Cobbers on the Brain

If you went around asking people what they think the cause of obesity is, they will most certainly tell you it is overeating. Even though they are right, they usually ignore other factors that lead to obesity. The notion that obesity is a disease is still not well accepted by the public. In this blog I will try to demonstrate how other factors can put a person at a high risk of being obese.
But before we dig into the all sciencey stuff we have to understand what obesity is.
What is obesity?
Obesity is excess adipose (fat) tissue. What is this, you ask? So a fat cell is an endocrine cell and adipose tissue is an endocrine organ. Significantly, excess adiposity or obesity causes increased levels of circulating fatty acids and inflammation. You can look at obesity as excessive body fat.

So how do I know if am obese?
Excess fat tissues can be determined by the use of a Body Mass Index (BMI). BMI is a mathematical calculation involving height and weight, irrespective of family history, gender, age or race. BMI is calculated by dividing a person’s body weight in kilograms by their height in meters squared (weight [kg] height [m] ^2) or by using the conversion with pounds (lbs) and inches (in) squared.

Other factors to known.
Insulin:  we usually associate insulin with low blood sugar and diabetes. Most people know that the role of insulin is to regulate metabolic processes like glucose uptake and lipid synthesis. What they don’t know is that insulin and insulin signaling plays a big role in obesity. Insulin acts on two neurons in the brain.

• The POMC neurons which signals us to stop eating
• The AgRP neurons which signals us to eat

But what happens is

• Over nutrition leads to
• Hyperinsulinemia (too much insulin)
• Which leads to insulin resistance
• That causes inhibition of the POMC neurons that tell you to stop eating
• Leaving the AgRP neurons that do not tell to stop eating so you over eat

Leptin: Leptin is a hormone that is produced by the fat cells in the body. Its main role is regulating how many calories we eat and burn, as well as how much fat we carry on our bodies. The more body fat they carry, the more leptin they produce. What happens is that,

• Eating->Increased body fat->Increased leptin->Decreased appetite, increased energy expenditure

But in leptin resistance, leptin does not signal to the brain that we are full and so we keep eating.

• Overeating ->increases body fat-> increased leptin( too much this time)-> blockage of signaling to the brain -> obesity

And just a reminder, obesity is not joke. It puts individuals at risk for more than 30 chronic health conditions. They include: type 2 diabetes, high cholesterol, hypertension, gallstones, heart disease, fatty liver disease, sleep apnea, GERD, stress incontinence, heart failure, degenerative joint disease, birth defects, miscarriages, asthma and other respiratory conditions, and numerous cancers. Think twice before you eat that box of pizza for a second time in a week.
 
 

Obesity rates are skyrocketing, and there is no denying that it is a large problem for our country. There are many contributing factors that lead to the development of obesity. As our diets has become more and more heavily composed of fat, sugar, and carbs, our bodies are undergoing changes that are leading to extreme health problems, including Type 2 diabetes and Obesity. Processed foods have become more addictive, because of the high amounts of fat, sugar, and additives they contain. These components in our food are altering the normal signaling within our bodies, leading to the development of chronic metabolic illnesses.
 
The Role of Insulin
Insulin is a key factor that our bodies use in maintaining energy homeostasis. Insulin is used to regulate the amount of energy your body needs and expends.
After we eat, insulin is released into the bloodstream, causing the food (glucose) that we consumed can be absorbed into our cells and used for energy. Insulin also acts in the brain where it binds to its receptors on neurons in the hypothalamus, causing an anorexigenic response. The anorexigenic response is one that lets you know you are full and should stop eating.
 
Insulin and Reward
Insulin also acts on dopaminergic neurons in the midbrain (involved in the reward pathway) The desire to eat is not only driven by the body’s current nutritional state, but also by the rewarding aspect of food. Reward- based eating behavior is likely linked strongly with obesity because the signaling in these circuits can eventually override the signaling in the hypothalamus. Insulin is able to change reward-related behavior by decreasing sucrose intake and conditioned preference for high-fat food. Therefore, insulin signaling is involved with the regulation of energy homeostasis and food intake in these neurons as well. When fed, insulin signals for you to stop eating for pleasure, and attempts to control your food intake.
 
