Posts Tagged ‘appetite’

Childhood Obesity Crisis Over?

February 20th, 2014

On January 28, 2014, President Barack Obama said in the State of the Union speech,” As usual, our First Lady sets a good example.  Michelle’s Let’s Move partnership with schools, businesses, and local leaders has helped bring down childhood obesity rates for the first time in thirty years – an achievement that will improve lives and reduce health care costs for decades to come. “ Really? We’ve already reviewed Michelle Obama’s premature “Mission Accomplished”. Perhaps the President and First Lady should take note of recent research which indicate the childhood obesity crisis is far from over.

Just two days after the State of the Union, the New England Journal of Medicine published a study by Cunningham and colleagues, “Incidence of Childhood Obesity in the United States.” Much attention has been paid to the prevalence of obesity, meaning the total number of persons with the condition in the population. Incidence, on the other hand, is the number of new cases appearing in the population at a given time. So Cunningham et al, looked at a database of 7,738 children who were in kindergarten in 1998 and were measured 7 times between 1998 and 2007.

They found that, on entering kindergarten (age 5.6 years) 12.4% were obese and another 14.9% were overweight. In eighth grade (age 14.1 years) 20.8% were obese and 17% were overweight. The incidence dropped between fifth and eighth grade. Overweight 5-year-olds were four times as likely as normal weight children to become obese. Among children who became obese between 5 and 14, nearly half had been overweight and 75% were above the 70th percentile. Hispanic and non-Hispanic black children had higher rates of obesity than white children. Children from the wealthiest 20% of families had the lower prevalence of obesity in kindergarten than those in all other socioeconomic groups and this difference increased through the eighth grade.

Overweight kindergartners had 4 times the risk of becoming obese by age 14 as normal weight kindergartners. Overweight children from the two highest socioeconomic groups had five times the risk of becoming obese as normal-weight children of similar socioeconomic status.

The incidence of obesity between the ages of 5 and 14 years was 4 times as high among children who had been overweight at age of 5 as among children who had a normal weight at that age. The researchers’ findings are significant in addressing public policies regarding obesity. “First,” they state, “a component of the course to obesity is already established by age of 5 years…Second, obesity incidence among overweight children tended to occur early in elementary school. “ The study supports closer examination of the roles of the early-life home and pre-school environments, intrauterine factors and genetic predisposition.

(Although not discussed in the paper, age 5-6 is regarded as the time of a child’s lowest Body Mass Index (BMI) and the beginning of “adiposity rebound” – a period of increasing weight into adulthood. This is a normal phenomenon all children go through.)

New studies show how babies might be already programmed for excessive weight gain. One study, by Jane Wardle and colleagues, show that greater appetite (either due to higher food responsiveness or lower satiety responsiveness predicted rapid growth up to 15 months of age among twins. The second study by the same group showed that low satiety responsiveness is one of the mechanisms by which genetic predisposition leads to weight gain in an environment rich with food.

A New Understanding of Body Weight Regulation

September 17th, 2012

John Blundell and colleagues have come out with an interesting new paper, “Role of resting metabolic rate and energy expenditure in hunger and appetite control: A New Formulation.” The paper provides a fascinating insight into human body weight regulation, appetite and the recurring drive to eat. The  resting metabolic rate (RMR) refers to the energy needed to keep our bodies functioning. Of all of the components of energy expenditure, it is the largest, accounting for about 50%-70% of total energy expenditure.  The liver contributes about 20% to the RMR, the brain another 20%, the heart 11%, the GI tract 9% and skeletal muscle another 20%. The drive to eat is predicated on getting enough energy to these systems to keep them running.

