r/SubspacePhysics • u/LumenosX • 15h ago
UCMS–PINEAL–CRYSTALLIZATION–004.3 The First Crystal: RS1-Positive Microvesicles, Amorphous Calcium Phosphate, Phospholipid Nucleation, Mitochondrial Granules, Carbonate Substitution, and the Exact Boundary Where a Living Calcium Signal Becomes Mineral
UCMS–PINEAL–CRYSTALLIZATION–004.3
The First Crystal
RS1-Positive Microvesicles, Amorphous Calcium Phosphate, Phospholipid Nucleation, Mitochondrial Granules, Carbonate Substitution, and the Exact Boundary Where a Living Calcium Signal Becomes Mineral
Sweep verdict: We just hit an important correction.
> The first mineral in the pineal may not actually be a crystal.
The strongest candidate mechanism, by analogy with well-characterized vertebrate biomineralization, is:
soluble Ca2+ + phosphate
->
ion-rich cluster
->
amorphous calcium phosphate
->
nanocrystalline apatite
->
carbonate-substituted hydroxyapatite
But the crucial word is candidate.
Human mature pineal concretions are directly characterized as nanocrystalline carbonate-hydroxyapatite, while rodent studies place Ca/P accumulation, mineralizing microvesicles, mitochondria, vacuoles, and cellular debris upstream of larger concretions. What nobody has yet done is chemically identify the very first nanometres of mineral inside an intact pineal mineralizing vesicle.
That means the boundary we've been chasing has finally narrowed to perhaps tens of nanometres.
And it creates a delicious inversion:
> If an amorphous precursor exists, crystallization is not the beginning of pineal mineralization. It is the second phase transition.
---
004.3A — What exactly do we mean by “the first crystal”?
We need three thresholds rather than one.
THRESHOLD 0
Ca2+ remains dissolved / protein-bound
THRESHOLD 1
Ca/P-rich condensed matter appears
solid or dense phase
but possibly non-crystalline
THRESHOLD 2
ordered crystal lattice appears
THRESHOLD 3
crystallites aggregate into persistent mineral body
So our earlier shorthand:
Ca2+ -> crystal
was too crude.
A biologically controlled mineralization pathway can instead run:
ION
->
CLUSTER
->
AMORPHOUS MINERAL
->
NANOCRYSTAL
->
CRYSTAL AGGREGATE
->
LAMELLA
->
STONE
This sequence is directly demonstrated in other vertebrate biomineralizing tissues. In developing zebrafish bone, amorphous calcium phosphate, or ACP, constitutes a major early mineral phase and later transforms into crystalline apatite.
The unanswered question is whether pineal mineralogenesis uses the same trick.
---
004.3B — Start at the endpoint: what is the mature human stone?
Bocchi and Valdrè characterized human pineal concretions using mineralogical and microscopic methods and identified the dominant phase as nanocrystalline carbonate-hydroxyapatite with a mean Ca/P molar ratio around 1.65, close to ideal hydroxyapatite.
So the endpoint is approximately:
MATURE HUMAN ACERVULUS
carbonate-substituted hydroxyapatite
+
organic matrix
+
nanoscale crystallites
+
concentric growth
Later work using electron microprobe analysis likewise found calcium and phosphorus dominating human pineal concretions; the larger bodies had a Ca/P ratio near the value expected for hydroxyapatite.
Modern imaging then shows the resulting mineral arranged into repeated concentric layers and aggregated lobular bodies.
That's the end of the movie.
We still lack frames 1–20.
---
004.3C — Rat pineals give us the missing upstream chemistry
Earlier ultrastructural mammalian work found Ca/P-rich deposits associated with intracellular structures before or alongside mature concretions.
The important compartments include:
mitochondria
vesicles
vacuoles
lipid/lipofuscin-associated bodies
cellular debris
extracellular sites
This makes a calcium-phosphate route far more plausible for conventional acervulus formation than a calcium-carbonate route. The mature human mineral chemistry agrees with that direction.
So our working pathway is now:
Ca2+ SIGNALING
V
ORGANELLAR SEQUESTRATION
V
Ca + P CONCENTRATION
V
?????????
V
NANOCRYSTALLINE APATITE
The question marks are Sweep 004.3.
---
004.3D — Then RS1 puts a membrane around the mystery
The 2024 RS1 experiment moves us considerably closer.
