Friedman’s articulation of the lipostat model — one account of fat-mass regulation, and a contested one.
What the evidence says
- On the lipostat model the body defends a “set point” for fat mass — *`cls04` is Friedman’s perspective piece, and Friedman discovered leptin; this is the model’s clearest articulation by its own champion, not an independent test*[1]
- Leptin signals current fat stores to brain[1]
- Hypothalamus compares current to set point[1]
- Deviations trigger corrective responses[2],[1]
- On that account the system evolved to prevent starvation[1]
- Obesity heritability is 0.7–0.8, equivalent to height and greater than schizophrenia, breast cancer or heart disease. Read it beside `kls04`’s companion figure: a GWAS of 123,865 people found 32 genome-wide-significant variants explaining 1.5% of BMI variance. Both are real; a page carrying one without the other misleads in whichever direction it picked And the two files give DIFFERENT heritability ranges, which this cross-reference did not say (added 2026-09-05, card MERNGY): `kls04` carries 50–70% from `cls01` (Speakman 2011), against the 0.7–0.8 here from `cls04` (Friedman 2004). The ranges barely overlap, and the difference is not noise — Speakman qualifies his own figure in the sentence after stating it, noting that estimates ”vary according the study design”, run ”higher when derived from twin studies”, and that classic twin studies ”will overestimate h2″. So do not present 0.7–0.8 as the corpus’s heritability figure. Give a range and say the estimate depends on study design, or attribute each figure to its source. Friedman’s is the higher end of a contested quantity, stated in a perspective piece this library holds abstract-only[1]