Blundell and colleagues’ paper explores a long-running research question as to the influence energy expenditure has on energy intake. As many people know, one of the problems with the ‘eat less, exercise more’ prescription is that exercising often leads to greater hunger, then to more eating, negating or lessening the weight-related benefits of exercise in the first place.  They noted previous research that found that exercise caused a significant increase in levels of hunger but this was highly variable between individuals. However, they also observed an increase in post-feeding satiety signalling. What the researchers found was that fat-free body mass but not fat mass or BM is strongly correlated with meal size and daily energy intake. The write, “The strong implication of this relationship is that some privileged molecules arising from FFM (fat free mass) or some physiological consequences that reflect the activity of FFM, act as a signal to drive food intake.” They note, further, that RMR is positively associated with meal size and daily energy expenditure. It is also a strong predictor of fasting levels of hunger and influences the daily profile of hunger. Ergo, RMR is the driver of food intake. They suggest three components of appetite regulation: a drive for food arising from the physiological demand for energy; an inhibition of eating arising from signals of energy storage, primarily adipose tissue; and additional inhibitory signals arising from the mouth and GI tract.

Regarding weight management, the authors note that their observations bring additional dissatisfaction with the Body Mass Index (BMI) as a measure of excess weight. They note that persons with obese, as well as people with large muscle mass, would have a higher tendency to consume larger meals just to maintain their RMR and greater difficulty in tolerating dietary restrictions. RMR is not the cause of obesity; it is the mechanism for preserving body weight. The amount of food actually consumed is determined by energy density. A high RMR could influence weight gain by maintaining a high level of hunger but a positive energy balance (i.e. gaining additional weight) would “depend on the energy density and palatability of the diet.” Increasing fat-free mass and RMR would increase the drive to eat “meaning that weight gain becomes part of a positive, rather then a negative, feedback system. Increasing body weight therefore could facilitate further weight gain and increase the difficulty of weight loss or maintenance.” See PubMed: Role of Resting Metabolic rate and Energy Expenditure

The universal call to “maintain a healthy weight”, “avoid weight gain” and “eat less to lose weight” begs the question, “How many calories should I be consuming?” The answer is your resting metabolic rate. Going well below that rate induces strong hunger signals and a return to earlier calorie consumption levels. Almost all diet advice tries to get dieters to consume just about their RMR to encourage weight loss and avoid triggering hunger cues. RMR can be measure in the laboratory using very sophisticated tools. But most consumers will look to web-based calculators. And this is a sorry story indeed.

 

Downey Fact Sheet 1 – About Obesity

September 27th, 2009

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Obesity is a global epidemic and a major health concern because of its premature mortality and extensive comorbidities. Obesity is a common, complex, multifactorial disease with a high degree of heritability. Between 25 and 40% of person with obesity have a parent who is obese. There are several significant facts to bear in mind when discussing obesity:

By Julie Snider for the Downey Obesity Report

By Julie Snider for the Downey Obesity Report

Every individual inherits a certain number of fat cells or adipose tissue. Obesity requires (a) a large number of fat cells or (b) a large volume in each fat cell or (c) both. Adipose tissue continues throughout the lifespan. Weight loss, including surgically-induced weight loss, does not remove fat cells. This is why weight regain is so common. Individuals with obesity have significantly more fat cells than the non-obese, 23-65 billion compared to 37-237 billion for persons with obesity . Early onset obesity is associated with increase adipose cell number while adult obesity is associated with normal cell number. There are two phases of life in which growth of adipose cells are likely to develop: very early, within the first few years of life and between the ages of 9-13 years of age. Those who become very obese early in life are the ones who have nearly normal cell size but have the greatest increase in cell number; whereas those with onset of obesity between 9-13 have more change in cell size than cell number. Salans LB, Cushman SW, Weisman RE, Studies of human adipose tissue. Adipose cell size and number in non0bese and obese patients. J. Clin Invest. 1973 Apr’ 52(4): 929-41)

Extremely obese individuals may have four times the number of fat cells as lean counterparts. http://www.jpp.krakow.pl/journal/archive/1205_s6/pdf/5_1205_s6_article.pdf

Human food intake and energy expenditure are controlled by complex, redundant and distributed neural systems that reflect fundamental biological reaction to food supply and energy balance. The hypothalamus and caudal brainstem play a critical role. The limbic system is important for processing information regarding previous experience with food, reward and emotion. The predisposition to store considerable amounts of energy as fat for later use is now a major health risk. Brain, appetite and obesity – PubMed Results

