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.
