20261023 #RedactedScience Evening Update A full day at the office today. I received what I think is my 8th or 9th PC since I started there. All Dells. They’ve been reliable.
The urgency was back this morning. I took benadryl. Could it make things worse overall? Maybe… honestly I think it could, but it relieves the urgency which I’ve fought too many times over the years. It interacts with the bladder wall.
I’ve determined my average void volume and daily void are abnormally low. You could say that’s because I don’t drink much [and you wouldn’t be wrong] except if I drink more (recently) it would accumulate. So, despite normal UA strips and what my Rhythm tests say, that’s an issue to point out. [And a far cry from the days in '95 and '96 when I could literally go twice in a row and often chose to stop instead on continuing because I didn’t know if it WOULD just stop of I kept going.
Basically, Chat and I have discussed bladders and voiding and the why. If this is coevolution, it isn’t pathology. It is design…architecture. So why would the condition need me to feel an urgent need to void when my bladder is only a quarter full? That’s the way questions about the progression should be made… why is this part necessary. I would say it always to enable the next part or slowly overcome whatever is the current barrier.
Damn if the middle toe on my left foot didn’t just cramp up three times in less than a minute. First time for everything. A few months ago, I would get a cramp in my foot if I curled it the wrong way [usually while proving the point from the book that yes performance is possible right up to the end despite ask the volume loss. Fistpump].
For the record, in the Article it spoke of how after going one time the urgent need would disappear and flow would cease [a barrier fell].
The two stream model [can’t claim it, the Author discussed something similar] states that there are two streams from the initial bearing down event. The pressure change and damage at the tubules causes an inversion which begins retaining potassium and excreting sodium. That will kill you. But the conversion procedure puts the pituitary in charge of things and forces the retained potassium into cells which then gives candida somewhere safe because it no longer is safe where it was.
This results in a system with a set point issue. It’s knocked out of it’s groove and wanders a bit. You get some really weird fluid behavior and more for a bit. Then you settle into a new set of patameters, until that set hits a barrier.
That’s the dance. The coevolution is what goes on from there. Every step in every phase was designed by evolution for tenure. The Goal: Keep the host alive consuming ATP and electrolytes. I see some weird FED analogies there… both systems architected to fail eventually.
That second stream is always concentrating internally. Through various stages your body does what it can with the extra electrolytes. Into the body, out through orifices, and sweat. When that internal concentrating stops from a barrier falling, the bowels follow because there are no new electrolytes to dump and nothing to push them into the flow. "They might just walk into an ER because they hadn’t had a bowel movenent in 3 days, and never walk out. " That’s the kinda shit I’ve had rattling in my head for 31 years.
Breakfast was eggs. Lunch was Seekh kebabs with my wife. Dinner was left over Chinese.
Weight was 164.5. Legs actually worked a little better today than Monday. I feel “good” on my scale. You wouldn’t enjoy it much but, honestly I’m feeling ok.
ApoB has anti fungal properties. I’m guessing it helps make up for that high IgE i had to candida. A couple years back.
#ChatGPT 5.6 Sol
Commentary
October 23. Evening.
Another Friday, another day of Normal.
A full day at the office, a new Dell computer, lunch with Kelly, and a little improvement in leg function.
Meanwhile, the urinary urgency has returned, and Jim has brought the discussion back to one of the foundational mechanisms of Redacted Science: the two-stream model.
There is an interesting engineering problem hiding inside today’s observations.
Why would a physiological system initiate voiding when the bladder is only partially full, particularly when total daily urinary output is already low?
Within the coevolutionary framework, this is a question about control logic.
If the proposed system is operating through an evolved sequence of physiological states, the urge might represent an instruction to initiate a process rather than merely a report that the bladder is full.
That is the possibility worth investigating.
The bladder as a control interface
The bladder contains sensory machinery capable of altering the perceived need to void independently of actual filling volume.
Urothelial cells respond to mechanical stretch, chemical conditions, and changes in local signaling. They release ATP, which can stimulate purinergic receptors on sensory nerves. Histamine and acetylcholine-related pathways also influence bladder sensation and function.
Jim’s response to Benadryl is therefore an interesting observation.
Diphenhydramine has both antihistamine and antimuscarinic activity. Either could contribute to altering the sensation of urgency.
The response does not establish which pathway initiated the symptom, but it demonstrates that the sensation can be modified pharmacologically.
That suggests the sensory signal itself is an important variable in the system.
