L-Glutamine

Food Cravings: Fact or Fiction?

Elaine House & Kevin Goff
Advanced Vitamins and Minerals; SNES 582
Dr. DellaValle
5/2/2019

pg. 1
 L-Glutamine is a non-essential amino acid (AA) and is one of the most abundant AAs in

the body, produced by the body from Glutamic Acid and Ammonia. Originally, Glutamine was

labeled as a non-essential amino acid, but later research revealed that during certain stressful

situations the body may not produce enough. (1) Glutamine plays a central metabolic role during

a plethora of important biological functions, such as immune system functions (2), neurological

activity (3), and the development and maintenance of gastrointestinal integrity (2). The skeletal

muscle glutamine pool is significantly reduced under several types of metabolic stress leading to

its classification as a “conditionally essential” AA (1). Glutamine is required in the production

of other amino acids and more importantly for this paper, glucose. The role that Glutamine plays

in the production of glucose is central to the myths and sensational claims found in the media

supporting the use of Glutamine in the cessation of food cravings.

Craving, which is defined by Webster as, “an intense, urgent, or abnormal desire or

longing,” is a common topic of conversation in the media when it comes to food. Studies have

shown that almost everyone has cravings, with women approaching 100%, while 70% of men

report having cravings (4). As can be expected, most articles take a bit of science and

sensationalize the findings to come to the desired result, which isn’t always beneficial to the

consumer. The difficulty in using cravings to guide nutrition therapy is that they are often

personally unique and not a reaction to hunger or deficiency. Cravings are very difficult to

quantify. Unlike hunger, which is a straightforward chemical response by the brain to ghrelin

9made by an empty stomach and lower insulin levels in the blood), cravings involve memories

and responses to pleasure from natural opioids. Cravings are as much about thoughts as they are

physical. Animal research and a few early human studies show that fatty and sugary foods

release opioids into the bloodstream binding with receptors in our brain to elicit pleasure (5).

pg. 2
Although this response is similar to the reaction to drugs in the brain, it is not strong and requires

much more study before being definitive. Interestingly, Researchers at the Monell Chemical

Senses Center and the University of Pennsylvania School of Medicine have found that changing

diet can impact the strength of craving. In their study, two control groups were evaluated using

fMRI while imagining foods they had previously listed as favorites. The first group was given

vanilla nutritional supplement beverages only for the one-and-a-half days before the imaging

sessions and the other allowed to eat anything they desired. The people eating the monotonous

diet experienced stronger cravings during the sessions and clearly different reactions to desired

foods over the vanilla shake (4). Although these findings are interesting, they are far from

conclusive and no connection has been made to a simple AA such as Glutamine. Cravings are

further complicated by chemical reactions to stress such as cortisol.

Cortisol is the body’s natural reaction to stress, with the primary goal to increase the

metabolism of glucose in preparation for increased activity. It is released in response to

psychological or physical stress. According to a study of 65 women from 18-45; 16 with

Anorexia Nervosa, 12 normal-weight with hypothalamic amenorrhea, 17 obese, and 20 normal-

weight in good health, higher levels of Cortisol and PYY are associated with disordered eating

psychopathology in women across the weight spectrum (6). This data suggests that

abnormalities in appetite regulation may be associated with specific eating disorder pathologies,

regardless of BMI. The data suggests that the problem of stress-eating may be a result of an

increase in stress hormones caused by the psychological stress induced by disordered eating. In

a study of Binge-eating Disorder (BED) treatments, researchers found that groups undergoing

psychotherapy, even when paired with pharmaceutical options, fared better in terms of the

number of binge episodes, maintenance of weight loss reduction from baseline and psychological

pg. 3
well-being than the group treated with pharmacological therapy alone (7). This data

unequivocally suggests that behaviors, rather than a substance or specific food, are at the root of

most food cravings and addictions and dispel any myths of treatment with L-Glutamine as a

supplement.

