Content Warning: Discussion of food, eating, and hunger. 

*Disclaimer: This essay is strictly in the context of TPN use and not eating disorders. I am by no means a medical professional or a psychologist. This is solely my personal experience and some information I gathered from my own research and should be interpreted as such.

As a person who was a “foodie” and was lucky enough to genetically have a fast metabolism, food and I were great friends. I grew up never having any dietary restrictions and was always known to go back for seconds, thirds, and even fourths, of food servings.

Once I began having health issues and dietary restrictions in 2020, it was much more frustrating to not be able to eat what I had wanted, and I ended up triggering a lot of small flares (1-3 days) because I didn’t have all of the restrictions memorized yet and figured “it can’t be that bad if I eat this right?”

When I was put on total parenteral nutrition (TPN) (intravenous nutrition through the veins) in August of 2021, I had already picked out my meal for when I would be able to eat again; a double beef patty burger from Smashburger with a side of fries.

Most of my family is from Spain so in our culture food is very important and a key part of pretty much every social gathering.

Having this change to not be able to tolerate food was one of my toughest battles and something that I’m still trying to figure out today.

I began getting hunger cravings on TPN after I had been switched from all lipid bags to 4 lipid bags and 3 non lipid bags per week. I had gotten this switch in January 2022 after getting parenteral nutrition associated liver disease (PNALD).

The switch did end up helping my liver enzymes, but my stomach began grumbling every evening and eventually the hunger cravings became a new daily thing to cope with.

Ever since starting on TPN, my sense of smell was heightened, and I could smell what food someone was eating from down the hall.

I had begun trying some methods to help with the hunger cravings such as watching food videos on Instagram and YouTube which helped me get through the first couple months. I then would ask family members or friends who were eating if I could watch them eat because it helped with how much I had missed even the smell of food just being in the house.

But unfortunately, it wasn’t enough to suffice me from my hunger cravings. I then began eating (more than what I had been doing just to keep my stomach from shutting down,) and would run into the kitchen in a hunger “craze” and would start smelling everything and grabbing food to figure out what I was going to eat. This was always the most dangerous times for me since I was willing to eat a chair and deal with the consequences later. (Read more on this in my article “Hunger Cravings”)

Unfortunately, pretty much every food I ate during one of these “lapses” resulted in week-long flares from ingesting things as small as the size of a cheerio. (Read my article “Egg the size of a cheerio”).

This bizarre relationship between my particular scenario of being “nourished” but being psychologically hungry made me ask the question:

Why is hunger still present in most who are “nourished” with parenteral nutrition?

This question still stumps me and it’s one that I took upon myself to research since I had posed the question to many medical professionals, and many had not had an answer.

As I had begun communicating with other tube fed patients on feeling this “hunger”, I had found that those who were on enteral feeding (tube feeding that goes through the digestive system) generally did not experience this “hunger craving” that PN consumers did.

This made me narrow my research to determine what was responsible within the digestive system to notify the brain that the body was nourished and how that compared to parenteral nutrition, regular hunger and psychological hunger (that then stimulates the gut into a response, i.e., feeling psychological hunger first and then getting a stomach grumble).

If we look at Maslow’s hierarchy of needs (which is a 5-tier pyramid used to represent human needs), the bottom tier represents physiological needs which includes food and water (1). In order to make it to the top of the pyramid to reach self-actualization, your needs at the bottom of the pyramid must be met first. From this, we can tell that this “hunger” is not true hunger as defined here by Maslow’s chart (which determines physiological needs) because otherwise, one wouldn’t be able to reach self-actualization.

Many including myself have been able to reach the top of Maslow’s pyramid while on parenteral nutrition, which shows that once again the body is being nourished but there’s a component of psychology that is sending signals to the brain and gut that are playing into this “hunger” feeling.

To preface, as noted by the Journal of Neuroendocrinology, “the regulation of appetite and energy intake is multifaceted and involves a number of organs and tissues,” so I will be breaking down some of these systems and will be explaining their component in this (2).

THE VAGUS NERVOUS SYSTEM

 The first potential cause is the vagus nervous system which is responsible for the vagus nerve. The vagus nerve is the “conduit” in transmitting gut hormones which suppress appetite to the brain (3). And while the vagus nerve can break down even further into more components (like cholecystokinin-a gut peptide, ghrelin-a “hunger” hormone, leptin-a hormone that helps regulate body fat, and more) I am going to focus on more generalized versions of the systems (4). The vagus system sends helps transmit satiety inducing hormones to the brain after meal ingestion (which again, these hormones are some of the ones I mentioned above) (5). The reason why this is significant is because a lot of the vagus system functions in result to the GI system secreting hormones after ingesting food (which makes sense) however, if you take this basis and apply it to parenteral and enteral nutrition, this is where you find a potential source of these “hunger cravings”. Since enteral nutrition is run through the digestive system (even if it’s parts of it), these hormones are still being released. Parenteral nutrition is going through the bloodstream and therefore the gut is not producing these chemicals from this particular system (my speculation) since no food is being taken in orally for the GI tract to be able to release the satiety hormones to then have the vagus nerve relay this further (specific to those who are NPO).  

