• Mayuri Vaish

What the Dopamine Diet REALLY Says About Dopamine

Many of us have heard, or read, about the neurotransmitter molecule called ‘dopamine’, but what really is it? Broadly said, dopamine is a chemical produced in our brains that is responsible for producing feelings of pleasure. There are many factors that stimulate the production of dopamine, such as exercise, romantic love, addictive drugs, and food. The internet contains a vast network of information regarding how dopamine is produced in response to these factors. Some of the information on the internet is well-informed, accurate, and backed by scientific research. However, a large portion of the internet contains misinformed, inaccurate ideas that are either not backed, or are falsely supported, by scientific research. One of these ill-formed, prevalent ideas is the ‘dopamine diet’—a diet composed of healthy foods that contain properties which boost the brain’s dopamine production, thereby making us feel good and consequently crave fewer unhealthy ‘junk’ foods.


The misinformed notion that the ‘dopamine diet’ reduces cravings by encouraging the consumption of healthy foods that contain dopamine-stimulating properties is relatively well-established, as it is found on a number of popular media sources online. Such online sources range from food websites, such as BBC Good Foods [1], to online fashion magazines, such as Sheer Luxe [2]. To summarize, these discussions claim that the ‘dopamine diet’ works because it promotes the ingestion of certain foods that contain chemicals which specifically heighten our brain’s dopamine production. Since dopamine induces feelings of pleasure, this corresponding increase in dopamine consequently elevates mood and therefore reduces cravings for unhealthy food items. The ‘dopamine diet’ primarily consists of high-protein foods such as red meat, fish, eggs, and dairy, as well as nuts such as almonds and walnuts. Other foods that are a component of the dopamine diet include dark chocolate, bananas, green tea, vanilla, sesame seeds and spirulina.


The popular media articles base their claim regarding the ‘dopamine diet’ on the fact that the aforementioned dopamine-producing foods contain a large amount of a chemical called ‘tyrosine’. Specifically, tyrosine is an ‘amino acid’, which is the smallest unit of a protein that acts as the building block of a protein molecule. The amino acid tyrosine has several functions inside the body, one of which is in the production of the neurotransmitter dopamine. Particularly, tyrosine acts as a ‘dopamine precursor’—i.e, it is one of the molecules in a series of steps leading to the production of dopamine. Therefore, these media articles claim that because tyrosine is present in one of the steps for synthesizing dopamine, foods containing large amounts of tyrosine must consequently lead to a large synthesis of dopamine.


In order to comprehend the basis for the articles’ claim in greater detail, we need to understand the mechanism of dopamine production, and how tyrosine plays a role in this phenomenon. Dopamine is a complex chemical that is synthesized from a series of simpler molecules which become progressively more complex. This series of steps, originating as a relatively simple molecule and terminating as a more complex substance, is called a ‘chemical pathway’. As this chemical pathway progresses, several chemical reactions occur in order to make the simpler molecules more complex. These chemical reactions are sped up via molecules called ‘enzymes’; without enzymes, the reactions within a chemical pathway would proceed incredibly slowly. Consequently, enzymes are called ‘catalysts’ as they increase the rate of a reaction, and the process of quickening a reaction is called ‘catalyzing’ a reaction.


The chemical pathway for dopamine production begins with an amino acid that is even simpler than tyrosine, called phenylalanine. Phenylalanine undergoes a reaction, catalyzed by an enzyme called phenylalanine hydroxylase, to produce the amino acid in the second step in the dopamine chemical pathway, called tyrosine. Tyrosine then converts into a molecule called ‘DOPA’, catalyzed by an enzyme called tyrosine hydroxylase. Finally, ‘DOPA’ undergoes a chemical reaction, also catalyzed by an enzyme named amino acid decarboxylase, to produce the complex neurotransmitter dopamine.


This pathway provides a further basis for understanding the articles’ claim that certain healthy foods can boost dopamine production. Based on the chemical pathway, it seems logical to conclude that because tyrosine is an essential step preceding the production of dopamine, consuming more tyrosine will allow for greater dopamine production. Furthermore, because dopamine is a pleasure-inducing chemical, a heightened dopamine production in the brain would promote pleasure and consequently, reduce cravings.