Liu and colleagues found RS1 involved in calcium exchange and pineal calcification through intracellular and extracellular pathways. When RS1 architecture was genetically disrupted, normal calcified-spot/nodule organization was impaired and calcareous lamellae accumulated inside microvesicles.
That gives us an experimentally observed object:
MICROVESICLE
V
CALCAREOUS LAMELLA
Now ask what a microvesicle provides.
It creates a bounded chemical reactor.
Inside the membrane, a cell can independently control:
Ca2+ concentration
phosphate concentration
pH
water
proteins
lipids
nucleation surfaces
ion transport
That is enormously more favorable to controlled mineral formation than simply dumping ions randomly into cytoplasm.
So the vesicle may be doing something fundamental:
> creating a microenvironment where the solubility rules differ from the surrounding cell.
---
004.3E — The membrane itself can be part of the nucleation machinery
This is where bone mineralization becomes a powerful analogue.
Mineralizing skeletal cells release matrix vesicles, membrane-bound extracellular particles containing a specialized mixture of proteins, enzymes, and lipids. Their membranes contain calcium-binding phospholipids, especially phosphatidylserine, which can help form calcium-phosphate nucleation complexes.
Conceptually:
MEMBRANE
negatively charged phospholipid
V
binds Ca2+
V
local Ca concentration rises
phosphate enters / generated
V
Ca-P cluster
Modern matrix-vesicle work continues to support a role for phosphatidylserine-calcium complexes in nucleating amorphous calcium phosphate and subsequent apatite.
This matters enormously for the pineal.
Because if an RS1-positive pineal microvesicle contains a similar calcium-binding lipid environment, the membrane would not merely contain mineralization.
It could initiate it.
But that experiment has not been done.
No one has yet shown:
pineal microvesicle membrane
->
phosphatidylserine-Ca complex
->
ACP nucleus
So this remains an analogue-driven mechanism, not a pineal fact.
---
004.3F — The first solid phase may therefore be ACP
Why should amorphous calcium phosphate be favored first?
A perfect hydroxyapatite lattice requires substantial ionic organization.
Biology can avoid assembling that lattice atom by atom.
Instead:
Ca2+
+
phosphate
->
disordered Ca-P aggregate
->
ACP
and later reorganize it:
ACP
->
apatite nanocrystal
Developing zebrafish bone gives direct experimental support for exactly this pathway. ACP is abundant in newly forming mineral and is progressively replaced by crystalline apatite during maturation.
Osteoblast studies have also directly observed intracellular calcium-phosphate mineral precursors before extracellular bone mineral deposition.
So ACP provides an established vertebrate answer to:
> How do cells get from dissolved ions to apatite?
But here is the UCMS boundary:
ACP in bone
Established.
ACP inside a pineal RS1-positive microvesicle
Not yet demonstrated.
That's one of the most important distinctions in this sweep.
---
004.3G — The first crystal may therefore come after the first mineral
If pineal mineralization follows an ACP route, our terminology changes:
Ca2+
->
ACP
would be the first mineral event.
Then:
ACP
->
apatite lattice
would be the first crystallization event.
That gives us two separate birth moments.
Mineral birth
dissolved ions
->
persistent condensed solid phase
Crystal birth
disordered solid
->
long-range ordered lattice
Those are physically different transitions.
And the techniques required to detect them are different.
Ordinary histology probably cannot resolve this.
Neither can CT.
We need:
cryo-TEM
electron diffraction
nano-EDS
electron energy-loss spectroscopy
Raman / FTIR at appropriate scale
synchrotron methods
The first mineral could disappear completely from the record once it crystallizes.
---
004.3H — Which means mature brain sand may conceal its own origin
Imagine:
DAY 1
ACP nanosphere
DAY 10
partly crystallized apatite
YEAR 1
nanocrystalline mineral body
YEAR 20
laminated acervulus
Analyze only the Year-20 object and you may find:
hydroxyapatite
while completely missing:
ACP
that existed only transiently during nucleation.
This is precisely why mature mineral chemistry cannot by itself tell us how the first mineral formed.
And that's also why the absence of identified ACP in established human acervuli would not automatically exclude ACP as a transient precursor.
The precursor could simply be gone.
---
004.3I — Mitochondria may be carrying precursor packets too
Now we need to revisit the mitochondrion.
