Mr. Heart: “Not well, and I think I might be coming down with something serious…”

Dr. McCondo: “Alright, let’s take a look.”

Mr. Heart: “Okay…hey do you think it’s going to be something serious? Do you think it might be because of the new neighbourhood I moved into? Ever since my buddies Turk and Burke helped me move in I started feeling a little weird. I mean, it was nice to relocate to a new place and all because my old one….well let’s just say my old one is a goner. But I feel like I’m not fitting into the new environment too well. I feel…rejected, almost.”

Dr. McCondo: “I see. Well, nothing to worry about right now. I’ll prescribe some medicine right now which should make you feel a bit better. We’ll also run some tests too just to be sure. The result will be available in the next hour or two.”

Mr. Heart: “Okay, thanks doc.”

Dr. McCondo: “No problem, see you in a bit.”

*cue corny fadeout music*

Sounds ludicrous? (That was a rhetorical question.)

But would it be useful if doctors could actually “communicate” with the heart and provide the necessary management at the time of, or better yet, BEFORE the injury (major problem) occurs? Absolutely.

Although the conversation above may never take place in the future despite our current technological advancements, scientists are still exploring, discovering, and utilizing various biological molecules and traits, known as “biomarkers”, as a means to gain insight into the status and wellbeing of the organ and, consequently, the patient.

A biomarker, according to the Merriam-Webster Medical Dictionary Online, is defined as “a distinctive biological or biologically derived indicator of a process, event, or condition.”
More specifically, these biomarkers or “indicators” can also be described as “cellular, biochemical or molecular alterations that are measurable in biological media such as human tissues, cells, or fluids.” [1, 2] This also means specific proteins, metabolites (substances produced from your metabolism), or even unique changes in gene expressions in your body can all be potentially used as biomarkers for diagnosis or even prognosis of injury or diseases.

Whether it’s for the diagnosis of cancer or assessment of organ-specific damage and/or diseases, a myriad of biomarkers have been identified and are currently used clinically everyday. However, as heart / cardiovascular disease is the leading cause of death in North America and a major contributor to the global disease burden, this paper will focus primarily on the (protein) biomarkers of the heart – from the classic markers of heart injury to the ones being used clinically today, and from the ones used today to those scientists are looking into for the use tomorrow. [3, 4]
Past, present, future…and beyond.

First stop, 1954!!

Classic Cardiac Marker(s) – Oldies but Goodies?

One of the most well known cardiovascular diseases is probably myocardial infarction (MI; also known as a “heart attack”). This is not surprising, considering it is thought to be the most common cause of morbidity and mortality in developed countries such as the United States and Canada. [5]

Myocardial infarction is a condition which occurs when an area of the heart is damaged or dies due to insufficient or complete lack of oxygen / blood supply. [6, 7] Traditionally, myocardial infarctions have often been diagnosed based on clinical presentations (i.e. “Doctor, I feel chest pain, shortness of breath, and squeezing pain which radiates to my jaw and left arm) and electrocardiogram (ECG, which measures electrical activity in the heart over time). [8, 9] However, since these clinical and ECG findings may often be atypical or absent, the use of serum markers / cardiac markers are becoming more and more essential for the diagnosis of myocardial infarction. [8, 9]

I. In the beginning, there was AST

In 1954, Dr. Arthur Karmen and his colleagues reported what is probably now considered the first known marker of AMI, called aspartate transaminase (AST), in the Journal of Clinical Investigation. [5, 10] More specifically, AST, which is a type of enzyme predominantly present in heart tissue, liver and skeletal muscle, was found to be at an elevated level in patients with heart attacks. [9]

At this point, you might say, “Hey! You said these markers are abundant in liver and skeletal muscle as well! Why would you use it as a cardiac marker!?”

