imaging (fMRI), Stice’s team measured the extent to which a certain area of the brain (the dorsal striatum) was activated in response to the individual’s consumption of a taste of chocolate milkshake (versus a tasteless solution). Researchers tracked participants’ changes in body mass index over six months.

Results indicated those participants who gained weight showed significantly less activation in response to the milkshake intake at six-month follow-up relative to their baseline scan and relative to women who did not gain weight.

“This is a novel contribution to the literature because, to our knowledge, this is the first prospective fMRI study to investigate change in striatal response to food consumption as a function of weight change,” said Stice. “These results will be important when developing programs to prevent and treat obesity.”

To sum it up: There is genetic variability in the population when it comes to brain dopamine receptors.  Particularly if you have a low number of these receptors and you overeat, you will need to overeat further to get the same satiability you once got with less food.  The solution to obesity, short of gene therapy, is to not start overeating.

There are many parallels between feeding behavior and drug addiction and the reason is that the same dopamine reward system is typically utilized.  Drug addicts don’t become addicts overnight.  They start out with small doses but as the reward feedback system demands higher and higher doses, the addiction becomes more and more pronounced.  Given the many parallels between food and drug cravings, it would make sense to use lessons from drug addiction to aid in the fight against obesity.  But then again, we are not too good at fighting drug addiction, either.

  1. Stice, E. et al. 2010. Weight gain is associated with reduced striatal response to palatable food.  Journal of Neuroscience, 30(39):13105-13109.