Reflections on the AMA Decision – Part 2

July 4th, 2013 No comments »

Sugarpova

One of the more curious comments on the AMA decision came from Hank Cardello of the Hudson Institute. Hank (with whom I have broken bread a couple of times) is a former food industry executive who believes that the food industry can basically down-shift the calories in the marketplace, resulting in lower obesity rates. Writing in Forbes Magazine, Why the AMA’s Obesity Ruling is Bad Medicine, Hank appears offended that doctors went off to decide what is a disease without checking first with the food industry. If they had, Hank would have told them how declaring obesity a disease gives health activists and policymaker a “new blunt instrument to use against the food industry.” Those crazy folks will now revive calls for Twinkie taxes, soda cup size bans and restrictions on full-fat pizza. Writes Hank,“These newly ignited brushfires, fanned and fed by social media and zealous lawmakers, could cost the food and restaurant industries enormous time and money to fight. If the activists were to claim that the industries are selling products that worsen a disease called obesity, they would have no choice but to lawyer up and defend themselves. As the decades-long tobacco wars proved, this would only greatly delay getting both parties to come to an equitable agreement.”

Whoa! Hank! Take a breath! Walk around the block.

First, numerous authorities have recognized obesity as a disease. It has been in the International Classification of Diseases for at least 20 years. The Social Security Administration, Food and Drug Administration, National Institutes of Health, Internal Revenue Service have described obesity as a disease for about 10 years or so. So, it isn’t new. If the ‘health activists’ will now ‘use’ it, where have they been? Do you really want to draw a parallel between the food industry and the tobacco industry? I don’t think it is apt and I would think you wouldn’t either.

But Hank presses on predicting (threatening?) that the food industry will now back off creating more healthy foods because they are being demonized “as purveyors of disease.” Well, it didn’t take any time to throw in the towel on the food industry meeting consumer demands for healthier alternatives! That was quick. Was the industry looking for a way out? It certainly feels that way since there is nothing really new in the AMA policy.

But it is next part of Hank’s paper that is embarrassing. It is like being at a party with a friend who starts to say something really unfortunate. You know it is too late to stop them. So, Hank goes on,

“Labeling obesity as a disease also ignores the almost taboo subject of personal responsibility. Describing obesity as purely a disease overlooks the complex role of a person’s psychological profile and attitudes. A study led by Angela Sutin of the National Institutes of Health highlighted that the most disciplined consumers had lower rates of obesity while larger weight gains were linked to personality factors such as impulsiveness, low conscientiousness, and a willingness to take risks. The authors concluded that any obesity solution must address these psychological factors, which general practitioners cannot.”

Well, I guess ‘personal responsibility’ isn’t so taboo after all. Never too late to call obese people damaged in the head. Persons with obesity have been called worse but trying to rope in a researcher from NIH for support was novel.

A few things are wrong with Hank’s description of this paper. First, it appears the study sample had many more ‘normal’ weight participants than the general population (45% to 31%) which might affect the outcomes. Second, Sutin and her co-authors acknowledge the possibility of reverse causation, i.e. that excess weight and the health and stigma attendant thereto can affect personality development. Hank ignores this. Third, while Hank is trying to say these overweight/obese customers can’t control themselves, Sutin points out, “Individuals high on Neuroticism, in particular the impulsiveness facet, and low on Conscientiousness have elevated triglycerides, hypertension, and clinically elevated levels of inflammation, even after controlling for differences in adiposity. Abnormal weight may be one mechanism that partially mediates the relationship between personality and these health outcomes.” (Emphasis added.) Sutin’s paper concludes, “The cognitive, emotional, and behavioral patterns associated with personality traits likely contribute to unhealthy weight and difficulties in weight management. Identifying the personality traits associated with obesity may help to elucidate the role of personality traits in disease progression.” Whoops! Did she just call obesity a disease?

This paper was published in 2011. To pull it out, Hank had to skip over 2 of her papers published earlier this year which have produced some dramatic and unexpected findings.

In the first 2013 paper, she and her colleagues found that individuals who rated high on impulsiveness and lacked discipline or low conscientiousness had high circulating levels of leptin, which plays a critical role in regulating body weight, even after controlling for body mass index, waist circumference or inflammatory markers.