You are right, and that is one of the main reasons AST has not endured the test of time as a cardiac marker – because of its abundance in liver and skeletal muscles. [6] In fact, the clinical use and significance of AST nowadays is limited mainly to the assessment of hepatocellular (liver) and skeletal muscle diseases. [6, 9] This makes sense as the basic idea behind most of the biomarkers (of organ damage) is that, when cells die, they are no longer biochemically compartmentalized properly. As a result, contents inside the cells (i.e. proteins) can spill out into the blood, which can then be measured and analyzed. [6]

II. The perfect test

Once released into the blood, the cardiac biomarkers can then be, in an ideal setting, measured by an assay or a biochemical test which is both sensitive and specific (the ability to detect the marker and the ability to distinguish a cardiac and non-cardiac problem, respectively). [8, 9, 11] As well, the test should be widely available and, most importantly, inexpensive! [11]

As Rolling Stones’ Mick Jagger once sang, “you can’t always get what you want.” Assuming that he was talking about the cardiac marker test (which he wasn’t), he’d be correct; no perfect test exists.

Likewise, the perfect cardiac injury marker has yet to be found (if there is one). Nonetheless, many of markers used today encompass various attributes of “the perfect biomarker.”

III. “The important thing is that it’s from the heart…” – No, I’m not talking about gifts.
Some ideal features of marker of heart injury

As one might imagine based on the example mentioned previously, one of the ideal characteristics of cardiac biomarker / marker of myocardial injury is for it to be found at high concentration in the myocardium (heart muscle tissue), while absent – or present at very low level – in other organs/tissues. [8] Also, the marker should appear very rapidly in plasma of patients experiencing myocardial infarction or ischemia, but should “not” be present in plasma at any other time. [8] The reason for this is pretty straightforward. If the marker is quickly elevated in the plasma of MI patients, then there may be less delay in diagnosing the cardiac problem. [8, 9] In other words, physicians can potentially have more time to “save” the myocardium from dying. Lastly, the ideal cardiac marker should remain in plasma / blood long enough to be detected and measured for diagnostic purposes, but it should not remain for too long.

”Why don’t you want it in the blood for too long?” you might ask.

In essence, the reason is to avoid confusion and allow diagnosis of recurrent injury. [8] Imagine a cardiac marker which was found to be significantly elevated in a patient. The patient was diagnosed with MI and was treated by the doctor. However, this marker is one which continues to be elevated because it doesn’t get cleared or degraded. Then, two days later, the patient comes in, complaining about chest pains again. Now the scenario gets confusing – is this person getting a heart attack or is the marker still elevated from the first heart attack?
Luckily, there are markers, some of which are very organ-specific, for dealing with scenarios such as this.

Modern Marker of Choice? CK vs. Tn – The Showdown

Creatine Kinase (CK), an enzyme generally involved in ATP (a type of energy currency in cells) regeneration in contractile systems and found in muscle of all types (skeletal, cardiac and smooth), is routinely measured as a marker of cardiac injury. [8, 9] In particular, CK-MB, an isoenzyme of CK (imagine the same CK enzyme but with small modification / difference), is found predominantly in cardiac tissues. [8, 9] Although CK-MB can be found in small amounts in other tissue (i.e. skeletal muscle), it’s still relatively specific to myocardium, which is basically the only tissue from which CK-MB “leaks” into the blood in significant amounts (and there’s typically more CK-MB released into blood when cardiac muscle dies than when skeletal muscle dies). [8, 9] More importantly, CK-MB level in blood generally elevates almost as quickly as Troponin (Tn) after cardiac injury, but drops back down (to the reference interval) a lot faster, making it a potentially better marker for assessing reinfarction. [7-9]

Troponins (Tn), on the other hand, are non-enzyme contractile proteins associated with myofibrils (filaments found in muscle cells); each troponin helps regulate muscle contractions and is composed of 3 subunits: TnC, TnI and TnT. [8, 9]

Luckily for the physicians, cardiac-specific TnT and TnI (i.e. cTnT and cTnI) exist! Even better, relative to other cardiac markers, cTnT and cTnI are nearly absent from normal serum! [6] Although these two markers aren’t exactly specific to the “cause” of the injury (i.e. myocarditis – inflammation of the myocardium, can also cause Tn elevation), they are still the preferred markers and probably the most clinical significant cardiac injury markers in the diagnosis of MI (a.k.a. heart attack). [7, 9] This is because of their superior sensitivity and tissue-specificity compared to the others known at this time. [6, 9, 11]

“But what about the prognosis? What about cardiac injury due to rejection after transplantation?” you ask.

It gets more complicated.

