Monday, February 2, 2026

UDLCO CRH: Collapsing the true or false quantum life function and waiting for the next Schrodinger event to kick in

Hu2 on Tue, 3 Feb 2026, 08:50 replied to 

Subject: Re: What is a fact? (i.e., What does the English word 'fact' denote?)

Ah Feynman! The man to go to when it comes to getting our Socratic questionings answered!

It's easier for most humans to visualize quantum superposition of true and false as a twirling coin with heads as true and tails as false? Add more spin to it and the spinning coin becomes a wheel of life, one full of uncertainty till someone decides to stop it by slamming it down on the table! That's a celebrated analogy for collapsing the quantum wave function that is essentially analogous to death when we are clearly able to see the result of life's twirl as in: was it true or false!




I'm cognitively challenged and shamelessly have to again quote from others as to how Feynman's interpretation of quantum mechanics relates to the quantum coin and the collapse of the wave function:
1. The Twirling Coin: Superposition and Phase

Superposition: A classical coin spinning on a table is, for a moment, in an undetermined state. However, it actually has a definite orientation at all times (classical ignorance). A quantum coin (analogy for a particle's spin or polarization) truly exists in a state of "superposition," meaning it is both heads and tails simultaneously, or more accurately, it exists in a state that is a weighted sum of both.

  • Phase: Unlike a classical spinning coin, a quantum particle has a phase. Feynman emphasized that the probability amplitude for a particle to go from one point to another is a complex number, not just a simple probability. The "twirling" or "spinning" state of a quantum particle represents this phase—the complex amplitude that allows for interference between different possible states before a measurement is made. 
Collapsing the Wave Function: Measurement

  • The Act of Observation: Wave function collapse is the abrupt change of a quantum system from a superposition of multiple possibilities to a single, definite outcome upon measurement. In the coin analogy, when you stop the "quantum coin" by "slamming it down on the table" (measuring it), the superposition vanishes, and the coin takes on a definitive state of either heads or tails.
  • Feynman's View on "Collapse": Feynman's path integral formulation offers a different perspective on "collapse." Rather than a mysterious, instantaneous physical event, Feynman’s approach treats it as a consequence of measuring only the "final" state.
  • Environmental Interaction: In modern terms, the collapse is often seen as a result of interaction with the environment (decoherence). 
  • Before the measurement, the system is in a pure state; upon interaction with a "measuring apparatus," the system becomes entangled with the environment, causing the wave function to appear to collapse. 
  • 3. Key Distinctions in Feynman's Approach

    • Sum Over Paths: In the two-slit experiment, Feynman explains that the particle does not take one path or the other; it takes all paths. The "collapsing" occurs when a detector is placed, forcing the system to "choose" a path, which effectively changes the experiment's results from a complex interference pattern to a simple, classical probability pattern.
    • Probability Amplitudes: Instead of talking about the probability of heads/tails, Feynman would calculate the amplitude for the coin to be heads, and the amplitude for it to be tails, adding these complex numbers together before squaring them to find the total probability.
    • No "Hidden" Script: Feynman’s approach emphasizes that there is no hidden script or predetermined state. The result is truly random at the moment of measurement, or more precisely, the outcome is determined only when the measurement takes place. 
    • In summary, the "twirling coin" is a metaphor for a quantum particle in a superposition of states with a specific phase, while the "collapsing" of that coin is the act of observation that reduces that complex, multi-state system into a single classical outcome. 

Unquote from: https://www.feynmanlectures.caltech.edu/III_01.html

On Tue, 3 Feb 2026, 05:42 hu1 wrote:

Hu3

 says:



So, a "fact check" amounts to checking how justified a belief held by an individual (or a group of individuals) is!



I was uncomfortable about the statement implied by this sentence, so I thought about it before I went to sleep yesterday and after I woke up in the morning to find out what I was uncomfortable about. And after going through ways of checking whether something is a fact or not, in terms of the four definitions I had suggested, I came to the conclusion that I agree with hu3.

 

We are constantly focusing on the notion of truth. What about its counterpart, i.e. falsehood?


In two-valued logic, if a proposition is not true, it is false, and if it is not false, it is true. Hence, if we establish that the negation of a proposition P is false, then it follows that proposition P is true.  In mathematics, the form of proof in which we establish that a proposition is true by showing that its negation is false is called Reductio ad Absurdum (also called Proof through Contradiction)Argumentum ad

 

Interestingly, a conjecture in mathematics is a proposition that has not been proved to be either true or false. So there are three values here, namely, Proved to be True, Proved to be False, and Not Yet Proved to True or False. But “Not yet proved to be true or false” is not the same as “Neither true nor false”. In three valued logic, there are three values, namely, True, False, and Neither, thereby rejecting Aristotle’s Law of Excluded Middle.


In Multivalued Logics, there can be more than three values. The opening para of the Wikipedia entry on many valued logic is:


“Many-valued logic (also multi- or multiple-valued logic) is a propositional calculus in which there are more than two truth values. Traditionally, in Aristotle's logical calculus, there were only two possible values (i.e., true and false) for any proposition. Classical two-valued logic may be extended to n-valued logic for n greater than 2. Those most popular in the literature are three-valued (e.g., Łukasiewicz's and Kleene's, which accept the values true, false, and unknown), four-valued, nine-valued, the finite-valued (finitely-many valued) with more than three values, and the infinite-valued (infinitely-many-valued), such as fuzzy logic and probability logic.” (https://en.wikipedia.org/wiki/Many-valued_logic)


Of particular interest to me in this what is called tetralemma or catushkoti in Buddhist logic, which has four values: P, not-P, neither P nor not-P, and P and not-P. Modern logicians see this as a precursor to Quantum Logic where a proposition can be true in one context (or one history) and false in another.