Sutin’s second 2013 paper, “I Know Not To, but I Can’t Help It: Weight Gain and Changes In Impulsivity Related Personality Traits,” has much greater implications. In this study, Sutin and colleagues picked up where the 2011 study left off. They looked to see whether weight gain or loss of 10% or more led to personality changes, specifically impulsiveness and deliberation. They found that, compared to participants to stayed weight-stable, those who gained weight became more impulsive. Those who did not gain weight showed a predicted loss in impulsiveness. Then came the surprise. Contrary to their hypothesis, weight gain was also associated with increases in deliberation. That is, with gaining weight, subjects became more thoughtful before acting. This was especially strong among younger participants. The authors considered that, as participants gained weight, they bought into the American stereotypes about persons with obesity. So they saw themselves as more impulsive even as they were increasing in deliberativeness. They had no change in self-discipline. The authors speculate further, “A second possibility is that physiological mechanisms associated with weight gain could contribute to the relation between weight gain and changes in personality. For example, overweight and obese individuals tend to have higher levels of inflammation and chronic inflammation may reduce the ability to effectively regulate emotions and control behavior.”

Sutin et al suggest more research to help identify how considerations of personality traits can enhance interventions. For example, information on healthy lifestyles may be less useful for some than information on emotional aspects of impulsivity.

Finally, Hank concludes that the ‘disease’ label will be a crutch and cause people to stop making lifestyle changes and probably backslide. Why do these pundits make such negative generalizations about 2/3 of the population? Has the food industry decided just to insult its customers? You may want to see what happened with Michael Jefferies, the head of the head of Abercrombie & Fitch who said he did not want fat customers in his store. Donny Deutsch, advertising executive and TV personality, recently called him “disgusting” and “vile.” or University of New Mexico professor Geoffrey Miller who said he did not want students with obesity to apply to his Ph.D. program. He is being investigated by his university.

Oh, if only we would just leave obesity in the hands of the benevolent food industry!

Remember, those are the folks who are re-introducing Twinkie’s to America’s stores.

Twinkies

The same folks who have brought us  tennis superstar Maria Sharapova whole line of candy called, Sugarpova. (Get it?) See picture above.

 

And let’s not forget Sonic’s new 1,700 calorie peanut butter and bacon milk shake.

Sonic" peanut butter and bacon milk shake

Oh, and then there is Safeway’s leadership to shift the costs of health insurance onto overweight and obese employees based on dubious representation of their program and Kroger’s and Safeway’s efforts to derail front of package calorie labeling in supermarkets. Yeah, let’s all follow those guys.

 

Snacking is Bad. Right?

June 12th, 2013 No comments »

In this uncertain world, one thing we can be sure of is that adolescent snacking is contributing to the obesity epidemic. Right? Well, er, no. Actually, young snackers (you know who you are) are likely to be less obese.

According to a literature review from 2000 to 2011 by Nicole Larson  and Mary Story at the University of Minnesota, “Although snacks can contribute to intake of key nutrients, frequent snacking has been associated with higher intake of total energy and energy from added and total sugars. Assessments in schools and retail stores have further indicated that energy-dense, nutrient-poor snacks are widely available in settings where youth spend their time. The majority of studies either found no evidence of a relationship between snacking behavior and weight status or found evidence indicating that young people who consumed more snacks were less likely to be obese; however, additional research is needed to address various methodological limitations.”

Picture: Selena Gomez snacking. Source: teennowmagazine.uk

 

Look AHEAD Crashes

October 22nd, 2012 No comments »

 

Behind Look Ahead

The National Institutes of Health (NIH) has announced that the Look AHEAD trial has been stopped in its 11th year, two years short of completion. The extensive trial, involving over 5,000 patients at 16 centers, was intended to find out if there was increased mortality from intentional weight loss and to see if intentional weight loss among obese patients with type 2 diabetes would result in fewer cardiovascular (CV) events. At the end of the trial, there was no difference between the study group, which received intensive behavioral counseling and the control group which received standard diabetes education and occasional support group meetings.  The NIH press release indicates that both arms had lower CV rates that reported for patients with diabetes in previous studies. NIHNEWS: Weight Loss Not Reduce CV events in Type 2 diabetes

While this is news is something of a shock, many folks saw it coming. Two years into the trial, which began in 2001, the monitoring board noticed that the event rate in the control arm was much lower than expected. The expected CVD event rate in the control arm was 3.125% per year; in fact it was 0.7%. A committee was formed and made changes to the original study protocol designed to capture more events. These changes went into effect in 2008. There appeared to be three reasons for the lower event rate. First, while cardiovascular disease (CVD) is still the major cause of death in the United States, mortality has gone down, resulting from better control of dyslipidemia and high blood pressure and improved care of chronic and acute coronary syndromes. (See NCHS Data Brief, NCHS DataBrief: Prevalence of Uncontrolled Risk Factors for CVD)  Second, study participants who choose to involve themselves in a long clinical trial may well be healthier than a community sample and more motivated to follow the diet and exercise and participation requirements. Finally, the Look AHEAD trial employed the Graded Exercise Test which excluded participants most likely to develop CVD. Because of the low event rate, an additional primary endpoint was added (hospitalized angina) and the trial was extended for 2 years. (See PubMed: Brancati_Midcourse Correction to clinical trial whe the event rate is underestimated: the Look Ahead Study) Readers may recall that the SCOUT trial of sibutramine also had to revise its protocol midway through the study for the same reason, resulting in a population which was older and sicker than typical clinical population. In both cases, revising the protocol did not favor the intervention.