New playing field, new challenges – Cardiac Biomarkers in Transplantation

For patients with life-threatening, end-stage heart failure, cardiac transplantation, the surgical procedure of putting a donor heart into the “foreign” environment of the recipient body, is currently considered as the primary therapy of choice. [7] Unfortunately, after transplantation, the donor’s heart, known as a cardiac allograft, may be attacked by both immune and non-immune elements in the recipient’s body, leading to dysfunction or rejection of the organ. [7] Heart rejection may occur in 20-50% of recipients at least once within the first year after transplant, while10-year cardiac allograft survival is only about 50%. [12, 13]

Normally, endomyocardial biopsies (essentially cutting a small piece of the heart muscle for examination!) are carried out post-transplant to monitor potential rejection episodes. [13] Not only is this a very invasive procedure, but the results often also suffer from reproducibility and interpretation issues. [13, 14]

This is where biomarkers come into play.

Researchers are attempting to use them to develop non-invasive, inexpensive and reliable tests to contribute to the diagnosis (is there rejection?), as well as prognosis (is there “going” to be a rejection?) of the patient and the transplanted heart. [13, 14]

”Why not just use Tn or CK?” you might ask.

One reason is because some of the aforementioned cardiac markers, such as cardiac troponin, are elevated post-heart transplant but are “not” specific to rejection. Also, it has been suggested that troponins may lack diagnostic sensitivity during the early post-operative period. [13, 15] This is also why researchers are looking into other areas for markers – such as markers of inflammation / immune process. But even those markers have their own potential advantages (i.e. prognosis of rejection before sufficient immune process occurs to damage the heart) and disadvantages (i.e. the immune marker is elevated, but is it actually a rejection or is it just an infection which caused the immune system to become activated). [15]

From the present….to the future….and beyond!

The general consensus among the research community is that, instead of finding that single “miracle” marker of rejection, multiple biomarkers (i.e. proteins, genes, metabolites) are going to be necessary to achieve the desired prognostic and diagnostic values. [11, 14] But just exactly which “ones” are clinically most useful and relevant? That’s the million dollar question researchers are trying to answer.

Large-scale “biomarker-searching” projects, such as the one funded by Genome Canada (called “the Better Biomarkers of Acute and Chronic Allograft Rejection” project), are currently underway and are using cutting-edge technologies to discover biomarkers (i.e. genes, proteins, metabolites) which might help pave the way for future diagnosis and prognosis of organ rejection. Furthermore, in addition to finding better biomarkers, the path to finding them has also helped scientists gain insight into the mechanisms involved in transplant rejection.

Conclusion – They are just cardiac markers, not doctors

After this brief overview of some of the classic markers of cardiac injury and their advantages and disadvantages, as well as a quick look at the current investigation for markers of cardiac allograft rejection and the rationale behind it, it’s not difficult to see how cardiac biomarkers can have such an important impact, both clinically and in regards to research.

It’s important to remember, however, that even with the availability of these newer, better biomarkers in the future, diagnosis for cardiac injuries will still require astute physicians’ clinical observations and the correct interpretation of the serum marker test results.

Nonetheless, the search continues.

Who knows, maybe that perfect cardiac marker is out there after all.

Mr. Heart: “Hey Doc”

Dr. McCondo: “Hello. So, how are you feeling now?”

Mr. Heart: “A little better I think…Did the test result come back?”

Dr. McCondo: “Good….Yes, the biomarkers test came back. Everything seems normal”

Mr. Heart: “Phew, that’s good news”

Dr. McCondo: “Yup. That is. Mr. Heart, don’t worry about feeling rejected. I think you are going to fit into the new environment just fine. Enjoy your new life there.”

*cue corny fade out music, part 2*

References

1. Biomarker. Available here. Accessed March, 2007.

2. Hulka BS, Griffith JD, Wilcosky TC. Biological Markers in Epidemiology. New York: Oxford University Press; 1990.

3. Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics–2006 update: A report from the american heart association statistics committee and stroke statistics subcommittee. Circulation. 2006;113:e85-151.

4. Navas-Acien A, Guallar E, Silbergeld EK, Rothenberg SJ. Lead exposure and cardiovascular Disease—A systematic review. Childhood. 2007;115.

5. Fuster V, Sanz J, Viles-Gonzalez JF, Rajagopalan S. The utility of magnetic resonance imaging in cardiac tissue regeneration trials. Nat Clin Pract Cardiovasc Med. 2006;3 Suppl 1:S2-7.

