Growing Brainless Human Bodies

The Three-Step Recipe

Step 1: Create a patient-matched embryo. Either via somatic cell nuclear transfer (SCNT — the Dolly-the-sheep technique, demonstrated in sheep, cattle, pigs, dogs, cats, horses, and monkeys but never in humans) or iPSC reprogramming (Yamanaka's 2006 Nobel Prize discovery). R3 Bio uses a histone demethylase (KDM5B) to boost cloning efficiency — the same protein used in the first monkey clone (2018).

Step 2: Edit out brain development. CRISPR-Cas9 to knock out genes required for brain formation. The goal: a body that develops functional organs but lacks consciousness-generating neural structures. Requires multiplex editing of 2–4 genes simultaneously. A January 2026 genome-wide CRISPR screen (Shifman/Yalcin, Nature Neuroscience) identified 331 genes essential for neuronal differentiation, providing a comprehensive map.

Step 3: Gestate. The edited embryo grows in either a surrogate pregnancy (ethically fraught), an animal surrogate (biologically difficult), or an artificial womb (doesn't exist for humans). Organs need to reach transplant-ready size — for kidneys, that means growing to roughly adult size, which takes 12–15 years.

Target Genes

Brain development is orchestrated by cascading transcription factors. The key targets:

• FOXG1 (Forkhead Box G1) — Telencephalon (cerebral hemisphere) development. Knockout mice have severely reduced cerebral hemispheres but intact brainstem and body. Most promising target for selectively eliminating higher brain regions.
• LHX2 (LIM Homeobox 2) — Cerebral cortex formation. Knockout mice lack cortex but develop other structures relatively normally.
• EMX2 (Empty Spiracles Homeobox 2) — Forebrain patterning. But also needed for urogenital development — knockout mice die at birth from kidney failure. New research shows EMX2's kidney defects may be pharmacologically rescuable via prostaglandin E2 supplementation.
• PAX6 (Paired Box 6) — "Master control gene" for eyes, also key for forebrain. Mutations cause aniridia and brain structural abnormalities.
• OTX2 — Entire future forebrain and midbrain. Homozygous deletion produces "headless phenotype." Knockout lethal at gastrulation — poor standalone target.
• FGF8 (Fibroblast Growth Factor 8) — Forebrain patterning. Null mutation lethal at day 8.5 — too early for any organs.

The core problem: Many of these genes have roles outside the brain (pleiotropic effects). Neural crest cells form parts of the heart, face, gut, and peripheral nervous system. A combinatorial, possibly conditional, editing strategy will likely be needed — turning off genes only in the brain at specific times using brain-specific promoters like the Emx1-Cre system.

The Brainstem Dilemma

This may be the single most challenging biological obstacle.

• If you remove the brainstem: the organism can't regulate heartbeat, breathing, blood pressure, or hormones. Even in utero, the fetus's brainstem manages practice breathing (critical for lung development) and amniotic fluid swallowing (critical for gut development).
• If you keep the brainstem: you preserve autonomic functions, but the organism may have reflexive behaviors, basic sensory processing, and arousal states. Research on hydranencephalic children (no cortex, brainstem intact) shows discriminative awareness, emotional responses, and associative learning. A 2025 review concluded subcortical structures alone may be compatible with basic experience.

The hypothalamus-pituitary problem: These structures at the brain's base control growth hormone, thyroid hormone, cortisol, and sex hormones. Without them, you need exogenous replacement of multiple hormones throughout years of development. Preserving them raises consciousness concerns since the hypothalamus mediates emotional states, hunger, and thirst.

The innervation problem: Organs developing without any neural input may not develop normally. Denervated hearts show reduced exercise capacity; severing the vagus nerve disrupts gastric function; the enteric nervous system (100-600 million neurons) is required for coordinated gut peristalsis. This is an open question with limited data.

What Has Actually Been Demonstrated

Demonstrated

• Headless frog embryos (Slack, 1997) High
• Gene knockout mice without complete brains/faces/limbs (Kind Bio patents) Medium
• Synthetic mouse embryos with beating hearts, blood flow, cranial folds (Hanna/Renewal Bio) High
• Human embryo models to 14-day equivalent (Hanna, 2024-2025) High
• Anencephalic pregnancies: organs develop without a cortex; longest survival 28 months High
• Pig-to-human kidney transplant surviving 271 days (eGenesis) High
• First pig-to-human liver in living patient (171 days, China) High
• First pig-to-human lung xenotransplant (216 hours, China) High
• Artificial womb (BioBag) supporting premature lambs for weeks High
• Human uterus kept alive outside body for 1 day (PUPER device, March 2026) High
• Blastocyst complementation: growing organs of one species inside another in rodent models High
• 331 genes essential for neuronal differentiation identified via genome-wide CRISPR screen (Jan 2026) High

Not Demonstrated

• A complete organ sac in any species Not done
• Maintaining a brainless mammal alive for weeks/months Not done
• Growing a brainless organism to adult size Not done
• Harvesting functional organs from a bodyoid Not done
• Full ectogenesis (artificial womb, embryo to term) in any mammal Not done
• Human SCNT for reproductive purposes Not done
• Brain transplant surgery Not done

What Anencephaly Teaches Us

Anencephaly — naturally occurring absence of most of the brain — is the closest real-world analog to a bodyoid:

• Occurs in ~1 in 1,000 pregnancies naturally
• Organs develop and function normally (hearts beat, kidneys produce urine, livers metabolize)
• Average survival after birth: 51 minutes. But 40%+ survive past 24 hours, 5% past one week
• Longest documented survival: 28 months without life-sustaining interventions
• Infants retain brainstem reflexes: sucking, breathing (often irregular), startle responses

Encouraging (organs work without a cortex) but also shows that even without higher brain function, these bodies exhibit significant brainstem activity. The bodyoid concept requires eliminating more than anencephaly does.

The Artificial Womb Bottleneck

Without an artificial womb, every human bodyoid requires a surrogate pregnancy. This is the most underappreciated constraint.

• CHOP BioBag (2017): Supported premature lambs for weeks — but only late-term fetuses (23-24 weeks equivalent), not from conception.
• FDA Breakthrough Device Designation: Artificial womb technology has received breakthrough designation. First-in-human clinical trials projected 2026-2028 — highly selective feasibility trials at the very limit of viability (22-24 weeks).
• PUPER device (March 2026): Kept a human uterus alive outside the body for one day — a record, but far from supporting pregnancy.
• Key distinction: Partial ectogenesis (supporting premature infants from ~23 weeks) is approaching clinical reality. Full ectogenesis (growing from embryo to term) is fundamentally different and requires breakthroughs in placental bioengineering, infection control, and initiating embryo growth outside the uterus.

Full ectogenesis for humans: 20–30+ years away. This is a binding constraint on bodyoid technology. The two-bottleneck problem: bodyoids need both reliable brain deletion AND artificial wombs. Neither is close to solved.