Tony Huge

Gene Editing and the Future of Human Performance: What CRISPR Means for Enhancement

Table of Contents

The Technology That Will Change Everything

CRISPR-Cas9 gene editing — the technology that allows precise modification of DNA sequences — has moved from theoretical possibility to practical reality in less than a decade. While its current applications are focused on genetic diseases (sickle cell disease became the first CRISPR-treated condition to receive FDA approval in 2023), the implications for human performance enhancement are profound and closer than most people realize.

As someone who’s spent a decade on the cutting edge of legal performance optimization, I watch genetic technology developments closely. CRISPR won’t replace the Natty Plus Protocol any time soon, but it will eventually transform what’s possible — and understanding the trajectory helps frame the current optimization landscape in proper context.

Myostatin: The First Target

Myostatin is a protein that limits muscle growth — it acts as a natural brake on how large muscles can become. Naturally occurring myostatin mutations in animals (like the Belgian Blue cattle breed, which is massively over-muscled) demonstrate what happens when this brake is removed. Myostatin knockout mice show 200-300% increases in muscle mass. A human boy with a natural myostatin mutation was documented with extraordinary muscle development from birth.

CRISPR-mediated myostatin inhibition is one of the most studied gene editing applications in animal models. Chinese researchers have successfully created myostatin-knockout dogs, goats, and pigs with dramatically increased musculature. The technology to do this in humans exists — the ethical and regulatory barriers are what prevent it, not technical limitations.

Current pharmaceutical approaches to myostatin inhibition (anti-myostatin antibodies like domagrozumab) have shown modest results in clinical trials for muscle-wasting conditions. Gene editing would provide a more permanent, potent solution — but one that raises fundamental questions about what constitutes acceptable human modification.

Other Enhancement Targets

Beyond myostatin, several genetic targets are relevant to performance enhancement. The ACTN3 gene (the “speed gene”) encodes a protein found exclusively in fast-twitch muscle fibers. The RR variant is associated with sprint/power performance and is found in virtually all elite sprinters. Gene editing could theoretically shift an individual’s ACTN3 status. The EPO receptor gene influences red blood cell production — the same pathway targeted by blood doping and EPO injections. Genetic modification of EPO signaling could create permanent endurance enhancement. PPARGC1A (PGC-1alpha) regulates mitochondrial biogenesis. Enhanced expression could create a permanent increase in mitochondrial density, improving endurance and metabolic health. Follistatin overexpression (follistatin is a myostatin antagonist) has been demonstrated in gene therapy models to increase muscle mass. A company called BioViva claimed to have performed this modification on its CEO in 2015, though the claims remain controversial and unverified.

The Timeline and Ethics

Genetic performance enhancement in humans is likely 10-20 years from becoming practically available (underground or medical tourism contexts may be sooner). The technical barriers are being resolved rapidly — delivery methods are improving, off-target effects are being minimized, and tissue-specific expression is becoming more precise.

The ethical questions are enormous and unresolved. Should genetic performance enhancement be legal? If so, should it be regulated? Would it create permanent genetic inequality between those who can afford it and those who can’t? Would it constitute “cheating” in athletic competition? Would modifications be heritable — passed to children who didn’t consent?

These questions will define the next era of performance enhancement debate, making the current “natural vs. steroids” discussion seem quaint by comparison.

What This Means for the Natty Plus Framework

The coming age of genetic enhancement reinforces the core Natty Plus principle: use the minimum effective intervention that preserves optionality. Genetic modifications are (currently) irreversible. Steroid cycles are partially reversible. Natty Plus interventions are fully reversible. As more powerful tools become available, the wisdom of starting with the gentlest effective intervention only grows.

For now, the Natty Plus Protocol represents the state of the art in legal, health-preserving performance optimization. It will continue to evolve as new compounds, peptides, and eventually genetic tools become available. But the philosophy — informed optimization, transparent risk assessment, and prioritizing long-term health — will remain relevant regardless of the specific tools available. The principles transcend any particular era of technology.

Interesting Perspectives

While mainstream discussion focuses on disease treatment, the biohacking and performance communities are already exploring the conceptual edges of gene editing. Some futurists and transhumanists view CRISPR not just as a medical tool, but as the first step toward deliberate human evolution, allowing us to engineer traits like enhanced cognition, extended lifespan, and superior physical resilience beyond natural human limits. This aligns with the core biohacking ethos of self-directed human optimization, but at a foundational genetic level. The conversation often centers on “gene doping” for athletics, but the more profound application may be in creating a new baseline of human health and capability, effectively rewriting the genetic code that currently limits peak performance. This is a direct application of the Tony Huge Laws of Biochemistry Physics—by permanently altering the source code of our biochemistry, we can change the physical limits of the system itself. The irreversible nature of these edits creates a stark contrast with the reversible, dose-dependent interventions like peptides and SARMs that form the current Natty Plus framework.

Citations & References

  1. FDA Approval of First CRISPR-Based Therapy for Sickle Cell Disease. U.S. Food and Drug Administration. 2023.
  2. Mosher, D.S., et al. A mutation in the myostatin gene increases muscle mass and enhances racing performance in heterozygote dogs. PLoS Genetics. 2007.
  3. Yang, J., et al. Generation of myostatin-knockout goats mediated by CRISPR/Cas9. Scientific Reports. 2016.
  4. McPherron, A.C., et al. Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature. 1997.
  5. Schuelke, M., et al. Myostatin mutation associated with gross muscle hypertrophy in a child. New England Journal of Medicine. 2004.
  6. Yang, N., et al. ACTN3 genotype is associated with human elite athletic performance. American Journal of Human Genetics. 2003.
  7. BioViva CEO Liz Parrish’s gene therapy claims. Various media reports. 2015-2016.