The stopping of Look AHEAD raises a host of questions. Was the study protocol correct? Did it end up studying healthy obese diabetics? Do long-term studies produce more noise than insight? Are we really studying the aging process when we cannot control for changes in health status, drug utilization (including drugs which can increase weight) and changes in energy intake, fitness levels, etc.? What is the picture for sub-groups, such as the 60-74 age group which had good weight loss in the DPP and 4 year results of Look AHEAD? Were there specific improvements, such as reductions in medications usage, fewer hospitalizations or shorter length of stays, improvements in quality of life? Did the presence of any the alleles associated with success in bariatric surgery affect outcomes? PubMed: High allelic burden of four obesity SNPs associated with poorer wt loss.  Should future efforts be devoted to cases where the disease process is already well-established or where high-risk populations can be identified and appropriate interventions evaluated? In future trials, should comorbid management be left to the local standards of care or defined in the study protocol?

Looking Ahead of Look Ahead

Whither behavioral lifestyle interventions?

The lifestyle interventions in the DPP and Look AHEAD were regarded as the ‘gold standard.’ They involved recruiting and training health professionals who provided not only the intervention but provided a supportive environment and a community spirit. Extensive communication with the patient was maintained. PUBMED: Look AHEAD: Description of the Lifestyle Intervention. Look AHEAD  participants even received an honoraria of $100 at each annual visit to improve adherence. (FDA EMDAC Hearing, March 28, 2012, Dr. Rena Wing, transcript, p. 169).

Recently the CDC and the NIH were looking at ways to take the DPP/Look AHEAD model to a more replicable model. The CDC’s National DPP program awarded $6.75 million in grants to develop lifestyle interventions program among people at high risk. One involves using the YMCA to provide lifestyle counseling. http://www.ymca.net/diabetes-prevention/ Questions will certainly be asked if highly trained professionals with incentives for participants did not produce better results will a down-scale program do better?

Whither diabetes prevention?

Look AHEAD was designed following the Diabetes Prevention Program (DPP). The DPP established that both lifestyle changes and metformin could reduce the incidence of type 2 diabetes, through weight loss, although lifestyle was superior to metformin alone. Look AHEAD was taking this important finding one step further asking whether weight loss among type 2 diabetics would reduce the incidence of cardiovascular events.

Even though the DPP has been promoted as a model for preventing the development of type 2 diabetes through weight loss, there were problems.

Dr. William Knowler of the National Institute on Diabetes, Digestive, and Kidney Disease (NIDDK) told the FDA Advisory Committee earlier this year,that, after three years of the DPP,

“the rates (of development of type 2 diabetes) have tended to flatten out and become parallel among all three groups. The rate of new development of diabetes has actually slowed down in the placebo and metformin groups, compared to what it was in the first three years. And the lifestyle group has flattened out a little bit at the end, but the difference that was attained has been largely maintained over time.  Notice, though, that over 10 years, although there still are remarkable treatment effects, if you look at things in an absolute sense, we can’t say that we still know how to prevent diabetes because, still, close to half of the people who enrolled in the trial developed diabetes over a 10-year period. But at least it’s been substantially delayed in those who have had the interventions.” ( FDA Endocrinologic and Metabolic Drug Advisory Committee Hearing on assessing cardiovascular safety of obesity drugs, March 28, 2012, Transcript, p 131-2).


(Figure: Diabetes Prevention Program Outcomes Study, Lancet (2009) 374; 1677-1686)

Is ‘delaying’ diabetes onset as powerful as ‘preventing’ diabetes from occurring in the competitive race for health care dollars and public attention?

Furthermore, a study earlier this year indicate poor outcomes in drug treatment of adolescents with type 2 diabetes with barely half showing glycemic control with metformin. PubMed: Clinical Trial to Maintain Glycemic Control in Youth with Type 2 Diabetes

Will the Look AHEAD experience affect FDA approval of drugs and devices to treat obesity?