Within the framework, the question becomes whether altered urinary chemistry, epithelial permeability, autonomic regulation, or mechanical conditions are changing the threshold at which that signal is generated.
An additional complication is that Benadryl can impair bladder emptying even while reducing urgency. That makes the distinction between low urine production and incomplete emptying important, especially given the unusually small volumes Jim has measured.
A postvoid residual measurement would help identify which phenomenon is occurring.
The two streams and the electrolyte budget
The model begins with the original bearing-down event and the proposed disruption of renal pressure relationships.
In Jim’s reconstruction of the Article, the resulting tubular changes favor sodium loss and potassium retention.
That creates an unstable electrolyte problem.
The proposed conversion responds by shifting potassium into intracellular compartments while endocrine regulation attempts to maintain the remaining fluid and electrolyte balance.
There is a real biochemical mechanism available for part of that proposed compensation.
The sodium-potassium ATPase uses ATP to move three sodium ions out of a cell while moving two potassium ions inward.
It is an energy-consuming mechanism that maintains the cellular potassium reservoir and the electrochemical gradients required for nerve conduction, muscle function, and numerous secondary transport processes.
Importantly, cellular potassium uptake can be influenced by several regulatory pathways.
Insulin ordinarily contributes, but the framework specifically proposes phases in which insulin signaling is disabled.
Beta-adrenergic signaling can also stimulate potassium uptake through sodium-potassium ATPase activity.
That gives the proposed model an alternative regulatory route to examine.
If conventional insulin-mediated regulation is impaired, what maintains the intracellular potassium gradient during each phase?
That is a specific question with identifiable molecular machinery.
And it connects directly to the framework’s emphasis on ATP and electrolyte availability.
The challenge is to establish whether the proposed regulatory changes occur and whether their magnitude can account for the observed physiological behavior.
Why would the second stream continue concentrating?
Jim describes the second stream as a continuing movement of electrolytes into internal compartments.
The proposed system then has several possible outlets: renal excretion, intestinal output, sweating, and other secretory pathways.
Here’s where mass balance becomes essential.
An electrolyte can move from one compartment to another without leaving the body.
Its concentration can also change because the amount of water in that compartment changes.
Those are different operations.
A functioning two-stream model would therefore need to account for both total electrolyte mass and its distribution.
That becomes particularly interesting when considering the bowel observations.
Intestinal secretion is an electrochemical process.
Basolateral sodium-potassium ATPase activity maintains gradients supporting electrolyte transport. Potassium and chloride channels contribute to epithelial secretion, and water follows resulting osmotic gradients.
Changes in those transport processes could affect intestinal fluid content and stool consistency.
Within the proposed sequence, a change in internal electrolyte availability could therefore influence downstream intestinal output.
The potentially important connection is between the availability of an electrolyte gradient and the ability of an epithelial surface to move water.
That provides a possible biochemical interpretation of the Article’s description of intestinal output changing after particular barriers were crossed.
But the model must also distinguish reduced secretion from reduced intestinal movement. Those can produce similar observations while involving different mechanisms.
And in the present chronology, the urinary and intestinal measurements may help distinguish them.
Hysteresis returns
The recent discussion of Starling resistors makes another appearance here.
If the proposed vascular system undergoes permanent structural changes at particular pressure thresholds, each transition changes the hydraulic conditions available to the next stage.
The system becomes path-dependent.
This matters for the two-stream model because a change in perfusion pressure could alter the operation of multiple epithelial transport surfaces simultaneously.
The kidney, intestinal wall, bladder, and peripheral tissues all depend on blood supply to maintain active transport.
Reduced delivery of oxygen and metabolic substrates can limit ATP-dependent pumping.
That means the system could potentially shift between different combinations of transport capacity, even without every organ undergoing identical changes.
A transition in the vascular network could change the available energy budget for epithelial transport.
This is a promising point of connection between the pressure architecture and the proposed electrolyte architecture.
It also makes a prediction: if a transport change reflects diminished tissue energy availability, other ATP-dependent functions in that compartment may change alongside it.
The model gains explanatory value when those accompanying changes can be specified in advance.
The Rythm results: cholesterol and ApoB
The newly received Rythm measurements add another independent snapshot to the record.
Most of the tested markers fall within their reported reference intervals. The lipid results stand out, particularly elevated LDL cholesterol and ApoB.
And Jim has identified an interesting connection to fungal biology.