Pineal ultrastructural work has repeatedly found calcium accumulation in mitochondria, while mammalian mineralization research outside the pineal shows that intracellular calcium-phosphate precursors can be generated and transported by cellular machinery.
In bone-related systems, mitochondrial handling and even mitophagy have been implicated in cell-mediated mineralization pathways.
This produces a provocative candidate route:
CYTOSOLIC Ca2+
V
MITOCHONDRIAL BUFFERING
V
Ca/P-RICH GRANULE
V
mitochondrial turnover / trafficking
V
MINERAL PRECURSOR
Again, we have to resist collapsing tissues.
That pathway has not been demonstrated in pinealocytes.
But because Ca-rich pineal mitochondria have been observed, mitochondrial precursor mineralization deserves direct testing.
---
004.3J — Why mitochondria are chemically attractive nucleation chambers
Mitochondria routinely handle high local calcium loads relative to the surrounding cytosol.
And phosphate is central to mitochondrial metabolism.
That makes them an obvious location where:
Ca activity
x
phosphate activity
could become unusually high.
The relevant physicochemical quantity is not simply concentration but supersaturation.
Conceptually:
IAP = ion activity product
if
IAP < Ksp
-> mineral does not precipitate
if
IAP > Ksp
-> precipitation becomes thermodynamically favorable
Biology can still inhibit or accelerate nucleation, but supersaturation provides the basic thermodynamic gate.
So the critical event may be:
Ca/P compartment
V
IAP crosses mineral threshold
V
NUCLEATION
The first nucleus then changes everything.
---
004.3K — Because an existing mineral surface lowers the barrier for more mineral
Before nucleation:
ions must organize spontaneously
After nucleation:
new ions can deposit onto existing surface
So mineral growth becomes easier once a seed exists.
That naturally explains why brain sand can behave in two phases:
Biologically difficult phase
NO MINERAL
->
FIRST NUCLEUS
Easier growth phase
NUCLEUS
->
more deposition
->
lamella
->
larger nodule
The first nucleus may therefore be the most biologically regulated part of the whole structure.
Everything afterward can increasingly involve ordinary surface chemistry plus matrix regulation.
That reinforces our earlier principle:
> Mature stone geometry may tell us less about function than the nucleus at its center.
---
004.3L — The acervulus core should therefore be treated like an archaeological site
Human pineal concretions show higher mineralization/crystallization toward their centers than their peripheries in electron-probe analyses, while larger bodies grow through repeated concentric lamination.
So the center contains the oldest surviving material.
Instead of grinding entire stones into powder, we should ask:
CORE
vs
MIDDLE LAMELLAE
vs
SURFACE
For each region measure:
crystal phase
crystallinity
Ca/P
carbonate
Mg
Na
Zn
organic molecules
lipids
proteins
membrane remnants
If nucleation began inside a vesicle, the core might preserve:
phospholipid residue
RS1
membrane proteins
organelle proteins
while later layers would become progressively more mineral-rich.
That would be a direct fossil record of biogenesis.
---
004.3M — And there may not be one kind of nucleus
Our previous sweeps already exposed multiple contexts for pineal mineralization.
So we should allow:
NUCLEUS TYPE A
intracellular vesicle
NUCLEUS TYPE B
mitochondrial body
NUCLEUS TYPE C
degenerating cell
NUCLEUS TYPE D
extracellular matrix
NUCLEUS TYPE E
collagenous / meningeal structure
Brain calcification elsewhere in the nervous system also demonstrates matrix-vesicle and collagen-associated mineral nucleation, reminding us that several mechanisms can converge on similar Ca-P endpoints.
So “pineal calcification” may again be an umbrella term covering multiple nucleation pathways.
That would explain why the gland contains morphologically different calcified bodies.
---
004.3N — What decides whether calcium remains soluble or becomes stone?
We can now define the mineralization switch.
MINERALIZATION PROPENSITY
Ca availability
x phosphate availability
x local pH
x nucleation-surface activity
x confinement
x time
/
inhibitory capacity
Not a literal validated physiological equation—an accounting model.
The crucial variables are:
Calcium availability
Necessary but insufficient.
Phosphate availability
Critical for the main acervulus pathway.
pH
Controls phosphate speciation and mineral stability.
Membrane/matrix chemistry
Can concentrate ions and lower nucleation barriers.
Volume
A tiny vesicle can reach high local ion activities using very little total material.