6. McPherson RA, Pincus MR. McPherson & Pincus: Henry’s Clinical Diagnosis and Management by Laboratory Methods. 21st ed. ed. Philadelphia, PA: W. B. Saunders/Elsevier; 2006.

7. Goldman L, Ausiello D. Cecil Textbook of Medicine. 22nd ed. ed. Philadelphia, PA: W. B. Saunders/Elsevier; 2004.

8. Rajappa M, Sharma A. Biomarkers of cardiac injury: An update. Angiology. 2005;56:677-691.

9. Bishop ML, Fody EP, Schoeff L. Clinical Chemistry: Principles, Procedures, Correlations. 5th ed. ed. Baltimore, MD: Lippincott Williams & Wilkins; 2005.

10. Karmen A, Wróblewski F, LaDue JS. Transaminase activity in human blood. J Clin Invest. 1955;34:126-131.

11. Maisel AS, Bhalla V, Braunwald E. Cardiac biomarkers: A contemporary status report. Nat Clin Pract Cardiovasc Med. 2006;3:24-34.

12. Starling RC, Pham M, Valantine H, et al. Molecular testing in the management of cardiac transplant recipients: Initial clinical experience. Journal of Heart and Lung Transplantation. 2006;25:1389-1395.

13. McManus CA, Rose ML, Dunn MJ. Proteomics of transplant rejection. Transplant Rev. 2006;20:195-207.

14. Mehra MR, Feller E, Rosenberg S. The promise of protein-based and gene-based clinical markers in heart transplantation: From bench to bedside. Nat Clin Pract Cardiovasc Med. 2006;3:136-143.

15. Trull AK, Akhlaghi F, Charman SC, et al. Immunosuppression, eotaxin and the diagnostic changes in eosinophils that precede early acute heart allograft rejection. Transpl Immunol. 2004;12:159-166.

You’re glad to be home, because it was just one of those laborious and stressful days in the lab when nothing seemed to work. Maybe the ELISA didn’t work; maybe the bands you were looking for on the gel were MIA; maybe someone accidentally left a male mouse in your cage and it decided life was too short to not get frisky with your precious female transgenic mice.
It’s just one of those days.

And now you’ve got the munchies.

You walk towards the fridge and open it.

”Crap,”
”I’m out of beer.”

You stick your head in closer and scan the other parts of the fridge, including the freezer, hoping to find some other beverage or food that will be the remedy to your overall unimpressive day.

A few of things you see:
1) Leftover bacon from this morning’s breakfast
2) Leftover salad from yesterday’s dinner
3) Big slice of apple pie
4) Cake from your birthday party
5) Leftover Chinese food from god-knows-when
6) A tub of vanilla ice cream and a tub of rocky-road ice cream

“Score,” you say as you reach out to grab your food of choice. Because you know after you finish eating it, you will feel that much better – or at the very least, feel that much fuller.

For most people, there are certain types of food that we associate with comfort and happiness growing up – although depending on your ethnicity and cultural background, you might have a slightly different take on what your ideal “comfort food” is. Whether it’s ice cream, macaroni and cheese, or chocolate chip cookies, the term “comfort food”, which was added to the Webster’s Dictionary in 1972, is generally defined as “food that gives a sense of emotional well-being,” or “any food or drink that one turns to for temporary relief, security or reward.” [1]

Although by definition comfort food can be anything the person chooses, the recipes for the majority of comfort foods consist of at least one of the 3 major ingredients: lots of carbohydrates and sugar, high levels of fat, and plenty of love (this last opinion being the author’s own). [2] In general, the overall effects of comfort food are believed to be partly psychological, through conditioning or cognitive response (i.e. parents giving ice cream to a kid when he/she is sad throughout childhood so that over a period of time, the child associates negative feelings with a craving for ice-cream), and partly biochemical/neurochemical. [2, 3] While the jury is still out on which is the major contributing factor, recent studies in the science community have provided further evidence that comfort food, particularly those high in carbohydrates and fat content, can in fact influence a person’s mood. [2-5]

As such, this paper will discuss some of the proposed biochemical/neurochemical mechanisms behind fat and carbohydrates that are believed to be responsible for bringing you the comfort in your food. Both fat and carbohydrates will be discussed, with a particular emphasis on the latter as it’s the more widely studied component of comfort food.

