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The Parametric g-Formula · Tutorial 315 of 501

Positivity Limits and Parametric Extrapolation

Learn to distinguish supported intervention predictions from model-based extrapolations, including the special support and smoothness issues for continuous treatments.

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What You'll Learn

  • Define treatment positivity over histories relevant to a target regime.
  • Distinguish structural lack of support from sparse, near-violated support.
  • Identify when a parametric g-formula prediction depends on extrapolation.
  • Explain why exact-dose identification with continuous treatment needs care.
  • Compare extrapolation with restricting or changing the intervention target.
  • Interpret unsupported longitudinal regime estimates cautiously.

Why Support Matters for Parametric g-Computation

Parametric g-computation uses fitted outcome and covariate-transition models to predict outcomes under specified treatment regimes. Those models can return predictions for histories not observed in the data. This computational ability is not, by itself, evidence that those predictions are identified by the data. When a treatment value or history is absent from the relevant observed population, the model must extend its fitted relationships beyond the empirical support. The resulting estimate may be precise numerically while remaining highly dependent on assumptions that the data cannot check.

The issue is not limited to treatment assignment. A regime may create covariate histories rarely or never seen in the observed data, and transition models may then be asked to predict the next covariate distribution in those histories. Positivity is the condition that connects the histories required by an intervention to histories for which the observed data provide information.

Definition: For a discrete treatment at time \(t\), sequential positivity for a regime requires \(P(A_t=d_t(H_t)\mid H_t=h_t)>0\) for almost every history \(h_t\) that can occur under that regime. Here \(H_t\) denotes the measured covariate and treatment history available just before \(A_t\), and \(d_t(H_t)\) is the regime’s treatment at that history. “Almost every” is with respect to the history distribution induced by the regime; it does not mean only histories having positive probability as individual points. For a stochastic intervention, the corresponding requirement is that its treatment distribution be supported by the observed treatment distribution at almost every relevant history.

In a longitudinal analysis, positivity must hold at each treatment decision, not merely at baseline or for the marginal treatment frequency. For example, both treatments may be common overall while treatment \(A_t=1\) is never observed among patients with a particular earlier treatment and covariate history. A regime that assigns \(A_t=1\) in that history has a support problem.

With continuous treatment, the statement needs additional care. An observed treatment distribution with a density does not assign positive probability to an exact dose. A density condition can describe local support, but it does not automatically identify a conditional mean at one exact dose: a conditional expectation is defined only up to sets of treatment values having probability zero. Point-dose identification generally requires an additional regularity condition, such as continuity of the response surface at the target dose. The earlier material on Continuous Treatment Levels and Parametric G-Formula develops the continuous-treatment setup; here the emphasis is on what limited support permits us to interpret.

Support, Identification, and Extrapolation

For a categorical regime, the parametric g-formula averages conditional outcome and covariate-transition distributions over the histories that the regime generates. Under consistency, sequential exchangeability, and positivity, those conditional distributions can be learned from the corresponding observed histories. The following result states the support implication precisely.

Theorem: Suppose consistency and sequential exchangeability hold, the required conditional distributions exist, and a discrete regime \(d\) satisfies sequential positivity at every decision for almost every history generated under \(d\). Then the regime-specific mean is identified by the g-formula, formed by integrating the observed conditional outcome and covariate-transition distributions along histories generated under \(d\). If positivity fails on a set of regime-generated histories with positive probability, the observed conditional distributions need not identify the regime-specific mean on that set.

The first assertion follows by iterated conditioning. At each decision, exchangeability allows the conditional counterfactual distribution under the assigned treatment to be represented by the corresponding observed conditional distribution; consistency equates the observed outcome for that treatment with its counterfactual outcome. Positivity ensures that this observed conditional distribution is available at almost every history to which the regime assigns positive probability. Applying these equalities successively through the covariate transitions and final outcome yields the g-formula integral. If positivity fails on a positive-probability set, the observed data place no restriction on the treatment-specific conditional outcome distribution there. The next example shows why that gap cannot generally be filled by data alone. \(\square\)

Worked Example: An Unsupported Covariate–Treatment Cell

Let baseline \(L\) and treatment \(A\) be binary, with \(P(L=1)=0.4\). Suppose \(P(A=1\mid L=0)=0.8\) and \(P(A=1\mid L=1)=0\). The observed risks in the three observed cells are \(E(Y\mid A=0,L=0)=0.10\), \(E(Y\mid A=1,L=0)=0.15\), and \(E(Y\mid A=0,L=1)=0.20\). Consider the regime that assigns \(A=1\) to everyone.