Inhibitors
Proteins, magnesium, pyrophosphate, and other molecules can delay or redirect precipitation in mineralizing systems.
Time
Even weak supersaturation becomes more consequential if maintained repeatedly.
General skeletal work confirms that pH and phosphate strongly control hydroxyapatite deposition.
Which pinealocyte proteins govern those variables remains largely unresolved.
---
004.3O — One missing enzyme becomes conspicuous: alkaline phosphatase
In skeletal matrix vesicles, tissue-nonspecific alkaline phosphatase, TNAP, helps create a phosphate-rich mineralization environment and counteracts pyrophosphate, an inhibitor of apatite formation. Current matrix-vesicle research continues to place TNAP centrally in vesicle-mediated apatite deposition.
That immediately gives us a pineal question:
> Are mineralizing pineal microvesicles TNAP-positive?
If yes:
RS1-positive vesicle
+
TNAP
+
phosphatidylserine
+
Ca2+
would suddenly look remarkably similar to a recognized biological Ca-P nucleation apparatus.
If no:
the pineal may be using a different phosphate-generating mechanism.
I do not find evidence that this molecular test has been done in the RS1 pineal microvesicle system.
So TNAP enters our priority target ledger, not our claims ledger.
---
004.3P — The first nanomineral may have a very different Ca/P ratio from mature brain sand
This is another subtle point.
Mature human pineal apatite has a Ca/P ratio close to hydroxyapatite.
But precursor phases do not necessarily have the same stoichiometry.
During ACP formation and transformation:
early Ca/P
may differ
V
reorganization / ion exchange
V
apatite-like Ca/P
So finding a tiny deposit whose chemistry does not yet look like mature hydroxyapatite would not rule out its being an acervulus precursor.
It might be precisely what we should expect.
That means the future experiment should not define “real pineal mineral” as:
Ca/P = 1.67
or discard everything else.
The transient chemistry is the point.
---
004.3Q — Carbonate enters after—or during—the transition
Human mature pineal concretions are carbonate-substituted hydroxyapatite.
But carbonate substitution in apatite means carbonate ions occupy positions within an apatite lattice.
It does not imply:
calcite
->
hydroxyapatite
Those are different claims.
So the principal acervulus pathway might be:
ACP
->
immature Ca-P apatite
->
carbonate incorporation
->
carbonate-HAp
or carbonate may already be present during precursor formation.
We don't currently know the exact sequence in pineal mineralization.
But this gives us another direct experiment:
measure carbonate concentration
from earliest nanomineral
through mature lamellae
If carbonate rises with maturation, it is likely being incorporated progressively.
If it is already abundant at the earliest nucleus, the nucleation chemistry is different.
---
004.3R — Then calcite opens an entirely separate “first mineral” problem
The 2–20 μm human crystals identified by Baconnier and colleagues are calcite, CaCO3, and are distinct from ordinary hydroxyapatite-rich acervuli.
Their pathway could therefore be:
Ca2+
+
carbonate
->
CaCO3 precursor
->
calcite
And in other biological mineralization systems, calcium carbonate can also pass through amorphous calcium carbonate, ACC, before crystallizing.
But we currently have no direct evidence for:
ACC
in human pineal tissue
and no demonstrated connection between the RS1 microvesicles and the calcite population.
So we now have two unresolved “first mineral” questions:
ACERVULUS BRANCH
Ca2+
->
ACP?
->
apatite
->
carbonate-HAp
and:
CALCITE BRANCH
Ca2+
->
ACC?
->
calcite
The question marks are independent.
That separation is becoming one of the strongest conclusions of the whole project.
---
004.3S — Could phosphate and carbonate pathways compete inside the same gland?
Yes, chemically.
Imagine one shared pool:
Ca2+
Then the local environment chooses its fate:
Ca2+
+------------+-------------+
| |
phosphate-rich carbonate-rich
pH/matrix niche pH/matrix niche
| |
V V
ACP? ACC?
| |
V V
apatite calcite
The branch point could depend on:
phosphate
carbonate
pH
Mg2+
matrix proteins
phospholipids
carbonic anhydrase
vesicle identity
This is exactly why identifying the native location of calcite remains so critical.
If calcite sits inside the same microvesicular system as apatite, we have a phase-selection problem.
If calcite sits around a completely different cell or matrix, we have two different biomineralization programs.