Insulin Defects= Bad News
Eating a high saturated fat diet causes disruptions in the insulin signaling pathway, thus interfering with energy homeostasis and the sending of messages to stop eating. This leads to inflammation in the brain and causes lots of stress in the cells. A cascade of inflammation begins; making the insulin receptor unable to continue the cascade that is supposed to occur once insulin is bound. This particular problem is what is known to be Type 2 diabetes. Insulin is present, and so is its receptor, but the rest of the pathway is dysfunctional.
 
Effects of Processed Foods
Since processed foods contain fat and sugar than we are not meant to consume, when we them, we start to crave them because the chemicals, fats and sugars they contain are causing chemical changes in our brains. This can lead to insulin resistance and the dopamine reward pathway can eventually override the hypothalamus, since we develop such a strong desire to eat these foods. It is a cascade that can very quickly get out of control and manifest into what is essentially brain disease, presenting itself visually as obesity.
 
Treatment
Hedonic feeding, the term used to describe the drive to eat to obtain pleasure, without actually having an energy deficit, is the type of hunger that most weight-loss programs are targeting. They are focused on relieving cravings, instead of targeting the hypothalamus and the inflammation/stress that occurs there due to the insulin resistance that occurs. There are several different medications available that can be used to treat food cravings in order to lose weight. Gastric bypasses are also common and effective. They bypass most of the stomach so that the individual will feel full much faster and not physically be capable of eating any more.
 
Regulations?
Since it seems like the cause of this obesity problem all comes back to the ingredients in the food we are eating, shouldn’t there be more restrictions and regulations on what companies are allowed to put in processed foods? Other countries have more restrictions on certain food preservatives and contents that they are allowed to include, and overall this seems to be an intelligent, logical idea. Until any laws are passed, however; all that we can do to steer clear of Type 2 diabetes and obesity is to eat whole, nutritious foods and get plenty of exercise. Food companies can tempt us all they want with the high-fat, high-sugar foods they process, but we must look out for our health and do the best we can to resist these foods that will give us brain disease.
 
 
For more information related to insulin signaling, energy homeostasis, and glucose metabolism, please visit:
https://moodle.cord.edu/pluginfile.php/625315/mod_resource/content/0/2013%20CNS%20insulin.pdf
 
 

Throughout our media, we see headlines about obesity and the plague-like effect it has over our country. Shows and lifestyle programs are dedicated to stopping obesity. Michele Obama advocated for the elimination of obesity in schools. Messages infiltrate our TVs and radios that tell us to eat less processed food and exercise daily to combat obesity. However, is it possible to avoid or eliminate obesity by simply changing our diet and lifestyle? Or is there more to the problem… Is obesity an actual disease that must be treated with more finesse?
Obesity is indeed an actual disease and despite contrary belief, is not based on laziness or lack of self-control.
In a normal functioning brain, when we consume food, insulin and leptin proteins activate a very specific pathway that leads to ion efflux from specialized brain cells called neurons. This ion efflux of potassium leads to an action called hyperpolarization. Hyperpolarization is important because it slows the neuron firing that tells us to eat more. There are two types of neurons that control our eating: POMC-neurons, which tell us to stop eating, and AgRP-neurons, which tell us to eat more. Insulin acts on these neurons by decreasing the number of AgRP-neurons in the brain and increasing POMC-neurons. Therefore, when we eat and our body releases insulin, we respond by stopping our eating. However, in people who suffer from obesity, overnutrition occurs and normal cellular function becomes cellular stress. Specifically, ER stress leads to physical inflammation of the brain and this inflammation creates insulin resistance. Therefore, the insulin in the brain of someone suffering from obesity does not function properly and cannot tell the body to stop obtaining food. Overall, the effect of overnutrition and obesity becomes a deadly cycle of continual eating and weight gain.
The biological cycle of obesity occurring in the brain cannot be fixed by exercise or dietary changes alone. Drugs that can block the pathway or stimulate normal pathways are more likely to create brain reversals that have a positive effect.
So, the next time we see a show or program about obesity and we are quick to judge the lack of self-control, let us remember that obesity is a disease that physically effects the brain and requires medication or surgery in most cases. It is not a matter of laziness, but of better treatment options and open-mindedness.
http://www.cell.com/trends/endocrinology-metabolism/pdf/S1043-2760(12)00204-4.pdf