Mmm…delicious knowledge on fat and carbs…Let’s dive right in, shall we?

Fat – Even the cavemen loved it. (or) Give me butter, and dunk my hand in ice-cold water.

Many types of comfort food contain both high levels of fat and sugar (Timbits, anyone?), but how can fat or a high-fat meal, in particular, affect a person’s mood?

In a study conducted by Sue Zmarzty and colleagues at the Northern General Hospital Trust / Centre for Human Nutrition in UK, the effects of a high-fat meal on a person’s mood – or more specifically, the influence of a fatty meal on a person’s reception to pain – have been demonstrated. In this particular experiment, 16 volunteers (8 male and 8 female) were treated to pancake meals with varying fat content before being subjected to a Cold Pressor Test (CPT), which is essentially a cold-induced pain tolerance test involving sticking your hand in ice-water. After all, there’s no such thing as a free lunch, right?

What the researchers found was interesting. It appeared that the people who ingested the high-fat, low carbohydrate pancake meals 1.5 hour before the CPT experienced a greater reduction in pain reception compared to those who had the low-fat (high-carbohydrate) meals of the equal calorie content.

The researchers concluded from their study that food, especially when rich in fat, may reduce the amount of pain a person feels. [6]

Even though the exact mechanism through which fat may directly trigger this comforting effect is still unknown, several have been suggested:

I. Fat and Cholecystokinin (CCK) – That satisfying feeling of a full tummy

CCK, a hormone naturally found in our brain and gut, is thought to mediate many of the behavioural responses to fat, such as satiety and tranquilization. [2, 6, 7] Shortly after a person begins to eat, CCK is released in the gut in response to food (particular if fatty food is being ingested). [6, 7] Researchers have suggested that as the level of CCK in the blood rises, it begins to slow stomach emptying and triggers CCK-induced analgesia through the activation of opioid pathways. [2, 6, 7] Eventually, once the blood CCK level reaches a critical level, the person feels satiated, satisfied, and stops eating. As Dr. John Francis, a psychology professor at the Sheffield Hallam University in UK, explained in an interview with Nature news, the effects of CCK after fat ingestion could be one of the reasons that people find high-fat meals more satisfying. [2] Supersize me, please.

II. Palatability and Fat – Feels good on your tongue because it’s smooth like butter…(and probably because it IS butter!!!)

In addition to the release of CCK in the gut in response to food, it has been suggested that the palatability of foods plays a major role in their ability to relieve negative mood and anxiety in stressful situations; therefore, it’s not hard to imagine the importance of fat (and sugar) in comfort foods. [3, 4, 8] In essence, several researchers proposed that the oral sensation of high-fat food may indirectly cause the feeling of comfort and pleasure in a person by triggering his or her endogenous opioid peptide system (a.k.a. activating the “pleasure pathway”). [2, 3, 9]

Carbohydrate and Sugar – Fuel up!

Not surprisingly, carbohydrates, which make up the majority of the organic matter on Earth, are also found in a variety of foods. [10] Ranging from milk (seriously! check out that milk carton in your fridge) to pasta to cookies, carbohydrates can be considered the staple ingredient in most people’s diets.

Before jumping into theories which associate carbohydrates and sugar consumption with mood alterations, it is important to recognize that the basic building blocks of carbohydrates are, in fact, monosaccharide / sugar molecules. The term “sugar”, or “table sugar”, that we commonly use, actually refers to sucrose, a simple carbohydrate / disaccharide composed of two basic sugar molecules (glucose and fructose). Regardless of the source, the fate of most digestible carbohydrates, once ingested, are essentially the same – they are broken down by the digestive system into individual sugar molecules such as glucose, which can then be used for processes such as ATP (a type of energy currency in the body) generation and serve as building blocks for other molecules. [10]

I. Carbohydrates and Sugar – To energy and beyond?

In addition to being an excellent source of energy (i.e. ATP generation), various studies have demonstrated evidence which suggest that carbohydrates and sugar molecules may have an effect on animals’, as well as peoples’, moods and emotional states. [3, 9, 11, 12]

