Thursday, September 18, 2025

Alamania punicea: What #AgingReversal #GeneticDrugTherapies are likely to work for #MuscleWastingReversal & #SpinalCompressionReversal & possibly per 1 variable - #heightWUaS? What #YogaGenetics with #YogaEthics for performance - #HigherFasterStronger & more supple bodies https://scott-macleod.blogspot.com/2025/09/alamania-punicea.html ? * * * What genes to add to #CElegans (nematode worm w 302 backbone neurons) to 100x lifespan, from 3 weeks to 300 weeks re #ExtremeLongevity #AgingReversal & per @geochurch https://youtu.be/bnCEIPQFNnk ? #AddGeneCopies with food somehow? How w #PhysicalDigitalSim in #RealisticVirtualEarth?



What #AgingReversal #GeneticDrugTherapies are likely to work for #MuscleWastingReversal & #SpinalCompressionReversal & possibly per 1 variable - #heightWUaS? What #YogaGenetics with #YogaEthics for performance - #HigherFasterStronger & more supple bodies https://scott-macleod.blogspot.com/2025/09/alamania-punicea.html ?

https://x.com/WorldUnivAndSch/status/1968853051143287102

https://x.com/Q_YogaMacFlower/status/1968853256680976415



* 



* 
Gemini - 
What #Aging Reversal #Genetic Drug Therapies are likely to work for #Muscle Wasting Reversal & #Spinal Compression Reversal & possibly per 1 variable - #height? What #Yoga Genetics with #Yoga Ethics #Aging Reversal #Genetic Drug Therapies are open targets or good candidates for randomized clinical trials for #Higher Faster Stronger & more supple bodies performance? 

This is a very complex and multi-faceted question that touches on areas of cutting-edge research, speculative science, and philosophical concepts. I'll break down the response into the different components you've asked about, based on the most current information available from scientific and medical research.

1. Genetic Drug Therapies for Muscle Wasting Reversal

Significant progress is being made in genetic and molecular therapies to address age-related muscle wasting, known as sarcopenia. The primary goal is to restore the function of muscle stem cells and improve muscle regeneration. Some of the most promising avenues include:

  • Prostaglandin E2 (PGE2): Recent studies on mice have shown that a single dose of a stable form of this naturally occurring molecule, when combined with exercise, can rejuvenate aged muscle stem cells and lead to long-lasting improvements in muscle mass and strength. The research suggests that PGE2 works by reversing age-related epigenetic changes on the DNA of muscle stem cells. This is a very promising candidate for further research and clinical trials due to its potent and durable effects.

  • NANOG Protein: Named after the mythical land of youth, the NANOG protein has been shown to reverse aging in skeletal muscle cells. Researchers found that overexpressing NANOG in senescent muscle cells improved their ability to divide and grow. This is another area of active research, with the goal of identifying "druggable targets" that can mimic the anti-aging effects of NANOG.

  • Telomerase Reverse Transcriptase (TERT): A key hallmark of aging is the shortening of telomeres, the protective caps on our chromosomes. Research has shown that restoring youthful levels of TERT, an enzyme that maintains telomeres, can improve muscle performance and reduce inflammation in preclinical models. A small molecule compound, a "TERT activating compound" (TAC), has been identified that can epigenetically restore TERT levels and reverse hallmarks of aging.

  • Gene Therapies for Muscular Dystrophies: While not strictly "aging reversal," the development of gene therapies for genetic muscle-wasting conditions like Duchenne muscular dystrophy (DMD) is highly relevant. These therapies use adeno-associated viruses (AAVs) to deliver functional genes (e.g., a truncated or full-length dystrophin gene) to muscle cells. The technology developed here could potentially be adapted for broader age-related muscle issues.

2. Genetic Drug Therapies for Spinal Compression Reversal

Spinal compression, often associated with degenerative disc disease, is a complex issue. While there is no current "magic bullet" genetic therapy to reverse it, research is exploring several approaches:

  • Gene Therapy for Spinal Muscular Atrophy (SMA): The success of gene therapies for SMA, such as onasemnogene abeparvovec (Zolgensma), is a significant breakthrough. These therapies use AAV vectors to deliver a functional copy of the SMN1 gene to motor neurons in the spinal cord. This success demonstrates the feasibility of using gene therapy to target and treat conditions affecting the spine and nervous system. The technology and delivery methods could be adapted for other spinal conditions.