There are no observations with \(A=1,L=1\), even though this cell contains 40% of the target population. A linear probability model with an \(A\)-by-\(L\) interaction can represent the observed cell means as \(m(a,l)=0.10+0.05a+0.10l+\gamma al\). For the three observed cells, this gives \(0.10\), \(0.15\), and \(0.20\), respectively, whatever value \(\gamma\) takes. But the unsupported cell prediction is \(m(1,1)=0.25+\gamma\).

If \(\gamma=0\), the g-computation risk under \(A=1\) is \(0.6(0.15)+0.4(0.25)=0.19\). If \(\gamma=0.25\), it is \(0.6(0.15)+0.4(0.50)=0.29\). Both models agree on every observed cell; the difference comes entirely from the assumed interaction in the unobserved cell. These are model-based extrapolations, not two estimates distinguished by the observed data. The numerical predictions are risks between zero and one, so both are admissible as conditional means.

This example also illustrates why “the software fit a model” is not an answer to a support problem. A parametric form can impose relationships across cells, but the resulting prediction inherits those restrictions. If the unobserved cell is given a prediction by an additive model, the additivity assumption supplies information that the data did not provide. A more flexible model may expose the lack of information by leaving that cell’s prediction unstable or undetermined; it does not create support.

Continuous Treatment: Local Support Is Not the Same as Point Identification

For a continuous treatment \(A\), positivity is often described by requiring the conditional density of treatment to be positive around the target dose at relevant histories. This is useful for assessing whether nearby doses are represented. However, it is not the same as the discrete condition \(P(A=a\mid H=h)>0\), since that probability is zero for any single dose under a continuous distribution. Moreover, if the target dose lies outside the observed support, nearby observations do not directly identify its response.

Key distinction: If the target dose is in the interior of an observed continuous-treatment region, a conditional mean at that exact dose is identified from the observed conditional-mean function only under an appropriate version and regularity condition, such as continuity at that dose. If the target dose is outside the observed support, identification requires an extrapolation assumption beyond the data support. A fitted parametric curve can provide such a prediction, but cannot verify the assumption that makes it credible.

Worked Example: A Point Dose and a Dose Beyond Support

Suppose \(A\) is uniformly distributed on \([0,1]\), and the observed conditional mean is \(m(a)=0.20+0.20a\) over that interval. Under the continuity assumption, the mean at dose \(a=0.5\) is the limit of the conditional means as doses approach \(0.5\): \(m(0.5)=0.20+0.20(0.5)=0.30\).

Without continuity, the observed distribution cannot distinguish this response surface from one that equals \(0.20+0.20a\) for every \(a\ne0.5\), but has mean \(0.60\) at exactly \(a=0.5\). Since \(P(A=0.5)=0\), changing the value at that one dose does not change the observed-data distribution. The two surfaces yield different point-dose means, so the dose-specific mean is not identified from the observed data alone in that unrestricted model.

Now consider a target dose \(a=1.2\), outside the observed interval. One possible extension is \(m_1(a)=0.20+0.20a\), which predicts \(m_1(1.2)=0.44\). Another extension agrees with it on \([0,1]\) but, for \(a>1\), is \(m_2(a)=m_1(a)+0.30(a-1)\). It is continuous at the boundary and predicts \(m_2(1.2)=0.50\). Both predictions are valid probabilities and both fit the same observed support. The observed data cannot choose between these extensions.

Longitudinal Support Can Fail Along a Path

A longitudinal regime is a sequence of treatment decisions. Even if each prescribed treatment occurs in the data somewhere, the complete histories leading to those decisions may not. The g-formula needs transition and outcome distributions at histories generated by the intervention, so a lack of support at a later decision can affect the regime-specific mean.