The discussions further support their point by claiming that the reason people overeat, or consume primarily sugar-rich or carbohydrate-rich foods, is because they seek to experience the pleasure caused by the production of dopamine upon consuming these foods. Thus, the ‘dopamine diet’ replaces these unhealthy sugar-rich foods with healthy tyrosine-rich foods that, based on the mechanism described above, must also stimulate dopamine production due to their tyrosine content. Consequently, the ‘dopamine diet’ keeps one happy to the same extent as if they ate sugary foods, except it also maintains health because the foods in this diet are healthy. Therefore, with the same level of pleasure achieved upon eating healthy diet foods, a follower of the dopamine diet will not feel a further need to crave or seek out unhealthy, fattening food.


Lastly, the articles attempt to support their claim by citing research suggesting that eating a high-protein breakfast is effective in reducing mid-morning cravings. They use this research as evidence to suggest that if a high-protein meal, which is a component of the dopamine diet, reduces cravings, then the dopamine diet must work via the mechanism described above.


To summarize, these discussions on the ‘dopamine diet’ suggest that eating tyrosine-rich foods enhances dopamine production in the brain, due to tyrosine’s role as a precursor to the formation of dopamine. This increase of dopamine induces pleasure that compensates for the pleasure produced by eating junk foods, and therefore reduces food cravings.


Despite the seemingly logical flow of the discussions’ claim, the premise of this argument is flawed. The articles’ primary claim is based on two major statements. The first statement claims that certain foods, such as high-protein foods and nuts, are rich in tyrosine. The second statement is that tyrosine is a precursor to dopamine in the chemical pathway for the synthesis of dopamine. Both these statements are, in fact, entirely correct. However, their claim falls short when it attempts to link the two statements by inferring that because certain foods are rich in tyrosine, and tyrosine is a precursor to dopamine, therefore, eating these tyrosine-rich foods will elevate dopamine production and consequently, reduce cravings.


This inference is incorrect, because in actuality, there is no evidence concluding that increasing dietary tyrosine actually causes a rise in dopamine synthesis via the chemical pathway described above. This lack of conclusive evidence has been documented in several studies [3, 4, 5, 6]. In these studies, the effect of tyrosine on dopamine synthesis was studied by providing tyrosine to rats, either via injection or via food, and then measuring corresponding dopamine concentrations in the brain. From these experiments, results consistently showed no conclusive effect of increased dietary tyrosine on dopamine production in the brain.


In addition to not being supported by research evidence, the discussions’ inference is flawed based on the mechanism of dopamine synthesis itself. The articles argue that because tyrosine is a precursor to dopamine in the dopamine synthesis pathway, elevating tyrosine will augment dopamine production. Although this inference appears logical, upon a closer look at the dopamine synthesis pathway, it is apparent that this inference is not supported by the mechanism of dopamine synthesis.


In the dopamine-synthesis pathway, tyrosine is converted into DOPA, which then forms dopamine. The conversion of tyrosine to DOPA is catalyzed by the enzyme tyrosine hydroxylase. Therefore, increasing tyrosine intake will only elevate dopamine production if the rate of reaction converting tyrosine to DOPA increases. Since this rate of reaction is controlled by the enzyme tyrosine hydroxylase, increased tyrosine will only elevate dopamine synthesis if tyrosine hydroxylase uses this increased availability of tyrosine to allow the reaction to proceed at a faster rate. However, in reality, the amount and effect of tyrosine hydroxylase remains unchanged, as it is independent of any increases in tyrosine content. Consequently, adding tyrosine does not alter the rate of tyrosine’s conversion to DOPA, and consequently has no significant effect on the synthesis of dopamine. Therefore, although the claim that more tyrosine produces more dopamine is ostensibly logically derived from the chemical pathway of dopamine synthesis, in reality, the role of enzymes in the dopamine-synthesis pathway limit the effect of increased tyrosine availability on dopamine production. Consequently, the chemical pathway of dopamine synthesis demonstrates how the articles’ inference that more tyrosine produces more dopamine. is a misunderstood claim.