Using animal models, Dr. Mary F. Dallaman and her colleagues reported their observations in the Proceedings of the National Academy of Sciences in 2003. When rats were subjected to stress (no, they didn’t dip their hands in ice water this time; rather, it was periods of cold environmental “stress”) consumed “comfort foods” (lard and sucrose in this case), a change in their stress-related hormonal system could be detected in their blood. The authors described this change as a reduction in dysphoric effects of the corticotropoin-releasing-hormone (a type of neurotransmitter) driven stress-response, and believe this change can influence the mood of stressed-out rats and may ultimately make them feel better. [11] Likewise, the association between the ingestion of high-carbohydrate meals and improved mood has also been suggested in human studies. In an experiment conducted by Dr. Lloyd and colleagues, 16 people were given breakfasts of the same calorie value but of varying carbohydrate and fat content. To evaluate the test subject, a series of cognitive performance tasks and mood ratings were conducted before and during the three hours following breakfast. Although the results revealed no clear difference in cognitive performances between the test subjects, researchers noticed a significant mood improvement (i.e. decline in dysphoria) in subjects following the high-carbohydrate/low fat breakfast, relative to those who received different diets. [12]

Unfortunately, the exact details behind how carbohydrates and sugars could potentially induce mood improvement are still unclear. However, several intriguing biological and neurochemical mechanistic explanations have been proposed, which are currently under heated debate and investigation within the research community.

II. Carbohydrates and Your Brain – The ‘S’’s in Happiness stand for…Serotonin?

One of the predominant theories (and perhaps the most widely discussed one), is that carbohydrates increase the level of serotonin synthesis in the brain. [4, 6] This idea is often refer to as the Wurtman hypothesis, proposed by Richard and Judith Wurtman back in the early 70’s.

Serotonin, a type of neurotransmitter found in the nervous system, is known to be involved in mood modulation. [2, 4, 5] The level of serotonin synthesis in the brain is limited by the availability of tryptophan, a type of essential amino acid (building blocks of proteins) we obtain from our diets. [6, 7] This also means that under normal circumstances, when the brain tryptophan level increases, more serotonin is made. [7]

So where do carbohydrates come into the picture?

According to the theory proposed by Wurtmans, the quick answer is that a high-carbohydrate meal can alter the level of amino acids in the blood. [8] When carbohydrate is ingested, it triggers the release of insulin in the body, which signals the glucose uptake by the cells. [8] As well, insulin promotes the uptake of most of the large neutral amino acids (LNAA; such as valine, leucine, tyrosine..etc), but not tryptophan, into the muscles. [7, 8] This is because tryptophan is normally bound to serum albumin (a type of protein found in blood), and insulin essentially increases the number of albumin which bind to tryptophan and prevent it from being taken up by the muscles. [8] The end result is an increase in ratio of tryptophan to the total amount of other LNAAs, which ultimately means more tryptophan ends up crossing the blood brain barrier into the brain, and more serotonins are synthesized!!! (This potentially means improved mood!)

Although this theory appears plausible, some researchers have argued that there’s a potential flaw in it – the presence of protein in a high carbohydrate meal. [2, 4, 8] Several researchers believe that if proteins are also ingested during the high-carbohydrate meal, the level of many amino acids (including other LNAAs) will increase, which ends up competing with tryptophan and lowering the tryptophan to LNAA ratio, leading to decreased serotonin synthesis. [4, 7] Furthermore, they argue that as little as ~5% of protein in a high-carbohydrate meal, which is rare in human diets, may be sufficient trigger this counter effect. [4, 6]

As such, it’s hard to say exactly how much this theory contributes to the “feeling good” effects of comfort foods. Currently, both sides of the theory are continually being investigated. Perhaps on rare occasions, with the right carbohydrate-rich/protein-poor combination (the Atkins dieter’s worst nightmare), comfort food can help a person feel better through this potential mechanism.