The FDA has viewed obesity as a cosmetic issue and only recently acknowledged it as a disease, worthy of attention as other cardiovascular risk factors. They (meaning the FDA Endocrinologic and Metabolic Drug Advisory Committee and FDA staff) have started, just barely, to view obesity as a cardiovascular disease risk factor, like hypertension. They have also opined, from time to time, that if folks only ate less and exercised more, they would not need drugs. So how does this decision play into these views? On one hand, they may be convinced that obesity is not so easy to treat as they thought by diet and exercise. On the other hand, they may think that there is less need for anti-obesity medications because other treatments, e.g. statins, lipid-lowering drugs, anti-hypertensives, are doing their job in reducing CV risk factors. So, this view may raise the bar for approval of new anti-obesity medications. On the other (the third?) hand, we may need a re-definition of obesity which tones down its “diabetes-metabolic syndrome-mortality” axis and raises its “disability-mobility-quality of life” axis. (Running out of hands here, I would not underestimate the potential for greater evidence of obesity’s role in the development of various cancers).

The recent trend in thinking at the FDA Endocrinologic and Metabolic Drug Advisory Committee (EMDAC) has been to view anti-obesity medications narrowly as cardiovascular disease treatments. The EMDAC met on March 28th and 29th,2012  and discussed how to assess the cardiovascular benefits and safety of anti-obesity medications. At the end of March 28, Dr. Rasmussen, who is the Industry Representative on the committee had the following exchange with Dr. Eric Coleman of the FDA.

Dr. Rasmussen: In your (Dr. Colman’s) presentation, you showed that there are different            populations pre-approval and in post-approval studies. ..Are we compromising the risk-            benefit evaluation if we impose more risk-based patients pre-approval?

Dr. Colman: I’m not sure I understood your question. Could you rephrase it?

Dr. Rasmussen: Maybe I’m preempting some of the discussion that we’ll be having                        tomorrow, whether we should require more high-risk CV patients pre-approval to rule out        a upper bound of the 95 percent confidence interval. But by doing so, we will likely be                including older patients with established cardiovascular risk disease. And I’m wondering          whether including more of those types of patients will compromise the benefits side of                doing the benefit-risk evaluation.

Dr. Coleman: Yes. And it might be that if the program had the resources to do this, that              that would just be one component of the program, and that there would be other be other,        smaller, shorter-term studies where they could study lower-risk individuals, younger                   individuals for shorter periods of time.

Dr. Rasmussen: But my concern was based on the fact that the SCOUT study didn’t really – I      mean, it looks like it wouldn’t be actually be able to be approved if it was submitted pre-            approval. ..(FDA EMDAC, March 28, 2012, transcript at p. 334-5)

On the second day of the hearing, Dr. Rasmussen returned to the topic.

Dr. Rasmussen: So I would just like to add a little bit of perspective on what “enrichment”          (Editor: “enrichment” is the term used here by the FDA referring to adding persons at high        risk of CVD to the pool of subjects in obesity drug trials) in this context will mean. I mean, I      did a little bit of “back-of-the-envelope” calculation, and maybe we’ll have that confirmed        after lunch. But, I mean, current programs, approximately 3,000 patient-years of                        exposure generate 15 MACE events or so. Even if we were to double that patient-year                  exposure with a population of a 3-percent annual event rate coming to additional 60                    events, we would still only be able to exclude a doubling of the hazard ratio. So, I mean,              what we’re talking about here is actually completely shifting the population that we’re                going to study in obesity programs to establish cardiovascular disease and not necessarily        the population that we know actually seek treatment in the real world. So, I think that’s              worth keeping in mind, that enrichment may sound appealing because it sounds like we will       add a fraction of sick patients, but in reality, this will be a complete shift of the population.        (FDA, EMDAC, March 29, 2012, at p. 169)

(Dr. Rasmussen’s calculations appear correction. The cardiovascular safety trial the FDA asked Orexigen Therapeutics to undertake surpassed its original goal of 7,000 patients in process of enrolling 9,000 patients to find 87 major CV events earlier than expected. Orexigen: Press Release Contrave CV study.)

A bit later, Dr. Rena Wing was asked about the influence of statins on the Look AHEAD trial. She responded:

Number one, that more and more people are being treated with statins. There’s better                blood sugar control. There’s better hypertension control. So you’re going to have to look          at what’s going to happen to the event rates in these studies. I was very surprised that your      event rates that you’re showing me in many of these trials looked so high compared to the        event rates we’re seeing in Look AHEAD. Now, some of that is because we did do GXTs.                (Editor: Graded Exercise Tests.) We did select healthier patients. But I also think that if you      are doing trials, in the United States especially, and with diabetics where there’s more and        more emphasis on increasing the use of lipids, increasing their blood pressure control, that      you’re going to be driving down your risk factors, and you’re going to have more and more      confounds with medication. (FDA, EMDAC, March 29, 2012 transcript, at p. 346)

