Hello all,
I'm running a difference GMM model for the first time to address a potential reverse causality issue. I have panel data covering every other year from 2009-2019 (six waves), and I have about 10,000 panelists (unbalanced panel).
I have four questions:
(1) I have read Leszczenky and Wolbring (2019). They compare difference GMM with (1) contemporaneous Xs, (2) lagged Xs, and (3) both contemporaneous and lagged Xs. Can anyone explain to me the appropriateness of each with respect to the reverse causality issue. If my IV theoretically would influence my DV at time t, can I use contemporaneous and sleep well about reverse causality? If my IV theoretically could influence my DV at t and t-1, should I run the model with both contemporaneous and lagged Xs?
(2) I use two different dependent variables. For both DVs, my Hansen tests suggest overidentification (DV1, P = 0.073; DV2, P=0.000). The former p value is too close to 0.05 for comfort; the latter is troubling. What is the solution for the Hansen test violation?
(3) Similarly, DV2 model is suffers from AR2 serial correlation (also p value of 0.064). My understanding is the fix for AR(2) is to use 3 lags. Is this correct?
(4) On a practical note, my IV of interest is insignificant in all of my models. However, this is an important finding. It it worth fixing the overidentifying restrictions and the AR(2) issue? That is, will fixing these only make my insignificant results even less significant? Or is there reason to think that the significance would improve?
Thanks!
I'm running a difference GMM model for the first time to address a potential reverse causality issue. I have panel data covering every other year from 2009-2019 (six waves), and I have about 10,000 panelists (unbalanced panel).
I have four questions:
(1) I have read Leszczenky and Wolbring (2019). They compare difference GMM with (1) contemporaneous Xs, (2) lagged Xs, and (3) both contemporaneous and lagged Xs. Can anyone explain to me the appropriateness of each with respect to the reverse causality issue. If my IV theoretically would influence my DV at time t, can I use contemporaneous and sleep well about reverse causality? If my IV theoretically could influence my DV at t and t-1, should I run the model with both contemporaneous and lagged Xs?
(2) I use two different dependent variables. For both DVs, my Hansen tests suggest overidentification (DV1, P = 0.073; DV2, P=0.000). The former p value is too close to 0.05 for comfort; the latter is troubling. What is the solution for the Hansen test violation?
(3) Similarly, DV2 model is suffers from AR2 serial correlation (also p value of 0.064). My understanding is the fix for AR(2) is to use 3 lags. Is this correct?
(4) On a practical note, my IV of interest is insignificant in all of my models. However, this is an important finding. It it worth fixing the overidentifying restrictions and the AR(2) issue? That is, will fixing these only make my insignificant results even less significant? Or is there reason to think that the significance would improve?
Thanks!
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