Extensive research over the past 10 years has shown that appetite is regulated by a complex system of central and peripheral signals which interact in order to modulate the individual response to nutrient ingestion. Satiety signals include cholecystokinin, glucagon-like peptide and peptide YY which originate from the gastrointestinal tract during a meal and through the vagus nerve reach the caudal brainstem. Here the signals move to the arcuate nucleus where satiety signals are integrated with adiposity signals, namely leptin and insulin, and with several other inputs create a neural circuit which controls the individual’s response to a meal, i.e. keep eating or stop. Neuro-hormonal control of food intake: basic mecha…[J Physiol Pharmacol. 2005] – PubMed Result

Adipose tissue, rather than some inert, jello-like, substance is an active hormonal tissue, secreting many hormones which are involved in creating signals from the gut to the brain, indicating hunger or satiety. These hormones include insulin, leptin, ghrelin, PYY-33-6, adiponctin, resistin and visfatin as well as cytokines and chemokines, such as tumor necrosis factor-alpha, interleukin-6 and others. These can lead to a chronic sub-inflammatory state which plays a critical role in the development of insulin resistance, type 2 diabetes, increased risk of cardiovascular disease associated with obesity. Adipokines: the missing link between insulin resis…[Diabetes Metab. 2008] – PubMed Result

Research

September 26th, 2009

                                                                                                                                                                                                                                                                              

Research is fundamental to understanding, preventing and treating obesity. And yet research reports are often not accepted by the public or policy-makers. One reason is that almost every adult is their own self-study of weight control. A study might have the most precise protocol, a powerful sample size and control for a variety of factors but if it does not comport with what “I” experience, I am not likely to believe it. But research itself in obesity is not without its difficulties. Many studies are ‘underpowered”, i.e. they have too few subjects to draw a conclusion from. That is why many preliminary studies do not pan out in larger tests. Also, in many cases, especially in drug trials, researchers try to remove “confounders” from the test subjects so they can see if there is an effect of the drug. That means that many patients who are sick, smoke, take other drugs, etc. are excluded from the trial. When the drug, for example, gets used by a more ‘real-world’ sample, the effects sometimes vanish. Studies that rely on self-reported weights or dietary recall or physical activity diaries are sometimes less reliable than studies where a more objective measurement is needed. Self-reported weight and height — Rowland 52 (6): 1125 — American Journal of Clinical Nutrition and COMPARISON OF SELF-REPORTED AND MEASURED HEIGHT AND WEIGHT — PALTA et al. 115 (2): 223 — American Journal of Epidemiology

There also may be a bias from the funding source (See Conflict of Interest in Medical Research, Education, and Practice – Institute of Medicine, Relationship between funding source and conclusion…[PLoS Med. 2007] – PubMed Result, Scope and impact of financial conflicts of interes…[JAMA. 2003 Jan 22-29] – PubMed Result) or a selection of participants which may skew the results one way or another. Currently, there is a lot of concern about ghost written scientific articles. Ghostwriting Widespread in Medical Journals, Study Says – NYTimes.com

What’s a reader to do? The first is to read skeptically. The second is to go to several different papers or research articles. If different authors appear to agree upon key points, chances are that they are on to something. Remember, extraordinary claims require extraordinary evidence. Research is a communications process among researchers and it should be thought of as a dialogue to which we can all listen.

Many readers may find useful this site, The Little Handbook of Statistical Practice. It is a handy guide to understanding some of the statistical issues involved…like association is not causation.

Research is key. If you are interested in furthering research, you should look into participating in a clinical research activity. To see what clinical trials are underway in obesity research, see www.ClinicalTrials.gov/Search of: Open Studies | “Obesity” – List Results – ClinicalTrials.gov

A major NIH initiative is support for Obesity and Nutrition Research Centers. In addition to the research they carry out, these centers are critical training facilities for new investigators exploring obesity. Most have their own websites which can provide additional, valuable information. Their sites may provide you with helpful information. Also included are their annual reports.