At the Cleveland Clinic’s Obesity Summit earlier this month, I asked cardiologist Steve Nissen about the FDA’s pushing companies to undertake clinical trials to rule out a CVD risk. He responded that one of the challenges of cardiovascular outcome studies of obesity drugs is that in order to get enough cv events you have to study patients with existing heart disease or at very high risk of a cv event . This pushes the trial into populations which are considerably sicker than the population likely to take the obesity drug. He suggested that FDA should look at absolute risk rather than the relative risk of the drug. If one looks at the absolute risk, you can study any reasonable population likely to take the drug. This change in the statistical approach allows one to study more typical populations.

 

In any event, it will be sometime before we know how the newer anti-obesity medications, like Contrave if approved), Belviq™ and Qysemia™ will impact cardiovascular disease risk factors.

Bariatric Surgery: Last Man Standing?

A study out of the Cleveland Clinic published in the New England Journal of Medicine in April, 2012 followed over 90% of 150 patients for 12 months. The study, a face to face comparison of medical therapy versus surgery in patients with uncontrolled type 2 diabetes, showed a clear superiority for bariatric surgery.  The proportion of patients achieving a hemoglobin A1c level of 6% after 12 months by medical therapy alone was 12%; for those in the medical plus gastric bypass surgical group it was 42% and for the medical plus sleeve-gastrectomy group it was 37%. Weight loss was greater in the gastric bypass group (-24kg) and sleeve gastretcomy group (-25.1kg) than in the medical therapy group (-5.4kg). Use of drugs for glucose control, lipids and blood pressure control decreased in the surgical group but increased in the medical group. PubMed: Bariatric surgery versus intensive medical therapy in obese patients with diabetes

In regard to cardiovascular risk factors, a systematic review of the literature on bariatric surgery analyzed over 60 studies involving 19,543 patients. At baseline, the mean patient was 41.7 years old, female and had a BMI of 47.1. Baseline prevalence of comorbid conditions which increase risk of CVD was hypertension (44.4%), diabetes (24%) and hyperlipidemia (43.6%). After correcting for publication bias, 36% of subjects had improvements in hypertension, 26% for diabetes and 34% for hyperlipidemia. Calculating the changes for mean participants, the authors found that a woman, without baseline CVD, diabetes or smoking, who is taking anti-hypertensive drugs, will move from an 8.6% 10 year global risk for CVD to a 3.9% risk. A man, with no CVD or smoking but whose diabetes and need for anti-hypertensive drugs resolves after surgery, will move from a 10 year global risk of 18.4% to 4.7%. PubMed: Bariatric Surgery and Cardiovascular outcomes: a systematic review

So, where are we? The gold standard of lifestyle change is tarnished. The drug story is muddy at best. Bariatric surgery is clearly producing the superior results. However, access to surgery is, and will remain, a problem. The challenge for the leaders in the field is to find ways to have surgery reach more people and not be a procedure for the 1 percent. Even with greater access to surgery, the obesity-diabetes epidemic will continue to be a major health crisis. It’s time to be humble in the face of this disease and realize a lot more research is going to be needed…and soon.

 

Brain and Gut

September 26th, 2009 No comments »

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

Behavior

September 26th, 2009 No comments »

Understanding the gene-environment-behavior connections Implications of gene-behavior interactions: preven…[Obesity (Silver Spring). 2008] – PubMed Result

Some see eating as an automatic behavior over which individuals have less control than they think Eating as an automatic behavior. [Prev Chronic Dis. 2008] – PubMed Result

While controversial, the view of eating or hunger as an addiction has many interesting parallels with studies of addictive behavior The neurobiology of appetite: hunger as addiction. [Int J Obes (Lond). 2009] – PubMed Result

It is generally accepted that humans have a genetic predisposition to obesity which is fueled by our modern environments. However, not everyone is becoming obese. Why? Individual differences in the neurophysiology of r…[Int J Obes (Lond). 2009] – PubMed Result Obese-resistant individuals may sense changes in their energy intake more quickly than persons who are obese. The effects of overfeeding and propensity to weigh…[Physiol Behav. 2009] – PubMed Result

Obese individuals may have evolved weak mechanism which favor overeating. Control of food intake in the obese. [Obes Res. 2001] – PubMed Result High concern over food intake may, paradoxically, lead to higher intake Determinants of food choice: relationships with ob…[Obes Res. 2001] – PubMed Result

Stringent parental controls may also disrupt a child’s development of internal cues for controlling eating. Development of eating behaviors among children and…[Pediatrics. 1998] – PubMed Result