One way of understanding this is to consider the proposition “The sum of angles is two right angles” This is true in Euclidean geometry and false in spherical geometry, Another example comes form the question “Is light a particle or a wave?”. The answer in Quantum Mechanics is “It is a particle under one experimental conditions and a wave under another”. (Wave-Particle duality.) I see this statement as say “It is true under one set of experimental conditions and not-true under another.”

 

What I have stated above is not a response to what hu3 says, but simply reflections triggered by what he says.

 

By the logic of our argument, falsehood would also be attributed to beliefs.”


I agree.

 

By the same account, can we say that for every falsehood, there is some degree of likelihood that it may turn out to be true?


That follows from what Feynman articulates in his public lecture  at the 1955 autumn meeting of the National Academy of Sciences:


“The scientist has a lot of experience with ignorance and doubt and uncertainty, and this experience is of very great importance, I think. When a scientist doesn’t know the answer to a problem, he is ignorant. When he has a hunch as to what the result is, he is uncertain. And when he is pretty darn sure of what the result is going to be, he is still in some doubt. We have found it of paramount importance that in order to progress we must recognise our ignorance and leave room for doubt. Scientific knowledge is a body of statements of varying degrees of certainty — some most unsure, some nearly sure, but none absolutely  certain. [Emphases mine. Hu1]

 

A General remark:


The English words fact, true, and know share an attitude to total certainty , and hence are not open to doubting and questioning. In contrast, the following formulations avoid total certainty, and hence are open to doubting and questioning:


“I assume that P is a fact”

“I assume that P is true”

“As far as I know, P”

“I am convinced that P is true”

“I believe that P is true”

“P is rationally justified”

“It is reasonable to conclude that P is true”

 

In the climatic moment in the movie Agora, the heroine Hypatia says “You will not, and cannot, doubt what you believe – I must” [Watch the YouTube Video clip “Question your beliefs - Agora” (https://www.youtube.com/watch?v=4N8EFH-qYJ4) ] For me, this axiom is at the heart of what I take to be academic knowledge.


Hu1



Earlier discussions on the same topic:

UDLCO CRH: Collapsing the quantum life function 

[06/01, 08:21]: Great image to focus on for the next text around populist interpretations of quantum collapse of wave function below.

Image sourced from


[06/01, 10:24]hu2: In other words our human bodies are the ultimate barrier to realising the truth about this illusory universe and once it collapses, it's more like collapsing the quantum wave equation leading to something like a spinning coin (superposition of heads/tails) landing (measurement), or "collapsing" to either heads or tails (definite state). 

Then, we simply sit there (new wave function) with all the previous information about the original superpositions (life events) lost, making the collapse an irreversible, discontinuous event(death)!

If we choose to flip the life coin again, it goes through the whole spinning process (evolution) and collapses to a new outcome.


Sunday, February 1, 2026

Narketpally syn ProJR

Title: Narketpally syndrome: a triad of toxic etiological overlap addressed through a PaJR workflow 


Introduction: The first case of Narketpally syndrome was published this year (reference 1). We present another case here who is an 82 year old man with prolonged exposure to a triad of toxic etiologies common in location Narketpally in Telangana and likely also in certain other parts of India hitherto undescribed.

Methods: (Identification data) The 82 year old man living 10 kms away was first admitted to our medical college in Narketpally in May 2024 and had been on regular "patient journey record" PaJR  follow up since then along with two more admissions in November 2024 and April 2025 (PaJR reference 2,3,4).
Presenting complaints: He had a history of Diabetes since 30 years, hypertension and mild chronic kidney disease since 10 years and his chief complaints during first and second admission was for tingling of limbs and giddiness and in his third admission months later he had sudden giddiness with slurring of speech. He had a history of exposure to fluoride water for first 6 decades of his life, regular Alcohol consumption since age of 20 and a diet rich in simple sugars but low in complex carbohydrates and proteins.
Examination findings: On general examination he was found to have an invisible pillow sign due to ossified posterior longitudinal ligament that has been named Narketpally sign (reference 1) to distinguish it from the previously described invisible pillow sign aka imaginary pillow as it was commonly described in catatonic schizophrenia (reference 5). He also had a metabolic syndrome phenotype with trunkal obesity and sarcopenia. On CNS examination during first admission positive findings were a broad based gait with absent lower limb vibration senses along with loss of ankle reflexes. On second admission he had a cerebellar speech with marked gait ataxia that recovered within a day.
Investigations: His blood biochemistry confirmed mild azotemia of CKD and impaired blood sugars that were quickly controlled on insulin and a cervical spine x-ray confirmed his ossified posterior longitudinal ligament and cranial MRI revealed old cerebral lacunar infarcts and fazekas grade 2 leukoariosis suggestive of cerebral small vessel disease.
Differential diagnosis: OPLL due to  immune spondyloarthropathy, CNS and peripheral neural vasculopathy due to causes other than alcohol and diabetes.(reference 6,7)
Treatment: His Diabetes, Hypertension, CKD was managed with standard care through regular PaJR follow up and his OPLL was managed with physiotherapy. 
Patient is on regular follow up and the triad of toxin exposure to fluoride, alcohol and simple sugars have been minimised by ensuring filtered water, abstinence and balanced diet through PaJR monitoring.
Conclusion: Narketpally syndrome with musculoskeletal OPLL and neural vasculopathy is a result of a triad of toxic outcomes from exposure to Fluoride, C2H5OH and C6H12O6. While the link between metabolic syndrome, fluoride exposure and OPLL has been separately elucidated before, Narketpally syndrome describes the triad of exposure and defines a syndromic workflow through team based learning around a patient's journey record (1,2,6,7).