  • Neuronal Regeneration and Gene Editing: Research is ongoing to promote the regeneration of spinal neurons and reverse damage from injuries or degenerative diseases. Gene therapies and editing techniques like CRISPR-Cas9 are being investigated to activate the regenerative ability of endogenous glial cells, which can help repair neural pathways.

  • Connective Tissue and Bone Regeneration: The reversal of spinal compression would require the regeneration of intervertebral discs and possibly bone. While this is a nascent field, research into gene therapies that promote the growth of cartilage and bone is underway. For example, some studies are looking at genetic mutations associated with bone growth (e.g., in achondroplasia) and exploring how those pathways can be modulated to promote growth and regeneration.

3. The Variable of Height

The idea of genetic therapies to "reverse" a variable like height is largely in the realm of science fiction, with a few key exceptions. Height is a polygenic trait, meaning it's influenced by hundreds of genes, and is also heavily dependent on environmental factors during development.

  • Height in Genetic Disorders: The primary area where genetic therapies are currently being explored to increase height is in specific genetic disorders that cause short stature, such as achondroplasia. The drug vosoritide (Voxzogo) is an FDA-approved medication that works by targeting the underlying genetic pathway in achondroplasia to increase growth velocity in children with open growth plates. This is a targeted therapy for a specific condition, not a general "height reversal" for the average person.

  • Spinal Compression and Height: From a biomechanical perspective, reversing spinal compression could lead to a small increase in height (on the order of a few centimeters) as the spinal column is decompressed. However, this is a restoration of a natural state, not a genetic alteration to increase overall height.

4. Yoga Genetics and Aging Reversal

The concept of "Yoga Genetics" is not a formal scientific discipline, but rather a way to describe the interplay between lifestyle practices like yoga and meditation and our genetic expression. This is rooted in the field of epigenetics, which studies how environmental factors and behaviors can alter how our genes are expressed without changing the underlying DNA sequence.

  • Epigenetic Modulation: Several studies have shown that mind-body interventions like yoga and meditation can lead to beneficial epigenetic changes. For example, they have been linked to:

    • Decreased inflammation: Yoga and meditation have been shown to decrease the production of a molecule called NF-kB, which regulates gene expression and can lead to inflammation. By reducing this pro-inflammatory gene expression pattern, these practices can help reverse a key molecular marker of aging and disease.

    • Increased Telomerase Activity: Some research suggests that yoga and meditation can increase the activity of telomerase, the enzyme that protects telomeres. While not a significant effect in a single short study, it points to a potential long-term benefit for cellular aging.

    • Reduced Stress Hormones: These practices can lower levels of cortisol, a stress hormone, which is known to accelerate aging and damage at a cellular level.

5. Candidates for Randomized Clinical Trials for "Higher, Faster, Stronger, and More Supple Bodies"

Combining these ideas into a framework for clinical trials is speculative but offers a look at a potential future for human performance optimization. A conceptual trial might focus on:

  • Target Population: Healthy, middle-aged or older adults who are physically active (e.g., athletes, yoga practitioners).

  • Intervention Groups:

    1. Yoga and Ethics Group (Control): A rigorous yoga and meditation program (including specific poses for muscle and spinal health) combined with a focus on ethical principles of well-being.

    2. Genetic Drug Therapy Group: Participants receive a specific genetic drug therapy targeting a mechanism of aging (e.g., a PGE2 or TERT-activating compound).

    3. Combination Group: Participants receive both the yoga/ethics program and the genetic drug therapy.

  • Measured Outcomes:

    • Physiological: Muscle mass and strength (e.g., using DEXA scans, grip strength tests), spinal flexibility and range of motion, and biomarkers of cellular aging (telomere length, inflammatory markers).

    • Performance: Measures of speed, endurance, and suppleness (e.g., standardized athletic tests, yoga flexibility metrics).

    • Psychological/Ethical: Self-reported well-being, stress levels, and adherence to ethical principles.

The goal of such a trial would be to investigate whether a synergy exists between these two approaches, and if a combination of lifestyle interventions and targeted genetic therapies could provide a more profound and holistic reversal of aging and enhancement of physical performance. The "Yoga Ethics" component would be crucial, as it would explore the moral and philosophical implications of using such powerful technologies and ensure they are used for well-being, not just enhancement without consideration for the consequences







* * 
What are the specific genes for higher, faster, stronger (more supple too) athletics?

more supple also re "Yoga genetics"


Add to - 



What are the specific genes for higher faster stronger (more supple too) athletics ... and with application to people who might live over 122 years of age?


