I wonder if the disease I invented is realistic or a total fiction.

In my story The Transcendence of Adolescence, there is a 17 years old homosexual (or lesbian if you want) transgender woman named Wilhelmina Karen Molina. She has a strange genetic trait: she produces much more brown fat than the average non-infant human being. That syndrome is named "brown fat-related hypertrophy".

In my story, brown fat-related hypertrophy is inherited by the incomplete dominance mode: when heterozygous to the mutated allele, people have slightly more brown fat than white fat, when homozygous, people have almost no white fat. Molina has inherited the mutant allele from both her parents.

If this genetic disease is real (assuming it is autosomal), what chromosome is linked? Chromosome 1 (like Hutchinson-Guilford progeria), chromosome 2 (like Ehlers-Danlos syndrome), chromosome 3 (like retinitis pigmentosa), chromosome 4 (like achondroplasia), chromosome 5 (like Sotos syndrome), chromosome 6 (like hemochromatosis), chromosome 7 (like tritanopia), chromosome 8 (like Werner syndrome), chromosome 9 (like cartilage-hair hypoplasia), chromosome 10 (like type 2 multiple endocrine hyperplasia), chromosome 11 (like sickle-cell anaemia), chromosome 12 (like phenylketonuria), chromosome 13 (like Wilson disease), chromosome 14 (like Krabbe disease), chromosome 15 (like Marfan syndrome), chromosome 16 (like Morquio syndrome), chromosome 17 (like type 1 neurofibromatosis), chromosome 18 (like type-C Niemann-Pick disease), chromosome 19 (like Donohue syndrome), chromosome 20 (like adenosine deaminase deficiency), chromosome 21 (like autoimmune polyendrocrinopathy-candidiasis-ectodermal-dystrophy), or chromosome 22 (like type 2 neurofibromatosis)?

I know I made an extremely long enumeration because the vast majority of the human genome is nuclear and autosomal, sorry.

Also, what would be the implications of having much more brown fat than white fat? Would these humans be able to swim in cold waters for an extremely long time? Would they be much less likely to get type 2 diabetes?

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    $\begingroup$ This is far from a proper answer but Wim Hof, a Dutch motivational speaker, is famous for enduring extremely cold temperatures. He credits practice but his identical twin brother has performed the cold resistance without training. Anyhow, both were noted as having higher amounts of brown-fat than average. The article also said that this alone didn't account for their resistance. ncbi.nlm.nih.gov/pmc/articles/PMC5605164 $\endgroup$ Commented Mar 20, 2022 at 2:45
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    $\begingroup$ Brown fat and white fat are misleading. They aren’t even derived from the same tissues and are not related to each other. If white fat disappears, it’s because the brown fat is metabolizing all the calories to make heat. $\endgroup$
    – DWKraus
    Commented Mar 21, 2022 at 19:41
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    $\begingroup$ You could have a brown fat benign tumor. I’m not aware of any such, but it would make more sense to me. $\endgroup$
    – DWKraus
    Commented Mar 21, 2022 at 19:43

1 Answer 1


Deletion of the MSTN gene results in an increase in conversion of white adipose tissue to brown adipose tissue. Presumably, someone born with this mutation would develop a higher ratio of BAT to WAT. This gene is on the tail end of Chromosome 2 in humans. Additional effects of this mutation are increased muscle mass, delayed wound healing, increase obesity resistance, and increased insulin sensitivity, among other conditions.

Information from "Myostatin knockout drives browning of white adipose tissue through activating the AMPK-PGC1α-Fndc5 pathway in muscle" and "Myostatin-null mice exhibit delayed skin wound healing through the blockade of transforming growth factor-β signaling by decorin"


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