Don’t Mess with your Appetite Hormones

New research confirms that yo-yo dieting can cause a communication breakdown in your appetite hormones, leading to more fat accumulation and a resistance to weight loss.

appetite hormonesThis recent study published in the Journal of Clinical Endocrinology & Metabolism shows that dieting can lead to hormonal imbalances and resistance in the appetite hormones ghrelin and leptin.

These hormones control your food cravings, hunger, satiation and how calories are put to work. However, these hormones can become ineffective when they are subjected to too much dieting and subsequent overeating.

The evidence from this study shows the importance of maintaining a healthy lifestyle once you’ve made the decision to lose weight. Through a healthy, low-calorie diet and regular exercise, you can achieve so much more than starving yourself and going on a diet every time you gain weight.

Besides eating healthy and becoming more active, there are a few other things you can do to help keep the weight off.

While there are conflicting views of whether eating before bed is good or bad, if your goal is to lose weight, then not eating before bed is good advice. This will encourage the body to use up stored fat for nightly metabolic functions rather than accessing readily available calories in the blood stream. The general rule is to cease eating three hours before you retire for bed.

Just because our society is geared towards eating three meals a day doesn’t mean that our bodies are evolved to handle such large quantities of food in one sitting. In fact, dividing your calories into 5 or 6 smaller meals throughout the day will help you to maintain blood sugar levels and decreases your risk of diabetes. It also helps to sustain energy levels so you’re not on a roller coaster, peaking and crashing all day long.

Chew your food properly to trigger digestive hormones and appetite control. Each mouthful should be chewed for 20-40 bites. The physical motion of the jaw when you’re chewing sends a signal to the brain and it judges by the number of chews whether you’re full or not. If you gulp your food, you will end up eating too much and putting on weight. By chewing your food properly, you will absorb more nutrients, vitamins and minerals, which will improve your health.

Avoid processed food all together. Science is discovering more and more evidence that proves the true harm processed food is doing to our digestive systems. With little nutritional value and an abundance of starch and sugar, these processed foods create spikes in your blood sugar and render your appetite hormones ineffectual to the point that they don’t comprehend whether to burn fat, store fat or to keep eating.


Bending the Brain to Find the Roots of Hunger and Eating

Bending the Brain to Find the Roots of Hunger and EatingSynaptic plasticity – the ability of the synaptic connections between the brain’s neurons to change and modify over time — has been shown to be a key to memory formation and the acquisition of new learning behaviours. Now research led by a scientific team at Beth Israel Deaconess Medical Center (BIDMC) reveals that the neural circuits controlling hunger and eating behaviours are also controlled by plasticity.

Described in the February 9, 2012 issue of the journal Neuron, the findings show that during fasting, the AgRP neurons that drive feeding behaviours actually undergo anatomical changes that cause them to become more active, which results in their “learning” to be more responsive to hunger-promoting neural stimuli.

“The role of plasticity has generally not been evaluated in neuronal circuits that control feeding behaviour and with this new discovery we can start to unravel the basic mechanisms underpinning hunger and gain a greater understanding of the factors that influence weight gain and obesity,” explains senior author Bradford Lowell, MD, PhD, an investigator in BIDMC’s Division of Endocrinology, Diabetes and Metabolism and Professor of Medicine at Harvard Medical School (HMS).

Adds BIDMC Chairman of Neurology Clifford Saper, MD, PhD, “For most animals, finding enough food to survive is their biggest daily challenge, and so the brain’s increase in feeding drive may be adaptive. But, for humans who are overweight, reducing this drive to the AgRP neurons may prove to be a path to future weight loss therapies.”

The roots of hunger, eating, and weight are based in the brain’s complex and rapid-fire neurocircuitry. Over the years, nerve cells containing agouti-related peptide (AgRP) protein and pro-opiomelanocortin (POMC) protein have emerged as critical players in feeding behaviors. Located in the hypothalamus, the brain area that controls automatic body functions, AgRP neurons have been shown to drive eating and weight gain while POMC neurons inhibit feeding behaviours, causing satiety and weight loss.

Previous work by the Lowell lab and others had demonstrated that when AgRP neurons in mice are artificially switched on, the animals eat voraciously, consuming four times more than control animals. “The ‘switched-on’ animals search in an unrelenting fashion for food, and when given a task to obtain pellets, will work five times harder to get them,” Lowell explains. “Given the important role played by AgRP neurons, we had a great interest in understanding the factors that regulate their activity.” While much focus had centered on hormones, including leptin, insulin and ghrelin, the Lowell team hypothesized that other nerve cells might be the mechanisms that were regulating neuronal activity.

Neurons communicate with one another via neurotransmitters, chemical messengers that traverse synapses, the specialized junctions between upstream and downstream neurons. Glutamate is one such excitatory neurotransmitter.

“Studies in other regions of the brain [for example those controlling learning and reward and addiction behaviours] have demonstrated that glutamate synapses are highly plastic, changing in their strength and sometimes even in their number,” explains Lowell. Shown to exert powerful control over behaviour, synaptic plasticity is brought about when glutamate binds to NMDA receptors on downstream neurons.