  1. University of Alabama Nutrition & Obesity Research Center | Nutrition & Obesity Research Center Annual report at http://www2.niddk.nih.gov/NR/rdonlyres/E6AE7940-23AC-402E-BCAC-D4F11A9213B0/0/Alabama.pdf
  2. University of Colorado at Denver and Health Science Center. No website. Annual report at http://www2.niddk.nih.gov/NR/rdonlyres/061BCC83-261E-4B39-95CC-226C97B03ED2/0/Colorado.pdf
  3. Pennington Biomedical Research Center PBRC – Nutrition Obesity Research Center. Annual report at: http://www2.niddk.nih.gov/NR/rdonlyres/841B5FA5-7AC1-4DDB-AD3F-300B94468560/0/Pennington.pdf
  4. University of Maryland, http://medschool.umaryland.edu/cnru/index.asp. Annual report at http://www2.niddk.nih.gov/NR/rdonlyres/BF6E7D31-948E-450A-AFF5-B863FF427B24/0/Maryland.pdf
  5. Boston, MA  Boston Obesity Nutrition Research Center Annual report at: http://www2.niddk.nih.gov/NR/rdonlyres/83F114DD-E707-4623-BA20-BCE02C33ADF6/0/Boston.pdf
  6. Harvard,MA,  no website. Annual report at: http://www2.niddk.nih.gov/NR/rdonlyres/9AFA2465-42C0-40CB-87DB-35813E80A978/0/Harvard.pdf
  7. University of Minnesota. Minnesota Obesity Center | College of Food, Agricultural and Natural Resource Sciences | University of Minnesota Annual Report at http://www2.niddk.nih.gov/NR/rdonlyres/78A3842A-030C-45F7-856E-5C27BE202C15/0/Minnesota.pdf
  8. Washington University, Missouri http://www2.niddk.nih.gov/NR/rdonlyres/BB5BBA2D-AA63-4B73-99D6-56741BB220B3/0/WashingtonUniversity.pdf
  9. Columbia/Cornell, New York, NY http://www.nyorc.org/favicon.ico Annual Report at: http://www2.niddk.nih.gov/NR/rdonlyres/28E027FF-5212-4F15-960B-4E5C84FF952A/0/NewYork.pdf
  10. University of North Carolina at Chapel Hill. No website. Annual report at: http://www2.niddk.nih.gov/NR/rdonlyres/8836D29C-0AF8-4C6A-914E-9D12828A1A82/0/NorthCarolina.pdf
  11. University of Pittsburgh. No web site. Annual Report at: http://www2.niddk.nih.gov/NR/rdonlyres/C8B65B24-EE7A-495C-B441-05EAD3372283/0/Pittsburgh.pdf
  12. University of Washington. http://depts.washington.edu/favicon.ico. Annual Report at: http://www2.niddk.nih.gov/NR/rdonlyres/739D3F88-98FE-4733-9D31-6BB81A1DA915/0/Washington.pdf

 

New Studies , updated October 16, 2009

Obesity driven GERD drives up health care visits Trends in Gastroesophageal Reflux Disease as Measu…[Dig Dis Sci. 2009] – PubMed Result

Psychiatrists survey on attitudes to obese patients Psychiatrists’ perceptions and practices in treati…[Acad Psychiatry. 2009 Sep-Oct] – PubMed Result

More evidence for role of FTO gene in obesity via loss of control and selecting diet high in fat The FTO gene rs9939609 obesity-risk allele and los…[Am J Clin Nutr. 2009] – PubMed Result

AHRQ summarizes evidence on breast-feeding, finds reduced risk of obesity, type 2 diabetes A Summary of the Agency for Healthcare Research an…[Breastfeed Med. 2009] – PubMed Result

Weight loss after bariatric surgery may be explained by changes in gut hormones controlling appetite. The Gut Hormone Response Following Roux-en-Y Gastr…[Obes Surg. 2009] – PubMed Result

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