III. Carbohydrate, Sugar and Cholecystokinin (CCK) – That satisfying feeling of a full tummy…again

(Similar idea as to how fat relates to CCK after a person begins to eat)

IV. Palatability and Sugar / Carbohydrate – Sweet! It feels good on your tongue.

As mentioned earlier in this paper, palatability has been suggested to be an important factor in comfort foods’ ability to alleviate negative moods. It has also been proposed that, similar to ingesting fatty foods which have rich fatty texture, the oral-sensory response to sweet/sugary food may stimulate the release of endorphins in the brain. [2-4, 8] Endorphins, a type of endogenous (i.e. produced in your body) neurochemical compound, are thought to be able to interact with the opiate receptors in the brain and induce a sense well-being, improve mood and alleviate pain. [13, 14] Moreover, the link between sweet, palatable taste in comfort foods and analgesia has been reported in a study conducted by Dr. Maxim Lewkowski and his colleagues. In their rather interesting experiment, 72 young adults held solutions of various tastes in their mouth before and during a cold pain stimulus test; what they found was a significant increase in pain tolerance in the group who received sweet tastes compared with those who were given bitter or water conditions. [15]

Needless to say, although some researchers believe that the release of endogenous endorphins after ingesting palatable food (those with high fat or sugar/carb content) is more likely the mechanism behind “comfort foods”, this theory is still up for debate and currently under investigation. [4]

Conclusion – Read and eat at your own discretion

After this brief look at some of the theories that have been proposed to explain the effects of “comfort foods”, it is important to remember that these theories are still being tested. (So don’t change the way you eat and what you eat just yet!)

Nonetheless, there appears to be a growing consensus in the scientific community that comfort foods (i.e. those high in carbohydrates/sugar or fat) can improve a person’s mood. The exact relationship between the comfort food and mood, while remaining unclear, is probably a complex one. Factors like the time of eating, the composition and the amount of foods consumed, along with the age, health status and dietary history of the person may all come into play. [7] Moreover, it is likely that the interaction between comfort food and mood may be a circular one (i.e. how we feel affects how we eat, and how we eat affects how we feel). [2, 4, 14]

As you finish eating the food you picked out earlier from the fridge, you think to yourself,

”That was some good food. Hmm…I wonder if what I just ate has both psychological and physiological effects on me, and if there are any scientific theories that try to associate comfort food and a person’s mood…Maybe it’s—“ you stop your train of thought.

“Nah…I think too much. It’s just food; there’s probably only so much it CAN do anyway.”

“I think I’m gonna take a nap…”

References
1. Comfort Food. Available here. Accessed 2007, Feburary, 2007.

2. Abdulla S. Food and mood. Available here. Accessed 2007, Feburary, 2007.

3. Dube L, LeBel JL, Lu J. Affect asymmetry and comfort food consumption. Physiol Behav. 2005;86:559-567.

4. Benton D, Donohoe RT. The effects of nutrients on mood. Public Health Nutr. 1999;2:403-409.

5. Canetti L, Bachar E, Berry EM. Food and emotion. Behav Processes. 2002;60:157-164.

6. Zmarzty SA, Wells AS, Read NW. The influence of food on pain perception in healthy human volunteers. Physiol Behav. 1997;62:185-191.

7. Prasad C. Food, mood and health: A neurobiologic outlook. Braz J Med Biol Res. 1998;31:1517-1527.

8. Benton D. Carbohydrate ingestion, blood glucose and mood. Neurosci Biobehav Rev. 2002;26:293-308.

9. Drewnowski A, Krahn DD, Demitrack MA, Nairn K, Gosnell BA. Taste responses and preferences for sweet high-fat foods: Evidence for opioid involvement. Physiol Behav. 1992;51:371-379.

10. Berg JM, Tymoczko JL, and Stryer L. Biochemistry. 5th ed. New York: W. H. Freeman and Co.; 2002.

11. Dallman MF, Pecoraro N, Akana SF, et al. Chronic stress and obesity: A new view of “comfort food”. Proc Natl Acad Sci U S A. 2003;100:11696-11701.

12. Lloyd HM, Rogers PJ, Hedderley DI, Walker AF. Acute effects on mood and cognitive performance of breakfasts differing in fat and carbohydrate content. Appetite. 1996;27:151-164.

13. Purves D, Augustine GJ, Fitzpatrick D, et al. Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates, Inc.; 2001.

14. Gibson EL. Emotional influences on food choice: Sensory, physiological and psychological pathways. Physiol Behav. 2006;89:53-61.

15. Lewkowski MD, Ditto B, Roussos M, Young SN. Sweet taste and blood pressure-related analgesia. Pain. 2003;106:181-186.