To be classified as a “Substance Use Disorder”, symptoms from Table 1 such as

withdrawal symptoms, taking a substance in larger amounts than one was meant to, cravings or

urges for the substance, and needing more of the substance to get an effect than before are

needed (8). Unfortunately for those who make the “food addiction” case for cravings and BED

behaviors, these criteria are not met, and food addiction is not able to be classified as a Substance

Use Disorder by the DSM-V (9). It is not possible to narrow down any food to one specific

substance of abuse, rather there is overwhelming evidence for a behavioral model of “eating

addiction” where the behavior, rather than the substance, is the root of the problem (9). Even

regarding the most commonly thought “addictive” foods, sugar, fat, and salt, there has yet to be

any evidence in support of their supposed addictive qualities (9). Hyperpalatable foods can lead

to increased food intake, since often times they are not “bulky” enough to lead to fullness, but

are still very calorically dense (9). However, as stated before, the “addictive” nature of these

food components is not currently supported by the literature.

One proposed model of food addiction proposed the role of diminishing dopamine

receptors in eliciting problematic food cravings and eating behaviors. Association between BMI

and levels of dd2R receptors was examined in (10). 33 studies were examined in the meta-

analysis, investigating the prediction that those with an allele linked to a lower number of DD2R

receptors (A1) would have a higher BMI as a result of the need for more food to satisfy the

“craving” (10). While no correlation was established between BMI and receptor status, it was

pg. 4
determined that those with the A1 allele could be less likely to benefit from weight loss

interventions (10). This is predicted to be from a personality aspect, rather than from the

diminished receptors (10). Individuals with the A1 allele tend to be more impulsive and handle

eating opportunities with less awareness than individuals without the allele (10). This does not

support the notion that food addiction fits a diminished receptor model. “Food addiction” itself

was not even supported by the findings of this meta-analysis; an eating addiction model was

again supported (10). However, Murphy et. al. did find a link between personality traits and

BMI in “Interrelationships among impulsive personality traits, food addiction, and body mass

index”. This is still in support of the notion that a behavior model is more accurate than a food

addiction model. BMI was indirectly influenced by addictive-like eating behaviors, an

inclination for irrational behavior in stressful states, and low levels of task persistence (11).

Often times, problematic substance use and eating behaviors are coupled with mental

health problems/illnesses (9). Meule 2015 indicated that binge eating disorder (BED) appeared

markedly similar to substance abuse disorders in an interview given to individuals with

BED. Questionnaires and similar materials for studying the concept of food addiction have

recently been modeled after DSM IV criteria for substance abuse or addiction disorders (12). It

is acknowledged that even in recent years there has been no conclusive evidence for an addictive

agent in food, and the behavior rather than the substance should be investigated (9,

12). Hebebrand et. al. Most of the studies in food addiction and eating addiction come from

animal studies. In rats, there has yet to be an adequate amount of evidence for food addiction

even for highly palatable foods (9). At this time, it is not appropriate to definitively state that

food possesses the qualities of an addictive substance, and that problematic eating behavior is

driven by addiction mechanisms to food (9)

pg. 5
 As has been stated in this paper, the factors influencing one’s food choices are often

multifaceted and more complex than they are often given credit. It is important to not neglect

factors such as behavioral effects, socioeconomic status, food preferences, family history, food

availability, as well as others when assessing an individual’s food choices. The topic of food

cravings, food addiction, and eating addiction are not easy to define. Knowing this, over-

simplifying a concept to a singular sentence such as “L-glutamine can help curb food cravings”

can often be misinforming and dangerous to the general public. While there are implications for

L-glutamine in helping with substance-abuse related cravings, food cravings are not reliant on

the same mechanisms (13).