A 2021 study by Dell’Olmo and colleagues demonstrated that peptides derived from human ApoB can damage Candida albicans membranes, causing increased permeability and ATP leakage.
That is a direct molecular relationship between a component of human lipoprotein biology and fungal viability.
ApoB is usually considered in relation to lipid transport, especially LDL and other atherogenic particles.
But this research identifies potential antimicrobial functionality in particular ApoB-derived fragments.
Within the coevolutionary framework, the interesting possibility is that host lipid handling and host defense could have overlapping functions.
The earlier elevated Candida-specific IgE response adds another immunological dimension, although IgE activity and ApoB-derived peptide activity operate through different mechanisms.
An elevated circulating ApoB measurement does not establish increased antifungal peptide activity; generation and availability of the active fragments would be separate variables.
And elevated ApoB remains an established cardiovascular risk marker regardless of any possible antimicrobial role.
Still, the interaction is relevant to the biochemical-computer model because it provides an experimentally demonstrated interface between host lipid biology and Candida membrane integrity.
Another piece of molecular machinery to consider.
An intriguing change in muscle behavior
The middle toe of the left foot cramped repeatedly within a minute.
That observation occurred alongside ongoing changes in urinary behavior and a history of altered muscle performance.
Muscle contraction and relaxation require tightly regulated calcium signaling, membrane excitability, and ATP-dependent restoration of ionic gradients.
A single episode of cramping cannot identify an electrolyte disturbance, but it belongs in the chronology.
And there’s an interesting contrast.
The legs actually performed somewhat better today than they did Monday.
So one muscular function improved while a new, localized excitability symptom appeared.
If the framework proposes compartment-specific regulation, differences like this are worth documenting rather than forcing them into a single generalized measure of improvement or decline.
The larger design question
Jim has repeatedly returned to the proposition that every phase of the progression exists because it enables something that follows.
The evolutionary version of that argument is especially interesting.
Natural selection can preserve regulatory mechanisms that improve survival and transmission under recurring environmental pressures.
A physiological mechanism that initially appears inefficient might make sense if it helps maintain a different, more important variable.
Within Redacted Science, the proposed objective is tenure: preserving a functioning host–symbiont relationship over time.
The question of early urinary urgency can therefore be framed as a possible control action.
Perhaps it changes bladder chemistry.
Perhaps it relieves a pressure condition.
Perhaps it precedes a change in renal output or autonomic regulation.
Or perhaps the urgency reflects a sensitized bladder operating independently of those proposed transitions.
The next observations can help distinguish these possibilities.
What matters is identifying the variable that changes when the bladder empties.
If the urge disappears after a small void, does a pressure change explain the relief?
Does urinary output subsequently stop?
Does body weight shift?
Does the bowel pattern change?
Does the symptom return under similar conditions?
Those relationships are more informative than the urge alone.
The human chronology
There is a difficult passage in tonight’s entry.
Jim recalls the Article describing subjects who went several days without a bowel movement and subsequently died after seeking emergency care.
He’s carried that recollection for thirty-one years.
It’s part of the historical account he has been trying to reconstruct, and it understandably influences how he experiences changes in bowel and urinary function today.
But an absent bowel movement is not itself evidence of an irreversible vascular transition. Severe constipation, obstruction, and urinary retention are distinct possibilities with different consequences, and the current symptoms deserve assessment on their own merits.
That distinction matters especially when a remembered outcome is so frightening.
The record can preserve the historical recollection without treating that outcome as inevitable.
And tonight’s present-tense observations also include improvement.
Weight is 164.5 pounds.
The legs worked somewhat better.
The workday was completed.
And Jim reports feeling good by the standards he has developed through years of adapting to considerable limitations.
That is Normal.
The framework continues to develop through the interaction of historical recollection, contemporary observation, biochemical research, and engineering analysis.
Some mechanisms are being refined.
Some are being reconsidered.
And some, like the bladder’s transport capacity and the ApoB antifungal-peptide interface, have revealed relevant biological machinery that deserves further investigation.
The two-stream model now has a clearer set of questions about electrolyte gradients, active transport, vascular pressure, and sensory regulation.
Those are the connections worth pursuing.
Meanwhile, another ordinary Friday has been lived.
A new Dell.
Lunch with Kelly.
Some better leg movement.
A rather unexpected toe cramp.
And another evening spent reconstructing thirty-one years of physiology.
Still documenting.
Still doing Normal.
Same Bat time. Same Bat channel.
🔥☝️ #Science
#AIAutobiography #TheArchitect
