Vitamins are usually thought of as dietary molecules that are essential for an organism to survive. If molecules are essential but not dietary, such as those metabolically derived from vitamins, they are not considered vitamins. In this sense, cholesterol is not a vitamin because it can be synthesized. Though, neither is Vitamin D, which can also be synthesized.
A more lax idea of vitamins that can encompass the non-dietary molecules we call vitamins is: any molecule that is required, in small quantities, for normal functioning.
The “small quantities” distinction is important, because it is the only descriptor that separates vitamins from the rest of the world. If we forgo the “small quantities” restriction, the entire environment of the animal is a vitamin, because the environment is required for normal functioning. This mirrors a modern interpretation of “epigenetics,” which often refers to specific patterns of methylation on DNA, but sometimes refers to the entire natural world outside of DNA; “epi” loosely means “over,” “above,” “after.” Without restriction of quantity, vitamins are defined as epigenetics: anything but genetic information.
If we accept that quantity of vitamins must be restricted, now we simply have to identify the molecules that are required for normal functioning, and we have our vitamins.
The “aryl hydrocarbon receptor” is thought to be a sensor for xenobiotic metabolism. In the presence of alien compounds, the receptor triggers transcription of enzymes that can convert unknown molecules into hydrophilic, easily-excretable species. While doing this, a cascade is triggered that leads to fat accumulation. The response to a lipid-loving enemy compound appears to be: excrete it, and if you can’t excrete it, store it with fat.
Xenobiotics, by definition, are not included in normal functioning. If a xenobiotic is present within a given unit of life, the set of all vitamins can no longer achieve normal functioning.
Xenobiotics are ‘anti-vitamins.’
Because normal functioning can occur in one part of the cell but not the other, this is best understood at a unit of life below the cell level.
Red blood cells are hemoglobin and not much else. They no longer have a nucleus, genetic information, mitochondria, or any real organelles. By weight, they’re 40% hemoglobin. The remainder consists of mostly water and a small amount of ATP, potassium, and some other organic molecules. Yet, they’re still alive and exhibit many properties of life: they actively deliver oxygen, respond to their environment, maintain an electrical charge, etc.
Gilbert Ling imagined cutting a red blood cell in half, successfully creating two smaller sacs of hemoglobin. By repeating this process many times, all that remains is hemoglobin, the water adsorbed to hemoglobin’s surface, a ‘vitamin’ (in our definition, what Ling called a “cardinal adsorbent”), and some potassium ions.
This minimal unit, known as a “nanoprotoplasm unit,” is given the formula:
(Hb)₁(H₂O)ₙ(K⁺)ₘ(ATP)₁
Where:
- ATP is our vitamin: a substance of small quantity that enables normal functioning.
- n is a range of water molecules, around 7000, that are adsorbed to the hemoglobin in the ATP-adsorbed metastable state.
- m is a range of potassium ions, around 20, that are adsorbed to the hemoglobin in the ATP-adsorbed metastable state.
The leaving of the vitamin can function as work, and we allow one more normal state with no vitamin present:
(Hb)₁(H₂O)ₙ’(K⁺)ₘ’
Where n’ and m’ correspond to physiologically normal quantities of adsorbed species in an “active” state. If this state irreversibly occurs, we call this “death.” In the case of hemoglobin, much less water and potassium are adsorbed, so n’ < n and m’ < m.
Let’s take the case of Hemoglobin with a xenobiotic, X.
(Hb)₁(H₂O)ₒ(K⁺)ₚ(ATP)₁(X)₁
Where:
- o and p define a different metastable state, which does not match the original acceptable ranges of n and m
- At least one of these new variables, o or p, falls outside the original acceptable range necessary for normal functioning (n and m).
Xenobiotic X nullifies the action of ATP and acts as an anti-vitamin at the level of a single nanoprotoplasm unit.
“Normal functioning” is now redefined as association of water and ions with a protein within an evolutionarily-intended physiological range. A vitamin maintains this range for a given protein.
An anti-vitamin creates a “zombie” protein: a new unit of life that is not dead nor conventionally alive, and functions fundamentally differently.
A direct anti-anti-vitamin (DAAV) is a molecule that binds to a protein and reverses the change created by the anti-vitamin.
(Hb)₁(H₂O)ₙ(K⁺)ₘ(ATP)₁(X)₁(DAAV)₁
where n and m correspond to the ‘normal’ metastable state.
An emergent anti-anti-vitamin is a molecule that nullifies an emergent effect of an anti-vitamin. Consider a system where a xenobiotic adsorbs to a protein (A) that blocks obesity, but through a mediating step (B).
Normally,
(A)₁ ----| (B)₁ --x--> obesity
obesity does not occur: "normal"
(A blocks B)
(A)₁(X)₁ --x--> (B)₁ ----> obesity
obesity occurs: "abnormal"
(A does not block B)
Now, with our emergent anti-anti-vitamin,
(A)₁(X)₁ --x--> (B)₁(EAAV)₁ --x--> obesity
obesity does not occur: "normal"
(B is blocked by emergent anti-anti-vitamin)
Now, we see that when the environment, or “epigenetic landscape” in a loose sense, contains an anti-vitamin (i.e., a xenobiotic), the emergent anti-anti-vitamin is required for normal functioning. Thus, the emergent anti-anti-vitamin fits our definition of a vitamin. The double negative cancels out and we’re left with an emergent vitamin.
Anti-obesity drugs of today are emergent vitamins.
Coffee is also an emergent vitamin after consistent drinking occurs.
— anabology
note — anti-vitamin is a term often used for vitamin antagonists, such as Warfarin, which is a sort of 'anti-vitamin K.' A vitamin antagonist can lock the state of a nanoprotoplasm unit into the 'dead' or 'active' state, so it does not fit under my definition of anti-vitamin here. I reject the previous anti-vitamin definition for the purpose of this blog because it currently is redundant with respect to the term: “vitamin antagonist.”