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Compromising improves forecasting.

ABSTRACT: Predicting the future can bring enormous advantages. Across the ages, reliance on supernatural foreseeing was substituted by the opinion of expert forecasters, and now by collective intelligence approaches which draw on many non-expert forecasters. Yet all of these approaches continue to see individual forecasts as the key unit on which accuracy is determined. Here, we hypothesize that compromise forecasts, defined as the average prediction in a group, represent a better way to harness collective predictive intelligence. We test this by analysing 5 years of data from the Good Judgement Project and comparing the accuracy of individual versus compromise forecasts. Furthermore, given that an accurate forecast is only useful if timely, we analyze how the accuracy changes through time as the events approach. We found that compromise forecasts are more accurate, and that this advantage persists through time, though accuracy varies. Contrary to what was expected (i.e. a monotonous increase in forecasting accuracy as time passes), forecasting error for individuals and for team compromise starts its decline around two months prior to the event. Overall, we offer a method of aggregating forecasts to improve accuracy, which can be straightforwardly applied in noisy real-world settings.

SUBMITTER: Ferreiro DN

PROVIDER: S-EPMC10189590 | biostudies-literature | 2023 May

REPOSITORIES: biostudies-literature

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Compromising improves forecasting.

Ferreiro Dardo N DN Deroy Ophelia O Bahrami Bahador B

Royal Society open science 20230517 5

Predicting the future can bring enormous advantages. Across the ages, reliance on supernatural foreseeing was substituted by the opinion of expert forecasters, and now by collective intelligence approaches which draw on many non-expert forecasters. Yet all of these approaches continue to see individual forecasts as the key unit on which accuracy is determined. Here, we hypothesize that compromise forecasts, defined as the average prediction in a group, represent a better way to harness collectiv ...[more]

PMID: 37206966

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Project description:BackgroundLysinuric protein intolerance is a rare autosomal disorder caused by mutations in the Slc7a7 gene that lead to impaired transport of neutral and basic amino acids. The gold standard treatment for lysinuric protein intolerance involves a low-protein diet and citrulline supplementation. While this approach partially improves cationic amino acid plasma levels and alleviates some symptoms, long-term treatment is suggested to be detrimental and may lead to life-threatening complications characterized by a wide range of hematological and immunological abnormalities. The specific cause of these hematopoietic defects-whether intrinsic to hematopoietic cells or driven by external factors-remains unclear. Given the limitations of current citrulline-based treatments and the unknown role of SLC7A7 in red blood cell production, there is an urgent need to investigate the pathways affected by SLC7A7 deficiency.MethodsWe employed total inducible and cell type-specific Slc7a7 knockout mouse models to determine whether the hematological abnormalities observed in LPI are due to the loss of Slc7a7 function in hematopoietic cells. We analyzed erythropoiesis in these mice and performed bone marrow transplantation experiments to assess the role of Slc7a7 in erythroblasts and myeloid cells. The statistical significance of differences between groups was evaluated via standard statistical tests, including Student's t test and ANOVA.ResultsWhole-body Slc7a7 knockout mice presented impaired erythropoiesis. However, this defect was not replicated in mice with Slc7a7 deficiency restricted to erythroblasts or myeloid cells, suggesting that the observed hematopoietic abnormalities are not due to intrinsic Slc7a7 loss in these cell types. Additionally, bone marrow transplants from control mice did not rescue the hematopoietic defects in Slc7a7-deficient mice, nor did the transplantation of Slc7a7-deficient cells induce defects in control recipients. Further investigation indicated that defective erythropoiesis is linked to impaired erythropoietin production in the kidney and subsequent iron overload.ConclusionsThe hematopoietic defects in the Lysinuric protein intolerance mouse model are not caused by intrinsic Slc7a7 loss in hematopoietic cells but rather by impaired erythropoietin production in the kidney. This finding opens potential avenues for therapeutic strategies targeting erythropoietin production to address hematological abnormalities in humans with lysinuric protein intolerance.

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Compromising improves forecasting.

Publications

Compromising improves forecasting.

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