For higher, faster, and stronger athletic performance, the genes ACTN3 (also known as the "speed gene") and ACE are the most studied and well-documented, with ACTN3 influencing fast-twitch muscle fibers and ACE impacting endurance and cardiovascular efficiency. 
Here's a more detailed explanation:
  • ACTN3 (alpha-actinin-3):
    • This gene codes for a protein found in fast-twitch muscle fibers, which are crucial for explosive movements and power. 
    • A common polymorphism (R577X) in the ACTN3 gene has two main variants:
      • RR genotype: Individuals with this genotype tend to have more fast-twitch muscle fibers and are often associated with strength and power-based sports. 
      • XX genotype: Individuals with this genotype have a complete deficiency of the alpha-actinin-3 protein, which leads to a lower proportion of fast-twitch muscle fibers and is more common in endurance athletes. 
  • ACE (angiotensin-converting enzyme):
    • This gene regulates blood pressure and cardiovascular efficiency, playing a role in both endurance and power performance. 
    • The ACE gene has two main variants:
      • II genotype: This genotype is associated with better endurance performance and higher exercise efficiency. 
      • DD genotype: This genotype is associated with strength and power performance

--


Society, Information Technology, and the Global University (2025, forthcoming) 

- Scott GK MacLeod  
Founder, President, CEO & Professor
CC-4 licensed MIT OCW-centric, Wiki, 
World University & School (WUaS) 
- USPS US Post Office, General Delivery, Canyon, CA 94516 


1) non-profit 501(c)(3) Public Charity 
MIT OCW-centric, 
 World University and School - http://worlduniversityandschool.org  

2) for profit general stock company WUaS Corporation in CA - http://worlduniversityandschool.org/AcademicPress.html

(m) 412 478 0116 - sgkmacleod@gmail.com 


World Univ & Sch Innovation Research -  scottmacleod.com 




* * 

higher, faster, stronger all re Olympics too & more supple also re "Yoga genetics"

"A Billion Years of Evolution in a Single Afternoon — George Church"

Height

12 minute marker
Multigenic trait



The phrase "Faster, Higher, Stronger" (Latin: Citius, Altius, Fortius) is the long-standing motto of the Olympic Games, embodying the pursuit of athletic excellence. In 2021, the International Olympic Committee added "– Together" (Latin: Communis) to the motto, emphasizing unity and solidarity. 
Your question also touches on the concept of being "more supple" in relation to "Yoga genetics", suggesting a connection between athletic performance, flexibility, and genetic predispositions. 
The role of yoga in enhancing athletic performance and suppleness
Yoga, a holistic practice combining physical postures, breath control, and mental focus, offers numerous benefits that contribute to athletic performance, including improved flexibility and suppleness. 
  • Improved Flexibility: Yoga poses are designed to stretch and lengthen muscles, increasing the range of motion in joints like the hips, shoulders, and knees. Regular practice can significantly enhance flexibility, with one study showing an increase of up to 35% within 8 weeks.
  • Enhanced Strength and Balance: Many yoga poses are weight-bearing and engage core muscles, leading to improved strength and endurance. Yoga also cultivates better balance and coordination, crucial for many sports.
  • Injury Prevention and Recovery: By strengthening stabilizing muscles, improving flexibility, and promoting better posture, yoga can help reduce the risk of injuries. It can also aid in recovery by relieving muscle tension and enhancing blood circulation.
  • Mental Well-being: Beyond physical benefits, yoga helps athletes manage stress, reduce anxiety, improve concentration, and enhance mental focus, which are critical for optimal performance. 
The influence of genetics on flexibility and suppleness
While lifestyle factors such as regular yoga practice can significantly improve flexibility, genetic factors also play a role in determining an individual's natural range of motion. 
  • Genetic Contribution: Scientists estimate that around 50% of an individual's flexibility is hereditary. Specific genes, such as ACTN3, COL5A1, and ESR1, influence the structure and function of muscles, tendons, and ligaments, impacting flexibility.
  • Connective Tissue Disorders: Certain genetic conditions, like Ehlers-Danlos Syndrome, cause hypermobility, resulting in excessively flexible joints.
  • Age and Sex: Flexibility naturally declines with age, and females tend to be more flexible than males due to differences in hormones and bone structure. 
Conclusion
Both genetic predispositions and lifestyle choices, such as incorporating yoga into one's routine, contribute to an individual's flexibility and overall physical performance. While genetics may set a baseline, consistent practice and dedicated training can significantly enhance an athlete's potential to be "faster, higher, stronger – together," and more supple. 