**also, I did want to add a piece in here saying that dysautonomia and gastroparesis both include a disfunction of the vagus nerve, so these could also be playing into this “hunger” however this would need to be a separate meta-analysis to see how the different conditions relate to hunger and those on TPN in addition to having these conditions.

HOWEVER, this whole theory gets cracked right open when you look into orosensory stimulation which is for example, when you chew gum in order to help with “hunger sensations” which in turn do  stimulate the gut (even when you aren’t swallowing the gum) and release these satiety hormones (6, 7).  I can also personally attest to this working as one of my “tricks” to help with my hunger is to chew gum (this was even recommended to me by one of my GI doctors to encourage gut movement in order to not have everything shut down).

CHEWING MECHANICS IN PROMOTING DIGESTION

Chewing is an important factor when it comes to satiety and feeling full (8). Chewing is said to, “provide motor feedback to the brain related to mechanical effort reflecting food texture and…flavor,” (9). A meta-analysis from 2018 done by the University of Leeds studied how chewing impacted satiety. They found that with a fixed amount of food to chew, more chewing resulted in higher satiety than less chewing (10). Through this chew number increasing, more gut hormones were released which included these “satiety” hormones (11).

Through a different meta-analysis on the effects of chewing gum, they mention that “appetite suppression was found in the studies on chewing gum,” and that, “chewing [gum] significantly increased fullness and reduced hunger, desire to eat, and desire to eat sweet snacks,” (12).

This then brings up another method of how some who are unable to eat deal with this “hunger”- using a method known as the “chew-and-spit” method. I personally never felt comfortable in trying this method since it is most commonly known and associated with eating disorders. I was also concerned that even some of the food would mix with the saliva and this would be swallowed which could still result in flares (for me personally- since my body is so sensitive). My hypothesis of this method still resulting in some food being ingested through saliva is backed up with a study from the American Journal of Gastroenterology which states that, “the chew-and-spit technique is esthetically distasteful and difficult to perform without some of the food being swallowed,” (13).

HYPOTHALAMUS

In terms of the hypothalamus, this is usually known as the “control center” for hunger and satiety (14). The hypothalamus, “coordinates the various hormonal inputs,” in, “maintaining homeostatic balance in appetite and satiety control,” (15).  As I had mentioned in the vagus nerve section, all of those hormones (like ghrelin, leptin, and cholecystokinin) are interpreted by the hypothalamus (16).

If we take ghrelin for example (a hormone-releasing peptide that is known as the “hunger hormone”) it has been found that the “sympathetic and parasympathetic pathways each play major roles in signaling our brain when to eat,” which ghrelin, “[promotes] feelings of hunger and food anticipation,” (17). This means that the situation once again could be further impacted by conditions that affect autonomic function and those who are unable to eat using their digestive system, since the release of these hormones may be impacted.

A study that was done in 2006 had, “patients receiving parenteral nutrition [who] still [felt] hungry despite adequate provision of calories intravenously,” wanted to test, “whether PN or its constituent macronutrients acutely affect appetite and to what degree this may be mediated by ghrelin and peptide YY,” (18). They found that infusing patients with PYY and ghrelin did not impact patient’s appetites which means there is definitely some other factor at play that is contributing to this potentially more “psychological-related” hunger.

HEDONIC HUNGER

Another more ‘psychological’ effect that could be impacting this “hunger” is called hedonic hunger which is, “one’s preoccupation with and desire to consume foods for the purposes of pleasure and in the absence of physical hunger,” (19). The term originally, “[referred] to one’s desire or drive to consume food for pleasure, in the absence of caloric need,” which is true for patients who use parenteral nutrition (20). Furthermore, it’s said that people, “who think a lot about eating in the absence of a need for calories could be in a state of hedonic or pleasure-based hunger,” (21). A study done in 2018 for Obesity Science & Practice  found that an individual’s neural activation in their “[brains] [suggested] that hedonic hunger is associated with elevated drives to consume regardless of hunger state,” (22). For further research diving into this topic, I highly recommend reading this study from Obesity Science & Practice as it has a lot more information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6009994/ .

