Posts Tagged ‘food environment’

Schools and Children

September 27th, 2009

As concern about childhood obesity has increased, the school environment has received increased attention.

Retooling school food offerings can help. The Somerville MA experiment Retooling food service for early elementary school…[Prev Chronic Dis. 2009] – PubMed Result

A very positive study on the value of nutrition education in the schools Effectiveness of school programs in preventing chi…[Am J Public Health. 2005] – PubMed Result

Effect of the school food environment Association between school food environment and pr…[J Am Diet Assoc. 2009] – PubMed Result

School food environments and practices affect diet…[J Am Diet Assoc. 2009] – PubMed Result

Schools are making progress in addressing obesity. Schools and obesity prevention: creating school en…[Milbank Q. 2009] – PubMed Result

International Journal of Obesity – Abstract of article: Childhood overweight and elementary school outcomes

Overweight affect school performance in girls but not boys. See: http://www.rand.org/pubs/reprints/2008/RAND_RP1315.pdf

Impact of removing low nutrition foods in schools. The Impact of Removing Snacks of Low Nutritional V…[Health Educ Behav. 2009] – PubMed Result

Food use in middle and high school fundraising: do…[J Am Diet Assoc. 2009] – PubMed Result

School Environment gets worse with higher grades. School food environments and policies in US public…[Pediatrics. 2008] – PubMed Result

BMI measurement in schools Body mass index measurement in schools. [J Sch Health. 2007] – PubMed Result

Journal of Public Health Policy – Disparities in Physical Activity and Sedentary Behaviors Among US Children and Adolescents: Prevalence, Correlates, and Intervention Implications

Journal of Public Health Policy – Arkansas Act 1220 of 2003 to Reduce Childhood Obesity: Its Implementation and Impact on Child and Adolescent Body Mass Index

Journal of Public Health Policy – Early Impact of the Federally Mandated Local Wellness Policy on Physical Activity in Rural, Low-Income Elementary Schools in Colorado

Journal of Public Health Policy – Preventing Childhood Obesity through State Policy: Qualitative Assessment of Enablers and Barriers

Journal of Public Health Policy – Correlates of Walking to School and Implications for Public Policies: Survey Results from Parents of Elementary School Children in Austin, Texas

Journal of Public Health Policy – Sociodemographic, Family, and Environmental Factors Associated with Active Commuting to School among US Adolescents

Journal of Public Health Policy – Implementation of Texas Senate Bill 19 to Increase Physical Activity in Elementary Schools

Genetic Basis of Obesity

September 26th, 2009

Often one hears it stated that obesity is not a genetic disease. If by that the speaker is saying that obesity is probably not due to a single genetic change they are not quite right. There are some rare forms of obesity which are due to a single gene change. Genetic obesity syndromes. [Front Horm Res. 2008] – PubMed Result; Genetic and hereditary aspects of childhood obesit…[Best Pract Res Clin Endocrinol Metab. 2005] – PubMed Result But if they mean a single genetic change cannot account for a worldwide epidemic of obesity occurring over the last 30 years they are probably right. If the speaker means it is unlikely that there will be a treatment for obesity based on gene therapy, they are probably correct. (Although who can predict the future?) However, they miss the point if they do not understand that for millions of years of evolution, the species we call humans have favored genes which maximize its chances for survival and reproduction. So our taste preferences, our physical activity preferences and the like are passed on in the genome and our part of our inheritance. The problem is that for centuries we humans lived in an environment which was totally different than the one we live in now. The disconnect is that our bodies have not yet adapted to this new world where tasty, nutritious food is readily available and where most of us do not have to expend anything other than a minimal effort to obtain it, survive and flourish. Anything policy-makers or parents want to do about obesity must be understood in the context of the powerful force evolution has been in designing how humans acquire, store and use energy from food.

According the CDC:

  1. Biological relatives tend to resemble each other in many ways, including body weight. Individuals with a family history of obesity may be predisposed to gain weight.
  2. Different responses to the food environment are largely due to genetic variation between individuals.
  3. Fat stores are regulated over long periods of time by complex systems that involve input and feedback from fat tissue, the brain and endocrine glands like the pancreas and the thyroid. http://www.cdc.gov/genomics/training/perspectives/files/obesknow.htm,
  4. The tendencies to overeat and be sedentary, the diminished ability to use dietary fat as fuel and enlarged, easily stimulated capacity to store body fat are all genetically influenced. The variation in how individuals respond to the food rich environment and the differences in acquiring obesity related comorbid conditions are also genetically determined. http://www.cdc.gov/Features/Obesity/

Since 1997, published studies have found that variation in BMI is largely due to heritable genetic differences, with estimates ranging from 55% to 85%. A 2008 study found that 77% of the adiposity in preadolescent children born since the start of the obesity epidemic was due to genetic inheritance compared to 10% for the environment. Evidence for a strong genetic influence on childho…[Am J Clin Nutr. 2008] – PubMed Result