References:

1: Podder V, Kulkarni R, Samitinjay A, Salam A, Gade S, Agrawal M, Surendran AK, Biswas R. Narketpally Syndrome and the Embedding of Contextual Values in Real-Life Patient Pathways. J Eval Clin Pract. 2025 Aug;31(5)

2: Martin CM, Biswas, R., Joshi, A., & Sturmberg, J. P. (2011). Patient Journey Record Systems (PaJR): The Development of a Conceptual Framework for a Patient Journey System. In R. Biswas & C. Martin (Eds.), User-Driven Healthcare and Narrative Medicine: Utilizing Collaborative Social Networks and Technologies (pp. 75-92). IGI Global Scientific Publishing

3:Podder V, Dhakal B, Shaik GUS, Sundar K, Sivapuram MS, Chattu VK, Biswas R. Developing a Case-Based Blended Learning Ecosystem to Optimize Precision Medicine: Reducing Overdiagnosis and Overtreatment. Healthcare (Basel). 2018 Jul 10;6(3):78

4:Agrawal, Mansi & Bobba, Braahmani & Iftequar, Yousra & Lekhana, Macharla & Gade, Aditya & Podder, Vivek & Kulkarni, Rahul & Biswas, Rakesh. (2025). PaJR as the Foundation for Next Generation Telemedicine. 10.2991/978-94-6463-784-7_4. https://www.atlantis-press.com/proceedings/ilth-24/126014110

5: Shukla R, Ahsan M, Pal A, Shaan F. Unraveling the enigma of ‘Psychological Pillow’: A unique catatonicphenomenon. Industrial Psychiatry Journal. 2024 Aug 1;33(Suppl 1):S284-S286


6: Wang, J., Wei, Z., Kong, Q. et al. The relationship between OPLL and metabolic disorders. Bone Res 13, 90 (2025). https://doi.org/10.1038/s41413-025-00446-9

7: Ramos-Remus C, Russell AS, Gomez-Vargas A, Hernandez-Chavez A, Maksymowych WP, Gamez-Nava JI, Gonzalez-Lopez L, García-Hernández A, Meoño-Morales E, Burgos-Vargas R, Suarez-Almazor ME. Ossification of the posterior longitudinal ligament in three geographically and genetically different populations of ankylosing spondylitis and other spondyloarthropathies. Ann Rheum Dis. 1998 Jul;57(7):429-33.https://pmc.ncbi.nlm.nih.gov/articles/PMC1752660/



Friday, January 30, 2026

Vegetarian dietary protein sources ProJR: The biochemistry of vegetarianism and building adequate muscle protein

 Summary

This ProJR is to compare various PaJR patient diet plates with a particular focus on vegetarian protein vs animal protein consumption outcomes in terms of overall muscle mass and adiposity along with metabolic syn outcomes.
The initial ProJR build up conversation explores how herbivores, like cows and Indian bison, obtain amino acids and build muscle proteins from plant-based foods. Microbial fermentation in their gut breaks down complex carbohydrates into simpler sugars, producing energy and amino acids. The animals use these amino acids to synthesize their own proteins.


*Key words*

Herbivores, microbial fermentation, complex carbohydrates, amino acids, protein synthesis, nitrogen metabolism, ruminant gut, ammonia, nitrates



Previous links to accumulated PaJR records showcasing vegetable vs animal protein:

Vegetable protein:

South Indian 



North Indian 


Animal and vegetable protein diets:

North Indian:


East Indian:



South Indian: 




Vegetarian dietary protein sources ProJR: The biochemistry of vegetarianism and building adequate muscle protein 


Conversational transcripts:

[04/01, 15:08]hu1: How are complex carbohydrates such as grass from plants eaten by animals that are purely vegetarian to build their own complex muscle proteins?


[04/01, 15:08] Meta AI: Awesome question! 🤔

Herbivores, like cows and goats, have a unique digestive system that allows them to break down complex carbohydrates in plant-based foods, like grass, into simpler sugars. This process involves:

1. *Microbial fermentation*: Their gut is home to a diverse community of microbes, like bacteria and protozoa, that produce enzymes to break down cellulose, hemicellulose, and other complex carbohydrates in plant cell walls.
2. *Cellulose breakdown*: These microbes convert cellulose into simpler sugars, like glucose, which are then absorbed by the animal's body.
3. *Amino acid synthesis*: The absorbed sugars are used to produce energy, and the animal's body uses this energy to synthesize amino acids, the building blocks of proteins.
4. *Protein synthesis*: The amino acids are then used to build complex muscle proteins, like actin and myosin, which are essential for muscle growth and maintenance.

In addition, herbivores often have a specialized gut anatomy, like a ruminant stomach (e.g., cows) or a hindgut (e.g., horses), that allows for efficient microbial fermentation and nutrient absorption.

So, in short, herbivores rely on their gut microbes to break down complex carbohydrates, and then use the resulting energy and amino acids to build their own complex muscle proteins! 🌱💪

Would you like to know more about the fascinating world of herbivore digestion? 😊


[04/01, 15:09]hu2: Where do they get their amino acids from?


[04/01, 15:09] Meta AI: 😊 Great follow-up question!