*


Hi Pin, Ed, Ma, how are you today this Wednesday? I just shared this with my mother ... Thoughts, and regarding KP and genetics Ed, and HHS and genetics too Pin?  - "Trimming the front hedge wiped me out, Ma ... Hmm ... seeking some aging reversal genetic drug therapies  for energy in the future ... and will  aging reversal genetic drug therapies for height also be extensible to higher, faster, stronger all re Olympics too & more supple also re "Yoga genetics" esp and newly 

"For #Olympics? #YogaGenetics? For performance - higher faster stronger athletics - & #ETHICS? What? How? If & when #vaccines for #YogaAthletes w #WUaSLongevity & #WUaSAgingReversal genetic drugs develop & give us younger -at age 150 years' old?, -more supple bodies, how #YogaEthics work?"

Hippy-anjali Yoga Notations

Hippy-anjali Yoga Notations 

...  and for muscle wasting reversal ... and so energy especially? 10,000 genes are what inform height George Church suggests here - "A Billion Years of Evolution in a Single Afternoon — George Church"

Height

12 minute marker
Multigenic trait
... and with no side effects ... & This may all happen incrementally between now and 2060 when you'd be 125 years old ðŸ™‚, Love, Scott (http://scott-macleod.blogspot.com/search/label/Cuttyhunk








* * * 

Caenorhabditis elegans 
100x lifespan by adding copies of genes back into this organism per George Church's 
How soon could humans reverse the aging process with genetic engineering?
How ?




What genes to add to #CElegans (nematode worm w 302 backbone neurons) to 100x lifespan, from 3 weeks to 300 weeks re #ExtremeLongevity #AgingReversal & per @geochurch https://youtu.be/bnCEIPQFNnk ? #AddGeneCopies with food somehow? How w #PhysicalDigitalSim in #RealisticVirtualEarth?

https://x.com/WorldUnivAndSch/status/1968719765762896099

https://x.com/sgkmacleod/status/1968720126783418511

https://x.com/WUaSPress/status/1968720423169790433

https://x.com/Q_YogaMacFlower/status/1968719916485210536

https://x.com/HarbinBook/status/1968720994362618140

https://x.com/scottmacleod/status/1968721284579094619

https://x.com/TheOpenBand/status/1968721350668742686



Caenorhabditis elegans


The organism with 302 neurons serving as its backbone is the nematode worm

3 weeks lifespan





*

What genes to add to #CElegans (nematode worm w 302 backbone neurons) to 100x lifespan, from 3 weeks to 300 weeks re #ExtremeLongevity #AgingReversal & per @geochurch https://youtu.be/bnCEIPQFNnk ? #AddGeneCopies with food somehow? How w #PhysicalDigitalSim in #RealisticVirtualEarth?



Gemini AI excerpt :
​The concept of extending lifespan in C. elegans has been explored extensively in genetic research. Some genes and pathways identified as influencing longevity in these worms include:
​Insulin/IGF-1 signaling pathway: Mutations in genes like daf-2 can double the lifespan of the worm, from a typical 2-3 weeks to around 6 weeks. When combined with other mutations like clk-1, this effect can be even greater, though not a 100-fold increase.
​Mitochondrial respiration pathways: Mutations in genes such as clk-1 and isp-1 have been shown to extend lifespan.
​Genes involved in mRNA translation and stress resistance.




*
From 
Based on the information available, there is no mention in the provided YouTube video of specific genes to add to C. elegans to increase its lifespan by 100x. The video focuses on gene therapy in mice to reverse aging and improve organ function, with plans to move to other animals like spaniels. The speaker, George Church, clarifies that this is about adding new copies of genes to boost their function, not editing them.


​The concept of extending lifespan in C. elegans has been explored extensively in genetic research. Some genes and pathways identified as influencing longevity in these worms include:
​Insulin/IGF-1 signaling pathway: Mutations in genes like daf-2 can double the lifespan of the worm, from a typical 2-3 weeks to around 6 weeks. When combined with other mutations like clk-1, this effect can be even greater, though not a 100-fold increase.
​Mitochondrial respiration pathways: Mutations in genes such as clk-1 and isp-1 have been shown to extend lifespan.
​Genes involved in mRNA translation and stress resistance.
​The hashtags you included in your query reference "Physical Digital Sim" and "Realistic Virtual Earth." These terms appear to be related to the concept of digital twins, where a virtual model of a physical object or system is created and continuously updated with real-time data from the physical counterpart. This allows for testing and analysis in a virtual environment. In the context of longevity research, this could hypothetically be used to model and simulate the effects of genetic changes in a virtual organism, before applying them in the real world.
​For more on the work of George Church, you can watch this video on his ideas about rewriting genomes to eradicate disease and aging.