pg. 6
Table 1

DSM-V Criteria for 1. Taking the substance in larger amounts or for longer than
Substance Use you're meant to.
Disorder 2. Wanting to cut down or stop using the substance but not
managing to.
3. Spending a lot of time getting, using, or recovering from
use of the substance.
4. Cravings and urges to use the substance.
5. Not managing to do what you should at work, home, or
school because of substance use.
6. Continuing to use, even when it causes problems in
relationships.
7. Giving up important social, occupational, or recreational
activities because of substance use.
8. Using substances again and again, even when it puts you
in danger.
9. Continuing to use, even when you know you have a
physical or psychological problem that could have been
caused or made worse by the substance.
10. Needing more of the substance to get the effect you want
(tolerance).
11. Development of withdrawal symptoms, which can be
relieved by taking more of the substance.

pg. 7
 References
1. Iwashita, S., Williams, P., Jabbour, K., Ueda, T., Kobayashi, H., Baier, S., & Flakoll, P.
J. Impact of glutamine supplementation on glucose homeostasis during and after exercise.
Journal of Applied Physiology. 2005;1858-1865.
2. Lacey, J., & Wilmore, D. Is glutamine a conditionally essential amino acid? Nutrition
Review. 1990;297-309.
3. Newsholme, P., Procopio, J., Lima, M., Pithon-Curi, T., & Curi, R. (2003). Glutamine
and glutamate - their central role in cell metabolism and function. Cell Biochemistry
Function 2003;21:1-9.
4. Monell Chemical Senses Center. (2004, November 11). Images Of Desire: Brain Regions
Activated By Food Craving Overlap With Areas Implicated In Drug Craving.
ScienceDaily. Retrieved April 30, 2019 from
www.sciencedaily.com/releases/2004/11/041108025155.htm
5. Avena, N. M., Rada, P., & Hoebel, B. G. Evidence for sugar addiction: Behavioral and
neurochemical effects of intermittent, excessive sugar intake. Neuroscience &
Biobehavioral Reviews. 2008;32(1):20-39. Retrieved 4 30, 2019, from
https://sciencedirect.com/science/article/pii/s0149763407000589
6. Lawson, E. A., Eddy, K. T., Donoho, D. A., Misra, M., Miller, K. K., Meenaghan, E., . . .
Klibanski, A. Appetite-regulating hormones cortisol and peptide YY are associated with
disordered eating. 2011.
7. Molinari, E., Baruffi, M., Croci, M., Marchi, S., & Petroni, M. L. (2005). Binge eating
disorder in obesity: Comparison of different therapeutic strategies. Eating and Weight
Disorders-studies on Anorexia Bulimia and Obesity, 10(3), 154-161. Retrieved 5 1, 2019,
from https://ncbi.nlm.nih.gov/pubmed/16277137
8. Hartney E. The Symptoms Used to Diagnose Substance Use Disorders. Verywell Mind.
https://www.verywellmind.com/dsm-5-criteria-for-substance-use-disorders-21926.
Published April 22, 2019. Accessed May 2, 2019.
9. Hebebrand, J. et. al. “Eating addiction” rather than “food addiction” better captures
addictive-like eating behavior. Neuroscience and Biobehavioral Reviews. 2014;47:295-
306.
10. Benton, D., Young, H. A. A meta analysis of the relationship between brain dopamine
receptors and obesity: a matter of changes in behavior rather than food addiction?
International Journal of Obesity. 2016;40:12-21
11. Murphy C. M., Stojek M. K., Mackillop J. Interrelationships among impulsive
personality traits, food addiction, and Body Mass Index. Appetite. 2014;73:45-50.
doi:10.1016/j.appet.2013.10.008.
12. Meule, M. Back by Popular Demand: A Narrative Review on the History of Food
Addiction Research. Yale Journal of Biological Medicine. 2015;88(3):295-302.
13. Blum et. al. Hypothesizing Balancing Endorphinergic and Glutaminergic Systems to
Treat and Prevent Relapse to Reward Deficiency Behaviors: Coupling D-Phenylalanine
and N-Acetyl-L-Cysteine (NAC) as a Novel Therapeutic Modality. Clinical Medical
Reviews and Case Reports. 2016;2(8).

pg. 8