Abstract
Hemoglobin levels are believed to be regulated as per a set point model of regulation. This model of regulation, by which specific levels of a parameter are targeted and defended by physiological systems, implies a particular population correlation between the parameter and its controlling hormone. Empirical population correlations of other parameters and their controlling hormones, have denied the presence of such set point‐based regulation. To assess if hemoglobin is regulated according to a set point model we performed a systematic search of PubMed/MEDLINE and Web of Science identifying relevant reports published up to November 2018. Population hemoglobin/erythropoietin level correlations were retrieved, and these empirically derived correlations were compared with the positive correlation implied by a set point model of regulation. Authors of papers containing potentially suitable data were contacted with requests for further analyses, and a meta‐analysis was performed. Twelve correlations between hemoglobin and erythropoietin levels from eleven papers were analyzed. None of these correlations were significantly positive, three, restricted to the normal range of hemoglobin, were significantly negative. All but one of the other correlations showed a negative trend. New analyses of previously published data sets resulted in similar findings. In particular a new analysis of large data sets of males (n = 2417) and females (n = 2592) with normal range hemoglobin levels, revealed significantly negative correlations. A meta‐analysis of our results indicated that the data overall are not consistent with a positive relationship between hemoglobin and erythropoietin (P < 0.0001). Population data indicate that individuals do not have set point levels of hemoglobin.
Highlights
“Set points” are a fundamental part of models of homeostasis (Modell et al 2015; Goldstein 2017)
We have previously shown that a set point model of regulation implies a particular population correlation between a parameter and its regulating hormone, that is, the population correlation should be in the direction of the effect of the controlling hormone on the parameter (Fitzgerald et al 2017; Fitzgerald and Bean 2018a). (The concept of an adjustable set point (Cabanac 2006) does not affect this property of a set point model.) For example, if regulation were according to a set point model, for glucose the population correlation should be negative, and for calcium it should be positive (Fitzgerald and Bean 2018a)
We found six studies that included a correlation for hemoglobin and erythropoietin through the anemic and normal ranges (Beguin et al 1993; Schrieber et al 1996; Roque et al 2001; Fehr et al 2004; Artunc and Risler 2007; Grote Beverborg et al 2015).We did not include two further studies (Malagarnera et al 1996; Panjeta et al 2017) reporting correlations between renal function and erythropoietin, and renal function and hemoglobin but not directly between hemoglobin and erythropoietin
Summary
“Set points” are a fundamental part of models of homeostasis (Modell et al 2015; Goldstein 2017). A “set point” is a target or ideal level of a parameter which the body defends by physiological processes, including negative feedback loops (Romanovsky 2004; Modell et al 2015). Set points have been likened to thermostat or cruise control settings (Modell et al 2015). A variety of parameters, including body temperature, blood levels of sodium
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