Worked Example: A Regime Reaches an Unsupported History

Suppose everyone follows \(A_0=0\) initially, and the resulting covariate \(L_1\) is binary with \(P(L_1=1\mid A_0=0)=0.25\). At the next decision, \(A_1=1\) is observed when \(L_1=0\), but \(P(A_1=1\mid A_0=0,L_1=1)=0\). Consider regime \((A_0,A_1)=(0,1)\).

Assume the observed outcome risk under this regime’s supported history is \(0.10\) when \(L_1=0\). A parametric outcome model might predict risk \(0.30\) at the unsupported history \(L_1=1,A_1=1\); another model, agreeing on all observed histories, might predict \(0.60\) there. The respective regime risks are \(0.75(0.10)+0.25(0.30)=0.15\) and \(0.75(0.10)+0.25(0.60)=0.225\). The difference, \(0.075\), is wholly attributable to the unsupported history. These calculations show what each model implies; they do not establish that either regime risk is identified.

What to Check and What the Estimate Means

Support should be assessed against the intervention and target population, not only by looking at overall treatment frequencies. Useful checks include tabulating treatment frequencies across important history strata, plotting continuous treatment distributions within those strata, and identifying histories that the regime generates but the observed data scarcely represent. For continuous treatment, inspect whether the target dose is inside the observed range at relevant histories, and distinguish a thinly represented neighborhood from a dose outside the range.

Sparse observations are a practical warning even when formal positivity holds. Estimates can then be driven by a small number of observations or by the chosen functional form. Exact zero support is more fundamental: no amount of increasing the number of observations from the same data-generating process fills a cell that has probability zero. A model can conceal this distinction by returning a smooth prediction in both situations.

A common mistake is to argue, “The parametric g-formula predicts every regime, so positivity is unnecessary.” The correction is that prediction and identification are different. Parametric restrictions may yield a number in an unsupported region, but the number is identified only if those restrictions or other assumptions justify extending the observed relationships there. That justification is not supplied merely by successful model fitting.

The main alternatives address the target or the assumptions, not the missing information by magic. One can restrict the target population or regime to histories with support, accepting that the estimand changes. One can consider a stochastic intervention that assigns treatment values represented in the observed data, rather than forcing an unsupported value; its support must still be checked. Inverse-probability weighting and other g-methods also depend on support, although the way the problem appears in their calculations differs. Parametric extrapolation is therefore not a way to evade positivity.

Interpretation should state where the estimate relies on extrapolation. If only a small share of the regime-generated population falls outside well-supported regions, the estimate may still be useful, but its uncertainty about model assumptions is not captured simply by a narrow simulation or sampling interval. If substantial population mass is unsupported, a single marginal estimate can obscure that its key contribution is assumption-driven. The appropriate response is to clarify the estimand, report the unsupported regions, and avoid presenting the model prediction as an empirical comparison.

Check Your Understanding

Answer each question, then compare with the solutions below.

  1. Why is positivity for a continuous covariate stated almost everywhere with respect to its target distribution rather than only at covariate values with positive point probability?
  2. In the first worked example, what part of the risk estimate changes when \(\gamma\) changes?
  3. Why does a positive density near a continuous target dose not, by itself, identify the conditional mean at that exact dose?
  4. What is the support failure in the longitudinal example?
  5. Name one way to respond to lack of support and state what it changes or assumes.

Solutions. (1) A continuously distributed covariate typically assigns probability zero to each individual value, even though its regions are populated. The relevant condition must therefore cover almost every value under the target covariate distribution. (2) Only the predicted risk in the unobserved cell \(A=1,L=1\) changes; its contribution to the marginal risk is weighted by \(P(L=1)=0.4\). (3) Conditional expectations are determined only up to treatment values of probability zero; continuity, or another suitable regularity condition, is needed to determine the value at the point from nearby values. (4) Under the regime, the history \(A_0=0,L_1=1\) occurs with probability \(0.25\), but \(A_1=1\) is never observed there. (5) Restricting the target to supported histories changes the estimand; using a supported stochastic intervention changes the intervention; parametric extrapolation instead requires additional assumptions about how relationships extend beyond observed support.

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