When I look at myself in the mirror, I think, how did my brain allow this to happen? My brain’s job is to protect me. Yet here I stand, 500 plus pounds, at the edge of my grave, which I, basically, dug with a fork. To understand where you are, you have to know where you have been. I have been overweight ever since I learned how to feed myself. Most kids’ parents had to force them to eat all of the food on their plates. My parents had to stop me from licking the pattern off my plate.
I have always preferred palatable foods. Palatable foods are calorie dense foods that have high concentrations of fat and sugars. Of the palatable foods, I have always gone for the high-fat foods. While other kids were eating candy and drinking Grape Kool-aid, I was popping pork chops as if they were M&M’s and drinking gravy through a straw.
Palatable foods are also the most energy dense foods, and subsequently evolution predisposed human taste to prefer them. Regardless, preferring calorie dense food is one thing, however most compulsive overeaters’ relationships with palatable foods go way beyond anything evolution had in mind. Studies have shown that palatable foods not only stimulate the appetite they stimulate the rate at which we eat them. This explains a great deal: at times, I eat so voraciously people get up to dance. Eating rapidly lends to overeating because it obscures the amount of food consumed.
Studies have also shown that palatable foods affect the brain’s reward system in the same manner as opioids. Thus, consumption of palatable foods predisposes humans to addictive behavior. Addiction is just habit formation in the brain, which I discuss in my first post: “Compulsive Overeating and Habit Formation.”
Homeostatic function, (calories in vs. calories out) regulates the metabolic consequences of food (energy, fat storage, weight loss), where as the reward function of food in the brain controls the pleasurable consequences eating. In addition, studies have shown that consuming palatable foods in tandem with weight gain, cause de-sensitization of the D2 dopamine receptors in the reward system in the brain. Less reward translates into increased consumption of palatable foods, which in turn leads to more weight gain, which results in further de-sensitization of dopamine receptors and decreased reward value, which promotes further excessive consumption of palatable foods, etc. This downward synergistic inscription on homeostatic function is the signature of obesity that sentences obese people to a cavalcade of negative health consequences.
In retrospect, I realize the availability of palatable foods was also a major contributing factor. Evolution did not anticipate technology’s influence on the availability of food. We are not the ancients roaming around collecting nuts and berries, feasting on the occasional suckling beast. Most humans have much more food than they need—especially palatable foods. I grew up very poor and with the exception of one prolonged UAW strike; we always had plenty of food. On the darker side of town, two things were readily available, and palatable food was the other one.
Like many kids, I grew up in a “functional alcoholic” home (as oxymoronic as that sounds). Emotional, physical, sexual and psychological abuse dominated my early years. Countless studies have shown that early life trauma causes hypothalamic remodeling. This is very important because the hypothalamus is the key brain structure in homeostatic maintenance. The highly adaptive brain wires itself according to its circumstance. If the circumstances are severe, the adaptations are maladaptive because desperate survival is seldom pretty. In addition, when persistent stress, emotional and psychological factors are present, the hedonic factors will override the homeostatic control of food intake. This is because the survival dial is on desperate. When this occurs the brain utilizes dopamine derived from food’s hedonic value as a drug to intervene on the pathophysiology of stress. Hence, food goes from being a fuel to being an opiate to intervene on suffering, which is rather ironic considering mµ opioid receptors are involved.
Key Signaling Hormones
Leptin and ghrelin, which are hormones that regulate food intake and fat storage, are also important. Leptin secreted by adipose tissue and the stomach mediates long-term regulation of energy balance by suppressing eating, which thereby causes weight loss. Ghrelin on the other hand, produced solely in the stomach is a fast-acting hormone that causes appetite. Leptin from adipose tissue and ghrelin are both released into the blood stream and travel across the blood-brain-barrier and binds to receptors found mostly in the hypothalamus, but also in other brain regions. Gastric leptin and ghrelin also travel to the brain via the vagal nerve and nucleus tractus solitarus. This leptin signal predicts satiety, based on nutrient content information in the stomach and inhibits the reward circuitry in the brain that regulates the hedonic value of eating. Leptin and ghrelin both stimulate and suppress hypothalamic neurons containing various neuropeptides, which result in orexic (appetite) and anorexic (loss of appetite) effects.
Because leptin suppresses appetite and ghrelin encourages eating, one would expect to find decreased serum leptin levels and increased ghrelin levels in the blood. I would have bet the farm that my ghrelin levels were at flash flood status. Not so, it is exactly the opposite. The fatter you are, the higher your serum leptin levels and the lower your ghrelin.
Leptin and Overeating
When leptin is functioning properly, it prevents excess eating, by telling insulin to shut off after you have had enough. When you over eat, it causes a surge in circulating leptin and insulin. Sustained exposure to these elevated leptin levels damages the hypothalamus making it less sensitive to leptin, which eventuates in leptin resistance. Conversely, high fat content foods decrease circulating leptin in the bloodstream because it decreases leptin secretion in the adipose tissues. Defective leptin transport across the blood-brain-barrier also contributes to leptin resistance. In addition, obesity exacerbates defective leptin transport across the blood-brain-barrier. Animal studies have shown evidence of this.
Connecting the Dots
In a healthy individual, the body is able to communicate effectively with the brain via hormones such as leptin, ghrelin, insulin and other informational substances. In the obese individual’s unhealthy body, converging reasons breach communication between the brain and the body.
1) Hypothalamic remodeling resulting from early life trauma compromises leptin receptors.
2) Elevated serum leptin levels from obesity and overeating damage the hypothalamus and resulting in leptin insensitivity.
3) The downward synergy of palatable food consumption in tandem with weight gain causes de-sensitization of the D2 dopamine receptors in the reward system in the brain. Less reward translates into increased consumption of palatable foods, which in turn leads to more weight gain, which results in further de-sensitization of dopamine of receptors, etc.
4) Maladaptive stress regulatory strategies by that utilize the dopamine from hedonic food value to offset cortisol surges, concomitant with the availability of palatable foods.
5) Processed foods further confuse the signaling mechanisms in the brain. The result of this is you overfeed your body because your brain believes you are starving. Like a helpless child, at the hand of an abusive parent, and silent witnesses, your body screams out helplessly to deaf ears, as it slowly dies.
My body has been screaming for years at my deaf brain. That is how I got here. Fortuitously, I have a brilliant cardiologist. He suggested not eating after 6:00 p.m. and before 10:00 a.m. This has tremendous neurochemical and hormone signaling benefits. After several months of this, for the first time in my life the fat stores in my body are beginning to communicate their status to my brain.
‘Forever’, came this day! Remain fabulous and phenomenal.
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