In addition, the few studies suggesting a potential relationship between tyrosine intake and dopamine production are based on tyrosine levels that are considerably higher than what is found in dietary foods [7]. Thus, even if tyrosine potentially yielded more dopamine, the amount of tyrosine needed for this effect would greatly exceed what can be achieved through a single high-protein meal as a part of the ‘dopamine diet’. Specifically, tyrosine levels administered in these studies were approximately 50 times greater than the tyrosine content in foods. The exact amount of tyrosine administered varied among studies, but on average, an amount of 150 mg/kg tyrosine was administered at once in order to study its effects on dopamine production. For an average adult human weighing 62 kg or 137 lbs, this quantity would be equivalent to receiving 9.3 grams of tyrosine at once. Consuming this amount within one day would be excruciatingly difficult: for reference, one egg contains approximately 250 mg of tyrosine. Therefore, one would have to consume approximately 37 eggs at once in order to receive the same dose of tyrosine that was documented to potentially increase dopamine production! Consequently, even if tyrosine were to potentially document an increase in dopamine production, the amount of tyrosine required would be much greater than the amount that can be obtained via diet.


The idea that tyrosine-rich foods produce dopamine upon consumption is further rebuked by the fact that the minimal research outlining a potential relationship between tyrosine and dopamine release found the dopamine increase to occur approximately one to two hours after consumption [8, 9]. Therefore, the relatively rapid pleasure experienced upon immediate consumption of ‘dopamine diet’ foods cannot be even potentially created due to dietary tyrosine consumption, and must be attributed to some other factor. Consequently, the premise that tyrosine-rich foods produce a surge of dopamine release cannot be substantiated based on existing literature.


In summary, due to these reasons, the authors of popular media discussions on the ‘dopamine diet’ falsely argue that tyrosine-rich foods promote dopamine release because tyrosine is a precursor to dopamine. Firstly, it is false because in the dopamine-synthesis pathway, the enzyme tyrosine hydroxylase prevents additional tyrosine from increasing the amount of dopamine produced by controlling the rate of reaction. Secondly, their premise is false because in order to achieve an effect on dopamine production in the brain, the amount of tyrosine ingested must be significantly greater than can be found in a single meal or meals. Lastly, their premise is false because any potential increase has only been documented to occur hours after tyrosine consumption, and therefore the pleasurable feelings resulting from consuming tyrosine-rich foods cannot be attributed to its role as a precursor in the dopamine-synthesis pathway. Consequently, the articles’ inference that because food has tyrosine, and tyrosine plays a role in dopamine production, tyrosine-rich foods must induce dopamine release is a poorly understood inference that is not backed by scientific research.


However, one objection to my argument that could potentially be raised by the authors of these popular media discussions proceeds as follows: proponents of the ‘dopamine diet’ argue that eating tyrosine-rich foods generally provides them a feeling of pleasure and satisfaction. Since dopamine is undoubtedly connected to pleasure, it must be true that upon eating tyrosine-rich foods, our bodies produce dopamine in our brains. Thus, how does my argument account for the fact that eating tyrosine-rich foods undoubtedly triggers a release of dopamine in our brains, without inevitably concluding that this dopamine rise is due to the tyrosine content in these foods from the ‘dopamine diet’?


In response to this objection, I will acknowledge that the two statements mentioned above are certainly true: First, specific foods are rich in tyrosine. Second, we often experience pleasure upon consuming them, which may definitely be associated with a rise in dopamine in our brains. However, here, the authors of discussions on the ‘dopamine diet’ make an unsubstantiated inference that because tyrosine-rich foods stimulate dopamine release, this dopamine production must be due to the tyrosine present in such foods, and not due to any other factor. This inference rests on the assumption that due to its role in dopamine-synthesis, tyrosine is the only factor in healthy foods that can cause any changes in the brain’s dopamine levels.