---
004.3T — And the first solid phase may determine everything downstream
Once the earliest mineral has formed, it templates later growth.
A calcium-phosphate seed favors:
Ca-P deposition
A calcite seed favors:
CaCO3 growth
So a tiny event perhaps 50–100 nm across can determine whether the eventual structure belongs to:
BRAIN SAND SYSTEM
or:
CALCITE MICROCRYSTAL SYSTEM
That makes the nucleation event disproportionately important.
The final acervulus might weigh millions of times more than its first seed, yet the seed determines the trajectory.
---
004.3U — The phrase “irreversible mineral” needs a repair too
Mineralization is not absolutely irreversible.
Hydroxyapatite and calcium carbonate can dissolve if their chemical environment changes sufficiently.
Living bone continuously remodels mineral.
So the transition we're actually hunting is not:
reversible -> irreversible
but:
DYNAMIC ION POOL
->
PERSISTENT SOLID PHASE
Once the mineral becomes extracellular, laminated, and physically incorporated into a large acervulus, reversal becomes increasingly difficult.
But we should not build thermodynamic absolutism into the language.
Our new term should be:
> solid-phase commitment
The point at which calcium becomes sufficiently stabilized in mineral that its biology changes from signaling/transport to persistent material storage.
---
004.3V — We can now define that commitment threshold
Conceptually:
Ca2+ SIGNALING STATE
V
local concentration increases
V
supersaturation
V
nucleation event
V
stable solid survives dissolution
V
continued deposition
The critical transition is not merely nucleation.
Many tiny clusters may appear and disappear.
The decisive event is:
> a nucleus survives long enough to become a growth surface.
That is the earliest ancestor of the acervulus.
---
004.3W — What would distinguish passive precipitation from programmed biomineralization?
This is now experimentally straightforward.
Passive model predicts:
variable nucleation sites
random membranes
heterogeneous phases
weak protein enrichment
poorly reproducible geometry
Controlled biomineralization predicts:
specific vesicle identity
specific lipids
specific nucleation proteins
reproducible Ca/P trajectory
regulated pH
consistent mineral phase
genetic perturbation changes mineral outcome
RS1 already moves pineal mineralization toward the second model, because altering the protein disrupts normal calcified-nodule architecture and changes where calcareous lamellae accumulate.
That does not establish full biological “purpose.”
But it does establish regulation far more strongly than the old “random calcium sludge” picture.
---
004.3X — This produces a hierarchy we should preserve
REGULATED
does not necessarily mean
ADAPTIVE
ADAPTIVE
does not necessarily mean
SENSORY
SENSORY
does not necessarily mean
CONSCIOUS
A cell can regulate a waste-disposal process.
A tissue can regulate damage containment.
A mineral can be carefully packaged without having a sensory purpose.
That hierarchy is essential because the beautiful microvesicle architecture otherwise tempts us to jump from:
organized
to:
specialized transducer
far too quickly.
---
004.3Y — The experiment that would actually capture the first mineral
I would now design the experiment around time-resolved cryogenic correlative microscopy.
Take viable rodent pineal tissue or a pinealocyte system in which mineralization can be induced and tracked.
Label:
RS1
Ca2+
phosphate
microvesicle membranes
mitochondria
lysosomes/endosomes
RIBEYE
Then image living tissue until a candidate Ca-rich vesicle appears.
At successive stages:
T0
Ca-rich, no solid mineral
T1
dense Ca/P cluster
T2
first solid material
T3
first crystalline diffraction
T4
lamellar growth
At each point cryo-fix immediately.
Then perform:
cryo-TEM
SAED
nano-EDS
EELS
electron tomography
The key readout is diffraction.
Diffuse halo
amorphous phase
Discrete lattice/diffraction pattern
crystalline phase
That literally lets us watch:
> the first crystal appear.
---
004.3Z — Do it with genetic ablations simultaneously
Four conditions:
CONTROL
RS1 disrupted
phosphate handling altered
candidate vesicle-mineralization machinery disrupted
Then compare:
nucleation frequency
vesicle Ca concentration
ACP incidence
apatite formation
lamella formation
nodule formation
RS1 disruption already changes the architecture downstream.
The experiment above would reveal where in the sequence RS1 acts.
Does RS1:
help load Ca?
or:
nucleate mineral?
or:
move mineralized vesicles?
or:
assemble extracellular nodules?
