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📣VERY exciting announcement… 📣 @tony_breu and I are writing a book, to be published by @wwnorton! Working title is: WHY DOESN’T YOUR STOMACH DIGEST ITSELF? It’s all about the wondrous ways that the human body is resilient, and we can’t wait to share it with you 😊 Also:

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Congratulations to @BostonChiefs on their new fellowships and jobs!

@tony_breu Thanks for that really interesting thread. A review that has just been published may be of interest to you and your audience: https://t.co/qBjnP7mbdj

1/ Does the tryptophan in turkey really cause a food coma? I've heard this repeatedly, while also being told that it is a myth. Let's have a look at the physiology of a Thanksgiving meal...

9/9 💧 An increase in effective osmoles (e.g., sodium) produces thirst via the movement of water out of cells (i.e., intracellular dehydration) 💧Urea and other ineffective osmoles don't produce the same shifts and, therefore, lead to less thirst

8/ The mechanism described above helps explain why other ineffective osmoles that increase serum osmolarity (e.g., glucose) are not independent drivers of thirst. https://t.co/XUj21fUWQE

7/ The explanation above leads to a beautiful symmetry of thirst promoters. Either... ➤EXTRAcellular volume depletion ...or... ➤INTRAcellular volume depletion... ...will make you seek water.

6/ What is the "sensor" for cellular dehydration? It appears that transient receptor potential vanilloid 1 (TRPV1) is key. TRPV1 is a non-selective cation channel that detects harmful stimuli like heat and capsaicin. 💡 It is also activated by cell shrinking!

5/ Based on this experiment, Gilman concluded that it is INTRAcellular dehydration that leads to thirst. This results from a hypertonic extracellular space (e.g., hypernatremia) and the movement of water outside of cells. https://t.co/tPm7OVivDS

4/ Gilman then made another crucial observation: 💡Only NaCl led to a reduction in serum specific gravity. This suggested a shift of water from the intracellular to the extracellular space. This only occurs with an effective osmole (e.g., sodium) and not an ineffective osmole

3/ After 30 minutes, the dogs were offered water, and had blood work drawn. Gilman made two key observations: 🔑 The increase in serum osmolarity with hypertonic NaCl and urea were nearly identical 🔑 Dogs drank significantly more water after hypertonic NaCl injection

2/ We've known for nearly a century that an increase in serum urea is not a significant driver of thirst. In 1937, Alfred Gilman published an experiment in which dogs received an IV injection of either: ➤20% NaCl ➤40% urea Both are hypertonic solutions.

1/9 🤔 Why doesn't an elevated BUN lead to extreme thirst? If increased serum osmolarity compels us to seek water, uremia should be a significant driver of this craving. And yet, it isn't. Let's examine why.

If you missed our 100th episode, where we recapped our favorite Curious Clinicians podcast episodes, you can also watch it on YouTube! https://t.co/0E1TBuLKHw

cc: @CarterBaughman_ & @BostonChiefs

4/4 It will be interesting to see if nemolizumab, an interleukin-31 receptor alpha antagonist, helps mitigate lymphoma-associated pruritus in the rare case when it becomes refractory. This drug has been tested in atopic dermatitis with pruritus and was effective.

3/ The mechanism involves a cytokine unfamiliar to me: IL-31. In one study of HL and angioimmunoblastic T-cell lymphoma, those with pruritis had higher serum levels of IL-31, IL-1β, and IL-1α than those with lymphoma and no pruritis compared with controls.

2/ The association between HL (and other lymphomas) and pruritus has prompted many to recommend a chest x-ray as part of the initial work-up when a primary skin disorder isn't present. A 2013 NEJM review suggests this, as does Up-To-Date. https://t.co/eggAkzJ8Ks