In reality, however, the pleasurable dopamine release experienced upon eating certain healthy foods from the ‘dopamine diet’ is independent of the foods’ tyrosine content. This is because, as delineated in my main argument, although tyrosine is important in dopamine synthesis, increased tyrosine intake from foods cannot induce any additional releases of dopamine immediately after consumption. How, then, must we account for the pleasure and dopamine rise experienced after eating a meal?


As it turns out, the rise in dopamine upon consuming food, whether healthy or unhealthy, is more closely related to the food’s energy content as opposed to its tyrosine content [10, 11]. From an evolutionary standpoint, humans obtained a survival benefit from consuming energy-rich and energy-dense foods, such as protein, fats, and carbohydrates, because it enabled them to more efficiently escape predators. In addition, the consumption of high-energy foods enabled humans to accumulate stored energy in order to prepare for times when they may need them, such as during periods of food scarcity or famine. Moreover, maximising energy consumption and energy storage enabled humans to survive in times of food insecurity during the prehistoric ‘hunter-gatherer’ phase. In this phase, humans relied on catching prey for food consumption. The availability of prey and the success of catching prey varied, as it depended on several ecological, social and health factors. Consequently, the availability of food was not always guaranteed. Thus, humans needed energy to not only survive times of low food availability, but also to retain enough energy to continue to hunt for food despite a paucity of prey. This need to retain energy therefore became a survival mechanism that evolved into a neural circuit which assigned ‘reward values’ to high-energy foods. By assigning a high reward value, humans would experience immense pleasure upon consuming high-energy foods. These feelings of pleasure would, consequently, encourage humans to seek and to continue to consume energy-rich foods. As humans evolved, this neural circuit remained within our bodies. It is called the dopamine system, and the molecule promoting feeling of pleasure upon consuming energy-dense foods is called dopamine.


A majority of the foods in the ‘dopamine diet’ comprise of high-protein and high-fat foods. These foods have a large evolutionary reward value due to their high energy content [12, 13]. Specifically, the reward value of foods is measured by the energy content that each food provides. This energy content in foods is measured, at least partly, by the foods’ energy density. The ‘energy density’ of a food describes the amount of energy provided by a food per unit mass of consumption. Its value is reported in kJ/g. Here, one kilojoule (kJ) is equivalent to 1000 joules (J) of energy, and joule (J) is the unit of energy. The energy density of a food is determined by the nutrient composition of the food. This is because each nutrient has a relatively fixed energy density. For example, fats have an energy density of 37 kJ/g, while proteins have an energy density of 17 kJ/g, which is equal to the energy density of carbohydrates, also at 17 kJ/g [14]. Consequently, fats and proteins both have high energy densities. Therefore, consuming them as a part of the ‘dopamine diet’ will stimulate dopamine production in the brain due to their evolutionary reward value and not due to their tyrosine content, subsequently promoting feelings of pleasure. For example, sesame seeds, almonds and walnuts are recommended as a part of the ‘dopamine diet’. All three of these items contain fat as their primary nutrient content. Since fat has the highest energy density among all nutrients, it is evolutionarily beneficial to associate fat with a high reward value. As such, fat consumption induces a release of dopamine in the brain, which promotes feelings of pleasure and satisfaction post-consumption. Similarly, high-protein foods such as red meat, fish, eggs and dairy products have an energy density that is similar to that of carbohydrates at 17 kJ/g. Therefore, the dopamine rise experienced upon eating high-protein meals is similar, if not more, than that of consuming high-carbohydrate meals. Consequently, the pleasure experienced by eating high-protein and high-fat foods are not due to the foods’ tyrosine content, but are more related to their energy densities that are similar or greater than that of carbohydrates.


