People with rare mutations in the myostatin gene have 5–8% more total skeletal muscle mass and at least 10% more muscle in areas like the glutes, along with less body fat, as measured by whole-body MRI.
See the scientific wording
Humans carrying rare, function-disrupting variants in the myostatin gene (MSTN) exhibit, on average, a 5–8% increase in total skeletal muscle mass and a 10% or greater increase in specific muscle groups such as the gluteus muscles, alongside a measurable reduction in body adiposity, as confirmed by whole-body MRI in over 77,000 individuals.
Correlational — new studies may shift this
ObservationalOne moderate-quality study links this claim to the outcome, but causation is not established.
What the research says
1 study reviewedSupporting (1)
Cohort StudyHuman2026
People born with a rare genetic change that turns down myostatin naturally have more muscle—up to 10% more in some areas like the buttocks—and less body fat, which scientists confirmed using detailed body scans in over 77,000 people.
Contradicting (0)
No contradicting studies found yet
That doesn't mean it's settled — it just means no study has tested the opposite.
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Scores reflect study quality, not just count.
When the myostatin protein is disrupted, it can no longer turn off muscle growth signals. This allows muscle cells to grow larger and multiply more, increasing total muscle mass. The extra muscle tissue burns more energy, which causes the body to store less fat.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting study
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People with rare mutations in the myostatin gene have 5–8% more total skeletal muscle mass and at least 10% more muscle in areas like the glutes, along with less body fat, as measured by whole-body MRI.
Mechanism
1 studyWhen myostatin doesn't work, muscles grow bigger because their growth signals are no longer turned off. Bigger muscles use more energy, so the body stores less fat.
When the myostatin protein is disrupted, it can no longer turn off muscle growth signals. This allows muscle cells to grow larger and multiply more, increasing total muscle mass. The extra muscle tissue burns more energy, which causes the body to store less fat.
Function-disrupting variants in the myostatin gene alter the structure of the myostatin precursor protein, leading to impaired processing or stability of the mature ligand
Reduced levels of bioactive myostatin ligand decrease binding to ActRIIA/B and ALK4/5 receptors on skeletal muscle cells
Diminished receptor activation suppresses phosphorylation and nuclear translocation of SMAD2/3 transcription factors
De-repression of SMAD2/3 signaling increases satellite cell activation, myoblast proliferation, and myofiber protein synthesis
Increased skeletal muscle mass elevates basal metabolic rate and shifts systemic energy partitioning toward lean tissue retention and away from adipose storage
Evidence from Studies
Supporting (1)
Community contributions welcome
People born with a rare genetic change that turns down myostatin naturally have more muscle—up to 10% more in some areas like the buttocks—and less body fat, which scientists confirmed using detailed body scans in over 77,000 people.
Contradicting (0)
Community contributions welcome
Score Breakdown
No multi-axis breakdown available yet. The overall Pro / Against score above is the best signal.
- No clinical evidence is available; the score reflects mechanistic plausibility only.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Systematic Review of MSTN Loss-of-Function Variants and Muscle Mass/Adiposity Outcomes in Human Populations
Population: Humans with confirmed rare MSTN loss-of-function variants; Intervention: None (natural genetic variant); Comparator: Individuals without MSTN variants; Outcome: Total skeletal muscle mass, specific muscle group hypertrophy, body adiposity measured by MRI; Duration: Cross-sectional assessment
Longitudinal Cohort Study of MSTN Variant Carriers vs Non-Carriers for Muscle Mass and Adiposity Trajectories
Population: Adults with and without rare MSTN variants identified by genetic screening; Intervention: None; Comparator: Non-carriers matched for age, sex, and activity level; Outcome: Serial measurements of skeletal muscle mass and body adiposity via MRI over 5–10 years; Duration: 5–10 years
Cross-Sectional Analysis of MSTN Variant Carriers and Non-Carriers for Muscle Mass and Adiposity Using Whole-Body MRI
Population: Over 77,000 individuals with genetic data and whole-body MRI scans; Intervention: None; Comparator: Non-carriers of rare MSTN variants; Outcome: Total skeletal muscle mass, gluteal muscle volume, body fat percentage; Duration: Single time point
Detailed Phenotypic Characterization of Individuals with Rare MSTN Loss-of-Function Variants and Extreme Muscle Hypertrophy
Population: Individuals with genetically confirmed rare MSTN variants; Intervention: None; Comparator: None; Outcome: Quantitative muscle and adipose tissue measurements via MRI, clinical history; Duration: Single assessment
In Vitro Analysis of Myostatin Loss-of-Function Mutations on Human Myoblast Proliferation and Differentiation
Population: Human myoblasts and adipocytes derived from individuals with and without MSTN variants; Intervention: Genetic knockout or silencing of MSTN; Comparator: Wild-type cells; Outcome: Myotube formation, myofiber size, lipid accumulation; Duration: 7–21 days