A fast rate of eating appears to be heritable. Eating rate is a heritable phenotype related to we…[Am J Clin Nutr. 2008] – PubMed Result Differences in responding to the obesogenic environment may also be heritable Genetic influence on appetite in children. [Int J Obes (Lond). 2008] – PubMed Result and Appetite is a Heritable Phenotype Associated with …[Ann Behav Med. 2009] – PubMed Result. The FTO gene may be involved. The FTO gene and measured food intake in children. [Int J Obes (Lond). 2009] – PubMed Result and Increasing heritability of BMI and stronger associ…[Obesity (Silver Spring). 2008] – PubMed Result Parental leanness appears to provide strong protection against the development of obesity in children. Development of overweight in children in relation …[Obesity (Silver Spring). 2009] – PubMed Result

There is an interesting scientific debate about what is called the “thrifty gene” hypothesis about how a genetic preference for storing extra energy on our bodies might have developed. Thrifty genes for obesity, an attractive but flawe…[Int J Obes (Lond). 2008] – PubMed Result and The clinical biochemistry of obesity. [Clin Biochem Rev. 2004] – PubMed Result. Some think that childhood obesity is increasing due to ‘associative mating’ by overweight parents who pass on their genetic disposition to obesity to their children. Childhood obesity: are genetic differences involve…[Am J Clin Nutr. 2009] – PubMed Result

The evidence for the genetic basis of obesity, in addition to environmental changes is quite strong. See Implications of gene-behavior interactions: preven…[Obesity (Silver Spring). 2008] – PubMed Result; Genome-wide association scan shows genetic variant…[PLoS Genet. 2007] – PubMed Result and The genetics of obesity. [Metabolism. 1995] – PubMed Result

The environment is thought to be responsible for variations between populations but genetics is responsible for the variations within a given population. Obesity – Missing Heritability and GWAS Utility and Genetic and environmental factors in relative body…[Behav Genet. 1997] – PubMed Result. Genetics may account for many cases of morbid obesityFamilial aggregation of morbid obesity. [Obes Res. 1993] – PubMed Result.

Genetics may play an important role in determining who can benefit from different types of intervention. Implications of gene-behavior interactions: preven…[Obesity (Silver Spring). 2008] – PubMed Result or who is more likely to be affected by obesity Ethnic variability in adiposity and cardiovascular…[Int J Epidemiol. 2009] – PubMed Result. Or experience a comorbid condition like Type 2 diabetes Mechanisms of disease: genetic insights into the e…[Nat Clin Pract Endocrinol Metab. 2008] – PubMed Result

The FTO gene is currently under active research interest for providing a link to how obesity related conditions might arise and how patients can benefit from this knowledge. FTO: the first gene contributing to common forms o…[Obes Rev. 2008] – PubMed Result Genome-wide association scan shows genetic variant…[PLoS Genet. 2007] – PubMed Result

The FTO gene may explain different responses to exercise. FTO Genotype Is Associated With Exercise Training-…[Obesity (Silver Spring). 2009] – PubMed Result .Physical activity and the association of common FT…[Arch Intern Med. 2008] – PubMed Result

A factor in the resistance to describe obesity as a genetic disease may be in the assumption that the human genome does not change rapidly whereas the increase globally in the rates of obesity have occurred in the last 40-50 years. However, evolutionary biologists are debating the speed of genetic change. In “Catching Fire, How Cooking Made us Human” (Basic Books, New York, 2009) Richard Wrangham, the Ruth Moore Professor of Biological Anthropology at Harvard University writes,

A long delay between the adoption of a major new diet and resulting changes in anatomy is also unlikely. Studies of Galapagos finches by Peter and Rosemary Grant showed that during a year when finches experiences an intense food shortage caused by an extended drought, the birds that were best able to eat large and hard seeds – those birds with the largest beaks- survived best. The selection pressure against small-beaked birds was so intense that only 15 percent of birds survived and the species as a whole developed measurably larger beaks within a year. Correlations in beak size between parents and offspring showed that the changes were inherited. Beak size fell again after the food supply returned to normal, but it took about fifteen years for the genetic changes the drought had imposed to reverse. The Grants’ finches show that anatomy can evolve very quickly in response to dietary changes…Other data show that if an ecological change is permanent, the species also changes permanently, and again the transition is fast…The adaptive changes brought on by the adoption of cooking would surely have been rapid. (p. 93-94, emphasis added.) (See Book Reviews)

Brain and Gut

September 26th, 2009

Frequently, when persons with obesity are depicted in the media, they are headless forms (butts and guts I call the pictures) for we think of obesity in terms of body fat accumulation. But obesity really starts in the brain with multiple signals coming from the gut. Adipose tissue itself generates hormones such as leptin and adiponectin; the GI tract generates ghrelin which signals the brain to initiate feeding . Other products which may stimulate feeding or signal time to stop feeding include leptin, insulin neuropeptide Y among others. Parts of the brain involved are the hypothalamus, the dorsal vagal complex and the reward system.