The idea that dopamine levels rise due to the energy content of foods accounts for the feelings of pleasure experienced upon consuming ‘dopamine diet’ foods without turning to their tyrosine content as an explanation. The authors of popular discussions on the ‘dopamine diet’ incorrectly attribute the rise in pleasure post-consumption to the tyrosine content of these foods due to their false premise that because tyrosine is a precursor to dopamine, consuming tyrosine will raise dopamine levels. In reality, as discussed, this is not the case, and instead this connection can be explained by the evolutionary origins of dopamine and how dopamine interacts with the various energy contents of foods.


A second objection to my argument, however, may be raised. The authors may counter my argument with the statement that, even though tyrosine-rich foods may not be responsible for the immediate rise in dopamine levels, followers of the dopamine diet do experience increased satiety, satisfaction and reduced cravings, which helps them lose weight. For example, chef Tom Kerridge, creator of the ‘dopamine diet’, lost 70 kilograms of weight while maintaining a high level of satisfaction when following this diet. If tyrosine-rich foods do not contribute to the short-term rise in pleasure, does the ‘dopamine diet’ still work because continuously consuming high-tyrosine foods ultimately induces long-term increments in overall happiness?


The answer to this would be that based on current knowledge, this is unlikely; however, we do not know for sure. It is very dubious that the long-term consumption of ‘dopamine diet’ foods would contribute to any substantial changes in happiness due to their tyrosine content. This is because as mentioned previously, based on existing literature and the nature of the dopamine-synthesis pathway, it is highly improbable that additional tyrosine impacts dopamine production. In addition, potential effects on dopamine production are found with an extremely high one-time dose of tyrosine, and occur hours after the tyrosine intake.


Theoretically, if a high dose of tyrosine potentially induced changes in dopamine levels in the brain, then it is logical to suggest that repeated consumption of tyrosine-rich foods may create a similar effect. However, several spaced-out small doses is not the same as a single high dose of tyrosine on the dopamine-synthesis pathway. Thus, although we could theoretically make the assumption that a 9.3 g dose of tyrosine at once may raise our brain’s dopamine levels, we cannot make the assumption that 37 250 mg doses spaced apart throughout a day will have the same effect as the single 9.3 g dose. Simply, that would be a very broad leap to make, and we do not have any evidence indicating that such an inference may be possible. For example, there are no publicly available studies on the effect of long-term, consistent tyrosine consumption on overall, long-term dopamine production. Therefore, making such an assumption, that is not backed by evidence and cannot be clearly inferred, would be illogical and unsubstantiated. Consequently, the idea that following the ‘dopamine diet’ would eventually raise overall happiness due to repeated tyrosine consumption seems incredibly unlikely. Instead, it is more likely that followers of the ‘dopamine diet’ feel generally happier because they repeatedly consume foods that have a high evolutionary reward value, and thus consistently experience a pleasurable dopamine rise after their meals.


How, then, do we explain the reduction of cravings and weight loss associated with the ‘dopamine diet’? In reality, these long-term feelings of satiety and suppressed appetite are due to factors that are not associated with dopamine or tyrosine in any manner.


Firstly, the dopamine diet consists largely of high-protein meals. Such meals have been documented to be satiating due to their high energy density [15]. In addition, high-protein foods such as meats are thought to be satiating in the long-run due to their effects on the digestive tract. For example, cholecystokinin (CKK) is the name of a type of chemical messenger called a ‘hormone’, and it is found in the gut and in the brain. This hormone is released into the gut when amino acids, such as tyrosine, are consumed. The release of CKK helps increase satiety, and reduce meal size. Consequently, the production of CKK is one mechanism by which proteins such as tyrosine act to induce satiety without acting on the dopamine-synthesis chemical pathway. Furthermore, proteins are responsible for increasing the amount of heat, or energy, that is constantly produced by the body [16]. The release of heat from the body is called ‘thermogenesis’, and proteins heighten thermogenesis in humans. Increased thermogenesis is associated with greater satiety: consequently, high-protein foods as a part of the ‘dopamine diet’ do reduce appetite and increase satiety, but not due to the foods’ tyrosine’s role in dopamine production.