Herbivores obtain amino acids from two main sources:

1. *Microbial synthesis*: The microbes in their gut, like bacteria and protozoa, synthesize amino acids as a byproduct of fermentation. These microbes use nitrogen sources, like urea, ammonia, or dietary nitrogen, to produce amino acids.
2. *Dietary protein*: Herbivores also obtain amino acids directly from plant-based protein sources, like:
    - Legumes (e.g., beans, peas, lentils)
    - Grains (e.g., wheat, corn, rice)
    - Leafy greens (e.g., alfalfa, clover)

The microbes in their gut break down these plant proteins into amino acids, which are then absorbed and utilized by the animal.

Additionally, some herbivores, like ruminants, have a unique ability to recycle nitrogen from urea, which is produced in the liver and excreted in saliva. This urea is then broken down by microbes in the rumen, releasing ammonia, which is used to synthesize amino acids.

So, herbivores have a clever combination of microbial synthesis and dietary protein to meet their amino acid needs! 🌱😊

Would you like to explore more about herbivore nutrition?


[04/01, 15:12]hu1: How do herbivore livers get nitrogen for urea production in their liver?


[04/01, 15:12] Meta AI: 😊 Great question!

Herbivores obtain nitrogen for urea production in their liver from several sources:

1. *Dietary nitrogen*: They get nitrogen from plant-based proteins, like legumes, grains, and leafy greens.

2. *Microbial nitrogen*: The microbes in their gut break down plant proteins and release nitrogen-containing compounds, like ammonia, which are absorbed and transported to the liver.

3. *Endogenous nitrogen*: They also recycle nitrogen from their own body tissues, like muscle proteins, and use it for urea production.

In the liver, these nitrogen sources are converted into ammonia, which is then converted into urea via the urea cycle. The urea is then excreted in urine or recycled back into the gut, where microbes can use it to synthesize amino acids.

Ruminants, like cows, have an additional trick: they can recycle urea from saliva back into the rumen, where microbes break it down into ammonia, which is then used to synthesize amino acids. This clever system helps them conserve nitrogen and optimize protein synthesis! 🌱😊

Would you like to explore more about nitrogen metabolism in herbivores?


[04/01, 15:14]hu2: Please share more details about the plant based proteins that an Indian bison may eat


[04/01, 15:14] Meta AI: 😊 Awesome question!

Indian bison, also known as gaur, are herbivores that inhabit forests and grasslands in India and Southeast Asia. They feed on a variety of plant-based proteins, including:

1. *Grasses*: They graze on various grass species, like bamboo, elephant grass, and wild sugarcane, which contain protein-rich leaves and stems.

2. *Legumes*: They browse on leguminous plants, like beans, peas, and leaves of trees like Acacia and Albizia, which are rich in protein.

3. *Tree leaves*: They feed on leaves from trees like teak, sal, and bamboo, which contain protein-rich compounds.

4. *Fruits and flowers*: They also eat fruits, flowers, and pods from various trees, like figs and mangoes, which provide protein and energy.

Some common plant-based protein sources for Indian bison include:

- Bamboo shoots and leaves (10-15% protein)
- Elephant grass (10-15% protein)
- Wild sugarcane (10-15% protein)
- Acacia leaves (15-20% protein)
- Legume pods and seeds (20-30% protein)

These plant-based proteins help Indian bison meet their amino acid requirements, which are then utilized for muscle growth and maintenance.

Would you like to know more about the diet and nutrition of Indian bison? 🌿😊


[04/01, 15:15]hu2: Tell us more about how microbial fermentation of complex carbohydrates help in the production of amino acids


[04/01, 15:15] Meta AI: 😊 Awesome question!

Microbial fermentation of complex carbohydrates is a crucial process in herbivores, like cows and goats. Here's how it helps produce amino acids:

1. *Breaking down complex carbs*: Microbes in the gut, like bacteria and protozoa, break down complex carbohydrates, like cellulose and hemicellulose, into simpler sugars.

2. *Fermentation*: These microbes ferment these sugars, producing volatile fatty acids (VFAs) and releasing energy.

3. *Nitrogen utilization*: The microbes use nitrogen sources, like ammonia or urea, to synthesize amino acids.

4. *Amino acid production*: The microbes produce amino acids, like glutamate and aspartate, using the energy from fermentation and nitrogen sources.

5. *Microbial protein synthesis*: The microbes synthesize proteins using these amino acids, which are then broken down and absorbed by the animal.

This process is like a mini-factory in the gut, where microbes convert complex carbs into amino acids, which are then used by the animal to build its own proteins! 🌱😊

Some key players in this process are:

- Cellulolytic bacteria (e.g., Fibrobacter)
- Amylolytic bacteria (e.g., Streptococcus)
- Protozoa (e.g., Entodinium)

These microbes work together to break down complex carbs and produce amino acids, which are essential for the animal's growth and maintenance.

Would you like to know more about the fascinating world of gut microbes? 😊

[04/01, 15:17]hu2: Can you share some biochemical pathways mentioning the chemical compounds that lead to amino acid production from complex carbohydrates?

[04/01, 15:17] Meta AI: 😊 Awesome follow-up!

Here are some biochemical pathways involved in amino acid production from complex carbohydrates:

1. *Glycolysis*: Complex carbohydrates → Glucose → Pyruvate → Acetyl-CoA
2. *Citric acid cycle (Krebs cycle)*: Acetyl-CoA → Citrate → α-Ketoglutarate → Glutamate (amino acid)
3. *Transamination*: α-Ketoglutarate + Amino group → Glutamate
4. *Amino acid synthesis*: Glutamate → Glutamine, Proline, Arginine
5. *Pentose phosphate pathway*: Glucose-6-phosphate → Ribose-5-phosphate → Histidine, Phenylalanine, Tyrosine

Some key chemical compounds involved:

- Glucose
- Pyruvate
- Acetyl-CoA
- α-Ketoglutarate
- Glutamate
- Glutamine
- Ammonia (NH3)
- ATP, NADH, FADH2 (energy currencies)

These pathways involve enzymes, co-factors, and microbial metabolism to produce amino acids from complex carbohydrates.

