Doing Science for understanding or changing the world

I recently had this thought that there are two kinds of scientists, or at least two different approaches to getting into science. We either want to understand the world, or we want to change the world.

This is a frequent contention in refereeing both articles and grants. Some will ask you in what way you are describing a new phenomenon or mechanism, while others will ask how your results are likely to change the world.

Physiology is by nature more of a science that tries to understand the world.

Clinical trials is the archetype of science that tries to change the world.

It is by no means necessary to understand the world in order to change it. A true trialist will answer the question of how does your intervention work with a disdainful: "I don't care".

The same goes for the risk factors identified in epidemiological research. They are risk factors because they are associated with some deleterious outcome, not because they are causal, or because we know how it works.

So, the question arises. Why do you do your science?

Angiotensin II and allostasis

Recently, we talked about allostasis, which is an extension of classical homeostatic regulation to include neural and hormonal signals that can reset homeostatic set points to anticipate changes in the environment.

As I was preparing to submit an abstract to Experimental Biology, which is the major conference in physiology, I realised that a paper that we published recently includes a potential example of allostatic regulation.

It turns out that the hormone angiotensin II that works to retain sodium and increase blood pressure also leads to increased production of the transcription factor NFAT5. This would be allostatic because when the kidney retains sodium the amount of sodium in the interstitial fluid in the medulla of the kidney increases, which means that its tonicity (the number of molecules per volume fluid) also increases and in turn causes osmotic stress. Normally, NFAT5 that is also known as Tonicity-responsive enhancer binding protein (TonEBP) reacts to changes in tonicity to activate genes that protect the cells. In this setting, it appears that the cells can anticipate increased tonicity by sensing angiotensin II directly and increasing the production of NFAT5 to be better prepared to respond to the change in osmotic stress that will come as an effect of the increased angiotensin II concentration.

I was happy to have the abstract well-received and actually got a talk, as well as a fair bit of interest at the poster.