 FINAL THOUGHTS

Hunger and satiety and how they work are a complex dynamic which has only been further complicated with modern day use of technology and advertisement of food in the media. The ways that hunger can derive are not only from physiological need but also from psychological “craving” which as I learned (mentioned above) can come even if the body has met its caloric intake.

While I may not know the exact reason for my and other’s hunger while being on parenteral nutrition, I am now more aware of all of the factors that may be contributing to this likely “psychological” or hedonic need.

If you found this essay interesting, please head over to my ‘Research’ tab which is a page focused on pieces just like this but are even more research focused!!

SOURCES:

1.     McLeod, S. (2007). Maslow's hierarchy of needs. Simply psychology, 1 (1-18), https://canadacollege.edu/dreamers/docs/Maslows-Hierarchy-of-Needs.pdf.

2.     Cork S. C. (2018). The role of the vagus nerve in appetite control: Implications for the pathogenesis of obesity. Journal of neuroendocrinology, 30(11), e12643. https://doi.org/10.1111/jne.12643.

3.     Cork S.C. (2018) pg 2.

4.     Owyang, C., & Heldsinger, A. (2011). Vagal control of satiety and hormonal regulation of appetite. Journal of neurogastroenterology and motility, 17(4), 338–348. https://doi.org/10.5056/jnm.2011.17.4.338.

5.     Cork S.C. (2018) pg 4.

6.    Hetherington, M. M., & Boyland, E. (2007). Short-term effects of chewing gum on snack intake and appetite. Appetite, 48(3), 397–401. https://doi.org/10.1016/j.appet.2006.10.001.

7.     Hetherington, M. M., & Regan, M. F. (2011). Effects of chewing gum on short-term appetite regulation in moderately restrained eaters. Appetite, 57(2), 475–482. https://doi.org/10.1016/j.appet.2011.06.008.

8.    Krop, E. M., Hetherington, M. M., Nekitsing, C., Miquel, S., Postelnicu, L., & Sarkar, A. (2018). Influence of oral processing on appetite and food intake - A systematic review and meta-analysis. Appetite, 125, 253–269. https://doi.org/10.1016/j.appet.2018.01.018.

9.    Miquel-Kergoat, S., Azais-Braesco, V., Burton-Freeman, B., & Hetherington, M. M. (2015). Effects of chewing on appetite, food intake and gut hormones: A systematic review and meta-analysis. Physiology & behavior, 151, 88–96. https://doi.org/10.1016/j.physbeh.2015.07.017.

10.  Krop, E.M., Hetherington, M. M., Nekitsing, C., Miquel, S., Postelnicu, L., & Sarkar, A. (2018) pg 14.

11.   Miquel-Kergoat, S., Azais-Braesco, V., Burton-Freeman, B., & Hetherington, M. M. (2015) pg 92.

12.  Miquel-Kergoat, S., Azais-Braesco, V., Burton-Freeman, B., & Hetherington, M. M. (2015) pg 92.

13.   Helman C. A. (1988). Chewing gum is as effective as food in stimulating cephalic phase gastric secretion. The American journal of gastroenterology, 83(6), 640–642, https://pubmed.ncbi.nlm.nih.gov/3376919/.

14.   Austin, J., & Marks, D. (2009). Hormonal regulators of appetite. International journal of pediatric endocrinology, 2009, 141753. https://doi.org/10.1155/2009/141753.

15.   Yeung AY, Tadi P. Physiology, Obesity Neurohormonal Appetite And Satiety Control. [Updated 2021 Nov 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK555906/.

16.  Yeung AY, Tadi P. (2021).

17.   Yeung AY, Tadi P. (2021).

18.  Murray, C. D., le Roux, C. W., Gouveia, C., Bassett, P., Ghatei, M. A., Bloom, S. R., ... & Gabe, S. M. (2006). The effect of different macronutrient infusions on appetite, ghrelin and peptide YY in parenterally fed patients. Clinical Nutrition, 25(4), 626-633. https://www.sciencedirect.com/science/article/abs/pii/S0261561405002281.  

19.   Espel-Huynh, H. M., Muratore, A. F., & Lowe, M. R. (2018). A narrative review of the construct of hedonic hunger and its measurement by the Power of Food Scale. Obesity science & practice, 4(3), 238–249. https://doi.org/10.1002/osp4.161.

20. Espel-Huynh, H. M., Muratore, A. F., & Lowe, M. R. (2018).

21.  Espel-Huynh, H. M., Muratore, A. F., & Lowe, M. R. (2018).

22.  Espel-Huynh, H. M., Muratore, A. F., & Lowe, M. R. (2018).