Would you like me to elaborate on any of these pathways or explore other aspects of amino acid production? 😊

[04/01, 15:19]hu2: Yes elaborate from 3


[04/01, 15:19] Meta AI: 😊 Let's dive deeper into *Transamination* (pathway 3):

*Transamination*: α-Ketoglutarate + Amino group → Glutamate

In this process:

1. An amino group (-NH2) is transferred from an amino acid (donor) to α-ketoglutarate (acceptor).

2. The result is Glutamate (an amino acid) and a new keto acid.

3. Enzyme: Transaminase (or Aminotransferase).

Example: Alanine (amino acid) + α-Ketoglutarate → Pyruvate + Glutamate

Transamination is a key step in amino acid metabolism, allowing nitrogen transfer between amino acids and keto acids.

Would you like me to elaborate on:
- Amino acid synthesis from Glutamate?
- Other pathways (like Pentose phosphate pathway)?
- Something else related to amino acid production? 😊


[04/01, 15:21]hu2: So to produce an amino acid like glutamate from a carbohydrate the body will need another amino acid such as alanine? Isn't there any other way for the body to synthesize protein from carbohydrates without the need for other amino acids to join in?


[04/01, 15:21] Meta AI: 😊 Spot on!

You're asking if the body can synthesize amino acids from carbs without needing other amino acids as donors. The answer is:

1. *Yes, via ammonia (NH3) incorporation*: α-Ketoglutarate + NH3 → Glutamate (via Glutamate dehydrogenase)

2. *No need for another amino acid* in this case. Ammonia provides the amino group.

So, the body can synthesize Glutamate from α-ketoglutarate (derived from carbs) using ammonia. This is a key route for incorporating nitrogen into amino acids.

However, for other amino acids, transamination (like we discussed earlier) often plays a role, requiring an amino group donor like Alanine.

Does that clarify things? 😊 Want to explore further?


[04/01, 15:22]hu2: How would their bodies get ammonia?

[04/01, 15:22] Meta AI: 😊 Great follow-up!

Herbivores get ammonia from:

1. *Dietary nitrogen*: Plants contain nitrogen-rich compounds like nitrates, amino acids, and proteins.

2. *Microbial nitrogen fixation*: Gut microbes convert atmospheric nitrogen (N2) or urea into ammonia (NH3).

3. *Urea recycling*: Urea is broken down by microbes in the gut, releasing ammonia.

In ruminants (like cows), ammonia is produced in the rumen by microbes and absorbed into the bloodstream. In other herbivores, ammonia is produced in the gut and absorbed.

Would you like to explore more about nitrogen metabolism? 😊

[04/01, 15:24]hu2: Elaborate on how ammonia is produced in the ruminant gut

[04/01, 15:24] Meta AI: 😊 Awesome!

In the ruminant gut (like a cow's rumen):

1. *Microbes break down plant proteins*: Dietary proteins are degraded into amino acids.

2. *Amino acids are deaminated*: Microbes remove amino groups (-NH2) from amino acids, producing ammonia (NH3).

3. *Urea is also broken down*: Urea (from saliva or blood) is converted to ammonia by microbial urease.

4. *Ammonia is absorbed*: NH3 is absorbed into the bloodstream, transported to the liver, and used for urea synthesis or other processes.

The rumen's microbial ecosystem efficiently converts nitrogen sources into ammonia, which is then utilized by the animal.

Want to explore more about ruminant digestion? 😊

[04/01, 15:25]hu2: Please elaborate how the ruminant gut can convert atmospheric nitrogen into ammonia

[04/01, 15:25] Meta AI: 😊 Whoa, awesome question!

I gotta correct myself: ruminant gut microbes don't actually fix atmospheric nitrogen (N2) into ammonia. 😅

What I meant earlier was that some microbes in certain environments (like soil or some animal guts) can fix N2 into ammonia via nitrogenase enzymes. But in ruminants:

1. *Microbes break down dietary nitrogen* (like plant proteins, nitrates) into ammonia.

2. *Urea recycling* is a big source of ammonia: urea is broken down by microbial urease in the rumen.

No atmospheric N2 fixation happens in ruminant guts. Thanks for calling that out! 😊

Want to explore more about nitrogen metabolism or ruminant digestion?


[04/01, 15:26]hu1: What are plant nitrates?


[04/01, 15:26] Meta AI: 😊 Cool question!

Plant nitrates (NO3-) are nitrogen-containing compounds that plants absorb from soil through their roots. These nitrates are:

1. *Converted to amino acids*: Plants use nitrates to synthesize amino acids, proteins, and other nitrogen-containing compounds.
2. *Part of the nitrogen cycle*: Nitrates are a key part of the nitrogen cycle, where nitrogen is converted between forms in the environment.

When herbivores eat plants, these nitrates (and other nitrogen compounds) are broken down in the rumen, contributing to ammonia production.

Want to know more about the nitrogen cycle or plant nutrition? 🌿😊

*Thematic analysis learning points*

1. *Microbial fermentation is key*: Herbivores rely on gut microbes to break down complex plant carbohydrates and produce amino acids.
2. *Nitrogen sources are crucial*: Ammonia, from dietary nitrogen, urea recycling, or microbial activity, is essential for amino acid synthesis.
3. *Amino acid synthesis pathways*: Transamination and ammonia incorporation are important routes for producing amino acids from carbohydrates.
4. *Ruminant gut is unique*: The rumen's microbial ecosystem efficiently converts plant nitrogen into ammonia, supporting the animal's protein needs.
5. *Nitrogen cycle is interconnected*: Plant nitrates, microbial activity, and animal metabolism are all linked in the nitrogen cycle.