Meanwhile, although high-fat foods do not promote satiety to the same extent as in proteins, certain properties of the high-fat foods recommended in the ‘dopamine diet’ elevate satiety and suppress appetite [17]. For example, the nutrients and energy from nuts are poorly absorbed within the body. Consequently, the amount of energy required to absorb the nutrients from nuts increases from baseline. Due to this, the nuts, similar to proteins, cause an increase in thermogenesis in the body [18]. This rise in thermogenesis contributes to feelings of increased satiety. Therefore, it is likely that the high-fat ‘dopamine diet’ foods also promote satiety in manners that are independent of their tyrosine content.


So far, I have shown that we do not know whether the long-term consumption of ‘dopamine diet’ foods can promote pleasure, but we do know that based on existing knowledge and information, this is unlikely. In addition, we know that with regards to satiety, the long-term consumption of ‘dopamine diet’ foods can suppress appetite and promote weight loss. However, these effects occur through various mechanisms that are related to energy, hormones, and metabolism, but are not associated with the tyrosine content of these foods. As such, in response to the authors’ potential second objection, I will state that the ‘dopamine diet’ is unlikely to increase pleasure, and does not increase appetite, simply due to the foods’ tyrosine content. Instead, the weight loss experienced by followers of the ‘dopamine diet’ likely occurs due to non-dopaminergic mechanisms mediating satiety.


Now that the primary misunderstanding surrounding the popular media discussions on the ‘dopamine diet’ is clarified, what can truly be said regarding dopamine and diet?


For one, it is clear that the basis upon which the dopamine diet is designed is false. The logic behind this diet is that if tyrosine is a dopamine precursor, then foods that contain a large amount of tyrosine must consequently augment dopamine levels in the brain. This premise rests on two true claims. First, certain foods are rich in tyrosine. Second, tyrosine is a precursor to dopamine. However, the media’s inference—that if certain foods contain high levels of tyrosine, and tyrosine is used to synthesize dopamine, then tyrosine-containing foods will elevate dopamine release——is unsupported by the mechanism of dopamine production and by current scientific literature.


Particularly, it is unbacked by the mechanism of dopamine synthesis because the rate of reactions occurring in the chemical pathway for dopamine production are controlled by enzymes. Specifically, the rate of conversion of tyrosine to DOPA before eventually forming dopamine is controlled by the enzyme tyrosine hydroxylase. Therefore, although consuming tyrosine-rich foods may result in a greater availability of tyrosine, the amount of tyrosine hydroxylase in the body remains unchanged. Consequently, the rate of conversion of tyrosine to DOPA remains the same, and any additional tyrosine does not affect the amount of or rate at which dopamine is synthesized. In addition, existing research supports the argument that tyrosine does not impact dopamine levels in the brain. Moreover, the minimal research suggesting a potential relationship between tyrosine and dopamine utilizes extremely high doses of tyrosine, and notices these effects hours after consumption.


Secondly, we can state that the feelings of pleasure experienced soon after consuming ‘dopamine diet’ foods occur due to a rise in dopamine levels. However, this increase in dopamine levels is due to the evolutionary reward value of the food as determined by its energy density, and not due to the amount of tyrosine that the food contains.


Thirdly, we can assert that we do not know for sure whether long-term, repeated consumption ‘dopamine diet’ foods can promote overall happiness due to their tyrosine content: however, given the lack of existing literature and the large assumptions made in such a claim, this statement seems unlikely. In order to reach a more certain conclusion, long-term studies on the effect of repeated, small-dose tyrosine intake on pleasure and satisfaction must be conducted. If these studies reveal any impact of tyrosine consumption on mood, then a plausible chemical mechanism of how this may occur must be developed. If these studies do not reveal any association between tyrosine intake and contentedness, then we can safely conclude that the repeated consumption of tyrosine-rich foods in the ‘dopamine diet’ has no effect on mood whatsoever, and that any rise in pleasure must be attributed to dopamine increases due to the evolutionary reward value of the food items consumed.


Lastly, it can be said that ‘dopamine diet’ foods are effective in promoting weight loss and suppressing appetite. However, these effects are due to non-dopaminergic mechanisms such as energy, hormones, and metabolism, and not due to the effect of tyrosine content of these foods on dopamine production in the brain.


