Taste and Smell, they changed drastically

And I wondered why. So, off to Google I went to do some reading. It seems the leading suspect is a substance called ghrelin. Ghrelin is responsible for enhancing exploratory sniffing and olfactory sensitivity in order to locate, identify, and select foods. In a 2011 study, Tong et al concluded that lower ghrelin production equaled increased satiety and pleasantness ratings for food odors were reduced dramatically in humans.

 Ghrelin is a hormone produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas that stimulates hunger. Ghrelin levels increase before meals and decrease after meals. It is considered the counterpart of the hormone leptin, produced by adipose tissue, which induces satiation when present at higher levels. In some bariatric procedures, the level of ghrelin is reduced in patients, thus causing satiation before it would normally occur.

So, with the removal of most of the stomach, the production level of ghrelin is greatly reduced. This causes changes in the need or desire for food and thus the olfactory stimulus normally associated with many foods.

Ghrelin has emerged as the first identified circulating hunger hormone. Ghrelin is also the only known circulating orexigen, or appetite enhancing hormone. It is produced mainly in the small and large intestines, but can also be secreted by the lungs, pancreatic islets, gonads, adrenal cortex, placenta, kidney and brain (Ariyasu, 2001). Again the diversity in areas of ghrelin production indicates that this hormone has widespread and numerous biological function. Ghrelin and synthetic ghrelin mimetics (the growth hormone secretagogues) increase food intake and increase fat mass^[16][17] by an action exerted at the level of the hypothalamus. They activate cells in the arcuate nucleus^[18][19] that include the orexigenic neuropeptide Y (NPY) neurons.^[20] Ghrelin-responsiveness of these neurons is both leptin- and insulin-sensitive.^[21] Ghrelin also activates the mesolimbic cholinergic-dopaminergic reward link, a circuit that communicates the hedonic and reinforcing aspects of natural rewards, such as food, as well as of addictive drugs, such as ethanol.^[21][22][23] Indeed, central ghrelin signalling is required for reward from alcohol.^[24] and palatable/rewarding foods.^[25][26] There is also strong evidence that ghrelin has a peripheral appetite modulatory effect on satiety by affecting the mechanosensitivity of gastric vagal afferents, making them less sensitive to distension resulting in over eating.^[5]


I had many issues with the last sentence above. I would eat, eat some more and be hungry. So I would eat some more. And feel hungry. And then, after stuffing myself with entirely too much food I would suddenly feel full.

Body weight is regulated through energy balance, the amount of energy taken in versus the amount of energy expended over an extended period of time. Studies have shown that ghrelin levels are negatively correlated with weight. This data suggests that ghrelin functions as an adiposity signal, a messenger between the body’s energy stores and the brain (Schwartz, 2000). When a person loses weight their ghrelin levels increase, which causes increased food consumption and weight gain. Conversely, when a person gains weight, their ghrelin levels drops, leading to a decrease in food consumption and weight loss (Tung, 2005). This suggests that ghrelin acts as a body weight regulator, continually keeping one’s body weight and energy stores in check.

This, of course, is assuming that your body functions properly.

The change in taste and smell actually have a much researched name. It can present in people who have not had surgery for various reasons.

 Disorders of taste and smell may be overlooked in aspects of medical practice because these senses are not considered critical to life. However, it is important to diagnose and treat dysguesia and dysosmia because these disorders could possibly lead to nutritional deficiencies (which in turn could cause other more severe problems), if they prevent a patient from consuming adequate food and/or supplements.


The disorders of smell are classified as "-osmias" and those of taste as "-geusias."

• Anosmia - Inability to detect odors
• Hyposmia - Decreased ability to detect odors
• Dysosmia - Distorted identification of smell
  

  • Parosmia - Altered perception of smell in the presence of an odor, usually unpleasant
  • Phantosmia – Perception of smell without an odor present
  • Agnosia - Inability to classify or contrast odors, although able to detect odors
• Ageusia - Inability to taste
• Hypogeusia - Decreased ability to taste
• Dysgeusia – Distorted ability to taste
  
  

 In 2008, a case study on RYGB detailed how postoperative food aversions, taste changes, and loss of appetite affected one patient and described nutrition intervention techniques employed by the treating clinician. At seven weeks post-RYGB, the patient had lost 47 pounds, but due to lack of appetite, the result of a “phobia” of food textures and taste alterations, her dietary intake had not progressed beyond clear liquids. The patient complained of a “gag response” when eating, or even thinking about eating, certain foods. The nutritional intervention employed by the treating registered dietitian (RD) focused on adding all textures and types of foods back into the diet with sips of water to cleanse the mouth after eating. Additionally, the patient adhered to bi-weekly and eventually monthly phone visits with the RD to review oral intake. During these phone calls, the RD provided encouragement and emotional support to the patient. At one year postoperative, the patient had achieved a total weight loss of 109 pounds and was tolerating all foods with the exception of hamburger and breads.


So I'm fascinated and anxious to discover what else smells different and what else tastes different. I know that chocolate milk is off the edible list. That was a most disgusting experiment.