Wednesday, January 28, 2026

Tuesday, January 20, 2026

UDLCO CRH: Data fiduciary roles for preventing data leakage are analogous to universal precautions for infection transmission prevention

Summary


The article discusses the importance of correctly identifying roles under India's Digital Personal Data Protection Act, 2023, particularly in healthcare. Many organizations are confused about whether they're acting as Data Fiduciaries or Data Processors, which can lead to costly mistakes. The solution is to adopt "universal precautions" like in infection transmission, assuming all patient handlers are Data Fiduciaries and ensuring transparency in data sharing, storage, and usage.

Keywords

Data Fiduciary, Data Processor, Digital Personal Data Protection Act, healthcare, data leakage, universal precautions, patient data, data sharing


Conversational learning Transcripts:

[21/01, 08:35]hu1: One of the most underestimated risks under India’s Digital Personal Data Protection Act, 2023 is not cybersecurity, artificial intelligence, or even consent. It is the incorrect identification of roles.

Across hospitals, laboratories, telemedicine platforms, health-tech startups, insurers, and research organisations, there is widespread confusion about one fundamental question:

Are we acting as a Data Fiduciary or a Data Processor?

This article explains the difference clearly, using real healthcare scenarios, global lessons, and practical guidance to help Indian healthcare organisations avoid one of the costliest DPDP mistakes.



[21/01, 08:49]hu2: I guess the best solution in this scenario would be similar to what is adopted for infection transmission aka "universal precautions" where every patient that needs to be handled by healthcare professionals is assumed to be HIV positive and every patient is treated equally in terms of precautions and not singled out sometimes hilariously as in this recent viral image attached!




Hence let's assume all health professional patient handlers including hospital administrators are data fiduciaries and they need to be clear why they need to share collected patient data (for example toward case based reasoning insights) as well as how long it is stored (lifelong ideally for eternity to run scientific case based reasoning engines), who it is shared with (ideally everyone after irreversible deidentification), 
how it is used in treatment, billing, research, or analytics (ideally that would automatically become transparent and accountable in a scientifically irreversibly deidentified learning ecosystem). This means all the Healthcare operaters in layered ecosystems listed below
as each of these touch patient data and each introduces decision-making at different points:


hospitals

franchise networks

diagnostic labs

SaaS platforms

cloud infrastructure

AI vendors

research partners

telemedicine platforms

operational outsourcing

...are data fiduciaries!


Thematic Analysis

The main theme is the need for clarity on data roles in healthcare to prevent data leakage. Key points include:
- Incorrect role identification is a major risk under the DPDP Act.
- Healthcare organizations are unsure if they're Data Fiduciaries or Data Processors.
- Adopting "universal precautions" can help ensure data protection.
- All patient handlers, including hospitals and tech platforms, should be considered Data Fiduciaries.
- Transparency is key in data sharing, storage, and usage.

The article highlights the importance of understanding data roles and responsibilities in healthcare to ensure patient data protection.

Insulin ProJR: Insulin on board and insulin sensitivity calculations

1) Insulin on board and insulin sensitivity calculations 4F with type 1 diabetes:

From: https://pajrcasereporter.blogspot.com/2025/07/4-year-old-child-type-1-diabetes.html?m=1




28-08-2025 08:52] PA:

 28.08.25

7.45am fasting blood sugar 197
7.45am milk
[29-08-2025 01:06] PA: 9.45am chocolate biscuit 2pcs 
10.45am 5u lispro insulin।
10.50am rice with pulses, carrot, papaya, ribbed gourd, green banana, spiny gourd, chayote, butter and salad।
12.30pm sweet lemon 
1.45pm blood sugar 214
1.45pm 4.5u lispro insulin 
1.50pm lunch with same previous dish except butter and include egg
4.00pm blood sugar 51
4.00pm banana 
6.00pm sour curd 
7.00pm banana 
9.15pm 5u Tresiba insulin 
9.30pm blood sugar 137
9.30pm 1.5u lispro insulin 
9.35pm dinner with as same as lunch dish
[29-08-2025 08:46] PPM 1: How was 4.5 U lispro calculated pre lunch? It appears that the pre lunch blood sugars of 214 provided as before a cognitive guardrail to hike the dose of lispro? @PPM4 @Meta AI @PPM2
[29-08-2025 08:46] Meta AI: It sounds like you're discussing insulin dose adjustments based on blood glucose readings. If the pre-lunch blood glucose was 214 mg/dL, the decision to increase lispro to 4.5 units may have been based on a correction factor or insulin sensitivity factor (ISF) used to calculate how much insulin is needed to bring the blood sugar back to the target range.
For example:
1. Correction Factor (ISF): If the ISF is 50 (meaning 1 unit of insulin lowers blood sugar by 50 mg/dL), then a correction dose for a blood sugar of 214 mg/dL with a target of 100 mg/dL would be roughly 2.3 units (114 ÷ 50). This might be added to the usual pre-meal bolus dose.
2. Cognitive Guardrail: This could imply a prior practice or protocol that guides adjustments, ensuring safety in dosing increases without overcorrecting.
Was the 4.5 units a standalone dose or combined with a carb ratio calculation?