Overall, it is evident that the ‘dopamine diet’ is based on the false premise that because certain foods are rich in tyrosine, a precursor of dopamine, consuming high-tyrosine foods stimulate dopamine production in the brain. This idea is misunderstood because in reality, consuming more tyrosine does not elevate dopamine production. Instead, the pleasure and satiety derived from consuming ‘dopamine diet’ foods is due to the food’s evolutionary reward value and other non-dopaminergic factors. Ultimately, the only true statement we can make regarding dopamine and food is that dopamine is produced upon the consumption of energy-dense foods due to their evolutionary reward value, and not due to their dietary tyrosine content.






References

[1] Lienard, S., Parker, K., & Gregory, C. (1970, October 7). What is the dopamine diet? Retrieved from https://www.bbcgoodfood.com/howto/guide/what-dopamine-diet

[2] Cardona, T. (n.d.). What Is The Dopamine Diet? Retrieved from https://sheerluxe.com/2017/08/11/what-dopamine-diet

[3] Briguglio, M., Dell'Osso, B., Panzica, G., Malgaroli, A., Banfi, G., Zanaboni Dina, C., … Porta, M. (2018, May 10). Dietary Neurotransmitters: A Narrative Review on Current Knowledge. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986471/

[4] Peuhkuri, K., Sihvola, N., & Korpela, R. A. (2015, July 1). Dietary proteins and food-related reward signals. Retrieved from https://researchportal.helsinki.fi/en/publications/dietary-proteins-and-food-related-reward-signals

[5] Fernstrom, J. D., & Fernstrom, M. H. (2007, June). Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17513421/

[6] Choi, S. J., DiSilvio, B., Fernstrom, M. H., & Fernstrom, J. D. (2011, November). Effect of chronic protein ingestion on tyrosine and tryptophan levels and catecholamine and serotonin synthesis in rat brain. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22053757

[7] Acworth, I. N., During, M. J., & Wurtman, R. J. (1988, September). Tyrosine: effects on catecholamine release. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/3214752

[8] Wurtman, J, R., Wurtman, J, J., Regan, Meredith, … J, J. (2003, January 1). Effects of normal meals rich in carbohydrates or proteins on plasma tryptophan and tyrosine ratios. Retrieved from https://academic.oup.com/ajcn/article/77/1/128/4689642

[9] van de Rest, O., Bloemendaal, M., de Heus, R., & Aarts, E. (2017, November 23). Dose-Dependent Effects of Oral Tyrosine Administration on Plasma Tyrosine Levels and Cognition in Aging. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5748730/

[10] Wiss, D. A., Avena, N., & Rada, P. (2018, November 7). Sugar Addiction: From Evolution to Revolution. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6234835/

[11] Hoertel, H. A., Will, M. J., & Leidy, H. J. (2014, August 6). A randomized crossover, pilot study examining the effects of a normal protein vs. high protein breakfast on food cravings and reward signals in overweight/obese "breakfast skipping", late-adolescent girls. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249715/

[12] Luca, F., Perry, G. H., & Di Rienzo, A. (2010, August 21). Evolutionary adaptations to dietary changes. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163920/

[13] Mann, N. (2000, April). Dietary lean red meat and human evolution. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/10918988

[14] (n.d.). Retrieved from http://www.fao.org/3/Y5022E/y5022e04.htm

[15] Berti, C., Riso, P., & Porrini, M. (2008, April). Satiating properties of meat-preparations: role of protein content and energy density. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/18689555

[16] Paddon-Jones, D., Westman, E., Mattes, R. D., Wolfe, R. R., Astrup, A., & Westerterp-Plantenga, M. (2008, May). Protein, weight management, and satiety. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/18469287

[17] Samra, R. A. (1970, January 1). Fats and Satiety. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK53550/

[18] Mattes, R. D., & Dreher, M. L. (2010). Nuts and healthy body weight maintenance mechanisms. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20199999