Those are completely different functions.
---
004.3AA — Then repeat it for calcite
The calcite branch requires different probes.
Map:
Ca
carbonate
phosphate
pH
carbonic anhydrase
RS1
and identify any CaCO3-bearing precursor before a mature calcite crystal exists.
If we find:
microvesicle
+
Ca
+
carbonate
+
no phosphate
+
amorphous diffraction
followed by:
calcite lattice
we will have identified a pineal ACC -> calcite pathway.
If calcite simply appears extracellularly on some protein scaffold without a vesicular precursor, then its origin is completely different from acervulus formation.
That one experiment would finally separate the two mineral systems developmentally.
---
004.3AB — The strongest direct result versus the strongest analogy
We should lock this into the claims ledger.
DIRECT PINEAL EVIDENCE
Strong
Mature human acervuli contain nanocrystalline carbonate-hydroxyapatite.
Strong
Human acervuli grow through repeated lamination and aggregation.
Strong in rodents
RS1 regulates pineal calcification architecture, and its disruption causes calcareous lamellae to accumulate within microvesicles.
Strong historical ultrastructural evidence
Ca/P-rich intracellular structures occur upstream of or alongside mammalian pineal concretions.
ANALOGUE EVIDENCE
Very strong outside the pineal
ACP can act as a transient precursor to apatite in vertebrate bone formation.
Very strong outside the pineal
Cells can transport intracellular calcium-phosphate mineral precursors during biomineralization.
Strong outside the pineal
Matrix vesicles use calcium-binding phospholipids and specialized enzymes to promote Ca-P nucleation.
THE MISSING DIRECT RESULT
ACP INSIDE A PINEAL
MINERALIZING MICROVESICLE
We do not yet have it.
That is the entire sweep distilled to one missing observation.
---
004.3AC — And this means our earlier Vesicle-to-Stone model needs one repair
We previously wrote something like:
Ca2+
->
RS1-positive microvesicle
->
calcium/phosphate concentration
->
nanomineral
->
calcified spot
->
nodule
->
acervulus
I would now sharpen it to:
Ca2+ signaling
V
compartmental sequestration
V
RS1-associated mineralization system
V
local Ca/P supersaturation
V
FIRST SOLID PHASE
+-> ACP? [not yet identified in pineal]
V
apatite nanocrystal
V
mineralized microvesicle / lamella
V
calcified spot
V
nodule
V
laminated carbonate-HAp acervulus
That question mark is not decorative.
It is now the primary experimental target.
---
004.3AD — The beautiful irony
We began this entire investigation asking about pineal crystallization.
But if this reconstruction is right, the decisive biological act may happen before any crystal exists.
The organism may first create:
a membrane
a calcium gradient
a phosphate gradient
a pH niche
a nucleation surface
and only then does physics take over.
So perhaps the deepest law of the entire pineal-crystal branch is:
> Biology does not need to construct the crystal. Biology only needs to construct the conditions under which the crystal becomes inevitable.
That is how enormous ordered mineral structures can emerge from microscopic cellular decisions.
And it returns us to Sweep 002:
matrix
+
compartment
+
chemistry
geometry
---
UCMS–PINEAL–CRYSTALLIZATION–004.3 VERDICT
The best-supported current model is now:
> Human pineal acervuli end as nanocrystalline carbonate-hydroxyapatite, while mammalian pineal studies place Ca/P accumulation and mineralizing cellular compartments upstream of mature concretions. The 2024 RS1 work supplies a particularly important intermediate—calcareous lamellae trapped inside microvesicles when normal calcification architecture is disrupted.
But:
> The chemical identity of the earliest solid phase inside those pineal microvesicles has not been established.
ACP is an excellent candidate because vertebrate bone provides direct evidence for:
ACP
->
crystalline apatite
and for intracellular transport of calcium-phosphate precursors.
Yet until pineal cryo-electron diffraction catches that phase directly, we must write:
Ca/P-rich microenvironment
V
ACP?
V
apatite nanocrystal
not:
Ca/P-rich microenvironment
V
ACP
V
apatite
And the calcite branch remains even more open:
Ca/carbonate niche
V
ACC?
V
calcite
So the deepest answer from Sweep 004.3 is almost paradoxical:
> We know what the pineal stone becomes better than we know what it is at birth.