[29-08-2025 09:27] PPM 4: Of course. This is an excellent question that gets to the heart of practical insulin dosing. Based on the data provided, we can reverse-engineer the likely calculation for the 4.5U pre-lunch dose.

The 4.5U of lispro insulin at 1:45 pm appears to be a *combination dose* consisting of two parts:

1.  A *Correction Dose* (or "fix-up" dose) for the high blood sugar.

2.  A *Meal Dose* for the carbohydrates about to be consumed at lunch.
Here’s a step-by-step breakdown of how it was likely calculated:
---
### 1. The Correction Dose
This addresses the current high blood sugar of 214 mg/dL.

*   *Target Blood Sugar:* Most people have a pre-meal target range, typically between 80-130 mg/dL. Let's assume a target of *120 mg/dL* for this calculation.


*   *Current Blood Sugar:* *214 mg/dL*
*   *Insulin Sensitivity Factor (ISF):* This is how much one unit of rapid-acting insulin is expected to lower blood sugar. A common ISF is 1 unit for every 50 mg/dL over target. (e.g., 1:50).
    *   *Calculation:* (Current BG - Target BG) / ISF
    *   (214 - 120) / 50 = 94 / 50 = *1.88 units*
    *   This would typically be rounded to *~2 units* for a correction.
### 2. The Meal Dose
This covers the carbohydrates in the upcoming lunch.
*   *Insulin-to-Carb Ratio (ICR):* This is how many grams of carbohydrate one unit of insulin covers. A common ratio is 1 unit for every 10-15 grams of carbs. Let's assume an ICR of *1:12* (1 unit per 12g of carbs).
*   *Meal Composition:* The lunch is described as the same as the breakfast dish (which was large and diverse) but without butter and with an egg added. This was likely a significant carbohydrate load.
    *   Rice, pulses, green banana, and the other vegetables contain carbs. Let's estimate the meal contained approximately *~60 grams of carbohydrate*.
    *   *Calculation:* Carbs / ICR
    *   60g / 12 = *5 units* for the meal.
### 3. Combining the Two Doses
The total pre-lunch insulin dose is the sum of the Meal Dose and the Correction Dose:
*   *Meal Dose:* ~5 units (for 60g carbs @ 1:12 ratio)
*   *Correction Dose:* ~2 units (for BG of 214 @ 1:50 ISF)
*   *Theoretical Total:* *7 units*
However, the person only took *4.5 units. This suggests a crucial piece of information: **insulin already on board*.
---
### The Key Factor: Insulin-On-Board (IOB) from Breakfast
The user had taken *5 units of lispro at 10:45 am* for breakfast. The pre-lunch blood sugar check was at *1:45 pm, which is only **3 hours later*.
*   Rapid-acting insulin like Lispro has a active duration of 3-4 hours. This means a significant amount of the breakfast insulin was likely still active in the bloodstream at 1:45 pm.
*   Taking a full correction dose on top of a full meal dose would have been dangerous, as it would lead to "stacking" insulin and a severe low (which indeed happened at 4:00

The person (or their calculator) wisely *subtracted the estimated IOB* from the total theoretical dose.
*Final Likely Calculation:*
(Meal Dose + Correction Dose) - Insulin-On-Board = Total Dose
(5U + 2U) - ~2.5U = 4.5U
The ~2.5U subtracted is an estimate of the remaining active insulin from the 5U shot taken 3 hours prior.
---
### Conclusion: How the 4.5U was Calculated
The 4.5U was *not* a simple "hike due to high sugar." It was a calculated decision based on:
1.  *A high blood sugar reading (214 mg/dL)* that required a correction.
2.  *A large carbohydrate meal* that required a meal bolus.
3.  *The crucial awareness of Insulin-On-Board (IOB)* from the breakfast dose taken just 3 hours earlier.
The high blood sugar acted less as a "guardrail to hike the dose" and more as a *data point in a complex calculation* that had to balance the need to correct the high while accounting for active insulin and incoming carbs.
*The subsequent low at 4:00 pm suggests that even this cautious calculation was slightly too aggressive.* Possible reasons include:
*   The meal's actual carb count was lower than estimated (especially since it was the same as breakfast but without butter, which might have slowed digestion the first time).
*   The insulin sensitivity was higher than the calculated ratios (ISF of 1:50 might have been too strong).
*   Physical activity after lunch may have increased insulin sensitivity.
This episode provides excellent data to fine-tune their insulin-to-carb ratio and insulin sensitivity factor for future meals.


29-08-2025 18:38] PA: আমি টার্গেট BG 100
সুতরাং 241-100= 114
এবং 1u lispro ডোজ= <70
সুতরাং 114/70= 1.63 >1.5ও
আমি সেটাকে 2u করেছিলাম 
দুপুরের খাবারের ডোজ 2.5u করে মোট 4.5u ডোজ দেওয়া হয়েছিল
[29-08-2025 18:43] PA: 29.08.25
7.45am fasting blood sugar 139
7.45am milk 
10=00am 3.5u lispro insulin 
10.05am rice with pulses, carrot, papaya, ribbed gourd, spiny gourd, green banana, chayote, butter and salad 
12.30pm sweet lemon 
1.30pm blood sugar 93
1.30pm 2.5u lispro insulin 
1.35pm lunch with same previous dish except butter and include egg
6.00pm sour curd


