The commentary from Aunt Roberta is all to familiar – Grandpa Scott is snoozing because of the tryptophan in the turkey. Wherever you might be for Thanksgiving, the mention of tryptophan paired with turkey is a constant -- like a requisite side dish.
Well, the myth has been explored in reasonable depth and has led to the commonly held conclusion that no, tryptophan is not the culprit for that post-meal lethargy. Try telling your aunt that.
What is the real truth behind the tryptophan conspiracy though? We all know that humans make notoriously bad research subjects. We don’t adhere to dietary protocols, we false report, and well, we are extremely complex animals genetically, metabolically, and behaviorally. Moreover, it does not appear that rigorous scientific and clinical studies have been performed to definitively support or refute the link.
It could be that despite our scientific knowledge regarding metabolism and biochemistry, there is a pathway or a process in which the right combination of factors results in this post-feast narcolepsy.
Let’s explore this further and start with what is known.
- Tryptophan (Trp) is an amino acid (AA), among the 20 natural amino acids that make up the bulk of proteins in our bodies. The L-isomer cannot be biosynthesized in the body and must be obtained strictly through the diet.
- Trp is no more abundant in turkey than in other protein rich foods such as chicken, fish, beef, and dairy foods. In fact, pound for pound chicken has more Trp than turkey.
- As thanksgiving eating commences, the stomach is filled with a complex mixture of proteins, lipids, carbohydrates, and liquid – in all likelihood gravy.
- Proteins (and other nutrients) are broken down in the stomach and intestines, absorbed, and used in various biosynthetic pathways from cell metabolism, to muscle repair, to hair growth.
- At the blood brain barrier, Trp lines up with the other AA, lipids, and carbs, and waits its turn for entry.
- Satiety, arising from that full feeling, is signaled from the stomach to the brain via the peptide hormone leptin and other factors -- although no amount of normal signalling can stop the inevitable overeating and brain circuitry overload.
- Trp is a key factor in niacin, which in turn plays important roles in digestion, skin, and nerve function.
- Trp is a known precursor to serotonin, a neurotransmitter that controls mood, well-being, and relaxation.
- Serotonin in turn is used to make melatonin, a hormone that controls sleep and wakefulness.
Thus, the link from turkey to sleep is complete…Trp-rich turkey leads to serotonin production, which leads to melatonin signalling, relaxation, and sleepiness…Case closed…
Not so fast...nutritionists and clinicians have infused logic, evidence, and skepticism into this argument, therefore offering alternative explanations...
- If turkey makes you sleepy, then other foods rich in Trp should do the same, right? There is no evidence to suggest this.
- Turkey is high in Trp and therefore boosts levels of serotonin in the brain, right? This has not been demonstrated and neither has it been shown for other Trp rich foods – at least not by themselves.
- Eating turkey alone will cause the same sleepy effects as the entire meal, right? Again, there is no conclusive evidence to suggest this.
The experts say instead it is the sheer act of overeating and the resulting overload to metabolic and brain circuitry in combination that causes the drowsiness effect.
Seems like a rational conclusion, but a letdown just the same, huh? Cast your mind out a bit…ok, a bit more…
- What if certain breeds of turkeys have in fact elevated levels of Trp?
- What if certain brines or prep techniques lead to elevated available levels of Trp in the bird?
- Trp alone won’t lead to the drowsiness effect, and experts say it’s the additional carbohydrates in food that enhance effects in the brain. Well then, what if levels of Trp are kept strictly in line with carbohydrate dosages in turkey to deliver the precise sleep-inducing effect?
Interesting albeit crazy hypotheses, right?
One way to investigate these dubious notions is to start by measuring actual Trp levels in food and in the body. Below are a few common methods in this regard.
- L-Tryptophan fluorescence assays measure L-Trp derived from native tissue or ex vivo by the use of reagent kits such as the Bridge-It assay from Mediomics. The presence of the tryptophan repressor protein (TrpR) results in DNA-binding in a Trp-dependent manner. The assay includes the use of two fluochrome-labeled DNA-half fragments that each contain portions of the TrpR binding site. When brought into proximity by Trp-dependent interactions, fluorescence is enhanced in a concentration dependent manner, thereby permitting Trp measurement over several orders of magnitude. The assay can be performed using high throughput microtiter plates allowing large cohort analysis of turkeys and eaters alike.
- Intrinsic Trp fluorescence stems from it’s aromatic ring structure. Multi-mode microplate readers such as the BMG Labtech CLARIOstar can detect this fluorescence down to a concentration of 2 nM. The signal is linear over a large concentration range and can be detected regardless of filters of monochromators using this system.
- Trp non-enzymatic fluorometric assays measure free and bound Trp in blood serum and other biological fluids. Detection is based on a non-enzymatic reaction in which Trp serves as a building block to generate a fluorometric product. Other AA do not interfere and the assay can be adapted to high throughput format, with limits of detection down to 2.5 µm
- Of course, we probably should abide by the AACCI Method for Trp Analysis by Alkaline Hydrolysis when measuring Trp content in food. The alkaline hydrolysis technique is based on original literature published in 1972 where proteins are hydrolysed by sodium hydroxide and heating, followed by neutralization with mildly acidic buffer. Trp is then resolved via ion exchange chromatography and the resulting Trp concentrations can be measured over a wide linear range.
- Modern semi-automated amino acid analyzers perform at levels of accuracy and precision far superior to any manual method.
In the end, use of one or more of the above methods may prove compatible with the Trp source in question – turkey, blood serum, brain (post mortem I hope).
This is turn may help answer the first two questions – are genetic or environmental factors responsible for increased Trp concentrations in a given turkey.
As far as the third question -- whether precise levels of carbs and other nutrients are present to drive the observed effect…
Looks like it's time for seconds... We’ll pick this back up after a nap.