“NMDA receptors are unusual and really interesting,” he adds. “When glutamate gets released by upstream neurons and binds to NMDA receptors, calcium enters the downstream neuron. This, in turn, engages signal transduction pathways that cause synaptic plasticity. In other parts of the brain, such as the hippocampus, NMDA receptors drive plasticity which serves to encode memories.”

Led by co-first authors Tiemin Liu, PhD, Dong Kong, PhD, Bhavik P. Shah, PhD, and Chianping Ye, PhD, the investigators created and studied mice genetically engineered to lack glutamate-binding NMDA receptors on the AgRP neurons. For the sake of comparison, they also created mice genetically engineered to lack NMDA receptors on POMC neurons.

They found that while mice lacking NMDA receptors on POMC neurons showed no change in feeding behaviour, the situation was dramatically different in the mice lacking NMDA receptors on AgRP neurons. “These mice ate a lot less and were much skinnier than a group of control mice,” explains Lowell. Furthermore, the scientists found that a 24-hour period of fasting — which causes intense hunger in the control mice — was associated with a 67 percent increase in the number of dendritic spines on the AgRP neurons.

“Dendritic spines are tiny structures attached to the neuron’s dendrites, the tree-like branches that receive incoming signals from upstream neurons,” explains Lowell. “These structures are the physical site, the subcellular communication hub, where synaptic input from upstream glutamate-releasing neurons is received, typically one synaptic input per spine.”

“I’ve been studying spines for a long time and I’ve never before seen a manipulation that triggered such rapid and robust changes in spine number,” says coauthor Bernardo Sabatini, MD, PhD, a Howard Hughes Medical Institute investigator in the Department of Neurobiology at Harvard Medical School. “Clearly, feeding is plugging in to the most basic mechanisms that control synapse and spine number in these cells. This may be a great system to understand not only feeding behaviour, but also to understand the cell biology behind dynamic synapse formation and retraction.”

When the control mice were refed — and their hunger alleviated — the number of spines dropped back to normal. (In contrast, fasting had no effect on spine number in the mutant mice lacking NMDA receptors on AgRP neurons.) These dramatic changes in spine number and their tight association with states of hunger and satiety in control mice — and the absence of changes in spine number in mice lacking NMDA receptors on the downstream AgRP neurons- strongly suggests that structural plasticity of excitatory glutamate synapses on AgRP neurons is an important regulator of feeding behaviour, says Lowell.

“Obesity is a major risk factor for type 2 diabetes, cardiovascular disease, and certain types of cancer,” he adds. “By understanding the neurobiological mechanisms underlying feeding behaviours, we can work on treatments for a problem that has now become a global epidemic. These findings move us closer to a mechanistic understanding of how various factors controlling hunger might work.”

This study was supported by grants from the National Institutes of Health and the American Diabetes Association, as well as support from the Shapiro Predoctoral Fellowship and the Parkinson’s Disease Foundation Postdoctoral fellowship programs.

In addition to Lowell, Sabatini and the paper’s first authors, other coauthors include BIDMC investigators Shuichi Koda and Zongfang Yang and HMS investigators Arpiar Saunders and Jun B. Ding.

Journal Reference:

  1. Matthew R. Banghart, Bernardo L. Sabatini.Photoactivatable Neuropeptides for Spatiotemporally Precise Delivery of Opioids in Neural TissueNeuron, 2012; 73 (2): 249 DOI: 10.1016/j.neuron.2011.11.016


Beth Israel Deaconess Medical Center (2012, February 8). Roots of hunger and eating: Plasticity in the brain’s wiring controls feeding behavior in mice. ScienceDaily. Retrieved February 21, 2012, from­/releases/2012/02/120208132253.htm

Appetite Hormone Ghrelin could Be the Answer to Obesity

Ghrelin is a digestive hormone that regulates our appetites, our hunger pangs and tells us when to stop eating. It is a vital hormone in the study of obesity.

Appetite Hormone Ghrelin could Be the Answer to ObesityNew research to be presented at the upcoming annual meeting of the Society for the Study of Ingestive Behavior, the foremost society for research into all aspects of eating and drinking behavior, finds that increasing the level of ghrelin in the blood can modify a person’s ability to taste food and alter their brain chemistry. Ghrelin is the cause of these food-related clues and as a result, increases dopamine levels in the brain at the most prominent reward center.

Scientists measured dopamine levels in rats as they enjoyed a highly rewarding diet of sugar. Administering ghrelin to rats while they ate sugar increased peak dopamine “spikes” within the reward center of the brain, whereas administering a drug that blocks ghrelin’s actions significantly reduced dopamine levels during sugar intake.

Study author Dr. Mitch Roitman from the University of Illinois at Chicago says, “The modulation of brain dopamine reward signals by a gut hormone that regulates appetite strongly supports this interaction as a way to direct the organism’s behavior towards further intake, perhaps by making food more rewarding. The results shed light on how peripheral body signals in general can shape brain-directed behavior.”

What this means is that this could be a means to treat obesity and over-eating disorders.


Society for the Study of Ingestive Behavior. “Feeding hormone ghrelin modulates ability of rewarding food to evoke dopamine release.” ScienceDaily, 12 Jul. 2011. Web. 14 Jul. 2011.

Originally published @ FITLODE.COM