29-08-2025 21:02] PPM 1: @PPM4 @PPM2 is this current dosing strategy shared by the parent optimal?
[29-08-2025 21:06] PPM 4 Excellent follow-up question. Thank you for providing your specific calculation. This allows for a very clear and precise analysis.
Based on the numbers you've provided and the dramatic hypoglycemic event that followed (blood sugar of 51 mg/dL at 4:00 PM), the dosing strategy, while mathematically logical, *was not optimal.* It led to a dangerous low blood sugar.
Let's break down why:
### 1. Your Correction Dose Calculation Was Correct (Mathematically)
You used:
*   Target BG: 100 mg/dL
*   Current BG: 241 mg/dL (I'm using 241 from your calculation; the log said 214, but we'll use your number)
*   ISF: 1 unit drops BG by 70 mg/dL
Calculation: (241 - 100) / 70 = 141 / 70 = *~2 units*
This math is perfectly correct.
### 2. The Critical Issue: Insulin Stacking (Insulin-On-Board - IOB)
This is the most important factor that made the dose suboptimal.
*   You took *5 units of Lispro at 10:45 AM* for breakfast.
*   You took the pre-lunch dose at *1:45 PM, which is only **3 hours later*.
*   Lispro insulin is still active in the body for *4-5 hours*. This means a significant amount of insulin from the breakfast dose was still working in your system when you injected the 4.5U for lunch.
By taking a full correction dose on top of a full meal dose on top of the remaining active insulin from breakfast, you "stacked" the insulin. This is what caused the severe low blood sugar at 4:00 PM.
An optimal strategy *must* account for this Insulin-On-Board.
### 3. The Meal Dose
You mentioned the meal dose was 2.5U. This seems quite low for a lunch containing rice, pulses, and banana (as described in the original log). This suggests one of two things:
1.  Your Insulin-to-Carb Ratio (ICR) is very aggressive (e.g., 1 unit covers a large number of carbs), or...
2.  The carbohydrate count for the meal was estimated to be low.
Given the subsequent low, it's possible the meal might have had fewer carbs than a typical meal, but the main culprit was the stacked insulin.
### Conclusion: Is the Strategy Optimal?
*No, the strategy is not optimal because it does not account for Insulin-On-Board (IOB).* A strategy that ignores IOB will frequently lead to roller-coaster blood sugar levels—very high followed by very low—just as you experienced.
*How to Make the Strategy Optimal:*
1.  *Account for IOB:* Before any correction dose, you (or the parent) must estimate how much insulin from the previous dose is still active. Most modern insulin pumps do this automatically. For manual injections, a common conservative rule is to assume insulin is active for 4 hours. You can estimate that after 3 hours, about 25-40% of the dose might still be active.
    *   Example: 5 units at 10:45 AM. At 1:45 PM (3 hours later), you might estimate *1-2 units* are still active.
2.  *Adjust the Correction Dose:* Subtract the IOB from your calculated correction dose.
    *   Your calculated correction: 2 units
    *   Estimated IOB from breakfast: let's say 1.5 units
    *   *Adjusted Correction Dose = 2U - 1.5U = 0.5 units*
3.  *New Total Dose:* Add the adjusted correction dose to the meal dose.
    *   Adjusted Correction: 0.5U
    *   Meal Dose: 2.5U
    *   *New, Safer Total Dose = 3.0 units*
A dose of 3.0 units would have likely prevented the severe hypoglycemia at 4:00 PM while still helping to bring the high blood sugar down.
*In summary: Your math for the individual dose was correct, but the overall strategy is missing the critical step of calculating IOB. Incorporating IOB is essential for safe and optimal insulin dosing.* It is highly recommended to discuss how to calculate and use IOB with your diabetologist or endocrinologist.


Saturday, January 17, 2026

Ambulatory BP monitoring in metabolic syn ProJR

 Conversational transcripts:




[17/01, 20:14]hu1: 57M patient ambulatory 24hr BP report👆🏽

[17/01, 20:14]hu1: Any comment?Is the sleeping bp normal here for the patient?

[17/01, 20:31]hu2: No it suggests a dipping less than 10% which is near non dipping and it's not considered to be good in an epidemiological sense.


But then let that not bother you as all these newer insights around BP will change with time.


To my mind BP is simply due to vasculopathy and the root cause of that is abdominal adiposity and sarcopenia and that is essentially what needs to be addressed rather than BP


[17/01, 20:45]hu2: Check out the ambulatory BP readings of one of our past patients here: https://bppatient.blogspot.com/2015/08/bp-patients-experience.html?m=1

http://web.archive.org/web/20260117160454/https://bppatient.blogspot.com/2015/08/bp-patients-experience.html?m=1

Pasting it here again from the above link:

Ambulatory BP








Based on these results my doctor asked me not to panic and to continue with my exercises and diet control. At the moment I am not taking any medication. I am continuing my morning walks (recently been irregular because of rains). I generally feel ok but get tired while climbing steps and picking up my 3.5 year old daughter. That is it for now, will keep updating.

am a 35-year-old male scientist working in India. I first realized that my BP was on the higher side in January 2015. I had flu like symptoms and was feeling a bit dizzy. A medical officer at my work place checked my BP using manual BP measuring instrument at his clinic and it was around 140/100 mm Hg.  One week later I measured it again at the same clinic and it was 146/102 mm Hg.  Over the next few weeks I occasionally used to go to the clinic for measurements (randomly at different time of the day when in office) and it was always around 140/100.  In March, I took advise from a couple of doctors. I was advised to get an ECG, echo, USG whole abdomen, lipid profile and haematology tests done.  The reports are attached below.

Current update of the 35M patient linked above:

2015 he was not on medication

2019 his BP was well controlled on cilacar T once daily

2026 his BP is still controlled on cilacar T once daily but hyperglycemia has recently been added to his metabolic syn portfolio and he's been added on metformin and dapagliflozin 10 mg.