* 



Caenorhabditis elegans The organism with 302 neurons serving as its backbone is the nematode worm lifespan


The roundworm Caenorhabditis elegans (C. elegans) is the nematode with exactly 302 neurons in the adult hermaphrodite. This nervous system is considered the "backbone" of its biology and has been completely mapped. The typical lifespan for C. elegans is about two to three weeks. 
Caenorhabditis elegans
  • A simple but powerful model: Measuring about 1 millimeter long and being transparent, C. elegans is an ideal organism for studying nervous system development.
  • Fixed cell count: The adult hermaphrodite has an invariant number of 959 somatic cells, of which 302 are neurons.
  • The connectome: The complete neuronal "wiring diagram," or connectome, of C. elegans was fully mapped in 2019, making it the only organism to have such a comprehensive neural map.
  • Neurobiology research: The simple and well-defined nervous system of C. elegans allows scientists to study how neurons work together to generate behavior, including complex decision-making, despite its low neuron count compared to the human brain's 100 billion neurons. 
Lifespan
  • Typical duration: Under laboratory conditions, the average lifespan of a C. elegans is approximately 2 to 3 weeks, though this can vary slightly depending on the exact strain and temperature.
  • Aging research: Because of its short lifespan and transparent body, C. elegans is a valuable model for studying the biology of aging and various human disorders.
  • Longevity influenced by environment: Environmental factors can affect the worm's longevity. For example, caloric restriction can extend its lifespan, while higher temperatures can shorten it.
  • Survival mode: Under harsh conditions like overcrowding or food scarcity, the worm can enter a dormant "dauer" larval stage, halting aging for months


* 

What does Caenorhabditis elegans eat?


Caenorhabditis elegans (C. elegans) is a nematode worm that feeds primarily on bacteria. In their natural environment, they consume soil bacteria, such as Pseudomonas, Bacillus, and Enterobacter. 
In laboratory settings, C. elegans are typically fed a diet of Escherichia coli (E. coli) bacteria, which are easy to grow and maintain in culture. Other bacterial species that can be used as food for C. elegans include: 
Enterococcus faecalis, Staphylococcus aureus, Serratia marcescens, and Klebsiella pneumoniae. 
It's important to note that C. elegans can also consume other microorganisms, such as yeast and protozoa, but these are not their primary food source. Their diet can influence their growth, development, and lifespan





* * 


Genes, Neurons, and Their Relationship


Created with 2.5 Flash September 18, 2025 at 03:20 PM
Published September 18, 2025 at 03:20 PM

How do genes relate to neurons and are genes smaller than neurons and do they make up neurons?




Google Search
Genes do not "make up" neurons in the sense that they are a structural component. Instead, genes contain the instructions for building and operating neurons. Genes are much smaller than neurons and direct the development, function, and connections of neurons by controlling which proteins are produced





--

--

Society, Information Technology, and the Global University (2025, forthcoming) 

- Scott GK MacLeod  
Founder, President, CEO & Professor
CC-4 licensed MIT OCW-centric, Wiki, 
World University & School (WUaS) 
- USPS US Post Office, General Delivery, Canyon, CA 94516 


1) non-profit 501(c)(3) Public Charity 
MIT OCW-centric, 

2) for profit general stock company WUaS Corporation in CA - http://worlduniversityandschool.org/AcademicPress.html

(m) 412 478 0116 - sgkmacleod@gmail.com 


World Univ & Sch Innovation Research - 






*


 



























https://en.wikipedia.org/wiki/Sesbania_punicea

https://commons.wikimedia.org/wiki/Category:Sesbania_punicea


and / or 

https://war.wikipedia.org/wiki/Alamania_punicea 

https://commons.wikimedia.org/wiki/Alamania_punicea 

https://commons.wikimedia.org/wiki/Category:Alamania_punicea?uselang=war 

https://commons.wikimedia.org/wiki/Category:Alamania_punicea

https://species.wikimedia.org/wiki/Alamania_punicea



https://en.wikipedia.org/wiki/Alamania

...


Posted by at
Labels: , , , , , , , , , , , , , , , ,

No comments:

Post a Comment

Subscribe to: Post Comments (Atom)