Researchers now appreciate that food acquisition, preparation, and intake are the result of a several physical signals by which the body communicates to the brain that it is hungry and needs to start feeding or full and needs to stop. MD

Brain

So, just how does the body regulate its weight? The body needs to get its weight just right. Too little nourishment and the body becomes ill and cannot reproduce. Too much also a problem. Look at the precision needed. If one ate the recommended 2,200 calories per day (and a lot eat a lot more) they would consumer 792,000 calories in a year. If they are just 1% more calories, they would add 2 pounds per year or 20 pounds over a decade of life. That’s just an extra 22 calories a day – about half a lower fat Oreo cookie. 100 extra calories a day – about 2/3 of 1 ounce of potato chips – can result in a 5-pound weight gain a year. To keep within these narrow boundaries of health body weight, our bodies have evolved a sophisticated, redundant system to gauge its body weight and when to feed and when to stop feeding.

The four parts of this system are (1) the nervous system which connects the brain, gut and adipose tissue, (2) hormones, including those made by fat cells, (3) neuropeptides which act as messengers and (4) messenger molecules in the immune system called cytokines. These molecules control body weight. The pancreas and adipose tissue make leptin, insulin, adiponectin, visfatin and resistin. The brain makes NPY, melanocortin and cocaine and amphetamine regulated transcript called CART. The stomach makes ghrelin, PYY and CCK.

The process can begin before you eat. Even the sight, smell or thought of food can trigger the “cephalic response.” This can start the production of insulin. Ghrelin increases the desire to eat. PYY can signal an end to feeding. Under stress, the sympathetic nervous system is activiated. This promotes storage of fat, decreases metabolism and promotes insulin resistance. Weight increases and metabolism slows down when this system is activated. The key hormone is insulin which is produced in the pancreas. It is designed to use carbohydrates or store them for later use.

The signals to the brain come from both the central nervous system and the peripheral nervous system Central and peripheral regulation of food intake a…[Obesity (Silver Spring). 2008] – PubMed Result

They appear to converge in the hypothalamus region of the brain.Hypothalamic control of energy balance. [Curr Drug Targets. 2004] – PubMed Result

No fewer than ten possible automatic and largely uncontrollable responses to the modern food environment have been proposed to understand why people can consume more calories than they need without their full awareness or control over their behavior Neurophysiological pathways to obesity: below awar…[Diabetes. 2008] – PubMed Result

Obese individuals appear to respond differently to food visual cues Obese adults have visual attention bias for food c…[Int J Obes (Lond). 2009] – PubMed Result

Obese and overweight persons appear to have lower brain volume Brain structure and obesity. [Hum Brain Mapp. 2009] – PubMed Result

Gut Hormones

Leptin has been identified as one of the most powerful hormones involved in appetite regulation. Appetite control and energy balance regulation in …[Int J Obes (Lond). 2009] – PubMed Result Now, newer techniques like brain imaging can be used to understand the role the brain and central nervous system play in eating behaviours.Leptin regulates striatal regions and human eating…[Science. 2007] – PubMed Result and Neuroimaging and obesity: mapping the brain respon…[Ann N Y Acad Sci. 2002] – PubMed Result

Another class of signaling substances are neuropeptides. Orexin is one of several currently of interest to scientists. Orexin/Hypocretin: a neuropeptide at the interface…[Pharmacol Rev. 2009] – PubMed Result and Orexin neuronal circuitry: role in the regulation …[Front Neuroendocrinol. 2008] – PubMed Result

Chronic stress and obesity: a new view of “comfort…[Proc Natl Acad Sci U S A. 2003] – PubMed Result

Maternal corticotropin-releasing hormone levels du…[Obesity (Silver Spring). 2006] – PubMed Result

The role of gut hormones in the regulation of body…[Mol Cell Endocrinol. 2009] – PubMed Result

Gut hormones: a weight off your mind. [J Neuroendocrinol. 2008] – PubMed Result

Gut hormones and appetite control. [Gastroenterology. 2007] – PubMed Result

Cord blood leptin and adiponectin as predictors of…[Pediatrics. 2009] – PubMed Result

The leptin/adiponectin ratio in mid-infancy correl…[J Pediatr Endocrinol Metab. 2008] – PubMed Result

As research progresses, new theories of evolutionary development are looking at Build-ups in the supply chain of the brain: on the…[Front Neuroenergetics. 2009] – PubMed Result

Ghrelin is a gut hormone which appears to be very significant and is the subject of much research.Lean Mean Fat Reducing “Ghrelin” Machine: Hypothal…[Neuropharmacology. 2009] – PubMed Result

Appetite

Viewing photographs of fattening foods, compared to non-food objects can result in greater activiation in parts of the brain. Activation in brain energy regulation and reward c…[Int J Obes (Lond). 2009] – PubMed Result In one study, obese women had greater brain activity in response to pictures of high fat foods than did non-obese women. Widespread reward-system activation in obese women…[Neuroimage. 2008] – PubMed Result and Effective connectivity of a reward network in obes…[Brain Res Bull. 2009] – PubMed Result

Gut peptides and the regulation of appetite. [Obes Rev. 2006] – PubMed Result